Tag Archives: ALS

Pre-hospital thoracotomy

The London Helicopter Emergency Medical Service provides a physician / paramedic team to victims of trauma. One of the interventions performed by their physicians is pre-hospital resuscitative thoracotomy to patients with cardiac arrest due to penetrating thoracic trauma. They have published the outcomes from this procedure over a 15 year period which show an 18% survival to discharge rate, with a high rate of neurologically intact survivors1.
The article was submitted for publication on February 1, 2010, and in the discussion mentions a further two survivors from the procedure performed after conducting the study. It is likely therefore in the year and a half since submission still more patients have been saved. It will be interesting to read future reports from this team as the numbers accumulate; penetrating trauma missions are sadly increasing in frequency.
Having worked for these guys and performed this procedure in the field a few times myself, I can attest to the training and governance surrounding this system. The technique of clamshell thoracotomy is well described 2 and one I would recommend for the non-surgeon.

BACKGROUND: Prehospital cardiac arrest associated with trauma almost always results in death. A case of survival after prehospital thoracotomy was published in 1994 and several others have followed. This article describes the result of prehospital thoracotomy in a physician-led system for patients with stab wounds to the chest who suffered cardiac arrest on scene.
METHODS: A 15-year retrospective prehospital trauma database review identified victims of stab wounds to the chest who suffered cardiac arrest on scene and had thoracotomy performed according to local standard operating procedures.
RESULTS: Overall, 71 patients met inclusion criteria. Thirteen patients (18%) survived to hospital discharge. Neurologic outcome was good in 11 patients and poor in 2. Presenting cardiac rhythm was asystole in four patients, pulseless electrical activity in five, and unrecorded in the remaining four. All survivors had cardiac tamponade. The medical team was present at the time of cardiac arrest for six survivors (good neurologic outcome): arrived in the first 5 minutes after arrest in three patients (all good neurologic outcome), arrived 5 minutes to 10 minutes after arrest in two patients (one poor neurologic outcome), and in one patient (poor neurologic outcome) the period was unknown. Of the survivors, seven thoracotomies were performed by emergency physicians and six by anesthesiologists.
CONCLUSIONS: Prehospital thoracotomy is a well-established procedure in this physician-led prehospital service. Results from this and other similar systems suggest that when performed for the subgroup of patients described, significant numbers of survivors with good neurologic outcome can be expected.

1. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician-Performed Resuscitation Procedure That Can Yield Good Results
J Trauma. 2011 May;70(5):E75-8
2. Emergency thoracotomy: “how to do it”
Emerg Med J. 2005 January; 22(1):22–24
Full text available here

Exsanguinating cardiac arrest not always fatal

The British Military has developed a reputation for aggressive pre-hospital critical care including (but not limited to) the use of blood products and tourniquets, and coordinated field hospital trauma care. They now report the outcomes for patients with traumatic cardiac arrest, mainly from improvised explosive devices. Of 52 patients, 14 (27%) demonstrated return of spontaneous circulation (ROSC), of whom four (8%) survived to hospital discharge with a neurologically good recovery. Resuscitative thoracotomy (RT) was performed on 12 patients (8 in the ED), including all four survivors. RT enabled open-chest CPR, release of pericardial tamponade, lung resection and compression of the descending thoracic aorta for haemorrhage control.
No patients who arrested in the field survived, although one of the neurologically well-recovered survivors arrested during transport to hospital and was in cardiac arrest for 24 minutes. The authors propose this individual’s survival was in part due to ‘the high level of care that he received during retrieval, including haemorrhage control, tracheal intubation and transfusion of blood products‘.
Asystole was universally associated with death but agonal / bradycardic rhythms were not. In keeping with other studies, cardiac activity on ultrasound was associated with ROSC.


AIM: To determine the characteristics of military traumatic cardiorespiratory arrest (TCRA), and to identify factors associated with successful resuscitation.

METHODS: Data was collected prospectively for adult casualties suffering TCRA presenting to a military field hospital in Helmand Province, Afghanistan between 29 November 2009 and 13 June 2010.

RESULTS: Data was available for 52 patients meeting the inclusion criteria. The mean age (range) was 25 (18-36) years. The principal mechanism of injury was improvised explosive device (IED) explosion, the lower limbs were the most common sites of injury and exsanguination was the most common cause of arrest. Fourteen (27%) patients exhibited ROSC and four (8%) survived to discharge. All survivors achieved a good neurological recovery by Glasgow Outcome Scale. Three survivors had arrested due to exsanguination and one had arrested due to pericardial tamponade. All survivors had arrested after commencing transport to hospital and the longest duration of arrest associated with survival was 24min. All survivors demonstrated PEA rhythms on ECG during arrest. When performed, 6/24 patients had ultrasound evidence of cardiac activity during arrest; all six with cardiac activity subsequently exhibited ROSC and two survived to hospital discharge.

CONCLUSION: Overall rates of survival from military TCRA were similar to published civilian data, despite military TCRA victims presenting with high Injury Severity Scores and exsanguination due to blast and fragmentation injuries. Factors associated with successful resuscitation included arrest beginning after transport to hospital, the presence of electrical activity on ECG, and the presence of cardiac movement on ultrasound examination.

Outcomes following military traumatic cardiorespiratory arrest: A prospective observational study
Resuscitation. 2011 Sep;82(9):1194-7

Still no cardiac arrest survival benefit from epinephrine?

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

Pre-hospital ECMO

Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

How much oxygen after ROSC?


I reported a previous JAMA publication demonstrating an association between hyperoxia and mortality in patients resuscitated post-cardiac arrest. The same authors have published furthur data to better define the relationship between supranormal oxygen tension and outcome in postresuscitation patients. They hypothesised that a linear dose-dependent relationship would be present in the association between supranormal oxygen tension and in-hospital mortality.

Background– Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.

Methods and Results– This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 [95% confidence interval 1.18 to 1.31]. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.

Conclusion– In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.

Relationship Between Supranormal Oxygen Tension and Outcome After Resuscitation From Cardiac Arrest
Circulation. 2011 Jun 14;123(23):2717-2722
Australasian investigators provided the following critique of the original JAMA study:

Unfortunately, these investigators used only the first set of arterial blood gases in the ICU to assess oxygenation, excluded close to 30% of patients because of lack of arterial blood gas data and did not adjust for standard illness severity scores. Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. Thus, their results are of uncertain significance and require confirmation.

They undertook their own study of 12,108 patients:

INTRODUCTION: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients.
METHODS: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined ‘hyperoxia’ as PaO2 of 300 mmHg or greater, ‘hypoxia/poor O2 transfer’ as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, ‘normoxia’ as any value between hypoxia and hyperoxia and ‘isolated hypoxemia’ as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.

RESULTS: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).

CONCLUSIONS: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
Crit Care. 2011 Mar 8;15(2):R90. [Epub ahead of print]
Open Access Full Text
What’s the best approach in the light of these differing results? My approach is to avoid hypoxia, since that’s probably bad, and to actively avoid overoxygenating as part of my general neuroprotection checklist in a post-cardiac arrest patient. It would seem prudent to follow the recommendations of ILCOR, summarised by the European Resuscitation Council guidelines as:

Recognition of the potential harm caused by hyperoxaemia after ROSC is achieved: once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry and/or arterial blood gas analysis), inspired oxygen is titrated to achieve a SaO2 of 94–98%

Drugs in cardiac arrest – guess what works?

Just like epinephrine (adrenaline), amiodarone does not increase survival to hospital discharge in cardiac arrest patients. I doubt his will deter the people in the resuscitation room with their stopwatches from handing me these drugs and telling me I ought to be giving them though.

Amiodarone - a load of balls

 

AIMS: In adult cardiac arrest, antiarrhythmic drugs are frequently utilized in acute management and legions of medical providers have memorized the dosage and timing of administration. However, data supporting their use is limited and is the focus of this comprehensive review.

METHODS: Databases including PubMed, Cochrane Library (including Cochrane database for systematic reviews and Cochrane Central Register of Controlled Trials), Embase, and AHA EndNote Master Library were systematically searched. Further references were gathered from cross-references from articles and reviews as well as forward search using SCOPUS and Google scholar. The inclusion criteria for this review included human studies of adult cardiac arrest and anti-arrhythmic agents, peer-review. Excluded were review articles, case series and case reports.

RESULTS: Of 185 articles found, only 25 studies met the inclusion criteria for further review. Of these, 9 were randomised controlled trials. Nearly all trials solely evaluated Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF), and excluded Pulseless Electrical Activity (PEA) and asystole. In VT/VF patients, amiodarone improved survival to hospital admission, but not to hospital discharge when compared to lidocaine in two randomized controlled trials.

CONCLUSION: Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.

The use of antiarrhythmic drugs for adult cardiac arrest: A systematic review
Resuscitation. 2011 Jun;82(6):665-70

ECLS on Japanese, in Japanese

A review of extracorporeal life support for out-of-hospital cardiac arrest was undertaken, looking specifically at studies published in the Japanese literature. The abstract is shown below. Based on these findings, inclusion criteria for a multicentre, prospective non-randomised cohort study were established. The ‘SAVE-J: Study of advanced life support for ventricular fibrillation with extracorporeal circulation in Japan’ was launched and has been ongoing since October 2008 to compare the proportion of patients with a favourable neurological outcome by intention-to-treat in an ECPR group with a non-ECPR group. Inclusion criteria for this new study are:

  1. shockable rhythm on the initial ECG
  2. cardiac arrest on arrival at hospital regardless of the presence of recovery of spontaneous circulation before arrival
  3. arrival at hospital within 45 min of the call for an ambulance or cardiac arrest;
  4. cardiac arrest remaining for more than 15 min after arrival at hospital.

I look forward to seeing the results SAVE-J. If you wish to read more, you can check out the SAVE-J study website.

AIM: Although favourable outcomes in patients receiving extracorporeal cardiopulmonary resuscitation (ECPR) for out-of-hospital cardiac arrest have been frequently reported in Japanese journals since the late 1980s, there has been no meta-analysis of ECPR in Japan. This study reviewed and analysed all previous studies in Japan to clarify the survival rate of patients receiving ECPR.
MATERIAL AND METHODS: Case reports, case series and abstracts of scientific meetings of ECPR for out-of-hospital cardiac arrest written in Japanese between 1983 and 2008 were collected. The characteristics and outcomes of patients were investigated, and the influence of publication bias of the case-series studies was examined by the funnel-plot method.
RESULTS: There were 1282 out-of-hospital cardiac arrest patients, who received ECPR in 105 reports during the period. The survival rate at discharge given for 516 cases was 26.7±1.4%. The funnel plot presented the relationship between the number of cases of each report and the survival rate at discharge as the reverse-funnel type that centred on the average survival rate. In-depth review of 139 cases found that the rates of good recovery, mild disability, severe disability, vegetative state, death at hospital discharge and non-recorded in all cases were 48.2%, 2.9%, 2.2%, 2.9%, 37.4% and 6.4%, respectively.
CONCLUSIONS: Based on the results of previous reports with low publication bias in Japan, ECPR appears to provide a higher survival rate with excellent neurological outcome in patients with out-of-hospital cardiac arrest.

Extracorporeal cardiopulmonary resuscitation for out-of-hospital cardiac arrest: a review of the Japanese literature
Resuscitation. 2011 Jan;82(1):10-4

Which cardiac arrest survivors have a positive angio?

A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.

OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors.
METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site.
RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6).
CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.

Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients
Eur J Emerg Med. 2011 Apr;18(2):73-6

In V.Fib and talking to you!

Some patients with severe refractory heart failure are kept alive thanks to implantable pumps such as the left ventricular assist device (LVAD). Many emergency physicians are likely to be unfamiliar with these but could encounter patients who have them. One particular peculiarity is that latter generation devices maintain non-pulsatile flow and provide or assist cardiac output independent of cardiac rhythm. In extreme situations patients can have life-sustaining cardiac outputs without palpable pulses or even audible heart sounds.

Click on image for Wikipedia article

A great example of how weird this can get is provided by a case of a 66 year male with an LVAD (HeartMate II (Thoratec Corporation)) who presented due to spontaneous discharge of his internal cardioverter-defibrillator (ICD). He was alert but had no pulses, and no detectable blood pressure using both a manual sphygmomanometer and an automated non-invasive blood pressure device. His 12 lead showed ventricular fibrillation. An invasive blood pressure showed a mean arterial pressure (mAP) of 80 mmHg. Several hours later his VF was successfully terminated and his mAP remained 80 mmHg
Some interesting points made by the authors include:

  • CPR was unnecessary in this guy but in cases of severe RV dysfunction it might need to be done to provide flow into the LV.
  • A danger of CPR in patients with an LVAD is the risk of damage to the device or ventricular rupture

LVAD use is significantly increasing so we can expect to encounter more episodes of previously impossible presentations to our emergency departments.

ABSTRACT
Optimal medical treatment, cardiac resynchronization, and the use of an implantable cardioverter defibrillator are established therapies of severe congestive heart failure. In refractory cases, left ventricular assist devices are more and more used not only as bridging to cardiac transplantation but also as destination therapy. Ventricular arrhythmias may represent a life-threatening condition and often result in clinical deterioration in patients with congestive heart failure. We report a case of asymptomatic sustained ventricular fibrillation with preserved hemodynamics caused by a nonpulsatile left ventricular assist device. Consecutive adequate but unsuccessful discharges of the implantable cardioverter defibrillator were the only sign of the usually fatal arrhythmia, prompting the patient to consult emergency services. Electrolyte supplementation and initiation of therapy with amiodarone followed by external defibrillation resulted in successful restoration of a stable cardiac rhythm after 3.5 hours.

Asymptomatic Sustained Ventricular Fibrillation in a Patient With Left Ventricular Assist Device
Ann Emerg Med. 2011 Jan;57(1):25-8.

Nasal cooling method

More data on the RhinoChill device from an in-hospital study of post-cardiac arrest patients in Germany. The RhinoChill device (BeneChill Inc., San Diego, USA) allows evaporative cooling by spraying an inert liquid coolant (a perfluorochemical) into the nasal cavity. The liquid evaporates instantaneously, thereby removing heat. It can make your nose discoloured, and in one patient with cardiogenic shock, tissue damage of nose and cheeks due to freezing occurred. Several of the authors are linked with the company that manufactures the device.

AIM: Mild therapeutic hypothermia improves survival and neurologic recovery in primary comatose survivors of cardiac arrest. Cooling effectivity, safety and feasibility of nasopharyngeal cooling with the RhinoChill device (BeneChill Inc., San Diego, USA) were determined for induction of therapeutic hypothermia.
METHODS: Eleven emergency departments and intensive care units participated in this multi-centre, single-arm descriptive study. Eighty-four patients after successful resuscitation from cardiac arrest were cooled with nasopharyngeal delivery of an evaporative coolant for 1h. Subsequently, temperature was controlled with systemic cooling at 33 degrees C. Cooling rates, adverse events and neurologic outcome at hospital discharge using cerebral performance categories (CPC; CPC 1=normal to CPC 5=dead) were documented. Temperatures are presented as median and the range from the first to the third quartile.
RESULTS: Nasopharyngeal cooling for 1h reduced tympanic temperature by median 2.3 (1.6; 3.0) degrees C, core temperature by 1.1 (0.7; 1.5) degrees C. Nasal discoloration occurred during the procedure in 10 (12%) patients, resolved in 9, and was persistent in 1 (1%). Epistaxis was observed in 2 (2%) patients. Periorbital gas emphysema occurred in 1 (1%) patient and resolved spontaneously. Thirty-four of 84 patients (40%) patients survived, 26/34 with favorable neurological outcome (CPC of 1-2) at discharge.
CONCLUSIONS: Nasopharyngeal evaporative cooling used for 1h in primary cardiac arrest survivors is feasible and safe at flow rates of 40-50L/min in a hospital setting.
Safety and feasibility of nasopharyngeal evaporative cooling in the emergency department setting in survivors of cardiac arrest
Resuscitation. 2010 Aug;81(8):943-9