Category Archives: Guidelines

Guidelines relevant to the critically ill patient

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Caution with intraosseous adenosine

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Two cases of failed cardioversion of SVT after tibial intraosseous administration of adenosine in infants are described in this month’s Pediatric Emergency Care. Both cases were subsequently cardioverted by intravenous adenosine. The maximum intraosseous dose given was 0.25 mg/kg. The successful IV doses were not higher than the IO doses.
It has been noted before that infants may require relatively higher doses of adenosine than children and that 0.2 mg/kg might even be considered a starting dose in infancy. I wonder if a bigger IO dose would have been effective, or whether a proximal humeral insertion site would make a difference. IO adenosine has been successfully used in infants and piglets.
This interesting case series provides a helpful caution in the management of paediatric SVT.

ABSTRACT: Supraventricular tachycardia (SVT) is a common tachyarrhythmia in the pediatric population that can necessitate immediate treatment. Adenosine has been well studied as a mainstay treatment, but the methods of adenosine administration have not been very well delineated. The intraosseous technique has presented itself as a possible method of administration. We describe 2 cases in which adenosine was administered through bone marrow infusion to convert SVT without success. The cases we describe show that intraosseous is not a reliable method of administering adenosine to stop SVT. Both patients presented with SVT refractory to vagal maneuvers and difficult intravenous placement. Intraosseous access was achieved, but administration of adenosine at increasing doses was unable to successfully convert the arrhythmia.

Intraosseous Infusion Is Unreliable for Adenosine Delivery in the Treatment of Supraventricular Tachycardia
Pediatr Emerg Care. 2012 Jan;28(1):47-8

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Two new anaphylaxis guidelines

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Many local and national guidelines for the management of anaphylaxis exist, but did you know there was a World Allergy Organization, and it has a very detailed guideline on this important life threatening condition?

Some interesting snippets from the guideline are included here

Anaphylaxis and cardiac disease

  • Anaphylaxis can precipitate acute myocardial infarction in susceptible individuals: in patients with ischemic heart disease, the number and density of cardiac mast cells is increased, including in the atherosclerotic plaques. Mediators released during anaphylaxis contribute to vasoconstriction and coronary artery spasm.
  • Epinephrine is not contraindicated in the treatment of anaphylaxis in patients with known or suspected cardiovascular disease, or in middle-aged or elderly patients without any history of coronary artery disease who are at increased risk of ACS only because of their age. Through its beta-1 adrenergic effects, epinephrine actually increases coronary artery blood flow because of an increase in myocardial contractility and in the duration of diastole relative to systole.
  • Glucagon has noncatecholamine-dependent inotropic and chronotropic cardiac effects, and is sometimes needed in patients taking a beta-adrenergic blocker who have hypotension and bradycardia and who do not respond optimally to epinephrine.
  • Anticholinergic agents are sometimes needed in beta-blocked patients, for example, atropine in those with persistent bradycardia or ipratropium in those with epinephrine-resistant bronchospasm.

How quickly can untreated anaphylaxis kill you?

Studies show median times to cardiorespiratory arrest after exposure to the offending stimulus were 5 minutes after administration of contrast media or drugs, 15 minutes after an insect sting, and 30 minutes after food ingestion.

What about confirming the diagnosis with serum tryptase measurements?

  • Blood samples for measurement of tryptase levels are optimally obtained 15 minutes to 3 hours after symptom onset.
  • Blood samples for measurement of histamine levels are optimally obtained 15–60 minutes after symptom onset. These tests are not specific for anaphylaxis.
  • Increased serum tryptase levels are often found in patients with anaphylaxis from insect stings or injected medications, and in those who are hypotensive
  • However, levels are often within normal limits in patients with anaphylaxis triggered by food and in those who are normotensive
  • Serial measurement of tryptase levels during an anaphylactic episode, and measurement of a baseline level after recovery are reported to be more useful than measurement at only one point in time.
  • Normal levels of either tryptase or histamine do not rule out the clinical diagnosis of anaphylaxis


How does epinephrine help?

  • Epinephrine is life-saving because of its alpha-1 adrenergic vasoconstrictor effects in most body organ systems (skeletal muscle is an important exception) and its ability to prevent and relieve airway obstruction caused by mucosal edema, and to prevent and relieve hypotension and shock.
  • Other relevant properties in anaphylaxis include its beta-1 adrenergic agonist inotropic and chronotropic properties leading to an increase in the force and rate of cardiac contractions, and its beta-2 adrenergic agonist properties such as decreased mediator release, bronchodilation and relief of urticaria
  • Epinephrine in a dose of 0.01 mg/kg of a 1:1,000 (1 mg/mL) solution injected promptly by the intramuscular route is effective and safe in the initial treatment of anaphylaxis. In other anaphylaxis scenarios, this low first-aid dose is unlikely to be effective. For example, if shock is imminent or has already developed, epinephrine needs to be given by slow intravenous infusion, ideally with the dose titrated according to noninvasive continuous cardiac monitoring.

What is the empty ventricle syndrome?

  • Patients with anaphylaxis should not suddenly sit, stand, or be placed in the upright position.
  • Instead, they should be placed on the back with their lower extremities elevated or, if they are experiencing respiratory distress or vomiting, they should be placed in a position of comfort with their lower extremities elevated.
  • This accomplishes 2 therapeutic goals: 1) preservation of fluid in the circulation (the central vascular compartment), an important step in managing distributive shock; and 2) prevention of the empty vena cava/empty ventricle syndrome, which can occur within seconds when patients with anaphylaxis suddenly assume or are placed in an upright position.
  • Patients with this syndrome are at high risk for sudden death. They are unlikely to respond to epinephrine regardless of route of administration, because it does not reach the heart and therefore cannot be circulated throughout the body

Should we give antihistamines, beta 2 agonists, and steroids?

The evidence base for use of these second line medications in the initial management of anaphylaxis, is extrapolated mainly from their use in treatment of other diseases such as urticaria (antihistamines) or acute asthma (beta-2 adrenergic agonists and glucocorticoids). Concerns have been raised that administering one or more second-line medications potentially delays prompt injection of epinephrine, the first-line treatment


Is ‘biphasic anaphylaxis’ a real phenomenon we should be concerned about?

  • Biphasic anaphylaxis occurs when symptoms recur within 1–72 hours (usually within 8–10 hours) after the initial symptoms have resolved, despite no further exposure to the trigger.
  • It occurs in up to 23% of adults and up to 11% of children.
  • After apparent resolution of symptoms, duration of monitoring in a medically supervised setting should be individualized. For example, patients with moderate respiratory or cardiovascular compromise should be monitored for at least 4 hours, and if indicated, for 8–10 hours or longer.
  • Protracted uniphasic anaphylaxis is uncommon, but can last for days.

World Allergy Organization Guidelines for the Assessment and Management of Anaphylaxis
World Allergy Organization Journal 2011;4(2):13-37 Full Text
[EXPAND click for abstract]

The illustrated World Allergy Organization (WAO) Anaphylaxis Guidelines were created in response to absence of global guidelines for anaphylaxis. Uniquely, before they were developed, lack of worldwide availability of essentials for the diagnosis and treatment of anaphylaxis was documented. They incorporate contributions from more than 100 allergy/immunology specialists on 6 continents. Recommendations are based on the best evidence available, supported by references published to the end of December 2010. The Guidelines review patient risk factors for severe or fatal anaphylaxis, co-factors that amplify anaphylaxis, and anaphylaxis in vulnerable patients, including pregnant women, infants, the elderly, and those with cardiovascular disease. They focus on the supreme importance of making a prompt clinical diagnosis and on the basic initial treatment that is urgently needed and should be possible even in a low resource environment. This involves having a written emergency protocol and rehearsing it regularly; then, as soon as anaphylaxis is diagnosed, promptly and simultaneously calling for help, injecting epinephrine (adrenaline) intramuscularly, and placing the patient on the back or in a position of comfort with the lower extremities elevated. When indicated, additional critically important steps include administering supplemental oxygen and maintaining the airway, establishing intravenous access and giving fluid resuscitation, and initiating cardiopulmonary resuscitation with continuous chest compressions. Vital signs and cardiorespiratory status should be monitored frequently and regularly (preferably, continuously). The Guidelines briefly review management of anaphylaxis refractory to basic initial treatment. They also emphasize preparation of the patient for self-treatment of anaphylaxis recurrences in the community, confirmation of anaphylaxis triggers, and prevention of recurrences through trigger avoidance and immunomodulation. Novel strategies for dissemination and implementation are summarized. A global agenda for anaphylaxis research is proposed.

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This month has also seen the publication guidelines from the UK’s National Institute for Health & Clinical Excellence, entitled ‘Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode’
Their guideline summary is as follows:

After a suspected anaphylactic reaction in adults or young people aged 16 years or older, take timed blood samples for mast cell tryptase testing as follows:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

After a suspected anaphylactic reaction in children younger than 16 years, consider taking blood samples for mast cell tryptase testing as follows if the cause is thought to be venom-related, drug-related or idiopathic:

  • a sample as soon as possible after emergency treatment has started
  • a second sample ideally within 1–2 hours (but no later than 4 hours) from the onset of symptoms.

Patients who have had emergency treatment for suspected anaphylaxis should be observed for 6–12 hours from the onset of symptoms, depending on their response to emergency treatment
After emergency treatment for suspected anaphylaxis, offer people a referral to a specialist allergy service (age-appropriate where possible) consisting of healthcare professionals with the skills and competencies necessary to accurately investigate, diagnose, monitor and provide ongoing management of, and patient education about, suspected anaphylaxis.
After emergency treatment for suspected anaphylaxis, offer people (or, as appropriate, their parent and/or carer) an appropriate adrenaline injector as an interim measure before the specialist allergy service appointment.
Before discharge a healthcare professional with the appropriate skills and competencies should offer people (or, as appropriate, their parent and/or carer) the following:

  • information about anaphylaxis, including the signs and symptoms of an anaphylactic reaction
  • information about the risk of a biphasic reaction
  • information on what to do if an anaphylactic reaction occurs (use the adrenaline injector and call emergency services)

Anaphylaxis: assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode
CG134 Anaphylaxis: NICE guideline

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Myoclonus no longer a show-stopper

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In comatose survivors of cardiac arrest, myoclonus is considered a grave prognostic sign. The American Academy of Neurology stated in 20061 that:
After cardiac arrest, the following clinical findings accurately predict poor outcome;

  • myoclonus status epilepticus within the first 24 hours in patients with primary circulatory arrest
  • absence of pupillary responses within days 1 to 3 after CPR
  • absent corneal reflexes within days 1 to 3 after CPR
  • and absent or extensor motor responses after 3 days.

However in the age of targeted temperature management the presence and/or timing of these signs needs to be re-evaluated. It has been suggested that therapeutic hypothermia and sedation required for induced cooling might delay recovery of motor reactions up to 5–6 days after cardiac arrest. Now a series of three survivors of cardiac arrest who had massive myoclonus in the first four hours after return of spontaneous circulation (ROSC) is reported2, all of whom were treated with TTM and experienced good neurologic outcomes.


Early myoclonus in comatose survivors of cardiac arrest, even when it is not myoclonic status epilepticus (MSE), is considered a sign of severe global brain ischemia and has been associated with high rates of mortality and poor neurologic outcomes. We report on three survivors of primary circulatory cardiac arrests who had good neurologic outcomes (two patients with a CPC score=1 and one patient with a CPC score=2) after mild therapeutic hypothermia, despite exhibiting massive myoclonus within the first four hours after return of spontaneous circulation. The concept that early myoclonus heralds a uniformly poor prognosis may need to be reconsidered in the era of post-cardiac arrest mild therapeutic hypothermia.

1. Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology
Neurology. 2006 Jul 25;67(2):203-10 Full Text
2. Neurologic Recovery After Therapeutic Hypothermia in Patients with Post-Cardiac Arrest Myoclonus
Resuscitation published on line 03 October 2011

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Offensive medicine: CT before LP

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I’m getting worn down by clinicians – often other specialists – who insist that CT imaging of the brain is mandatory prior to lumbar puncture in all patients. There is surely a subgroup of patients (especially young ones) in whom the benefit:harm balance of CT comes out in favour of NOT doing the imaging. In these cases, getting the scan is not ‘defensive medicine’ but ‘offensive medicine’ – offending the principle of primum non nocere. During ED shifts I have recently had to perform online searches in order to furnish colleagues and patients’ medically qualified relatives with printouts of the literature on this. This page is here to save me having to repeat those searches. Regarding the practice of performing a routine head CT prior to lumbar puncture to rule out risk of herniation:

  • Mass effect on CT does not predict herniation
  • Lack of mass effect on CT does not rule out raised ICP or herniation
  • Herniation has occurred in patients who did not undergoing lumbar puncture because of CT findings
  • Clinical predictors of raised ICP are more reliable than CT findings
  • CT may delay diagnosis and treatment of meningitis
  • Even in patients in whom LP may be considered contraindicated (cerebral abscess, mass effect on CT), complications from LP were rare in several studies

Best practice, it would seem, is the following

  • If you think CT will show a cause for the headache, do a CT
  • If a CT is indicated for other reasons (depressed conscious level, focal neurology), do a CT
  • If a GCS 15 patient is to undergo LP for suspected (or to rule out) meningitis, and they have a normal neurological exam (including fundi), and are not elderly or immunosuppressed, there is no need to do a CT first.
  • If you’re seriously worried about meningitis and are intent on getting a CT prior to LP, don’t let the imaging delay antimicrobial therapy.

Here are some useful references:

1. The CT doesn’t help

CT head before lumbar puncture in suspected meningitis BestBET evidence summary: In cases of suspected meningitis it is very unlikely that patients without clinical risk factors (immunocompromise/ history of CNS disease/seizures) or positive neurological findings will have a contraindication to lumbar puncture on their CT scan If CT scan is deemed to be necessary, administration of antibiotics should not be delayed. BestBETS website

Computed Tomography of the Head before Lumbar Puncture in Adults with Suspected Meningitis Much cited NEJM paper from 2001 which concludes: “In adults with suspected meningitis, clinical features can be used to identify those who are unlikely to have abnormal findings on CT of the head” N Engl J Med. 2001 Dec 13;345(24):1727-33 Full Text

Cranial CT before Lumbar Puncture in Suspected Meningitis Correspondence in 2002 NEJM including study of 75 patients with pneumococcal meningitis: CT cannot rule out risk of herniation Cranial CT before Lumbar Puncture in Suspected Meningitis N Engl J Med. 2002 Apr 18;346(16):1248-51 Full Text

2. The CT may harm

Cancer risk from CT Paucis verbis card, from the wonderful Academic Life in EM

3. Guidelines say CT is not always needed

National (UK) guidelines on meningitis (community acquired meningitis in the immunocompetent host) available from meningitis.org. , including this box:

Practice Guidelines for the Management of Bacterial Meningitis These 2004 guidelines from the Infectious Diseases Society of America provide the following table listing the recommended criteria for adult patients with suspected bacterial meningitis who should undergo CT prior to lumbar puncture:

Clin Infect Dis. (2004) 39 (9): 1267-1284 Full text

4. This is potentially even more of an issue with paediatric patients

Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma

An excellent summary of the above mentioned issues presented in a paediatric context, including the following:

On initial consideration a cranial CT would seem to be an appropriate and potentially useful diagnostic study for confirming the diagnosis of cerebral herniataion. The fallacy in this assessment has been emphasized by the finding that no clinically significant CT abnormalities are found that are not suspected on clinical assessments. Further, as previously noted, a normal CT examination may be found at about the time of a fatal herniation. Thus, the practical usefulness of a cranial CT in the majority of pediatric patients is limited to those rare patients whose increased ICP is secondary to mass lesions, not in the initial approach to acute meningitis.

Pediatrics. 2003 Sep;112(3 Pt 1):e174-6 Full Text

The last words should go to Dr Brad Spellberg, who in response to the IDSA’s guidelines wrote an excellent letter summarising much of the evidence at the time, confessed:

Why do we persist in using the CT scan for this purpose, despite the lack of supportive data? I am as guilty of this practice as anyone else, and the reason is simple: I am a chicken.

Clin Infect Dis. (2005) 40 (7): 1061 Full Text

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Prehospital Spine Immobilisation for Penetrating Trauma

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The Executive Committee of Prehospital Trauma Life Support, comprised of surgeons, emergency physicians, and paramedics, has reviewed the literature and produced the following recommendations on Prehospital Spine Immobilisation for Penetrating Trauma:


PHTLS Recommendations

  • There are no data to support routine spine immobilization in patients with penetrating trauma to the neck or torso.
  • There are no data to support routine spine immobilization in patients with isolated penetrating trauma to the cranium.
  • Spine immobilization should never be done at the expense of accurate physical examination or identification and correction of life-threatening conditions in patients with penetrating trauma.
  • Spinal immobilization may be performed after penetrating injury when a focal neurologic deficit is noted on physical examination although there is little evidence of benefit even in these cases.

Prehospital Spine Immobilization for Penetrating Trauma—Review and Recommendations From the Prehospital Trauma Life Support Executive Committee
Journal of Trauma-Injury Infection & Critical Care September 2011;71(3):763-770

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Still no cardiac arrest survival benefit from epinephrine?

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A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

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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

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Pre-hospital NIV

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"The driver's dyspneic - pass the Boussignac valve!"

Pre-hospital non-invasive ventilation for patients with acute dyspnoea features in two journals this month. Researchers at the Ambulance Service New South Wales published an evidence-based review of pre-hospital NIV for acute cardiogenic pulmonary oedema, concluding that there are probable benefits.

Background Non-invasive ventilation (NIV) is increasingly being implemented by many ambulance jurisdictions as a standard of care in the out-of-hospital management of acute cardiogenic pulmonary oedema (ACPO). This implementation appears to be based on the body of evidence from the emergency department (ED) setting, with the assumption that earlier administration by paramedics would give benefits with regard to inhospital mortality and the rate of endotracheal intubation beyond those seen when initiated in the ED. This paper sought to identify and review the current level of evidence supporting NIV in the prehospital setting.

Methods Electronic searches of Medline, EMBASE, CINAHL, Cochrane Database of Systematic Reviews and Cochrane Database of Controlled Trials were conducted and reference lists of relevant articles were hand searched.

Results The search identified 12 primary studies documenting the use of NIV, either continuous positive airway pressure or bi-level non-invasive ventilation, for ACPO in the out-of-hospital setting. Only three studies were randomised controlled trials, with none addressing inhospital mortality as a primary outcome measure. The majority of articles were non-comparative descriptive studies.

Conclusion Early prehospital NIV appears to be a safe and feasible therapy that results in faster improvement in physiological status and may decrease the need for intubation when compared with delayed administration in the ED. There is weak evidence that is may decrease mortality. The cost versus benefit equation of system-wide prehospital implementation of NIV is unclear and, based on the current evidence, should be considered with caution.

Prehospital non-invasive ventilation for acute cardiogenic pulmonary oedema: an evidence-based review.
Emerg Med J. 2011 Jul;28(7):609-12
At the same time, the National Association of EMS Physicians has published a position statement on noninvasive positive pressure ventilation, for the general indication of acute dyspnoea. It states:

The general indication for NIPPV is dyspnea accompanied by early respiratory failure in patients with intact protective airway reflexes and mental status. The majority of NIPPV studies have focused on patients with acute pulmonary edema.

However, NIPPV may prove useful with other reversible disease processes such as chronic obstructive pulmonary disease or asthma exacerbations. While utilized in in-hospital practice, the role of NIPPV for pneumonia-associated respiratory failure is less clear. While some clinicians advocate the use of NIPPV to augment oxygenation prior to ETI in the in- hospital setting, there are no studies evaluating this strategy in the prehospital setting.

 
Noninvasive positive pressure ventilation: resource document for the National Association of EMS Physicians position statement.
Prehosp Emerg Care. 2011 Jul-Sep;15(3):432-8
Full Text of Position Statement

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Central lines in coagulopathic patients

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If a patient needs a central line, he/she needs one. Often low platelets or a deranged coagulation profile are cited as reasons for omitting or delaying the procedure, but this is not based on evidence of increased complications. A recent Best Evidence Topic Review concludes:

“…insertion of CVC lines do not require correction of haemostatic abnormalities prior to intervention. Rates of haemorrhage are low in patients with elevated PT, APTT or low thrombocyte count and appear to be closely related to the level of experience of the physician … rather than the defects of haemostasis. “

Links to the abstracts of a couple of relevant articles reviewed are included below.
Central line insertion in deranged clotting
Emerg Med J. 2011 Jun;28(6):536-7 Full text
Low levels of prothrombin time (INR) and platelets do not increase the risk of significant bleeding when placing central venous catheters.
Med Klin (Munich). 2009 May 15;104(5):331-5
US-guided placement of central vein catheters in patients with disorders of hemostasis
Eur J Radiol. 2008 Feb;65(2):253-6