Chetanvalte007@bloggers. com

      Osh state Medical University

Name:chetan vijay valte
Teacher :Aipiry
Sub:Hematemesis



                      Hematemesis
A multitude of reasons contribute to gastrointestinal hemorrhage, hemobilia being less frequent. Here we present a
case of hematemesis who was later found to have bleeding from the biliary tract that was due to pseudo-aneurysm
arising from the hepatic artery. The diagnosis was supported by angiogram. He underwent coil embolization post
which bleeding stopped. We present this case since hemobilia is a rare event and classical finding of blood clot on the
ampulla on endoscopy is rare as seen in our case.
Key words: Hemobilia, pseudoaneurysm, right hepatic artery, coil embolization.

                          introduction

Gastrointestinal bleeding is among
the most common emergency dealt by gastro-
enterologists needing quick initial triage assess-
ment and appropriate resuscitation. Its incidence
is about 50 to 150 per 1 lakh patients each year,
with highest among areas of lower socioeco-
nomic status.[1] Upper gastrointestinal bleeding
(UGB) is associated with morbidity and mortality
in India. It can be attributed to NSAID use viz.
Ibuprofen, Diclofenac and Ketorolac. Peptic
ulcer bleed is associated with whopping 60%
of cases of UGB, while esophageal varices
contribute to about 6%.[2] Less common causes
include Mallory-Weiss tear, gastritis, duodenitis,
arteriovenous malformations, malignancy,
     and use of anti-platelets like clopidogrel, aspirin,
anticoagulants viz. warfarin, low molecular
weight heparin and unfractionated heparin.
Upper endoscopy needs to be performed to exclude
other causes of gastrointestinal bleed.
Hemobilia (bleeding in the biliary tree)
occurs when conditions produce an abnormal
communication between blood vessels and bile
ducts.[4] It can present many weeks after the
initial injury.[5] Bleeding can lead to biliary
obstruction. The most common cause is live

               Background

o Bleeding from GI tract proximal to ligament of Treitz

2.General information 

o Upper GI bleeding commonly presents with hematemesis (vomiting of bright 

red blood or "coffee ground" material [blood altered by gastric acid])

o May also have melena (dark colored, tarry stools)

o Massive upper GI bleed can present with hematochezia (bright red, bloody 

stools)

o Bleeding not explained by hemoptysis, epistaxis, or other non-GI source

                    

                             History

o Bleeding characteristics 

 Timing and quantity? 

 Helps determine severity of bleeding

 Site? 

 Helps determine source of bleeding (nasopharynx/oropharynx?) 

 Color? 

 "Coffee ground" emesis suggests blood altered by gastric acid

o Exposure to ill contacts or contaminated food? 

 Consider esophagitis, gastritis

o Recent ingestion of NSAIDs? 

 Consider gastric or duodenal ulceration

o Vomiting, retching, or paroxysmal cough preceding hematemesis? 

 Consider Mallory-Weiss tear

o Abdominal pain? 

 Consider ulceration, gastritis, esophagitis

      

                       Pathophysiology

1.Pathology 

o Neonates 

 Esophagitis, gastritis, gastroduodenal ulcers

 Mallory-Weiss tear, congenital malformations

 Intestinal duplication, heterotopic pancreatic tissue

 Liver failure, coagulopathy

 Cow's milk allergy

2.Incidence/prevalence 

o GI bleeding is rare in the general pediatric population and is not well 

documented

o Published data are limited to pediatric ICU patients

o One pediatric ICU study reported an incidence of 6.4% (63 episodes in 984 

pediatric ICU patients) - only 0.4% were considered life threatening

o Another study reported an incidence of 25% among pediatric ICU patient

                       Diagnoses

Mortality is low in children with upper GI bleeding 

 High potential for recovery

 Few comorbid conditions

 Attentive care usually given

 In contrast to significant mortality in elderly patients despite aggressive 

treatment

o Some specific fatalities reported: 

 Candida esophagitis in child with AIDS

 Perforated ulcers

 Sulindac-induced gastritis

 Vascular anomalies

                      Mortality

Variceal bleeding

Mallory-Weiss tear

Peptic ulcer disease

Erosive gastritis

Hemosuccus pancreaticus

Arterioenteric fistula 

Perforation*

Pseudohematemesis*

Hemoptysis*

Epistaxis*

Esophagitis

Prolapse gastropathy C

Duodenitis A

Dieulafoy’s lesions B,C

       

                Prognosis

  

1.In most cases prognosis is good if follow-up and preventative measures are in place

2.Prognosis may be worse if: 

o Pt has severe persistent underlying condition, such as: 

 Liver disease with portal hypertension

 Coagulopathy

 Congenital vascular malformation

o Cause of bleeding has left damage that increases risk for future 

complications, such as: 

 Caustic ingestion

 Pill esophagitis or ulcers

                    Risk factors

o Medications (NSAIDs, corticosteroids, anticoagulants, etc.)

o Bleeding diathesis / disorder

o Chronic liver disease

o Major illness / PICU patient

o Genetic, age, and environmental factors related to the conditions causing the 

bleeding

                    Endoscopy

 Dx test of choice for upper GI bleed

 Done only after acute volume resuscitation has been initiated

 Diagnostic upper endoscopy indicated: 

 For active, persistent, or recurrent bleeding

 For hemodynamically significant hemorrhage

 To distinguish between variceal and non-variceal bleeding

 When sampling of tissue/fluid is indicated

                   Prevention

1.Related to patient's underlying condition and cause for bleeding

2.Avoid risk factors for bleeding including medications, when possible

      

               Acute Treatment

1.ABCs, assess hemodynamic stability

2.Rehydration with NS prn 

o If hypotensive, 20 ml/kg bolus until BP improves 

o May repeat x2

o If still low BP, consider transfusion

3.Resuscitation 

o Volume expansion

o Oxygen

o Foley catheter

o Central venous line

o Blood transfusion

o Replacement of clotting components as needed / indicated (platelets, vitamin

                  Medical therapy

.

o H2 blockers 

 Ranitidine 

 Neonates: 2 mg/kg/d div q8hr IV

 Infants/children: 2-4 mg/kg/d IV div q6-8h

 Continuous infusion: give daily IV dose over 24 h

 Cimetidine

 Neonates (<28 do): 5-20 mg/kg/d div q8-12hr IV/IM/PO

 Infants/children: 10-20 mg/kg/d div q6-12hr IV/IM/PO

 Famotidine

 0.25 mg/kg IV q12hr OR

 0.5 mg/kg PO qHS OR

 0.5 mg/kg/d div q12hr PO 

 May prevent secretion of acid, though it may not be helpful in 

controlling ulcer bleeding

           Thank you.....