American Journal of Emergency Medicine xxx (2014) xxx–xxx

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Case Report

Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients☆ ,☆☆ ,★ Abstract Pediatric cerebrospinal fluid shunt malfunctions can present with varying complaints. The primary cause is elevated intracranial pressure (ICP). Malfunctioning sites are the proximal or distal sites [1-4]. A rare presenting complaint is cardiac arrest. Immediate ICP reduction is the only reversible option for this type of cardiac arrest. Cerebral oximetry (rcSO2) with blood volume index (BVI) has been used in pediatrics especially in shunt malfunction (Table). Review of 14 shunt malfunction shunts patients: 13 in cardiac arrest and one with severe bradycardia with rcSO2 with BVI. Age: 5.56 SD + 3.4 years; 63% males, 34.8°C SD + 1.9 years; during cardiac arrest: end-tidal CO2, 25.7 SD + 5.6 mmHg; and postcardiac arrest: end-tidal CO2, 37.5 SD + 3.6 mm Hg. Cardiac arrest duration: distal, 32.16 SD + 9.3 minutes; proximal, 59.9 SD + 15.35 minutes. Pediatric malfunctioning cerebrospinal fluid (CSF) shunts in cardiac arrest are resistant to routine resuscitation and 3% hypertonic saline (HTS) therapy. Cerebral physiology improved, and cardiac arrest resolved with intracranial pressure (ICP) reduction. This was achieved via shunt tap in distal shunt malfunction or via external ventricular drain (EVD) in proximal shunt malfunction. Cerebral oximetry (rcSO2) and BVI changes occurred before cardiac arrest resolution. In these patients, rcSO2 with BVI can detect cerebral physiology changes during cardiac arrest, ICP reduction, arrest resolution, and postarrest. Cerebral oximetry with BVI has shown its usefulness in malfunctioning CSF shunts causing cardiac arrest. Ventricular shunt failure is common with CSF shunt failure rate at 39%, 1 year and 53%, 2 years after initial shunt placement [1-3]. During episodes of shunt malfunction, increased ICP results in changes in brain tissue perfusion, metabolism, and oxygen extraction. Pediatric patients with malfunctioning shunts can present with varying complaints and symptoms. Headache, nausea and/or vomiting, lethargy, and irritability are all common presenting symptoms [1-4]. In developmentally challenged patients, these signs and symptoms can be subtle. In rare incidents, these patients can develop significantly increased ICP causing cardiovascular compromise and asystole. This occurrence is known to be a rare complication of ☆ Financial support: Somanetics Corporation (Boulder, CO) provided near-infrared spectroscopy (NIR) machines and limited number of NIR probes used in the study. Company representatives otherwise had no input into the design, execution, data analysis, or preparation of this manuscript. ☆☆ The authors have no conflicts of interest to disclose. ★ Thomas Abramo and Mark Meredith wrote the first draft of the manuscript, and no honorarium, grant, or other form of payment was given to anyone to produce the manuscript.

malfunctioning shunts and not commonly reported in the literature. However, pediatric emergency physicians, emergency medicine physicians, and neurosurgeons have known of its occurrence or have had personal patient experience. In these clinical scenarios resulting in cardiac arrest, the only therapeutic option for reversal of the cardiac arrest is to decrease the increased ICP by removal of CSF fluid through a shunt tap or other means of CSF diversion [4-11]. The assumption is that CSF removal will lead to a reduction in the increased ICP, thus reducing pressure on the brain stem, restoring the cardiovascular system, and restoring systole. To the emergency physician, this is only successful in distal shunt malfunctions, where fluid can be easily removed. In the proximal malfunctioning shunts, a shunt tap will produce little to no fluid removal therefore making restoring systole more problematic. The only therapeutic intervention for proximal malfunctioning shunt is by placement of an EVD, a difficult procedure for the untrained emergency physician [1-4]. Cerebral oximetry is not pulse dependent for reliable tissue monitoring [4,11]. 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) [4,11-18]. Cerebral oximetry detects tissue venous area’s oxyhemoglobin (O2Hgb) to deoxyhemoglobin (Hgb) ratio as expressed as rcSO2[4,11-19]. These rcSO2 readings are reflective of tissue physiology, tissue oxygen levels, blood flow, oxygen extraction, and other underlying variables in the brain [4,11-18]. In pediatric patients, the normal rcSO2 readings are 60% to 80% (O2Hgb) [4,11-13]. In pediatric shunt patients, their normal rcSO2 readings are patient specific and can range from 15% to 95% (O2Hgb), whereas in the malfunctioning state, they retain their unique rcSO2 readings [4,1418,20]. In our prior study, we have demonstrated relative rcSO2 readings in hydrocephalus subjects with malfunctioning ventricular shunts [4]. Shojima et al [5] investigated the reliability of cerebral near-infrared spectroscopy system (NIRS) monitoring in adult subjects with dilated ventricles without ventricular shunts with CSF removal by a lumbar drainage system. They demonstrated in malfunctioning shunt patients that cerebral blood oxygenation changes were recognized after CSF removal using cerebral NIRS monitoring [5]. We have demonstrated the effects of CSF shunt taps on distal compared with proximal malfunctioning shunts by the rcSO2 changes [4]. The degree of rcSO2 changes occurring from a shunt tap predicts either distal or proximal shunt malfunctions [4-8]. The rcSO2 with BVI measured by the NIRS INVOS 5100v during cardiovascular surgery has been shown to predict blood flow during cardiac arrest and postoperative ischemia-related cerebral injury [1118]. The INVOS NIR rcSO2 machine has capability of detecting and

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Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

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T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

Table Cerebral oximetry with BVI monitoring in malfunctioning CSF shunts by site, during cardiac arrest, and postcardiac arrest Malfunctioning site rcSO2 with BVI Cardiac arrest, n = 13 Distal, n = 5 Proximal, n = 8 Postarrest postintervention, n = 13 Distal: shunt taps, n = 5 Proximal: EVD, n = 8

Left rcSO2 Mean (15%-99%) 24.5% SD ± 2.7% 16.9% SD ± 5.7%

Right rcSO2 Mean (15%-99%) 16.5% SD ± 3.0 15.5% SD ± 5.9%

Left BVI Mean (−50-+50) −31.3 SD ± 10.1 −48.3 SD ± 10.1

Right BVI Mean (50-+50) −49.1 SD ± 6.3 −49.1 SD ± 7.3

60.4% SD ± 18.5% 67.3% SD ± 11.5%

52.3% SD ± 12.5% 62.5% SD ± 14.4%

+13.6 SD ± 16.1 +7.7 SD ± 17.8

−1.7 SD ± 24.2 −10.2 SD ± 21.2

trending the regional tissue blood flow expressed as BVI [15-18]. The BVI is a number displayed from − 50 to + 50 [12-18]. The − 50 value is set by internal calibration by the monitor at start-up before patient measurement [12-18]. This signal strength is proportional to the total hemoglobin level passing through the light path emitted on the tissue vascular bed [14-18]. If a negative BVI reading occurs, there is less Hgb flow through the tissue area then interpreted as very little blood tissue flow, and if there is a positive or increase in BVI reading, there is an increased Hgb flow in the tissue bed indicating increased tissue blood flow [14-18]. Cerebral oximetry is not pulse dependent for reliable tissue monitoring and can measure rcSO2, in patients with hypotension, hypothermia, and/or circulatory arrest [14-18,20,13,21-25]. Cerebral oximetry in cardiac arrest has shown its potential in the quality of cerebral and cardiac resuscitation in the adult and pediatric studies [20,13,21-25]. The brain has limited energy stores, dependent on constant oxygen and glucose delivery, which makes the brain more susceptible to tissue ischemic events and global cerebral ischemia [12-18,20-25]. Global cerebral ischemia due to cardiac arrest results in an acute drop of oxygen delivery to the brain as a result of limited tissue oxygen; a high metabolic demand and limited oxygen and glucose tissue desaturations occur promptly [7,20,13,21-25]. This acute decrease in global oxygen delivery during cardiac arrest is associated with significant drops in cerebral tissue oxygen rSO2 in the normal brain. In rcSO2 arrest studies, rcSO2 readings decrease before loss of pulses, and rcSO2 appear to increase before cardiac arrest resolution and return of spontaneous circulation (ROSC) in normal cerebral architecture and physiology [20,13,21-25]. Ahn et al [25] demonstrated that the mean rcSO2 measured during cardiac arrest was significantly higher in patients who achieved ROSC compared with no ROSC. In a limited pediatric case series with normal cerebral physiology and architecture, the rcSO2 and BVI changes during pediatric cardiac arrest and postcardiac arrest have been described [20]. In pediatric CSF shunt malfunction patients, rcSO2 studies have shown their unique abnormal cerebral physiology and very patientspecific left and right cerebral rcSO2 readings, which are the results of the patient’s varying degrees specific increased ICP as a result of their unique CSF shunt malfunction [4-12]. The utilization of rcSO2 with BVI in pediatric hydrocephalus patients with malfunctioning shunts as a result of severe increased ICP causing cardiac arrest or severe bradycardia has never been reported. We would like to present rcSO2 with BVI monitoring in a series of pediatric hydrocephalus patients in cardiac arrest or with severe bradycardia as a result of their significant malfunctioning shunts and during therapeutic interventions. We will show the potential utility of rcSO2 with BVI monitoring in detecting the cerebral physiology changes during treatment interventions in these arrested malfunctioning shunt patients, distal vs proximal. We present a retrospective case series from 2007 to 2013 of pediatric hydrocephalus patients with malfunctioning CSF shunts who presented to a pediatric emergency department (PED) (Vander-

bilt Children’s PED) (level one pediatric trauma center with annual 54 000 visits) and Arkansas Children’s PED (level one pediatric trauma center with annual 54 000 visits) in cardiac arrest or with severe bradycardia. Only CSF shunt patients in cardiac arrest or with severe bradycardia who had rcSO2 with BVI monitoring were selected for review and analysis (Diagram). Cerebral oximetry monitoring with BVI in the PED is a common noninvasive neurologic monitoring for neurologic emergencies (suspected malfunctioning CSF shunts, strokes, altered mental status, and seizures) and cardiac arrest. The patients were selected from the PED cardiac arrest database and PED census database cross-reference to recorded rcSO2 data files. Patients fulfilling the inclusion criteria had review of their emergency medical services (EMS) run sheet, PED electronic medical records, intubation records, code sheet, respiratory, and nursing documentation. The selected patients had their operative note reviewed for the type of CSF shunt malfunction, distal or proximal. These patients had rcSO2 with BVI monitoring by the INVOS 5100 (Somanetics) with left (rcSO2) and right (rcSO2) probes place on the forehead area and with readings every 5 second. This monitoring was begun within minutes of arrival to the PED, during resuscitation, and until departure to the operating room for surgical repair. All patients received airway stabilization, continuous cardiopulmonary resuscitation (CPR), masked inline endtidal CO2 (a mask attached to an End-Tidal CO2 (ETCO2)mainstream capnography and anesthesia bag), and medication administered per pediatric advance life support protocols. During every cardiac resuscitation, the patient had their CSF shunt reservoir tapped by the pediatric emergency medicine (PEM) attending or PEM fellow under the direct supervision by the PEM attending using a 23-gauge butterfly needle, extension tubing stopcock, and 10-mL syringe with aspirating. Ten milliliters or more of CSF was aspirated by puncturing the CSF shunt reservoir. All patients who had successful shunt taps had eventual externalization of their shunt in the PED. All patients with unsuccessful shunt taps underwent placement of an EVD by the neurosurgery residents. A retrospective PED chart review for patients with CSF shunt malfunction, cardiac arrest, or only severe bradycardia with rcSO2 and BVI monitoring. A total of 14 CSF shunt malfunction patients who presented in cardiac arrest or only severe bradycardia with cerebral and BVI monitoring fulfilled the inclusion criteria. Of the 14 patients fulfilling the inclusion criteria, there were 13 cardiac-arrested shunt malfunction patients, 5 distal and 8 proximal; and one proximal CSF shunt malfunction patient with no arrest, only severe bradycardia (heart rate of 30-40 beats per minute). The mean age was 5.56 SD + 3.4 years, and 63% were males. All patients had a CSF shunt for many years, and 75% of these patients had undergone prior shunt revisions (0-12 times). None of the patients had shunt revisions in the preceding 4 months. All 14 shunt malfunction patients had varying degrees of neurologic devastation and limited communicative ability per chart review. No patient had subjective or documented fever. The patients’ shunt malfunction complaints included increased sleeping (100%; 24-96 hours), headache (per parental

Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

description, 85%; 24-168 hours), vomiting (100%; 24 hours to 2 weeks), change in mental status (per parental description, 100%; 24 hours to 4 weeks), and increased seizure activity (64%; 8-36 hours). All had varying times from symptoms onset to presentations ranging from days to weeks. No patient had a prior cardiac arrest history related to a CSF shunt malfunction. Three patients had active seizures or a seizure-related occurrence during their shunt evaluation at the referral centers. Five patients were transported by EMS from home for complaints of headache (24 hours to 2 weeks duration), vomiting (24 hours to 2 weeks duration), and altered level of mental status (24-168 hours duration). Four of these patients developed cardiac arrest within a few minutes before arrival to the PED. These 4 EMS transported patients who went into cardiac arrest, had assisted ventilation with Bag Valve Mask, and no epinephrine given due to the short transport time from occurrence of cardiac arrest to arrival to the PED. The fifth patient developed bradycardia during EMS transport from home and within minutes of arrival to the PED developed cardiac arrest. No EMS intervention occurred for this patient. Nine patients were referred from outside emergency departments with clinical signs and symptoms highly suggestive of CSF malfunctioning shunts per referring emergency department physician: vomiting (100%; 24 hours to 1 week), altered mental status (100%; 24120 hours duration), increase or seizure activity (45%; 24-96 hours duration), and confirmed by computed tomographic (CT) scan. The average EMS transport time was 1.57 hours SD + 38 minutes. None were transport by pediatric specialty team. Eight of these patients developed bradycardia and then cardiac arrest within 10 minutes before arrival or upon arrival to the PED. Of these 8 patients who went into cardiac arrest, all 8 had assisted bag mask ventilation, 4 received epinephrine by intravenous, and none were intubated. One transferred patient developed severe bradycardia (heart rate, 30-50 beats per minutes; duration, 67 minutes) during EMS transport with no interventions, and the severe bradycardia continued in the PED. No EMS-transported patients received any treatment for the patient’s bradycardia or cardiac arrest indicating increased ICP: HTS, mannitol, or elevation of the patient’s head by the EMS crew. A total of 14 patients had CSF shunt malfunctions; 5 patients had distal, and 9 patients had proximal shunt malfunctions per their operative report. None of patients had a shunt infection based on CSF culture. All patients went to the operating room without CT scans or fast magnetic resonance imaging. Patient’s average hospital length of stay was 123 + 33 hours. All patients survived to discharge. It was difficult to discern the effects of the cardiac arrest on their neurologic state upon the patient’s discharge note due to their prior significant neurologic impairment and no documentation of parental assessment of their child’s neurologic state at discharge. Upon review of all the patients’ physicians hospital discharge summary, all patients were discerned to be back at their limited neurologic baseline upon discharge. All 14 patients had continuous rcSO2 with BVI monitoring within minutes of their PED arrival, during resuscitation, and until PED departure for the operating room. Fourteen patients had rcSO2 with BVI monitoring during their neurosurgical interventions: CSF shunt tap, EVD placement, and shunt externalization with drainage. The timing of the patients’ shunt taps or EVD placement varied as shown in their rcSO2 with BVI graphs. The initial average temperature for the 13 arrested patients was 34.8°C (SD + 1.9); baseline ETCO2, 25.7 (SD + 5.6) mm Hg during cardiac arrest; and ETCO2, 37.5 (SD + 3.6) mm Hg postcardiac arrest. All 13 patients had effective change in ETCO2 with chest compression. In all 13 patients when CSF was removed, there was a corresponding ROSC, increase in heart rate, and rise in baseline ETCO2. When the shunt or ventricular tap occurred, there was a corresponding positive change in the left and right rcSO2 and BVI readings. All patients received weight-based doses of epinephrine, atropine, and 5 mL/kg of 3% HTS over 5 to 10 minutes. All cardiac arrest patients were intubated by rapid sequence intubation method with age-

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appropriate endotracheal tube, weight-based dosing for atropine, etomidate, and rocuronium in the PED. All cardiac arrest patients had shunt taps before intubations. In proximal CSF shunt malfunction, patients all were intubated before neurosurgical interventions, EVD, except for one proximal CSF shunt malfunction patient. All distal CSF shunt malfunction patients received 2.45 + 0.7 doses of atropine, 2.5 + 0.5 dose of epinephrine, 1.7 + 0.5 dose of 3% HTS, and no bicarbonate and proximal CSF shunt malfunction patients received 3.1 + 1.2 doses of atropine, 5.75 + 1.1 doses of epinephrine, and 2.3 + 0.9 doses of 3% HTS by the PED staff. In the 14 (13 arrested and one severe bradycardia) malfunctioning shunt patients, their left and right rcSO2 and BVI were individually specific in all aspects from their cerebral physiology, cardiovascular system, etiology for the malfunctioning shunt (distal vs proximal), and their therapeutic interventions. The pharmacologic ICP reduction therapy by 3% HTS 5 mL/kg in the arrested patients was not successful as defined by no change in the rcSO2 (15% rcSO2) and BVI (− 50) readings after 3% HTS infusion. In the one nonarrested proximal shunt malfunction patient who had severe bradycardia after the HTS infusion, there was a corresponding positive rcSO2 and BVI change before the increased heart rate. In the 13 arrested patients when CSF fluid was removed by CSF shunt tap or ventricular tap, there was a corresponding positive change in the left and right rcSO2 and BVI readings and resolution of cardiac arrest. The patients’ shunt malfunction complaints included increased sleeping (100%; 24 hours to 1 week), headache (per parental description, 85%; 24-168 hours), vomiting (100%; 24 hours to 1.75 weeks), change in mental status (per parental description, 100%; 24 hours to 4 weeks), and increased seizure activity (7%; duration, 8 hours). Average cardiac arrest duration for the distal malfunctioning shunt patients was 32.16 (SD + 9.3) minutes. From the 5 distal malfunctioning shunt patients, their rcSO2 with BVI, cardiac arrest, and interventions graphs, the trends and postulation are presented. In these patients, removal of CSF fluid by shunt tap correlated with distal malfunctioning shunt by CT scan and operative note. In these patients, removal of CSF fluid led to corresponding positive changes in rcSO2 and BVI readings and subsequent cardiac resolution as shown graphically. Distal patient E had a repeat episode of decreasing rcSO2 and BVI readings with corresponding severe bradycardia. Distal patient E had a repeat shunt tap with immediate positive change in rcSO2 and BVI readings and increased heart rate. Distal patient E had the shunt externalized by the neurosurgery resident to prevent reoccurrence of the bradycardia. This patient was taken immediately to the operating room for repair. From the rcSO2 with BVI and cardiac arrest graphs of the 5 distal shunt malfunction patients (Fig. 1A-E), the following trends are postulated. The patients’ shunt malfunction complaints included increased sleeping (100%; duration, 24-96 hours), headache (per parental description, 85%; duration, 24 hours to 2 weeks), vomiting (100%; duration, 24 hours to 2 weeks), change in mental status (per parental description, 100%; duration, 24 hours to 2 weeks), and increased seizure activity (93%; duration, 8-36 hours). In 8 patients with cardiac arrest due to proximal malfunctioning shunt, the average cardiac arrest duration was 59.9 (SD + 15.35) minutes. From the 8 arrested proximal shunt malfunction patients, their rcSO2 with BVI, cardiac arrest, and intervention graphs, the trends and postulation are presented. In these patients, proximal shunt malfunction shunt was confirmed by CT scan and operative note. In these patients, if no CSF fluid was removed during shunt tap, there was no change in rcSO2 or limited to no change in BVI and no resolution of cardiac arrest. When EVD placement was performed with CSF drainage, there was a corresponding positive change in left and right rcSO2 and BVI readings, and cardiac arrest resolved as shown graphically (Fig. 2A-H). Proximal malfunctioning shunt patients (Fig. 2C and D, F) who underwent placement of an EVD had a corresponding positive change in rcSO2 and BVI readings with subsequent cardiac arrest resolution. These patients subsequently developed another episode of cardiac arrest with a

Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

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T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

Fig. 1. A, Cerebral oximetry and BVI graph: 1.875-year–arrested distal malfunctioning shunt patient. B, Cerebral oximetry and BVI graph: 2.125-year–arrested distal malfunctioning shunt patient. C, Cerebral oximetry and BVI graph: 3.125-year–arrested distal malfunctioning shunt patient. D, Cerebral oximetry and BVI graph: 6.5-year–arrested distal malfunctioning shunt patient. E, Cerebral oximetry and BVI graph: 7.56-year–arrested distal malfunctioning shunt patient.

preceding negative change in rcSO2 and BVI readings. These occurrences were related to an obstructed external ventricular catheter. Two patients (Fig. 2C and D) had a second external ventricular drainage system placed

with an immediate positive change in rcSO2 and BVI readings and restoration of cardiac function. One patient (Fig. 2F) had manipulation of the ventricular catheter with flushing of the tubing, which unclogged the

Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

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Fig. 2. A, Cerebral oximetry and BVI graph: 1.72-year–arrested proximal malfunctioning shunt patient. B, Cerebral oximetry and BVI graph: 2.9-year–arrested proximal malfunctioning shunt patient. C, Cerebral oximetry and BVI graph: 3.75-year–arrested proximal malfunctioning shunt patient. D, Cerebral oximetry and BVI graph: 5.6-year–arrested proximal malfunctioning shunt patient. E, Cerebral oximetry and BVI graph: 6.35-year–arrested proximal malfunctioning shunt patient. F, Cerebral oximetry and BVI graph: 9.125year–arrested proximal malfunctioning shunt patient. G, Cerebral oximetry and BVI graph: 13.5-year–arrested proximal malfunctioning shunt patient. H, Cerebral oximetry and BVI graph: 16.9-year–arrested proximal malfunctioning shunt patient. I, Cerebral oximetry and BVI graph: 1.35-year proximal malfunctioning shunt patient with severe bradycardia.

system causing an immediate positive change in rcSO2 and BVI readings and resolution of cardiac arrest. One proximal CSF shunt malfunction patient (Fig. 2H) who presented with vomiting (36 hours duration) and altered mental status (per parental description, 100%; 36 hours duration) and severe bradycardia had low rcSO2 and BVI readings received 3% HTS 5 mL/kg. This intervention resulted in improvement in rcSO2 and BVI readings, heart rate, and activity per parent’s perception and description of the patient’s normal activity (the patient was noted to have significant neurologic devastation per PED electronic medical records). While waiting for CT scan, the patient developed decreasing rcSO2 and BVI readings and proceeded to cardiac arrest. Upon cardiac arrest, the patient had assisted bag anesthesia mask, inline end-tidal CO2 ventilation, continuous chest compression, and one dose of weightbased epinephrine until neurologic intervention occurred. The patient had ventricular tap by the neurosurgical resident with 20 cm 3 of CSF removed whereupon there was a positive change in rcSO2 and BVI readings before the resolution of cardiac arrest and ROSC. The patient was then intubated before the patient underwent an EVD placement with CSF drainage with weight-based dosing of atropine, etomidate,

and rocuronium with age-appropriate endotracheal tube confirmed by end-tidal CO2 monitoring. No hypoxia or bradycardia or cardiac arrest occurred during the intubation process. Patient then immediately went to the operating room for shunt replacement and had a confirmed proximal shunt malfunction. One patient (Fig. 2I) with vomiting (duration, 36 hours), altered mental status changes (per parental description duration, 96 hours), and severe bradycardia by EMS (transport time, 38 minutes) presented to the PED. The patient received no intervention for the bradycardia or of increased ICP by EMS during transport to the PED. The patient upon arrival to the PED had severe bradycardia 30 to 40 beats per minute with altered mental status changes, and periods of apnea was given 5 mL/kg of 3% HTS to relieve the increased ICP producing the bradycardia and head elevation, 30°. The patient’s heart rate, rcSO2, and BVI readings improved after HTS as shown graphically. The patient’s repeat bradycardia episode did not respond to further HTS therapy. A shunt tap was performed, and no CSF was returned indicating a proximal shunt malfunction. This patient was taken immediately to the operating room for shunt repair and had a confirmed proximal shunt malfunction.

Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

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T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

This is the first reported case series of pediatric CSF shunt malfunction patients in cardiac arrest with noninvasive neurologic monitoring during their cardiac arrest, therapeutic interventions, and postresuscitation monitoring. We were able to noninvasively capture and detect the effects of severe increased ICP and its effect on the patient’s cerebral physiology, cerebral perfusion, and cardiovascular system. We also showed the effects of the neurologic interventions on the patient’s cerebral and cardiac physiology as expressed by their rcSO2 with BVI readings changes and cardiac arrest resolution. These patients showed the effects of the severely increased ICP on the cardiovascular system and the ineffectiveness of the standard pediatric advance lifer support system (PALS) pharmacologic interventions on this particular type of cardiac arrest. In these patients, their cardiac arrest phase was only resolved by decreasing the ICP pressure by CSF drainage. This reduction in ICP pressure alleviated its effect on the brain stem shown by the earlier positive changes in rcSO2 and BVI readings, which preceded the cardiac arrest resolution and ROSC. In all 13 cases, the various episodes of cardiac arrest was associated with low rcSO2 and BVI readings and presumed secondary to the increased ICP. When this increased ICP was reduced, the reduced ICP effect on the brainstem cardiovascular control center caused resolution of cardiac arrest and ROSC. In comparing proximal with distal CSF shunt malfunction arrest patients, there was a longer time to ICP reduction causing greater cardiac arrest phase duration and significant delay in ROSC because of a more difficult neurosurgical technique and limited personal to reduce this type of severe increased ICP. The positive rcSO2 and BVI changes occurred before the cardiac arrest resolution showing an earlier improvement in cerebral reperfusion and metabolism before the cardiovascular system in these particular patients. Furthermore, in proximal CSF shunt malfunction patient with bradycardia, there was improvement in cerebral physiology detected by rcSO2 with improved rcSO2 and BVI readings after ICP reduction using 3% HTS. A rise in ICP causes diminished cerebral perfusion, oxygen delivery, and higher oxygen extraction rate therefore explaining the decreased cerebral rSO2 readings during malfunctioning shunts [12-18]. In the cardiac arrest secondary to the significant elevated ICP, the expectation is that the patient’s cerebrum has very limited to no perfusion, and the tissue oxygenation would be extremely low. This low tissue oxygenation has been well documented in numerous adult cardiac arrest patients with rcSO2 monitoring [20,13,21-25]. In adult and pediatric cardiac arrest studies using rcSO2 monitoring during the cardiac arrest phase, the rcSO2 readings were 15% O2Hgb [4,20,13,21-25]. This 15% rcSO2 readings represent 25% of oxygen that is irreversibly bound to hemoglobin level in the tissue vascular bed and no tissue metabolism or perfusion [12-18,20-25]. These 13 malfunctioning shunt patients had similar presenting 15% rcSO2 readings during their cardiac arrest phase, which indicated neither cerebral tissue perfusion nor tissue metabolism as in similar cerebral cardiac arrest studies [12-26]. As in the adult cerebral arrest studies with resolution of the arrest, there was a corresponding change in their rcSO2 readings, which indicated reperfusion of the cerebral tissue and improved tissue metabolism [14-20,13,21-26]. The 13 arrested shunt patients did not responded to pharmacologic attempts at ICP reduction as shown by the lack of change in their rcSO2 (15% rcSO2) and BVI (−50) readings or asystole. These arrested shunt patient demonstrated similar rcSO2 (15% rcSO2) trends as reported in the adultarrested rcSO2 studies [20,13,21-25]. These arrested shunt patient’s arrest resolution only occurred after ICP reduction via CSF removal. This was demonstrated by the positive change in rcSO2 and BVI readings, which indicated cerebral tissue reperfusion and metabolism, before the restoration of the cardiovascular system [20,13,21-25]. When ICP is lowered, cerebral reperfusion occurs as is reflective in increased BVI readings. Tissue oxygenation and metabolism improve and are reflected in increased rcSO2 reading. [20-25]. During the process of CSF shunt tap or ventricular tap, there is a release of fluid, which reduces the pressure in the intracranial space [4,7-16]. This release of ICP pressure should, as demonstrated in other studies,

improve cerebral perfusion, oxygenation, and tissue metabolism, which was demonstrated in these malfunctioning shunt patients. In the distal shunt malfunctions, the obstruction occurs distal to the valve or reservoir. The fluid and pressure buildup is due to the blockage of CSF fluid distally or at the emptying site causing a back pressure buildup in the shunt system [4,7-10]. When tapping a distal malfunctioning shunt, the expectation is that significant fluid will be aspirated thereby a decreasing ICP and leading to a more dramatic improvement in cerebral perfusion, oxygen delivery, and greater change in rcSO2 readings. [4,5,12,13]. In the proximal malfunctioning shunt, the obstruction is proximal, and during the ventricular shunt tap, there will be minimal to no fluid removed because the obstruction is before the valve, and fluid collects in the ventricles. In cardiac-arrested distal malfunctioning shunt patients, the shunt tap produced earlier CSF fluid drainage, decreasing ICP producing a positive rcSO2 and BVI change, which preceded the cardiac arrest resolution. In the proximal malfunctioning shunts patients, the shunt tap produced no CSF fluid drainage, no decrease ICP, persistently low rcSO2 and BVI readings, and most importantly, no cardiac arrest resolution. As expected in these proximal shunt patients, once there was reduced ICP with EVD placement, there was resolution of the cardiac arrest. In these proximal malfunctioning cardiac arrest patients when 3% HTS was given as medical therapy for increased ICP, it did not reduce the ICP nor improve the cerebral physiology as represented by persistently low rcSO2 and BVI readings and no cardiac arrest resolution. One proximal shunt patient had only severe bradycardia, and arrested was given 3% HTS to decrease the increased ICP and reverse the bradycardia. The patient’s response to 3% HTS was resolution of the severe bradycardia. Cerebral oximetry and BVI monitoring was able to detect the reduction in the ICP with improvement in cerebral physiology and perfusion as reflective of the positive changes in the rcSO2 and BVI readings. This proximal malfunctioning shunt patient’s response to HTS therapy during bradycardiac events has possible effectiveness. This also implies that, in proximal malfunctioning shunts, there is varying degrees of the malfunction shunt producing varying degrees of ICP. In comparison with the 8 other arrested proximal malfunctioning shunt patients, this patient responded well to 3% HTS therapy by the relieve of the bradycardia and positive rcSO2 and BVI changes. The assumption in proximal malfunctioning shunt that there should be little or no ICP reduction related to 3% HTS therapy needs further investigation as a result of this patients responsiveness to 3% HTS as detected by the positive rcSO2 and BVI readings and relieve of bradycardia. For the emergency physician from these 13 malfunctioning shunt patients who presented in cardiac arrest, the probable cause is severe increased ICP and its persistent effect on the cardiac arrest phase. The resistance to continuous CPR and PALS interventions is related to the persistent severe ICP. The tapping of the shunt with fluid removal may indicate the location of the malfunction. In distal-arrested malfunctioning patients, tapping the shunt should remove fluid and correct the severe increased ICP and produce resolution of the cardiac arrest. In the arrested proximal malfunctioning shunt patients, the shunt tap will produce little to no fluid, no reduction in ICP, and no resolution of cardiac arrest. Continuous CPR and PALS protocol must be continued in these patients until the definitive therapy with CSF drainage is accomplished by a neurosurgeon. The cardiac arrest phase was related to the severe increased ICP as expressed by the persistently low rcSO2 readings, 15% rcSO2 (O2Hgb), and negative BVI, during the arrest [20-25]. Once there was a reduction in the ICP by CSF drainage, there was a corresponding positive rcSO2 and BVI change, improved cerebral perfusion, and metabolism and physiology as detected by rcSO2 with BVI reading. Cerebral oximetry in these particular patients has shown its usefulness in detecting the degrees of ICP, ICP’s effect on the cardiovascular system, and cerebral physiology and most importantly, detecting the responsiveness of therapeutic interventions. From this rare complication of malfunctioning shunts, limited assumptions have been derived, but a detailed prospective investigation will be difficult to accomplish.

Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007

T.J. Abramo et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

These 14 malfunctioning shunt patients showed the effects of increased ICP on cerebral perfusion and metabolism and the cardiovascular system. The improved cerebral rcSO2 and BVI changes and resolution of cardiac arrest only occurred after successful shunt tap was reflective of distal shunt malfunction. While in the proximal shunt malfunction, the improved cerebral rcSO2 with BVI changes, and cardiac arrest resolution occurred only with ventricular taps and drainage. Pharmacologic ICP reduction therapy by 3% HTS was not successful in the arrested patients except in one bradycardiac proximal malfunction shunt patient, there was an improvement in the cerebral rcSO2 and BVI readings and heart rate. There was an earlier resolution of cardiac arrest in the distal compared with the proximal malfunctioning shunt patients as the result of degree of complexity for the therapeutic interventions shunt tap vs EVD placement. This is the first reported case series of malfunctioning shunt patients in cardiac arrest who had noninvasive cerebral physiology monitoring. Cerebral oximetry with BVI monitoring demonstrates the effectiveness of ICP reduction, by either shunt taps for distal or ventricular taps for proximal malfunctioning shunts and the corresponding effect on cerebral physiology and cardiac arrest phase. This ICP reduction’s effect on the cerebral physiology and cardiovascular system were detected by the positive changes in rcSO2 and BVI readings and before cardiac arrest resolution. In this clinical state of malfunctioning shunts producing cardiac arrest, rcSO2 with BVI monitoring has shown its practicality and potential utility as a noninvasive cerebral physiologic monitor. Thomas J. Abramo, MD Department of Pediatrics Division of Pediatric Emergency Medicine University of Arkansas College of Medicine Little Rock, AR E-mail address: [email protected] Mark Meredith, MD Department of Pediatric University of Tennessee Health Science Center Le Bonheur Children’s Hospital Memphis, TN Mathew Jaeger, MD Bradford Schneider, MD Holli Bagwell, MD Department of Pediatrics Division of Pediatric Emergency Medicine University of Arkansas College of Medicine Little Rock, AR Eleym Ocal, MD Gregory Albert, MD Department of Neurosurgery Division of Pediatric Neurosurgery University of Arkansas College of Medicine Little Rock, AR http://dx.doi.org/10.1016/j.ajem.2014.04.007

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Please cite this article as: Abramo TJ, et al, Cerebral oximetry with blood volume index in asystolic pediatric cerebrospinal fluid malfunctioning shunt patients, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.007