Aeromedical retrieval specialists in Scotland developed a simple, cheap, effective in-flight cooling protocol using intravenous (IV) cold Hartmann’s solution and chemical cooling packs. Fluids cooled in a fridge (4°C) were transported in an insulated cool box; the patient was sedated, paralysed and intubated, and controlled ventilation started. The patient was then cooled by IV infusion of 30 ml/kg of cold Hartmann’s. Chemical ice packs were activated and placed in the axillae and groin. The time interval between successful resuscitation and the patient being retrieved and flown to an Intensive Care Unit (ICU) was at least 3.5 h. Cooled patients had a mean decrease in body temperature during retrieval compared to patients not cooled (−1.6 °C vs. +0.9 °C, p = 0.005) and a lower body temperature on ICU arrival (34.1 °C vs. 36.4 °C, p = 0.05). Two of the 5 cooled patients achieved target temperature (<34 °C) before ICU arrival. No complications of in-flight cooling were reported.
Emergency physicians at Hennepin County Medical Centre (HCMC) are trained in skull trephination (drilling a burr hole) for patients with coma, anisocoria and epidural (extradural) haematoma (EDH) who have not responded to osmotic agents and hyperventilation. This may be particularly applicable in centres remote from neurosurgical centres where delays caused by interfacility transfer are associated with increased morbidity and mortality.
Dr Smith and colleagues from HCMC describe a series of five talk-and-deteriorate patients with EDH who underwent skull trephination. 3 had complete recovery without disability, and 2 others had mild to moderate disability but with good to excellent cognitive function. None had complications from the procedure other than external bleeding from the already lacerated middle meningeal artery. In 4 of 5 cases, the times were recorded. Mean time from ED presentation to trephination was 55 min, and mean time from ED to craniotomy was 173 min. The mean time saved was 118 min, or approximately 2 h.
All trephinations were done by emergency physicians, who had received training in skull trephination as part of the HCMC Emergency Medicine Residency or as part of the Comprehensive Advanced Life Support (CALS) course. Training was very brief and involved discussion of the treatment of EDH, review of a CT scan of EDH, and hands-on practice on the skull of a dead sheep, using the Galt trephinator.
An excellent point made by the authors reminds us that patients with EDH who talk-and-deteriorate (those with the traditionally described “lucid interval”) have minimal primary brain injury and frequently have no brain parenchymal injury. Thus, if the EDH is rapidly decompressed, the outcome is significantly better than for deterioration due to other aetiologies. The authors recommend in EDH that the procedure should be done within 60–90 min of onset of anisocoria. A review of other studies on the procedure would suggest that case selection is critical in defining the appropriateness of the procedure: talk-and-deteriorate, coma, anisocoria, and a delay to neurosurgical decompression. Emergency Department Skull Trephination for Epidural Hematoma in Patients Who Are Awake But Deteriorate Rapidly J Emerg Med. 2010 Sep;39(3):377-83
Over a thousand patients in North America with blunt traumatic head injury and coma who did not have hypovolaemic shock were randomised to different fluids pre-hospital. 250 ml Hypertonic (7.5%) saline was compared with normal (0.9%) saline and hypertonic saline dextran (7.5% saline/6% dextran 70). There was no difference in 6-month neurologic outcome or survival.
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
Symptomatic cerebral vasospasm occurs in nearly one-third of patients with aneurysmal subarachnoid hemorrhage and is a major cause of disability and mortality in this population.
Magnesium (Mg) acts as a cerebral vasodilator by blocking the voltage-dependent calcium channels.. Experimental studies suggest that Mg also inhibits glutamate release by blocking N-methyl-D-aspartate receptors, decreases intracellular calcium influx, and increases red blood cell deformability; all these changes may reduce the occurrence of cerebral vasospasm and minimise brain ischemic injury occurring after SAH.
One hundred and ten patients within 96 hours of admission for aneurysmal subarachnoid haemorrhage (SAH) were randomised to receive iv magnesium or placebo. Nimodipine was not routinely given. Twelve patients (22%) in the magnesium group and 27 patients (51%) in the control group had delayed ischemic infarction – the primary endpoint (p< .0020; odds ratio [OR], 0.28; 95% confidence interval [CI], 0.12– 0.64). Mortality was lower and neurological outcome better in the magnesium group but these results were not statistically significant.
Larger trials of magnesium in SAH are ongoing. Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: A randomized, placebo-controlled, clinical study Crit Care Med. 2010 May;38(5):1284-90 Update September 2012:
A multicentre RCT showed intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended. Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial Lancet 2012 July 7; 380(9836): 44–49 Free full text
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Background Magnesium sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed cerebral ischaemia. We did a trial to test whether magnesium therapy improves outcome after aneurysmal subarachnoid haemorrhage.
Methods We did this phase 3 randomised, placebo-controlled trial in eight centres in Europe and South America. We randomly assigned (with computer-generated random numbers, with permuted blocks of four, stratified by centre) patients aged 18 years or older with an aneurysmal pattern of subarachnoid haemorrhage on brain imaging who were admitted to hospital within 4 days of haemorrhage, to receive intravenous magnesium sulphate, 64 mmol/day, or placebo. We excluded patients with renal failure or bodyweight lower than 50 kg. Patients, treating physicians, and investigators assessing outcomes and analysing data were masked to the allocation. The primary outcome was poor outcome—defined as a score of 4–5 on the modified Rankin Scale—3 months after subarachnoid haemorrhage, or death. We analysed results by intention to treat. We also updated a previous meta-analysis of trials of magnesium treatment for aneurysmal subarachnoid haemorrhage. This study is registered with controlled-trials.com (ISRCTN 68742385) and the EU Clinical Trials Register (EudraCT 2006-003523-36).
Findings 1204 patients were enrolled, one of whom had his treatment allocation lost. 606 patients were assigned to the magnesium group (two lost to follow-up), 597 to the placebo (one lost to follow-up). 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio [RR] 1·03, 95% CI 0·85–1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·86–1·08).
Interpretation Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.
Lactate may be an important metabolic substrate for injured brain and sodium lactate may have beneficial effects on cerebral oedema and cerebral blood flow. Sodium lactate was compared with 20% mannitol in severely brain injured patients with cranial hypertension in a randomised controlled trial. Sodium lactate was more likely to lower ICP, and to have a sustained effect on ICP. A nonsignificant improvement in one year outcome was seen with sodium lactate, although the study was not powered for this endpoint. These promising findings should prompt a larger multicentre study. Sodium lactate versus mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients Intensive Care Med. 2009 Mar;35(3):471-9