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
[EXPAND Click to read abstract]
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.
A review article in Anesthesia and Analgesia provides a summary of the literature surrounding RSI controversies.
Should a pre-determined dose of induction drug be given or should it be titrated to effect prior to giving suxamethonium?
Should fast acting opioids be coadministered to blunt the pressor response?
What is the optimal dose of suxamethonium?
Should defasciculating doses of neuromuscular blocking drugs be given?
What is the ‘priming’ technique with rocuronium and is it necessary?
Is it really bad to bag-mask ventilate the patient after induction prior to intubation? Which patients might this benefit?
Should patients with full stomachs be anaesthetised sitting up, supine, or head down?
Is cricoid pressure a good or a bad thing?
Not surprisingly the jury is still out on these, which is of course why they remain ‘controversies’. The review article provides a readable, interesting, and up to date summary of the evidence to date.
A case is reported of a stroke patient who aspirated his nasopharyngeal airway, resulting in coughing and desaturation. After iv propofol and topical anaesthesia to the oropharynx and hypopharynx, it was seen on laryngoscopy to be within the trachea but could not be retrieved with Magill forceps. Instead, his doctors inserted a well lubricated 14 Fr foley catheter through the lumen of the tube, inflated the balloon, and pulled it out. Retrieval of Aspirated Nasopharyngeal Airway Using Foley Catheter Anesth Analg. 2010 Apr;110(4):1245-6
While clearing up after teaching with my bald colleague Dr Phil Hyde yesterday I noticed his bulging scalp veins and this reminded me that we don’t talk about this route much in our Paediatric Emergency Medicine Course.
This prompted me to look up the complications of scalp vein access in neonates and infants, which include:
scalp abscess
alopecia
intracranial abscess
thrombophlebitis
intracranial venous sinus air embolism
scalp necrotising fasciitis
Phil's bulging scalp veins
Suggested ways to decrease the risk of complications include:
A vein should not be used for more than 24 h at a time
The needle entry point should not be covered
The butterfly needle should be immobilized to avoid movements of the needle into the tissue with consequent extravasation of fluid
The infusion site should be monitored by regular examination
If a swelling or leakage of fluid is noted, the infusion should be discontinued immediately from that site
The hair should be properly shaved
If the line is required for more than 24 h, a peripheral venous cutdown or central venous line should be considered, after initial resuscitation
An alternative route for rehydration (e.g. intraosseous infusion) should be considered initially, rather than risk multiple, unsuccessful attempts at scalp vein cannulation.
Update 2013: since this post was written in 2010, new guidelines have been written entitled: “Management of bleeding and coagulopathy following major trauma: an updated European guideline” which are available here
The 2007 guidelines on management of bleeding in trauma have been updated in the light of new evidence and modern practice. The guideline group summarises their recommendations as:
We recommend that the time elapsed between injury and operation be minimised for patients in need of urgent surgical bleeding control. (Grade 1A).
We recommend adjunct tourniquet use to stop life-threatening bleeding from open extremity injuries in the pre-surgical setting. (Grade 1C).
We recommend that the physician clinically assess the extent of traumatic haemorrhage using a combination of mechanism of injury, patient physiology, anatomical injury pattern and the patient’s response to initial resuscitation. (Grade 1C).
We recommend initial normoventilation of trauma patients if there are no signs of imminent cerebral herniation. (Grade 1C).
We recommend that patients presenting with haemorrhagic shock and an identified source of bleeding undergo an immediate bleeding control procedure unless initial resuscitation measures are successful. (Grade 1B).
We recommend that patients presenting with haemorrhagic shock and an unidentified source of bleeding undergo immediate further investigation. (Grade 1B).
We recommend early imaging (FAST or CT) for the detection of free fluid in patients with suspected torso trauma. (Grade 1B).
We recommend that patients with significant free intraabdominal fluid and haemodynamic instability undergo urgent intervention. (Grade 1A).
We recommend further assessment using computed tomography for haemodynamically stable patients who are either suspected of having torso bleeding or have a high risk mechanism of injury. (Grade 1B).
We do not recommend the use of single haematocrit measurements as an isolated laboratory marker for bleeding. (Grade 1B).
We recommend both serum lactate and base deficit measurements as sensitive tests to estimate and monitor the extent of bleeding and shock. (Grade 1B).
We recommend that routine practice to detect post-traumatic coagulopathy include the measurement of international normalised ratio (INR), activated partial thromboplastin time (APTT), fibrinogen and platelets. INR and APTT alone should not be used to guide haemostatic therapy. (Grade 1C) We suggest that thrombelastometry also be performed to assist in characterising the coagulopathy and in guiding haemostatic therapy. (Grade 2C).
We recommend that patients with pelvic ring disruption in haemorrhagic shock undergo immediate pelvic ring closure and stabilisation. (Grade 1B).
We recommend that patients with ongoing haemodynamic instability despite adequate pelvic ring stabilisation receive early preperitoneal packing, angiographic embolisation and/or surgical bleeding control. (Grade 1B).
We recommend that early bleeding control of the abdomen be achieved using packing, direct surgical bleeding control and the use of local haemostatic procedures. In the exsanguinating patient, aortic cross-clamping may be employed as an adjunct. (Grade 1C).
We recommend that damage control surgery be employed in the severely injured patient presenting with deep hemorrhagic shock, signs of ongoing bleeding and coagulopathy. Additional factors that should trigger a damage control approach are hypothermia, acidosis, inaccessible major anatomic injury, a need for time-consuming procedures or concomitant major injury outside the abdomen. (Grade 1C).
We recommend the use of topical haemostatic agents in combination with other surgical measures or with packing for venous or moderate arterial bleeding associated with parenchymal injuries. (Grade 1B).
We recommend a target systolic blood pressure of 80-100 mmHg until major bleeding has been stopped in the initial phase following trauma without brain injury. (Grade 1C).
We recommend that crystalloids be applied initially to treat the bleeding trauma patient. (Grade 1B) We suggest that hypertonic solutions also be considered during initial treatment. (Grade 2B) We suggest that the addition of colloids be considered within the prescribed limits for each solution in haemodynamically unstable patients. (Grade 2C).
We recommend early application of measures to reduce heat loss and warm the hypothermic patient in order to achieve and maintain normothermia. (Grade 1C).
We recommend a target haemoglobin (Hb) of 7-9 g/dl. (Grade 1C).
We recommend that monitoring and measures to support coagulation be initiated as early as possible. (Grade 1C).
We recommend that ionised calcium levels be monitored during massive transfusion. (Grade 1C) We suggest that calcium chloride be administered during massive transfusion if ionised calcium levels are low or electrocardiographic changes suggest hypocalcaemia. (Grade 2C).
We recommend early treatment with thawed fresh frozen plasma in patients with massive bleeding. (Grade 1B) The initial recommended dose is 10-15 ml/kg. Further doses will depend on coagulation monitoring and the amount of other blood products administered. (Grade 1C).
We recommend that platelets be administered to maintain a platelet count above 50 × 109/l. (Grade 1C) We suggest maintenance of a platelet count above 100 × 109/l in patients with multiple trauma who are severely bleeding or have traumatic brain injury. (Grade 2C) We suggest an initial dose of 4-8 platelet concentrates or one aphaeresis pack. (Grade 2C).
We recommend treatment with fibrinogen concentrate or cryoprecipitate if significant bleeding is accompanied by thrombelastometric signs of a functional fibrinogen deficit or a plasma fibrinogen level of less than 1.5-2.0 g/l. (Grade 1C) We suggest an initial fibrinogen concentrate dose of 3- 4 g or 50 mg/kg of cryoprecipitate, which is approximately equivalent to 15-20 units in a 70 kg adult. Repeat doses may be guided by thrombelastometric monitoring and laboratory assessment of fibrinogen levels. (Grade 2C).
We suggest that antifibrinolytic agents be considered in the bleeding trauma patient. (Grade 2C) We recommend monitoring of fibrinolysis in all patients and administration of antifibrinolytic agents in patients with established hyperfibrinolysis. (Grade 1B) Suggested dosages are tranexamic acid 10-15 mg/kg followed by an infusion of 1-5 mg/kg per hour or ε-aminocaproic acid 100-150 mg/kg followed by 15 mg/kg/h. Antifibrinolytic therapy should be guided by thrombelastometric monitoring if possible and stopped once bleeding has been adequately controlled. (Grade 2C).
We suggest that the use of recombinant recombinant activated coagulation factor VII (rFVIIa) be considered if major bleeding in blunt trauma persists despite standard attempts to control bleeding and best-practice use of blood components. (Grade 2C).
We recommend the use of prothrombin complex concentrate for the emergency reversal of vitamin K-dependent oral anticoagulants. (Grade 1B).
We do not suggest that desmopressin (DDAVP) be used routinely in the bleeding trauma patient. (Grade 2C) We suggest that desmopressin be considered in refractory microvascular bleeding if the patient has been treated with platelet-inhibiting drugs such as aspirin. (Grade 2C).
We do not recommend the use of antithrombin concentrates in the treatment of the bleeding trauma patient. (Grade 1C).
As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and antithrombin therapy have been offered, formally assess individual risk of future adverse cardiovascular events using an established risk scoring system that predicts 6-month mortality (for example, Global Registry of Acute Cardiac Events [GRACE]).
Consider intravenous eptifibatide or tirofiban as part of the early management for patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.
Offer coronary angiography (with follow-on PCI if indicated) within 96 hours of first admission to hospital to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%) if they have no contraindications to angiography (such as active bleeding or comorbidity). Perform angiography as soon as possible for patients who are clinically unstable or at high ischaemic risk.
When the role of revascularisation or the revascularisation strategy is unclear, resolve this by discussion involving an interventional cardiologist, cardiac surgeon and other healthcare professionals relevant to the needs of the patient. Discuss the choice of the revascularisation strategy with the patient.
To detect and quantify inducible ischaemia, consider ischaemia testing before discharge for patients whose condition has been managed conservatively and who have not had coronary angiography.
Before discharge offer patients advice and information about:
– their diagnosis and arrangements for follow-up
– cardiac rehabilitation
– management of cardiovascular risk factors and drug therapy for secondary prevention
– lifestyle changes
One of the most potentially confusing areas is the choice of antithrombin therapy. Whereas the low molecular weight heparin enoxaparin is currently widely used, the guideline recommends the following:
The guideline summary is here and the full guideline is here
In a randomised study of more than 1072 patients for emergency intubation using rapid sequence induction, single-use metal blades were associated with fewer failed first attempts and fewer poor grade laryngeal views than reusable metal blades. Improved illumination may be a factor. Comparison of Single-use and Reusable Metal Laryngoscope Blades for Orotracheal Intubation during Rapid Sequence Induction of Anesthesia Anesthesiology. 2010 Feb;112(2):325-32
Patients with symptomatic severe carotid artery stenosis do better with carotid endarterectomy than with medical therapy alone. Surgical complications such as bleeding and cranial nerve damage make the alternative strategy of carotid stenting attractive, but a new randomised trial of 1710 patients with over 50% stenosis and symptoms suggests otherwise.
In favour of stenting, there was one event of cranial nerve palsy in the stenting group compared with 45 in the endarterectomy group, and fewer haematomas of any severity in the stenting group than in the endarterectomy group (31 vs 50 events; p=0.0197).
However the incidence of stroke, death, or procedural myocardial infarction was 8.5% in the stenting group compared with 5.2% in the endarterectomy group (72 vs 44 events; HR 1.69, 1.16-2.45, p=0.006). Risks of any stroke (65 vs 35 events; HR 1.92, 1.27-2.89) and all-cause death (19 vs seven events; HR 2.76, 1.16-6.56) were higher in the stenting group than in the endarterectomy group. Three procedural myocardial infarctions were recorded in the stenting group, all of which were fatal, compared with four, all non-fatal, in the endarterectomy group.
The authors point out that longer term follow up remains to be looked at, but that carotid endarterectomy should remain the treatment of choice for symptomatic patients with severe carotid stenosis suitable for surgery. However most patients had no complications from either procedure and stenting is also likely to be better than no revascularisation in patients unwilling or unable to have surgery because of medical or anatomical contraindications. Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomised controlled trial Lancet. 2010 Mar 20;375(9719):985-97
The American Heart Association recommends cardiopulmonary resuscitation (CPR) by bystanders with chest compression only for adults who have cardiac arrests, but not for children. These recommendations have new support in a large observational study from Japan examining outcomes in 5170 out-of hospital paediatric arrests over a 3 year period.
For children who had out-of-hospital cardiac arrests from non-cardiac causes, conventional CPR (with rescue breathing) by bystander was associated with improved outcomes compared with compression-only CPR (7·2% [45/624] favourable one month neurological outcome vs 1·6% [6/380]; OR 5·54, 2·52–16·99). In children who had arrests of cardiac causes conventional and compression-only CPR were similarly effective. Infants < 1 year had uniformly poor outcomes.
An editorial points out that this is the largest study that has analysed out-of-hospital cardiac arrest in children, and the overall survival of 9% with only 3% of children having a good neurological outcome, is consistent with previous reports. Conventional and chest-compression-only cardiopulmonary resuscitation by bystanders for children who have out-of-hospital cardiac arrests: a prospective, nationwide, population-based cohort study Lancet. 2010 Apr 17 345:1347-54
One of the key changes in international resuscitation guidelines between the 2000 and 2005 has been to minimise potentially deleterious hands-off time, so that CPR is interrupted less for pulse checks and DC shocks.
These two approaches have been compared in a randomised controlled trial of 845 patients in France requiring out of hospital defibrillation, in which the control group were shocked using AEDs with prompts based on the 2000 guidelines (3 stacked shocks before CPR resumed, and pulse checks done), and the intervention group were shocked using devices that prompted according to the 2005 guidelines, in which there were fewer and shorter intervals for which the AED required the rescuer to stay clear of the patient (single shocks, no pulse checks).
There was no difference in the primary endpoint of survival to hospital admission (43.2% versus 42.7%; p=0.87), or in survival to hospital discharge (13.3% versus 10.6%; p=0.19). The study was not powered to assess one year survival. In the authors’ words: “our randomized controlled trial now provides more definitive evidence that this combination of Guidelines 2005 CPR protocol changes does not measurably improve outcome. Although the protocol changes accomplish the desired effect of increasing chest compressions, they may also cause other effects, such as earlier refibrillation and more time spent in VF, with as yet unknown consequences.”
Interestingly the Cardio-pump was used in this study to provide chest compressions, which is an active compression-decompression device, potentially limiting the generalisability of the findings to manual compression-only CPR situations. Potential bias was also introduced by the exclusion of patients in whom consent from relatives was not obtained. Nevertheless it’s good to see such rigorous clinical research applied to this area. DEFI 2005. A Randomized Controlled Trial of the Effect of Automated External Defibrillator Cardiopulmonary Resuscitation Protocol on Outcome From Out-of-Hospital Cardiac Arrest Circulation. 2010;121:1614-1622
