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Clinical Course: We present a potentially fatal case of acute methaqualone (M) poisoning with very low serum concentrations of M but extremely high levels of its metabolite, 2-methyl-3-(2-hydroxymethyl-phenyl)-4 (3H)-chinazoline (Met-1). A 23-year-old man was admitted to the intensive care unit 2 days after ingestion of 4-5 g M in an suicidal attempt. On admission he was somnolent and poorly responsive to painful stimuli. Physical examination revealed a heart rate of 95 bpm, a blood pressure of 125/65 mmHg, and a normal body temperature. His chest was clear to auscultation, respirations were shallow, and the skin was cyanotic. The electrocardiogram was unremarkable. The chest radiograph showed a normal heart size without pulmonary infiltrates or venous congestion. The pupils were dilated but reactive to light. The neurologic examination was further remarkable for increased limb reflexes, myoclonia, and positive pyramidal signs. During the next 2 days the patient became comatose and developed respiratory insufficiency due to non-cardiogenic pulmonary oedema, which was confirmed by chest radiograph and haemodynamic investigations by means of right heart catheterisation. He required mechanical ventilation for 6 days. Finally, he recovered completely and was discharged in good condition.Diagnostics: A lumbar puncture revealed neither blood nor pleocytosis in the cerebrospinal fluid. Cranial computed tomography was carried out on an emergency basis, but no abnormality was disclosed. An electroencephalogram did not exhibit any significant pathological findings. Testing for infectious diseases or porphyria gave negative results. Toxicological screening based on enzyme immunoassays (ELISA) was negative for alcohol, tricyclic antidepressants, benzodiazepines, barbiturates, and morphine, but gave a positive result for M. From the moment of admission daily blood samples were taken and analysed by combined gas chromatography and mass spectrometry. These showed very low levels of M but extremely high levels of Met-1.Therapy: After gastric lavage, continuous enteric lavage with activated charcoal and mannitol was initiated to minimise intestinal absorption. Since M was hardly detectable in the serum, haemoperfusion was not regarded as indicated for drug elimination and treatment was restricted to general supportive measures. To rule out a central anticholinergic syndrome, an anticholinesterase drug (physostigmine) was administered but remained without therapeutic effect.Conclusions: The presented case is the first report of a life-threatening intoxication after M ingestion primarily caused by Met-1. It supports the significance of this metabolite for the toxic effects of the drug. A toxicological screening test based on ELISA proved helpful due to its cross-reactivity with metabolites. In cases similar to ours, resin haemoperfusion may be indicated to remove the metabolites despite low detectable concentrations of the parent substance in the serum. [ABSTRACT FROM AUTHOR]

Polycytemia vera (PV) is a rare myeloproliferative neoplasm associated with microcirculatory disturbances, thrombosis and bleeding. Patients suffering from PV have a high risk of perioperative adverse events, but the literature regarding on-pump procedures in PV patients is scarce. We report two cases of acute and severe oxygenator failure during cardiopulmonary bypass and present valid exit scenarios., (© 2020 The Authors. Journal of Cardiac Surgery Published by Wiley Periodicals LLC.)

Previous exposition to heparin and protamine in patients undergoing cardiopulmonary bypass and postoperative therapeutic anticoagulation with LMWH may lead to the development of heparin-induced thrombocytopenia (HIT) and/or protamine-induced thrombocytopenia (PIT). This case deals with a rare clinical presentation of circulating IgG antibodies against heparin/platelet factor 4 complexes and heparin/protamine complexes after cardiac surgery. Ensuing purpura and skin necrosis (blisters) at the injection sites of LMWH and clinical symptoms improved rapidly after replacement of LMWH by an alternative anticoagulant. The aim of this report is to draw attention to the several different clinical manifestations of heparin- and/or protamine-induced thrombocytopenia and shows a possible course of treatment and recovery., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Caroline Holaubek et al.)

Introduction: We report a rare but severe pacemaker complication of a pacemaker lead perforating the papillary muscle. This induced severe tricuspid regurgitation and right heart failure. Patients suffering from right heart failure have an increased operative risk of open-heart surgery and therefore represent a clinical challenge due to the lack of clear guidelines., Case Presentation: A 70-year-old male patient presented with severe tricuspid regurgitation and a history of decompensated right heart failure. One pacemaker lead was described as 'whipping'. Four years earlier he had received a VVIR pacemaker with a passive lead. This lead failed after three years and a new ventricular lead had been placed. We performed on-pump beating heart surgery after a multidisciplinary decision process. One lead was perforating the posterior papillary muscle, severely impairing valve movement. The tricuspid valve was replaced with a stented bioprosthesis. Epicardial pacemaker wires were placed on the right and left ventricle to enable cardiac resynchronization therapy in the case of postoperative heart failure. However, the patient recovered quickly without left ventricular pacing and could be discharged home 12 days after surgery., Conclusion: This particular case emphasizes the importance of meticulous surgical technique during pacemaker lead implantation and a tight postoperative follow-up including echocardiography in complicated cases. The management of patients with an indication for lead removal having developed secondary severe tricuspid valve dysfunction inducing ventricular impairment represents a clinical challenge and should be approached by a multidisciplinary team.

1. Reocclusion is still a significant complication after percutaneous transluminal coronary angioplasty. The injury of coronary arteries resulting from PTCA plays an important role in the pathophysiology of both abrupt closure and late restenosis after an initially successful procedure. Cytokines play a pivotal role in the accumulation of circulating blood cells at the endothelium and are known to regulate their interaction with the vessel wall. 2. To obtain further information about this interaction, serum concentrations of soluble endothelial leukocyte adhesion molecule 1 (sELAM-1), leucocyte endothelial cell adhesion molecule 1 (sL-selectin), intercellular adhesion molecule 1 (sICAM-1), interleukin 2 receptor (sIL-2R) and interleukin 8 (IL-8) detected by enzyme-linked immunosorbent assay were monitored in 30 consecutive patients referred for elective PTCA. Fifteen patients who underwent elective coronary angiography without PTCA served as controls. 3. All patients underwent successful first PTCA. Within 24 h the serum concentrations of sELAM-1 increased gradually from 21.7 (SD 7.1) to 48.2 (SD 8.6) ng/ml (P < 0.01); levels of sL-selectin rose from 982.1 (SD 128.7) to 1541.3 (SD 104.6) ng/ml after 48 h (P < 0.01). Serum levels of IL-8 remained stable initially, but peaked at the end of the observation time of 72 h (9.4, SD 3.8, versus 16.1, SD 4.9 ng/ml; P < 0.05). A positive correlation was found between the number of dilatations and the rise in these parameters (P < 0.01). No significant changes were found in the serum concentrations of sICAM-1 and sIL-2R after PTCA or in any of the parameters in patients after coronary angiography. 4. We conclude that PTCA induces a significant rise in the concentration of certain adhesion molecules in serum. Thus, we provide preliminary data on the potential role of cytokines for blood cell-endothelium interaction after PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: To evaluate the effect of acute cardiogenic pulmonary edema on the concentrations of immune parameters in serum., Design: Prospective, controlled study., Setting: Medical ICU., Patients: Twenty-four consecutive patients with acute pulmonary edema who had significant clinical improvement within 30 mins and did not show any evidence of either tissue damage or infection. For comparison, 25 healthy, age-matched controls and 25 patients with mild chronic heart failure were also studied., Interventions: Treatment with oxygen, nitrates, and loop diuretics., Measurements: Lymphokines, acute-phase reactants, and cortisol concentrations were measured in serial serum and plasma samples., Main Results: Serum concentrations of soluble CD-8 antigen (soluble CD-8) decreased from 928 +/- 124 (SEM) U/mL on admission to 712 +/- 112 and 579 +/- 67 U/mL after 2 and 6 hrs, respectively (p less than .05, p less than .01), and returned to baseline values within 48 hrs (853 +/- 109 U/mL). Concentrations of soluble interleukin-2 receptor increased from 721 +/- 71 to 1078 +/- 112 and 1226 +/- 128 U/mL 12 and 36 hrs, respectively, after admission (p less than .05, p less than .01). Plasma cortisol concentrations were markedly increased on admission (56.9 +/- 4.7 vs. 13.1 +/- 1.3 micrograms/dL after recovery, p less than .001). Increased cortisol concentrations coincided with the nadir of soluble CD-8. Tumor necrosis factor-alpha remained within normal limits in all patients. Neither acute-phase reactants nor angiotensin converting enzyme activity showed significant changes during the observation period., Conclusion: The present results indicate significant alterations in the serum concentrations of immune parameters as an effect of an uncomplicated acute cardiogenic pulmonary edema.

A 65-year-old, previously healthy man developed acute renal failure, severe thrombocytopenia and hepatic icterus after a small dose of mefenamic acid (Parkemed). Drug-dependent antibodies reacting against platelets could be identified as the most probable cause for this acute and rapidly reversible disorder. A concomitant hemolytic reaction was not observed and accordingly no drug-dependent red cell antibodies could be demonstrated. The drug-specific antibodies were found only during the acute phase using the platelet immunofluorescence test and a solid-phase immunoassay but not with the monoclonal antibody specific immobilization of platelet antigens assay. After discontinuation of the drug the patient steadily improved and fully recovered until day 22 after admission and drug removal. The clinical course strongly suggests that drug-dependent antibodies against mefenamic acid and/or its metabolites reacting by immune complex mechanism were responsible not only for the thrombocytopenia but also for the renal and hepatic failure.

Critically ill patients with intracerebral hemorrhage require immediate treatment in an intensive care unit. In the acute phase of the disease the patients are endangered from increased intracerebral pressure, respiratory disorders (aspiration!) and hypertension. An adequate intensive care management consisting of sedation, analgesia, intubation and mechanical ventilation, correct body positioning and treatment of hypertension is of decisive importance for the prognosis of these patients. The aim of this report is to discuss the most important therapeutic strategies and arising problems in the course of intracerebral hemorrhage.

The clinical relevance of daily measurement of beta 2-microglobulin in serum and urine was evaluated in 49 patients undergoing renal transplantation. The changes in beta 2-microglobulin levels were compared to standard parameters for assessment of renal function. One hundred episodes of acute deterioration of renal function, clinically diagnosed as rejection, were analyzed retrospectively: (1) In 18 episodes renal malfunction did not respond to methylprednisone but improved immediately upon dose reduction of ciclosporin A, thus indicating a nephrotoxic effect of the drug. In these cases a mean increase of beta 2-microglobulin in urine as high as 7.9 mg/l was observed while serum values decreased. (2) Fifty episodes of apparent rejection (responsive to steroids) were preceded by a 3-day lasting continuous rise of beta 2-microglobulin in serum of up to 3.6 mg/l as a mean with only a moderate elevation in urine. (3) In 13 episodes antirejection treatment could have been avoided as continuously declining laboratory parameters indicated spontaneous improvement of renal function. We conclude that parallel determination of beta 2-microglobulin in serum and urine allows to differentiate between ciclosporin A nephrotoxicity and rejection in 91% of the cases.

Stress ulcer bleeding is a serious complication of critical illness and is associated with increased morbidity and mortality. For the prophylaxis of stress ulcers, antacids, H2-blockers, or sucralfate are prescribed. While H2-blockers inhibit the secretion of gastric acid, sucralfate appears to provide protection without reducing levels of gastric acid. Inhibition of acid secretion increases gastric pH, allowing bacterial overgrowth of the stomach by Gram negative bacteria, which colonize the pharynx and trachea and increase the risk of nosocomial pneumonia. For this reason, H2 blockers appear disadvantageous, though they offer adequate prophylaxis for stress ulcer bleeding. As it does not increase gastric pH, sucralfate provides adequate protection against Gram negative gastric overgrowth, however its prophylactic efficacy is not generally accepted. Therefore, we compared the H2-blocker ranitidine to sucralfate in the prophylactic treatment of stress ulcer bleeding and studied the incidence of positive bacteriological findings in the blood and bronchial secretions of the two groups. In a randomized study, 84 patients undergoing general intensive care received either ranitidine (6 x 50 to 6 x 100 mg daily i.v.) or sucralfate (6 x 1 g via gastric tube or per os). Both groups were comparable with respect to age, underlying disorders, and factors predisposing to the development of stress ulcers.(ABSTRACT TRUNCATED AT 250 WORDS)

Nephrotoxicity is the main side effect of cyclosporine therapy. In this study 2 groups consisting of 6 kidney transplant recipients were investigated. The oral cyclosporine daily dose was in the first group 13 mg/kg, in the second 11 mg/kg, respectively. In both groups, the daily dose was divided on the first day of investigation in 2 equal portions given at an interval of 12 hours. On the second day, the same dose was divided in 3 equal portions given at an interval of 8 hours. After cyclosporine administration twice a day very high blood cyclosporine peak concentrations (two to three times higher than the therapeutic range) were measured. These potential nephrotoxic cyclosporine concentrations could be prevented by cyclosporine application in 3 equal portions. A reduction of the daily dose in the early period after kidney transplantation to a starting daily dose of 12 mg/kg or even 10 mg/kg can be recommended.