Rate and pattern of antibiotic resistance in microbiological cultures of sepsis patients in a low-middle-income country's ICU.

BACKGROUND: In this prospective, observational study, the rate of antibiotic resistance in cultures sampled from sepsis patients was determined in an intensive care unit of a low-middle income country. METHODS: Critically ill patients suffering from bacterial sepsis were eligible for enrollment. Aside from demographic, disease-related and sepsis-specific parameters, the type of microbiological sample and cultured microorganism as well as the resistance pattern (extensively resistant bacteria, multi-drug resistant bacteria) were documented. Descriptive statistical methods, parametric and non-parametric tests were used. RESULTS: 215 sepsis patients were included. 193 ofthe 410 cultured organisms (47.1%) showed antibiotic resistance [extensively resistant bacteria, n = 90 (11%); multi-drug resistant bacteria, n = 103 (25.1%)]. 51.6% of the patients were infected by > or = 1 resistant bacteria. Bacteria with an exceptionally high rate of antibiotic resistance were Acinetobacter baumannii (90%), Enterobacter spp (60%) and coagulase-negative Staphylococci (60%). Patients infected with resistant bacteria more often received inadequate empirical antibiotic therapy (36.9 vs. 13.5%, p < 0.001), required mechanical ventilation (66.7 vs. 42.3%, p < 0.001) and renal replacement therapy (28.8 vs. 9.6%, p < 0.001) more frequently, and had a longer stay in the intensive care unit [5 (3-9.5) vs. 5 (2-8)%, p < 0.001] than patients with sepsis due to non-resistant bacteria. There was a trend towards a higher mortality in patients with resistant bacteria (43.2 vs. 31.7%, p = 0.09). CONCLUSION: Resistant bacteria were detected in up to 50% of microbiological samples from critically ill sepsis patients in the intensive care unit of a low-middle-income country. Antibiotic resistance appears to be a relevant problem of sepsis management in a resource-limited setting.

Dear vasopressin, where is your place in septic shock?

Cardiovascular failure is one of the central therapeutic problems in patients with severe infection. Although norepinephrine is a potent and, in most cases, highly effective vasopressor agent, very high dosages leading to significant side effects can be necessary to stabilize advanced shock. As a supplementary vasopressor, arginine vasopressin can reverse hemodynamic failure and significantly decrease norepinephrine dosages. Whether the promising possibility of 'bridging' advanced septic shock when the benefit/risk ratio of catecholamine therapy leaves a clinically tolerable range may improve quantitative and qualitative patient outcome can only be determined by a large, prospective, randomized study.

Prolonged bilateral reactive miosis as a symptom of severe insulin intoxication.

BACKGROUND: Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase the cholinergic tone, or exert sedative-hypnotic effects, but has not been reported in insulin poisoning. CASE REPORT: A 64-year- old woman without co-morbidities was found unconscious next to an empty insulin pen. Her Glasgow Coma Scale was 3 with absent reflexes, bilateral reactive miosis, and injection marks across the abdominal wall. The patient was endotracheally intubated, mechanically ventilated, and transferred to this hospital. At admission, the blood glucose level was 34 mg/dL. Glasgow Coma Scale remained at 3, with persistent bilateral reactive miosis. The toxicology screening was negative for ethanol, barbiturates, tricyclic antidepressants, phenothiazines, amphetamines, cannabinoids, salicylates, acetaminophen, and cocaine. Cranial computed tomography with angiography and magnetic resonance imaging (MRI) did not show any structural brain lesions. Intravenous glucose was continued at 6-14 g/h for 3 days. On repeated neurological examinations, the patient remained deeply comatose, with partial loss of cranial nerve function. Bilateral reactive miosis persisted for 4 days. From day 5 on, the patient awoke progressively. At discharge, the patient was fully alert and orientated, without a focal neurological deficit. CONCLUSIONS: Prolonged bilateral reactive miosis can be a clinical symptom accompanying metabolic encephalopathy in severe insulin poisoning. Functional impairment of the pons due to relative hypoperfusion during hypoglycemia may serve as a reasonable pathophysiologic explanation for this phenomenon.