Showing posts with label Intensive Care. Show all posts
Showing posts with label Intensive Care. Show all posts

Tuesday, July 1, 2014



Adrenal response after trauma is affected by time after trauma and sedative/analgesic drugs.

Brorsson C, Dahlqvist P, Nilsson L, Thunberg J, Sylvan A, Naredi S
 Injury. 2014 Aug;45(8):1149-55

The aim of this study was to assess the early adrenal response after trauma.

METHODS:

Prospective, observational study of 50 trauma patients admitted to a level-1-trauma centre. Serum and saliva cortisol were followed from the accident site up to five days after trauma. Corticosteroid binding globulin (CBG), dehydroepiandrosterone (DHEA) and sulphated dehydroepiandrosterone (DHEAS) were obtained twice during the first five days after trauma. The effect of time and associations between cortisol levels and; severity of trauma, infusion of sedative/analgesic drugs, cardiovascular dysfunction and other adrenocorticotropic hormone (ACTH) dependent hormones (DHEA/DHEAS) were studied.

RESULTS:

There was a significant decrease over time in serum cortisol both during the initial 24h, and from the 2nd to the 5th morning after trauma. A significant decrease over time was also observed in calculated free cortisol, DHEA, and DHEAS. No significant association was found between an injury severity score≥16 (severe injury) and a low (<200nmol/L) serum cortisol at any time during the study period. The odds for a serum cortisol <200nmol/L was eight times higher in patients with continuous infusion of sedative/analgesic drugs compared to patients with no continuous infusion of sedative/analgesic drugs.

CONCLUSION:

Total serum cortisol, calculated free cortisol, DHEA and DHEAS decreased significantly over time after trauma. Continuous infusion of sedative/analgesic drugs was independently associated with serum cortisol <200nmol/L.


Intracranial pressure response after pharmacologic treatment of intracranial hypertension.

J Trauma Acute Care Surg. 2014 Jul;77(1):47-53.

Patients older than 17 years, admitted and requiring ICP monitoring between 2008 and 2010 at a high-volume urban trauma center, were retrospectively evaluated. Timing and dose of ICP-directed therapy were recorded from paper and electronic medical records. ICP data were collected automatically at 6-second intervals and from manual charts
A total of 117 patients met inclusion criteria; 450 treatments were administered when nursing records indicate an ICP greater than 20 mm Hg, while 968 treatments were given when ICP was greater than 20 mm Hg by automated data.
 Pharmacologic treatments identified include hypertonic saline (HTS), mannitol, barbiturates, and dose escalations of propofol or fentanyl infusions.
Treatment with HTS resulted in the largest ICP decrease of the treatments examined, with a 1-hour ICP reduction of 8.8/9.9 mm Hg (for a small/large dose) according to manual data and a reduction of 3.0/2.4 mm Hg according to automated data. Propofol and fentanyl escalations resulted in smaller but significant ICP reductions. Mannitol (n = 8) resulted in statistically insignificant trends down in the first hour but rebounded by the second hour after administration. The average ICP in the hour before medication administration was higher for barbiturates (27 mm Hg) and mannitol (32 mm Hg) than for the other interventions (18-19 mm Hg).

CONCLUSION:

ICP fell after administration of HTS, mannitol, or barbiturates and showed continued improvement after 2 hours. ICP fell initially after treatment with short-acting propofol and fentanyl but trended back up after 2 hours

Thursday, June 19, 2014


Early Administration of Hydrocortisone Replacement After the Advent of Septic Shock: Impact on Survival and Immune Response


Katsenos, Chrysostomos S. et  al on behalf of the Hellenic Sepsis Study Group


Critical Care Medicine:
July 2014 - Volume 42 - Issue 7 - p 1651–1657



Over a 2-year period, 170 patients with septic shock treated with low doses of hydrocortisone were enrolled. Blood was sampled from 34 patients for isolation of peripheral blood mononuclear cells and cytokine stimulation before and 24 hours after the start of hydrocortisone.
 After adjusting for disease severity and type of infection, a protective effect of early hydrocortisone administration against unfavorable outcome was found (hazard ratio, 0.20; p = 0.012).
Time of discontinuation of vasopressors was earlier among patients with initiation of hydrocortisone within 9 hours. Production of tumor necrosis factor-α was lower among patients who had had hydrocortisone early,
This resulted in improved survival.