Near-fatal intra-abdominal bleeding from a ruptured follicle during thrombolytic therapy.
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Biomedical subjects
Publications and source records attributed to P G Lankisch.
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CONCLUSION: Pleural infiltrates are indicative of severe acute pancreatitis and a negative prognostic parameter for the course of the disease. BACKGROUND: The purpose of this study was to determine the frequency of pulmonary infiltrates in acute pancreatitis and their importance for evaluating the severity of the disease. METHODS: Incidence and localization of pulmonary infiltrates were evaluated in 140 patients with acute pancreatitis. Chest X-ray was obtained within 24 h, and a contrast-enhanced computed tomography within 72 h after admission. Ranson's prognostic parameters were estimated within the first 48 h. RESULTS: Patients with pulmonary infiltrates (n = 36, 26%) had a significantly higher Ranson's score and pancreatic necroses more frequently than patients without this complication, plus a higher mortality rate.
Results of the SPT and the ERCP staged for their severity were compared in 202 patients. The correlation between both investigations was significant (p < 0.001); however, ERCP showed significantly more severe changes (p = 0.04). Furthermore, we found that 129 (64%) patients had parallel SPT and ERCP results, matching in all four gradings of severity. Forty-three (21%) patients had abnormal results for both SPT and ERCP, but the severity gradings did not parallel. Finally, 30 (15%) patients showed totally nonparallel results, a normal SPT and abnormal ERCP, or vice versa. Abnormal ERCP but normal SPT results were found in 23 of these 30 patients (group 1), and normal ERCP but abnormal SPT results in the seven remaining cases (group 2). In the first group, more patients had a history of acute pancreatitis compared to the second group (19 vs. one, p < 0.005). Based on medical history, laboratory and functional test results, and other morphological tests, chronic pancreatitis was diagnosed in two of 23 patients in group 1 and in all seven patients in group 2. Follow-up interviews (86 +/- 54 months) were possible in 20 of the remaining 21 patients in group 1 and showed definite chronic pancreatitis in one and probable chronic pancreatitis in another two of them, whereas in the other 17 patients no symptoms of acute pancreatitis or abdominal pain suggestive of chronic pancreatitis had occurred. In conclusion, both SPT and ERCP should be used to complement each other when chronic pancreatitis is suspected. ERCP seems to over-diagnose the disease since duct changes may only reflect scars after severe acute pancreatitis, or old age, and are not necessarily a sign of chronic pancreatitis. SPT seems to diagnose chronic pancreatitis with more reliability.
The course of a first attack of acute pancreatitis was evaluated in a retrospective study of 602 patients, who were admitted between 01.01.1980 and 30.09.1993 to the Centers of Internal Medicine and Surgery of the University of Göttingen (n = 417) and from 16.11.1986 to 30.06.1994 to the Municipal Hospital of Lüneburg (n = 185). Etiology was biliary tract disease in 227 (37.7%), alcohol abuse in 177 (29.4%), unknown in 133 (22.1%), and other causes in 65 (10.8%) patients. Mean hospital stay was 27.9 +/- 24 days (x +/- SD), median 23 days. Pancreatic pseudocysts developed in 14.3% of the patients, and surgical treatment was necessary in 11.1%. Within the first 48 hours, respiratory insufficiency was observed in 63.2% of the 204 patients undergoing arterial blood gas analysis while renal impairment occurred in 32.6% of 602 patients. Artificial ventilation was indicated in 12.5%, and dialysis in 7% of the patients. Mortality rate was 6.1%, correlating significantly with respiratory and renal impairment and procedures in connection with these complications and also with transfers from other hospitals.
The aim of this retrospective study was to determine the time intervals between the onset of symptoms and diagnosis of celiac disease on the basis of a questionnaire that was published in the journal of the German Celiac Society (Verbandszeitschrift der Deutschen Zöliakie-Gesellschaft). 408 adult patients in whom the diagnosis of celiac disease was made after the age of 15 responded to the questionnaire. The time interval between the onset of symptoms and diagnosis (total diagnostic interval) was 5.4 (median) and 10.1 +/- 12.3 (mean +/- SD) years, interval-1 (time interval between the onset of symptoms and the first visit to a doctor) was 0.4 (median) and 2.2 +/- 6.6 (mean +/- SD) years, and interval-2 (time interval between the first visit to a doctor and the diagnosis) was 3.9 (median) and 8.0 +/- 10.4 (mean +/- SD) years. The time intervals shortened only a little over the years. At all times, interval-2 was significantly longer than interval-1. There were no differences between female (n = 328) and male (n = 80) patients and between the age groups. Furthermore, none of the gastrointestinal and non-gastrointestinal symptoms had had a distinct influence on all diagnostic intervals and also the fact that other family members having the disease did not shorten any of the intervals. In summary, the diagnostic intervals for recognizing celiac disease are still unacceptably long. More public awareness work has to be done so that patients can recognize their symptoms and doctors especially can suspect celiac disease sooner and perform the necessary diagnostic procedures when patients present with suggestive symptoms.
In 38 patients, exocrine pancreatic function was tested by means of the secretin-pancreozymin test (SPT) and pancreatic duct system with endoscopic retrograde cholangiopancreatography (ERCP) 34 +/- 36 mo (mean +/- SD, range 1-156 mo) following acute pancreatitis. SPT and ERCP results were both normal in 19 (50%). They were both abnormal in four (11%) patients (group 1). Fourteen (37%) patients with normal SPT had abnormal ERCP test results (group 2), and one (3%) patient with normal ERCP had abnormal SPT (group 3). All patients except one of group 2 could be followed up within a mean observation time of 105 +/- 46 mo (range 24-168 mo): Chronic pancreatitis developed in all four patients of group 1, in one patient of group 2, and in the single patient of group 3, and suspected chronic pancreatitis in another patient of group 2. Eleven of the remaining 12 patients with abnormal ERCP results, but normal exocrine pancreatic function (group 2), showed no signs or symptoms of acute or chronic pancreatitis. It is concluded that (1) recovery to normal does not necessarily occur after acute pancreatitis, (2) progression to chronic pancreatitis is possible at a considerable percentage, and (3) duct changes demonstrated by ERCP may persist without any later signs and symptoms of acute or chronic pancreatitis.
The natural course of pain in chronic pancreatitis was followed up in 318 patients over 10.6 +/- 8.0 years (median, 9.0 years). By the end of our follow-up, a significant decline in pain in alcoholics (n = 228) and nonalcoholics (n = 90) (p < 0.001 and p < 0.03) was marred by the fact that, even after more than 10 years, 50% of alcoholics and 62% of nonalcoholics still reported pain attacks (difference insignificant). Only alcoholics had pain relief with increasing exocrine pancreatic insufficiency (p < 0.02), but 54% of alcoholics and 73% of nonalcoholics still had pain attacks despite severe, enzyme substitution-requiring exocrine pancreatic insufficiency. The development of severe endocrine pancreatic insufficiency did not significantly influence the course of pain. It is concluded that no clinically relevant differences exist in the course of pain in alcoholic and nonalcoholic chronic pancreatitis.
Painful acute pancreatitis masking pancreatic carcinoma and painless acute pancreatitis with shock or coma as leading symptoms have been described before. We report a first case of almost-painless pancreatitis mimicking pancreatic carcinoma with spontaneous normalization of symptoms and biochemical as well as imaging procedure findings.
To determine the incidence and severity of drug induced acute pancreatitis, data from 45 German centres of gastroenterology were evaluated. Among 1613 patients treated for acute pancreatitis in 1993, drug induced acute pancreatitis was diagnosed in 22 patients (incidence 1.4%). Drugs held responsible were azathioprine, mesalazine/sulfasalazine, 2',3'-dideoxyinosine (ddI), oestrogens, frusemide, hydrochlorothiazide, and rifampicin. Pancreatic necrosis not exceeding 33% of the organ was found on ultrasonography or computed tomography, or both, in three patients (14%). Pancreatic pseudocysts did not occur. A decrease of arterial PO2 reflecting respiratory insufficiency, and an increase of serum creatinine, reflecting renal insufficiency as complications of acute pancreatitis were seen in two (9%) and four (18%) patients, respectively. Artificial ventilation was not needed, and dialysis was necessary in only one (5%) case. Two patients (9%) died of AIDS and tuberculosis, respectively; pancreatitis did not seem to have contributed materially to their death. In conclusion, drugs rarely cause acute pancreatitis, and drug induced acute pancreatitis usually runs a benign course.
An alcoholic, 67-year old retired male nurse complained of abdominal pain, loss of appetite and weight loss of 10 kg within one year. Based on elevated serum enzyme levels, ultrasonography and computed tomography examinations, an acute attack of chronic pancreatitis with several pancreatic pseudocysts was diagnosed. Ultrasonographically, an 1.8 cm phi, echo-free, pulsatile, space-occupying lesion, suggestive of a pancreatic pseudoaneurysm, was found at the right lateral margin of an almost echo-free pseudocyst measuring 6.8 x 5.6 x 5.0 cm in the head of the pancreas. Shortly before the planned discharge when the patient felt well, he developed acute abdominal pain. An immediate ultrasound examination showed an inhomogenous and echo-dense pseudocyst, in short, an acute hemorrhage. Rupture of the pseudoaneurysm of the Arteria gastroduodenalis was suspected and later confirmed by angiography and laparotomy. After proximal an distal ligation of the vessel and fibrin sealing of the inner surface of the cyst, the patient recovered and, under alcohol abstinence, has been free of symptoms since one year.
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The natural course of the classical symptoms of chronic pancreatitis, i.e. pain, exocrine and endocrine pancreatic insufficiency, was followed up in 335 patients over a median of 9.8 years (mean 11.3 +/- 8.3 years). Pain relief was not obtained in the majority of patients, even after a longterm observation of > 10 years, and severe exocrine and/or endocrine insufficiency, severe duct abnormalities and pancreatic calcifications developed. Alcohol abstinence failed to have a significant beneficial effect on pain. Pancreatic surgery led to pain relief immediately after operation, but later on the pain course between operated and nonoperated patients was not significantly different. Repeated exocrine pancreatic function tests in 143 patients showed that functional exocrine impairment came to a standstill (46%), or improved (11%). At the end of the observation, 22% of 335 patients still had normal endocrine function and only 40% required insulin treatment. Alcohol abstinence had a significant beneficial effect on endocrine, but not on exocrine pancreatic insufficiency. Chronic pancreatitis led to a sharp increase in unemployment and retirement. Pancreatic carcinoma occurred in 3% and extrapancreatic carcinoma in 4%. The mortality rate within the observation period was 22%, pancreatitis-induced complications accounted for 13% of these deaths.
The clinical, biochemical (serum enzymes), and morphologic course of acute pancreatitis was studied in 83 consecutive patients from time of admission until 3 months after discharge. At discharge, all 75 surviving patients had no more symptoms of acute pancreatitis, even though amylase (in 11%) and lipase (in 25%) were still elevated, computed tomography (CT) findings still abnormal (in 81%), and necrosis amounting up to 50% of the gland still present (in 24%). There was no significant correlation between serum enzymes and CT findings at discharge. Three months later, with the exception of one patient with an acute relapse of the disease, all followed-up patients were free of symptoms and had normal serum amylase, whereas lipase was still elevated in 10%, and CT findings abnormal in 23%. Subsiding symptoms provided a more accurate picture of the patients' recovery than the biochemical markers, and even more so that the morphologic findings.
A longterm review (median follow up 11 years) of the postoperative course of pancreatic pseudocysts was undertaken in 55 patients with chronic pancreatitis. While 96% of the patients were free of pain immediately after the operation this figure fell to 53% subsequently. Alcohol abstinence did not significantly reduce pain. Endocrine pancreatic deterioration (60%) was significantly (p = 0.0059) more frequent than exocrine (38%). Unemployment increased from 2 to 41%; retirement rose from 0 to 33%, mainly as a result of pancreatitis. Twenty one (38%) patients died. Chronic pancreatitis related death rate was 14%. Three patients died of extrapancreatic carcinomas.
The value of the lipase/amylase ratio for early etiological differentiation of acute pancreatitis was tested in 103 consecutive patients with acute pancreatitis from an ongoing prospective study. On admission, amylase, but not lipase, was significantly lower in alcoholics than in nonalcoholics in general and especially in patients with biliary pancreatitis. Alcoholics as a group had significantly higher lipase/amylase ratios than non-alcoholics and patients with acute biliary pancreatitis. But although the mean values of the ratio were significant, sensitivity, specificity, positive and negative predictive values of lipase/amylase ratio were insufficient to separate alcoholics from nonalcoholics, patients with alcohol-induced pancreatitis from those with biliary etiology, and patients with biliary pancreatitis from those with pancreatitis of other etiologies in the individual case. Finally, there was no correlation between the ratio and the amount of pancreatic changes as judged from computed tomography. We concluded that the ratio does not allow for early routine clinical differentiation between etiologies of pancreatitis and evaluation of the severity of the disease.
Serum amylase, lipase and C-reactive protein (CRP) levels upon and CRP again within 72 hours after admission were estimated in 115 consecutive patients with acute pancreatitis and correlated with contrast-enhanced computed tomography (CT) results performed within 72 hours after admission and scored for morphological changes and necroses. Serum enzyme levels > or = 3 times the upper limit of normal and CRP levels > or = 10 times on admission and maximal CRP levels > or = 10 times within 72 hours after admission significantly correlated with severe pancreatic morphological changes. Thus, contrary to previous belief, high, not low, enzyme levels indicate severe acute pancreatitis. Furthermore, maximal CRP levels > or = 10 times the upper limit of normal within 72 hours in all patients and amylase admission levels of > or = 3 times the upper limit of normal in alcoholics were significantly indicative of pancreatic necroses. Thus, serum enzyme estimation upon, and maximal CRP levels within 72 hours after, admission may help the clinician to evaluate the severity of acute pancreatitis when imaging procedures are not immediately available.
OBJECTIVE: To evaluate the incidence, localization, and size of pleural effusions in 133 patients with acute pancreatitis. METHODS: A contrast-enhanced computed tomographic scan was prospectively obtained within 72 h after admission. RESULTS: Patients with pleural effusions (66 = 50%) had significantly more severe morphological changes of the pancreas and necroses (independent of the size and localization of the effusions and etiology of the acute pancreatitis), more often had a pancreatic pseudocyst, and had a higher mortality rate than patients without this complication. CONCLUSION: Pleural effusions are indicative of severe acute pancreatitis and are a negative prognostic parameter for the course of the disease.