| Abstract|| |
Context: The spectrum of the etiology of out-of-hospital cardiopulmonary arrest (OHCPA) has not been established. We have performed perimortem computed tomography (CT) during cardiopulmonary resuscitation. Aims: To clarify the incidence of non-cardiac etiology (NCE), actual distribution of the causes of OHCPA via perimortem CT and its usefulness. Settings and Design: Population-based observational case series study. Materials and Methods: We reviewed the medical records of 1846 consecutive OHCPA cases and divided them into two groups: 370 showing an obvious cause of OHCPA with NCE (trauma, neck hanging, terminal stage of malignancy, and gastrointestinal bleeding) and others. Results: Of a total OHCPA, perimortem CT was performed in 57.5% and 62.5% were finally diagnosed as NCE: Acute aortic dissection (AAD) 8.07%, pulmonary thrombo-embolization (PTE) 1.46%, hypoxia due to pneumonia 5.25%, asthma and acute worsening of chronic obstructive pulmonary disease 2.06%, cerebrovascular disorder (CVD) 4.48%, airway obstruction 7.64%, and submersion 5.63%. The rates of patients who survived to hospital discharge were 6-14% in patients with NCE. Out of the 1476 cases excluding obvious NCE of OHCPA, 66.3% underwent perimortem CT, 14.6% of cases without obvious NCE and 22.1% of cases with perimortem CT were confirmed as having some NCE. Conclusions: Of the total OHCPA the incidences of NCE was 62.5%; the leading etiologies were AAD, airway obstruction, submersion, hypoxia and CVD. The rates of cases converted from cardiac etiology to NCE using perimortem CT were 14.6% of cases without an obvious NCE.
Keywords: Etiology of out-of-hospital cardiac arrest, out-of-hospital cardiac arrest with non-cardiac etiology, perimortem computed tomography, perimortem imaging
|How to cite this article:|
Moriwaki Y, Tahara Y, Kosuge T, Suzuki N. Etiology of out-of-hospital cardiac arrest diagnosed via detailed examinations including perimortem computed tomography. J Emerg Trauma Shock 2013;6:87-94
|How to cite this URL:|
Moriwaki Y, Tahara Y, Kosuge T, Suzuki N. Etiology of out-of-hospital cardiac arrest diagnosed via detailed examinations including perimortem computed tomography. J Emerg Trauma Shock [serial online] 2013 [cited 2020 Mar 30];6:87-94. Available from: http://www.onlinejets.org/text.asp?2013/6/2/87/110752
| Introduction|| |
The accurate spectrum of the etiology of out-of-hospital cardiopulmonary arrest (OHCPA) has not yet been established. Usually the etiology of OHCPA can only be speculated on in the emergency department (ED) on the basis of very little information. We can confirm that patients with OHCPA have a non-cardiac etiology (NCE) only if they present with a clear cause of OHCPA other than cardiac diseases.  Although autopsy is a good method for detecting the actual cause of OHCPA, the opportunity to perform autopsies is decreasing in most countries. In recent years, postmortem imaging, autopsy imaging, virtual autopsy, or virtopsy including postmortem computed tomography (CT) have become more common as alternatives to conventional autopsy. However, these procedures have not been established scientifically or legally and are not socio-economically viable in many countries.
In our ED, we have aggressively performed brain CT and body CT as optional advanced examinations for detecting the cause of OHCPA during cardiopulmonary resuscitation (CPR) and before death certification.  This practice is not postmortem CT but should be called as "perimortem CT." The characteristics and usefulness of perimortem CT for diagnosis are the same as those of postmortem CT. The purpose of this study is to clarify the usefulness of perimortem CT, to clarify how many patients with OHCPA can be diagnosed as having a NCE via aggressive examinations including perimortem CT, and to clarify more actual distribution of the causes of OHCPA using perimortem CT than distribution of the cause of OHCPA suspected without perimortem CT in an urban setting.
| Materials and Methods|| |
Emergency medical service system in the study area
In Japan, an out-of-hospital emergency medical service (EMS) system has been established that involves ambulance services and Emergency Life Saving Technicians (ELST) belonging to fire departments and in-hospital EDs. The ELST license was established in 1991, and the activities performed by these technicians have expanded to include defibrillation by automated defibrillator, cannulation into veins and infusion of Ringer solution, insertion of laryngeal mask airways, Esophageal gastric tube airway, and insertion of laryngeal tubes. Today, some of them who have received proper prearranged training can be permitted to perform endotracheal intubation (beginning in 2004) and can administer adrenaline (beginning in 2006) under restricted conditions. 
We are establishing a pre-hospital and inter-hospital EMS system for critical and severe patients including OHCPA in our city. Yokohama is the second largest city in Japan, and our institute is located in the center of Yokohama. The area of Yokohama is 434 km 2 with a population of 3.37 million. We selected 12 hospitals, whose EDs can receive and treat the severest patients including OHCPA patients, and which have to receive patients with OHCPA independent of their capacity. One EMS director (a medical doctor) who belongs to the 12 hospitals is stationed in the central operation center in the fire department of the city. This director advises ELSTs, orders treatment through them, and notifies the hospitals when OHCPA patients are being transferred to them. OHCPA patients are transferred to the ED of the nearest of the 12 hospitals [Figure 1]. For each hospital, including our hospital, all data concerning OHCPA patients are population-based. ,,
|Figure 1: Map of Yokohama city indicating the 12 hospitals to which the emergency medical service system transfers out-of-hospital cardiopulmonary arrest (OHCPA) patients based on the nearest emergency department and which must receive OHCPA patients. For each hospital in Yokohama including our hospital, all data concerning cardiopulmonary arrest patients are population-based|
Click here to view
We evaluated and treated patients with OHCPA in our ED according to our strategy based on the International Liaison Committee on Resuscitation (ILCOR) guideline throughout the study period. This strategy includes continuous long chest compression for over 30 min, airway management with mask or intubation, regular ventilation using a respirator, infusion of cristaloid, administration of adrenalin every 3 min, and special treatment for specific pathological conditions such as glucose administration for hypoglycemia during the resuscitation period before death certification. We also perform basic examinations, such as blood tests including creatin kinase and its isozyme, troponin I, arterial blood gas analysis, chest and abdominal simple X-rays, and body ultrasonography including the heart, thoracic cavity, neck-chest-abdominal great vessels and abdominal cavity for all patients.  If we could confirm the lethal cause of OHCPA via these basic examinations, via physical findings and/or the patient's history such as severe trauma, neck hanging, terminal stage of malignancy, or gastrointestinal bleeding, we determined the cause of OHCPA without advanced examinations. In other cases, during this resuscitation period, we have aggressively performed brain CT and body CT as optional advanced examinations after performing all of these aggressive resuscitation effort and before the declaration of the patient's death. In conditions when more than two OHCPA patients are simultaneously in our ED, we did not perform these optional advanced examinations. If the return of spontaneous circulation was established, we performed examinations to detect the etiology of OHCPA including CT, ultrasound (US), electrocardiography, etc. based on the physician's decision [Figure 2].
|Figure 2: Standard and optional advanced examination and evaluation of out-of-hospital cardiopulmonary arrest patients in our emergency department|
Click here to view
Study protocol and data collection
This was a population-based observational case series study. We reviewed the medical records of OHCPA patients in our ED, intensive care unit and wards, for patients treated in our hospital in two different 2.5-year periods (from September 2002 to February 2005 and from September 2007 to February 2010) and evaluated the etiologies of 1846 consecutive OHCPA cases using the patients' histories and information obtained from the patients' families or from lay persons, from physical findings and from the examinations performed. Cases of OHCPA that occurred after contact with the EMS team at the scene and before arrival at the hospital were included. We chose theses non-consecutive period because we and laypersons became familiar with the different two guidelines for resuscitation in these different periods, which were published in 2001 and 2006, respectively. Before September 2002 and September 2007, these guidelines were not diffusely received by all laypersons.
Based on the patients' histories and information, OHCPA patients were divided into two groups: 370 patients who showed an obvious cause of OHCPA with NCE and were confirmed to have a NCE (trauma 222, neck hanging 91, terminal stage of malignancy 35, gastrointestinal bleeding 22) and 1476 patients who did not show an obvious non-cardiac cause. OHCPA patients with hypoxia due to pneumonia were diagnosed based on their histories, clinical findings, the character and volume of sputa and intratracheal aspirates after intratracheal intubation, and via the ruling out of intracranial diseases using perimortem CT in some cases. In this study, positive perimortem CT findings refer to fresh intracranial bleeding and infarction, Acute aortic dissection (AAD) and its main branches, arterial thrombo-embolization including pulmonary thrombo-embolization (PTE), lethal internal bleeding, signs of massive pulmonary infiltration, atelectasis and aspiration, and signs of other critical diseases. All patients underwent intratracheal intubation and aspiration and sampling of sputa and other intratracheal findings including aspirated materials.
The procedures were in accordance with the Helsinki Declaration.
| Results|| |
Of a total of 1846 OHCPA cases, perimortem CT was performed in 1062 cases (57.5%), and 1153 (62.5%) were finally diagnosed as NCE. Of all of the OHCPA cases, the numbers and the incidences of OHCPA due to various causes were as follows: AAD 149 (8.07%), PTE 27 (1.46%), hypoxia due to pneumonia 97 (5.25%), asthma and acute worsening of chronic obstructive pulmonary disease (COPD) 38 (2.06%), cerebrovascular disorder (CVD) 83 (4.48%), epilepsy 2 (0.11%), organ failure 37 (2.01%), intra-abdominal bleeding 1 (0.04%), dehydration and malnutrition 12 (0.65%), airway obstruction 141 (7.64%), hypoglycemia 34 (1.84%), hypothermia 17 (0.92%), toxic substances 35 (1.90%), and submersion 104 (5.63%) [Table 1]. The rates of patients who survived to hospital discharge were 18-46% in patients with cardiac etiologies, which was higher than that in patients with NCE; 11.1% in patients with PTE; 10.5% in patients with asthma and acute worsening on COPD; 14.2 in patients with airway obstruction; 11.4% in patients subjected to toxic substances; and 6.3% in trauma patients [Table 1].
|Table 1: The incidence of each etiology in out-of-hospital cardiopulmonary arrest with non-cardiac etiology and their survival rates|
Click here to view
Perimortem CT can confirm the cause of OHCPA or rule out specific pathological conditions such as cerebral hemorrhage. The numbers and incidences of patients showing an obvious cause of NCE were as follows: 222 trauma (12.03%), 91 neck hanging (4.92%), 35 terminal stage of malignant disease (1.90%), and 22 non-traumatic gastrointestinal bleeding (1.19%). Out of the 1476 cases excluding these obvious non-cardiac causes of OHCPA, 978 cases (66.3%) underwent perimortem CT and 216 (14.6% of cases without obvious non-cardiac cause and 22.1% of cases with perimortem CT) were confirmed as having some NCE by perimortem CT findings; i.e., their etiologies were changed from cardiac etiology to NCE. Perimortem CT was performed in 98.8% of CVD patients; only one case that did not undergo perimortem CT underwent spinal puncture, which confirmed the cause of OHCPA [Table 2], [Figure 3].
|Figure 3: The relation of out-of-hospital cardiopulmonary arrest patients and the performance of perimortem computed tomography|
Click here to view
|Table 2: The relation between each etiology and the performance of perimortem computed tomography|
Click here to view
| Discussion|| |
It is difficult to determine an accurate spectrum of the actual etiology of OHCPA because we can only contact and evaluate these patients at some interval after the OHCPA event. Utstein's templates for resuscitation registries say that "an arrest is presumed to be of cardiac etiology unless it is known or likely to have been caused by trauma, submersion, drug overdose, asphyxia, exsanguination, or any other non-cardiac cause as best determined by rescuers."  Pell, et al.  reported that presumed cardiac etiology is 82% in OHCPA. Some recent studies demonstrated a variable rate of NCE from 19.9% to 34.1% among OHCPA cases. ,,,, Yoshida, et al.  reported 58.5% of OHCPA cases being NCE. The rate of OHCPA with cardiac origin appears to be decreasing.
This tendency is thought to be due to a real decrease in actual cardiogenic OHCPA. The successful prevention of sudden OHCPA in patients with cardiac disease can extend the lives of these patients, resulting in an increase in the rate of OHCPA with NCE and an increase in the rate of in-hospital and in-home natural death, cases in which death certification can be made without resuscitation. Some authors found a decreasing number of OHCPA due to ventricular fibrillation (VF), which is a contributing factor to the increasing proportion of OHCPA with NCE observed in the out-of-hospital setting, and which is caused in part by the usage of implantable cardiac defibrillators and the primary prevention of coronary artery disease. ,,
Also, this tendency may be due to the relative decrease of cardiogenic OHCPA with presumed cardiac etiologies. The earnest and aggressive examination to determine the cause of OHCPA with NCE can result in a decrease in the number of cases in which a cardiac etiology is presumed, despite there being no change in the rate of real cardiogenic OHCPA. This phenomenon should be referred to as "etiology migration." Kuisma and Alaspδδ  showed that if the determination of etiology had only been based on clinical suspicion, over one-third of cases with NCE would have been missed. Yoshida et al.  also showed that of the witnessed OHCPA cases diagnosed as having cardiac etiology in the ED using the Utstein style of diagnosis, 42% were re-classified as NCE on the basis of scrutiny after admission or of postmortem findings (44% of the total witnessed OHCPA underwent postmortem CT). A Czech group reported that postmortems were performed on 31% of the total, with 34% of the cases undergoing postmortems being found to be NCE and 16% being revised from cardiac to NCE. 
In this study, we showed a lower incidence of cardiac etiology in OHCPA using consecutive population-based data in our district using aggressive examination, with a higher rate of perimortem CT than in any other report: 57.5% of all OHCPA cases and 66.3% of cases without an obvious non-cardiac cause. We can detect subarachnoid hemorrhage (SAH), cerebral hemorrhage, AAD, and ruptured aortic aneurysm in OHCPA patients only after an advanced examination such as US or CT. These patients may be misjudged as cardiac OHCPA if physicians do not perform these aggressive examinations. Our data are thought to be more accurate than those reported in previous studies.
Concerning the detailed spectrum of causes of OHCPA with NCE, some authors reported chest disease as a predominant cause. Yoshida et al.  reported that the etiologies of OHCPA with NCE cases re-classified from cardiac etiology were as follows: Respiratory disease 20.3%, aortic disease 14.5%, PTE 2.9%, CVD 5.8%, malignancy 14.5%, and aggravated chronic renal failure 10.1%. Hess et al.  reported that the etiologies of OHCPA with NCE were as follows: Respiratory failure 35.6%, PTE 13.3%, intracranial process 3.3%, overdose 10.0%, non-traumatic bleeding 8.9%, sepsis 4.4%, drowning 2.2%, and malignancy 1.1%. Kuisma and Alaspδδ  reported that the leading etiologies of OHCPA with NCE excluding trauma were PTE (8.4%), drug overdose (14.5%), non-traumatic bleeding (16.8%), and near drowning (10.3%). In our data, the leading etiologies were different from those in these previous data, as follows: Pulmonary diseases 7.3% and airway obstruction 7.6%, AAD 8.1%, PTE 1.46%, CVD 4.5%, toxic substances 1.9%, organ failure 2.0%, submersion 5.63%, and hypoglycemia 1.84% of all OHCPA cases. The differences were thought to be due to the differences in the local EMS and in the method of analysis.
The reported survival-to-discharge rates for OHCPA with NCE in the previous studies varied from 2.4% to 11.3%. ,,, Hess et al.  reported survival-to-discharge rates of 6.25% in cases of respiratory failure, 16.7% in PTE, 11.1% in overdose, 12.5% in non-traumatic bleeding, and 0% in sepsis, drowning and intracranial process. Our study showed similar rates of survival-to-hospital discharge: 11.1% in patients with PTE, 10.5% in asthma and acute worsening on COPD, 14.2% in airway obstruction, 11.4% in exposure to toxic substances and 6.3% in trauma. All studies including ours showed worse outcomes for OHCPA with NCE than for cardiac OHCPA or OHCPA showing VF as an initial rhythm.
CPR for OHCPA with NCE is sometimes regarded as futile, ,,, and OHCPA patients with NCE require complex and definite procedures other than standard CPR during resuscitation, such as tube drainage, keeping the airway open (for children), transfusion and various surgical procedures. Some authors reported that the outcomes of OHCPA with NCE are strongly related to the sequential performances of the EMS and hospital staff.  In some areas, it is recommended that a regionalization strategy including a high-volume OHCPA center and the securing of the safety of bypassing community hospitals should be devised. , However, these strategies are not always applicable in districts with different contexts and backgrounds.
At the start of CPR, it is not important to clarify the accurate etiology of OHCPA because this information would not lead to a change in treatment strategy. However, it is important to evaluate the etiology in order to perform the most proper advanced treatment for OHCPA patients, particularly for NCE. It is also important to determine the spectrum of etiologies from the viewpoint of public health and preventive medicine. Although the etiology of OHCPA is difficult to diagnose based on a patient's present status and clinical data in the ED, many authors have found that taking the patient's pre-arrest medical history is important for diagnosing their etiology and to improve the survival rate, and finding new independent quantitative variables is the next challenge. ,, In our ED, one medical doctor gathered information on the patient in as much detail as possible without directly treating the patient.  Accurately determining the etiology of OHCPA in every case is necessary for these feedback to ED staffs and their strategies. We should accurately evaluate the etiology of OHCPA patients with NCE and determine the proper treatment, a practice for which perimortem imaging is thought to be useful.
Postmortem imaging is emerging as an effective technique to augment forensic autopsy. Postmortem imaging has several forensic, legal, ethical, and medical problems. Applying medical intervention to a dead body after death certification is prohibited in some countries including Japan. Also, it has been found that there are many false-positive postmortem CT findings.  However, we were able to perform CT in 1062 OHCPA cases before death certification without legal problems, and this practice can easily demonstrate a variety of special pathological conditions which might be misdiagnosed without CT. This study showed that, of OHCPA cases without an obvious cause, 66.3% could be determined to be OHCPA with NCE using perimortem CT. Without perimortem CT, most of these cases would be diagnosed as cardiac OHCPA. Perimortem or postmortem imaging can more accurately determine the spectrum of etiologies of OHCPA. Some authors reported that postmortems were performed on from 31% to 44% of total cases, , that was lower than our rate.
The usefulness of postmortem CT for detecting the cause of OHCPA is still unclear because there is no standard method of evaluating its usefulness. Candidates for such a method include using the rate of cases in which the cause of OHCPA can be detected by postmortem CT; the rate of cases in which the cause of OHCPA was changed by postmortem CT from common clinical findings; and the rate of positive findings of postmortem CT as a fraction of total OHCPA cases, total OHCPA cases with NCE, cases that underwent postmortem CT or cases in which the cause of OHCPA was not detected via medical histories, clinical findings or common examinations other than postmortem CT.  Moreover, in different studies, the subjects were obtained from different sources, such as pathological departments and EDs. Postmortem CT is also thought to be useful to rule out specific pathological conditions among OHCPA cases with presumable cardiac etiology according to the Utstein method. This usefulness is difficult to describe and evaluate with a quantifiable and comparable method.
In this study, we demonstrated the conversion rate from cardiac etiology to NCE as a percentage of total OHCPA cases without obvious non-cardiac causes to be 14.6%, and the rate as a percentage of cases without obvious non-cardiac causes that underwent perimortem CT to be 22.1%. These data indicated the usefulness of perimortem CT for determining the treatment strategy for each victim and for accurately evaluating the spectrum of etiologies of OHCPA patients. However, we cannot compare these data with those from previous reports because the data in each report including ours were calculated and described using different methods. It is thought that the data should be described based on a standard evaluation method.
| Limitations|| |
The major limitations of this study are as follows. First, in some cases, we were not able to determine a final and conclusive etiology for OHCPA even if we could independently comprehend all pathological conditions because OHCPA is usually a very complex condition; for example, SAH and consequent coronary ischemia and airway obstruction followed by vomiting. There is always a possibility that the etiology of OHCPA is not SAH, even if a brain CT shows SAH. We can always indicate a lethal pathological condition which may be related to a patient's OHCPA. However, this study is meaningful for clarifying major etiologies of the patient with OHCPA.
Second, we perform perimortem CT for patients with OHCPA not only in order to detect or to neglect the cause of OHCPA but also to evaluate the life and neurological expectancy, particularly for patients who were successfully resuscitated. Third, we did not evaluate the usefulness of US in this study because the procedure of US for neck, neck vessels, chest, aortic arch, sign of AAD, and signs of PTE are not established and not standardized. Their accuracy for diagnosis is also not established. However, we performed US in all OHCPA patients. Fourth, the rate of OHCPA with NCE is dependent on the total number of subjects; it differs when computed as a percentage of all OHCPA patients including those with traumatic OHCPA, including those with obvious OHCPA with NCE, including those with non-sudden OHCPA, including non-resuscitated cases in the ED, etc. The EMS system in each district may treat different a spectrum of OHCPA. Thus, it is difficult to compare the rates among different reports.
| Conclusions|| |
We have demonstrated higher incidences of OHCPA with NCE (62.5%) than those reported previously based on the high performance rate of perimortem CT (57.5%). Of total OHCPA cases, the leading etiologies were AAD (8.07%), airway obstruction (7.64%), submersion (5.63%), hypoxia due to pneumonia (5.25%), CVD (4.48%), organ failure (2.01%), exposure to toxic substances (1.90%), hypoglycemia (1.84%), and PTE (1.46%). Perimortem CT can confirm the cause of OHCPA or rule out specific pathological conditions. The rates of cases converted from cardiac etiology to NCE that were confirmed as NCE by perimortem CT findings were 14.6% of cases without an obvious non-cardiac cause and 22.1% of cases that underwent perimortem CT.
| References|| |
|1.||Jacobs I, Nadkarni V, Bahr J, Berg RA, Billi JE, Bossaert L, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports: Update and simplification of the Utstein templates for resuscitation registries. A statement for healthcare professionals from a task force of the international liaison committee on resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Southern Africa). Resuscitation 2004;63:233-49. |
|2.||Moriwaki Y, Tahara Y, Arata S, Toyoda H, Iwashita M, Kosuge T, et al. Etiology of out-of-hospital cardiac arrest due to non-cardiac origin in Japan. Intensive Care Med 2009;35:S144. |
|3.||Moriwaki Y, Sugiyama M, Hayashi H, Mosiello G, Cremonese F, Altomani V, et al. Emergency medical service system in Yokohama, Japan. Ann Hosp S. Camillo Forlanini 2001;3:344-56. |
|4.||Moriwaki Y, Sugiyama M, Toyoda H, Kosuge T, Tahara Y, Suzuki N. Cardiopulmonary arrest on arrival due to penetrating trauma. Ann R Coll Surg Engl 2010;92:142-6. |
|5.||Moriwaki Y, Sugiyama M, Yamamoto T, Tahara Y, Toyoda H, Kosuge T, et al. Outcomes from prehospital cardiac arrest in blunt trauma patients. World J Surg 2011;35:34-42. |
|6.||Moriwaki Y, Sugiyama M, Tahara Y, Iwashita M, Kosuge T, Harunari N, et al. Complications of bystander cardiopulmonary resuscitation for unconscious patients without cardiopulmonary arrest. J Emerg Trauma Shock 2012;5:3-6. |
|7.||Pell JP, Sirel JM, Marsden AK, Ford I, Walker NL, Cobbe SM. Presentation, management, and outcome of out of hospital cardiopulmonary arrest: Comparison by underlying aetiology. Heart 2003;89:839-42. |
|8.||Kuisma M, Alaspää A. Out-of-hospital cardiac arrests of non-cardiac origin. Epidemiology and outcome. Eur Heart J 1997;18:1122-8. |
|9.||Engdahl J, Bång A, Karlson BW, Lindqvist J, Herlitz J. Characteristics and outcome among patients suffering from out of hospital cardiac arrest of non-cardiac aetiology. Resuscitation 2003;57:33-41. |
|10.||Pleskot M, Babu A, Kajzr J, Kvasnicka J, Stritecky J, Cermakova E, et al. Characteristics and short-term survival of individuals with out-of-hospital cardiac arrests in the East Bohemian region. Resuscitation 2006;68:209-20. |
|11.||Hess EP, Campbell RL, White RD. Epidemiology, trends, and outcome of out-of-hospital cardiac arrest of non-cardiac origin. Resuscitation 2007;72:200-6. |
|12.||Ro YS, Shin SD, Song KJ, Park CB, Lee EJ, Ahn KO, et al. A comparison of outcomes of out-of-hospital cardiac arrest with non-cardiac etiology between emergency departments with low- and high-resuscitation case volume. Resuscitation 2012;83:855-61. |
|13.||Yoshida T, Nakao H, Itagaki Y, Kato T, Kawashima T, Ishii N, et al. Actual situation regarding cardiac etiology determined by clinical diagnosis of and medical examiner's postmortem findings on witnessed out-of-hospital cardiac arrest cases. Kobe J Med Sci 2011;57:E17-25. |
|14.||Bunch TJ, White RD, Friedman PA, Kottke TE, Wu LA, Packer DL. Trends in treated ventricular fibrillation out-of-hospital cardiac arrest: A 17-year population-based study. Heart Rhythm 2004;1:255-9. |
|15.||Raitt MH. Have increasing rates of defibrillator implantation reduced the incidence of out-of-hospital cardiac arrest? Heart Rhythm 2004;1:260-1. |
|16.||Stockinger ZT, McSwain NE Jr. Additional evidence in support of withholding or terminating cardiopulmonary resuscitation for trauma patients in the field. J Am Coll Surg 2004;198:227-31. |
|17.||Cera SM, Mostafa G, Sing RF, Sarafin JL, Matthews BD, Heniford BT. Physiologic predictors of survival in post-traumatic arrest. Am Surg 2003;69:140-4. |
|18.||Nichol G, Aufderheide TP, Eigel B, Neumar RW, Lurie KG, Bufalino VJ, et al. Regional systems of care for out-of-hospital cardiac arrest: A policy statement from the American Heart Association. Circulation 2010;121:709-29. |
|19.||Martin-Gill C, Dilger CP, Guyette FX, Rittenberger JC, Callaway CW. Regional impact of cardiac arrest center criteria on out-of-hospital transportation practices. Prehosp Emerg Care 2011;15:381-7. |
|20.||Aurore A, Jabre P, Liot P, Margenet A, Lecarpentier E, Combes X. Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients. Eur J Emerg Med 2011;18:73-6. |
|21.||Kürkciyan I, Meron G, Behringer W, Sterz F, Berzlanovich A, Domanovits H, et al. Accuracy and impact of presumed cause in patients with cardiac arrest. Circulation 1998;98:766-71. |
|22.||Charlier P, Carlier R, Roffi F, Ezra J, Chaillot PF, Duchat F, et al. Postmortem abdominal CT: Assessing normal cadaveric modifications and pathological processes. Eur J Radiol 2012;81:639-47. |
|23.||Iwase H, Yajima D, Hayakawa M, Yamamoto S, Motani H, Sakuma A, et al. Evaluation of computed tomography as a screening test for death inquest. J Forensic Sci 2010;55:1509-15. |
Critical Care and Emergency Center, Yokohama City University Medical Center, 4-57 Urafune-cho, Minami-ku, Yokohama
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]