Plasma exchange treatment for acute hyperlipidemic pancreatitis with falsely low levels of serum triglycerides - a case report.

Hypertriglyceridemia is a well-recognized cause of acute pancreatitis. We present a patient with acute hypertriglyceridemic pancreatitis. At presentation serum triglycerides were severely elevated (104 mmol/l) and were decreasing the next day (11 mmol/l). However, based on increasing levels of serum lipase, worsening respiratory failure and evidently lipemic serum, we decided to perform plasma exchange, and patient's condition improved dramatically. Repeated laboratory test of the serum obtained before the first plasma exchange revealed that the actual value of serum triglycerides was 57 mmol/l. A clinically-driven decision is crucial when treating patients with hypertriglyceridemic acute pancreatitis as the serum triglyceride levels can be falsely low.

Upper gastrointestinal haemorrhage: predictive factors of in-hospital mortality in patients treated in the medical intensive care unit.

This prospective, cohort study assessed the independent predictors of in-hospital mortality in patients with acute upper gastrointestinal haemorrhage admitted to the medical intensive care unit (MICU) at the University Clinical Centre Maribor, Slovenia. Using univariate, multivariate and logistic regression methods the predictors of mortality in 54 upper gastrointestinal haemorrhage patients (47 men, mean ± SD age 61.6 ± 14.2 years) were investigated. The mean ± SD duration of treatment in the MICU was 2.8 ± 2.9 days and the mortality rate was 31.5%. Significant differences between nonsurvivors and survivors were observed in haemorrhagic shock, heart failure, infection, diastolic blood pressure at admission, haemoglobin and red blood cell count at admission, and lowest haemoglobin and red blood cell count during treatment. Heart failure (odds ratio 59.13) was the most significant independent predictor of in-hospital mortality. Haemorrhagic shock and the lowest red blood cell count during treatment were also important independent predictive factors of in-hospital mortality.

Severe carbon monoxide poisoning treated by hyperbaric oxygen therapy--a case report.

Carbon monoxide (CO) poisoning is an important cause of mortality and late neurological sequelae such as memory loss, personality changes, psychosis, dementia, and so on. The benefits of hyperbaric oxygen (HBO) therapy are still discussed, but the majority of trials recommend it in severe cases with coma and/or hemodynamic instability, irrespective of carboxyhemoglobin (COHb) level, to prevent permanent neurological deficits. We present a 35-yr-old woman who underwent accidental CO poisoning. Although breathing 100% oxygen by mask during transfer to the hospital, she was in deep coma, hypotensive, cyanotic, and hypoxic (arterial pO(2) 7,41 kPa, HbO(2) 87.8%), with serum COHb 26.7% on hospital admission. Orotracheal intubation, mechanical ventilation, iv fluids, dobutamin, and norepinephrine were administered. COHb level decreased to 17.2% within 1 h. To prevent severe neurological sequelae, the patient was transferred as soon as possible to an HBO center 60 km distant to perform HBO therapy twice at 3.0 and once at 2.2 atm within 24 h. After the second HBO session, the patient regained consciousness, and respiratory failure and shock resolved. She was transferred to our hospital and discharged few weeks later with discrete paresis of peripheral nerves, discrete ischemic brain lesions on computed tomography (CT) scan, and moderately abnormal electroencephalogram (EEG) without cognitive disturbances. She was able to resume her daily activities. We conclude that in severe CO poisoning, normobaric oxygen therapy and resuscitation by fluids, inotropic agents, and catecholamines is essential for survival, but additional HBO therapy seems to prevent major neurological sequelae.

Plasminogen activator inhibitor-1 in patients with atrial arrhythmias during acute myocardial infarction, treated with streptokinase.

Atrial arrhythmias (AA), especially atrial fibrillation (AF), during acute myocardial infarction (AMI) are often associated with increased mortality and heart failure. Impaired fibrinolysis with elevated plasminogen activator inhibitor-1 (PAI-1) activity is associated with resistance to fibrinolytic therapy in AMI patients, but it is also found in patients with AF. Our aim was a prospective study of the role of pre-treatment PAI-1 levels for the presence of AA in AMI patients and the influence of AA on in-hospital mortality. In 116 AMI patients, treated with streptokinase, pre-treatment PAI-1 levels were estimated by the chromogenic method (normal levels, 0.3-3.5 U/ml) and in-hospital AA were assessed as atrial fibrillation, flutter and/or tachycardias. Between patients with and without AA, a significant difference was observed in mean pre-treatment PAI-1 levels, in several in-hospital complications and mortality (24 versus 4.4%; P < 0.01; odds ratio, 6.45; 95% confidence interval, 1.66-25.0). The PAI-1 level > 7 U/ml was the most significant independent pre-treatment risk factor for AA (P < 0.05; odds ratio, 3.5; 95% confidence interval, 1.15-10.6). We conclude that AA were a significant risk for in-hospital mortality of AMI patients, treated with streptokinase. A pre-treatment PAI-1 level > 7 U/ml was the most significant pre-treatment risk for AA in these patients.

Prognostic role of plasminogen-activator-inhibitor-1 levels in treatment with streptokinase of patients with acute myocardial infarction.

BACKGROUND: The antifibrinolytic effect of plasminogen-activator-inhibitor type 1 (PAI-1) may be responsible for delays in reperfusion and/or reinfarctions after streptokinase (STK) therapy in patients with acute myocardial infarction (AMI). HYPOTHESIS: This study aimed to demonstrate the prognostic role of pretreatment PAI-1 levels for the outcome of STK therapy in patients with AMI, depending on reperfusion and/ or reinfarction. METHODS: The mean pretreatment PAI-1 level of 104 patients with AMI, treated with STK, determined by chromogenic method, was 5.8 +/- 8.6 U/ml, range 0.3-66.2 U/ml. Streptokinase therapy was successful when reperfusion was achieved, as assessed noninvasively, without subsequent reinfarction; it failed when reperfusion was delayed and/or reinfarction developed. RESULTS: Fibrinolysis with STK failed significantly in patients with elevated pretreatment PAI-1 levels (p < 0.05), especially with levels >4.0 U/ml (p< 0.01). The mean pretreatment PAI-1 level was significantly higher in unsuccessfully treated patients. Multivariate statistical testing demonstrated that among pretreatment variables, elevated PAI-1 activity was the most significant independent risk factor of failed fibrinolysis with STK. CONCLUSIONS: Among pretreatment variables, elevated pretreatment PAI-1 activity in patients with AMI was the most significant independent risk factor of failed fibrinolysis with STK, especially at levels > 4.0 U/ml.

Rhabdomyolysis and acute renal failure in intensive care unit.

Rhabdomyolysis is common clinical and laboratory syndrome resulting from skeletal muscle injury and acute renal failure is the most important complication. Acute renal failure is common in critically ill medical patients. The aim of our study was to determine the prevalence of rhabdomyolysis induced acute renal failure in these patients and to established the prognosis of critically ill patients with acute renal failure and rhabdomyolysis. In the study were included 1557 patients treated in our medical intensive care unit. Seventy-three patients had criteria for acute renal failure. Twelve of them (16.4%) had rhabdomyolysis, eight were women and four were men (average age was 71 years). Sixty-one patients (83.6%) had acute renal failure without rhabdomyolysis, 33 were women and 28 were men (average age was 69 years). We found no difference in age and sex between patients with acute renal failure with or without rhabdomyolysis. Ten patients (83.3%) with rhabdomyolysis and 39 patients (63.9%) without rhabdomyolysis had multiorgan failure syndrome. In patients with rhabdomyolysis, the number of failing organs were statistically significantly higher (p < 0.027). Nine patients (75%) with rhabdomyolysis and 27 patients (44.3%) without rhabdomyolysis died. Mortality was statistically significantly higher (p < 0.05) in patients with rhabdomyolysis. Rhabdomyolysis with acute renal failure was frequently observed in patients treated in our medical intensive care unit. Multiorgan failure syndrome was common in these patients and mortality was higher compared to patients without rhabdomyolysis.

Acute hemorrhage into the peritoneal cavity--a complication of chronic pancreatitis with pseudocyst: a case report from clinical practice.

Acute hemorrhage due to a pseudocyst of the pancreas is a dangerous complication of chronic pancreatitis (CP). Without operative treatment, mortality is as high as 90%. Immediate recognition of this complication as well as urgent operative treatment allowing the survival of 70% of patients is imperative. Described is the case of a patient with CP and pseudocyst in which hyperamylasemia and unclarified anemia developed following sudden abdominal pain. The suspicion of hemorrhage into the peritoneal cavity was confirmed by selective visceral angiography showing hemorrhage from the splenic artery in the region of the hilus of the spleen. Operative treatment was successful. During the procedure, a ligature was applied to the hemorrhaging splenic artery and a splenectomy was carried out with 2500 ml of bloody contents being removed from the abdominal cavity. Acute hemorrhage into the peritoneal cavity as a complication of chronic pancreatitis with pseudocyst (CPP) requires immediate identification, confirmation by visceral angiography, and urgent operative treatment.

Pretreatment plasminogen activator inhibitor-1 (PAI-1) levels and the outcome of thrombolysis with streptokinase in patients with acute myocardial infarction.

BACKGROUND: The risk for reinfarctions and delays in reperfusion after streptokinase therapy may be caused by the antifibrinolytic effect of platelet-derived type 1 plasminogen activator inhibitor (PAI-1). This study aims to show the relation of pretreatment PAI-1 levels of patients with acute myocardial infarction treated with streptokinase therapy and the outcome of fibrinolysis, with the emphasis on reperfusion and reinfarction. METHODS: Pretreatment PAI-1 levels of 60 patients with acute myocardial infarction, treated with streptokinase, were determined by the chromogenic method. Failure of thrombolysis with streptokinase was present when reperfusion was delayed as assessed by noninvasive reperfusion criteria, or reinfarctions developed. RESULTS: Mean pretreatment PAI-1 level of patients was 6.3+/-1.2 U/ml; span 1.2 U/ml to 34.0 U/ml. Thrombolysis with streptokinse failed significantly in patients with pretreatment PAI-1 levels >4.0 U/ml (p < 0.05), mainly because of significant occurrence of reinfarction (p < 0.05), but less to delayed reperfusion (p > 0.05). CONCLUSION: Failure of thrombolysis with streptokinase is significantly associated with pretreatment PAI-1 levels of >4.0 U/ml.

Rhabdomyolysis and acute renal failure following cardioversion and cardiopulmonary resuscitation.

A 39-year-old male suffered a myocardial infarction at work and cardiopulmonary resuscitation was initiated immediately. After 15 cardioversions, ventricular fibrillation converted to sinus rhythm. Rhabdomyolysis with a 100-fold increase of serum creatine kinase level and myoglobinuria with acute renal failure ensued, requiring hemodialysis treatment. The patient died and autopsy revealed acute posterior myocardial infarction. Prolonged cardiopulmonary resuscitation involving repeated cardioversion may predispose to myoglobinuric renal failure.