Perhaps you’ve read the blog post and heard the podcast about the excellent NAP4 airway audit…..now you can start putting the learning points into action with the intubation checklist, developed by the regional trainee-led collaborative ‘RTIC Severn’. Thanks to Dr Tim Bowles for the link:
I’ve used an RSI checklist for both in-and-out of hospital intubations for the last seven years. The beauty of this one is the potential for it to become a standard within and between hospitals, so wherever you work the team will be on the same page when preparing for intubation.
Further details are at http://saferintubation.com
Category Archives: Resus
Life-saving medicine
NAP 4 Podcast
Check out EMCrit.org for our Podcast interview with Professor Jonathan Benger, the Emergency Physician who contributed to the design, execution, and analysis of the important NAP 4 national airway audit, which has important learning points for all of us involved in pre-hospital, emergency, or ICU airway management.
EMCrit Podcast
2016 Update
An important follow up study showing the effect of the NAP 4 Audit:
A national survey of the impact of NAP4 on airway management practice in United Kingdom hospitals: closing the safety gap in anaesthesia, intensive care and the emergency department
Br. J. Anaesth. (2016) 117 (2): 182-190.
Predicting neurological outcome after cardiac arrest
Predicting neurological recovery after successful cardiac arrest resuscitation has always been tricky, with clinical signs on day one being unreliable, but absent pupillary responses or absent or extensor motor responses to painful stimuli being predictive of a poor outcome on day three. However, the use of therapeutic hypothermia, and its frequent associated need for sedation, appear to make even these downstream assessments inclined to give false positive predictions for a poor outcome, potentially resulting in withdrawal of intensive care in patients who may have recovered. A review recommends a multimodal approach to prognostication.
Regarding physical examination, the authors state:
In summary, therapeutic hypothermia and sedation required for induced cooling might delay recovery of motor reactions up to 5–6 days after cardiac arrest. Corneal/ pupillary reflexes and myoclonus are more robust predic- tors of poor outcome after cardiac arrest, but their absence is not an absolute predictor of dismal prognosis
PURPOSE OF REVIEW: Therapeutic hypothermia and aggressive management of postresuscitation disease considerably improved outcome after adult cardiac arrest over the past decade. However, therapeutic hypothermia alters prognostic accuracy. Parameters for outcome prediction, validated by the American Academy of Neurology before the introduction of therapeutic hypothermia, need further update.
RECENT FINDINGS: Therapeutic hypothermia delays the recovery of motor responses and may render clinical evaluation unreliable. Additional modalities are required to predict prognosis after cardiac arrest and therapeutic hypothermia. Electroencephalography (EEG) can be performed during therapeutic hypothermia or shortly thereafter; continuous/reactive EEG background strongly predicts good recovery from cardiac arrest. On the contrary, unreactive/spontaneous burst-suppression EEG pattern, together with absent N20 on somatosensory evoked potentials (SSEP), is almost 100% predictive of irreversible coma. Therapeutic hypothermia alters the predictive value of serum markers of brain injury [neuron-specific enolase (NSE), S-100B]. Good recovery can occur despite NSE levels >33 μg/l, thus this cut-off value should not be used to guide therapy. Diffusion MRI may help predicting long-term neurological sequelae of hypoxic-ischemic encephalopathy.
SUMMARY: Awakening from postanoxic coma is increasingly observed, despite early absence of motor signs and frank elevation of serum markers of brain injury. A new multimodal approach to prognostication is therefore required, which may particularly improve early prediction of favorable clinical evolution after cardiac arrest.
Predicting neurological outcome after cardiac arrest
Status epilepticus review
A review on status epilepticus, differentiating complex partial status from generalised convulsive status:
PURPOSE OF REVIEW: Status epilepticus is one of the most common emergencies in neurology, and every third patient does not respond to adequate first-line treatment. Refractory status epilepticus may be associated with increased morbidity and mortality, and new treatment options are urgently required. This review critically discusses recently published data regarding the role of ‘new’ antiepileptic drugs, the efficacy and safety of anesthetic agents, and the overall clinical outcome that is an integral part of treatment decisions.
RECENT FINDINGS: In complex partial status epilepticus, levetiracetam may be administered after failure of first-line and/or second-line agents. Lacosamide may be an interesting new adjunct, but reliable data are pending. In the treatment of refractory generalized convulsive status epilepticus, propofol seems to be as efficient as barbiturates. The latter are associated with prolonged ventilation times due to redistribution kinetics, whereas the former bears the risk of propofol infusion syndrome if administered continuously. Even after prolonged treatment with anesthetics over weeks, survival with satisfactory functional outcome is possible.
SUMMARY: Unambiguous recommendations regarding treatment strategies for refractory status epilepticus are limited by a lack of reliable data. Therefore, randomized controlled trials or at least prospective observational studies based on strict protocols incorporating long-term outcome data are urgently required.
Treatment strategies for refractory status epilepticus
Curr Opin Crit Care. 2011 Apr;17(2):94-100
STEMI criteria vary with age and sex
On reading through the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 10: Acute Coronary Syndromes, I found a reminder that the ECG criteria for diagnosing ST-elevation myocardial infarction (STEMI) vary according to age and sex. From the original article in the Journal of the American College of Cardiology:
The threshold values of ST-segment elevation of 0.2 mV (2 mm) in some leads and 0.1 mV (1 mm) in others results from recognition that some elevation of the junction of the QRS complex and the ST segment (the J point) in most chest leads is normal. Recent studies have revealed that the threshold values are dependent on gender, age, and ECG lead ([8], [9], [10], [11] and [12]). In healthy individuals, the amplitude of the ST junction is generally highest in leads V2 and V3 and is greater in men than in women.
Recommendations
- For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.
- For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).
- For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.
- For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.
- For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
- For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.
What does establishment of abnormal J-point mean for STEMI diagnosis? The AHA/ECC guidelines state the following:
ST-segment elevation… is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are:
- J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old);
- J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old);
- J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).
So, in summary:
Older men – 2mm in V2/V3 and 1mm everywhere else
Younger men – 2.5 mm in V2/V3 and 1mm everywhere else
Women – 1.5 mm in V2/V3 and 1mm everywhere else
Shouldn’t be too difficult to remember.
Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010 Nov 2;122(18 Suppl 3):S787-817
AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.
J Am Coll Cardiol. 2009 Mar 17;53(11):1003-11
Intravenous lipid emulsion as antidote
Emergency physician intensivist Grant Cave and colleagues review the literature on intravenous lipid emulsion (ILE) therapy for human poisoning in this month’s Emergency Medicine Australasia
Intravenous lipid emulsion (ILE) has been demonstrated to be effective in amelioration of cardiovascular and central nervous system sequelae of local-anaesthetic and non-local-anaesthetic drug toxicity in animal models. Sequestration of lipophilic toxins to an expanded plasma lipid phase is credited as the predominant beneficial mechanism of action of ILE. Systematic review of published human experience is however lacking. We determined to report a comprehensive literature search of all human reports of ILE application in drug poisoning. Forty-two cases of ILE use (19 local-anaesthetic, 23 non-local-anaesthetic) were identified, with anecdotal reports of successful resuscitation from cardiovascular collapse and central nervous system depression associated with ILE administration in lipophilic toxin overdose. Although significant heterogeneity was observed in both agents of intoxication, and reported outcomes; case report data suggest a possible benefit of ILE in potentially life-threatening cardio-toxicity from bupivacaine, mepivacaine, ropivacaine, haloperidol, tricyclic antidepressants, lipophilic beta blockers and calcium channel blockers. Further controlled study and systematic evaluation of human cases is required to define the clinical role of ILE in acute poisonings.
Review article: Intravenous lipid emulsion as antidote: A summary of published human experience.
Emerg Med Australas. 2011 Apr;23(2):123-41
An editorial by Guy Weinberg, the researcher who first demonstrated the effect of ILE on bupivacaine toxicity, has some interesting observations and recommendations:
- Each of the first six case reports of lipid resuscitation from local anaesthetic systemic toxicity (LAST) were noted to have one or more of either underlying ischaemia, conduction defect or low cardiac output. For patients in these susceptible groups, reduce the dose of local anaesthetics used in nerve blocks
- There is laboratory evidence that epinephrine (adrenaline) can impair lipid resuscitation. Weinberg believes that epinephrine should be used only in small doses, if at all, in treating LAST
- In bupivacaine toxicity, use it early rather than later, as outcomes are likely to be better when intervention occurs before tissue perfusion has been compromised and too much pressor therapy has been used
Weinberg informs us that more examples of lipid resuscitation can be found at the educational website: http://www.lipidrescue.org/ and the registry site: http://www.lipidregistry.org/.
Intravenous lipid emulsion: Why wait to save a life?
Emerg Med Australas. 2011 Apr;23(2):113-5
In his editorial Weinberg refers to the review article by Jamaty et al, whose suggested regimen included 20% ILE 1.5mL/kg bolus then 0.25–0.5 mL/kg/min for 30–60 min.
OBJECTIVE: To assess the evidence regarding the efficacy and safety of intravenous fat emulsion (IFE) in the management of poisoned patients.
METHODS: We performed a systematic review of the literature with no time or language restriction. The electronic databases were searched from their inception until June 1, 2009 (Medline, EMBASE, ISI web of science, Biological abstract, LILACS, ChemIndex, Toxnet, and Proquest). We also examined the references of identified articles and the gray literature. The target interventions eligible for inclusion were administration of any IFE before, during, or after poisoning in human or animals. All types of studies were reviewed. Eligibility for inclusion and study quality scores, based on criteria by Jadad and the STROBE statement, were evaluated by independent investigators. The primary outcome was mortality. Secondary outcomes included neurologic, hemodynamic, and electrocardiographic variables, as well as adverse effects.
RESULTS: Of the 938 publications identified by the search strategies, 74 met the inclusion criteria. We identified 23 animal trials, 50 human, and 1 animal case reports. Overall, the quality of evidence was weak and significant heterogeneity prevented data pooling. Available data suggest some benefits of IFE in bupivacaine, verapamil, chlorpromazine, and some tricyclic antidepressants and beta-blockers toxicity. No trial assessed the safety of IFE in the treatment of acute poisoning.
CONCLUSION: The evidence for the efficacy of IFE in reducing mortality and improving hemodynamic, electrocardiographic, and neurological parameters in the poisoned patients is solely based on animal studies and human case reports. The safety of IFE has not been established.
Lipid emulsions in the treatment of acute poisoning: a systematic review of human and animal studies.
Clin Toxicol (Phila). 2010 Jan;48(1):1-27
The Guidelines from the Association of Anaesthetists of Great Britain and Ireland, also endorsed by the Australian and New Zealand College of Anaesthetists, outline the dose and indications for ILE in LAST. The full guideline can be accessed by clicking the image below:
Triple marker panel for AMI
A large Asian/Australasian study examined a 2hr triple-marker test in patients presenting with chest pain.
BACKGROUND: Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome.
METHODS: This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279.
FINDINGS: 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11.8%) patients had a major adverse cardiac event. The ADP classified 352 (9.8%) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0.9%) of these patients, giving the ADP a sensitivity of 99.3% (95% CI 97.9-99.8), a negative predictive value of 99.1% (97.3-99.8), and a specificity of 11.0% (10.0-12.2).
INTERPRETATION: This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide.
A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study.
Lancet. 2011 Mar 26;377(9771):1077-84
Full text link available at time of writing
In an accompanying editorial, nicely entitled ‘Acute MI: triple-markers resurrected or Bayesian dice?’ Dr Rick Body notes that the point-of-care triple-marker test has a relatively low sensitivity, at just 82.9%, when used alone, and the sensitivity only increased to 99.3% in the current study because it was used in an already-selected low-risk population. He writes: “Most people will probably consider this net risk to be statistically acceptable. However, if properly informed, low-risk patients might feel differently about the relative merits of waiting for definitive six-hour laboratory-based troponin testing or going home after two hours on the basis of results from a test that correctly identifies serious coronary disease, when present, in just over eight of 10 occasions.”
Dr Body has a new blog at The Bodsblog where we’re likely to be informed other data relevant to emergency cardiology as they emerge.
Point-of-care panel assessment using a similar triple-marker test at presentation and 90 minutes was also examined in the RATPAC study, in which it increased successful discharge home and reduced median length of stay, but did not alter overall hospital bed use.
Colorimetric CO2 detectors and newborns
Colorimetric CO2 detectors may fail to indicate successful tracheal tube placement in adults in certain circumstances, such as low cardiac output states, and waveform capnography is considered the gold standard. We now have data that demonstrate their inadequacy for neonatal intubation. Ideally, waveform devices should be used by all professionals who intubate patients – from paramedics to neonatologists.
AIM: Clinical assessment and end-tidal CO(2) (ETCO(2)) detectors are routinely used to verify endotracheal tube (ETT) placement. However, ETCO(2) detectors may mislead clinicians by failing to identify correct placement under a variety of conditions. A flow sensor measures gas flow in and out of an ETT. We reviewed video recordings of neonatal resuscitations to compare a colorimetric CO(2) detector (Pedi-Cap®) with flow sensor recordings for assessing ETT placement.
METHODS: We reviewed recordings of infants <32 weeks gestation born between February 2007 and January 2010. Airway pressures and gas flow were recorded with a respiratory function monitor. Video recording were used (i) to identify infants who were intubated in the delivery room and (ii) to observe colour change of the ETCO(2) detector. Flow sensor recordings were used to confirm whether the tube was in the trachea or not. RESULTS: Of the 210 infants recorded, 44 infants were intubated in the delivery room. Data from 77 intubation attempts were analysed. In 35 intubations of 20 infants both a PediCap® and flow sensor were available for analysis. In 21 (60%) intubations, both methods correctly identified successful ETT placement and in 3 (9%) both indicated the ETT was not in the trachea. In the remaining 11 (31%) intubations the PediCap® failed to change colour despite the flow wave indicating correct ETT placement.
CONCLUSION: Colorimetric CO(2) detectors may mislead clinicians intubating very preterm infants in the delivery room. They may fail to change colour in spite of correct tube placement in up to one third of the cases.
Assessment of flow waves and colorimetric CO2 detector for endotracheal tube placement during neonatal resuscitation
Resuscitation. 2011 Mar;82(3):307-12
LRAs for acute asthma?
As far as I’m concerned the jury is still out here since this small study was terminated early, more patients in the montelukast group received magnesium and / or aminophylline, and it is unclear how the groups compared with regard to other other acute therapies such as beta-agonists and steroids.
BACKGROUND: Although leukotriene receptor antagonists have an established role in the management of patients with chronic asthma, their efficacy in an acute asthma exacerbation is not fully known.
METHODS: 87 adults with acute asthma requiring hospitalisation were randomly assigned to receive either montelukast 10 mg or placebo on admission and every evening thereafter for 4 weeks (when they were reviewed as outpatients). All patients were admitted under the care of a consultant chest physician and received full care for acute asthma according to the British Thoracic Society guidelines. The primary end point was the difference in peak expiratory flow (PEF) between active and placebo treatment the morning following admission.
RESULTS: Primary end point data were analysed for 73 patients. At study entry, patients who received montelukast (n=37) had a mean (±SD) PEF of 227.6 (±56.9) l/min (47.6% predicted) and those who received placebo (n=36) had a PEF of 240.3 (±99.8) l/min (49.6% predicted). The morning after admission, patients who received montelukast achieved a PEF of 389.6 (±109.7) l/min (81.4% predicted) compared with 332.3 (±124.9) l/min (69.8% predicted) for placebo (p=0.046). The mean difference between treatment groups was 57.4 l/min (95% CI of 1.15 to 113.6 l/min or 1.95-21.2% predicted).
CONCLUSION: In acute asthma exacerbations the additional administration of oral montelukast results in a significantly higher PEF the morning after admission than that achievable with current standard treatment.
Oral montelukast in acute asthma exacerbations: a randomised, double-blind, placebo-controlled trial
Thorax. 2011 Jan;66(1):7-11
Vasoactive drugs in cardiogenic shock
I’m always on the look-out for evidence to guide vasoactive drug therapy, an area where much dogma is spouted by many who have not read the literature. Here’s a small (note: pilot) study comparing two strategies for cardiogenic shock. The higher heart rate and lactate with epinephrine (adrenaline) are consistent with the findings of the great CAT study; this is of interest, but not necessarily clinically significant nor practice changing.
OBJECTIVE: There is no study that has compared, in a randomized manner, which vasopressor is most suitable in optimizing both systemic and regional hemodynamics in cardiogenic shock patients. Hence, the present study was designed to compare epinephrine and norepinephrine-dobutamine in dopamine-resistant cardiogenic shock.
DESIGN: Open, randomized interventional human study.
SETTING: Medical intensive care unit in a university hospital.
PATIENTS: Thirty patients with a cardiac index of <2.2 L/min/m and a mean arterial pressure of <60 mm Hg resistant to combined dopamine-dobutamine treatment and signs of shock. Patients were not included in cases of cardiogenic shock secondary to acute ischemic events such as myocardial infarction. Noninclusion criteria also included immediate indication of mechanical assistance.
INTERVENTIONS: Patients were randomized to receive an infusion of either norepinephrine-dobutamine or epinephrine titrated to obtain a mean arterial pressure of between 65 and 70 mm Hg with a stable or increased cardiac index.
MAIN RESULTS: Both regimens increased cardiac index and oxygen-derived parameters in a similar manner. Patients in the norepinephrine-dobutamine group demonstrated heart rates lower (p<.05) than those in the epinephrine group. Epinephrine infusion was associated with new arrhythmias in three patients. When compared to baseline values, after 6 hrs, epinephrine infusion was associated with an increase in lactate level (p<.01), whereas this level decreased in the norepinephrine-dobutamine group. Tonometered PCO2 gap, a surrogate for splanchnic perfusion adequacy, increased in the epinephrine-treated group (p<.01) while decreasing in the norepinephrine group (p<.01). Diuresis increased in both groups but significantly more so in the norepinephrine-dobutamine group, whereas plasma creatinine decreased in both groups.
CONCLUSIONS: When considering global hemodynamic effects, epinephrine is as effective as norepinephrine-dobutamine. Nevertheless, epinephrine is associated with a transient lactic acidosis, higher heart rate and arrhythmia, and inadequate gastric mucosa perfusion. Thus, the combination norepinephrine-dobutamine appears to be a more reliable and safer strategy.
Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study
Crit Care Med. 2011 Mar;39(3):450-5