Analysis of hyperamylasemia in patients with severe head injury

To evaluate the influence of severe head injury (SHI) on amylase activity, we studied the amylase profile of 60 patients with SHIs and Glasgow Coma Scores less than 10. Fourteen additional multiple trauma patients without head injuries were studied as a control group. We excluded patients with pancreatic injury and abdominal trauma. Total serum amylase (TA), pancreatic isoamylase (PA), and nonpancreatic isoamylase (NPA) levels were measured on Days 0, 2, 4, 7, and 14 postinjury. Values greater than 2 SD above the normal mean were considered elevated. All SHI patients were comatose; 14 died. In the SHI group, TA increased in 23 patients, PA increased in 40, and NPA increased in 14. The source of hyperamylasemia was PA in 14, NPA in one, and mixed in 8 patients. While PA increases occurred throughout the study, NPA elevations occurred early. These increases did not correlate with shock (BP less than 80 mm Hg; 17 patients), facial trauma (24 patients), or associated injury (29 patients). On Day 7 postinjury, the mean TA (215 du%) and the mean PA (203.8 du%) were significantly elevated in the SHI patients compared to controls (122.1 du%, P less than 0.05, Wilcoxon's rank sum test). These data indicate that serum amylase is not a reliable index of pancreatic injury in patients with SHI. Severe head injury and multiple trauma activate pathways that increase amylase levels in the blood, suggesting a central nervous system regulation of serum amylase levels.     

Isoamylase levels in bone marrow transplant patients are affected by total body irradiation and not by graft-versus-host disease

Abstract. The mean total serum amylase levels in patients was 3.2 ± 0.5 μkat/l (± SE) before total body irradiation (TBI) prior to bone marrow transplantation of which 50% was due to pancreatic isoamylase and 50% salivary isoamylase. Total serum amylase increased to a maximum of 100.3 ± 12.3 μkat/l on the first dayafter TB Iandmostofthis increase was due to an increase in salivary isoamylase (90.0 ± 12.1 μkat/l). In association with this, all patients had clinical symptoms of parotitis. An increase in pancreatic isoamylase was found in 27% of the patients; however, none of them had clinical symptoms of pancreatitis. Serum amylase levels returned to normal within 5 days after TBI but then decreased to subnormal values, remaining below the normal range for 3 weeks. Pancreatic isoamylase returned to pre-irradiation levels 1.5 months after TBI, while salivary isoamylase remained low for the rest of the observation time. TBI of 7.5 Gyat 26 cGy/min gave significantly lower salivary amylase at 2 days after TBI compared with 10 Gy at 4 cGy/min: 32 ± 4 versus 76 ± 13 μkat/l ( P < 0.05). At 2.5 and 6 months after TBI significantly higher total amylase levels were recorded for patients treated with 7.5 Gy of TBI compared with 10 Gy: 2.5 ± 0.4 and 2.7 ± 0.3 versus 2.0 ± 0.5 and 0.8 ± 0.3 μkat/1, respectively ( P < 0.01, P < 0.05, respectively). Acute or chronic GVHD did not affect acinar cells in this investigation.     

Hyperamylasemia after cardiopulmonary bypass

Postpump pancreatitis has been described to occur in patients undergoing cardiac surgery with cardiopulmonary bypass. Twenty patients were prospectively analyzed with sera drawn for total serum amylase, pancreatic isoamylase, and nonpancreatic isoamylase levels. Six of 19 patients were found to be hyperamylasemic postoperatively, the majority of which were not due to pancreatic isoamylasemia . No patient had clinical pancreatitis. These findings suggest that elevations of serum amylase is common after cardiopulmonary bypass and is not indicative of pancreatitis.     

Hyperamylasemia after cardiac surgery. Incidence, significance, and management

The significance of hyperamylasemia and its relationship to pancreatitis after cardiac surgery is controversial. Three hundred consecutive patients undergoing cardiopulmonary bypass were prospectively studied to determine the incidence and significance of postoperative hyperamylasemia. Ninety-six of three hundred patients (32%) developed hyperamylasemia. Fifty-six patients (19%) were classified as having isolated hyperamylasemia because they were asymptomatic and had normal serum lipase. Thirty-two patients (10.7%) had subclinical pancreatitis defined as elevation of serum amylase and lipase or pancreatic isoamylase. Many of these patients had mild gastrointestinal symptoms that were self-limited. Eight patients (2.7%) had overt pancreatitis documented by clinical findings, biochemical abnormalities, and computed tomography (CT) scan or autopsy. Isoamylase analysis demonstrated that isolated hyperamylasemia usually originated from nonpancreatic sources. However, hyperamylasemia occurring in conjunction with abdominal signs and symptoms or elevated serum lipase was almost always pancreatic in origin. Patients with hyperamylasemia had a significantly higher mortality rate (seven of 96 patients, 7.5%) than those with normal serum amylase (two of 204 patients, 0.9%) (p less than 0.01) even when the amylase was nonpancreatic in origin (five of 56 patients, 9%). The reason that nonpancreatic hyperamylasemia is associated with increased postoperative mortality is not established but may represent a variety of metabolic aberrations or tissue injuries. It is concluded that 1) hyperamylasemia after cardiopulmonary bypass is a marker of potential clinical importance, and 2) pancreatitis in this setting is more common than previously recognized and is a potentially lethal complications. Successful treatment depends on early diagnosis and aggressive treatment.     

Foregut mucosal defects: an etiology of hyperamylasemia

To evaluate a preliminary correlation of hyperamylasemia to upper gastrointestinal bleeding, total serum amylase and serum isoamylase profiles were determined in 50 patients with upper gastrointestinal bleeding. Etiologies of the bleeding were determined in 46 patients including gastritis or duodenitis in 25, gastric ulcers in 12, duodenal ulcers in 3, Mallory-Weiss tears in 3, gastric carcinoma in 2, and esophageal varices in 1. Gastritis or duodenitis was seen incidentally in 14 more patients. Hyperamylasemia was seen in 38 patients, most commonly being due to a rise of both nonpancreatic and pancreatic isoamylases (18 patients). In 13 patients it was due to an elevation of nonpancreatic amylase alone, and in 7 patients secondary to elevated pancreatic isoamylase alone. Acute pancreatitis raises only the pancreatic component and cannot explain the hyperamylasemia in most of these patients. Hyperamylasemia did not correlate to etiology of the bleeding; gastritis or duodenitis present in the majority of these patients appears to be the unifying factor. Since both nonpancreatic and pancreatic amylases are present in the duodenum and the stomach with pyloric reflux, reabsorption of intraluminal amylase across damaged mucosa is postulated as a mechanism to explain the observed isoamylase patterns. The possibility of decreased amylase clearance as an explanation is unlikely. An alternative central nervous system mechanism might be invoked. It is concluded that hyperamylasemia is a complex event which the use of isoamylase analysis is beginning to elucidate. The hyperamylasemia seen commonly in patients presenting with upper gastrointestinal bleeding does not imply the presence of acute pancreatitis.     

Gelegenheitstrinker und chronische Alkoholiker

Patients who suffer an accident after alcohol consumption can be differentiated into 2 groups: patients which drink alcohol occasionally and chronic alcoholics. We examined prospectively in-patients treated after suffering a trauma in an alcoholised state. The diagnosis acute alcohol intoxication was made by a breath-alcohol-analysis, the diagnosis chronic alcoholism by a shortened MAST-test. In the average chronic alcoholics were 12 years older than acute intoxicated. Family backgronnd of chronic alcoholics was more often disrupted and social status lower than in acute alcoholics. For the acute alcoholics a car crash, for the chronic alcoholics a fall was the main trauma cause. In over 50% both patient groups suffered a minor head injury. Chronic alcoholics had a twice as long hospital stay (16.1±3.2 vs. 8.5±1.1 days), needed more specialist consultations (84% vs. 60%) and developed more complications (40% vs 16%) than the acute alcohol intoxicated. The ISS (Injury Severity Score) was the same for both patient groups (6.7±0.7 vs. 7.1±0.8) and had no prognostic value for the group of the chronic alcoholics. On the basis of the present findings it is advisable to check the diagnosis alcohol intoxication and to look whether chronic alcoholism is present whenever a drunken patient is admitted.     

Diagnostic value of serum elastase 1 in pancreatic disease

We studied serum elastase 1 concentrations in patients with pancreatic disease to assess its diagnostic value and compare its sensitivity and specificity with that of amylase and pancreatic isoamylase. Markedly raised concentrations of elastase 1 were found in all twenty-nine patients with acute pancreatitis (amylase was elevated in all but three and pancreatic isoamylase in all but one). Serial measurements of the three enzymes in acute pancreatitis showed that elastase remained elevated longer than amylase and pancreatic isoamylase. The majority of chronic pancreatitis patients studied during a painful relapse (16 out of 21, 76 per cent) had elastase concentrations above the upper normal limit. Amylase and pancreatic isoamylase were elevated in 11 (52 per cent) and in 13 (62 per cent), respectively. Most patients with chronic pancreatitis studied during clinical remission (39 out of 43) had serum elastase levels either within (n = 24) or below (n = 15) the control range. The latter had severe exocrine pancreatic insufficiency and steatorrhoea. In carcinoma of the pancrease, 20 out of 32 (63 per cent) had abnormal serum elastase concentrations; 16 were higher and 4 lower than the control range. Amylase was abnormal in 10 (31 per cent) (8 high, 2 low), and pancreatic isoamylase was abnormal in 16 (50 per cent) (11 high, 5 low). In 46 control patients with non-pancreatic abdominal pain, serum elastase concentrations were not significantly different from those in healthy controls. Elastase was slightly raised in two, whereas amylase and pancreatic isoamylase were elevated in seven and eight, respectively. We conclude that serum elastase 1 is a highly sensitive and specific indicator of pancreatic disease.     

24-hour pulsatile and circadian patterns of cortisol secretion in alcoholic men

Pulsatile and circadian patterns of cortisol secretion during acute (3 to 16 days) and chronic (29 to 39 days) abstinence were examined in alcoholic men with no clinical or laboratory evidence of hepatic dysfunction or nutritional deficiencies. Mean and integrated 24-hour serum concentrations of cortisol determined by sampling the blood every 20 minutes over a 24-hour period were increased in six out of 10 alcoholic subjects during acute abstinence when compared with normal controls. Sustained abstinence in seven subjects with follow-up studies caused significant decreases in the mean maximal cortisol peak amplitude (13 +/- 1.0 SEM acutely vs. 10.3 +/- 0.52 micrograms/dl follow-up; P = 0.01), mean 24-hour serum cortisol concentrations (10.9 micrograms/dl +/- 1.2 vs. 8.5 micrograms/dl +/- 0.26; P = 0.047), interpulse valley mean (9.3 micrograms/dl +/- 0.88 vs. 6.5 micrograms/dl +/- 0.34; P = 0.007), and valley nadir (7.9 micrograms/dl +/- 0.69 vs. 5.4 micrograms/dl +/- 0.30; P = 0.0036) concentrations. Cortisol pulse frequency was normal. Although circadian cortisol rhythmicity was maintained in alcoholics, the timing of the circadian acrophase was delayed significantly (P = 0.006) during acute abstinence (1022 [clocktime] +/- 34 min) as compared with normal controls (0743 [clocktime] +/- 34 min), and the amplitude of circadian cortisol rhythms exceeded normal in five of 10 alcoholics. Analysis of data in one alcoholic subject by a new multiparameter deconvolution method demonstrated increases in secretory burst amplitude (0.64 microgram/dl +/- 0.08 SD), mass of cortisol released per burst (9.8 micrograms/dl +/- 1.2 SD), and daily endogenous cortisol production rate (22 mg +/- 2.4 SD) during acute abstinence. These values were statistically different when compared with seven normal controls and the subjects' values during sustained abstinence (P less than 0.02). In conclusion, the results of the present study suggest increased daily production of cortisol as a possible mechanism underlying the elevated serum cortisol concentrations in chronic alcoholics during acute abstinence. This abnormality is shown to be reversible with sustained abstinence from alcohol.     

A correlation between clinical pancreatitis and isoenzyme patterns of amylase

Fifty-seven patients admitted with the clinical diagnosis of acute pancreatitis had isoamylase analysis on their sera to determine the source of their hyperamylasemia. Our objective was to correlate the isoamylase pattern with our clinical observations. Thirty-nine of 57 patients (68%) had pancreatic hyperamylasemia as expected, but 18 of 57 patients (32%) had normal levels of pancreatic amylase. The hyperamylasemia in the latter group was due either to nonpancreatic hyperamylasemia (16 of 57) of macroamylasemia (2 of 57). Consequently, hyperamylasemia associated with abdominal pain, nausea, and vomiting led to the incorrect diagnosis of acute pancreatitis in 32% of the patients. The measurement of isoamylase profiles can be done rapidly and inexpensively. Knowledge that hyperamylasemia is nonpancreatic in origin may have an important influence on treatment, hospitalization, and the extent of laboratory and radiologic investigation.     

Isoamylase levels in bone marrow transplant patients are affected by total body irradiation and not by graft-versus-host disease

The mean total serum amylase levels in patients was 3.2±0.5 kat/l (±SE) before total body irradiation (TBI) prior to bone marrow transplantation of which 50% was due to pancreatic isoamylase and 50% salivary isoamylase. Total serum amylase increased to a maximum of 100.3±12.3 kat/l on the first day after TBI and most of this increase was due to an increase in salivary isoamylase (90.0±12.1 kat/l). In association with this, all patients had clinical symptoms of parotitis. An increase in pancreatic isoamylase was found in 27% of the patients; however; none of them had clinical symptoms of pancreatitis. Serum amylase levels returned to normal within 5 days after TBI but then decreased to subnormal values, remaining below the normal range for 3 weeks. Pancreatic isoamylase returned to pre-irradiation levels 1.5 months after TBI, while salivary isoamylase remained low for the rest of the observation time. TBI of 7.5 Gy at 26 cGy/min gave significantly lower salivary amylase at 2 days after TBI compared with 10 Gy at 4 cGy/min: 32±4 versus 76±13 kat/l (P<0.05). At 2.5 and 6 months after TBI significantly higher total amylase levels were recorded for patients treated with 7.5 Gy of TBI compared with 10 Gy: 2.5±0.4 and 2.7±0.3 versus 2.0±0.5 and 0.8±0.3 kat/l, respectively (P<0.01, P<0.05, respectively). Acute or chronic GVHD did not affect acinar cells in this investigation.     

The poor man's isoamylase analysis (wheat inhibitor). Does it work?

The value of a wheat inhibitor assay to measure the pancreatic isoamylase fraction in the serum was evaluated in a clinical trial. Fifty-four patients with a variety of disorders and wide range in serum amylase levels were studied comparing pancreatic isoamylase levels measured by both cellulose acetate membrane electrophoresis and wheat inhibitor assay. The overall correlation was excellent (r = 0.96), and was best when the total serum amylase was high. The predominate serum isoamylase was correctly predicted in 45 of 54 (83%) patients, with an overall specificity of 73 per cent and sensitivity of 96 per cent. Because it is easy to perform, the test is recommended for clinical use by those without access to more sophisticated forms of isoamylase analysis.     

Serum amylase and its isoenzymes: a clarification of their implications in trauma

Previous reports on the use of the serum amylase level to assess pancreatic injury in patients with blunt abdominal trauma have been disappointing. The availability of methods to measure the serum isoamylases (P & NP) might be expected to improve the accuracy with which the serum amylase level is used. Sixty-one patients treated for a variety of blunt trauma injuries were studied. All categories of injury were included. Isoamylase levels were determined from admission sera and were compared to injuries found at laparotomy. Three patients had major pancreatic injury but only two of these patients showed a rise in the pancreatic isoamylase. Sixteen additional patients had a rise in the pancreatic isoamylase without evidence of pancreatic injury. Eight of these patients had no component of abdominal injury whatsoever. Two patients with isolated head injury had substantial elevations of pancreatic isoamylase. The regulation of serum amylase is multifactorial and variable. The measurement of serum isoamylase levels does not offer great improvement over the serum amylase in evaluating patients with blunt abdominal trauma.     

Acute pancreatitis and normoamylasemia. Not an uncommon combination.

A consecutive series of 352 attacks of acute pancreatitis (AP) was studied prospectively in 318 patients. AP was ascertained by contrast-enhanced CT scan in all but four cases in which diagnosis was made at operation or autopsy. Sixty-seven of these cases (19%) had normal serum amylase levels on admission (i.e., less than 160 IU/L, a limit that includes 99% of control values), a figure considerably higher than generally admitted. When compared to AP with elevated serum amylase, normoamylasemic pancreatitis was characterized by the following: (1) the prevalence of alcoholic etiology (58% vs. 33%, respectively, p less than 0.01), (2) a greater number of previous attacks in alcoholic pancreatitis (0.7 vs. 0.4, p less than 0.01); and (3) a longer duration of symptoms before admission (2.4 vs. 1.5 days, p less than 0.005). In contrast AP did not appear to differ significantly in terms of CT findings, Ranson's score, and clinical course, when comparing normo- and hyperamylasemic patients, although there was a tendency for normoamylasemic patients to follow milder courses. Serum lipase was measured in 65 of these normoamylasemic cases and was found to be elevated in 44 (68%), thus increasing diagnostic sensitivity from 81% when amylase alone is used to 94% for both enzymes. A peritoneal tab was obtained in 44 cases: amylase concentration in the first liter of dialysate was greater than 160 IU/L in 24 cases (55%), and lipase was greater than 250 U/L in 31 cases (70%). Twelve of these 44 cases had low peritoneal fluid and plasma concentrations for both enzymes. Thus little gain in diagnostic sensitivity was obtained when adding peritoneal values (96%) to serum determinations. AP is not invariably associated with elevated serum amylase. Multiple factors may contribute to the absence of hyperamylasemia on admission, including a return to normal enzyme levels before hospitalization or the inability of inflamed pancreases to produce amylase. Approximately two thirds of cases with normal amylasemia were properly identified by serum lipase determinations. AP does not appear to behave differently when serum amylase is normal or elevated, and should therefore be submitted to similar therapeutic regimens in both conditions.     

Timing of surgical drainage for pancreatic pseudocyst. Clinical and chemical criteria.

Traditional concepts of managing pancreatic pseudocysts have changed with the advent of computerized tomography (CT) and ultrasound scanning, but new misconceptions related to spontaneous resolution have replaced some old ones. This report shows a difference in natural history and treatment requirements when pseudocysts are associated with acute versus chronic pancreatitis. There were 42 consecutive patients with pseudocysts treated over 5 years. Thirty-one were known alcoholics, two had gallstone pancreatitis, and nine had idiopathic pancreatitis. An attack of acute pancreatitis was identifiable within 2 months preceding in 22 patients, but there were only chronic symptoms in 20. Spontaneous resolution of the pseudocyst occurred in three patients (7%), all of whom had recent acute idiopathic pancreatitis, normal serum amylase levels, and pancreatograms showing normal pancreatic ducts freely communicating with the pseudocyst. Factors associated with failure to resolve included known chronic pancreatitis, pancreatic duct changes of chronic pancreatitis, persistence greater than 6 weeks, and thick walls (when seen) on scan. Nearly all (18/19) patients with known chronic pancreatitis had successful internal drainage of the pseudocysts immediately upon admission, whereas 6/20 patients with antecedent acute pancreatitis were found to require external drainage at the time surgery was eventually elected. Isoamylase analysis, performed on serum from 19 patients by means of polyacrylamide gel electrophoresis, detected the abnormal pancreatic isoamylase pattern described as "old amylase" in 15. When old amylase was present in the serum, internal drainage was always possible (14/14). In four of five patients whose serum contained no detectable old amylase, internal drainage was not possible regardless of the length of prior observation. There were four nonfatal complications arising from an acute pseudocyst during the wait for maturity. It is concluded that prolonged waiting is expensive and unnecessary for pseudocysts in chronic pancreatitis when there has been no recent acute attack. However, pseudocysts developing after identifiable acute pancreatitis should be observed in the safety of a hospital for up to 6 weeks to allow for either spontaneous resolution or maturation of the cyst wall. The appearance of old amylase in the serum suggests that the pseudocyst wall has achieved sufficient maturity to allow safe internal anastomosis.     

Effect of chronic alcoholism on semen—studies on lipid profiles

The effect of chronic alcoholism on various seminal parameters (sperm concentration, rate of forward motility, percentage of abnormal spermatozoa, lipid profiles of seminal plasma and spermatozoa) was studied together with the serum levels of testosterone and oestradiol. In chronic alcoholics there was a marked reduction in sperm concentration and in the rate of their forward motility, and increase in the number of spermatozoa with morphological abnormalities when compared to age-matched normal fertile subjects. Serum levels of testosterone were decreased while oestradiol levels were increased in chronic alcoholic men. Studies of lipid profiles showed a marked decrease in the total phospholipid concentration in spermatozoa, primarily in sphingomyelin, phosphatidyl choline and ethanolamine fractions. The cholesterol phospholipids ratio in spermatozoa was increased in alcoholics. In the seminal plasma of chronic alcoholics, there was a decrease in total lipid, in glyceride glycerol and in free and esterified cholesterol. Of the phospholipid classes, sphingomyelin and phosphatidyl ethanolamine showed a significant reduction. In general, the present study provides evidence for the adverse effects of chronic alcoholism on serum hormones, sperm count, morphology, motility and seminal lipid profiles. These may be responsible for the fertility disorders common in chronic alcoholics.     

Effect of long-term alcohol abuse on male sexual function and serum gonadal hormone levels

Purpose The relationship between chronic alcohol abuse and male sexual dysfunction and pituitary gonadal function abnormalities remains uncertain. The purpose of this study was to assess the effect of chronic alcoholism on sexual functions and serum hormone levels. Materials and methods Forty-five chronically alcoholic men and a control group of thirty healthy non-alcoholic, volunteers were enrolled in the study. Each of the men in the study and control group were interviewed according to a sexual dysfunction questionnaire by an urologist. Blood samples were collected for evaluation of hormone levels. Sera were stored at-70°C for analysis. Results The sexual desire and erection scores of alcoholic men were not statistically different from those of the control group. Fourteen out of the 45 alcoholic men complained of loss of erection during sexual activity. No significant difference in hormone levels between groups was found except for FSH. Conclusion In the absence of hepatic and gonadal failure in chronically alcoholic men, there is no significant difference in serum hormonal levels, sexual dysfunction form, and sexual functions between alcoholics and normal healthy nonalcoholic men.     

A method of measuring quantitative hepatic function and hemodynamics in cirrhosis: the changes following distal splenorenal shunt

Quantitative measurement is required to define the severity of chronic liver disease and the effects of therapy on its complications. This paper presents a method of such assessment based on measurement of hepatocyte function, liver volume, functional liver blood flow, portal perfusion and cardiac output. Data are presented on 54 patients evaluated prior to, and one year after DSRS for variceal bleeding. Preoperative testing showed that alcoholics (n = 24) had significantly (p less than 0.05) larger liver and smaller spleen volumes than nonalcoholic cirrhotics (n = 22) and patients with portal vein thrombosis (n = 8), but that the other parameters were not significantly different by etiologies. At one year after DSRS: all groups showed a significant (p less than 0.01) reduction of 41 per cent in spleen size: liver volume was significantly (p less than 0.05) reduced in cirrhotics: there was a significantly (p less than 0.01) greater loss of portal perfusion in alcoholic cirrhosis: liver blood flow showed a significant (p less than 0.05) rise in alcoholics when compared to nonalcoholics and portal vein thrombosis patients: cardiac output rose in alcoholic cirrhosis: hepatocyte function was not significantly different in any group. This study shows that in patients all doing well clinically one year after DSRS, there are markedly different hemodynamic responses. Further studies on cirrhosis aimed at improving therapy for its complications should include some objective, quantitative assessment, first to define the study population, and second to measure the effect of the therapy.     

Relationship between degree of renal failure and impairment of intestinal calcium absorption.

The coefficient of true intestinal calcium absorption (a value) was measured by a double radioisotope technique in 29 chronic renal failure patients (serum creatinine levles 2.5-19.5 mg%) aged 20-75 years. The mean log 10 a (+/- standard error) of these subjects (1.197 +/- 0.031) was significantly lower (p less than 0.001) than that of 52 controls (1.532 +/- 0.024), the geometric mean of the renal failure group (15.7%) being approximately half (46%) of that of the controls (33.9%). The decrease of a value of the uremic patients was more pronounced in the younger than in the older subjects as shown by a statistically significant (r = 0.570; p less than 0.001) positive curvilinear, relationship between a value and age. The lowest intestinal calcium absorptions were observed in patients with a serum creatinine level of approximately 11 mg%, the a values increasing progressively with lower or larger than 11 mg% serum creatinine levels, as shown by a statistically significant (r = 0.485; p less than 0.01) parabolic relationship between a value and serum creatinine. The possible mechanism(s) of this relationship are discussed.     

Alcohol intoxication, injuries, and dangerous behaviors--and the revolving emergency department door

Suicides, homicides, motor vehicle crashes, and other violent deaths and injuries are linked inextricably to alcoholism. The association of injury and alcoholism should be particularly obvious to Emergency Department (ED) physicians. We sought to determine the extent to which intoxicated patients in an ED were properly diagnosed, counselled, and referred for substance abuse care. We reviewed the charts of 153 consecutive patients seen in a teaching hospital ED who had blood alcohol levels above 100 mg%. Most were male (70%), white (62%), young (mean age, 34 years) and severely intoxicated (mean BAL, 245; range, 109-558 mg%). Forty-six per cent of visits were for trauma; half of the patients were victims of violent assaults. The intoxicated patients received extensive medical and surgical management: an average of five tests or X-rays were performed per patient; 75% received at least one medication; at discharge 48% were referred for followup to medical or surgical clinics. In contrast, few patients were evaluated for dangerous behaviors or referred for treatment of alcoholism: only 19 patients (12.5%) were asked about depression, suicide, or homicide; 15% were advised to stop drinking; 13% received a referral to a psychiatrist, mental health worker, or alcohol rehabilitation facility. Forty-seven per cent of patients received "stat" intravenous thiamine (although the Wernicke-Korsakoff syndrome is rare). In contrast, only 16% received a stat on-site psychiatric consultation (although dangerous behaviors are common in alcoholics). There was a strong, statistically significant negative association between the occurrence of an injury and the decision to initiate treatment and referrals for alcoholism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Compartment syndrome in a young male caused by acute alcoholic rhabdomyolysis

We report a case of young male who developed compartment syndrome of his left leg caused by rhabdomyolysis following a heavy binge of alcohol. The laboratory data on his admission revealed extremely elevated serum levels of CPK (108,021 IU.l-1). The serum levels of potassium and creatinine were within normal ranges. He also had myoglobinuria. He required fasciotomy after admission. Diuretics and a large volume of fluids were given to prevent the renal failure. His postoperative course was uneventful. The direct toxic effects of alcohol and the prolonged ischemia of his lower leg induced by acute alcoholic intoxication, are thought to have played a major role in the triggering of the acute rhabdomyolysis. Acute alcoholic rhabdomyolysis should be considered in any intoxicated patient who presents muscle tenderness and weakness. The early recognition and prompt treatment are essential to prevent serious complications.