Early Phase Of Critical Illness Research Articles

Modalités pratiques de l'insulinothérapie en réanimation

Critical illness associated hyperglycemia is a common problem in the intensive care unit. Its mechanisms are still unclear. The very early phase of critical illness induced stress is associated with exaggerated hormone response including high circulating levels of adrenaline, glucagon and cortisol. These hormones activate glycogenolysis and neoglucogenesis. Subsequently, insulin resistance develops within muscles, adipose and liver tissues contributing further the rise in the blood glucose levels. The mechanisms of the insulin resistance likely involve breakdown in GLUT 4 levels in cells as a consequence of pro-inflammatory cytokines induced down regulation of GLUT 4 gene transcription. Hyperglycemia with levels exceeding 2 g/l are very likely contributing to mitochondrial dysfunction and critical illness associated morbid-mortality. Tight control of glucose levels may then help improving ICU patients outcome. Nonetheless, the potential serious side effects associated with severe hypoglycemia should urge physicians to be cautious in managing patients with intensive insulin therapy. So far, except in selected surgical ICU patients, physicians should not target normo-glycemia and only avoid blood glucose to exceed 2 g/l. Ongoing clinical trials will help clarifying in the next future which category of ICU patients benefits more from normo-glycemia.

The impact of weekends on outcome for emergency patients

Levels of staffing and access to diagnostics at weekends are recognised to be significantly lower than on weekdays. It is unclear if subsequent inpatient mortality and readmission rates for acute medical admissions are increased for weekend admissions compared to those on a weekday. A large Canadian study demonstrated increased weekend mortality but does the Edinburgh healthcare model support these findings? This study analysed all hospital admissions in 2001 to the Royal Infirmary of Edinburgh for six predetermined diagnoses (total 3,244): chronic obstructive pulmonary disease, cerebrovascular accidents, pulmonary embolism, pneumonia, collapse and upper gastrointestinal bleed. We compared hospital mortality rates, readmission rates and hospital length of stay for weekend admissions as compared to those on a weekday. Weekend admission was not associated with significantly higher in-hospital mortality, readmission rates or increased length of stay compared to the weekday equivalent for any of the six conditions. The implementation of an acute medical admissions unit in the Royal Infirmary of Edinburgh, with consistent staffing levels and 24-hour access to diagnostics for the early phase of critical illness, may have helped address the discrepancy in care suggested by previous studies.

Plasma renin activity and aldosterone behavior in critically ill patients

To investigate the influence of critical illness on plasma renin activity and aldosterone levels and to examine potential inhibitory effects of dopamine therapy on aldosterone responsiveness, we measured plasma renin activity, and potassium and creatinine in serum, as well as the responses of aldosterone, cortisol and prolactin levels to TRH 200 micrograms i.v. + Synacthen 0.25 mg i.v. in 63 unselected, critically ill patients (32 females, 31 males, aged 18-84 years). Of the patients 19 received dopamine treatment (3-13 micrograms/kg/min i.v.); 21 of the patients died in the further course of their disease. Plasma renin activity was increased in 66.7% of the patients and aldosterone levels were elevated in 90.5% of the patients. There were correlations (P less than 0.05) of lethality with plasma renin activity and cortisol levels and correlations (P less than 0.01) of aldosterone concentrations with plasma renin activity and cortisol levels. Whereas dopamine treatment had no inhibitory effect on aldosterone levels before and after stimulation, prolactin stimulation was decreased in dopamine-treated patients. Thus, dopamine does not generally lose its potency of hormone inhibition in critically ill patients, but has no influence on the secondary aldosteronism developing regularly in the early phase of critical illness, which is apparently mainly due to the stimulatory effect of ACTH (or ACTH-related pituitary peptides) and is considered an epiphenomen of the stress mechanisms acting upon the patients in this condition.