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Objectives: To investigate the effect of low-dose hydrocortisone on time to shock reversal, the cytokine profile, and its relation to adrenal function in patients with early septic shock., Design: Prospective, randomized, double-blind, single-center study., Setting: Medical intensive care unit of a university hospital., Patients: Forty-one consecutive patients with early hyperdynamic septic shock., Interventions: After inclusion and a short adrenocorticotropic hormone test, all patients were randomized to receive either low-dose hydrocortisone (50-mg bolus followed by a continuous infusion of 0.18 mg/kg body of weight/hr) or matching placebo. After shock reversal, the dose was reduced to 0.06 mg/kg/hr and afterward slowly tapered. Severity of illness was estimated using Acute Physiology and Chronic Health Evaluation II score and Sequential Organ Failure Assessment score., Measurements and Main Results: Time to cessation of vasopressor support (primary end point) was significantly shorter in hydrocortisone-treated patients compared with placebo (53 hrs vs. 120 hrs, p < .02). This effect was more profound in patients with impaired adrenal reserve. Irrespective of endogenous steroid production, cytokine production was reduced in the treatment group with lower plasma levels of interleukin-6 and a diminished ex vivo lipopolysaccharide-stimulated interleukin-1 and interleukin-6 production. Interleukin-10 levels were unaltered. Adverse events were not more frequent in the treatment group., Conclusions: 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.

Group A streptococcal necrotizing fasciitis is a rare disease associated with high mortality. Since severe toxic shock syndrome is a common complication, only immediate and aggressive surgical intervention, adequate antimicrobial therapy and supportive intensive care can be life-saving. We report about successful treatment of a 60-year old patient with necrotizing fasciitis and multiple organ failure.

A 36-year-old male with a known history of sickle cell disease (SCD) and acute chest syndrome (ACS) was treated in our hospital. Gas exchange deteriorated and the patient was transferred to our intensive care unit (ICU). Low dose inhaled nitric oxide (iNO) during pressure controlled mechanical ventilation (pcMV) induced a clinically relevant increase in arterial oxygenation. The patient was weaned from pcMV after five days and discharged home 14 days later. ACS evolving to acute respiratory distress syndrome (ARDS) is a rare but severe complication. In ACS iNO should be considered a beneficial therapeutic option.

A possible diagnostic role of procalcitonin (PCT) as a marker for ventilator associated pneumonia (VAP) in patients with an already triggered acute phase response after successful cardiopulmonary resuscitation (CPR) was investigated. In 28 patients with return of spontaneous circulation (ROSC) after out of hospital CPR, measurements of PCT, C-reactive protein (CrP), white blood cell count (WBC) and body temperature were compared with the clinical course of the patients. In this setting, PCT was the only marker to differentiate between patients with and without VAP (median value on day 1, 6.0 vs. 0.5 ng/ml; P<0.001). Using a cut off value of 1 ng/ml during the first 7 days after ROSC PCT had a sensitivity of 100% and a specificity of 75% to indicate VAP. PCT was elevated a median of 2 days earlier than the clinical diagnosis of VAP. Elevations in PCT can, therefore, indicate bacterial complications in cardiac arrest patients with a non-infectious acute phase response.

Intensive care medicine currently accounts for about 20% of the overall budget of a hospital. A certain reduction of these expenses may be reached through a rationalisation of medical care procedures and structures. The evaluation of procedure efficacy and outcomes, however, is mandatory for the quality assurance of treatment results. A possible rationing of intensive care therapy is difficult to imagine since the current practice of intensive care medicine is also based on humanitarian grounds. The associated costs have to be born by society as a whole. Intensive care medicine though, has to continuously reevaluate and discuss its goals with society.

Objectives: To compare cortisol levels during "low-dose" hydrocortisone therapy to basal and ACTH-stimulated endogenous levels and to assess whether clinical course and the need for catecholamines depend on cortisol levels and/or pretreatment adrenocortical responsiveness., Design and Setting: Prospective observational study in a medical ICU of a university hospital., Patients: Twenty consecutive patients with septic shock and a cardiac index of 3.5 l/min or higher, started on "low-dose" hydrocortisone therapy (100 mg bolus, 10 mg/h for 7 days and subsequent tapering) within 72 h of the onset of shock., Measurements and Results: Basal total and free plasma cortisol levels ranged from 203 to 2169 and from 17 to 372 nmol/l. In 11 patients cortisol production was considered "inadequate" because there was neither a response to ACTH of at least 200 nmol/l nor a baseline level of at least 1000 nmol/l. Following the initiation of hydrocortisone therapy total and free cortisol levels increased 4.2- and 8.5-fold to median levels of 3,587 (interquartile range 2,679-5,220) and 1,210 (interquartile range 750-1,846) nmol/l on day 1, and thereafter declined to median levels of 1,310 nmol/l and 345 nmol/l on day 7. Patients with "inadequate" steroid production could be weaned from vasopressor therapy significantly faster, although their plasma free cortisol concentrations during the hydrocortisone treatment period did not differ., Conclusions: (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.

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.

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.

Carbromal is metabolized extensively in humans. The major metabolites known to date are bromoethylbutyramide, ethylbutyrylurea and inorganic bromide. After ingestion of a therapeutic dose of 1.0 g carbromal (4.2 mmoles) by four healthy volunteers highest concentrations in serum were found to be for carbromal 30 mumoles/l, for bromoethylbutyramide up to 20 mumoles/l and for ethylbutyrylurea 2--3 mumoles/l. In patients acutely poisoned by carbromal-containing sedatives serum concentrations measured were in the range of 200 mumoles/l carbromal, 350 mumoles/l bromoethylbutyramide and 50 mumoles/l ethylbutyrylurea. These patients were comatose, apneic, had isoelectric encephalographic records and decreased body temperature. The degree of central nervous depression as judged by clinical signs was found to correlate with the serum concentrations of carbromal and of bromoethylbutyramide. Pharmacological activity and acute toxicity of carbromal and its two metabolites were examined in rats and compared with the activity of phenobarbitone. For intraperitoneal injection LD-50 values were found to be for carbromal 1.8 mmoles/kg, for bromoethylbutyramide 1.5 mmoles/kg, for ethylbutyrylurea 5.0 mmoles/kg and for phenobarbitone 0.9 mmoles/kg. Carbromal and bromoethylbutyramide severely decreased body temperature. The relative narcotic activity was estimated to be for carbromal = 100; bromoethylbutyramide = 66; ethylbutyrylurea = 33; phenobarbitone = 100. The anticonvulsive activity against pentetrazol-induced generalized seizures was nearly identical for carbromal, bromoethylbutyramide and phenobarbitone. Anticonvulsant activity of ethylbutyrylurea was two to three times less than that of carbromal. Inorganic bromide was found to increase the narcotic activity of carbromal and of bromoethylbutyramide. The findings show that the clinical signs of central nervous system depression seen in patients acutely poisoned with carbromal are caused mainly by unchanged carbromal and by its metabolite bromoethylbutyramide.

The effect of an i.v. injection of 100 mg pentoxifylline on cardiac output, stroke volume, heart rate, atrial pressure, pulmonary arterial, pulmonary capillary and aortic pressure in normal myocardial function and in myocardial insufficiency was investigated in 8 patients with peripheral-arterial occlusive disorders. In normal myocardial function there was a brief, statistically significant increase in cardiac output of +9.6% and a simultaneous reduction in total peripheral resistance of -7.6%. No increase in cardiac output was recorded in patients with myocardial insufficiency. None of the other parameters monitored showed any statistically significant change.