Cerebral oximetry and cerebral blood flow monitoring in 2 pediatric ...

20 downloads 2515 Views 821KB Size Report
In pediatric out-of-hospital cardiac arrest (POHCA), cardiovascular monitoring tools have improved resuscitative endeavors and cardio- vascular outcomes but ...
American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

Contents lists available at ScienceDirect

American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem

Case Report

Cerebral oximetry and cerebral blood flow monitoring in 2 pediatric survivors with out-of-hospital cardiac arrest☆ Abstract In pediatric out-of-hospital cardiac arrest (POHCA), cardiovascular monitoring tools have improved resuscitative endeavors and cardiovascular outcomes but with still poor neurologic outcomes. Regarding cardiac arrest in patients with congenital heart disease during surgery, the application of cerebral oximetry with blood volume index (BVI) during the resuscitation has shown significant results and prognostic significance. We present 2 POHCA patients who had cerebral oximetry with BVI monitoring during their arrest and postarrest phase in the emergency department and its potential prognostic aspect. Basic procedures include left and right cerebral oximetry with BVI monitoring at every 5-second interval during cardiac arrest, resuscitation, and postarrest in 2 POHCA patients in the pediatric emergency department. Regional cerebral tissue oxygen saturation (rSO2) with BVI readings in these 2 POHCA survivors demonstrated interesting cerebral physiology, blood flow, and potential prognostic outcome. In 1 patient, the reference range of cerebral rSO2 with positive blood flow during arrest and postarrest phases consistently occurred. This neurologic monitoring had its significance when the resuscitation effectiveness was used and end-tidal CO2 changes were lost. The other patient's cerebral rSO2 with simultaneous BVI readings and trending showed the effectiveness of the emergency medical services (EMS) resuscitation. Cerebral oximetry with cerebral blood flow index monitoring in these POHCA survivors demonstrates compelling periarrest and postarrest cerebral physiology information and prognostication. Cerebral oximetry with cerebral BVI monitoring during these arrest phases has potential as a neurologic monitor for the resuscitative intervention's effectiveness and its possible neurologic prognostic application in the pediatric OCHA patients. Thousands of children experience pediatric out-of-hospital cardiac arrest (POHCA) each year in North America, with high mortality and poor functional outcome for those who survive [1,2]. Currently, the measurement of end-tidal CO2 (ETCO2) is the best resuscitative tool that prehospital and emergency department providers have for hemodynamic monitoring in cardiac arrest (CA) and post-CA patients [3-5]. Compelling studies have shown that ETCO2 monitoring should be used for continuation of resuscitative interventions and prognostication during the patient's arrest and postarrest states [3-5]. This noninvasive monitoring parameter represents the global state of the cardiovascular physiology but not the neurologic physiology [5-7]. The brain is the most susceptible internal organ to ischemic events, and global cerebral ischemia is closely associated with poor outcome ☆ The authors have no conflicts of interest to disclose.

0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.

of POHCA [5-7]. One of the major hurdles in improving the quality of CA resuscitation has been the lack of a real-time noninvasive cerebral physiology monitoring system in the emergency department for the POHCA patients [6,7]. Cerebral oximetry by a near-infrared spectroscopy device (INVOS, Somanetics, Troy, MI) is a regional tissue monitoring technique that assesses and trends the regional cerebral tissue oxygen saturation (rSO2) [8-11]. These cerebral rSO2 readings are reflective of tissue physiology, tissue oxygen levels, blood flow, oxygen extraction, and other underlying variables in the brain [8-13]. In comparison, the pulse oximetry readings reflect the relative pulsating oxygenated hemoglobin in the arteries. The pulse oximetry can also detect the relative changes in arterial blood volume by detecting changes in oxygenated hemoglobin representing the trending of the regional perfusion. The INVOS NIR cerebral oximetry machine has this similar capability of detecting and trending the regional tissue blood flow and volume changes expressed as blood volume index (BVI) [14-18]. The relative rSO2 with BVI measured by the NIR INVOS 5100v during cardiovascular surgery has been shown to predict blood flow and postoperative ischemia-related cerebral injury [14-16]. The BVI is a number displayed from −50 to +50 [14-18]. The −50 value is set by internal calibration by the monitor at startup before patient measurement [14-18]. This signal strength is proportional to the total hemoglobin passing through the light path; if the BVI number is negative, there is a very little blood flow, and if it is positive, the blood flow increases [14-18]. If the hemoglobin concentration is not changing, this signal strength should be proportional to the cerebral blood volume in the light path, giving rise to the designation cerebral blood volume index [14-18]. During CA and resuscitative phase, better end points are needed to guide cardiovascular and cerebral resuscitation efforts and to determine when to stop resuscitation [6,7]. Near-infrared spectroscopy has been evaluated in a wide range of neonatal and pediatric conditions and has been demonstrated to be especially useful in patients who are in cardiopulmonary compromise or near arrest [19-26]. Near-infrared spectroscopy has been used in adult resuscitations as a predictor for survival and poor neurologic outcome. A 15% rcSO2 readings represents 25% of oxygen that is irreversibly bound to Hgb in the tissue vascular bed and no tissue metabolism [4,12,13]. A 95% rSO2 (%O2HgB) is interpreted as increased perfusion or pool oxygenated hemoglobin with little or no oxygen tissue extraction [12,13,19,21-23]. Although this technology has been validated and used extensively as a tool for cerebral perfusion monitoring in many clinical scenarios, to date, there have been very limited studies or reported cases using cerebral oximetry during adult CA and none in pediatrics [8-11]. Preliminary adult out-of-hospital studies have indicated that a low cerebral rSO2 may predict poor outcomes and may have a role in correlating with OHCA patients' outcomes [19-26].

394.e6

T. Abramo et al. / American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

In the prehospital and the emergency department, the criteria for continuation of resuscitative measures are limited and driven by the health care provider' experience. The various resuscitative courses give limited information on continuation of resuscitative interventions in the pediatric arrest and postarrest patients [1-5]. We would like to present 2 POHCA patients with standard prehospital and emergency department resuscitation interventions and monitoring who also had cerebral oximetry monitoring upon presentation to the pediatric emergency department (PED). The patient in case 1 was monitored during his continued CA and postarrest period in the PED. The patient in case 2 was monitored during her postarrest period in the PED. In the first POHCA patient, the ETCO2 readings were unrecoverable because of pulmonary hemorrhage, and using the ETCO2 readings, the criteria for continuation and/or cessation were not possible. The patient's cerebral oximetry and BVI readings presented compelling information about the patient's cerebral physiology, which facilitated the clinical decision for continuation of resuscitative arrest interventions. The second POHCA patient's cerebral oximetry and BVI readings in the PED, besides the current postarrest criteria, demonstrated the effectiveness of the EMS intervention for this patient. We would like to present 2 POHCA survivors with their cerebral oximetry and BVI readings, cerebral physiology, and the potential of cerebral oximetry with blood flow monitoring during arrest and postarrest phases in the PED. These 2 cases also present the potential prognostic outcome relevance of using cerebral oximetry with blood flow monitoring system in POHCA patients and warrant further detailed investigation. The patient in case 1 is a 15-year-old boy with no medical history who presented with CA. The patient's medical, surgical, family, and social histories were all noncontributory to his current presentation. He had been complaining of intermittent headaches for the past several months but had otherwise been healthy, and as per family, he had no other complaints recently. He was at the church when he was noted to have a syncope-like event where he went from a sitting position to a standing position and collapsed. He was found lying on the floor when a nurse in the crowd examined him. A femoral pulse could not be palpated, and bystander cardiopulmonary resuscitation (CPR) was immediately initiated. Ten minutes of bystander CPR was performed before EMS arrived at the church. The patient was still noted to be pulseless and was found to have a rhythm consistent with ventricular fibrillation. The patient was under the care of EMS for 15 minutes and was defibrillated 3 times over this duration. Cardiopulmonary resuscitation was continued during this time. The patient received a total of 3 mg intravenous (IV) epinephrine per advance cardiac life support protocol. His rhythm continued to be ventricular fibrillation, and he was undergoing chest compressions on arrival to the PED. On arrival to the PED, the patient was undergoing chest compressions. Cerebral oximetry probes were placed on the patient's left and right foreheads, with cerebral rSO2 and BVI readings recorded every 5 seconds (Fig. 1A [14-year-old rSO2 and ETCO2 and Fig. 1B [14year-old BVI and ETCO2]). He had a Glasgow Coma Scale score of 3 and had agonal respirations on arrival. Pupils were 4 mm and unreactive on arrival, and a definitive airway was not in place. Chest compressions were continued with good correlation with ETCO2 reading of 30 to 59 mm Hg. Ventricular fibrillation was confirmed on the monitor, and he was defibrillated twice with 200 J. The patient received a total of 2 mg of epinephrine. He was loaded with 300 mg amiodarone. A 7-0 endotracheal tube was placed without any difficulty on first-pass attempt without any drugs. There was blood noted in his posterior oropharynx during the intubation attempt. After 6 minutes of resuscitation, the patient was noted to be in pulseless electrical activity. He received 1 mg epinephrine, sodium bicarbonate, insulin, and glucose and 4 minutes of additional CPR, after which he was noted to have a palpable femoral pulse and a wide complex tachycardia on the monitor. He went into a PEA rhythm after

2 minutes of this rhythm. He was in PEA for 3 minutes before a wide complex tachycardia was noted after he received 1 mg epinephrine. He went into a PEA rhythm again after 4 minutes. He was started on an epinephrine drip at 0.1 μg/kg per minute and received 2 additional doses of 1 mg epinephrine before return of spontaneous systemic circulation was attained after 4 minutes. He received one more round of sodium bicarbonate, insulin, and glucose in addition to calcium chloride. During this period, there was always good correlation with chest compression and ETCO2 readings. The patient's EMS and PED total ventricular fibrillation time was 31 minutes, and the total PEA time was 11 minutes. After 30 to 40 minutes into the resuscitation, the respiratory therapy noticed difficulty with bagging the patient. After this occurrence, the patients developed large amounts of blood coming up the ETT. A positive end-expiratory pressure of approximately 20 cm H2O was required to ventilate the patient effectively. The effectiveness of correlating chest compression and perfusion to the ETCO2 reading was lost. During this period, the cerebral rSO2 readings were 50% to 60% for both the right and left cerebrum. The patient was cooled using external ice packs to 34°C. The patient received IV methylprednisolone, IV vancomycin, IV Zosyn, and fresh frozen plasma prior to transfer to the intensive care unit (ICU). The patient was cooled with ice packs after ROSC. A computed tomography of his head, C-spine, and face was obtained en route to the ICU and was found to have normal findings. In the ICU, he required significant vasopressor support early in his clinical course. He was on epinephrine, dopamine, and vasopressin drips for the first 48 hours to maintain a mean arterial pressure greater than 70. He was then placed on milrinone for the next 48 hours. During this time, he developed nonoliguric renal failure and subsequently developed hypertension, which was thought to be due to decreased renal perfusion from acute tubular necrosis. He required a nicardipine drip and clonidine patch for blood pressure control. He underwent hemodialysis on hospital days 7, 8, and 12, which decreased his antihypertensive needs. On admission, he required a high-frequency oscillatory ventilator for 3 days, after which he was transitioned to a conventional ventilator. He was extubated to room air on hospital day 11. From a neurologic perspective, by the end of hospital day 1, he was awakening to voice, blinking to questions, and appeared to comprehend basic instructions. He had continued improvement in his mental status after hemodialysis and would open eyes to command consistently on hospital day 8. He was extubated on hospital day 11 and had ICU delirium for the next week. His first cognitive evaluation showed that he had mild-moderate cognitive-communication deficits consistent with a Rancho VII score (automatic and appropriate) on hospital day 16, which improved to a Rancho VIII score (highest score possible, purposeful and appropriate) by day 22. He was discharged on hospital day 24 and was fully ambulatory, performing all his activities of daily living and asking whether he could start playing basketball. A cognitive assessment performed 2 weeks after discharge showed mild-moderate inefficiencies in memory and new learning. The patient in case 2 is a 14-year-old girl who presented to an outside emergency department after an incident that occurred while she was playing in a softball game. She hit a triple and was rounding third base when she raised her hands to celebrate and suddenly collapsed without warning. Her father, the third base coach, reported that she demonstrated shaking movements. Her grandfather, a CPR instructor, could not feel a pulse and initiated CPR. Cardiopulmonary resuscitation continued for 7 to 10 minutes until EMS arrival. Per EMS, the patient was in asystole and apneic when they arrived. Cardiopulmonary resuscitation was continued by EMS, and 2 minutes after EMS arrival, the patient was intubated without complications. An IV dose of 1 mg of 1:10 000 epinephrine was administered 3 minutes after EMS arrival. At the next rhythm check, the patient was noted to be in ventricular fibrillation, and she received a shock at 120 J. She received

T. Abramo et al. / American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

394.e7

Fig. 1. The patient's graph of cerebral oximetry left and right rcSO2 and left and right BVI, heart rate, and ETCO2.

another 1-mg dose of epinephrine 8 minutes after EMS arrival and was given a 300-mg bolus of amiodarone 9 minutes after EMS arrival. At the next rhythm check, the patient was in ventricular tachycardia with a pulse and spontaneous respirations. The patient's rhythm transitioned to sinus tachycardia with pulses and occasional premature ventricular contractions. She was transported in a stable condition to Vanderbilt Children's Hospital. Total estimated CPR time was 16 to 19 minutes. She had no family history of congenital heart disease, sudden cardiac death, arrhythmias, or unexplained childhood deaths. The patient's PED course upon arrival is as follows: she had a confirmed airway and was in sinus tachycardia. Cerebral oximetry probes were placed on the patient's left and right foreheads with cerebral rSO2 and BVI readings recorded every 5 seconds (Fig. 2). She

was given an normal saline bolus for initial blood pressure of 80/40 mm Hg. An electrocardiogram was performed, which showed slightly prolonged corrected QT interval (493 milliseconds). The patient was cooled using external ice packs to 33°C. A bedside echo was performed by a cardiologist that demonstrated globally depressed biventricular function, and a milrinone infusion was started. Owing to brief oxygen desaturations to the 70s and a large leak, the patient's size of 5.5 ETT was exchanged for a 6.5 ETT without complications. The patient's hospital course is as follows: the patient was admitted to the pediatric ICU and kept on a cooling protocol for 24 hours. Her milrinone infusion was gradually weaned because serial echocardiograms demonstrated improved function. She was extubated to room air on hospital day 3. She was transferred to the floor and underwent further cardiac testing including serial electrocardiograms, cardiac

394.e8

T. Abramo et al. / American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

Fig. 2. The patient's graph of cerebral oximetry left and right rcSO2 and left and right BVI.

magnetic resonance imaging, exercise stress test, and electrophysiology study, none of which conclusively diagnosed the etiology of her CA. An internal cardiac defibrillator was placed on hospital day 12, and the patient was discharged home on hospital day 13. Both of these patients survived their POHCA and were discharge home with an excellent to very good neurologic state. With these 2 patients, we have demonstrated interesting cerebral rSO2 and BVI readings during their pediatric CA, resuscitation, and post-CA state in the PED. In case 1, the initial and subsequent rSO2 readings during resuscitation were consistently within the normal pediatric range (50%-70%) for regional cerebral tissue oxygenation and compelling cerebral blood flow dynamics during the CA, chest compression, unstable cardiovascular system, and through pharmacologic support. There were consistent normal rSO2 readings despite the poor cardiovascular system, but effective chest compression and airway management. Because the ETCO2 readings were lost due to pulmonary hemorrhage and the use of these accepted criteria for the effectiveness and prognosis of resuscitation became unavailable, the use of cerebral oximetry readings became the clinical decision tree beside the cardiovascular system for continuation of resuscitative interventions in the PED. Case 2 demonstrated the effectiveness of the EMS resuscitative interventions and the postarrest interventions for this patient. Also, these 2 cases demonstrate the effectiveness of CA resuscitative interventions on cerebral physiology and the potential prognostic outcome relevance of cerebral oximetry rSO2, along with cerebral BVI readings in POHCA. These 2 pediatric cases present compelling evidence for further research in the use of cerebral oximetry along with cerebral BVI during adult and pediatric in-house and out-of-house CA. The improvement in the management of pediatric CA and their successful resuscitation can be attributed to the quality of CPR resuscitation efforts of prehospital care or in-hospital (“no flow” and “low flow” durations) [1-7]. There are no specific clinical signs or global monitoring tools that can predict the patient's short- or longterm outcome [5-7]. In adult and pediatric arrest patient, the ETCO2 changes from baseline to 10 minutes or significant ETCO2 changes with effective chest compression can predict the ROSC and possible outcome [4-6]. Measurement of ETCO2 is currently perceived as the best tool that prehospital and emergency department providers have

for the monitoring of hemodynamics in peri- and post-CA patients in an out-of-hospital setting [4-6]. This parameter does not assess real time the cardiocerebral resuscitation efforts, cerebral perfusion, cerebral oxygen delivery, or the patient's neurologic outcome. The human brain is a highly aerobic organ with limited energy stores, making neuronal activity and energy metabolism dependent on constant oxygen and glucose delivery, which makes it more susceptible to ischemic events and global cerebral ischemia and is closely associated with poor outcome of patients with OHCA [5-7]. Global cerebral ischemia due to CA results in an acute drop of oxygen delivery to the brain [12-17]. Although minimal blood flow may persist for some minutes, tissue oxygen is rapidly metabolized and anaerobic glycolysis ensues [12-17]. Because the brain has a high metabolic rate of oxygen without having large oxygen stores, critical desaturations occur quickly and tissue saturation plummets asymptotically until all available oxygen is consumed. Acute cessation of global oxygen delivery during CA is associated with an exponential drop in cerebral tissue oxygen. The degree of cerebral tissue desaturation depends on the oxygen level before CA, and the duration of CA depends on hematocrit, brain tissue pH, and brain temperature. Impaired oxygen supply to the brain as well as enhanced oxygen consumption due to hyperthermia may cause secondary injury to the brain in this critical phase. The impact of these factors may go unnoticed [7,12-17]. In patients resuscitated from CA, neurologic outcome depends on the duration of ischemia and the restoration of systemic circulation and oxygenation [7,13-18]. To avoid additional detrimental effects of cerebral hypoperfusion and maximize the potential beneficial effect of induced hypothermia in the post-CA patient, it is necessary to detect episodes of cerebral hypoxia or inadequacy of cerebral perfusion [7,18-26]. Unfortunately, many of these CA patients may have inadequate cerebral regional tissue oxygen delivery, extraction, and altered metabolism despite apparent adequate systemic perfusion parameters, especially during arrest, resuscitation, and post-CA syndrome [1,2,7]. Traditional methods of identifying these patients with the adequacy of CPR resuscitative efforts carry inherent flaws and currently cannot assess the inadequacy of cerebral tissue resuscitation [1,2,5,7,18-22]. Patients who are perceived to be fully resuscitated, when resuscitation is directed by global methods alone, may have markedly significant cerebral tissue hypoxia and go undetected by the health care provider.

T. Abramo et al. / American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

Cardiocerebral resuscitation is crucially important in patients with OHCA or in-hospital CA (IHCA) [1,2,5,7,18-21]. There is no established real-time indicator of cerebral perfusion or metabolic demands during the periarrest and postarrest in neonatal or pediatric arrest. The primary objective for the arrest and or post-CA syndrome patients is to obtain survival with no or little neurologic sequels [1,2,5,7]. By influencing the vital and functional prognosis of patients, cerebral protection is now an essential part of the management of patient undergoing CA [5-7,23-26]. Cerebral oximetry has potential to aid in the early detections and possibly preventions of these cerebral hypoxia or to decrease cerebral perfusion times resulting in improved neurologic outcomes, as demonstrated in these 2 cases. Cerebral oximetry may further aid in the prognostication of individual outcome during CPR and also after ROSC and could track the quality of cerebral reperfusion and reoxygenation and the degree of dysfunction of the cerebral autoregulation [21-26]. Brain protection therapy for patients with OHCA has greatly improved in recent years owing to the development of emergency post-CA interventions, for example, mild therapeutic hypothermia and extracorporeal CPR in pediatrics [1,2,5,7]. These interventions are extremely burdensome and costly, especially when the patient outcome is unknown. However, defined criteria for these POHCA patients with outcome indicators for these costly interventions have not yet been established in adults or in pediatrics mainly because of difficulty in prognosticating neurologic outcomes at hospital discharge [5,7]. Currently, there are limited prognostic indicators for OHCA patients on whether or not highly intensive continuation for post-CA interventions should be performed [1,2,5,7]. An adult and pediatric OHCA patient's prognostic index that can be used immediately upon emergency department arrival is needed to determine posttreatment strategies. Many studies have identified factors associated with poor functional outcome after resuscitation; no study has shown a reliable predictor of neurologic outcomes [15,7,19-26]. Previous cerebral oximetry reports have described that inadequate intraoperative cerebral rSO2 readings and trending are a significant predictor of postoperative neurologic complications after cardiovascular surgery [11,15-17,21-26]. Cerebral rSO2 does not require vascular pulsation and can measure rSO2, even in patients with hypotension, hypothermia, and/or circulatory arrest. In small arrest cerebral oximetry studies, these cerebral rSO2 readings appear to decrease prior to loss of pulses and appear to be a rapid increase in rSO2 with ROSC [21-26]. In these adult studies, there appears to be a constant level of rSO2 in those patients who did not experience rearrest [21-26]. This suggests that decreases in rSO2 may be specific to hemodynamic instability and used as a marker for the need of additional interventions that may prevent rearrest, such as aggressive blood pressure management, because catecholamines administered during the CA wear off [21-26]. Cerebral oximetry major use and focus has been in the anesthesia, ICU, and cardiac intensive unit realm [8-10]. The application outside these arenas has been limited by certain misconceptions by the health care providers about the technology, interpretation of the readings, and trending, along with its clinical applications. Part of the difficulty in demonstrating the value of a monitoring device is that monitoring results can prompt a variety of interpretations and clinical responses. If a monitor is used without a concomitant understanding of the interplay of what the monitoring is detecting and trending, along with the interpretation of the interplay of the local area sampling and global physiology, then it is likely to be easily misinterpreted. Health care providers tend to focus more on the immediate and absolute values vs interpreting all the parameters producing the readings and trending. Although the pulse oximetry and/or capnography readings can serve as an adjunct tool for the patient's ventilator management, it is the health care provider's critical thinking of the monitor's results that drives the ventilator management strategy and not solely the pulse oximetry and/or capnography that drives interventions and

394.e9

impacts patient outcome. This concept must be retained when using cerebral oximetry in any clinical situation. In adult CA studies, use of cerebral oximetry has been demonstrated to have potential for optimizing cerebral perfusion during CPR to predict neurologic outcomes at hospital discharge in patients with OHCA and IHCA [21-26]. Measuring cerebral tissue oximetry using a cerebral oximetry has a potential role in assisting the prehospital and emergency department providers in the neurologically monitoring of the periarrest and postarrest for OHCA and IHCA patients [21-26]. The ability for early detection of cerebral hypoxia/ischemia and cerebral hemodynamic instability could be used to proactively prevent neurologic deterioration and contribute to a better neuroprotective approach producing improved patient neurologic outcomes [21-26]. Future detailed research is needed to determine the full capabilities of cerebral oximetry and cerebral BVI in OHCA and IHCA and how this technology could be combined with clinical practice to improve outcomes in the vulnerable peri- and post-CA adult and pediatric patient population. These 2 POHCA survivors' cerebral oximetry with BVI use presents interesting POHCA cerebral physiology information, prognostic appeal, and, potentially, a new adjunct resuscitation monitoring tool that needs further detail research. Cerebral oximetry along with cerebral BVI monitoring during periarrest and postarrest has potential to be a noninvasive neurologic monitor for the effectiveness of the resuscitative interventions and a possible prognostic neurologic indicator for further interventions for the adult and pediatric OHCA patients. Thomas Abramo MD Department of Pediatrics Division of Pediatric Emergency Medicine Vanderbilt University School of Medicine Nashville, TN Nitin Aggarwal MD Department of Emergency Medicine Vanderbilt University Nashville, TN Ian Kane MD Kristen Crossman MD Division of Pediatric Emergency Medicine Department of Pediatrics, Vanderbilt University Nashville, TN Mark Meredith MD 1 Department of Pediatrics Division of Pediatric Emergency Medicine Vanderbilt University School of Medicine Nashville, TN http://dx.doi.org/10.1016/j.ajem.2013.10.039 1

Current affiliation: Emergency Services LaBonheur Children's Hospital, Memphis, TN.

References [1] Moler FW, Meert K, Donaldson AE, et al. Pediatric Emergency Care Applied Research Network. In-hospital versus out-of-hospital pediatric cardiac arrest: a multicenter cohort study. Crit Care Med 2009;37:2259–67. [2] Nolan JP, Neumar RW, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication: a scientific statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (part II). Int Emerg Nurs 2010;18:8–28. [3] Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care 2001;10:391–8.

394.e10

T. Abramo et al. / American Journal of Emergency Medicine 32 (2014) 394.e5–394.e10

[4] Kolar M, Krizmaric M, Klemen P, et al. Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care 2008;12:R115. [5] Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122: S729–67. [6] Atkins DL, Everson-Stewart S, Sears GK, et al. Epidemiology and outcomes from out-of-hospital cardiac arrest in children: the Resuscitation Outcomes Consortium Epistry-Cardiac Arrest. Circulation 2009;119:1484–91. [7] Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation 2008;118:2452–83. [8] Scheeren TW, Schober P, Schwarte LA. Monitoring tissue oxygenation by near infrared spectroscopy (NIRS): background and current applications. J Clin Monit Comput 2012. [9] Murkin JM, Arango M. Near-infrared spectroscopy as an index of brain and tissue oxygenation. Br J Anaesth 2009;103:i3–i13. [10] Scheeren TW, Schober P, Schwarte LA. Monitoring tissue oxygenation by near infrared spectroscopy (NIRS): background and current applications. J Clin Monit Comput 2012;26:279–87. [11] Moerman A, Vandenplas G, Bove´ T, et al. Relation between mixed venous oxygen saturation and cerebral oxygen saturation measured by absolute and relative near-infrared spectroscopy during off-pump coronary artery bypass grafting. Br J Anaesth 2013;110(2):258–65. [12] Schwartz G, Litscher G, Kleinert R. Cerebral oximetry in dead subjects. J Neurosurg Anesthesiol 1996;8:189–93. [13] Figaji AA, Kent SJ. Brain tissue oxygenation in children diagnosed with brain death. Neurocrit Care 2010;12:56–61. [14] Andropoulos D, Stayer S, McKenzie D, et al. Regional low-flow perfusion provides comparable blood flow and oxygenation to both cerebral hemispheres during neonatal aortic arch reconstruction. J Thorac Cardiovasc Surg 2003;126(6): 1712–7.

[15] Pigula FA, Nemoto EM, Griffith BP, et al. Regional low-flow perfusion provides cerebral circulatory support during neonatal aortic arch reconstruction. J Thorac Cardiovasc Surg 2000;119:331–9. [16] Brady K, Joshi B, Zweifel C, et al. Real-time continuous monitoring of cerebral blood flow autoregulation using near-infrared spectroscopy in patients undergoing cardiopulmonary bypass. Stroke 2010;41:1951–6. [17] Jaeger M, Soehle M, Schuhmann MU, et al. Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen. Acta Neurochir (Wien) 2005;147:51–6. [18] Roberts IG, Fallon P, Kirkham FJ, et al. Measurement of cerebral blood flow during cardiopulmonary bypass with near infrared spectroscopy. J Thorac Cardiovasc Surg 1998;115:94–102. [19] Ito N, Nanto S, Nagoa K. Regional cerebral oxygen saturation on hospital arrival is a potential novel predictor of neurological outcomes at hospital discharge in patients with out-of-hospital cardiac arrest. Resuscitation 2012;83:46–50. [20] Lemiale V, Huet O, Vigue B. Changes in cerebral blood flow and oxygen extraction during post–resuscitation syndrome. Resuscitation 2008;76:17–24. [21] Nagdyman N, Fleck TPK, Ewert P, et al. Cerebral oxygenation measured by nearinfrared spectroscopy during circulatory arrest and cardiopulmonary resuscitation. Br J Anaesth 2003;91:438–42. [22] Parnia S, Nasir A, Shah C, et al. A feasibility study evaluating the role of cerebral oximetry in predicting return of spontaneous circulation in cardiac arrest. Resuscitation 2012;83:982–5. [23] Mayr PN, Martin K, Hausleiter J, et al. Measuring cerebral oxygenation helps optimizing post–resuscitation therapy. Resuscitation 2011;82:1110–1. [24] Suffoletto B, Kristan J, Rittenberger JC, et al. Near-infrared spectroscopy in post– cardiac arrest patients undergoing therapeutic hypothermia. Resuscitation 2012;83:986–90. [25] Paarmann H, Heringlake M, Sier H, Schön J. The association of non-invasive cerebral and mixed venous oxygen saturation during cardiopulmonary resuscitation. Interact Cardiovasc Thorac Surg 2010;11:371–3. [26] Nemoto EM, Yonas H, Kassam A. Clinical experience with cerebral oximetry in stroke and cardiac arrest. Crit Care Med 2000;28:1052–4.