Gastroenterology & Hepatology Unit

Orientation and Clinical Care Guidelinesfor Junior Doctors

Authors: Dr Marcus Robertson

Dr Ray Boyapati

Contributions: Prof. William Sievert

Last Revised October 2019

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WelcomeWelcome to the Gastroenterology and Hepatology Unit at Monash Health. We hope your enjoy the rotation and learn a great deal.

This orientation guide contains most of the important information you will need for your Gastroenterology term – please familiarise yourself with it.

We pride ourselves on being a very approachable and friendly Unit. If you have any questions or concerns feel free to approach any of the Registrars or Consultants.

A/Prof. Sally BellDirector, Gastroenterology and Hepatology Unit

We would like to acknowledge Prof. Peter Hayes and the Royal Infirmary of Edinburgh who provided many resources that assisted in the development of these guidelines.

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Clinical Care Guidelines for Junior Doctors

CONTENTS Pages

Orientation 2-7Important Numbers / Bullying & HarassmentMonash Health Gastroenterology Consultants Unit timetables + Education opportunities

Gastroenterology ward procedures 8-16Admission Preparation of patients for invasive GI procedures Practical procedures at the bedside Performing a liver screen Common problems on the ward 17-201. Fever 2. Increasing confusion 3. Low Na+ 4. Poor urine output 5. Alcohol withdrawal/ DTs Common Liver conditions/related problems 21-281. Alcoholic Hepatitis2. SBP 3. Hepatorenal syndrome 4. Encephalopathy 5. Ascites 6. Variceal bleeding

Management of acute Upper GI bleeding 28

Common GI conditions 32-411. Inflammatory bowel disease 2. Diarrhoea 3. Management of acute pancreatitis

What to check prior to discharge 42

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MMC• Home ward is 34: 43460 or 43461• MMC Endoscopy: 43185 (Reception) 43188 (Scope room)

MMC Gastro Junior staff pager numbers:• Ward Reg # 474• Scopes Reg # 1043• 5th Reg # 928• RMO # 414• Intern # 4103

DDH• Home Ward is North 3 48551 or 48162 • DDH Endoscopy room 48633• DDH Endoscopy recovery 48342

DDH Gastro Junior staff pager numbers:• Ward Reg # 7219• Scopes Reg # 7393• RMO # 7747• RMO # 7786

Important contacts:• Heidi Harron (Gastro secretary): ph: 43177 fax: 46250• MMC Peg outreach (Jenny/Megan): 43090• MMC Liver research nurses: 43088• IBD clinical/research nurses: 43577

• IBD pharmacist: # 5019

IMPORTANT NUMBERS

BULLYING / HARRASSMENT

Monash Health and the Gastroenterology unit have very strong policies regarding this.

It is not acceptable in any form

You can report an incident to Sally Bell, Anouk Dev, Dilip Ratnam, Marcus Robertson or the Medical Workforce Unit.

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Name Role / Subspeciality A/Prof. Sally Bell Director, Hepatology, IBD

A/Prof. Anouk Dev Deputy Director, Hepatology, General Gastro, HCC

Michael Swan Director of Endoscopy, Interventional Endoscopy, General Gastro

A/Prof. Greg Moore Head of IBD, General Gastro, Capsule Endoscopy

A/Prof. Stephen Pianko Head of Clinical Trials, Hepatology, General Gastro

Malcom Barnes Interventional Endoscopy, General Gastro

Ian Bejer General Gastro

Ray Boyapati IBD, General Gastro

Chris Desmond General Gastro, EUS

David Devonshire Interventional Endoscopy, General Gastro

Rimma Goldberg IBD, General Gastro

Simon Hew Interventional Endoscopy, General Gastro

Alex Hodge Hepatology, General Gastro, FibroScan

Darcy Holt Clinical Nutrition, IBD, General Gastro

Suong Le Hepatology, General Gastro

Gauri Mishra Hepatology, HCC, FibroScan

Debbie Nathan General Gastro, Fiboscan

Fiona Nicholson Colorectal Cancer/Genetics, General Gastro

Lani Prideaux IBD, General Gastro

Dilip Ratnam Hepatology, General Gastro

Marcus Robertson Hepatology, General Gastro, FibroScan

David Rubinstein General Gastro

Ferry Rusli Hepatology, General Gastro

Ed Shelton IBD, General Gastro

Prof. William Sievert Hepatology, General Gastro

Cathy Sorrell General Gastro

Shireen Tabatabai Hepatology, General Gastro

Poornirma Varma Interventional Endoscopy, General Gastro

CONSULTANTS

Gastro Executive Committee: A/Prof Sally Bell, A/Prof Anouk Dev, Prof William Sievert, A/Prof Greg Moore, A/Prof Stephen Pianko, Dr Dilip Ratnam, Dr Michael Swan, Dr Marcus Robertson

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Basic Timetable - Meetings & Clinics

Monday Tuesday Wednesday Thursday Friday

0800 -0900

Radiology / Pathology,HCC MDT (Alt weeks)

Gastro meeting

(alt weeks journal club

/ clinical sciences)

AM Clinical trials clinic

Cirrhosis Clinic

MMC Gastro Clinic

(Clinic B); DTC clinic

PM DDH Gastro Clinic

Cranbourne Liver Clinic (alt weeks)

IBD MDT (alt weeks)

Springvale Liver Clinic

IBD Clinic MMC

Berwick IBD Clinic

Registrar Clinic(DTC)

Education opportunities for Junior Medical staff

• MDT meetings: General Gastro & HCC (Wed mornings 8-9am) and IBD (1pm alt weeks) in Pathology meeting room on Level 3.

• Friday morning Journal Club and Clinical Sciences meeting (8-9am alt between Lecture Theatre 3 and Seminar Room 2)

• Gastroenterology registrar teaching (co-ordinated by Dr Ray Boyapati) – generally alternate Friday mornings from 7.15 – 8am. This is not compulsory but you are more than welcome to attend.

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Endoscopy Rosters

MMCMonday Tuesday Wednesday Thursday Friday

AM Dev

Croagh

Bell

Barnes /

Varma

Devonshire (alt public / private

list)

Goldberg

Swan

Hodge/Prideaux

(alternating)

PM Moore / Nicholson

Croagh

Mishra (MBS)

Boyapati / Shelton

Desmond (EUS)

Croagh

Pianko

Swan

Devonshire

Monday Tuesday Wednesday Thursday Friday

AM Moore / Nicholson

Swan Ratnam(alt weeks)

PM Rubinstein Robertson Robertson/ Swan

Holt

Dandenong

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WARD PROCEDURES

ADMISSIONS

ALL PATIENTS admitted to the ward need to be FULLY clerked including a review of the patient’s drug chart, recent blood results and imaging. It is also advisable to check that all investigations have been requested for the next day e.g. endoscopy, ultrasound or blood tests.

IT IS THE RESPONSIBILITY OF THE WARD DAY STAFF TO ADMIT PATIENTS PRESENTING DURING THE DAY AND SHOULD NOT BE LEFT FOR DOCTORS WHO ARE COVERING THE WARD OUT OF HOURS.

Salient points in the history that should be documented for all patients:• Full history of presenting problem and systemic inquiry,

including any prior abdominal surgery • Aetiology and accurate time course of illness and effect on

QOL• Accurate current and recent drug history• Full family and social history• Details of relevant investigations (e.g. endoscopy, blood tests,

imaging, liver biopsy, Fibroscan) and relevant treatments

For patients with liver disease:• Episodes of decompensation for patients with liver disease

(e.g. ascites, variceal bleed and encephalopathy)• Whether patient is up-to-date with HCC and variceal screening • All patients with ascites should be considered for a diagnostic

tap on admission to the ward if this has not been performed prior

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to transfer of the patient. This should be sent for biochemical (total protein) and microbiological analysis (PMN count and MCS) with the results documented clearly in the notes.

PREPARATION OF PATIENTS FOR ENDOSCOPIC/RADIOLOGICAL GI PROCEDURES

• ALL PATIENTS requiring endoscopy need an inpatient REA (canary) form filled in and given to Endoscopy ANUM

• ALL PATIENTS must have a working cannula and a signed consent form which should accompany the patient.

• ALL PATIENTS undergoing interventional radiological procedures should have a FBE and COAG screen checked prior to the procedure with the results documented clearly in the case notes. Patients on anticoagulant medications or with coagulopathy (INR >1.5; platelets <50) should be discussed with the Registrar as reversal of coagulopathy with blood products may sometimes be required prior to the procedure.

• ALL PATIENTS should be FASTED FROM MIDNIGHT on the evening prior to a morning procedure or if on afternoon list, patients can have LIGHT BREAKFAST ONLY at 6am and then fast till the procedure.

It is important to clearly document if a patient is oninfectious precautions (VRE, C. difficile) etc. as this

affects the order in which patients are placed on the list

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ENDOSCOPIC PROCEDURES

It is important patients receive their usual medication prior to procedures (e.g. anti-hypertensive medication) unless there is a reason to withhold. If patient is on a morning list, oral medications should be taken with a sip of water (withhold diabetic oral hypoglycaemic agents).

Consent for endoscopic procedures

Written consent is required in all patients and should be obtained prior to the procedure by an HMO or Registrar. Endoscopy is a common and safe procedure, however during the consent process all patients should be aware of the following risks:• Anaesthetic risk• Bleeding (bleeding risk increases with procedures such as

polypectomy, dilatation)• Infection (including aspiration)• Perforation (Gastroscopy – 1:10,000 risk, Colonoscopy: 1:1000 risk)

In addition, patients undergoing ERCP also need to be consented for:• Risk of pancreatitis (5%)• Damage to other structures

Colonoscopy

The bowel preparation of choice is

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• 2 sachets of Picoprep → patient must drink 2-3 glasses of water after each sachet

• 1 litre of Glycoprep (1 litre)

3 L of glycoprep is another regimen, particularly in the elderly or those with multiple comorbidities.

ERCP:

• Antibiotic prophylaxis is not routinely given pre-procedure• In certain scenarios (eg. biliary stasis, pancreatic pseudocyst),

antibiotic prophylaxis may be given at the discretion of the treating physician– this is generally CIPROFLOXACIN 750mg orally or IV TAZOCIN 4.5 gram 1-hour pre-procedure

PEG (percutaneous endoscopic gastrostomy):

• Antibiotic prophylaxis should be given for all patients undergoing PEG insertion

• FBE and Coags should always be performed prior to procedure

RADIOLOGY PROCEDURES

TIPSS insertion

• Antibiotic prophylaxis (I.V CEFTRIAXONE 2 grams) should be given 2 hours PRE-PROCEDURE TO ALL PATIENTS.

Liver biopsy (percutaneous or trans-jugular)

• It is important to check with the interventional radiologist performing the procedure as requirements vary

• Generally for a percutaneous liver biopsy, platelets should be >50 and INR <1.5

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GASTROENTEROLOGY COMMON BEDSIDE PROCEDURES

• Informed consent should be obtained prior to all procedures (generally by the doctor completing the procedure)

• Platelet count and prothrombin time/INR checked prior to all procedures. LFTs and renal function is also checked for patients having ascitic drains.

• Aseptic technique should be adopted for all invasive procedures.

• All procedures should be documented clearly in case notes. In particular, the colour of ascitic fluid should be documented in addition to any immediate complications

This section covers a) diagnostic ascitic tap, and b) insertion of paracentesis drain. Important Note: these procedures require marking by ultrasound (either in radiology or by the gastroenterology registrar).

A) DIAGNOSTIC ASCITIC TAP

Should be performed in all patients with ascites on admission and if sepsis/SBP is suspected.• To minimize complications, avoid areas of prominent veins,

infected skin or scar tissue. • All patients should empty bladder prior to procedure

Procedure:1. Correctly position patient - lying supine with one pillow (if gross

ascites present) or at 30o elevation (moderate ascites)2. Area at right or left iliac fossa (approx. 3-5cm superior and

medial to anterior superior iliac spine) should be marked after suitable percussion note is detected:

3. Clean skin with antiseptic solution and apply a sterile drape.

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4. Using a 20ml syringe and 18 gauge needle, advanced slowly. Aspirate every 0.5cm to determine when the peritoneum is entered and ascitic fluid aspirated freely. If fluid cannot be freely aspirated consider another site or obtain assistance from the Registrar.

5. Once 25ml of fluid has been aspirated withdraw the needle and syringe and apply a dressing to the area.

6. Place ascitic fluid into: sterile yellow-topped urine container, purple-topped blood tube and blood culture bottles.

Fluid should be sent for: • BIOCHEM: protein/albumin, LDH• CELL COUNTS: PMN and RBC count• MICROBIOLOGY: MCS. Blood culture bottles should

also be sent.• If malignancy is suspected then a sample should also

be sent for CYTOLOGY (ideally a large amount of fluid obtained at paracentesis rather than 10mls obtained at time of diagnostic tap).

Note: A serum/ascites albumin gradient (SAAG) >11g/L is consistent with ascites secondary to portal hypertension

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B) INSERTION OF PARACENTESIS DRAIN

1. Ensure patient has emptied bladder prior to procedure2. Position patient - lying supine with one pillow 3. Mark site of drain insertion:

• Preferred site of drain insertion is the right or left iliac fossa (3-5 cm superior and medial to the ASIS)

• Drain can also safely be inserted 2-3cm below the umbilicus in the mid-line (ensure no large umbilical hernia)

• If unsure of appropriate site then ultrasound with marking of aspiration site can be performed prior to procedure

4. Wash hands and put on sterile gloves. Clean skin with antiseptic solution and apply sterile drape.

5. Using 10ml syringe and 25 gauge needle draw up 5-10mls of 1 or 2% lignocaine.

6. After infiltrating the skin, advance needle towards peritoneum, alternating aspiration and injection until ascitic fluid is noticed to be aspirated freely. Note depth at which the peritoneum is entered.

7. Use a scalpel blade to make a small nick in the skin to allow easier insertion of the paracentesis catheter.

8. Insert paracentesis catheter gradually with the needle directly perpendicular to the entry point on the skin. Continually apply negative pressure to the syringe as the needle is advanced. Entry into the peritoneal cavity is associated with loss of resistance and free aspiration of ascitic fluid. Now advance catheter over the needle into the peritoneal cavity.

IF ANY RESISTANCE IS FELT WHEN ADVANCING THE CATHETER THEN SEEK REGISTRAR ASSISTANCE OR ABANDON THE PROCEDURE AS THE CATHETER IS LIKELY TO BE MISPLACED.

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9. If safe to do so, advance catheter fully while withdrawing the needle and then attach drainage bag. Secure drain in place with Tegaderm and tape (+/- polystyrene cup).

Dispose of all sharps safely.10. Prescribe Albumin fluid replacement regimen (use dedicated

ascites order sheet):• Usually 100ml of 20% Albumin is given for every 2 litres

drained• Each bottle of 20% Albumin is given over 60min (note:

more rapid administration may result in acute circulatory overload and pulmonary oedema)

11. Drainage should be free (i.e. rapid) and the drain removed within 6-8 hours. • There is no upper limit to the amount of fluid that can be

drained and patients should be drained to dryness 12. If there is ongoing leakage from the drain site a stoma bag can

be applied. Losses from here should also be recorded and albumin given if total losses amount to >2L.

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PERFORMING A LIVER SCREEN

This usually should include:

• FBE, U&E• LFT’s• Coags• Viral serology: • Hep A, B and C, CMV, EBV, HSV (+ consider HDV and

HEV)• Autoantibodies: • ANA, AMA, Anti-smooth muscle ab, Anti-LKM Ab• Immunoglobulins• Fe studies• Alpha-1-antitrypsin• Copper, ceruloplasmin • Paracetamol level if required

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COMMON PROBLEMS ON THE WARD

Covered in this section:

A. FeverB. Increasing confusionC. Low Na+D. Poor urine outputE. Alcohol withdrawal

A. FEVER

• Not every fever will be sepsis (e.g. alcoholic hepatitis, pancreatitis)

• Sepsis will not always be accompanied by fever. Think of sepsis also when unexplained in BP and in HR or unexplained deterioration in patient condition e.g. GCS or

urine output

What to do:1. Examine patient looking for sites of infection (chest, urinary

tract, abdomen and lines/catheters)2. Carry out a full sepsis screen which includes blood cultures,

MSU, sputum, ascitic tap, and swab any breakages in the skin (esp. old cannula sites). Send stool cultures if appropriate and update CXR if respiratory symptoms or signs present.

3. Commence broad spectrum antibiotics after cultures have been taken as per Therapeutic Guidelines

4. Consider U/S to exclude intraabdominal collection/biliary sepsis.

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B. INCREASING CONFUSION

• Not all confusion in patients with liver disease is due to encephalopathy

• Not all intracranial pathology results in localising signs

What to do:1. Full neurology examination. Document any signs of external

head injury2. Document any hepatic flap/ fetor3. CHECK SPOT GLUCOSE4. Examine for any signs of sepsis and carry out full sepsis

screen. Consider supplementary IV fluids and broad spectrum antibiotics.

5. If acute GCS or seizure activity- consider URGENT CT Brain to exclude SOL/ICH or subdural.

6. Regular neuro obs with early anaesthetic referral if airway could be compromised.

C. LOW NA+• A low serum Na+ rarely indicates depletion of whole body

Na+; in patients with liver cirrhosis it more often represents total body water and Na+ overload (H2O>Na+)

• Symptoms and signs relate to rate of onset rather than the degree of hyponatraemia

• In most patients with liver disease the cause will be diuretic use or cirrhosis

What to do:1. Assess volume status of patient and check SERUM and

URINARY OSMOLARITY and URINARY Na+.2. Review previous biochem results to assess rate of fall in Na+.

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If not related to liver disease, check serum glucose (exclude ADDISON’S DISEASE), TFTs (exclude HYPOTHYROIDISM) and request CXR if no recent CXR (exclude SIADH).

3. Management depends on degree of hyponatraemia and rate of fall. If appropriate, fluid restrict (1.5L daily) patients and stop all diuretics when serum Na+ < 125 mmol/L.

D. POOR URINE OUTPUT

• Hepatorenal syndrome is common in patients with cirrhosis and ascites

• More that one aetiology may be present at one time e.g. volume depletion (including bleeding, excess diuretics, poor oral intake), sepsis, drug toxicity.

What to do:1. Assess volume status of patient (clinically and by reviewing

fluid balance charts for previous 24-48hours).2. Examine patient for signs of sepsis or GI blood loss.3. Check U&Es. If acidotic, also check ABGs.4. If clinically hypovolaemic: Stop any diuretics and give IV

fluid challenge (usually with IV Albumin)5. Consider empirical broad spectrum antibiotics if underlying

sepsis is a possibility.

If no improvement occurs then discuss with senior colleagues as CVP monitoring +/- inotropic support may be required.

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E. ALCOHOL WITHDRAWAL/DTS

• Is associated with significant morbidity and mortality. Alcohol withdrawal should be considered in all patients admitted to the ward (not just “liver” patients)

• Electrolyte disturbance e.g. gluc, Na+, K+, Ca+ may predispose patients to seizures or DTs.

• Look for associated problems e.g. aspiration pneumonia, rhabdomyolysis

What to do:1. Correct electrolyte disturbance and treat hypoglycaemia if

present.2. IV Thiamine 100-300mg TDS.3. Exclude underlying sepsis.4. Cautiously sedate the patient with Diazepam as per alcohol

withdrawal scale5. Consider CT Brain if fluctuating GCS or ongoing seizures/

agitation.

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COMMON LIVER CONDITIONS AND THEIR MANAGEMENT

Covered in this section:

A. Alcoholic HepatitisB. Spontaneous Bacterial Peritonitis (SBP)C. Hepatorenal syndromeD. EncephalopathyE. AscitesF. Variceal bleeding

A. ALCOHOLIC HEPATITIS

• Is defined as acute inflammation of the liver that is related to recent excess alcohol intake. If severe it is associated with high morbidity and mortality

• Only occurs in a minority of patients with alcoholic liver disease• Often develops during hospital admission.

The diagnosis is mainly clinical: patients have bilirubin on background of recent alcohol excess. ALT is often normal or minimally elevated (transaminases are usually <300 U/L) and the serum AST:ALT ratio can be >2. Alcoholic hepatitis can cause fevers (although sepsis must be excluded); CRP is typically <45. Not all patients with alcoholic hepatitis will have cirrhosis.

What to do:1. Exclude underlying sepsis (as cause of WCC) 2. RISK STRATIFICATION with Maddrey’s Discriminant function

(we typically use an on-line calculator to obtain this) → this

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determines whether the patient could be considered for Prednisolone therapy

3. DAILY U&Es, LFTs, FBC and COAG4. Consider Prednisolone 40mg daily if Maddrey’s discriminant

function is >32a) All patients must have sepsis excluded prior to

commencing steroidsb) Calculate Lille score on Day 7 to decide whether steroids

will be continuedc) Note: prednisolone therapy may confer a short term (28

day) benefit but no long term (90 day) reduction in mortality has been shown. Serious infection is more common in PNL treated patients (N Engl J Med 2015;372:1619-28)

5. All patients require formal dietetic assessment – the majority of patients will require nutritional supplementation (high protein, low salt diet)

B. SPONTANEOUS BACTERIAL PERITONITIS (SBP)

• Often asymptomatic• Common cause of confusion/ encephalopathy/ sepsis• Common in hospital in-patients

SBP is defined as a PMN count >250/mm3 in ascitic fluid, in the absence of an obvious source of peritonitis (e.g. bowel perforation).

Diagnosis:• Diagnostic ascitic tap. • Ascitic fluid should be sent for WCC count and MCS (10mls

universal container, ascitic fluid in a purple-topped blood tube and set of blood culture bottles should be sent to micro).

• Bedside inoculation of ascitic fluid to blood culture bottles will increase bacterial yield.

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Presence of >1 type of organism should raise the possibility of intra-abdominal pathology such as a bowel perforation.

Treatment: • Avoid NSAIDs, ACE inhibitors/A2RB and aminoglycosides in

patients with ascites• If patients are on non-selective beta blockers (propranolol,

carvedilol) for prophylaxis of varices consider ceasing these during an episode of SBP

• Antibiotics covering Gram negative organisms; typically IV Ceftriaxone 1-2g OD or IV Tazocin 4.5g TDS for 5 days

• IV Albumin – generally 1.5g/kg per day on days 1, 1g/kg on day 3

• A repeat diagnostic tap to assess progress is not currently routine practice

SBP Prophylaxis • Recommended in all patients following SBP and in all patients

with ascitic albumin concentration <15g/L → this is continues long-term.

• First-line therapy is Bactrim DS 160/800mg – 1 tablet daily• Second-line therapy is Norfloxacin 400mg – 1 tablet daily

C. HEPATORENAL SYNDROME( HRS)

• Patients with liver disease can develop renal impairment for numerous reasons e.g. pre-renal (excess diuretic use, sepsis, haemorrhage, inadequate volume replacement post paracentesis), nephrotoxic drugs (GN, ATN)

• NOT all renal impairment in patients with liver disease is due to HRS

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HRS is a clinical condition that occurs in patients with advanced liver disease and portal hypertension. Ascites must be present for a diagnosis of HRS to be made. It is characterised by impaired renal function and marked abnormalities in the arterial circulation and activity of the endogenous vasoactive systems. HRS carries an extremely poor prognosis and the treatment of choice remains liver transplantation if appropriate.

Types of HRS:• Type 1 = a rapid deterioration with doubling of serum

creatinine to >220 µmol/l or a reduction in creatinine clearance of >50% within two weeks (survival is 2-3 weeks without renal replacement therapy or OLT).

• Type 2 = a more moderate or stable reduction in renal function

Diagnosis of HRSFor the diagnosis of HRS to be made the following should be present:

1. Acute or chronic liver disease with advanced liver failure and portal hypertension

2. Creatinine >130 µmol/L or creatinine clearance < 40 ml/min (often associated with oliguria or anuria)

3. Absence of shock, bacterial infection, current or recent nephrotoxic drugs and exclusion of GI or renal fluid loss

4. No sustained improvement after diuretic withdrawal and plasma expansion with 1.5L saline or Albumin 1g/kg/day (max 100g/day) → caution needs to be given to avoid volume overload

5. Proteinuria should be <0.5g/day with absence of ultrasound, renal obstruction or parenchymal disease

6. Urinary sodium is typically <10mmol/day

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Treatment of HRS1. Exclude causes of pre-renal failure, stop diuretics (Frusemide

can be considered if necessary but cease Spironolactone)2. Ensure adequate filling especially with intravenous albumin

(CVP monitoring sometimes helpful)3. If no improvement in renal function consider the use of

vasoconstrictors, particularly Terlipressin initially 1 mg 4-6 hr with intravenous albumin (40g/day)• Terlipressin is contraindicated in patients with

significant IHD or PVD• Patients must be adequately filled prior to Terlipressin use • All patients on Terlipressin must have BD vascular obs

and daily review of hands and feet as peripheral necrosis is a known complication

4. If the above treatments fail, the prognosis is extremely poor. Consideration can be given to the use of renal replacement therapy (RRT) and liver transplantation, although it is appropriate only in a minority of patients.

D. ENCEPHALOPATHY

• Clinical signs can vary greatly e.g. from mild confusion to deep coma

• Diagnosis is made on clinical grounds (investigations such as EEG rarely required)

• Encephalopathy confers a very poor prognosis with approximately 50% mortality in the next 12-months

Management:1. Investigation and management as per “the confused patient”

(refer to earlier section).2. Stop diuretics for 24 - 48hours and look for obvious precipitants

e.g. sepsis, UGI bleeding, dehydration, constipation, drugs,

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over sedation.3. First-line management is regular oral Lactulose aiming for 3-4

bowel actions daily. Movicol, enemas or PR Lactulose can also be considered if required

4. Consider broad spectrum antibiotics once cultures taken (infection is a common cause)

5. Early ICU referral if airway compromised6. Consider Rifaximin therapy (550mg BD) for patients with

recurrent encephalopathy

E. ASCITES MANAGEMENT

• Ascites is defined as the presence of fluid in the peritoneal cavity and is the most common decompensation event in cirrhosis

• Ascites also carries a very poor prognosis long-term• All patients with ascites need exclusion of SBP

Management:

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F. VARICEAL BLEEDING

• All cases of GI bleeding in patients with known cirrhosis should be assumed to be variceal bleeding until proven otherwise

• In the majority of cases, bleeding is from oesophageal varices

What to do:1. Large bore IV access x22. URGENT BLOODS- FBE, U&E, LFT, COAG, Xmatch or G+H3. Fluid resuscitation:

a. Aim only for a Haemoglobin of 70-80 (do NOT over transfuse as this is associated with poorer outcomes)

b. Aim for “hypotensive resuscitation: - Systolic bp around 90-100mmHg

c. Fluid resuscitation with IV colloids, albumin or pRBC4. Ensure Gastro Registrar is aware5. All cirrhotic patients with haematemesis should be intubated

for airway protection6. Correct coagulopathy (this should NOT delay urgent

Endoscopy) 7. ALL patients should receive empiric IV antibiotics – either

IV Ceftriaxone 1-2g OD or IV Tazocin 4.5g TDS which should be continued for 3-5 days. Antibiotics improve prognosis in patients with cirrhosis irrespective of source of bleeding.

8. Early and urgent endoscopy is the hallmark of treatment – pt must be adequately resuscitated prior

9. Commence vasoactive therapy either Octreotide infusion or IV Terlipressin 2 mgs as a bolus followed by 1mg 4-6hrly.

Very rarely does a Sengstaken tube need to be passed pre-UGIE but if required this should be ONLY be passed by GI team or someone experienced in inserting the tube (incorrect placement is associated with serious complications such as oesophageal rupture)

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ACUTE UPPER GI BLEEDING (UGIB)

• This is a common medical emergency and continues to have a 4-10% mortality

• All patients with cirrhosis presenting with UGIB should be assumed to be having a variceal bleed until proven otherwise

• Never dipstick vomitus for the presence of blood as this is NOT accurate

Definitions• Haematemesis: Vomiting of fresh or altered blood• Coffee ground vomiting: Vomiting of dark (“coffee-like”)

material – isolated coffee ground vomiting is rarely associated with significant upper GI lesions

• Melaena: Passage of black, tarry stool. Melaena is NOT solid • PR bleeding: Passage of fresh, cherry-coloured or maroon

blood PR. This usually indicates a lower GI source of bleeding but in an unstable patient may result from rapid-transit bleeding (usually from an ulcer)

• Shock: Pulse >100 bpm; Systolic blood pressure <100 mmHg. Beware of patients on rate-limiting cardiac medications and young, fit patients who may remain compensated until major blood loss has occurred.

a) Variceal bleeding: See section (F) in the previous chapter

b) Non-variceal bleeding:

Risk stratification of upper GI bleeding

The AIMS65 score is a simple risk stratification score that can very accurately predict the risk of inpatient mortality following a GI bleed.

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• An AIMS65 score of 0 is associated with a 0% chance of inpatient mortality

• Any patient with an AIMS65 ≥2 should be considered high-risk (AIMS65 score of 3, 4 and 5 is associated with a mortality rate of 7%, 26% and almost 100% respectively)

Management of haematemesis and melaena:

Routine management in all patients:• Secure adequate IV access (2 x large-bore cannulas) • Resuscitation – generally IV fluid replacement is with Normal

Saline or CSL (Avoid Saline in patients with liver disease – albumin is preferred in these patients if possible). o Send blood tests including a Group and Hold or Xmatch o Do NOT over transfuse. A restrictive transfusion policy

aiming for a Hb of 70-80 (Hb 80-90 in patients with significant heart disease) is associated with improved outcomes

o Keep NBM and obtain informed consent for Endoscopy o Note any previous history of:

i. peptic ulcer diseaseii. NSAID use

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iii. Anticoagulants or anti-platelet agentsiv. Liver diseasev. Dyspeptic symptoms vi. Significant co-morbidities – eg. Cardiovascular, respiratory, renal, malignancy

• Look for evidence of chronic liver disease (eg. jaundice, spider naevi)

• Ask for a descriptive bowel chart to document melaena• PPI infusion:

i. Pantoprazole 80 mg IV stat followed by 80mg in 100ml given as a 10 hour infusion (8mg/hr)

ii. IV Pantoprazole (40mg IV BD) can also be used in many cases

• If a variceal bleed is suspected, commence empiric IV antibiotics and vasoactive therapy as per the variceal bleeding guidelines

Features of a major GI bleed:• Tachypnoea• Tachycardia >100 bpm• Hypotension (SBP <100 mmHg) or a postural drop• Clammy, cold, peripherally shut down• Reduced conscious level and/or confusion• Syncope or collapse

Timing of endoscopy:• This will be determined by the Gastroenterology Consultant

and Registrar. • Patients MUST be adequately resuscitated prior to endoscopy• All patients should receive Endoscopy within 24 hours, however

many patients are able to safely wait until an endoscopy list the following day

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COMMON GI CONDITIONS AND THEIR MANAGEMENT

Covered in this section:

A. Inflammatory bowel disease (IBD) A1. Management of acute severe ulcerative colitis (UC) A2. Management of Crohn’s disease (CD)B. Investigation of diarrhoea C. Management of acute pancreatitis

A. INFLAMMATORY BOWEL DISEASE

• The IBD nurse should be informed of the admission of all IBD patients (via email or phone)

• The IBD pharmacist (pager 5019) should be contacted with regards to all patients commencing or having their thiopurines adjusted. The IBD pharmacist can assist with blood monitoring and dose adjustment post discharge.

• Patients should be seen in IBD clinic (Monash or Berwick) within 2-4 weeks post discharge (depending on clinical circumstance)

Commonly used medications in IBD• Immunosuppressive (steroids and steroid sparing) therapies

are commonly used in IBD• All patients starting immunosuppressive therapy should have

the following tested: HBsAg, HBsAb, HBcAb, HCV Ab, HIV, QuantiFeron Gold, CXR, VZV IgG and EBV IgG (for thiopurines). A history of tuberculosis or chicken pox infection should be taken.

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• Annual influenza and 5 yearly pneumococcal vaccination should be recommended

• The following live vaccines are to be avoided whilst taking immunosuppressant therapy:

o Tuberculosis vaccine (BCG)o MMR (measles/mumps/rubella)o Varicella Zoster (VZV) vaccineo Oral typhoid vaccineo Yellow fever vaccineo Japanese encephalitis (Imojev brand)o Rotavirus vaccine

Thiopurines (azathioprine (pro-drug) / 6-mercaptopurine (active form of drug))• These agents are usually initiated in patients with steroid

dependency in UC or CD.• Approximately 1 in 300 patients have a genetic predisposition

of altered metabolism of thiopurine and are at risk of profound bone marrow suppression. All patients treated with thiopurines should have a thiopurine S-methyltransferase (TPMT) assay done on the wards and the result checked in clinic (results take at least 2 weeks). Low TPMT predicts bone marrow suppression (however, marrow suppression can still occur with normal TMPT)

• Patients should also be educated about:o Increased risk of skin cancers (fastidious skin care and

yearly skin check recommended)o Risk of hepatitis and/or pancreatitis (idiosyncratic reactions)o Increased risk of lymphoma

• Azathioprine/6MP take at least 3 months (and up to 6 months) for optimum effect.

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• If TPMT is unknown, starting dose should be 50mg per day (azathioprine) or 25mg per day (6MP). If TPMT is normal, dosing regime is 2-2.5mg/kg (azathioprine) or 1mg/kg (6MP).

• Be careful with drug interactions – allopurinol (a xanthine-oxidase inhibitor will lead to high levels of thiopurines and should only be used by IBD specialists).

• Close monitoring of FBE and LFT is mandatory after starting and adjusting therapy with thiopurineso The IBD pharmacist should be contacted for all of these

patients as they will help in monitoring post dischargeo A pathology slip with FBE, LFT and CRP should be provided

to the patient to get done one-week post commencing thiopurine therapy

o Another pathology slip for FBE, LFT and CRP as well as “thiopurine metabolites”) should be performed four weeks after the target dose is commenced

Monoclonal antibodies to TNFa(e.g. infliximab and adalimumab)• Sepsis must be rigorously excluded e.g. urine and blood

cultures taken.• Infliximab is generally given at 5mg/kg every 8 weeks (with

loading doses at 0, 2 and 6 weeks).o Infusion reactions are not uncommon – if occurs (even mild

episodes), infusion should be discontinued. Antihistamines can be used (together with co-administered hydrocortisone).

• Adalimumab is generally given at 40mcg fortnightly (with loading doses of 160mg at week 0 and 80mg at week 2)

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A1. Management of inpatient IBD - acute severe ulcerative colitis• Acute severe UC is a medical emergency requiring urgent

admission and close monitoring on the wards• It is defined by the Trulove and Witt criteria

o Bloody diarrhoea >6 bowel actions in 24 hours AND ≥ 1 of the following:

• Tachycardia (Resting pulse >90 bpm) • Fever (>37.8oC) • Anaemia (Hb <105 g/L) • Elevated inflammatory markers (ESR >30) [CRP can be used as a surrogate]

• Patients who satisfy criteria for severe disease have a 30-40% likelihood of not responding to standard medical therapy (e.g. high dose corticosteroids) and will require careful monitoring and consideration of rescue medical therapies or colectomy

• It is imperative that the surgeons are involved early in the admission for all patients with severe UC.

History and examination:• Colitis diagnosis (year of diagnosis, gastroenterologist/unit

who usually manages patient, UC or indeterminate), past and current treatments

• Previous episodes of severe flares requiring intravenous steroids

• Recent disease activity: latest endoscopy result, faecal calprotectin, blood results

Note:• Colicky lower abdominal pain can be present, but constant

severe abdominal pain is NOT typical.• Remember travel and infectious contacts• Patients already on prolonged courses of oral steroids prior to

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presentation, may not have classical signs of perforation• Fever, tachycardia and abdominal tenderness should be

regarded seriously.

Investigations:• Routine bloods (Beware of very high CRP and WCC – these are

not typical of UC, increase index of suspicion for perforation).• Hypoalbuminaemia is a consistent predictor of poor outcome.• Abdominal X-ray should be performed on day 1.

o Colonic dilatation (Transverse colon >5.5cm or caecal pole >9cm with loss of haustration).

o Mucosal oedema (Thickened colon with loss of haustration)o Presence of 3 or more dilated small bowel loops (often

heralds development of colonic dilatation).• Multiple stool cultures must be sent (up to 10% patients

are Clostridium difficile positive. This is often associated with medically refractory disease)

• Flexible sigmoidoscopy should be performed within 48-72 hours of admission. This can confirm a new diagnosis of colitis, assess endoscopic severity (e.g. the presence of deep ulcers is associated with a reduced response to steroids) and extent of disease (20-30% of proctitis becomes more extensive in 5 year follow-up). Biopsies are taken during endoscopy in formalin (for histology) and saline (for CMV).

Management:• Management of severe UC is typically multi-disciplinary with

gastroenterologists and colorectal surgeons • IV Hydrocortisone 100mg QID is typical first-line management• 5-ASA medications: may be started during admission or at

time of discharge (eg. Mezevant 4.8g daily or Pentasa 2g bd).

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• All patients should receive thromboembolic prophylaxis (Enoxaparin 40mg daily), even if they have rectal bleeding

• Exclude concurrent infection (stool cultures, biopsies for CMV)

Progress:• Patients should be assessed twice daily by medical staff• Patient should be assessed at day 3 of therapy to ascertain

need for 2nd line (rescue) medical therapy or early surgery • Medical rescue therapies include infliximab or cyclosporine

infusion • Patients refractory to medical therapy need to be considered

for colectomy which is curative in UC

A2. Management of inpatient IBD - Crohn’s disease

Patients with Crohn’s disease may present acutely in several ways:• Obstructive abdominal pain• Diarrhoea• Profuse bleeding• Complications relating to malnutrition• Perianal disease

History and examination:• Crohn’s diagnosis (year of diagnosis, gastroenterologist/unit

who usually manages patient), past and current treatments• Previous episodes of admission – what was the reason for

admission (e.g stricture, fistula, perianal disease, malnutrition or luminal inflammation)

• Extent of disease – gastric, proximal small bowel, terminal ileum, colonic, perianal etc. Commonly patients with ileal/ileo-colonic disease can present with acute luminal/obstructive symptoms

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• Signs of active disease – fever, elevated inflammatory markers.• Patients with full-thickness inflammation can have localized

peritonism.• Observations – watch for fever and tachycardia, etc.

Investigations:• Routine bloods: beware of very high WCC, CRP levels (consider

perforation, abscess formation or septic complication)• Nutrition screen• AXR• If disease extent unclear, investigations such as gastroscopy,

colonoscopy, small bowel MRI and pelvis MRI may be required during the admission or as an outpatient

• Multiple stool cultures should be sent if diarrhoea is a presenting symptom.

Management:

Small bowel disease with obstruction• Usual conservative management such as bowel rest• Consider NGT if profuse vomiting and pain or low-residue diet

if symptoms sub-acute• A trial of corticosteroids (IV or oral) can be considered• All patients should have their disease staged (e.g. small bowel

MRI) to delineate extent and activity of disease.• Patients with long strictures, multiple segments of active

disease or fistulising disease often will not settle with simple medical management and may require more complex solutions e.g. combined immunosuppressive therapies +/- surgery

• Symptomatic fibrotic disease often requires surgery

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Colonic disease• 1st line therapies usually involve corticosteroids and 5-ASA

medication• Patients who fail to settle with IV corticosteroids as an

inpatient for inflammatory colonic Crohn’s disease will require consideration of an anti-TNF agent (infliximab or adalimumab). In patient with corticosteroid-dependent disease, azathioprine or 6-mercaptopurine should be considered (note these medications take months to take full effect).

B. INVESTIGATION OF DIARRHOEA

Most patients admitted for investigation of diarrhoea fall into 2 groups:1. They have profound symptoms which are well documented

with or without a previous diagnosis; OR 2. There is doubt about the degree and/or cause of diarrhoea

Important points to consider in the patient history:• Acute or chronic (>2 weeks)?• Recent episode of gastroenteritis or travel abroad?• Any blood or steatorrhoea?• Nocturnal symptoms?• Associated symptoms - weight loss, systemic upset, pains• Any medications (e.g. recent use of antibiotics, NSAIDs, PPI)?• Diabetes? Recent cholecystectomy?• History of IBD / pancreatic disease / diverticular disease?• History of previous stomach or bowel surgery?• Family Hx of IBD or coeliac disease?

Approach to the patient with diarrhoea during hospitalisation• Observation of behavioural and diet habits of patient very

important

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• Completion of a diarrhoea chart stating time, amount, consistency and presence of blood or mucous mandatory.

• Examine patient carefully; do not miss abdominal masses• Do not miss overflow diarrhoea in a constipated patient – PR

examination mandatory• Monitor weight

Investigations (extensiveness is driven by clinical suspicion):• All patients should have stool samples sent for MCS and ova,

cysts and parasites (OCP) along with C. difficile • Basic bloods including: FBC, LFTs, U&Es, TFTs, coeliac

screen, blood glucose• Depending on the clinical suspicion colonoscopy or flexible

sigmoidoscopy may be performed after infection is excluded

Second line investigations: To exclude more unusual causes or atypical presentations of common diseases• Faecal calprotectin – typically raised in IBD and normal in IBS• Faecal elastase - reduced in chronic pancreatitis with exocrine

insufficiency• Hydrogen Breath test for bacterial overgrowth• Serum LDH (? Lymphoma)• Laxative abuse screen (requires urine sample)• Testing for neuroendocrine tumour – Chromogranin A is an

excellent screening test; 24-hour urinary 5-HIAA is useful if carcinoid syndrome is suspected

• Unexplained diarrhoea (from all above testing) and weight loss in an unwell patient should prompt testing for TB.

• Consider specialised imaging (if still suspicion of IBD) such as small bowel CT, small bowel MRI

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C. MANAGEMENT OF ACUTE PANCREATITIS

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What to check prior to ward discharge

• Effective patient care does not stop at discharge. The patient’s outcome is heavily dependent on your effective communication with the patient’s GP and organisation of outpatient services

• All patients need a discharge summary with detailed management plan completed within 24 hours of discharge

• For all patients that have had a variceal bleed during admission, please ensure that they have a repeat gastroscopy booked for 2-3 weeks post index scope

• For patients who have had SBP, please ensure they are discharged with SBP prophylaxis

• Please ensure the IBD nurse (and IBD pharmacist if new or altered thiopurine prescription) have been notified of IBD patients

• Ensure Outpatient clinic visit is booked – please specify which clinic and what timeframe

• Ensure that any further investigations are requested following discharge and record in the case notes and discharge summary.

• Discharge summaries should be brief and to the point

• Please ensure that all patients have their discharge weight documented in the discharge summary, especially those with cirrhosis and ascites