Archive for the ‘.trauma-general’ Category

Big Trauma: Before the CT

November 28th, 2016
by reuben in .trauma-general

  Efforts to standardize the approach to trauma have led to an algorithmic, thoughtless approach to trauma that over-utilizes CT in well patients and delays CT in ill patients. In critically injured blunt trauma patients, CT is a fantastically useful test and should be prioritized as the critical diagnostic step to be taken as quickly as feasible. Classic teaching is that unstable patients should be stabilized prior to CT, but this is an outdated, dangerous paradigm; optimal care in severe trauma rapidly implements key resuscitative maneuvers so that resuscitation can continue simultaneously with CT. I have witnessed many cases where persistently hypotensive patients were observed in the trauma bay because “the patient might need to go direct to the OR,” but direct to the OR means direct to the OR; observation of an unstable trauma patient prior to elucidation of the injuries is usually the wrong strategy. Know exactly what the initial resuscitative priorities are in trauma so that as soon as they’re done, the patient can be taken to their next destination (CT, OR, IR). The following are carried out in parallel with universal first steps of resuscitation and the primary survey. 1. Staunch external bleeding. This can be accomplished with pinpoint pressure in almost all cases, occasionally a proximal tourniquet is required. 2. Resuscitative vascular access. Short, wide peripheral lines or a sheath introducer in a central vein is an immediate priority. Know the flow rates of commonly used catheters. 3. Blood. Do not delay initiation of your massive transfusion protocol in the unstable trauma patient when ongoing internal bleeding is likely….

In this month’s Canadian Journal of Emergency Medicine, Filanovsky et al describe how studies in the 70s associate rises in ICP to ketamine, and review more recent, higher quality evidence to the contrary. They do not mention that several of the early studies examined the influence of ketamine on ICP in non-intubated patients. Ketamine is well-known to cause brief periods of apnea, especially if pushed quickly; these short episodes are clinically inconsequential when ketamine is used for PSA and irrelevant when ketamine is used for RSI, where patients are simultaneously paralyzed. However, transient rises in pCO2 will cause cerebral vasodilation and a rise in ICP. Apnea time should therefore be minimized in patients potentially susceptible to ICP fluctuations, but this strategy applies to all induction agents used for RSI. Filanovsky et al also review evidence suggesting that ketamine may in fact be neuro-protective in head trauma, though the jury is still out on this question. They also note the concerns around the adrenal effects of etomidate, the induction agent most often used in polytrauma. While we know that etomidate infusions increase ICU mortality, it’s so far unclear if single-dose etomidate used for RSI causes clinically consequential adrenal suppression. Irrespective of these two issues, given the tendency of ketamine to increase blood pressure, it should be the induction agent of choice in the hypotensive trauma patient, with or without head injury. CJEM 2010;12(2):154-157

Critical Care 2007 11_R1