Critical Care Aspects of Alcohol Abuse

Ibrahim Al-Sanouri MD; Matthew Dikin MD; Ayman O. Soubani MD

Disclosures

South Med J. 2005;98(3):372-381. 

In This Article

Gastrointestinal Complication

Upper gastrointestinal bleeding

Alcoholics with cirrhosis or portal hypertension are at a considerable risk of development of upper gastrointestinal (UGI) bleeding. Causes of UGI bleeding are alcohol-induced gastric mucosal injury and, more commonly, esophageal or gastric varices.

Major hemorrhage from gastritis is rare,[71] and it virtually never leads to life-threatening bleeding or transfusion requirements.[72,73]

Varices develop in 12 to 77% of patients with alcohol-related liver cirrhosis, and they are encountered as the most common cause of UGI bleeding in alcoholics.[74] Fortunately, only one third of these patients bleed from their varices, with an acute mortality rate of 15 to 40% that reaches up to 80% over 1 to 4 years of follow-up.[75]

Patients with esophageal variceal bleeding usually present with hematemesis with or without melena. Often, on physical examination, patients have stigmata of liver disease including ascites, hepatic encephalopathy, jaundice, spider angiomas, and coagulopathy. Treatment is directed to hemodynamic stability and cessation of the UGI hemorrhage. Fluid and blood resuscitation is immediately instituted if there are signs of shock. Two large-bore intravenous lines should be placed and crystalloid infused. Blood products are given if there is evidence of coagulopathy, thrombocytopenia, and blood volume deficit. If there is an alteration of mental status from hepatic encephalopathy, airway protection with endotracheal intubation should be considered. Resuscitation goals include adequate urine output, stable blood pressure, adequate peripheral perfusion, and hematocrit range of 25 to 30%. Recent data have shown that patients with cirrhosis and UGI bleeding should receive somatostatin (250 µg bolus followed by infusion of 250 µg/h) or its long-acting analog, octreotide (50 µg bolus and infusion of 25 to 50 µg/h), for up to 5 days.[76] These infusions decrease portal and intravariceal pressures by blocking the release of vasodilator substances such as glucagon. Endoscopy is best performed once the patient is stabilized, active bleeding is stopped, and treatment to reverse coagulopathy is initiated. Band ligation has proven superior to sclerotherapy for esophageal varices, but both have been shown to decrease rebleeding and the need for blood transfusions when used in combination with somatostatin or octreotide.[77]

Gastric variceal bleeding is often more difficult to treat. Standard sclerotherapy has been rendered relatively ineffective in achieving control of active hemorrhage.[78] Newer sclerosing agents, including cyanoacrylate and thrombin, are currently being investigated as adjunctive agents. Transhepatic portal systemic shunts have been used extensively for prevention of recurrent UGI bleeding in cirrhotic patients.[79] Cirrhotic patients with UGI bleeding have an increased risk of developing a bacterial infection. Current data suggest that 22% of MICU patients have an infection by 2 days and 35 to 66% at 7 to 14 days.[80] Infection has been shown to correlate with failure to control bleeding because of alterations in homeostasis.[81] Prophylactic antibiotics have been shown to decrease bacteremia and spontaneous bacterial peritonitis and increase overall survival compared with those treated without antibiotics.[81] Multiple antibiotic regimens have been studied, but the current recommendation for prophylaxis is to use an intravenous fluoroquinolone during active UGI bleeding, followed by oral treatment for 3 days after bleeding has been controlled.[82]

Acute Necrotizing Pancreatitis

Alcohol abuse is the most common cause of the first episode of acute pancreatitis in Americans and usually occurs after 4 to 7 years of heavy drinking. Acute necrotizing pancreatitis occurs in 20 to 30% of all cases and is the most common reason for treatment in the MICU. It carries a mortality rate of 10% that increases up to 30% if associated with infection.[83]

The pathophysiology of alcoholic pancreatitis is unclear. Acinar cell injury and subsequent leakage of pancreatic enzymes into the interstitium are the main findings. Free radical release from injured acinar cells act as a chemoattractant to neutrophils, and subsequent cytokine release worsens the inflammatory reaction.

Furthermore, necrotic tissue might get infected as the result of bacterial translocation from the colon to the mesenteric lymph nodes, peritoneal fluid, blood, and the pancreas itself.[84] Ethanol has been suggested to cause dysfunction in the sphincter of Oddi, with subsequent biliary, duodenal, and pancreatic secretion reflux.[85] Ethanol may also stimulate pancreatic enzyme release and thus enhance the inflammatory response.[86] Last, chronic ethanol intake may enhance pancreatic juice, with a higher protein concentration that may plug the small ductules and cause pancreatitis.[87] The clinical manifestations of acute pancreatitis include epigastric pain radiating to the back associated with nausea and vomiting, flank ecchymosis, and signs of hypovolemic or septic shock. Routine laboratory tests include determination of serum amylase and lipase levels. However, the most accurate indicator for acute pancreatitis is serum trypsin level, which is not readily available. Most authorities recommend obtaining abdominal and chest radiographs to exclude bowel obstruction, pancreatic calcifications, free air under the diaphragm, and early signs of pulmonary disease. Ultrasonography of the abdomen is indicated only if concomitant biliary disease is suspected. Computed tomography (CT) scan of the abdomen helps delineate the degree of pancreatic inflammation and any signs of early or delayed complications. Thus, it is indicated in all cases of severe acute pancreatitis and when there is suspicion of infected necrosis.[88] Standard treatment of severe pancreatitis in the MICU setting has not been established. Multiple medical regimens have been proposed, but none have been found to be superior. Aggressive hydration and analgesia are well accepted, as well as the use of H2-antagonists.[88] Placement of a nasogastric tube has not been proven to be a routine therapeutic measure unless there is bowel obstruction on radiography or if there is protracted emesis.[89] Patients should not be fed in the acute stage, especially if there is severe ileus or signs of hypovolemic or septic shock. Enteral feeding preferably beyond the ligament of Treitz may begin within 48 hours in most patients. Routine total parental nutrition is not recommended and has been shown to increase infectious complication.[90]

Empiric use of parental antibiotics in acute necrotizing pancreatitis is recommended whether infection is present or not. Current parental regimens include imipenem-cilastin, cefuroxime, ceftazidime, amikacin, metronidazole, or a fluoroquinolone.[91,92] Furthermore, if there is persistent leukocytosis and lack of improvement, CT-guided needle aspiration of the pancreas is recommended to rule out an infected necrosis of the pancreatic bed.[93,94] Infected pancreatic necrosis is uniformly fatal without intervention.[95] The treatment of choice in these circumstances is open surgical necrosectomy.[96] Other surgical treatments include CT-guided percutaneous drainage and irrigation of the pancreatic bed with multiple large-bore catheters or an endoscopic debridement through transgastric or transduodenal drainage catheter.[97] No controlled trials of these novel surgical treatments have been performed. A biochemical approach to inhibiting pancreatic secretions with agents such as atropine, glucagon, somatostatin, and calcitonin has not been yet established.

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