Upper GI Bleed

Dr. Syed Muhammad Ali ShahRMO

Dept. of MedicineABSTH/NSMC

History

Name XYZAge 75 YearsSex MaleOccupation TailorResident Jalalpur Jattan GujratDOA 1-7-14

Presenting Complaints

• Abdomen distension 1 month• Epigastric discomfort 10 days• Black stools 4 days• Hematemesis 4 episodes – 2

hours• Altered sensorium 1 hour

History of Present Illness

• Abdominal distension• Pedal edema• Epigastric discomfort• Malena • Hematemesis• Altered sensorium• Loss of appetite• On & off constipation

Past History

• Known patient Chronic Hep. C• h/o admission 6 months back due to same

problem• No h/o IHD, HTN, DM, Joint Pain, TB or

Asthma• No h/o of NSAID or anticoagulant intake• No h/o any bleeding tendency

• PERSONAL HISTORY:– Smoker having h/o 25 pack years– Non-addict

• FAMILY HISTORY:– No h/o IHD, HTN, DM, Joint Pain, TB, Asthma or

Chronic Viral Hepatitis• DRUG HISTORY:– Took some drugs from hakeems from time to time

• SOCIOECONOMIC HISTORY:– Low class– No facility of clean drinking water

GPE

• An ill looking old man, sweating heavily, lying in bed in semiconscious state, disoriented in time, place and person with red stains on his clothes.

• VITAL SIGNS:– Blood Pressure 90/60 mmHg– Temp.98 F– Resp. Rate 24/min– Pulse 117/min

GPE• Pallor +++• Jaundice +• Pedal Edema +++• Cold Extremities ++• Clubbing Absent• Cyanosis Absent• Koilonychea Absent• Leuconychea Absent• JVP Not raised• Lymph Nodes Not Palpable• Thyroid Gland Not Palpable

Pedal Edema

ABDOMINAL EXAMINATION

• Distended• Umbilicus protuberant • No veins visible• Tenderness in epigastric region.• Liver, spleen, kidneys not palpable• Fluid thrill present • Bowel sounds audible• No hepatic, renal or splenic bruit

CNS Examination• GCS 10/15• Disoriented in time place and person• Confused• Motor system intact• Sensory system intact• Reflexes normal• Planters down going

Respiratory ExaminationCVS Examination

INITIAL RESUSITATION

• Passed 2 IV lines – 14-16 G• Placed patient in left lateral position• Passed Folley catheter and monitored urine output• Monitored vital signs after every 15 min• Kept NPO• Sent blood for CBC, LFTs, BSR, PT, aPTT, grouping

and cross-match• Arranged 4 pints of fresh blood

• Haemacel infusion 500 ml IV stat• Inj. N/S 1000 ml IV infusion• Inj. Sandostatin 50ug IV stat then 50ug/hour

continuous infusion started• Inj. Omeprazole 80 mg in 100 ml N/S IV over

half hour• Inj. Metoclopramide 20 mg IV TDS• Inj. Ceftriaxone 1g IV BD• Inj. Vit. K 10 mg IM stat• Blood transfusion @ 1 unit/hour until vitally

stable

INVESTIGATIONS

Hb: 6.1 g/dLHct: 21.1Platelets: 85 WBCs: 3300

BSR: 138mg/dL

RFTs & LFTs

Serum Urea 56 mg/dLSerum Creatinine 1.0 mg/dL

Total Bilirubin 0.9 mg/dL

Serum ALT 46 U/L

Serum Alkaline phosphatase 172 U/L

Hepatitis & HIV Screening

HBsAg Negative

Anti-HCV-AbPositive

HIV Screening Negative

Coagulation Profile

• PT 18 sec (prolonged)• aPTT 30 sec (normal)

USG ABDOMEN

• Liver cirrhosis with small size of liver• Massive ascities• No other remarkable findings

DIAGNOSIS

DECOMPENSATED CHRONIC LIVER DISEASE WITH ASCITIES AND ESOPHAGEAL VARICES

Upper GI EndoscopyORAL CAVITY:

Poor hygiene.ESOPHAGUS:

Four columns of high grade esophageal varices in middle and distal third of esophagus.STOMACH:

Mild to moderate portal hypertensive gastropathy was present in body and antrum.DUODENUM:

1st and 2nd part of duodenum were normal.

ENDOSCOPIC DIAGNOSIS:High grade esophageal

varices. Endoscopic variceal band ligation was done.

TREATMENT

• Syp. Lactulose 60 ml PO TDS• Tab. Spironolactone 100 mg PO BD• Inj. Furosemide 40 mg IV TDS• Inj. Metoclopramide 20 mg IV TDS• Inj. Omeprazole 40 mg in 100 ml N/S IV BD• Tab. Inderal 40 mg PO BD

CASE DISCUSSION

UPPER GI BLEED

Defined as…• Bleeding from a lesion in esophagus / stomach

/ duodenum above the ligament of Treitz is called upper GI bleeding..

Ligament ofTreitz

CLINICALLY PRESENTS AS:

• Hematemesis – (vomiting of bright red / coffee grounds in blood)

• Melena – (passage of black tarry stools)

• Hematochezia – (in 10% of massive bleeds :bright red blood in stools)

• Shock– (pallor, cold nose, systolic BP below 100 mmHg, pulse

>100 b.p.m.)

Epidemiology• Upper vs Lower GI bleeding = 5:1• Incidence: 170 patients/ 100,000 /year(USA data)• 38% due to peptic ulcer (Most common).• 80% are self-limited.• Patientss on anti platelet therapy has two fold

increase in bleed as compared to normal ones. (annual UGI Bleed incidence > 13%).

• 20% of pts of moderate to high risk, who have recurrent bleeding (within 48-72 hrs) have poor prognosis.

• The mortality rate is 5% to 10% for severe UGI bleed

CAUSES OF SEVERE UGI BLEED• Peptic ulcer 38 %• Oesophageal varices & Gastric varices 16%• Esophagitis 13%• No cause found 8%• Upper gastrointestinal tract tumor 7%• Angioma 6%• Mallory Weiss tear 4%• Erosions 4%• Dieulafoy’s lesion 2%• Other 2%

Uncommon Causes of Non-Variceal Bleed (< 5%)

• Gastroesophageal reflux disease

• Trauma from foreign body• Esophageal ulcer• Cameron lesion• Stress ulcer• Drug induced erosions• Angioma• Watermelon stomach• Portal hypertensive gastropathy• Aorta-enteric Fistula• Radiation telangiectasis/

Enteritis• Benign tumours• Malignant tumour• Blue rubber bleb nevus

syndrome • Osler-Weber-Rendu syndrome• Haemobilia• Hemosuccus pancreatitis• Infections(CMV,HSV)• Stomal ulcer• Zollinger-ellison syndrome

ESOPAHGEAL VARICES

DEVELOPMENT OF VARICES:• The rise in portal pressure is associated with the

development of collateral circulation which allows the portal blood to be diverted into the systemic circulation.

• Varices develop and enlarge with time.• The two factors that appear to determine the

development of varices are – Continued hepatic injury– The degree of portosystemic shunting.

Natural History• A cirrhosis patient who does not have varices has not yet developed

portal hypertension, or his portal pressure is not yet high enough for varices to develop.

• As portal pressure increases, the patient may progress to having small varices.

• With time, and as the hyperdynamic circulation increases, blood flow through the varices will increase, thus raising the tension in the wall.

• Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension.

Natural History

Sites of Varices

These spontaneous shunts occur:

– At the cardia of stomach through the intrinsic and extrinsic gastro-oesophageal veins

– In the anal canal where the superior haemorrhoidal vein belonging to the portal system anastomoses with the middle and inferior haemorrhoidal veins which belong to the caval system

– In the falciform ligament of the liver through the para-umbilical veins which are the remains of the umbilical circulation of the fetus.

– In the abdominal wall and the retroperitoneal tissues, from the liver to the diaphragm, veins in the lienorenal ligament, in the omentum and lumbar veins.

Esophageal Varices

VARICEAL HAEMORRHAGE

• Variceal haemorrhage is defined as bleeding from an oesophageal or gastric varix at the time of endoscopy or the presence of large oesophageal varices with blood in the stomach and no other recognizable cause of bleeding.

• An episode of bleeding is clinically significant when there is a – Transfusion requirement of 2 units of blood or more

within 24 hours of the time zero.

– A systolic blood pressure of less than 100 mm Hg or a postural change of greater than 20 mm Hg

– Pulse rate greater than 100 beat/min at time zero

– Time zero is the time of admission to the first hospital the patient is taken to.

TIME FRAME OF ACUTE BLEEDING

• The acute bleeding episode is represented by an interval of 48 hours from time zero with no evidence of clinically significant bleeding between 24 and 48 hours.

• Evidence of any bleeding after 48 hours is the first rebleeding episode.

VARICEAL REBLEEDING

• Variceal rebleeding is defined as the occurrence of new haematemesis or malena after a period of 24 hours or more from the 24 hour point of stable vital signs.

• All bleeding episodes regardless of severity should be counted in evaluating rebleeding.

GRADING OF VARICESAlthough numerous methods have been described for grading

varices, the simplest method is to divide them into three grades:

Grade 1 – Small, straight esophageal varices

Grade 2 – Enlarged, tortuous esophageal varices occupying less than one third of the lumen

Grade 3 – Large, coil-shaped esophageal varices occupying more than one third of the lumen

PRIMARY PROPHYLAXIS• Pharmacological therapy with propranolol is the best available

modality at present. • Aim of therapy with propranolol: Reduction in hepatic venous

pressure gradient to less than 12mmHg. • Dose: Starting dose 40 mg twice daily, increasing to 80 mg twice daily

if necessary. • In case of contraindications or intolerance to propranolol, variceal

band ligation is the treatment of choice. • In difficult situations where neither propranolol nor variceal band

ligation can be used, isosorbide mononitrate is the treatment of first choice (20 mg twice daily).

Management of Active Variceal Haemorrhage

RESUSCITATION• Site: Where haemodynamic monitoring is

possible• Protect the airway: position the patient on

side.• Protection of the airway by elective intubation:

– Severe uncontrolled variceal bleeding;– Severe encephalopathy;– Inability to maintain oxygen saturation above 90%;– Aspiration pneumonia.

• IV access: use 2 large bore (14-16G) cannulae into peripheral vein for initial fluid resuscitation. – If peripheral access is difficult, access via jugular,

subclavian, or femoral vein may be necessary.

• Take blood for Hb, CBC, Platelet count, Blood glucose, PT and LFTs, Group and X-match

• Arrange at least 4 pints of fresh whole blood

• Restore the circulating volume– If there are no signs of haemodynamic compromise use a slow infusion

of N saline (0.9%) to keep the iv line patent and for maintenance fluids.

– Tachycardia, hypotension, or a postural fall in BP or a postural increase in HR (by > 30 bp) suggests a low intravascular volume. Give 500 -1L colloid over 1 hour (e.g. Haemaccel) and then crystalloid and continue until blood is available.

– Use compatible blood when it is ready (give 1unit/h) until volume is restored.

– If the rate of bleeding is slow, packed cells are preferred. – If there is massive haemorrhage, ask for O-negative blood which may

be given without cross-matching.

• Monitor urine output and catheterize the patient if there are signs of haemodynamic compromise. Aim for >30ml/h. Prompt rescuscitation should restore urine output.

• Watch for the usual signs of overload (raised JVP or CVP, pulmonary oedema, peripheral oedema). Too rapid transfusion may precipitate pulmonary oedema even before the total lost volume has been replaced.

• Commence intravenous PPI---Intravenous omeprazole (80mg iv, followed by 8mg/h for 72 hours) decreases the risk of rebleeding from >20% to ~7% after endoscopic therapy.

• Give a bolus dose of metoclopramide 20mg iv. This transiently increases the lower oesophageal pressure and decreases azygous blood flow.

• Antibiotics: Take blood, urine, and ascitic cultures ± microscopy. – Start broad-spectrum antibiotics. – Several studies have shown that variceal bleeding is associated

with sepsis. – Commence a third-generation cephalosporin or ciprofloxacin and

amoxycillin. Treat for 5 days.

• Terlipressin (2mg initially, and then 1-2mg every 4-6 hours for up to 72 hours) is effective in controlling variceal bleeding by causing splanchnic vasoconstriction (relative reduction in mortality of ~34%).

OR

• Octeotride - 50ug bolus then 50ug/hr infusion for 5 days

• Consider passing an NG tube: this may help confirm coffee-grounds or blood in the stomach and is useful in diagnosing re-bleeding.

• Keep the patient nil by mouth for the endoscopy.

Correct any Coagulopathy

• Platelet count below 50 000/mm3 should be treated with platelet support (6-12 units of platelets).

• Otherwise give fresh frozen plasma (2-4units) and iv vitamin K (5-10mg).

• Serum calcium may fall after several units of citrate containing blood transfusion.

– Give 10 ml (4.5mEq) of calcium gluconate for

every 3-4 units transfused.

• Tranexamic acid (0.5-1.5g iv tds, or 1-1.5g tds po) increases the levels of fibrinogen and may be helpful.

Blatchford Scoring System(Pre-endoscopic Assessment)

Variables Points * SBP(mm Hg) 100-109 1 90-99 2 <90 3 * BUN (mg/dl) 39.0-47.4 2 48.0-59.4 3 60.0-149.4 4 >150 6 * Hb(g/dl) In Male 12.0-12.9 1 10.0-11.9 3 <10.0 6 * Other variables pulse >100 1 Presentation with melena 1 Hepatic disease 2 Cardiac failure 2

Most patients need intervention if their score is 6 or higher.

TIMING OF UPPER GASTROINTESTINAL ENDOSCOPY – As soon as the patient is haemodynamically

stable. CONTROL OF BLEEDING– Variceal band ligation is the method of first choice.– If banding is difficult because of continued

bleeding or this technique is not available, endoscopic variceal sclerotherapy should be performed.

• WHO SHOULD HAVE SURVEILLANCE FOR VARICEAL BLEEDING?– All patients with cirrhosis should be endoscoped at the time of

diagnosis.

• HOW OFTEN SHOULD CIRRHOTIC PATIENTS BE ENDOSCOPED?– If at the time of first endoscopy no varices are observed, patients

with cirrhosis should be endoscoped at three year intervals.– If small varices are diagnosed, patients should be endoscoped at

yearly intervals.

• WHICH PATIENTS WITH CIRRHOSIS SHOULD HAVE PRIMARY PROPHYLAXIS?– If grade 3 varices are diagnosed, patients should have primary

prophylaxis irrespective of the severity of the liver disease.– If patients have grade 2 varices and Child class B or C disease, they

should have primary prophylaxis.

FAILURE TO CONTROL ACTIVE BLEEDING• In case of bleeding that is difficult to control, a

Sengstaken tube should be inserted until further endoscopic treatment, TIPSS, or surgical treatment.

• Specialist help should be sought at this time and transfer to a specialist centre should be considered.

Sengstaken-Blackmore Tube

Secondary prophylaxis of varicealbleeding in cirrhosis

VARICEAL BAND LIGATION• Following control of active variceal bleeding the varices

should be eradicated using endoscopic methods. The method of first choice is variceal band ligation.

• It is recommended that each varix is banded with a single

band at weekly intervals until variceal eradication. • Following successful eradication of the varices, patients

should be endoscoped:– three months– six monthly thereafter.

ENDOSCOPIC VARICEAL SCLEROTHERAPY

• If banding is not available, sclerotherapy should be used.

• The interval between treatments should be the same as those outlined above for banding.

NON-SELECTIVE BETA BLOCKER WITH OR WITHOUT ENDOSCOPIC THERAPY

• Either combination treatment of sclerotherapy and non-selective beta blocker or non-selective beta blocker alone may be used.

• If the latter strategy is used then it is recommended that patients should have the hepatic venous pressure gradient measured to confirm that this has been successfully reduced to less than 12 mm Hg.

Trans-jugular Intra-hepatic Porto-Systemic Shunts (TIPSS)

• TIPSS is more effective than endoscopic

treatment in reducing variceal rebleeding

• Does not improve survival and is associated with more encephalopathy.

• It is a treatment option that may be used in certain centres with particular expertise.

Adverse Prognostic Factors in UGIB

1. Age over 602. Shock(SBP<100mmhg), pulse >1003. Malignancy or varices as bleeding source.4. Sever coagulopathy5. Co-morbid medical illness6. Continued or recurrent bleeding7. Severe active Bleeding (Hypotension, multiple transfusion,

bright red nasogastric aspirate)8. Endoscopically identified arterial bleeding or visible vessel9. Ulcer location10. Emergency surgery if surgical complication

PEPTIC ULCERPATHOGENESIS:

Due to decrease in mucosal defense mechanism: aspirin, other NSAIDS, H.Pylori or both.

H.PYLORI: NSAIDS:* involves antrum * gastric ulcers > common *duodenal ulcers * 15-45% patients develop * 3%(USA) & 25%(Japan) ulcers on regular use lifetime risk of peptic ulcer

PPI-Based Triple Therapies

• PPI-based triple therapies are a 14-day regimen as shown below:– Oral PPI (Omeprazole 20 mg PO bid)

Plus– Clarithromycin 500 mg PO bid

and– Amoxicillin 1 g PO bid

Quadruple Therapy

• Quadruple therapies for H pylori infection are generally reserved for patients in whom the standard course of treatment has failed.

• Quadruple treatment includes the following drugs, administered for 14 days:– PPI, standard dose, or ranitidine 150 mg, PO bid– Bismuth 525 mg PO qid– Metronidazole 500 mg PO qid– Tetracycline 500 mg PO qid

Primary prevention of NSAID-induced ulcers

• Primary prevention of NSAID-induced ulcers includes the following:– Avoid unnecessary use of NSAIDs– Use acetaminophen or nonacetylated salicylates

when possible

Prophylactic or Preventive Therapy

• Consider prophylactic or preventive therapy for the following patients:– Patients with NSAID-induced ulcers who require chronic, daily NSAID

therapy– Patients older than 60 years– Patients with a history of PUD or a complication such as gastrointestinal

bleeding– Patients taking concomitant steroids or anticoagulants or patients with

significant comorbid medical illnesses

• Misoprostol 100-200 mcg PO 4 times per day• Omeprazole 20-40 mg PO every day• Lansoprazole 15-30 mg PO every day

MALLORY WEISS SYNDROME / TEARS

• Mallory-Weiss tears are mucosal or submucosal lacerations that occur at the gastroesophageal junction and usually extend distally.

• Patients generally present with hematemesis or coffee-ground emesis after alcohol intake & have a history of recent non-bloody vomiting with excessive retching followed by hematemesis

• Endoscopy usually reveals a single tear that begins at the gastroesophageal junction and extends several millimeters distally within cardiac portion of stomach

Mallory-Weiss tear at the gastroesophageal junction.

• Occasionally, more than one tear is seen.

• Bleeding stop spontaneously in 80 – 90% of the patients

• In 0 – 5% of the patient bleeding recurs– Endoscopic electro-coagulation of the tears–Angiography therapy with intra arterial

infusion of vasopressin or embolisation.–Operative therapy with oversewing of tear.

HAEMORRAGIC OR EROSIVE GASTRITIS

• Stress related mucosal injury– Occur only in extremly sick patients

• Serious trauma• Major Surgery• Burn Covering > 1/3 of Surface area• Major intracranial disease • Severe medical illness (Ventilator dependence, coagulopathy)

– Significant bleeding probably does not develop unless ulceration occurs.

– Intravenous H2-receptor antagonist is the treatment of choice. Sucralfate also effective

• Aspirin and NSAIDS– Half of the patient who chronically ingest NSAIDS

have Erosions. (15 – 30% have Ulcers)– Most Frequently and severely affected site is

gastric antrum.

NSAIDS Induced Gastric Ulcers

PORTAL GASTROPATHY• On endoscopic examination mucosa is engorged and friable.

• Portal hypertensive gastropathy (PHG) is caused by increased portal venous pressure and severe mucosal hyperemia

• It results in ectatic blood vessels in the proximal gastric body and cardia and oozing of blood.

• Less severe grades of PHG appear as a mosaic or snake skin appearance and are not associated with bleeding.

PORTAL GASTROPATHY

Esophagitis• 8% of all UGI bleeding was caused by erosive esophagitis.

• Independent risk factors for bleeding esophagitis were grade 3 or 4 (moderate to severe) esophagitis.

• A history of heartburn was obtained in only 38% of patients.

• Severe bleeding from gastroesophageal reflux–induced esophagitis is treated medically with a PPI

• Upper endoscopy is critical to diagnosing severe erosive esophagitis.

• Endoscopic therapy generally has no role unless a focal ulcer with a stigma of recent hemorrhage is found.

• These patients should be treated with a daily

PPI for 8 to 12 weeks and undergo repeat endoscopy to exclude underlying Barrett's esophagus

Upper Gastrointestinal Malignancy

• Malignancy accounts for 1% of severe UGI bleeds.

• The tumors are usually large, ulcerated masses in the esophagus, stomach, or duodenum.

• Endoscopic hemostasis with Monopolar electro cautary, laser, injection therapy, or hemoclips can temporarily control acute bleeding.

• External beam radiation can provide palliative hemostasis for patients with bleeding from advanced gastric or duodenal cancer

Gastric Antral Vascular Ectasia

• Gastric antral vascular ectasia (GAVE), also described as watermelon stomach.

• Characterized by rows or stripes of ectatic mucosal blood vessels that emanate from the pylorus and extend proximally into the antrum .

• GAVE is most commonly reported in older women and also seems to be more common in patients with end-stage renal disease

• GAVE has been associated with cirrhosis and scleroderma.

• Patients with GAVE who do not have portal hypertension

demonstrate linear arrays of angiomas (classic GAVE).

• Whereas those with portal hypertension have more diffuse antral angiomas.

• Endoscopic therapy with argon plasma coagulation has been shown to be equally (80%) effective in cirrhotic and noncirrhotic patients with GAVE.

Gastric Antral Vascular Ectasia

Aortoenteric Fistula• Bleeding is usually acute and massive, with a high mortality

rate(30-100%).

• A primary aortoenteric fistula is a communication between the native abdominal aorta (usually an atherosclerotic abdominal aortic aneurysm) and, most commonly, the third portion of the duodenum.

• Often, a self-limited herald bleed occurs hours to months before a more severe, exsanguinating bleed.

• On endoscopy obscure site of bleeding.

• Demonstration of an aortic aneurysm and fistulous track on abdominal CT angiogram.

• Secondary aortoenteric fistula between the third portion of the duodenum and the proximal end of the graft but may occur elsewhere in the GI tract.

• Therapeutic endoscopy plays no role in the management of bleeding from an aortoenteric fistula.