Upper GI tract bleed
 Upper GI bleed presents with
hematemesis
 Hematemesis means vomiting of blood
 The appearance of hematemesis
resembles coffee grounds
 It indicates bleeding from upper GI
usually from esophagus, stomach and
duodenum above ligament of treitz
 Conditions which cause hematemesis can
also cause melena
Causes of Upper GI bleed
 Peptic ulcer
 Esophageal varices
 Erosive gastritis
 Esophagitis
 Mallory weiss syndrome
 Carcinoma stomach
 Hereditary hemorrhagic telengeictasia
 Bleeding disorders
Peptic ulcer
 It means ulcers in those parts of the gut
which are exposed to acid.
 Common sites are duodenum , stomach and
can also occur in lower esophagus.
 Causes:
 Increase acid secretion(duodenal ulcer)
 Decrease mucosal resistance(gastric ulcer)
 NSAIDs ingestion
 H.Pylori infection
 Zollinger Ellison syndrome (uncommon)
 Peptic ulcer pain is felt in the epigastrium and is well
localized. Patient points with one finger to the site of
pain- the ‘pointing sign’-
 Duodenal ulcer
 Occurs in the 1st part of duodenum.
 Symptoms include
 Pain epigastrium aggravated by empty
stomach(hunger pain), relieved by food and antacids
 Nocturnal pains occur
 Pain in the morning is not due to peptic ulcer
 History of periodicity may be present.
 Signs
 Localized tenderness in the epigastrium
Investigation
 Barium meal shows duodenal
deformity/ulcer crater.
 Endoscopy confirms ulcer presence.
Gastric ulcer
 Symptoms
 Relation of pain to meals and timings is variable
 May be relieved or aggravated by food
 Nocturnal pain is uncommon
 Signs
 Epigastric tenderness
 Investigation
 Barium meal shows ulcer crater
 Endoscopy confirms
 Every gastric ulcer must be biopsied to exclude
malignancy
Treatment
 1st line therapy includes
 PPI ,Antibiotics( clarithromycin and amoxicillin)
 2nd line therapy includes quadruple therapy
 PPI ,Antibiotics(clarithromycin and amoxicillin)
bismuth
 For long term ulcer use only PPI
 Complications of peptic ulcer
 Bleeding
 Perforation
 Chronicity
 Gastric outlet obstruction
Esophageal varices
 These are dilated tortuous veins in the
esophagus
 These are communication channels
between the portal and systemic venous
systems and become dilated in portal
hypertension
 Most common cause of portal
hypertension is hepatic cirrhosis
 Symptoms
 Hematemesis is massive and recurrent
 Distention of abdomen due to ascites
 History of jaundice
 Hematemesis may be the first manifestation of
cirrhosis
 Signs
 Jaundice
 Dependent edema
 Gynecomastia and testicular atrophy
 Palmar erythema, dupuytren’ contracture, Spider
angiomas, parotid swelling (common in alcoholic
cirrhosis)
 Veins of abdominal wall may be prominent
 Liver may be enlarged/shrunken
 Palpable spleen
 Ascites in advanced disease
Investigation
 Endoscopy
treatment
 I.V fluid replacement with 0.9% saline
 Vasopressor
 Prophylactic antibiotics (cephalosporin)
 Variceal band ligation
 PPI
 Lactulose
Erosive gastritis
 In addition to inflammation of stomach, there are multiple
mucosal erosions and petechiae.
 Causes
 A. drugs
 Aspirin and NSAIDS
 Theophylline
 Potassium chloride
 B. stress
 Head injury
 Shock
 Trauma
 Burns
 Sepsis
 Hepatic encephalopathy
Symptoms
 Hematemesis with or without epigastric
pain
 h/o drug intake
Signs
 Tenderness in the epigastrium
Investigation
 Endoscopy
Esophagitis
 Abnormal reflux of gastric contents into
lower esophagus is the most common
cause of esophagitis
 Smokers and obese are more prone
Symptoms
 Retrosternal burning and pain(heart
burn), increases on bending forward or
lying flat
 Relieved by antacids
 History of regurgitation
 Water brash
 Bitter taste in the morning
 Persistent dysphagia indicates peptic stricture
 Aspiration of regurgitant material cause
laryngitis and aspiration pneumonia
 Signs
 Pallor may occur
 Investigation
 Barium swallow demonstrates reflux
 Esophageal ulcers may be seen
 Endoscopy shows
 Hyperemic mucosa with or without ulcers
 If mucosa looks normal , biopsy will
demonstrate microscopic inflammation
 PH monitoring <4 for >4% of time is
suggestive of acid reflux
 Treatment
 Lifestyle modification
 PPI
 H2 antagonists
 Prokinetic drugs
Mallory weiss syndrome
 Repeated retching and vomiting can cause
vertical mucosal tear at gastroesophageal
junction
Symptoms
 H/o repeated vomiting and retching
before hematemesis
Sign
 Epigastric tenderness
Investigation
 Endoscopy
Carcinoma stomach
 Occurs after age of 40 years
 Risks include
 Pernicious anemia
 Partial gastrectomy
 Gastroenterostomy
 Symptoms
 Loss of appetite, nausea and discomfort after meal
 Vague epigastric pain and feeling of distention after
meals
 Early satiety is common
 Persistent vomiting if gastric outlet obstruction
 Marked loss of weight
 Signs
 Pallor
 Epigastric mass may be palpable
 In later stages, patient may have enlarged scalene lymph
nodes, nodular liver and ascites due to metastases
 Investigation
 Iron deficiency anemia
 Barium meal shows filling defect
 Endoscopy shows mass/ulcer
 Biopsy confirms diagnosis. In case of ulcer, six biopsies
should be taken
 Treatment
 Gastrectomy (partial and complete)
 Palliative treatment
Hereditary hemorrhagic
telengeiectasis
 It is an autosomal dominant disease.
 Bleeding occurs from multiple
telangiectasias which consists of localized
collection of non-contractile capillaries.
Symptoms
 Recurrent
hematemesis/epistaxsis/hemoptysis
 Sites of telangiectasias
 Face
 Hands
 Mucous membranes of nose, oral cavity
and GIT
Investigation
 Telengiectasia may be seen in gastric
mucosa on Gastroscopy
Bleeeding disorders
 Causes
 A. Defects of blood vessels:
 Vascular purpura
 Hereditary hemorrhagic telengiectasia
 B. Platelet disorders
 Thrombocytopenia
 Thrombocythemia
 Thromboasthenia
 C. Clotting disorders
 Hereditary
 Hemophilia
 Christmas disease
 Von willebrand disease
 Acquired
 Vitamin K deficiency
 Oral anticoagulant therapy
 Advanced liver disease
 D. Consumption coagulopathy
 DIC
Basic investigations
 Full blood count show anemia
 Urea and electrolytes :elevated urea with
normal creatinine concentration implies
severe bleeding
 Liver function tests may show evidence of
chronic liver disease
 Prothrombin time shows bleeding
disorders and liver synthetic dysfunctions
Management of upper GI bleeding
 Intravenous access using one large bore cannula
 Initial clinical assessment
 Define circulatory status
 Seek evidence of liver disease
 Identify other comorbidity
 Resuscitation with crystalloids or transfusion in severe
bleeding
 Ventilation with oxygen mask
 Monitoring of B.P and urinary output
 Endoscopy should be performed within 24 hours. It is used
in treatment of bleeding from peptic ulcer using injection of
epinephrine and thermal clips.in varicial bleeding band
ligation is also done endoscopically.
 Surgery
History taking related to GI
bleeding
 Duration
 Episodes of hematemesis
 Quantity
 Color(coffee ground appearance)
 Blood in stools (maroon colored stools can be
present in acute severe upper GI bleeding)
 History of jaundice(cirrhosis)
 History of epigastric pain (peptic ulcer,
esophagitis, erosive gastritis)
 Weight loss (carcinoma stomach)
Signs in upper GI bleeding
 Anemia
 Epigastric tenderness
 Ascites
 Hepatomegaly and spleenomegaly
 Jaundice
 Palmar erythema ,dupuytren contracture,
Spider angiomas ,parotid swelling in alcoholic cirrhosis
 Gynecomastia and testicular atrophy
 Prominent abdominal veins
 Dependent edema
 Abdominal mass
 Palpable scalene, paraumblical , virchow’ lymph nodes
Thanks

Upper gi tract bleed

  • 1.
  • 2.
     Upper GIbleed presents with hematemesis  Hematemesis means vomiting of blood  The appearance of hematemesis resembles coffee grounds  It indicates bleeding from upper GI usually from esophagus, stomach and duodenum above ligament of treitz  Conditions which cause hematemesis can also cause melena
  • 3.
    Causes of UpperGI bleed  Peptic ulcer  Esophageal varices  Erosive gastritis  Esophagitis  Mallory weiss syndrome  Carcinoma stomach  Hereditary hemorrhagic telengeictasia  Bleeding disorders
  • 4.
    Peptic ulcer  Itmeans ulcers in those parts of the gut which are exposed to acid.  Common sites are duodenum , stomach and can also occur in lower esophagus.  Causes:  Increase acid secretion(duodenal ulcer)  Decrease mucosal resistance(gastric ulcer)  NSAIDs ingestion  H.Pylori infection  Zollinger Ellison syndrome (uncommon)
  • 5.
     Peptic ulcerpain is felt in the epigastrium and is well localized. Patient points with one finger to the site of pain- the ‘pointing sign’-  Duodenal ulcer  Occurs in the 1st part of duodenum.  Symptoms include  Pain epigastrium aggravated by empty stomach(hunger pain), relieved by food and antacids  Nocturnal pains occur  Pain in the morning is not due to peptic ulcer  History of periodicity may be present.  Signs  Localized tenderness in the epigastrium
  • 6.
    Investigation  Barium mealshows duodenal deformity/ulcer crater.  Endoscopy confirms ulcer presence.
  • 7.
    Gastric ulcer  Symptoms Relation of pain to meals and timings is variable  May be relieved or aggravated by food  Nocturnal pain is uncommon  Signs  Epigastric tenderness  Investigation  Barium meal shows ulcer crater  Endoscopy confirms  Every gastric ulcer must be biopsied to exclude malignancy
  • 8.
    Treatment  1st linetherapy includes  PPI ,Antibiotics( clarithromycin and amoxicillin)  2nd line therapy includes quadruple therapy  PPI ,Antibiotics(clarithromycin and amoxicillin) bismuth  For long term ulcer use only PPI  Complications of peptic ulcer  Bleeding  Perforation  Chronicity  Gastric outlet obstruction
  • 9.
    Esophageal varices  Theseare dilated tortuous veins in the esophagus  These are communication channels between the portal and systemic venous systems and become dilated in portal hypertension  Most common cause of portal hypertension is hepatic cirrhosis
  • 10.
     Symptoms  Hematemesisis massive and recurrent  Distention of abdomen due to ascites  History of jaundice  Hematemesis may be the first manifestation of cirrhosis  Signs  Jaundice  Dependent edema  Gynecomastia and testicular atrophy  Palmar erythema, dupuytren’ contracture, Spider angiomas, parotid swelling (common in alcoholic cirrhosis)
  • 11.
     Veins ofabdominal wall may be prominent  Liver may be enlarged/shrunken  Palpable spleen  Ascites in advanced disease Investigation  Endoscopy
  • 12.
    treatment  I.V fluidreplacement with 0.9% saline  Vasopressor  Prophylactic antibiotics (cephalosporin)  Variceal band ligation  PPI  Lactulose
  • 13.
    Erosive gastritis  Inaddition to inflammation of stomach, there are multiple mucosal erosions and petechiae.  Causes  A. drugs  Aspirin and NSAIDS  Theophylline  Potassium chloride  B. stress  Head injury  Shock  Trauma  Burns  Sepsis  Hepatic encephalopathy
  • 14.
    Symptoms  Hematemesis withor without epigastric pain  h/o drug intake Signs  Tenderness in the epigastrium Investigation  Endoscopy
  • 15.
    Esophagitis  Abnormal refluxof gastric contents into lower esophagus is the most common cause of esophagitis  Smokers and obese are more prone Symptoms  Retrosternal burning and pain(heart burn), increases on bending forward or lying flat  Relieved by antacids
  • 16.
     History ofregurgitation  Water brash  Bitter taste in the morning  Persistent dysphagia indicates peptic stricture  Aspiration of regurgitant material cause laryngitis and aspiration pneumonia  Signs  Pallor may occur  Investigation  Barium swallow demonstrates reflux  Esophageal ulcers may be seen
  • 17.
     Endoscopy shows Hyperemic mucosa with or without ulcers  If mucosa looks normal , biopsy will demonstrate microscopic inflammation  PH monitoring <4 for >4% of time is suggestive of acid reflux  Treatment  Lifestyle modification  PPI  H2 antagonists  Prokinetic drugs
  • 18.
    Mallory weiss syndrome Repeated retching and vomiting can cause vertical mucosal tear at gastroesophageal junction Symptoms  H/o repeated vomiting and retching before hematemesis
  • 19.
  • 20.
    Carcinoma stomach  Occursafter age of 40 years  Risks include  Pernicious anemia  Partial gastrectomy  Gastroenterostomy  Symptoms  Loss of appetite, nausea and discomfort after meal  Vague epigastric pain and feeling of distention after meals  Early satiety is common  Persistent vomiting if gastric outlet obstruction  Marked loss of weight
  • 21.
     Signs  Pallor Epigastric mass may be palpable  In later stages, patient may have enlarged scalene lymph nodes, nodular liver and ascites due to metastases  Investigation  Iron deficiency anemia  Barium meal shows filling defect  Endoscopy shows mass/ulcer  Biopsy confirms diagnosis. In case of ulcer, six biopsies should be taken  Treatment  Gastrectomy (partial and complete)  Palliative treatment
  • 22.
    Hereditary hemorrhagic telengeiectasis  Itis an autosomal dominant disease.  Bleeding occurs from multiple telangiectasias which consists of localized collection of non-contractile capillaries. Symptoms  Recurrent hematemesis/epistaxsis/hemoptysis
  • 23.
     Sites oftelangiectasias  Face  Hands  Mucous membranes of nose, oral cavity and GIT Investigation  Telengiectasia may be seen in gastric mucosa on Gastroscopy
  • 24.
    Bleeeding disorders  Causes A. Defects of blood vessels:  Vascular purpura  Hereditary hemorrhagic telengiectasia  B. Platelet disorders  Thrombocytopenia  Thrombocythemia  Thromboasthenia
  • 25.
     C. Clottingdisorders  Hereditary  Hemophilia  Christmas disease  Von willebrand disease  Acquired  Vitamin K deficiency  Oral anticoagulant therapy  Advanced liver disease  D. Consumption coagulopathy  DIC
  • 26.
    Basic investigations  Fullblood count show anemia  Urea and electrolytes :elevated urea with normal creatinine concentration implies severe bleeding  Liver function tests may show evidence of chronic liver disease  Prothrombin time shows bleeding disorders and liver synthetic dysfunctions
  • 27.
    Management of upperGI bleeding  Intravenous access using one large bore cannula  Initial clinical assessment  Define circulatory status  Seek evidence of liver disease  Identify other comorbidity  Resuscitation with crystalloids or transfusion in severe bleeding  Ventilation with oxygen mask  Monitoring of B.P and urinary output  Endoscopy should be performed within 24 hours. It is used in treatment of bleeding from peptic ulcer using injection of epinephrine and thermal clips.in varicial bleeding band ligation is also done endoscopically.  Surgery
  • 28.
    History taking relatedto GI bleeding  Duration  Episodes of hematemesis  Quantity  Color(coffee ground appearance)  Blood in stools (maroon colored stools can be present in acute severe upper GI bleeding)  History of jaundice(cirrhosis)  History of epigastric pain (peptic ulcer, esophagitis, erosive gastritis)  Weight loss (carcinoma stomach)
  • 29.
    Signs in upperGI bleeding  Anemia  Epigastric tenderness  Ascites  Hepatomegaly and spleenomegaly  Jaundice  Palmar erythema ,dupuytren contracture, Spider angiomas ,parotid swelling in alcoholic cirrhosis  Gynecomastia and testicular atrophy  Prominent abdominal veins  Dependent edema  Abdominal mass  Palpable scalene, paraumblical , virchow’ lymph nodes
  • 30.