Acute abdomen


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Acute abdomen

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