Upper Gastro Intestinal Bleed

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Upper GI Bleed

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  • Upper GI Bleed Dr. Syed Muhammad Ali Shah RMO Dept. of Medicine ABSTH/NSMC
  • History Name XYZ Age 75 Years Sex Male Occupation Tailor Resident Jalalpur Jattan Gujrat DOA 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 Examination CVS 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/dL Hct: 21.1 Platelets: 85 WBCs: 3300 BSR: 138mg/dL
  • RFTs & LFTs Serum Urea 56 mg/dL Serum 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-Ab Positive 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 Endoscopy ORAL 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 of Treitz
  • 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% Dieulafoys 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 represent