Patient with melaena

A 72 yrs old gentleman on aspirin was admitted with history of passage of black stool for last 3 days. On examination, he lookedpale, his pulse rate was 110/min, BP 110/ 70mmHg. Abdomen- soft, epigastric tenderness present with increased bowel sounds. Investigations revealed Hb of 6.9gm%, WBe 10,800, normal platelet counts, normal coagulation profile, normal liver function test, normal creatinine with raised urea, amylase -was normal. USGexamination of abdomen did not reveal anything specific. After transfusing him with 3 units of blood, gastroscopy was performed which showed a large posterior duodenal ulcer.

Diagnosis: Duodenal ulcer presenting with melaena.
Acute upper gastrointestinal haemorrhage is not uncommon presentation in day to day hospital practice. Common causes encountered are:
Peptic ulcer
Variceal bleeding
Mallory Weiss tear
Oesophagitis, gastritis and deodenitis
Vascular
Tumours

There is often history of steroid and NSAID ingestion. Any bleeding beyond the attachment of ligament of Teitz usually causes melaena rather than haematemesis. However massive small intestinal bleeding can also cause haematemesis. While dealing with such patients haematemesis should be differentiated from haemoptysis as it may sometimes confuse the clinical picture. Haemoptysis is usually of bright red in colour.
Bleeding from Mallory Weiss tear may be bright red colour. Haematemesis is acidic where as haemoptysis is alkaline in nature.
 
Relevant history taking will solve the issue. In peptic ulcer disease there may be history of aspirin, NSAID and steroid intake. In patients with chronic liver disease, variceal bleeding is the cause although in 25% of case peptic ulcer disease may co-exist. Sudden haematemesis (with bright red colour) following vomiting or retching points towards the diagnosis of Mallory Weiss tear.

Recent history of aortic -graft insertion would suggest aorto-duodenal fistula. Presence of telangiectatic lesion in the FTlouth may indicate hereditary haemorrhagic telangiectasia. Presence of Virchow's nodes in the neck may point towards an underlying gastric malignancy. Other causes like gastric antral vascular ectasia, Dieulafoy's lesion, gastric lymphoma etc needs endoscopic examination for proper diagnosis.
.
In critically ill patients, upper gastrointestinal bleeding is a common problem and it is usually multifactorial like severe thrombocytopenia due to DIC, in septicaemic patients, stress ulceration and use of anticoagulants like heparin etc.

Investigations
Full blood count
Coagulation screening
Liver function test
Urea, creatinine, electrolytes
Gastroscopy

Management
While the diagnostic work up is on, full resuscitative measures should be taken. Haemodynamically unstable patient should be preferably managed in High Dependency Unit with CVP monitoring. Fluids in the form of crystalloids (Normal saline) should be given with appropriate CVP monitoring.

Blood transfusion should be targeted at a Hb level of approximately 10gm%. Endoscopy should only be done after appropriate fluid resuscitation otherwise it can cause morbidity particularly in elderly population.

Majority of the patients presenting with upper GI bleeding settle with conservative treatment. However, occasional patients need endoscopic therapy. The situations are:
Bleeding oesophageal varices.
Peptic ulcer with stigmata of recent haemorrhage.
Vascular malformations.

Bleeding peptic ulcer
Injection of adrenaline (1:10,000) - This is very effective in controlling bleeding. Addition of sclerosant like polydocanol, ethanolamine do not give any additional benefit. On the contrary they can cause necrosis of the injected area.

Heat probe - Application of heat proble over the bleeding area is an equally effective way of securing haemostasis. Application of Argon plasma coagulator (APC) via an endoscopically placed catheter is one of such ways of securing haemostasis.
Combination of injection of adrerlaline and application of heat probe does not add on to the efficacy of each other.

Indication of endoscopic therapy
Not all patients will need endoscopic therapy. There are certain endoscopic stigmata of impending rebleeding with attendant high mortality. The stigmata are:

Active spurting haemorrhage
Non bleeding visible vessel
Adherent blood clot over the arterial defect.
The aforementioned findings are associated with high chance of rebleeding which may prove catastrophic.

Medication
Gastric pH should be kept above 6.8 as acid environment destabilizes the clot. Injecting Omeprazole (bolus 80mg followed by 72 hrs infusion in a dose of 80mg/Hr) has been shown to reduce the incidence of rebleeding. H2 blocker although widely used do not decrease the risk of rebleeding from duodenal ulcers.
Continuous infusion of somatostatin has been shown to reduce the Incidence of rebleeding. The mechanism of action is by reduction 01 mesenteric blood flow and suppression of acid secretion.
Tranexamic acid, by way of its antifibrinolytic activity with stabillsation of the blood clot, can reduce the chance of rebleeding.

Surgical therapy
Now a days, it is rarely needed. However, in occasional elderly patients, medical therapy along with endoscopic therapy may fail. In such situations emergency surgery is the way forward. In duodenal ulcer, under running of the ulcer with pyloroplasty and in gastric ulcer, Pariiai gastrectomy is all that is required. Vagotomy is not done nowadays because of acid suppressing effects of proton pump inhibitors.

In critically ill patients stress ulcer bleeding is common and the risk factors are mechanical Ventilation, renal failure and coagulopathy. The best treatment is prophylaclic use of H2 blockers, Sucralfate and antacids.

After successful treatments, the patients should receive H.pylori eradication therapy. PPI should be prescribed with NSAID in patients needing long term NSAID.

The index patient underwent gastroscopy which showed a moderately large posterior duodenal ulcer and the endoscopist thought it to be prudent to be treated with local adrenaline injection therapy. He received blood transfusion and fluid resuscitation and fortunately there was no recurrence of the GI bleeding. He was given a course of H pylori eradication therapy and was discharged with 6 months course at omeprazole therapy.  (Reprint)

 

Patient with melaena

A 72 yrs old gentleman on aspirin was admitted with history of passage of black stool for last 3 days. On examination, he lookedpale, his pulse rate was 110/min, BP 110/ 70mmHg. Abdomen- soft, epigastric tenderness present with increased bowel sounds. Investigations revealed Hb of 6.9gm%, WBe 10,800, normal platelet counts, normal coagulation profile, normal liver function test, normal creatinine with raised urea, amylase -was normal. USGexamination of abdomen did not reveal anything specific. After transfusing him with 3 units of blood, gastroscopy was performed which showed a large posterior duodenal ulcer. Diagnosis: Duodenal ulcer presenting with melaena. Acute upper gastrointestinal haemorrhage is not uncommon presentation in day to day hospital practice. Common causes encountered are: Peptic ulcer Variceal bleeding Mallory Weiss tear Oesophagitis, gastritis and deodenitis Vascular Tumours There is often history of steroid and NSAID ingestion. Any bleeding beyond the attachment of ligament of Teitz usually causes melaena rather than haematemesis. However massive small intestinal bleeding can also cause haematemesis. While dealing with such patients haematemesis should be differentiated from haemoptysis as it may sometimes confuse the clinical picture. Haemoptysis is usually of bright red in colour. Bleeding from Mallory Weiss tear may be bright red colour. Haematemesis is acidic where as haemoptysis is alkaline in nature. Relevant history taking will solve the issue. In peptic ulcer disease there may be history of aspirin, NSAID and steroid intake. In patients with chronic liver disease, variceal bleeding is the cause although in 25% of case peptic ulcer disease may co-exist. Sudden haematemesis (with bright red colour) following vomiting or retching points towards the diagnosis of Mallory Weiss tear. Recent history of aortic -graft insertion would suggest aorto-duodenal fistula. Presence of telangiectatic lesion in the FTlouth may indicate hereditary haemorrhagic telangiectasia. Presence of Virchows nodes in the neck may point towards an underlying gastric malignancy. Other causes like gastric antral vascular ectasia, Dieulafoys lesion, gastric lymphoma etc needs endoscopic examination for proper diagnosis. . In critically ill patients, upper gastrointestinal bleeding is a common problem and it is usually multifactorial like severe thrombocytopenia due to DIC, in septicaemic patients, stress ulceration and use of anticoagulants like heparin etc. Investigations Full blood count Coagulation screening Liver function test Urea, creatinine, electrolytes Gastroscopy Management While the diagnostic work up is on, full resuscitative measures should be taken. Haemodynamically unstable patient should be preferably managed in High Dependency Unit with CVP monitoring. Fluids in the form of crystalloids (Normal saline) should be given with appropriate CVP monitoring. Blood transfusion should be targeted at a Hb level of approximately 10gm%. Endoscopy should only be done after appropriate fluid resuscitation otherwise it can cause morbidity particularly in elderly population. Majority of the patients presenting with upper GI bleeding settle with conservative treatment. However, occasional patients need endoscopic therapy. The situations are: Bleeding oesophageal varices. Peptic ulcer with stigmata of recent haemorrhage. Vascular malformations. Bleeding peptic ulcer Injection of adrenaline (1:10,000) - This is very effective in controlling bleeding. Addition of sclerosant like polydocanol, ethanolamine do not give any additional benefit. On the contrary they can cause necrosis of the injected area. Heat probe - Application of heat proble over the bleeding area is an equally effective way of securing haemostasis. Application of Argon plasma coagulator (APC) via an endoscopically placed catheter is one of such ways of securing haemostasis. Combination of injection of adrerlaline and application of heat probe does not add on to the efficacy of each other. Indication of endoscopic therapy Not all patients will need endoscopic therapy. There are certain endoscopic stigmata of impending rebleeding with attendant high mortality. The stigmata are: Active spurting haemorrhage Non bleeding visible vessel Adherent blood clot over the arterial defect. The aforementioned findings are associated with high chance of rebleeding which may prove catastrophic. Medication Gastric pH should be kept above 6.8 as acid environment destabilizes the clot. Injecting Omeprazole (bolus 80mg followed by 72 hrs infusion in a dose of 80mg/Hr) has been shown to reduce the incidence of rebleeding. H2 blocker although widely used do not decrease the risk of rebleeding from duodenal ulcers. Continuous infusion of somatostatin has been shown to reduce the Incidence of rebleeding. The mechanism of action is by reduction 01 mesenteric blood flow and suppression of acid secretion. Tranexamic acid, by way of its antifibrinolytic activity with stabillsation of the blood clot, can reduce the chance of rebleeding. Surgical therapy Now a days, it is rarely needed. However, in occasional elderly patients, medical therapy along with endoscopic therapy may fail. In such situations emergency surgery is the way forward. In duodenal ulcer, under running of the ulcer with pyloroplasty and in gastric ulcer, Pariiai gastrectomy is all that is required. Vagotomy is not done nowadays because of acid suppressing effects of proton pump inhibitors. In critically ill patients stress ulcer bleeding is common and the risk factors are mechanical Ventilation, renal failure and coagulopathy. The best treatment is prophylaclic use of H2 blockers, Sucralfate and antacids. After successful treatments, the patients should receive H.pylori eradication therapy. PPI should be prescribed with NSAID in patients needing long term NSAID. The index patient underwent gastroscopy which showed a moderately large posterior duodenal ulcer and the endoscopist thought it to be prudent to be treated with local adrenaline injection therapy. He received blood transfusion and fluid resuscitation and fortunately there was no recurrence of the GI bleeding. He was given a course of H pylori eradication therapy and was discharged with 6 months course at omeprazole therapy. (Reprint)