Category Archives: Resus

Life-saving medicine

All Updates, PHARM, Resus, Trauma

Traumatic Aortic Injury

Two recent papers expand our knowledge of blunt traumatic aortic injury.
UK crash data identified risk factors for low impact blunt traumatic aortic rupture, or ‘LIBTAR’ (crashes at relatively low speed): age >60, lateral impacts and being seated on the side that is struck are predictive of LIBTAR. This study should raise our index of suspicion of aortic injury in low-impact scenarios since low-impact collisions account for two thirds of fatal aortic injuries.
Low-impact scenarios may account for two-thirds of blunt traumatic aortic rupture
Emerg Med J. 2010 May;27(5):341-4

Data from the Victorian State Trauma Registry showed pre-hospital mortality from traumatic thoracic aortic transection was approximately 88.0%, whereas patients who survive to reach hospital have a much lower hospital mortality (33.3%, and once patients who arrived in extremis were removed hospital mortality was reduced to 5.9%). Repair was performed in 46 patients, with 22 receiving initial endovascular repair and 24 receiving initial open repair. Mortality rates following surgery were 9.1% and 16.7%, respectively.

The majority of patients arriving at hospital (57.1%) had an ISS of over 40 highlighting that these patients are unlikely to have only one serious injury and are likely to be more seriously injured than the normal trauma population. An ISS greater than 40 was a main predictor of mortality before repair.

Aortic transection: demographics, treatment and outcomes in Victoria, Australia
Emerg Med J. 2010 May;27(5):368-71

All Updates, ICU, Kids, Resus

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

All Updates, ICU, Resus

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

All Updates, Guidelines, ICU, Kids, Resus

Post cardiac arrest guideline

A patient is resuscitated from an out-of-hospital cardiac arrest and is in your emergency department, comatose, with a pulse.
You know that therapeutic hypothermia is indicated and are happy with the protocol for that. You clinically assess for the underlying cause with history, examination, ECG, and other investigations as indicated.
Someone asks you if you want to give some magnesium “as per the guidelines”. As you are wondering what that’s for someone else asks you how long myocardial stunning lasts for and whether that’s the likely cause of hypotension now.
Luckily you avoid getting annoyed with all these reasonable questions by suddenly remembering that there are international recommendations for the management of ‘Post–Cardiac Arrest Syndrome’. You excuse yourself from the room on the pretext of going to the lavatory and quickly find a quiet area where you scan the following article for help:
Post–Cardiac Arrest Syndrome Epidemiology, Pathophysiology, Treatment, and Prognostication
A Consensus Statement From the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council
Circulation 2008;118;2452-2483 Full Text Article

All Updates, Kids, Resus

Early CPAP versus Surfactant in Extreme Prems

In a randomised, multicentre trial of 1316 infants born between 24 weeks 0 days and 27 weeks 6 days of gestation, infants were randomly assigned to intubation and surfactant treatment (within 1 hour after birth) or to CPAP treatment initiated in the delivery room, with subsequent use of a protocol-driven limited ventilation strategy. The primary outcome was death or bronchopulmonary dysplasia as defined by the requirement for supplemental oxygen at 36 weeks.

Infants who received CPAP treatment, as compared with infants who received surfactant treatment, less frequently required intubation or postnatal corticosteroids for bronchopulmonary dysplasia (P<0.001), required fewer days of mechanical ventilation (P=0.03), and were more likely to be alive and free from the need for mechanical ventilation by day 7 (P=0.01). However the rates of the primary outcome did not differ significantly between the CPAP group and the surfactant group (47.8% and 51.0%, respectively; relative risk with CPAP, 0.95; 95% confidence interval [CI], 0.85 to 1.05).
The infants randomised to CPAP could receive limited invasive ventilation if necessary; 83.1% of the infants in the CPAP group were intubated. They did not include infants who were born at a gestational age of less than 24 weeks, since the results of a pilot trial showed that 100% of such infants required intubation in the delivery room.
This study had a 2-by-2 factorial design in which infants were also randomly assigned to one of two target ranges of oxygen saturation.
Early CPAP versus Surfactant in Extremely Preterm Infants
N Engl J Med. 2010 May 16. [Epub ahead of print]

Acute Med, All Updates, Resus

Bloodtest Not Pertinent (BNP)

Despite a lack of evidence that it’s useful, many emergency departments have introduced BNP testing. Some smart Australians decided to properly evaluate its benefit the best way possible – with a randomised controlled trial on 612 patients with acute severe dyspnoea. Guess what? Clinician knowledge of BNP values in patients who presented with shortness of breath to the emergency department did not reduce the probability of hospital admission or alter management or length of hospital stay. The study findings do not support indiscriminate BNP testing in all dyspnoea patients, but do not rule out a possible role in patients with milder dyspnoea.
B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial
Ann Intern Med. 2009 Mar 17;150(6):365-71

Acute Med, All Updates, ICU, Resus

PCI and therapeutic hypothermia

Percutaneous coronary intervention did not increase the risk of dysrhythmia, infection, coagulopathy, or hypotension associated with therapeutic hypothermia after cardiac arrest. Intensivists and cardiologists should perhaps agree that this adds to existing evidence that the two therapies are not mutually exclusive.
Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest
Resuscitation. 2010 Apr;81(4):398-403

All Updates, PHARM, Resus, Trauma

The myth of ketamine and head injury

A literature review addresses the myth that ketamine is contraindicated in head injured patients. They summarise articles from the 1970’s which identified an association between ketamine and increased ICP in patients with abnormal cerebrospinal fluid pathways (such as those caused by aqueductal stenosis, obstructive hydrocephalus and other mass effects). In more recent studies no statistically significant increase in ICP was observed following the administration of ketamine in patients with head injury; some of the studies showed a net increase in CPP following ketamine administration. They list ketamine’s stable haemodynamic profile and potential neuroprotective effects as further rationale for its use.
The authors boldly summarise:
‘Based on its pharmacological properties, ketamine appears to be the perfect agent for the induction of head-injured patients for intubation.’
Myth: ketamine should not be used as an induction agent for intubation in patients with head injury
CJEM. 2010 Mar;12(2):154-7

Acute Med, All Updates, Resus

Rapid discharge in AF

The Ottawa Aggressive Protocol is used to treat recent onset (< 48 hours) atrial fibrillation or flutter with procainamide and/or cardioversion to allow discharge from the emergency department.
A cohort of 660 patient visits is described in a paper in the Canadian Journal of Emergency Medicine, 95.2% involving atrial fibrillation and 4.9% involving atrial flutter. The mean age of patients enrolled was 64.5 years. In total, 96.8% were discharged home and, of those, 93.3% were in sinus rhythm. All patients were initially administered intravenous procainamide, with a 58.3% conversion rate. A total of 243 patients underwent subsequent electrical cardioversion with a 91.7% success rate. Adverse events occurred in 7.6% of cases: hypotension 6.7%, bradycardia 0.3% and 7-day relapse 8.6%. There were no cases of torsades de pointes, stroke or death. The median lengths of stay in the ED were as follows: 4.9 hours overall, 3.9 hours for those undergoing conversion with procainamide and 6.5 hours for those requiring electrical conversion.
This proactive approach by emergency physicians seems excellent for patients who in some centres probably still get admitted for this presentation. I’m not sure why they continue to use a drug with a conversion percentage in the 50’s, which the authors have demonstrated before. Many of us routinely use flecainide for recent onset AF in patients likely to have structurally normal hearts, as it has been shown to be superior to procainamide in AF.
Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter
Canadian Journal of Emergency Medicine 12.3 (May 2010): p181(11)

All Updates, Kids, Resus, Trauma

Vital signs of severely injured children

Systolic blood pressures of severely injured children are very often hypertensive compared with APLS ‘norms’. A lower pulse rate is associated with more severe brain injury

SBP (Mean+/- 95% confidence limits) in moderately injured children with and without TBI by age and Advanced Paediatric Life Support (APLS) range for normal systolic blood pressure (shaded region)

Comparing the systolic blood pressure (SBP) and pulse rate (PR) in injured children with and without traumatic brain injury
Resuscitation. 2010 Apr;81(4):418-21