Printer Friendly

Critical care aspects of alcohol abuse.

The authors reviewed MEDLINE and references of major articles in the published literature over the last 30 years regarding the complications of alcohol abuse and discuss the critical care aspects of alcohol abuse. This article discusses the severe medical conditions associated with alcohol abuse that lead to admission to the medical intensive care unit. The clinical manifestations, pathophysiology, diagnostic studies, and management of these conditions are discussed in detail.

Key Words: alcohol abuse, critical care, delirium tremens, liver disease, upper gastrointestinal bleeding, Wernicke encephalopathy, withdrawal


Alcohol abuse is defined as the regular and excessive use of alcohol that is associated with concomitant physical, emotional, and social problems. During the 20th century, alcohol abuse has emerged as a major problem with global health implications. In Westernized countries, more than 50% of adults can be classified as alcohol consumers. For most of these people, drinking is a safe, pleasurable experience with minimal health consequences. However, about 10% of alcohol consumers will at some point experience serious health problems related to their drinking habit. (1) Although difficult to accurately quantify, in the United States, approximately 11 to 15 million people report heavy alcohol intake. (2,3) The costs of medical complications related to alcohol abuse in the United States are also astonishing, and are estimated to be nearly $100 billion per year. (2,3) Moreover, tobacco and alcohol account for approximately three quarters of the substance abuse-related intensive care admissions and costs. Similar statistics are reported in other parts of the world. (4)

Alcohol-related medical problems in the medical intensive care unit (MICU) involve almost every system, including the neurologic, respiratory, gastrointestinal, cardiovascular, and renal systems (Table 1). The frequency of adult surgical and medical ICU admissions related to substance abuse was determined at a large community trauma and tertiary referral hospital. It was found that 9% of ICU admissions were alcohol related, generating 13% of costs. It was also noted that ICU admissions in patients with a history of alcohol abuse were longer and more costly than admissions not associated with alcohol abuse. (5)

This review will discuss the alcohol emergencies that require prompt attention, as most of these complications are reversible if they are recognized early and treated properly.

Neurologic Complications

Alcohol withdrawal syndrome

Alcohol withdrawal syndrome (AWS) consists of a spectrum of clinical manifestations that vary in severity and duration upon cessation of alcohol intake in the alcohol-dependent patient. (6) Presentations to the MICU are part of a clinical continuum, but the sequence of events may be inconsistent, and is dependent on the degree of alcohol abuse. There are four stages of alcohol withdrawal. The first stage is autonomic hyperactivity, in which clinical symptoms appear within hours of the last drink and peak within 24 to 48 hours. There is usually a clear sensorium, but this is often accompanied by tremulousness, sweating, anxiety or agitation, insomnia, and nausea and vomiting. This stage is secondary to sympathetic outflow, documented by increased circulating catecholamine levels in the urine, serum, and the cerebrospinal fluid. (7,8)

Most symptoms resolve within 24 to 36 hours, but approximately 25% of patients progress to a more severe stage. (9) The second stage is hallucinations, which are usually visual and occur in one quarter of all patients presenting with alcohol withdrawal. (10) They occur within 8 to 48 hours after a decrease in alcohol intake and may last from 1 to 6 days. (10,11) The third stage is neuronal excitation, which is accompanied by seizure activity that occurs in up to 10% of patients (9) and within 12 to 48 hours of abstinence or decreased alcohol intake. (12) The seizures are usually single, short, and generalized tonic-clonic. Importantly, status epilepsy lasting more than 6 hours is suggestive of another underlying neurologic disorder such as idiopathic epilepsy, trauma, or other toxic-metabolic causes. (13) The fourth stage is delirium tremens. This occurs in up to 5% of patients and usually begins at 48 to 72 hours but may be delayed up to 4 to 5 days. (14,15) Approximately 30% of alcoholics with seizures progress to this stage. (15) Delirium tremens is characterized by disorientation, confusion, impaired attention, pronounced autonomic hyperactivity, and visual and auditory hallucinations. If left untreated, mortality rates may reach 15% (14,16); death is usually due to cardiovascular or respiratory collapse. (6) In an effort to objectively assess the severity of AWS, a scale called the Clinical Institute Withdrawal Assessment for Alcohol Scale was developed. (17) This scale is a 10-step assessment (scored from 0 to 67 points) of signs and symptoms of AWS. The initial score can be administered upon admission to the hospital and repeated hourly thereafter for signs of progression. Patients with a score of greater than 20 should be transferred to the MICU immediately, with the goal of reducing their score to less than 10 within the first 24 hours. (17)

The pathophysiology of AWS is not well known. There are various interactions between neurotransmitters and neuromodulators that contribute to this condition. One of the most widely accepted theories is the upregulation of cyclic adenosine 3', 5'-monophosphate that occurs in certain regions of the brain, including the locus ceruleus, nucleus accumbens, and the ventral tegmental area. (18) This receptor upregulation represents a physiologic dependence. With removal of alcohol in acute withdrawal, the cyclic adenosine 3', 5'-monophosphate pathway "overshoots," and the clinical signs of withdrawal become evident. (19) A "kindling phenomenon" may occur whereby patients may become sensitized to this upregulation and subsequent withdrawals become progressively more severe. (20)

The diagnosis of AWS is initially made by a history of heavy drinking. The well-established CAGE (cut down, annoyed, guilty, eye-opener) questionnaire has been shown to correlate with the Diagnostic and Statistical Manual criteria for alcohol dependence (21,22) but has limited utility in the MICU, since many patients are poorly responsive. In addition, the blood-alcohol concentration is often negative in chronic alcoholics. (23) Conventional markers for the detection of chronic alcohol abuse such as the mean corpuscular volume, the [gamma]-glutamyl-transferase, the aspartate aminotransferase, and the alanine transferase are reported to be neither sensitive nor specific. (24) In more recent studies, an elevation in carbohydrate-deficient transferrin level was shown to be a more sensitive and specific biologic marker for detecting alcohol abuse. (25)

Treatment of AWS is challenging and varies among clinicians. Goals of therapy are to alleviate the symptoms, prevent further progression, treat underlying comorbidities, and plan for long-term rehabilitation. (26) Treatment should be started promptly, with intensive care monitoring, intravenous access, hydration, and parental thiamine with dextrose bolus instituted immediately. If the patient has an altered mental status, supplemental oxygen and airway protection is needed. Endotracheal intubation may be necessary in the presence of seizures or risk of pulmonary aspiration. Benzodiazepines are the mainstay of therapy for AWS. (27) They enhance the activity of endogenous neurotransmitter [gamma]-aminobutyric acid, which essentially is a replacement for alcohol. Benzodiazepines alleviate the excitatory manifestations of AWS and reduce the risk of seizures and delirium. (28) The dose required is variable, and frequent adjustment is based on withdrawal severity. With adequate benzodiazepine "sedation" treatment, the patient should rest comfortably but be easily awakened. Agents such as diazepam 10 to 40 mg, lorazepam 1 to 8 mg, or chlordiaz-epoxide 50 to 100 mg may be used as long as reassessment and titration is performed on a regular basis. None of these drugs have been shown to be superior to others in this setting. Some investigators, however, report a decrease in seizure activity and a smoother withdrawal course with longer-acting benzodiazepines such as diazepam. (29) A fixed schedule regimen may be used and gradually tapered off, once symptoms are suppressed. In addition, beta-blockade may be used adjunctively for excessive autonomic activity and has been shown to decrease the manifestations of alcohol withdrawal. (30) These agents should be used with caution, as they may mask some of the withdrawal symptoms in cases of inadequate treatment, such as tachycardia and hypertension. (30) Beta-blockade has also been reported to precipitate delirium. (31) Central alpha agonists such as clonidine are used to attenuate central sympathetic outflow and reduce plasma catecholamine levels. (32) This class of medication decreases tachycardia, tremor, and diaphoresis but has no effect on delirium or seizures. (33) Thus, they should only be used in conjunction with sedatives. (33) Neuroleptics, such as haloperidol, have been shown to increase mortality rates if used as monotherapy and therefore are used only in synergistic combination with benzodiazapines. (34) Carbamazepine is used in Europe and has been shown to decrease withdrawal symptoms, especially with seizure, (35) but does not prevent delirium. (36) It may also retard the "kindling phenomenon" described above. Ethyl alcohol, either enteral or through central venous access, may be used, but no controlled trials have compared the safety or efficacy with that of benzodiazepines. (37) Finally, propofol is an aromatic sedative-hypnotic used for severe cases of AWS. It acts on a subunit of the [gamma]-aminobutyric acid receptor-ionophore complex that increases chloride conductance and inhibits the N-methyl-D-aspartate subtype of the glutamate receptor. (38) Its major utility is for refractory agitation seen with benzodiazepine failure. Its rapid penetration into the central nervous system and rapid elimination kinetics make it an ideal drug for short-term therapy. (39) Significant side effects associated with propofol include hypotension, hypertriglyceridemia, and a risk of infection caused by the infusate medium.

Wernicke encephalopathy

Wernicke encephalopathy (WE) is an important cause of mental status change in chronic alcoholics and carries a 10 to 20% mortality rate if left untreated. WE is an important syndrome to recognize because it is fatal but easily reversed. This syndrome is characterized by nystagmus, gaze palsies, gait ataxia, and mental confusion. Korsakoff amnestic state is a unique mental disorder in which retentive memory is impaired in greater proportion compared with other cognitive dysfunction and is closely associated with WE. These two disorders may present together in critically ill alcoholic patients. WE occurs as a result of thiamine deficiency, (40) which is an important cofactor for several enzymatic systems, such as transketolase and pyruvate dehydrogenase, (41,42) that are responsible for cerebral glucose utilization and glutamate elimination. Therefore, thiamine deficiency results in an alternation of cerebral metabolism leading to a diminished nerve impulse transmission at various synapses. (43)

Only one third of patients present with the classic triad described by Wernicke: confusion, ataxia, and ophthalmoplagia. (44) Most of the patients, on the other hand, present with a change in mental status or some degree of Korsakoff psychosis. Other manifestations include meiotic or nonreactive pupils, postural hypotension with accompanying syncope caused by impaired autonomic dysfunction, and hypothermia caused by loss of central thermoregulation. (45) The diagnosis of WE is made by a high index of suspicion. In the appropriate clinical settings, low levels of serum thiamine, pyruvate dehydrogenase, and transketolase activity might confirm the diagnosis. (46) Magnetic resonance imaging is used to support the diagnosis by demonstrating high-intensity lesions in the paraventricular regions of the thalamus, hypothalamus, mamillary bodies, periaqueductal region of the midbrain, fourth ventricular floor, and superior cerebellar vermis. (46)

Treatment of WE in the MICU is a medical emergency. Patients should receive immediate parental thiamine as a 100-mg bolus. However, only 2 to 3 mg is needed to reverse the ocular symptoms. Thereafter, daily intravenous infusion of 100 mg of thiamine is given until the patient resumes a normal diet. (47) Improvement of the ataxia and confusion is usually seen within 1 to 6 hours of treatment.

Hepatic encephalopathy

Portal systemic encephalopathy or hepatic encephalopathy is a potentially reversible decrease in neurologic function seen in critically ill chronic alcoholics. The syndrome is characterized by irritability, impaired attention, poor memory, and even somnolence that may progress to stupor and coma. Precipitating factors unique to alcoholics include gastrointestinal hemorrhage, hypokalemia, metabolic alkalosis, and excessive diuresis. It is also imperative to rule out sources of infection, including meningitis, pneumonia, urinary tract infection, and spontaneous bacterial peritonitis. Furthermore, the use of benzodiazepines in the treatment in AWS may precipitate hepatic encephalopathy in patients with underlying alcoholic liver disease. (48)

The onset is insidious and is marked by subtle changes in memory and concentration. The syndrome is divided into four stages. The first stage involves higher cortical function and may be manifested by a decrease in attention span, depression, tremor, personality changes, incoordination, apraxia, and irritability. The second stage is marked by exaggeration of the first stage and includes poor memory and computation, disordered sleep, slowed speech, ataxia, and even drowsiness. The third and fourth stages include increasing obtundation, amnesia, nystagmus, clonus, and muscular rigidity and may progress to coma, decerebrate posturing, dilated pupils, and poor response to painful stimuli.

The diagnosis of portal systemic encephalopathy is made on a clinical basis but can be supported by laboratory data, electroencephalogram (EEG), and neuropsychiatric testing. The most reliable assessment is the Portal Systemic Encephalopathy Index, which contains five parameters, including (1) a clinical assessment of mental status, (2) trail-making time, (3) EEG, (4) the presence of asterixis on physical examination, and (5) an arterial ammonia level. The trail-making test is a semiquantitative measure whereby the subject connects 25 consecutive numbered circles, and the time (in seconds) is noted. (49) Figures may be used if the patient is not able to recognize numbers. (50) The EEG is sensitive and reliable for all stages of portal systemic encephalopathy and will display subtle slowing in stage 1, slow rhythms and triphasic waves at the frontal regions in stages 2 and 3, and severe slowing with theta and delta waves in stage 4. (51) An elevation of the arterial ammonia level does not confirm or exclude the diagnosis of portal systemic encephalopathy, but increased levels parallel changes in the EEG and can be helpful in guiding the response to treatment in the MICU. (52)

The goals of portal systemic encephalopathy treatment in the MICU include identification and correction of precipitating causes, initiation of ammonia-lowering therapy, and minimizing potential medical complications of cirrhosis and decreased consciousness. Initial management includes elimination of sedatives and tranquilizers that may contribute to the mental status change, adequate volume repletion, correction of metabolic derangements, treating infection, and halting active bleeding. After initial management, it is imperative to lower elevated serum ammonia levels. A dietary protein restriction of 60 g/d of vegetable protein will effectively decrease ammonia levels. (53) Lactulose is given by nasogastric tube (30 to 60 mL every 2 hours or until a bowel movement) or by enema if the patient has an ileus (300 mL of 50% lactulose + 700 mL water) to increase bowel transit time and to decrease the stool pH. (54) Lactulose is a nonabsorbable synthetic disaccharide that is metabolized by colonic bacteria to lactic, acetic, and other organic acids, which stimulate peristalsis and trap ammonia in the gut as an ammonium ion. (55,56) The remainder of the compound acts as an osmotic laxative. Another ammonia-lowering therapy includes antibiotics such as neomycin, rifaximin, ampicillin, and metronidazole. (57,58) Keeping the head of the bed elevated to decrease risk of aspiration, treating agitation, gastrointestinal bleeding prophylaxis, and minimizing medications metabolized by the liver are part of the management of portal systemic encephalopathy in the MICU. Corticosteroids have been suggested in the management of severe alcoholic liver disease; however, this should only be considered after excluding acute infection and confirming the diagnosis by a liver biopsy. (59)

Respiratory Complications

Respiratory infections

Alcohol has been observed to be a common comorbidity in MICU patients with pneumonia. (60) Interestingly, there is a 60% increase in the use of the MICU when an alcoholic has pneumonia compared with a nonalcoholic patient. Moreover, the length of stay is increased compared with a nonalcoholic patient. (61) The mortality rate of pneumonia with alcohol-related diagnoses was reported to be 10%; however, in the case of Klebsiella pneumoniae, there was a higher incidence of bacteremia, with mortality up to 66%. (62) In addition, the incidence of tuberculosis, pleurisy, bronchitis, and empyema are significantly higher among alcoholics compared with nonalcoholics. (63)

The pathophysiology of pneumonia in alcoholics is primarily due to depression of normal defense mechanisms. Alcohol is known to depress normal mucociliary function. (64) Furthermore, the ability of neutrophils and macrophages to fight against infection is hampered. (65,66) Other inhibited lower respiratory tract defenses include nonspecific antibacterial activity of surfactant, opsonization by immunoglobulin or complement, and intracellular killing by alveolar macrophages. (67) Aspiration of material from the mixed oropharyngeal flora may be due to a diminished cough or epiglottic reflex seen during alcoholic withdrawal seizures or a decrease in level of consciousness associated with heavy drinking. (67) Other contributors to an increased risk of development of pneumonia include poor nutrition, immunosuppression from alcohol-related liver disease, and smoking abuse.

The symptoms of pneumonia in alcoholics are similar to those with community-acquired pneumonia but may be more severe. The organisms most commonly isolated are Streptococcus pneumoniae, Haemophilus influenza, and K pneumoniae. (68) In addition, because of the frequent occurrence of poor oral dentition, seizures, and subsequent aspiration, alcoholics are susceptible to a variety of anaerobic pleuropulmonary diseases, including anaerobic pneumonitis, necrotizing pneumonia, primary lung abscess, and empyema.

Treatment of alcoholics with pneumonia in the MICU is challenging. Mechanical ventilation for pneumonia is often required in severe hypoxemia, significant aspiration, and/or acute alcohol-withdrawal seizure. Antibiotic therapy for severe pneumonia or suspected aspiration must be started as early as possible for better outcome. Treatment options include cefotaxime or certriaxone plus a macrolide or a fluoroquinolone. If aspiration is suspected, ampicillin/sulbactam, ticarcillin/clavulanate, or piperacillin/tazobactam may be used as monotherapy, or a fluoroquinolone plus clindamycin or metronidazole can be used as an alternative for penicillin allergy. Last, surgical intervention with decortication or chest thoracostomy for necrotizing aspiration pneumonia, lung abscesses, and empyema may be required. Supportive therapy with adequate hydration, bronchodilators, chest physiotherapy, and nutrition are also essential in the treatment of these patients.

Acute respiratory distress syndrome

A history of chronic alcohol abuse significantly increases the risk of developing acute respiratory distress syndrome (ARDS) in critically ill patients, regardless of the inciting illness. (69) Risk factors of developing ARDS in chronic alcohol abuse include severe pancreatitis, hypertransfusion caused by gastrointestinal bleeding, aspiration pneumonia, hepatic failure, trauma, and sepsis.

The pathophysiology of alcoholic-related ARDS is complex. Alcohol may directly interact with the pathogenic cascade leading to ARDS. In vitro

studies have shown an increase in neutrophil adherence, phagocytosis, and chemotaxis when alcohol levels consistent with intoxication are found in experimental animals. In addition, other in vivo studies have shown upregulation of CD 11b/CD 18 receptors, which recognize the intercellular adhesion molecule, ICAM-1, on endothelial cells, an important step in cell requirement at the site of inflammation. This would increase oxidative free radical production and enhance the inflammatory process seen with ARDS.

The management of ARDS in alcoholics in the MICU is similar to that of nonalcoholics. Treatment is directed at supportive care, mechanical ventilation, and treatment of the underlying illness. The outcome of alcoholic patients with ARDS appears to be worse than in nonalcoholics. In-hospital mortality rates may be as high as 65% in patients with a history of alcohol abuse, compared with 36% in those without a history of alcohol abuse. (70)

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 [micro]g bolus followed by infusion of 250 [micro]g/h) or its long-acting analog, octreotide (50 [micro]g bolus and infusion of 25 to 50 [micro]g/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 [H.sub.2]-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.

Metabolic and Renal Complications

Metabolic derangements in chronic alcoholics are frequent in the MICU setting. These occur in patients with acute intoxication, withdrawal, or even with chronic ethanol exposure. The most common and potentially life-threatening abnormalities include hypokalemia, hypomagnesemia, hypophosphatemia, hypoglycemia, ketoacidosis, and lactic acidosis.

The pathophysiology of hypophosphatemia in heavy drinkers is multifactorial. Poor intake, ethanol-enhanced urinary excretion, emesis, and antacid use are some of the most common causes of low serum phosphorus. In addition, if there is alcoholic ketoacidosis or vitamin D deficiency, there may be phosphaturia and subsequent hypophosphatemia. Severe hypophosphatemia (<1 mEq/dL) may lead to seizures, hypoventilation, or even coma. In addition, it may result in rhabdomyolysis and subsequent acute renal failure. Moreover, tissue hypoxia may ensue because of a decrease in 2,3 DPG level. Low levels of ATP secondary to hypophosphatemia increase the incidence of bacterial or fungal infections because of poor phagocytosis or opsonization.

Hypomagnesemia in alcoholics commonly develops because of a decrease in renal reabsorption of magnesium, poor nutritional status, and nasogastric suctioning. Furthermore, during an acute alcoholic withdrawal, there is a shift of magnesium, phosphorus, and potassium into the cells and ensuing hypomagnesemia. Manifestations of severe hypomagnesemia (<1 mEq/dL) include muscle weakness, increased deep tendon reflexes, and cardiac dysrhythmias triggered by prolonged PR or QT intervals.

Hypokalemia occurs because of emesis, skin or gastrointestinal losses, or concomitant hypomagnesemia. Patients with severe hypokalemia (level <2.5 mEq/L) display weakness, hypoventilation, paralytic ileus, and ventricular dysrhythmias.

Hypoglycemia is common and is due to a decrease in endogenous glucose production and a decrease in glycogenolysis.

Alcoholic ketoacidosis is an important syndrome to recognize because it is potentially fatal but easily reversed. Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde, which in turn is metabolized to acetyl-CoA. This process generates hydrogen ions and reduces nicotinamide adenine dinucleotide (NADH):

CH3CH2OH + NAD [right arrow] CH3CHO + NADH + H

Ethanol [right arrow] Acetaldehyde

The accumulation of reduced NADH leads to a reduction in oxidized NAD+. Since gluconeogenesis depends on the availability of NAD+, ethanol intoxication impairs the generation of glucose. When glycogen stores are depleted, hypoglycemia ensues. The resultant low insulin state promotes the breakdown of fatty acids, which are then metabolized to ketone bodies. (98)

Lactate dehydrogenase catalyzes the synthesis of lactate from pyruvate, using NADH as a cofactor and generating NAD+:

CH3COCOO + NADH + H [right arrow] CH3CHOHCOO + NAD+

Pyruvate [right arrow] Lactate

Accumulating NADH by ethanol favors the generation of lactate and causes lactic acidosis. (98) Patients with alcoholic ketoacidosis are usually hypoglycemic, stuporous, and prone to have nausea, vomiting, and aspiration. At this stage, ethanol may be completely metabolized and no longer detectable. These patients are usually acidotic, with the presence of ketones as well as lactic acid. Treatment consists of hydration with intravenous fluids and glucose.

Alcohol-induced acute renal failure may be due to prerenal azotemia, rhabdomyolysis, or hepatorenal syndrome. In addition, Newell et al (99) reported that 50 to 100% of patients with hepatic cirrhosis caused by alcohol have an associated glomerulonephropathy, histologically identical with immunoglobulin A nephropathy.

The treatment of these common metabolic derangements is supportive and includes prompt electrolyte and glucose replacement, dehydration, and maintaining adequate nutritional status.

Cardiovascular Complications

The direct effect of ethanol on the heart and long-term neurohumoral influence are the main causative factors in cardiac dysfunction caused by alcohol abuse.

The three main complications of cardiac dysfunction from ethanol requiring MICU care include cardiomyopathy, atrial and ventricular dysrhythmias, and variant angina.

Alcoholics may develop dilated cardiomyopathy with intake of more than 90 g/d of alcohol for at least 5 years. (100,101) A dilated left ventricle, normal or decreased left ventricular wall thickness and an increase in left ventricular mass characterize this type of cardiomyopathy. (102,103) The pathophysiology is not well understood, but mechanisms may include histologic and cellular changes, including myocyte loss, (104,105) intracellular organelle dysfunction, (106-108) decrease in contractile proteins, and changes in calcium regulation. (109,110)

The mechanism of dysrhythmias is also not known, but structural changes including myofibrillar necrosis, interstitial fibrosis, and dysfunction of myocyte sarcolemma and mitochondria alter the normal conduction system of the heart in chronic alcohol abuse. Ethanol or its metabolite acetylaldehyde may change the electrolyte balance at the cellular level and trigger cardiac dysrhythmias. Moreover, the combination of the increase in catecholamines along with electrolyte derangements may contribute to dysrhythmias. Finally, coronary vasospasm has been shown to occur in response to ethanol, which leads to angina. (111) The elevation in catecholamines and the poor cardiac contractility may also increase the coronary demand and cause variant angina.

The clinical signs and symptoms of cardiac dysfunction in alcoholic patients are similar to those in patients without a history of alcohol abuse. The diagnostic workup includes standard electrocardiogram, cardiac enzymes, thyroid function tests, chest radiogram, and cardiac echocardiogram. Endomyocardial biopsy is indicated in alcoholic cardiomyopathy if the diagnosis is not clear. (111) The biopsy will demonstrate myocyte hypertrophy, enlarged nuclei, and lymphocytic infiltrates.

Treatment of cardiac dysfunction from alcohol abuse in the MICU should focus on ruling out true coronary ischemia, controlling dysrhythmias, and improving cardiac function. Standard medical therapy for chest pain including aspirin, nitrates, and oxygen is similar in this population. Appropriate preload and afterload reduction is necessary if signs of congestive heart failure are present as a result of cardiomyopathy or dysrhythmias. Heart rate control with beta-blockade, calcium-channel blockers, and digitalis are indicated for a variety of dysrhythmias. Furthermore, beta-blockade for the increased neurohormonal activity in alcoholics has been shown to decrease further cardiac dysfunction (111). Correction of nutritional and electrolyte deficits are also an important part of treatment for cardiac disease in this population. Acute atrial fibrillation induced by acute alcohol intoxication (holiday heart syndrome) is a benign condition with spontaneous recovery in the majority of cases. (112)


Management of alcohol-related disorders in the MICU is challenging. Patients often present with multisystem dysfunction and require aggressive care. Because of the significant morbidity and mortality rates from acute alcohol-related disorders in the ICU setting, early recognition and treatment of alcohol-related disorders is imperative. The cost of medical care for these patients is extraordinary, and the best strategy in dealing with alcohol abuse-related problems, both acute and chronic, is a preventive one. It is the responsibility of primary care physicians to recognize alcohol abuse in their office by using different types of screening methods and informing their patients of the serious complications that could result from their continued drinking.
Table. Critical care complications of alcohol abuse

 Alcohol withdrawal syndrome
 Wernicke encephalopathy
 Hepatic encephalopathy
 Respiratory infections
 Acute respiratory distress syndrome
 Upper gastrointestinal bleeding
 Alcohol-induced gastritis
 Esophageal varices
 Gastric varices
 Acute necrotizing pancreatitis
Metabolic and renal
 Electrolyte disturbances
 Alcohol ketoacidosis
 Acute renal failure
 Variant angina

Accepted November 10, 2004.


1. Lowenfels AB. Epidemiologic studies of alcohol-related disease in the 20th century. J Epidemiol Biostat 2000;5:61.

2. Grant FF. Alcohol consumption, alcohol abuse and alcohol dependence: the United States as an example. Addiction 1994;89:1357-1365.

3. National Institute on Alcohol Abuse and Alcohol Abuse. Eighth Special Report to the US Congress on Alcohol and Health. Rockville, MD, 1993, DHHS Publication No. ADM:281-91-0003.

4. Chagas Silva M, Gaunekar G, Patel V, et al. The prevalence and correlates of hazardous drinking in industrial workers: a study from Goa, India. Alcohol Alcohol 2003;38:79-83.

5. Baldwin WA, Rosenfeld BA, Breslow MJ, et al. Substance abuse-related admissions to adult intensive care. Chest 1993;103:21-25.

6. Hall W, Zador D. The alcohol withdrawal syndrome. Lancet 1997;349:1897-900.

7. Bartug B, Fullwood J. Delirium tremens in acute myocardial infarction. Heart Lung 1994;23:21-26.

8. Agartz I, Shoaf S, Rawlings RR, et al. CSF monoamine metabolites and MRI brain volumes in alcohol dependence. Psychiatry Res 2003;20;122:21-35.

9. Chiang WK, Goldfrank LR. Substance withdrawal. Emerg Med Clin North Am 1990;8:613-631.

10. Surawicz FG. Alcoholic hallucinosis: a missed diagnosis. Can J Psychiatry 1980;25:57-63.

11. Victor M, Adams RD. The effects of alcohol on nervous system. Proc Assoc Res Nerv Ment Dis 1953;32:526-532.

12. Victor M, Brausch C. The role of abstinence in the genesis of alcoholic epilepsy. Epilepsia 1967;8:1-20.

13. Thompson WL. Management of alcohol withdrawal syndromes. Arch Intern Med 1978;138:278-283.

14. Turner RC, Lichstein PR, Peden JG Jr, et al. Alcohol withdrawal syndromes: a review of pathophysiology, clinical presentation, and treatment. J Gen Intern Med 1989;4:432-444.

15. Morris JC, Victor M. Alcohol withdrawal seizures. Emerg Med Clin North Am 1987;5:827-839.

16. Smith GS, Falk H. Unintentional injuries. Am J Prev Med 1987;3:143-146.

17. Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br J Addict 1989;84:1353-1357.

18. Ortiz J, Fitzgerald LW, Charlton M, et al. Biochemical actions of chronic ethanol exposure in the mesolimbic dopamine system. Synapse 1995;21:289-298.

19. Nestler EJ, Aghajanian GK. Molecular and cellular basis of addiction. Science 1997;278:58-63.

20. Klinker JF, Lichtenberg-Kraag B, Damm H, et al. Activation of pertussis toxin sensitive G-protein in membranes of SH-SY5Y human neuroblastoma cells and bovine transducin by ethanol. Neurosci Lett 1996;213:25-28.

21. Ewing JA. Detecting alcohol abuse: the CAGE Questionnaire. JAMA 1984;252:1905-1907.

22. Buchsbaum DG, Buchanan RG, Centor RM, et al. Screening for alcohol abuse using CAGE scores and likelihood ratios. Ann Intern Med 1991;115:774-777.

23. Soderstrom CA, Dischinger PC, Smith GS, et al. Psychoactive substance dependence among trauma center patients. JAMA 1992;267:2756.

24. Stibler H. Carbohydrate-deficient transferrin in serum: a new marker of potentially harmful alcohol consumption reviewed. Clin Chem 1991;37:2029.

25. Figlie NB, Benedito-Silva AA, Monteiro MG, et al. Biological markers of alcohol consumption in nondrinkers, drinkers, and alcohol-dependent Brazilian patients. Alcohol Clin Exp Res 2002;26:1062-1069.

26. Brown CG. The alcohol withdrawal syndrome. Ann Emerg Med 1982;11:276-280.

27. Wax PM. Withdrawal syndromes, in Rippe JM, Irwin RS, Fink MP, et al (eds): Intensive Care Medicine. 3rd edition. Boston, Little, Brown & Company, 1996, pp 1718-1726.

28. Mayo-Smith MF. Pharmacological management of alcohol withdrawal: a meta analysis and evidence based practice guideline. JAMA 1997;278:144-151.

29. Ritson B, Chick J. Comparison of two benzodiazepines in the treatment of alcohol withdrawal: effects on symptoms and cognitive recovery. Drug Alcohol Depend 1986;18:329-334.

30. Kraus ML, Gottlieb LD, Horwitz RI, Anscher M. Randomized clinical trial of Atenolol in patients with alcohol withdrawal. N Engl J Med 1985;313:905-910.

31. Sellers EM, Zilm DH, Degani NC. Comparative efficacy of propranolol and chlordiazepoxide in alcohol withdrawal. J Stud Alcohol 1977;38:2096-2108.

32. Liskow BI, Reed J. Atenolol for alcohol withdrawal. N Eng J Med 1986;314:782-784.

33. Cushman P Jr, Forbes R, Lerner W, et al. Alcohol withdrawal syndromes: clinical management with Lefoxidine. Alcohol Abuse 1985;9:1103-1108.

34. Bjorkqvist SE. Clonidine in alcoholic withdrawal. Act Psychiatr Scand 1975;52:256-263.

35. Adams F, Fernandez F, Anderson BS. Emergency pharmacotherapy of delirium in the critically ill cancer patient. Psychomatics 1986;27:33-38.

36. Bjorkqvist SE, Isohanni M, Makela R, et al. Ambulant treatment of alcohol withdrawal symptoms with carbamazepine: a formal multicenter double blind comparison with placebo. Acta Psychiatr Scand 1976;53:333-342.

37. Ballenger JC, Post RM. Kindling as a model for the alcohol withdrawal syndromes. Br J Psychiatry 1978;133:1-14.

38. Funderburk FR, Allen RP, Wagman AM. Residual effect of ethanol and chlordiazepoxide treatment for alcohol withdrawal. J Nerv Ment Dis 1978;166:195-203.

39. Crippen D, Ermakov S. Titrated treatment of delirium tremens using continuous Propofol infusion. St Francis J Med (on line). Available at\journal\v. 2_n. 1\clinical\clinical.htm. Accessed May 1999.

40. Singleton CK, Pekovich SR, McCool BA, et al. The thiamine-dependent hysteric behavior of human transketolase: implications for thiamine deficiency. J Nutr 1995;125:189-194.

41. Blass JP, Gibson GE. Abnormality of a thiamine enzyme in-patients with Wernicke-Korsakoff syndrome. N Engl J Med 1977;297:1367.

42. Fawcett S, Young GB, Holliday RL. Wernicke encephalopathy after gastric partitioning for morbid obesity. Can J Surg 1984;27:169.

43. Schenker S, Henderson GI, Hoyumpa AM Jr, et al. Hepatic and Wernicke encephalopathies: current concepts of pathogenesis. Am J Clin Nur 1980;22:2719.

44. Victor M, Adams RD, Collins TG. The Wernicke-Korsakoff syndrome: a clinical and pathological study of 245 patients, 82 with post-mortem examinations. Contemp Neurol Ser 1971;7:1-206.

45. Kearsly JH, Musso AF. Hypothermia and coma in the Wernicke-Korsakoff syndrome. Med J Aust 1980;2:504.

46. Torvik A, Lindboe CF, Rogde S. Brain lesion in alcoholics: a neuropathological study with clinical correlation. J Neuro Sci 1982;56:233.

47. Feinnman L, Lieber C. Modern nutrition, in Shils M (ed): Health and Disease. 9th edition. Philadelphia, Lea and Febiger, 2000, p 1538.

48. Basile AS, Hughes RD, Harrison PM, et al. Elevated brain concentrations of 1,4-benzodiazepines in fulminant hepatic failure. N Engl J Med 1991;325:473.

49. Sleisenger MH, Fordtran JS. Gastrointestinal and Liver Disease. Philadelphia, Saunders, 1998, ed 6, 1334-1354.

50. Victor M, Ropper AH. Adams and Victor's Principles of Neurology. New York, McGraw-Hill, 2000, ed 7, 1205-1211.

51. Amodio P, Marchetti P, Del Piccolo F, et al. Spectral versus visual EEG analysis in mild hepatic encephalopathy. Clin Neurophysiol 1999;110:1334-1344.

52. Parsons-Smith BG, Summerskill WHJ, Dawson AM, et al. The electroencephalogram in liver disease. Lancet 1957;2:867-871.

53. Lockwood AH. Hepatic Encephalopathy. Boston, Butterworth-Heineman, 1992, pp 65-72.

54. Simons F, Goldstein H, Boyle JD. A controlled trial of lactulose in hepatic encephalopathy. Gastroenterology 1970;59:827-832.

55. Conn HO, Floch MH. Effects of lactulose and lactobacillus acidophilous on the fecal flora. Am J Clin Nutr 1970;23:1588-1594.

56. Price JB, Sawoda M, Voorhees AB. Clinical significance of intraluminal pH in intestinal ammonia transport. Am J Surg 1970;119:595-598.

57. Atterbury CE, Maddery WC, Conn HO. Neomycin, sorbitol and lactulose in the treatment of acute portal systemic encephalopathy: a controlled double blind clinical trial. Am J Dig Dis 1978;23:398-406.

58. Puxeddu A, Quartini M, Massimetti A, et al. Rifaximin in the treatment of chronic hepatic encephalopathy. Curr Med Res Opin 1995;13:274-228.

59. Mathurin P, Mendenhall CL, Carithers RL Jr, et al. Corticosteroids improve short-term survival in patients with severe alcoholic hepatitis (AH): individual data analysis of the last three randomized placebo controlled double blind trials of corticosteroids in severe AH. J Hepatol 2002;36:480-487.

60. Capps JA, Coleman GH. Influence of alcohol on prognosis of pneumonia in Cook County Hospital. JAMA 1923;80:750-752.

61. Saitz R, Ghali WA, Moskowitz MA. The impact of alcohol-related diagnoses on pneumonia outcomes. Arch Intern Med 1997;157:1446-1452.

62. Jong GM, Hsiue TR, Chen CR, et al. Rapidly fatal outcome of bacteremic Klebsiella pneumoniae pneumonia in alcoholics. Chest 1995;107:214-217.

63. Lebowitz MD. Respiratory symptoms and diseases related to alcohol consumption. Am Rev Respir Dis 1981;123:16-19.

64. Krumpe PE, Cummiskey JM, Lillington GA, Alcohol and the respiratory tract. Med Clin North Am 1984;68:201-219.

65. Glassman AB, Bennett CE. Effects of ethyl alcohol on human peripheral lymphocytes. Arch Pathol Lab Med 1985;109:540-542.

66. Mili F, Fanders WD, Boring JR, et al. The associations of alcohol drinking cessation to measures of the immune system in middle aged med. Alcohol Clin Exp Res 1992;16:688-694.

67. Guarneri JJ, Laurenzi GA. Effect of alcohol on the mobilization of alveolar macrophages. J Lab Clin Med 1968;72:40-51.

68. Saitz R, Ghali WA, Moskowitz MA. The impact of alcohol-related diagnoses on pneumonia outcomes. Arch Intern Med 1997;157:1446-1452.

69. Moss M, Bucher B, Moore FA, et al. The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults. JAMA 1996;275:50-54.

70. Balla AK, Doi EM, Wunder PR, et al. Human polymorphonuclear leukocyte (PMN) priming and activation by acute ethanol intoxication. Adv Exp Med Biol 1993;335:165-168.

71. Laine L. Upper gastrointestinal hemorrhage. West J Med 1991;155:274.

72. Laine L, Weinstein WM. Subepithelial hemorrhage and erosions of human stomach. Dig Dis Sci 1988;33:490.

73. Larine L, Weinstein WM. Histology of alcoholic hemorrhage "gastritis": a prospective evaluation. Gastroenterology 1988;94:1254.

74. Valencia Parracen J. Alcoholic gastritis. Clin Gastroenterol 1981;10:289-399.

75. Graham D, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology 1981;80:800.

76. Imperiale TF, Teran JC, McCullough AJ. A meta analysis of somatostatin versus vasopressin in the management of acute esophageal variceal hemorrhage. Gastroenterology 1995;109:1289-1294.

77. Laine L, Cook D. Endoscopic ligation compared with sclerotherapy for the treatment of esophageal variceal bleeding: a meta analysis. Ann Intern Med 1995;123:280-287.

78. Lo GH, Lai KH, Cheng JS, et al. Emergency banding ligation versus sclerotherapy for the control of active bleeding from esophageal varices. Hepatology 1997;25:1101-1104.

79. Jalan R, John TG, Redhead DN, et al. A comparative study of emergency transjugular intrahepatic portal systemic stent shunt and esophageal transection in the management of uncontrolled varices hemorrhage. Am J Gastroenterol 1995;90:1932-1937.

80. Deschenes M, Villenceuve JP. Risk factors for the development of bacterial infections in hospitalized patients with cirrhosis. Am J Gastroenterol 1999;94:2193-2197.

81. Goulis J, Armonos A, Patch D, et al. Bacterial infection is independently associated with failure to control bleeding in cirrhotic patients with gastrointestinal hemorrhage. Hepatology 1998;27:1207-1212.

82. Beranard B, Grange JD, Khac EN, et al. Antibiotic prophylaxis for the prevention of bacterial infection in cirrhotic patients with GI bleeding: a meta analysis. Hepatology 1999;29:1655-1661.

83. Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med 1999;340:1412-1417.

84. Pratt DS, Epstein SK. Recent advances in critical care gastroenterology. Am J Respir Crit Care Med 2000;161:1417-1421.

85. Guelrud M, Mendoza S, Rossiter G, et al. Effect of local institution of alcohol on sphincter of Oddi motor activity: combined ERCP and manometry study. Gastrointest Endosc 1999;37:428.

86. Gronroos JM, Aho HJ, Nevalainen JJ. Cholinergic hypothesis of alcoholic pancreatitis. Dig Dis Sci 1992;10:38.

87. Renner IG, Rinderknecht H, Valenznela JE, et al. Studies in pure pancreatitis secretions in chronic alcoholic subjects without pancreatic insufficiency. Scand J Gastroenterol 1980;15:241.

88. Reynaert MS, Dugernier TH, Kestens PJ. Current therapeutic strategies in severe acute pancreatitis. Intensive Care Med 1990;16:352.

89. Steinberg W, Tenner S. Acute pancreatitis. N Engl J Med 1994;330:1198-2076.

90. Kalfarentzos F, Kehagias J, Mead N, et al. Enteral nutrition is superior to parental nutrition in severe acute pancreatitis: results of a randomized prospective trial. Br J Surg 1997;84:166-169.

91. Sainio VE, Kemppainen P, Puolakkainen M, et al. Early antibiotic treatment in acute necrotizing pancreatitis. Lancet 1995;346:663-667.

92. Ho HS, Frey CF. The role of antibiotic prophylaxis in severe acute pancreatitis. Arch Surg 1997;132:487-492.

93. Pederzoli P, Bassi C, Vesentinin S, et al. A randomized multicenter clinical trial of antibiotic prophylaxis of septic complications in acute necrotizing pancreatitis with imipenem. Surg Gynecol Obstet 1993;176:480-483.

94. Rau B, Pralle U, Mayer JM, et al. Role of ultrasonographically guided fine needle aspiration cytology in the diagnosis of infected pancreatic necrosis. Br J Surg 1998;85:179-184.

95. Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med 1999;340:1412-1417.

96. Mier J, Leon EL, Castillo A, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997;173:71-75.

97. Baron TH, Thaggard WG, Morgan DE, et al. Endoscopic therapy of organized pancreatic necrosis. Gastroenterology 1996;111:755-764.

98. Turner RC, Oakley NW, Nabarro JDN. Changes in plasma insulin during ethanol-induced hypoglycemia. Metabolism 1973;22:111.

99. Newell GC. Cirrhotic glomerulonephritis: incidence, microbiology, clinical features. Am J Kidney Dis 1987;9:183-190.

100. Fauchier L, Babuty D, Poret P, et al. Comparison of long term outcome of alcoholic and idiopathic dilated cardiomyopathy. Eur Heart J 2000;21:306-314.

101. McKenna CJ, Codd MB, McCann HA, et al. Alcohol consumption in idiopathic dilated cardiomyopathy: a case control study. Am Heart J 1998;135:833-837.

102. De Keulenaer GGW, Brutsaert DL. Dilated cardiomyopathies: pathophysiology concepts and mechanisms of dysfunction. J Card Surg 1999;14:64-74.

103. Dancy M, Bland JM, Leech G, et al. Preclinical left ventricular abnormalities in alcoholic are independent of nutritional status, cirrhosis and cigarette smoking. Lancet 1985;1:1122-1125.

104. Haunstetter A, Izumo S. Apoptosis: basic mechanisms and implications for cardiovascular disease. Circulation 1998;82:1111-1129.

105. Cartwright MM, Smith SM. Increased ceel death and reduced neural creast cell numbers in ethanol-exposed embryos: partial basis for the fatal alcohol syndrome phenotype. Alcohol Clin Exp Res 1995;19:378-386.

106. Segel LD, Rendig SV, Mason DT. Alcohol-induced hemodynamic and CA+2 flux dysfunctions are reversible. J Mol Cell Cardiol 1981;13:443-455.

107. Segel LD, Rendig SV, Choquet Y, et al. Effects of chronic graded ethanol consumption on the metabolism function of the real heart. Cardiovasc Res 1975;9:649-663.

108. Sarma JS, Ikeda S, Fischer R, et al. Biochemical and contractile properties of heart muscle after prolonged alcohol administration. J Mol Cell Cardiol 1976;8:951-972.

109. Preedy VR, Peters TJ. The acute and chronic effects of ethanol on cardiac muscle protein synthesis in the rat in vivo. Alcohol 1990;71:97-102.

110. Preedy VR, Patel VB, Why HJF, et al. Alcohol and the heart: biochemical alternations. Cardiovasc Res 1996;31:139-147.

111. Piano MR. Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. Chest 2002;121:1638-1650.

112. Lowenstein SR, Gabow PA, Cramer J, et al. The role of alcohol in new-onset atrial fibrillation. Arch Intern Med 1983;143:1882-1885.


* This report describes the critical illnesses related to alcohol abuse.

* The pathophysiologic mechanisms of these illnesses are discussed.

* The role of the different diagnostic studies and the management approaches to these critical illnesses are discussed.

Ibrahim Al-Sanouri, MD, Matthew Dikin, MD, and Ayman O. Soubani, MD

From the Division of Pulmonary, Critical Care, and Sleep Medicine, Wayne State University School of Medicine, and Detroit Medical Center, Detroit, MI.

Reprint requests to Dr. Ayman O. Soubani, Harper University Hospital, Division of Pulmonary, Critical Care and Sleep Medicine, 3990 John R-3 Hudson, Detroit, MI 48201. Email:
COPYRIGHT 2005 Southern Medical Association
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2005, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Review Article
Author:Soubani, Ayman O.
Publication:Southern Medical Journal
Date:Mar 1, 2005
Previous Article:Strategies for insulin therapy in type 2 diabetes.
Next Article:Pulmonary sarcoidosis presenting with acute respiratory failure.

Related Articles
A new prescription: investing in substance-abuse treatment would take a big bite out of crime.
Lawyers and substance abuse.
Substance abuse and the elderly: unique issues and concerns. (Substance Abuse and the Elderly).
Substance addiction treatment information.
Drug (Ab)use research among Rural African American males: an integrated literature review.
Substance abuse in African Americans: in search of a culturally competent research agenda.
Older women & substance abuse: there are no age limits when it comes to substance abuse. Girls as young as 10 or 11 can be found in treatment...

Terms of use | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters