GI Disorders

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GI Disorders
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Upper Gastrointestinal Hemorrhage

• Causes
• Peptic ulceration
• Gastritis/esophagitis NSAIDs/aspirin
• Esophageal varices cirrhosis
• Clinical features
• Hematemesis (vomiting blood)
• Melena (tarry stool)
• Shock
• Epigastric pain/tenderness
• Hepatosplenomegaly
• Anorexia, weight loss, lymph nodes, and
  epigastric mass associated with gastric Ca

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• Investigation
• Blood tests
• Hb may be normal or decreased
• Microcytic, hypochromic anemia suggests previous
  chronic bleeding
• Elevated urea indicates the bleed is upper GI
  rather than lower GI
• Liver function tests and coagulation profile
  assess liver and clotting dysfunction
• Radiology
• Air beneath the diaphragm indicates perforation
  of the viscus
• Gastroscopy can locate and tx the bleed
• Antiography can locate the bleed if gastroscopy
  doesnt
• Exploratory lap is done if bleed is
  life-threatening or you cant find the cause any
  other way

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• General management
• Prophylactic
• Enteral nutrition
• Gastric acid suppression
• Gastric mucosal coating
• General
• Early consult to GI specialist/surgeon
• O2
• NG tube
• Resuscitation
• Plasma expanders
• Blood transfusions
• Fresh frozen plasma/platelets

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Peptic Ulcer

• H2 receptor antagonists or proton pump inhibitors
  should be administered with peptic ulcers and
  gastritisboth speed healing
• Endoscopy with thermal coagulation
  (electrocautery) or injection therapy
  (epinephrine) reduces the bleed
• Surgery is required for large hemorrhages
• Arterial embolization controls the bleeding but
  may cause gastric necrosis

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Esophageal varices

• Sclerotherapy
• Injection of an agent to control the bleed
• Alcohol, ethanolamine
• Tx of choice
• Endoscopic variceal ligation/banding
• Pharmacotherapy
• Vasopressin causes vasoconstriction
• Beta blockers decrease portal HTN
• Balloon tamponade
• Blakemore tube is an NG with ballons on it
• One balloon inflates in the stomach and puts
  pressure on the fundus part to occlude the veins
• Another balloon in the esophagus is inflated
• This is a temporary measure to control massive
  bleeds

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Esophageal varices

• Transjugular intrahepatic portal stent
• A stent is placed in the portal vein
• This decreases portal hypertension and
  decompresses the portal system
• Surgery
• Variceal ligation
• Portocaval shunting

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Lower GI Bleeds

• Causes
• Angiomas
• Carcinoma/polyps
• Upper GI bleeding
• Diverticular dx
• Colitis
• Present with either frank rectal bleeding or
  melena (tarry stool)
• Sigmoidoscopy, colonoscopy are done if OGD
  (gastroscopy) is inconclusive
• Exploratory lab is done if nothing else is
  conclusive

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Lower GI Bleed

• Management
• Most bleeds stop spontaneously but may recur
• General management is the same as for upper GI
  bleeds
• Specific
• Endoscopy electrocoagulation or laser therapy
  can stop the bleeds
• Elective surgery
• Arterial embolization

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Liver Failure

• Primary
• Occurs in previously healthy patients
• Evolves over less than a month and is fatal most
  of the time
• Viral hepatitis and tylenol toxicity are the most
  common causes
• Secondary
• More common than primary
• Occurs when acute illness/stress causes
  decompensation in pre-existing liver dx
  (cirrhosis, hepatitis)
• Acute failure is due to ischemia or toxic damage

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Clinical Features

• Pre-existing chronic liver disease
• Spider nevi
• Palmar erythema
• Ascites
• Metabolic dysfunction
• Hypoglycemia
• Lactic acidosis
• Elevated liver function tests
• Serum aminotransferase
• Increased bilirubin
• Sweet smelling breath (exhaled mercaptans)
• Increased ammonia levels
• Electrolyte disturbances
• Hyponatremia
• Hypokalemia
• Secondary hyperaldosteronism

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Clinical Features

• Synthetic dysfunction
• Hypoalbuminemia
• Clotting factor deficiencies
• Decreased immunity
• Phagocytic dysfunction
• Infections common organisms are staph, strep,
  and gram- rods
• Spontaneous bacterial peritonitis
• Due to splanchnic hypoperfusion which allows
  bacteria to move from inside the bowel to outside
  the bowel infecting the peritoneal cavity
• Fever, abdominal discomfort, and encephalopathy
  are signs/symptoms
• E coli is most common organism

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Clinical Features

• Organ dysfunction
• Respiratory complications
• Pulmonary edema from hypoalbuminemia
• Pneumonia, atelectasis, pulmonary shunting lead
  to hypoxemia
• Renal failure
• Cerebral edema
• Hepatic encephalopathy
• Most common fatal complication
• Toxin-laden blood bypasses the liver and is
  shunted into the systemic circulation
• Precipitated by GI bleed, hypovolemia, renal
  failure, and infection
• Altered mental status, irritability, confusion
• Diagnosed by elevated ammonia levels and/or EEG
  findings

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Management

• General
• Early consult to liver specialist
• Tx hypoglycemia with glucose
• Tx infection with ATB
• Potassium supplements
• H2 blockers/antacids
• Avoid high protein feeds and limit sodium intake
• Cardiorespiratory
• Fluid therapy but avoid pulmonary edema
• Early intubation/ventilation if signs of
  hypoxemia, aspiration risk

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Management

• Ascites
• Treated with potassium-sparing diuretics
• Bleeding
• Fresh frozen plasma
• Cerebral edema
• Hyperventilation
• Mannitol
• Encephalopathy
• Avoid sedation
• Correct precipitating factors
• Specific tx
• Mucomyst for tylenol OD
• Liver transplant
• May work for tylenol OD, but less successful with
  alcohol dx
• 50 of candidates die while waiting for a liver

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Pancreatitis

• Mild cases resolve with analgesia and fluid
  therapy
• Severe cases require greater degree of management
  with about a 25 mortality rate
• Etiology
• Gallstones and alcohol cause 80 of cases
• Ductal obstruction (gallstones) or cytotoxic
  injury (alcohol) cause the pancreas to start
  digesting itself

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Clinical Features

• Severe, persistent, boring epigastric and/or back
  pain
• Nausea, vomiting, low grade fever common
• Tachycardia, hypotension, and shock of fluid loss
  occurs
• Acute lung injury can lead to ARDS
• Two distinct clinical phases
• Early phase (0-14 days)
• Inflammation/mediator release/SIRS
• Large fluid shifts causing shock, ARDS, ARF,
  coagulopathy, fat necrosis, and hypocalcemia
• Late phase (gt14 days)
• Pancreatic necrosis
• Infection
• Pseudocyst/fistula
• Ascites
• Strictures
• Ileus
• Portal vein thrombosis
• diabetes

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Investigation

• Laboratory
• Elevated WBC
• Uremia
• Hypocalcemia
• Hypoglycemia
• Hypoalbuminemia
• Elevated serum amylase
• Elevated serum lipase
• Radiology
• Localized ileus on abdominal x-ray
• Abdominal ultrasound detects gallstones, biliary
  duct dilation, and pancreatic pseudocysts
• CT best shows the pancreas and associated
  complications

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Prognosis

• Mortality is 10 in sterile and 35 in infected
  pancreatitis
• Early deaths (within 14 days) due to SIRS and
  MSOF
• Late deaths usually due to infection
• Scoring systems, such as Apache, can assess the
  severitypancreatic hemorrhage carries the worst
  prognosis
• With MSOF, the more organs that are failing the
  higher the mortality rate

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Management

• Uncomplicated, edematous pancreatitis
• Fluid resuscitation and electrolyte replacement
• Corrects hypovolemia from 3rd spacing and GI loss
• May need inotropes
• Nutrition
• Withhold oral feeding
• NG tube
• Enteric feeding thru NJ tube
• Pain control
• Prophylactic ATB indicated with gallstones
• Stress ulcer prophylaxis
• Early gallstone extraction reduces mortality
  and complications
• Specific meds dont influence the outcome in
  uncomplicated cases

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Severe necrotizing pancreatitis

• Treated like uncomplicated but infected necrosis
  increases mortality rate
• Antibiotics reduce infection and mortality
  ratehigh dose cefuroxime or meropenem
• Surgery
• Infected necrotizing pancreatitis is usually
  fatal without surgical debridement
• Endoscopic debridement with irrigation a bit less
  invasive
• Somatostatin and octreotide improve outcome by
  reducing pancreatic secretions