Acute Abdominal Disorders

Question 1

Acute Pancreatitis

Pathophysiology

Answer 1

• 20% will develop a severe necrotizing form of the disease that is characterized by necrosis, abcess and psuedocyst formation, and multi-organ dysfunction.
• the pancreas secretes trypsinogen, and inactive pro-enzyme that is normally converted into typsin an the duodenum to aid protein digestion
• Activation of trypsinogen and other pancreatic enzymes inside the pancreas initiates an inflammatory process that destroys tissue in and around the pancreas.
• Cell distruction can cause edema, vascular damage, interstitial hemorrhage, and fat necrosis within the pancreas, but can extend to other tissues and organs
• acute pancreatitis occurs when pancreatic enzymes are activated prematures causing autodigestion of the pancreas
  
  • obstuction of the pancreatic duct system, injury or infection involving acinar cells within the pancreas, and defensive intracellular transport of proteolytic enzymes are three possible mechanisms
• once activated, trypsin starts a domino effect on other pancreatic enzymes
  
  • pancreatic tissue damage activates the inflammatory response leading to extravascular movement of serum albumin, third-spacing, and pancreatic edema.
  • the cellular release of inflammatory mediators (or cytokines) contributes to the development of shock, acute respiratory distress syndrome, acute tubular necrosis, and multisystem organ dysfunction

Question 2

Acute Pancreatitis

Triggers

Answer 2

• biliary disease
• alcohol consumption
• abdominal trauma
• hypertriglyceridemia
• medications
• surgery
• post-ERCP (endoscopic retrograde cholongiopancreatography)
• idopathic

Question 3

Acute Pancreatitis

Clinical Manifestations

Answer 3

• severe upper quadrant abdominal pain - can radiate
• pain described as sudden, knifelike, and twisting
• pain typically worsens if the patient lies down, eats a fatty meal, or drinks alcohol
  
  • pain caused by one or a combination of the following:
    
    • edema and distention of the pancreatic capsule
    • pancreatic enzymes causing a chemical-like burn to the peritoneum
    • release of kinin peptides
    • obstruction of the biliary tree\
• nausea and vomiting
• abdominal distension and guarding
• tachycardia
• hypotension
• jaundice
• low-grade fever
• decreased breath sounds
• lab findings include:
  
  • increased leukocytes
  • increase amylase
  • increased lipase
  • increased alkaline phosphate with billiary obstruction
  • increased aminotransferases (ALT, AST)
  • increased glucose
  • decreased calcium
• CT scans done to monitor progression and improvement of pancreatitis

Question 4

Acute Pancreatitis

Complications

Answer 4

1. Abcess or pseudocyst formation
   
   • a collection of fluid, often with high levels of pancreatic enzymes, enclosed in a non-epithelialized wall
   • may become infected or enlarged, compressing on other structures or blocking a duct
   • may also erode surrounding blood vessels causing a hemorrhage
   • abcess/pseudocyst may rupture causing wide-spread infection
2. Intravascular volume depletion
   
   • hypotension and possible relative hypovolemic shock due to the movement of fluid from the intravascular space into the abdominal cavity
   • relative hypovolemia worsens as sepsis progresses and capillary leakage becomes systemic
3. Acute Renal Failure
   
   • hypovolemia and persistent hypotension may lead to renal failure as blood flow to the kidneys decreases
   • microemboli in sepsis may occlude renal vasculature and result in acute tubular necrosis
4. Respiratory Insufficiency
   
   • enxyme leakage into the pleural space and inflammation may lead to pleural effusions
   • direct damage to the lungs by pancreatic enzymes may occur thus decreasing surfactant levels and leading to alveolar instability
   • atelectasis with alveolar collapse may result from abdominal distension and/or pain preventing deep inspiration
5. Electrolyte Abnormalities
   
   • hypocalcemia
     
     • decreased oral intake
     • altered absorption secondary to a decrease in the enzymes that facilitate calcium transport (trypsin inactivates parathyroid hormone)
     • leaking of albumin from intravascular space to peritoneum (majority of calcium is bound to albumin)
     • precipitation of serum calcium in areas of fat necrosis
   • hypokalemia/hyperkalemia
     
     • decreased potassium with vomiting
     • elevated potassium with renal failure
   • hyperglycemia
     
     • glucose will be elevated in the pancreatic endocrine function is impaired
     • decreased insulin release increases glucagon release and increases output of adrenal glucocorticosteroids and catecholamines

Question 5

Acute Pancreatitis

Management

Answer 5

1. Adequate Nutritional Support
   
   • traditional methods were designed to “reset the pancreas” by making the patients NPO and administering TPN. TPN, however, has been associated with catheter related sepsis and hyperglycemia
   • now early enteral NJ feeding (within 48 hours) helps promote a positive nitrogen balance, maintains the integrity of the GI mucosa (thereby decreasing bacterial translocation) and lowers the incidence of infection
2. Hemodynamic Stability
   
   • aggressive fluid resuscitation with crystalloid or colloids
   • fluid status can be monitored clinically or via central venous monitoring
   • a septic presentation may require additional vasoactive medications to increase systemic vascular resistance
3. Pain Control
   
   • Parenterally administered narcotics are indicated to relieve the debilitating pain associated with pancreatitis
   • morphine is prefered over meperidine because it has a longer duration and no toxic metabolites
   • surgical debridement
   • endoscopic removal of gallstones via ECRP if duct blocked
   • prophylactic antibiotic therapy in cases of severe pancreatitis is controversial
     *

Question 6

Fulminant Hepatic Failure

Pathology

Answer 6

• medical emergency that is best described as severe acute liver failure (hepatocellular necrosis) accompanied by coagulopathy and hepatic encephalopathy
• mortality rate of 75-80% and generally occurs in patients without pre-existing liver disease
• development of acute liver failure over 1 to 3 weeks, followed by the developments of hepatic encephalopathy within 8 weeks in a patient with a previously healthy liver
• the underlying cause is massive necrosis of the hepatocytes
• impaired bilirubin conjugation, decreased production of clotting factors, depressed glucose synthesis, and decreased lactate clearance
  
  • results in jaundice, coagulopathies, hypoglycemia, and metabolic acidosis
• hypoalbuminemia, fluid and electrolyte imbalances, acute portal hypertension
• hepatic encephalopathy is thought to result from failure of the liver to detoxify various substances and may be worsened by metabolic and electrolyte imbalances
• may also experience cerebral edema, dysrhythmias, acute respiratory failure, and acute renal failure
  
  • hepatorenal syndrome - severe liver failure alters blood flow to the kidney resulting in intense intrarenal vasoconstriction and thus oliguria and sodium retention

Question 7

Fulminant Hepatic Failure

Signs and Symptoms

Answer 7

• headache
• hyperventilation
• jaundice
• personality changes
• palmary erythema
• spider nevi
• petechiae
• bruises
• bleeding
• edema

Question 8

Fulminant Hepatic Failure

Assessment and Diagnosis

Answer 8

• asterixis - the involuntary downward flapping of the hands when the patient is asked to maintain extension of the arms and dorsiflexion of the wrists - hepatic encephalopathy
• elevated serum
  
  • bilirubin
  • AST
  • Alkaline phosphate
  • ammonia
  • PT
  • fibrin
• decreased serum
  
  • albumin
  • plasmin
  • plasminogen
  • platelets
• respiratory alkalosis and/or metabolic acidosis
• hypoglycemia
• hypokalemia
• hyponatremia

Question 9

Staging of Hepatic Encephalopathy

Answer 9

Grade 1 - mild confusion, euphoria, anxiety, shortened attention span, slurred speech, abssent-mild asterixis, normal EEG

Grade 2 - lethargy, personality changes, inappropriate behaviour, confusion, marked asterixis, abnormal EEG

Grade 3 - stuporous, incoherent speech, gross disorientation, asterixis remains

Grade 4 - coma, asterixis absent

Question 10

Fulminant Hepatic Failure

Management

Answer 10

• management of symptoms and prevention of multisystem complications
• intracranial pressure monitoring is required to effectively manage cerebral edema
  
  • mannitol may be used to pull intracellular water to the intravascular compartment for excretion
• ammonia levels are treated with lactulose or antibiotics by enchancing the removal of nitrogenous wastes
  
  • lactulose inhibis bacterial growth and ammonia production through alteration of intestinal pH
  • antibiotics such as amoxicillin or rifamixin reduce the bacteria flora in the intestine responsible for protein breakdown
• coagulopathy is managed with the administration of fresh frozen plasma to replace clotting factors along with vitamin K and platelets
• CRRT is used in the case of acute renal failure