Pass Critical Care Liver GIT

Dr Ali Ragab (www.facebook.com/groups/pass.critical.
care/)
Pass Critical Care

Essential ICU study notes
GIT and Liver

Dr. Ali Ragab
1
Dr Ali Ragab (www.facebook.com/groups/pass.critical.care/)
Table of Contents
Gastro intestinal bleeding (GIB) .............................................................................................. 3
Stress Ulcer Syndrome ............................................................................................................ 8
Variceal bleeding .................................................................................................................. 11
GIT motility disorders in ICU ................................................................................................. 17
Fulminant Colitis and Toxic Megacolon ................................................................................. 21
Hepatic dysfunction .............................................................................................................. 26
Acute liver failure (ALF) ........................................................................................................ 30
Fulminant hepatic failure...................................................................................................... 30
Chronic liver failure .............................................................................................................. 35
Diarrhea ............................................................................................................................... 40
Severe and Complicated Biliary Tract Disease ....................................................................... 46
2
Gastro intestinal bleeding (GIB)

Definition
• Upper GIB à blood loss proximal to ligament of Treitz.
• Lower GIB à blood loss distal to ligament of Treitz.
Etiology
Upper GIB
Common causes
• Ulcer à duodenal and gastric ulcers (most common).

• Drugs à NSAIDs.
• Infection à Helicobacter pylori infection.
• Inflammation à esophagitis (rarely associated with severe bleeding).
• Severe vomiting à Mallory–Weiss tears.
• Varices à esophageal – gastric – duodenal.
Uncommon causes
• Vascular à angiodysplasia – telangiectasia.

• Fistula à aorto–enteric fistula.
• Benign tumors à gastrointestinal stromal tumor.
• Malignant tumors à adenocarcinoma – lymphoma.
Lower GIB
Common causes
• Diverticulosis à most common.

• Anorectal à hemorrhoids – anal fissures.
• Colitis à IBD – infectious colitis – ischemic colitis.
• Vascular à angiodysplasia.
• Tumors à benign – malignant – polyps.
Uncommon causes
3
• Ulcers à rectal ulcer.

• Vascular à vasculitis – colonic varices.
• Fistula à aorto–enteric fistula.
• Radiation à proctopathy and colopathy.
• Meckel diverticulum.
• Intussusception.
Clinical presentation
Hematemesis
• Definition à vomiting of blood or altered blood (coffee–ground).
• Indicative of à acute upper GIB.
Hematochezia
• Definition à passage of bright or dark red blood through the anus.
• Indicative of à lower GIB or brisk upper GIB.
Melena
• Definition à passage of (black + sticky + tarry) stools.
• Indicative of à upper GIB or slow lower GIB.
• Melena can persist for several days after GIB has ceased (stool may
remain positive for occult blood for up to 2 weeks).
Diagnostic tests
Nasogastric aspiration and lavage
• Aspiration of red blood à urgent endoscopy.
• Lavage à remove clots from stomach in preparation for endoscopy.
NG aspirate may be non–bloody if tightly closed pylorus prevents

reflux of blood from duodenal bleeding site.
Endoscopy
Ideally performed when the patient is hemodynamically stable
4
Esophagogastroduodenoscopy (EGD)
• Evaluates and treats upper GIB.

• Should be performed within 24 hours of presentation in patients with
evidence of acute blood loss of suspected upper GI origin.
Colonoscopy
• Detect and treat the source of lower GIB.

• Should be performed after adequate resuscitation and bowel
cleansing (the presence of stool and blood in the colon lumen
obscures visualization and prevent treatment of culprit lesion).
Push enteroscopy
• Evaluates proximal small bowel when bleeding site is not found in
upper GI tract or colon on EGD or colonoscopy.
Imaging studies
Technetium99m labeled red blood cell scan
• Detect bleeding rates as low as 0.1 mL/minute.
Angiography
• Detect bleeding rates of 0.5–1 mL/minute.

• If bleeding source is detected à embolization or infusion of
vasopressin can be therapeutic.
Clinical manifestation
• Shock à ¯ BP – confusion – agitation – cold extremities.
• Abdominal pain
o Abdominal pain is not common with GIB.
o May indicate à haemobilia – intestinal infarction – perforation.
• Chest pain à superimposed ACS – anemia – hypotension.
• Aorto–enteric fistula à history of abdominal vascular graft surgery.
5
Initial blood testing

• CBC à initial blood count may not reflect the degree of blood loss.
• Coagulation parameters à PTT – PT – INR – BT – CT.
• Complete metabolic profile à LFTs – KFTs – ABG – electrolytes.
• Type and cross–match blood à for transfusion.
Treatment
Resuscitation (takes priority over other treatments)
• Airway à massive hematemesis may require ETT.
• Breathing à keep adequate oxygenation and ventilation.
• Circulation à aggressive administration of fluids or blood products.
• Exsanguinating hemorrhage à immediate surgical management.
Pharmacologic therapy in upper GIB

Non–variceal bleeding
• Acid suppression à IV PPI (standard in acute upper GIB).

• Prokinetics à IV erythromycin or metoclopramide.
Variceal bleeding
• Octreotide
o Bolus à 25–100 mcg IV.
o IV infusion à 25–50 mcg/h for 2–5 days.
• Antibiotics (IV ceftriaxone or ciprofloxacin).
Endoscopy
• Injection à sclerosing solutions – hypertonic saline – epinephrine.
• Thermal devices à heater probe – electrocoagulation – laser.
• Banding devices.
• Hemoclips.
Recurrent bleeding occurs in 30% of cases with bleeding ulcers despite

successful endoscopic therapy à continue observation for 72 hours.
6
Angiographic therapy
• Intra–arterial vasopressin à for upper and lower GIB.
• Intra–arterial vasopressin à ↑ risk of cardiovascular complications.
• Gel foam or metal coil embolization à localized thrombosis.
Non–surgical management in variceal bleeding

Trans–jugular intra–hepatic portosystemic shunt (TIPS)
• Indications
o Variceal bleeding refractory to endoscopic management.
o Multiple episodes of variceal bleeding.
Balloon tamponade
• Temporary measure when alternate therapeutic procedure is planned

within 24 hours.
Surgery
Indications
• Massive ongoing hemorrhage that overwhelms resuscitative effort.

• Failure to respond to endoscopic or angiographic management.
7
Stress Ulcer Syndrome

Definition
• Mucosal damage in upper GIT that occurs with extreme physiologic
stress associated with clinical bleeding or perforation.
Description
• In the fundus and body of stomach (common).
• Duodenal ulcers (uncommon).
Etiology
Critically ill patient with
• Mechanical ventilation > 48 hours.
• Sepsis.
• Hypotension and shock.
• Major burns >35% BSA (Curling ulcer).
• Acute intracranial head trauma and coma (Cushing ulcer).
• Coagulopathy.
Pathogenesis
Mucosal damage
• Stress à splanchnic VC à ↓ synthesis of mucus + ↓ intramucosal
pH à gastric mucosal ischemia à ulceration.
• Reperfusion à hyperemia + ↑ inflammatory response à injury.
• Hematemesis – gross blood from NGT – melena.
• Abdominal pain (unusual) à consider perforation.
Endoscopy
Findings
8
• Early à mucosal changes à pallor – mottling – petechiae.

• Then à superficial linear erosions and ulcers.
• Eventually à diffuse mucosal damage + bleeding.
Treatment
Prophylaxis
H2 receptor antagonists
• Route à IV bolus or continuous IVI.

• CrCL <30 ml/min à give ½ recommended dose.
• Adverse effects à thrombocytopenia.
• Benefits à ↓ Incidence of bleeding without ↑ risk for VAP.
Proton pump inhibitors (PPI)
• Strongest antisecretory agents.
Antacids
• Dose à 10–80 mL through NGT q1–2h.

• Target à titrate to gastric pH > 4.0.
• Adverse effects à diarrhea – ↓ bioavailability of oral medications.
• Renal failure à contraindicated.
Sucralfate
• Dose à 4–6 gm/day through NGT.

• Chronic renal insufficiency à be Cautious.
• Benefits à lower incidence of nosocomial pneumonia.
• Mechanism à sucralfate coats the early shallow mucosal lesions and
protects them from further acid and pepsin damage without altering
gastric pH.
Endoscopy
• Upper GI endoscopy à diagnosis + local control of bleeding.
• Management à injection – clipping – thermal therapy.
9
Angiography
• Failure of endoscopic measures à angiography using intra–
arterial vasopressin or embolization.
Surgical therapy
• Indication à severe hemorrhage unresponsive to all other measures.
• Management
o Total or subtotal gastrectomy.
o Vagotomy + sewing of remaining ulcers during subtotal
gastrectomy.
Complications
• Stress ulcers
o Stress ulcer à bleeding – perforation.
• Nosocomial pneumonia
o Stress ulcer prophylaxis à gastric alkalinization à ↑
colonization of upper GIT with potentially pathogenic
organisms.
• Clostridium diffcile infection
o Gastric acid protects against Clostridium diffcile infection.
10
Variceal bleeding
Pathophysiology
• Increased intrahepatic resistance to portal venous flow à portal
hypertension à portosystemic pressure gradient >10 mmHg à
portosystemic collateral circulation progressively enlarges à varices.
Etiology
• Hepatic fibrosis and cirrhosis.
• Portal vein and hepatic vein thrombosis.
• Congenital hepatic fibrosis.
• Schistosomiasis.
Risk factors for variceal rupture

• Large size.
• Portosystemic pressure gradient ≥12 mm Hg.
• Red wale marks.
• Decompensated cirrhosis.
• Active infection.
• Variceal bleeding à hematemesis – melena – hematochezia.
• Hemodynamic instability à varying degrees.
Endoscopy (gold standard)

Endoscopic findings supporting variceal bleeding
• Active bleeding.
• Fresh fibrin clot protruding from varix.
• Nipple–like protrusion from varix.
• Red wale marks.
• Large varices with no other potential bleeding source.
11
Treatment
Initial resuscitation
• Airway à ETT may be indicated in massive bleeding or DCL.
• Breathing à maintain adequate oxygenation and ventilation.
• Circulation à fluid resuscitation + transfusion ± vasopressors.
Nasogastric aspiration
• Fears of trauma to varix from NGT largely are unfounded.
• Good lubrication and careful technique are recommended.
• NG aspiration à clear stomach of blood before upper endoscopy for
better visualization.
Pharmacological therapy
Octreotide
• Vasoconstrictor of choice in acute variceal bleeding.

• Mechanism (long–acting analog of somatostatin) à inhibits release
of vasodilators à ↓ splanchnic blood flow and portal pressure.
• Dose (bolus 50 mcg then IVI 50 mcg/h for 3–5 days).
• Side effects (transient nausea and abdominal pain).
Somatostatin is not available in United States (when available should be

given as 250 mcg bolus followed by IVI 250 mcg/h).
Vasopressin
• Used only when octreotide is not available.

• Mechanism (VC) à ↓ splanchnic blood flow and portal pressure.
• Dose (0.2–0.4 U/min) – titrate to max 0.8 U/min for 24 hours.
• Side effects à myocardial ischemia, arrhythmias, hypertension, and
peripheral and bowel ischemia.
Concurrent nitroglycerin IVI at 40 mcg/min (titrated to keep SBP of 90

mmHg) à ↓ systemic side effects of vasopressin.
12
Terlipressin
• Synthetic analog of vasopressin with slower release and fewer side

effects (not available in the United States).
• Dose (2 mg q4h) and can be titrated down.
Endoscopic therapy
Band ligation (technique of choice)
• Elastic rings are placed endoscopically over varices à strangulation

of the vessel à sloughing and fibrosis of the varix à decompressing
downstream veins.
Sclerotherapy
• Injecting sclerosant solution into variceal lumen or into adjacent

submucosa à vascular obliteration.
• Indication
o Bleeding refractory to band ligation.
o Gastric variceal bleeding.
o Massive bleeding (inadequate visualization of variceal columns
to perform band ligation).
• Sclerosant solutions
o Sodium tetradecyl sulfate.
o Ethanolamine oleate.
o Ethanol.
o Hypertonic dextrose.
o Phenol.
Variceal obturation
• Injection of tissue adhesives à cyanoacrylate and thrombin.

• Complications à rebleeding due to extrusion and distant
embolization.
Complications of endoscopic therapy
13
• Esophageal ulceration – bleeding – stricture formation – dysmotility –

perforation and mediastinitis – aspiration.
Balloon tamponade
• Balloons à Sengstaken Blakemore – Minnesota – Linton Nachlas.
• Balloon tamponade à temporary measure until definitive therapy
can be arranged within 24–48 hours of balloon inflation.
• Gastric and esophageal balloon à direct tamponade of bleeding
varices (severe or persistent bleeding refractory to endoscopic and
pharmacologic treatment).
Complications
• Esophageal/gastric necrosis and perforation.

• Aspiration.
• Balloon migration.
• ETT intubation before balloon placement for airway protection.
Given these potentially lethal complications à balloons should be

inflated for maximum of 24 hours.
Trans–jugular intrahepatic portosystemic shunt (TIPS)
• TIPS à shunt between hepatic and portal veins à ↓ portosystemic
pressure gradient to <12 mmHg.
• Cross–sectional imaging or Doppler US à before TIPS to evaluate
patency of portal vessels and to rule out liver masses.
Indications
• Bleeding refractory to pharmacologic and endoscopic therapy.

• Recurrent bleeding or bleeding from gastric varices.
• Portal hypertensive gastropathy.
Thirty percent of patients develop transient deterioration of liver

function after elective shunt placement and up to 25% of patients may
experience new or worsened hepatic encephalopathy.
14
Balloon–occluded retrograde transvenous obliteration (BRTO)

• Left adrenal venography à identify gastro–renal shunt à occluded
with balloon à then sclerosant is injected proximally to obliterate
gastric varices.
Other measures
Surgical shunts
• Portocaval and distal splenorenal shunts may be considered in

patients with good long–term prognosis (Pugh Childs class A
cirrhosis and patients with non–cirrhotic portal hypertension).
Non–shunting operations
• Sugiura procedure à mucosal transection and devascularization of

esophagus (varices reform and bleeding recur in 20% of patients).
• Embolization of short gastric veins in gastric variceal bleeding and
splenectomy in splenic vein thrombosis are other potential
management options.
Complications
Rebleeding
Β–blockers
• Non–selective β–blockers à ↓ COP (β1) and splanchnic

vasoconstriction (β2) à ↓ portal pressures à ↓ rebleeding.
• Nadolol (40 mg q24h) or propranolol (20 mg q12h) à titrate up
according to BP.
• Avoid β–blockers in acute variceal bleeding à hypotension + block
physiologic increase in HR à may be initiated once acute bleeding
has resolved and if the patient is hemodynamically stable.
Band ligation
• Serial endoscopic band ligation à ↓ rebleeding rates.
15
• Scheduled sessions at weekly or biweekly intervals are recommended

until obliteration of the varices is achieved.
Bacterial infections
• Antibiotic prophylaxis à ↓ (mortality – infections – rebleeding).
• Oral Norfloxacin à 400 mg q12h for 5–7 days.
• IV Ciprofloxacin à 400 mg q12h for 5–7 days.
• IV Ceftriaxone à 1 gm q24h for 5–7 days.
Portosystemic encephalopathy
• Precipitating factor à GIB.
• Treatment à lactulose and rifaximin.
• Endoscopy à evaluate for occult bleeding may à consider in
patients with encephalopathy when no other trigger is identified.
Renal failure
• Etiology à ATN or HRS.
• Prevention à early resuscitation.
Patients with alcoholism

• Should receive thiamine.
• Monitor closely for alcohol withdrawal.
16
GIT motility disorders in ICU

Etiology
Gastric stasis (delayed gastric emptying/gastroparesis)
• Inflammation à infection – sepsis.
• Neurologic à trauma – parkinsonism – neuropathy – pain.
• Organ failure à cirrhosis – ESRD.
• Electrolytes à hypercalcemia – hypokalemia – hypomagnesemia.
• Metabolic à hyperglycemia – acidosis – alkalosis – hypothyroidism.
• Medications à vasopressors – narcotics – propofol.
• Diseases that alter the mucosa à amyloidosis – scleroderma.
Colonic dysfunction (distension/constipation)

• Medications – metabolic disturbances – medical comorbidity.
• Systemic or GI infection à Clostridium diffcile – CMV.
• Ischemia à intestinal – cerebrovascular.
• Nutritional à withholding or strict limitation of luminal nutrition.
Diarrhea
• Enteral feedings à hyperosmolar formulas – high infusion rates –
colonic fermentation of malabsorbed carbohydrates.
• Infections à clostridium diffcile – opportunistic pathogens (CMV).
• Medications à antacids – antibiotics – lactulose – sorbitol.
• Impaction à fecal impaction with fecal overflow around impaction.
Diagnosis
Gastric stasis
Gastric stasis is suspected with
• Impaired tolerance to gastric feeding.

• Gastric residual volumes ≥200 mL suggest retention.
17
Mechanical obstruction is evaluated by
• Upper endoscopy.
• Imaging à abdominal plain films – CT scan.
GERD
• Gastric stasis à GERD à heartburn and regurgitation.

• Endoscopy à reserved to evaluate GERD complications (e.g. GIB).
Acute colonic pseudo–obstruction (Ogilvie syndrome)

• Presentation à marked abdominal distension and pain.
• Complications à colonic ischemia and perforation.
• Plain abdominal films or CT images
o Diffuse colonic dilatation + normal mucosal markings.
o Absence of small bowel dilatation.
Diarrhea
• Diarrhea à change in stool frequency or consistency.
• Medications à review medications that may precipitate diarrhea.
• Antibiotic–associated diarrhea à unexplained TLC à diagnose
via detection of stool PCR for C. diffcile.
• Rectal examination à exclude distal impaction.
• Abdominal radiographs à exclude proximal impaction.
• Colonoscopy with biopsy à when diarrhea remains unexplained.
Treatment
Gastric stasis
• Eliminate iatrogenic factors and exclude mechanical obstruction.
• Minimize or eliminate narcotics and other provoking medications.
• Improve feeding tolerance by positioning feeding tube ports beyond
the pylorus (jejunal or gastro–jejunal feeding tube).
• Consider parenteral nutrition if enteral feeds are not tolerated.
18
Medical treatments
• Metoclopramide
o Increases gastric emptying but does not prevent aspiration.
o Side effects à confusion – agitation – somnolence – dystonic
reactions.
• Intravenous erythromycin
o Increases gastric emptying (motilin agonist).
o Dose à 1–3 mg/kg 3–4 times daily.
o Side effects à nausea – vomiting – diarrhea.
o Tolerance to prokinetic effect à due to motilin receptor down–
regulation with repeated use.
Management of GERD
• Conservative measures
o 45–degree elevation to head of bed.
o Avoid large–bolus tube feedings.
o Post–pyloric feeding tube placement.
• Pharmacologic treatment
o PPIs are the most effective acid–suppressant agents.
Acute colonic pseudo–obstruction (Ogilvie syndrome)

• Recognize and correct of reversible causes.
• Exclude fecal impaction and place rectal tube.
• Opioid–induced intestinal dysfunction à newer opioid receptor
antagonists (alvimopan – methyl naltrexone) may be helpful in.
Neostigmine
• Dose à 2 mg IV over 5 min.

• Mechanism à inhibit acetyl–cholinesterase.
• Indications à failure of conservative measures and reversal of
underlying factors.
19
• Contraindications à bradycardia – active bronchospasm –

mechanical bowel obstruction.
Colonic decompression
• Colonoscopy for decompression à consider when distension

worsens, and clinical condition appears compromised.
Diarrhea
• Decrease feeding rate in tube–fed patients.
• Correct electrolyte and metabolic abnormalities.
• Discontinue medications potentially responsible for diarrhea.
• Incontinence devices (e.g. rectal tube) à ↓ skin complications.
Pharmacologic treatment
• Metronidazole
o Drug of choice for Clostridium diffcile infection.
o When suspected à initiate therapy in severely ill patient.
o Continue treatment for at least 14 days in confirmed cases.
o Response of diarrheal symptoms may take 7–10 days.
o IV route is required in patients intolerant of oral metronidazole.
o If systemic antibiotics cannot be discontinued à maintain
metronidazole until their treatment courses are completed.
o Relapse of clostridium diffcile infection à requires retreatment.
• Oral vancomycin and fidaxomicin
o Reserved for patients with intolerance or who fail to improve
with metronidazole.
Adjunct approaches
• Colestipol or cholestyramine à toxin binder and probiotics.

• Sequestrant agents à bind oral vancomycin à avoid administration
at the same time.
20
Fulminant Colitis and Toxic Megacolon

Definitions
Fulminant colitis
• Severe progressive colonic mucosal inflammation à extending
into deeper layers of the colon à severe bloody diarrhea +
abdominal tenderness + systemic toxicity.
Toxic megacolon
• Systemic toxicity à colonic circular muscle paralysis à acute
colonic dilatation or toxic megacolon.
Etiology
• Inflammatory
o IBD – Behcet disease – collagenous colitis.
• Tumors
o Lymphoma – cancer colon – Kaposi sarcoma – chemotherapy.
• Colonic infections
o Bacterial à salmonella – shigella – E. coli – C. diffcile.
o Parasitic à Entamoeba – Cryptos poridium.
o Fungal à Aspergillosis.
o Viral à CMV – rotavirus.
• Other causes
o Idiopathic colitis.
o Ischemia – volvulus – diverticulitis.
o Hirschsprung disease – chronic constipation – intestinal pseudo
obstruction.
Clinical manifestations
Inflammatory colitis
• Progressive bloody diarrhea + crampy abdominal pain.
• Extra–intestinal manifestations à joint – eye – skin – liver.
21
Factors contributing to the development of the condition
• Barium enema or colonoscopy.

• Electrolyte imbalances and pH disturbances.
• Medications à laxatives – antidiarrheal – anticholinergic.
Infectious colitis
• Clostridium diffcile à due to ↑ use of broad–spectrum antibiotics.
Systemic toxicity
• ↑ T – ↑ HR – ↓ BP – confusion – agitation.
Local examination
• Abdomen examination à tenderness + distension + ↓ bowel sounds.
• Peritoneal signs à transmural inflammation or perforation.
Laboratory studies
• Routine à CBC – RFTs – KFTs – electrolytes – CRP – ESR – ABG.
• Stool à C. diffcile PCR toxin and other pathogens.
• HIV +ve patients à consider CMV and Cryptosporidium.
• Blood cultures à assess for bacterial translocation.
Radiologic studies
Abdominal imaging (plain X–ray or CT)
• Loss of colonic haustrations.
• Segmental or total colonic dilatation (>6 cm).
Endoscopy
Limited proctoscopic examination
• Extensive ulceration + friable bleeding mucosa.

• Biopsies à if the etiology of colitis is uncertain.
• Extensive endoscopic examination à ↑ risk of perforation (avoid).
22
Diagnostic criteria require all components below

Dilated colon on imaging +
At least three of the following
1. Fever >38 degrees.

2. Tachycardia >120.
3. Leukocytosis >10500 with left shift.
4. Anemia.
At least one of the following

1. Dehydration.
2. Low blood pressure.
3. Altered mental status.
4. Electrolyte abnormalities.
Treatment
General measures
• Maintain hemodynamics à Fluid ± transfusion ± vasopressors.
• Electrolytes replacement à correct (↓ K – ↓ PO4 – ↓ Mg – ↓ Ca).
• Small bowel ileus à NPO + NG suction.
• Drugs à stop anticholinergic and narcotic agents.
• Prophylaxis against à stress ulcer + DVT.
Monitoring
• Serial abdominal exams.

• Serial abdominal x–rays.
Inflammatory bowel disease

Corticosteroids
• Indication à if IBD is diagnosed or suspected.

• Dose à IV hydrocortisone 100 mg q6h.
23
Cyclosporine
• Indications
o Severe ulcerative colitis + no improvement after 7–10 days of
intensive IV steroids.
o In toxic megacolon à controversial.
• Dose
o IV cyclosporine 2–4 mg/kg/day.
Infliximab
• Indication à steroid refractory severe colitis.
Amino salicylates (e.g. mesalamine – sulfasalazine)
• No role in the treatment of fulminant colitis or toxic megacolon.

• Withheld until the patient has recovered and has resumed eating.
IV broad–spectrum antibiotics
• Indication à suspected toxic megacolon or transmural inflammation.
• Continued until patient stabilizes over several days to week.
Clostridium diffcile infection
• IV metronidazole (500mg q8h) or

• PO vancomycin (500mg q6h).
• Discontinue any unnecessary antibiotics.
Surgical management
Indications
• No improvement after 24 hours of intensive medical management.

• Failure to respond to IV steroids or IV cyclosporine after 7 days.
• Progressive dilation.
• Imminent transverse colon rupture (diameter >12 cm).
• Colonic perforation.
• Uncontrollable bleeding.
24
• Septic shock.
Surgical options
• Limited abdominal colectomy + ileostomy.
25
Hepatic dysfunction
Pathophysiology
Bilirubin metabolism
• Erythrocytes à heme à unconjugated bilirubin à transported
bound to albumin to liver à bilirubin is made soluble by conjugation
with glucuronic acid within hepatocytes à conjugated bilirubin is
transported into the bile canaliculus à bile duct à intestine.
Drug metabolism
Phase I
• Oxioreductases and hydrolases à ↑ water solubility of substances

and potentially generate toxic metabolites.
Phase II
• Transferases à produce less active metabolites.

Hemostasis – liver produces
• Coagulation à vitamin K–dependent coagulation factors.
• Anticoagulation à protein C and protein S.
Etiology
Ischemic Hepatitis
• Hypoxemia.
• Shock à hypovolemic – cardiogenic.
• Sickle cell crisis.
• Hepatic artery occlusion à especially post liver transplantation.
Congestive hepatopathy
• RSHF or pericardial disease or pulmonary HTN à ↑ hepatic vein
pressures à hepatic congestion à mild ↑ (serum aminotransferases –
alkaline phosphatase – bilirubin).
26
• Long–standing hepatic venous congestion à cardiac cirrhosis.
Differential diagnosis
• Budd–Chiari syndrome à hepatic vein thrombosis.

• Sinusoidal obstruction syndrome à veno–occlusive disease.
• IVC thrombosis at hepatic portion à obliterative hepatocavopathy.
TPN–related liver injury

• Hepatic steatosis and steatohepatitis.
• Cholestasis and cholecystitis.
Sepsis
• Sepsis à alterations in hepatic blood flow + activation of reticulo–
endothelial cells + release of inflammatory cytokines à hepatic
dysfunction à ↑ serum aminotransferases 2–3 times upper limits of
reference range may occur 2–3 days after the onset of bacteremia.
• Sepsis–induced cholestasis à jaundice + ↑ serum ALP.
Drug hepatotoxicity
• Depends on dose/duration of drug exposure and host susceptibility.
• Idiosyncratic reactions (isoniazid – phenytoin) à damage is dose
independent and unpredictable.
• Intrinsic hepatotoxicity (acetaminophen – methotrexate) à
damage is dose dependent.
History
• Episodes of symptomatic hypotension.
• Right or biventricular heart failure.
• New medications associated with liver injury.
• Abdominal or right upper quadrant abdominal pain à suggest
mechanical biliary obstruction.
Physical examination
27
• Physical findings of congestive hepatopathy à jaundice – tender

hepatomegaly – ↑ JVP – edema – ascites.
Laboratory studies
• Ischemic hepatitis à ↑ serum aminotransferases 10–40 times upper
limits of the reference range.
• In hyperbilirubinemia à measure both direct (conjugated) bilirubin
and indirect (unconjugated) bilirubin.
Indirect hyperbilirubinemia
• Hemolysis.
• ↓ Hepatic clearance (impaired bilirubin conjugation).
• Gilbert syndrome and Crigler–Najjar syndrome à inherited
disorders resulting in decreased bilirubin conjugation.
Mixed direct and indirect hyperbilirubinemia or pure direct

hyperbilirubinemia
• Heritable disorders of bilirubin canalicular excretion.
• Liver disease.
• Biliary obstruction.
Radiographic studies
Sonography (with Doppler studies) evaluates
• Liver architecture.
• Biliary system à intra–hepatic and extra–hepatic bile ducts.
• Hepatic circulation à hepatic veins – portal vein – hepatic artery.
Combined right heart and trans–jugular portal pressure measurements

• Can differentiate ascites development due to chronic passive
congestion from hepatic cirrhosis.
Treatment
Supportive treatment
28
• Maintain adequate perfusion and adequate venous return.

• Correction of fluid and electrolyte imbalances.
• Introduction of enteral feeding as soon as clinical condition permits.
Cholestasis of sepsis
• Treatment of the underlying infectious process.
TPN steatosis
• Decrease carbohydrate load + decrease total calories.
• Ursodeoxycholic acid à 10–45 mg/kg/day PO.
Drug hepatotoxicity
• Stop medications responsible for liver injury.
• Consider liver transplantation.
• Consider corticosteroids in
o Drug hypersensitivity (drug rash with eosinophilia).
o Drug–induced autoimmune reactions.
29
Acute liver failure (ALF)

Fulminant hepatic failure
Definitions
• ALF = development of coagulation disturbance + encephalopathy
without cirrhosis + <26 weeks duration.
Wilson disease and autoimmune hepatitis can be included in this

diagnosis when the initial presentation is acute illness even if cirrhosis is
present.
Etiology
• Acetaminophen overdose (most common cause)
o Hepatotoxicity occurs when dosages exceed 150 mg/kg.
• Hepatotoxicity with acetaminophen dose 3–4 gm/day
o Depletion of intracellular glutathione (chronic alcohol use).
o ↑ Cytochrome P–450 2E1 activity (chronic antiepileptic therapy).
• Viral hepatitis
o HAV – HBV – HEV – (HCV is extremely rare).
o CMV – VZV – adenovirus – paramyxovirus – EBV – Herpes.
• Metabolic disorders
o Acute fatty liver of pregnancy.
o HELLP syndrome.
o Wilson disease.
o Reye syndrome.
• Cardiovascular disorders
o Budd–Chiari syndrome.
o Sinusoidal obstruction syndrome.
o Cardiogenic shock.
• Drug and toxins
o Acetaminophen – Sodium valproate – Isoniazid – Halothane –
Amanita phalloides.
Complications
30
Encephalopathy and cerebral edema

• Encephalopathy à confusion (grade 1) up to coma (grade 4).
• Cerebral edema (80%) à brain herniation à death.
Coagulopathy
• ↓ Vitamin K–dependent coagulation factors à ↑ INR and PTT.
Cardiorespiratory complications
Hemodynamic changes in ALF mimic distributive shock
• ↑ COP + ↓ SVR + ↓ peripheral oxygen extraction.
Renal failure
Causes of renal failure in ALF
• Acute tubular necrosis.

• Prerenal azotemia.
• Hepato–renal syndrome (HRS).
Metabolic disorders
Lactic acidosis
• ↑ Lactate production (e.g. hypoxia).

• ↓ Hepatic metabolism of lactate.
Hypoglycemia
• Severe hepatocellular injury à ↓ gluconeogenesis + ↓ glycogenolysis.
Infection
• Organisms à Staph. – Strept. – enteric organisms – candida spp.
• Signs of infection à may be absent (no fever – no leukocytosis).
Treatment
General measures
31
• Early identification and treatment of the cause is critical.

• Invasive hemodynamic monitoring is useful in the management of
hemodynamic changes associated with ALF.
Sepsis
• Cultures à blood – sputum – urine.
• Low threshold for the use of empiric antibacterial ± antifungal.
• The use of prophylactic antibiotics remains controversial.
Coagulopathy
FFP or platelet transfusion
• Indication
o Active bleeding.
o Prevention of bleeding during invasive procedures.
o Excessive blood product transfusion à worsen cerebral and
pulmonary edema.
Vitamin K
• Vitamin K administration à safe but ineffective.
Parenteral recombinant factor VIIa
• Reverse coagulopathy.
• Benefits à avoid large volumes associated with FFP.
Encephalopathy and cerebral edema

Frequent assessment
• Level of consciousness – pupillary response to light – motor reflexes.
ICP monitoring
• CPP = MAP – ICP.

• Target à CPP >50 mmHg and ICP <15 mmHg.
32
• ICP monitoring à identification and treatment of cerebral edema in

patients candidate for liver transplantation and progress beyond
grade 2 encephalopathy.
• Risks of ICP monitoring à bleeding and infection.
Management of increased ICP
• Avoid excessive à oral suctioning – visual and auditory stimuli.

• Head of bed à >30–degree elevation.
• Serum sodium à permissive hypernatremia.
• Hypertonic saline à keep PNa 145–155 mmol/L.
• Dehydrating measures à IV mannitol (0.5–1 gm/kg).
• Hypothermia à core body temperature 32°C.
• Hyperventilation à keep PaCO2 25–30 mmHg.
Metabolic disorders
• Hemodialysis à may be required (continuous modes are preferred).
• Prevention of hypoglycemia à BG monitoring ± IV dextrose.
Acetaminophen toxicity
• N–acetyl cysteine
o Lifesaving antidote to acetaminophen toxicity.
o Effective within the 1st 24 hours after ingestion.
o NAC may still be useful even when treatment is delayed >24
hours or when signs and symptoms of ALF have developed.
• Dosing of NAC
o Oral dose
§ Loading dose à 140 mg/kg.
§ Maintenance à 17 doses of 70 mg/kg q4h.
o IV infusion dose
§ 1st dose à 150 mg/kg over 15 minutes then
§ 2nd dose à 50 mg/kg over 4 hours then
§ 3rd dose à 100 mg/kg over 20 hours.
• Role of NAC in non–acetaminophen ALF
33
o Administration of NAC to non–acetaminophen ALF appeared

to improve spontaneous survival when given during the early
stages of encephalopathy.
Viral hepatitis
• Treatment of HAV is supportive.
• Treatment of known or suspected HSV hepatitis à acyclovir (5–10
mg/kg IV q8h) may be lifesaving.
Electrolyte imbalances
• Correction of electrolyte disorders (particularly ¯ PO4).
Liver transplantation (LT)

• ALF without contraindications to LT à manage at LT center.
King's College Criteria for Liver Transplantation for ALF

Non–acetaminophen ALF
INR >7.7 or any three of the following
1. Age <10 or >40 years.
2. Unfavorable cause
o Non–A Non–B hepatitis.
o Drug.
o Wilson disease.
3. Period of jaundice to encephalopathy >7 days.
4. Serum bilirubin > 17 mg/dL.
5. INR > 3.85.
Acetaminophen–related ALF
pH <7.3 or all three of the following
1. Grade III–IV encephalopathy.

2. INR > 7.7.
3. Serum creatinine > 3.4 mg/dL.
34
Chronic liver failure

Etiology
• Hepatitis à HBV – HCV.
• Autoimmune hepatitis.
• Hereditary hemochromatosis.
• Wilson disease.
• Alpha1 antitrypsin deficiency.
• Primary biliary cirrhosis.
• Primary sclerosing cholangitis.
• Non–alcoholic fatty liver disease.
• Alcohol–related liver disease.
Pathophysiology
Portal hypertension
• Cirrhosis à endothelial dysfunction + ↑ resistance to flow within the
hepatic sinusoids à sinusoidal hypertension à portal hypertension.
• Portal hypertension is responsible for
o GIB – ascites – encephalopathy.
o Hepato–renal syndrome.
o Hepato–pulmonary syndrome.
o Porto–pulmonary hypertension.
Salt and water retention

• ↑ Resistance to mesenteric flow à activation of compensatory
systems to maintain effective arterial volume à Na and water
retention à ↑ intra–vascular volume.
• Common symptoms à fatigue – ↑ abdominal girth – emotional
lability – day/night sleep reversal – poor mental concentration.
35
• Common physical findings à jaundice – temporal wasting – ascites
– splenomegaly – asterixis – spider angiomata – male gynecomastia.
Blood tests
• CBC à anemia – thrombocytopenia – leucopenia (hypersplenism).
• Serum transaminases à elevated.
• Alkaline phosphatase à variable.
• Synthetic dysfunction à ↓ albumin and ↑ INR.
• Bilirubin à mixed direct and indirect hyperbilirubinemia.
• Serum ammonia à elevated (common with encephalopathy) – there
is modest correlation with the magnitude of the elevation and the
severity of the encephalopathy.
Ascites studies
• Ascites from portal hypertension à SAAG > 1.1 gm/dL.
• SBP à (neutrophil in ascites fluid >250/mL) or (when bacteria can
be cultured from ascites).
Peritonitis from abdominal perforation or abdominal abscess should

be considered when multiple organisms are cultured from ascites or
neutrophil count is high. The ascites in these conditions should fulfill two
of the following criteria
1. Total protein > l gm/dL.
2. Glucose < 50 mg/dL.
3. LDH greater than upper limit of the reference range.
Urine studies
• UNa <20 mmol/L à typical (but not required) for diagnosis of HRS.
Treatments
Ascites
36
Sodium restriction (1st line treatment)
• Dietary Na restriction to <2 gm/day.
Diuresis
• Furosemide (20–160 mg/day) + spironolactone (50–400 mg/day).

• IV diuretics should be avoided and may precipitate renal failure.
Intermittent large–volume paracentesis
• Ascites refractory to diuretics.

• Intolerance of diuretics à e.g. hyponatremia – renal insufficiency.
Spontaneous bacterial peritonitis

• Antibiotics of choice
o IV 3rd generation cephalosporins à effective against gram –ve
enteric organisms.
• IV albumin
o Dose à 1.5 gm/kg on day 1 and 1 gm/kg on day 3 à ↓ rate of
infection–related renal dysfunction.
Encephalopathy
• Management of precipitants
o GIB – infection – renal failure.
• Lactulose PO
o Dose à 15–60 mL q4–12h à titrate to 3–4 soft bowels daily.
• Rifaximin
o Dose à 550 mg q12h à ↓ frequency encephalopathy.
Variceal hemorrhage
• See variceal hemorrhage.
Hepatorenal syndrome
• Expand intravascular volume
o Avoid diuretics.
37
o Volume replacement à IV saline 1.5L.

o IV albumin à 25–75 gm daily.
• Other lines of treatment
o Octreotide à 100 mcg SC q8h.
o Midodrine à 7.5–12 mg q8h.
o Consider LT in appropriate subjects.
Hepato–pulmonary syndrome
• Disorder characterized by
o Portal hypertension (with or without cirrhosis).
o Arterial hypoxemia (A–a gradient >15 mmHg on room air).
o Evidence of pulmonary vascular dilation.
• Investigation
o Contrast–enhanced echo à delayed (>3 cardiac cycles) passage
into the left heart of injected agitated saline bubbles.
• Management
o Supplemental O2 administration.
o Exclusion of other causes of shunt.
o Consider LT.
Porto–pulmonary hypertension
• Disorder characterized by
o Liver disease à portal hypertension.
o Mean PAP à > 25 mm Hg (at rest).
o Mean PCWP à < 15 mm Hg.
o Pulmonary vascular resistance à >3 Woods units.
• Diagnosis
o Right heart catheterization with measurement of pulmonary
artery pressure is the gold standard for diagnosis.
• Management à liver transplantation
o Indication à patients responding to PO or IV vasodilators.
o Contraindication à severe portal hypertension (mean PAP > 50
mm Hg).
38
Liver transplantation
• LT à effectively treat all complications of end–stage liver disease.
• LT à determined by calculation of the model for end–stage liver
disease (MELD) score.
MELD calculator is available at

• Http://ww.unos.org/resources/meld-PeldCalculator.asp.
39
Diarrhea
Definition
• Diarrhea = ↑ frequency or ↓ consistency of stool.
• Other definitions à three or more loose or watery stools per day
and stool weight > 200 gm/day.
Classification
• Acute à diarrhea ≤ 14 days.
• Chronic à diarrhea >30 days.
• Persistent à diarrhea > 14 days and < 30 days.
Etiology
Infectious causes
• Viral infection
o Norovirus (most common) – rotavirus – adenovirus – astrovirus.
o Immunosuppressed and elderly à CMV or HSV.
• Bacterial infection
o Salmonella and Campylobacter (most common).
o Shigella and E. coli 01 57:H7 (bloody diarrhea).
o Clostridium diffcile toxin–induced colitis.
• Others causes
o Amebiasis (bloody diarrhea and dysentery).
o Fungal and mycobacterial diarrhea (rare).
Medications
• Antibiotics (erythromycin – ampicillin – clindamycin –
cephalosporins – azithromycin) à
o Alterations in intestinal flora.
o Breakdown of dietary carbohydrate products.
o Prokinetic effects e.g. from erythromycin.
• Other medications
40
o Magnesium containing antacids – magnesium and phosphorus

– lactulose – colchicine – digitalis – theophylline –
levothyroxine – aspirin – NSAIDs – diuretics – β blockers –
chemotherapy – PPIs – antiretroviral medications.
Enteral feeding
• Osmolarity of enteral solution may precipitate diarrhea.
• Enteral formulas high in lactose or fat may precipitate diarrhea.
Inflammatory bowel disease (IBD)

• Crohn's disease à affects any part of the luminal gut.
• Ulcerative colitis à affects the colon within the luminal gut.
• Less common causes
o Lymphocytic colitis – collagenous colitis – autoimmune
enteritis – celiac disease – sarcoidosis – GVHD.
Malignancy
• Adenocarcinoma – lymphoma – carcinoid – gastrinoma – VIPoma –
somatostatinoma.
Anatomical causes
• Short gut syndrome à <200 cm of functional small intestine.
• Subtotal gastrectomy – ileocolonic resection and subtotal colectomy.
• Roux–en–Y gastric bypass.
Other causes
• GIB – ischemic bowel – fecal impaction – opiate withdrawal.
History
• Diarrhea (onset – duration – character).
• Relation to antibiotic or enteral feeding.
• Clostridium diffcile related diarrhea may occur up to 8 weeks after
the offending antibiotic is discontinued.
41
• Abdominal pain à ischemia – infection – inflammatory conditions.
• Bloody diarrhea à GIB – ischemia – pseudomembranous colitis.
• Hypotension à volume loss – adrenal insufficiency – neuropathy.
• Fever à infection – vasculitis – hyperthyroidism.
• Abdominal tenderness à infection – ischemia – vasculitis.
• Rectal examination à partially obstructing fecal impaction.
• Skin rashes or mucosal ulcers à GVHD – IBD – vasculitis.
Laboratory studies
• Metabolic acidosis and hypokalemia à suggest severe diarrhea.
• Hyperkalemia à suggest adrenal insufficiency or uremia.
• Leukocytosis à suggest infection or ischemia.
• Neutropenia à suggest immunosuppressed state or sepsis.
• Falling hematocrit à suggest GI bleeding.
Additional tests
• TSH à hyperthyroidism.
• Celiac serology à celiac disease.
• Urine 5–HIAA and serum chromogranin à carcinoid.
• Serum vasoactive intestinal peptide à VIPoma.
• Serum gastrin à gastrinoma.
• Somatostatin à somatostatinoma.
• Serum calcitonin à C-cell hyperplasia – medullary thyroid cancer.
• Stool magnesium and laxative screen à laxative abuse.
• Anti–enterocyte antibody à autoimmune enteropathy.
Stool studies
• Fresh stool specimens à C. difficile toxin assay and culture.
• Stool PCR à C. difficile (more sensitive and specific).
42
• Sudan stains for fecal fat à malabsorption of fat.

• Stool pH <5.6 à carbohydrate malabsorption.
• High–volume stool that persists with fasting à secretory origin.
Stool osmolar gap
• Stool osmolar gap = expected – calculated stool osmolarity.

• Expected stool osmolarity = 290 mOsm/kg.
• Calculated stool osmolarity = (stool Na + stool K) x 2.
• Distinguish between osmotic and secretory causes
o Stool osmolar gap >70 mOsm/L à suggests osmotic causes.
Immunosuppressed patients need more extensive stool tests
• Ova and parasite evaluation.

• Concentration for isolation of à Cryptosporidium – Microsporidium
– Isospora belli.
Imaging studies
Plain abdominal radiographs
• Can detect partial obstruction or perforation.
• Can detect changes associated with enteritis or colitis.
Contrast studies
• CT à bowel wall thickening – tumors – obstruction.
• MREnterography or CTEnterography à better examination of the
small bowel for abnormality and IBD.
Endoscopy
• Flexible Sigmoidoscopy
o Indication à bright red rectal bleeding or distal colitis.
o Diagnosis of à pseudomembranous colitis – ischemic colitis –
CMV colitis – herpetic proctocolitis – GVHD.
• Mucosal biopsies
43
o When endoscopic findings are nonspecific or absent.

• Colonoscopy
o In chronic (IBD – microscopic inflammatory disorders –
neoplasia).
• Upper endoscopy with small bowel biopsies
o Diagnose à celiac – giardiasis – Crohn – Whipple – amyloid –
eosinophilic gastroenteritis.
• Duodenal aspirate
o Diagnose à Giardia or small intestinal bacterial overgrowth.
Treatment
General measures
• Correct of fluid and electrolyte imbalance.
• CVC à for severe fluid loss and monitoring.
• Iatrogenic causes à withdraw the offending medications.
Diarrhea due to enteral feedings

• Reduce volume or temporarily discontinue of enteral feedings.
• Some suggest continuous infusion over bolus infusions.
• Addition of fiber to continuous infusions.
• TPN in severe cases (temporary measure).
Consider elemental diet formulas in
• Short bowel syndrome – pancreatic insufficiency – radiation enteritis

– fistula – IBD.
Clostridium diffcile colitis

• Antibiotic related à stop the offending antibiotic (if possible).
• Antibiotic therapy
o Metronidazole PO 500mg q8h or
o Vancomycin PO 125–500mg q6h.
o Vancomycin is reserved for treatment failures and severe cases
(contribute to selection for vancomycin–resistant bacteria).
44
• Duration à continue for 7–14 days.

• If relapse à longer and multiple courses of treatment are required.
• Improvement à expected within 24–48 hours.
Symptomatic ttt (when the cause of diarrhea is not found)

• Anti–motility agents
o Loperamide (4–16 mg/day).
o Diphenoxylate with atropine (diphenoxylate 20 mg q6h).
o Complications (CNS side effects – gut hypomotility).
• Octreotide (indication)
o Acquired immunodeficiency syndrome.
o GVHD.
o Hormone–producing tumors.
45
Severe and Complicated Biliary Tract Disease

Etiology
Biliary obstruction
• Intrinsic lesions
o Gall stones – cholangiocarcinoma – benign stricture.
• Extrinsic lesions
o Liver à hepatic cyst.
o Biliary à choledochal cyst.
o Pancreatic à carcinoma – pseudocyst – ampullary stenosis.
o GIT à duodenal diverticulum.
o Tumors à metastatic carcinoma – lymphadenopathy.
o Vascular à visceral artery aneurysm.
o Operative à injury – post operative stricture.
o Parasites.
Bile leak
• Cholecystectomy – hepatic resection – liver transplantation – trauma.
Acalculous cholecystitis
• Acalculous cholecystitis is typically seen in critically ill patients and
can result in significant morbidity and mortality.
• Physical examination à icterus – ascites – focal RUQ tenderness.
Cholangitis
Charcot triad
1. Fever.
2. Pain à right upper quadrant abdomen.
3. Jaundice.
46
Reynold pentad (severe cases)
1. Fever.
2. Pain à right upper quadrant abdomen.
3. Jaundice.
4. Hypotension.
5. Mental state changes.
Biliary obstruction
• Jaundice.
• Pain à right upper quadrant abdomen.
• Painless à consider neoplasm.
Bile leak
• Bile leak à peritonitis à abdominal pain – ascites – ↑ TLC – ↑ T.
Laboratory evaluation
• Bilirubin à elevated à obstructive process – sepsis – hemolysis.
• ALP à elevation is not specific for biliary disease.
• ↑ ALP + ↑ GGT à confirm hepatobiliary origin.
• Transaminases à elevated (can be seen with bile duct obstruction).
Imaging
Plain abdominal radiograph
• Usually shows nonspecific findings.
• Air in the biliary tree can result from
o Prior sphincterotomy.
o Biliary–enteric fistula or surgical anastomosis.
o Infection with gas–producing organisms.
Ultrasonography
• Detect à biliary ductal dilatation – cholecystitis – cholelithiasis.
47
• Limited accuracy in choledocholithiasis (gas in the duodenum can

obscure visualization of the distal bile duct).
Radionuclide scanning
• Technetium hepatic iminodiacetic acid (HIDA) scans yield
physiologic and structural information regarding the biliary tract.
CT and MRI can detect

• Level and cause of biliary obstruction.
• Visualization of pancreas.
• Biloma or free fluid in the abdominal cavity.
• MRCP provides high–resolution images of pancreatobiliary system.
These studies are impractical in ICU patients who are too sick for transport.
Endoscopic ultrasound (EUS)
• Visualize entire biliary tree and pancreas without intestinal gas
interference (more sensitive than transabdominal US).
Treatment
Cholangitis and biliary obstruction
• Broad spectrum antibiotics.
• Aggressive supportive measures.
• Emergent ERCP with sphincterotomy and biliary stenting.
Bile leaks
• ERCP à biliary decompression + stenting à allow leak site to heal.
• Broad spectrum antibiotics à protect against sepsis.
Acute cholecystitis
• IV fluids + antibiotics + nasogastric suction.
• Operative cholecystectomy.
• Percutaneous cholecystostomy (alternative in unstable patients).
48
Acute gallstone pancreatitis

• Conservative therapy
o Majority will improve with conservative therapy.
• Early ERCP
o Indication à severe pancreatitis – persistent jaundice –
cholangitis.
• Definitive therapy
o Elective cholecystectomy.
o Endoscopic sphincterotomy with stone extraction in non–
operative candidates after pancreatitis has subsided.
Complications
Cholangitis and biliary obstruction
• Failed ERCP à percutaneous transhepatic cholangiography.
Bile leaks
• Bilomas à percutaneous drainage + ERCP.
Cholecystitis
• GB perforation or emphysematous cholecystitis à
cholecystostomy and drainage catheter is left in place until acute
symptoms resolve.
Acute gallstone pancreatitis

• Pseudocyst and bacterial colonization à abscess à mandates
(endoscopic or surgical or percutaneous) drainage.
49

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Dr Ali Ragab (www.facebook.com/groups/pass.critical.

Pass Critical Care

GIT and Liver

Gastro intestinal bleeding (GIB)

• Ulcer à duodenal and gastric ulcers (most common).

• Vascular à angiodysplasia – telangiectasia.

• Diverticulosis à most common.

• Ulcers à rectal ulcer.

NG aspirate may be non–bloody if tightly closed pylorus prevents

• Evaluates and treats upper GIB.

• Detect and treat the source of lower GIB.

• Detect bleeding rates as low as 0.1 mL/minute.

• Detect bleeding rates of 0.5–1 mL/minute.

Initial blood testing

Pharmacologic therapy in upper GIB

• Acid suppression à IV PPI (standard in acute upper GIB).

Recurrent bleeding occurs in 30% of cases with bleeding ulcers despite

Non–surgical management in variceal bleeding

• Temporary measure when alternate therapeutic procedure is planned

• Massive ongoing hemorrhage that overwhelms resuscitative effort.

Stress Ulcer Syndrome

• Early à mucosal changes à pallor – mottling – petechiae.

• Route à IV bolus or continuous IVI.

Proton pump inhibitors (PPI)

• Strongest antisecretory agents.

• Dose à 10–80 mL through NGT q1–2h.

• Dose à 4–6 gm/day through NGT.

Risk factors for variceal rupture

Endoscopy (gold standard)

• Vasoconstrictor of choice in acute variceal bleeding.

Somatostatin is not available in United States (when available should be

• Used only when octreotide is not available.

Concurrent nitroglycerin IVI at 40 mcg/min (titrated to keep SBP of 90

• Synthetic analog of vasopressin with slower release and fewer side

• Elastic rings are placed endoscopically over varices à strangulation

• Injecting sclerosant solution into variceal lumen or into adjacent

• Injection of tissue adhesives à cyanoacrylate and thrombin.

Complications of endoscopic therapy

• Esophageal ulceration – bleeding – stricture formation – dysmotility –

• Esophageal/gastric necrosis and perforation.

Given these potentially lethal complications à balloons should be

• Bleeding refractory to pharmacologic and endoscopic therapy.

Thirty percent of patients develop transient deterioration of liver

Balloon–occluded retrograde transvenous obliteration (BRTO)

• Portocaval and distal splenorenal shunts may be considered in

• Sugiura procedure à mucosal transection and devascularization of

• Non–selective β–blockers à ↓ COP (β1) and splanchnic

• Serial endoscopic band ligation à ↓ rebleeding rates.

• Scheduled sessions at weekly or biweekly intervals are recommended

Patients with alcoholism

GIT motility disorders in ICU

Colonic dysfunction (distension/constipation)

• Impaired tolerance to gastric feeding.

Mechanical obstruction is evaluated by

• Gastric stasis à GERD à heartburn and regurgitation.

Acute colonic pseudo–obstruction (Ogilvie syndrome)

Acute colonic pseudo–obstruction (Ogilvie syndrome)

• Dose à 2 mg IV over 5 min.

• Contraindications à bradycardia – active bronchospasm –

• Colonoscopy for decompression à consider when distension

• Colestipol or cholestyramine à toxin binder and probiotics.

Fulminant Colitis and Toxic Megacolon

Factors contributing to the development of the condition