**3.3 Elements of an ECPR program**

this. Though the AHA recommends considering ECMO for pediatric IHCA, there are no specific guidelines for the actual implementation of ECMO during CPR. Site of cannulation varies in pediatrics and could be central or peripheral. Central (transthoracic) cannulation is more frequently performed in cardiac surgical patients, some of whom may already have an open sternum [52–54] . Peripheral cannulation could be via right neck vessels (internal jugular vein and carotid artery) or femoral vessels. Data is conflicting on the presence of a correlation between

Questions also remain surrounding (i) the appropriate timing of initiating a request for ECMO implementation during CPR, (ii) the use of timed cycled interruptions of chest compressions to allow for cannulation, and (iii) the ongoing administration of epinephrine (adrenaline) during ECPR cannulation. From a review of the literature, clinical practice varies in regard to how long after the initiation of chest compressions that ECMO is requested for pediatric IHCA [57, 60, 63–66]. A cross-sectional survey of pediatric cardiac intensive care practitioners published in 2018 showed that 38% of respondents reported activating ECMO after just one dose of epinephrine, while more than 80% called for ECMO after the second dose [67]. The timing of initiation of ECMO cannulation during CPR is important because it contributes to total CPR duration. Based on this, it would seem prudent to request ECMO early into the resuscitation effort. But caution must also be taken to avoid deployment prematurely, for example, if return of spontaneous circulation (ROSC) could have been achieved without ECMO. The effect of total CPR duration on survival and neurological outcomes after pediatric ECPR is unclear. In a recent large study using data from both ELSO and GWTG-R registries, a linear relationship was demonstrated between CPR duration and odds of death before hospital discharge [68]. Multiple single-center studies have also shown worse outcomes from pediatric ECPR if duration of CPR is longer [52, 60, 63, 64, 66, 69–72]. However, still other studies have shown no correlation between ECPR duration and outcomes [37, 53, 57, 73–79]. The patient population possibly dictates the effect of ECPR duration on outcome. Compared to other illness categories, pediatric cardiac surgical patients have been shown to have a higher probability

of favorable neurologic outcomes despite ECPR of prolonged duration [37]. The use of timed cycled interruptions of chest compressions to facilitate cannulation during ECPR is practiced in some centers, but there is no literature to show how widespread this practice is or whether it has positive effects on outcomes. Without timed cycled interruptions, chest compressions are paused randomly, usually at the discretion of the cannulating surgeon, and they are paused for varying amounts of time. With timed cycled interruptions, pauses in chest compressions are on a cycle—compressions are not paused unless a minimum time has passed (e.g., 2 min), and they are only paused for a maximum amount of time (e.g., 30–45 s). With the cycled method, the cannulating surgeon is only able to work in short bursts of time, and it is possible that overall CPR duration is therefore longer. However, it is also likely that CPR "no-flow" time is less. This is an area that needs to be studied. Epinephrine administration for CPR during ECMO cannulation is also an area of research interest. Proponents of the cessation of epinephrine administration during ECMO cannulation for CPR argue that ongoing administration would only increase systemic vascular resistance (which would impede ECMO flow subsequently and hamper myocardial recovery) and is futile for ROSC since the decision would have already been made to cannulate. However, the 2009 study of 199 pediatric ECPR recipients from GWTG-R registry demonstrated no statistically significant difference between survivors and non-survivors in cumulative dose of epinephrine received during ECPR [73]. Also, in the cross-sectional survey of pediatric cardiac critical care clinicians published in 2018, only 19% of respondents reported limiting

epinephrine to 1–3 doses during CPR before ECMO cannulation [67].

**34**

cannulation site and outcomes in pediatric ECPR [55–62].

*Sudden Cardiac Death*

Deployment of ECPR requires that a well-coordinated, streamlined, and efficient sequence of activities takes place. For success of an ECPR program, it is essential that clinical teams are always ready since time is of the essence. Important elements to a successful ECPR program include (i) prior identification of patients that would be offered ECMO in the case of cardiac arrest, (ii) prior establishment of a system of emergently notifying all required parties in the event of cardiac arrest (e.g., through paging), (iii) ready availability of primed ECMO circuits and blood products, and (iv) effectively trained and prepared team members [80, 81].

Some ECPR programs have crystalloid-primed or non-blood colloid-primed circuits always on standby [57, 76, 81, 82]. Sixty-five percent of 1828 pediatric ECPR cases reported to ELSO from 2011 to 2015 had an ECMO circuit primed with blood products [44]. Different considerations go into the choice of prime solution for rapid deployment. Blood-primed circuits are dependent on the rapid availability of blood products and cannot be stored long-term. Some programs do not keep preprimed circuits if blood can be obtained quickly [83]. Crystalloid-primed circuits may be stored for up to 30 days but may require adjustment of pH and addition of blood prior to use [57, 76, 81]. Cost must also be considered in the decision to have pre-primed circuits on standby. For example, as published in 2017 by Erek et al., their pediatric ECPR program in Turkey avoids pre-primed ECMO circuits due to cost. Instead they emergently deploy cardiopulmonary bypass circuits for ECPR then transition to ECMO circuits later in the course [52].

Teams must be effectively trained and prepared. Simulation has proven to be an effective method for ECPR team training and has been used in many programs around the world with good results [84–86].

### **3.4 Pediatric ECPR outcomes**

Survival after ECPR in pediatrics is around 43% in all age groups, according to ELSO [44]. Only a few pediatric studies have compared conventional CPR (CCPR) with ECPR [48, 87, 88]. In an analysis published in 2016 of almost 600 pediatric IHCA patients from the GWTG-R registry, there were increased odds of survival to hospital discharge for patients who received ECPR compared to CCPR only (adjusted OR 2.76; 95% CI 2.08–3.65; *p* < 0.0001) [87]. An earlier study published in 2013 did not demonstrate an association between ECPR and improved survival to discharge compared to CCPR, but that study had a small ECPR subgroup and was unable to match controls [48].

Taeb et al. compared CPR quality between ECPR and CCPR in pediatric cardiac intensive care patients. They found that CPR duration was significantly longer for patients who received ECPR than those who received CCPR [30 min (9.5–33 min) vs. 5.5 min (4–12.5 min); *p* = 0.016]. Rate of ROSC, intensive care unit length of stay, and hospital length of stay were not different between the groups [88].

Neurological outcomes after ECPR are important metrics, but there is a general paucity of data on this topic. Multiple single-center and registry studies have reported on neurologic status at hospital discharge using the Pediatric Cerebral Performance Category (PCPC) scale [37, 57, 61, 64, 73, 81, 87, 89–91]. However, many of those studies have incomplete data, and designation of a patient's PCPC is also subjective. In addition, the definition of favorable neurologic outcome scores using PCPC varies. All these make interpretation of the data somewhat difficult. In the 2019 study of merged ELSO and GWTG-R data, discharge PCPC was only available in 48% of 241 pediatric ECPR survivors; 93% of those had a PCPC ≤2 which was considered favorable [68].

There is limited data on functional and neurobehavioral status in pediatric ECPR patients beyond hospital discharge [60, 63, 92–95]. Torres-Andres et al. assessed healthrelated quality of life after pediatric ECPR. Children with normal brain imaging at the time of ECMO decannulation had statistically higher quality of life scores compared to other children, and those with ischemic changes on brain imaging at decannulation had higher quality of life scores than those with hemorrhagic changes [96].

cardiac arrest, and patient's prearrest state of health. The mechanism of post-cardiac arrest brain injury is complex and includes excitotoxicity, disrupted calcium homeostasis, free radical formation, protease cascades, and activation of cell death signaling pathways. Post-cardiac arrest brain injury is also influenced by what is often hyperemic reperfusion and frequent failure to achieve adequate cerebral reperfusion. Post-cardiac arrest myocardial dysfunction describes the transient global dysfunction that is seen immediately after ROSC. The systemic ischemia/ reperfusion response describes the whole-body ischemia/reperfusion that occurs with hypoxia-induced activation of immunologic and coagulation pathways that is seen with cardiac arrest. Clinically this appears as intravascular volume depletion, impaired vasoregulation, impaired oxygen delivery, and increased susceptibility to infection. The persistence of the precipitating cause of the cardiac arrest often complicates the pathology of post-cardiac arrest syndrome. Specific treatment of the cause must be aligned with treatment of the PCAS [101]. In 2019, the AHA scientific statement estimated that more than 1800 children and infants were at risk for PCAS annually [102]. The individual components of PCAS are potentially treat-

able, and this has led to an emphasis on post-cardiac arrest care (PCAC).

**4.2 Hemodynamics**

*Pediatric Cardiac Arrest*

*DOI: http://dx.doi.org/10.5772/intechopen.92381*

PCAC varies depending on the phase of post-cardiac arrest syndrome and the setting in which care is being delivered. PCAC requires multisystem support and must begin promptly after ROSC. The goal of the treatment is to support end-organ function, treat PCAS, and correct the causal factor for the arrest. PCAC begins with the initiation of monitoring as soon after ROSC as feasible. This monitoring includes continuous cardiac telemetry, pulse oximetry, continuous capnography, continuous temperature monitoring, blood pressure measurement, and monitoring of urine output. Laboratory analysis is also important and includes blood gases, serum electrolytes, serum glucose, and calcium. Other monitoring to consider includes arterial lactate, central venous oxygen saturation, chest x-ray, renal function, hemoglobin concentration, coagulation function, and monitoring for signs of inflammation. Neurologic monitoring is useful in a comatose post-cardiac arrest patient. The goal of neurologic monitoring is to prevent secondary neurological injury and aid in prognostication. This monitoring could include serial exams and electroencephalogram [103]. Appendix **Figure A1** shows an example of a post-arrest care checklist.

There is no high-quality evidence to support a single strategy for providing optimal hemodynamic support in pediatric patients post-cardiac arrest. Postcardiac arrest myocardial dysfunction treatment can be aided by monitoring arterial lactate and central venous oxygen saturation. Parenteral fluids, inotropes, and vasoactive medications are to be used as needed to provide hemodynamic support. Optimal use of parenteral fluids vs. vasopressors/inotropes has not yet been determined. At times hemodynamic stability will include management of arrhythmias. Medications to treat arrhythmias are dependent on the underlying cardiac pathology. Hemodynamic treatment should be adjusted to account for the patient's PCAS and prearrest characteristics. At times extracorporeal membrane oxygenation is initiated during CPR as described earlier in the chapter. The efficacy of ECMO for

Optimizing oxygenation and ventilation after ROSC is essential and may be hindered by the cause of the arrest and the ongoing PCAS. Providing oxygen is a common therapy in critically ill children. There is no consistent data on the

hemodynamic support after ROSC is unclear [104].

**4.3 Oxygenation and ventilation**

**37**

#### **3.5 Transportation of pediatric cardiac arrest patients to ECMO centers**

The decision to transport pediatric cardiac arrest patients with active chest compressions to a hospital that performs ECPR must be considered carefully. Literature on this subject is minimal. Prolonged CPR before ECMO cannulation has been shown in some studies to not result in worse mortality, especially in patients with cardiac diagnoses [77, 97, 98]. However, Eich et al. describe the outcomes of 12 pediatric patients who suffered near-drowning episodes between 1987 and 2005 and who were transported to a tertiary center in Germany for emergent cardiopulmonary bypass [45]. Only 5 of the 12 survived to hospital discharge, of which 3 were in a persistent vegetative state.

In deciding to transport pediatric patients receiving CPR, one must consider the following: etiology of cardiac arrest, origin of transport (i.e., out-of-hospital transport vs. interhospital transfer), the duration of "no-flow" time, the anticipated total duration of CPR, the physical distance to the ECMO center, effectiveness of CPR during transport, and safety of medical personnel performing compressions during transport. Safety and effectiveness of CPR during transport of children has not been studied [99].

#### **3.6 Summary**

In summary, ECPR use in pediatrics is on the rise. There is evidence of its positive impact, and it has been included in resuscitation guidelines for pediatric inhospital cardiac arrest, in specific patients and where existing programs are available. It is important that hospitals establishing and running ECPR programs have detailed protocols and repeated training and rehearsing for ECPR.

#### **4. Pediatric post-arrest care**

#### **4.1 Introduction**

In 1966, the National Academy of Sciences published a consensus statement on CPR describing the ABCDs of resuscitation. In this document A denoted airway opened; B denoted breathing restored; C denoted circulation restored; and D denoted definitive therapy. Definitive therapy was described as therapy for the management of the cause(s) of the arrest and management of resulting pathology from the arrest [100]. Successful return of spontaneous circulation (ROSC) that is sustained often results in post-cardiac arrest syndrome (PCAS). PCAS is described in phases defined by time. The immediate post-arrest phase is described as the first 20 min after ROSC. This is followed by the early post-arrest phase which is described as between 20 min through 6–12 h after ROSC. The intermediate phase follows lasting up to 72 h following ROSC. Afterwards the recovery phase starts and lasts until disposition when the rehabilitation phase begins. These last two phases vary in duration [101].

Post-cardiac arrest syndrome encompasses (1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischemia/reperfusion response, and (4) persistent precipitating pathology. The severity of illness from this pathology varies based on the extent of the ischemic insult, the cause of the

#### *Pediatric Cardiac Arrest DOI: http://dx.doi.org/10.5772/intechopen.92381*

There is limited data on functional and neurobehavioral status in pediatric ECPR patients beyond hospital discharge [60, 63, 92–95]. Torres-Andres et al. assessed healthrelated quality of life after pediatric ECPR. Children with normal brain imaging at the time of ECMO decannulation had statistically higher quality of life scores compared to other children, and those with ischemic changes on brain imaging at decannulation had

higher quality of life scores than those with hemorrhagic changes [96].

**3.5 Transportation of pediatric cardiac arrest patients to ECMO centers**

survived to hospital discharge, of which 3 were in a persistent vegetative state.

**3.6 Summary**

*Sudden Cardiac Death*

**4.1 Introduction**

**36**

**4. Pediatric post-arrest care**

The decision to transport pediatric cardiac arrest patients with active chest compressions to a hospital that performs ECPR must be considered carefully. Literature on this subject is minimal. Prolonged CPR before ECMO cannulation has been shown in some studies to not result in worse mortality, especially in patients with cardiac diagnoses [77, 97, 98]. However, Eich et al. describe the outcomes of 12 pediatric patients who suffered near-drowning episodes between 1987 and 2005 and who were transported to a tertiary center in Germany for emergent cardiopulmonary bypass [45]. Only 5 of the 12

In deciding to transport pediatric patients receiving CPR, one must consider the following: etiology of cardiac arrest, origin of transport (i.e., out-of-hospital transport vs. interhospital transfer), the duration of "no-flow" time, the anticipated total duration of CPR, the physical distance to the ECMO center, effectiveness of CPR during transport, and safety of medical personnel performing compressions during transport. Safety and effectiveness of CPR during transport of children has not been studied [99].

In summary, ECPR use in pediatrics is on the rise. There is evidence of its positive impact, and it has been included in resuscitation guidelines for pediatric inhospital cardiac arrest, in specific patients and where existing programs are available. It is important that hospitals establishing and running ECPR programs have

In 1966, the National Academy of Sciences published a consensus statement on CPR describing the ABCDs of resuscitation. In this document A denoted airway opened; B denoted breathing restored; C denoted circulation restored; and D denoted definitive therapy. Definitive therapy was described as therapy for the management of the cause(s) of the arrest and management of resulting pathology from the arrest [100]. Successful return of spontaneous circulation (ROSC) that is sustained often results in post-cardiac arrest syndrome (PCAS). PCAS is described in phases defined by time. The immediate post-arrest phase is described as the first 20 min after ROSC. This is followed by the early post-arrest phase which is described as between 20 min through 6–12 h after ROSC. The intermediate phase follows lasting up to 72 h following ROSC. Afterwards the recovery phase starts and lasts until disposition when the

Post-cardiac arrest syndrome encompasses (1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischemia/reperfusion response, and (4) persistent precipitating pathology. The severity of illness from this pathology varies based on the extent of the ischemic insult, the cause of the

rehabilitation phase begins. These last two phases vary in duration [101].

detailed protocols and repeated training and rehearsing for ECPR.

cardiac arrest, and patient's prearrest state of health. The mechanism of post-cardiac arrest brain injury is complex and includes excitotoxicity, disrupted calcium homeostasis, free radical formation, protease cascades, and activation of cell death signaling pathways. Post-cardiac arrest brain injury is also influenced by what is often hyperemic reperfusion and frequent failure to achieve adequate cerebral reperfusion. Post-cardiac arrest myocardial dysfunction describes the transient global dysfunction that is seen immediately after ROSC. The systemic ischemia/ reperfusion response describes the whole-body ischemia/reperfusion that occurs with hypoxia-induced activation of immunologic and coagulation pathways that is seen with cardiac arrest. Clinically this appears as intravascular volume depletion, impaired vasoregulation, impaired oxygen delivery, and increased susceptibility to infection. The persistence of the precipitating cause of the cardiac arrest often complicates the pathology of post-cardiac arrest syndrome. Specific treatment of the cause must be aligned with treatment of the PCAS [101]. In 2019, the AHA scientific statement estimated that more than 1800 children and infants were at risk for PCAS annually [102]. The individual components of PCAS are potentially treatable, and this has led to an emphasis on post-cardiac arrest care (PCAC).

PCAC varies depending on the phase of post-cardiac arrest syndrome and the setting in which care is being delivered. PCAC requires multisystem support and must begin promptly after ROSC. The goal of the treatment is to support end-organ function, treat PCAS, and correct the causal factor for the arrest. PCAC begins with the initiation of monitoring as soon after ROSC as feasible. This monitoring includes continuous cardiac telemetry, pulse oximetry, continuous capnography, continuous temperature monitoring, blood pressure measurement, and monitoring of urine output. Laboratory analysis is also important and includes blood gases, serum electrolytes, serum glucose, and calcium. Other monitoring to consider includes arterial lactate, central venous oxygen saturation, chest x-ray, renal function, hemoglobin concentration, coagulation function, and monitoring for signs of inflammation. Neurologic monitoring is useful in a comatose post-cardiac arrest patient. The goal of neurologic monitoring is to prevent secondary neurological injury and aid in prognostication. This monitoring could include serial exams and electroencephalogram [103]. Appendix **Figure A1** shows an example of a post-arrest care checklist.

#### **4.2 Hemodynamics**

There is no high-quality evidence to support a single strategy for providing optimal hemodynamic support in pediatric patients post-cardiac arrest. Postcardiac arrest myocardial dysfunction treatment can be aided by monitoring arterial lactate and central venous oxygen saturation. Parenteral fluids, inotropes, and vasoactive medications are to be used as needed to provide hemodynamic support. Optimal use of parenteral fluids vs. vasopressors/inotropes has not yet been determined. At times hemodynamic stability will include management of arrhythmias. Medications to treat arrhythmias are dependent on the underlying cardiac pathology. Hemodynamic treatment should be adjusted to account for the patient's PCAS and prearrest characteristics. At times extracorporeal membrane oxygenation is initiated during CPR as described earlier in the chapter. The efficacy of ECMO for hemodynamic support after ROSC is unclear [104].

#### **4.3 Oxygenation and ventilation**

Optimizing oxygenation and ventilation after ROSC is essential and may be hindered by the cause of the arrest and the ongoing PCAS. Providing oxygen is a common therapy in critically ill children. There is no consistent data on the

usefulness of hyperoxia after cardiac arrest in children. Treatment with a goal of providing normal paO2 using the lowest possible fraction of inspired oxygen to maintain an oxygen saturation of 94–99% is the current strategy [102]. It is important to manage ventilation as both hypercarbia and hypocarbia have deleterious effects on cerebral perfusion. Current data suggest that it is appropriate to target normocapnia or a PaCO2 specific for the patient's condition while minimizing hypercapnia and hypocapnia [24, 105]. While providing strategies to optimize oxygenation and ventilation, we must be mindful that therapeutic hypothermia can alter the arterial oxygen saturation and affect carbon dioxide production which will be reflected in the minute ventilation [106].

**4.6 Neurologic monitoring**

*DOI: http://dx.doi.org/10.5772/intechopen.92381*

*Pediatric Cardiac Arrest*

**4.7 AKI and glucose control**

control on PCAC pediatric patients.

pediatric post-cardiac arrest patients [102].

**4.8 Rehabilitation**

**4.9 Summary**

**5. Conclusions**

**39**

Continuous EEG monitoring for pediatric patients who are encephalopathic following cardiac arrest and ROSC is recommended. This recommendation came forth from the recent consensus statement from the American Clinical Neurophysiology Society Critical Care Continuous EEG Guidelines Committee [111]. It is recommended that EEG monitoring be initiated as soon as possible and continue for 24–48 h. The recommendation also advises to continue monitoring for 24 h after patients treated with hypothermia are rewarmed to normothermia. There have not been studies to evaluate the effect of treatment of seizures in the post-cardiac arrest period on patient outcomes. Generally, most clinicians treat seizures as they can

The impact of the management of AKI and glucose control during PCAC is unclear. Data evaluating pediatric post-cardiac arrest AKI and glucose control management is scarce. AKI in critically ill children is associated with increased mortality and morbidity [112, 113]. It is important to monitor kidney function during PCAC as these patients are at risk to develop AKI. During PCAC, it is important to monitor for and treat hypoglycemia and hyperglycemia in post-cardiac arrest patients. Both hypoglycemia and hyperglycemia have been associated with poor outcomes in children [114]. There is no data that evaluates interventional studies of glucose

Rehabilitation following cardiac arrest is vital. Children surviving cardiac arrest

are at risk for alterations in their quality of life from physical, cognitive, and emotional disabilities. They are at risk for significant declines in neurobehavioral function across multiple functional domains [115]. There is also evidence that postcardiac arrest patients are at risk for developing delirium [116]. There is little data on specific interventions during PCAC that will improve functional outcomes in children after cardiac arrest. More information is needed to identify specific rehabilitation interventions that can be used in PCAC that will improve outcomes for

To summarize, how we care for pediatric patients post successful ROSC after cardiac arrest critically influences their outcomes. Each component of post-cardiac arrest care requires focused management. This care is highly complex and time sensitive. Despite knowing how crucial this management is to the outcomes of patients post-cardiac arrest, significant gaps in knowledge remain. More work is needed to identify the most efficient approaches to provide this care for pediatric patients.

Many of the recommendations regarding CPR quality metrics in children are based on extrapolation of adult and animal data, given the scarcity of pediatric literature. Although current AHA guidelines focus on "provider"-centric CPR, the evidence for transitioning to a "patient"-centric guided CPR is growing. Along with

increase metabolic demand and contribute to secondary brain injury.

#### **4.4 Targeted temperature management (TTM)**

The 2019 American Heart Association update for Pediatric Advanced Life Support included endorsement of post-cardiac arrest continuous maintenance of patient temperature, also referred to as TTM. In 2019 ILCOR pediatric CoSTR summarized evidence supporting the use of TTM (32–34°C) in infants and children after cardiac arrest [107]. Referring to their work, the American Heart Association recommends continuous measurement of core temperature during TTM. Additionally, for infants and children between 24 h of age and 18 years of age who remain comatose after out of hospital cardiac arrest or IHCA, it is reasonable to use TTM at 32–34°C followed by TTM at 36–37.5°C. Initiating hypothermia can be achieve in many ways including cooling blankets, surface cooling with ice packets, or gastric lavage. Electrolyte derangements including hyperglycemia, hypokalemia, hypophosphatemia, hypomagnesaemia, and hypocalcemia can occur during induction of hypothermia. This electrolyte instability can lead to arrhythmias. While maintaining hypothermia, careful monitoring is required. The ideal strategy for rewarming has not yet been identified. In children, the rewarming is usually done at a rate no faster than 0.5°C every 2 h. This reduces the risk of cerebral hyperperfusion, vasogenic edema, and acute systemic hypotension [102]. During PCAC, a temperature >37.5°C should be avoided and aggressively treated [108].

There was data suggesting that earlier timing of hypothermia was associated with better outcomes. Moler and colleagues developed a trial to investigate if shorter time to goal temperature was associated with improved outcomes at 1 year. Using data from the Therapeutic Hypothermia After Pediatric Cardiac Arrest Outof-Hosptial Trial (ThAPCA –OH), critically ill children from 38 pediatric intensive care units in the United States and Canada were randomized to therapeutic hypothermia or normothermia [109]. Median time to goal temperature in group 1 was 5.8 h and in group 2 was 8.8 h. However, outcomes between the groups did not differ. They concluded that earlier time to goal temperature was not associated with better outcomes [110].

#### **4.5 Sedation**

Similarly, to other critically ill children, children with PCAS will likely require treatment with sedatives, analgesics, and possibly neuromuscular blockade. There is insufficient data to describe optimal management of sedation and analgesia for pediatric patients with PCAS. With the use of TTM sedation, analgesia and neuromuscular blockade may be used to facilitate cooling and prevent shivering. Caution is advised when using neuromuscular blockade as this will hinder the clinical neurologic exam and will mask seizures.
