Yearly Archives: 2011

Acute Med, All Updates, ICU, Resus

Early CT may rule out subarachnoid haemorrhage

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A multicentre Canadian study challenges the practice of routine lumbar puncture after negative CT in patients with suspected subarachnoid haemorrhage. CT scanning within six hours was highly sensitive, although a few cases of initially misinterpreted CTs “illustrate the importance of having a qualified radiologist with a high level of skill interpreting the head scans in a timely manner“.

Nearly 2% of patients were lost to all follow-up; the authors point out that even if a quarter of these patients could have experienced a subarachnoid haemorrhage, the corresponding negative likelihood ratio for a computed tomography performed within six hours rises to only 0.024 (0.007 to 0.07). They assert:

Such a likelihood ratio could be incorporated into the informed discussion surrounding the risks and benefits of lumbar puncture after negative results on computed tomography for this diagnosis

They point out that when CT imaging is obtained more than six hours after headache onset, clinicians should continue to be cautious because of the decreasing sensitivity for subarachnoid haemorrhage beyond this time.


Objective To measure the sensitivity of modern third generation computed tomography in emergency patients being evaluated for possible subarachnoid haemorrhage, especially when carried out within six hours of headache onset.

Design Prospective cohort study. Setting 11 tertiary care emergency departments across Canada, 2000-9.

Participants Neurologically intact adults with a new acute headache peaking in intensity within one hour of onset in whom a computed tomography was ordered by the treating physician to rule out subarachnoid haemorrhage.

Main outcome measures Subarachnoid haemorrhage was defined by any of subarachnoid blood on computed tomography, xanthochromia in cerebrospinal fluid, or any red blood cells in final tube of cerebrospinal fluid collected with positive results on cerebral angiography.

Results Of the 3132 patients enrolled (mean age 45.1, 2571 (82.1%) with worst headache ever), 240 had subarachnoid haemorrhage (7.7%). The sensitivity of computed tomography overall for subarachnoid
haemorrhage was 92.9% (95% confidence interval 89.0% to 95.5%), the specificity was 100% (99.9% to 100%), the negative predictive value was 99.4% (99.1% to 99.6%), and the positive predictive value was 100% (98.3% to 100%). For the 953 patients scanned within six hours of headache onset, all 121 patients with subarachnoid haemorrhage were identified by computed tomography, yielding a sensitivity of 100% (97.0% to 100.0%), specificity of 100% (99.5% to 100%), negative predictive value of 100% (99.5% to 100%), and positive predictive value of 100% (96.9% to 100%).

Conclusion Modern third generation computed tomography is extremely sensitive in identifying subarachnoid haemorrhage when it is carried out within six hours of headache onset and interpreted by a qualified radiologist

Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study
BMJ. 2011 Jul 18;343:d4277

All Updates, ICU, Resus, Trauma

CRASH-2 and head injury

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The overall effect of the antifibrinolytic drug tranexamic acid on outcome from major trauma was assessed in the CRASH-2 trial, reported here and here. Its effect on a nested cohort of 270 patients from the trial who had traumatic brain injury has now been published1.
Previous evaluation in nontraumatic subarachnoid haemorrhage patients showed tranexamic acid to be associated with cerebral ischaemia, whereas in CRASH-2 (in which a lower dose of tranexamic acid was used) there was a trend to fewer ischaemic lesions as well as smaller haematoma growth and decreased mortality. None of these outcomes were statistically significant so further research is warranted.
An accompanying editorial2 states:

…the CRASH-2 study also justifies a re-evaluation of the possible benefit of low dose short term TXA in patients with other types of intracranial haemorrhage. Many patients with aneurysmal subarachnoid haemorrhage still have to wait for one or two days before the aneurysm is occluded. In addition, at least 30% of patients with spontaneous intracerebral haemorrhage experience substantial haematoma growth in the first 24 hours after the onset of the haemorrhage. As well as the CRASH-2 trial we therefore need new trials investigating short course low dose TXA in patients with aneurysmal subarachnoid haemorrhage and intracerebral haemorrhage.

It looks like considerable enthusiasm for this drug will be around for a while. I look forward to more outcome data, particularly in regard to this challenging group of patients with traumatic and non-traumatic intracranial bleeding.


OBJECTIVE: To assess the effect of tranexamic acid (which reduces bleeding in surgical patients and reduces mortality due to bleeding in trauma patients) on intracranial haemorrhage in patients with traumatic brain injury.

METHODS: A nested, randomised, placebo controlled trial. All investigators were masked to treatment allocation. All analyses were by intention to treat. Patients 270 adult trauma patients with, or at risk of, significant extracranial bleeding within 8 hours of injury, who also had traumatic brain injury.

INTERVENTIONS: Patients randomly allocated to tranexamic acid (loading dose 1 g over 10 minutes, then infusion of 1 g over 8 hours) or matching placebo.

MAIN OUTCOME MEASURES: Intracranial haemorrhage growth (measured by computed tomography) between hospital admission and then 24-48 hours later, with adjustment for Glasgow coma score, age, time from injury to the scans, and initial haemorrhage volume.

RESULTS: Of the 133 patients allocated to tranexamic acid and 137 allocated to placebo, 123 (92%) and 126 (92%) respectively provided information on the primary outcome. All patients provided information on clinical outcomes. The mean total haemorrhage growth was 5.9 ml (SD 26.8) and 8.1 mL (SD 29.2) in the tranexamic acid and placebo groups respectively (adjusted difference -3.8 mL (95% confidence interval -11.5 to 3.9)). New focal cerebral ischaemic lesions occurred in 6 (5%) patients in the tranexamic acid group versus 12 (9%) in the placebo group (adjusted odds ratio 0.51 (95% confidence interval 0.18 to 1.44)). There were 14 (11%) deaths in the tranexamic acid group and 24 (18%) in the placebo group (adjusted odds ratio 0.47 (0.21 to 1.04)).

CONCLUSIONS: This trial shows that neither moderate benefits nor moderate harmful effects of tranexamic acid in patients with traumatic brain injury can be excluded. However, the analysis provides grounds for further clinical trials evaluating the effect of tranexamic acid in this population

1. Effect of tranexamic acid in traumatic brain injury: a nested randomised, placebo controlled trial (CRASH-2 Intracranial Bleeding Study)
BMJ. 2011 Jul 1;343:d379 (free text available)
2. Tranexamic acid for traumatic brain injury
BMJ. 2011 Jul 1;343:d3958

Acute Med, All Updates, Guidelines, Resus

What do I do with a high sensitivity troponin?

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Newer high-sensitivity troponin tests can be positive in patients who would have negative tests with the ‘traditional’ assay, which can result in confusion about what to do with the patient, particularly those patients without an obvious cardiac presentation. A recent study1 shows that the majority of patients that fall into this group had non-cardiac discharge diagnoses.


Background: High sensitivity troponin T (hsTnT) detects lower levels of troponin T with greater precision than the 4th generation (cTnT) assay. However, the clinical implications of this are uncertain.

Objectives: Primary: Describe the proportion of patients who test ‘positive’ with hsTnT but negative with cTnT. Secondary: Determine proportion in each group with an adverse event (representation, AMI or died) within 90 days of the index test.

Method: 161 patients samples were tested with cTnT and hsTNT assays. McNemar’s test was used to compare paired samples. Electronic medical records were reviewed, with discharge diagnosis and 90 day outcomes determined blind to hsTnT results. Patients were then classified as ‘TnT negative’ (hsTnT was <0.014 mcg/mL), 'new positive' (hsTnT was ≥0.014 mcg/mL and cTnT <0.03 mcg/mL) and 'TnT positive' (cTNT was ≥0.03 mcg/mL)
Results: Positive results more than doubled with the hsTnT assay (50% vs 22%, P < 0.001). 81 patients were ‘TnT negative’, 44 were ‘new positive’ and 36 ‘cTnT positive’. The discharge diagnosis for ‘new positives’ was AMI in 4 (9%), other cardiac in 13 (30%) and non-cardiac in 27 (61%). At 90 days adverse events occurred in 30%, 54% and 50% of the groups respectively. There were no late cases of AMI or cardiovascular death in ‘new positive’ patients.

Conclusion: Many patients with diagnoses other than AMI will have hsTNT above the reference level. Indiscriminate testing with hsTnT might lead to more patients requiring serial troponin testing and/or invasive further tests, which will have process and resource implications for EDs and health services.

An accompanying editorial2 highlights that:

Elevations are seen in pathological conditions, including structural heart disease, renal impairment and pulmonary embolism, but might also be seen in extreme exertion, such as marathon runners. It is now clear that when using a highly sensitive assay, circulating levels of troponin will be detected in many normal people.

The editorial makes the interesting observation that the duration of rise may help elucidate the cause; ischaemic elevation of troponin falls rapidly, since the rise might be due to the release of small amounts of troponin that exist free within the cytoplasm, in contrast to the more persistent elevation seen with myocardial necrosis. The editorialist provides the following caution:


Overall, our practice for ordering troponin will need to be urgently reviewed. Single troponin values will continue to be of little to no use in defining disease states in the ED. Identifying a chronic versus an acute elevation will only be revealed by serial troponin testing. The time interval between testing is currently contentious.

High sensitivity troponins are referred to in the newly published 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes (full text link below)3:

RECOMMENDED PROTOCOL FOR TROPONIN TESTING USING HIGH SENSITIVITY ASSAYS IN “RULING-OUT” ACS

  • All patients with a suspected ACS should undergo troponin testing on arrival at ED to ‘rule in’ ACS within the differential diagnosis
  • For a patient with a positive troponin result or a change in troponin levels over time, neither ACS nor other significant pathology (e.g. pulmonary embolus, aortic dissection, and sepsis) can be excluded. These patients are at higher risk of subsequent events. A positive result should be considered within the entire clinical context (history, examination, ECG findings and other investigations). Further investigations directed at all plausible clinical diagnoses should be considered and, if ACS is thought to be the likely cause, these patients may require cardiology assessment.
  • All patients with a negative result should undergo repeat testing 3–4 hours later.
  • The testing interval to ‘rule out’ MI may be reduced to 3 hours, provided that one sample is taken at least 6 hours after symptom onset:
  • Patients with a negative result at 3 hours after presentation and at least 6 hours after the onset of pain should be considered for early assessment by non-invasive anatomic or functional testing, as determined by local availability.
  • For patients presenting more than 6 hours after pain onset, a single high sensitivity troponin assay is sufficient to rule out myocardial infarction in the absence of ongoing chest pain.

High sensitivity troponin assays have an increased sensitivity for the detection of “myonecrosis”, but a reduced specificity for the diagnosis of “MI”. A positive result (≥99th centile for reference population OR where there is a change of ≥50% above an initial baseline level) should be interpreted in the context of the entire clinical presentation and does not necessarily represent an indication for coronary angiography. The management MI secondary to other conditions (e.g. anaemia, thyrotoxicosis, and sepsis) should be primarily directed at those conditions.
The finding of troponin concentrations that remain stable over time suggests that the presence of troponin is due to chronic disease. Acute exacerbations of chronic disease that result in elevated troponin levels can mimic an MI release pattern.

1. Clinical diagnosis and outcomes for Troponin T ‘positive’ patients assessed by a high sensitivity compared with a 4th generation assay
Emerg Med Australas. 2011 Aug;23(4):490-501
2. Troponin: A risk-defining biomarker for emergency department physicians
Emerg Med Australas. 2011 Aug;23(4):391-4
3. 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes
Heart, Lung and Circulation 2011 Aug;28(8):487-502 Free Full Text

All Updates, ICU, Resus, Trauma

Better than FFP in trauma?

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Replacement of clotting factors in bleeding trauma patients seems to be of benefit, but are coagulation factor concentrates safer than fresh frozen plasma? This retrospective study suggests they might be; prospective studies are recommended.

INTRODUCTION: Clinical observations together with recent research highlighted the role of coagulopathy in acute trauma care and early aggressive treatment has been shown to reduce mortality.
METHODS: Datasets from severely injured and bleeding patients with established coagulopathy upon emergency room (ER) arrival from two retrospective trauma databases, (i) TR-DGU (Germany) and (ii) Innsbruck Trauma Databank/ITB (Austria), that had received two different strategies of coagulopathy management during initial resuscitation, (i) fresh frozen plasma (FFP) without coagulation factor concentrates, and (ii) coagulation factor concentrates (fibrinogen and/or prothrombin complex concentrates) without FFP, were compared for morbidity, mortality and transfusion requirements using a matched-pair analysis approach.
RESULTS: There were no major differences in basic characteristics and physiological variables upon ER admission between the two cohorts that were matched. ITB patients had received substantially less packed red blood cell (pRBC) concentrates within the first 6h after admission (median 1.0 (IQR(25-75) 0-3) vs 7.5 (IQR(25-75) 4-12) units; p
CONCLUSION: Although there was no difference in overall mortality between both groups, significant differences with regard to morbidity and need for allogenic transfusion provide a signal supporting the management of acute post-traumatic coagulopathy with coagulation factor concentrates rather than with traditional FFP transfusions. Prospective and randomised clinical trials with sufficient patient numbers based upon this strategy are advocated.

The impact of fresh frozen plasma vs coagulation factor concentrates on morbidity and mortality in trauma-associated haemorrhage and massive transfusion.
Injury. 2011 Jul;42(7):697-701

All Updates, PHARM, Resus, Trauma, Ultrasound

Open book fractures and ultrasound

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For me, this is one of those ‘why didn’t I think of that?!’ studies… extending the FAST scan to measure pubic symphyseal widening to detect open-book pelvic fractures. A pubic symphysis width of 25 mm was considered positive; the authors state that this width is considered diagnostic for anterior-posterior compression fracture of the pelvis in the non-pregnant patient.
Since only four of the 23 patients studied had radiological widening, the authors’ conclusions make sense: Further study with a larger cohort is needed to confirm this technique’s validity for diagnosing PS widening in APC pelvic fractures.
A reasonable question might be: ‘so what?’, especially if pelvic binders are routinely applied to polytrauma patients and radiographs are rapidly obtained. However as a retrieval medicine doctor working in remote and austere environments I wonder whether this could be useful to us. Perhaps if combined with this intervention?

BACKGROUND: The focused abdominal sonography in trauma (FAST) examination is a routine component of the initial work-up of trauma patients. However, it does not identify patients with retroperitoneal hemorrhage associated with significant pelvic trauma. A wide pubic symphysis (PS) is indicative of an open book pelvic fracture and a high risk of retroperitoneal bleeding.

STUDY OBJECTIVES: We hypothesized that an ultrasound image of the PS as part of the FAST examination (FAST-PS) would be an accurate method to determine if pubic symphysis diastasis was present.

METHODS: This is a comparative study of a diagnostic test on a convenience sample of 23 trauma patients at a Level 1 Trauma Center. The PS was measured sonographically in the Emergency Department (ED) and post-mortem (PM) at the State Medical Examiner. The ultrasound (US) measurements were then compared with PS width on anterior-posterior pelvis radiograph.

RESULTS: Twenty-three trauma patients were evaluated with both plain radiographs and US (11 PM, 12 ED). Four patients had radiographic PS widening (3 PM, 1 ED) and 19 patients had radiographically normal PS width; all were correctly identified with US. US measurements were compared with plain X-ray study by Bland-Altman plot. With one exception, US measurements were within 2 standard deviations of the radiographic measurements and, therefore, have excellent agreement. The only exception was a patient with pubic symphysis wider than the US probe.

CONCLUSION: Bedside ultrasound examination may be able to identify pubic symphysis widening in trauma patients. This potentially could lead to faster application of a pelvic binder and tamponade of bleeding.

Ultrasonographic determination of pubic symphyseal widening in trauma: the FAST-PS study
J Emerg Med. 2011 May;40(5):528-33

All Updates, Resus, Trauma, Ultrasound

E-FAST for pneumothorax

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Some further evidence of the superiority of ultrasound over chest x-ray for the detection of pneumothorax (although it’s not perfect):

INTRODUCTION: Early identification of pneumothorax is crucial to reduce the mortality in critically injured patients. The objective of our study is to investigate the utility of surgeon performed extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax.
METHODS: We prospectively analysed 204 trauma patients in our level I trauma center over a period of 12 (06/2007-05/2008) months in whom EFAST was performed. The patients’ demographics, type of injury, clinical examination findings (decreased air entry), CXR, EFAST and CT scan findings were entered into the data base. Sensitivity, specificity, positive (PPV) and negative predictive values (NPV) were calculated.
RESULTS: Of 204 patients (mean age–43.01+/-19.5 years, sex–male 152, female 52) 21 (10.3%) patients had pneumothorax. Of 21 patients who had pneumothorax 12 were due to blunt trauma and 9 were due to penetrating trauma. The diagnosis of pneumothorax in 204 patients demonstrated the following: clinical examination was positive in 17 patients (true positive in 13/21, 62%; 4 were false positive and 8 were false negative), CXR was positive in 16 (true positive in 15/19, 79%; 1 false positive, 4 missed and 2 CXR not performed before chest tube) patients and EFAST was positive in 21 patients (20 were true positive [95.2%], 1 false positive and 1 false negative). In diagnosing pneumothorax EFAST has significantly higher sensitivity compared to the CXR (P=0.02).
CONCLUSIONS: Surgeon performed trauma room extended FAST is simple and has higher sensitivity compared to the chest X-ray and clinical examination in detecting pneumothorax.

Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center
Injury. 2011 May;42(5):511-4

Acute Med, All Updates, ICU, Resus

Verapamil vs adenosine for SVT

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Most people reach for the adenosine once vagotonic manouevres have failed in SVT, but some patients find the side effects – albeit short-lived – pretty unpleasant. For this reason I’ve heard Jerry Hoffman espouse the relative benefits of verapamil in patients without contra-indications. A recent meta-analysis suggests both verapamil and adenosine have about a 90% success rate. The study did not look at recurrence rates of SVT, which one might expect to be higher with the shorter-acting adenosine.
The authors conclude:
The choice between the agents should be made on a case by case basis with awareness of the respective adverse effect profiles, and should involve informed discussion with the patient where appropriate.

OBJECTIVE: Verapamil and adenosine are the most common agents used to treat paroxysmal supraventricular tachycardia (PSVT). We performed a systematic review and meta-analysis to determine the relative effectiveness of these drugs and to examine their respective adverse effect profiles.
METHODS: We searched MEDLINE, EMBASE, CINAHL, the Cochrane database, and international clinical trial registers for randomized controlled trials comparing adenosine (or adenosine compounds) with verapamil for the treatment of PSVT in stable adult patients. The primary outcome was rate of reversion to sinus rhythm. Secondary outcome was occurrence of pooled adverse events. Odds ratios and 95% confidence intervals (CIs) were calculated using a random effects model (RevMan v5).
RESULTS: Eight trials were appropriate and had the available data. The reversion rate for adenosine was 90.8% (95% CI: 87.3-93.4%) compared with 89.9% for verapamil (95% CI: 86.0-92.9%). The pooled odds ratio for successful reversion was 1.27 (95% CI: 0.63-2.57) favouring adenosine. This was not statistically significant. There was a higher rate of minor adverse effects described with adenosine (16.7-76%) compared with verapamil (0-9.9%). The rate of hypotension was lower with adenosine [0.6% (95% CI: 0.1-2.4%)] compared with verapamil [3.7% (95% CI: 1.9-6.9%)].
CONCLUSION: Adenosine and verapamil have similar efficacy in treating PSVT. Adenosine has a higher rate of minor adverse effects, and of overall adverse effects, whereas verapamil has a higher rate of causing hypotension. A decision between the two agents should be made on a case-by-case basis and ideally involve informed discussion with the patient where appropriate.

The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis
Eur J Emerg Med. 2011 Jun;18(3):148-52

All Updates, Resus

It's up to you….

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Sometimes you have nothing to lose by doing a procedure that you may never have done before, if the patient is going to die or deteriorate without it.
In today’s competency-based-training-and-accreditation climate (a good thing), how does one achieve competence in a procedure that may be too rare to have even been seen, let alone practiced under supervision and formally assessed?
I spend a lot of time and energy trying to convince colleagues and trainees that there are situations where the benefit-harm equation is in favour of acting, despite reservations they may have about inadequate experience or training. These situations often require ‘surgical’ procedures. What they have in common is that they are all relatively simple to perform, but may save a life, a limb, or sight which otherwise may almost certainly be lost.
How best to train for these procedures, some of which may be too rare even for ‘see one, do one, teach one’ in an entire residency program? Simulators? Animal labs? Cadavers?

Slide from 'Making Things Happen' Course

In my view, the answer is to use the most high fidelity simulator in the universe – the human brain. It is those professionals who mentally rehearse the scenario and visualise the procedure over and over who are most likely to act when the patient needs it most. Several colleagues of mine over the years can recount incidents in which the indications for a thoracotomy or hysterotomy were present but they failed to act, talking themselves out of doing the procedure with a range of excuses from ‘I hadn’t had enough training’ to ‘No-one in the room wanted to do it’. Don’t be one of those! Get simulating now – you have all the equipment you need!

Ten steps to making it happen – be prepared
1. Pick a procedure (eg. thoracotomy)
2. Be ABSOLUTELY CLEAR on the indications – this helps remove any doubt when the time comes
3. Learn how to do it (talk to colleagues, read a book)
4. Know where the required equipment is kept
5. Start practicing in your mind – visualise seeing the patient, what you will say to your staff, where you will locate your equipment, what you will do procedurally step-by-step
6. Visualise possible outcomes and what your next steps would be (tamponade plus cardiac wound in a beating heart, tamponade plus wound plus VF, return of spontaneous circulation with bleeding from internal mammary arteries)
7. Read more and talk to more colleagues based on questions arising from your ‘simulations’
8. Travel, go on a course, get access to animal or cadaver labs if that’s an option in your setting
9. Speak to people who have done it in YOUR context (eg. for a resus room thoracotomy, talk to emergency physicians who have done it there, rather than a cardiothoracic surgeon who has only ever done them in the operating room)
10. Find an excuse on shift to talk about it to colleagues and rehearse the steps, locate the equipment, and so on. Remember: REPETITION IS THE MOTHER OF SKILL!

What’s on your list of life/limb/sight-saving procedures that can’t wait for someone else to do? Did I miss any? Should skull trephination be there? Comments welcome!

All Updates, Kids, Resus

Prehospital resuscitative hysterotomy

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My colleagues and I describe a tragic case in this month’s European Journal of Emergency Medicine1. Our physican-paramedic team was called to the home of a collapsed 38-week pregnant female who was in asystolic cardiac arrest. A peri-mortem caesarean delivery was performed by the physician in the patient’s home and the delivered newborn required intubation and chest compressions for bradycardia before resuming good colour and heart rate. Sadly there was ultimately a fatal outcome for both patients, but this case reminds us of the indications for this intervention and for emergency and pre-hospital physicians to be prepared to do it. A literature search yielded only one other reported prehospital case in recent medical literature2.

1.Prehospital resuscitative hysterotomy
Eur J Emerg Med. 2011 Aug;18(4):241-2
2.Out-of-hospital perimortem cesarean section
Prehosp Emerg Care. 1998 Jul-Sep;2(3):206-8