Tag Archives: outcome

Terlipressin for refractory cardiac arrest in kids

Okay so it’s a small case series – but the results warrant further investigation: 10-20 mcg/kg terlipressin was given to five infants and children who arrested in the paediatric intensive care unit and who had not responded to several doses of adrenaline (epinephrine)1. Sustained return of spontaneous circulation (ROSC) was achieved in four, and two survived to be discharged home without sequelae and with good neurologic status at 6 and 12 month follow up. Interestingly, the four patients who had ROSC all had septic shock as the cause of their arrest. The two survivors had severe bradycardia and severe bradycarda-asystole as the arrest rhythms, and both received 20 mcg/kg terlipressin.
Terlipressin is a synthetic arginine vasopressin analog with a significantly longer duration of effect, which previously showed positive effects when administered to a small group of children unresponsive to prolonged resuscitative efforts2.
1. Pediatric cardiac arrest refractory to advanced life support: Is there a role for terlipressin?
Pediatr Crit Care Med. 2010 Jan;11(1):139-41
2. Beneficial effects of terlipressin in prolonged pediatric cardiopulmonary resuscitation: A case series.
Crit Care Med. 2007 Apr;35(4):1161-4

Paediatric Retrieval – what's the rush?

The Children’s Acute Transport Service (CATS) in the UK performed 2106 interfacility transports between April 2006 and March 2008. The stabilisation time averaged just over 2 hrs. Stabilisation time was prolonged by the number of major interventions required to stabilise the patient before transfer and differed significantly between various diagnostic groups. The length of time spent by the retrieval team outside the intensive care environment had no independent effect on subsequent patient mortality.

They have shown that stabilisation time can be influenced by a number of patient- and transport team-related factors, and that time spent undertaking intensive care interventions early in the course of patient illness at the referring hospital does not increase patient mortality. In the authors’ words: ‘the “scoop and run” model can be safely abandoned in favor of early goal-directed management during interhospital transport for intensive care.
There’s NO rush guys!
Effect of patient- and team-related factors on stabilization time during pediatric intensive care transport
Pediatr Crit Care Med. 2010 May 6

Control oxygenation after resuscitation

How much oxygen should we give patients after successful cardiac arrest resuscitation? Too little oxygen may potentiate anoxic injury. Too much oxygen may increase oxygen free radical production, possibly triggering cellular injury and apoptosis. A multicentre ICU database of over 6300 post-arrest patients was analysed and demonstrated an association between ‘hyperoxia’ and in-hospital mortality.
Adult patients who sustained nontraumatic cardiac arrest and were admitted to the ICU at a participating center between 2001 and 2005 were included. Specifically, inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival.
The cohort was divided into 3 exposure groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg (39.5 kPa) or greater; hypoxia, PaO2 of less than 60 mm Hg (7.9 kPa) (or ratio of PaO2 to fraction of inspired oxygen [FIO2] <300); and normoxia, cases not classified as hyperoxia or hypoxia.
Exposure to hyperoxia was found to be a significant predictor of in-hospital death (OR, 1.8 [95% CI, 1.5-2.2]; this was an independent effect that persisted after adjusting for all other significant risk factors
The authors acknowledge that association does not necessarily imply causation, but add that these data support the hypothesis that high oxygen delivery in the postcardiac arrest setting may have adverse effects.
Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality
JAMA. 2010;303(21):2165-2171

Early CT and post-arrest outcome

A study on the early CT appearances of post-cardiac arrest patients shows two signs to be of importance – loss of boundary (LOB) between white and grey matter (at the level of the basal ganglia), and cortical sulcal effacement (SE). These features were more prevalent in patients who had > 20 minutes of arrest time and were associated with a worse neurological outcome at six months.
Early CT signs in out-of-hospital cardiac arrest survivors: Temporal profile and
prognostic significance

Resuscitation. 2010 May;81(5):534-8

High BMI and frontal crashes

In adult patients injured in front impact motor vehicle collisions, the outcomes of obese patients with a Body Mass Index greater than 30 kg/m2 was compared with those less than 30 kg/m2. Obese patients were more likely to suffer a severe head injury from a frontal collision.
J Trauma. 2009 Mar;66(3):727-9
Traumatic Brain Injury After Frontal Crashes: Relationship With Body Mass Index

Blood product ratios and survival bias

Haemostatic resuscitation of trauma patients, using high ratios of fresh frozen plasma (FFP) to packed red cells (PRBC), is growing in popularity as a result of military experience. Few data support the practice in civilian trauma. It is possible that some of the demonstrated mortality benefit is a result of survival bias: it takes time to obtain FFP, by which time severely injured patients may be dead. Therefore, those that receive large ratios of FFP:PRBC must have survived long enough to receive it. In other words FFP doesn’t lead to survival, but survival leads to FFP. Some evidence in favour of this explanation is provided on a study of 134 patients in the Journal of Trauma. Reanalysing data to correct for survival bias made an apparently significant survival benefit from high FFP:PRBC ratios go away. An interesting paper, although unlikely to dissuade us from paying attention to coagulopathy in trauma. I suspect the debate on optimal blood product resuscitation will be around for a while.
The Relationship of Blood Product Ratio to Mortality: Survival Benefit or Survival Bias?
J Trauma. 2009 Feb;66(2):358-62

Transfusion and ARDS

Blood transfusion in trauma is a risk factor for acute respiratory distress syndrome (ARDS). An analysis of 14070 patients in a trauma database showed that 521 (4.6%) developed ARDS. Logisitc regression analysis demonstrated that, independent of injury type, injury severity, or pneumonia, (1) early PRBCs transfusion of more than 5 units during the first 24 h of hospital admission predicted ARDS and (2) each unit of PRBCs transfused early after admission increased the risk of ARDS by 6%.
Early packed red blood cell transfusion and acute respiratory distress syndrome after trauma.
Anesthesiology. 2009 Feb;110(2):351-60

Delays to neurosurgery

Further evidence from the UK shows that patients with acute traumatic brain injury suffer delays in the neurosurgical evacuation of intracranial haematomas which are increased from an average of 3.7 hours to 5.4 hours if they have to undergo interhospital transfer. Coordinated regional trauma systems please!
A prospective study of the time to evacuate acute subdural and extradural haematomas.
Anaesthesia. 2009 Mar;64(3):277-81

Physicians in pre-hospital care

This systematic review by Scandinavian authors examined controlled studies comparing physician with non-physician treatment in pre-hospital care. Fourteen of the 26 studies identified demonstrated significantly improved survival in the intervention (physician-treated) group. Most survival benefit has been demonstrated in trauma and cardiac arrest, reflecting the fact that these two areas are the most studied. The authors rightly remind us of the paucity of pre-hospital controlled studies of sufficient quality and strength.
A systematic review of controlled studies: do physicians increase survival with prehospital treatment?
Scand J Trauma Resusc Emerg Med. 2009 Mar 5;17(1):12
Full text available at http://www.sjtrem.com/content/pdf/1757-7241-17-12.pdf

oxygen for myocardial infarction – harmful?

Hyperoxia may reduce coronary artery blood flow, increase systemic vascular resistance, and decrease cardiac output. This paper argues that if the baseline arterial oxygen saturations are >90%, high concentration oxygen does not increase oxygen transport, as the reductions in cardiac output are in excess of the increase in oxygen content. The balance of the limited evidence that exists suggests that the routine use of oxygen in uncomplicated MI (no failure or shock) may increase infarct size and possibly increase the risk of mortality, owing to its haemodynamic effects, including a reduction in coronary blood flow.
Routine use of oxygen in the treatment of myocardial infarction: systematic review
Heart. 2009 Mar;95(3):198-202