Category Archives: ICU

Stuff relevant to patients on ICU

Single bag for adults and kids

A nice idea – using a single adult self-inflating bag for the resuscitation of adult and paediatric patients, marked to identify compression points that deliver specific tidal volume ranges. Might be useful in situations where equipment needs to be minimised, such as military or pre-hospital settings.

AIM: To overcome limitations of inaccurate tidal volume (TV) delivery by conventional selfinflating paediatric and adult bags during paediatric and adolescent resuscitation, we designed a novel target volume marked bag (TVMB) with four compression points marked on an adult bag surface. The aim of this study was to evaluate the TVMB in delivering preset TV.

METHODS: Fifty-three subjects (28 doctors, 17 nurses, 8 paramedics) participated in this simulation trial. TVMB, paediatric bag and adult bag were connected to a gas flow analyser for measuring TV and peak inspiratory pressure (PIP). In a random cross-over setting, participants delivered 10 ventilations using the adult bag, paediatric bag or TVMB in each of four target volume ranges (100-200ml, 200-300ml, 300-400ml, 400-500ml). We compared TV and PIP for the adult bag, paediatric bag and TVMB in each subject.

RESULTS: Compared with the paediatric bag, TVMB showed higher rates of accurate TV delivery in the 200-300ml target volume range (87-90% versus 32-35%; p<0.05). Compared with the adult bag, TVMB showed higher rates of accurate TV delivery in all target volume ranges (75-90% versus 45-50%; p<0.05). The frequency of too high or low TV delivery was higher with the adult bag than TVMB (20-30% versus 0-5%; p<0.05). There was no significant difference in PIP between the paediatric bag and TVMB (within 5cm H(2)O; p<0.05).

CONCLUSIONS: TVMB could deliver accurate TV in various target volume ranges for paediatric and adolescent resuscitation.

Resuscitation. 2011 Jun;82(6):749-54

Decompressive craniectomy for high ICP head trauma

Bilateral decompressive craniectomy for severe diffuse traumatic brain injury and intracranial hypertension that was refractory to first line therapies did not improve neurological outcome. This was the Australasian DECRA study.

Emergency Medicine Ireland reviews the paper here.
Another study on decompressive craniectomy, the RESCUE-ICP study, is ongoing, with 306/400 patients now recruited. The RESCUE-ICP investigators make the following comment on the DECRA trial:
“The study showed a significant decrease in intracranial pressure in patients in the surgical group. However, although ICP was lowered by surgery, ICP was not excessively high in the medical group (mean ICP below 24 mmHg pre-randomisation).
RESCUE-ICP differs from DECRA in terms of ICP threshold (25 vs 20 mmHg), timing of surgery (any time after injury vs within 72 hours post-injury), acceptance of contusions and longer follow up (2 years).
The cohort profiles and criteria for entry and randomisation between the DECRA and RESCUE-ICP are therefore very different. Hence the results from the DECRA study should not deter recruitment into RESCUE-ICP. Randomising patients into the RESCUE-ICP study is now even more important!”

Background
It is unclear whether decompressive craniectomy improves the functional outcome in patients with severe traumatic brain injury and refractory raised intracranial pressure.
Methods
From December 2002 through April 2010, we randomly assigned 155 adults with severe diffuse traumatic brain injury and intracranial hypertension that was refractory to first-tier therapies to undergo either bifrontotemporoparietal decompressive craniectomy or standard care. The original primary outcome was an unfavorable outcome (a composite of death, vegetative state, or severe disability), as evaluated on the Extended Glasgow Outcome Scale 6 months after the injury. The final primary outcome was the score on the Extended Glasgow Outcome Scale at 6 months.
Results
Patients in the craniectomy group, as compared with those in the standard-care group, had less time with intracranial pressures above the treatment threshold (P<0.001), fewer interventions for increased intracranial pressure (P<0.02 for all comparisons), and fewer days in the intensive care unit (ICU) (P<0.001). However, patients undergoing craniectomy had worse scores on the Extended Glasgow Outcome Scale than those receiving standard care (odds ratio for a worse score in the craniectomy group, 1.84; 95% confidence interval [CI], 1.05 to 3.24; P=0.03) and a greater risk of an unfavorable outcome (odds ratio, 2.21; 95% CI, 1.14 to 4.26; P=0.02). Rates of death at 6 months were similar in the craniectomy group (19%) and the standard-care group (18%).
Conclusions
In adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but was associated with more unfavorable outcomes

Decompressive Craniectomy in Diffuse Traumatic Brain Injury
N Engl J Med. 2011 Apr 21;364(16):1493-502

Thrombolysis in submassive PE – still equipoise?

The AHA has produced a comprehensive guideline on venous thromboembolic disease. Here are some excerpts pertaining to resuscitation room decision making, particularly: ‘should I thrombolyse this patient?’

Definition for massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).
Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.
RV dysfunction means the presence of at least 1 of the following:

  • RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
  • RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
  • Elevation of BNP (>90 pg/mL)
  • Elevation of N-terminal pro-BNP (>500 pg/mL); or
  • Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Myocardial necrosis is defined as either of the following:

  • Elevation of troponin I (>0.4 ng/mL) or
    Elevation of troponin T (>0.1 ng/mL)

Odds ratio for short-term mortality for RV dysfunction on echocardiography = 2.53 (95% CI 1.17 to 5.50).
Troponin elevations had an odds ratio for mortality of 5.90 (95% CI 2.68 to 12.95).
Definition for low risk PE: those with normal RV function and no elevations in biomarkers with short-term mortality rates approaching ≈ 1%

Recommendations for Initial Anticoagulation for Acute PE

  • Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
  • Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C).

 
Patients treated with a fibrinolytic agent have faster restoration of lung perfusion. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. However, by 7 days, blood flow improves similarly (≈65% to 70% reduction in total defect).
Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
When Wan et al restricted their analysis to those trials with massive PE, they identified a significant reduction in recurrent PE or death from 19.0% with heparin alone to 9.4% with fibrinolysis (odds ratio 0.45, 95% CI 0.22 to 0.90).
Data from registries indicate that the short-term mortality rate directly attributable to submassive PE treated with heparin anticoagulation is probably < 3.0%. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment.
Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. Patients with low-risk PE have an unfavorable risk-benefit ratio with fibrinolysis. Patients with PE that causes hypotension probably do benefit from fibrinolysis. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment.

An algorithm is proposed:

Two criteria can be used to assist in determining whether a patient is more likely to benefit from fibrinolysis: (1) Evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.
Evidence of circulatory failure includes any episode of hypotension or a persistent shock index (heart rate in beats per minute divided by systolic blood pressure in millimeters of mercury) >1
The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).
Evidence of moderate to severe RV injury may be derived from Doppler echocardiography that demonstrates any degree of RV hypokinesis, McConnell’s sign (a distinct regional pattern of RV dysfunction with akinesis of the mid free wall but normal motion at the apex), interventricular septal shift or bowing, or an estimated RVSP > 40 mm Hg.
Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides.
Two trials are currently ongoing that aim to assess effect of thrombolysis on patients with submassive PE: PEITHO and TOPCOAT

Recommendations for Fibrinolysis for Acute PE

  • Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
  • Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
  • Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
  • Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).

Recommendations for Catheter Embolectomy and Fragmentation

  • Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
  • Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
  • For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C).
  • Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
  • Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C).

 
Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension
Circulation. 2011 Apr 26;123(16):1788-1830 (Free Full Text)

It's a bit quiet in here

Blogging has slowed a bit as I’ve been travelling to the UK and am running courses here all week.
Just in case you’re desperate to read something useful, I came across a guideline on The Management of Diabetic Ketoacidosis in Adults by the Joint British Diabetes Societies Inpatient Care Group
The guideline contain the following approaches:

  • Measurement of blood ketones, venous (not arterial) pH and bicarbonate and their use as treatment markers
  • Monitoring of ketones and glucose using bedside meters when available and operating within their quality assurance range
  • Replacing ‘sliding scale’ insulin with weight-based fixed rate intravenous insulin infusion (IVII)
  • Use of venous blood rather than arterial blood in blood gas analysers
  • Monitoring of electrolytes on the blood gas analyser with intermittent laboratory confirmation
  • Continuation of long acting insulin analogues (Lantus® or Levemir®) as normal
  • Involvement diabetes specialist team as soon as possible

There is also a section on ‘Controversial Areas’, discussing such issues as bicarbonate therapy, rate of fluid therapy, and even 0.9% saline versus Hartmann’s (Ringer’s Lactate) solution, although this part was desperately disappointing, with the following bizarre excuse given for not recommending the latter:
In theory replacement with glucose and compound sodium lactate (Hartmann’s solution) with potassium, would prevent hyperchloraemic metabolic acidosis, as well as allow appropriate potassium replacement. However, at present this is not readily available as a licensed infusion fluid.
Apart from that, this appears to be an interesting and potentially useful document.
The Management of Diabetic Ketoacidosis in Adults
Joint British Diabetes Societies Inpatient Care Group

Intubation checklist

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

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

Curr Opin Crit Care. 2011 Jun;17(3):254-9

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

  1. 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.
  2. 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).
  3. 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.
  4. 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.
  5. For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
  6. 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: