Category Archives: All Updates

Emergency physicians providing stroke 'lysis in the UK

Although the worldwide emergency medicine community is split in its support for stroke thrombolysis, those who work in centres where it is provided might be interested in systems to optimise its effectiveness.
A study from the UK showed that emergency physicians can provide the majority of the service, with outcomes similar to the SITS-MOST data.
Interestingly there was only one (suspected) major intracranial haemorrhage case.
The best resource for reducing door-to-tPA time in ischaemic stroke, with heaps of related discussion, is here at EMCrit

Image from EMJ Open Access. Click for PubMed image source


BACKGROUND: Stroke thrombolysis is strongly supported as an effective therapy for selected cases of early stroke. The absence of 24 h stroke specialists in district general hospitals (DGHs) has led to the suggestion that regional hyper-acute stroke centres should be developed. This paper describes a cooperative model that uses the skills already present in a DGH to deliver a thrombolysis service initiated in the emergency department by the emergency physicians, and describes the outcomes of that service in comparison with the SITS-MOST trial.

METHOD: The outcomes of all stroke patients thrombolysed at Scarborough DGH from 2004 to January 2009 were reviewed. Outcome was defined using a three-part scale. Data at Scarborough DGH were compared with data from the SITS-MOST European-wide study of stroke thrombolysis.

RESULTS: Data were available for 98 of 110 patients thrombolysed during the study period. Fifty (51%) had a good outcome, seven (8%) had partial resolution of their symptoms, and 41 (42%) showed no improvement or deterioration. These outcomes were comparable to those in the European database.

CONCLUSION: Stroke thrombolysis can be effectively delivered in a non-specialist (a non-hyper-acute stroke centre) DGH in the UK. An audit of cases completed describes complications seen.

An analysis of outcomes of emergency physician/department-based thrombolysis for stroke
Emerg Med J. 2012 Aug;29(8):640-3
Free Full Text

Extracorporeal cardiopulmonary resuscitation

You have a patient in cardiac arrest who has had excellent resuscitation from the point of collapse, and who has treatable underlying pathology (eg. PE or STEMI). However you’re unable to get return of spontaneous circulation so you call it. Someone just died for whom the technology exists to save them. Extracorporeal life support (ECLS) supports heart and lung function by externally providing circulatory flow and gas exchange until the patient’s underlying cause of arrest is treated or recovers.
ECLS requires an extracorporeal membrane oxygenation (ECMO) circuit to be placed during the cardiac arrest resuscitation. This may sound like extreme stuff, but there have been some amazing saves with this technology, and large numbers of in-hospital and out-of-hospital arrest patients have been treated in Japan, Korea, and Taiwan. ECMO has even been commenced in the field by prehospital emergency physicians.
An inspiring EMCrit podcast with Dr Joe Bellezzo described how this technology is applied at Sharp Memorial Hospital in San Diego. Bellezzo and colleagues have now published a series of their out-of-hospital arrest cases who received ECLS initiated by emergency physicians(1).
Coming back to the Japanese, a multicentre prospective cohort study of ECLS for out-of hospital cardiac arrest (the ‘SAVE-J’ study) selected patients with VF or pulseless VT in whom no ROSC was achieved with standard resuscitative measures. Their striking results mirror other ECLS studies and were published in abstract form in November 2011(2).
To me, the overwhelming take home messages from what I’ve seen and read on this are:


1. ECLS can provide dramatic saves with neurologically intact survival in cardiac arrest cases that otherwise would be dead.

2. The critical factor for successful clinical outcomes and avoidance of wasted resources and clinical futility is case selection. The underlying cause of arrest needs to be reversible (eg. myocarditis) or treatable (eg. STEMI) and good resuscitation needs to have been in place prior to ECLS.

3. In the right hospital with the right resuscitation team, it can be done.

1. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation
Resuscitation. 2012 Aug;83(8):966-70
[EXPAND Click for abstract]


CONTEXT: Extracorporeal cardiopulmonary resuscitation (ECPR) refers to emergent percutaneous veno-arterial cardiopulmonary bypass to stabilize and provide temporary support of patients who suffer cardiopulmonary arrest. Initiation of ECPR by emergency physicians with meaningful long-term patient survival has not been demonstrated.

OBJECTIVE: To determine whether emergency physicians could successfully incorporate ECPR into the resuscitation of patients who present to the emergency department (ED) with cardiopulmonary collapse refractory to traditional resuscitative efforts.

DESIGN: A three-stage algorithm was developed for ED ECPR in patients meeting inclusion/exclusion criteria. We report a case series describing our experience with this algorithm over a 1-year period.

RESULTS: 42 patients presented to our ED with cardiopulmonary collapse over the 1-year study period. Of these, 18 patients met inclusion/exclusion criteria for the algorithm. 8 patients were admitted to the hospital after successful ED ECPR and 5 of those patients survived to hospital discharge neurologically intact. 10 patients were not started on bypass support because either their clinical conditions improved or resuscitative efforts were terminated.

CONCLUSION: Emergency physicians can successfully incorporate ED ECPR in the resuscitation of patients who suffer acute cardiopulmonary collapse. More studies are necessary to determine the true efficacy of this therapy.

[/EXPAND]
2. Multicenter Non-Randomized Prospective Cohort Study of Extracorporeal Cardiopulmonary Resuscitation for Out-of Hospital Cardiac Arrest: Study of Advanced Life Support for Ventricular Fibrillation with Extracorporeal Circulation in Japan (SAVE-J)
Circulation 2011; 124: A18132
[EXPAND Click for abstract]


Background: This study is aimed to examine the efficacy of extracorporeal cardiopulmonary resuscitation (ECPR) for patients in out-of hospital cardiac arrest (OHCA) with ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT).

Method: The design of this study is a multicenter non-randomized prospective cohort study. Hypothesis is that the outcome of OHCA with VF or pulseless VT is similar between ECPR and conventional advanced life support (ALS). During from Oct. 2008 to Dec. 2010, forty six tertiary emergency hospitals were participated in this study. Patient inclusion criteria were 1) VF or pulseless VT on scene, 2) cardiac arrest on arrival at hospital, 3) within 45 minutes from a call to an arrival of hospital, and 4) non-ROSC by conventional ALS during 15 minutes after an arrival at hospital. Exclusion criteria were 1) age: 75 yr, 2) poor activities of daily livings, 3) non-cardiac verified cardiac arrest, and 4) hypothermia. According to the inclusion criteria, ECPR was adopted for OHCA in 26 hospitals (ECPR group) and conventional ALS was planned in 20 hospitals (non-ECPR group). Both groups (Intention-to-treat) were analyzed about the proportion of patients with favorable outcome (CPC1 or 2) assessed with the Glasgow-Pittsburgh Cerebral Performance and Overall Performance Categories at 1 month by chi square test and Fisher exact probability test.

Results: One hundred and eighty patients of ECPR group and 134 patients of non-ECPR group were enrolled. There was no difference between the background of ECPR group and non-ECPR group; Average age (56.0 VS 56.9), Witnessed (72.8% VS 75.4%), Lay-rescuer CPR (49.4% VS 45.5%), Acute coronary syndrome (65.6% VS 61.4%), Minutes from collapse to emergency department (26.8 VS 30.0). The favorable outcome rate in ECPR group (12.4%, 22 patients) was statistically higher than the rate in non-ECPR group (1.6%, two patients) (p<0.001).

Conclusion: Extracorporeal cardiopulmonary resuscitation may improve the outcome of out-of hospital cardiac arrest with VF or pulseless VT without ROSC by conventional ALS during 15 minutes after an arrival at hospital.

[/EXPAND]

Superglue for CVCs

In resuscitation situations, the securing of vascular catheters is an important but sometimes cumbersome process, particular when sutures are required for central lines or arterial lines.

Medical grade ‘superglue’ (cyanoacrylate) can be used and this has been described in the anaesthetic literature before(1). Now, further in vitro work shows the glue does not weaken the intravenous catheter and is not associated with bacterial colonisation(2).

I think this is perfect for resuscitation lines. Just last night I used this technique to secure a femoral arterial line during a cardiac arrest resuscitation. It was great not to have to faff around with sharp suture needles during CPR and the line felt very secure after just a few seconds.

1. Tissue adhesive as an alternative to sutures for securing central venous catheters
Anaesthesia. 2007 Sep;62(9):969-70

2. Cyanoacrylate tissue adhesives – effective securement technique for intravascular catheters: in vitro testing of safety and feasibility
Anaesth Intensive Care. 2012 May;40(3):460-6

Hypothermia after long down times

You receive a patient resuscitated from cardiac arrest to a perfusing rhythm in your emergency department. History suggests a long ‘down time’: There was a ten minute duration of ‘no-flow’ (time from collapse to the start of resuscitation attempts).
Would this make you more likely or less likely to initiate targeted temperature management (TTM) and cool the patient to the recommended 32-34 degrees?
A recent study supports the suggestion that a longer no-flow time is associated with greater odds of survival with TTM compared with no TTM, than patients with shorter no-flow times. In other words, cooling the patient is more likely to make a difference in the ‘long down time’ patient, even though the overall survival in that group is obviously less.


Aim Mild therapeutic hypothermia has shown to improve long-time survival as well as favorable functional outcome after cardiac arrest. Animal models suggest that ischemic durations beyond 8 min results in progressively worse neurologic deficits. Based on these considerations, it would be obvious that cardiac arrest survivors would benefit most from mild therapeutic hypothermia if they have reached a complete circulatory standstill of more than 8 min.

Methods In this retrospective cohort study we included cardiac arrest survivors of 18 years of age or older suffering a witnessed out-of-hospital cardiac arrest, which remain comatose after restoration of spontaneous circulation. Data were collected from 1992 to 2010. We investigated the interaction of ‘no-flow’ time on the association between post arrest mild therapeutic hypothermia and good neurological outcome. ‘No-flow’ time was categorized into time quartiles (0, 1–2, 3–8, >8 min).

Results One thousand-two-hundred patients were analyzed. Hypothermia was induced in 598 patients. In spite of showing a statistically significant improvement in favorable neurologic outcome in all patients treated with mild therapeutic hypothermia (odds ratio [OR]: 1.49; 95% confidence interval [CI]: 1.14–1.93) this effect varies with ‘no-flow’ time. The effect is significant in patients with ‘no-flow’ times of more than 2 min (OR: 2.72; CI: 1.35–5.48) with the maximum benefit in those with ‘no-flow’ times beyond 8 min (OR: 6.15; CI: 2.23–16.99).

Conclusion The beneficial effect of mild therapeutic hypothermia increases with cumulative time of complete circulatory standstill in patients with witnessed out-of-hospital cardiac arrest.

The beneficial effect of mild therapeutic hypothermia depends on the time of complete circulatory standstill in patients with cardiac arrest
Resuscitation. 2012 May;83(5):596-601

Hyperosmolar therapy

A great review article from the New England Journal of Medicine summaries the current knowledge base regarding the use of hypertonic saline and mannitol for raised intracranial pressure.

Hyperosmolar Therapy for Raised Intracranial Pressure 
N Engl J Med. 2012 Aug 23;367(8):746-52
Full text access is only available to New England Journal subscribers, but I’ve summarised some of the interesting bits in a short quiz you can take to test your knowledge. Just 13 True/False questions.

If you liked the quiz and want to use it at your local teaching sessions, here’s a Keynote Version and a PowerPoint Version

From BURP to BILP: backwards internal laryngeal pressure

A burns patient whose tracheal tube was accidentally dislodged and ended up placed in the oesophagus on day 2 of his ICU stay continued to spontaneously ventilate and maintain saturations on a midazolam infusion. The oesophageal tube was left in during laryngoscopy (after propofol but no muscle relaxant due to anticipated difficult airway) which revealed a cormack-lehane grade 3 view. The operator’s hand which was holding a bougie rested on the oesophageal tube, which displaced it backwards. This resulted in backwards displacement of the larynx and improved the glottic view to 2b, facilitating intubation.
The discovery of this ‘backwards internal laryngeal pressure’ manoeuvre led the authors to make the recommendation that during difficult intubation an inadvertently placed oesophageal tube should be left in place to allow a BILP manouevre, but removed if it impedes the passage of the tracheal tube.
I love anything that might improve success rates of critical procedures and this one could conceivably come in handy. I can just see Minh Le Cong inventing a transoesophageal posterior laryngal retractor for under 50 bucks…
The use of “Internal Laryngeal Pressure” to improve the laryngeal view following inadvertent oesophageal intubation in a patient with difficult airway
Anaesth Intensive Care. 2012 Jul;40(4):736-7

The opposite of acute kidney injury?

Prescribing in the critically ill patient can be a challenge due to a number of factors impacting on pharmacology:

  • variable enteral absorption and interaction with enteral feed
  • less protein binding in hypoalbuminaemic states
  • extravascular volume expansion with fluid loading and capillary leak can alter the volume of distribution
  • altered hepatic metabolism of drugs
  • impaired renal excretion
  • accumulation of toxic metabolites
  • removal by renal replacement therapy
  • interaction with other drugs

There’s another factor to bear in mind, though, which has been recently highlighted in the context of antibiotic prescription: that of Augmented Renal Clearance (ARC).
Some ICU patients have supraphysiologic renal function. Several studies have demonstrated significant numbers of ICU patients with higher than normal creatinine clearance. This is thought to be due to varying combinations of the following factors:

  • Low systemic vascular resistance and increased cardiac output leading to increased renal blood flow
  • Above factors enhanced by aggressive fluid and vasoactive therapy in pursuit of haemodynamic targets
  • These lead to increase delivery of solute to the kidneys and increased clearance

This can have implications for prescribing: the serum creatinine will not identify these patients, but it is possible that ARC will result in less effective therapy for a given dose of a renally-excreted drug, for example beta-lactam antibiotics.
An editorial by critical care physician Dr Andrew Shorr highlights the inadequacy of basing prescribing recommendations on data from the ex-vivo interaction between drug and pathogen:

‘To believe that all patients will respond in the same fashion and with the same trajectory is to become handcuffed by the median response noted in clinical trials……….The central fallacy of the bug-drug approach is that it misses the key role of the host.’

Sub-therapeutic initial β-lactam concentrations in select critically ill patients: association between augmented renal clearance and low trough drug concentrations
Chest. 2011 Dec 22. [Epub ahead of print] Free Full Text
Antibiotics in the critically ill: the bug, drug, host triad
Chest. 2012 Jul 1;142(1):8-10 Free Full Text

Don't ignore the diastolic

Most of us are pretty good at spotting hypotension and activating help or initiating therapy.
But ‘hypotension’ in many practitioners’ minds refers to a low systolic blood pressure. Who pays serious attention to the diastolic blood pressure? A low diastolic in a sick patient to me is a warning sign that their mean arterial pressure (MAP) is – or will be – low. After all, we spend about twice as long in diastole as in systole, so the diastolic pressure contributes more to the MAP than does the systolic.
A recent study showed that a low diastolic BP was one of several factors predictive of cardiac arrest on hospital wards: the most accurate predictors were maximum respiratory rate, heart rate, pulse pressure index, and minimum diastolic BP. These factors were more predictive than some of the variables included in the commonly used Early Warning Scores that trigger an emergency review.
The ‘pulse pressure index’ examined in the study is the pulse pressure divided by the systolic blood pressure (ie. [SBP-DBP]/SBP) which of course will be higher with lower diastolic blood pressures.
Importantly, the authors point out:


“In addition, our findings suggest that for many patients there is ample time prior to cardiac arrest to provide potentially life-saving interventions.”

…suggesting that there is still room for improvement in the identification and management of patients at risk for cardiac arrest, as the NCEPOD report ‘Cardiac Arrest Procedures: Time to Intervene?’ also showed.
They also recommend:


“…although systolic BP is commonly used in rapid response team activation criteria, incorporation of pulse pressure, pulse pressure index, or diastolic BP in place of systolic BP into the predictive model may be superior.”

Perhaps this may remind all of us to keep an eye on the diastolic as well as systolic BP when patients first present to us, and to include the importance of recognising diastolic hypotension in the teaching we provide our medical, paramedical and nursing students.

Predicting Cardiac Arrest on the Wards: A Nested Case-Control Study
Chest. 2012 May;141(5):1170-6 Free Full Text here
[EXPAND Click to read abstract]


Background: Current rapid response team activation criteria were not statistically derived using ward vital signs, and the best vital sign predictors of cardiac arrest (CA) have not been determined. In addition, it is unknown when vital signs begin to accurately detect this event prior to CA.

Methods: We conducted a nested case-control study of 88 patients experiencing CA on the wards of a university hospital between November 2008 and January 2011, matched 1:4 to 352 control subjects residing on the same ward at the same time as the case CA. Vital signs and Modified Early Warning Scores (MEWS) were compared on admission and during the 48 h preceding CA.

Results: Case patients were older (64 ± 16 years vs 58 ± 18 years; P = .002) and more likely to have had a prior ICU admission than control subjects (41% vs 24%; P = .001), but had similar admission MEWS (2.2 ± 1.3 vs 2.0 ± 1.3; P = .28). In the 48 h preceding CA, maximum MEWS was the best predictor (area under the receiver operating characteristic curve [AUC] 0.77; 95% CI, 0.71-0.82), followed by maximum respiratory rate (AUC 0.72; 95% CI, 0.65-0.78), maximum heart rate (AUC 0.68; 95% CI, 0.61-0.74), maximum pulse pressure index (AUC 0.61; 95% CI, 0.54-0.68), and minimum diastolic BP (AUC 0.60; 95% CI, 0.53-0.67). By 48 h prior to CA, the MEWS was higher in cases (P = .005), with increasing disparity leading up to the event.

Conclusions: The MEWS was significantly different between patients experiencing CA and control patients by 48 h prior to the event, but includes poor predictors of CA such as temperature and omits significant predictors such as diastolic BP and pulse pressure index.

[/EXPAND]

COPD and heart disease interactions

Ischaemic heart disease (IHD) and chronic obstructive pulmonary disease (COPD) often affect the same patient; in fact, more than one-third of patients with angiography-proven IHD also have COPD on spirometry(1).
A recent study suggests COPD exacerbations in patients with IHD were associated with longer (5 more days) recovery times and suffered more severe breathlessness between exacerbations(2).
An accompanying editorial highlights some important points:

  • Patients admitted with COPD exacerbations are more susceptible to myocardial infarction during the admission.
  • Infective COPD exacerbations may contribute to heart failure through systemic inflammation, autonomic activation, and increased fluid in the lung. Lung infection can increase ventilation/perfusion mismatch and increased work of breathing, further straining the heart.
  • Heart failure can be very difficult to diagnose during a COPD exacerbation because cough, dyspnoea and wheeze are common to both disorders. Physical examination may not be discriminatory, and chest radiography is insensitive to milder degrees of heart failure.

The authors recommed a high index of suspicion combined with consideration of biomarkers (BNP or pro-BNP) and imaging such as echocardiography or even nuclear medicine scans, cardiac MRI, and cardiac catheterisation.
So, next time you’re managing a COPD exacerbation, ask yourself:

  • Could there be concomitant heart failure contributing to symptoms?
  • If not, is the patient at risk of cardiac events during this admission, for which we need to be vigilant?
  • Do I need to consider additional laboratory (BNP) or imaging (echo) investigations? Remember BNP may be elevated in pneumonia and other non-cardiac critical illness, although a normal BNP rules out heart failure.
  • Should I add empiric anti-failure therapy to the acute treatment regimen?
  • If there is combined COPD exacerbation and heart failure, are there any conflicting priorities in therapy (eg. the pros and cons of beta-agonists, anticholinergics, and steroids)?

1. The complex relationship between ischemic heart disease and COPD exacerbations
Chest. 2012 Apr;141(4):837-8
2. The impact of ischemic heart disease on symptoms, health status, and exacerbations in patients with COPD
Chest. 2012 Apr;141(4):851-7
[EXPAND Click to read abstract]


BACKGROUND: Comorbid ischemic heart disease (IHD) is a common and important cause of morbidity and mortality in patients with COPD. The impact of IHD on COPD in terms of a patient’s health status, exercise capacity, and symptoms is not well understood.

METHODS: We analyzed stable-state data of 386 patients from the London COPD cohort between 1995 and 2009 and prospectively collected exacerbation data in those who had completed symptom diaries for ≥ 1 year.

RESULTS: Sixty-four patients (16.6%) with IHD had significantly worse health status as measured by the St. George Respiratory Questionnaire (56.9 ± 18.5 vs 49.1 ± 19.0, P = .003), and a larger proportion of this group reported more severe breathlessness in the stable state, with a Medical Research Council dyspnea score of ≥ 4 (50.9% vs 35.1%, P = .029). In subsets of the sample, stable patients with COPD with IHD had a higher median (interquartile range [IQR]) serum N-terminal pro-brain natriuretic peptide concentration than those without IHD (38 [15, 107] pg/mL vs 12 [6, 21] pg/mL, P = .004) and a lower exercise capacity (6-min walk distance, 225 ± 89 m vs 317 ± 85 m; P = .002). COPD exacerbations were not more frequent in patients with IHD (median, 1.95 [IQR, 1.20, 3.12] vs 1.86 (IQR, 0.75, 3.96) per year; P = .294), but the median symptom recovery time was 5 days longer (17.0 [IQR, 9.8, 24.2] vs 12.0 [IQR, 8.0, 18.0]; P = .009), resulting in significantly more days per year reporting exacerbation symptoms (median, 35.4 [IQR, 13.4, 60.7] vs 22.2 [IQR, 5.7, 42.6]; P = .028). These findings were replicated in multivariate analyses allowing for age, sex, FEV(1), and exacerbation frequency where applicable.

CONCLUSIONS: Comorbid IHD is associated with worse health status, lower exercise capacity, and more dyspnea in stable patients with COPD as well as with longer exacerbations but not with an increased exacerbation frequency.

[/EXPAND]

Is it time to abandon plain radiography in the trauma room?

For patients who will be having a chest CT, perhaps sonography could replace chest radiography in the resus room as the initial imaging step; this recent prospective study shows its superiority over the ‘traditional’ ATLS approach.

In haemodynamically stable patients with prophylactic pelvic splints in place, one could easily argue against plain pelvis films too (the caveat being rapid access to CT is necessary). The arguments against resus-room lateral cervical spine x-rays were made ages ago and these are now rarely done in the UK & Australia.

Is it time to abandon plain radiography altogether for stable major trauma patients?


Background: The accuracy of combined clinical examination (CE) and chest radiography (CXR) (CE + CXR) vs thoracic ultrasonography in the acute assessment of pneumothorax, hemothorax, and lung contusion in chest trauma patients is unknown.

Methods: We conducted a prospective, observational cohort study involving 119 adult patients admitted to the ED with thoracic trauma. Each patient, secured onto a vacuum mattress, underwent a subsequent thoracic CT scan after first receiving CE, CXR, and thoracic ultrasonography. The diagnostic performance of each method was also evaluated in a subgroup of 35 patients with hemodynamic and/or respiratory instability.

Results: Of the 237 lung fields included in the study, we observed 53 pneumothoraces, 35 hemothoraces, and 147 lung contusions, according to either thoracic CT scan or thoracic decompression if placed before the CT scan. The diagnostic performance of ultrasonography was higher than that of CE + CXR, as shown by their respective areas under the receiver operating characteristic curves (AUC-ROC): mean 0.75 (95% CI, 0.67-0.83) vs 0.62 (0.54-0.70) in pneumothorax cases and 0.73 (0.67-0.80) vs 0.66 (0.61-0.72) for lung contusions, respectively (all P < .05). In addition, the diagnostic performance of ultrasonography to detect pneumothorax was enhanced in the most severely injured patients: 0.86 (0.73-0.98) vs 0.70 (0.61-0.80) with CE + CXR. No difference between modalities was found for hemothorax.
Conclusions: Thoracic ultrasonography as a bedside diagnostic modality is a better diagnostic test than CE and CXR in comparison with CT scanning when evaluating supine chest trauma patients in the emergency setting, particularly for diagnosing pneumothoraces and lung contusions.

Diagnostic accuracy of ultrasonography in the acute assessment of common thoracic lesions after trauma
Chest. 2012 May;141(5):1177-83