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Biomedical subjects

D L Bouwman

Publications and source records attributed to D L Bouwman.

At least 37 records · Page 2Linked to original sources

Interpretation of serum amylase levels in the critically ill patient.

To understand better the incidence and meaning of hyperamylasemia in the intensive care setting, cellulose acetate membrane electrophoresis was used to measure the isoenzymes of serum amylase in 192 patients with a variety of critical illnesses. Seventy of these patients had elevated serum amylase levels, but none had clinical or biochemical evidence of acute pancreatitis or renal failure. Of the 70 patients who had hyperamylasemia, in only 18 (26%) was it due solely to an elevation of the pancreatic isoamylase fraction. The remaining 52 patients were hyperamylasemic due to elevations in the nonpancreatic isoamylase fraction or elevations in both pancreatic and nonpancreatic isoamylase fractions. These data indicate that hyperamylasemia in the absence of clinical pancreatic disease is common in the ICU and is frequently caused by nonpancreatic production of serum amylase. Caution is, therefore, advised in interpreting elevated serum amylase levels in critically ill patients.

Amylases↗

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.

Acute Disease↗

Alcohol-induced salivary hyperamylasemia.

The effects of alcohol intoxication on serum amylase levels were tested in both normal subjects and chronic alcoholics. Paired samples of ethanol levels and isoamylase levels in the normal subjects (n = 11) showed a rise in both total serum amylase (P less than 0.01) and nonpancreatic isoamylase (P less than 0.05) after drinking. Unpaired cohort groups of sober chronic alcoholics at a rehabilitation facility (n = 46) and intoxicated chronic alcoholics in an emergency room (n = 58) were also compared. Average blood alcohol levels in the intoxicated controls were 93 mg% compared to a level of 301 mg% in the intoxicated chronic alcoholic. Intoxication superimposed on chronic alcoholism caused a moderate rise in the total serum amylase (NS) and a significant elevation of the nonpancreatic isoamylase (P less than 0.01). Sober chronic alcoholics had a significantly greater average total serum amylase (P less than 0.001) and nonpancreatic isoamylase (P less than 0.01) than the normal controls. No difference in the average pancreatic isoamylase levels was seen in any group. These data suggest a biphasic response to alcohol on the serum amylase level. Acute and chronic changes appear to operate independently. The cause for these effects is speculative. Isoamylase analysis is needed in the alcoholic population to sort out the meaning of hyperamylasemia.

Abdomen↗

Isoamylase determinations in patients undergoing endoscopic retrograde cholangiopancreatography.

The isoamylase profile in 24 patients undergoing ERCP were prospectively studied. Serum samples were obtained prior to and 4 hours following ERCP. All patients had the bile duct successfully visualized and in all but one patient the pancreatic duct was seen. Twenty-two of the 24 patients had a rise in the total serum amylase following ERCP. Most often this was from pancreatic sources, but two patients had a substantial rise in the salivary isoamylase. No patient developed clinical signs of acute pancreatitis. The patients in whom ductal pathology was found had a significant rise in pancreatic isoamylase following ERCP. Patients with normal pancreatic ducts did not show a significant rise in the pancreatic isoamylase. Patients who were hyperamylasemic prior to ERCP had a statistically significant post-ERCP rise in pancreatic isoamylase. In contrast, those who were normoamylasemic had no significant change in their pancreatic isoamylase level following the procedure. Development of hyperamylasemia is an expected sequela of ERCP, most often is due to pancreatic sources, and is rarely of clinical significance.

Amylases↗

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.

Adult↗

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.

Adolescent↗

Outcome after peritoneo-jugular shunting of pancreatic ascites.

Three patients with pancreatic ascites documented by ascitic fluid protein greater than 2.5 g/dl and elevated amylase in their peritoneal fluid were treated by peritoneo-jugular shunting (PJS). Patient 1 was so treated inadvertently; Patient 2 had resolving amylase levels but increasing amounts of ascites; Patient 3 had clear, active pancreatic ascites. None incurred untoward effects from this procedure. Ventilatory compromise from reduced diaphragmatic excursion was ameliorated in all patients. Two patients required no further therapy. The third patient was greatly improved in preparation for definitive surgical therapy for a leaking pancreatic pseudocyst. The infusion of enzyme-rich fluids into the circulation may be responsible for certain systemic effects of pancreatitis. Coagulation defects are a known complication of PJS for the ascites of Laennec's cirrhosis. There was no evidence of histamine-mediated cardiovascular collapse, exacerbation of respiratory failure, or coagulation defects in these patients. We conclude that these complications are not the inevitable results of PJS of pancreatic ascites.

Adult↗

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.

Amylases↗

Acute alcohol intoxication: significance of the amylase level.

To evaluate the effects of acute alcohol intoxication on serum amylase and isoamylase levels, 58 clinically intoxicated patients with blood alcohol levels greater than 100 mg/dL were studied. Comparisons were made to normal control and a sober chronic alcoholic group. Admitting serum isoamylase levels were determined by cellulose acetate membrane electrophoresis and serum amylase levels measured by the Amylochrome technique. The average blood alcohol level in the intoxicated group was 301 +/- 99 mg/dL. Thirty of the 58 patients had hyperamylasemia (greater than 207 IU). Twenty-five of these 30 patients had hyperamylasemia from nonpancreatic sources (increased salivary isoamylase). Two of the 30 patients had pancreatic hyperamylasemia and three patients had elevated levels of both isoamylases. Neither of the patients with pancreatic hyperamylasemia had clinical evidence of acute pancreatitis. Although nine of the 58 patients had abdominal pain and clinical symptoms suggestive of acute pancreatitis, none of these patients had elevated pancreatic isoamylase. The finding of hyperamylasemia in acutely intoxicated patients is common. This is most frequently due to a rise in the salivary (nonpancreatic) isoamylase. The reliability of the total serum amylase as an indication of pancreatic disease in the intoxicated patient is questioned.

Acute Disease↗

Hyperamylasemia: a result of intracranial bleeding.

The unexpected finding of hyperamylasemia in a patient with isolated head injury prompted a study of amylase levels in patients with various degrees of cranial trauma. None of seven patients with isolated maxillofacial trauma had hyperamylasemia. This group was studied to discount injury to salivary glands as a source of elevated amylase levels. Only one of ten patients with simple cranial injury without computerized tomographic (CT) scan evidence of intracranial bleeding had hyperamylasemia. Six of ten patients with CT scans positive for intracranial bleeding had hyperamylasemia. Isoamylase analysis showed that the source of the hyperamylasemia was varied. These results suggest a central neural control of serum amylase levels. The reliability of the serum amylase level as an indication of pancreatic trauma in a patient with concomitant head injury is questioned.

Amylases↗

Aged amylase: a valuable test for detecting and tracking pancreatic pseudocysts.

Amylase-rich fluid that incubates ("ages") within a pancreatic pseudocyst undergoes a change that can be detected by isoenzyme analysis of amylase from the serum. This aging is a result of deamination of the asparagine and glutamine residues on the amylase molecule. Eighteen of 20 patients with surgically proved pseudocysts had greater than 15% aged (deaminated) amylase in their serum. Levels of aged amylase returned to normal following treatment of their pseudocysts. Twenty of 23 patients with acute pancreatitis had levels of aged amylase below 15% (P less than .05). A criterion of 15% aged amylase resulted in 87% specificity, and 91% sensitivity for the diagnosis of pseudocysts. Because this test is noninvasive and easy to perform, it should become the ideal screen for patients at risk of development of pseudocysts, Endoscopic retrograde pancreatography, ultrasonography, and abdominal computed tomographic scanning should be reserved for confirmation of the diagnosis when the result of isoenzyme analysis is positive.

Amylases↗

A continuing appraisal of pancreatic ascites.

Pancreatic ascites is a distinct clinical entity characterized by elevated amylase and protein levels in the ascitic fluid. This should be distinguished from the ascites of cirrhosis, tuberculosis or metastatic carcinoma. Precise delineation of the ductal anatomy by endoscopic retrograde pancreatography preoperatively will enhance the ability of the surgeon to plan a rational operation and will, thereby, provide the best results. Medical treatment may obviate surgical intervention in a small number of instances but contains intrinsic hazards and should not be prolonged beyond three weeks. In carefully selected patients, limited pancreatic resection, encompassing the site of leakage, produces excellent results.

Adult↗

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.

Acute Disease↗

Differential serum protein changes following supplemental albumin resuscitation for hypovolemic shock.

The effects of supplemental albumin infusion on serum protein homeostasis were studied in 94 seriously injured patients who received an average of 14.4 transfusion, 9.2 L electrolyte solution, and 829 ml fresh frozen plasma before and during operation. Based on randomization, 46 patients received an average of 31 gm albumin during operation followed by 150 gm/day for 5 days; 48 patients received no albumin. Supplemental albumin caused a significant (p = less than 0.05) increase in total serum protein and albumin concentrations. In contrast, supplemental albumin caused a significant decrease in alpha 1 globulin, alpha 2 globulin, beta globulin, gamma globulin, and fibrinogen levels. The prothrombin time used as index of prothrombin concentration was significantly prolonged in albumin patients. These changes, not previously documented, need further evaluation to determine clinical significance.

Adult↗

A logical solution to the perforated ulcer controversy.

Until recently, the Graham patch was the undisputed method of management for a perforated duodenal ulcer. Results of our experience with 186 patients treated at Wayne State University Affiliated Hospitals from 1970 through 1978 dispute this concept and suggest that a definitive operation is the procedure of choice. One hundred and thirty-seven of the patients were treated with an omental patch, and 47 underwent a definitive operation; 114 of the patients were available for an 18 month follow-up study. It was found that previous ulcer symptoms were not an accurate predictor of the need for a subsequent definitive operation and that mortality was determined by the age and condition of the patient at the time of operation rather than by the choice of operation itself. It is recommended that the perforation itself is an indication for a definitive operation unless the patient is in a state of shock at the time of operation. Vagotomy and pyloroplasty have proved to be safe, reliable, definitive operations in this situation.

Aged↗

Early sympathetic blockade for frostbite--is it of value?

Sympathectomy has been advocated in the therapy of acute frostbite because ischemia is one determinant of injury severity. Among 66 frostbite victims treated from 1976 through 1978, a group of 15 patients with acute, bilaterally equal injuries judged to be third or fourth degree were treated with immediate intra-arterial reserpine (IAR) in one limb and ipsilateral sympathectomy. Three additional patients who were excellent candidates underwent immediate sympathectomy. The average interval from injury to IAR injection was 3 hours (range 1 to 24 hours). The average interval from injury to sympathectomy was 3 days (range, 12 hours to 10 days). Efficacy of therapy was assessed by comparison of the sympathectomized limb to the contralateral untreated limb. There was no conservation of tissue, resolution of edema, pain reduction, or improved function in sympathectomized limbs compared with those treated with IAR. One patient demarcated more rapidly and one other patient appeared to be protected from recurrent injury. Sympathectomy was not effective therapy for acute frostbite even when achieved early with IAR. Late protection against subsequent cold injury appears to be the only benefit of sympathectomy for frostbite.

Adolescent↗