thiopental and Pneumonia

The role of barbiturate therapy in the development of pneumonia in head trauma patients in the intensive care unit of a university hospital was studied retrospectively. A total of 151 ventilated head trauma patients were included in the study. Intravenous thiopentone was administered to 75 patients (Group A), and 76 patients were managed without thiopentone therapy (Group B). Pneumonia was diagnosed when a new persistent pulmonary infiltrate appeared, with at least two of the following: (a) fever greater than 38 degrees C, (b) a white blood cell count greater than 15,000/mm3, or (c) the presence of purulent bronchial secretions. On admission, there were no differences in the acute physiology and chronic health evaluation 2 revision (APACHE II) and Glasgow Coma Score between Groups A and B. Fifty-three per cent of the patients treated with thiopentone (Group A) developed pneumonia compared with 35% in Group B (odds ratio 1.85, 95% confidence interval 0.97-3.51). Gram-negative and Staphylococcus aureus organisms were the most frequently isolated in all cases. No differences in age, sex, APACHE II, Glasgow Coma Score, nutritional status or dexamethasone treatment were observed between the groups with and without pulmonary infection. In the multivariate analysis, prolonged mechanical ventilation before pneumonia and thiopentone treatment remained as the only independent risk factors for the appearance of pneumonia in head trauma patients (p = 0.001 for both). Nevertheless, thiopentone did not increase the rate of mortality in patients with pneumonia. In conclusion, head trauma victims treated with thiopentone have a greater risk for the development of nosocomial pneumonia independent of mechanical ventilation.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Confidence Intervals; Craniocerebral Trauma; Female; Humans; Hypnotics and Sedatives; Incidence; Intensive Care Units; Male; Middle Aged; Odds Ratio; Pneumonia; Prognosis; Respiration, Artificial; Survival Rate; Thiopental

We report on three acute encephalitis patients with refractory, repetitive partial seizures (AERRPS). All three suffered acute febrile episodes associated with status epilepticus, which necessitated high-dose barbiturate therapy under artificial ventilation for several weeks. Electroencephalography (EEG) revealed a predominance of diffuse epileptiform discharges initially, subsequently developing into periodic bursts of these discharges. Reduction of the barbiturate dosage resulted in clinical and subclinical partial seizures appearing repetitively in clusters. Prolonged fever persisted for 2-3 months, even several weeks after normalization of cell counts in the cerebrospinal fluid. The EEG showed an improvement after resolution of this fever, and seizures became less frequent, although still intractable. Oral administration of high-dose barbiturate and benzodiazepines were partially effective during the acute phase, and a barbiturate dependency, lasting for years, was noted in one patient. Steroid administration was effective in stopping the febrile episodes in one patient, with concurrent improvement in seizure control. Magnetic resonance imaging showed enhancement of bitemporal cortical areas in one patient, and high signal intensity on T2 weighted image in the bilateral claustrum in another patient. Diffuse cortical atrophy appeared within two months after the onset of encephalitis in all patients. The evolution of the seizures and EEG findings suggested a high degree of cortical excitability in AERRPS. In this report, we propose a tentative therapeutic regimen for seizure control in this condition. We also hypothesize that a prolonged inflammatory process exists in the cerebral cortex with AERRPS, and may be pivotal in the epileptogenesis.

Topics: Acute Disease; Anti-Inflammatory Agents; Anticonvulsants; Brain; Cell Count; Cerebrospinal Fluid; Child; Delirium; Drug Resistance; Electroencephalography; Encephalitis; Epilepsies, Partial; Female; Fever; Humans; Magnetic Resonance Imaging; Male; Midazolam; Pneumonia; Status Epilepticus; Thiopental; Tomography, X-Ray Computed; Treatment Outcome; Unconsciousness

Several studies suggest that anesthetics modulate the immune response. The aim of this study was to investigate the effect of halothane and thiopental on the lung inflammatory response. Rats submitted or not to intratracheal (IT) instillation of lipopolysaccharides (LPS) were anesthetized with either halothane (0. 5, 1, or 1.5%) or thiopental (60 mg. kg(-1)) and mechanically ventilated for 4 h. Control rats were treated or not by LPS without anesthesia. Lung inflammation was assessed by total and differential cell counts in bronchoalveolar lavage fluids (BALF) and by cytokine measurements (tumor necrosis factor-alpha [TNF-alpha], interleukin-6 [IL-6], macrophage inflammatory protein-2 [MIP-2], and monocyte chemoattractant protein-1 [MCP-1]) in BALF and lung homogenates. In the absence of LPS treatment, neither halothane nor thiopental modified the moderate inflammatory response induced by tracheotomy or mechanical ventilation. Cell recruitment and cytokine concentrations were increased in all groups receiving IT LPS. However, in halothane-anesthetized rats (halothane > or = 1%), but not in thiopental-anesthetized rats, the LPS-induced lung inflammation was altered in a dose-dependent manner. Indeed, when using 1% halothane, polymorphonuclear leukocyte (PMN) recruitment was decreased by 55% (p < 0.001) and TNF-alpha, IL-6, and MIP-2 concentrations in BALF and lung homogenates were decreased by more than 60% (p < 0.001) whereas total protein and MCP-1 concentrations remained unchanged. The decrease of MIP-2 (observed at the protein and messenger RNA [mRNA] level) was strongly correlated to the decrease of PMN recruitment (r = 0.73, p < 0.05). This halothane-reduced lung inflammatory response was transient and was reversed 20 h after the end of the anesthesia. Our study shows that halothane > or = 1%, delivered during 4 h by mechanical ventilation, but not mechanical ventilation per se, alters the early LPS-induced lung inflammation in the rat, suggesting a specific effect of halothane on this response.

Topics: Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Base Sequence; Bronchoalveolar Lavage Fluid; Escherichia coli; Halothane; Lipopolysaccharides; Lung; Male; Molecular Sequence Data; Pneumonia; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; Respiration, Artificial; Specific Pathogen-Free Organisms; Thiopental; Time Factors

The development of pneumonia was monitored in head-trauma patients requiring mechanical ventilation. Of the 66 patients studied, 15 (23%) developed pneumonia within 14 days after ICU admission. In each case the diagnosis was based on x-ray evidence and at least two of the following: increased white blood cell count, increased fever, and/or increased sputum production with a predominant organism on the sputum stain. Coagulase-positive Staphylococcus aureus was the most common etiologic agent. There was no difference in the occurrence of pneumonia between patients treated with no steroids or with low, moderate, or high steroid doses. Although there was an association between thiopental use and the development of pneumonia, dexamethasone treatment was not a significant risk factor in the development of pneumonia in this patient population.

Topics: Adrenal Cortex Hormones; Cell Count; Craniocerebral Trauma; Critical Care; Dexamethasone; Fever; Humans; Intensive Care Units; Pneumonia; Respiration, Artificial; Sputum; Thiopental

Topics: Anesthesia; Anesthesia, General; Anesthesia, Spinal; Bronchitis; Cyclopropanes; Ether; Halothane; Hernia, Inguinal; Meperidine; Muscle Relaxants, Central; Nausea; New York; Nitrous Oxide; Pneumonia; Postoperative Complications; Respiratory Tract Infections; Surgical Procedures, Operative; Thiopental; Toxicology; Urinary Catheterization; Vomiting