Acute abdomen
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Acute abdomen






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Acute abdomen Presentation Transcript

  • 1. Acute Abdomen Dr. Andey Rahman
  • 2. Objective
    • On completion of this lecture you will be able to:
      • Define the acute abdomen.
      • Describe the cause and pathophysiology of the following acute abdominal diseases:
        • Acute appendicitis
        • Intestinal obstruction
        • Acute mesentric ischemia
        • Gastritis, peptic ulcer disease
        • Peritonitis
        • Acute pancreatitis
        • Acute cholangitis
        • Cholecystitis
      • Identify and describe the symptoms, signs, clinical course and laboratory and x-ray findings for the acute abdominal diseases listed under Objective 2.
      • Identify the clinical features that help to distinguish the surgical from the non-surgical acute abdomen.
      • Construct an approach to evaluation and management of the acute abdomen.
  • 3. Definition
    • Intra-abdominal process causing severe pain and often requiring surgical intervention
    • It is a condition that requires a fairly immediate judgement or decision as to management
    • Identify, diagnosis
  • 4. General causes
    • Inflammatory
      • Bacterial – acute appendicitis
      • Chemical – PGU lead to spillage of gastric content
    • Mechanical – obstructive condition such as; intestinal obstruction, intussesception, adhesion
    • Vascular - mesenteric arterial thrombosis or embolism. When the blood supply is cut off, necrosis of tissue results, with gangrene of the bowel
  • 5. Cont…
  • 6. Acute appendicitis
    • Caused by luminal obstruction of the vermiform appendix, typically by a fecalith
    • Continuous mucus secretion – increase intraluminal pressure – appendicceal vascular insufficiency – bacterial proliferation/inflammation – perforation – peritonitis
  • 7. Clinical feature
    • Early
      • Malaise
      • Indigestion
      • Bowel irregularity
      • Anorexia
    • Periumbilical pain, nausea, vomitting, flank pain, dysuria
    • RIF pain, rebound tenderness, guarding, rovsig sign, psoas sign
  • 8. Diagnosis
    • CLINICAL!!!
    • Alvarado score – aid in diagnosis
    • Investigation – FBC/BUSE/creat/GSH/UFEME/UPT
    • Xray, US
  • 9. Management
    • Appendicectomy – prompt surgical referral
    • NBM
    • Fluid resus/maintainance
    • Antiemetic
    • Analgesia
    • Antibiotics
  • 10. Acute pancreatitis
    • acute inflammatory process of the pancreas that may involve surrounding tissue and remote organ systems
    • mild inflammation to severe extensive pancreatic necrosis and multi-organ failure
    • The specific mechanism that triggers pancreatic inflammation remains unclear
  • 11. Causes
    • Gallstone
    • Alcohol
    • HyperTG
    • ERCP
  • 12. Pathophysiology
    • Unregulated activation of trypsin – activation of digestive enzymes, complement, kinins – antudigestion of pancreas – pancreas injury, inflammation – acinar cells necrosis- multiorgan failure
  • 13. Clinical feature
    • Persistent abdominal pain
      • Epigastric area
      • Radiate to the back
      • Worse in supine, relieved by sitting up with the trunk flexed and knees drawn up
    • Physical findings
      • Fever
      • Tachycardia
      • Hypotension/shock
      • Absent bowel sound
      • Cullen sign, turner sign – uncommon, late indicate retroperitoneal and intra-abdominal hemorrhage and severe necrotizing pancreatitis
      • Hypoxemia, ARDS
  • 14. Cont…
    • Cullen sign
    • Grey-Turner sign
  • 15. Diagnosis
    • Diagnosis of acute pancreatitis is generally made in the presence of two of the following three features;
      • characteristic abdominal pain
      • serum amylase and/or lipase levels three times or more the upper limit of normal
      • characteristic findings of acute pancreatitis on US or CT scan
  • 16. Amylase vs lipase
    • The sensitivity and specificity of amylase level as a diagnostic test depends on the cutoff value
    • Serum amylase concentrations exceeding three times the normal upper limit support the diagnosis in the setting of abdominal pain
    • When the cutoff level is raised to 1000 IU/L (more than three times the upper limit of normal), specificity approaches 95% but sensitivity remains about 61
    • Lipase catalyzes the breakdown of triglycerides into fatty acids and monoglycerides
    • Pancreatic inflammation leads to increased enzyme levels
    • The accuracy of lipase level is better than that of amylase level in the diagnosis of acute pancreatitis, and it is the preferred test when available
    • cutoff activity of 600 IU/L, most studies have reported specificities above 95%, with sensitivities ranging between 55% and 100%
  • 17. Prediction
    • used to determine the severity of acute pancretitis
    • Because the Ranson criteria are applied after 48 hours, criteria are less useful for ED assessment
  • 18. Treatment
  • 19. Acute Cholangitis
    • requires the presence of biliary obstruction and an infected biliary tract
    • Causes of biliary obstruction include choledocholithiasis, biliary tract strictures, stricture of a biliary anastomosis, and compression caused by malignant disease
    • Charcot triad: fever, jaundice, and right upper quadrant pain
    • The Reynolds pentad is altered mental status, shock, fever, jaundice, and abdominal pain
    • ED treatment is aggressive volume replacement, administration of broad-spectrum antibiotics, and consultation for emergency surgical or endoscopic decompression of the biliary tract
  • 20. Cholecystitis
    • inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis
    • Obstruction of cystic duct – distention gallbladder – compromised blood flow and lymphatic drainage – mucosal ischemia and necrosis
  • 21. Clinical feature
    • RUQ pain sometimes radiated to Rt scapula
    • Fever
    • Tachycardia
    • Palpable gallblader
    • Murphy sign/ US Murphy sign
  • 22. Management
    • Analgesic
    • Antibiotic
    • Fluid resus
    • Surgical consultation
  • 23. Intestinal obstruction
    • inability of the intestinal tract to allow for regular passage of food and bowel contents secondary to mechanical obstruction or adynamic ileus
    • Adynamic ileus (paralytic ileus) is more common but is usually self-limiting and does not require surgical intervention.
    • Mechanical obstruction can be caused by either intrinsic or extrinsic factors and generally requires definitive intervention
  • 24. Pathophysiology
    • Intraluminal accumulation of gastric, biliary, and pancreatic secretions
    • the bowel becomes congested and intestinal contents fail to be absorbed
    • combination of decreased absorption, vomiting, and reduced intake leads to volume depletion with hemoconcentration and electrolyte imbalance and ultimately can cause renal failure or shock
    • increase in intraluminal pressure
    • intraluminal pressure exceeds capillary and venous pressure in the bowel wall, absorption and lymphatic drainage decrease, the bowel becomes ischemic, and septicemia and bowel necrosis can develop
  • 25. Clinical feature
    • Abdominal pain
      • Crampy
      • Colicky/intermittent
    • Vomitting
    • No BO, No flatus
    • Abdominal distention
    • Bowel sound - active to absent
  • 26. Management
    • Investigation
      • Blood – FBC/BUSE/GSH/VBG
      • Radiography – AXR, CXR
    • Nasogastric tube is often unnecessary, but could be considered in the presence of severe distention and vomiting
    • Vigorous IV fluid replacement is needed because of loss of absorptive capacity, decreased oral intake, and vomiting
    • Administer preoperative broad-spectrum antibiotics in the ED
    • Surgical referral
  • 27.  
  • 28. PUD & Gastritis
    • acute or chronic inflammation of the gastric mucosa and has various etiologies
    • Dyspepsia is continuous or recurrent upper abdominal pain or discomfort with or without associated symptoms
  • 29. Pathophysiology
    • HCL destroy gastric mucosa
    • Mucus and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production and by enhancing mucosal blood flow
    • The balance between these protective and destructive forces determines whether peptic ulcer disease occurs
    • H. pylori infection or NSAIDs are thought to be the causal agents of peptic ulcer disease in almost all cases
  • 30. Clinical feature
    • Burning epigastric pain
    • pain also may be described as sharp, dull, an ache, or an "empty" or "hungry" feeling
    • Pain may be relieved by ingestion of milk, food, or antacids, presumably due to buffering and/or dilution of acid
    • Pain recurs as the gastric contents empty, and the recurrent pain may classically awaken the patient at night
  • 31. Diagnosis
    • Uncomplicated peptic ulcer disease can be strongly suspected in the presence of a "classic" history, including epigastric burning pain; relief of pain with ingestion of milk, food, or antacids; and night pain accompanied by "benign" physical examination findings, including normal vital signs with or without mild epigastric tenderness
    • The gold standard for diagnosis of peptic ulcer disease is visualization of an ulcer by upper GI endoscopy
  • 32. Investigation
    • To rule out other emergencies
    • ECG
    • CXR
    • Amylase
    • FBC
  • 33. Treatment
    • Goal of treatment is to heal the ulcer while relieving pain and preventing complications and recurrence
    • PPI, H2 receptor antagonist, antacids
    • Eradication of H. Pylori
    • No NSAID
  • 34. Acute Mesentric Ischemia
    • Mesenteric artery occlusion can result from thrombosis or embolism which usually arises from a recent myocardial infarction or atrial fibrillation
    • rare but serious cause of an acute abdomen, characterized by sudden onset of severe diffuse abdominal pain associated with nausea, vomiting, progressive distention, and sometimes bloody diarrhea
    • pain is out of proportion to the physical findings which are minimal at the onset
  • 35. Cont…
    • Initially peristalsis is hyperactive, then gradually diminishes
    • When peristalsis is absent, the bowel wall is usually not viable
    • Signs of peritonitis develop rapidly with distinctly elevated white cell count and elevated temperature
    • X-ray films of the abdomen may reveal wide-spread gas and fluid filled loops of bowel but negative x-ray findings do not exclude this diagnosis
  • 36. AAA
    • An abdominal aortic aneurysm is defined as an aneurysm 3.0 cm in diameter, and repair is considered for an aneurysm 5.0 cm in diameter
    • Clinical feature;
      • Syncope
      • flank, back, or abdominal pain – severe, tearing
      • GI bleeding from an aortoduodenal fistula
      • extremity ischemia from embolization of a thrombus in the aneurysm
      • Shock
      • sudden death
      • Pulsatile mass
  • 37. Cont…
    • Investigation
      • US
      • AXR – calcified aorta
      • CT scan with contrast
  • 38. Treatment