KEVAN AKRAMI MD, LAUREN EDWARDS MD,MONIQUE MAHLUM MD AND EB SLADEK MD

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It is impossible to begin to learn that which one thinks one already knows.

- Epictetus

The editors and authors of this handbook would like to thank the following faculty and staff fortheir assistance with this publication:

Derek Patel MD Ronelle Campbell MD Lori Wan MD

Peter Fedullo MD Joshua Fierer MD Timothy Morris MD

Melly Sani MD Hiroke Shike MD Thomas Lane MD

C. Ann Reardon MD Dzung T. Le MD Lane Campbell

Eliza Wang PharmD Gregory Maynard MD Maria Stubbs, RPh.

Brian Clay MD Ian Jenkins MD Sundar Mudaliar MD

Michael Docherty MD Elaine Muchmore MD Kalli Hose MD

Gregory Seymann MD Daniel Davis MD

Previous Editors: Carrie Chun MD (2004-2005), Keola Beale MD (2005-2006), Carrie ConstantiniMD (2006-2007), Ni-Cheng Liang MD (2007-2008), Erica Boettcher MD (2008-2009), JonathanLyons and Tricia Santos (2009-2010), Matthew Crull and Emmet Ratigan (2010-2011)

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PAPERWORK, COMPUTERS, AND DICTATION 1NATALIE GARCIA MD AND CHHAVI GANDHI MD

QUICK REFERENCE GUIDE - VA 1QUICK REFERENCE GUIDE - UCSD 3COMPUTING TIPS 4WEBSITES 6DISCHARGE PROCEDURES 7VA FORMULARY 8DEATH PROCEDURE 8TRANSFERS AND DISCHARGES 9GRADUATION REQUIREMENTS 10

PULMONARY CRITICAL CARE 12PATRICK LEW MD, DEBBY NGO MD, MARISA MAGANA MD, REBECCA SELL MD, THOMAS KIM MD, JOSHUA STERNBACH MD, CAROLINE SUL PHARMD, AND JENNIFER REAL MD

MECHANICAL VENTILATION 12VENT TERMS & DEFINITIONS 12COMMON MODES OF VENTILATION 13HIGH AIRWAY PRESSURES 15LIBERATION 16NON-INVASIVE POSITIVE PRESSURE VENTILATION (NIPPV) 16ARDS AND ACUTE LUNG INJURY 18HYPOXIA 20SHORTNESS OF BREATH 21ANAPHYLAXIS 21SEPSIS 22EARLY GOAL DIRECTED THERAPY 23CORTICOSTEROIDS 25ACTIVATED PROTEIN C 25PRESSORS 26PARALYTICS 27SEDATIVES 28SEVERE METABOLIC ACIDOSIS 29VENT TROUBLESHOOTING 30PULMONARY FUNCTION TESTING 31COPD 32CYSTIC FIBROSIS 33

CODE ALGORITHMS 35DANIEL DAVIS MD

PERFUSING PATIENT 35ARRESTED PATIENT 36

CARDIOLOGY 37Derek Juang MD, Leo Slavin MD, Ramin Shadman MD, Jonathan Lyons MD, Thomas Ro MD, Cynthia Kao MD, Gautam Lalani MD, CharlesParise MD, Mitul Patel MD, Andrew Dublin MD and Hong Nguyen MD

CHEST PAIN AND ACUTE CORONARY SYNDROME 37EKGS 38CHF 40CARDIAC BIOMARKERS 42TACHYCARDIA AND TACHYARRHYTHMIAS 42ATRIAL FIBRILLATION 43ANTIARRHYTHMIC THERAPY 44HYPERTENSION 44HYPOTENSION 45PACEMAKERS 46STRESS TESTS 46THE "POST CATH CHECK" 46HEMODYNAMICS AND SWAN-GANZ CATHETERS 47HYPERLIPIDEMIA MANAGEMENT 48PERIOPERATIVE CARDIAC RISK ASSESSMENT 49CARDIOLOGY LITERATURE 51

PROCEDURES 56JONATHAN LYONS MD, REBECCA SELL MD, AND BRIAN KOLSKI MD

CENTRAL VENOUS CATHETERS: AN INTRODUCTION 56INTERNAL JUGULAR VENOUS CATHETER 57SUBCLAVIAN VENOUS CATHETER 57FEMORAL VENOUS CATHETER 59

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CENTRAL LINE REMOVAL 59THORACENTESIS 59PARACENTESIS 60LUMBAR PUNCTURE 60SUBACROMIAL INJECTION 61KNEE ASPIRATION/INJECTION 62

INFECTIOUS DISEASE 63PHILIP LEDERER MD, BENJAMIN WESTLEY, MD, ERIC ROELAND MD, RONELLE CAMPBELL MD, DAVID WYLES MD, DAVID BUTLER MD, MAILE YOUNG MD, JI CHAE

MD, AND JENNIFER BLANCHARD MD

FEVER 63CLINICAL PEARLS 63MENINGITIS 64PNEUMONIA 64LINE ASSOCIATED INFECTIONS 67UTI 68PATHOGENIC ORGANISMS BY GRAM STAIN 68HIV 69OPPORTUNISTIC INFECTION: PRIMARY PROPHYLAXIS 70OPPORTUNISTIC INFECTION: SECONDARY PROPHYLAXIS 71OPPORTUNISTIC INFECTION: TREATMENT 71ANTIBIOTICS 72

GASTROENTEROLOGY 74CAINAN FOLTZ MD, ARTHUR YAN MD, JULIO GUTTIEREZ MD PHD, MICHAEL DOCHERTY MD, ERICA BOETTCHER MD, DEREK PATEL MD, TRENT TAYLOR MD

CALLING A CONSULT 74ACUTE PANCREATITIS 74ACUTE GI BLEED 75CLOSTRIDIUM DIFFICILE COLITIS 78GERD AND PEPTIC ULCER DISEASE 78ULCER PROPHYLAXIS 79SMALL BOWEL OBSTRUCTION 80

HEPATOLOGY 81MATTHEW CRULL MD, ARTHUR YAN MD, JULIO GUTTIEREZ MD PHD, MICHAEL DOCHERTY MD, ERICA BOETTCHER MD, DEREK PATEL MD, TRENT TAYLOR MD

END STAGE LIVER DISEASE & CIRRHOSIS 81ASCITES 81SPONTANEOUS BACTERIAL PERITONITIS 82HEPATIC ENCEPHALOPATHY 83ESOPHAGEAL VARICES 83ABNORMAL LFTS 84LESS COMMON LIVER DISEASE 85

RENAL 87Emmett Ratigan MD, Graham Abra MD, Ken Park MD, and Carrie Chun MD

CALLING A CONSULT 87ACUTE KIDNEY INJURY 87HEPATORENAL SYNDROME 90CHRONIC KIDNEY DISEASE 91CONTINUOUS RENAL REPLACEMENT THERAPY 92MAINTENANCE INTRAVENOUS FLUIDS 93CONTRAST INDUCED NEPHROPATHY 92NEPHROGENIC SYSTEMIC FIBROSIS 93ELECTROLYTE REPLACEMENT 93SODIUM BALANCE

HYPERNATREMIA 94HYPONATREMIA 95

POTASSIUM BALANCE

HYPERKALEMIA 96HYPOKALEMIA 96

CALCIUM BALANCE

HYPERCALCEMIA 97HYPOCALCEMIA 97

PHOSPHATE BALANCE

HYPERPHOPHATEMIA 98HYPOPHOSPHATEMIA 98

HYPOMAGNESEMIA 98

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EQUATIONS 99ACID-BASE DISTURBANCES 99METABOLIC ACIDOSIS 100METABOLIC ALKALOSIS 100RESPIRATORY ACIDOSIS 101RESPIRATORY ALKALOSIS 101GENERAL CONCEPTS 101

ENDOCRINE 103PATRICIA LIAO MD, MATTHEW CRULL MD, KIMBERLY MAXON, MD, JEN KERNS MD, AND LI TAI MD

CORRECTING SUGARS 103DIABETES MELLITUS 103INPATIENT DIABETES MANAGEMENT 105MANAGEMENT OF DKA & HHS 106ADRENAL INSUFFICIENCY 107PRIMARY HYPERPARATHYROIDISM 108OSTEOPOROSIS 109VITAMIN D DEFICIENCY 110

HEME/ONC 111SOAMES BOYLE MD, JUSTIN PERSICO MD, KRISTEN RICE MD, MARYANNE BHOJWANI MD, PAUL CHENG MD PHD, AND STINA MUI MD PHD

ANEMIA 111DISSEMINATED INTRAVASCULAR COAGULATION 112HYPERCOAGUABLE DISORDERS 113VENOUS THROMBOEMBOLISM PROPHYLAXIS 113THROMBOCYTOPENIA 114BLOOD PRODUCTS 115DEEP VEIN THROMBOSIS 115CHEMOTHERAPY & COMPLICATIONS 117

NEUROLOGY 120TERRY FAN MD

ALTERED MENTAL STATUS 120SEIZURES & STATUS EPILEPTICUS 121STROKE CODE 122

PALLIATIVE CARE 123TERRY FAN MD

CONSTIPATION 123INSOMNIA 123NAUSEA 123

PREVENTATIVE MEDICINE/EBM/STATS 124JEFF WEISSMAN MD AND TERRY FAN MD

CARDIOVASCULAR RISK MODIFICATION 124PSYCHOSOCIAL SCREENING 124CANCER SCREENING 125PRIMARY PREVENTION 126EVIDENCE BASED MEDICINE & STATISTICS 127

MEDICAL SPANISH: THE BASICS 128WINSTON TILGHMAN MD

CONVERSIONS & TABLES 130CORTICOSTEROID CONVERSION TABLE 130INTRAVENOUS FLUIDS 130NARCOTIC & OPIOID CONVERSION 130ENTERAL FORMULARY 132

PHONE NUMBERS 133VAMC 133HILLCREST 134THORNTON 135OUTSIDE HOSPITALS 136

DOOR CODES 137

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PAPERWORK, COMPUTERS, AND DICTATION

QUICK REFERENCE GUIDE - VA

Admissions:1. Medicine Admit pager 619-290-71732. The “PHYSICIAN ADMISSION H&P” template must be filled out for each admission UNLESS

a patient has had one filed within 30 days of their admission. If there is an H&P done within 30days, an accept note can be written, referencing the prior H&P and with any new or changedinformation.

3. If your patient is not assigned a room yet (located on top of the screen), write admission ordersunder the “Delayed Orders” tab—if you don’t, you will find that your orders have been lost andthen must be rewritten.

4. If your patient is assigned a room and it states it on the top of his screen (eg 3N, DOUMED)write admission orders under the “Active Orders” tab.

5. Admission order sets under medicine specialties help ensure you don’t miss anything.6. All patients admitted through the ED require orders before going to their assigned floor.7. Food for thought: (guidelines, not necessarily rules)

- Afib/flutter, CHF requiring DOU level of care -> VICU team admits- CHF admitted from cardiomyopathy clinic -> VICU team admits- Post procedure cardiac patients, EP patients -> VICU team admits- Unstable angina requiring heparin drip -> VICU team admits

Blood Draws/Labs:1.2. Lab draws are done @ 6am, 10am, 2pm, 4pm (drug levels only), 6pm, 10pm, or 2am, 7 days a

week. If you need a stat lab, call x3668 or page the phlebotomist.3. Floor RNs DO NOT DRAW BLOOD, so if you need it stat, call the phlebotomist (above) or

you can always do it yourself. DOU and ICU RN’s will do blood draws.4. Floor RN’s also DO NOT DRAW FROM CENTRAL LINES. If a patient has a Groshong or

Hickman for instance, you have to do their blood draws. They can draw from portacaths andPICC lines.

Central Lines:1. ICU RN’s can d/c IJ or SC central lines but NOT FEMORAL lines.2. Floor RN’s CANNOT d/c ANY central line; you have to d/c it yourself (under supervision –

please see procedure section)

CPRS: see Section: Computing Tips

DISPO Clues…- Talk with SW early and often. Try to anticipate placement needs at admission. Patients

usually CANNOT be transferred to SNFs over the weekend and SW is not in house on theweekend. For help with SNF placement (including 4 South):

- 4S transfers/admissions —2279- Home health needs are taken care of by the discharge planners:- 3N—Linda Suchocki 2973; 5E—Pat Pelican 3094- ALL patients will need a DISCHARGE SUMMARY completed prior to transfer- to a SNF or 4S (SW needs to fax to the facility for the patient to be considered).

Echocardiograms: Order in CPRS under “CONSULTS” cardiology echo. If urgent, call the EchoLab (1127) and/or page the Cardiology Fellow. Prelim results are available at the heart station(4N); final reads usually take 3-5 days to show up in CPRS and a viewable under Tools –> VistaImaging.

EKGs: Order in CPRS under “Orders ->Cardiology->Procedure Orders->ECG/Holter Menu”Done by EKG techs M-F 6am-7pm and 6am-12pm on weekends and holidays (x3644, x6363); after7pm and on the weekends/holidays after 12pm, call the ICU Gas Lab (x7264, pager 66131) for statEKGs.

Grand Rounds: Short & Post call teams are excused. Wednesdays at 7:30am on the med schoolcampus. Grand rounds is now also being broadcast to Hillcrest and Thornton and can be watchedfrom any internet-connected computer using:

http://neurofms.ucsd.edu/streaming/live.html, password: vmg001

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Home Oxygen: Pts only qualify if they have on ABG PaO2 < 55 on RA or RA finger sat SaO2 <88%.Consider getting this info before ordering a Home Oxygen Consult.

IV MEDS (including antibiotics): All IVs expire after 96 hours. For antibiotics, total duration can bewritten in the comments section, which will extend expiration date. Certain antibiotics require IDapproval or they will expire after 24hrs. Page the on-call fellow for approval.

IV Push Medications on Floor: For Metoprolol, Labetalol, Verapamil, Diltiazem and Adenosine youmust place an order for telemetry in CPRS, notify the nurse you’ll be giving med, contact pharmacyfor the med, administer the med yourself and remain on the unit for at least one hour. The patientshould remain on telemetry or be moved to higher level floor. Not applicable in the DOU or ICU.

Library: Located on 4W; can be accessed after-hours with your ID badge.

Meals: Cafeteria hours: 6:30am-6pm M-F (Grill closes at 5:30pm), closed Sat and Sun. Mealsprovided for on-call housestaff Sat/Sun in the kitchen of the call rooms suite. Meal times: breakfast at8am; lunch at 12pm; dinner at 5:45pm.

Meal cards: $5 deposit, see personnel in the medicine office by CMR’s office on 3rd floor.

PICC Lines: Look for lists of PICC nurses in team offices. Place order for PICC AND call a PICCnurse. IR won’t do them unless a PICC nurse has tried and failed, and left a note in the chart sayingthey have done so. Expect long waits and try to order them early if possible. At times PICC lines canbe speeded up if they are hindering discharge by calling the bed coordinator and letting them knowabout the patient.

Radiology:1. PACS and Web 1000 access/login: There is a PACS station across from the DOU on the 5th

floor and several computers now have PACS loaded on them (look for the green rectangleicon). Log-in/password: er/vhasdc#1. For Web 1000, in CPRS, go to "Tools" menu, there isan option for "Online Radiology Web1000,” use your vhasdc login/password

2. Impax: Use Weboutlook email login and password.3. Radiology Rounds: Friday morning at 9am after morning conference. Keep a running list of

interesting or confounding images to give to your CMR each week.4. Ultrasound: techs work on Saturdays, but only come in on Sundays for EMERGENCIES, page

the radiologist on call – 619-290-5063.5. Prelim reads: Look at the I-box on the PACS system, or call radiology.6. Central lines: PICC lines, GROSHONGs, HICKMANs can be ordered under

“ANGIO/NEURO/INTERVENTIONAL” in the imaging orders.7. DEXA scans: can be ordered under “GENERAL RADIOLOGY.”8. IR Procedures: Know the patients coags/platelets and be sure they are NPO prior to the

procedure. Go to the IR suite or call (x6915) to discuss your case.9. Radiologist on-call: page 619-290-5063 (after 5pm on weekdays/weekend reads)

Transfers:1. Inter-team transfers:

- VICUWard team transfers: The VICU team writes transfer orders.- Ward teamVICU transfers: The VICU team writes transfer orders.- “Code Status” and “Diagnosis” orders drop off when transferred and need to be rewritten.

2. Level of care transfers:NEW transfer orders must be written when patients transfer between DOU and FLOOR. Neworders are NOT needed between TELE and FLOOR – tele orders can just be discontinued oradded.

3. Transfer to 4S (Extended Care Center):4 South is considered an outpatient facility; when patients are transferred there, it is actually aDISCHARGE and requires DISCHARGE ORDERS. The DISCHARGE SUMMARY must bewritten PRIOR to discharge as the 4S team uses it to determine whether or not they can/willaccept the patient.

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QUICK REFERENCE GUIDE - UCSD

Admissions:1. Medicine Admit pager 290-1150 for Hillcrest2. Orders need to be done before ED patients can go to the floor.3. Each patient MUST have a UCSD H&P in EPIC. This MUST be completed by either the intern

or the resident NOT the medical student (unless it is a sub-intern).4. Orders for patients stuck in the ED have become somewhat confusing since the transition to

EPIC. “EDIP” refers to ED Inpatient. If a patient is EDIP’d, the nurse should be following theadmission orders in EPIC (for dosing meds, labs, meals, etc). To add new orders to suchpatients, re-enter the “Admissions Tab” and enter single orders. If a patient is NOT EDIP’d, butstill in the ED, then orders should be entered in Webcharts until the patient makes it up to thefloor. Call to clarify with the nurse taking care of the patient where active orders shouldbe entered for ED patients. It is not always clear is a patient is EDIPed or if the EPIC ordersare actually being heeded.

5. Food for thought (guidelines, not necessarily rules):- New onset heart failure CCU team admits- Rule out MI CCU team admits

Antibiotics: Simply type in the name of the antibiotic you wish to use in the orders section. Whenfiling in the details of administration, you will see whether or not an antibiotic is restricted under the“Order Inst” tab. You must speak with the ID fellow on call within 24 hours of starting a restrictedantibiotic to continue its use.

Blood Draws/Labs: 24 hour phlebotomy. Nurses will draw from central lines. DO NOT ACCESSDIALYSIS CATHETERS. Only dialysis nurses should draw from them.

Call rooms: Located on the 3rd floor main hospital access from the patient elevators. Keys availablefrom med office will open large double doors outside of elevators and call rooms. Rooms have acomputer, phone and shared bathroom.

Central Lines: Floor RNs DO NOT d/c central or arterial lines. ICU nurses do.

Copiers: There are copiers on most floors; use 5436272 as password (the medicine dept. phone).

DISPO Clues… The Case Managers are your KEY to DISPO. They generally think ahead for you,but keep in touch with them because their help can MAKE or BREAK getting a patient dispo’d. Thereis a weekend Social Worker and Case Manager on call, but it’s easiest to have things arrangedalready.

Pts going to SNF need to be sitter free for 24 hours prior to leaving.Not every SNF will take patients with feeding tubes. Ask.Patients going to Hospice or SNF need d/c summaries done prior to transfer.

Echocardiograms:- Order in PCIS, may want to call the Heart Station (3-6399) to confirm. For urgent echos,

page the Cardiology Fellow.- Prelim reads can be found in the Reading Room @ the Heart Station located on the3rd floor

near the noon conference room.

ER Computers:- Online access at: webcharts.ucsd.edu. This can be accessed from most hospital computers.

Talk to any ER attending for a login and password.

EKG’s:- Online access at: webcharts.ucsd.edu.- Once in ANY pt’s record, click on EKG on top menu bar.- Login: ad/emergency Password: Emer!gency

Library: (UCSD Medical Library); located behind the hospital, Mon-Fri 7am-8pm, Sat-Sun 1pm-5pm

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Meals:- Scan your ID card to pay for meals. Money at the end of the month keeps rolling over from

month to month but is zero’d at the beginning of the academic year.- Cafeteria Hours

Hillcrest: 6:30am-8pm, then 11:30pm-2:30am, 7 days a week.Thornton: 6:30am-8pm (grill closed 3-4:30, after 7pm) M-F, 6:30am-7pm Sat/Sun.

Page Forwarding: Each team intern must forward pages to the covering physician after sign out. Allpagers start with “290.” It is optional for residents to forward pagers, however if not forwarded, pagesmust be returned.

- Dial your pager, then enter 01234 (access code)- Enter 166 (to access system and forward; 163 to cancel page forward)- Enter the 7 digit pager number to which you are forwarding followed by #.- Re-Enter the 7 digit pager number again; press # (to confirm)

Parking:1. Parking Office @ Hillcrest in Bachman Structure (2nd Floor). Mail Code 8205; x36524.

Housestaff must obtain parking permits from this office (not from office on UCSD campus).You have the option of paying via automatic paycheck deduction. Get chip from this office toplace on back of ID badge so that you may open security gate.

2. Renew your parking pass each June; you’ll get a renewal form in UCSD mailbox.

PICC Lines: Order in PCIS, will usually be done in 1-2 days by PICC nurse. If urgent, page theinfusion nurse under “vascular access team” in webpaging. IR won’t do it unless the infusion centerhas tried.

Phones:1. To dial out: 8 + 1 Phone Number. Some phones require you to hit 9 first, to turn “tone sender

on” on the phone.2. To page: go to webpaging.ucsd.edu.3. To tag your pages: always include your call-back phone number AND your pager number.

Radiology: PACS Access: Same user name and password as your UCSD email account.1. MRIs: You can ONLY get MRI with sedation on Wednesdays from 9:30am-2:30pm. They will

collaborate with Anesthesia. Keep this in mind if you have a claustrophobicpatient. Write an order in the chart AND call 32940 for scheduling.

2. IR Procedures: Know the patients coags/platelets and be sure they are NPO prior to theprocedure. Go to the IR suite or give them a call (x32138/32476/35747) to discuss your case.

3. Radiologist on-call: 290-5063 (for reads after 5pm, and weekend reads)

Swallow studies: speech path x36530 Write an order in PCIS. You can page them if urgentby calling the operator to see which pathologist is on duty.

Transfers:1. Inter-team transfers: The accepting team is responsible for writing TRANSFER orders.2. Level of care transfers: NEW transfer orders must be written when patients transfer between

IMU, FLOOR and TELEMETRY.

COMPUTING TIPS

CPRS Quick Tips:1. HELP = vaww.san-diego.med.va.gov/ITS/cprs or call x47672. ACCESS from home/UCSD medicine office computers is available. Visit Jesse Christmas

(ext 7802) at Computer Information Office in SCI basement to get paperwork. You must havepaperwork completed to access UCSD computers even if you don’t have home access.

3. Discharge orders must be written under “ACTIVE ORDERS”; if you use the “DISCHARGE”section, nurses can’t view them, and you’ll have to re-write them.

4. Try to anticipate a discharge time and date and order it under Discharge time for planning.5. Transfer orders must be written under “TRANSFER” section as DELAYED.6. How to create your own inpatient list: go to TOOLS, then OPTIONS, then Lists/Teams, then

Personal Lists, then New List (must name the list first), then begin adding patients, click Saveto save changes.

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7. How to create a list of commonly accessed tests- On “LABS” tab, choose “WORKSHEET”- List up to 7 labs that you would like to group together- In top right-hand corner, choose “NEW” and your group has been created.- Every time you use the worksheet function, your test groups will be listed in the top half of the

window for easy access.8. How to create templates

- Under “OPTIONS” header, select “CREATE NEW TEMPLATE”- Type in the name of your template- Begin typing your template in the bottom half of the window- Press “OK” to save it.

9. How to get to the medicine resident note template- This will automatically import the most recent vitals, chem., CBC, and coags- Go to “Shared Templates” at the side tool bar- Select General Medicine

10. How to create a list of your most frequently used notes- Under “TOOLS” header, select “OPTIONS”- Choose “Document Titles”- Select the type of note you would like added to your list (ie, MED/GEN/RESIDENT)- Press “ADD” to add it to your list- Press “SAVE CHANGES”- Now your list will pop up whenever you start a new note, and you’ll have ready-access to the

most titles of the notes you most frequently use11. Accessing remote records in CPRS

- Choose “REPORTS” tab- If remote records are available, a tab in the upper right-hand corner of the screen will have

“Remote Records” in blue; if it is in grey, then there are none available.- Click on the “Remote Records” tab and activate the sites in which you want.- In the Left-Hand column, you will see “Clinical Reports”- Expand the menu and choose items of interest.

12. How to alert yourself when lab/imaging/consult results are available- Select the lab/image/consult that you want to be alerted about.- Select the “VIEW” header.- Choose “Alert When Results”

13. Access to UCSD Webproxy: for Online Clinical Library on your VA desktop type inww.cwp.ucsd.edu. Same username and password are the same as your weboutlook email.

14. Access to UCSD Webpaging: Same as at Hillcrest or Thortontype in webpaging@ucsd.edu.

EPIC Quick Tips:1. 24 hour help: ie. If you can’t remember login/pswd x374742. Home access: @ www.cwp.ucsd.edu. Click on EPIC icon to enter. Use your AD username and

password.3. How to create your own inpatient list:

-click on “My Patient Lists” on the upper left column in the “Patient Lists” tab (thenameless icon tab to the far left)-click on “Create” and then type in the name you want for your list and selectparameters to be displayed (especially useful are Patient Name/Age/Sex, Room, MRN,Arrival Date and whatever else you see fit)-add patients by either clicking on “Add Patient” from the icons at the top and enteringyour patient’s name or MRN or by copy and pasting them from the “Systems Lists” onthe left hand column. Most useful System Lists include Units – Hillcrest (choose a flooror ED Inpatient for patients still downstairs) and Service Teams (scroll down to find theMed Hillcrest team your patients belong to)

4. Find finger stick blood sugars under Results Review tab at the bottom of the list: “GlycemicControl – POCT”

5. Inpatient medication profile: under the “Medications” tab. The best way to review whichmedications your patient has actually received is to click on the “Patient Summary” tab andthen type in “IP MAR Current” or “IP MAR History” into the white box next to the word “report.”You can add this to your permanent tabs on this screen by clicking on the wrench icon next tothe box and type in your choice into the matrix.

6. Outpatient medication profile: under the “Medications” tab. Select “Prior to Admission”medications.

7. Lab Reference Guide: click on “Web Ref” (just next to the word EPIC at the top left of thescreen) and choose “Laboratory Information” and then Lab Reference Guide.

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8. Nursing Policies: there are a number of useful resources listed under the “Nursing Standardsand Guidelines” tab of the “Web Ref” (see #8 above). Choose “Standards” and you can thenselect “Level of Care Criteria,” which helps you determine whether a patient with a certain dripor nursing requirement is appropriate for a certain floor (the message may not be consistentamong all nurses asked…) or “Paging Standard RN – Physician Team” to determine whetheror not it is appropriate to correct a nurse about a particular instance of paging.

9. How to find out who a patient’s primary care physician is and what their insurance is: click onthe “Facesheet” icon at the top of the “Patient Summary” tab.

WEBSITES

1. Organizations & ServicesAmerican College of Physicians www.acponline.orgCalifornia Medical Board www.medbd.ca.govCPRS (remote access) citrix.san-diego.med.va.govDEA www.deadiversion.usdoj.govEpocrates www.epocrates.comHopkins Curriculum www.hopkinsilc.org/JAMA jama.ama-assn.orgNew England Journal of Medicine www.nejm.orgNew Innovations www.new-innov.comPCIS (remote access) cwp.ucsd.eduPubMed www.pubmed.govUCSD ER Charting System webcharts.ucsd.eduUCSD Healthcare health.ucsd.eduUCSD Library gort.ucsd.edu/clinlibUCSD Medicine Residency imresidency.ucsd.eduUCSD Pharmacy health.ucsd.edu/pharmacyUCSD Webmail (Popmail) acs-webmail.ucsd.eduUCSD Weboutlook weboutlook.ucsd.eduUCSD Webpaging webpaging.ucsd.eduUCSD Web-based Signouts www.mypatientyourpatient.com/ucsdUCSD Web1000 web1000.ucsd.edu/LaunchUp-to-Date www.utdol.comVerizon Wireless Online Paging www.myairmail.com

2. Evidence Based MedicineACP Journal Club www.acpjc.orgCenter for Evidence Based Medicine www.cebm.netCochrane Library www.cochrane.org

3. Palm Resources- palm.stanford.edu/quicksoftware.html - Stanford Med’s palm resource page.- www.guideline.gov/resources/pda.aspx - A list of pocket guidelines for your PDA. There are a

lot so you may have to pick a few to download and try.- www.statcoder.com - Check out the free cardiac clearance, LDL cholesterol, and JNC 7

guidelines.- www.timi.org - The TIMI risk calculator is an interactive and easy to use tool developed by

the authors of the TIMI trials.- www.memoware.com - A collection of free software, including some medical software.- www.freewarepalm.com - Check out eponyms and some of the useful calculators.- eponyms.net/palm.htm - A useful website filled with links to several palm resources.- www.healthypalmpilot.com - A useful website with downloads to tons of resources.

4. MiscellaneousBalboa Park Visitor’s Information www.balboapark.orgFederal Loan General Website www.dl.ed.govFederal Loan Consolidation www.loanconsolidation.ed.gov/indexSan Diego Special Events Calendar www.sandiego.gov/specialevents/indexSan Diego Union Tribune signonsandiego.com

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DISCHARGE PROCEDURES

UCSD1. Residents are responsible for writing discharge summaries in EPIC. Patients being

discharged to a SNF or hospice need a DISCHARGE SUMMARY written that can go withthem at the time of discharge. Often times this is the discharge documentation so thedescription needs to be complete.

2. Security Prescription Forms: The State of California has mandated that as of January 1,2005, ALL controlled drugs in schedules 2, 3, 4, and 5 must be prescribed on a tamperresistant security form. All attendings will have security forms and the residency programprovides licensed residents with a DEA number and their own forms as well.

3. Handwritten Prescription Forms: For patients going to SNF, select the “Yes” button on the“Facility Discharge?” tab from the Discharge menu. This will default all prescriptions tohandwritten format. Once the discharge orders are signed, a prescription sheet will print at thenursing station on the patient’s floor and you must sign this form in orderyou're your patient tosuccessfully leave the hospital.

4. ALL PATIENTS MUST HAVE SOME SORT OF FOLLOWUP.

VAMC1. Discharge planning rounds for residents are every Wednesday.2. Discharge summaries are REQUIRED for all patients (regardless of length of stay) and are

due within 24 hours of discharge.3. If a pt is going to 4S/SNF, a discharge summary will be needed prior to DC.4. Interns are responsible for all D/C summaries, unless they have >6. In this case, the

residents are responsible for pts with SSN ending in numbers 0-4; interns are responsible forpts whose SSN ends with the numbers 5-9.

5. If the patient is discharged on the intern’s day off, the resident is responsible for the summaryand vice versa.

6. Medical students following the patient should write the summary; however, they cannot write itunder the discharge summary tab. They should write it as a regular progress note but shouldnot sign it. The note can then be pasted into the discharge summary note by theintern/resident with credit being given to the student. The draft progress note can then bedeleted.

7. Discharge orders should be written under active impatient orders. (Under “Main Inpatient\)Menu” choose “Discharge Instructions” to launch the order set.)

8. Medications at discharge:

- Review your pt’s outpt medication profile and compare it to the inpt med regimen beforewriting your orders. Discontinue any meds no longer required.

- Order only meds the patient requires at discharge.

- Do not discontinue and re-enter all of your patients’ meds if nothing has changed.

- Refill any active outpatient prescription. This avoids unnecessary co-pays.

- Renew expired or zero refill prescriptions if appropriate.

- If you have a STAT discharge, then enter your meds in STAT (recommend 2 hours of turnaround time).

- IV antibiotics are coordinated through the discharge planner.- Patients being sent to a nursing facility need a 5-day supply of medications.- Patients being sent to a board and care facility need a 30-day supply of meds.

9. For patients being sent to 4 South (VAMC Extended Care Center), this is a discharge.However, you do not need to order their medications—just type a list of their medications inyour discharge summary.

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VA Formulary

Pearls:1. Meds that are non-formulary (NF) require consult approval before they can be dispensed.2. ID restricted antibiotics can be given for 24 hours but then will require ID approval within

24h.

To access the formulary:1. CPRS Tools Menu: select Pharmacy References and Formulary, then click Formulary2. VA Web page: Services Pharmacy Formulary (on left side menu)

Submitting an NF/PA Consult:1. Go to ORDER tab, select CONSULT (inpt or outpt use)2. Click on NON-Formulary/Prior Auth Drug Request. There are specific consults for select

medications and a generic NF form for all other medications.3. You must enter a CPRS medication order for the requested drug. Page your area pharmacist if

you cannot enter the drug order in CPRS.

Most common consults:1. ARBs: valsartan for CHF, losartan for DM, need consult.2. Ezetimibe: monotherapy in pt with CI to statin and niacin. Combo with max statin and CI to

niacin/cholestyramine OR needs a 3rd agent.3. Glargine: recurrent symptomatic hypoglycemia OR intensive insulin therapy and documented

improvement during first 6 months.4. Tamsulosin: documented orthostatic hypotension/syncope on alpha-blocker.5. Zolpidem: NF consult needed, except in sleep apnea w/documented desaturation.6. Plavix/Lovenox/Formoterol/ IV PPI (pantoprazole)/COX 2

Can’t find your med to order…1. You are not alone. Some meds are only found under “Quick PO Meds,” in the “Meds” menu.

These include: Clopidogrel, Carvedilol, Rosiglitizone,Simvastatin, Zolpidem2. Controlled substances: not orderable via CPRS. Give green script form to pharmacist.3. IV antibiotics: many are listed underOrders tabMeds (inpt)quick IV abx.

Medication Conversions: see Pharmacist for questions on conversion.

Death Procedure

Prior to pronouncing the death:1. Speak to nursing staff to get details about the patient, family, family dynamics and the

circumstances of the death.2. Determine if there are any special problems or concerns.3. Assess the immediate situation.

- Was the death expected or unexpected?- Was the family present? If not have they been notified?

4. Find out about autopsy and organ donation from next of kin.- Has family requested an autopsy? Is there an indication for an autopsy?- Is the patient an organ donor? If not, has family considered organ donation? If patient is a

possible organ donor, contact Life Share (ask nursing staff for details).

Evaluate the patient:1. Identify the patient by the hospital identification tag or bracelet.2. Note the general appearance of the patient’s body.3. Determine that the patient will not rouse to verbal or tactile stimuli.4. Listen for the absence of heart sounds; feel for the absence of a carotid pulse.5. Look and listen for the absence of spontaneous respirations.6. Check the position of the pupils and the absence of the pupillary light reflex.7. Note the time your assessment was completed. This is recorded as the official time of death.

Contact any next of kin inquire about autopsy, organ donation. Contact Organ Donation/LifeShare if indicated.

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Put Death Note in the medical record1. State name of the provider. Write “Called to pronounce (Insert patient's name).”2. Chart findings of physical examination, including absence of pulse, respirations, pupil

response.3. Note date and time of death.4. Indicate in chart if patient's family was notified.5. Chart if family declines or accepts autopsy.6. Document if the coroner or medical examiner was notified. If the death might be a

coroner/medical examiner case, contact the medical examiner. If the medical examiner waivesthe case, get a “waiver number” for the death packet.

7. Document notification of attending, pastoral care, social work, or others as indicated.8. Fill out Death Packet (different for UCSD Hillcrest/Thornton and VA).

Notify the patient’s attending: Even if it isn’t your attending and it is 3am, send them a text page.

TRANSFERS AND DISCHARGES

Transfer Summaries:- Date of admission / Date of transfer- Attending Physician / Resident / Intern- Procedures/Radiologic studies- Consultations- Problem List- Brief HPI / PMH / PSH / FamHx / SocHx- Hospital course by problems- Medication list

Discharge Summaries:- Date of admission / Date of discharge- Attending Physician / Resident / Intern- Procedures/Radiologic studies- Consultations- Problem List- Brief HPI / PMH / PSH / FamHx / SocHx *- Admission physical exam *- Initial laboratory studies, radiology *- Hospital course by problems- Disposition- Condition on discharge- Discharge medication list- Followup

* If there is a dictated History and Physical in the computer you may reference it

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Graduation Requirements

.PROCEDURES:Required: Elective (examples):Abdominal paracentesis (3) Arterial line placement (5)**ACLS certification Bone marrow aspiration (5)**Arterial puncture (5) *Central venous line placement: Femoral (5)Arthrocentesis of the knee (3) Elective cardioversion (requires supervision)*Line placement: IJ (5) or Subclavian (5)*Central line removal (5)

Endotracheal intubation (req. supervision)

**IV access (5) Flexible sigmoidoscopy (25)Lumbar puncture (5) Holter monitor interpretation**Pap smear and endocervical cx (5) Nasogastric intubation (3)Thoracentesis (5) S-G catheter placement (req. supervision)**Venopuncture Temp. pacemaker (requires supervision)

Treadmill testing and interpretVascath placement (requires supervision)

*Placement of central lines in the UCSDMC CCU requires direct supervision by the fellow orattending physician regardless of the number of procedures previously done by the resident.**Required procedures to sit for the American Board of Internal Medicine (ABIM)

CLINICAL EVALUATION EXERCISES (CEX):1. One “long” CEX2. Two “mini” CEXs/year3. Med/peds: one “long” and three “mini” total

EVIDENCE BASED MEDICINE:1. 2nd/3rd year ward residents2. 5 minute presentation at morning report addressing a focused clinical question3. Email a copy to medicine office to be filed away4. A minimum of five EBMs to graduate (for both categorical and med/peds residents)

MECHANISM OF MEDICINE PRESENTATIONS:1. 2nd/3rd year consult residents2. 5 minute presentation at morning report addressing mechanism (molecular, cellular, or

physiologic) and, if applicable, therapeutic potential.3. Email a copy to medicine office to be filed away

JOURNAL CLUB PRESENTATIONS: One presentation is required of all residents completing theprogram.

SCHOLARLY ACTIVITY REQUIREMENT (SAR): One scholarly activity project is required for allresidents completing training in Internal Medicine. Options for completing the project include thefollowing which must be done and published by May 15th of the graduating year:1. Research Project: Culminating in written abstract, poster presentation, original manuscript for

submission, or written description in manuscript, and presenting your findings at the AnnualResident Research Symposium.

2. Case Report and case conference presentation3. “State of the Art” Review of Topic: Review article and presenting your findings at a noon

conference or grand rounds

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JOHN HOPKINS CURRICULAR REQUIREMENT FOR AMBULATORY CARE:

Categorical Medicine Residents Required Modules (15 total out of 33):PGY-1: 4 modules

Cancer screeningImmunizationsProfessionalismLow Back Pain

PGY-2: 7 modules (3 new + 4 were assigned last year as PGY-1s)All of the above 4 modules ANDPreoperative AssessmentAny 2 of the 30 modules not done above

PGY-3: 15 modules (8 new + 7 were assigned as PGY-1-2s)All of the above 7 modules ANDDermatitisOphthalmologyAny 6 not done above

Med/Peds Required Modules (10 total out of 33):PGY-1: 3 modules

ImmunizationsProfessionalismCancer Screening

PGY-2: 4 modules (1 new +3 were assigned last year as PGY-1s)All of the above ANDLower Back Pain AND

PGY-3: 5 modules (1 new + 4 were assigned as PGY-1-2s)All of the above ANDPreoperative Assessment

PGY-4: 10 modules (5 new + 5 were assigned last year as PGY-1-3s)All of the above ANDDermatitisOphthalmologyAny 3 not done above

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Pulmonary/Critical Care

Mechanical Ventilation

Indications for Intubation:1. Airway protection from obstruction or aspiration

- GCS <8, airway obstruction, or laryngeal edema2. Failure to ventilate. PaCO2 > 55 mmHg with acute acidosis (pH < 7.25)

- Hypoventilation, neurologic compromise, muscular weakness, anatomical restrictions,gas exchange abnormality.

3. Failure to oxygenate. PaO2 < 60 mmHg despite max FiO2 delivered non-invasively- Diffusion abnormality, V/Q mismatch, inability to extract O2 at cellular level.

4. Clinical judgment. Note that these are not hard and fast rules, just some parameters.Trending of these parameters should be analyzed. Decision for intubation and initial ventsettings should be discussed with the ICU Fellow/Attending.- Respirations > 35/min for prolonged period of time (leads to exhaustion)- PaO2 < 55 mmHg- Minute ventilation > 10 L/min- A-a gradient* > 350 mmHg on 100% oxygen- PaCO2 (arterial partial pressure of carbon dioxide) > 55 mmHg (except in chronic

retainers)

*A-a gradient = Difference between Alveolar oxygen and arterial oxygen, or PAO2 – PaO2.PAO2 = (FiO2 x (Patm – PH2O)) – (PaCO2/0.8) where Patm-PH2O = 760-47 = 713Expected A-a gradient = (patient's age divided by 4) + 4

VENT TERMS/DEFINITIONS

1. Control/mode: parameter that determines how the ventilator controls pressure, volume, andflow within a given breath as well as how it manages the sequence of mandatory andspontaneous breaths.

2. Cycling: parameter that determines when the change from inspiration to exhalation occurs- Time-cycled- Volume-cycled (can also add inspiratory pause to make it both volume- and time-cycled)- Flow-cycled as in pressure support

3. Triggering: parameter that determines when the ventilator delivers the breath- Time- Pressure – pt generates negative pressure and breath is delivered. Usually -1 to -2 cmH2O.- Flow – most ventilators use “flow by” which is a constant flow of air within the circuit; when

the pt attempts inhalation there is a change in this flow. This is sensed by vent and a breathis delivered.

4. Breaths: three types: mandatory, assisted, or spontaneous- Mandatory = delivered completely by the ventilator, independent of pt- Assisted = pt effort to breathe is sensed by the ventilator, which then delivers a full breath- Spontaneous = pt breaths on his/her own, without help from the ventilator

5. Extrinsic PEEP: positive end expiratory pressure provided by the ventilator to prevent alveolifrom collapsing at the end of expiration. This recruits alveoli, thereby improving gas exchangeand therefore oxygenation.- Indications for PEEP:

- Improve gas exchange (and decrease intrapulmonary shunt as well as decrease theamount of FiO2 needed)

- Increase lung compliance- Prevent lung injury by minimizing volutrauma and stress of shear forces when alveoli

repeatedly open and close- Prevent end-expiratory airway collapse (as in obstructive lung disease) and thus

decrease work of breathing.

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- Adverse Effects:- Increases intrathoracic pressure and reduces venous return to the right heart (can

cause hypotension).- Can over-distend alveoli and redirect blood to diseased areas (thus increasing dead

space).

6. Plateau Pressure (Pplateau): pressure needed to keep alveoli open at the end of inspiration.- Ppeak – Pplateau ≈ airflow resistance (normal = 5 mmHg, but definitely <10 mmHg) - Increased Ppeak with unchanged Pplateau means increased airflow resistanceDDx: ETT obstruction, increased secretions, bronchospasm- Increased Ppeak with Pplateau ≈ decreased distensibility of lung and chest wall DDx: PTX, atelectasis, acute pulmonary edema, worsening pneumonia or ARDS, increased

abdominal pressure, auto-PEEP- Decreased Ppeak ≈ air leak DDx: disconnected tube, cuff leak, hyperventilation

7. Static Compliance (Cstatic) :PEEPP

TV

plateau , normal= 50-80 cmH2O. A measure of the

distensibility of the lung.- To calculate Dynamic compliance simply use peak inspiratory pressure (PIP) instead of the

plateau pressure.- Chest wall can account for 35% of total static compliance.

8. Airway Resistance (Rinsp):insp

plateaupeak

V

PP , where Vinsp is the inspired volumetric flow rate.

- Minimal flow resistance in typical ETT is 3-7 cmH2O/L/sec

9. Determinants of Oxygenation (determinants of PO2):- FiO2

- PEEP- Mean Airway Pressure (this is why APRV and inverse ratio can improve oxygenation)

10. Determinants of Ventilation (determinants of PCO2):- Minute Ventilation = RR x TV- Dead Space (dramatic increases/changes in dead space will effect ventilation – a common

example: massive PE increases dead space because alveoli are ventilated but there is noperfusion).

Common Modes of Ventilation

Volume Control: Mandatory breaths deliver a pre-set volume. Pressure is determined by lung andchest wall mechanics.

1. Continuous Mandatory Ventilation (CMV): mandatory breaths are delivered at a set RR andvolume. Commonly used in the OR, but not well tolerated in pts with intact respiratory drive.

2. Assist-Control (AC): Mandatory breaths are delivered at a set rate and volume, and“triggered breaths” (when pt’s effort sensed by vent) are assisted in the same manner as themandatory breaths (vent delivers same volume or driving pressure) and have the samelimits/cycling as a mandatory breath).- Advantage: Good for pts with impaired respiratory drive- Disadvantages:

- Excessive pt-triggered breaths may lead to respiratory alkalosis or breath stacking(“auto-PEEP”).

- Usually not well tolerated without sedation.- May increase the work of breathing if: a)_sensitivity to pt effort is inadequate for the pt

to trigger assisted breaths, or b) flow rate is insufficient for pt comfort and thus ptexerts persistently increased respiratory effort.

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- Example of initial settings:- RR 10-12- TV 6-12 mL/kg [NOTE: In ARDS, goal is usually 6-8cc/kg (ideal body weight)]- Normal Flow = 60-80mL/min- Flow rate can be increased to decrease the Inspiratory time and thereby increase

expiratory time. This is useful in pts with severe obstructive physiology and/or auto-PEEP.

- PEEP = 5 cmH2O (if PEEP is necessary, it often isn’t)- FiO2 = 1.00. This is then titrated down according to ABG or pulse oximetry.

3. Synchronous Intermittent Mandatory Ventilation (SIMV): Mandatory breath rate is set andthese breaths are volume-controlled. The TV for the spontaneous breaths will be determinedby chest wall/lung mechanics/compliance and pt effort. Spontaneous breaths are thereforeunsupported, but pressure-support can be added to assist these breaths. Mandatory breathsare synchronized with spontaneous breaths.

- Advantages:- Very useful in the post-operative period.- May be helpful in brain injury when there is centrally-mediated increase in respiratory

rate which causes respiratory alkalosis when AC mode is used.- Mandatory breaths are synchronized with spontaneous breaths, thus preventing

breath stacking (“auto-PEEP”). This also leads to greater pt comfort. If asynchronous,then the mandatory breaths can be delivered at any time in the respiratory cycle (pureIMV).

- Disadvantages:- If spontaneous breaths are not sufficiently supported with pressure-support (i.e. TV is

low), may stimulate tachypnea and increased work of breathing.- The work of breathing may also be high if the mandatory rate is set too low.

- Example of initial settings:- Similar to AC mode (see above).- In addition, may add pressure support to the spontaneous breaths.

Pressure Control: Delivers a pre-set pressure, usually for a set time. TV is determined by lung andchest wall mechanics as well pt effort.

1. Pressure Controlled Ventilation (PCV): In our ICU, most commonly used in AC mode. Thus,for each breath, whether mandatory or pt-triggered, a given driving pressure is used to inflatelungs. The pressure is held for a certain time (time-cycled) and then released.- Advantages:

- High flow rates are usually more comfortable and therefore lead to decreased work ofbreathing.

- Prolonging inspiratory time allows distribution of ventilation and may improveoxygenation by allowing recruitment of more stiff alveoli (i.e. increasing mean airwaypressure). This may help refractory hypoxemia. Note that once the inspiratory timeexceeds the expiratory time, then inverse ratio ventilation is being used.

- Disadvantages:- Poor lung compliance may lead to low TVs or minute ventilation and therefore

hypercapnea (although this is usually well tolerated).- The longer the inspiratory time, the more improved the oxygenation. However, more

air trapping (“auto-PEEP”) occurs as the time for expiration decreases.- Minute ventilation is not guaranteed (TV determined by lung and chest wall

mechanics), therefore more monitoring by physician and RT is needed.- Example of initial settings: more difficult than in other modalities.

- The pt must be monitored to ensure the desired minute ventilation is being reachedwith the set driving pressure or goal TV (usually 6-8 cc/kg).

- Attempts are made to keep Peak Airway Pressures < 35-40 cmH2O.- Inspiratory time (time that pressure is held) must be set as well (usually 1 sec). On

some ventilators this is set as the fraction of an entire inspiration/expiration cycle.

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1. Airway Pressure Release Ventilation (APRV): A form of time-cycled/pressure-controlledventilation. In this mode, inspiratory pressure is kept high through most of the respiratory cyclewith occasional drops in pressure to allow for ventilation. Most often used in severe refractoryhypoxemia and ARDS. See figure below.- Advantages:

- Pts can usually spontaneously breathe throughout the cycle. Therefore, less sedationcan be used.

- Majority of ventilation occurs during expiratory phase (decreased pressure), thuspreventing barotrauma and volutrauma.

- Disadvantages:- Cannot use in pt who are difficult to ventilate, such as pts with severe COPD and

cannot empty their lungs quickly or in pts with increased airway resistance.- Example of initial settings:

- Expiratory time should be short enough to prevent de-recruitment and long enough toobtain suitable TV. Usually 0.4-0.6 sec. Target TV is 4-6 mL/kg.

- High PEEP usually set at 28 cmH2O (to help recruit more alveoli) and titrated down.- If transitioning from another mode, then use the old mean airway pressure.- Low PEEP usually set at 0 cmH2O.- Inspiratory time usually set at 4-6 sec. Target rate is 8-12/min.

High Airway Pressures

If sats dropping or hemodynamicallyunstable then disconnect circuit andbag while determining cause.

If stable then check Ppeak, Pplateau and end-expiratory pressures (pressure at end-inspiration, ie. inspiratory hold maneuver,pressure at end-expiration is determined bypause at expiration)

↑ Resistance

Ppeak ↑ (> 35 cmH2O) andPplateau normal (≤ 35 cmH2O)- mucus plug

suctioning- biting ETT ↑sedation- tracheal obstruction

reposition ETT- bronchospasm

bronchodilators

Decreased CompliancePeak and Plateau P ↑ > 35 cmH2O

Check CXR and ABG while you are thinking about thesepossible causes:- ETT dislodgement, ie. in right mainstem bronchus

reposition ETT- Dysynchrony (“bucking the vent”, look at flow-pressure

waveforms) ↑sedation- Auto PEEP (pressure at expiratory pause will be greater

than your set PEEP, or flow at end-expiration is not 0)increase expiratory time by ↓RR and/or TV, ↑ inspiratory flow rate (decreases inspiratory time), or in severe cases(hemodynamic effects) disconnect pt from vent and allowfor a full expiration. Sometimes increased sedation (orparalysis in severe cases) is needed.

- Atelectasis, PNA, CHF treat underlying cause- Pneumothorax chest tube

HIGH PIP

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Liberation

This process accounts for up to 40% of time that patient is on the ventilator.

1. Assessing Readiness:- Respiratory criteria:

o Oxygenation: PaO2 > 60 mmHg on FiO2 < 0.40 and PEEP 5-8 cmH2Oo Ventilation: PaCO2 at baseline (unless permissive hypercapnea)o Strength: Patient able to initiate respiratory effort/lift head off bed

- Cardiovascular criteria: No evidence of myocardial ischemia; HR 140; BP normal without orwith minimum vasopressors.

- Mental status: Arousable; GCS ≥ 13.- Initial cause for intubation reversed or significantly improved.

Typical Bedside Weaning Parameters

Parameter Normal Adult Range Weaning ThresholdPaO2/FiO2

Tidal VolumeRespiratory RateVital CapacityMinute Ventilation

>4005-7 cc/kg

14-1865-75 cc/kg5-7 L/min

2005 cc/kg

<4010 cc/kg

< 10 L/minMax inspiratory Pressure

RSBI (RR/TV ratio)*

> -90 cmH2O (women)> -120 cmH2O (men)

< 50/min/L

-25 cmH2O

< 100/min/L

2. Sprinting:- CPAP is often used as a means of minimal pressure support so that the patient can

overcome the resistance of the ventilator circuit. In this mode, the patient is initiating eachbreath but ventilatory parameters can still be monitored. RSBI (rapid shallow breathing index,RR/TV) holds the greatest predictive value for success. For patients with neuromuscularweakness, maximal inspiratory pressure is also very helpful.

*RSBI > 105 predicts 95% failure rate for weaning.*RSBI < 105 predicts 80% success rate for weaning.

References: Tobin, MJ. “Mechanical Ventilation.” N Engl J Med 1994; 330:1056-1061. Marino, P. The ICU Book. 3nd

Ed. Lippincott. New York2007: 457-511.

NON-INVASIVE POSITIVE PRESSURE VENTILATION (NIPPV)

Several studies have shown that using NIPPV can prevent intubation and thus decrease length ofhospital stay and mortality. Consider a trial of NIPPV in pts with moderate to severe respiratorydistress and good mental status (they must be able to work with RT in order to be effective). Be sureto check serial ABGs and don’t hesitate to intubate if pt is not improving. (See Cross Cover Clues:Dyspnea).

**Note that NIPPV does not prevent the need to re-intubate or reduce mortality in a pt with respiratoryfailure after extubation (NEJM 2004; 350(24): 2452-60).

1. Indications for NIPPV- COPD exacerbations. BiPAP has been shown to decrease mortality rates, intubation rates,

length of hospital stay, and complication rates such as PNA. This is probably related todecreased intubations. BiPAP, specifically EPAP assists in decreasing the work ofbreathing.

- Cardiogenic pulmonary edema. CPAP (usually started at 10cm H2O) has been shown todecrease the work of breathing and thereby increase cardiac output. It is thought to increasethe functional residual capacity and thus place the lung/chest wall system on a morecompliant part of the curve. Decreases rate of intubation with no significant changes notedwith mortality. There may be increased mortality in pts with active ischemia, so use caution inthese pts.

- Immunocompromised patients with hypoxemic respiratory failure. A study with 40 pts(mostly solid organ transplant pts or hematologic malignancy) showed decreased need forintubation, serious complications, and mortality.

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2. Contraindications for NIPPV- Altered mental status or inability to cooperate- Severe upper GI bleed- Cardiac or respiratory arrest or other organ failure- Inability to clear secretions or high aspiration risk- Hemodynamic instability- Surgery or trauma to face or neurological system- Recent upper airway or GI surgery – think carefully: may be at risk of viscus perforation- Mask or nasal prongs cannot be fitted

3.4. Types of NIPPV

- Continuous positive airway pressure (CPAP): delivers continuous positive airwaypressure throughout the respiratory cycle. Similar to breathing with your head stuck out of amoving car.

- Counteracts intrinsic PEEP

- Decreases preload and afterload and improves lung compliance in CHF

- Decreases the work of breathing- Bi-level positive airway pressure (BiPAP): delivers CPAP but also senses when an

inspiratory effort is being made and delivers a higher pressure during inspiration. Pressurereturns to CPAP level when flow stops.

- Increased positive pressure unloads diaphragm during inspiration thus decreasing thework of breathing.

- Can be used for chronic respiratory failure due to neuromuscular problems or chestwall abnormalities.

5. Level of Care:- VA: ICU or ICU boarder. MUST have Pulmonary consult.- UCSD: nasal bipap in IMU. Otherwise, ICU. If BiPAP/CPAP is being used to treat respiratory

failure, you should have the ICU team involved or at least aware.

6. Other references:- www.ccmtutorial.com- “Review of indications and data for NIPPV.” Chest 2003; 124: 699-713.- “Non-invasive Positive Pressure Ventilation.” Am J Med 2005; 118: 584-91.

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19

ARDS AND ACUTE LUNG INJURY

Definitions1. Acute lung injury (ALI) = a syndrome of acute and persistent lung inflammation with

increased vascular permeability. Characterized by three clinical features:- PaO2/FiO2 = 201-300 mmHg (regardless of PEEP).- No evidence of left atrial pressure (pulmonary capillary wedge pressure < 18 mmHg).- Bilateral radiographic infiltrates.

2. Acute Respiratory Distress Syndrome (ARDS) = meets above criteria for ALI, exceptPaO2/FiO2 ≤ 200 mmHg. Additionally:- For both ALI and ARDS, the degree of gas exchange disturbance does not correlate with the

extent of the underlying pathology.- Severity of hypoxia on presentation does not predict the clinical course or survival.- Most cases of ARDS require positive pressure mechanical ventilation. Mechanical ventilation

itself, however, may cause additional lung injury – barotrauma (i.e. pneumothorax) orventilator-associated lung injury (VALI) from over-distension of non-diseased lung regions.

Lung Protective Ventilation Strategies1. ARDS Network Trials: low tidal volume ventilation decreased mortality in ALI/ARDS (ARMA

trial). Low PEEP in ALI/ARDS had similar outcomes as higher PEEP (ALVEOLI trial).- Tidal volume of 6 mL/kg ideal body weight, plateau airway pressure ≤ 30 cmH2O- Average PEEP approximately 9 cmH2O- ARMA Trial: “Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal

Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome.” N Engl J Med2000. 342(18): 1301-8.

- Multicenter randomized trial involving 861intubated patients with ALI/ARDS comparing“traditional ventilation treatment” with initial tidal volume 12 mL/kg predicted body weightand plateau pressure 50 cmH2O vs. tidal volume 6 mL/kg predicted body weight andplateau pressure 30 cmH2O.

- Mortality lower in the lower tidal volume group than in traditional tidal volume group(31.0% vs. 39.8%, p = 0.007; ARR 8.8%, NNT 11).

- By day 28, 65.7% breathing without assistance and had 12±11 ventilator-free days inlow tidal volume group, compared with 55.0% and 10±11 days in traditional tidal volumegroup (p < 0.001 and p = 0.007, respectively).

- Conclusion: Using tidal volume of volume 6 mL/kg predicted body weight and plateaupressure ≤ 30 cmH2O reduces mortality, decreased time on ventilator, and increased number of ventilator-free days compared to traditional ventilation volumes.

- ALVEOLI Trial: “Higher versus Lower Positive End-Expiratory Pressures in Patients with theAcute Respiratory Distress Syndrome.” N Engl J Med 2004; 351(4): 327-36.

- Multicenter randomized trial involving 549 intubated patients with ALI/ARDScomparing low PEEP (average 8.3±3.2 cmH2O) vs. higher PEEP (average 13.2cmH2O) (p < 0.001). Tidal volume 6 mL/kg predicted body weight with plateaupressure ≤ 30 cmH2O.

- Rates of death before hospital discharge 24.9% in low PEEP group vs. 27.5% inhigher PEEP group (p = 0.48).

- By day 28, low PEEP group with 14.5±10.4 days breathing unassisted vs. 13.8±10.6days in high PEEP group (p = 0.50).

- Conclusion: In ventilated patients with ALI/ARDS, clinical outcomes similar whetherlow and high PEEP used, if tidal volume 6 mL/kg predicted body weight and plateaupressure ≤ 30 cmH2O.

2. Permissive hypercapnea: not a ventilatory strategy per se, but is a common consequence oflow tidal volume ventilation. This is acceptable if oxygenation is maintained. Contraindicationsinclude: Predisposition to increased intracranial pressure, hemodynamic instability, andtreatment with -blockers (adequate catecholamine response is required to maintainhemodynamic stability during hypercapnea).

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HYPOXIA

Evaluation: Get other vitals and see patient to assess the level of distress. Many causes overlapwith the Shortness of Breath section (next), but important to think of mechanism.

1. Identify Underlying Cause: Anything creating an Aa-gradient (preventing blood flow orpreventing air flow to alveoli) or depressing Respiratory Drive.

2. Evaluate the Patient: for below causes of SOB. Assess ability to protect airway – if no gag,call ICU resident immediately for possible intubation (see below). Examine other cranial nerves(e.g. blown pupil concerning for herniation, fixed dilated pupils concerning for opiate overdose).

3. If not dyspneic: Evaluate medications and timing of meds given, also look at renal/hepaticfunction for clearance issues.

4. Give Narcan: For suspected Narcotic Overdose (remember the short half-life: may need tostart a gtt).

5. Workup: stat ABG, chem panel, CXR, cardiac markers, ECG, consider AMS work-up.6. When to intubate: You should have called your resident by now, but if patient looks like tiring

out (persistently tachypneic, retracting, pCO2 up-trending) call ICU team for evaluation.Respiratory failure is defined as PO2 <50 or PCO2 >50 (exception: chronic CO2 retainers), pH<7.30, almost all with pH <7.20 (acute change) will require intubation. However, withresident/ICU input, you may consider a trial of NIPPV if not contraindicated (i.e. not obtunded).

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SHORTNESS OF BREATH

Evaluation: Get vitals (including oxygen sats), see patient to assess the level of distress.

Things Not to Miss:1. PE: Check if on proper prophylaxis to stratify suspicion. Check O2 sats, ABG, D-dimer (only

useful to r/o PE if low pre-test probability), EKG for classic S1/Q3/T3, but most often see sinustachycardia, and if high suspicion order a CTPA vs. V/Q scan. If you can’t give contrast (i.e.high creatinine) or V/Q (COPD or its midnight) and suspicion high, can treat presumptively withheparin gtt/enoxaparin 1mg/kg bid. Consider Lower Extremity Dopplers.

2. Lung collapse (mucus plugging): Patients with pneumonia and poor ability to clear secretions.ON EXAM: Decreased breath sounds with dullness to percussion in focal region, and trachealdeviation toward region. Get CXR. Call RT for aggressive suctioning & CPT. If collapse isstrongly suspected, call pulm for bronchoscopy.

3. Pneumothorax: Consider risk factors (recent central line, thoracic procedure, right sidedendocarditis, and PE): ON EXAM: Absent breath sounds with hyperresonance to percussion inregion, and tracheal deviation away from region. If evidence of tension PTX: DON’T WAITFOR CXR emergently decompress with 14 or 16 gauge needle in 2nd intercostal space inmidclavicular line (to avoid internal thoracic artery). Call CT Surg/Pulm for chest tubeplacement (stable patients will still need if PTX >20% of lung field).

4. Aspiration: Witnessed? Consider risk factors (emesis, AMS, seizures, ETOH). Keep HOBelevated while waiting for CXR. Debate continues as to microbiology of aspiration PNA. Ingeneral, use Abx w/ good gram negative coverage (Zosyn/Ceftaz) and consider addinganaerobic coverage (Clinda/ Flagyl) for pts w/ poor dentition, and if hospital stay >3 days, addnosocomial coverage (Vanc and Cipro). FYI: Not all aspirations are the same. Be sure toalso consider aspiration pneumonitis, which usually resolves within 24-48 hrs without antibiotictreatment, however primary team can always reassess in AM and d/c Abx.

5. COPD/Asthma: (use care with O2 as can cause decreased respiratory drive and CO2retention: goal saturations 90 - 92%) – consider IV steroids with Combivent (COPD) oralbuterol (asthma) MDI (if tachycardic with albuterol – can substitute with Levalbuterol).

6. Cardiac: Ischemia can cause acute rise in pulm pressures & subsequent SOB. Always bewareof “flash” pulmonary edema from papillary muscle rupture. Watch for CHF (use IV lasix andraise head of bed) and tamponade – look for signs of R sided failure (JVD, LE Edema).

7. Other: Metabolic Acidosis, Anxiety, and Pain are also common causes of SOB, but other moreserious causes should be excluded first. Sepsis can induce tachypnea in attempt to blow offCO2 and compensate. Be vigilant of this in the setting of increased RR with good O2saturations.

ANAPHYLAXIS

Evaluation and Treatment:- Start with ABCs—Airway, Breathing, Circulation- EPINEPHRINE 0.5 cc of 1:1000 IM or SQ- Solumedrol 125mg IV x 1; H-2 blocker IV x 1; Benadryl 50mg IV x 1- Consider albuterol nebulizers if the patient is wheezing or stridorous- Close observation and call resident f/b anesthesia for intubation if necessary

22

SEPSIS

SIRS (2 of 4)

- Temp > 100.3 or < 96.8- Heart rate > 90 bpm- Respiratory Rate > 20 or PaCO2 < 32- WBC > 12 K or < 4K or > 10% bands

Suspected Infection

Venous Lactate > 35 mg/DL or> 1 organ dysfunction

Initiate Sepsis Pathway

Corticosteroid Evaluation /Replacement (B)

Blood Cultures / Early BroadSpectrum Antibiotic Initiation

Early Goal Directed Therapy(A)

If ARDS,Low Volume Ventilation (E)

Xigris Eligibility (C)

Tight Glycemic Control (D)

Systolic Blood Pressure < 90after fluid bolus

Sepsis Pathway

23

Definitions of Sepsis1. Bacteremia: Positive blood cultures without evidence of systemic inflammation.

2. Systemic inflammatory response syndrome (SIRS): a widespread inflammatory responseto a variety of severe clinical insults. Must have two or more of the following:- Temperature > 38.0ºC (100.4ºF) or < 36.0ºC (96.8ºF)- Heart rate > 90- Respiratory rate > 20 or PaCO2 < 32 mmHg- WBC > 12,000 or < 4000 or > 10% bands

3. Sepsis: clinical signs describing SIRS along with suspected infection

4. Severe sepsis: sepsis associated with organ dysfunction, hypoperfusion, or hypotension (SBP< 90 mmHg or decrease of 40 mmHg from baseline). For example: lactic acidosis (lactate > 35mg/dL) or evidence of > 1 organ system dysfunction (e.g. oliguria or acute AMS)

5. Septic shock: severe sepsis with hypotension despite adequate fluid resuscitation (> 20-30mL/kg) combined with perfusion abnormalities and requirement of inotropic or vasopressorsupport.

6. Multiple organ dysfunction syndrome: presence of altered organ function in an acutely illpatient such that homeostasis cannot be maintained without intervention. End of SIRS/sepsisspectrum.- Increasing abnormalities in the following organ-specific parameters are correlated with a

higher mortality: PaO2/FiO2, creatinine, platelet count, Glasgow Coma Scale, total bilirubin,

pressure-adjusted HR ( HR CVP

MAP)

EARLY GOAL DIRECTED THERAPY

Management of severe sepsis/septic shock: Based on a randomized trial of 263 pts comparingstandard therapy vs. early goal directed therapy (EGDT) in pts with suspected sepsis. The in-hospitalmorality rate was 30.5% in the EGDT group vs. 46.5% in the standard group (NNT = 6). Inclusioncriteria included at least 2 of 4 criteria for systemic inflammatory response syndrome (SIRS) pluseither lactate > 4 mmol/L (35 mg/dL) or SBP < 90 mmHg after 20-30 mL/kg fluid resuscitation. Theinitial EGDT guidelines were published in 2004 and updated in 2008. Start EGDT within six hours ofdiagnosis. All pts will need an arterial or central line in order to monitor BP/CVP and to send blood forcentral or mixed venous O2 sat.

1. Initial resuscitation: should be started in the first six hours (1C). Can use either crystalloidsor colloids (no difference). Goals are (1C):- CVP 8-12 mmHg (12-15 mmHg if mechanically ventilated or pre-existing decreased

ventricular compliance)- MAP > 65 mmHg- Urine output ≥ 0.5 mL/kg/hr- Central venous O2 sat ≥ 70% or mixed venous O2 sat ≥ 65%. If venous O2 sat not met,

then can give more fluid, transfuse PRBCs to Hct ≥ 30%, or start dobutamine drip (max 20 mcg/kg/min) (2C)

2. Diagnosis: culture everything immediately (1C). Can perform imaging studies promptly if safeto do so (1C).

3. Antibiotics: begin broad-spectrum IV antibiotics as early as possible and within the firsthour of recognizing severe sepsis (1D) and septic shock (1B).- Vancomycin + Zosyn, Imipenem or 3rd/4th generation cephalosporin, etc. (1B)- Anti-fungals or anti-virals when indicated (1B)- Reassess regimen daily to optimize efficacy, reduce toxicity, and prevent resistance (1C)- Consider combination therapy in Pseudomonas infections (2D) or in neutropenia (2D).- Duration of therapy usually 7-10 days, but can be longer if response is slow (1D)- Stop antibiotics if cause is non-infectious (1D)

4. Source control: find the focus of infection as soon as possible (1C). If it is potentially infected(lines, etc), remove it (1C). If there is an abscess, necrotic tissue, etc, then take care of it assoon as resuscitation is complete (1C).

24

5. Pressors and Inotropes (please also refer Pressors section): maintain MAP ≥ 65 mmHg (1C)- Norepinephrine and dopamine are the preferred agents in septic shock (1C)- Consider Vasopressin 0.03-0.04 units/min (may decrease stroke volume) (2C)- Consider Epinephrine if blood pressure poorly responsive to norepinephrine or dopamine

(2B)- Dobutamine in myocardial dysfunction/low cardiac output (after adequate fluid resuscitation

and left ventricular end diastolic pressure) in combination with vasopressors (1C)6. Steroids (please also refer to Corticosteroids in the ICU section): do not use corticosteroids to

treat sepsis in absence of shock unless patient has endocrine need or is steroid dependent(1D)- Consider IV hydrocortisone if hypotension poorly responsive to adequate fluids and

vasopressors (2C)- CORTICUS 2008 study demonstrated that hydrocortisone did not improve survival or

reversal of shock in septic shock. However, in those patients who did have eventual reversalof shock, hydrocortisone did hasten the reversal.

7. Activated protein C (please also refer to Activated Protein C section): patients with low risk ofdeath (APACHE II <24 or one organ failure) should not receive APC (1A).

8. Blood products: TRICC trial suggested that in absence of significant CAD, acute hemorrhageor lactic acidosis, transfuse for target Hgb 7.0-9.0 (1B)- Transfuse to Hct ≥ 30% in first 6 hours if mixed venous O2 sat < 70% (2C)- Give FFP if coags abnormal AND bleeding OR procedure planned (2D)- Give platelets if < 5000 or < 30,000 and bleeding or < 50,000 and invasive procedure

planned (2D)- Even in the setting of ischemic cardiac disease, if hemodynamically stable, studies suggest

that transfusions are associated with INCREASED mortality. More definitive studies pending.9. Sepsis-induced ALI (please also refer to ARDS/ALI section): follow ARDSnet protocol

- Conservative fluid strategy if no evidence of tissue hypoperfusion (1C)10. Sedation, analgesics, and paralytics (please also refer to Sedatives section):

- Use intermittent boluses or continuous infusions, and have daily sedation vacations (1B)- Avoid neuromuscular blockade if possible (prolonged skeletal muscle weakness) (1B)

11. Glycemic control: insulin drip with target glucose < 150-200 mg/dL (2C)- a study by Van den Berghe et al. (2001) showed that tight glucose control (glucose 80-110

mg/dL) with intensive insulin therapy reduced morbidity in all medical ICU patients, but onlyreduced mortality in the subset of patients that stayed in the ICU > 3 days (these patientscould not be identified before entering the ICU). In contrast, a study by Van den Bergheshowed a morbidity and mortality benefit in all patients in a surgical ICU.

- The NICE-SUGAR Study (2009) showed that intense glucose control (target of 81 to 108)INCREASED mortality for adult ICU patients compared with conventional glucose control(target of 180 or less).

- D5 or D10 glucose infusions or enteral feeding and glucose monitoring while receiving insulindrip

12. Renal replacement: CVVHD or intermittent HD as needed (see Nephrology section) (2B)13. Bicarbonate therapy: No evidence that bicarbonate improves outcomes for pH > 7.15 and may

actually worsen outcome in lactic acidosis. Do not use for purpose of improving hemodynamicsor reducing vasopressors requirements (1B).

14. DVT prophylaxis: low-dose UFH or LWMH if not contraindicated (1A). If contraindicated, usecompression stockings or intermittent compression device (1A).

15. Stress ulcer prophylaxis: use H2 blocker (1A) or PPI (1B)16. Advance care planning: early and frequent discussions with patient and family. Describe

likely outcomes and set realistic expectations (1D)

References: NEJM 2009; 360(13): 1283-1297, NEJM 2008; 358(2): 111-24, NEJM 2006; 354(5): 449-61, NEJM 2001; 345(19): 1359-67.

25

CORTICOSTEROIDS

Use in the ICUThe incidence of adrenal insufficiency (AI) in the ICU is ~30% and even higher in patients with septicshock. Untreated, AI in the ICU has a high mortality. One should suspect AI in any septic patient thatdoes not hemodynamically respond to adequate fluid resuscitation (20-30 mL/kg) and becomespressor dependent.

1. Septic patients with known AI or at high risk for AI (on chronic steroids) should be startedempirically on hydrocortisone 50-100mg IV Q6-8 hr*.

2. For all others patients, check a random serum cortisol level.- > 34 mcg/dL = appropriate response in a severely stressed patient no steroids needed- < 15 mcg/dL = abnormal response start hydrocortisone- 15-34 mcg/dL* = equivocal response corticotropin (cosyntropin) stimulation test

3. Corticotropin stimulation test: measure serum cortisol give corticotropin IV 250mcg measure serum cortisol 30-60 min after administration- If you want to give steroids before the random cortisol level use dexamethasone 4-10mg IV- Change in serum cortisol < 9 mcg/dL = relative AI start hydrocortisone

4. Also consider adding fludrocortisone 50mcg po/ngt QD

- Note that a study by Sprung et al published in 2008 demonstrates that hydrocortisonetherapy in septic shock does not provide for a survival benefit, including those patients whodid not appropriately respond to corticotropin. However, hydrocortisone is still widely used.

- Cortisol level of 15-34 mcg/dL are suggested by Cooper and Stewart. Your attending maydisagree, as do other experts, and consider > 25-30 mcg/dL normal.

References: Marik PE and Zaloga GP. “Adrenal Insufficiency in the Critically Ill: a New Look at an Old Problem.” Chest 2002; 122(5): 1784-96. Keh Dand Sprung CL. “Use of Corticosteroid Therapy in Patients with Sepsis and Septic Shock: an Evidence-Based Review.” Crit Care Med 2004; 32(11Suppl): S527-33. Cooper MS and Stewart PM. “Corticosteroid Insufficiency in Acutely Ill Patients.” N Engl J Med 2003; 348(8): 727-34. Sprung CL, etal. “Hydrocortisone Therapy for Patients with Septic Shock.” N Engl J Med 2008; 358(2): 111-24.

ACTIVATED PROTEIN C (DROTRECOGIN ALPHA)

1. PROWESS: randomized, double-blinded, placebo-controlled, multicenter trial (2001) of 1690patients with severe sepsis- showed mortality benefit in using activated protein C (drotrecogin alfa, Xigris©)- 28 day mortality was significantly decreased in the activated protein C group: 24.7% vs

30.8% in the control group, a relative risk reduction 19% (NNT=16)- given as continuous infusion of 24 mcg/kg/hr x 96 hours- increased incidence of severe bleeding in the study group: 3.5% vs 2% (p=0.06)

- defined as intracranial hemorrhage, life threatening bleed, or transfusion requirementof > 3 PRBCs/day x 2 consecutive days.

- benefit was only shown in patients at high risk for death- APACHE II score > 24 AND > 1 organ system dysfunction.

2. ENHANCE: (2005)- confirmed the results of the PROWESS trial, including the increased risk of bleeding.- patients treated within the first 24 hours of organ dysfunction had higher survival rates

than patients treated later (22.9% vs. 27.4% mortality)

3. XPRESS: (2007)- prophylactic heparin safe to use with activated protein C and did not increase the risk of

bleeding.

*Note: At UCSD you must fill out the pre-printed form to use activated protein C

26

- PROWESS Inclusion criteria:- Known infection, or suspected infection- At least 3 of the 4 criteria for SIRS- One of the following criteria for organ system dysfunction:

- Cardiovascular: SBP < 90 or MAP < 70 despite adequate fluids, or use ofpressors

- Respiratory: PaO2/FiO2 < 200 (or < 250 in presence of other systemdysfunction)

- Renal: UOP < 0.5 mL/kg/hr despite adequate fluids- Hematologic: platelets < 80,000 or decreased by 50% in past 3 days- Metabolic acidosis: pH < 7.30 and serum lactate > 4.2 mEq/L

- PROWESS exclusion criteria:- Pregnant or breast-feeding- Age < 18 or weight > 135 kg- Platelets < 30,000- INR > 3- Conditions with increased risk of bleeding (recent or impending surgery, recent

trauma, GI bleed in past 6 weeks, h/o head trauma, CVA in past 3 months, intracranialAVM, surgery, or mass lesions)

- Known hypercoagulable state- Acute pancreatitis- Cirrhosis, jaundice, portal HTN, or chronic ascites- LP in past 12 hours- Heparin in past 8 hrs, LMWH in past 12 hrs, warfarin within past 7 days, elevated INR,

thrombolytics within past 3 days, ASA > 650 mg/day for past 3 days, GP IIb/IIIainhibitor within past 7 days, antithrombin III in past 12 hrs, protein C within past 24 hrs(prophylactic doses of heparin OK)

- Exclusions in original study but not considered absolute: AIDS with CD4 < 50, ESRDon dialysis, h/o bone marrow, lung, liver, or small bowel transplant

References: Bernard GR, et al. “Efficacy and safety of recombinant human activated protein C for severe sepsis.” N Engl J Med 2001; 344(10): 699-709.Laterre P. “Clinical trials in severe sepsis with drotrecogin alfa (activated).” Crit Care 2007; 11(Suppl 5): S5.

PRESSORS

**Always fill the tank first** i.e. large volume fluid resuscitation

1. Norepinephrine (Levophed) and dopamine are preferred agents in septic shock.Phenylephrine (Neosynephrine) is used once the patient is on the maximum doses ofnorepinephrine and dopamine.

2. Dopamine may be useful if patient is bradycardic.2. Vasopressin is useful as a second agent, not first line.3. Epinephrine is used for anaphylactic shock and codes.4. Dobutamine and isoproteronol are used only in cardiogenic shock5. Phenylephrine is very useful for sedation associated hypotension peri-operatively and in

liver patients.

Mechanism Major action Dose Use

Phenylephrine(Neosynephrine)

Pure SVR, / CO 10-200 mcg/min Septic shock, neurogenic shock,anesthesia-induced hypotension

Norepinephrine(Levophed)

>> SVR, / CO 0.01-0.3mcg/kg/min

Septic shock

Epinephrine 1 >> 2, CO, SVR (low dose)/ SVR (high dose)

0.01-0.5mcg/kg/min

Anaphylactic shock, code situations(last ditch effort)

Dopamine D, 1 CO (inotrope) 2-10 mcg/kg/min Septic shock, cardiogenic shock

1, > D SVR 10-20 mcg/kg/min Septic shock, cardiogenic shock

Dobutamine 1 > 2 CO, SVR 2-50 mcg/kg/min Cardiogenic shock

Isoproterenol 1, 2 CO (chronotrope), SVR

0.015-0.5mcg/kg/min

Only cardiogenic shock due tobradycardia

Vasopressin ADH analogue SVR 0.04 U/min Septic shock (useful as secondagent)

- vasoconstriction increased SVR, blood pressure- 1 increased heart rate and contractility increased CO- 2 vasodilation slight decrease SVR; also bronchodilation- D vasodilates kidney and viscera increased renal perfusion

27

PARALYTICS

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29

SEVERE METABOLIC ACIDOSIS

The initial therapeutic goal for patients with severe acidemia is to raise the systemic pH above 7.15-7.2, a level at which dysrhythmias become less likely and cardiac contractility and responsiveness tocatecholamines (pressors) will be restored.

1. Treatment of the Underlying Cause: is usually adequate for correction. (e.g. treat DKA withfluids and insulin drip and treat sepsis with fluids and antibiotics)

2. Bicarbonate therapy: Consider for pH < 7.15-7.2. The decision to give bicarbonate shouldbe based upon the pathophysiology of the specific acidosis, the clinical state of the patient,and the degree of acidosis.- In hyperchloremic acidosis (RTA and GI losses), the central problem is with the reabsorption

or regeneration of bicarbonate. In these conditions, therapy with bicarbonate makesphysiologic sense in severe acidosis.

- In renal failure, bicarbonate is renally lost, so it makes sense to replace it.- There is a possible benefit for bicarbonate as a short term therapy for salicylate intoxication

to create an alkalemic environment to enhance toxin elimination.- There is controversy regarding use of bicarbonate in lactic acidosis. It may only transiently

raise the serum bicarbonate concentration and cause an eventual worsening of metabolicacidosis. Discuss with ICU Fellow/Attending if bicarbonate therapy is appropriate.

- For all cases of diabetic ketoacidosis, the role of bicarbonate is controversial, regardless ofthe pH or bicarbonate level. Glaser et al suggested a possible increased risk of cerebraledema.

- Complications associated with bicarbonate therapy:- Hypernatremia, hypokalemia, hypocalcemia- Fluid overload,- Post-recovery metabolic alkalosis (as the excess lactate is converted back to

bicarbonate)- Decreased oxygen availability (due to left-shift of O2-Hb dissociation curve with

increasing pH)- Paradoxical CNS acidosis (CO2 diffuses through BBB while bicarbonate does not)

- Bicarbonate deficit = (Desired Bicarbonate – Measured Bicarbonate) x Weight (kg) x 0.6- The general recommendation is to replace only half of the total bicarbonate deficit

over several hours, then reassess.

3. Hemodialysis: for metabolic acidosis secondary to ingestions (e.g., salicylate, methanol,ethylene glycol)- Preferred treatment for patients with significant metabolic acidosis in the setting of renal

failure. Nephrology should be consulted.

4. Mechanical Ventilation: If the patient is on mechanical ventilation, ventilation can beincreased by increasing respiratory rate (maximum rate 35) or increasing tidal volume (peakpressure maximum 35- 40). However, increasing the respiratory rate excessively can causedecreased expiratory time and lead to CO2 retention → acidosis. Note, in ARDS, try not to greatly exceed plateau pressure of 30.

30

VENT TROUBLESHOOTING

31

PULMONARY FUNCTION TESTING

R(E) = extraparenchymal restrictive diseaseR(P) = parenchymal restrictive diseaseO = obstructive diseaseRV = residual volumeTLC = total lung capacity

32

SpirometryValue

ObstructiveDisease

Restrictive Disease

Parenchymal NeuromuscularChest walldeformity

TLC Normal to

RV

Depends onstrength

Dependson disorder

VC to normal

FEV1/FVC Normal to

Depends onstrength

Normal

MIP (maxinsp.

Pressure)Normal Normal Normal

COPD

Global initiative for chronic Obstructive Lung Disease (GOLD) guidelines, 2008

1. Indications for admission:- Marked increased intensity of symptoms- Severe background COPD- Onset of new physical signs (cyanosis, edema, etc.)- Failure of exacerbation to respond to initial medical management- Significant comorbidities- Frequent exacerbations- New arrhythmias- Older age- Insufficient home support- Diagnostic uncertainty

2. Assess severity:- ABG

- PaO2 < 60 and/or SaO2 < 90% with/without PaCO2 > 50 on room air respiratoryfailure

- pH < 7.36 + PaCO2 > 45-60 in a patient with respiratory failure indication forintubation

- CXR (PA and lateral): to identify alternative diagnoses- EKG: look for RVH, arrhythmia, or ischemia- Lab tests: sputum culture and sensitivities, chem panel, and CBC with diff.

3. Therapy:- Supplemental oxygen- Bronchodilators – combination therapy probably better than single agent

- albuterol 90mcg 4-8 puffs (MDI) or 2.5mg (neb) Q1-4h PRN [MDI equivalent to nebs]- Ipratropium 18mcg 2 puffs (MDI) or 500mcg (neb) Q4h PRN

- Steroids: methylprednisolone 60-125mg IV Q6-12h or prednisone 40-60mg po Qday x 7-10days (no need to taper if treatment less than 3 weeks)

- Antibiotics: indicated if intubated OR if increased dyspnea + increased sputum volume+ increased sputum purulence

- (-) risk factors for Pseudomonas: moxifloxacin OR ceftriaxone OR cefotaxime- (+) risk factors for Pseduomonas: cefepime OR ceftazidime OR Zosyn OR

levofloxacin

Risk factors = ≥4 courses of antibiotics in last year, recent hospitalization ≥ 2 days in past 90 days, past Pseudomonas infection, FEV1 < 50% predicted

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4. Chronic treatment for stable COPD:

CYSTIC FIBROSIS

Cystic fibrosis is a genetic disorder of the CFTR gene that presents with symptoms from birth.However, given advances in caring for CF, patients are now living much longer. Adults often presentfor acute care secondary to a CF exacerbation; acute, rather than chronic, care is discussed here.Remember that CF is a multisystem disorder, not just pulmonary.

Most common bacteria isolated in CF patients’ respiratory cultures: P. aeruginosa (55%), MSSA(52%), MRSA (19%), H. influenzae (17%), MDR P. aeruginosa (16%), Stenotrophomonas maltophilia(13%), Burkholdria cepacia (3%)

1. Symptoms of an exacerbation:- Increased cough, sputum production, or chest congestion- Decreased exercise tolerance/increased dyspnea with exertion- Increased fatigue- Decreased appetite- Shortness of breath or tachypnea- Change in sputum appearance- Fever- Increased nasal congestion or drainage

2. Antibiotic therapy:- PO for mild exacerbations: dicloxacillin, Augmentin, cephalexin, TMP-SMX, doxycycline, or

macrolide (may be resistant if receiving azithromycin chronically)- IV for severe exacerbations, resistance to PO antibiotics, or PO failure

- Usually based on susceptibilities, but studies show in vitro susceptibilities don’t matter(Smith AL et al. “Susceptibility Testing of Pseudomonas aeruginosa Isolates andClinical Response to Parental Antibiotic Administration: Lack of Association in CysticFibrosis.”

- Pseudomonas: TOBRAMYCIN or AMIKACIN or COLISTIN + [piperacillin,ceftazidime, cefepime, meropenem, doripenem]

- MSSA: cefazolin or nafcillin- MRSA: vancomycin or linezolid- Burkholderia: meropenem or per sensitivities

- Usually treat for 2 weeks; PICC line may be helpful if the patient has no long-termaccess like a port (but most do have a port).

- Remember to check serum peaks and troughs for aminoglycosides.- Many patients may be on inhaled tobramycin (tobi) or colistin as an outpatient. This is usually

a one-month-on/one-month-off regimen. If the patient is on tobi/colistin at admission,continue it.

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3. Other Affected Systems: continue their outpatient medications- PULM: oxygen, bronchodilators, mucolytics (DNAse, hypertonic saline, etc), chest

percussion therapy- GI: enzymes (Pancrease, etc), acid suppressants (H2 blockers, PPI), bowel regimen- FEN: vitamins (ADEK, etc), diet supplements (Ensure, etc)- ENDO: insulin if diabetic (pancreatic failure)- RENAL: may have kidney injury from repeated aminoglycoside use- ID: antibiotics as above. Remember to check for access site (PICC line, port) infections.

Sinusitis may be present. Patients are at increased risk for allergic bronchopulmonaryaspergillosis.

- PSYCH: treat depression if present

References: Chest 2003; 123(5): 1495-1502.

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CODE ALGORITHMS

PERFUSING PATIENT

36

ARRESTED PATIENT

37

CARDIOLOGY

CHEST PAIN AND ACUTE CORONARY SYNDROME

1. Cross Cover Clues:- Differential: MI, dissection, PTX, PE, pericarditis, PNA, GERD, PUD, esophageal spasm,

esophagitis, anxiety.- Primary goal is determine if it is life-threatening. Find out if CP is new, and if chest pain is

different. If h/o ACS is this the same pain they had before w/ MI?- Look at the signout: does the patient have chronic/recurrent CP that has been evaluated?- Recurrent CP still needs to be evaluated, but this may give you a sense of the source initially.- LOOK AT THE PATIENT: often you get alarming pages that turn out to be nothing.- Assess for the four major killer causes of chest pain: acute MI, aortic dissection, PE, and

tension pneumothorax.- Vital Signs are vital: ask the nurse for them with the initial call – including SaO2.- Stratify urgency with vitals and history: if you suspect a cardiac cause, get an urgent EKG

and compare it to previous EKGs for changes.- Initial workup, if serious cause suspected: EKG, STAT Cardiac Markers and serially, Chem

10, CBC, BNP, Coags, and CXR. If suspect PE, see section: Dyspnea- Initial interventions: can give trials of sublingual NTG if sbp >90 mm Hg (does not rule out GI

if relieves) or a GI cocktail (Maalox 30 cc, 10 cc viscous lidocaine). NSAIDs if MSK etiology.- If cardiac is suspected, and SL Nitro only temporarily relieves, move on to Nitro Paste; may

need Nitro gtt (call your resident or ICU/CCU team); assess likelihood of ACS and considerasa, b-blocker, and heparin drip (call CCU early if you suspect ACS – the fellow should beinvolved if you are starting heparin gtt for ACS)

- If CXR suspicious for aortic dissection (widened mediastinum) or if there are different BPs ineach arm, get CT chest with contrast and alert CT surgery, NO ANTICOAGULATION.

History Keys: description of pain including length, quality, radiation, duration, relieving factors.Functional status of patient, can he walk across a parking lot, up a flight of stairs? Increasing severity,frequency? Prior ischemic disease, CHF, or arrhythmias? Hx of HL, HTN, DM, PVD. Tobacco use?On aspirin? Allergy to contrast or shellfish? Track down previous EKG/Echo/Cath reports/CABGreports.

2. Risk Stratification:- TIMI score can be used to stratify chest pain patients

- Age over 65- 3 or more risk factors for CAD [Diabetes, cigarette smoking, HTN (BP 140/90 mm Hg or

on antihypertensive medication), dyslipidemia, Family history of premature CAD (CAD inmale first-degree relative 55 or younger, CAD in female first-degree relative 65 oryounger, Age (men 45 years; women 55 years)]

- Established CAD (Angiographic stenosis of ≥ 50%) - 2 or more angina episodes in past 24 hours- ASA use in the last 7 days- Elevated cardiac enzymes- ST depression ≥ 0.5 mm

- TIMI Scale- 0-2 = low risk- 3-4 = intermediate risk- 5-7 = high risk

*Negative cardiac markers 12hrs from onset of chest pain makes NSTEMI highly unlikely

3. Physical Exam: JVP, card (murmurs?), pulm (basilar crackles?), pulses in both arms,peripheral edema, femoral pulses, rectal w/heme if starting heparin

4. EKG: see section below, but for STEMI you are looking for:- EKG with >1mm ST elevation in >2 contiguous leads, OR- Left bundle branch block, not known to be old

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5. Initial Management for ACS: Antiplatelet, Antithrombotic and early revascularization.Decrease O2 demand and increase coronary perfusion (manage HTN, pain, HR)- ASA 325mg PO. Immediately in all patients, except for those with active hemorrhage or

allergy.- Heparin gtt: use in all patients without contraindications (hemorrhage).- BB: metop 5mg IV q2-5min x3. Goal to decrease myocardial demand. Follow this with PO

metoprolol. Contraindications: cardiogenic shock, hypotension, decompensated heartfailure, symptomatic bradycardia, 2nd or 3rd degree heart block w/o pacer, active wheezing.

- Activate cath lab: contact your fellow who will determine whether or not pt will needintervention. He will also determine whether to start a GIIb/IIIa inhibitor – the preferredreperfusion therapy in pts presenting <24h after onset of symptoms.

- Control pain with NTG:- SL NTG (400mcg) q5 min PRN chest pain, repeat PRN up to 3 doses and topical

Nitropaste (1-2 inches to chest wall)- If pain unrelieved by above, or pain recurs, begin IV NTG drip (20-200mcg/min)- You may consider morphine, however you need to be able to tell whether or not pt is

having cardiac pain. If you know cath lab is already going to intervene, then it is likelyOK.

6. Orders: ASA/Statin/BB/ACEI, Plavix?, Heparin/Lovenox (attn. dep), IIb/IIIa inhibitor (callfellow); NPO p MN, ECHO next day, Labs – CBC, CHEM10, coags, AM lipids, TSH, LFTs,BNP- Have all EKGs from admission (and old one if attainable); also CP patients need qAM EKG- Patient must be NPO and receive no Lovenox on day of cath. A copy of the H&P MUST be in

the chart for the cath lab.

7. Sub-acute Management:- monitor on tele- ASA 81-325mg PO daily- If received stent, Plavix 75mg PO daily continued at least 1 month for Bare Metal Stents, at

least 1 year for Drug-Eluting Stents- Heparin gtt for 48h or until trops downtrending or pt revascularized (stent placed).- Beta blocker: titrate up metoprolol to goal heart rate 55-60- ACE Inhibitor: helps prevent remodeling.- Statins: have shown benefit in the acute setting. Get a lipid panel immediately on admission,

as in the acute phase LDL levels will be lower by 25-50% for up to 6 weeks. Goal LDL<70.- Smoking Cessation- Exercise: goal 30-60 min of activity 5-7x/wk- Diet: cardiac diet

8. Consents: get release of info for all pts, then copy and fax to multiple hospitals, we need cathreports, EKGs, previous echos.

9. Device Interrogation: call rep phone# on signout sheet

EKGS

- Be sure to check out ECG Wave-Maven at http://ecg.bidmc.harvard.edu/maven/mavenmain.asp.

- Finding old EKG’s at Hillcrest/Thornton- Login to webcharts. Click on any patient’s chart. Click on ‘EKG’ from the top menu.

Username: ad/emergencyPassword: Emer!gency

1. Determine rate and rhythm: P-wave before QRS, upright P-wave lead II, III and aVF

2. Evaluate intervals:- PR < 0.12-0.20sec <5 boxes- QRS < 0.06-0.120sec <3 boxes- QTc < 0.48sec, less than ½ the R-R distance)

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3. Determine the Axis:- Normal: QRS upright in I and aVF- LAD: QRS up in I, down in aVF, II- RAD: QRS down in I, up in aVF

4. Evaluate for evidence of atrial and ventricular abnormalities:- LVH: HTN, HOCM, AS/AI, coarctation of aorta

- R in aVL > 9mm (female); 11mm (male) - most specific- R in aVL + S in V3 > 20mm (female); 28mm (male) - most sensitive- S in V1 or V2 + R in V5 or V6 >35mm

- RVH: cor pulmonale, congenital, MS, TR- RAD- R:S in V1 1- R in V1 > 7mm- R:S in V5 or V6 < 1

- Combined Right and Left Ventricular Hypertrophy:- Voltage Criteria for LVH + RAD

- LAE:- Notched P-wave in II (- Biphasic P-wave in V1 (terminal P-wave >1 small box)

- RAE:- Peaked P-wave (>2.5mm) in lead II- P-wave > 1.5mm in V1 or V2

5. Evaluate for evidence of bundle branch block:- QRS > 0.12sec (incomplete block QRS 0.10-0.12sec)- Look @ V1 & V6 draw vertical line down middle of QRS; portion to right of the verticalline = LATE component of QRS.- LBBB:

- Late V1 = downward; Late V6 = upward- Broad, slurred, monophasic R wave in I, V5 & V6. Absence of “septal” Q’s in I, V5 &

V6- Displacement of ST and T wave opposite to major deflection of QRS +/- PRWP, LAD,

Q’s in inferior leads LAFB:

- LAD- Small q (qR) in I, aVL, small r (rS) in II, III, aVF

LPFB:- RAD- Small r (rS) in I, aVL, small q (qR) in II, III, aVF- No evidence for RVH

RBBB:- Late V1 = upward; Late V6 = downward- RsR’ pattern in RIGHT precordial leads- Wide broad S wave in I, V5 & V6

6. Evaluate for evidence of ischemia/infarction: ST Elevation/Depression TWI Change from baseline Dominant R wave V1/V2 suggestive posterior MI (IMI)

7. Evaluate For Vascular Distribution:Territory ECG Distribution Vessel

Anterior wall of LV V1-V4 LADInferior wall of LV II, III, aVF RCA/PD, LCxLateral wall of LV I, aVL, V5, V6 LCxPosterior wall of LV V1-V2 (large R) RCA/PD, LCxSeptal Wall V1, V2 LAD/septal

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8. Diagnosis of MI in presence of bundle branch block:- No change in criteria in setting of RBBB, RBBB+LAFB and RBBB+LPFB- In LBBB, normally ST-T wave changes are in opposite direction of QRS

Diagnosis of acute MI in LBBB:>1mm concordant (in same direction of QRS) ST elevation>1mm ST depression in V1-3>5mm discordant (opposite direction of QRS) ST elevationQ waves in I, avL, V5-6 suggestive of Q wave infarction

9. Differential of EKG Findings: Q Waves:

- LBBB- WPW- HOCM- COPD- Pulmonary Embolism

ST Elevation:- Hypothermia (Osborne/J waves)- Acute Pericarditis (diffuse without anatomical distribution)- Myocardial Infarction (follows anatomical distribution)- LV aneurysm (persistent STE)- Early repolarization- Coronary vasospasm

QT Prolongation:- Congenital Long QT- Electrolytes (hypocalcemia, hypomagnesemia, hypokalemia)- Antipsychotics (e.g. haldol)- Antiarrhythmics- Bradycardia

CHF

3. History: orthopnea, PND, dyspnea on exertion, ask about functional status, weight gain,decreased exercise tolerance, medication/diet non-compliance

4. Etiology: CAD, HTN, idiopathic dilated cardiomyopathy, valvular heart disease, substances(Alcohol, cocaine, meth), infiltrative (amyloid, sarcoid), hemachromatosis, HIV, viral

5. Acute exacerbation: consider new ischemic event, arrhythmia, infection, hyperthyroidism,PE, medication and dietary non-compliance, recent increase in beta-blocker dose, renalfailure, HTN

- evaluate severity of exacerbation: warm/dry -> warm/wet -> cold/wet -> cold/dry

6. Physical Exam:- signs of left-sided failure: rales, tachypnea, S3- signs of right-sided failure: elevated JVP, ascites, peripheral edema, enlarged/tender liver- signs of low cardiac output: cachexia, muscle loss, cool extremities, tachycardia

5. Relevant Labs:- chem7, CBC, TSH, LFTs, BNP, lipid panel, cardiac enzymes- BNP: secreted by ventricles as a response to ventricular volume expansion/pressure

overload- Lower than expected BNP: obese, acute MR/MS, flash pulmonary edema- Higher than expected BNP: AKI, acute MI, lung dz with RHF, acute PE, cirrhosis,age- BNP levels <100 pg/ml essentially excludes heart failure as a cause of a patient’s symptoms

or physical exam (sens: 90%, spec: 73%, NPP: 90%)- not influenced by mild renal insufficiency, but may be increased in dialysis patients

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6. Treatment:- Aspirin, ACE-I, BB: shown to decrease mortality. If EF<40%, use carvedilol. Use BB when

pt’s are clinically stable, not necessarily during an exacerbation- digoxin: symptomatic improvement in pt’s with systolic failure, decreases morbidity- spironolactone: benefits pts NYHA Class III-IV (EF<40%), ischemic etiology- Diuresis: often starts with Lasix. Lasix has a threshold before it works, so if a pt is not

responding to his diuretics, the dose will need to be increased. 2:1 PO to IV conversion.Variable bioavaility.

- Bumex: 40x more potent than lasix with higher bioavailability (90%)- may need to add Metolazone (30 min before giving lasix) as a primer to make diuresis more

effective- if not responding to metolazone and lasix, may use Diurel (IV) instead- In everyone, monitor strict I/Os and daily weights. Always have I/Os for rounds. Place pts on

2g Na diet, 2L fluid restriction, while diuresing check lytes BID (K, Mg).- If bicarb is increasing rapidly, may consider acetazolamide

7. B-type Natriuretic Peptide (BNP):- A hormone that is synthesized de novo by cardiac ventricles in response to increased wall

stress and/or ischemia. (Note: there are other natriuretic peptides A-type and C-type but arenot as specific and are currently not being used for diagnostic purposes)

- released primarily by LV during CHF exacerbation to relieve ventricular wall stress and thusimprove cardiac function ("wet BNP")

Pro-BNP

BNP = C-terminal proBNP NT-proBNP = N-terminal proBNP

Potent Neurohormone Biologically Inactive peptide

Renally cleared (partially) Not renally cleared

Short half-life (21 min) Short half-life

Physiologic Actions of BNP:- Hemodynamic: - Renal:

- Vasodilation (venous > arterial) - Diuresis- Neurohumoral: - Natriueresis

- Aldosterone - Cardiac:- Norepinephrine - Fibrosis- Endothelin - Remodeling

When to order a BNP level:

Dyspnea - (Physical exam and BNP)

BNP < 100 BNP 100 - 400 BNP > 400

CHF veryunlikely (2%)

Known LV Dysfunction, Cor Pulmonale orAcute PE

CHF verylikely (95%)

Yes No

CHF exacerbation (25%) CHF exacerbation(75%)

Dry BNP Wet BNP

BNP level once euvolemia is reached Anything significant over the “dry BNP”Falls slowly with treatment Falls rapidly with treatmentMay be 20-1000 pg/ml depending onseverity of Heart Failure

Can be 2 – 4 fold the ‘dry BNP” thusworsening severity of HF to class III-IV

Correlates with NYHA functional class

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Heart failure patientswhose BNP level failsto fall over their hospitalstay have a higherincidence ofrehospitalization orcardiac death.

The closer the HFpatient gets to his/hereuvolemic weight, “dryBNP” level, the lesslikely to berehospitalized early.

CARDIAC BIOMARKERS

Troponin- serial testing at presentation, then 6-12hr after onset symptoms. Detectable 4-6hr after myocardialinjury- peaks at 24hr, may remain elevated 7-10 days after myocardial infarction- “false positive” – renal failure, demand ischemia

CKMB- useful for evaluating re-infarction, post CABG and PCI.- >3x UNL post-PCI suggests reinfarction, >5x UNL post-CABG suggests reinfarction

TACHYCARDIA AND TACHYARRHYTHMIAS

Initial Assessment: is pt symptomatic or hypotensive (SBP<80)?- If so, place pt in Trendelenburg. Give fluid bolus, begin ACLS if necessary.- place pt on cardiac monitor, get a 12 lead EKG/rhythm strip

Narrow Complex TachycardiaRegular (QRS<120msec)1. Sinus Tachycardia:

- could be caused by hypoxia, hypovolemia, fever, myocardial dysfunction, PE, pain, anxiety,EtOH withdrawal, hyperthyroid- usually has upright P waves in II, III, aVF followed by a QRS- treat underlying cause

2. AVNRT: AV nodal re-entrant tachycardia, usually rate 150-250- inverted P (or pseudo S) in II, III, aVF. P waves may be buried in QRS- if pt unstable, synchronized DC cardioversion- if no history of CVA/TIA/carotid bruit, try carotid massage or valsalva- if no history of asthma, can try adenosine to break it- put pt on rhythm strip, have atropine ready in case pt has a long pause- Adenosine 6mg IVP, then 12mg IVP, then repeat 12mg IVP- if doesn’t break with adenosine, can try Metop 5mg IV q5min x3 (pushed over 2 minutes,

then flush) or Dilt 15mg IV q5min3. Atrial Tachycardia:

- P waves before each QRS, usually with a P wave different from pt’s baseline P (atrialactivation does not start at sinus node)- treat with BB, CCB, or Class III antiarrhythmic (amiodarone, sotalol)

4. Atrial Flutter (with regular block):- flutter waves in II, III, aVF. Ventricular rate is some division of 300 (150, 100, 75).- can push adenosine 6/12/12 to reveal flutter waves- If stable, treat with BB, CCB, or digoxin- If unstable, synchronized DC cardioversion- may need anticoagulation

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Irregular (QRS<120msec)1. Atrial Fibrillation (see management below):

- caused by hypertension, pulmonary disease, idiopathic, ischemia, valvular heart disease,thyrotoxicosis, ethanol, sepsis

- NO p waves on EKG- If stable, treat with Metoprolol 5mg IV q5min x3 (if no COPD or low EF) or Diltiazem 10-15mg

IV q5min x3 (or dilt gtt)- If unstable, synchronized DC cardioversion or amiodarone 150mg IV over 10 min followed by

1mg/min x6h, then 0.5mg/min x18h2. Frequent PACs3. Multifocal atrial tachycardia: caused by multiple ectopic pacemakers

- EKG will have 3 distinct P wave morphologies with 3 different PR intervals- check magnesium, potassium

Wide Complex TachycardiaRegular (QRS>120msec)1. Ventricular Tachycardia (monomorphic):

- assume VT in all pts with heart disease- ACLS protocol – synchronized shock for perfusing VT and defibrillation for VF- check electrolytes

2. SVT with Aberrancy:- diagnosis of exclusion- check if pt has history of BBB, although sometimes this is not brought out until pt is

tachycardic- treat as SVT- check lytes- in any case, call your resident STAT

Irregular (QRS>120msec)1. VTach (polymorphic): DEFIBRILLATE2. Torsades de pointes (causes):

- Meds: antiarrhythmic drugs that prolong QT, TCAs, phenothiazines, H1 blockers(astemizole, terfinadine), pentamidine, erythromycin, antifungal agents

- Electrolyte abnormalities: hypokalemia, hypomagnesemia- Subarachnoid hemorrhage- Congenital long QT syndrome- EKG: twisting QRS complexes, prior EKGs may have long QT (QTc>450)- Treatment: defibrillate, Mg Sulfate 2mg IV over 1 min

3. Atrial fibrillation with Aberrancy or Accessory pathway:- diagnosis of exclusion. Treat as VT until proven otherwise

4. Frequent PVCs:- Frequently due to electrolyte abnormalities, hypoxemia, acidosis. - Check 12-lead EKG, CMs, Mag, chem 10 (replace Potassium & Magnesium), CBC, digoxin

level (if taking), consider ABG to r/o acidosis.

ATRIAL FIBRILLATION

Atrial Fibrillation w/ Rapid Ventricular Response (RVR)

1. OBTAIN VITALS and assess patient.- Even if patient appears stable, patient cannot be left w/ HR>100 as rhythm can degenerate

and vitals can deteriorate. Also, sustained tachycardia is a significant stress and if underlyingCAD, pt can develop demand ischemia.

2. UNSTABLE Patient:- DC CARDIOVERSION notify resident and prepare for it stat (follow ACLS).

3. Stable Patient:- EKG to see if truly Afib/flutter vs. SVT +/- abberency- Chem 10, Mag to ensure no electrolyte abnormalities.

4. Medical Interventions:- Diltiazem: Push q15 min x 3(can start at 5mg and increase to 0.35 mg/kg in increments of

5mg) until rate control. Will have some effect on BP. Can give 1-2amps of Ca Gluconate priorto dilt and with help negate effect on pressures. Once rate controlled give as gtt (5-15 mg/h)IV for up to 24 h. Often considered first-line in patients without a h/o CHF; Contraindicated insevere CHF, sick sinus syndrome, second- or third-degree AV block.

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- Metoprolol: Push 5-15 mg IV over 5-15 min (5-mg increments). Preferred in patients withCAD, thyrotoxicosis and increased sympathetic tone. Contraindicated in decompensatedCHF, bradycardia, asthma, cardiogenic shock, and AV conduction abnormalities.

- Digoxin: Loading regimen: 500mcg iv, f/b 250mcg 6h later, and another 250mcg 6h later(total 1gram); decrease doses by half in CKD. Ensure K is replaced as hypokalemia limitseffect. Obtain level 6h after last loading dose. Effect often not seen for several hours, butuseful especially in low output heart failure. Contraindicated in wet beriberi, idiopathichypertrophic subaortic stenosis, constrictive pericarditis, carotid sinus syndrome.

- Other Agents (these are typically only used on the Cards service with fellow/attendinginput): see below

ANTIARRHYTHMIC THERAPY

Antiarrhythmic Dosage Indications

Adenosine6 mg IVP 12 mg IVP if needed 12 mg IVP if needed

1. Stable narrow-complex AV nodal or sinus nodal re-entrytachycardia2. Unstable re-entry SVT prior to cardioversion3. Undefined stable narrow-complex SVT

Amiodarone150 mg IVP over 10 min 1 mg/minx 6 hr 0.5 mg/min x 18 hr

1. Narrow-complex re-entry tachycardia2. Stable VT, polymorphic VT, wide-complex tachycardia3. Rate control of due to accessory pathway

Calcium-channel blockers1. Stable narrow-complex re-entry tachycardia2. Stable narrow-complex automaticity tachycardia(junctional, ectopic, multifocal)3. Rate control of atrial fibrillation or atrial flutter (do notgive if WPW present)

Verapamil

1. 2.5-5 mg IV over 2 min 5-10 mg Q15-30 min (20 mg total)2. 5 mg IV bolus Q15 min (30mg total)

Diltiazem 0.25 mg/kg IV 0.35 mg/kg IV

-blockers

1. Narrow-complex re-entry tachycardia2. Narrow-complex automaticity tachycardia (junctional,ectopic, multifocal)3. Rate control of atrial fibrillation or atrial flutter(ventricular function preserved)

Atenolol5 mg IV over 5 min can giveanother dose 10 min later

Metoprolol 5 mg slow IVP Q5 min (15 mg total)

Propranolol0.1 mg/kg slow IVP divided into 3equal doses at 2-3 min intervals (nofaster than 1 mg/min)

Esmolol

500 mcg/kg IVP 50 mcg/kg/min x 4min (200 mcg/kg total) if needed,500 mcg/kg IV 100 mcg/kg/min IV(max 300 mcg/kg/min)

Sotalol 1-1.5 mg/kg IVP 10 mg/min IV1. Rhythm control of atrial fibrillation or atrial flutter withWPW2. Monomorphic VT

Others1. Cardioversion of atrial fibrillation or atrial flutter with orwithout WPW (<48 hr)2. Control rate in atrial fibrillation or atrial flutter

Ibutilide1 mg IV (0.01 mg/kg if < 60 kg) over10 can repeat 10 min later ifneeded

Lidocaine

0.5-0.75 mg/kg IVP (up to 1-1.5mg/kg) 0.5-0.75 mg/kg IVP Q5-10min (max 3 mg/kg) 30-50mcg/kg/min IV

1. Stable monomorphic VT with preserved ventricularfunction2. Polymorphic VT with normal baseline QT interval

Magnesium1-2 g IV over 5-60 min (stableslower, unstable faster)

Torsades de pointes

Procainamide

20 mg/min IV until suppression ofarrhythmia, hypotension, or QRSprolongation by 50% (max 17 mg/kg) 1-4 mg/min IV maintenance

1. Stable monomorphic VT with preserved ventricularfunction2. Rate control of atrial fibrillation or atrial flutter3. Rhythm control of atrial fibrillation or atrial flutter withWPW4. Narrow-complex AV re-entry tachycardia

Reference: American Heart Association. “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care – Part 7.3: Management of Symptomatic Bradycardia and Tachycardia.” Circulation 2005; 112(24 Suppl): IV-67-IV-77.

HYPERTENSION

1. Evaluation:- Assess initially if Hypertensive Emergency (end organ damage) or Hypertensive Urgency.

Both with BP>180/110.- Important to double check validity of reading, ask for recheck and you should CHECK

MANUALLY at bedside BP in both arms. Check CUFF SIZE.- PE: Fundoscopic exam (papilledema), neuro exam, lungs for edema, BP in both arms for

possible aortic dissection.2. Differential:

- OD (cocaine, meth)- Withdrawal (EtOH, cocaine, meth, narcs, anti-HTN)- Pain or anxiety- Increased intracranial pressure (Cushing’s reflex – associated w/ bradycardia)- Renal Artery Stenosis- Coarctation of the aorta- Endocrine (thyrotoxicosis, pheo, Cushing’s syndrome)

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** Do not lower BP too abruptly. Goal is 25% reduction in MAP or to reduce DBP to no lower than100-110mmHg in first 12-24 hrs.

3. Hypertensive URGENCY: HTN without evidence of end-organ damage- Labetalol: 10mg ivp, followed by 200-400mg po BID- Clonidine: 0.2mg orally, re-check BP in 30-60 minutes. May follow with 0.1mg q hour to total

of 0.8mg. Watch for sedation, bradycardia with AV nodal blockers. Rebound hypertension ifabruptly stopped.

- Captopril 12.5-25mg orally works in 15-30 minutes.- Metoprolol 12.5-100mg PO BID (ok to start titrating 25 mg po q6hrs x 48 hrs -> then convert

to BID). Try to avoid IV MTP as it lasts a short time. (2.5 mg PO MTP = 1 mg IV MTP)4. Hypertensive EMERGENCY: HTN associated w/ end-organ damage

- End-Organ Damage:- CNS: headache, mental status changes, seizure, stroke- Eyes: blurred vision, papilledema, exudates, flame hemorrhages- Cardiac: chest pain, EKG strain or ischemic changes, pulmonary edema- Vascular: aortic dissection- Renal: low urine output, edema, hematuria, azotemia

3. Management: admission to ICU- IV Nipride 0.2-5 mcg/kg/min: 1st line in most patients. Arteriolar and venous dilation.

Toxicity with thiocyanate and cyanide metabolite must be considered with several days oftherapy and with renal and hepatic insufficiency

- IV Nitroglycerin 10-400mcg/min: First choice agent for patients with myocardial ischemia.Venous dilation

- IV Labetalol (α1, β1, β2 antagonist) 20mg IV bolus, then 2mg/min: First choice agent forpatients with myocardial ischemia or acute aortic dissection

4. Special cases:- Cocaine or Pheochromocytoma, make sure you have alpha blockade (phenoxybenzamine

10mg BID) PRIOR to beta blockade or will have unopposed alpha tone.- Pulmonary edema/MI, nitroprusside is good choice, but if using for Aortic Dissection,

make sure you have β-blocker on board first.

HYPOTENSION

1. Initial Assessment:- Make sure reading is accurate, repeat manually in both arms. Check CUFF SIZE, may need

arterial line. Assess if patient is mentating well. Remember to treat the patient, not thenumbers. BP 90/50 may be normal, ex: CHF or end stage liver disease.

- Palpate Pulse: Radial ~SBP>80. Carotid/fem ~SBP>60, No pulse - start ChestCompressions, then call CODE BLUE

- Check for signs if hypoperfusion defects:- Brain: AMS- CV: MI, ischemia, arrhythmia- Renal: decreased uop- GI: LFT/lipase leak, can check lactate for ischemia

Check baseline BPs (low in ESLD, ESRD, cardiomyopathy), also check med list. Workup to order once patient is stable: CBC with diff, Chem 10, EKG (rule out Afib, SVT

Vtach), cardiac markers, consider lactate, ABG, blood cultures.2. Differential:

Hypovolemia: hemorrhage, dissection, GI loss, dieresis, third spacing Cardiogenic: MI, arrhythmia, valvular dysfunction Obstructive: PE, tamponade, tension pneumo Sepsis Anaphylaxis Medications (BP meds) Adrenal Insufficiency (primary or relative)

3. Management: will depend on the etiology, but some general considerations: place pt in Trendelenburg position to increase perfusion to the brain check for anti-hypertensives like nitropaste, clonidine patch if no evidence for CHF or renal failure, bolus with 1L NS and re-evaluate in CHF/Volume Overload diuresis often will increase pressure in Afib with RVR, rate control will often improve blood pressure

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PACEMAKERS

1. Nomenclature:- Position I – chamber paced (A – atrium, V – ventricle)- Position II – chamber sensed- Position III – response to event sensed (I – inhibitory, D – dual, T – triggered, O – none)- Position IV – rate modulation (R – rate response to activity, O – none)- Position V – multisite pacing (usually omitted)

2. Common Pacing Modes:- AAI/AAIR – for sinus node dysfunction. Need an intact AV node- VVI/VVIR – for bradycardias, afib w/ slow ventricular response- DDD/DDDR – for bradycardias, AV node dysfunction, physiology pacing

3. Complications after placement: Pneumothorax (check CXR) Hematoma formation (especially if patient on anticoagulation) Lead perforation of RA or RV (suspect if hemodynamically unstable) Lead dislodgment or pacemaker failure (suspect if failure to sense or capture)

STRESS TESTS

1. Exercise treadmill test: Excellent if pt has good exercise capacity; 85% sensitive. Do not use if pt unable to walk, is from jail (may not give maximal effort), has LBBB, WPW,

paced rhythm, or other EKG abnormalities that would make it uninterpretable.- Before ETT, HOLD beta blockers and nodal CCB (verapamil, diltiazem).

2. Adenosine sestamibi:- Causes direct coronary artery vasodilation, which is attenuated in diseased coronaryarteries—they have reduced reserve and can’t dilate in response to adenosine.- Can cause bronchospasm. Use if BBB.- Hold caffeine, which is a competitive inhibitor of adenosine.

3. Dobutamine stress echo:- stimulates beta-1 and beta-2.- Use in pt’s with RAD/asthma/COPD.- Before dobutamine echo, HOLD BB, dilt/verapamil. Nifedipine/amlodipine OK

*Many attending prefer patients to be NPO at midnight before stress test.

THE “POST-CATH CHECK”

Pt should be on bedrest with leg straight 6 hours afterwards At night, check the groin. Make sure there is no hematoma and distal pulse is palpable.

Listen to ensure no bruit. CBC and cardiac markers q6h (follow CKMB for pericath MI, significant if >3x upper limit of

nl) If there is an acute bleed, hold pressure ABOVE the puncture site, since the opening from

the femoral artery will be higher than the external puncture site Summarize cath report results on S/O sheet Post cath complications to watch for: MI >3x ULN CKMB, Renal failure, Stent thrombosis,

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HEMODYNAMICS AND SWAN-GANZ CATHETERS

Site Normal Pressure (mmHg)

Right AtriumRight VentriclePulmonary ArteryPulmonary Capillary Wedge PressureLeft AtriumLeft VentricleAortaPeripheral (measured blood pressure)

< 5 (3-5)< 25/5< 25/10< 12 (6-12) PA diastolic pressure< 12 ( PCWP)< 150/10< 150/90< 120/80

Cardiac output (CO) = (stroke volume) x (heart rate) normal 3-7 L/min Cardiac index (CI) normal 2.4-4 L/min/m2 Systemic vascular resistance (SVR) normal 800-1200 dynes-s/cm5 Mixed venous O2 saturation (SvO2) normal 70-75%

ConditionRight AtrialPressure

PCWP SVR CO

Septic shock

Hypovolemic shock

Cardiogenic Shock

Neurogenic Shock Normal to

Pulmonary Embolus Normal to Normal

Tamponade Normal to

RV Infarct

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HYPERLIPIDEMIA MANAGEMENT

1. Lipid Lowering Medications:

Drug class* Serum LDL Serum HDL Serum TGs

Bile acid sequestrants 15 to 30 percent 0 to slight increase No change*

Nicotinic acid 10 to 25 percent 15 to 35 percent 25 to 30 percent

HMG CoA reductaseinhibitors (statins)

20 to 60 percent 5 to 10 percent 10 to 33 percent

Gemfibrozil 10 to 15 percent 15 to 25 percent 35 to 50 percent

Fenofibrate(micronized form)

6 to 20 percent 18 to 33 percent 41 to 53 percent

Cholesterol absorptioninhibitors

17 percent No change No change

Neomycin 20 to 25 percent No change No change

2. Lipid Target Levels:

Risk category LDL goalLDL level at which toinitiate lifestylechanges

LDL level at which to considerdrug therapy*

High risk:Coronary heartdisease (CHD) orCHD riskequivalent (10-year risk >20percent)*

<100mg/dL;optionalgoal <70mg/dL invery highrisk

100 mg/dL100 mg/dL; <100 mg/dLconsider drug options

Moderately highrisk: 2 or more riskfactors (10-yearrisk 10 to 20percent)

<130mg/dL

130 mg/dL130 mg/dL; 100 to 129

mg/dL consider drug options

Moderate risk: 2 ormore risk factors(10-year risk <10percent)

<130mg/dL

130 mg/dL 160 mg/dL

Lower risk: 0 to 1risk factor

<160mg/dL

160 mg/dL190 mg/dL; 160 to 189

mg/dL consider drug options

Risk category LDL goalLDL level at which toinitiate lifestylechanges

LDL level at which to considerdrug therapy*

High risk:Coronary heartdisease (CHD) orCHD riskequivalent (10-year risk >20percent)*

<100mg/dL;optionalgoal <70mg/dL invery highrisk

100 mg/dL 100 mg/dL; <100 mg/dLconsider drug options

Moderately highrisk: 2 or more riskfactors (10-yearrisk 10 to 20percent)

<130mg/dL

130 mg/dL 130 mg/dL; 100 to 129 mg/dLconsider drug options¦

Moderate risk: 2 ormore risk factors(10-year risk <10percent)

<130mg/dL

130 mg/dL 160 mg/dL

Lower risk: 0 to 1risk factor

<160mg/dL

160 mg/dL 190 mg/dL; 160 to 189 mg/dLconsider drug options

* CHD equivalent: AAA, symptomatic carotid artery disease, DM, peripheral arterial disease*Adapted from Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation,and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Circulation 2002; 106:3143; withmodifications from Grundy, SM, Cleeman, JI, Merz, CN, et al, Circulation 2004; 110:227.

*Statins use should be maximized if possible before addition of other lipid lowering agents.

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PERIOPERATIVE CARDIAC RISK ASSESSMENT

1. General concepts:- The perioperative period can put patients with vulnerable coronary artery lesions at risk for MIor death due to stresses of surgery, anesthesia, and a prothrombotic postoperative state.- The ACC/AHA guidelines have been recently updated based on new evidence, which issummarized below

2. Who is at risk: Need to assess 3 components: functional status, surgical risk, and clinicalrisk- Functional status

- Surgical stress = approximately 4 METS on a treadmill test- 4 METS = climbing 2 flights of stairs, brisk walking on level ground for 4 blocks- If a patient can achieve 4 METS without angina equivalent, he likely can withstand thesurgical stress

- Surgical risk- Certain surgeries are inherently high risk (>5% risk of cardiac complications)

- Aortic or other major vascular surgery- Peripheral vascular surgery (not including CEA)- Anticipated major blood loss or prolonged surgery

- Clinical predictors of risk (use Revised Cardiac Risk Index [RCRI] Lee TH et al.Circulation. 1999; 100: 1043-9 ).

- Assign 1 point for each:- High risk surgery- CAD- CHF- Cerebrovascular disease- IDDM- Creatinine > 2.0

- For < 3 points, risk of cardiac event < 1%- For 3 or more points, risk > 6%

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3. How to risk stratify:

4. Estimated Energy Requirement:1 MET Self care

Eating, dressing, or using the toiletWalking indoors and around the houseWalking one to two blocks on level ground 2-3 mph

4 METs Light housework (e.g., dusting, washing dishes)Climbing a flight of stairs or walking up a hillWalking on level ground at 4 mphRunning a short distanceHeavy housework (scrubbing floor, moving furniture)Moderate recreational activities (e.g., golf, dancing, doubles tennis,throwing a baseball or football)

>10 METs Strenuous sports (e.g., swimming, singles tennis, football, basketball,skiing)

5. Four Active Cardiac Conditions: For Which the Patient Should Undergo Evaluation andTreatment Before Noncardiac Surgery (Class I, Level of Evidence: B)

Unstable Coronary Syndromes Unstable or Severe Angina,Recent MI

Decompensated HF NYHA Class IV,Worsening or New-onset HF

Significant Arrhythmias High-grade AV block,Mobitz II AV blockThird-degree AV heart blockVentricular arrhythmias*Supraventricular Arrhythmias*,Symptomatic bradycardia,Ventricular tachycardia

Severe Valvular Disease Severe Aortic Stenosis**,Symptomatic Mitral Stenosis

*HR greater than 100 or symptomatic, **gradient >40 mmHg, AoV <1.0 cm2

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6. Who needs preoperative testing:- Short answer: almost NO ONE who is an inpatient awaiting urgent surgery- Short answer #2: ask yourself “If I were seeing this patient for an office visit instead of for a

pre-op consult, would I recommend testing?” If the answer is “no,” you should probably notrecommend a test

- Neither stress testing nor revascularization has been shown to improve outcomespostoperatively, and several high quality trials have been done. (McFalls, et al. NEJM 2004v 351, Poldermans D, et al. JACC 2006; 48: 964-9.)

- However, in cases for which patients with significant ischemia on testing could reasonablydefer or delay the surgery, it is reasonable to test

- Remember, patients with stents need antiplatelet agents continued for 6-12 monthsminimum, so perioperative PCI will delay surgery unless it can safely be performed onantiplatelet agents

7. Who needs preoperative beta-blockers- Short answer: DO NOT STOP beta-blockers preoperatively in patients who are taking them

already, DO NOT START perioperative beta-blockers in naive patients.- Data from the POISE trial (Lancet 2008; 371: 1839-1847) suggest that starting beta-blockers

in naïve patients reduces cardiac events at a cost of increased mortality; there remainscontroversy about the design but we await results of DECREASE V to shed more light on theissue.

- IF you are using perioperative beta-blockers, adjust them regularly to a target HR of <75

8. Final thoughts- Avoid writing “cleared for surgery”- Better: “patient is at low risk for cardiac events, no further pre-op testing recommended,” or

“the patient’s cardiac risk factors are optimized”- Address other issues (e.g. management of diabetes, COPD, adrenal insufficiency, VTE

prophylaxis)

From ACC/AHA guidelines: Fleisher, L. A. et al. Circulation 2007;116:e418-e499

CARDIOLOGY LITERATURE

CHF Trials:

US Carvedilol Heart Failure Study GroupNEJM 1996; 334 (21): 1349-55Design: Double-blind, placebo-controlled; 1094 pts with chronic HF randomized to placebo orstratified to carvedilol with initial dosing of 6.25mg, 12.5mg, or 25mg BID based on exercise capacity.Pts assigned to mild-mod HF based on 6-min walk test; mean follow-up 6.5mo.Endpoint: Death or hospitalization for CV events.Results: Early termination; 65% RRR overall mortality (p <0.001); 27% reduction in hospitalizationfrom CV causes (p = 0.036); 38% reduction in combined risk of hospitalizationor death (p <0.001).Conclusion: Carvedilol reduces the risk of death and hospitalization from CV causes in pts w/ chronicHF (mostly pts in class II/III) with concurrent therapy of ACE-I, diuretics, and digoxin.

Carvedilol Prospective Randomized Cumulative Survival Trial (COPERNICUS)NEJM 2001; 344: 1651-8Design: Double blind RCT 2289 pts with NYHA III and IV pts w/ LV EF < 25%, but clinically stable (i.e.euvolemic and not on pressors) with chronic HF from ischemic or non-ischemic CM, but not fromvalvular disease. Pts on treatment group received carvedilol 3.125mg bid to target dose 25 mg BIDfor 11 months vs. placebo.Endpoint: Death from HF, cardiac causes and/or re-hospitalization.Conclusion: The Carvedilol group had a 35% RRR in death. A combined end point of death &hospitalization was signif for a 24% RRR compared to placebo. Prior studies show that not all b-blockers have this favorable mortality effect, bucindolol was tested and showed no effect.Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF)Lancet 1999; 353: 2001-7Design: Double-blind, placebo-controlled; 3994 pts w/ chronic HF in NYHA II-IV randomized toMetoprolol XL 12.5mg III-IV) or 25mg (II) daily vs placebo. Target dose 200mg once daily.Results: Early termination; lower all-cause mortality w/ metoprolol XL (7.2% pt-yr of f/u vs 11%, RR0.66); fewer sudden deaths (79 vs 132, RR 0.59); deaths worsening HF (RR .51).Conclusion: Metoprolol CR/XL daily, w/standard HF therapy, improves survival in pts w/ mild-severechronic ischemic or non-ischemic heart failure (>95 % of pts in class II-III).

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Randomized Aldactone Evaluation Study Investigators (RALES)NEJM 1999; 341: 709-17Design: Double-blind, placebo-controlled; 1663 pts with severe chronic HF (NYHA III-VI) fromischemic/non-ischemic causes randomized to 25mg spironolactone qd vs placebo.Results: Early termination; 30% RRR in mortality in the spironolactone group- attributed to lower risksof sudden cardiac death and death from progressive HF; 35% RRR in hospitalization for worseningHF; improvement in NYHA class HF sxs; all with p <0.001.*Beware of gynecomastia/breast pain and serious hyperkalemia (K >6)Conclusion: Addition of spironolactone to standard therapy reduces morbidity & mortality in pts withsevere HF. Of note, only 10% pts on a beta-blocker @ baseline during the trial (COPERNICUSpublished in ’01).

Digitalis Investigation Group (DIG Trial)NEJM 1997; 336: 525-33Design: Double-blind, placebo-controlled; in the main trial, pts w/ EF <45% (70% due to ischemia;>80% in NYHA Class II-III) randomized to digoxin (3397 pts) vs placebo (3403 pts) inaddition to diuretics and ACE-I; median dose digoxin 0.25mg daily. In the ancillary trial,pts w/ EF >45%; 492 pts assigned to digoxin and 496 to placebo.Conclusion: Digoxin reduced hospitalization rates both overall and for worsening heart failure;however, digoxin did NOT reduce overall mortality.

NSTEMI Trials TACTICS-TIMI 18NEJM. 2001;344:1879-87.Design: Blinded, randomized controlled trial; 2220 pts w/ ECG e/o ischemia, elevated troponin ordocumented CAD were randomized to cath < 48hrs after randomization vs medical tx and stress test.All pts received ASA, heparin, and tirofiban.Conclusion: Early invasive strategy was more effective with RRR of 30% at 30 days and 18% at 6mos. 19% mortality in conservative group vs. 14% mortality in early invasive group. Furthersubgroup analysis found that this benefit was only found in pts w/ a TIMI risk score >3, there was nobenefit in pts w/ a low TIMI risk score (0-2).

Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE)NEJM August 16, 2001Design: 12562 patients randomized within 24 hours after onset of non-ST elevation ACS to receiveeither ASA (75mg to 320mg) alone or with clopidogrel (300mg LD, then 75 mg daily).Results: Primary outcome occurred in 9.3% of the clopidogrel group & 11.4% of the ASA alone group(RR 0.8, p<0.001). Refractory ischemia occurred 16.5% in the clopidogrel group and 18.8% in theplacebo group (RR 0.86, p<0.001). Significantly more bleeding in the clopidogrel group (3.7% vs2.7%) but no difference in life threatening bleeding or hemorrhagic strokes.Conclusion: Clopidogrel + ASA has beneficial effects in ACS vs ASA alone. Majorbleeding and possible delay of CABG are the main drawbacks of the study.

The Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited byUnstable Signs and Symptoms (PRISM-PLUS)NEJM May 21, 1998Design: 1915 patients with unstable angina or NSTEMI randomized in a double-blind studyto receive tirofiban, heparin or both. Everyone received ASA.Results: Study was stopped prematurely for the group receiving tirofiban alone, who had excessmortality within the first 7 days. Primary endpoint was reached at 7 days for 12.9% in the groupreceiving tirofiban + heparin, and 17.9% in the heparin alone group (p=0.004). There was nosignificant difference in major bleeding between the two groups.Conclusion: When administered with ASA and heparin, tirofiban decreased incidence of ischemicevents in pts with ACS compared to those receiving ASA and heparin alone.

Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using IntegrilinTherapy (Pursuit)NEJM August 13, 1998Design: 10,948 patients with rest angina lasting >10 minutes in the previous 24 hours with ischemicEKG changes or CKMB elevation were randomized to receive either eptifibatide plus standardtherapy, or placebo.Results: Primary endpoint reached for 15.7% of placebo group and 14.2% of study group (p=0.04).Bleeding was more common in the study group, but there was no significant increase in hemorrhagicCVA.Conclusion: Eptifibatide reduced death & non-fatal MI in pts with ACS without persistent STE

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Electrophysiology Trials” Madit II (Multicenter Automatic Defibrillator Implantation Trial II)NEJM March 21, 2002Design: 1232 pts with prior MI (@ least >30dy prior), EF<30% randomized to receive prophylacticICD or conventional medical therapy.Results: Study terminated prematurely after f/u 20mo because ICD group had significantly reducedall-cause mortality (14.2 vs 19.8%) all due to reduction of sudden death.Conclusion: In pts with prior MI & LV dysfx (EF<30%) prophylactic implantation of a defibrillatorimproves survival.

SCD-HEFT (Sudden Cardiac Death in Heart Failure Trial)NEJM January 20, 2005Design: 2521 pts w/ NYHA class II/III CHF (ischemic/non ischemic) and an EF < 35% wererandomized to conventional drug therapy (CDT) + placebo vs. CDT + amio vs. CDT + ICD.Endpoint: Death from any cause.Results: At 45 months there were 244 deaths, 29% in the placebo group, 28% in the amio group, and22% in the ICD group. ICD had a 23% relative risk reduction (p<0.007) compared to CDT + placebo.This benefit did not differ between non ischemic and ischemic CHF.Conclusion: In pts w/ NYHA class II/III CHF and an EF < 35%, ICD therapy has improved survivalbenefit compared to amiodarone/placebo.

COMPANION (Comparison of Medical Therapy, Pacing and Defibrillation in Heart Failure)NEJM May 20, 2004Design: 1520 pts w/ NYHA class III/IV CHF were randomized to medical therapy vs. medical therapy+ cardiac resynchronization vs. medical therapy+ cardiac resynch + defibrillator.Results: For all cause death/hospitalizations, compared to med tx alone, med tx + resynch or med tx+esynch/defib had a 20% relative risk reduction. For CHF related death/hospitalization, compared tomed tx alone, med tx + resynch had RRR of 34% and med tx + resynch/defib had RRR of 40%. All p-values <0.05.Conclusion: Medical tx plus cardiac resynch/defib significantly decreases all causemortality/hospitalization. The use of resynch has been further validated by the CARE-HF trial (NEJMMarch 7, 2005).

DEFINITE (Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation)NEJM May 20, 2004Design: 458 pts w/ nonischemic cardiomyopathy, NYHA I – III, EF < 35% were randomizedto conventional drug therapy (CDT) vs. CDT + ICDEndpoint: Death from any cause.Results: ICD’s demonstrated a statistically significant reduction of 80% in arrhythmicmortality and a trend (P = 0.08) toward a reduction in all-cause mortality.Conclusion: In pts w/ nonischemic CM, NYHA class I-III Heart Failure, and EF < 35%ICD’s reduce arrhythmic mortality and show a trend toward reducing all-cause mortality.

AFFIRMNEJM 2002;347:1825-33Design: Randomized, multicenter. rhythm vs. rate control in 4060 pts w/ A-fib & highrisk of stroke or death.Rhythm-control: Sole or combination of: amiodarone, disopyramide, flecainide, moricizine,procainamide, propafenone, quinidine and sotalol.Rate-control: Target resting HR: 80 bpm or while walking: 100 bpm. Drugs: b-blockers, CCB, digoxinand combination of these drugs. INR of 2 – 3 maintained.Results: Trend towards increased mortality with the rhythm control strategy (p = 0.8). Torsades,bradycardic arrest, and cardiac related hospitalizations occurred more frequent in rhythm controlgroup.Conclusion: Rhythm controlled atrial fibrillation had more co-morbidities than rate control strategy.Therapeutic anticoagulation should be maintained to avoid risk of CVA.

Lipid Trials: Heart Protection Study (HPS)Lancet 2002 360:7Design: Randomized placebo controlled, 20,536 pts to either simvastatin 40mg qd or placebo.Endpoint: Mortality, fatal or non-fatal vascular events, average follow 5.5 yrsResults: Statin group: 13% reduction all-cause mortality, 24% reduction major CV events, 25%reduction In first stroke. 3982 diabetics without known CAD 28% reduction MI/Stroke. Reductionseen even with LDL<100.Conclusion: For a wide range of high risk populations, 40mg simvastatin reduces rates MI, stroke byabout one quarter irrespective of initial cholesterol concentrations.

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Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL)JAMA March 3, 2004Design: 654 patients randomized in a double-blind study to receive either 40mg of pravastatin or80mg of atorvastatin for 18 months.Results: Significantly lower progression rate in atorvastatin group (p=0.02), mean LDL of 150 reducedto 110 in the pravastatin group and 79 in the atorvastatin group (p<0.001), and CRP decrease 5.2%with pravastatin and 36.4% with atorvastatin.Conclusion: For patients with CAD, intensive lipid-lowering treatment with atorvastatin reducedprogression of coronary atherosclerosis compared with pravastatin.

Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in MyocardialInfarction 22 Investigators (PROVE IT-TIMI 22)NEJM April 8, 2004Design: 4162 pts hospitalized for ACS within the previous 10 days were randomized in a double-blindstudy to receive either 40mg of pravastatin or 80mg of atorvastatin.Endpoint: Death from any cause, MI, unstable angina requiring hospitalization, revascularization(performed at least 30 days after randomization), CVA.Results: Median LDL achieved was 95 in pravastatin group and 62 in atorvastatin group (p<0.001).Primary endpoint reached at 2 yrs in 26.3% of pravastatin group and 22.4% of atorvastatin group;16% reduction in hazard ratio (p=0.005, 95% CI 5-26%).Conclusions: Intensive lipid-lowering therapy (reduction of LDL to levels substantially below targetlevels at time of study) for patients with recent ACS provides greater protection against death ormajor CV events compared to a standard regimen. Intensive Lipid Lowering with Atorvastatin in

Patients with Stable Coronary Disease (TNT)NEJM April 7, 2005Design: 10,001 patients with CHD and LDL less than 130, randomly assigned, double-blind therapy,either 10mg or 80mg of atorvastatin per day, average follow up of 5 years.Results: Mean LDL=77 with 80 mg of atorvastatin , LDL=101 with 10 mg of atorvastatin. Primaryevent in 8.7% of pts receiving 80 mg, as compared with 10.9 % pts receiving 10 mg. ARR of majorCV events of 2.2% and a 22% relative reduction in risk (P<0.001). No difference between the twogroups in mortality. Persistent elevations in liver aminotransferase levels was 0.2 % in the groupgiven 10 mg and 1.2% in the group given 80 mg (P<0.001)

Conclusion: Intensive lipid-lowering therapy with 80 mg of atorvastatin per day in patientswith stable CHD provides significant clinical benefit beyond that afforded by treatment with 10 mg ofatorvastatin per day. Greater incidence of elevated aminotransferase levels.

Other CV/HTN Studies: COURAGENEJM 2007 Apr 12;356(15):1503-16.Design: 2287 pts with objective myocardial ischemia and stable CAD comparing PCI + optimalmedical therapy vs. optimal medical therapy.Results: Primary endpoint of all cause mortality and nonfatal MI, median 4.6 years. PCI group 19% vsmedical therapy group 18.5% (NS). Composite secondary endpoint of death, MI, and stroke 20% vs19.5 % (NS)..Conclusions: As an initial management strategy in patients with stable coronary arterydisease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascularevents when added to optimal medical therapy.

ALLHATJAMA 2002;288:2981-97Design: Double-blinded randomized controlled trial; patients with HTN and 1 other CADrisk factor treated with CCB or ACE-I vs. diuretic (chlorthalidone).Conclusion: There was no significant difference in primary outcomes in the two groups; all causemortality similar between the two groups. However, thiazide diuretics had significantly lower SBPsafter 5yrs. Thiazide diuretics were superior in preventing CAD & should be the FIRST LINEmedication used.

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HOPENEJM. 2000;342(3):145-53Design: Randomized controlled trial; 9297 “high risk” patients NOT known to have a low EF or CHFwere randomized to ramipril vs. placebo.Conclusion: Ramipril reduced the rate of death, MI and stroke in high-risk patients. RR=0.74 for MI;0.68 for stroke; 0.85 for revascularization procedures, 0.63 for cardiac arrest.SAVE study showed captopril reduced all-cause mortality (RRR 17%) and CV morbidity when started3-16 days after MI. RRR in cardiovascular death was 20%. (NEJM. 1992;327:669-77.)SOLVD study showed enalapril given to pts w/ low EF was associated w/ improved survival andslowed progression to decompensated heart failure. HOWEVER, the difference was NOTsignificant. (NEJM. 1991;325:293-302.)

CONCENSUS IINEJM. 1987;316:1429-35.Trial showed that enalapril given within 1 day of MI was NOT associated with a significant survivalbenefit.

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Procedures

CENTRAL VENOUS CATHETERS: AN INTRODUCTION

1. Indications:- continuous hemodynamic monitoring/transvenous pacing- continuous infusions of medications that could induce phlebitis- plasmapheresis/hemodialysis- lack of peripheral IV access

2. General Rules:- visualize anatomy – use portable u/s if possible.- be sterile – gown, gloves, mask/shield, sterile drapes, chlorhexidine.- position the patient – be comfortable.- have everything ready before hand (don’t forget flushes).- small amounts of sedation are OK, local anesthesia is essential- get consent (unless emergent)- if the patient is on the UCSD CCU SERVICE, YOU MUST HAVE FELLOW- SUPERVISION, even if you are signed off.

3. Types of central lines:- Triple Lumen Catheter (TLC) – 3 lumens for multiple drugs.- Cordis – this is a large lumen through which swan-ganz catheters, transvenous pacers, triple

lumens and large volume fluid resuscitation can be passed.- Vascath – these are large bore and for dialysis, they require fellow supervision.

4. Where to go:- Internal Jugular – cleaner, easy to access, low risk of PTX, easy to compress carotid artery if

punctured, but uncomfortable for patient. Excellent for swans and pacers.- Subclavian – cleanest, easy to access, most comfortable for patient but higher risk of PTX

and no ability to compress bleeding. Excellent for swans and pacers. Contraindicated ifcoagulopathic/thrombocytopenic.

- Femoral Vein – easy, especially during CPR, but increased risk of infection, retroperitonealbleed and thrombus formation.

5. Seldinger Technique:After identifying landmarks on a sterile field, the vein is cannulated with a needle and a guidewire is inserted. NEVER let go of the guide wire. The tract is then dilated and a catheterinserted over the guidewire. The wire is removed and the catheter stitched in place.

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INTERNAL JUGULAR VENOUS CATHETER

The IJ vein is internal and anterior to the carotid artery (except in 5-10% of patients therefore, U/Sis a good idea).

1. Positioning: The IJ vein is found at the apex of the triangle formed by the sternal andclavicular branches of the SCM with the clavicle. The carotid is medial to the vein. Tilt thepatient at 15-30% trendelenburg (less chance of air embolism) and turn the head 45 degreesaway from puncture site.

2. Preparation: Clean the site extensively with chlorhexedine. Open the sterile kit and fill thewells with sterile saline for flushes. Gown up and organize your kit by arranging materials,flushing lumens, drawing up lidocaine, etc. Drape your pt.

3. The needle:- Find and maintain continuous palpation of the carotid artery. Liberally inject local anesthetic

at the apex of the triangle. ALWAYS aspirate before injecting to avoid injectinganesthetic/air into the vessel.

- Using a finder needle, angle at 45-60 degrees, and aim toward ipsilateral nipple, advanceand aspirate until you find a flash w/ good flow. If it pulsates or is bright red, that is a badsign.

- Advance the introducer needle directly in front of the finder and aspirate. With good flow,remove the syringe (finger over the needle to prevent air entering) and thread the wire. Don’tforce it and NEVER let go. If the wire passes successfully, remove the needle.

- Enlarge the puncture site with the scalpel (blade away from the wire) and apply pressure withsterile gauze to prevent brisk bleeding. Advance the dilator over the wire, then remove thedilator.

- Thread the catheter over the wire – don’t let go. When in place, remove the wire, aspirateblood from all ports and then flush with sterile saline and suture in place with a 2.0 silksuture. Clean the site and cover with tegaderm.

4. Check a CXR: to confirm the catheter is in the SVC and there is no PTX. Don’t forget to cleanup.

SUBCLAVIAN VENOUS CATHETER

The subclavian vein is below the medial third of the clavicle, coursing just below the bone.

1. Positioning: Tilt the patient at 15-30 degrees Trendelenburg, the vein is found at the junctionof the proximal third with distal two-thirds of the clavicle, aiming toward the sternum. Place arolled up towel between the scapula to lower the ipsilateral shoulder. Preparation: liberallysterilize, local anesthetic – aspirate before injecting. Prep the kit as above.

2. The needle:- Place a finger on the sternal notch, and thumb on the clavicle at the junction between the

medial first third and the outer two-thirds.- Insert the needle 2 cm lateral to the clavicular curve and keep it parallel to the patient’s body

with bevel up. Do NOT enter at a steep angle, keep it low to avoid PTX.- Aspirate and advance by marching down the bone, aiming just above the sternal notch. If no

venous return, withdraw and re-direct.- Use the Seldinger technique to advance the catheter in place.

3. Check the CXR:4. NEVER attempt a line on the opposite side: without checking a CXR and ruling out a PTX

on the first side.5. TIPS: Have an assistant pull down on the ipsilateral arm, this will assist in successfully finding

the vein. Once you have inserted the needle bevel up, rotate the needle 90 degrees caudallyto assist in correct advancement of the wire.

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59

FEMORAL VENOUS CATHETER

The femoral vein is found medial to the artery. Some use the mnemonic NAVEL (from lateral tomedial Nerve, Artery, Vein, Empty Space, Lymphatics).This is opposite to the IJ vein which is lateralto the artery.

1. Positioning: The leg should be slightly abducted and externally rotated.2. Preparation: As above, sterilize well. This is a dirty site.3. The needle:

- Palpate the artery and advance a finder needle (or an introducer) with the other hand at a 45degree angle.

- Do not let go of the artery and continually aspirate as you advance. It can be very shallow(i.e. 2 cm) in thin people.

- If no flash, withdraw the needle slowly, but continue to aspirate – you may have compressedthe vein while advancing. *If you hit the artery, hold pressure for 15-20 minutes.

- With a good flash, use the Seldinger technique as described above. Never advance yourwire against resistance.

REMOVAL OF CENTRAL VENOUS CATHETERS

There is a small, but real risk of introducing an air embolus into the circulatory system any time acentral venous catheter is removed. This can be a fatal event, which is why removal of catheter Isnow also a supervised-to-signed-off procedure.

1. Gather supplies:The leg sterile scissors, gauze, sterile ointment (bacitraicin ointment packswork well), tape, chlorhexadine swabs

2. Positioning: position patient in Trendelenberg position3. Preparation: remove dressing and stitches and swab area with chlorhexadine swab. Squeeze

ointment onto the sterile gauze.4. Instruct patient on Valsalva maneuver (hum or bear down)5. While patient is humming, slowly remove catheter and immediately apply the ointment-laiden

gauze to the exit site and hold pressure6. Dressing should be left in place for 24 hours.

THORACENTESIS

1. Indications: Effusion (unilateral or bilateral but disparate sizes), or febrile, or havingassociated pleurisy. Need >1cm on lateral decubitus to be considered safe to tap. If smalleffusion or loculated consider US guided tap. If presents with CHF, b/l effusions, afebrile andwithout chest pain, may try diuretics first.

2. Contraindications: severe coagulopathy, mechanical ventilation (relative)

3. Positioning: Patient seated upright, bed raised for your comfort.4. Preparation: Review the CXR, percuss the patient. Your site should be 1-2 interspaces

below where the dullness ends and about midway between the spine and the posterior axillaryline. Liberally clean the site and drape the patient. You need a 50ml syringe, 22 g needle 1.5in long and lidocaine for local anesthesia.

5. The needle: After local lidocaine, advance your needle superiorly over the rib (to avoiddamage to the neurovascular bundle) and aspirate.

6. CXR is not required: (only 1 in 488 asymptomatic patients post-thoracentesis had PTX)although usually obtained regardless of the data.

7. Measurements: (patient needs serum LDH and total protein at the same time)- Appearance – bloody effusions concerning for malignancy- Cell count and differential - >10000 wbc usually empyema. >10% eosinophils, consider

trauma but also fungal/tb/parasite/malignancy- Gram stain and culture – can help with antibiotic choice- LDH, protein, pH and glucose to determine exudates vs. transudates- Cytology (need large volume)- at the very least 100 cc

8. Light’s Criteria: (Exudates have one or more of the below (98% sensitive))- fluid/serum protein ratio >0.5- fluid/serum LDH ratio > 0.6- OR fluid LDH >2/3 upper limit of normal- pH usually <7.2 with infection, indicates need for chest tube

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PARACENTESIS

1. Indications: new ascites, refractory ascites, rule-out SBP.2. Positioning: Patient supine in bed, raised for your comfort.3. Preparation: Abdominal wall is thinnest 2 fingerbreadths cephalad & 2 finger breadths medial

to the left anterior superior iliac spine, avoiding large umbilical veins and the large spleen.Sterilize the LLQ with chlorprep or betadine and drape the patient. Prepare your kit.

4. The needle: After injecting a few ml of lidocaine (aspirate first), advance your needle throughthe dermis using the “z”-technique. Lift the skin up to prevent your needle from entering theperitoneum in a straight path more prone to leaks. Withdraw fluid for diagnosis with largesyringe. If doing a large volume tap use the paracentesis catheter in the kit.- If large volume tap, give IV albumin ~8gm/L of fluid removed as may decrease risk of

hemodynamic compromise and acute renal failure.5. Measurements:

- Cell count (purple top): an ANC of greater than 250 is diagnostic of infection.- Chemistries (gold top): Measure albumin (for SAAG) and total protein. LDH, amylase,

and glucose can also be useful. The patient will also need a serum albumin and totalprotein from that same day.

- Gram stain and Culture (red top): At UCSD, send in syringe. At the VAMC, inoculate bloodculture bottles at bedside (increase sensitivity from 50%80%).

- Cytology: This requires large volumes (don’t forget labels)

LUMBAR PUNCTURE

1. Indications: Two out of the three findings: Altered Mental Status, Fever and/or Headache (orany HIV patient with any one of the above).

2. Contraindications: Focal neurological defect (check head CT) or Coagulopathy3. Positioning: Place the patient on their side with legs drawn up and chin to their chest. Raise

the bed for your comfort.4. Preparation: Find your mark – palpate the highest point of the iliac crests and locate the

L3/L4 or L4/L5 vertebral interspace. Liberally sterilize and drape the patient. Prepare your kitby putting together your manometer and arranging your test tubes.

5. The needle: Carefully inject a few ml of lidocaine (always aspirate first). Using your spinalneedle, bevel up, insert between the interspace angling toward the umbilicus and slightlycranially until you feel a pop. Transiently remove the stylet to confirm CSF flow.

6. Lay flat for 6-12 hours and encourage fluid intake to prevent headaches.7. Measurements:

- Opening Pressure: CSF < 15 cm = normal. >20 cm is abnormal.- Color: Should be clear, colorless- Lab analysis: (label your tubes)

- TUBE 1: Cell count (<5 cells, 0 PMNs)- TUBE 2: Glucose and Protein: About 1 ml.

- Normal Glucose: about 2/3 of blood sugar.- Normal Protein: <40. Blood raises protein concentration by 1/1000 RBCs.

- TUBE 3: Culture and gram stain: about 5 ml of CSF; also consider cryptococcalantigen, VDRL, cytology (may require larger volumes), AFB, fungal cultures, India ink,lyme titers, HSV/MTD/EBV/West Nile Virus/JC virus PCR where indicated. Alsooligoclonal bands (requires simultaneous red top tube).

- TUBE 4: repeat cell count, if traumatic, can subtract 1 WBC : 500 RBC

Test Bacterial Viral Fungal Tubercular

Open Pressure Elevated Usually normal Variable Variable

WBC count >=1,000 per mm3 <100 per mm3 Variable Variable

Cell differential PMNs* lymphocytes† lymphocytes lymphocytes

Protein Mild to marked elevation Normal to elevated Elevated Elevated

CSF-to-serumglucose ratio

Normal to markeddecrease

Usually normal Low Low

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SUBACROMIAL INJECTION

1. Indications: For symptomatic relief of pain from rotator cuff tendonitis, subacromial bursitis, orimpingement syndrome.

2. Contraindications: Absolute: severe coagulopathy, overlying cellulitis, allergy to injectables,joint replacement, fracture, septic joint- Relative: bacteremia, out of control diabetes, supratherapeutic INR

3. Informed Consent: Discuss risks including infection (~1:10,000), bleeding, no improvement,tendon/ligament rupture, steroid flare, skin/soft tissue depigmentation and atrophy. Havepatient sign consent

4. Positioning: Patient seated on exam table with shirt off5. Preparation: Palpate the spinous process of scapula until you reach the posterolateral corner

of the acromion. Mark your site 1cm below this posterolateral corner with cap of needle. Cleansite with 3 betadine swabs and an alcohol swab. For injection mix ~4 cc of anesthetic (1%lidocaine without epi or 0.25% marcaine) with 1cc (40mg) kenalog or equivalent steroid.

6. Procedure: After spraying ethyl chloride (optional), advance your needle into the markedspace usually all the way to the hub of the needle. Angle the needle towards the coracoidprocess and slightly up, just under the acromion. When injecting you should not encounterresistance, which could indicate you are in a tendon. Reposition the needle and re-inject.Remove needle and apply pressure with gauze. Apply bandaid.

7. Post-injection instructions: Inform patient to contact you if develop fevers, chills, erythema atinjection site or severe pain. The cortisone typically takes 3 days to take effect

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KNEE ASPIRATION/INJECTION

1. Indications: For diagnosis of septic joint, gout or hemarthrosis. For symptomatic relief of painfrom osteoarthritis, gout, bursitis.

2. Contraindications: Absolute: severe coagulopathy, overlying cellulitis, allergy to injectables,joint replacement, fracture, septic joint (for steroid injection)- Relative: bacteremia, out of control diabetes, supratherapeutic INR

3. Informed Consent: Discuss risks including infection (~1:10,000), bleeding, no improvement,tendon/ligament rupture, steroid flare, skin/soft tissue depigmentation and atrophy. Havepatient sign consent

4. Positioning: Patient seated upright with knees dangling (injection), or patient lying supine(aspiration or injection).

5. Preparation: Mark your site with cap of needle. For seated patient the space between thefemoral condyle, tibial plateau, patellar edge and patellar tendon either medially or laterally.For supine patient just under superolateral or supermedial patella. Clean site with 3 betadineswabs and an alcohol swab. For aspiration you need several 20 cc syringes and at least a 22gauge, 1 ½ inch needle. For injection mix ~4 cc of anesthetic (1% lidocaine without epi or0.25% marcaine) with 1cc (40mg) kenalog or equivalent steroid.

6. Procedure: After spraying ethyl chloride (optional), advance your needle into the markedspace and aspirate. For sitting patient the needle should be parallel to the floor and usually nofluid is able to be aspirated. For supine patients remember the angle of the patellar facetswhen introducing the needle. If performing injection you should not encounter resistance wheninjecting the fluid. Remove needle and apply pressure with gauze. Apply bandaid.

7. Post-injection instructions: Inform patient to contact you if develop fevers, days to takeeffect.

8. Measurements:- Cell count and differential- Gram stain and culture – can help with antibiotic choice- Crystal analysis

9. Joint Fluid Analysis:

Test Normal Non-inflam

Inflam Sepsis Crystal Hemo

Clarity Clear Slightlyturbid

Turbid Turbid Turbid Bloody

Color Yellow Yellow Yellow Gray/green

Yellow-milky

Red/Brown

Viscosity High Reduced Low Low Low Reduced

WBC/uL 0 - 200 0 - 2000 2000 -100,000

>50,000 500 -200,000

50 -10,000

%Polys <25 <30 >50 >90 <90 <50

Glucosedifference

0 - 10 0 -10 0-40 20-100 0-80 0-20

Crystals Absent Absent Absent Absent Present Absent

Culture Sterile Sterile Sterile Positive Sterile Sterile

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INFECTIOUS DISEASE

FEVER

1. Basic Concepts:- Defined variably as >38.5C (101.3F), unless immunosuppressed or neutropenic then asingle measurement >38.3C (101F) or >38.0C (>100.4F) over 1 hour.- Assess current and past antibiotic use.- Identify most likely source (GI vs. pulmonary vs. line vs. GU vs. CNS, etc.)- Differential is broad: infection (as above also sinus, decub ulcers, etc) vs. drug fever vs.autoimmune vs. neoplasm vs. PE/DVT.

2. Physical Exam: Vitals for hypotension, tachycardia, tachypnea, lung exam, oropharynx, lymphnodes, abdominal exam, decubs, check all lines.

3. Workup: CBC with diff, UA (eos, sediment), blood cultures x 2 BEFORE antibiotics (usuallydon’t need to repeat within 24-48hrs), urine cultures, CXR; consider sputum culture, LP, stoolstudies if clinically indicated. Consider upgrading level of care to DOU etc if patient meetingmultiple SIRS criteria or septic

4. Intervention: based on workup, but for unstable patients cover broadly AFTER blood cultures.Consider nosocomial pathogens if patient has been in house >3 days. If patient on antibiotics,get cdiff toxin along with stool cultures. If patient has been on broad spectrum antibiotics,consider fungal infections and get fungal blood cultures.- Note, for fever spike through antibiotics consider:

- Drug failure (not susceptible)- Development of resistance in previously susceptible organisms- Drug fever-

5. Neutropenic Fever (ANC <500): see Heme/Onc section. Treatment usually 3rd generationcephalosporin with pseudomonal coverage (eg Ceftaz) +/- Vancomycin (nearly always in our ptpop) if suspect line infection or colonization with MRSA. May consider adding Gentamicin forsynergy.

CLINICAL PEARLS

1. The way to think about antibiotics is to always ask yourself this question- “What organisms Inot covering with this antibiotic regimen?”

2. Review: Pathology and films yourself3. Find the Source: Cornerstone of effective infectious disease management is source control:

remove the foreign body ie infected line, even if it’s a tunneled catheter, drain the infected fluid,debride the infected tissue. Staph aureus and candidal line infections usually require removal.

4. Antibiotics are NOT antipyretics5. Treat the patient: NOT the culture. For example, positive sputum culture does not equal

clinical PNA. Also, in the absence of neutropenia, + UA without pyuria excludes a UTI.6. Antibiotic Misconceptions: IV vancomycin does not work for C. difficile colitis. Vancomycin is

not the best drug for MSSA and should not be used except in the setting of beta lactamallergy. Cephalosporins are safe in PCN allergies, unless there is a history of anaphylaxis.

7. Complex Regimen = Complex Change: Never add one drug to failing regimen (eg TB, HIV).8. Approach to Endocarditis: If you suspect BE get blood Cx before Abx. A negative TTE does

not rule out endocarditis (sensitivity ~50%). Aminoglycosides have no impact on the mortalityof Staph aureus bacteremia/endocarditis but they do decrease the duration of bacteremia solimit treatment to 14 days.

9. Candida as a Pathogen: Not in the sputum or bronch washes. Usually not in the urine(exceptions are renal transplant, stents, pyelonephritis). Candidemia requires catheterremoval, evaluation by Ophthalmology for retinal disease/endophthalmitis, and antifungaltherapy.

10. Hospital acquired infections due to gram negative bacteria are bad news. These organisms arehighly efficient at up-regulating or acquiring genes that code for mechanisms of antibiotic drugresistance, especially in the presence of antibiotic selection pressure. Furthermore, they haveavailable to them a plethora of resistance mechanisms, often using multiple mechanismsagainst the same antibiotic or using a single mechanism to affect multiple antibiotics Seerecent review, NEJM May 13, 2010 for details.

11. Community Acquired MRSA is bad news, just like hospital acquired MRSA. See review inLancet, May 1, 2010

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MENINGITIS

If you're worried about meningitis to treat it, attempt to obtain a sample of CSF after CT head if safe.

1. Common Bacterial Pathogens:- 16-50yo N meningitides, Strep pneumo- >50yo S pneumo, N meningitides, Listeria monocytogenes, Aerobic gram negative Bacilli

2. Antibiotics:- vancomycin + 3rd gen cephalosporin for pts 16-50yrs- add ampicillin for >50yrs or HIV+

3. Decadron: initiate with or prior to first dose of abx (10mg q6) and continue for 4 days.- Unclear benefit if started after the first dose of abxs; and no clear benefit in fungal meningitis

4. Fungal Meningitis: Crypto, Cocci, Histo in HIV or other immunocompromised patients.- For Crypto: 2 week induction with 5FC and Amphotericin B( with aggressive hydration and

premedication or liposomal preparation) followed by prolonged course of oral fluconazole.5. TB Meningitis: adjunctive Rx w/ IV decadron (0.4mg/kg x wk1, 0.3mg/kg x wk2, 0.2mg/kg x

wk3, and 0.1mg/kg x wk4, then po decadron taper) reduced mortality (RR 0.69).6. Nosocomial bacterial meningitis may result from invasive procedures (e.g., craniotomy,

placement of internal or external ventricular catheters, lumbar puncture, intrathecal infusions ofmedications, or spinal anesthesia), complicated head trauma, or in rare cases, metastaticinfection in patients with hospital-acquired bacteremia. January 14, 2010 NEJM

References: NEJM 2006;354:44-53, NEJM 2004;351:1741-1751

PNEUMONIA

1. Basic Concepts:- Pneumonia is one of the most common conditions you will see on the inpatient medical

wards and in the ICU. Over 1 million patients are hospitalized with pneumonia annually in theU.S., and it is the most common infectious cause of death.

- Pneumonia is not as simple as it used to be. Antibiotic therapy needs to be tailored to thepatient’s specific risks/comorbidities. Getting initial empiric antibiotic selection right isCRITICAL, as inpatient mortality rates more than double when antibiotic selection is notconsistent with guidelines, and 30-day mortality increases by a factor of 5.

- Pneumonia comes in several flavors: community-acquired (CAP), hospital-acquired (HAP),ventilator-associated (VAP), and healthcare-associated (HCAP). HAP, VAP, and HCAP areall treated the same, and require broader spectrum antibiotics than CAP. The definitions ofHAP and VAP are fairly self-explanatory, so we will focus on distinguishing CAP from HCAP,and the special circumstances of CAP treated in the ICU.

Apart from being associated with increased morbidity and mortality, suspected hospital-acquired pneumonia in the ICU can lead to the inappropriate use of antibiotic drugs,contributing to bacterial drug resistance and increases in toxic effects and health care costs.NEJM 5/13/10

- If you are too busy to read the rest of this section, all you really need to know is contained inthe PNEUMONIA ORDERSET on EPIC. If you use this to order antibiotics for all yourpneumonia patients you will get it right every time. (OK, it doesn’t work for specialcircumstances like TB or PCP…) The orderset is intended to speed the process of orderingtreatment for pneumonia patients, and its use is STRONGLY ENCOURAGED.

2. Community acquired pneumonia (CAP): pneumonia occurring the outpatient setting > 90days after a hospitalization and not meeting the criteria for healthcare associated pneumonia- Usual etiology: Streptococcus pneumonia, H. influenza, other gram negatives, atypical

(Mycoplasma, Chlamydia, Legionella), viral- Recommended treatment:- Non-ICU:

- 3rd generation Cephalosporin (e.g. Ceftriaxone) PLUS Macrolide (e.g. Azithromycinor doxycycline)

OR- Respiratory Fluoroquinolone (e.g. Moxifloxacin)

- ICU:- 3rd generation Cephalosporin (e.g. Ceftriaxone) PLUS Macrolide (e.g. Azithromycin)

or respiratory fluoroquinolone (e.g. Moxifloxacin)

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3. Healthcare associated pneumonia (HCAP): pneumonia occurring in any patient:- Hospitalized in an acute care hospital for > 2 days within 90 days of the infection- Residing in a SNF or long-term care facility- Receiving intravenous antibiotic therapy, chemotherapy, or wound care within the past 30

days of the current infection- Attending a hospital or hemodialysis clinic within the past 30 days- Family member with multidrug-resistant pathogen

- Usual etiology: Streptococcus pneumonia, enteric gram negatives, MSSA/MRSA, ESBLproducing gram negative rods, Pseudomonas, Acinetobacter

- Recommended treatment: Should cover MRSA and include 2 antipseudomonal agents- Vancomycin PLUS Piperacillin/tazobactam PLUS Ciprofloxacin

OR- Vancomycin PLUS Aztreonam PLUS Ciprofloxacin (if Penicillin Allergic)

4. Ventilator associated pneumonia (VAP): pneumonia occurring > 48-72 hr after endotrachealintubation and mechanical ventilation.- Recommended Treatment: Same as HCAP

5. Risk factors for multidrug-resistant (MDR) pathogens:- Antimicrobial therapy in last 90 days- Current hospitalization ≥ 5 days - High frequency of antibiotic resistance in community or hospital unit- Any of the HCAP criteria- Immunosuppressive disease or therapy

6. Consider ICU Admission in CAP if the patient has either:- One of the major criteria:

- Need for invasive mechanical ventilation- Septic shock with the need for pressors

- Three of the minor criteria:- Respiratory rate ≥ 30 or PaO2/FiO2 ≤ 250 or NIPPV - Multilobar infiltrates on CXR- Confusion or disorientation- Uremia (BUN ≥ 20 mg/dL) - Leukopenia (WBC < 4000) as a result of infection alone- Thrombocytopenia (platelets < 100,000)- Hypothermia (T < 36ºC)- Hypotension requiring aggressive fluid resuscitation

7. Other tips on pneumonia:- Whenever possible, obtain blood and sputum cultures, especially for HCAP/VAP/HAP. If

positive, it will allow you to narrow antibiotic therapy.- More commonly cultures will be negative or unobtainable. In that case, it is usually safe to

narrow antibiotic therapy for patients with HCAP who have achieved clinical stability.CLINICAL JUDGMENT is imperative here as there are no evidence-based guidelines.

- Patients rarely decompensate due to their pneumonia once they achieve clinical stability.There is no benefit to inpatient observation of a stable patient just to ensure they tolerate atransition from IV to oral antibiotics.

- Although important, obtaining blood and sputum cultures should not delay antibioticadministration. In general the yield of cultures is low, and delays in antibiotic administrationincrease mortality.

-In patients crashing on the floor with a suspected pneumonia versus volume overload, weoften simultaneously diuresis the patient if their vitals and renal function can handle it

Consider Influenza. Infection with the 2009 H1N1 virus caused a broad spectrum of clinicalsyndromes, ranging from afebrile upper respiratory illness to fulminant viral pneumonia.- May6, 2010 NEJM

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8. Quality control: National Pneumonia Project: www.nationalpneumonia.org- Abx given within 4hrs after arrival to ED was associated w/ reduced length of stay, 17%

reduction in mortality- Blood cultures before Abx.- Blood cultures within 24 hrs of admission or transfer to ICU.- Oxygen assessment- Antibiotic selection: consider hospital-acquired pneumonia in pts w/ recent previous

hospitalization(<90days) and fungal/PCP in immunocompromised.- Vaccination – pneumovax and influenza vaccine – prior to discharge.- Smoking cessation counseling, if appropriate- If indicated, urine antigen tests for Legionella pneumophila and S. pneumoniae (all common

serotypes). Both tests are specific but not completely sensitive.- PCP:

- Silver stain (cytology) of induced sputum (sensitivity 50% in HIV patients) orbronchoalveolar lavage (BAL); must fill out paper requisition.

- TMP-SMX always the first choice. If pt has sulfa or septra allergy, can use clinda +primaquine or IV pentamidine. If severe PCP, consider desensitization for septra (askpharmacist).

- Prednisone if paO2<70 or A-a grad >35 in RA ABG.40mg bid x 5 days, 40mg qday x 5days, then 20mg qday to complete 21 day course.

- Nasal swab or wash for influenza antigen. Most sensitive <48 hours- AFB smears and culture of sputum to diagnose Mycobacterial infections. If there is a +

smear, do a PCR assay to rule-out TB. All HIV+ patients should have a sputum PCR sent inaddition to 3 smears. Once positive TB identification, TB cultures can be repeated every 2weeks until negative.

- At VA: send one sputum q8h x 3 (one must be a morning sample).- At UCSD: send daily sputum x 3 days.

References: American Thoracic Society and Infectious Diseases Society of America. “Guidelines forthe Management of Adults with Hospital-acquired, Ventilator-associated, and Healthcare-associatedPneumonia.” Am J Respir Crit Care Med 2005; 171: 388-416. Infectious Diseases Society of Americaand American Thoracic Society. “Consensus Guidelines on the Management of Community-AcquiredPneumonia in Adults.” CID 2007; 44(Suppl 2): S27-72. Gilbert DN, et al. “The Sanford Guide toAntimicrobial Therapy 2007.” 37th ed. Antimicrobial Therapy Inc. 2007: 85-92. Arch Intern Med 2004;164:637–644 85-92. Arch Intern Med 2004; 164:637–644

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LINE ASSOCIATED INFECTIONS

Non-tunneled central venous catheters

Tunneled central venous catheters and implantable devices

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UTI

Tips: Never Collect urine for culture from a drainage bag. If a patient cannot provide a clean catch

specimen, catheterize the patient to obtain the urine. If a urine specimen is obtained from aurinary catheter - label it.

In men there are no guidelines for interpreting colony counts and the isolation of potentialurine pathogens in any number should be regarded with suspicion.

In women, a voided urine should have <104 CFU/ml; values greater than that are abnormal.However, you should not diagnose and treat urinary tract infections in patients with normal UA,as the culture results are either false positives or the patient has asymptomatic bacteriuria. Acatheterized urine should be sterile.

Pathogenic Organisms by Gram Stain

Gram Positive Cocci

in clusters - Staphin chains - Strep

Staph epi (coagulase negative)Staph aureus (coagulase positive)Strep pneumo (ovals in pairs)-hemolytic strepie, viridans, salivarius-hemolytic strepGroup A strep (this is what rapid streptests look for…)Group G strepGroups C, D, E, F, GEnterococcus species (also Group D)

Faecalis (sensitive to ampicillin)Faecium (resistant to ampicillin)

Gram Negative Cocci

Neisseria gonorrheaeMoraxella catarrhalis

(both are aerobic diplococci)

Gram Positive Rods

Actinomyces species*Bacillus anthracisClostridium species*Corynebacterium diphtheriaeListeria species (-hemolytic)Nocardia species (branching)Diphtheroids species (both aerobic andanaerobic)

*Anaerobic organisms

Gram Negative Rods

Escherichia coliProteus speciesKlebsiella speciesEnterobacter speciesCitrobacter species

Pseudomonas aeruginosaSalmonella speciesShigella speciesAcinetobacter species (coccobacillus)Haemophilus influenzaBordetella pertussisVibrio cholerae (comma shaped)Campylobacter species*Bacteroides species*Yersinia species

Brucella species*Pasteurella multocidaFrancisella species

Zoonoses

Coliform

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HIV

Guidelines for treatment of HIV change rapidly; up-to-date information may be obtained from:http://AIDSinfo.nih.gov

1. Indications for ARV*:- Any pt. with AIDS-defining illness or HIV nephropathy regardless of CD4 count (AI)- Asymptomatic patients with CD4 T cells <350 (AII)- Pregnant women (AI)- HBV coinfection when treatment for Hepatitis B is indicated (BIII)

- Regimen must include TDF and either FTC or 3TC- Consider ARV for asymptomatic patients with CD4 T cell counts >350 who also have plasma

HIV RNA >100,000 or rapid decline in CD4 count (>120 cells/mm3/annum)- Defer ARV for patients with CD4 T cell counts >350 and plasma HIV RNA <100,000.

*Delay initiation of HAART 2-8 weeks in setting of TB (BIII), PCP, MAC, or CM (CIII)

2. NNRTI-Based Regimens (1 NNRTI + 2 NRTIs):- Preferred NNRTI (AII):Efavirenz (except during 1st trimester of pregnancy or in women

w/high pregnancy potential*)- Alternative NNRTI (BII Nevirapine may be used as an alternative in adult females w/CD4 T

cell counts</=250 and adult males with CD4 T cell counts </= 400. Increase risk of hepatitiswhen Nevirapine is given to women whose CD4>250 and men whose CD4 >400.

- Women with high pregnancy potential are those who are trying to conceive or who aresexually active with men and not using effective and consistent contraception.

3. PI Based Regimens ( 1 or 2 PI’s + 2 NRTI) (alphabetical):

Preferred PIs: Alternative PIs (BII):atazanavir + ritonavir* (AIII) atazanavir**fosamprenavir + ritonavir* q 12 hrs(AII) fosamprenavirlopinavir/Ritonavir (Kaletra) q 12 hrs(AII) fosamprenavir + ritonavir* q daylopinavir/ritonavir (kaletra) q day saquinavir + ritonavir

- Ritonavir @ daily doses of 100 – 400 mg used as a pharmacokinetic-booster- Ritonavir 100 mg q day must be given when tenofovir or efavirenz is used with atazanavir.

4. Dual-Nucleoside Options as Part of Initial Combination Therapy:- Preferred dual NRTI (AII) (alphabetical)

- Abacavir/lamivudine (Epzicom)*(co-formulated) (in patients negative for HLA-B*5701)- Tenofovir/emtricitabine (Truvada)* (co-formulated)- Alternative dual-NRTI (BII) (in order of preference)- Zidovudine/lamivudine (Combivir)* (co-formulated)- Didanosine + (lamivudine or emtricitabine)

5. Drug Interactions:- PI: PIs are metabolized in the liver by the cytochrome P450 CYP 3A4. There are numerous

drugs with significant interactions with PIs. A few of the examples include statins, benzos,calcium channel blockers, cyclosporine, tacrolimus, dilantin, rifamycins, erectiledysfunction medications (eg. viagra), azole antifungals, macrolides, oral contraceptives(OCPs) and methadone.

- NNRTI: NNRTIs are substrates of CYP3A4 and in some cases are also inducers(nevirapine) or a mixed inducer and inhibitor (efavirenz).

- NRTI: NRTIs do not undergo metabolism through the CYP pathway. Beware ofinteractions.

- Zidovudine and ganciclovir or valganciclovir: additive bone marrow suppression- Zidovudine and Ribavirin: severe anemia may occur- Zidovudine and stavudine: Do not use together – pharmacologic antagonism- Tenofovir and Didanosine: Increased levels of Didanosine (adjust ddI dose)- Atazanavir and Tenofovir: Decrease levels of Atazanavir (interaction can be

overcome with addition of ritonavir)- Cidofovir/foscarnet/Amphotericin B/Aminoglycosides and Tenofovir: watch for renal

toxicity

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- CCR5 Antagonists: Maraviroc is metabolized by CYP 3A4. Requires decreased dosingwhen given with 3A4 inhibitors (eg ritonavir), and increased dosing when given with 3A4inducers (eg rifampin).

*Web Site for HIV drug interactions: HIVinsite.org and search for drug interactions.

References: Guidelines for the Use of Antiretroviral Agents in HIV-1 Infected Adults and Adolescents,Oct 10,2006. Benson CA, Kaplan JA, Masur H, Pau A, Holmes KK. Treating Opportunistic Infectionsamong HIV-Infected Adults and Adolescents: Recommendations from CDC, the National Institutes ofHealth, and the HIV Medicine Association/Infectious Diseases Society of America. Clinical InfectiousDiseases 2005;40:S131-235.

OPPORTUNISTIC INFECTION: PRIMARY PROPHYLAXIS

CD4 Count Pathogen Primary Regimen AlternativeRegimen

When to DC

<200/mm3 Pneumocystisjiroveci

TMP/SMX DS160 mg trimethoprim/800 mgSulfamethoxazole1 tablet q 24 hrsORTMP/SMX SS80 mg trimethoprim/400 mgSulfamethoxazole1 tablet q 24 hrs

Dapsone100 mg q 24 hrsORDapsone 100 mg q 24 hrs ANDPyrimethamine 50 mg q wk ANDleucovorin 25 mg po q wkORAerosolized Pentamidine300 mg q month via Respirgard IInebulizerORAtovaquone susp 1500 mg po q 24hrs.OR TMP/SMX DS 3X/wk

DC prophylaxiswhen CD4 >200for > 12 wks inresponse toHAART

< 100/mm3 ToxoplasmaGondii

TMP/SMX DS160 mg trimethoprim/800 mgSulfamethoxazole1 tablet q 24 hrs

Dapsone 50 mg q 24 hrs ANDPyrimethamine 50 mg q wk ANDleucovorin 25 mg q wkORMepron/Atovaquone susp750 mg q 6-12 hrs ANDPyrimethamine 25mg q24 hrs ANDleucovorin 10 mg q 24 hrs.

DC prophylaxiswhen CD4 >200for >12 wks inresponse toHAART

< 50/mm3 Mycobacterium Aviumcomplex

Azithromycin1200 mg q wkORClarithromycin500 mg q 12 hrs

Rifabutin 300 mg q 24 hrs DC prophylaxiswhen CD4 >100for 12 wks inresponse toHAART

< 50/mm3 CMV Valganciclovir 900mg q 24 hrs* Ophthalmic exam q3 mos to r/o CMVretinitis* May elect to followpts closely withoutprophylaxis (this iswhat we do at Owen)* Considerprophylaxis for highrisk groups: Gaymen: 35% risk, +plasma CMV PCR:43% risk

Ganciclovir 1 gm q 8 hr DC prophylaxiswhen CD4 >100 –150

Any CD4cell count

Mycobacteriumtuberculosis

Isoniazid 5 mg/kg q24 hrs (max 300 mgq 24 hrs)ANDPyridoxine (B6) 50mg po q 24 hrs X 9months

Rifampin 600 mg q24 hrs for 4monthsORRifabutin 300 mg q 24 hrs for 4months

*TBTC 26 is a multicenterrandomized study comparing dailyself administered INH 300 mg for 9months to Isoniazid 900 mg q wkAND Rifapentine 600 mg q wk for 12wks. Trial includes HIV+ and HIV-patients. Call Peach Francisco @543-7719 to enroll

NA

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OPPORTUNISTIC INFECTION: SECONDARY PROPHYLAXIS

Pathogen Regimen When to DC

Candida: frequent orsevere recurrences oforopharyngeal OResophageal candidiasis

Fluconazole 100 – 200 mg q 24 hrs Suppressive therapy should be balancedwith risk of fluconazole resistantcandidiasis, costs and severity/frequency ofcandidial infections.

Coccidioidomycosis Fluconazole 400 mg q 24 hrsOR Itraconazole 200 mg q 12 hrs(Liquid formulation is preferred)

Lifelong suppression required regardless ofCD4 count

Cytomegalovirus Retinitis(CMV)

Valganciclovir 900 mg q 24 hrs DC prophylaxis when CD4 >100-150for 6 monthsAND No evidence of CMV diseaseAND Ophthalmic exam w/o active disease

Cryptococcus Fluconazole 200 mg q 24 hrs. CD4 cell count > 100-200 X 6 monthsAND Pt has completed initial therapy

Histoplasmosis Itraconazole 200 mg q 24h(Liquid formulation is preferred)

Consider when CD4 >150AND s/p 12 months of anti-fungal therapyAND 6 months of ARV’s

Mycobacterium aviumcomplex(MAC)

Clarithromycin 500 mg q 12 hrs ANDEthambutol 15 mg/kg q 24 hrsPlus/minus Rifabutin 300 mg q 24 hrs.ORAzithromycin 500 mg q 24 hrs ANDEthambutol 15 mg/kg q 24 hrsPlus/minus Rifabutin 300 mg q 24 hrs.

CD4 cell count > 100 for 6 monthsAND s/p 12 months of MAC therapyAND Pt is clinically asymptomatic

Pneumocystis jiroveci(PCP)

Same as primary prophylaxis CD4 cell count >200 for > 12 wks

Toxoplasma gondii Same as primary prophylaxis CD4 > 200 for 6 monthsAND s/p Treatment for Cerebraltoxoplasmosis

OPPORTUNISTIC INFECTION: TREATMENT

Pathogen/Disease Preferred Regimen Comments

Esophageal Candidiasis Fluconazole 100 - 400 mg q24h x 14-21d Nystatin or Clotrimazole for oral candida;Consider endoscopy if no improvement in7 – 10 days

Coccidioidomycosis Itraconazole* 200mg BID OR Fluconazole 400-800mg;Ampho B 0.7-1mg/kg/d for disseminated diseaseFluconazole 800mg daily for CNS disease*Liquid formulation preferred

Ampho B in preganancy or if life-threatening disease; Intrathecal Ampho Bmay be needed in refractory CNS cases;Itraconazole preferred for non-CNSdisease by some experts

Cytomegalovirus (CMV)* Valganciclovir 900mg PO BID x3 wks then 900mg daily +/- ocular implant (retinitis);Ganciclovir 5mg/kg IV q12h PLUS Foscarnet90mg/kg IV q12h for encephalitis/myelitis

Treatment varies by site and severity ofinfection; no RCTs to validatecombination therapy in CNS disease,typically 3 weeks induction then maint.

Cryptococcus neoformansmeningitis*

Amphotericin B Liposomal complex 4mg/kg/d IVAND Flucytosine 25 mg/kg PO q6h x 14d; thenFluconazole 400 mg PO daily x 8 – 10 weeks;then 200 mg PO daily

If OP >25 cm H2O, take off CSF untilpressure decreases by 50% and do dailytherapeutic LP until OP <20 cm x2-3d.Consider following flucytosine levels,peak <100 µg/mL to minimize toxicity.Steroids not indicated in routine CM.

Histoplasma capsulatum Itraconazole* 200mg TID x3 d then 200mg BIDx12w;Amphotericin B 0.7 mg/kg IV q24h for severedisease until stable, then Itraconazole as above*Liquid formulation preferred

Itraconazole preferred over fluconazoleunless CNS disease, where 800mg/dfluconazole should follow 12-16 weeks ofAmpho B 0.7mg/kg IV q24h

Mycobacterium aviumcomplex (MAC)

Clarithromycin 500 mg q 12 hrs (AI) orAzithromycin 500 mg q 24 hrs (AII) ANDEthambutol 15-25 mg/kg q 24 hrsPlus/minus Rifabutin 300 mg q 24 hrs

Fluoroquinolone or amikacin may beadded in refractory cases. Cautionrifabutin interaction with ARVs; dose-adjustment of rifabutin may be necessary.

Pneumocystis jiroveci (PCP)* TMP/SMX 5mg/kg IV/PO q8 hours x 21 d.OR Pentamidine 4mg/kg IV dailyOR TMP 5mg/kg q8 plus Dapsone 100mg dailyOR Clindamycin 1.8-2.4 g/d PO/IV plusprimaquine 30 mg base/d PO

TMP/SMX preferredAdd prednisone if paO2<70 or A-a grad>35 in RA ABG. 40mg bid x 5 days, 40mgqday x 5 days, then 20mg qday tocomplete 21 day course.

Toxoplasma gondiiencephalitis

Pyrimethamine 200mg x1 then 75 mg/d ANDLeucovorin 10-20 mg/d AND Sulfadiazine 1.5gq6h x 6 weeks then ½ dose x 6 wks

Decadron if significant mass effect;treatment often empiric, consider biopsy ifno improvement in 1-2 weeks

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ANTIBIOTICS

Antibiotic Mechanism StaticorCidal

Spectrum Toxicities Common Clinical/EmpiricUsages

Vancomycin Inhibitspeptidoglycanchain formationin bacterial cellwall

cidal MRSA, MSSA,strep,enterococcus

Fever, chills, rash, nephrotoxicity(extremely rare), but vanc must berenally adjusted to avoid such thingsas ototoxicity. Redman syndromevery common with rapid infusion –infuse over 1-2 hrs

IV empiric therapy anyinfection requiring IV abx inwhich MRSA is suspected.Empiric oral therapy forrefractory C. dif or empiricallyin very old or very ill.

Nafcillin/Oxacillin

Inhibitscrosslinking ofpeptidoglycanchains, β-lactamaseresistant

cidal MSSA, strep All β-lactams may cause: GI UpsetHypersensitivity, Anaphylactic shock(rare), hepatic, hematologic andneurologic abnormalities .Nafcillin may cause neutropenia orinterstial nephritis.

IV therapy for MSSAbacteremia/endocarditis, MSSApneumonia, osteomyelitis, orMSSA skin infections.

Ampicillin/Amoxicillin

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall.

cidal Strep,enterococcus,Listeria,Menningococcus,M. catarrhalis, H.flu

HypersensitivityAnaphylactic shockGI upsetCandidiasis, TEN, Liver/Hematologicabnormalities, renal adjustment isnecessary

Ampicillin in meningitis iflisteria is suspected

Amoxicillin in sinusitis, otitismedia, or UTI with sensitiveorganisms, (must be taken q8h)

Augmentin(Amox/clavulanatic acid)

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall.Beta-lactamaseinhibitor:irreversiblybinds to beta-lactamases

cidal Strep,enterococcus,MSSA, listeria,many non-resistant GNRs,anaerobes

Similar to other β-lactams Extended courses may cause C. Dif

Sinusitis, UTIs, PNA withsensitive organism

Zosyn(Piperacillin/tazobactam)

β-lactam: Inhibitssynthesis of cellwallBeta-lactamaseinhibitor:irreversiblybinds to beta-lactamases

cidal Strep, MSSA,enterococcus,resistant GNRs,anaerobes

Diarrhea, GI upset, headache,candidiasis,

C. dif colitis

Empiric therapy forhospital/healthcare associatedpneumonia.

Carbapenems

Reuire IDapproval

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall

cidal Strep, MSSA,resistant GNRs,anaerobes

Similar to other β-lactams Infections with extended spectrum β-lactamase producing (ESBL) GNRs, includingmeningitis

1st

GenerationCephalosporin

CefazolinCephalexin

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall

Cidal Strep/MSSA (notgenerally drug ofchoice), some E.Coli, Klebsiella,and Proteus

Similar to other β-lactams Skin infections with strep/MSSA (although keflex isnot as effective against MSSA)

3rd

GenerationCephalosporin

CeftriaxoneCeftazidime

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall

Cidal CFT- strep,MSSA, most non-resistant GNRs ,oral anaerobesCTD- expandedcoverage ofpseudomonas,less effectiveagainst strep andMSSA

Similar to other β-lactams: Remember people on these drugs forextended periods need to bemonitored with periodic CBCs andliver panels.

CFT-empiric therapy for:Community acquiredpneumonia (with macrolide),UTIs/Pyelo requiring IV abx,MeningitisSBPCTD-Empiric therapy forSuspected pseudomonas

4th

GenerationCephalosporin

β-lactam: Inhibitssynthesis ofpeptidoglycanlayer ofbacterial cellwall

Cidal Strep, MSSA,many resistantGNRs, oralanaerobes

Similar to other β-lactams Infections with extended spectrum β-lactamase producing (ESBL) GNRs, includingmeningitis

Aztreonam Inhibitsmucopeptidesynthesis inbacterial cellwall

cidal GNRs Elevated LFTs, C. dif colitis, GIupset, hypersensitivity

Use for resistant GNRinfections when there is a trueβ-lactam allergy

Ciprofloxacin Inhibits DNAgyrase

cidal Non-resistantGNRs

Most frequent:CNS toxicity, GI upset.

Good choice for UTIs (although>20% E. Coli now resistant),often paired with metronidazoleas empiric therapy of entericinfections

Moxifloxacin Inhibits DNAgyrase andtopoisomerases

cidal Strep, non-resistant GNRs,oral anaerobes

Most frequent:CNS toxicity, GI upset. Rememberquinolones can also cause QTprolongation.

Empiric therapy for CAP(penetrates excellently intolungs and urine; but not FDAappeoved indication

Antibiotic Mechanism StaticorCidal

Spectrum Toxicities Common Clinical/EmpiricUsages

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Aminoglycocide

GentamicinAmikacinTobramycin

Blocks proteinsynthesis bybinding to 30Ssubunit ofbacterialribosome

cidal Primarily for mostGNRs includingpseudomonas;adjunctive therapyfor complicatedMSSA infectionsand used forenterococcalinfectionscombined with acell wall inhibitor

Most frequent: AuditoryNeurotoxicity, CNS Toxicity,Nephrotoxicity (cumulative effect, Ingeneral, one dose of AG does not domuch harm to kidneys), Ototoxicity,Renal Disease

Empiric therapy for in whichpseudomonas is possiblepathogen, GU infections if thereis allergy to alternative.

Also used synergistically forgram-positive bloodstreaminfections

Macrolides

AzithromycinClarithromycinErythromycin

Binds reversiblyto 50S subunitof bacterialribosomepreventingpeptideelongation

static Strep, legionella,mycoplasma,chlamydophiliaOral anaerobes

GI upsetHepatotoxicityPruritisHypersensitivityProlonged QT

Community acquired/atypicalpneumonia

Tetracyclines

Doxycycline

Bind to 30Ssubunit toprevent peptidelongation

static MRSA > MSSA,atypicalpneumonaorganisms

GI upset, CNS Toxicity, DentalDiscoloration Photosensitivity

Atypical pneumonia, COPDexacerbation, sensitivecommunity acquired MRSAskin/soft tissue infections,suppressive therapy for chronicosteo.

TMP-SMX TMP- inhibitsfolic acidbiosyntheticpathwaythroughdihydrofolatereductase

SMX- inhibitsfolic acidnucleic acidsynthesis

cidal MRSA>MSSA,50% of GNRs thatcause UTIs arenow resistant totmp-smx. DOCfor PCP

Most frequent: GI upset, allergy/rash,photosensitivity, headache/dizziness

Less frequent: AIN, hepatitis,Stevens-Johnson/TEN, a wide varietyof hematologic disorders

Skin and soft tissue infectionswith MRSA (95 % of MRSA incommunity are sensitive), butdoes not cover strep well, whichis most common cause ofcellulitis.

Rifampin Inhibits RNApolymerase

Both MSSA, MRSA,never used asmonotherapy

GI upset, discoloration of bodilyfluids, allergy/rash,flu like symptoms,hepatotoxicity,

Use in RIPE therapy for TB; it’suse as an adjunt to treat MRSAinfections is controversial

Metronidazole Disrupts DNAsynthesis?

cidal Anaerobesamoebas

Nausea/Vomiting, xerostomia, CNSeffects, hypersensitivity, disulfiram-like effect if taken with EtOH

C. difficile colitis, Empirictherapy in which anaerobes aresuspected, often used incombination with cipro or CFTfor empiric coverage of entericinfections.

Clindamycin Binds to 50Ssubunit, similarto macrolides

static Oral anaerobes,strep, MSSA,MRSA

Abdominal pain, nausea/vomiting,esophagitisC. dif colitis, hypersensitivity

Aspiration pneumonia, oralinfections, infections withsensitive community acquiredMRSA.

Antibiograms:- UCSD: EPIC -> Web References -> InfectionControl/Epidemiology.- VAMC: CPRS -> Services -> Infection Control -> Antibiograms.

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GASTROENTEROLOGY

CALLING A CONSULT

1. When you call, have a question. For example, instead of calling the Fellow and saying “Ihave a patient with pancreatitis…” you might say “I have a patient with pancreatitis and I’m notsure if he/she needs an ERCP…”

2. Call the consult after you examine the patient yourself (including rectal exam). In regardsto the rectal exam, stool color is most important – black, red or brown.

3. Understand the limitations of endoscopy. In the GI bleeder, resuscitation is most importantand endoscopy will be delayed until the pt. is stable enough to undergo endoscopy. Also, ifyou have a very unstable bleeder, consider calling GI and Surgery/IR to evaluate them.

4. Anemia. You won’t likely get GI to scope an inpatient for anemia if there is no evidence ofblood loss (melena, hematochezia or hematemesis).

5. PEGs. GI won’t do a PEG on an emergent basis. Also, consider previous abdominal surgerywhen considering a PEG (contraindication).

ACUTE PANCREATITIS

1. Treatment Goals: Rest the pancreas/gut and provide supportive care

2. General Considerations:- Ranson’s criteria: although these have largely fallen out of favor, they can still help identify

patients with high risk pancreatitis.- Amylase vs. Lipase: Around 25% of patients with acute pancreatitis have a normal amylase.

Lipase is more sensitive and specific than amylase.- Early Nutrition: Has been demonstrated to improve outcomes. Earyl oral feeding is a

reasonable approach in cases of mild-to-moderate pancreatitis. Whereas PPN/TPN may benecessary until jejunal feedings are initiated in severe cases.

3. Etiologies:- Alcohol and gallstones (most common); Trauma - blunt and iatrogenic (2%-5% after ERCP).- Others: hypertriglyceridemia (when greater than 1000 mg/dl); hypercalcemia; medications

such as pentamidine, antiretrovirals, thiazides, diuretics, and sulfa antibiotics; pancreaticdivisum; infections such as mumps, CMV, HIV, and E. coli; and the dreaded scorpion sting.

4. Signs: Quiet, distended and painful abdomen with rebound and guarding.- Cullen’s sign: periumbilical discoloration- Turner’s sign: flank ecchymoses, from retroperitoneal tracking of blood

5. Therapeutics:- NG tube decompression if significant nausea and vomiting- NPO while in pain. If your patient is critically ill for an extended period of time, consider

feeding distal to the ligament of Treitz (jejunum) – you’ll need to call IR to place this tube.- Aggressive IVF; approximately 250 to 300 cc of intravenous fluids per hour are required for

48 hours if the cardiac status permits. One of the biggest mistakes in pancreatitis isunderhydration. Follow K+, Mg++, and replete as necessary.

- Pain Managment: Morphine is commonly used for analgesia, although in theory it can causespasm of the sphincter of Oddi. Consider a PCA. Meperidine may cause seizures andhypotension in large amounts, although it is the 'textbook' favorite. Also, if you believe thatcause of the pancreatitis is ETOH, remember withdrawal and consider librium taper / PRNativan. Watch the patient’s mental status and vital signs. Take care not to overmedicate,because it is easy to send people over the edge with benzos.

- Trending Laboratories: QD: CBC, lytes, BUN, creatinine, glucose, calcium, LDH, LFTs. It isnot necessary to follow pancreatitic enzymes.

- Further Studies: ABG and CXR if any evidence of respiratory compromise. Abdominal CTsshould include IV and oral contrast with a ‘rapid bolus’ or ‘dynamic’ or ‘pancreatic’ protocol(with thin cuts through the pancreas) to delineate necrosis from edema. Non-necrotizingdisease generally has an excellent prognosis, whereas necrotizing pancreatitis markedlyincreases the risk of complications (see below).

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6. Complications:- In general, with clinical deterioration do the following: pan culture, CT the abdomen

(pancreatic protocol), and cover for bowel flora. Use of empiric antibiotics should be limited topatients with severe, necrotizing disease, and even in this setting, is still somewhatcontroversial. Imipenem has the best pancreatic penetration and tissue levels. Look forpancreatic necrosis (that may be sterile or infected) and abscesses. To rule out infectednecrosis, especially with continued fevers, consider a FNA for organisms on gram stain. IfFNA is positive, this represents infected necrosis and is generally managed with surgicaldebridement/necrosectomy.

- Pulmonary: atelectasis, effusion, ARDS.- Renal failure: from severe intravascular volume depletion.- Sepsis/multisystem organ failure.

7. Ranson's Criteria: Severe acute pancreatitis if > 3 Ranson criteria or if any of the following:shock, renal insufficiency, or respiratory distress.- At Admission: Glucose >200, AST >250, LDH >350, Age >55yo, WBC >16000- At 48h: Ca <8, Hct drop >10%, PaO2 <60mm, BUN rise >5, Base deficit >4, IVF >6L

Reference: Whitecomb D. NEJM 2006; 354: 2142.

Admission 48 hrsNon–gallstone pancreatitis

Age > 55 Decrease in Hct > 10%WBC > 16K Increase in BUN > 5 mg/dlGlucose > 200 mg/dl Ca++ < 8 mg/dlLDH > 350 U/L PO2 < 60 mmHgAST > 250 u/L Base deficit > 4 mM

Fluid deficit > 6 LGallstone pancreatitis

Age > 70 Decrease in Hct > 10%WBC > 18K Increase in BUN > 2 mg/dlGlucose > 220 mg/dl Ca++ < 8 mg/dlLDH >400 U/L Base deficit > 5 mMAST >250 u/L Fluid deficit > 4 L

Risk factors Mortality1–2 < 1%3–4 15%6–7 100%

ACUTE GI BLEED

1. Treatment Goals: Stabilize a bleeding patient and determine the site of the bleed as best youcan.

2. Etiologies: The H&P is key. Remember melena is an UGIB until proven otherwise and briskupper GI bleeding can cause BRBPR/hypotension. Conversely a slow, right-sided colonicbleed can supposedly cause melena. However, the presumed location of bleed will help guideappropriate studies: EGD, colonoscopy, sigmoidoscopy, angiography, radionuclide scan, etc.

3. Don’t forget to ask about prior bleeds, prior abdominal surgery, trauma, ETOH use, liverdisease, coagulopathy, anticoagulant meds, NSAID use.

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4. Predisposing Risk Factors for GI Bleed:

Risk factors Symptoms/signsUpper GIBleed

NSAID use Previous ulcer disease GERD/esophagitis

Retching/emesis Known liver disease EtOH abuse

Epigastric pain Hematemasis Melena

Lower GIBleed

Diverticulosis Angiodysplasia Colon cancer

Bowel ischemia IBD

Hematochezia (BRBPR)

*Clinical judgment always comes first. Use this to help determine need for ICU care, and need for GIto see the patient.

5. Patient Risk Stratification prior to Endoscopy:

Low risk Moderate risk High risk

Age <60 Age >60 Age > 60Initial SBP >100; vital signs

now normalSBP <100 on admission and/or

mild ongoing tachycardiaCurrent SBP <100 and/or

severe ongoing tachycardiaTransfusion <2 units Transfusion >2 units Transfusion >5 unitsNo active major co-morbid

disease*Stable major co-morbid

disease*Unstable major co-morbid

disease*No liver disease Liver disease without

coagulopathy orencephalopathy

Decompensated liver disease

No moderate or high-riskclinical features

No high-risk clinical features

* Major co–morbid disease defined as CAD, CHF, acute renal failure, sepsis, disseminatedmalignancy, altered mental status, pneumonia, COPD, asthma

6. Clinical Evaluation and Stabilization:

Low risk Moderate risk High risk

Vital signs q30 min Single IV okay T&C 2 units PRBC

Continuous ECG Vital signs q15 min with BP

and O2 sat Two IVs with isotonic fluid T&C 2-4 PRBC

Continuous ECG Vital signs q15 min with BP and

O2 sat Two IVs with isotonic fluid T&C 2-4 units PRBC Foley catheter Transfuse if no response to

crystalloid, Consider airway protection and surgery consult

*Remember that most deaths occur from respiratory, cardiovascular, and renal complicationsassociated with bleeding, not exsanguination.

7. Endoscopic risk stratification:

Low risk Moderate risk High risk Gastritis Esophagitis Malloy-Weiss tear Clean-based ulcer

Ulcer with clot Dieulafoy’s ulcer

Varices Actively bleeding ulcer Ulcer with visible vessel

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8. Labs/Studies: Check serial CBC (q4-6h at least until it is clearly stable), lytes, coags, LFTs,and a CXR. Get a KUB for abdominal distention, pain, or peritoneal signs; get an ECG forhistory of coronary artery disease or age >45. In an upper GIB, you will see high BUN/Cr ratio2/2 blood absorbed in small intestine. NGT can help identify if bleeding is upper. Using a stiffcold NGT with lidocaine jelly is kinder to the patient, and be sure to keep the neck against thechest. Placing an NGT in a patient with suspected variceal bleeding is probably notrecommended, although somewhat controversial. If no blood is visible and content is clear,bleeding is not likely to be from stomach (duodenal bleeding cannot be assessed). If content isbilious, there is likely no active duodenal bleed but the visual assessment of the presence ofbile is inaccurate. No role for guiaic of stomach contents.

9. Therapeutics:- Volume resuscitate with IV NS to correct vital signs. Patient should have two large-bore IVs,

and be typed and crossed.- Transfusion of PRBCs to maintain hematocrit of >25% (>30% if CAD) and platelets >50K.- FFP and vitamin K should be considered if INR >1.5, DDAVP (0.3 mcg/kg IV q12h x 2) if

uremic bleeding.- Octreotide drip for patients with acute bleeding and evidence of advanced liver disease or

portal HTN. Dosing: 50 mcg bolus then 50 mcg/hr x 72h.- Ceftriaxone (1gm IV q24h) for SBP prophylaxis in patients with cirrhosis and ascites- NPO until after endoscopy- IV PPI drip in patients with presumed nonvariceal UGI bleeding. Avoid NSAIDs, ASA,

anticoagulants.- Propranolol or Nadolol should be initiated in patients with variceal bleeds from portal

hypertension after the acute bleed has resolved. Titrate to a dose that lowers the baselineheart rate 25%.

- If pt. is unstable, call the ICU, transfuse, call GI and surgery. Can consider tagged RBC scanor IR eval for coiling (if active blood loss continues without an identified source).

10. Post-endoscopy treatment:- Ask GI when it is okay for the patient to eat. They are guided by endoscopic risk factors, the

matter simply being that GI wants an empty stomach for a re-scope, if needed.- Generally if patients are admitted they are often observed for re-bleeding after endoscopy.

Length of time depends on endoscopic and clinical risk criteria. Rapid post-endoscopydischarge is reasonable for some patients with low-risk endoscopic findings; others, withhigh-risk stigmata, will generally be observed for up to 72 hours.

11. Lower GI bleeding: follow the same guidelines above for ER evaluation and stabilization aswell as resuscitation. For brisk lower GI bleeds, consult GI and consider proceeding to taggedRBC scan (nuclear medicine) which can detect bleeding at a rate of 0.1 - 0.5 cc/minute. Oncebleed is localized, consult interventional radiology for angiography and embolization/coiling toachieve hemostasis. Often, the bleed has stopped by the time the patient has finished thebowel prep and GI recommends a push enteroscopy or pill endoscopy. Some studies haveshown that the pill is better at picking up occult small intestinal bleeding.

References: Baradarian, R, et al. Am J Gastroenterol 2004; 99: 619. Barkun, A, et al. Ann Intern Med 2003; 139: 843.Fernandez, J, et al.Gastroenterology 2006; 131: 1049.Leontiadis, GI, et al. BMJ 2005; 330: 568.

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CLOSTRIDIUM DIFFICILE COLITIS

1. Treatment Goals: Treating diarrhea.

2. Etiologies: The focus is usually on recent antibiotic use, but the biggest risk is being exposedto C. diff spores, which usually means proximity to another infected patient or MD/RN vectors.PPI and antibiotics are also linked to C. diff. IDSA guidelines discourage performing repeattesting, however, sensitivity of current tests is not perfect and some still advocate for sending 3samples. Think about C. diff in hospitalized patients with new nausea, vomiting, leukocytosisand (obviously) diarrhea.

3. Definitions: To help guide treatment

- Mild/Moderate Infection: WBC <15K AND Cr < 1.5x baseline- Severe Infection: WBC > 15K OR Cr > 1.5x baseline- Severe w/ Complications: WBC > 15K OR Cr > 1.5x baseline with hypotension/shock,ileus, megacolon

4. Therapeutics: First stop the offending antibiotic.- Mild to moderate infection: Metronidazole 500mg PO tid x 10-14d with 1st and 2nd episode.- Severe infection: Vancomycin 125mg QID x10-14d for the 1st and 2nd episode.- Severe Infection w/ Complications: Vancomycin 500mg PO QID AND Metronidazole

500mg IV q8h. If NPO, vanco can be given in a rectal solution, but it is in a large volume (1-2Liters) and if the patient is awake, is miserable for all involved.

- 3rd episodes: Vancomycin 250-500mg PO qid x 10d, then 250mg po daily x 14-21d orVancomycin 125mg po qid + Rifampin 600mg po bid x 7-10d

- Cholestyramine: can be used to bind the toxin but cannot be given at the same time asantibiotics (i.e. 2 hours after).

- Probiotics: Once therapy is completed can try adding probiotics, but remember the antibioticswill kill the probiotics too.

5. Lactobacillus for Antibiotic-Associated Diarrhea Prophylaxis:Lactobacillus has been studied in several trials for its theoretical efficacy in reducing the risk ofantibiotic-associated diarrhea by maintaining the gut microflora. The data appear to beconflicting, with several studies (including a double-blinded randomized controlled trial)showing benefit but at least one randomized, controlled double blinded study by the MayoClinic showing none in a group of patients with previous episodes of pseudomembranouscolitis. However, Lactobacillus is by and large without adverse effects other than cost. Patientcharacteristics and flaws varied from study to study, and clear guidelines are few. Decisionson whether or not to administer lactobacillus as diarrheal prophylaxis may be made on a case-by-case basis. If given, the VA pharmacy suggested dose is two capsules orally three timesdaily with meals.

References: Surawicz CM. Best Pract Res Clin Gastroenterol 2003;17:775-83. Schroeder MS. Am Fam Physician. 2005 Mar 1;71(5):921-8. InfectionControl and Hospital Epidemiology 2010; 31:431-455

GERD AND PEPTIC ULCER DISEASE

1. GERD:- In patients with moderate to severe GERD who are NPO, it is reasonable to use IV

lansoprazole 30 mg daily until such time as the patient can have oral or enteral medication.- Oral lansoprazole at 30 mg daily should be given to patients who are taking a PPI chronically

for moderate to severe GERD.- For inpatients with mild to moderate GERD, oral H2 blockers (or IV H2 blockers in patients

who are NPO) should be the first line agents instead of lansoprazole.

2. Peptic Ulcer Disease:- For inpatients that are taking a PPI for the chronic treatment of peptic ulcer disease, oral

lansoprazole 30 mg daily should be given. In the case where patients are NPO, IVpantoprazole 40mg daily should be given until such time as the patient can have oral orenteral medication.

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3. H. Pylori Treatment:- First Line:

P – PPI bidA – Amoxicillin 1g bidC – Clarithromycin 500mg bid

- First Line, PCN-allergic:P – PPI bidM – Metronidazole 500mg bidC – Clarithromycin 500mg bid

- Salvage Quadruple Therapy:P – PPI bidB – Bismuth subsalicyclate 525mg qidM – Metronidazole 250mg qidT – Tetracycline 500mg qid

- Eradication: Generally should be checked if there was a significant complication from theulcer (GI bleed, stricture, perforation, etc) or if patient is high risk. If you want to proveeradication after treatment, don’t recheck serology (which will stay positive) or repeatendoscopy (which has low sensitivity). You need to either order an H. pylori breath test (anoutpatient procedure) or an H. pylori stool antigen.

Note: All regimens should be continued for 10-14d to achieve 80-95% efficacy, Metronidazoleresistance >> clarithromycin >> amoxicillin.

ULCER PROPHYLAXIS

- The development of stress ulcers is due to local tissue hypoperfusion in the gastric lining, which isusually present only in critically ill patients. Despite this, the popularity of PPIs has led to substantialoveruse of this class of medications for the purpose of “GI prophylaxis.”

- New stress ulcer prophylaxis guidelines have been developed by a multidisciplinary team at UCSD(see below). One should note that the vast majority of the patients who would benefit fromprophylaxis are in the intensive care unit.

1. Risk Factors for the Development of Stress Ulcers: In a review by Cook et al, over 2800critically ill inpatients were studied to determine risk factors for stress ulcer bleeding.- Only two risk factors were found to be significant:

- mechanical ventilation for >48 hours (odds ratio 15.6)- coagulopathy not due to warfarin or heparin (odds ratio 4.3)- one or both of these risk factors had a bleeding rate of 3.7% vs 0.1%.

2. Therapeutics:- IV H2 blockers (ranitidine 50mg iv q8h)- enteral PPIs (lansoprazole 30mg PO/NGT daily)- IV PPIs (pantoprazole 40mg iv daily) reserved for patients whom are NPO

3. Patients requiring stress ulcer prophylaxis:1. ICU patients with at least one of the following risk factors:

- Mechanical ventilation > 48 hours- Coagulopathy not due to anticoagulant medication (INR > 1.5, PTT > 2x normal,

platelet count < 50K)- Glasgow Coma Score < 10- Burn injury with >35% body surface area involved- Acute spinal cord injury- Transplant patients in the perioperative period- Multiple trauma (Injury Severity Score > 15)- Hepatic failure

2. History of PUD/UGIB plus at least two of the following risk factors:- Sepsis- ICU stay > 7 days- Occult bleeding lasting > 6 days- High-dose corticosteroids (>250 mg hydrocortisone/day or the equivalent)

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4. Discontinuation of stress ulcer prophylaxis:- Stress ulcer prophylaxis may be discontinued once risk factors have resolved.- Stress ulcer prophylaxis is rarely warranted in adult patients in non-ICU settings, with the

exception of those patients who meet the criteria listed above.

References: Geerts et. Al, Chest 2001; 119:132-175. Ching, Drug Therapy Topics 2004, 33(1):1-8. Anderson et. al, Ann Intern Med 1991; 115:591-595.Alikhan et. al, Arch Intern Med 2004; 164:963-968 Cade, Crit Care Med 1982; 10(7):448-450. Gardlund et. al, Lancet 1996; 347:1357-1361.Gallus et. al,NEJM 1973;288(11)545-551. Belch et. al, Scott Med J 1981;26:115-117. Samama et. al, NEJM 1999;341(11):793-800. Cook et al, JAMA 1996 275 (4),308-314. Kantorova et al, Hepatogastroenterology 2004 51(57), 757-761. Cook et al, NEJM 1994 330(6), 377-381

SMALL BOWEL OBSTRUCTION

- Although generally considered a surgical problem, SBO is something we see on the wards. It isimportant to be able to recognize SBO and to be able to initiate treatment.

- The surgeons say: “Never let the sun rise or set on a small bowel obstruction”

1. Risk Factors:-Crohn’s disease-Previous abdominal surgery or radiation-Intra-abdominal malignancy-Hernias

2. Clinical features:-Nausea/vomiting (bilious vomiting)-Decreased bowel sounds or high pitched “tinkling” bowel sounds-Abdominal distention-Abdominal pain-Constipation

3. Diagnosis:-Acute abdominal series – Look for air fluid levels, volvulus or free air under the diaphragm(could indicate perforation)-Labs:-CBC: Marked leukocytosis could indicate ischemia-Chem panel: Electrolyte abnormalities 2/2 dehydration and N/V-Consider CT scan of the abdomen-Consider other diagnoses including ileus or pseudo-obstruction

4. Initial management:-NG tube to intermittent suction-NPO-Stat surgical consult-Correct the hypovolemia/electrolyte disturbances-Treat the pain and nausea/vomiting

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HEPATOLOGY

END STAGE LIVER DISEASE & CIRRHOSIS

1. Treatment Goals: These patients often present with numerous complications of theiradvanced disease, including AMS, infection, and metabolic derangement. Initially, the goal inthese patients is to control massive ascites, GI bleeding, bacterial pathogens translocatingfrom the gut and hepatic encephalopathy.

2. Etiologies: The number one cause of end stage liver disease in the US is HCV. ETOH andHBV follow after HCV, and rare causes of liver disease including AIH, hemochromatosis, PBC,PSC, and Budd-Chiari syndrome. NAFLD / NASH are emerging causes of chronic liverdisease. Use the Child-Pugh classification (below) to evaluate patient’s survival. MELD scorewas developed to assess patient’s surgical risk when undergoing TIPS, but is now used inUNOS organ allotment.

3. Child-Pugh Classification:

Points scored 1 2 3Encephalopathy grade None 1–2 (mild confusion/lethargy) 3–4 (marked

confusion/coma)Bilirubin (mg/dl)* < 1.5 1.5–2.3 > 2.3Ascites None Easily controlled Poorly controlledAlbumin (mg/dl) > 3.5 2.8–3.5 < 2.8PT (sec >control) < 4 4–6 > 6

* Does not apply to primary cholestatic liver disease (e.g. primary biliary cirrhosis)

Total points Classification 1 & 2 year survival

5–6 Class A 100%, 85%

7–9 Class B 80%, 60%

10–15 Class C 45%, 35%

4. MELD Score:3.8 × Ln (bilirubin mg/dL) + 11.2 × Ln (INR) + 9.6 Ln (creatinine mg/dL) + 6.4 × (etiology – 0 forAlcohol / Cholestasis)- Scoring ranges from 6 (least ill) 40 (most ill)

- 4 special cases in which higher MELD score assigned includes HCC,Hepatopulmonary Syndrome, Familial Amyloidosis, and Primary Oxaluria (pediatricmetabolic disorder)

- Average MELD for pt underoing liver transplantation is 20.

ASCITES

1. Treatment Goals: Usually fluid management and determining if the patient has SBP.

2. Etiologies: Most commonly ESLD with portal HTN, but other causes include cardiac (rightsided heart failure, constrictive pericarditis); noncardiac (Budd-Chiari, cirrhosis, etc.); lymphaticobstruction (from TB or peritoneal carcinomatosis); pancreatitis; nephrotic syndrome.

3. Paracentesis: Tap the belly if the etiology is not clear, or if you have any suspicion of SBP, asSBP can often be present without symptoms. Many patients present simply with anuncomfortable and swollen belly, but best to rule SBP ASAP. Coagulopathies are high in thispatient population and prior to performing any procedure check coagulation studies. Use anultrasound to decide if there is enough to tap. The fluid appears dark on ultrasound, andusually the right or left LQ are popular locations. If you doubt whether the fluid can be tappedIR can help, but you may miss the diagnosis by waiting. Send a cell count, and cultures toevaluate for infection. Send albumin to calculate the SAAG and lipase and amylase if youthink pancreatitis is involved.

4. Fluid Analysis: Calculate the SAAG (serum ascites-albumin gradient) by subtracting theascites albumin from the serum albumin. A high gradient (> 1.1) means there is portalhypertension. The total protein concentration of the ascites, a proxy for complement levels,predicts risk of SBP (< 1 g/dl is high risk). A high total protein (> 2.5 g/dl) with portalhypertension can be seen in congestive heart failure.

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High gradient (> 1.1 g/dl) Low gradient (< 1.1 g/dl)

CirrhosisAlcoholic hepatitisCardiac failureMassive liver metastasesFulminant hepatic failureBudd–Chiari syndromePortal vein thrombosisVeno–occlusive diseaseFatty liver of pregnancyMyxedema“Mixed” ascites

Peritoneal carcinomatosisPeritoneal TBPancreatic ascitesBiliary ascitesNephrotic syndromeSerositisBowel obstruction/infarction

5. Treatment of Ascites due to Cirrhosis: If the patient is drinking, cessation of ETOH ishelpful. Liver usually starts patients on lasix 40mg and spironolactone 100mg daily, andadjusts depending on the patient’s response. Sodium restriction 2 grams/day (without Narestriction diuretics rarely work). Large volume paraecentesis are reserved for refractoryascites (meaning unresponsive to diuretics). TIPS is often performed in these patients as well,but it often results in worsening or new encephalopathy.

References: Moore, K.P., Aithal G.P. Guidelines on the management of ascities in cirrhosis. Gut 2006 55vi1-vi12.

SPONTANEOUS BACTERIAL PERITONITIS

1. Treatment Goals: Treating and preventing peritonitis in cirrhotics.

2. Etiologies: In patients with cirrhosis & ascites SBP is thought to be secondary to translocationof gut flora. Debatable on whether it goes directly into the peritoneum or blood first.Classically, SBP presents as a patient with pre-existing ascites who develops abdominal pain,fever, decreased bowel sounds, worsened hepatic encephalopathy, and hypotension.However, fever is present only 70% of the time, abdominal pain 60%, and encephalopathy only50%. One in ten patients with SBP will have no symptoms at all.

3. Fluid Analysis: PMN > 250/mm3: The sensitivity and specificity of this value is above 90%,but only in cirrhotics (can’t use same diagnostic method in patients with peritoneal cancer orascites due to cardiac or other causes). Traumatic taps generate 1 WBC per 250 RBCs, and 1lymph per 750 RBCs. WBC greater than 10,000 is suggestive of secondary peritonitis. PMN<250 and other signs/symptoms of infection should be treated empirically while awaitingculture results. A positive Gram stain occurs 5-20% of the time, and is not only diagnostic, butcan quickly rule-in bowel perforation when polymicrobial. A positive culture is diagnostic ofSBP and will narrow therapy. Most common organisms are E. coli, Strep species, andklebsiella pneumoniae.

4. Therapeutics: Treat with third generation cephalosporin (e.g. ,cefotaxime or ceftriaxone). Givealbumin on day 1 (1.5 g/kg of 25% albumin) and day 3 (1.0 g/kg of 25% albumin). In high-riskpatients (those with total protein in ascites < 1.0, previous SBP, or s/p recent GI bleed),consider initiating SBP prophylaxis with ciprofloxacin 500mg po daily.

5. SBP Prophylaxis:- During GI bleed, Ceftriaxone x 5-7 days for prevention of SBP.- Indications for SBP Prophylaxis: Previous SBP, ascites Total Protein <1.5gm/dL and with at

least one of the following: a) Child-Pugh ≥9 points and serum bilirubin ≥3 mg/dL or b) serum creatinine ≥1.2 mg/dL or blood urea nitrogen ≥25 mg/dL or serum sodium ≤130 mEq/L .

- Above patients should receive daily fluoroquinolone indefinitely (theoretical risk of selectionfor resistance with intermittent FQ).

References: Runyon B. Hepatology 2009, 49; 2087. Sort P, et al. NEJM 1999; 341: 403-409. Runyon BA, et al. Gastroenterology 1991; 100:1737-1742.

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HEPATIC ENCEPHALOPATHY

1. Treatment Goals: Improving mental status in cirrhotics

2. Etiology/Precipitating Causes: Most commonly, it is an exacerbation in a patient who is nottaking lactulose. But can also be worsened by GI bleeding, increased protein intake, infection,hypovolemia, sedatives/tranquilizers (narcotics also constipate), hypokalemia, andhypoglycemia.- Checking Ammonia levels rarely useful but can help to determine if there is a hepatic etiology

for delirium / encephalopathy or to monitor the efficacy of ammonia-lowering treatment (e.g.rifaximin, lactulose).

3. Grading:

Grade Level ofConsciousness

IntellectualFunction

Neuro Findings

1 Day/night reversalLack of awareness

Short attention Incoordination

2 Lethargic &inappropriatebehavior

Disoriented Asterixis & abnlreflexes

3 Asleep but arousable Loss ofmeaningfulcommunication

Asterixis & abnlreflexes

4 Unarousable Comatose Decerebrate

4. Therapeutics: ID and treatment of precipitating event. Lower blood ammonia: Give 20ml oflactulose q2-4h to tirate to about 4 BM/day. If the pt is NPO for some reason, you can also dolactulose enemas, but it won’t make you friends with the nursing staff. Starting rifaxamin400mg TID will also help.

References: Ferenci P, et al., 1998. Hepatology. 2002; 35:721. Garcia-Tsao, Wongcharatrawee. Leevy CB, et al.. Am J Gastroenterol 2005; 100(suppl)t S134. Mas AR, et al. J Hepatol 2003; 38:51-5

ESOPHAGEAL VARICES

1. Treatment Goals: Controlling active variceal hemorrhage

2. Etiology: From portal HTN.

3. Therapeutics:

- Hemodynamic Resuscitation:

- 2 large bore IVs

- Type and Cross

- IVF: goal SBP>70, HR<100 and Hct 27-30; Permissive anemia better; over-aggressive transfusionleads to increased Portal Pressure leading to rebleeding

- Octreotide: 50mcg bolus IV, then 50 mcg/hour x 2-5 days

- Endoscopic Therapy: Sclerotherapy or Esophageal Variceal Ligation (EVL)

- SBP Prophylaxis: Ceftriaxone x 5-7 days preferred over Fluoroquinolone (IV or PO) BID

4. Options when endoscopy fails (10-20% of patients):- Repeat Endoscopy- Balloon Tamponade (initial control of bleeding observed in 30-90% of pts)- TIPS (early on can provide hemostasis and survival benefit)- Surgical consultation for surgical shunt placement or other nonshunt options.

5. Primary Prevention of Variceal Hemorrhage:

- Nonselective blockers decrease risk of 1st variceal hemorrhage by 50%: It has beenrecently shown that BB were not effective in preventing development of varices

- Prophylactic EVL c/w blockers decreased risk of 1st bleed, but no difference inbleeding-related mortality or all cause mortality (2 RCT’s comparing EVL and BB areconflicting). Therefore, data exist only to support EVL for 1º prophylaxis onlyin pts intolerant to BB.

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6. Secondary Prevention of Variceal Hemorrhage:

- Nonselective blockers- Block adrenergic dilatory tone in mesenteric arterioles causing unopposed adrenergic

mediated vasoconstriction leading to decreased portal inflow causing decreased portalpressure

- Decrease risk of rebleeding by 40% (1 study showed survival benefit).- EVL plus blockers reduce rebleeding much more than banding alone.- Start with propranolol 20 mg BID (or nadolol 40 mg QD) and titrate dose to achieve

25% reduction in HR or resting HR of 50-60.

7. TIPS: decompresses portal vn. without risks of general anesthesia. TIPS has been shown to rebleeding c/w sclerotherapy (but assoc with survival & cost). Considered salvagetherapy for pts who rebleed despite adequate endoscopic and medical therapy.- Adverse effects: encephalopathy, TIPS stenosis portal pressure.

References: Garcia-Tsao, et. al. Hepatology 2007;46:922-938. Sung JY, et al. The Lancet 1993, 342: 637-641.Bernard B, et al. Hepatology1999; 29: 1655-1661. Bildoza M, et al.. Scand J Gastroenterol 2000; 35:419.Loannou G, et al. Cochrane Database Syst Rev 2003; CD002147 NEJM1992; 326: 1527.Chojkier M, et al. Gastroenterology 1996; 111: 138. Laine L, et al.. Ann Intern Med 1995; 123:280.Pascal JP, et al. NEJM 1987;317:856.

ABNORMAL LFTS

Remember the normal range for a lab test = mean value in a healthy group ± 2 SD. Therefore 5% ofthe results from normal pts fall outside the defined range of “normal.”

1. Sources of Individual Liver Tests:- AST: liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs- ALT: mostly liver and is therefore a more specific marker.- Alk phos: liver, bone, placenta. Levels inc with age (65yo ~150% seen in 30 yo).- GGT: hepatocytes and biliary epithelium. Sens for detecting ETOH ingestion: 52-94%.- 5NT: 5’ Nucleotidase produced by the liver and specific for hepatobiliary etiology for

elevated alk phos.

CAUSES OF CHRONICALLY ELEVATED AMINOTRANSFERASE LEVELS

Hepatic Causes Nonhepatic Causes

Alcohol Abuse Celiac sprue

Medications Muscle disorders (polymyositis, rhabdo)

Chronic HBV and HCV Strenuous activity

Steatosis and NASH

Autoimmune Hepatitis

Hereditary Hemochromatosis

Wilson’s disease

Alpha1- antitrypsin deficiency

HEPATIC CAUSES OF CHRONICALLY ELEVATED ALK PHOS LEVELS

Obstructed bile ducts

Drug-induced Cholestasis

Primary Biliary Cirrhosis

Primary Sclerosing Cholangitis

Infiltrative disease (sarcoid)

Bile Ductopenia of adulthood

2. Helpful Patterns of LFT Abnormalities:- AST:ALT>2 is >90% sens for ETOH liver- AST:ALT> 3 is >96% sens for ETOH liver- GGT 2x normal and AST:ALT > 2 very suggestive of Alcoholic Liver Disease- AST or ALT>1000 usually seen only in Acute Viral Hepatitis, Ischemic Injury, Fulminant

Failure, or after Chemo-Embolization (TACE)- In acute biliary obstruction, elevation of alk phos and GGT often lags symptoms or rise in

ALT (~24 hours).- Elevated Alk Phos and GGT in non-dilated biliary tree suggests cholestatis or hepatic

infiltration (sensing). If GGT normal, suggestive of non-hepatic source (bone or placenta).

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3. Work up of chronic LFT abnormalities:- RUQ Ultrasound- Hepatitis Panel- Screen for the below conditions based on clinical scenario

LESS COMMON LIVER DISEASE

Most LFT abnormalities and liver disease encountered in our hospitals is secondary to Alcohol, ViralHepatitis, and Medications. Below are a few well characterized, but less common liver diseases thatyou may encounter.

1. Auto-Immune Hepatitis: SPEP is a useful screening test as >80% of patients with AIH havehypergammaglobulinemia. A finding of >2x nl polyclonal Ig’s is most suggestive of AIH. (WhileANA, anti-smooth muscle and anti-liver-kidney microsomal Ab are commonly ordered, theseare all relatively insensitive and routine use is discouraged).

2. Non-alcoholic Fatty Liver Disease NAFLD: Ranges from simple Hepatic steatosis to Non-Alcoholic SteatoHepatitis (NASH) and Cirrhosis: See AST/ALT <1. US or CT demonstratesfatty infiltration. The diagnosis of NASH is a histologic one and requires liver biopsy(demonstrating pericentral fibrosis, inflammation or hepatocyte necrosis).

3. Hereditary Hemochromatosis: Transferrin saturation (serum Iron/TIBC) >45% is highlysuggestive (94% sens and 94% specific). Confirmation should include Ferritin and genetictesting for HFE gene.- If C282Y homozygote patient has HH- If C282Y/H63D heterozygote – HH most likely- If H63D homozygote –HH likely, but must r/o other causes of elevated LFTs.

4. Primary Biliary Cirrhosis: Pathognomic finding is anti-mitochondrial antibody positive with aflorid duct lesion on biopsy. Clinically, these patients are women more than 90% of the timewith an insidious onset of their disease usually associated with fatigue and other autoimmunedisease. Ursodiol has been shown to improve transplant free survival, and vitamin D has beenassociated with an improvement in fatigue.

5. Primary Sclerosing Cholangitis: The man’s version of PBC, usually diagnosed by ERCP orMRCP. MRCP is preferable for diagnosis to save the extrahepatic ducts from further damage.Associated with cholangiocarcinomas, ulcerative colitis and ANCA positivity. Walter Paytondied of this.

6. Wilson’s Disease: consider in pts <40 yo. Screen with serum cerruloplasmin (decreased in85% of cases) & ophtho exam looking for Kayser Fleischer rings. If highly suspicious,measure urine copper excretion (>100mcg per day is suggestive). Copper stain of liver biopsyis gold standard.

7. Alpha1-Antitrypsin Deficiency is diagnosed by either:- Direct measurement of alpha1-antitrypsin (careful: it’s an acute phase reactant).- Lack of peak in alpha globulin bands on SPEP.

8. Nonhepatic causes of elevated LFTs:- Celiac Sprue: 10% of cases of asymptomatic elevated LFT’s (check anti-endomysial and

antigliadin Ab)- Polymyositis: check CK and aldolase levels- Strenuous exercise: check CK and aldolase levels

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King’s College Criteria for Liver Transplantaion in Fulminant Hepatic Failure

Acetaminophen-Induced Disease: Other Causes of Fulminant Liver Failure:

Arterial pH < 7.3or

The three following:1. Grade III/IV Encephalopathy2. PT > 100 sec3. Cr > 3.4 mg/dL

PT > 100 secor

Any three of:1. Age ≤10 or > 40 yrs 2. Non-A, Non-B hepatitis, drug toxicity3. Jaundiced > 7 days before HE onset4. PT > 505. Serum Bilirubin > 18 mg / dL

References: Pratt DS, Kaplan MM, NEJM 2000; 342: 1266-1271. Tavill AS, Hepatology 2001, 33: 1321-1328.

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RENAL

CALLING A CONSULT

1. Have a question beyond elevated Cr. Think about what your differential is and how youwould like nephrology to help. For example, instead of saying “I have a patient with a Cr of 3.0”you might say “I have a cirrhotic patient with AKI who hasn’t responded to a volume challengeand I’m concerned about HRS”

2. Know the time course of Cr rise and history of urine output.3. Realize that setting up dialysis takes time. Calling sooner rather than later on AKI patients

who are not turning the corner in terms of urine output, acid base or electrolyte regulation isnever a bad idea. Getting dialysis going requires renal seeing the patient, consent for bothaccess and dialysis, placing access (which may require reversing coagulopathy or plateletdysfunction), dialysis prescription, lining up nursing and equipment and finally putting thepatient on.

4. If admitting a chronic dialysis patient call Nephrology. Schedules for the next day’sinpatient dialysis are made the night prior so get the basic info and call ASAP. Ask the patientwhat schedule they are on (MWF, TThSat), when they were last dialyzed, where they areusually dialyzed, what their access is (fistula, graft, permacath) and current/dry weights toasses degree of overload.

5. Renal transplant patients. Call Nephrology for renal related admits and FYI for unrelated (iepneumonia). Remember that transplant meds interact with lots of other medications alwaystalk with pharmacy or the renal fellow if unsure. Ask when immunosuppressant levels shouldbe drawn, random levels are rarely useful.

ACUTE KIDNEY INJURY

When you see a patient with renal failure of any kind (any elevation in creatinine or anuria),follow the following steps, in order.

A.) Rule Out KillersDetermine if there is any related problem that will quickly kill the patient. The following disordersare potentially lethal and often times require hemodialysis. Remember them with AEIOU:Acidosis - Renal failure oftentimes causes a nongap acidosis in its early stage but with accumulationof organic ions a gap acidosis later predominates.Obtain ABG to determine degree of acidosis/compensation and calculate gap as described below torule out other acid-base disturbances that may be present.Electolytes- specifically potassium- if >6.0, obtain EKG, treat as below. If patient does not respond totreatment then should prepare for dialysis.Intoxication- Lithium is classic example of toxic med that is dialyzableOverload (of fluid)-

If respiratory rate is >30, O2 sat <90%, then goal is to remove fluid fast.Try furosemide (patients with renal failure will only respond to high doses- try 80mg IV),if not responding then patient will require urgent hemodialysis. Note If patient Is anuricthis is less likely to work.

Uremia- Uremic syndrome includes confusion, pericarditis, and cardiomyopathy and should betreated with urgent dialysis.

For uremic bleeding expected or ongoing- Trial DDAVP followed by estrogens andcryoprecipitate. If not reversing, may need dialysis.

B) Workup:1. History and Physical exam: Attention to urine output/color, recent procedures and medications,

vital signs, volume status, signs of obstruction/vascular disease/systemic disease. If urine

output has slowed/stopped, what was happening when it stopped? (new medications-

especially NSAIDS, hypovolemia, fever, etc)

2. Check the creatinine.

What is it today? What was it yesterday? A few months ago?

The trend in the creatinine is the ONLY true way to know if the failure is acute or chronic.

3. Urine evaluation: Output, urinalysis, sediment, electrolytes (Na, Cr, UN), osmolality

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4. Fractional Excretion of sodium/urea: (UNa/PNa)/(Ucr/PCr): If FeNa is <1% then likely prerenal,

contrast-induced, or glomerulonephritis. If >2% then ATN

In setting of diuretics, then check FeUN: <35% is prerenal.

5. Additional workup: If indicated renal ultrasound, serologies, urine eos.

C) Treat the patient: In order to treat the patient, you should try to determine the diagnosis. Much ofthis can be determined by history and physical.If it is determined that the renal failure is acute, the next question to ask what kind of renal failure is it.A simple algorithm is to determine if the renal failure is pre-renal, intra-renal, or post-renal. Thisallows you to form a more narrow differential and focus therapy better.

1. Is this Pre-renal? This is the second most common cause of acute renal failure and generally an easy one to fix,

so it is good to think about it first.

Prerenal is caused by:

1) Decreased intravascular volume (dehydration, blood loss, sepsis) - patients look dehydrated2) Renal Vasoconstriction (NSAIDs, ACE/ARB, hepatorenal syndrome, CHF) - patients maylook euvolemic or even overloaded

Diagnosis: Check history and physical: Is the patient dehydrated? Low blood pressure? Elevated heart

rate? Did they have a reason to lose volume, ie vomiting, diarrhea or blood loss? Did they

take NSAIDs or ACE? Do they have cirrhosis or CHF?

Check course of creatinine rise: It should have been over only a few days (a few weeks at

most) if this is pre-renal.

Check urine: Patients should have a very concentrated urine (look at the specific gravity-

concentrated is >1.020. Pre-renal patients should be making only small amounts of urine or no

urine. Urine osmolality frequently >450 mosm/kg and urine sodium <25 meq/l

Compare the urine creatinine to the serum creatinine. This ratio can help determine the type

of acute renal failure

If it is >40, that is consistent with pre-renal, if it is less than 20 then it is more consistent withtubular necrosis

If not volume overloaded, provide patient with fluid challenge. Give a few liters of fluid over one

day, and then recheck the creatinine and urine output the next day. If there is improvement

this is most likely prerenal.

Consider renal ultrasound if diagnosis of renal failure unclear.

Note if the patient appears volume overloaded and urine studies are consistent with prerenal

azotemia, then the effective arterial blood volume is low such as in CHF or Hepatorenal

Syndrome (HRS discussed in separate section).

Treatment: If fluid depleted, hydrate with normal saline and then recheck creatinine and urine output over

the next day. If they are improving, continue hydration until creatinine normalizes or reaches a

nadir.

If blood loss caused the renal insufficiency, then give blood.

If due to CHF, treatment involves improving cardiac output

If due to hepatorenal syndrome then treatment is with midodrine/ocreotide/albumin (MOA)

cocktail.

If sepsis (can be pre-renal early in the course), use fluid and antibiotics

Treat underlying problems (ie those causing the vomiting or diarrhea)

Stop offending medications like NSAIDs and ACE-I.

Renally dose all medications

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2. Is this post-renal?Diagnosis: Requires either bilateral obstruction (or unilateral obstruction with a single functioning kidney)

and is most commonly due to prostatic disease (hyperplasia or cancer) or metastatic cancer.

Can be acute or chronic.

Possible causes of acute urinary retention to consider:

BPH (53%), constipation, prostate cancer, postoperative, urethral stricture, neurologicdisorder, medications/ drugs (anticholinergics/sympathomimetics), UTI, urolithiasis, bladderneoplasm, spinal cord injury/compression, phimosis, pelvic masses, malpositioned foleycatheter, acute prostatitis.

Important to diagnose early since most causes of obstructive uropathy are reversible but can

lead to irreversible kidney damage if treatment is delayed

Feel suprapubic area for distended bladder, DRE for enlarged prostate. Perform neurologic

exam.

Realize that many patients with urinary obstruction can still make normal urine volumes!

Anuria 2/2 obstruction is rare and only occurs with acute obstruction.

If suspicious, check post void residual (have patient urinate, then place foley or obtain u/s

immediately after urinating). If >200ml remaining in the bladder after urination, this indicates

obstruction.

Order renal ultrasound to look for hydronephrosis, (acute obstruction or obstruction in volume

depleted patients may not show hydronephrosis)

Treatment: Place foley: serves 2 purposes

o Relieves possible bladder neck obstructions

o Helps with UOP measurement

o If decompressing high post void residual clamp foley ever 500cc for an hr or two to

reduce risk of hemorrhagic cystitis from decompressing too quickly

o Also be aware of post-obstructive diuresis- if patient is urinating large volumes (>5L

day), they will need fluid replacement to prevent dehydration. Aim to replace about

80% of what he is urinating each day so that the urine volume will eventually

decrease

Treat underlying cause of obstruction (ie BPH)

3. Is this intrinsic renal disease?Diagnosis: First rule out pre-renal and post-renal etiologies as above.

Causes of intrinsic renal problems to consider:

Vascular:o Acute

o Malignant Hypertensiono HUS/TTPo Vasculitis (Wegners)o Sclerodermao Cholesterol emboli (can be acute or chronic, but usually occurs post

procedure)o Chronic

o Unilateral or Bilateral renal artery stenosiso Nephrosclerosis

Glomerularo Nephritic: UA with RBCs, WBCs, casts (of rbc's or wbc's), variable proteinuria

o Nephrotic: Urine protein >3g/ 24h, few RBCs, WBCs The urine protein can be

measured for 24 hours or in a single sample of urine (spot protein/creatinine ratio):

o Urine protein in 24 hrs ~ urine protein in single sample / urine creatinine in

single sample x 8.8 for women OR x 13.2 for men)

o There are many different diseases that cause glomerular disease; they usually do not

cause renal failure but still can. There will be other times where a patient with an

underlying glomerular disease presents with acute renal failure from another cause

and the urine studies will reflect both problems.

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Tubularo Acute

ATN: UCr/SerumCr <20; FeNa>2%; muddy brown casts on UA(many underlying causes: sepsis that persists and the kidneys become ischemic,

rhabdomyolysis, meds,contrast, progression of pre-renal)

Note: Contrast Induced Nephropathy= 25% increase in serum creatinineafter exposure to contrast; usually transient: Creatinine peaks at 3 daysand returns to normal by day 10. Risk Factors: DM, Cr> 150, HTN,NSAIDS, proteinuria, periproceduere volume depletion, heart failure,cirrhosis

AIN (drug induced)Cast Nephropathy (multiple myeloma)Acute Phosphate Nephropathy (after bowel prep)Tumor Lysis Syndrome (with chemotherapy)

o Chronic

PolycysticHypercalcemiaAutoimmune (Sarcoid, Sjogren's)

Infectious (note, these can be glomurular, tubular or vascular): HIV, Malaria, Schistosomiasis,Bacterial , TB

Treatment: Two parts:0. Follow Guidelines for General Treatment (see below)1. Treat underlying disorder.

5. General Treatment of all Kidney Failure (prerenal, postrenal, intrinsic) Check all meds. Stop those that are nephrotoxic. Adjust doses as necessary using GFR

(remember that equations for GFR often underestimate true GFR in AKI). Common meds to

hold or dose adjust include ace -i, metformin, glimepizide, clonidine, atenolol, digoxin,

allopurinol, colchicine, metoclopromide, antibiotics, lamivudine, pyrazinamide, ethambutol

Avoid contrast

Monitor blood pressure and treat as needed (goal <130/80)

Monitor urine output and volume intake (IV AND ORAL) closely. Treat volume overload if

necessary. Kidney failure requires the use of HIGH doses of furosemide (around 80mg IV or

more) in cases of volume overload. Follow daily weights.

Monitor electrolytes daily at minimum (K, Phos, Ca). Phos Binders as needed.

Monitor creatinine daily at minimum

Monitor for acidosis. May need sodium citrate or sodium bicarbonate.

Encourage good nutrition. Avoid high potassium and high protein foods.

6. Consider a renal biopsy or dialysisConsider this if:Your patient is not improving with treatment outlined above.Your patient is quickly getting worse (rising creatinine, decreasing urine output, or an AEIOU)

HEPATORENAL SYNDROME

Development of acute renal failure due to cirrhotic liver disease and portal hypertension

through the generation of nitric oxide with resultant splanchnic vasodilation and steal from

effective arterial volume. Also component of renin-angiotensin mediated systemic

vasoconstriction. Diuretics can cause azotemia but they do not cause HRS.

Two types of hepatorenal syndrome: Type I HRS is the most severe and is defined as at least

a 50% decline in creatinine clearance over 2 week period; Type II HRS is more insidious and is

often described as ascites resistant to diuretics.

HRS Type I most commonly precipitated by GI bleeding, infection including SBP, large volume

paracentesis without albumin supplementation.

Criteria for diagnosis include

o Presence of cirrhosis with ascites

o Serum creatinine > 1.5

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o No improvement in creatinine after at least two days with diuretic withdrawal and

volume expansion with albumin. Recommended “challenge” dose is 1 g/kg of body

weight per day up to a maximum of 100 g/day.

o Absence of shock, recent treatment with nephrotoxic drugs.

o Absence of parenchymal kidney disease as indicated by proteinuria >500 mg/day,

microhaematuria (>50 red blood cells per high power field) and/or abnormal renal

ultrasonography.

Treatment

o Various small studies have shown benefit with combined therapy of

vasopressor/albumin in which roughly 2/3 of patients show improvement in serum

creatinine.

o Current recommendations are as follows:

1. Vasopressor: Include midodrine in combination with octreotide ornorepinephrine

Most commonly use midodrine 7.5 mg tid (increase to 12.5 tid ifneeded) in combination with octreotide 100 ug SQ tid (increased to 200ug tid if needed)

2. Albumin 1 gram/kg on day one followed by 20-40 grams daily3. Duration of therapy 5-15 days. End point: reduction of serum creatinineconcentration<1.5

o Other treatment modalities include TIPS (although not much data on this) and liver

transplantation.Genes Pere and Shrier. Renal Failure in Cirrhosis: Medical Progress. NEJM 2009;361:1279-90; Genes

Pere MD, Cardenas A, Vincente A, Rodes J. Management of Cirrhosis and Ascites Review. NEJM 2004;350:1646-54.

Prophylaxis: It is worth noting that up to 30 percent of patients with SBP develop HRS.

Studies have shown that in addition to antibiotics, cotreating them with IV albumin at 1.5 gm/kg

at diagnosis and 1 gram/kg 48 hours later helps prevent HRS and improve probability of

survival. In one study of 126 patients with cirrhosis and SBP who were randomized to

cefotaxime verusus cefotaxime + albumin, the development of renal dysfunction while in house

was reported in 33% of patients in the cefotaxime only group versus 10% in the cefotaxime +

albumin group. Survival at three months was 22% in the cefotaxime group versus 41% in the

cefotaxime + albumin group respectively. Sort P. Navasa et al. Effect of intravenous albumin on renal impairment and

mortality in patients with cirrhosis and SBP. NEJM. 1999; 341: 403-409.

CHRONIC KIDNEY DISEASE

>3 months of reduced GFR (<60 ml/min).

Multiple etiologies but diabetes and hypertension the most common

Five stages of chronic kidney disease based on GFR

o Stages I-III focused on slowing progression and treating complications: controlling

hypertension (treat with ACE/ARB) with goal <130/80, strict diabetic control, modify

cardiac risk factors, avoid contrast administration, monitor/treat anemia (goal Hgb 11-

12), secondary hyperparathyroidism, acidosis, hyperposphatemia/hypocalcemia.

Dietary restriction: Na/K, moderate protein restriction. Smoking cessation

o Stage IV (GFR15-29): as above, prepare for hemodialysis.

o Stage V (GFR<15): as above; dialysis. Avoid contrast as many patients are not

anuric and do have residual kidney function that can be adversely impacted. Patients

should fluid restrict and monitor their “dry weight”

Hemodialysis patients can be dialyzed through AV fistula, AV graft, tunneled catheter or

temporary hemodialysis catheter. Patients requiring dialysis need functioning access at all

times.

AV fistulas are the preferred method of access for long term patency and lower rate of

complications.Levy, A. Nondiabetic Kidney Disease: Review. NEJM. Vol. 347, No. 19 · November 7, 2002K/DOQI Clinical Practice Guidelines and Clinical Practice Recommendations 2006 Updates Hemodialysis adequacy Peritoneal DialysisAdequacy Vascular Access. Am J Kidney Dis 2006; 48(Suppl 1):S1.

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CONTINUOUS RENAL REPLACEMENT THERAPY

Indicated in patients with AKI and ESRD in need of hemodialysis who are unable to tolerate

fluid shift of intermittent hemodialyisis

Requires hemodialysis chatheter (temporary/tunneled)

Blood is filtered through hemodialysis membrane and filtrate is discarded.

Based on goal volume status (positive/even/negative) a replacement solution is infused at a

rate (greater/equal/or less than) the filtration rate of blood which is adjustable.

Citrate is infused prior to the hemodialysis filter as an anticoagulant (binds calcium which is

pro-coagulant) and is monitored by measuring post-filter ionized calcium which is maintained

at an appropriate level via a calcium infusion.

Typically nephrology team controls the infusate/dialysate/citrate infusion rate directly with the

nursing staff. However, goal volume status is to be determined by both ICU/nephrology teams.

MAINTENANCE INTRAVENOUS FLUIDS

In normal adults obligatory daily intake includes roughly 500 cc of ingested water, 800 cc of

water from food, and 300 cc of water from oxidation

Obligatory water output is roughly equal to 500 cc in urine, 500 cc from skin, 400 cc from

respiratory tract and 200 cc in stool.

Keep the above in mind as patients who are unable to eat, as all obligatory sources need

replacing, not just that of ingested water.

In the patient who is euvolemic with normal serum sodium then maintenance fluid can be

infused according to the following formula:

o Maintenance IV fluid infusion of 60 ml/hour plus 1 ml/kg per hour for each kilogram

over 20 kg up to a maximum of 120 ml/hour (or 3 liters per day). For example an

individual weighing 60 kg would have a maintenance fluid intake of approximately

1440 ml (60 ml/hour x24 hour) + 960 ml (40 kg x 1 ml x24 hours) or 2400 ml/day.

Increased water intake required in the setting of sweating, burns, tachypnea, surgical drains,

polyuria, or ongoing GI loss.

¼ NS or ½ NS with 20 meq KCL/liter are good choices of maintenance fluid in patients with

good renal function and normal sodium concentrations. Adjustments in concentration should

be made if hypo/hypernatremia develops.

Bicarbonate addition can be beneficial in setting of acidosis. Prior to administration of 1-3

amps (50-150 meq HCO3) to maintenance fluid calculate the bicarbonate deficit to further

guide therapy.

Be very cautious about providing maintenance fluids in patients who are overloaded and

especially if they are oliguric/anuric!

For fluid repletion in setting of hypo/hypernatremia see separate section below.Rose, Burton D. Maintenance and replacement fluid therapy in adults. Uptodate. January 2010.

CONTRAST INDUCED NEPHROPATHY

1. Definition: A fixed (0.5 mg/dl]) or proportionate (25 percent) rise in serum creatinine levelsafter exposure to contrast. Usually transient, Cr peak at 3 days and returns to normal by day10.

2. Risk factors: Diabetes, Cr>1.2-1.5 or GFR<50-60, age>75, periprocedure volume depletion,heart failure, cirrhosis, nephrosis, HTN, proteinuria, NSAIDS, intraarticular injection of contrast,and high dose of contrast

3. Intervention: Guidelines. Patients with normal kidney function do not require prophylacticintervention.- Patients with risk factors and GFR <50-60:- If the GFR is less than 50, consider alternative imaging approaches.- If contrast must be given, a low-osmolar agent should be used at the minimal dose

necessary.- Measurement of the serum Cr should be repeated 24 to 48 hours after the contrast.- NSAIDS and diuretics should be withheld for at least 24 hours before and after, if possible.- Metformin should be withheld for 48 hours before and until it is certain that CIN has not

occurred.- Hydration is key.

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- Normal saline 1ml/kg/hr for up to 12 hours pre and post is studied best.- Consider the IV bicarb (3cc/kg/hr x 1 hr, then 1cc/kg/hr x 6 hours) after (appears to be

better than saline) especially if the test is urgent.- No definitive data to support mucomyst, but It is cheap, harmless, and may work.

Barrett, B. J. et al. N Engl J Med 2006;354:379-386)

NEPHROGENIC SYSTEMIC FIBROSIS

1. General concepts:

- Originally case reports focused on skin findings and was first known as “NephrogenicFibrosing Dermopathy” subsequent reports have shown involvement of multiple organs.

- Caused by Gadollinium (Gd) induced activation of fibroblasts, has been reported with all fivemarketed forms of Gd.

- Unfortunately no widely accepted treatment though improvements have been seen inpatients in which renal function improved after disease development.

2. Clinical Presentation:- History of burning, itching, myalgias, arthralgias and skin hardening- Woody indurated skin, SC nodules, hyperpig plaques, waxy erythematous papules- Symmetric LE involvement most common, UE common as well but usually with LE first, trunk

late, face spared, can lead to severe contractures with pts becoming wheelchair bound anddeath 2/2 complications

- Yellow scleral papules- Can involve skeletal muscle, dura, rete testes, renal tubules, myocardium, pericardium,

pleura, lungs- Onset days to months post Gd exposure

3. Patients at Risk:- AKI or CKD with GFR <30- Any degree of renal dysfunction attributed to HRS

Any degree of renal dysfunction post liver transplant

4. Diagnosis: Skin biopsy in appropriate clinic setting

5. Prevention/Risk Management:- Does the pt need Gadolinium? Think hard about whether the study will change management

in a meaningful way.- If test is performed in patient with impaired GFR either you/nephrology will have to write a

note documenting that benefit clearly outweighs risks. If the patient is hemodialyzed, thenconsider three sequential dialysis sessions over three hours to remove 78%, 96%, and 99%of Gd respectively (although currently no studies show that this modifies risk of NSF)

- Watch for signs and sxs and make sure to document in discharge summary events so thatfuture symptoms can be interpreted appropriately

ELECTROLYTE REPLACEMENT

1. Calcium:

- 1 amp Ca-gluconate raises ionized Calcium by 0.032. Magnesium:

- For every 0.2 mg/dL below normal give 1g MgSO4 IV3. Phosphate:

- If replacing phosphate preferentially use oral phosphate, as IV formulations are potentiallydangerous as they can precipitate calcium. However they are preferred for severe/symptomatic hypophosphatemia.

-Note: 10meq = 6.8mmol = 212.5mg*for phosphate serum concentration below 0.5 mg/dl give 0.5 mmol/kg over 4-6 hours IV

and recheck/redose*for phosphate serum concentration between 0.5-1 mg/dl give 0.25 mmol/kg IV over 4-6

hours and recheck/redose*for serum concentrations between 1-1.5 mg/dl supplement with 15 mmol (or 0.2

mmol/kg) of phosphate (IV or oral=2 packets) and recheck/redose*for levels 1.5-2.5 give 6.8 mmol (1 packet) of phosphate*If patient is hypercalcemic dosage should be decreased by 25-50%

- Oral replacement preferable unless patient has symptomatic/severe hyophosphatemia.

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* Neutra-Phos-K Packet: Phos 250mg; K 14.3meq; Na 7.1meq* Neutra Phos Packet: Phos 250mg; K 7.1meq; Na 7.1meq* K-Phos-Neutral tablet: Phos 250mg; K 1.3meq; Na 1.1meq

-In general higher K containing preparations preferred if K<44. Potassium:

- For every 0.1meq below normal, replace with 10meq KCl.- If replacing via PIV then can replace no faster than 10meq/hr.- If replacing via central line then can replace at 20 meq/hour

HYPERNATREMIA

1. Definition: Na > 145 mEq/L (It’s a water not a salt problem)

2. Etiologies: Pt losing hypotonic fluid AND impaired access to free water (intubated, AMS andso on) rarely infusion of hypertonic fluid or mineralocorticoid excess with ADH suppression.

3. Hypovolemic hypernatremia: (most common situation) divided into extrarenal vs. renal waterloss.- Extrarenal losses- Diarrhea or insensible loss.- Renal losses- loop diuretics, osmotic diuresis (Glu, Urea, mannitol)

4. Euvolemic hypernatremia: DI is divided into central vs nephrogenic. Think of it when UOP>3L/day. If pt is ambulatory then hypernatremia is usually mild as thirst mechanism intact- Central- Multiple etiologies resulting in ADH deficiency, most commonly seen in patients

post-neurosurgical procedure.- Nephrogenic (ADH resistance); Li, Ca, postobstructive and recovery from ATN

5. Hypervolemic hypernatremia: Usually iatrogenic from injection of hypertonic saline orNaHCO3 (post code) also the rare case of mineralocorticoid excess

6. Symptoms: irritability, seizures, lethargy, coma and death.

7. Treatment:- Correct underlying etiology (address AMS, treat hyperglycemia, etc).- Calculate free water deficit ([Na]serum-140)/140 and then determine rate of sodium change per

liter of infusate: ([Na]serum-[Na]infusate)/TBW+1 where TBW=0.60x IBW (x0.85 if female/elderly).

- In cases of symptomatic hypernatremia, correct serum sodium rapidly with assistance ofnephrology team. Goal is to correct free water deficit by 50% over 12-24 hours. Serialelectrolyte measurements q2 hours should be performed along with neurologic exams. Rate ofcorrection should be tapered based on improvement in symptoms.

- For chronic hypernatremia with no or mild symptoms, rate of correction should not exceed 0.5meq/L/hour.

- If a volume deficit and hypernatremia are present. Intravascular volume should be restoredwith normal saline prior to free water administration.

- If having trouble after above measures or problem is chronic consider asking pharmacy tochange IV abx and other IVs from NS to D5W

- Remember to never give sterile water IV

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HYPONATREMIA

1. Definition: Symptomatic <115 mEq/L or rapid rate of change, Asymptomatic typically 120-135mEq/L or slow change

2. Etiologies: Can be hypertonic (excess of another effective osmole, glu, mannitol draws H2Oout of cells and dilutes serum Na), isotonic (rare lab artifact 2/2 hyperlipidemia orhyperproteinemia) or hypotonic which is the most common scenario and further subdivided byvolume status

o Hypovolemic Hyponatremia: Renal (thiazide diuretics) and Extrarenal (diarrhea, poorPO, insensible loss, third spacing as in pancreatitis)

o Euvolemic Hyponatremia: SIADH, Hypothyroidism, AI, Tea and Toast, BeerPotomania, massive polydipsia (>12L free water/d), Reset osmostat

o Hypervolemic Hyponatremia: CHF, Cirrhosis, Nephrotic Syndrome, Advanced CKD

6. Workup: Think about possibility of hypertonic or isotonic states (examples are hyperglycemicpt or pt with large protein gap) if you have clinical suspicion measuring serum osm helpsconfirm, in most cases the above are essentially ruled out by Hx/PE and basic labs, the nextand trickiest question is what’s the pt’s volume status- Use Hx/PE and vital signs (CVP, JVD, Orthostats, Skin turgor, mucus membranes) as first

line of investigation followed by…- Labs and imaging typically obtained in ED (Spec Grav on UA, BNP, BUN/Cr,

hemoconcentration, acid/base, CXR)- Check urine osmolality- A low value is seen in euvolemic or volume overloaded patients

whereas a high value is seen in hypovolemic patients or in those with SIADH.- Check TSH and Cortisol in patients who you are considering SIADH

7. Symptoms: Lethargy, altered mental status, seizures, and coma.

8. Treatment: Isotonic hyponatremia is a lab artifact; hypertonic hyponatremia is treated mycorrecting underlying etiology, hypotonic hyponatremia as below:- Severe Symptomatic Hyponatremia:

- Symptomatic (AMS, Sz) hyponatremia regardless of etiology is a medical emergencyrequiring ICU level care with Na q2h

- Use hypertonic 3% saline for initial rapid correction at a rate of 2 meq/L/hr for the first2-3 hours or until symptoms resolve. Remember that the max correction per 24 hourperiod is 10-12 mEq.

- Use equation 3 to estimate rate of Na increase- Hypovolemic:

- Volume repletion with normal saline to correct at a rate no greater than 0.5meq/L/hour; 10-12 meq/L/day to avoid osmotic demyelination.

- Euvolemic:- Low solute, feed pt regular diet- SIADH

- Free H20 restrict ~ can initially try placing 1 L/day fluid restriction and tighteningthis if needed.

- If fluid restriction fails to increase sodium consider hypertonic saline versusconivaptan gtt (V1a/V2 antagonist) which requires central line.

- Consider Lasix - low dose to poison loop (not as diuretic)- Hypervolemic:

- Free water restrict- Diuresis, consider colloid in cirrhosis

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HYPERKALEMIA

1. Definition: Mild 5.1-6.5 mEq/L, Moderate 6.5-8.0 mEq/L, Severe >8.0 mEq/L

2. Etiologies: Pseudohypokalemia, Transcellular shift, Decreased GFR, Normal GFR withdecreased potassium excretion (ie hypoaldosteronism). Most acute inpatient hyperkalemiadue to trancellular shift or AKI along with predisposing Renin-ATII-Aldo abnormality (DMII,ACE, NSAID so on)

3. Workup:- Rule out pseudohyperkalemia (repeat the lab if no good reason for elevated K) and

transcellular shift- Assess GFR- If GFR nml Calculate TTKG > 7, suggest nml aldo, if TTKG < 7, suggest hypoaldo state,

TTKG same as FeNa just put K in for Na and Osm in for Cr, think of it as a measure of aldoactivity (should be high in hyperK as body tries to kick K out)

- Check EKG for peaked T waves, flattening of p waves, prolonged PR interval, QRSwidening, ventricular arrythmias and eventually sine wave pattern and PEA.

4. Symptoms: Asx, weakness, cramps, arrhythmias, and sudden death.

5. Treatment:- Stabilize the Cardiac Myocyte Membrane:

- Any EKG changes start with 1-2 amps Ca gluconate (CaCl though it has more Ca istypically reserved for codes as extravasation from PIV can cause tissue necrosis)caution if Dig toxic

- Shift K intracellularly:- 10U Regular insulin, coadminister with 1 amp D50 to keep pt euglycemic (Don’t need

the D50 if the pt is hyperglycemic)- Consider albuterol 10-20mg neb, has little effect in up to 1/3 of pts, caution in pts who

are already tachycardic or arrythmia prone (h/o afib, SVT so on)- Consider 1-2amps NaBicarb if serum bicarb <22, if bicarb higher will have little effect- Can further temporize with insulin/D10 and bicarb ggt’s

- Decrease Total Body K:- Kayexalate 30-90mg PO/PR, consider rectal tube if using PO (kayexalate today to

lower K tomorrow)- Use the kidney, 90% of K excretion in the normal state, if pt eu- to hypovolemic

increase UOP with NS, once hydrated consider Lasix 40mg IV, assess response andrepeat

- Hold meds that impair K excretion (ACE/ARB, NSAID, Septra so on)- HD: severe hyperkalemia or EKG changes beyond peaked T waves are a medical

emergency, call nephrology sooner rather than later as it takes time to get vascath inand dialysis nurse with equipment

6. Tips:- Outpatients on ACE/ARB, K up to 5.5 mEq/L, manage with dose reduction, low dose lasix,

d/c other meds that impair K excretion (NSAIDs), eval dietary habits (salt substitutes withhigh K), NaHCO3 tabs in CKD pts with bicarb <22

- Don’t go nuts with kayexalate if am labs on an otherwise stable inpt have mildly elevated K,just give a little lasix if volume status allows, the nurse and pt will thank you

HYPOKALEMIA

1. Definition: K < 3.5 mEq/L.

2. Etiologies: divided into extrarenal vs. renal losses.- Extrarenal: include diarrhea, vomiting, and increased insensible losses.- Renal losses: diuretics, RTA, DKA, mineralocorticoid excess states.

3. Workup:- Calculate TTKG. If TTKG < 3, then extrarenal losses, if TTKG > 7 then renal losses.

- On EKG can see U waves, T wave flattening, and ST changes.- Should always check Mg since may be difficult to replace K if Mg is low

4. Symptoms: Fatigue, nausea, ileus, weakness, cramps, arrhythmias.

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5. Treatment:- Treat underlying etiology- For every 0.1meq below normal, replace with 10meq KCl.- Replace Mag to 2.0

HYPERCALCEMIA

1. Definition: Ca > 10.5 mg/dl

2. Etiologies: Can be divided into increased absorption vs. decreased excretion. MnemonicCHIMPANSEE (calcium excess, hyperparathyroidism, immobility, mild alkali syndrome/multiplemyeloma, Paget’s dz, Addison’s, neoplasm, sarcoidosis and granulomatous dz, excess vit D,excess vit A).

3. Symptoms: moans, stones, groans, psychatric overtones (nausea, anorexia, abdominal pain,kidney stones, altered mental status, polyuria). EKG: shortened QT.

4. Treatment: Fluids (2-4L NS) since most patients are hypovolemic, consider using diureticsbut need to hydrate prior to use, otherwise will worsen hypercalcemia. Consider calcitonin (4iu/kg SQ q12h) which decreases Ca by 1-2 mg/dl in 2-3 hrs. Other options includebisphosphonates and steroids for long term control.-Treat underlying etiology!

HYPOCALCEMIA

1. Definition: Ca < 8.5 mg/dl. Correct w/albumin since 40% of calcium is bound to albumin andonly ionized Ca is active. Every decrease in alb by 1 g/dl from 4, add 0.8 to measured Ca.

2. Etiologies decreased absorption, increased loss, and sequestration, decreased osteoclasticactivity- Decreased absorption- etiologies inclue vitamin D deficiency, hypoparathyroidism, calcium

chelators.- Increased losses usually through diuretic use- Sequestration-blood transfusion, pancreatitis, tumor lysis- Decreased bone turnover- hypoparathyroidism, cinacalcet, bisphosphonates

3. Workup: check PTH, Vitamin D-25, Vitamin D-1,25, mag, phos, albumin, alkalinephosphatase, urine calcium.

4. Symptoms: tetany, muscle spasms, weakness, paresthesia, hypotension, seizures, alteredmental status. On EKG can see prolonged QT.

5. Treatment:- Always check Mg and replace it, since difficult to replace Ca if low.- For mild hypocalcemia (Ca > 8.0 mg/dl or ionized Ca2+ > 0.8) give calcium carbonate.- For mod to severe hypocalcemia (Ca < 7.0 mg/dl or ionized Ca2+ of <0.7 mEq/dl) or

symptomatic, give 2 - 3 amps of calcium gluconate. Elevation in calcium only transient (2-3hrs) and should recheck Ca in several hours. May consider repeating dose in 6 hr orconsider starting calcium gtt at 0.5-1.5 mg/kg/hr for several hours.

- 15 mg/kg Ca needed to raise Ca by 2-3 mg/dl.- 1 amp Calcium gluconate has 90 mg Ca- 1 amp Calcium chloride has 272 mg Ca (although can cause tissue necrosis if extravasates).- 1000 mg Calcium carbonate has 400 mg Ca but keep in mind that this is slower acting.

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HYPERPHOSPHATEMIA

1. Definition: Phosphate > 4.5 mg/dl

2. Etiologies: divided into decreased excretion, increased intake, and shift from intracellular toextracellular space- Decreased excretion usually due to renal failure and hypoparathyroidism- Increased intake usually from vit D intoxication- Shift occurs in rhabdo, trauma, tumor lysis syndrome, insulin deficiency, acidosis

3. Symptoms: Usually asx but can result in calcium deposition and acute hypocalcemia.

4. Treatment: treat the underlying cause for chronic hyperphosphatemia, also can use oralphosphate binding drugs such as calcium carbonate, calcium acetate, and sevelamer.

HYPOPHOSPHATEMIA

1. Definition: phosphate < 2.6 mg/dl

2. Etiology: increased excretion, decreased intake, and EC to IC shiftsIncreased excretion occurs with hyperparathyroidism, thiazides, acetazolamide, andFanconi’s syndromeDecreased intake w vit D def., antacids, poor nutritionShifts can occur w/ refeeding (increase use of phosphate), tx of DKA or HNK, alkalosis

3. Symptoms: usually symptomatic when < 1.0 and include tremor, paresthesia, weakness,AMS, rhabdomyolysis

4. Treatment:- Remember that only phosphate checked while fasting is reliable.- If replacing phosphate preferentially use oral phosphate as IV formulations are potentially

dangerous as they can precipitate calcium but preferred for severe /symptomatichypophosphatemia.

-Note: 10meq = 6.8mmol = 212.5mg*for phosphate serum concentration below 0.5 mg/dl give 0.5 mmol/kg over 4-6 hours IV

and recheck/redose*for phosphate serum concentration between 0.5-1 mg/dl give 0.25 mmol/kg IV over 4-6

hours and recheck/redose*for serum concentrations between 1-1.5 mg/dl supplement with 15 mmol (or 0.2

mmol/kg) of phosphate (IV or oral=2 packets) and recheck/redose*for levels 1.5-2.5 give 6.8 mmol (1 packet) of phosphate*If patient is hypercalcemic dosage should be decreased by 25-50%

- Oral replacement preferable unless patient has symptomatic/severe hyophosphatemia.* Neutra-Phos-K Packet: Phos 250mg; K 14.3meq; Na 7.1meq* Neutra Phos Packet: Phos 250mg; K 7.1meq; Na 7.1meq* K-Phos-Neutral tablet: Phos 250mg; K 1.3meq; Na 1.1meq

-In general higher K containing preparations preferred if K<4

HYPOMAGNESEMIA

1. Definition: Mg < 1.8 mg/dl

2. Etiologies: include GI losses from diarrhea, malabsorption, vit D def, renal losses due todiuretics, hyperparathyroidism

3. Treatment:- Low magnesium can make correcting hypocalcemia and hypokalemia more difficult- For every 0.2 mg/dL below normal, give 1g MgSO4 IV. Should raise to goal above 2 mg/dl in

cardiac patients.- Oral mag used for dietary supplementation and mild hypomagnesemia and should be given

TID.- IV preparation is MgSO4 1000 mg (98 mg elemental Mg)

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- Oral replacements at University Hospital include Mg Oxide 250 mg (150 mg elemental Mg) or500 mg (300 mg elemental Mg), and Slow Mag (64 mg elemental Mg). At the VA, can giveMg Oxide 400 mg (242 mg elemental Mg).

EQUATIONS

- TBWater = WT(kg) x 0.6 (if male) or 0.5 (if female)- Free water deficit = TBW x (Serum Na – 140) ÷ 140

- Change in serum Na with 1L of IVFs = (Na in IVFs in mEq - Serum Na) ÷ (1+TBW)

- 24 creatinine clearance = [UCr x Volume (ml)] ÷ (PCr x 1440)

- TTKG = (UK x Posm) ÷ (PK x Uosm)

- Serum osmolarity = 2 x Na + BUN/2.8 + Glu/18- Electrolyte Free Water Clearance = 24 Hr Urine Volume [1- (UrineNa – UrineK/SerumNa)]- A-a gradient = [FiO2(713) – PaCO2/0.8] – PaO2- Expected A-a gradient = 0.21 x age + 2.5

ACID-BASE DISTURBANCES

Normal Values: pH 7.35-7.45pCO2 35-45pO2 80-100HCO3 22-26

To determine if the ABG is accurate, calculate H+=24 x pCO2/HCO3.

H+ 70 60 50 40 32 25

pH 7.16 7.22 7.30 7.40 7.50 7.60

Step 1: Look at the pH to determine the primary disturbance. Use pCO2 and HCO3

to determine if it is respiratory or metabolic and if appropriate compensationis present (see below).- pH < 7.35 = primary acidosis- pH > 7.45 = primary alkalosis

Step 2: Calculate the anion gap to determine if a gap metabolic acidosis is present.(Normal AG = 10 in young adults; 12 in older adults)

Anion Gap = Na+ (Cl-- + HCO3--)

Step 3: If an anion gap is present, calculate the excess gap to determine if aconcomitant non-gap metabolic acidosis or a concomitant metabolicalkalosis is present.

Excess AG = (Calculated AG – Normal AG) + Measured HCO3

Excess Anion Gap > 30 = metabolic alkalosisExcess Anion Gap < 22 = non-gap metabolic acidosis

Numbers to Remember:Acute Respiratory Process: pH changes 0.08 per 10mmHg increase in pCO2Chronic Respiratory Process: pH changes 0.03 per 10mmHg increase in pCO2A-a gradient = [FiO2(760-47) – PaCO2/0.8] – PaO2Expected A-a gradient ~ Patients Age/4 + 4

Example: 7.10/50/94/15, Na 145, Cl 100Step 1: Acidosis is present. Since pCO2 is elevated, there is a primary respiratory acidosis.However, an acute respiratory acidosis only accounts for a 0.08 drop in the pH.Step 2: The AG = 145 – (100+15) = 30. Therefore, there is an anion gap metabolicacidosis also present.Step 3: Excess AG = (30-12)+15=33. Therefore, a concomitant metabolic alkalosis isalso present.References: Haber, RJ. A practical approach to Acid-Base Disorders. Western J Med, Aug 1991;155(2):146-151

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METABOLIC ACIDOSIS

Gap Acidosis Non-Gap Acidosis

Methanol ingestionUremiaDiabetic KetoacidosisParaldehydeIntoxication (EtOH)Lactic acidosisEthylene glycolSalicylate ingestion

Diarrhea (GI losses)RTAEarly renal failureMineralocorticoidsAlkali intakePotassium depletion

1. Usually see pH < 7.35 and HCO3 < 22 mEq/L.2. Determine if Respiratory Compensation is adequate or if there is a secondary respiratory

disorder.Winters formula: pCO2 = 1.5 x HCO3 + 8.

3. If pCO2 is higher than expected, there is a secondary respiratory acidosis. If pCO2 is lowerthan expected, there is a secondary respiratory alkalosis.

4. Determine whether there is an anion gap. Anion gap = Na – (HCO3 + Cl). Normal anion gapis <12. If pt has low albumin, then need to adjust anion gap. This can be done by adding 1.5to the anion gap for every 1 g/dl decrease from 4 in albumin.

5. If anion gap is present, then check for serum ketones and/or lactate based on clinicalpresentation. If concerned about alcohol poisoning, calculate the serum osmolar gap. Ifosmolar gap is > 10, then consider methanol and ethylene glycol.

6. There may be a concomitant anion gap and nonanion gap acidosis or metabolicalkalosis. First calculate Delta gap (anion gap – 12). Delta + HCO3 > 30 suggests metabolicalkalosis. Delta + HCO3 < 23 suggests additional nonanion gap acidosis. Another method isto calculate delta gap/delta HCO3. If ratio > 1, then add’l metabolic alkalosis. If ratio < 1,then add’l nonanion gap metabolic acidosis.

7. For nonanion gap acidosis, etiology is divided between renal and extrarenal. Renal etiologiesinclude RTA. Extrarenal include diarrhea, pancreatic fistula, ureteral diversion. Todifferentiate between renal and extrarenal, calculate the urine anion gap = UNa + Uk – UCl. Ifextrarenal losses, then UAG will be negative since kidneys will be compensating by producingmore NH4+. If renal losses, then UAG will be positive.

METABOLIC ALKALOSIS

Low Urine Chloride NL/High Urine Chloride

VomitingDiureticsPost-hypercapnea

HypercortisolismSteroid use, CushingDiureticsIncreased renin, RAS

1. Usually see pH > 7.45 and HCO3 > 26 mEq/L.2. Determine if respiratory compensation is adequate or if there is a secondary respiratory

disorder. Formula is pCO2 = 0.7 x HCO3 + 20. If pCO2 is higher than expected, then there isa secondary respiratory acidosis. If pCO2 is lower than expected then there is a secondaryrespiratory alkalosis.

3. UCl< 20 indicates GI loss while UCl>20 indicates early diuretic use or hyperaldosteronism.

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RESPIRATORY ACIDOSIS

CNS/Respiratory Drive (Drug overdose, OSA)Lung Disease (ie, Acute COPD Exacerbation)Chest Cavity (neuromuscular, PTX)

1. Usually see pH <7.35 and HCO3 > 26 mEq/L for respiratory acidosis.2. Can estimate if pH is appropriate for given pCO2. pH decreases 0.08 per 10mmHg increase

in pCO2 for acute process. pH decreases 0.03 per 10mmHg increase in pCO2 for chronicprocess. Partial pressure of O2 decreases as pCO2 increases, resulting in severe hypoxemiaas a consequence of respiratory acidosis.

3. Determine if metabolic compensation is appropriate. For every 10 increase in pCO2,increase in HCO3 by 1 mEq/L for acute vs. 4 mEq/L for chronic. If HCO3 is higher thanexpected, then there is an underlying metabolic alkalosis. If HCO3 lower than expected, thenthere is an underlying metabolic acidosis.

RESPIRATORY ALKALOSIS

Anxiety/Pain/FeverHypoxia/Lung Disease (PE,early bronchospasm)CNS DiseaseMechanical VentilationCentral hyperventilation

Drugs (Aspirin, progesterone)PregnancyHepatic Encephalopathy/ESLDHyperthyroidismSepsis

1. Usually see pH >7.45 and HCO3 < 22 mEq/L for respiratory alkalosis.2. Determine if metabolic compensation is appropriate. For every 10 decrease in pCO2,

decrease HCO3 by 2 mEq/L for acute vs. 4 mEq/L for chronic. If HCO3 higher thanexpected, then also underlying metabolic alkalosis. If HCO3 lower than expected, thenunderlying metabolic acidosis.

3. Sepsis and salicylate toxicity are the only single disorders that cause both gap metabolicacidosis and respiratory alkalosis.

4. Cannot predict pH change with change in pCO2 for respiratory alkasosis. Only acid/basedisorder in which compensation can return pH to normal.

GENERAL CONCEPTS

- Insensible losses are about 500-1000 cc/day but increased in patients with fever, diarrhea,vomiting, intubated, etc. For every 1° F increase, insensible losses goes up by about 60-80cc/day

- Kidneys able to regulate osmolarity of urine between 50 mosm/kg to 1200 mosm/kg (basedupon low or high ADH levels repectively)

- Normal GFR is 100-125 cc/min in men, 85-105 cc/min in women- Oliguria is < 400 cc/24 hrs, Anuria is < 50 cc/24 hrs, Polyuria is > 3000 cc/24 hrs- MDRD is a better measure of GFR than Cockroft-Gault equation or 24 hr creatinine clearance- 24 hr creatinine clearance overestimates GFR with in pts with low GFR- Use of creatinine as measure of GFR during AKI is inaccurate- NS has 154 mEq/L of Na, ½ NS has 77 mEq/L, 3% NS has 512 mEq/L- FENa < 1% suggests prerenal azotemia, however, affected with use of diuretics. In diuretic

use, FEUrea < 35% suggests prerenal azotemia.

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ENDOCRINE

CORRECTING SUGARS

1. Hypoglycemia: If mild, can give orange juice (unless hyperkalemic); if severe D50 (1 ampiv); if low nl sugars, can hold short acting insulin/oral secretagogues; but if low nl andnurses ask to hold long acting, consider giving with close monitoring as sugars will be veryhigh by AM if you hold their basal insulin; hypo is almost always iatrogenic.

2. Hyperglycemia: If mild, can give additional SS dose of SQ short-acting insulin. Find out iftype 1 or 2 (risk for DKA vs. HONK); check chem for gap, serum/urine ketones for DKA,consider VBG if suspect DKA. If patient is in DKA, aside from w/u of cause, will needtransfer of care to at least IMU and likely ICU for insulin gtt and q 1-2 hour finger sticks.

DIABETES MELLITUS

Medications:

1. Insulin Types and Sliding Scale:Insulin Action Onset Peak Duration

Lispro/HumalogAspart/NovalogGlulisine /Apidra

Immediate 5-15” 1-2hrs 3-5hrs

Regular Short acting 30-60” 2-4hrs 4-8hrsNPH Intermediate 1-3hrs 4-10hrs 10-18hrs70/30 30-60” to 3-4hrs 2-10hrs 10-18hrs

Glargine/Lantus Long acting 2-3hrs No true peak ~24hrs

- U500: this is regular insulin that is 5x as concentrated and is useful for people who arevery insulin resistant and use more than 100 units of insulin (at regular concentration 1x)for each injection. U500 is give bid to qid and given before meals (in place of both shortand long acting insulin). For more info or dose conversion, consult endocrine.

2. Injectables:- Exenatide/Byetta: an incretin mimetic. Indicated for use w/metformin and/or

sulfonylurea. Start 5mcg bid w/in 1h of am/pm meal, may inc to 10mcg bid after 1mo.Induces some weight loss. Decrease HbA1c by 1%. Nausea can occur. Expensive.

- Pramlintide/Symlin: co-secreted w/ insulin. Suppresses glucagon secretion, delaysgastric emptying, promotes satiety, stabilizes post-prandial glucose, induces wt. loss.Adjunct use with meal time insulin. Start 30 mcg SC for type II, increase up to 120mcgqac. For type 1 DM, start 15 mcg SC qac, slowly increase to goal 45 mcg QAC if nauseamanageable. Need to reduce insulin by 50% when Symlin is started. Decreases A1c by0.5 %.

3. Oral Hypoglycemics:- Metformin: should be held when Cr >1.4 ( women), Cr > 1.5 (men), GFR < 70,

susceptible to lactic acidosis, decompensated CHF.- Hold on the day of IV iodine dye studies and restart 2 days after w/ normal Cr.- Titrate up at 500 mg interval every week to avoid GI upset.- First drug of choice for new type 2 diabetes. Helps with weight loss. Decrease A1c

by 1-2%.- Sulfonylurea: glyburide has active metabolites that also cause hypoglycemia. For

liver/renal dysfunction and in the elderly, glipizide is better tolerated. Decrease A1c by 1 to2%.

- Meglitinides: short acting insulin secretagogue. Useful for postprandial hyperglycemia.- Thiazolidinediones: not recommended for pt w/ severe liver dysfunction or CHF NYHA

III or IV.- LFTs before the start and later only if clinically indicated.

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- Side effects: weight gain, lower extremity edema and some reports of macularedema. Decrease A1c by 1-2 %.

- Alpha-glucosidase inhibitors: not for pts with GI illness or liver dysfunction. Acarboseshould be titrated at weekly interval. Decreases A1c by 0.5 - 1%. Check LFTs q3mon inthe 1st year.

Outpatient Diabetes Management:

1. Screening: Glucose: pt over age 45 q3yr, or earlier if BMI > 25, IFG/IGT*, physicalinactivity, FHx, Non-Caucasian, h/o GDM, components of dysmetabolic syndrome, PCOS,vascular disease, or insulin resistance.- Impaired fasting glucose (IFG) = glucose between 100 and 125 after fasting 8 hrs- Impaired glucose tolerance (IGT) = glucose between 140 to 199 2 hrs post-prandial.

2. Established Diabetes Patient Monitoring and Care:

OutcomeMeasures:

Frequency: Goal:

A A1C Q3-6 m < 7%B BP Every visit goal bp < 130/80 unless MA>30 mcg/g,

then consider ACE I and bp goal<125/75C Cholesterol Q1y if ctrl goal < 70-100 mg/dLD Diet Usually 1800, 2000, or 2200 kcal dietE Eye Exam Annually screen for retinopathy (Q1y in DMII, after 5

y Q1y in DMI)F Foot Exam Annually monofilament and tuning fork, refer to

vascular surg or podiatry when appropriateG Glucose As directed fasting fsg 90-130, postprandial < 180, fsg

as directed**fsg monitoring:oral agents/Qd insulin: 1-2x/d, BID insulin: 2-4x/d, TID-QID: 3-6x/d

H Healthy Living self mngmt goal, get active, healthy diet,smoke cessation, check fsg, daily footchecks, know meds. *At UCSD, can referto Project Dulce education program.

I Immunize Annually Flu shot annually, Pneumovaccine once,then repeat in five years once > 65 y.o.

J Join TobCess

call 1-800-NO-BUTTS, or begin Chantix

K Kidneys Annually microalbuminuria & eGFR yearly, goal MA< 30 mcg/gm

3. Diet Recs: If moderately active: 30-35 kcal/kg/day; for weight loss, can reduce to 20-30kcal/kg/day. Decrease of 500 kcal/day should result in gradual wt. loss of 1 lb/wk. Typical diet50-60% carbs w/ complex carbs emphasized, 10-20% protein (< 10%/d if overt diabeticnephropathy), <30% calories from fat/d, w/ < 10% saturated fat, and total cholesterol <300mg/d. Emphasize high fiber 20-35 gm sol/insoluble. If HTN: Na+ restrict to <2400 mg/d; ifnephropathy, Na+ < 2000 mg/d.

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INPATIENT DIABETES MANAGEMENT

When in doubt, use the EPIC inpatient subcutaneous insulin order set…

1. Target blood glucose range: Goal for in-hospital patients is controversial given recentreport of increase mortality for critically ill pt in MICU. Goal is to keep fsg close to 110fasting (90-130 according to ADA for non-critical ill patient, 100-150 in critically ill) and <180 postprandial (Standards of Medical care in Diabetes-2006, ADA, Diabetes care, 2006,29(S1), p. s29). Should get HbA1c if none in the last 3 months.

2. Stopping oral medications: In acute settings, it is prudent to stop oral hypoglycemics. Inaddition, metformin should be discontinued in patients with a serum creatinine >1.5 or inwhom there is a risk of nephrotoxicity (e.g., receiving iv contrast); sulfonylureas should notbe used in the NPO patient; and glitazones should be discontinued in patients with CHFdecompensation or volume overload.

3. For patients eating meals or receiving bolus tube feeds: Glargine insulin is the mostphysiologic basal insulin and is recommended in these patients. Lispro insulin is moreappropriate than regular insulin for nutritional doses due to its shorter, more predictablehalf-life and correspondence with UCSD inpatient meal times. If you choose to use NPHinstead of glargine, the distribution of TDD should be modified: Basal insulin: NPH -- 0.5 xTDD; dose 2/3 of this amount before breakfast and 1/3 of this amount at bedtime.Nutritional insulin: Lispro -- 0.17 x TDD, dosed with first bite of each meal.

4. For patients receiving continuous enteral or parenteral nutrition:- Consider using an insulin infusion for optimal control in this setting. Keep insulin separate

from TPN until a stable dose is reached. Glargine insulin is the most physiologic basalinsulin and is recommended in these patients, as it has no serum spike and thereforehas less hypoglycemia than NPH.

- Regular insulin is recommended as the nutritional insulin rather than lispro - because ofits longer half-life, it is better suited to continuous nutritional sources.

- If tube feeds or parenteral nutrition are held, the nutritional regular insulin doses shouldalso be held.

5. For the NPO patient: NPO patients have fewer episodes of hypoglycemia when given alow-dose dextrose infusion like D5 ½ NS at 75/hr along with their basal long acting insulin.Nutritional or scheduled short-acting insulin should not be given to patients without anutritional source. Sliding scale insulin should be offered in small doses only once FSG >200.- Type I Diabetes: Always require insulin, even when NPO, can become ketotic w/in 12-24h.- Type II Diabetes: Hold oral meds in general. TZD ok to ctn.- Type I and II DM: If on intermediate acting insulin (NPH), give ½ on the morning of

procedure. Patients on long acting HS insulin, reasonable to decrease dose by approx 10-20%.

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6. Starting/Adjusting Long Acting Insulin:

- Lantus/Glargine: When A1C> 9% and already on 2-3 PO agents: Start 10 U QHS, andd/c sulfonylurea. Adjust insulin Q3d by 2U HS until FSG < 130. If after 3 mo, A1C >7%, add pre-meal insulin or change to 70/30.

Intermediate/NPH Insulin

Calculate 0.5 U/kg/d body wt to estimateTDD. Give 2/3 am, 1/3 pm

AM dose If pre-lunch fsg > 120 Pre-dinner > 150 Inc am dose by 3U

Pre-dinner > 250 Inc am dose by 5UPM dose If HS > 150 Am > 150 Inc pm dose by 3U

Am > 250 Inc pm dose by 5U

MANAGEMENT OF DKA & HHS

Initial evaluation: plasma glucose, chemistry panel (calculate anion gap), osmolality, serum andurinary ketones, and UA, as well as initial ABG and a CBC with a differential. An ECG, CXR, andurine, sputum, or blood cultures should also be obtained based on clinical presentation.Precipitating factors should be identified and treated (infection, medication non-compliance, MI,etc).

Diagnostic Criteria:

• DKA: Blood glucose >250, pH < 7.3, bicarbonate < 15, ketonuria and ketonemia.• HHS: Blood glucose > 600, pH > 7.3, bicarbonate >15, osmolality >320.

Fluid Management:

• Replacement varies based on age, wt, hemodynamics and comorbidities.• Replace intravascular volume: Give 1L 0.9% NS over 30-60min. Give additional NS until

hemodynamically stable and urine output increased.• Replacement of total body water deficit: Calculate corrected Na. Low Na: Give 0.9% NS 250-

500ml/hr*. Normal/High Na: Give 0.45% NS 250-500ml/hr*. When BG <200 (DKA) or <300(HHS) add D5 and decrease rate to 100-200ml/hr.

*Rate dependent on volume status. Fluid replaced over 12-24hr. Generally patients in DKAdepleted 3-6L and in HHS 8-12L. Care taken in patients with CHF and renal disease.

Insulin Management:• Bolus: 0.1-0.15U/Kg of regular insulin IV and then start continuous infusion (DKA: Start at

0.1U/Kg/hr HHS:start 0.05U/Kg/hr)*. Check BG q1hr until 3 consecutive in target range of 50-75/hr.

• Decrease insulin by 50% if BG decreases >100 in any 1hr period.**• Increase insulin by 50% if BG decreases <50 in any 1hr period.• Decrease infusion by 50% once at target range (DKA 150-200, HHS 250-300). May need to

adjust again after adding D5 to fluid replacement.• Start SC insulin once patient able to eat AND AG closed and Bicarb >15 (DKA) or Mental

Status improved and normal osmolality (HHS).• Stop insulin gtt 1-2 hours after ensuring the patient has a meal, given twice the hourly rate of

infusion in the form of short acting insulin SC and Long acting insulin at 0.2-0.3U/kg or homeinsulin dose.

*Alternative to bolus regimen is to start the insulin gtt at 0.14U/kg/hr then giving 0.14U/Kg bolus ifnot achieving target decrease/hr.**Lowering glucose >100mg/dL/hr may cause osmotic encephalopathy.

Electrolyte Management: Repeat chem panel q2-4h based on imbalancePotassium:• K >5.5: No supplementation• K 4-5.4: add 20mEq of KCl/L to IVF• K 3-3.9: add 40mEq of KCl/L to IVF• K <3: add 60mEq of KCl/L to IVF

• In DKA, do not give insulin if initial K <3.3 until it has been supplemented (Risk of severehypoKalemia).

Bicarb replacement: Generally not needed.• Reasonable to give when pH <7, HCO3 <5-10, Cardiac instability related to acidosis, severe

hyperKalemia.Kitabchi, AE et. al. Diabetes Care. 2009; 32: 1335.

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ADRENAL INSUFFICIENCY

Primary Adrenal InsufficiencyEtiology:

1. Autoimmune (Addison’s Disease)2. Metastatic malignancy (lung, GI, breast, renal) or lymphoma3. Adrenal hemorrhage4. Infectious – TB, CMV, MAC, fungal, HIV5. Adrenoleukodystrophy6. Infiltrative d/o – amyloidosis, hemochromatosis7. Congenital adrenal hyperplasia8. Familial glucocorticoid deficiency and hypoplasia9. Drugs – ketoconazole, etomidate, suramin, aminoglutethimide and metyrapone

Signs and symptoms:Chronic primary adrenocortical insufficiency: weakness, fatigue, anorexia, wt loss,hyperpigmentation (tan, buccal mucosa, gums, palmar creases due to increasedhypothalamic pro-opiomelanocortin release), hypotension, GI disturbances, salt craving,postural symptoms, abdominal painAcute adrenal crisis: hypotension and shock, fever, dehydration, volume depletion, N/V, anorexia,weakness, apathy, depressed mentation, hypoglycemia

Secondary Adrenal InsufficiencyEtiology: Most commonly ACTH deficiency due to exogenous glucocorticoid therapy. Also maysee pituitary or hypothalamic tumors.

Signs and symptoms: Similar to primary adrenal insufficiency, but no hyperpigmentation ormineralcorticoid deficiency.

Diagnosis- Check early AM random serum cortisol: <3 μg/dl is diagnostic, >18 μg/dl rules out

diagnosis unless pt in critical illness, then proceed to cosyntropin test.- Cosyntropin stimulation test:

o Check random serum cortisolo Administer 250 μg cosyntropin (some advocate 1 μg for more

physiologic dosing)o Recheck serum cortisol 45-60 min post cosyntropin

Adrenal insufficiency diagnosed if serum cortisol increases by ≤9 μg/dl.

TreatmentAcute adrenal crisis:

1. Hydrocortisone 100mg IV q8h x 24 hrs (longer if major complications, ie sepsis).2. When stable, decrease to hydrocortisone 50mg q6h. In primary Addison’s disease,

add mineralocorticoid replacement with fludrocortisone (see below).3. Taper to maintenance dose of 10mg TID/QID by day 4 or 5.

Maintenance therapy:1. Hydrocortisone 10-15mg qAM, 5-10mg qPM2. Fludrocortisone 0.05-0.1mg qAM. (NOT needed for secondary adrenal insufficiency)3. Increase hydrocortisone dose during stress. Double oral dose for mild illness.

Provide pt with injectable form of glucocorticoid (ex: dexamethasone 4mg IM) foremergency use.

Steroid coverage for surgery:1. Hydrocortisone 100mg IM on call to OR.2. Hydrocortisone 50mg IM or IV in recovery room and then q6h x 24 hrs.3. If stable, reduce dose to 25mg q6h x 24 hrs then taper to maintenance dose over 3-

5 days. Resume fludrocortisone dose when pt taking PO meds.4. Maintain/increase hydrocortisone dose to 200-400mg/d if fever, hypotension or

other complications.

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PRIMARY HYPERPARATHYROIDISM

Etiology:- 80% parathyroid adenoma- 15% primary parathyroid hyperplasia- 1-2% parathyroid carcinoma

Signs and Symptoms:1. Bone disease:

- Osteitis fibrosa cystica: bone pain, pathologic fractures. Elevation of alk phos onlabs. Increase in osteoclasts, marrow fibrosis, cystic lesions that contain fibroustissue (brown tumors). Subperiosteal resorption of cortical bone most sensitiveradiologic finding.- Osteoporosis: preferential loss of cortical bone. Mass and mechanical strength oftrabecular bone are maintained in mild disease.

2. Kidney disease:- Ca oxalate stones: indication for parathyroidectomy.- Nephrocalcinosis: usually not clinically evident, but do see gradual loss of renalfxn.- Polyuria and polydipsia: from loss of renal concentrating ability due to chronichypercalcemia.

3. Nonspecific features: lethargy, fatigue, depression, difficulty concentrating, personalitychanges, muscle weakness, dyspepsia, nausea, constipation, chondrocalcinosis.

Labs:- hypercalcemia, low normal/low phosphorus (2/2 phosphaturic effects of PTH), mild

hyperchloremic metabolic acidosis (always check albumin at same time)- Intact PTH – elevated or upper normal- 24 hour urinary calcium and urinary Cr excretion to exclude FBHH

Imaging:- Sestamibi scanning, ultrasound, CT scan to localize abnormal gland for surgery ONLY ifhyperparathyroidism with clinically significant signs and symptoms (i.e. osteoporosis) or palpablenodule.

Treatment:- Indications for surgery: Serum Ca >1mg/dL above upper limit of normal, previous episode

of life threatening hyperCa, CrCl reduced below 70% normal, kidney stone, UCa>400mg/24h, BMD T< - 2.5 at lumbar spine, hip or distal radius, <50 yo, long term medicalsurveillance not possible.

- Parathyroidectomy: definitive treatment of primary hyperparathyroidism. High recurrencerates in patients with parathyroid hyperplasia. 95% cure rate for single parathyroidadenoma.

- Medical therapy: High dose estrogen, oral bisphosphonates and raloxifene can be tried inpostmenopausal woman. Cinacalcet for secondary hyperparathyroidism in pts on dialysis.

Variants of Primary Hyperparathyroidism1. Familial benign hypocalciuric hypercalcemia (FBHH)

- Autosomal dominant inheritance

- Mild hyperCa, mild hypophosphatemia, hypermagnesemia

- PTH normal/slightly elevated

- HYPOCALCIURIA, UCa <50mg/24h, Ca/CrCl ration <0.01

- Important to distinguish from primary hyperparathyroidism to avoid unnecessary

surgery.

2. MEN Syndromes: hyperparathyroidism seen in both MEN 1 and MEN 2A

3. Lithium therapy

- Exposure to extracellular lithium shifts set point higher for inhibition of PTH

secretion.

- Also produces hypocalciuria, looks similar to FBHH.

- Difficult to diagnose primary hyperparathyroidism in lithium treated patients.

However, primary hyperparathyroidism likely with serum Ca >11.5 mg/dL

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OSTEOPOROSIS

Definition: DEXA T score ≤ -2.5 (Osteopenia is T score between -1 and -2.5) OR dx of low-impact fracture (i.e. vertebral compression fracture). Low bone mass and deterioration of bonemicroarchitecture. This increases fracture risk.

Who to screen:- NOF recs: Women > 65yo, Men > 70yo, Younger postmenopausal women with a clinical

risk factor, Men 50-70yo with a clinic risk factor, personal hx of adult fracture.- USPSTF recs: Woman > 65 yo, woman 60-65 with a clinical risk factor

Medication risks: Glucocorticoids (equivalent of >5mg prednisone/d x 3 mos), dilantin,phenobarbital, suppressive doses of thyroxine, depoprovera , heparin, TCAs, antipsychotics,benzos, lithium, GnRH analogue, cyclosporin, tacrolimus, methotrexate

Disease risks: Primary hyperparathyroidism, hypogonadism, thyrotoxicosis, IDDM,hyperprolactinemia, premature ovarian failure, RA, SLE, Sprue, IBD, HIV/AIDS, Cushing’s,ESRD.

Who to treat:- Men > 50yo or postmenopausal women with T score ≤-2.5 - Men > 50yo or postmenopausal women with hx of hip or spine fracture- T score between -1 and -2.5 AND 10 yr hip fracture risk >3% OR 10 yr major osteoporotic

fracture risk >20%.- Calculate fracture risk with online FRAX: www.shef.ac.uk/FRAX

Treatment:- NOF recs for Ca/Vit D:

o <50 yo Ca 1000 mg/d, Vit D 400-800 IU/do >50 yo Ca 1200 mg/d, Vit D 800-1000IU/do Take Calcium in divided doses for better absorption

- Weight bearing exercise and muscle strengthening exercise- Avoid smoking and excess alcohol- Antiresorptives: fills in resorptive cavity, increases mineralization

o Estrogen: preserves/increases BMD, reduces spine, hip and nonvertebralfractures. Increases risk of breast cancer, VTE, coronary disease, stroke.

o Raloxifene: increases spine and hip BMD, reduces risk of vertebral fractures.Reduces risk of breast cancer. Increases risk of VTE, leg cramps.

o Bisphosphonates: Alendronate, Risedronate, Ibandronate, Zoledronate Spine fracture reduced by 50% in all Hip fractures reduced by 40% with alendronate, risedronate

and zoledronate Poorly absorbed, GI intolerance with oral agents 50% excreted by kidney, 50% binds to bone Not recommended for GFR <30-35 ml/min Risk of osteonecrosis of jaw, stronger association with IV

bisphosphonate for metastatic bone disease,risk of spontaneous subtrochanteric femur fxin those using bisphosphanates >10 y.

- Anabolic: produces osteoid, increases connectivityo Teriparatide: increases BMD at spine and hip, increases bone turnover

markers, decreases spine and nonvertebral fractures. Black box warning:osteosarcoma with lifetime use of this drug.

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VITAMIN D DEFICIENCY

Who is at risk:- African Americans, elderly, institutionalized, hospitalized patients, obese.- Vit D deficiency can precipitate osteopenia, osteoporosis, osteomalacia, muscle weakness

and increase risk of fracture.

Pathophysiology:- We get vitamin D from the sun, food or supplements.- Vitamin D metabolized in liver to 25-hydroxy vitamin D then metabolized by kidney to

active form, 1,25-hydroxy vitamin D.

Labs:- 25-hydroxy vitamin D used to determine vitamin D status.- <20 ng/mL = vitamin D deficiency- Goal level 30-40 ng/mL

Treatment:- 2 forms of vitamin D supplements: D3 and D2- Vitamin D3 (cholecalciferol) preferred, more physiologic, more effective

o 2000IU daily x 12 weekso Repeat vitamin D level, if <20 ng/mL, refer to endocrine.o If repeat 20-30 ng/mL, increase dose by 2000IU daily x 12 more weeks. Then

recheck, if <20ng/mL, refer to endocrine. If 20-30 ng/mL, continue increasingby 2000IU daily until levels normalize.

o If 30-40 ng/mL, decrease to maintenance dose 1000IU daily. Dose dependson body weight, ethnicity, sun exposure, co-morbidities.

- Vitamin D2 (ergocalciferol) is the only prescription vitamin D in USo 50,000IU qweek (equivalent to D3 2000IU daily) x 8 weekso Then repeat vitamin D level check, if still <30 ng/mL, repeat 50,000IU qweek

x another 8 weeks.o If 30-40 ng/mL, decrease to maintenance dose of 50,000IU q2-4weeks.

- Foods high in vitamin D: salmon, sardines, mackerel, tuna, cold liver oil, shiitakemushrooms, vitamin D fortified milk/orange juice/yogurts/margarine/cheeses/cereals.

- Exposure to sunlight: 10-15 min of full body summer noon-day sun or artificial UVBradiation (tanning beds) equals >10,000IU of vitamin D in light-skinned adults. Obviouscaution against risks of sun exposure.

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HEME/ONC

HEMATOLOGY/ONCOLOGY

ANEMIA

Microcytic Normocytic MacrocyticIron deficiency Iron deficiency (early) B12/FolateThalassemia Acute blood loss ETOHACD (late)Sideroblastic anemia

Anemia of Chronic DiseaseHypothyroidism

MDSLiver disease

Copper deficiency CKD HemolysisDrugs(AZT,HU)

Terminology Description Associated disease statesDiscocyteA.k.a. biconcavedisc

Disc form of RBC with twoconcentric concavities

Echinocyte (I-III)A.k.a. burr cell,crenated cell,berry cell

Spiculated RBC with shortequally spaced projectionsover entire surface;progressing from thecrenated disc (I) tocrenated sphere (IV) withnear complete loss ofspicules

UremiaPyruvate kinase deficiencyLow K+ red cellsImmediately post-transfusion with aged ormetabolically depleted bloodCarcinoma of the stomach or bleedingpeptic ulcer

AcanthocyteA.k.a. spur cell,acanthoid cell

Irregularly spiculated RBCwith projections of varyinglength and position

Alcoholic liver diseaseAbetalipoproteinemiaPostsplenectomyMalabsorptive state

StomatocyteA.k.a. mouth cell,cup form,mushroom cap,uni-concave disc

Bowl-shaped RBC withsingle concavityprogressing from shallowbowl to near sphere withsmall dimple (seen asmouth form on peripheralsmear)

Hereditary stomatocytosisAlcoholismCirrhosisObstructive liver diseaseErythrocyte sodium pump defect

SpherocyteA.k.a. prelyticsphere,microspherocyte

Spherical RBC with densehemoglobin content, EMshows persistent minimaldimple

Hereditary spherocytosis (cells actuallyspheromastocytes)Immune hemolytic anemiaPosttranfusionHeinz body hemolytic anemiaWater dilution hemolysisFragmentation hemolysis

SchistocyteA.k.a. helmet cell,fragmented cell

Split RBC, often showinghalf-disk shape with two orthree pointed extremities;may be small irregularfragment

Microangiopathic hemolytic anemia (TTP,DIC, vasculitis, GN, renal graft rejection)Heart-valve hemolysis (prosthetic orpathologic valves)Severe burnsMarch hemoglobinuria

ElliptocyteA.k.a. ovalocyte

Oval to elongated ellipsoidcell (with polarization ofhemoglobin)

Hereditary elliptocytosisThalassemia IrondeficiencyMyelophthisic anemiasMegaloblastic anemias

DrepanocyteA.k.a. sickle cell

Cells containingpolymerized Hgb S showingvarying shapes from bipolarspeculated forms to hollyleaf and irregularlyspeculated forms

Sickle-cell disorders (S, S trait, SC, SD, S-thal, etc.)HemoglobinopathyC-Harlem Hemoglobin Memphis/S

CodocyteA.k.a. target cell

On EM these bell-shapedcells assume a targetshape on dried films ofblood

Obstructive liver diseaseHemoglobinopathies (S, C)ThalassemiaIron deficiencyPostsplenectomyLCAT deficiency

DacrocyteA.k.a. teardropcell, tennis racketcell, poikilocyte

Cells with a singleelongated or pointedextremity

Myelofibrosis with myeloid metaplasiaMyelophthisic anemiasThalassemias

LeptocyteThin cell, wafercell

Thin, flat cell withhemoglobin at periphery

ThalassemiaObstructive liver disease(+/- iron deficiency)

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DISSEMINATED INTRAVASCULAR COAGULATION

Excessive thrombin causes massive activation of coagulation leading to hemorrhage andthrombosis. Underlying causes include sepsis, malignancy (AML M3, prostate cancer),trauma (head injury, crush), liver disease, and pregnancy (abruption, amniotic fluidembolism).

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HYPERCOAGULABLE DISORDERS

Virchow's triad:1. Alterations in blood flow2. Endothelial damage

3. Hypercoagulable state

Common inherited:1. Factor V Leiden

2. Prothrombin gene mutation3. Protein S deficiency*4. Protein C deficiency*5. Antithrombin deficiency*

6. Dysfibrinogenemia

Common acquired:1. Malignancy2. Surgery/trauma/burns

3. Pregnancy4. OCPs, HRT, Tamoxifen5. Immobilization6. CHF

7. Antiphospholipid antibodies8. Myeloproliferative disorders and PNH9. CKD, nephrotic syndrome10. Hyperhomocysteinemia

11. HIT

If age >50 and no family history of thromboembolism it is unlikely they have antithrombin deficiency, protein Cdeficiency or protein S deficiency

Thrombophilia workup: Effects of anticoagulant therapy and acute thrombosis

Hypercoagulable disorderAcute

Confounding Factors

Heparin Coumadin therapyfor testing Thrombosis therapy

Antithrombin (deficiency) Can be lowered* Lowered NC; Rarely increased

Antiphospholipid antibodies NC NC NC

Factor V Leiden NC NC NC

Factor VIII level Acute phase reactant. Do not test while inflammation is still present.

Lupus anticoagulant NC Cannot measure False positivespossible

Protein C (deficiency) Can be lowered* NC Cannot measure

Protein S (deficiency) Can be lowered* NC Cannot measure

Prothrombin gene mutation NC NC NC

Acquired AT deficiency: neonatal period, pregnancy, liver disease, DIC, nephrotic syndrome, major surgery,acute thrombosis, treatment with L-asparaginase, heparin, or estrogens

Acquired Protein C deficiency: neonatal period, liver disease, DIC, chemotherapy (CMF), inflammation,acute thrombosis, treatment with warfarin or L-asparaginase

Acquired Protein S deficiency: neonatal period, pregnancy, liver disease, DIC, acute thrombosis,treatment with warfarin, L-asparaginase, or estrogens

NC: not changed; CMF: cyclophosphamide, methotrexate, 5-fluorouracil.* Results can be affected by acute thrombosis; it is most cost effective to avoid testing for these deficiencies during theinitial presentation. However, if plasma levels are well within the normal range at presentation, deficiency of theseproteins is essentially excluded. ©2010 UpToDate

®

VENOUS THROMBOEMBOLISM PROPHYLAXIS

1. Pulmonary embolism: The major complication of venous thromboembolism (VTE)accounts for approximately 5-10% of hospital deaths. Many VTEs are asymptomatic andwill go undiagnosed, but some will present as symptomatic DVT or pulmonary embolism.Presenting symptoms of hypoxia, tachycardia, SOB, pleuritic/atypical chest pain. LargePE can present with hypotension, acute right heart failure.

2. Risk factors: The most significant risk factors found in inpatients- age > 50 yrs, Varicose Veins, CAD, Cancer, Ischemic stroke, DM2

3. Strategies to Prevent VTE:- Mechanical:

- Elastic compression stockings (TEDS)- Intermittent pneumatic compression devices: Also called SCDs or Venodynes,

have not been studied well in medical inpatients, but likely provide somesubstantial benefit to those patients who have contraindications to anticoagulants.Just as efficacicous when applied to upper extremities

- Pharmacological:- Unfractionated heparin 5000 units SQ q8h- Enoxaparin 40 mg SQ daily or Dalteparin 5000 units SQ daily (only in GFR > 30)

4. Role in Thrombocytopenia/Coagulopathy: There is no data at this time regardingpharmacologic DVT prophylaxis and liver failure or thrombocytopenia, however patientswith INR > 2.0 or a platelet count below 50,000 can be considered to havecontraindications to pharmacologic prophylaxis.

References: Geerts WH et al, Chest 2001; 119:132S-175S.Kikura M et al, Arch Surg 2005; 140:1210-17.Samama MM et al.” NEJM 1999;341(11):793-800.Leizorovicz A et al, Lechler E et al, “Haemostasis 1996; 26(Suppl 2):49-56. KleberFX et al, “Am Heart J 2003; 145(4). Bergmann JF et alThromb Haemost 1996 76(4):529-34

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THROMBOCYTOPENIA

1. Definition: platelet count less than 150k (normal in 2.5% of population)2. Bleeding Risk: prolonged lab bleeding time <100k, surgical <50k, spontaneous <10-20k

Decreased production Destruction Sequestration

Viral infection (rubella, mumps,

varicella, parvovirus, HCV, EBV)HIV direct megakaryocyte damageChemotherapy or XRT

Bone marrow aplasia or hypoplasia, EtOH

toxicity

ITP

TTPDIC antiphospholipid abHELLP

Drugs (heparin, quinine,quinidine, valproate) Infection(EBV, CMV, HIV) Physicaldestruction (CP bypass)Evans syndrome

Portal HTN

CirrhosisSplenomegalyHypothermia

3. General workup: cbc (isolated thrombocytopenia or other cell lines affected?), peripheralsmear (looking for schistocytes, immature forms, etc.), coags, DIC panel, chemistries toeval for hemolysis (bilirubin, reticulocyte count, LDH, haptoglobin if smear equivocal), andof course careful review of medications. Many medications are associated withthrombocytopenia.

4. DVT prophylaxis in thrombocytopenia: In general, platelet count <50k is a relativecontraindication to SQ heparin, <30k is absolute. For patients at very high risk for VTE,weigh the risks and benefits. Some may warrant prophylaxis no matter how low the plateletcount.

5. Heparin Induced Thrombocytopenia- Type I:

- Transient, mild, asymptomatic drop in platelet count (rarely below 100k)- Occurs during first 1-2 days of therapy.- Resolves spontaneously and does not require suspension of drug.

- Type II (the real deal):- Platelet count often falls below 50-60k or by 50% of baseline platelet count- Generally occurs on day 10-14. Can be earlier in pts who have had heparin in the

last 3-4 months; late presentations can occur even after heparin discontinued- Immune mediated disorder characterized by antibodies against heparin-pltF4

complexes leading to platelet activation.- Thrombotic sequellae occur in 30-80% of people (arterial and venous)- LMWH is less likely to cause HIT when used first line but has 100% cross-

reactivity with antibodies- HIPA (Heparin Induced Platelet Aggregation) protocol

- If scheduled and ordered STAT, test is run M-F 8:30-16:30. Routine tests are runM-F 11:00 a.m.

- Patient must be off of heparin therapy (including lines and flushes) for at least 18hours.

- Specimen must be delivered within 1 hour of collection. Specimen cannot befrozen, must be fresh... Must be in by 11:00 a.m.

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BLOOD PRODUCTS

1. Packed Red Blood Cells (PRBCs): based on hemoglobin and risk factors- Hgb < 7 gm/dL – PRBC transfusion is indicated- Hgb 7-10 gm/dL – Consider transfusing patients who are high risk:

- Age >65, ACS, hypoxic respiratory failure- Goal hgb 10 g/dL, hematocrit 30.

- Hgb > 10 gm/dL – PRBC transfusion not indicated- Each unit of PRBCs is 300mL and should raise the hemoglobin by about 1gm/dl and

hematocrit by 3-4 percentage points unless there is continued bleeding. Each unit ofPRBC also delivers about 200mg of iron, so iron studies in an anemia work-up should besent before transfusion.

- Consider volume status with each transfusion (ESRD, CHF patients). Each unit of bloodincreases intravascular volume ~1L of crystalloid. Post-treat with lasix if needed, considerslow transfusion to avoid flash pulmonary edema.- Leukoreduced PRBCs are preferable in: chronically transfused patients, potential

transplant recipients, patients with previous transfusion reactions, and cytomegalovirus(CMV) seronegative at-risk patients for whom seronegative components are notavailable.

2. Platelets: transfusion threshold varies based on risk of bleeding- Keep platelets > 10,000 if: low risk of bleeding, ecchymoses/petechiae as only

manifestation of thrombocytopenia, acute leukemia, hematopoietic cell transplantation,solid tumors

- Keep platelets > 20,000 for minor bleeding (eg. mucosal bleeding) and for bone marrowbiopsy

- Keep platelets > 50,000 for most invasive surgical procedures (as long as there aren’tany other coagulation abnormalities) or if actively bleeding

- In general, one random donor platelet concentrate is expected to increase the plateletcount by 5000 to 10,000/uL in a 70 kg patient who is not refractory. Refractoriness isroughly equivalent to an absolute platelet count increment of <2000/microL per unit ofplatelet concentrate given to an average-sized adult.

3. Fresh Frozen Plasma: contains coagulation factors- Indications: coagulopathy in warfarin overdose, vitamin K deficiency, liver failure, TTP-

HUS (plasmapheresis). FFP should not be used as primary therapy for a specificcoagulation defect (eg, hemophilia A, hemophilia B, factor VII or XIII deficiency) whenspecific coagulation factor concentrates are available.

- Each bag is about 250mL. Initial dose should be 15mL/kg.

4. Cryoprecipitate: contains factor VIII, factor XIIII, fibrinogen, fibronectin, and vonWillebrand factor- Indications: Low fibrinogen states (eg. DIC), bleeding in von Willebrand disease, factor

VIII deficiency, factor XIII deficiency- Each bag is 10-15mL. It is usually ordered as 10 bags, which contain 2 gm of fibrinogen

and will raise the fibrinogen level about 70 mg/dL in a 70 kg recipient.

*Nomenclature of red cell shapes and associated disease states.Williams, Beutler, Rundles, et.al. Hematology.For images: http://www.som.tulane.edu/classware/pathology/Krause/AbnormalRBC/AbnormalRBC.html

DEEP VEIN THROMBOS IS (ADAPTED FROM UP TO DATE)

Pathogenesis: Involves three factors known as Virchow's triad: damage to vessel wall (preventsthe endothelium from inhibiting anticoagulation and initiating local fibrinolysis), venous stasis(inhibits clearance of activated clotting factors), and hypercoagulability.

Risk factors: History of immobilization or prolonged hospitalization/bed rest, recent surgery,obesity, prior episode(s) of venous thromboembolism, lower extremity trauma, malignancy, oralcontraceptives or hormone replacement therapy, pregnancy or postpartum status, stroke

Diagnosis: classic symptoms of DVT are pain, unilateral swelling, discoloration of leg. Becausethese symptoms are relatively nonspecific, the Wells criteria were developed to aid in thediagnosis via assessment of the PRE-TEST probability that a DVT is present.

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Wells criteria: (patients get 1 point for having each of the following)

• History of active cancer (within the last six months)• Paralysis, paresis, or recent plaster immoblization of lower extremity

• Bedridden for > 3 days, or has has major surgery within the last 4 months• Localized tenderness along distribution of venous system• Entire leg is swollen• Asymmetric swelling of calf of > 3 cm (measured below tibial tuberosity)• Pitting edema greater in symptomatic leg• Presence of collateral superficial veinsThen SUBTRACT TWO POINTS IF THERE IS AN ALTERNATIVE DIAGNOSIS MORELIKELY THAT DVT AS ETIOLOGY OF SYMPTOMS• High probability: 3 or more points• Moderate probability: 1-2 points• Low probability: 0 points

If patient is LOW PROBABILITY - check D-dimer, if -, no further testing indicatedIf patient is MODERATE PROBABILITY - check D-Dimer. If -, unlikely patient has

DVT. If +, get ultrasoundIf patient is HIGH PROBABILITY - no need to check D-Dimer, proceed with ultrasound

Treatment: Treatment is indicated for all patients with proximal deep vein thrombosis. It isestimated that >50% of patients with symptomatic proximal DVT develop PE

• Initial anticoagulation: Unless patient has contraindication to anticoagulation (hemorrhagicCVA or other life threatening bleed, patients can be treated with low molecular weightheparin (LMWH), fondaparinux, or unfractionated heparin (either as continuous IV infusionor adjusted-dose given subcutaneously).

• Oral anticoagulation: For most patients, warfarin should be started at the same time to allowthe level to become therapeutic (an INR 2-3) over five days. Warfarin inhibits the vitamin Kdependent clotting factors, including protein C. However, levels of protein C fall before theother clotting factors, causing patients to become transiently hypercoagulable when startingwarfarin.

• Inferior vena caval filter placement is recommended if patient has contraindication toanticoagulation, a massive PE causing hemodynamic instability (indicating that the patientwould not tolerate further emoblization from the deep venous system into the pulmonaryvasculature), or massive iliofemoral thrombosis.

• Fibrinolytics: activate plasminogen to form plasmin, resulting in clot lysis. Not generally usedin isolated deep vein thrombosis unless DVT is limb or life threatening. Used in massive PEif patient is hemodynamically unstable or in cardiogenic shock.

Duration of treatment: duration of anticoagulation varies by clinical setting and patientpreferences.

• First DVT in setting of obvious precipitant (i.e. surgery): three months of treatment• First distal (vein below knee) DVT and unknown precipitant: three months of treatment

• First proximal (vein above knee) DVT and unknown precipitant: six months of treatment, canconsider longer therapy if bleeding risk is small

• Patients with active malignancy: consider life long anticoagluation, optimally with LMWH, butwarfarin can be used if LMWH not available.

• Recurrent DVT: consider lifelong anticoagulation.

Complication of heparin therapy: bleeding and heparin-induced thrombocyptopenia (HIT):• HIT type I: non immune mediated, platelets fall within three days after initiation of heparin.

No further treatment required.• HIT type II: immune medicated disorder in which antibodies form against the heparin-

platelet factor 4 complex. Platelets fall > 50% 5-10 days after exposure to heparin. Typicalnadir is 60,000.

• Heparin MUST BE STOPPED and direct thrombin inhibitors (i.e. argatroban, fondaparinux,bivalirudin) started. Although HIT is a clinical diagnosed based on a drop in platelet count by50% within 5-10 days of exposure to heparin, it is a hypercoagulable disorder characterizedby both arterial and venous thrombosis. Diagnosis should be made and treatment started(cessation of heparin and initiation of direct thrombin inhibitors) before confirmation studiesare back due risk of venous and arterial clots. HIT with thrombosis (HIT-T) carries a 30-50%mortality.

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CHEMOTHERAP Y & COMPLICATIONS

1. Tumor Lysis Syndrome (adapted from Up to Date)

Definition: oncologic emergency that is caused by massive tumor cell lysis with the release oflarge amounts of potassium, phosphate, and nucleic acids into the systemic circulation

Who is at risk?- Patients with bulky disease, mainly leukemia (especially ALL, sometimes AML) or poorly

differentiated/high-grade lymphomas- Patients treated with cytotoxic chemotherapy, though steroids may be sufficient to

precipitate- Particularly high risk if present with elevated lactate dehydrogenase (LDH), uric acid, or

creatinine levels

Pathogenesis: Initiation of chemotherapy in patients with a large tumor burden or highlyproliferating malignancies leads to rapid lysis of tumor cells. Massive quantities of intracellularcontents are released, leading to hyperkalemia, hyperphosphotemia, hypocalcemia (bindsphosphate in circulation and precipitates out), and hyperuricemia (from the cataboism of nucleicacids). Both uric acid deposition and calcium phosphate deposition in the renal tubules can leadto renal failure.

Clinical manifestations: related to underlying metabolic abnormality such as hyperkalemia,hyperphosphatemia, hypocalcemia or due to flank pain due to uric acid nephrolithiasis - nausea,vomiting, diarrhea, anorexia, lethargy, hematuria, heart failure, cardiac dysrhythmias, seizures,muscle cramps, tetany, syncope, and possible sudden death

Medical treatment options• IV fluid: In absence of contraindication (i.e. heart failure), patients should receive 2-3L per

day with goal urine output 80 to 100 cc/hour

• Sodium bicarbonate: the role of urinary alkalinization is unclear, only clear role is in patientswith metabolic acidosis.

• Allopurinol: blocks catabolism of hypoxanthine and xanthine into uric acid.• Rasburicase: lowers uric acid levels by catalyzing oxidation of uric acid to the much more

water-soluble compound allantoin

Risk stratification with prophylactic treatment recommendations:

• High Risk features: all patients with Burkitt NHL or Burkitt ALL, ALL with WBC > 100,000 orAML with WBC > 50,000 should receive aggressive IV hydration and prophylacticrasburicase instead of allopurinol if available PRIOR to initiation of treatment

• Medium Risk features: patients with diffuse large B cell lymphoma, non B-ALL with WBC50,000 to 100,000, AML with WBC between 10,000 to 50,000, patients with CLL receivingfludarabine with WBC between 10,000 and 50,000 should receive IV fluid resusitation andprophylactic allopurinol when pre treatment uric acid level is normal. If pre treatment uricacid level are elevated, can consider using one time rasburicase in addition to allopurinol

• Low Risk features: patients with indolent NHL, ALL with WBC < 50,000, AML or CLL withWBC < 10,000, all patients with solid tumors. Prophylaxis with IV hydration in generallysufficient prophylaxis

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2. Neutropenic Fever:

DefinitionFever: single oral T >38.3 (101.3) or sustained T >38.0 (100.4) for over 1 hour

• Neutropenia: ANC <500, or ANC 500-1000 with predicted decline within 48 hours

Etiology

• Similar incidence of gram negative and gram positive infection; therapy targeted togram negative infection, especially Pseudomonas, due to faster rate ofdecompensation and death

• Candida and Aspergillus most common fungal infections; become more prevalentwith increasing duration of neutropenia

• No infection found in 50-70% of cases; 10-20% bacteremia, 20-30% clinicallyevident infection

Initial Evaluation and Management• Physical exam looking carefully for catheter site infections, mucositis• Panculture including any lines and start empiric antibiotics immediately

Empiric antibiotics - IDSA guidelines:

• Monotherapy: Appropriate for uncomplicated neutropenic fever• Ceftazidime 2g IV q8h, cefepime 2g IV q8h, imipenem-cilastatin 500mg IV

q6h, or meropenem 1g IV q8h (for patients with normal renal function)• Combination therapy: Indicated in severe sepsis or septic shock or high prevalence of

multi- drug resistant gram negative rods, Includes any of the above plus aminoglycosideor ciprofloxacin (if low enough prevalence of FQ resistance)

• Vancomycin should not be part of empiric regimen unless (1) evidence of catheter orsoft tissue infection,(2) known colonization with MRSA or penicillin-resistant S.pneumoniae, (3) severe mucositis, or (4) severe sepsis/septic shock.

• Oral regimen consisting of amoxicillin/clavulanate and ciprofloxacin may beappropriate for certain very low risk patients

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NEUROLOGY

ALTERED MENTAL STATUS

- Investigate: circumstances and vitals- SAFETY FIRST: patients are often confused and agitated so keep yourself between the

patient and the door and ask for assistance if any doubts.- Things not to miss: meningitis, ICH or intracranial mass, delirium tremens, untreated

infection.- Obtain Medication List: (the elderly are especially affected); look for medications causing

delirium (Anticholinergics, Benzos, Narcotics).- Workup: FS glucose, Chem 10 (Ca, Na, BUN), CBC, TSH, NH3 if suspect hepatic, LFTs,

UA, Blood and Urine Cx. Consider ABG, EKG, non-con CT Head if h/o trauma or focalneuro exam, LP if suspect meningitis.

- PE: pupils, neuro exam for focality, asterixis, fundoscopic exam, Kernig’s/Brudinski’s forMeningitis, Battle’s/Raccoon’s eyes for basilar skull fracture (fall/trauma), skin forpetechiae.

- Once patient is stable consider Differential: MOVE STUPID

- Metabolic: hepatic encephalopathy, B12/thiamine deficiency, niacin deficiency(pellagra), Wilson’s disease, electrolyte abnormalities

- Oxygen: hypoxia, hypercarbia, anemia, sepsis, CO poisoning- Vascular: CVA, hemorrhage (intracranial, subdural, epidural, subarachnoid),

vasculitis, TTP- Endocrine: hyper/hypoglycemia, hyper/hypothyroid, high/low cortisol, HONK/DKA- Seizures: post-ictal confusion (ie. Todd’s paralysis), status epilepticus

(nonconvuslive), complex partial- Structural: mass effect, hydrocephalus (normal pressure hydrocephalus &

pseudotumor cerebri)- Tumor, Trauma, Temperature- Uremia- Psych: sundowning and ICU psychosis are dx’s of exclusion. Porphyria (rare)- Infection- Drugs: intoxication/withdrawal, neuroleptic malignant syndrome, serotonin

syndrome

- Intervention: Depends on cause (Benzos for withdrawal from ETOH, lactulose for hepaticencephalopathy, dialysis for uremia, etc),

- Medications: Haldol often used 2-5 mg IM/IV as it causes minimal respiratorydepression-but beware of QT prolongation, sudden death (very rare). For elderly andliver patients avoid Benzos. Risperdal* is useful in the elderly (dissolvable form: M-tab).Benzos and Narcotics may worsen delirium.

*Black Box Warning does exist with regard to this use, though it still is commonly used with good efficacy

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SEIZURES AND STATUS EPILEPTICUS

If you are concerned for status, get the Ativan (or your benzo of choice), and call your Residentand Neuro ASAP.

- Definition: the occurrence of a single unremitting seizure >5 to 30 minutes or frequentclinical seizures without an interictal return to the baseline clinical state.

- Risk factors: head injury, stroke, Alzheimer's disease, history of intracranial infection, andalcohol or drug abuse, electrolyte perturbation.

- PE: Assess ABCs, call anesthesia to intubate if necessary; Labs: Chem, FSBS- Initial Intervention: Lorazepam 2mg iv, Midazolam 5mg iv, or Diazepam 10mg iv- Follow Algorithm: if seizures are refractory to initial boluses of benzodiazepines, follow

the Status Algorithm for further evaluation and treatment

Status Epilepeticus Algorithm:

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STROKE CODE

- If you have high suspicion for CVA, call operator and call a “Stroke Code”. This will alertthe Stroke team to mobilize.

- Follow the Algorithm.

Reference: American Heart Association. “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care – Part 9: Adult Stroke.” Circulation 2005; 112(24 Suppl): IV-111-IV-120.

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PALLIATIVE CARE

CROSSCOVER TIPS

CONSTIPATION

1. Goal: Move the bowel2. Etiology: Important to determine. Obtain a KUB to check for signs of obstruction,

which may sometimes reveal impaction of bowel with stool. Always keep thepossibility of ischemic colitis in the back of your mind. Check for use of narcotics &check rectal exam.

3. Orders: KUB, and consider a CT scan. Decide if you want to move the bowel fromaboveor below. Starting from below first in severely constipated patients is probablysafest, then transition to oral laxatives after a BM. Miralax is a GI favorite. Use cautionwith fleet enemas and MOM in elderly or patients with renal insufficency. Lactuloseenemas work well but are messy. Senna is helpful in waking up sleepy bowels fromnarcotics. Methylnaltrexone can be used in a single dose with repeat if patient is onhigh dose narcotics. Ask nurses to carefully record stools.- From Below: Dulcolax suppository, enemas (Fleets vs tap water vs mineral oil)- From Above: MOM 30ml QID, MiraLax 17g in 8oz liquid qd to bid, Mag citrate,Lactulose- Bowel Stimulation: Senna 1-2 BID, oral dulcolax bid, Neostigmine (severe refractory)- Stool Softener: Docusate 250 mg BID- Gastroparesis: reglan, erythromycin (beware of QTc prolongation) (motilin agonist)

4. Keep An Open Mind: An insidious but potentially morbid process is always possible.- Ogilvie's Acute Colonic Pseudoobstruction: these patient are at risk of

perforation because of acute dilation (often >10-15cm) of colon.- Volvulus: Gastrograffin enema is both diagnostic and therapeutic- Toxic Megacolon: part of the spectrum of C.diff (can also be seen in Hirschsprung’s)

and can present without antecedant diarrhea.

INSOMNIA

* Beware of Benzos and Anticholinergics. Better to have a grumpy patient then one on thevent from aspiration, hypercarbic respiratory failure.

* Care with oversedation especially in COPD or ESLD patients.1. Medications:

- Neuroleptics: Risperdal 0.5mg, Seroquel 25mg, Haldol 0.5mg: better for insomniathat is associated with delirium, not first line for the average patient.- Zolpidem 5-10mg: decreased rebound, tolerance, dependence compared to Benzos.- Trazodone 50mg: good for elderly, okay in liver patients.- Benzodiazepines: Temazepam 15-30mg; beware of paradoxical response; can

cause delirium; potential for dependence; avoid in liver patients- Diphenhydramine 25mg: beware of anticholinergic effects

NAUSEA

1. First line:- Ondansetron (Zofran) 4-8 mg IV or PO q6 prn. Serotonin receptor antagonist- Prochlorperazine (Compazine) 10 mg PO/IM/IV q6h or 25 mg PR q12h PRN. Side

effects: Extrapyramidal symptoms, seizures (CI), QT prolongation,hyper/hypoglycemia, sleep disturbances, anticholinergic.

- Promethazine (Phenergan) 12.5-25 mg PO/PR/IM/IV q4-6h, SE: sedation, seizures,hallucinations, respiratory depression, & anticholinergic. Do not give with narcotics.

- Lorazepam (Ativan) 0.5-2.0 mg PO/IV q4-6h prn.- Metoclopramide (Reglan) 10 mg PO/IV q4-6h prn; good for gastroparesis (DMII),

SE: EPS, dystonia, tardive dyskinesia, fluid retention, AV block, insomnia/anxiety- Dexamethasone (Decadron) 10 mg PO/IV q6h prn.

2. Second line:- Dronabinol (Marinol) 2.5-10 mg po q6h

3. General tips:- Beware neuroleptic malignant syndrome or dystonic reaction with excessive

use of compazine or droperidol (treat with benadryl 50 mg IV/IM or Cogentin 10mg IV)

- Compazine and Marinol are relatively contraindicated in patients with seizure disorder.- A common side-effect of many anti-emetics is drowsiness.- Happy Bag: continuous gtt of famotidine, zofran, diphenhydramine, haldol, and ativan

124

PREVENTATIVE MEDICINE/EBM/STATS

CARDIOVASCULAR RISK MODIFICATION

1. Aspirin Therapy: 81mg qd, higher doses are associated w/ increased side effects andlittle, if any, increased benefit.- Primary Prevention: Recommended in patients who have a 10 year risk of CHD >6-

10%. The ADA recommends that clinicians consider aspirin in diabetic patients >30years old or in those who have risk factors for CVD and no contraindications to aspirintherapy.

- Secondary Prevention: Should be given to all patients with CHD/CHD risk equivalentswho do not have contraindications.

2. Diabetes mellitus: While A1c remains the best test for assessing management ofdiabetes, it remains to be added as an accepted screening test.- Fasting Glucose: ADA recommends fasting glucose q3yrs, starting at age 45.- Early Screening: Consider initiation of screening at an earlier age if the patient has risk

factors for diabetes present (ie, obesity, hyperlipidemia, family history of DM, etc).

3. Dyslipidemia:- Lipid Panel: every other year in men >35yrs or women >45yrs- Yearly screening: Consider if any of the following are present:

- Diabetes- Family history of early CAD (<50 in males; <60 in females)- A family history suggestive of familial hyperlipidemia- Multiple CAD risk factors (eg, tobacco use, hypertension) then start at age 20 for

men and women

4. Abdominal Aortic Aneurysm:- Abdominal Imaging (usually AAA Screen Ultrasound) one time for all men who have

smoked (>100 cigarettes: 5 packs)

PSYCHOSOCIAL SCREENING

1. Alcohol Abuse:- CAGE: To screen for at risk drinking

- Have you ever felt you should Cut down on your drinking?- Have people Annoyed you by criticizing your drinking?- Have you ever felt bad or Guilty about your drinking?- Have you ever had a drink first thing in the Early morning to steady your nerves or

get rid of a hangover?- A positive response to two or more questions suggests a high likelihood of alcohol

abuse.

2. Depression Screening:- During the past month have you often been bothered by feeling down, depressed or

hopeless?AND

- During the past month have you often been bothered by little interest or pleasure in doingthings?

- 97% sensitivity for depression when both positive

Reference: BMJ Nov 2003

125

CANCER SCREENING

1. Breast Cancer:- Self-breast exams: at age 20- Annual CBE: Clinical Breast exams after age 20 (10% of screening detected breast

cancer caught by exam despite negative mammogram).- Annual Mammogram: starting at age 40.- Early Screeing: At age 35 if family h/o breast cancer earlier than age 50 or 10yrs prior

to the age of diagnosis of breast cancer in first degree family member.- Discontinuation: Some evidence supports stopping screening after age 74, however,

most expert groups recommend continued screening if patient has >10 year lifeexpectancy.

2. Cervical Cancer:- Annual PAP smear starting 3 years after onset of sexual activity or at age 21, whichever

comes first (ACOG). This is based on the fact that it takes 3-5yrs after HPV infection todevelop dysplastic changes.

- Intervals: If 3 consecutive normal PAP smears AND patient has no risk factors forcervical cancer (ie not sexually active or in a monogamous relationship, no DESexposure, no history of abnormal pap, etc) PAP every 1-3yrs.

3. Colorectal Cancer:- Screening Initiation: For average risk patients >50 years old.- Annual fecal occult blood test FOBT(stool cards) WITH either Flexible sigmoidoscopy

every 5yrs, starting at age 50 (Not available at UCSD) OR double contrast bariumenema every 5yrs, starting at age 50

- Colonoscopy every 10yrs, starting at age 50

Increased risk patients:- Includes adenomatous polyps, IBD, genetic syndromes (ie. FAP and HNPCC), prior CRC

and family history of CRC in first degree relative.- Family history: if 1st degree relative developed CRC or adenoma >60 yo, then begin

colonoscopy at age 40, repeat q10yrs, if 1st degree relative developed CRC oradenoma<60 yo or two 1

stdegree relatives with disease at any age, then begin

colonoscopy at 10 yrs before earliest age of diagnosis OR at 40 years of age,whichever comes first, repeat q5yrs.

- Prior CRC: q3-5yrs- Prior adenomatous polyp:

- In 3-6 months – if large sessile adenoma (>2cm) and/or if poor prep- In 3 years – If adenoma >1cm or >2 adenomas found or adenoma with villous

histology or high grade dysplasia.- In 5 years – If 1-2 small adenomas (<1cm)

4. Prostate Cancer: Current guidelines recommend discussing the role of prostate screeningin asymptomatic men with them, but do not advocate any specific screening modality.- Consider annual DRE, starting at age 40 if African-American (there is an increased

incidence of prostate cancer in this group); age 50 for others. No controlled studies haveshown a reduction in the morbidity or mortality of prostate cancer when detected by DREat any age.

- Consider annual PSA, starting at age 40 if African-American; age 50 for others.- Start screening at age 40 if the patient has 1st degree relative w/history of prostate

cancer.- African-Americans have a 60% higher incidence rate of prostate cancer; screening

should be discussed earlier in this population- If PSA >7, refer for biopsy, if 4-7, repeat lab within few weeks and have patient refrain

from ejaculating and bike riding 48hrs before test.- If PSA <4.0, but rise of 0.75 ng/ml/year based on 3 measurements over 1-2yr period

then refer for biopsy.- Usually stop screening at 75 yo or when patient has <10yr life expectancy.

5. Testicular Cancer: The U.S. Preventive Services Task Force (USPSTF) recommendsagainst routine screening for testicular cancer in asymptomatic adolescent and adultmales.

126

PRIMARY PREVENTION

1. Osteoporosis:- Intiation: Bone densitometry screening starting at age 65yo or <65 yrs and

postmenopausal and at increased risk of fracture (i.e. wt <127lbs, smoking, fracture in 1st

degree relative, ETOH, immobility. Estrogen deficiency--> menopause < 45yo, BSO.- Medications Associated with Bone Loss: Synthroid, Seizure meds, Steroids- DEXA Scan: T score = the number of standard deviations (SD) above/below- the mean in young adults of same sex and race.- Osteopenia: T score of -1.0 to -2.5- Osteoporosis: T score of > - 2.5- Calcium: premenopausal: 1000mg daily, postmenopausal: 1500mg daily- Vitamin D: 400-800 IU Daily- Bisphosphonates: Indicated for osteoporosis

2. Vaccinations:- Influenza:

- Annually for adults with chronic medical problems- Annually for healthcare workers- As desired for healthy adults

- Pneumovax:- Once in any adult with chronic medical problems. Single booster should be given

at age 65 if patient received 1st dose >5 yrs previously.- Once in any immunocompromised adult (ie. HIV, malignancy, CRF, asplenia,

chemotherapy, post organ/bone marrow transplant). Single booster after >5 yrs- All adults > 65 years old.

- Tetanus: Booster should be given every 10 years.- Hepatitis A:

- All children at age 1 year- Children/adolescents ages 2-19 who live in states where mandated- Persons traveling to or working in countries with high or intermediate prevalence- Men who have sex with men- Users of illegal injection and noninjection drugs- Persons who have occupational risk for infection- Persons who have chronic liver disease- Persons who have clotting-factor disorders

- Hepatitis B:- Age 19-39: Universal immunization- Age 40 and over: Immunize high risk patients (MSMs, correctional facilities, IVDU,

HIV/AIDS, those exposed to high-risk patients)- Meningococcus:

- Routine vaccination of young adolescents or prior to high school entry- College freshman, military recruits, travelers to areas in which disease is

hyperendemic or epidemic, health-care workers exposed to Neisseria- Functional or anatomic asplenia or terminal complement deficiency

- Varicella:- Age 19-26: Verify second dose completed.- Age 27 and over: For all adults without evidence of immunity to varicella, give two

doses of varicella vaccine with at least 28 days between first and second doses.- HPV:

- Females age 11-12 (as young as 9); catch up vaccines for females age 13-26- Consider MSMs- NOT a substitute for routine cervical cancer screening

- Shingles: Immunize age 60 and over (single dose) irrespective of whether patientreports a prior episode of herpes zoster.

Grading of Recommendations:

1 = strong recommendation (benefitsclearly outweigh costs)2 = weak recommendation (benefitsprobably outweigh costs, but unsure)

A D = high grade of evidence verylow grade of evidence

127

EVIDENCE BASED MEDICINE & STATISTICS: THE 5 A’S

1. Assess: Information you need to take better care of your patient.

2. Ask: Focus in your information search by increasing the words in your query:- P: Word or phrase for patient or problem- I: Word for intervention you’re considering- C: Word for comparison intervention- O: Word for outcome important to you/ptExample: Will metoprolol, which is more affordable, provide as much mortality benefit as carvedilol?

P = heart failure or CHF; I = metoprolol; C = carvedilol; O = mortality

3. Acquire: Limit Medline using EBM criteria such as RCT, meta-analysis, or the extra limitsin Medline’s Clinical Queries. Consider using pre-appraised information:- ACP Journal Club (OCL) - Cochrane Library (OCL)- ACP’s PIER (thru STAT!Ref on OCL) - National Guideline Clearinghouse (OCL)- Clinical Evidence (free thru unitedhealthfoundation.org)

4. Appraise: Assess the article’s validity before proceeding to the results.- Validity: one method to assess the validity of an article/article type can be found in the

Users’ Guides at the OCL.- Results: methods to assess the results are also available via the Users’ Guides and

Center for EBM (OCL). For the common article types:

Appraising Treatments:- EER = the experimental event rate (512/1511 carvedilol patients died = 34%)- CER = the control event rate (600/1518 metoprolol patients died = 40%)- Statistical significance: p < 0.05 or CI not crossing null effect- RR = relative risk = EER/CER = 85%

(risk of death on carvedilol is 85% what it would have been on metoprolol)

- RRR = relative risk reduction = 100 – RR = 15%(risk of death on carvedilol is 15% LESS THAN it would have been on metoprolol)

- ARR = absolute risk reduction = CER – EER = 6%(proportion of population who will change outcome w/changing from metoprolol to carvedilol)

- NNT = number needed to treat = 100/ARR = 17(number of patients treated with carvedilol instead of metoprolol to save one life)

Appraising Diagnostic Tests:

Sensitivity: true +/all with dz = 167/197 = 85%- High Sensitivity: positively identifies most case but not just true cases, in other words, not

specific to disease; thus high false positive, but low false negative- Mnemonic: snout - high sensitivity and neg test rules out dz

Specificity: true -/all without dz = 670/980 = 68%- High Specifity: positively (and correctly) identifies true cases, but misses some due to

lack of sensitivity; thus low false positive, but high false negative- Mnemonic: spin - high specificity and pos test rules in dz

LR Likelihood Ratio: likelihood ratio (with 1 being no increased likelihood) that you havedisease for a given test result.- LR = proportion of pts w/ dz who came up + = 167/197 = sensitivity = 2.7

proportion of pts w/o dz who came up + 310/980 1 – spec- LR can be entered into a nomogram at OCL to obtain a post-test probability of disease.

5. Apply: your results to affect patient care

PE

w/ w/o

d-dimerr+

_

167 310

30 670

1977 980

47

701177

*Online Clinical Library (OCL) availablethru Users’ Guides or Center for EBMlinks on UCSD computers

128

MEDICAL SPANISH: THE BASICS

This guide is designed to get you through the basic admission work-up and daily pre-rounding. Since one of the hardest things about speaking Spanish to patients isunderstanding what they say back to you, most of what is included is in the form of yes/noquestions.

There are Two Basic Verbs for which you should learn conjugations:

1. Ser: to be, meaning a permanent state of being- Yo soy (I am); Tu eres (you are, informal); Usted es (you are, polite); Nosotros somos

(we are); Vosotros sois (you are, plural, rarely used except in Spain); Ustedes son (youare, plural)

2. Estar: meaning a temporary state of being- Yo estoy (I am); Tue estas (you are, informal); Usted esta (you are, polite); Nosotros

estamos (we are); Vosotros estais (you are, pleural, again never use this); Ustedes estan(you are, plural)

*Often you can just use the verb without the indicator in sentences. Examples:- Yo soy Doctor Smith (I am Doctor Smith, I will ALWAYS be Doctor Smith)- Donde estas? (Where are you at THIS moment?).

3. Greetings and formalities:- Buenos dias (good morning, good day), buenas tardes (good afternoon), buenas noches

(good evening)- Hola (hello)- Yo soy doctor (doctora) _______. - I am Doctor _______.- Como estas? - How are you?- Como te llamas? - What is your name?- Me llamo ______. - My name is _______.- Gracias - thank you- De nada - you are welcome- Chau/adios - bye

4. HPI:- Que problema tienes hoy? - What problem are you having today?- Tienes dolor? OR Estas con dolor? (Both mean “do you have pain?”)

- dolor del pecho (chest pain)- falta de aire (shortness of breath)- fiebre o escalofrios (fevers or chills)- dolor de la cabeza (headache)- nausea- vomitos (vomiting) – con sangre? (with blood?)- dolor del estomago/abdomen (abdominal pain)- cambios en la vista (visual changes)- dolor de la garganta (sore throat)- dolor al orinar (dysuria)- dificultad de hablar/tragar (difficulty speaking/swallowing)- tos (cough) - con sangre? (with blood?)- diarrea (diarrhea) - con sangre? (with blood?)- sangre en la orina - hematuria- sangre en el excremento - bloody stool- debilidad de un brazo o de una pierna (weakness in an arm or leg)- izquierdo/a (left)- derecho/a (right)

129

5. PMH/FH/SH:- Tienes algun problema medico? (Do you have any medical problems?)- Tienes ______ (do you have ______?)

- diabetes- presion alta (hypertension)- ataque del corazon OR coronaria OR infarto- cardiaco (MI)- enfermedades cardiacas (heart disease)- SIDA/VIH (AIDS/HIV)- Tuberculosis- Cancer (you can ask “donde?” for them to indicate where they have cancer)- Asma (asthma)- Enfermedades pulmonares (lung disease)- Problemas del higado/del pancreas (liver/pancreatic problems)- Hay historia en tu familia de ______ (do you have a family history of ______?)- Quien (who?): papa (father), mama (mother), abuelo (grandfather), abuela

(grandmother), hijo (son), hija (daughter), tio/a (uncle/aunt), primo/a (cousin),- nieto/a (grandson/daughter), hermano/a (brother/sister); Note: as a general- rule with many exceptions masculine words end with “o” and feminine words- with “a.”- Tomas alcohol? (Do you drink alcohol?); Tomas drogas? (do you use drugs?); if

yes, con agujas o sin agujas? (with or without needles if patient answers yes todrug use); fumas cigarillos? (do you smoke cigarettes?); donde vives (where doyou live?); con quien? (with whom); has viajado recien? (have you traveledrecently?); para donde? (to where?); has estado en la carcel? (have you been injail?); tienes trabajo? (do you work?); que tipo de trabajo haces? (what kind ofwork do you do?)

6. Allergies: tienes alergia a medicamentos o comidas? (do you have a medication or foodallergy?); a cuales (to which ones?)

7. Medications: que medicamentos tomas? (what medications do you take?); tienes unalista de los medicamentos? (do you have a list of your medications?)

8. Physical Exam:- Te voy a examinar ahora, OK? (I am going to examine you now, OK?)- Levantate (get up)- Acuestate (lie down)- Sientate (sit down)- Abra la boca y saque la lengua (open your mouth and stick out your tongue)- Por favor (please)- Te duele? (Does it hurt?)

9. AM rounds:- Como te sientes hoy? (How do you feel today?)- Tuviste algun problema por la noche? (Did you have any problems overnight?)- Tuviste ____ (did you have ____?, see above list for items to fill the blank.)- Te sientes mejor/peor/igual? (Do you feel better/worse/the same?)- Necesitas algo? (Do you need anything?)- Comida/bebida (food/drink)

130

CONVERSIONS & TABLES

CORTICOSTEROID CONVERSION TABLE

Drug Equivalentdose (mg)

Anti-inflammatory

potency

Mineralo-corticoidpotency

BiologicHalf-life(hours)

Cortisone 25 0.8 2 8-12Hydrocortisone* 20 1 2 8-12

Prednisone 5 4 1 18-36Prednisolone 5 4 1 18-36

Methylprednisolone 4 5 0 18-36Triamcinolone 4 5 0 18-36

Dexamethasone 0.75 20-30 0 36-54Betamethasone 0.6 20-30 0 36-54Fludrocortisone Not available 10 125 18-36

*roughly equivalent to endogenous Cortisol

INTRAVENOUS FLUIDS

Osmolality(mOsm/kg)

Glucose(g/L)

Sodium(mmol/L)

Chloride(mmol/L)

Other

D5W 278 50 0 0D10W 556 100 0 0D50W 2778 500 0 0½ NS 154 -- 77 77

NS 308 -- 154 1543% NS 1026 -- 513 513

LR 274 -- 130 109

K+ 4mmol/LCa++

1.5mmol/LLactate

28mmol/L

NARCOTIC & OPIOID CONVERSION

1. Commonly Used Orals: Morphine Equivalence:Tylenol #3

Acetaminophen 325mg+

Codeine 30mg

VicodinAcetaminophen 500mg

+Hydrocodone 5mg

PercocetAcetaminophen 325mg

+Oxycodone 5mg

Morphine 3-4mg PO Morphine 5-6mg PO Morphine 7-8mg PO

2. Opioid Conversion Table:Oral/Rectal Dose (mg) Analgesic IV/SC/IM Dose (mg)

150 Meperidine 50150 Tramadol -150 Codeine 5015 Hydrocodone -15 Morphine 510 Oxycodone -3 Hydromorphone 12 Levorphanol 1- Fentanyl 0.050 (50mcg)

131

3. Transdermal Fentanyl: (2:1 Rule)Morphine 50mg PO over 24 hours = Fentanyl 25mcg transdermal patch

- Serum Fentanyl takes 12-24 hours before reaching plateau so may need to continueto treat pain with other medication for at least first 12 hours.

- Do not use in opioid naïve pts or for post-operative pain; useful in chronic stable pain.- Heat & Fever increase absorption.- Never cut a fentanyl patch in half.- Remove patch when pt goes to MRI to avoid burns.

4. MethadoneDaily Morphine Dose

(mg/24hr PO)Conversion Ratios

Morphine PO : Methadone PO

<100 3:1101-300 5:1301-600 10:1601-800 12:1801-1000 15:1

>1001 20:1

5. Side Effects- Constipation – be sure to place all patients on bowel regimen.- N/V – treat w/ compazine, usually improves in 24-48 hrs.- Itching – treat w/ benadryl, usually improves in 48-72 hrs. (Hives are an allergic- reaction and med should be stopped)- Myoclonus/Hallucinations – these are signs/symptoms of opiate toxicity.

6. The Transition:- It is recommended to initially use lower than equivalent doses when switching between

different opioids, especially in the elderly.

132

ENTERAL FORMULARY

Two Cal HNHigh calorie: As well as high nitrogen, complete formula withreduced sodium for hypermetabolic patient requiring severe fluidrestriction.

Jevity 1.2High Fiber: Normalization of bowel function; isotonic, nutrientdense, high nitrogen, low residue, lactose free.

Promote w/ FiberHigh Fiber & Protein: Nutritionally complete high nitrogen, nearlyisotonic liquid with fiber for patients with increased protein needs.

PivotorPromote

High Protein: Nutritionally complete high nitrogen, nearly isotonicliquid with fiber for patients with increased protein needs.

NeproDialysis Patients: Nutritionally complete high nitrogen, nearlyisotonic liquid with fiber for patients with ESRD.

NutrihepESLD Patients: Rich in branched-chain amino acids and low inaromatic and ammonogenic amino acids. Calorically dense, with ahigh calorie-to-nitrogen ratio for patients with ESLD.

Peptamen AF

Elemental nutrition: complete and balanced tube feeding forhypermetabolic conditions requiring partially hydrolyzed protein(free amino acids, di and tri-peptides), -carotene and L-argininewith MCT oil. Useful in Pancreatic Insufficiency.

Glucerna 1.2Diabetic Patients: Calorically-dense formula with a uniquecarbohydrate blend for enhanced glycemic control, and fish oil toreduce glycemic response.

Ensure PlusHigh calorie, lactose free, nutrient dense formula when limitedvolume required.May be used orally or as tube feeding.

EnsureA concentrated high protein liquid food for patients requiringadditional calories, protein, vitamins and minerals.May be used orally or as tube feeding.

133

PHONE NUMBERS

VAMC PHONE NUMBERS

Main – (858) 552-8585AOD 2366/2367Chief residents

Inpatient 7622Outpatient 2759

Cast tech 3841p347-1391

Cath lab 3464Coding room 3950Computer Help 4767Coumadin clinic 3041CPRS

J. Christmas 7802B. Henry 1033

Cytology 7729DAV 7470Decedent Affairs 7568Diabetes Educ 7245ECG ((M-F 7-4pm) 3644EEG/EMG 3688/3685ER 2366Escort 3311/66-791Exercise Treadmill 3550Eye Clinic 2205FIRM (4N) 2907Heart Station 1127Hemodialysis 7517Home Health/HBPC 3064Home health planning

3N L. Suchocki 2973Linda’s pgr p347-1837

5E P. Pelican 3094Pat’s pgr p347-1818

Home Oxygen 3634Labs:

Add-On 7707ABG/Gas Lab 7264Blood bank 3200Chemistry 7750/7751Cytology 7729Hematology 3420Immunology 2383Micro 3367Pathology 7723Processing 7707Serology 2383

MAOD 4344Med Admit pager 290-7173Medicine Office 3481Mission Valley Firm 5051/5052Nuclear Med 7511/4385Nutrition 3373OT 7672PFT Lab 7352Pharmacy :

Outpatient 1669Inpatient

3N 2214p347-1408

5E 5343p347-1409

ICU/DOU 2377/5344p347-1444

Phlebotomy 3668/7707Physical Therapy 7487/3683PICCs

Andrea/Tracy 7979Myra Williams 2362

p347-1849Podiatry 3981Prosthetics 7415Psychiatry p347-1427Radiology: 3226

Main 1164Body 7773Bone Pit 7793, 7194Chest 7772/7774CT scanner 7796Head 2850IR 6903/7801MRI 2860/7980Neurorads 2850Ultrasound 7771Tech 6471

p347-1428RT 3518Security 3647Sleep study 2494/4701Social Work

3N Eric Ramirez 73914S Marita McGoldrick 2279

Or 858-699-3507 (cell)5E Katherine Ponchetti 3329

Speech path 7564Surg Path 7738Travel Office 7575/5848Transfer Office 7458Urgent Care 3386Vascular Lab 3290Floors:1E SCI 3185/31732S 37953N-Main 34463N-B Pod 7248/76473N-C Pod 7645/76483S-Infusion Center 35214S-Main 35645E 32955E-B Pod 5478/54795E-C Pod 54285S DOU 79795S VICU 5400Fax Machines:DOU (858) 642-3494UCC/ER (858) 552-7515FIRM (858) 642-6325

134

Main (619) 543-6222ACLS/PALS 294-5838Case management 33516Cath Lab 37166Chief residents

Inpatient 36297Computer help 34357

PACS 36760CMH 692-8200ER 32140

Nurses 32154ER fax 33122

4th & Lewis Clinic 294-9520471-9250

Back lines: 19270/19271Flow Cytometry (858) 642-4774GME Office 37768Heart Station 36399/36485

Echo 35715Telemetry 32703Fellow’s Rm. 37230

Hemodialysis 36871Infusion Center 32639Labs:

Blood gas 36536Blood bank 35640Chemistry 36020Cytology 35378Hematology 36020Micro 35940/32820Rheum 35773Surg path 35764Toxicology 36020Virology 35797Serology 35587, 32249

Medical Records 36700Med Rec Fax 33287Dictations 32720, 32867,

32936Med Admit pager 290-1150Notary public 33620Nuclear medicine 36680, 31985,

31991Nursing Supervisor p2616Owen Clinic 33995/33999Paging 36440Pharmacy:

Discharge 33279/32682Inpatient 35924Outpatient 36191CCU On-call p3535

Physical Therapy 36530

PPD/Skin Testing 35890Peach 37719

Path Hot Seat 33243Psych On-call 290-5050Rads On-call p5063, 37043Rads scheduling 33405/32280

Chest RR 37043/35389CT scanner 36893, 36894

Body CT RR 32511KUB 19476

Bone 35277Head CT RR 32566IR 32158, 32476,

32138MRI 36148, 32944,

32940MRI Body 33177MRI Neuro 32931, 10759File room 36586Ultrasound 32620/32621Risk management 36630/96468RTAS 37140San Ysidro Clinic 619-205-6306Security 33762Speech Pathology 220-7570Transfer Coord 35709Floors:2S SICU 374285E BICU 365025W IMU 36080533 363446E 320916E fax 362246W 328707IMU 19533/195538E 363808W 363059W MICU 3596010E 3630010W CCU 36592, 3313511E 3528011W 36450

Administrative Support StaffMPF Bldg, 402 Dickinson St, Suite 380

Chief Res Office fax 37186Residency Admin Offi fax 36529Anne Bamrick 36287abamrick@ucsd.eduERAS Coordinator, Payroll/PersonnelSpecialist, Duty Hours/New Innovations

HILLCREST PHONE NUMBERS

135

Main (858) 657-7000Case Managers 76063

Weekend p7578Elyse (3E) p0423

76067Irma (3W) p8078

76602Bonnie (2E) p3987

76805Vangie (2W) p3606

76815Liz (ER) p9861

77224CF Clinic 77073

Jessica Hill 77103, 76774p7255

Code Blue 76111Computer Help 3HELPEEG 76080ER 77600, 77660Fax (2W) 76061Flow Cytometry (858) 642-4774Heart Station 78530/78533

Tech p3960Infusion Center 76301Lab: 76595

Blood Bank 76161Chem 76169Cytology 35378Hematology 76165Microbiology 76959Other 76595

Med Admit pager p7268Med Records 76906Nursing Stations:

ICU (2 North) 76700IMU/2E (200s) 76295, 762902W (250s) 768863W/BMT (350s) 763903E (300s) 76340

Nursing Supervisor p2670Nutrition 76470OR 76500OT/PT 76590

Weekend PT p4924Weekend OT p1814Tracy (PT) p3986Tammy (PT) p4196Kelly (PT) p4172Jorge (PT) p3980Resie (OT) p3562Linda (OT) p7590

PACU 76540Pain Service 76035Pathology 76595Pharmacy (inpt) 600-2330

p395276679

Pgr 4142Pharm (outpt) 78512Phlebotomy 78690PTE Office 77100

Maureen p5141Pam p3863

RadiologyRTAS 37140Day Tech p3997Night Resident p5063Angio 76657CT Scanner 76667

Tech p3954Fileroom 76646IR 76657MRI 76671

Tech 76674Neuro CT 32566Nuc Med 76659Reading Rooms

CT Body 76779Bone 76780Chest 37043Ultrasound 76778

Radiation Oncology 26040Respiratory 76690

Pgr 4166, 41863972, 3585

Security Pgr 2660Speech Path 220-7570

Pgr 4288Social Work 76804

Pgr 4288Telemetry 76703Transfer Center 35709

Pgr 5673Urgent Care 77300Workrooms

2W 7688676282

3W 7638076382

3E 76340

Any phone number: PCISGeneral Menu UCSD PhoneBook

THORNTON PHONE NUMBERS

136

OUTSIDE HOSPITALS

Scripps Mercy (Hillcrest)Main Number: 619-294-8111Med Records: 619-260-8972Med Records Fax: 619-260-7369

Scripps Mercy Chula VistaMain Number: 619-691-7000Med Records: 619-691-7336Med Records Fax: 619-407-7677

Scripps Memorial La JollaMain Number: 858-626-4123Med Records: 858-626-6848Med Records Fax: 858-626-6141

Scripps GreenMain Number: 858-554-9100Med Records: 858-554-4757Med Records Fax: 858-554-2540

Sharp MemorialMain Number: 858-939-3400Med Records: 858-939-3404Med Records Fax: 858-939-3491

Sharp Grossmont HospitalMain Number: 619-740-6000Med Records: 619-740-3887Med Records Fax: 619-740-4442

Sharp Chula Vista HospitalMain Number: 619-482-5800Med Records: 619-482-3642Med Records Fax: 619-482-3483

Alvarado HospitalMain Number: 619-287-3270Med Records: 619-229-3175Med Records Fax: 619-229-3397

Paradise Valley HospitalMain Number: 619-470-4321Med Records: 619-470-4205Med Records Fax: 619-470-4102

Fallbrook HospitalMain Number: 760-728-1191Med Records: 760-731-8238Med Records Fax: 760-728-0617

El Centro Regional Medical CenterMain Number: 760-339-7100

Pioneers Memorial Hospital(Brawley)Main Number: 760-351-3333

137

DOOR CODES/PASSWORDS

Hillcrest- Copier code: Employee ID or 5-4-3-6-2-8-7- BICU: 5-4-3- CCU: 6-1-9-*- ER: 0-3-5-*- ER side door: 5-3-2-Enter- UCC: 1-5- 10E workroom: 3-5- Medicine office: 3-2-4-Enter- CCU Office: 3-2-4-Enter- Closet combo 3-1-5-3- PACU/OR 4-0-0-0-*- New PACU 7-7-8-8- Senior Behavioral Health: 8-6-3-1- SICU: 6-4-2- Clean Utility (most floors): 2-5-Enter- Storage Rooms (on ends): 3-5-1-Enter- Cath lab: 1-6-3-*- 4th & Lewis Clinic: 9-1-1-9-1- Owen’s Clinic: 8-5-4-*

Thornton- ER: 7-6-0-*- 2nd Floor Pharmacy: 6-0-1-0-#- ICU: 6-0-3-8- BMT Office: 6-3-9-0

VAMC- ER/UCC: 9-8-7-4- Area 2: 7-9-2- 3E call rooms (Main door): Check with VA chief at start of rotation- 3E call rooms 3288, -89, -97: 3-2-8-7- Team 3 work room: 3-2-1-4- 3W access clinic: 3-0-3-2- 5S VICU call rooms 5101: 3-0-0-4- Supply rooms: 1-7-4-7- Main medicine office: 3-0-1-8- Conf Room 3004: 1-3-7-9-5-5- 3S Lounge 3207B: 3-2-0-8- MV Firm: 4+5-2- MV Firm Copier Code: 1-2-0-4- Hemodialysis Unit: 1-8-0-7

PASSWORDSMUSE ECGs: Username: ad/emergency

Password: Emer!gency

MyFax http://www.myfax.comUsername: 888-569-7870 (same # as the fax)Password: ucsdmedres2