Gastrointestinal and Hepatic
Gastrointestinal haemorrhageHaemorrhage may occur in the upper (oesophagus, stomach, or duodenum) or lower GI tract (small bowel or colon). Severity can vary greatly from trivial to immediately life-threatening. It may be the cause of critical care admission, or occur as a complication of ICU care.
Causes
Upper GI
Pre-existing peptic ulcer disease (with/without Helicobacter pylori infection).
‘Stress’ ulceration which is associated with critical illness and shock, renal failure, or burns.
Drugs:
Oesophageal (or gastric) varices.
Malignancy.
Mallory-Weiss tear.
Lower GI
Infection or inflammation (e.g. diverticulitis, Crohn’s disease).
Malignancy (including polyps).
Trauma.
Angiodysplasia/vascular malformations.
Ischaemic colitis.
Radiation colitis/enteropathy.
Haemorrhoids.
Minor lesions (e.g. gastric erosions or haemorrhoids) may cause major GI bleeds where patients are coagulopathic (e.g. anticoagulated, or thrombocytopaenic).
Presentation and assessment
GI signs and symptoms may be relatively non-specific:
Abdominal pain (occasionally epigastric in nature).
Nausea, vomiting, or diarrhoea.
Evidence of chronic liver disease (e.g. jaundice, ascites, spider naevi, asterixis, encephalopathy).
Evidence of bleeding:
Haematemesis or blood aspirated from an NG tube (may be fresh blood or ‘coffee-ground’).
Small/occult GI bleeds may be a cause of unexplained anaemia.
Fresh PR blood (if source is below the duodenum/ligament of Treitz).
Melaena may occur with upper or lower GI bleeding, typically within 24-48 hours of a bleeding event.
Major bleeds may cause features associated with haemorrhage (see 
p.112), including:
p.112), including:
General: pallor and anaemia.
Cardiovascular: tachycardia, hypotension, ↑capillary refill time.
Respiratory: tachypnoea/dyspnoea.
Renal: oliguria (<0.5 ml/kg/hour), metabolic acidosis.
Neurological: syncope, ↓ consciousness.
Investigations
Crossmatch blood.
ABGs (acidaemia).
FBC (anaemia, thrombocytopaenia).
Coagulation screen, including fibrinogen (to identify new coagulopathy, or quantify the effects of anticoagulants):
Thromboelastography may help in rapid correction of coagulation
LFTs (liver failure/dysfunction may be present).
ECG (if cardiac ischaemia suspected).
CXR (subdiaphragmatic air will occur with perforation).
GI endoscopy (upper or lower GI endoscopy is the definitive way of diagnosing GI bleeds, although the presence of large volumes of blood may obscure the actual bleeding point).
Angiography, or radiolabelled bleeding scan.
Differential diagnoses
Haemoptysis.
Epistaxis/pharyngeal bleeding (swallowed blood may be regurgitated).
Occult haemorrhage from any cause; shock from any cause.
Immediate management
Give O2 as required, support airway, breathing, and circulation.
Endotracheal intubation may be required to protect the airway in certain situations:
Where there is ↓ consciousness
Where there is torrential bleeding and/or oesophageal manipulation (e.g. endoscopy or insertion of a Sengstaken tube)
Induction of anaesthesia may provoke cardiovascular instability
Obtain large-bore venous access (ideally 2 × 14g cannulae).
Ensure blood is crossmatched, aggressively correct coagulopathies.
Circulatory resuscitation will be required:
Start fluid resuscitation as clinically appropriate, initially with crystalloid/colloid followed by blood/blood products as required
Reverse anticoagulation if required
In major GI haemorrhage consider giving vitamin K IV 10 mg, and tranexamic acid IV 1 g (there is mixed evidence that tranexamic acid is beneficial)
Urinary catheterization and fluid balance monitoring is required
Invasive CVP monitoring may be required
Inotropic/vasopressor support for circulation as necessary
Lower GI bleeding
Colonoscopy (or sigmoidoscopy for distal sources) is the investigation of choice.
Alternatively consider CT/angiography in lower GI bleeding if the patient is stable.
Surgery or angiographic embolization may be required in severe cases.
Upper GI bleeding
Upper GI endoscopy is the investigation of choice in major GI haemorrhage:
Endoscopic therapies may be applied to bleeding lesions, visible vessels, or ulcers with an adherent blood clot
Adrenaline injections may be combined with thermal or mechanical treatments
Where endoscopic treatments are only partially successful (e.g. because of large volumes of blood), or if a rebleed would most likely be fatal, they should be repeated within 24 hours.
Where endoscopic treatments fail proceed to:
Interventional radiology (selective arterial embolization), or
Surgery
After endoscopy high-dose proton pump inhibition should be commenced using omeprazole IV 80 mg bolus followed by an infusion of 8 mg/hour for 72 hours (alternatively pantoprazole may be used).
Variceal upper GI bleeding
Terlipressin IV 2g 6-hourly should be administered before endoscopy.
Upper GI endoscopy should be undertaken with oesophageal variceal band ligation or gastric variceal sclerotherapy.
Uncontrollable variceal bleeding may require temporary insertion of a Sengstaken Blakemore (SSB) tube (or equivalent, e.g. Minnesota, or Linton Nachlas tubes).
Sedation (and almost certainly intubation/ventilation) is likely to be required in order to tolerate Sengstaken tubes
After endoscopic treatment terlipressin should be continued for 48 hours:
Further management
Careful cardiovascular monitoring and serial FBC measurement should be undertaken.
Avoid steroids, SSRIs, and NSAIDs where possible.
An NGT may be sited at endoscopy (depending upon the lesion); it should be left to drain.
In patients with chronic liver disease and upper GI variceal bleeding, antibiotic therapy should be commenced (e.g. ciprofloxacin IV 1 g daily for 7 days).
Further variceal bleeding may be prevented by commencing β-blocker or nitrate therapy.
Transjugular intrahepatic porto-systemic shunting (TIPSS) may be considered for patients with oesophageal varices.
H .pylori identification/eradication may be required in the long term.
Pitfalls/difficult situations
Patients should ideally be stabilized before endoscopy but this is not always possible with ongoing bleeding.
Endoscopy may need to be performed on ICU or in theatres; a surgical team may need to be ‘standing by’ in the end of a failure to endoscopically gain control of the bleeding
Rise in urea and drop in haemoglobin may be the only initial sign that a bleed is present in the intubated patient.
In some cases the source of bleeding may not be found, angiography or labelled scans should be considered.
Aortoenteric fistulas may present with relatively small GI bleeds prior to a catastrophic haemorrhage.
Prophylaxis against stress ulceration should include enteral feeding:
Further reading
Barkun A, et al. International consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding. Ann Internal Med 2010; 152(2): 101-13.
Jalan R, et al. UK Guidelines on the management of variceal haemorrhage in cirrhotic patients. BSG guidelines in gastroenterology. Gut. 2000; 46(S III): iii1-iii15.
Scottish Intercollegiate Guidelines Network. Management of acute upper and lower gastrointestinal bleeding. Edinburgh: Scottish Intercollegiate Guidelines Network, 2008.
Acute severe pancreatitisAcute inflammation of the pancreas may cause local tissue destruction and a generalized inflammatory response causing distal organ failure.
Causes
Post-procedure (e.g. after ERCP or biliary surgery).
Alcohol (up to 40% of cases).
Neoplasms (pancreatic).
Cystic fibrosis, or Cold (hypothermia).
Rheology (e.g. vasculitis/SLE, hypoperfusion, ischaemia).
Endocrine (hypercalcaemia).
Anatomical/functions abnormalities.
Triglycerides/hyperlipidaemia.
Idiopathic.
Trauma (especially blunt abdominal trauma).
Stones/gall stones (up to 35% of cases).
Toxins (e.g. steroids, azathioprine, didanosine, pentamidine, envenomation).
Presentation and assessment
General: pyrexia, marked ‘third-space’ loss (i.e. oedema, ascites, pleural effusions).
Abdominal/GI: abdominal pain (often radiating to the back):
Nausea and vomiting, diarrhoea may also occur
Cullen’s sign (umbilical bruising)
Grey Turner’s sign (flank bruising)
Cardiovascular: tachycardia, hypotension.
Respiratory: tachypnoea/dyspnoea due to pain or metabolic acidosis.
Respiratory distress and/or hypoxia may occur due to abdominal splinting or pleural effusion
Renal: oliguria (<0.5 ml/kg/hour), AKI, metabolic acidosis.
Other:
Super-added infection/sepsis (typically respiratory or abdominal)
Hypocalcaemia
Hyperglycaemia
Multiple organ failure
Investigations
ABGs (metabolic acidosis is common; hypoxia).
LFTs (jaundice or liver dysfunction, especially with gall stone disease or malignancy).
Serum amylase and lipase (raised in pancreatitis, but moderate rises may be non-specific).
Serum glucose (hyperglycaemia is common).
Serum calcium (hypocalcaemia is common).
Serum magnesium and phosphate, and serum CRP.
Blood, urine and sputum culture (if infection is suspected).
CXR, AXR (raised hemidiaphragm, pleural effusions, basal atelectasis, or pulmonary infiltrates may be present).
US abdomen (to evaluate the biliary tract or identify gall stones).
CT abdomen, contrast-enhanced (to confirm the diagnosis and assess severity); indications for CT include:
Hyperamylasaemia, clinically severe disease, temperature >39°C
Ranson score >3, APACHE II score >8
Failure to improve after 72 hours of conservative treatment
Acute deterioration
CT abdomen should be repeated after 48-72 hours to identify and delineate any complications/necrosis which may have developed.
Differential diagnoses
Bowel obstruction/perforation, or bowel ischaemia.
Cholecystitis/cholangitis.
Renal colic.
MI.
Pneumonia.
DKA.
Immediate management
Give O2 as required, support airway, breathing, and circulation.
In severe cases respiratory support may be required using NIV or mechanical ventilation:
Drainage of massive pleural effusions may improve lung function
Drainage of severe ascites to improve ventilation has been described
Aggressive fluid resuscitation is likely to be necessary, with inotropic/vasopressor support as required:
Urinary catheterization and fluid balance monitoring is required
Invasive monitoring of CVP may be required
Analgesia (e.g. morphine PCA or infusion) and antiemetics should be prescribed.
Correct coagulopathy/electrolyte disturbance:
Hypocalcaemia may be corrected with calcium chloride 10% IV (10 ml)
Hyperglycaemia is likely to require an IV insulin sliding scale
The severity of the pancreatitis should be assessed using a scoring system (
p.279).
Further management
Regular reassessment of oxygenation/fluid balance is required.
Maintain glycaemic control (serum glucose 6-10 mmol/L).
Intra-abdominal pressure monitoring should be commenced in patients with severe abdominal distension and/or oliguria unresponsive to blood pressure and fluid status correction.
Renal replacement therapy may become necessary.
NGT enteral feeding is possible in most patients (80%) but an NJ tube may be needed:
PN may be used in patients in whom a 7-day trial of enteral feeding has failed
If gallstone obstruction is suspected ERCP should be performed (ideally within 24-72 hours of onset):
Early cholecystectomy may be indicated
Be vigilant for complications, including:
Pancreatic necrosis, abscess or pseudocyst formation
Diabetes mellitus; hypocalcaemia
Pancreatic encephalopathy
Sepsis
Early sepsis is likely to be extra-pancreatic in origin (e.g. pneumonia).
Pancreatic necrosis may result in super-added pancreatic infection:
Routine antimicrobial prophylaxis is not generally recommended (although the evidence is inconclusive, and some centres still use prophylaxis)
Where infection is suspected (e.g. by the presence of gas on radiological imaging) radiologically-guided fine-needle aspiration should be attempted
Where infection or abscess is confirmed, antibiotics (e.g. meropenem 1 g IV 8-hourly) and radiologically guided drainage should be undertaken
In severe cases surgical pancreatic necrosectomy may become necessary, but it should be noted that delayed surgery is associated with better survival than surgery undertaken early
Indications for surgical referral include infected pancreatic necrosis or pancreatic abscess, persistent biliary peritonitis.
Pitfalls/difficult situations
An APACHE II score >8 is associated with a severe attack; identifying severe cases early enables rapid aggressive intervention.
CT scanning within 48 hours may underestimate necrosis but initial scan may help with differential diagnosis.
Timing of surgical intervention can be difficult, early intervention is associated with higher mortality.
Pseudocyst formation is common (10% of cases), but rarely needs urgent treatment.
There is little evidence at present that drug therapy such as octreotide is of any benefit.
Pancreatitis complicated by Candida infections is associated with worse outcomes, and empiric antifungal cover may be needed in severe infections (e.g. using an echinocandin such as caspofungin).
Other factors associated with severity/worse outcome include:
Pancreatitis severity scoring
Ranson criteria (score 1 for each of the following):1
At presentation:
Age >55
Blood glucose > 11 mmol/L
White cell count >16 × 109/L
Lactate dehydrogenase (LDH) >400 iu/L
AST >250 iu/L
Within 48 hours after presentation:
Haematocrit fall by >10%
Serum calcium <2 mmol/L
Base deficit >4 mmol/L
Blood urea rise >1 mmol/L
Fluid sequestration >6 L
PaO2 <8 kPa.
Score 0-2 < 1% mortality Score 3-4 15% mortality
Score 5-6 40% mortality Score >6 ˜100% mortality
Computed tomography grading
A radiological grading system is also used ranging from A (normal) to D (the most severe grade, associated severe inflammation, necrosis or infection).
1Reprinted with permission from the Journal of the American College of Surgeons, formerly Surgery Gynaecology & Obstetrics. ‘Prognostic signs and the role of operative management in acute pancreatitis’. Randon JHC, Rifkind KM, Roses DF, et al., Surg Gynecol Obstet 1974;139:69-81.
2Reproduced from Gut, S.L. Blamey et al., ‘Prognostic factors in acute pancreatitis’, 25, 12, pp.1340-1346, copyright 1984, with permission from BMJ Publishing Group Ltd.
Further reading
Balthazar et al. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002; 223(3): 603-13.
Mier J, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997; 173: 71-5.
Skipworth JRA, et al. Acute pancreatitis. Br J Intenisve Care 2010; 20(4): 105-15.
UK Working Party on Acute Pancreatitis. UK guidelines for the management of acute pancreatitis. Gut 2005; 54(SIII): iii1-iii9.
van Santvoort, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362: 1491-502.
Villatoro E, et al. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev 2010; 5: CD002941. DOI: 10.1002/14651858.CD002941.pub3.
Whitcomb, D. Acute pancreatitis. N Engl J Med 2006; 354: 2142-50.
The acute abdomen
