Paroxysmal autonomic instability with dystonia in a patient with tuberculous meningitis: a case report

<p>Abstract</p> <p>Introduction</p> <p>This case report describes an extremely rare combination of paroxysmal autonomic instability with dystonia and tuberculous meningitis. Paroxysmal autonomic instability with dystonia is normally associated with severe traumatic brain injury.</p> <p>Case presentation</p> <p>A 69-year-old man of Indonesian descent was initially suspected of having a community-acquired pneumonia, which was seen on chest X-ray and computed tomography of the chest. However, a bronchoscopy showed no abnormalities. He was treated with amoxicillin-clavulanic acid in combination with ciprofloxacin. However, nine days after admission he was disorientated and complained of headache. Neurological examination revealed no further abnormalities. A lumbar puncture revealed no evidence of meningitis. He was then transferred to our hospital. At that time, initial cultures of bronchial fluid for <it>Mycobacterium tuberculosis </it>turned positive, as well as polymerase chain reaction for <it>Mycobacterium tuberculosis</it>. Later, during his stay in our intensive care unit, he developed periods with hypertension, sinus tachycardia, excessive transpiration, decreased oxygen saturation with tachypnea, pink foamy sputum, and high fever. This constellation of symptoms was accompanied by dystonia in the first days. These episodes lasted approximately 30 minutes and improved after administration of morphine, benzodiazepines or clonidine. Magnetic resonance imaging showed an abnormal signal in the region of the hippocampus, thalamus and the anterior parts of the lentiform nucleus and caudate nucleus.</p> <p>Conclusions</p> <p>In patients with (tuberculous) meningitis and episodes of extreme hypertension and fever, paroxysmal autonomic instability with dystonia should be considered.</p

Irreversible Encephalopathy After Treatment With High-Dose Intravenous Metronidazole

Background: Encephalopathy associated with metronidazole is rare and, in most cases, reversible following discontinuation. Objective: We describe a case of fatal encephalopathy after treatment with high-dose intravenous metronidazole and the potential causes of the irreversibility. Case summary: A 38-year-old white woman (weight, 45 kg) received metronidazole among other medications to treat osteomyelitis for 74 days after surgery to correct a spinal neuroarthropathy. An initial dose of 500 mg IV QID was administered. After 6 weeks, the patient was discharged and the dose was changed to 1500 mg IV administered once dally (over 90 minutes) by a visiting nurse. Other treatments included teicoplanin 400 mg once dally and trimethoprim-sulfamethoxazole 480 mg BID for the infection, baclofen 25 mg TID for pain associated with a congenital spinal cord lesion with paraplegia, and omeprazole 20 mg once daily for pyrosis. Tell weeks after the start of metronidazole, the patient developed somnolence and dysarthria, changing to encephalopathy with coma on admission 2 weeks later. Despite discontinuation of all medication, including metronidazole, 2 days after admission, the patient's condition appeared to be irreversible. After 8 weeks, her coma was considered permanent, mechanical ventilation was discontinued, and she died. Evaluating all medicines administered, metronidazole, with a Naranjo adverse drug reaction score of 5 (probable), was the most plausible cause of the encephalopathy. The other medicines, including baclofen, had a negative score of -3 to -2 (doubtful). All tests on infections, metabolic disorders, or interactions between medications were negative. Conclusion: This patient had a fatal encephalopathy, probably associated with long-standing exposure to high plasma concentration peaks of metronidazole, due to a once-dally dose of 1500 ing IV over several weeks. (Clin Ther. 2010;32:60-64) (C) 2010 Excerpta Medica Inc

Tentamen suicidii met barbituraten van internet

BACKGROUND: Barbiturate intoxication is potentially lethal. With the availability of the newer anticonvulsants the use of barbiturates in treating epilepsy has decreased significantly, with a concurrent decrease in the incidence of overdose with these medications. There have, however, been recent alarm signals from governmental sources concerning the increase in the Internet purchase of illegal medications, including barbiturates, for use in attempted suicide. CASE DESCRIPTION: Here we describe two patient cases involving barbiturate intoxication with amobarbital and thiopental, respectively. They had both obtained the barbiturates via the Internet. Both patients were comatose and showed signs of respiratory depression; one of them was also haemodynamically unstable. Both patients recovered fully following intensive supportive therapy. CONCLUSION: In patients with coma, respiratory depression, absence of brainstem reflexes and shock with no evident cause one should be aware of the possibility of barbiturate intoxication, even when there is no indication that these have been prescribed or that the patient has direct or indirect access to barbiturates. Prompt, optimal supportive therapy will give a good chance of full somatic recovery

Tentamen suicidii met barbituraten van internet

BACKGROUND: Barbiturate intoxication is potentially lethal. With the availability of the newer anticonvulsants the use of barbiturates in treating epilepsy has decreased significantly, with a concurrent decrease in the incidence of overdose with these medications. There have, however, been recent alarm signals from governmental sources concerning the increase in the Internet purchase of illegal medications, including barbiturates, for use in attempted suicide. CASE DESCRIPTION: Here we describe two patient cases involving barbiturate intoxication with amobarbital and thiopental, respectively. They had both obtained the barbiturates via the Internet. Both patients were comatose and showed signs of respiratory depression; one of them was also haemodynamically unstable. Both patients recovered fully following intensive supportive therapy. CONCLUSION: In patients with coma, respiratory depression, absence of brainstem reflexes and shock with no evident cause one should be aware of the possibility of barbiturate intoxication, even when there is no indication that these have been prescribed or that the patient has direct or indirect access to barbiturates. Prompt, optimal supportive therapy will give a good chance of full somatic recovery

Pharmacokinetics of favipiravir during continuous venovenous haemofiltration in a critically ill patient with influenza.

Favipiravir is a novel antiviral drug approved for influenza treatment in Japan. Little is known about favipiravir pharmacokinetics in critically ill patients. Here, we report a patient with influenza treated with favipiravir and undergoing continuous venovenous hemofiltration (CVVH) on the Intensive Care Unit of a tertiary hospital in the Netherlands. Pharmacokinetic analyses showed increased clearance and decreased plasma levels compared to healthy volunteers. CVVH has no clinically relevant contribution to total clearance. Despite susceptibility to favipiravir, the influenza virus was not cleared. A multi-disciplinary approach is needed to ensure optimal favipiravir treatment in critically ill patients

Association of Whole Blood Tacrolimus Concentrations with Kidney Injury in Heart Transplantation Patients

Background and Objectives: Acute kidney injury (AKI) is frequently observed after heart transplantation and is associated with morbidity and mortality. However, many confounding factors also contribute to the development of AKI in heart transplants. We hypothesized that supratherapeutic whole-blood tacrolimus trough concentrations are associated with AKI. Methods: In a retrospective observational cohort from April 2005 to December 2012, all adult heart transplantation patients were included. AKI was assessed in the first 2 weeks after transplantation as classified by the Kidney Disease Improving Global Outcomes Network (KDIGO). Whole-blood tacrolimus trough concentrations were determined from day 1 to day 14 and at 1, 3, 6 and 12 months post-transplantation. The therapeutic range was 9 to 15 ng/ml in the first 2 months and tapered to 5–8 ng/ml thereafter. The relationship between supratherapeutic tacrolimus trough concentrations and AKI was evaluated. The impact of various potentially confounding factors on tacrolimus concentrations and AKI was considered. Results: We included 110 patients. AKI occurred in 57% of patients in the first week. Recovery from AKI was seen in 24%. The occurrence of chronic kidney disease (CKD) was 19% at 1 year. Whole-blood tacrolimus trough concentrations were often supratherapeutic and, despite correction for confounding factors, independently associated with AKI (OR 1.66; 95% CI 1.20–2.31). Conclusions: Supratherapeutic whole-blood tacrolimus trough concentrations are independently associated with the development of AKI in adult heart transplantation patients. More stringent dosing of tacrolimus early after transplantation may be critical in preserving the kidney function

Clinical Pharmacokinetics and Impact of Hematocrit on Monitoring and Dosing of Tacrolimus Early After Heart and Lung Transplantation

The calcineurin inhibitor tacrolimus is an effective immunosuppressant and is extensively used in solid organ transplantation. In the first week after heart and lung transplantation, tacrolimus dosing is difficult due to considerable physiological changes because of clinical instability, and toxicity often occurs, even when tacrolimus concentrations are within the therapeutic range. The physiological and pharmacokinetic changes are outlined. Excessive variability in bioavailability may lead to higher interoccasion (dose-to-dose) variability than interindividual variability of pharmacokinetic parameters. Intravenous tacrolimus dosing may circumvent this high variability in bioavailability. Moreover, the interpretation of whole-blood concentrations is discussed. The unbound concentration is related to hematocrit, and changes in hematocrit may increase toxicity, even within the therapeutic range of whole-blood concentrations. Therefore, in clinically unstable patients with varying hematocrit, aiming at the lower therapeutic level is recommended and tacrolimus personalized dosing based on hematocrit-corrected whole-blood concentrations may be used to control the unbound tacrolimus plasma concentrations and subsequently reduce toxicity