laboratory tests in the intensive care unit · 2016-12-01 · laboratory tests in the intensive...

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LABORATORY TESTS

IN THE

INTENSIVE CARE UNIT

JASSIN M. JOURIA, MD

DR. JASSIN M. JOURIA IS A MEDICAL DOCTOR, PROFESSOR OF ACADEMIC MEDICINE, AND MEDICAL AUTHOR. HE GRADUATED FROM ROSS UNIVERSITY SCHOOL OF MEDICINE AND HAS COMPLETED HIS CLINICAL CLERKSHIP TRAINING IN VARIOUS TEACHING HOSPITALS THROUGHOUT NEW YORK, INCLUDING KING’S COUNTY HOSPITAL CENTER AND BROOKDALE MEDICAL CENTER, AMONG OTHERS. DR. JOURIA HAS PASSED ALL USMLE MEDICAL BOARD EXAMS, AND HAS SERVED AS A TEST PREP TUTOR AND

INSTRUCTOR FOR KAPLAN. HE HAS DEVELOPED SEVERAL MEDICAL COURSES AND CURRICULA FOR A VARIETY OF EDUCATIONAL INSTITUTIONS. DR. JOURIA HAS ALSO SERVED ON MULTIPLE LEVELS IN THE ACADEMIC FIELD INCLUDING FACULTY MEMBER AND DEPARTMENT CHAIR. DR. JOURIA CONTINUES TO SERVES AS A SUBJECT MATTER EXPERT FOR SEVERAL CONTINUING EDUCATION ORGANIZATIONS COVERING MULTIPLE BASIC MEDICAL SCIENCES. HE HAS ALSO DEVELOPED SEVERAL CONTINUING MEDICAL EDUCATION COURSES COVERING VARIOUS TOPICS IN CLINICAL MEDICINE. RECENTLY, DR. JOURIA HAS BEEN CONTRACTED BY THE UNIVERSITY OF MIAMI/JACKSON MEMORIAL HOSPITAL’S DEPARTMENT OF SURGERY TO DEVELOP AN E-MODULE TRAINING SERIES FOR TRAUMA PATIENT MANAGEMENT. DR. JOURIA IS CURRENTLY AUTHORING AN ACADEMIC TEXTBOOK ON HUMAN ANATOMY & PHYSIOLOGY.

Abstract

When patients are brought to the intensive care unit, extensive

laboratory testing is often considered necessary in order to diagnose

and treat critical conditions. However, laboratory tests are not without

risk. Results can be misleading, and the testing itself can be harmful,

such as potentially causing iatrogenic anemia. Medical professionals

need to take a sensible approach to laboratory testing for patients in

the intensive care unit, focusing on the benefits and risks of each test

and being mindful of the probability of disease.


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Policy Statement

This activity has been planned and implemented in accordance with

the policies of NurseCe4Less.com and the continuing nursing education

requirements of the American Nurses Credentialing Center's

Commission on Accreditation for registered nurses. It is the policy of

NurseCe4Less.com to ensure objectivity, transparency, and best

practice in clinical education for all continuing nursing education (CNE)

activities.

Continuing Education Credit Designation

This educational activity is credited for 2.5 hours. Nurses may only

claim credit commensurate with the credit awarded for completion of

this course activity.

Statement of Learning Need

Clinicians caring for patients in the Intensive Care Unit are required to

interpret laboratory tests and be able to manage safe and appropriate

laboratory testing guidelines. Health professionals working with

critically ill patients need to take an evidenced-based and rational

approach to laboratory testing, including an understanding of the

benefits and risks of each test relative to a disease process.


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Course Purpose

To provide health clinicians with knowledge of different types of

laboratory testing for patients in the ICU as well as the benefits and

risks of varied tests.

Target Audience

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses

and Medical Assistants may obtain a Certificate of Completion)

Course Author & Planning Team Conflict of Interest Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article.

Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.


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1. Laboratory test sensitivity refers to the ability of a

a. patient to tolerate a test. b. test to identify the presence of a disease or condition

correctly. c. test to identify true negative. d. test to identify the absence of a disease or condition correctly.

2. Transfusion of whole blood, packed cells or blood

components has been a. shown to offer a survival advantage to patients. b. known to reduce production of erythropoietin. c. shown to depress new blood cells. d. associated with the risk of infection.

3. True or False: Wellness testing is not an aspect of lab

testing in the ICU setting. a. True b. False

4. Red blood cell transfusion is indicated for a patient

a. with adequate blood flow (hemodynamic stability). b. with acute hemorrhage but only in single units. c. with evidence of hemorrhagic shock. d. as an absolute method to improve tissue oxygen

consumption. 5. The Nyquist-Shannon Theorem posits that there is an

appropriate relationship between the number of samplings and the likelihood that a. a test will identify the presence of a disease. b. the risk of clinically inappropriate treatments c. there will be a medically appropriate solution. d. the sample signal will be properly determined.


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Introduction

There are surprisingly relatively few studies that address the question

of what tests are the most effective and offer the most benefit for

patients in the Intensive Care Unit. Evidence and data should drive

medical decisions as much as possible, particularly with critically ill

patients. The Intensive Care Unit is an environment where increased

patient monitoring, data acquisition and frequent testing are very

common. At first glance, one might reasonably believe that the more

data and information one could acquire, the better patient interests

can be served. However, frequent blood draws carry their own perils.

These include anemia, increased need for transfusions of whole blood

or blood components and infection. This course focuses on the

common laboratory tests requested by clinicians caring for critically ill

patients.

Overview Of Laboratory Testing For Critically Ill Patients

Studies focused on laboratory testing in the Intensive Care Unit (ICU)

have revealed that ICU patients had from 40 to 70 mL of blood drawn

daily, amounting to over 1 L of blood during their ICU stay;1 and, also

that conservative blood sampling strategies are not widely used. In a

recent review, the total blood volume removed from ICU patients was

299 ± 355 mL over 48 hours. Utilizing small-volume phlebotomy tube

(SVPT) versus conventional-volume phlebotomy tube (CVPT)

decreased this volume to 174 ± 182 mL.2

Another aspect related to the drawback of frequent blood draws

involved patient discomfort in the ICU setting at a time when they can


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often least endure more discomfort. Frequent blood draws can disrupt

needed sleep and cause additional stress to patients. There is also an

increased risk of false positive or false negative laboratory test results

that can increase the risk of clinically inappropriate treatments.

Test sensitivity is the ability of any test to correctly identify the

presence of a disease or condition (true positives) while specificity is

the ability of any test to correctly identify the absence of a disease or

condition (true negatives). Clinicians should only order those tests that

have a reasonable probability of providing useful information, either

for ruling in or for ruling out a particular diagnosis. Ruling out a

diagnosis with laboratory testing has the highest power for diagnoses

with a low probability.

Wellness Testing

Wellness testing is obviously not an aspect of lab testing in the ICU

setting. Lipid panels or blood glucose screening tests have a definite

place in populations at risk for hyperlipidemia or diabetes. Genetic

screening may make sense for newborns, but it has little application

for patients in the ICU. The general recommendation in the ICU is to

order tests for which, if the results indicate a problem, there is a

medically appropriate solution.

Nyquist-Shannon Theorem

The Nyquist-Shannon Theorem posits that there is an appropriate

relationship between the number of samplings and the likelihood that

the sample values will be properly determined; in other words, there is


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a relationship between how often one should sample a varying

laboratory test.3 For example, blood glucose values will vary based on

meal frequency or if the patient is receiving total parenteral nutrition.

Oversampling (for example) every 30 minutes will not reveal any more

information as compared to sampling 2 hours after a meal. With

oversampling, while sensitivity may be increased, specificity will

necessarily be decreased, which will reduce the accuracy of the test.

Undersampling, on the other hand, can be just as problematic.

Reflexive testing algorithms as well as reflective testing have

significant clinical utility. Using an algorithmic approach, clinicians are

able to order sequential laboratory tests or a laboratory specialist will

get straight to the point of a diagnostic concern through further

testing. There are a number of tools in the laboratory toolbox that can

be effectively utilized in the ICU setting.4 These include the following

strong tools adapted for the ICU setting.

Laboratory Utilization Toolbox

TOOL TARGET STRENGTHS WEAKNESSES

Laboratory Test Formulary

All tests, but particularly those with recognized (evidence-based) utility

Provides a uniform policy, similar to a pharmacy formulary. Exceptions can be determined as needed.

Requires a buy-in from all involved

Combining Intervention

Any test Combining interventions increase the effectiveness by allowing one intervention to

Can be logistically difficult and complex, particularly because it requires the involvement


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complement another

(buy-in) from all parties.

Banning Repetitive Orders

Daily testing Powerful way to reduce automatic testing. Often providers are not aware of automatic testing.

Providers are often concerned about missing important data. Indeed, there is some risk — i.e., not ordering coagulation studies for patients

Limit Ordering Privileges to Specific Providers

Complex tests, expensive tests or those tests that may provide questionable benefits.

Increases cost effectiveness and diagnostic yield.

Adds a layer of bureaucracy and possibly competitiveness.

Require Pre-approval for Tests

Complex tests, expensive tests or those tests that may provide questionable benefits.

Specialists may have a better understanding of necessary and effective testing

Time consuming, adds a layer of bureaucracy

Change Order Options

Primarily computerized ordering

Difficult to subvert or “get around”

Requires involvement of the IT department and universal cooperation and use of computer ordering

Encourage Reflexive Testing

Any test where a less expensive screening test can be used before a more expensive test

Allows for the use of ordering algorithms. Increases the efficacy of more expensive testing

Only useful for analytes with a less expensive screening test available (eg. TSH followed, if necessary with fT3, fT4, TRH, etc.)


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These tools are useful to keep in mind when thinking about the specific

tests that may be required for any patient, but particularly to minimize

the testing while maximizing the benefits for ICU patients.

Peripheral Blood Samples

Peripheral blood samples, also called peripheral sticks, may be needed

frequently or intermittently in the ICU, depending on the specific

patient’s condition and needs. Beyond blood tests, the patient will

generally require blood pressure monitoring, temperature

measurements, respiration rates, pulse, fluid intake and output levels

and pulse oximetry.

Frequent blood draws can destroy veins, cause pain and discomfort,

disturb a patient’s rest and, under some circumstances, cause anemia.

Placement of venous, arterial or intraosseous catheters can minimize

the damage and maximize the effectiveness of blood draws. However,

it is also critical to use blood conservation devices and only subject the

patient to blood draws when it is medically necessary.

Anemia is a significant concern in critically ill patients. In critically ill

patients, RBC life span is reduced, there is a decreased production of

erythropoietin and the bone marrow production of new blood cells is

often depressed. Additionally, the inflammatory response increases the

synthesis of hepcidin (a protein that regulates the entry of iron into

the blood circulation), which in turn increases the amount of iron

trapped in macrophages. Transfusion of whole blood, packed cells or


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blood components has not been shown to offer a survival advantage

and has been associated with a number of risks including infection,

febrile, allergic and hemolytic transfusion reactions, transfusion-

related circulatory overload and acute lung injury. In addition, the

significance of RBC storage duration and transfusion-associated end-

organ injury and immunomodulatory effects are becoming more

appreciated.

Recent research has shown that institutions involved in blood collection

and transfusion should explore strategies that assure blood

availability, while limiting the use of the oldest RBCs currently

approved by regulation.5 In the last decades, it has become realized

that the use of transfusions does not offer a survival benefit when the

hemoglobin concentration becomes greater than 7 g/dL. The current

recommendations for RBC transfusions in adults are highlighted below.

Indications related to RBC Transfusion in the General Critically

Ill Patient6

• RBC transfusion is indicated for patients with evidence of

hemorrhagic shock.

• RBC transfusion may be indicated for patients with evidence

of acute hemorrhage and hemodynamic instability or

inadequate oxygen delivery.

• A “restrictive” strategy of RBC transfusion (transfuse when

Hb< 7 g/dL) is as effective as a ‘liberal’ transfusion strategy

(transfusion when Hb < 10 g/dL) in critically ill patients with

hemodynamically stable anemia, except possibly in patients

with acute myocardial ischemia.


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• The use of only Hb level as a trigger for transfusion should be

avoided. Decision for RBC transfusion should be based on an

individual patient’s intravascular volume status, evidence of

shock, duration and extent of anemia, and cardiopulmonary

physiologic parameters.

• In the absence of acute hemorrhage RBC, transfusion should

be given as single units.

• Consider transfusion if Hb < 7 g/dL in critically ill patients

requiring mechanical ventilation (MV). There is no benefit of a

‘liberal’ transfusion strategy (transfusion when Hb < 10 g/dL)

in critically ill patients requiring MV.

• Consider transfusion if Hb < 7 g/dL in resuscitated critically ill

trauma patients. There is no benefit of a ‘liberal’ transfusion

strategy (transfusion when Hb < 10 g/dL) in resuscitated

critically ill trauma patients.

• Consider transfusion if Hb < 7 g/dL in critically ill patients

with stable cardiac disease. There is no benefit of a ‘liberal’

transfusion strategy (transfusion when Hb < 10 g/dL) in

critically ill patients with stable cardiac disease.

• RBC transfusion should not be considered as an absolute

method to improve tissue oxygen consumption in critically ill

patients.

• RBC transfusion may be beneficial in patients with acute

coronary syndromes (ACS) who are anemic (Hb ≤ 8 g/dL) on

hospital admission.


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Fluid And Electrolyte Balance In The ICU

Fluid and electrolyte balance is a critical issue in ICU patients. Often,

fluids can have unwanted effects on multiple organs, particularly in

patients with systemic inflammatory response. Electrolyte imbalances,

especially in patients with kidney dysfunction and impaired excretion

of fluids, are also critically important.

Sodium Overload

One liter of 0.9% saline infusion contains 3.4 g of sodium,

representing about eight 100 g packages of potato chips. Sources of

additional sodium include saline used to dilute medication and to keep

catheters open. This can result in hypernatremia in many patients —

recent studies have indicated that up to 7 % of ICU patients are

hypernatremic on admission. Hypernatremia is associated with disease

severity, kidney injury and dysfunction, mechanical ventilation, ICU

length-of-stay and higher in-hospital mortality. In many ICUs,

hypernatremia is considered a quality-of-care marker.

Chloride

Intravenous infusions such as 0.9% saline, Ringer’s lactate and

Plasmalyte contain 154, 109 and 98 mEq/L of chloride, respectively.

Initial chloride levels in patients are generally lower than initial sodium

concentrations; this can lead to uneven increases is chloride levels as

compared to sodium levels after infusions containing the same

amounts (in mEq/L) of each ion. Extra- to intravascular chloride shifts

can occur due to the combined effects of differences in transmembrane

potentials.


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The renal excretion of both sodium and chloride are often impaired in

many ICU patients, especially those with acute kidney injury (AKI).

This can result in a hyperchloremic metabolic acidosis or strong ion

difference (SID) acidosis, a condition associated with higher mortality,

particularly in septic patients.

Electrolyte overload has renal, hemodynamic, acid-base and

inflammatory consequences. These effects may be direct or indirect.

Fluid overload is also a concern in critically ill ICU patients and can

include renal, pulmonary and other end-organ consequences as well as

acid-base effects. A recent review on electrolyte and fluid imbalances

in critically ill patients recommended a patient-centered approach. This

includes the following approaches.

Fluid Resuscitation

Judicious fluid resuscitation includes timing. There is no evidence that

other than at the onset of injury (i.e., during surgery) or soon after

injury or insult (i.e., during the first hours of septic shock or major

surgery) infusion of supplemental fluids lead to improved results;

rather, the evidence suggests the opposite. Early use of vasopressors

may be beneficial, and repeated or excessive fluids should be avoided.

Acid-Base Monitoring

The acid-base status should be consistently monitored during fluid and

electrolyte resuscitation.

Active De-resuscitation


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Active de-resuscitation can involve the use of diuretics or, if necessary,

hemodialysis to maintain fluid and electrolyte balance.

Potassium

Hypokalemia can be defined as a serum potassium level of < 3.5

mEq/L. Potassium may be given by mouth of by intravenous (IV)

infusion. Potassium is usually replaced intravenously as KCl, which

raises the serum potassium levels quickly. Dosage is usually Oral: 40

meq three times to four times daily; IV: peripheral line 10 meq/hr.

With a central line, the dosage is usually 20 meq/hr. Potassium

bicarbonate/citrate/acetate is less commonly used, but may be used in

patients with metabolic acidosis. In general, every 10 mEq of K+ given

will raise the serum K+ by 0.1 mEq/L. Potassium levels should be

rechecked in 2-4 hours after an infusion. Potassium should be diluted

in saline as it may burn. Dextrose should be avoided as it can increase

potassium excretion. If infusing potassium, a femoral catheter is

recommended as using an internal jugular or subclavian can increase

potassium levels too rapidly.

Hypokalemia is usually secondary to GI losses (i.e., vomiting,

diarrhea) or urinary losses and often co-exists with other electrolyte

abnormalities. Symptoms include muscle weakness, cramps,

rhabdomyolysis, respiratory muscle weakness, anorexia, nausea,

vomiting.

Cardiac arrhythmias (atrial tachycardia, junctional tachycardia, AV

block, ventricular tachycardia or fibrillation) and ECG abnormalities

(PAC, PVC, sinus bradycardia, ST segment depression, decreased


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amplitude of T-wave, increased amplitude of U-wave (mostly in V4-

V6)) can be evident as well. Signs and symptoms include tetany,

seizures (in children and neonates), electrolyte imbalances

(hypokalemia, hypocalcemia), hypoparathyroidism (hypocalcemia),

vitamin D deficiency, ECG changes (widened QRS, peaked T-waves, PR

interval prolongation), and ventricular arrhythmias including torsades

des pointes.

Magnesium

Hypomagnesemia can be defined

as a serum magnesium level of

< 1.3mEq/L. In general, every 2 g

of MgSO4 will raise the serum Mg2+

by 0.5 mEq/L. Magnesium can be

given by mouth (usually as MgO)

or by IV (as MgSO4). Almost 12%

of hospitalized patients may have hypomagnesemia. It should be

suspected in patients with chronic diarrhea, other electrolyte

imbalances and ventricular arrhythmias.

Phosphorus

Hypophosphatemia can be defined as serum phosphorus of < 2.8

mg/dL. Phosphorus can be given by mouth or by IV.

Hypophosphatemia can occur in alcoholism, refeeding syndrome,

hyperalimentation, “Hungry Bone” syndrome, chronic antacid use,

primary or secondary hyperparathyroidism, Vitamin D deficiency and

Fanconi syndrome. Acute signs and symptoms of hypophosphatemia

IV MgSO4:

1.5-1.9mg/dL: 2g magnesium sulfate IV 1.2-1.4mg/dL:4g 0.8-1.1mg/dL: 6g <.8mg/dL: 8g Torsades des Pointes: 2g IV push Low K+/Ca2+ with tetany or arrhythmia 50meq (~6g) of IV Mg2+ given slowly over 8-24 hrs


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include encephalopathy, respiratory distress, decreased cardiac output,

proximal myopathies, elevated CPK and coagulopathy.

Chronic signs and symptoms of hypophosphatemia include

hypercalciuria and osteomalacia and rickets due to increased bone

resorption. Oral replacement is preferred. The dose should be adjusted

for patients with reduced glomerular filtration rate (GFR) (decreased

dose) and for certain patients with obesity. Phosphate levels should be

rechecked within 12 hours.

Calcium

Hypocalcemia can be defined as a

serum calcium < 8.4 mg/dL or an

ionized calcium < 4.2 mg/dL.

Calcium should only be given IV for

severe or symptomatic

hypocalcemia. Pseudohypcalcemia

should be ruled out by determining

the corrected calcium levels. As a

general rule, every 1 g of calcium

gluconate given will raise the serum

calcium by 0.5 mg/dL. Signs and

symptoms of acute hypocalcemia

include tetany, seizures, bronchospasm, papilledema, and cardiac

symptoms (prolonged QT, hypotension, heart failure, arrhythmia).

There may also be signs of psychiatric manifestations.

Corrected Ca2+ = [(4 – albumin) x 0.8] + measured calcium.

Symptomatic or acute serum Ca2+ <7.5 mg/dL: - IV Calcium gluconate 1-2 g (amp) over 10-20min.

- Temporary rise for 2-3 hrs, must be followed by slower infusion - 50 mL/hr if Ca2+ remains low) Asymptomatic and serum Ca >7.5 mg/dL or chronic: Oral therapy: calcium carbonate or citrate 1-2 g/day (500 mg bid-qid) Consider Vitamin D in following cases: Hypoparathyroidism: Vitamin D - Calcitriol: 0.25-0.5 mcg bid - Vitamin D deficiency: 50,000 IU/week for 6-8 weeks then 800-1000 IU daily.


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Complete Blood Count

Routine blood tests have not been shown to be of an overall benefit for

many critically ill patients and may actually cause harm. Recently, a

5-step quality improvement project was implemented to eliminate

unnecessary ordering of routine blood tests. The 5-steps used were

identified as:7

1. An educational component regarding the lack of evidence that

routine blood tests were medically justified and that repeated

blood draws could in fact prove deleterious.

2. An added checkbox to the ICU rounds checklist reminding

clinicians of the evidence presented in Step 1.

3. A rubber stamp made for orders and progress notes that read

‘No routine lab work indicated for tomorrow’.

4. Adding a prompt to the electronic ordering system that allowed

for acceptable indications when routine tests such as CBCs,

electrolytes, urea and creatinine were ordered.

5. Re-meeting with the staff reinforcing the first educational

component of the strategy.

It has been shown through studies that there was no increase in time-

critical orders, no differences in severity of illness or the duration of

ICU stays. Additionally, studies have shown that fewer blood tests

ordered (over a period of 3 months) are associated with significant

cost savings. The American Board of Internal Medicine and the Critical

Care Societies Collaborative which includes the American Association

of Critical Care Nurses, the American College of Chest Physicians, the


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American Thoracic Society and the Society of Critical Care Medicine

has made the following recommendations:8

• Diagnostic tests — including complete blood counts (CBCs), blood

chemistries, arterial blood gases and ECGs — should only be ordered

as a response to specific clinical questions and not as a matter of

routine.

• A ‘restrictive’ transfusion policy is recommended; hemodynamically

stable patients who are not bleeding and a hemoglobin

concentration of greater than 7 g/dL should not be transfused. An

exception may be patients with acute coronary syndrome. However,

most studies of aggressive transfusions indicate that harm may be

caused in these patients as well.

Critical CBC Values

There are a number of generally accepted critical or ‘alert’ values.

These values may vary slightly in different settings. Individual values

need to be interpreted for each individual patient. The values used at

Massachusetts General Hospital identified as life threatening or that

place the patient at serious risk if left untreated is listed below.9

• Hematocrit

− >56%

− ≤20%

• Platelet counts

− <40,000 (pediatric patients <20,000)

− >999,000

• White blood cells

− <1500

− >50,000


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• Hemoglobin

− <6.5 g/dL

• INR

− ≥4.0

CBCs after Bleeding Episodes

It is important to remember that many of the variables such as

hemoglobin and the hematocrit can remain unchanged for up to 12

hours. There is no absolute hematocrit or hemoglobin level that

universally should prompt a transfusion, though patients at risk for

myocardial ischemia are generally transfused when Hgb levels fall

below 7 g/dL. As stated above, repeated CBCs should be avoided as

much as possible due to the potential for inducing anemia and have

not been shown to add clinical value. Coagulation studies may also not

be useful because of the time delay in equilibration after hemorrhage

begins.

Coagulation studies may be useful for those patients on warfarin, low

molecular weight heparin, or antiplatelet medications or those patients

with severe preexisting hepatic insufficiency. Total bleeding time may

be useful, but is difficult to perform in a patient with acute

hemorrhage; aPTT and PT tests, if abnormal, require correcting. On

the other hand, arterial blood gas and pH levels can be good indicators

for oxygen imbalance at the tissue level. A pH of less than 7.25

generally requires intervention.


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Blood Chemistries

As with CBCs, blood chemistries should not necessarily be routinely

performed, but only if potentially critical and medically necessary

information can be obtained.

• Total bilirubin (neonates and infants)

− For infants between 0 and 3 months: >15 mg/dL

− For infants between 4 and 6 months: >20 mg/dL

• Calcium

− <6.5 mg/dL or > 14 mg/dL

• Total CO2

− <11 mmol/L or > 40 mmol/L

• Glucose

− <40 mg/dL

• Magnesium

− <1.2 mg/dL or >5.9 mg/dL

• Potassium

− <2.8 mmol/L or >6.0 mmol/L

• Sodium

− <120 mmol/L or >160 mmol/L

• Serum/Plasma osmolality

− <250 mOsm/kg water or >335 mOsm/kg water

• Anion Gap

− The anion gap is used primarily to evaluate metabolic

acidosis, though metabolic acidosis can exist with a normal

anion gap.

− An elevated anion gap suggests the presence of metabolic

acidosis (anion gap >30 mmol/L). The anion gap depends on

both serum phosphate and serum albumin levels; in patients


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with low albumin levels, a falsely normal anion gap may be

present.

− Anion Gap = Na+ – (Cl- + HCO3-)- 12 +/-2

ü Every 1g/L decrease in albumin will decrease the

anion gap by ≈0.25 mmol. The corrected anion gap

can be calculated: AG + (0.25 X (40-albuming/L).

ü A normal anion gap is ≈12 meq/L.

− Causes of a high anion gap can be caused by ketoacidosis

(diabetic, alcoholic, starvation), uremia (renal failure),

lactic acidosis and toxins (ethylene glycol, methanol,

paraldehyde, salicylates); Mnemonic: KULT. Another

mnemonic is MUDPILES (Methanol, Uremia, DKA,

Paraldehyde, INH, Lactic acidosis, Ethylene glycol,

Salicylate).

• Delta values (Delta ratio) or Δ/Δ

− The delta ratio can be used to determine if a mixed acid

base disorder exists.

− If Δ/Δ is < 0.4, suspect hyperchloremic AG acidosis

− If Δ/Δ is <1, suspect High AG and Normal AG acidosis

− If Δ/Δ is 1-2, suspect pure Anion Gap Acidosis, Lactic

acidosis (the average value is 1.6) or DKA. DKA is more

likely to have a ratio closer to 1 because of urinary loss of

ketones.

Arterial Blood Gas

Arterial blood gas samples are often obtained. Levels should be

maintained so that PaO2 is between 60-80mm Hg, representing 92-

100% saturation. The American Thoracic Society recommends a 6-step

approach to the interpretation of arterial blood gasses.10


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Step 1:

The internal consistence of arterial blood gas (ABG) measurements

should be assessed based on the Henderson-Hasselbach equation.

[H+] = (24 PaCO2)/[HCO3-]. As a rule, the pH is not consistent with the

ABG.

• If the pH is 7.00, the [H+] = 100 mmol/L



• If the pH is 7.15, the [H+] = 71mmol/L











Step 2:

• Determine if there is acidemia or alkalemia present based

on the measured pH levels.

− Acidemia: pH<7.35

− Alkalemia: pH>7.45

• To determine this, the PaCO2, the HCO3- and the anion gap

need to be determined.


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• Acidosis or alkalosis may be present with a normal pH

between 7.35 - 7.45.

Step 3:

• Differentiate between respiratory and metabolic

acidosis/alkalosis. In respiratory-based disorders the pH

and the PaCO2 change in the opposite directions while in

metabolically-based disorders change in the same

direction.

− In respiratory acidosis the pH decreases and the PaCO2

increases.

− In respiratory alkalosis the pH increases and the PaCO2

decreases.

− In metabolic acidosis the pH decreases and the PaCO2

decreases.

− In metabolic alkalosis the pH increases and the PaCO2

increases.

Step 4:

Determine if there is appropriate compensation for the

acidosis and alkalosis. If the observable compensation does

not match the expected compensation, it is likely there may

be more than one acid-base disorder present.

Step 5:

• If metabolic acidosis exists, calculate the anion gap.


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Step 6:

• The delta ratio may be used in the assessment of elevated anion

gap metabolic acidosis to determine if a mixed acid base disorder is

present. Albumin levels should be adjusted.

For mixed and complex acid-base disturbances, the following may be

helpful in determining the underlying causes.

• Respiratory acidosis associated with metabolic acidosis may be

characterized by:

− A decrease in pH

− A decrease in HCO3-

− An increase in PaCO2

− This situation may occur in some cases of cardiac arrest,

intoxications and multi-organ failure

Disorder Expected Compensation Correction Factor

Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 +/- 2

Acute respiratory acidosis

Increase in [HCO3-] = ∆ PaCO2/10 +/- 3

Chronic respiratory acidosis

Increase in [HCO3-] = 3.5(∆

PaCO2/10)

Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-

)

Acute respiratory alkalosis

Decrease in [HCO3-] = 2(∆ PaCO2/10)

Chronic respiratory alkalosis

Decrease in [HCO3-] =5(∆ PaCO2/10)

to 7(∆ PaCO2/10)


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• Respiratory alkalosis associated with metabolic alkalosis may be

characterized by:

− An increase in pH

− An increase in HCO3-

− A decrease in PaCO2

− This situation may occur in some cases of cirrhosis (with

diuretics), nausea of pregnancy, chronic obstructive

pulmonary disease (COPD) over-ventilation

• Respiratory acidosis associated with metabolic alkalosis may be

characterized by:

− Normal pH

− An increase in PaCO2

− An increase in HCO3-

− This situation may occur in some cases of COPD (with

diuretics, vomiting, NG suction), severe hypokalemia

• Respiratory alkalosis associated with metabolic acidosis may be

characterized by:

− Normal pH

− A decrease in PaCO2

− A decrease in HCO3-

− This situation may occur in some cases of uremia or

ketoacidosis with vomiting, NG suction, use of diuretics

Patients With Arrythmia And Laboratory Testing

Patients with arrhythmias should have magnesium, phosphate and

calcium levels carefully monitored. Electrolyte abnormalities can cause

or contribute to arrhythmias and cardiac arrest and may hamper

efforts at resuscitation.


26

Potassium

The potassium gradient across the myocardial cells can determine the

excitability of the myocardial cell membrane. The potassium gradient

(and the levels of serum potassium) is affected by acid-base balance

— when pH decreases, potassium levels in the serum can increase

because of an intracellular to extracellular shift. This is especially

critical in patients with arrhythmias and comorbidities that can affect

the acid-base balance including, for example, diabetic ketoacidosis.

Hyperkalemia is classified as moderate and severe: moderate (K+ 6-7

mEq/L) and severe (>7 mEq/L) hyperkalemia, which is life threatening

and is seen most commonly in end-stage renal disease. Other causes

include chronic renal failure, metabolic acidosis,

pseudohypoaldosteronism Type II, chemotherapy (with tumor lysis),

rhabdomyolysis, renal tubular acidosis, hemolytic disorders, Addison’s

disease and hyperkalemic periodic paralysis. Signs and symptoms of

hyperkalemia include weakness, generalized fatigue, paresthesias,

ascending paralysis, and respiratory failure. ECG changes include early

findings of peaked T waves (tenting). Later changes include flattened P

waves, prolonged PR interval (first-degree heart block), widened QRS

complex, deepened S waves, and a merging of S and T waves.

Untreated hyperkalemia can result in sine-wave patterns, and

idioventricular rhythms. Asystolic cardiac arrest can rapidly develop.

Diuretics (i.e., furosemide) and resins such as kayexalate may be used

for mild (5-6 mEq/L) hyperkalemia, while moderate hyperkalemia may

be treated with:


27

• Calcium gluconate or calcium chloride can be used to reduce the

risk of ventricular fibrillation

• Insulin plus glucose will induce an intracellular shift of potassium

because of the ‘dragging’ effect of glucose

• Alkalizing agents will increase the pH, also inducing an

intracellular shift of potassium

• Diuretics to induce renal excretion of potassium

• Beta-2-adrenergic agonist to promote intracellular uptake

• Binding resins, promoting K-Na exchange in the GI tract

Hypokalemia can be defined as a serum potassium level of <3.5

mEq/L. Common causes include loss from the GI tract, loss from renal

excretion (due to hyperaldosteronism, hyperglycemia (severe),

medications such as K+ depleting diuretics, amphotericin B, etc.),

alkalosis, and malnutrition. Mild hypokalemia can result in weakness,

fatigue, paralysis, respiratory difficulty, constipation, paralytic ileus,

and leg cramps. More severe hypokalemia can result in alterations in

myocardial excitability, changes in ECGs such as the presence of U

waves, T-wave flattening, and arrhythmias including ventricular

arrhythmias. Treatment of hypokalemia is generally by infusion and

minimizing loss.

Sodium

Sodium is the major extracellular ion involved in maintaining serum

osmolality and water/ion shifts between the inter- and extravascular

spaces. Hypernatremia is defined as a serum sodium concentration

greater than 145-150 mEq/L. Hypernatremia can be caused by excess

mineralocorticoid (i.e., hyperaldosteronism), excess glucocorticoid


28

(i.e., Cushing’s syndrome), excessive hypertonic saline infusion,

sodium bicarbonate administration and by excess dehydration through

GI or renal losses.

Symptoms of hypernatremia are primarily neurologic in nature and

include altered mental states, weakness, irritability, focal neurologic

deficits, coma and seizures. Treatment reduces the cause(s) of

dehydration and correcting any water deficit with normal saline or 5%

dextrose in half-normal saline. The water deficit is calculated and the

fluid is administered to lower the rate of sodium decrease by 0.5 to 1.0

mEq per hour over the first 24 hours.

Hyponatremia is defined as serum [Na+] levels lower than 130 mEq/L

and is commonly caused by reduced renal excretion of water or

urinary loss of sodium. Reduced renal excretion of water can be

caused by thiazide diuretics, renal failure, depletion of the extracellular

fluid (i.e., by vomiting), Syndrome of Inappropriate Antidiuretic

Hormone (SIADH) secretion, congestive heart failure, cirrhosis (with

ascites), hypothyroidism and adrenal insufficiency. Hypo-osmolar

hyponatremia is the most common, but in uncontrolled diabetes, there

may exist a hyper-osmolar hyponatremia. Hyponatremia is often

asymptomatic, but an acute drop in sodium levels can cause nausea,

vomiting, headache, lethargy, seizures, cerebral edema, coma and

death. Hyponatremia is treated by the administration of sodium and

the volume reduction. For gradual increases in sodium (0.5

mEq/L/hour) unless seizures are present, with seizures of other

neurologic symptoms, the serum level should be corrected more

rapidly, i.e., 2-4 mEq/L/hour.


29

Magnesium

Magnesium is one of the most common minerals in the body and is

required for a wide variety and large number of critical reactions. It is

bound to serum albumin and serum levels often do not reflect total

body levels; serum magnesium levels can appear to be normal in the

face of depleted bone stores. In addition, magnesium balance is

closely associated with sodium, calcium and potassium levels.

Hypermagnesemia ([Mg2+] >2.2mEq/L) is most commonly related to

renal failure and is characterized by muscular weakness, paralysis,

ataxia, drowsiness, and confusion. Hypermagnesemia can also produce

vasodilation and severe hypermagnesemia can result in severe

hypotension, bradycardia, cardiac arrhythmias, hypoventilation and

cardiorespiratory arrest. Hypermagnesemia is treated by chelation by

calcium. Severe cases may be treated with dialysis.

Hypomagnesemia ([Mg2+] < 1.3mEq/L) occurs in ~10% of all

hospitalized patients, and commonly results from decreased absorption

or increased loss from the GI and kidneys. The levels of T3/T4 can also

affect magnesium levels. Symptoms of low serum magnesium include

muscular fasciculations or tremors, ocular nystagmus, tetany, altered

mental state and cardiac arrhythmias such as torsades de pointes.

Patients may also have ataxia, vertigo, seizures, and dysphagia.

Severe hypomagnesemia is treated with MgSO4.


30

Calcium

Calcium is the most abundant mineral in the body, and, as

magnesium, is involved in a wide number and variety of cellular

reactions and processes. About 50% of all extracellular calcium,

regulated by parathormone and Vitamin D, is bound to albumin while

the other 50 % is in the active, ionized form. The levels of ionized

calcium levels are inversely related to the albumin levels and can

therapeutically act as an ionic antagonist to both magnesium and

potassium.

Hypercalcemia is defined as a serum calcium level of > 10.5 mEq/L or

an ionized calcium level of > 4.8mg/dL. Hypercalcemia is most

commonly due to primary hyperparathyroidism and the presence of a

malignancy. Neurologic symptoms of moderate hypercalcemia include

depression, weakness, fatigue and confusion. More significant

hypercalcemia can be characterized by hallucinations, disorientation,

hypotonicity, seizures, and coma. Further, hypercalcemia can affect

the renal concentration of urine and the resultant diuresis can cause

dehydration.

Serum calcium levels above 15 mg/dL can have cardiac effects

including depressed myocardial contractility, decreased automaticity

and shortened ventricular systole. Hypercalcemia can exacerbate

digitalis toxicity. Hypercalcemic individuals can also become

hypokalemic, contributing to potential arrhythmias. QT interval

shortening is often seen in calcium levels above 13mg/dL along with

prolonged PR and QRS intervals. At serum calcium levels above 15


31

mg/dL, atrioventricular blocks can occur, sometimes leading to cardiac

arrest.

Treatment should generally begin if a patient exhibits calcium levels

above 12 mg/dL and is often begun with saline diuresis, with

potassium and magnesium levels constantly monitored. Loop diuretics

may be used along with hydration. In patients with heart failure or

renal insufficiency, hemodialysis may be necessary as may be the use

of chelating agents. Bisphosphonates may be used in some cases,

though these may take up to 72 hours to reach therapeutic efficacy.

Hypocalcemia exists with a serum calcium levels below 8.5 mg/dL or

ionized calcium of less than 4.2 mg/dL. The more common causes of

hypocalcemia are toxic shock syndrome, alterations in magnesium

levels, post-thyroid surgery, tumor lysis syndrome and fluoride

poisoning. Symptoms generally appear with calcium levels below 2.5

mg/dL and include paresthesias of the extremities and face, muscle

cramps, carpopedal spasm, stridor, tetany, and seizures. Signs include

hyperreflexia and positive Chvostek and Trousseau signs. Decreased

myocardial contractility and heart failure can also occur. In addition,

hypocalcemia can exacerbate digitalis toxicity. Treatment is supportive

at first and may be followed with administration of calcium — acutely,

with 10% calcium gluconate or calcium chloride (used cautiously).

Nutrition And Laboratory Blood Values

The American Society for Parenteral and Enteral Nutrition (ASPEN)

along with the Society of Critical Care Medicine (SCCM) has produced a

series of guidelines for nutrition support therapy in critically ill


32

patients.11 The following guidelines for adults receiving enteral

nutrition (EN) and parenteral nutrition (PN) are necessary for ICU

clinicians to understand, and are outlined below.

Enteral Nutrition

Traditional nutrition assessment tools (albumin, prealbumin, and

anthropometry) are not validated in critical care. Before initiation of

feedings, assessment should include evaluation of weight loss and

previous nutrient intake prior to admission, level of disease severity,

comorbid conditions, and function of the gastrointestinal (GI) tract.

Nutrition support therapy in the form of enteral nutrition should be

initiated in the critically ill patient who is unable to maintain volitional

intake.

Enteral nutrition is the preferred route of feeding over parenteral

nutrition for the critically ill patient who requires nutrition support

therapy. Enteral feeding should be started early within the first 24-48

hours following admission. The feedings should be advanced toward

goal over the next 48-72 hours.

In the setting of hemodynamic compromise (patients requiring

significant hemodynamic support including high dose catecholamine

agents, alone or in combination with large volume fluid or blood

product resuscitation to maintain cellular perfusion), EN should be

withheld until the patient is fully resuscitated and/or stable.


33

In the ICU patient population, neither the presence nor absence of

bowel sounds nor evidence of passage of flatus and stool is required

for the initiation of enteral feeding.

When to Use Parenteral Nutrition

If early EN is not feasible or available the first 7 days following

admission to the ICU, no nutrition support therapy should be provided.

In the patient who was previously healthy prior to critical illness with

no evidence of protein-calorie malnutrition, use of PN should be

reserved and initiated only after the first 7 days of hospitalization

(when EN is not available). If there is evidence of protein-calorie

malnutrition on admission and EN is not feasible, it is appropriate to

initiate PN as soon as possible following admission and adequate

resuscitation.

In a patient expected to undergo major upper GI surgery where EN is

not feasible, PN should be provided under very specific conditions:

• If the patient is malnourished, PN should be initiated 5-7 days

preoperatively and continued into the postoperative period.

• PN should not be initiated in the immediate postoperative period

but should be delayed for 5-7 days (should EN continue not to be

feasible).

• PN therapy provided for a duration of <5-7 days would be

expected to have no outcome effect and may result in increased

risk to the patient. Thus, PN should be initiated only if the

duration of therapy is anticipated to be ≥7 days.


34

Dosing of Enteral Feeding

The target goal of EN (defined by energy requirements) should be

determined and clearly identified at the time of initiation of nutrition

support therapy. Energy requirements may be calculated by predictive

equations or measured by indirect calorimetry. Predictive equations

should be used with caution, as they provide a less accurate measure

of energy requirements than indirect calorimetry in the individual

patient. In the obese patient, the predictive equations are even more

problematic without availability of indirect calorimetry.

Efforts to provide >50% - 65% of goal calories should be made in

order to achieve the clinical benefit of EN over the first week of

hospitalization.

If unable to meet energy requirements (100% of target goal calories)

after 7-10 days by the enteral route alone, consideration should be

given to initiating supplemental PN. Initiating supplemental PN prior to

this 7-10 day period in the patient already receiving EN does not

improve outcome and may be detrimental to the patient.

Ongoing assessment of adequacy of protein provision should be

performed. The use of additional modular protein supplements is a

common practice, as standard enteral formulations tend to have a high

non-protein calorie:nitrogen ratio. In patients with body mass index

(BMI) <30, protein requirements should be in the range of 1.2 - 2.0

g/kg actual body weight per day, and may likely be even higher in

burn or multi-trauma patients.


35

In the critically ill obese patient, permissive underfeeding or

hypocaloric feeding with EN is recommended. For all levels of obesity

where BMI is >30, the goal of the EN regimen should not exceed 60%

- 70% of target energy requirements or 11 - 14 kcal/kg actual body

weight per day (or 22 - 25 kcal/kg ideal body weight per day). Protein

should be provided in a range ≥2.0 g/kg ideal body weight per day for

patients with BMI 30 - 40, ≥2.5 g/kg ideal body weight per day and for

BMI ≥ 40.

Monitoring Tolerance and Adequacy of Enteral Nutrition

In the ICU setting, evidence of bowel motility (resolution of clinical

ileus) is not required in order to initiate EN in the ICU. Patients should

be monitored for tolerance of EN (determined by patient complaints of

pain and/or distention, physical exam, passage of flatus and stool, and

abdominal radiographs).

Inappropriate cessation of EN should be avoided. Holding EN for

gastric residual volumes <500 mL in the absence of other signs of

intolerance should be avoided. The time period that a patient is made

nil per os (NPO) prior to, during, and immediately following the time of

diagnostic tests or procedures should be minimized to prevent

inadequate delivery of nutrients and prolonged periods of ileus. Ileus

may be propagated by NPO status.

Use of enteral feeding protocols increases the overall percentage of

goal calories provided and should be implemented. Patients placed on

EN should be assessed for risk of aspiration. Steps to reduce risk of


36

aspiration should be employed. The following measures have been

shown to reduce risk of aspiration:

• In all intubated ICU patients receiving EN, the head of the bed

should be elevated 30° - 45°.

• For high-risk patients or those shown to be intolerant to gastric

feeding, delivery of EN should be switched to continuous

infusion.

• Agents to promote motility such as prokinetic drugs

(metoclopramide and erythromycin) or narcotic antagonists

(naloxone and alvimopan) should be initiated where clinically

feasible.

• Diverting the level of feeding by post-pyloric tube placement

should be considered.

• Use of chlorhexidine mouthwash twice a day should be

considered to reduce risk of ventilator-associated pneumonia.

Blue food coloring and glucose oxidase strips, as surrogate markers for

aspiration, should not be used in the critical care setting. Development

of diarrhea associated with enteral tube feedings warrants further

evaluation for etiology.

Selection of Appropriate Enteral Formulation

Immune-modulating enteral formulations (supplemented with agents

such as arginine, glutamine, nucleic acid, ω-3 fatty acids, and

antioxidants) should be used for the appropriate patient population

(major elective surgery, trauma, burns, head and neck cancer, and

critically ill patients on mechanical ventilation), with caution in patients


37

with severe sepsis. ICU patients not meeting criteria for immune-

modulating formulations should receive standard enteral formulations.

Patients with acute respiratory distress syndrome (ARDS) and severe

acute lung injury (ALI) should be placed on an enteral formulation

characterized by an anti-inflammatory lipid profile (i.e., ω-3 fish oils,

borage oil) and antioxidants. To receive optimal therapeutic benefit

from the immune-modulating formulations, at least 50% - 65% of goal

energy requirements should be delivered.

If there is evidence of diarrhea, soluble fiber-containing or small

peptide formulations may be utilized.

Parenteral Nutrition

If EN is not available or feasible, the need for PN therapy should be

evaluated. If the patient is deemed to be a candidate for PN, steps to

maximize efficacy (regarding dose, content, monitoring, and choice of

supplemental additives) should be used.

In all ICU patients receiving PN, mild permissive underfeeding should

be considered at least initially. Once energy requirements are

determined, 80% of these requirements should serve as the ultimate

goal or dose of parenteral feeding. Eventually, as the patient

stabilizes, PN may be increased to meet energy requirements. For

obese patients (BMI ≥ 30), the dose of PN with regard to protein and

caloric provision should follow the same recommendations given for

EN.


38

In the first week of hospitalization in the ICU, when PN is required and

EN is not feasible, patients should be given a parenteral formulation

without soy-based lipids. A protocol should be in place to promote

moderately strict control of serum glucose when providing nutrition

support therapy. A range of 110 - 150 mg/dL may be most

appropriate. Additionally, when PN is used in the critical care setting,

consideration should be given to supplementation with parenteral

glutamine.

In patients stabilized on PN, periodically repeated efforts should be

made to initiate EN. As tolerance improves and the volume of EN

calories delivered increases, the amount of PN calories supplied should

be reduced. PN should not be terminated until ≥60% of target energy

requirements are being delivered by the enteral route.

Adjunctive Therapy

Administration of probiotic agents has been shown to improve outcome

(most consistently by decreasing infection) in specific critically ill

patient populations involving transplantation, major abdominal

surgery, and severe trauma. No recommendation can currently be

made for use of probiotics in the general ICU population due to a lack

of consistent outcome effect. It appears that each species may have

different effects and variable impact on patient outcome, making it

difficult to make broad categorical recommendations. Similarly, no

recommendation can currently be made for use of probiotics in

patients with severe acute necrotizing pancreatitis, based on the


39

disparity of evidence in the literature and the heterogeneity of the

bacterial strains utilized.

A combination of antioxidant vitamins and trace minerals (specifically

including selenium) should be provided to all critically ill patients

receiving specialized nutrition therapy.

The addition of enteral glutamine to an EN regimen (not already

containing supplemental glutamine) should be considered in burn,

trauma, and mixed ICU patients.

Soluble fiber may be beneficial for the fully resuscitated,

hemodynamically stable critically ill patient receiving EN who develops

diarrhea. Insoluble fiber should be avoided in all critically ill patients.

Both soluble and insoluble fiber should be avoided in patients at high

risk for bowel ischemia or severe dysmotility.

Pulmonary Failure

Specialty high-lipid low-carbohydrate formulations designed to

manipulate the respiratory quotient and reduce CO2 production are

not recommended for routine use in ICU patients with acute

respiratory failure. Fluid-restricted calorically dense formulations

should be considered for patients with acute respiratory failure. Serum

phosphate levels should be monitored closely and replaced

appropriately when needed.

Renal Failure


40

Patients in the ICU with acute renal failure (ARF) or acute kidney

injury (AKI) should be placed on standard enteral formulations, and

standard ICU recommendations for protein and calorie provision

should be followed. If significant electrolyte abnormalities exist or

develop, a specialty formulation designed for renal failure (with

appropriate electrolyte profile) may be considered.

Patients receiving hemodialysis or continuous renal replacement

therapy (CRRT) should receive increased protein, up to a maximum of

2.5 g/kg/d. Protein should not be restricted in patients with renal

insufficiency as a means to avoid or delay initiation of dialysis therapy.

Hepatic Failure

Traditional assessment tools should be used with caution in patients

with cirrhosis and hepatic failure, as these tools are less accurate and

less reliable due to complications of ascites, intravascular volume

depletion, edema, portal hypertension, and hypoalbuminemia. EN is

the preferred route of nutrition therapy in ICU patients with acute

and/or chronic liver disease. Nutrition regimens should avoid

restricting protein in patients with liver failure.

Standard enteral formulations should be used in ICU patients with

acute and chronic liver disease. Branched chain amino acid

formulations (BCAA) should be reserved for the rare encephalopathic

patient who is refractory to standard treatment with luminal acting

antibiotics and lactulose.


41

Acute Pancreatitis

On admission, patients with acute pancreatitis should be evaluated for

disease severity. Patients with severe acute pancreatitis should have a

nasoenteric tube placed and EN initiated as soon as fluid volume

resuscitation is complete.

Patients with mild to moderate acute pancreatitis do not require

nutrition support therapy (unless an unexpected complication develops

or there is failure to advance to oral diet within 7 days). The gastric or

jejunal route may be used to feed patients with severe acute

pancreatitis enterally.

Tolerance to EN in patients with severe acute pancreatitis may be

enhanced by the following measures:

• Minimizing the period of ileus after admission by early initiation

of EN.

• Displacing the level of infusion of EN more distally in the GI

tract.

• Changing the content of the EN delivered from intact protein to

small peptides, and long-chain fatty acids to medium-chain

triglycerides or a nearly fat-free elemental formulation.

• Switching from bolus to continuous infusion.

For the patient with severe acute pancreatitis, when EN is not feasible,

use of PN should be considered. PN should not be initiated until after

the first 5 days of hospitalization.


42

Nutrition Therapy in End-of-Life

Specialized nutrition therapy is not obligatory in cases of futile care or

end-of-life situations. The decision to provide nutrition therapy should

be based on effective patient/family communication, realistic goals,

and respect for patient autonomy.

Total Parenteral Nutrition

Total parenteral nutrition (TPN) or Total Enteral Nutrition (TEN) may

be needed for patients with some stages of ulcerative colitis, short

bowel syndrome, bowel obstruction and in certain pediatric disorders

such as congenital anomalies or prolonged diarrhea. The major

indication for TPN is some failure of the GI tract to perform normally.

Children may need more energy and amino acids and may have

different fluid requirements. Use of TPN requires adequate water,

calories, amino acids, essential fatty acids, vitamins and minerals.12

A recent systematic review indicated that between 38-78% of ICU

show signs of malnutrition — this increases re-admission, infections

and mortality.13 A NUTRIC scoring system can be used to determine

nutritional status and disease severity. A more comprehensive

nutritional assessment can include:

• Medical/surgical History

− History of weight loss

− Any conditions that may be associated with an acute

inflammatory response such as a major infection, major

abdominal surgery, closed head injuries, sepsis, adult


43

respiratory distress syndrome, severe burns and systemic

inflammatory response syndrome

− Chronic conditions that may predispose to nutritional risk.

Examples include GI surgery and hemorrhage, fistulas, GI

obstruction, ischemia, pancreatitis, inflammatory bowel

disease, malignancy, post-transplantation, major organ

failure and HIV-AIDs.

• Clinical diagnosis of conditions associated with inflammation and

malnutrition

• Physical exam including both specific or non-specific signs of

inflammation

• Anthropometric data

− Sudden or unexplained weight loss and underweight status

• Laboratory indicators such as albumin and prealbumin

• Dietary evaluation

• Functional outcomes (strength and physical performance related

to muscle mass)

Energy Estimation

Energy expenditure (EE) is often used to determine the caloric needs

of a patient in the ICU. During the early phases of a critical illness,

however, it is believed that the caloric needs are likely to be lower

than the EE while during later phases the caloric needs are likely to be

higher than the EE. In addition, patients with liver dysfunction may

have energy requirements significantly different than the EE. In

general, a fixed amount of calories (per kg of body weight) are


44

recommended. Many equations have been derived that may be

predictive for energy needs, but may be difficult to implement

clinically.

Total parenteral nutrition can be life saving in a number of clinical

conditions, but there are a number of serious adverse effects that

must be monitored and addressed. Nutritional support teams can often

provide specific advice for specific situations, but TPN can result in:14,15

• Re-feeding Syndrome

− Vitamin B1 deficiency and acute beriberi

− Volume overload, edema, cardiac insufficiency, pulmonary

edema

− Electrolyte disorders

− Arrhythmias

− Hyperglycemia

• Hyperglycemia, especially in pre-diabetic or diabetic patients

− Glucose should be monitored and maintained between 80-

145mg/dL

• Hypertriglyceridemia

− Triglycerides should be monitored and maintained below

400mg/dL

• Dyslipoproteinemia and EFA deficiencies

− A triene to tetraene ratio of > 0.1 is diagnostic of an EFA

deficiency

− Lipid emulsions with low amounts of polyunsaturated fatty

acids (PUFA) and low amounts of medium chain

triglycerides should be used with total calories of lipids

≤30%.


45

• Acid-base imbalances

− Serum electrolytes, blood gases must be consistently

monitored

• Liver dysfunction

− Using minimal enteral feeding may reduce the risk of

biliary complications (a trial of enteral feeding should be

used as soon as clinically possible)

− In liver dysfunction, the reduction of the use of lipids

should be considered

− Consider choline, glutamine and/or lecithin

supplementation

− Patients with liver dysfunction may require carnitine

supplementation to maintain levels between 30-60µmol/L

with free carnitine at 20µmol/L

• Bone demineralization/Osteoporosis

− Serum Ca2+ levels, parathyroid hormone levels, levels of

25-OH-vitamin D, urinary Ca2+ and Mg2+ should be

regularly monitored, particularly patients on long-term TPN

• Infections

− Infections should be monitored and treated aggressively

• Intestinal effects can include mucosal atrophy and leaky gut

syndrome

− Small intestinal bacterial overgrowth (SIBO) should be

aggressively treated

Strict sterile techniques must be consistently used and the central

venous catheter must be monitored for signs of infection. TPN is

generally begun starting at 50% of the expected requirements with

5% dextrose used to complete the fluid component. Insulin, if needed,


46

can be added to the TPN solution. Patient progress is generally also

constantly monitored; this usually entails weight measurements, CBCs,

electrolyte levels, BUN and blood glucose levels. Blood glucose

abnormalities are common and are an independent predictor or

mortality in patients treated with TPN.

Other common complications are catheter-related sepsis, liver

dysfunction, increased ammonia levels (particularly in infants), volume

overload, bone disease or demineralization, cholelithiasis, cholecystitis

and accumulation of ‘sludge’ in the gallbladder. More rarely, there are

adverse reactions to the use of lipid emulsions — these can include

dyspnea, nausea, headaches, allergic reaction, back pain, dizziness

and sweating.

Omega-3 and omega-6 essential fatty acids can be used to help

decrease inflammatory markers in all patients, including septic

patients. It should be mentioned that a recent meta-analysis indicated

that supplementation with omega-3 (ω-3) essential fatty acids do not

improve mortality, complications due to infections, and ICU length of

stay, though they do appear to reduce the total length of stay in

hospital. It should also be mentioned, however, that other larger,

meta-analyses have concluded that inclusion of omega-3 essential

fatty acids in TPN are safe, effective and reduce the rates of infection

in both surgical and in ICU patients and reduce the duration of stay in

both groups of patients.

The use of omega-3 supplementation with TPN in neonates had been

reviewed relative to parenteral nutrition-associated cholestasis (PNAC)


47

and reversal or prevention of PNAC in this patient population. It was

found that the while omega-3 containing emulsions were not effective

in preventing PNAC, the omega-3 containing emulsions were more

effective at reversing PNAC than were similar emulsions containing

either soybean or olive oil.

Liver Function Tests

Liver function tests are usually recommended at least weekly,

particularly in patients receiving total parenteral nutrition. Significant

percentages of patients on long-term TPN suffer deleterious liver

effects, primarily diagnosed by elevated bilirubin and liver enzymes.

Up to 40% of adult patients experience liver dysfunction and 22% of

deaths in long term TPN are related to liver disease. Other

complications include hypertriglyceridemia, hyperglycemia and fatty

liver disease. Adult patients on TPN are at higher risk of:16

• Steatosis

• Steatohepatitis

• Biliary sludge

• Fatty liver

• Cholelithiasis

• Cholestasis

• Fibrosis

• Micronodular cirrhosis

• Phospholipidosis

Infants and neonates are at higher risk of:

• Cholestasis


48

• Distended gallbladder (abdominal pseudotumor)

• Fibrosis

• Cirrhosis

• Biliary sludge

• Cholelithiasis

While the causes of liver dysfunction during TPN are not well

understood, they appear to be related to excess caloric intake,

impaired triglyceride secretion, increased hepatic fat deposition,

increased insulin secretion and deficiencies in essential fatty acids. Up

to 40% of adult patients experience liver dysfunction and 22% of

deaths in long term TPN are related to liver dysfunction. The

dysfunctions include hepatic steatosis, cholecystitis, biliary sludge and

cholestasis.

In very low birth-weight infants, cyclic/continuous TPN is also

associated with cholestasis. In these infants, the use of Di(2-

ethylhexyl) phthalate (DEHP)-containing polyvinylchloride infusion

systems may increase the risk. The risk in very low-birth-weight

infants may be decreased with the use of ursodiol (10-30 mg/kg/day)

within 14 days after cholestasis onset.

Liver function tests (LFT), including tests on hepatic enzymes such as

alanine transaminase (ALT or SGPT), aspartate transaminase (AST or

SGOT), alkaline phosphatase (ALP) and gamma-glutamyl

transpeptidase (GGT) should be routinely done as should liver protein

tests for albumin, globulin, prothrombin. Bilirubin, serum ammonia,

creatinine and other levels specific to the individual patient can also be


49

monitored. The timing of these tests may depend on clinical judgment

but should likely be done at least twice a week in the ICU. It should be

remembered that LFTs are not truly functional tests, but can allow the

health clinician to derive conclusions regarding the overall state of liver

functions and aid in differential diagnoses.

Prothrombin, prothrombin time (PT) and the International Normalized

Ratio (INR) can determine the presence and the severity of

coagulopathies and are sensitive markers for liver failure. Non-liver

causes such as Vitamin K deficiency, the presence of disseminated

intravascular coagulation (DIC) may complicate and worsen the

results.

Aminotransferase levels can be used to detect liver injury and to

monitor therapeutic progress. There are some ethnic differences; both

AST and ALT tend to be higher in non-Hispanic blacks and Mexican

Americans than in non-Hispanic whites. Elevations of both AST and

ALT are more common in persons over the age of 30 but tend to

decline after the age of 60. In all patients, elevations are associated

with hepatocellular injury due to ethanol, medications, hepatitis B or C

viruses, and, more rarely, underlying liver diseases. (i.e.,

hemochromatosis). Significant elevations of aminotransferase levels

can also occur in viral infections, ischemic injury and in drug-induced

liver disorders.

Moderate elevations of both AST and ALT can be seen in liver

dysfunction associated with TPN as well as non-alcoholic fatty liver

disease (NAFLD), chronic viral hepatitis, chronic cirrhosis and in


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cholestatic disease. Liver dysfunction as sequelae of TPN is associated

with significant elevations of transaminases, alkaline phosphatases and

conjugated bilirubin levels. GGT may be particularly useful in patients

undergoing TPN and associated cholestasis. Elevated GGT may be seen

in those patients undergoing TPN and with acute biliary tract stones.

In these cases, the aminotransferase levels may be elevated > 500U/l

and associated with either normal or mildly elevated ALP levels.

Bilirubinemia can occur in both chronic and in acute liver disease as

well as in congenital disorders. Unconjugated bilirubinemia may be

Gilbert’s syndrome, where hepatocytes have an impaired bilirubin

uptake, with a glucuronyl transferase deficiency (Crigler-Najjar’s

syndrome), in various forms of hemolysis or erythropoietic

dysfunction. Conjugated bilirubinemia occurs in impaired secretion.

Direct bilirubin levels ≥ 0.4mg/dL must be evaluated further; 5’

nucleotidase levels can be used to determine the likelihood of

cholestasis.

Low serum albumin is associated with a poor prognosis. Adding

albumin to the parenteral solution may allow for a slow and steady

increase in serum albumin. In general, however, adding albumin to the

parenteral solution is not recommended due to concerns surrounding

increased risk of infectious complications, flow rate and filter

questions.

A number of recent studies have examined the positive effects of fish-

oil based essential fatty acids (EFAs) on the reversal of TPN-associated

liver disease in both pediatric patients and in adults. Parenteral


51

nutrition-associated liver disease (PNALD) may occur in both adult and

in pediatric populations after recurrent septic events, delayed enteral

feeding, specific hepatotoxic medications, high caloric intake, high

levels of lipid infusions, various deficiencies such as cysteine, taurine

and choline deficiency as well as anatomic factors such as a short

bowel or, specifically in pediatric patients, gastroschisis and jejuna

atresia. In addition, underlying disease and the duration of parenteral

nutrition are important factors in the development of PNALD.

Finally, in pediatric populations, the situation is complicated by

prematurity and low birth weights. EFAs are essential because they are

needed for a wide array of cellular and organ functions including

platelet function, clotting, inflammation, immunocompetence, wound

healing, skin integrity and maintaining the barrier function and

prostaglandin synthesis. Intravenous fat emulsions (IVFE) can provide

the necessary fatty acids to maintain function and reduce the risk of

PNALD. IVFE can also allow for the reduction of the volume of the

parenteral fluids, potentially avoiding volume overload.

Coagulation Studies

Mechanical complications such as catheter dislodgement or occlusions

can result in a thrombosis. Complications in central lines most

commonly are pneumothorax and hemothorax while complications in

PICC lines commonly include thrombophlebitis. Prophylactic heparin

has not been shown to significantly reduce the incidence of

thromboembolic events.


52

Coagulation factors that should be monitored, usually weekly, include:

• Prothrombin time (PT):

The PT measures the time needed to generate fibrin after the

activation of Factor VII, measuring the extrinsic and common

coagulation factors VII, V, X, prothrombin and fibrinogen.

Acquired deficiencies are commonly due to liver disease, use of

anticoagulants, depletion of factors secondary to consumptive

coagulopathy, severe bleeding, or massive transfusion.

• Partial thromboplastin time (aPTT):

aPTT is used to determine inherited or acquired factor

deficiencies. In the ICU, a prolonged aPTT may indicate Vitamin

K deficiency, liver dysfunction, or the use of an anticoagulant. A

shortened aPTT may be indicative of a hypercoagulable stite and

possibly, the early stages of DIC, but is not diagnostic.

• Thrombin time (TT):

Thrombin time measures the integrity of fibrinogenà fibrin in the

presence of thrombin. An acquired deficiency is most commonly

due to consumptive coagulopathy or severe liver disease.

Glucose Monitoring

Glucose level is one of the most critical metabolic parameters to

monitor. A dextrose infusion of 4-5mg/kg/minute is most commonly

recommended. 50-60% of total calories should be derived from


53

dextrose. Those patients with Types 1 or 2 diabetes, sepsis, acute

pancreatitis, liver dysfunction and on corticosteroids are at greatest

risk of hyperglycemia. However, reactive hypoglycemia can also occur

within 60 minutes after cessation of parenteral feeding. Those patients

at greatest risk include patients with renal or liver disease, those who

are severely malnourished, septic patients and those patients with

hyperthyroidism.

Other Tests

• Fluid balance:

Fluids “in” versus fluids “out” should be strictly monitored to

prevent fluid overload and edema.

• Blood glucose levels:

Blood glucose levels should be closely monitored, particularly in

those patients receiving TPN or partial enteral nutrition.

Increased mortality is directly associated with hyperglycemia: in

patient with a mean blood glucose of 80-99 mg/dL, mortality

was 9.6%; in those patients with a mean blood glucose of 180-

199 mg/dL, mortality was 29.4%; in those with a mean blood

glucose greater than 300 mg/dL, mortality was 42.5%. Equally,

hypoglycemia is also associated with increased mortality,

prompting a mover away from intensive insulin therapy.

Diabetic and non-diabetic patients evidence different responses

to glucose variability, with high levels of variability associated

with greater mortality, particularly in non-diabetic patients.


54

While the benefits of continuous glucose monitoring have not

been rigorously established, the current guidelines recommend

initiating insulin infusions to maintain blood glucose <

180mg/dL.

• Blood lipid levels:

Blood lipid levels can rise, particularly when receiving lipid

infusion. In cases of hypertriglyceridemia, the dextrose load can

be reduced. If this does not correct the hyperlipidemia, cycling

lipid infusions as 250 mL of 20% IV fat emulsion twice weekly if

serum triglyceride > 400 mg/dL (4.5 mmol/L) can be

considered. If the patient is receiving propofol, the additional

kcal should be accounted for and included in the total kcal

provided. (propofol provides 1.1 kcal/mL of infusion). The goal

for serum triglycerides should be < 400 mg/dL (4.5 mmol/L) in

adult patients on continuous total parenteral nutrition.

• Blood Cultures/Fever Work-up:

Severe sepsis can be defined as sepsis-induced tissue

hypoperfusion or organ dysfunction. The diagnostic criteria

include a number of physical signs and symptoms, including

general variables such as body temperature, heart rate,

respiratory rates and mental status, but also include some

variables related to lab tests. In severe sepsis, the central

venous pressure (CVP) is of 8-12 mm Hg, a mean arterial

pressure (MAP) of ≥65mm Hg. These include:

− Significant edema/positive fluid balance

>20 mL/kg over 24 hr

− Hyperglycemia


55

Plasma glucose > 140 mg/dL or 7.7 mmol/L in non-

diabetic patients

− Leukocytosis

WBC count > 12,000/µL

− Leukopenia

WBC count < 4000/µL

− Normal WBC count with more than 10% immature forms

− Plasma C-reactive protein greater than two SD above

normal

− Plasma procalcitonin greater than two SD above normal

− Arterial hypoxemia

Pao2/Fio2 < 300

or

< 250 with no signs of pneumonia as the source of

infection

or

<200 with positive signs of pneumonia as the source

of infection

− Acute oliguria

Urine output < 0.5mL/kg/hr for a minimum of 2 hrs

in the face of appropriate fluids

− Creatinine increase

Greater than 0.5mg/dL (44.2µmol/L)

or

Greater than 2 mg/dL (176.8 µmol/L) in severe

sepsis

− Coagulation abnormalities

INR > 1.5

or


56

aPTT > 60 s

− Ileus (absent bowel sounds)

− Thrombocytopenia

Platelet count < 100,000/µL

− Hyperbilirubinemia

Plasma total bilirubin > 4 mg/dL (70 µmol/L)

− Hyperlactatemia

>1 mmol/L

Summary

There are a number of unresolved issues in patient care regarding the

interpretation of the various lab values that may be produced during

the patient’s time in the ICU. While individual clinical decisions must

be based on individual patients, reducing the number of laboratory

tests can be important to reduce patient discomfort as well as the risk

of additional injury. Several benefit to risk analyses have indicated

that laboratory blood draws may be reduced without reducing the

clinical benefit.

Please take time to help NurseCe4Less.com course planners evaluate the nursing knowledge needs met by completing the


57

self-assessment of Knowledge Questions after reading the article, and providing feedback in the online course evaluation.

Completing the study questions is optional and is NOT a course requirement. 1. Laboratory test sensitivity refers to the ability of a

a. patient to tolerate a test. b. test to identify the presence of a disease or condition

correctly. c. test to identify true negative. d. test to identify the absence of a disease or condition correctly.


components has been

a. shown to offer a survival advantage to patients. b. known to reduce production of erythropoietin. c. shown to depress new blood cells. d. associated with the risk of infection.


a. with adequate blood flow (hemodynamic stability). b. with acute hemorrhage but only in single units. c. with evidence of hemorrhagic shock. d. based on caloric needs.

4. The Nyquist-Shannon Theorem posits that there is an

appropriate relationship between the number of samplings and the likelihood that a. a test will identify the presence of a disease. b. the risk of clinically inappropriate treatments. c. there will be a medically appropriate solution. d. the sample signal will be properly determined.

5. There is no absolute hematocrit or hemoglobin level that

universally should prompt a transfusion, though patients at risk for myocardial ischemia are generally transfused when Hgb levels fall below


58

a. 13g/dL. b. 7g/dL. c. 8.7g/dL. d. 11g/dL.


testing in the ICU setting. a. True b. False

7. Additional sodium levels in an ICU patient may result from

saline used to dilute medication and to keep catheters open, which can result in

a. hyponatremia. b. the Gibbs-Donnan effect. c. hypernatremia. d. hypokalemia.

8. Active de-resuscitation can involve the use of ________________ or, if necessary, hemodialysis to maintain fluid and electrolyte balance. a. diuretics b. saline solutions c. phosphates d. liberal transfusions

9. Hypokalemia can be defined as a serum ____________

level of <3.5 mEq/L.

a. magnesium b. chloride c. potassium d. phosphorus

10. Diagnostic tests, i.e., complete blood counts (CBCs), blood chemistries, arterial blood gases and ECGs, should

a. be ordered liberally as a safety precaution. b. be ordered routinely in-hospital.


59

c. be restricted based on cost. d. be ordered only in response to specific clinical questions.

11. True or False: Initial chloride levels in patients are

generally lower than initial sodium concentrations. a. True b. False

12. __________ nutrition is the preferred route of feeding for

the critically ill patient who requires nutrition support therapy.

a. Parenteral b. Intravenous c. Subcutaneous d. Enteral

13. Administration of _______________ has been shown to

improve outcome (most consistently by decreasing infection) in specific critically ill patient populations involving transplantation, major abdominal surgery, and severe trauma.

a. parenteral nutrition b. probiotic agents c. liberal transfusions d. saline solutions

14. True or False: If early enteral nutrition is not feasible or

available the first 7 days following admission to the ICU, no nutrition support therapy should be provided.

a. True b. False

15. Energy expenditure (EE) is often used to determine the

___________________ of a patient in the ICU.

a. phosphorus levels


60

b. red blood count c. caloric needs d. the potassium levels

CORRECT ANSWERS:

1. Laboratory test sensitivity refers to the ability of a

b. test to identify the presence of a disease or condition correctly. p. 6: “Test sensitivity is the ability of any test to correctly identify the presence of a disease or condition (true positives) while specificity is the ability of any test to correctly identify the absence of a disease or condition (true negatives). Clinicians should only order those tests that have a reasonable probability of providing useful information, either for ruling in or for ruling out a particular diagnosis. Ruling out a diagnosis with laboratory testing has the highest power for diagnoses with a low probability.”


components has been

d. associated with the risk of infection. p. 9: “Transfusion of whole blood, packed cells or blood components has not been shown to offer a survival advantage and has been associated with a number of risks including infection; febrile, allergic and hemolytic transfusion reactions; transfusion-related circulatory overload and acute lung injury.”


c. with evidence of hemorrhagic shock. p. 10: “Recommendations for Indications related to RBC Transfusion in the General Critically Ill Patient: RBC transfusion is indicated for patients with evidence of hemorrhagic shock.”


61

4. The Nyquist-Shannon Theorem posits that there is an

appropriate relationship between the number of samplings and the likelihood that

d. the sample signal will be properly determined. pp. 6-7: “The Nyquist-Shannon Theorem posits that there is an appropriate relationship between the number of samplings and the likelihood that the sample values will be properly determined; in other words, there is a relationship between how often one should sample a varying laboratory test. For example, blood glucose values will vary based on meal frequency or if the patient is receiving total parenteral nutrition. Oversampling (for example) every 30 minutes will not reveal any more information as compared to sampling 2 hours after a meal. With oversampling, while sensitivity may be increased, specificity will necessarily be decreased, which will reduce the accuracy of the test. Undersampling, on the other hand, can be just as problematic.”

5. There is no absolute hematocrit or hemoglobin level that

universally should prompt a transfusion, though patients at risk for myocardial ischemia are generally transfused when Hgb levels fall below

b. 7 g/dL. p. 19: “There is no absolute hematocrit or hemoglobin level that universally should prompt a transfusion, though patients at risk for myocardial ischemia are generally transfused when Hgb levels fall below 7 g/dL.”


testing in the ICU setting.

a. True


62

p. 6: “Wellness testing is obviously not an aspect of lab testing in the ICU setting.”

7. Additional sodium levels in an ICU patient may result from

saline used to dilute medication and to keep catheters open, which can result in

c. hypernatremia. p. 11: “Sources of additional sodium include saline used to dilute medication and to keep catheters open. This can result in hypernatremia in many patients ….”

8. Active de-resuscitation can involve the use of

________________ or, if necessary, hemodialysis to maintain fluid and electrolyte balance.

a. diuretics p. 13: “Active de-resuscitation can involve the use of diuretics or, if necessary, hemodialysis to maintain fluid and electrolyte balance.”

9. Hypokalemia can be defined as a serum ____________

level of <3.5 mEq/L.

c. potassium p. 27: “Hypokalemia can be defined as a serum potassium level of <3.5 mEq/L.”

10. Diagnostic tests, i.e., complete blood counts (CBCs), blood

chemistries, arterial blood gases and ECGs, should

d. be ordered only in response to specific clinical questions. p. 17: “Diagnostic tests — including complete blood counts (CBCs), blood chemistries, arterial blood gases and ECGs — should only be ordered as a response to specific clinical questions and not as a matter of routine.”


63

11. True or False: Initial chloride levels in patients are

generally lower than initial sodium concentrations.

a. True p. 12: “Initial chloride levels in patients are generally lower than initial sodium concentrations; this can lead to uneven increases is chloride levels as compared to sodium levels after infusions containing the same amounts (in mEq/L) of each ion.”

12. __________ nutrition is the preferred route of feeding for

the critically ill patient who requires nutrition support therapy.

d. Enteral p. 32: “Enteral nutrition is the preferred route of feeding over parenteral nutrition for the critically ill patient who requires nutrition support therapy.”

13. Administration of _______________ has been shown to

improve outcome (most consistently by decreasing infection) in specific critically ill patient populations involving transplantation, major abdominal surgery, and severe trauma.

b. probiotic agents p. 38: “Administration of probiotic agents has been shown to improve outcome (most consistently by decreasing infection) in specific critically ill patient populations involving transplantation, major abdominal surgery, and severe trauma.”

14. True or False: If early enteral nutrition is not feasible or

available the first 7 days following admission to the ICU,


64

no nutrition support therapy should be provided.

a. True p. 32: “If early EN is not feasible or available the first 7 days following admission to the ICU, no nutrition support therapy should be provided.”

15. Energy expenditure (EE) is often used to determine the

___________________ of a patient in the ICU.

c. caloric needs p. 43: “Energy expenditure (EE) is often used to determine the caloric needs of a patient in the ICU. During the early phases of a critical illness, however, it is believed that the caloric needs are likely to be lower than the EE while during later phases, the caloric needs are likely to be higher than the EE.”

References Section

The References below include published works and in-text citations of published works that are intended as helpful material for your further reading.

1. Corwin HL, Parsonnet KC, Gettinger A. RBC transfusion in the ICU is there a reason? Chest. 1995; 108:767–71. 2. Dolman, HS., et al, Impact of minimizing diagnostic blood loss in the critically ill., Surgery, 158(4), 1083-1088, 2015. 3. Srivastava, R., Bartlett, WA., Kennedy, IM., Hiney, A., Fletcher, C., Murphy, MJ. Reflex and reflective testing: efficiency and effectiveness of adding on laboratory tests. Ann Clin Biochem. 47 (3) 223-227, 2010. 4. Baird, G., The laboratory test utilization management toolbox. Biochemia Medica 2014;24(2):223-34. 5. Flegel, WA., Natanson, C., Klein, HG. Does prolonged storage of red blood cells cause harm? Accessed at http://rdcr.org/wp-content/uploads/2012/08/BJH-2014.pdf (9/2016) 6. Napolitano, LM., et al, Clinical practice guideline: Red blood cell transfusion in adult trauma and critical care. Accessed at: http://www.learnicu.org/docs/guidelines/redbloodcell.pdf (9/2016)


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7. Iosfina, I. et al, Implementation Of An On-Demand Strategy For Routine Blood Testing In ICU Patients, D23. QUALITY IMPROVEMENT IN CRITICAL CARE. May 1, 2013, A5322-A5322. Accessed at http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2013.187.1_MeetingAbstracts.A5322 (Accessed 10/2016) 8. http://www.choosingwisely.org/societies/critical-care-societies-collaborative-critical-care/ (Accessed 10/2016) 9. http://mghlabtest.partners.org/criticalvalues.htm (Accessed 10/2016) 10. https://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/abgs.php (Accessed 9/2016) 11. http://www.lumen.luc.edu/Lumen/MedEd/nutrition/JPEN%2033%202009.pdf (Accessed 10/2016) 12. https://www.merckmanuals.com/professional/nutritional-disorders/nutritional-support/total-parenteral-nutrition-tpn (Accessed 10/2016) 13. Lew, CC., et al, Association Between Malnutrition and Clinical Outcomes in the Intensive Care Unit: A Systematic Review. J Parenteral Nutrition, Feb, 2016. 14. Hartl, WH., et al, Complications and Monitoring – Guidelines on Parenteral Nutrition, Chapter 11, Ger Med Sci, 7, Doc 17, 2009. 15. Rees Parrish, C.,(ed) Liver Dysfunction Associated with Parenteral Nutrition: What are the Options? Nutrition issues in Gastroeneterology, Series #4, Accessed at (10-2016) http://www.practicalgastro.com/pdf/December06/LeeArticle.pdf 16. Venecourt-Jackson, Esra, Simon J. Hill, and Russell S. Walmsley. "Successful treatment of parenteral nutrition–associated liver disease in an adult by use of a fish oil–based lipid source." Nutrition 29.1 (2013): 356-358.

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