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Gastrointestinal
bleeding
Bleeding from peptic ulcer
Features of ulcer associated with recurrent bleeding:
- spurting or oozing 85-90% risk of rebleeding
- protruberant vessel 35-55%
- adherent clot 30-40%
- flat pigmented spot on ulcer base 5-10%
Oesophageal variceal bleeding
- renal failure associated with worse prognosis and increased risk of bleeding
- ascites may cause rise in RAP
- ventilation and PEEP appear to decrease bleeding (NB clinical impression NO
data)
- over-transfusion causes marked increase in portal pressure
- treatment is based on directly therapy local therapy to varices and
reduction of portal pressure
- gastric variceal haemorrhage often more severe, more difficult to control
and more likely to recur than oesophageal variceal haemorrhage
Management
Algorithm for management of acute variceal haemorrhage
- Urgent endoscopy is required in order to confirm the diagnosis and to
allow endoscopic treatment. Consider intubation for airway protection in
patients with massive bleeding, altered mental state
- In a patient known or suspected to have varices terlipressin or octreotide
should be started while awaiting endoscopy.
Reduction of portal pressure
Vasopressin
- produces mesenteric vasoconstriction and thus decreases portal venous
inflow and pressure
- v. short t1/2 and therefore should be given by continuous infusion of 0.2-0.4
U/min. Max. 0.8 U/min
- if haemorrhage is controlled the dose can be tapered by 0.1 U/min every 4-6 h
- use should be restricted to 24 h
- adverse effects due to vasoconstriction: hypertension, LVF, arterial ischaemia.
Result in withdrawal in up to 25%
Terlipressin
- synthetic analogue of vasopressin
- fewer side effects than vasopressin
- longer half life means that it can be given as a bolus
Octreotide
- synthetic analogue of somatostatin
- mechanism of action unclear
- as effective as injection sclerotherapy in the immediate control of variceal
haemorrhage
- dose dependent symptoms of nausea, cramps, fat malabsorption and flatulence.
Appear following first administration but disappear after 1-2 weeks of treatment
- reduced glucose tolerance and hyperglycaemia (rarely a problem)
- (cholesterol gallstones are more common in patients taking octreotide for >
1 month)
- initial bolus of 50 mcg followed by infusion of 50 mcg/hr
- pharmacological treatment of choice
- as with all pharmacological treatments benefits cease as soon as treatment is
stopped and a definitive treatment is required to prevent re-bleeding
Further details
Nitrates
- not only counteract adverse effects of vasopressin but decrease portal
venous resistance and hence portal pressure
- effect is additive to that of vasopressin. Trials show benefit in terms of
bleeding but not survival
Propranolol
- contraindicated in acute phase
- reduces re-bleeding by causing splanchnic vasoconstriction
- titrate dose to reduce heart rate by 25%
Balloon tamponade
- use restricted to haemorrhage refractory to medical/endoscopic treatment or
when it is too massive to allow endoscopy
- predominant action is to reduce pressure in oesophageal varices by
occluding feeding vessels at the gastro-oesophageal junction using the
gastric balloon
- causes mucosal damage and therefore application should be limited to 12 h
- risk of aspiration pneumonia, oesophageal rupture and upper airway
obstruction
- tape tube to face do not hang bag of fluid on end
Further details
Staple transection of oesophagus
- effective and relatively easily applied means to stop variceal haemorrhage.
In experienced hands may take as little as 45 minutes to complete
- has been suggested that staple transection should be carried out in patients
who re-bleed after 2 sessions of sclerotherapy
- alternative procedures include oesophago-gastric devascularization
Transjugular intrahepatic portosystemic stent shunts
- indicated for uncontrollable variceal bleeding
- involves the creation of a fistula through the liver between the hepatic vein
and portal vein using an internal jugular vein catheter
- stops variceal haemorrhage by reducing portal pressure and reduces risk of
further bleeding as long as the shunt remains patent
- complications include:
- complications associated with internal jugular vein cannulation
- arrhythmias
- bile duct and hepatic artery injuries
- hepatic encephalopathy
- stenosis and dysfunction of shunt
- patients with advanced liver disease and multi-organ failure at the time
of shunting have a 30 day mortality approaching 100%
Direct therapy
Endoscopic sclerotherapy
- stops bleeding in 80-90% of patients
- complication rate of a single session of sclerotherapy 10-30%. Mortality
0.5-2%. Rate higher with emergency sclerotherapy than elective
- not effective for gastric varices due their position deeper in the
submucosa
- complications include oesophageal ulceration, perforation, bacteraemia,
pleural effusions, pulmonary oedema
Band ligation
- as effective as sclerotherapy with lower incidence of complications but
more difficult to perform
- not effective for gastric varices
Tissue glue
- N-butyl-2-cyanoacrylate
- useful for gastric varices which lie deeper in the submucosa than
oesophageal varices
Prophylaxis against encephalopathy
- lactulose if patient able to swallow. Otherwise phosphate enema
Prophylaxis against spontaneous bacterial peritonitis
- consider prophylaxis for patients with GI bleeding, cirrhosis and ascites
(20% already have SBP)
Prognosis
- each episode of variceal bleeding associated with a 25-40% mortality
- risk of re-bleeding very high with peak risk in first few days after index
haemorrhage. Risk remains high for 2-3 months
- rebleeding occurs in 70% in 1 year and risk of death is as high as 50% in 1
year
Lower GI haemorrhage
Aetiology
- diverticulosis
- colonic vascular ectasias
- inflammatory bowel disease
- colonic ischaemia
- infectious colitis due to a variety of parasitic and bacterial pathogens
including: Salmonella spp, Yersinia enterocolitica, Campylobacter jejuni,
schistomasiasis. Massive bleeding is unusual
- radiation colitis. Symptoms may occur early in course of treatment or many
years after completion
- neoplasms
- haemorrhoids
- rectal varices secondary to raised portal pressure
- rectal ulcers, can result from pressure necrosis due to faecal impaction
- Meckel's
- aortoenteric fistula. Major haemorrhage often preceded by a sentinel bleed
Diverticulosis
- only 3-5% of patients with diverticulosis develop bleeding but because
diverticulosis is so common it is one of the commonest causes of lower GI
bleeding
- bleeding arises from rupture of one of the branches of the vasa rectum
adjacent to a diverticulum, usually in the proximal colon
- bleeding is not due to inflammation. Gross bleeding rarely, if ever, occurs in
association with diverticulitis
- acute presentation (sudden onset of cramping abdominal pain associated with
urge to defaecate and subsequent passage of bright red/dark blood associated
with variable amounts of gelatinous clot) with no distinctive features that
allow diagnosis of diverticulosis
- usually resolves spontaneously after bleeding intermittently for a few days
Vascular ectasias
- asymptomatic vascular ectasias can be found in 25%
- 2/3 of patients > 70 yrs
- not associated with other vascular lesions
- bleeding usually subacute and recurrent
- amount of blood lost often varies in a single patient from one episode to
another. Stool may be bright red, dark red or melaena on separate occasions
- occult bleeding in 10-15%
- acute massive haemorrhage in 15%
- in > 90% bleeding stops spontaneously
Investigations
- FBC
- urea:creatinine ratio. Increased in majority of patients with an upper GI
bleed
- aspiration of gastric contents crucial as 10-15% of patients with an apparent
lower intestinal bleed actually have an upper GI bleed. Aspiration of gastric
fluid containing bile but not blood virtually excludes an upper GI bleed.
However if the fluid does not contain bile the bleeding may still be from the
duodenum as the pylorus may be closed or obstructed
- PR examination and sigmoidoscopy
- technetium-99m-labelled RBC scan. More sensitive and safer than angiography
but not as precise in identifying the site of bleeding. Can detect active
bleeding reliably at rates < 0.1 ml/min. Permits serial studies to be
obtained as long as 36 hours after a single injection of radionuclide, enabling
identification of lesions that bleed intermittently
- if scintigraphy fails to demonstrate a bleeding site or if a site is revealed
in the colon of a haemodynamically stable patient he should undergo colonoscopy
- if colonoscopy does not reveal the source of bleeding the patient should have
a barium enema
- patients with recurrent lower intestinal haemorrhage require angiography. Also
the procedure of choice in patients with continued severe active bleeding.
Bleeding can be demonstrated with rates as low as 0.5 ml/min
- other investigations of value when source of bleeding remains unclear: small
bowel enema, push enteroscopy, Sonde-type enteroscopy and intraoperative
enteroscopy
Management
- supportive treatment
- intra-arterial injection of vasopressin or embolization may be helpful
- vascular ectasia can usually be treated transendoscopically
- right hemicolectomy should be performed when an ectasia has been identified
and transendoscopic treatment is unsuccessful
- subtotal colectomy - last resort when active bleeding persists, the angiogram
is completely normal and colonoscopy and examination of the small bowel are not
diagnostic
Further reading
Ellis DJ, Reinus JF. Lower intestinal hemorrhage. Crit Care Clin, 1995;
11:369-89
Sharara AI, Rockey DC Gastroesophageal variceal hemorrhage N Engl J Med,
2001,345:669-81
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