Treatment with low-dose hydrocortisone accelerates shock reversal in early hyperdynamic septic shock. This was accompanied by reduced production of proinflammatory cytokines, suggesting both hemodynamic and immunomodulatory effects of steroid treatment. Hemodynamic improvement seemed to be related to endogenous cortisol levels, whereas immune effects appeared to be independent of adrenal reserve.
(a) During proposed regimens of "low-dose" hydrocortisone therapy, initially achieved plasma cortisol concentrations considerably exceed basal and ACTH stimulated levels. (b) Cortisol concentrations decline subsequently, despite continuous application of a constant dose. (c) "Inadequate" endogenous steroid production appears to sensitize patients to the hemodynamic effects of a "therapeutic rise" in plasma cortisol levels.
Since experience with primary and secondary detoxification in severe flecainide intoxications is limited, 2 different cases of flecainide intoxications are reported. In the first case, with plasma concentrations of 6500 ng/ml (therapeutic range: 200-980 ng/ml), the patient survived with a pacemaker and catecholamine support. In the second case, hemoperfusion terminated the need for emergency resuscitation during the initial phase, but was unsuccessful 3 h later. Even with a lower plasma concentration the patient died. Both patients had rapid onset of symptoms due to the very good bioavailability of the drug. Although it may be a rare intoxication, it is dangerous because of its quick onset and its efficiency in altering the cardiac stability. We recommend the prophylactic use of a pacemaker and gastric suction. The usefulness of hemoperfusion has not yet been proven.
No effective treatment is available for adult respiratory distress syndrome, pulmonary hypertension and progressive lung fibrosis in severe paraquat poisoning. A potentially beneficial effect of nitric oxide inhalation on the mean pulmonary artery pressure and gas exchange in a subject with advanced paraquat intoxication is reported. Eight days after the suicidal ingestion of an unknown dose of paraquat, a 52-year-old female had a PaO2 < or = 50 mm Hg despite ventilation with an FiO2 of 1 and a positive end-expiratory pressure of 14 to 18 cm H2O. After administration of 25 ppm nitric oxide, PaO2 increased and the mean pulmonary artery pressure and the right-to-left shunt decreased. Discontinuation of nitric oxide resulted in rapid reversal. Ventilatory function was stabilized for three days during nitric oxide inhalation but the patient developed massive pleural effusions and died on d 11 during an interruption of nitric oxide therapy. The response of serious paraquat intoxications to nitric oxide therapy may merit further study. A remarkable post-mortem finding was extensive myonecrosis supporting prolonged muscular retention of paraquat with toxic myopathy or neuromyopathy as a late manifestation of paraquat toxicity.
Patients with lower respiratory tract infection (LRTI) were randomized 2:1 to receive either cefepime 2 g i.v. bd or cefotaxime 2 g i.v. tds. Bronchopneumonia alone or associated with another LRTI was diagnosed in 30 of 37 cefepime recipients and in 11 of 18 cefotaxime recipients; other diagnoses included bronchitis, lobar pneumonia and aspiration pneumonia. The mean duration of treatment was 5.9 days in the cefepime group and 5.4 days in the cefotaxime group. There were no significant differences between the two groups with regard to clinical or bacteriological outcome. Treatment was associated with a satisfactory clinical response in 27 (73%) of 37 evaluable cefepime patients and in 10 (56%) of 18 evaluable cefotaxime patients. Treatment resulted in eradication of 33 (89%) of 37 pathogens in the cefepime group, including 13 of 15 strains of Staphylococcus aureus, and of 16 (73%) of 22 pathogens in the cefotaxime group, including eight of ten strains of S. aureus. Two Pseudomonas aeruginosa strains persisted in the cefotaxime group. The sole clinical adverse event reported was a rash in one cefepime patient which did not require discontinuation of treatment. No clinically relevant changes in laboratory test results were attributed to either agent. Cefepime twice daily and cefotaxime three times daily were of comparable safety and efficacy in the treatment of bronchopneumonia and other LRTIs.
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