Download - Upper GI bleed Approach and Management

UGI bleed

Dr Manoj K Ghoda M.D., M.R.C.P.Consultant GastroenterologistVisiting faculty, GCS hospital

[email protected]

Gujarat gastro group

45 years old male

Referred for UGI endoscopy for “hematemesis”

Vomited blood previous nightSince then he has blood collecting in his mouth

No h/o drug ingestionNo alcohol, no tobaccoPreviously diagnosed to have hypertension and on medication but otherwise fit and well

When confronted with such a case scenario what should you check?

When confronted a patient with “hematemesis” you should have following check list

•Is it really hematemesis?•If it is, is patient stable?•How bad is hematemesis? What is the estimated amount of blood loss?•What could be the lesion?•Where could be the lesion?•What could be its blood supply?

Is it really hematemesis?

•Vomiting of blood from GI tract is called hematemesis. •Apart from UGI tract, blood could be from respiratory tract, from mouth, and from nose.

•Unless a careful history is taken, wrong assumption could be made leading to diversion to a system actually not responsible in the first place, causing delay in diagnosis and even death, not to speak of unnecessary expense and hardship to patient.

Is it Hematemesis?......... Some clinical considerations..

•Bright red blood is less likely to be from upper GI. Consider epistaxis, hemoptysis or bleeding gums and of course, fictitious bleeding.•Frothy blood or blood in lumps is more likely to be from lungs. •Epistaxis is never a part of hemetemesis. More likely that blood from epistaxis is swallowed and brought out as hematemesis. Blood pressure in such cases is very high.•A small amount of blood, mostly red, after several bouts of violent retching and non-bloody vomiting, is almost certainly a Mallory-Weiss tear, and if this is followed by severe chest pain, a transmural esophageal tear, the “Boerhaave syndrome”.

•Blood accumulating in mouth requiring patient to spit it out is either dental bleed or epistaxis. Dental or gum disorders may be present in the past.

•Coffee colored or black vomiting is hematemesis, due to bleeding from upper GI, unless otherwise proved. History and physical findings of portal hypertension or acid peptic disease may be present. This preliminary inquiry will always lead you to the correct line of investigation and treatment.

It always help to check visually...

Patient with hematemesis usually requires a bucket; whereas patient with hemoptysis usually requires a small bowl

Is it hematemesis?

How bad is the bleeding?…………. Assessing the blood loss.

•Resting pulse and B.P. normal = < 500 ml. blood loss.

•Resting tachycardia and postural drop of B.P. = up to 2.0 L loss.

•Shock = > 2.0 l blood loss.

What could be the cause of bleeding?Common causes of UGI bleed in Indian context.Remember!! Ca esophagus or Ca stomach rarely, if ever, present with GI bleed. They always have other features of presentation.

Esophageal Gastric varices are now one of the commonest cause of upper GI bleed in pediatric population

•Peptic ulcer, duodenal or gastric. Related or unrelated to H. Pylori.•NSAID induced mucosal injury, erosions, and ulcers.•Esophageal varices are now one of the commonest cause of upper GI bleed in India.•Mallory-Weiss tear.•Gastric varices.•Portal hypertensive gastropathy.•Dieulafoy lesion.

Dieulafoy lesionVarices

Gastric erosions

Where could be the lesion?

What is the blood supply of the lesion?

Could you name these blood vessels ?

Blood supply of the lesionEsophagus: •Upper esophagus is supplied from superior and inferior thyroid arteries.

•Mid-esophagus by the bronchial, right intercostal arteries and descending aorta.

•Distal esophagus by left gastric left inferior phrenic and splenic arteries.

•The venous drainage of upper esophagus is through the superior vena cava. •Mid esophagus through azygous veins.•Distal esophagus through portal vein by means of left and short gastric veins. Through these veins there is a porta-systemic communication.

There is an extensive submucosal venous anastomotic network which is very important because in portal hypertension blood is diverted from high pressure portal venous systems to low pressure systemic circulation via this network resulting in esophageal varices.

X

X

X

X

X

X

Vascular supply of stomach


Stomach:Arterial supply is from celiac artery; through common hepatic, left gastric and splenic arteries, which form two arterial arcades along lesser curvature and lower two thirds of greater curvature. Gastric fundus and left upper aspect of greater curvature are supplied via short gastric arteries, which arise from the splenic artery. Greater curvature below fundus is supplied from above by left gastroepiploic artery, a branch of splenic artery and from below by right gastroepiploic artery, a branch of gastroduodenal artery and these two usually anastomose.Lesser curvature is supplied from above by left gastric artery and from below by right gastric artery or gastroduodenal artery, branches of common hepatic artery.

X

X

Duodenum:Celiac trunk supplies proximal duodenum via hepatic artery, from which arises gastroduodenal artery, which in turn branches into superior pancreaticoduodenal artery, which gives off anterior and posterior branches to duodenum.

Distal duodenum is supplied by branches the superior mesenteric artery.


Branches of Common Hepatic Artery?

Remember, the celiac trunk has three main branches

1--Left gastric artery (supplies L greater curvature of stomach)

2--Splenic artery (spleen, pancreas, left greater curve of stomach)

3--Common hepatic artery (liver, gall bladder, right greater curvature, head of the pancreas)

Clinical presentation of UGI bleed:•Presentation may be as coffee-brown vomiting known as hematemesis, or there may be frank red blood.•Mallory-Weiss tear usually presents with one or more clear vomits followed by reddish, rather than coffee brown blood.•Some patients present with dark black, like coal tar, stool known as melena.•Some people with massive bleed will have both Hemetemesis and bleeding PR which is not dark black but red.•There may be nausea, dizziness, and perspiration related to hypovolemia and hypotension•Patients with acid-peptic disease give a history of epigastric pain for sometime before the illness and there may be history of analgesic ingestion.•There may be past history of jaundice, ascites or other features of chronic liver disease.

How will you decide if the patient needs admission or could be discharged home?

Identifying high risk patients.

•When the patient is in shock.•Patients above the age of 65 years.•Patients with co-morbid conditions like IHD, hypertension, diabetes, coagulopathy or chronic liver disease.•Where there is simultaneous upper and lower GI bleeding.•Previous ulcers/bleed•Patient having rebleed during the same admission•On steroids or NSAIDs•Alcoholic or tobacco smokerCan you Identifying high risk Doctors ?

These patients are preferably treated in intensive care unit.

The Rockall Score for stratifying riskVariable

0 Score

1 2

3

Age (yrs) < 60 60-79 ≥ 80

Comorbidity No or mild coexisting

Moderate coexisting (e.g., hypertension)

Severe coexisting (e.g., CHF)

Life threatening (e.g., RF)

Hemodynamic status

No shockP < 100Syst BP ≥ 100

P ≥ 100 plusSys BP ≥ 100

Hypotension

Diagnosis MW tear, normal endoscopy with no blood seen

All other diagnosis

Malignancy of UGI tract

Major stigmata of recent hemorrhage

None or dark spot

Blood in UGI tractAdherent clot, visible or spurting vessel

Rockall, Lancet 1996

ROCKALL System - Rebleeding According to Risk Score Category

Rockall et al. Gut 1996;38:316

Rockall score

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Enns RA, W J Gastroenterol, 2006

The Glasgow-Blatchford Bleeding Score

• GBS superior to total/clinical Rockall scores (ROC curves, P<0.05)

• 123 patients (22%) classified as low risk, with 84 (68%) were managed as outpatients safely

• Proportion admitted fell (96% to 71%, p<0·00001)

Stanley, Lancet 2008

Score-value

Blood urea (mmol/L)

6.5-7.9 2

8.0-9.9 3

10.0-25.0 4

>25.0 6

Haemoglobin for men (g/L)

120-129 1

100-119 3

<100 6

Haemogolbin for women (g/L)

100-119 1

<100 6

Systolic blood pressure (mmHg)

100-109 1

90-99 2

<90 3

Other markers

Pulse >100/min 1

Presentation with melaena 1

Presentation with syncope 2

Hepatic disease* 2

Cardiac failure** 2*Known history, or clinical and laboratory evidence, of chronic or acute liver disease.** Known history, or clinical and echocardiographic evidence, of cardiac failure.

Admission risk markers for GBS

Who could be Discharged from ER?

Who can be sent home from the emergency room?

Gralnek, NEJM, 2008

These patients represent upto 20-40% of all patientspresenting with PUB

Investigations:

•CBC with indices.•Where indicated liver function test and coagulation profile.•Renal function tests.•Endoscopy, once the patient is stable.•Sonography when portal hypertension is suspected.•Abdominal angiography in selected cases.

Managing UGI bleed:Some fundamentals: • Rule of 18; 18 G venflon, 18 F Ryle’s tube, endoscopy in 18 hrs,• Irrespective of degree of blood loss it is always safer to cross

match at least one unit of PCV to cope with any unexpected requirement.• This is a volume loss so..replace volume, use pressure agents

as last resort• A large bore, 18F, Ryle’s tube is passed and stomach washed

off any blood clots in anticipation of urgent endoscopy. • Cold saline lavage has no benefit and will cause unnecessary

delay and temperature disturbances. Similarly lavage with adrenaline, noradrenalin and various “coagulating agents” have very little to offer.• If pt has no vomiting, clear fluid is allowed.

Resuscitation:•For small amount of blood loss with normal pulse and B. P., crystalloids like normal saline etc. are enough.

•For moderate blood loss crystalloids plus colloids like dextran 70/40 %, hydroxyethyl starch, are required to maintain B.P. Blood may be required as well, depending upon the patient’s fitness and previous hemoglobin levels.

•For large blood loss, colloids and crystalloids and blood are all required, sometimes simultaneously.

•Fluid input is monitored by central venous pressure, pulse, blood pressure, and hourly urine output and hemoglobin level. Blood transfusion is given to keep Hb around 10 Gms.

•Pressure agents like dopamine 2.5 to 10 mcg/kg/min, and dobutamine 2.5 to 10 mcg/kg/min as infusion, Noradrenalin 3mg. /Hr as infusion may be required, as a last resort, to maintain peripheral perfusion.

•IV Erythromycin and Metochlopromide may be used to increase forward motility to clear the stomach of clots for better visualization.•Somatostatin, 250 mcg bolus and then 250 mcg/ hr as infusion may be helpful in variceal bleed, and perhaps bleed of hypertensive gastropathy and ulcer bleed by way of producing splanchnic vasoconstriction; and is started while awaiting definitive treatment.•IV Omeprazole / Pantaprazole is given 40 mg. diluted in saline, and then 4mg/ hr. and 8mg//hr as infusion respectively for bleeding ulcers. •Any disturbance of coagulopathy is corrected using vitamin K, fresh frozen plasma, platelet infusion and where appropriate specific clotting factors.

•For patients requiring large numbers of blood, i.v. calcium is supplemented; platelet infusion, one unit for 4 PCV and fresh frozen plasma, 2 units for 4 PCV, are also required in these circumstances.

•For known or possible cirrhotic, lactulose is given orally 30 ml. Every 2 hours till the diarrhea establishes when the dose is reduces to produce two stools / day. If oral lactulose is not possible lactulose enema is given.•Once the patient is stable, endoscopy is done.

Variceal bleeding

Pharmacotherapy consists of•splanchnic vasoconstrictors (vasopressin and analogues, somatostatin and analogues, •nonselective -blockers) and •venodilators (nitrates)

AASLD PRACTICE GUIDELINES

Effect of drugs used for varices


Patients with Cirrhosis and an AcuteEpisode of Variceal Hemorrhage

Antibiotic prophylaxis• Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in

any patient with cirrhosis and GI hemorrhage (Class I, Level A). • Oral norfloxacin (400 mg BID) or intravenous ciprofloxacin (in patients in

whom oral administration is not possible) is the recommended antibiotic (Class I, Level A).

• In patients with advanced cirrhosis intravenous ceftriaxone (1 g/day) may be preferable particularly in centers with a high prevalence of quinolone-resistant organisms (Class I, Level B).

Pharmacological therapy• Pharmacological therapy (somatostatin or its analogues octreotide and

vapreotide; terlipressin) should be initiated as soon as variceal hemorrhage is suspected and continued for 3-5 days after diagnosis is confirmed (Class I, Level A).


Interventions• OGD, performed within 12 hours, should be used to make the

diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy (Class I, Level A).

• Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy (e.g., TIPS or endoscopic therapy) is planned (Class I, Level B).

• TIPS is indicated in patients in whom hemorrhage from esophageal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy (Class I, Level C).


Tips

Tips

PEPTIC ULCER BLEED

Overall management ABC’s and adequate resuscitation Early risk stratification

o pre-endoscopyo at early endoscopy

Very Low risk patients discharge home

All other patients admit

High-risk patients Endoscopic hemostasis Initiate high-dose IV PPI

Consider secondary prophylaxis H pylori testing and treating NSAID/COX2 use ASA use

Low-risk patients Initiate daily dose PPI

Ulcer bleed

•Adrenalin Injection•Heater prob•Hemoclip application

THANK YOU

Dr Manoj K Ghoda

Consultant Gastroenterologist Visiting faculty, GCS hospital

[email protected]

Gujarat gastro group