Cases reported "Critical Illness"

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1/25. Falsely increased immunoassay measurements of total and unbound phenytoin in critically ill uremic patients receiving fosphenytoin.

    BACKGROUND: Fosphenytoin, a phosphate ester prodrug of phenytoin, is metabolized to phenytoin in vivo. phenytoin metabolites accumulate in renal insufficiency and cross-react in some phenytoin immunoassays. Our aim was to determine the accuracy of phenytoin immunoassays in renal patients treated with fosphenytoin. methods: We measured phenytoin with HPLC and with the aca, ACS:180, TDx phenytoin II, Vitros, and AxSYM methods. Specimens were collected 2-120 h after fosphenytoin administration from 17 patients with renal insufficiency. RESULTS: The AxSYM, TDx phenytoin II, ACS:180, and Vitros assays displayed falsely increased phenytoin results up to 20 times higher than the HPLC results. The aca Star results for these specimens were comparable to the HPLC results. Although fosphenytoin can cross-react with phenytoin immunoassays, no fosphenytoin was detected by a sensitive HPLC method in any sample that was tested for its presence. CONCLUSION: These results are consistent with the formation of one or more novel metabolites or adducts of fosphenytoin that accumulate in some critically ill patients with renal insufficiency and that display significant cross-reactivity with some, but not all, phenytoin immunoassay methods.
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2/25. Severe non-infectious circulatory shock related to hypopituitarism.

    The authors report a case of refractory non-infectious circulatory shock with catecholamine and massive fluid loading-resistant features related to hypopituitarism. A 76-year-old man was admitted for shock after suffering from gastroenteritis for 3 days. He was pale and had sparse axillary and pubic hair and small testes. Right catheterization showed shock with low preload pressure and a low oxygen extraction ratio relevant for septic shock. Ultrasound tomography revealed a distended gallbladder due to a stone without peritoneal effusion. A non-inflammatory hydrops of the gallbladder was removed surgically. No microorganism was isolated. Cerebral computed tomography (CT) scan showed a pituitary mass. In the post-surgical period the shock became uncontrollable. Cortisol replacement therapy was instituted and clinical and hemodynamic improvement occurred after 2 h. Hormonal screening on admission before catecholamine administration showed a major decrease in all the hypothalamic-pituitary hormone concentrations. The patient died on day 15 with multiple organ failure. hypopituitarism, probably owing to pituitary adenoma, was the only disease identified in this case. hormone replacement therapy dramatically improved the clinical and hemodynamic status, although the role of an abdominal sepsis could not be eliminated. Arguments that pituitary hormone deficiency might increase the hemodynamic consequences of adrenal deficiency are discussed.
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3/25. acyclovir induced coma in the intensive care unit.

    A 73-year-old man with multiorgan failure requiring mechanical ventilation and haemodialysis developed herpes labialis infection during his stay in the ICU. This was treated with enteral acyclovir. He developed persistent neurologic impairment soon after acyclovir administration, which, over the course of seven days, progressed to coma, the aetiology of which was unclear. The computed tomograph (CT) of the brain and the cerebrospinal fluid (CSF) examination was normal. The electroencephalogram (EEG) showed generalized slowing. The possibility of acyclovir neurotoxicity was considered and the drug was discontinued. Haemodialysis was instituted and the patient made a complete neurological recovery. We believe that this is the first reported case of coma due to enteral acyclovir.
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4/25. life-threatening bleeding and acquired factor v deficiency associated with primary systemic amyloidosis.

    Acquired factor x deficiency has been described in patients with amyloidosis but acquired factor v deficiency is quite rare. We report here a case of life-threatening bleeding and acquired factor v deficiency associated with primary amyloidosis. A 50-year-old man who had no previous hemorrhagic diathesis was referred to our hospital because of recurrent epistaxis, gingival bleeding and hemospermia. The laboratory examination revealed that both the prothrombin time (PT) and the activated partial thromboplastin time (aPTT) were significantly prolonged, and factor V activities were markedly decreased to 14-39% of the normal value. Other coagulation factors such as fibrinogen, prothrombin, factor VII, factor viii, factor ix and factor X were subnormal and normal. transaminases were slightly elevated but serological tests of hepatitis b and hepatitis c were negative. Mild hepatosplenomegaly was noted without sign of liver cirrhosis. The PT and aPTT obtained 8 years ago when he received a cholecystectomy due to cholecystitis were both normal. Specific assays for the detection of factor V inhibitor were repeatedly performed but no factor V inhibitor was found. Furthermore, a significant recovery of the infused factor V was noted shortly after an intravenous administration of 5-10 U fresh frozen plasma, but it did not last more than 6 h. melena, bleedings into the left shoulder and buttock, and finally mortal retroperitoneal hemorrhage developed despite repeated infusions of large amounts of fresh frozen plasma. Acquired factor v deficiency associated with primary amyloidosis was suspected but histological diagnosis was not obtained because of the severe bleeding tendency. autopsy revealed hepatosplenomegaly and massive deposits of AL amyloid in the liver, spleen, heart and other parenchymal organs. Perivascular amyloid deposition and factor v deficiency are both thought to be the cause of the severe hemorrhagic tendency seen in this patient.
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5/25. Excessive argatroban anticoagulation for heparin-induced thrombocytopenia.

    OBJECTIVE: To report 4 patients who became excessively anticoagulated with the recommended or lower starting doses of argatroban during treatment for heparin-induced thrombocytopenia type II (HIT-II) in a cardiothoracic intensive care unit. CASE SUMMARY: Four patients were treated with argatroban after confirmation of HIT-II after cardiac surgery. In 3 patients, argatroban was initiated at the recommended starting dose of 2 micro g/kg/min; in 1 patient, therapy was initiated at 1 micro g/kg/min. All patients had relatively normal hepatic function. In all cases, the resulting activated partial thromboplastin time was supertherapeutic and exceeded 100 seconds in 3 patients. Additionally, argatroban clearance appeared to be prolonged upon discontinuation. DISCUSSION: Argatroban pharmacokinetics in critically ill patients have not been investigated. Our case series demonstrates the potential over-anticoagulation that can occur in this patient population despite relatively normal hepatic function. An objective causality assessment revealed that the adverse drug event in these patients was probably caused by administration of argatroban. CONCLUSIONS: Formal pharmacokinetic studies of argatroban are needed in critically ill patients in order to optimize therapy.
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6/25. Case report: requirement of supplemental morphine during sedation with propofol in a critically ill patient undergoing hemodiafiltration.

    OBJECTIVE: propofol has been shown to produce a predictable and easily attainable level of sedation in postcardiac, head-injured, general trauma patients. The commencement of hemodiafiltration itself has not been shown to significantly influence the requirement for propofol. We report on a patient who underwent binephrectomy complicated by sepsis-induced adult respiratory distress syndrome (ARDS). DESIGN: Case report. SETTING: Largest nonteaching hospital in Southern italy. patients/SUBJECTS: An 18-year-old male underwent a surgical procedure for splenectomy and right nephrectomy for severe abdominal trauma. On the 10th postoperative day, the patient was admitted into our intensive care unit (ICU) for acute respiratory and renal failure due to ARDS and left renal infarction. INTERVENTIONS: Continuous venovenous hemodiafiltration was carried out through a double-lumen cannula. Sedation was initially achieved with propofol up to standard doses into a nonfemoral venous site. Because the optimal level of sedation was not achieved, the initial propofol infusion rate was increase to 3.5 mg/kg, and then an intravenous bolus of morphine (.01 mg/kg) was administered twice daily. RESULTS: The administration of morphine was fundamental to achieving an optimal level of sedation. ARDS resolved and, 10 days later, the patient was transferred to the surgical unit, then discharged home after 14 days. CONCLUSION: hemodiafiltration was found to influence the clinical requirement for propofol. The optimal level of sedation is achieved with the addition of morphine.
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7/25. critical illness myopathy associated with hyperthyroidism.

    A 51-year-old woman was admitted to the intensive care unit for exacerbation of chronic obstructive pulmonary disease. She received antibiotics, neuromuscular blocking agents, and steroids. After 8 days in the intensive care unit, she was noted to be severely weak, her serum creatine kinase had risen to 1,692 U/L (normal, 20-220 U/L), and a muscle biopsy was consistent with critical illness myopathy. As a result of evaluating for resting tachycardia, the patient was found to be hyperthyroid. Her weakness rapidly improved within 1 month after treatment of her hyperthyroidism with iodine-131 and methimazole. The metabolic alterations associated with hyperthyroidism may enhance the risk of developing critical illness myopathy after the administration of antibiotics, neuromuscular blocking agents, and steroids in the intensive care unit.
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8/25. Prolonged cardiac repolarization after tacrolimus and haloperidol administration in the critically ill patient.

    A 42-year-old woman who underwent single lung transplantation who received tacrolimus and a 58-year-old woman with pneumonia and multiple comorbidities who received haloperidol both experienced drug-induced prolongation of cardiac repolarization. The second woman also developed torsade de pointes. Critically ill patients are particularly susceptible to developing torsade de pointes due to various comorbidities, electrolyte disturbances, and receipt of numerous drugs. These two case reports illustrate the increased risk for drug-induced cardiotoxicity in the critically ill patient. They also indicate the need for current knowledge derived from basic research and retrospective case reports on drug-induced torsade de pointes to be integrated into the existing body of knowledge. Guidelines can then be developed to help prospectively reduce the frequency of adverse effects in intensive care patients. research is necessary regarding identification of high-risk patients before drugs are administered, and clarification of the proper role of therapeutic QT monitoring in clinical practice.
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9/25. life threatening hyperphosphataemia after administration of sodium phosphate in preparation for colonoscopy.

    An elderly woman developed severe hyperphosphataemia, hypocalcaemia, and cardiac arrest after oral administration of sodium phosphate in preparation for colonoscopy. This is an unusual complication and is attributed to decreased phosphate excretion by the kidneys. At increased risk are patients with impaired renal function, age more than 65 years, and presenting with intestinal obstruction or decreased intestinal motility, increased intestinal permeability, liver cirrhosis, or congestive heart failure. Though there are no accepted guidelines for anticipation and prevention of this adverse effect, it may be desirable to check serum phosphate concentrations before choosing the method for colonic preparation and before giving the second oral dose of sodium phosphate in patients at risk. Hyperphosphataemia should be suspected if a patient develops hypotension or neuromuscular irritability after administration of sodium phosphate. Haemodialysis for direct removal of phosphate and intravenous calcium for treatment of symptomatic hypocalcaemia may be life saving.
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10/25. Unusual hypersensitivity to warfarin in a critically ill patient.

    A patient was admitted to the intensive care unit because of respiratory failure, and warfarin therapy was started at 2 mg/day for the treatment of pulmonary embolism, together with other medications. Despite the low dosage of warfarin, international normalized ratio (INR) was markedly elevated from 1.15 to 11.28 for only 4 days, and bleeding symptoms concurrently developed. Vitamin K2 was infused along with discontinuation of warfarin. One day later, the INR was found to have decreased, and bleeding was also improved. An objective causality assessment indicated a probable relationship between clotting abnormality and warfarin administration, although the degree of elevation of the INR was unusual in the light of the daily warfarin dose and duration of its exposure. Based on the clinical status of the patient, it was suspected that several conditions contributed to the abnormal hypersensitivity to warfarin. Contributory factors probably included pharmacokinetic interactions with co-administrated drugs, vitamin k deficiency caused by decreased dietary intake, reduced gut bacterial production, impaired intestinal absorption and hepatic synthetic capacity, and increased consumption of clotting factors. In view of our experience in the present case, it should be stressed that close monitoring of coagulation capacity is necessary in critically ill patients in order to avoid fatal haemorrhage after initiating warfarin therapy regardless of the dosage.
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