ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Initial post-cardiac arrest care in children

Initial post-cardiac arrest care in children
Literature review current through: Jan 2024.
This topic last updated: Dec 07, 2023.

INTRODUCTION — This topic discusses post-cardiac arrest care in children. The epidemiology, recognition, and treatment of cardiac arrest are discussed separately. (See "Pediatric basic life support (BLS) for health care providers", section on 'Epidemiology and survival' and "Pediatric advanced life support (PALS)".)

DEFINITIONS — Important definitions for this topic include:

Return of spontaneous circulation (ROSC) – ROSC describes a patient with a perfusing heart rhythm and a palpable central pulse.

Return of circulation – Return of circulation applies to ROSC or extracorporeal circulation established with extracorporeal membrane oxygenation (ECMO).

Active temperature control (also called targeted temperature management) – Active temperature control targets normal core body temperature (36oC to 37.5oC) or hypothermia (32oC to 34oC) using cooling devices or ECMO.

Post-cardiac arrest syndrome (PCAS) – PCAS and associated clinical manifestations are described in the figure. The key components consist of [1]:

Post-cardiac arrest brain injury

Post-cardiac arrest myocardial dysfunction

Systemic ischemia/reperfusion response

Precipitating pathophysiology

PRIORITIES IN CARE — Priorities in post-cardiac arrest care include (table 1) [1-3]:

Prevent secondary brain injury caused by hypoxemia or shock with decreased cerebral perfusion

Identify and manage cardiovascular dysfunction (eg, recurrent arrhythmias, high or low systemic vascular resistance, and impaired cardiac contractility)

Treat reversible causes of cardiac arrest

Identify and manage systemic ischemia/reperfusion injury manifested by hyperglycemia, coagulopathy, systemic inflammatory response with capillary leak, acute ischemic kidney and liver injury

APPROACH TO STABILIZATION — The approach to post-cardiac arrest stabilization consists of ongoing monitoring of oxygenation, ventilation, and hemodynamic status with continued management of the airway, breathing, and circulation. Active temperature control and rapid treatment of seizures, increased intracranial pressure, and hyperglycemia are also critically important.

Monitoring — As soon as return of spontaneous circulation (ROSC) occurs, the resuscitation team should ensure continuous monitoring of:

Cardio-respiratory status

Blood pressure (BP)

Pulse oximetry

End-tidal capnography (intubated patients)

Core body temperature

After ROSC, the blood pressure is frequently labile. Close BP monitoring is achieved with continuously cycled non-invasive BP monitoring or insertion of an intra-arterial catheter. Efforts to obtain intra-arterial access should not interfere with post-cardiac arrest stabilization. In many hospitals, arterial access is obtained after transfer to the pediatric intensive care unit. Procedures for obtaining intra-arterial access in children are discussed separately. (See "Arterial puncture and cannulation in children", section on 'Arterial cannulation'.)

Airway (C-spine motion restriction) — After ROSC, airway assessment and management should occur simultaneously with support of breathing (oxygenation and ventilation) and circulation. C-spine motion restriction should be maintained or, if not present, initiated for patients with a history or suspicion of trauma until appropriate imaging can be performed. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Cervical spine imaging'.)

Airway management depends upon interventions performed during cardiac arrest [1,2]:

Unintubated — For unintubated children with ROSC, the clinician must determine if the airway is maintainable or needs to be secured. Most children with altered mental status, respiratory distress, or shock after ROSC require endotracheal intubation. Prior to rapid sequence intubation (RSI) and if it does not delay timely airway management, the clinician should perform a focused neurologic examination to determine level of responsiveness (AVPU), pupillary response, and presence of key reflexes prior to neuromuscular blockade. (See 'Disability/Dextrose' below.)

These children are at increased risk of hypotension during RSI. Furthermore, any sedative or analgesic medication can result in hypotension during the post-arrest period. For this reason, intermittent doses of short-acting sedatives are good choices. Medications traditionally used for RSI in patients with hemodynamic instability such as etomidate, ketamine, midazolam, or fentanyl are potential candidates. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis".)

Our approach is as follows:

If airway reflexes are absent, suggesting deep coma, we perform RSI with rocuronium as a paralytic in a dose of 1.2 mg/kg to promote rapid onset of intubating conditions; we do not provide a sedative.

If airway reflexes are present, we perform RSI with low-dose sedatives, as above, and rocuronium as a paralytic in a dose of 1.2 mg/kg to promote the rapid onset of intubating conditions.

RSI and the technique for emergency endotracheal intubation in children are described in detail separately. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Approach" and "Technique of emergency endotracheal intubation in children".)

Children who are awake and without signs of shock after ROSC should receive supplemental oxygen as needed (table 2) to maintain pulse oximetry 94 to 99 percent. Patients who have acute hypoxemic respiratory failure but are awake and can maintain their airway may be candidates for high-flow nasal cannula oxygen therapy or non-invasive ventilation. (See "High-flow nasal cannula oxygen therapy in children" and "Noninvasive ventilation for acute and impending respiratory failure in children".)

Intubated — All intubated children require continued assessment to ensure proper endotracheal tube positioning, including auscultation and capnography (EtCO2). Insertion of a gastric tube helps to relieve gastric distension and may prevent vomiting. If not already obtained, the child should have a chest radiograph to ensure correct endotracheal tube position. (See "Technique of emergency endotracheal intubation in children", section on 'Post-intubation care'.)

Breathing

Oxygenation (pulse oximetry target) — After ROSC, the clinician should avoid hypoxemia using initial measurement of arterial oxygen to correlate with continuous pulse oximetry. For children with ROSC, we suggest supplemental oxygen to maintain pulse oximetry between 94 and 99 percent or, if the child has congenital heart disease, the baseline value appropriate for the child's condition [2-5]. The clinician should avoid oxygen toxicity by gradually lowering inspired supplemental oxygen, as tolerated, to keep oxygen saturation <100 percent while avoiding hypoxemia.

An association between post-arrest arterial oxygenation and mortality in resuscitated children has been inconsistent but supports the harmful effects of insufficient or excess oxygenation [5-9]. In one large, retrospective, multicenter observational pediatric study of 1875 infants and children who survived to pediatric intensive care unit (PICU) admission, multivariate analysis found that both hypoxemia (PaO2 <60 mmHg) and hyperoxemia (PaO2 ≥300 mmHg) were associated with an increased estimated risk of death [4]. Overall mortality prior to PICU discharge was 39 percent in this study. However, this study did not adjust for cardiac arrest characteristics and almost one-third of patients did not have arterial measure of PaO2 within one hour of ROSC, indicating a high risk for bias [3]. In a separate retrospective cohort study of 1500 post-cardiac arrest patients admitted to a pediatric ICU, the probability of death using a validated mortality score was not related to the initial paO2 obtained within one hour of admission despite one-quarter of patients having hypoxia (PaO2 <50 mmHg) or hyperoxia (paO2 >300 mmHg) [5]. However, overall mortality in this cohort was high (63 percent). In addition, all of these patients had monitoring and targeting of arterial oxygenation to avoid persistent hypoxemia or hyperoxia.

Adverse effects of hyperoxia are discussed in greater detail separately. (See "Adverse effects of supplemental oxygen".)

Ventilation (PaCO2 target) — After ROSC, the clinician should target normocapnia (eg, PaCO2 35 to 45 mmHg) using initial arterial blood gas measurements and correlated with continuous quantitative end-tidal capnography. Severe hypocapnia (PaCO2 <30 mmHg) or hypercapnia (PaCO2 >50 mmHg) should be avoided [3,10-12]. For patients with chronic lung disease with hypercapnia at baseline, target the PaCO2 near their baseline but ensure that the pH is ≥7.3. Exceptions to the target PaCO2 include permissive hypercapnia in patients with chronic lung disease or emergency hyperventilation with hypocapnia in patients with increased intracranial pressure and impending herniation [3]. (See "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Ventilation'.)

In one prospective, multicenter observational study of 223 infants and children who sustained an in-hospital arrest, PaCO2 30 to 50 mmHg was associated with lower mortality (33 percent) compared with PaCO2 <30 mmHg (50 percent) or >50 mmHg (59 percent) [6].

Mechanical ventilation — For children receiving mechanical ventilation after ROSC, consultation with an expert in the mechanical ventilation of children (eg, pediatric intensivist or pediatric anesthesiologist) is strongly encouraged. Lung protective strategies including low-inspiratory volume and use of positive end-expiratory pressure are typically warranted (table 3) [1]. (See "Initiating mechanical ventilation in children", section on 'Inadequate oxygenation'.)

For these patients, the physician must assess oxygenation and ventilation by measurement of an arterial blood gas shortly after initiation of mechanical ventilation and adjust settings based upon repeat arterial blood gases or correlated pulse oximetry, and/or capnography. When using non-invasive monitoring, the clinician should be aware of the errors associated with pulse oximetry (table 4) and the limited accuracy of capnography in ROSC patients due to changing cardiac output and alveolar dead space. If there is concern for an inaccurate reading, the clinician should obtain an arterial blood gas. (See "Pulse oximetry", section on 'Troubleshooting sources of error' and "Carbon dioxide monitoring (capnography)", section on 'Limitations'.)

The approach to stabilized patients who abruptly decompensate during mechanical ventilation is provided in the algorithm (algorithm 1) and discussed separately. (See "Initiating mechanical ventilation in children", section on 'Approach to decompensation'.)

Circulation

Vascular access — To optimize management, a second vascular access should be obtained after ROSC. In the emergency department, either a peripheral intravenous (IV) or intraosseous catheter (IO) is an acceptable second form of access. However, patients with persistent altered mental status or fluid-refractory shock may eventually need central venous access to permit measurement of central venous pressure and oxygen saturation and to provide central access for vasopressor administration.

Maintain blood pressure and treat shock — After ROSC in children, the general aims are to maintain a normal blood pressure that ensures adequate cerebral perfusion and to avoid shock [10,11,13]:

Maintain blood pressure – After cardiac arrest, autoregulation of cerebral perfusion is impaired. In children, most experts try to achieve a near-normal blood pressure (table 5 and table 6 and table 7) that is well above the 5th percentile threshold for shock, although precise thresholds have not been established. Preliminary evidence suggests improved clinical outcomes with this approach. For example, in a secondary analysis of almost 700 prospectively collected blood pressure measurements obtained within 6 hours of an in-hospital pediatric cardiac arrest, a higher survival to discharge with a favorable neurologic outcome was associated with a systolic blood pressure threshold >10th percentile (adjusted relative risk [RR] 1.2, 95% CI 1.1 to 1.3) and a diastolic blood pressure >50th percentile threshold (adjusted RR 1.2 (95% CI 1.1 to 1.4). Limitations of this study included lack of standardized post-arrest care, use of systolic and diastolic blood pressure rather than mean arterial pressure as the key measures, and inability to correct for the presence of post-cardiac arrest myocardial dysfunction.

Evidence in adults suggests that higher-than-normal blood pressures are needed to maintain cerebral perfusion and improve clinical outcomes after cardiac, as discussed separately. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Determining blood pressure goals'.)

Treat shock – The physician should rapidly treat shock in post-arrest pediatric patients, especially hypotensive shock, as indicated by a systolic blood pressure <5th percentile for age [10,11] (see "Pediatric advanced life support (PALS)", section on 'Shock'):

Term neonates (0 to 28 days): <60 mmHg

Infants (1 to 12 months): <70 mmHg

Children (1 to 10 years): <70 mmHg + (child's age in years x 2)

Children >10 years: <90 mmHg

Initial treatment of post-arrest shock consists of rapid infusion of isotonic fluid (lactated Ringer's or normal saline). The typical volume and rate is 10 to 20 mL/kg over 10 to 20 minutes with the lower volume used for patients with suspected or confirmed myocardial dysfunction [2]. After the fluid bolus, provide further treatment based upon clinical response such as improvement in skin perfusion, quality of pulses, blood pressure, mental status, and, when rapidly available, serum lactate. Also assess for signs of fluid overload and right-sided congestion (eg, pulmonary edema, hepatomegaly, or jugular venous distention) (algorithm 2). (See "Shock in children in resource-abundant settings: Initial management", section on 'Volume and rate'.)

Children with fluid-refractory post-arrest shock also require vasopressor support. In patients with ongoing shock despite fluid administration, start a vasoactive infusion, typically epinephrine. For patients without central venous access, epinephrine may be started via the IV or IO route at a dose of 0.03 to 0.05 mcg/kg per minute and titrated as needed up to 1 mcg/kg per minute. Other agents may be used in addition to or instead of epinephrine depending upon the patient's hemodynamic status and response to epinephrine. (See "Shock in children in resource-abundant settings: Initial management", section on 'Vasoactive agents'.)

Vasoactive agent options according to blood pressure and suggested by Pediatric Advanced Life support include [2]:

Hypotensive shock – For patients with hypotensive shock, the physician may administer a continuous infusion of epinephrine or norepinephrine. The choice between epinephrine and norepinephrine is guided by preference of the physician, patient physiology, and local system factors. Typically, epinephrine is used in patients with signs of myocardial dysfunction, and norepinephrine is used in patients with signs of low systemic vascular resistance or vasodilation. This suggestion is based upon indirect evidence of benefit of epinephrine or norepinephrine in children and adults with fluid-refractory septic shock. (See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)", section on 'Hypotensive patients' and "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Vasopressors'.)

Normotensive shock – For patients with signs of shock (poor perfusion, delayed capillary refill, thready peripheral pulses, and/or persistent lactic acidosis) without hypotension, epinephrine is the most commonly used agent. Milrinone is an alternative option that is sometimes used in patients with known or suspected cardiac dysfunction and high systemic vascular resistance (SVR). It can be used alone or in combination with epinephrine. However, milrinone has a substantial risk of causing hypotension and requires careful titration. For this reason, milrinone should only be used by experienced clinicians in a setting where the child can be adequately monitored (ie, an intensive care unit).

Patients with recurrent or persistent shock require central venous access, preferably with a central line catheter equipped with multiple ports to permit administration of resuscitation fluids and vasopressors, as well as measurement of central venous pressure (CVP). (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies".)

After cardiac arrest, circulatory instability may recur as the result of ongoing fluid loss, decreased cardiac function, and/or changes in systemic vascular resistance. In several retrospective, observational studies, hypotension after ROSC has been associated with decreased survival to hospital discharge [14-18] and, for infants and children with an inpatient arrest, decreased survival with favorable neurologic outcome [14]. High-quality evidence is lacking regarding the benefit of vasoactive agents and the preferred vasoactive agent or combination of agents for the treatment of fluid-refractory shock after cardiac arrest [1].

Treat arrythmias — Recurrent arrest and arrhythmias that occur after ROSC and compromise circulation should receive treatment according to Pediatric Advanced Life Support with correction of any identified reversible causes:

Recurrent pulseless arrest (algorithm 3 and algorithm 4)

Tachyarrhythmias with a pulse (algorithm 5) – For patients with recurrent ventricular arrhythmias who are hemodynamically compromised, synchronized cardioversion is the initial treatment. If drugs are necessary, our approach is to use lidocaine to avoid medications such as amiodarone or procainamide, which are arrhythmogenic. Such patients may have a congenital conduction defect such as Brugada or Long QT syndrome as the cause of the initial arrest. Early consultation with a pediatric cardiologist is recommended.

Bradyarrhythmias with a pulse (algorithm 6) – Primary bradyarrhythmias are rare in children. Bradycardia commonly accompanies therapeutic hypothermia but does not require treatment if perfusion is adequate [1]. Recurrent bradycardia may suggest a toxic ingestion (eg, beta blocker or calcium channel blocker) or intracranial pathology (eg, ruptured arteriovenous malformation with intracranial hypertension).

Ongoing arrhythmias after ROSC require pediatric cardiology consultation to identify cardiac pathology and to select the optimal antiarrhythmic therapy [1].

Extracorporeal membrane oxygenation (ECMO) — For patients with recurrent arrest or persistent post-arrest shock, ECMO may be an option if there is an underlying condition with potential for recovery. Examples include ingestions of cardiotoxic medications or thrombosis of an aorta-pulmonary shunt following surgical palliation procedures. Rapid consultation with a pediatric critical care specialist is recommended as soon as ECMO is being considered. In general, ECMO is not indicated following unwitnessed or prolonged out-of-hospital cardiac arrest due to associated hypoxic-ischemic organ injury unless there are mitigating circumstances such as moderate to severe environmental hypothermia. (See "Hypothermia in children: Management".)

The use of ECMO during cardiopulmonary resuscitation (ECPR) is discussed separately. (See "Pediatric advanced life support (PALS)", section on 'Extracorporeal membrane oxygenation (ECMO) with CPR (ECPR)'.)

Disability/Dextrose — Soon after ROSC, essential interventions related to disability include:

Check rapid blood glucose and treat hypoglycemia (table 8); initiate blood glucose monitoring (see 'Glucose homeostasis' below)

Assess neurologic status before sedation and neuromuscular blockade or, if performed, initiation of hypothermia including:

Glasgow coma scale

Mental status using AVPU: alert, responds to voice, responds to pain, or unresponsive

Pupil responses

Gag, corneal, and, for patients with no concern for C-spine trauma, oculocephalic (doll's eyes) reflex (figure 1)

Muscle tone and presence of myoclonus

Gross sensory or motor deficits

Upper and lower extremity reflexes

Babinski sign

If signs of impending brain herniation (table 9), treat per the algorithm (algorithm 7) and obtain emergency consultation with a neurosurgeon with pediatric expertise

Treat seizures (algorithm 8)

Initiate active temperature control (see 'Active temperature control' below)

For patients with adequate blood pressure and perfusion:

Elevated head of the bed 15 to 30 degrees and keep head midline

Maintain oxygenation and normocarbia (see 'Breathing' above)

Exposure — Fully undress the patient, perform a complete examination, and then initiate continuous core body temperature monitoring with active temperature control. Since fever is associated with worse outcomes following cardiac arrest, aggressively treat temperature >37.5°C with cooling measures and acetaminophen. (See 'Active temperature control' below.)

Accurate monitoring of core body temperature requires the use of a low-reading thermometer and is best obtained with a flexible temperature probe. Sites of measurement include the bladder, rectum, esophagus, nasopharynx, and central vein. Rectal temperatures, though widely used, are prone to artifact and may lag significantly behind changes in true core temperature. (See "Hypothermia in children: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Ancillary studies — Children should undergo the following studies as soon as possible after ROSC:

Arterial blood gas

Rapid blood glucose

Complete blood count with differential and, whenever available, point-of-care hematocrit

Electrolytes

Ionized or serum calcium

Serum lactate

Blood urea nitrogen and creatinine

Serum alanine aminotransferase (ALT), (AST) aspartate aminotransferase, and total/direct bilirubin

Prothrombin/international normalized ratio (PT/INR)

Partial thromboplastin time (PTT)

Type and screen

Urine rapid dipstick and urinalysis

Urine beta hCG (post-menarchal females)

ECG

Chest radiograph

If a trained and experienced provider is present, point-of-care ultrasonography to assess for pericardial tamponade, pneumothorax, and poor myocardial function

Febrile patients and those with suspected sepsis should also undergo:

Cultures of blood, urine, and, if hemodynamically stable with a secured or maintainable airway, cerebrospinal fluid

Cultures from other sites of infection (eg, skin lesions or abscess)

Blood polymerase chain reaction or respiratory molecular panel for viral and bacterial pathogens

Other studies may also be indicated based upon the suspected cause of arrest such as:

Head CT – Unknown cause of arrest, suspected brain lesion or intracranial hemorrhage with increased intracranial pressure (ICP), or suspected child abuse (table 10 and table 11)

Type and cross – Hemorrhage or severe anemia

Blood ammonia – Patients with elevated liver enzymes, PT/INR, or total/direct bilirubin suggesting liver failure; concern for inborn error of metabolism

Urine testing for drugs of abuse and other toxicology testing – Suspected poisoning, other testing is based on history of exposure, medications or other substances (including illicit drugs) available in the home, or found near the patient (see "Testing for drugs of abuse (DOAs)" and "Approach to the child with occult toxic exposure", section on 'Toxicology screens')

Troponin I or T and brain natriuretic peptide (BNP; or N-terminal BNP) – Primary cardiac etiology (h/o congenital heart disease, heart failure, or primary arrhythmia)

D-dimer – Patients at risk for thrombosis (eg, sickle cell disease or pro-thrombotic conditions such as nephrotic syndrome, protein C deficiency, Protein S deficiency)

TRANSFER TO DEFINITIVE CARE — After return of spontaneous circulation, children should receive post-cardiac arrest care under the direction of a pediatric critical care specialist in a pediatric intensive care unit. If the child is not being treated in a center with pediatric critical care expertise, the child should be stabilized and rapidly transferred for definitive care at a regional pediatric center with a full complement of pediatric specialty care and advanced technologic capabilities including dialysis and, whenever available, Extracorporeal membrane oxygenation (ECMO). Critically ill or injured children typically benefit from transport by a team with pediatric expertise and advanced pediatric treatment capability as well, although in some isolated cases more rapid transport by an immediately available non-pediatric team may be acceptable. (See "Prehospital pediatrics and emergency medical services (EMS)", section on 'Inter-facility transport'.)

Prior to transfer, the physician responsible for the child's care at the transferring hospital should speak directly to the physician who will be taking charge of the patient at the receiving hospital. All documentation of care (eg, medical chart, medication administration record, laboratory results, copies of ancillary studies [radiographs, ECGs]) should be sent with the patient. (See "Prehospital pediatrics and emergency medical services (EMS)", section on 'Inter-facility transport'.)

TREATMENT OF REVERSIBLE CAUSES — Reversible causes of cardiac arrest and their initial treatment are provided in the table (table 1) [19]:

For children with an inpatient cardiac arrest, the cause and relevant comorbidities are frequently known. For these patients, specific treatment is continued with escalation of therapies as indicated.

When the cause is unclear (eg, previously healthy child without a known precipitating illness or event), a comprehensive evaluation should include close examination for signs of child abuse (table 10), especially in infants in young children, and testing for drugs of abuse and other signs of occult toxic exposure. (See "Physical child abuse: Recognition" and "Approach to the child with occult toxic exposure", section on 'Ancillary studies'.)

In addition, pediatric survivors of sudden cardiac arrest should undergo a comprehensive evaluation under the direction of a pediatric cardiologist as described separately. (See "Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) in children", section on 'Survivors of SCA'.)

ONGOING MANAGEMENT — Ongoing post-cardiac arrest care in children should be directed by a pediatric critical care specialist in a pediatric intensive care unit.

Oxygenation and ventilation — Ensuring that oxygenation and ventilation goals are met is a critical aspect of post-cardiac arrest care:

Oxygenation – For children with return of spontaneous circulation (ROSC), give supplemental oxygen to maintain pulse oximetry between 94 and 99 percent or the value appropriate for the child's condition if the child has cyanotic congenital heart disease [2-5]. Adjust supplemental oxygen to avoid hyperoxia (oxygen saturation 100 percent). (See 'Oxygenation (pulse oximetry target)' above.)

Ventilation – After ROSC, maintain normocarbia (PaCO2 35 to 45 mmHg) using initial arterial blood gas measurements and correlated with continuous quantitative end-tidal capnography. Avoid severe hypocapnia (PaCO2 <30 mmHg) or hypercapnia (PaCO2 >50 mmHg). (See 'Ventilation (PaCO2 target)' above.)

Cardiovascular dysfunction — Children who are comatose after ROSC often have derangements in vascular tone. In addition, impaired cardiac contractility commonly occurs within hours after ROSC in children and significantly raises the risk of mortality. Peak impairment is typically 8 hours after arrest with improvement at 24 hours and resolution by 72 hours [1].

Management of cardiovascular function after ROSC requires careful monitoring of measures of perfusion including:

Arterial blood pressure

Capillary refill time

Quality of pulses

Mental status

Urine output

Serial arterial blood gases and blood lactate

In patients with evidence of cardiovascular dysfunction, central venous pressure and oxygen saturation (ScvO2)

Treatment of cardiovascular dysfunction includes:

Correct metabolic abnormalities – Correction of metabolic derangements such as hypocalcemia, hypoglycemia and severe metabolic acidosis. (See 'Glucose homeostasis' below and 'Electrolyte abnormalities' below.)

Fluid resuscitation – Judicious use of fluid resuscitation with crystalloid solution (lactated Ringer's or normal saline) to ensure adequate venous pressure.

Vasoactive agents – Vasoactive infusions to provide support for cardiac contractility. Epinephrine infusion is often needed soon after ROSC to manage ongoing shock and cardiac dysfunction. For patients with severe cardiac dysfunction, milrinone infusion may also be needed to support cardiac contractility while reducing afterload. (See "Shock in children in resource-abundant settings: Initial management", section on 'Vasoactive agents'.)

Hypoxic-ischemic brain injury — After a cardiac arrest, it is essential that the clinician optimize cerebral oxygenation and perfusion and avoid increased metabolic demand caused by fever and seizures. In addition, general measures to address increased intracranial pressure (ICP) should be employed.

Active temperature control — Active temperature control (ATC; also called targeted temperature management) after cardiac arrest refers to the practice of continuously monitoring core body temperature and actively intervening (typically with cooling blankets and antipyretics [eg, acetaminophen]) to maintain core temperature in a narrow pre-defined range.

ATC is a broad term that includes targeted normothermia (maintaining core temperature 36 to 37.5°C [96.8 to 99.5°F]), mild hypothermia (core temperature 34 to 36°C [93.2 to 96.8°F]), and therapeutic hypothermia (core temperature 32 to 34°C [89.6 to 93.2°F]). The optimal temperature is uncertain, as discussed below.

The rationale for ATC following cardiac arrest is based upon observations that fever is common in the initial days after cardiac arrest and that fevers are associated with worse outcomes [20]. Thus, avoiding fever is an important part of post-resuscitation care. The rationale for therapeutic hypothermia is to reduce cerebral metabolic demand, which may reduce the risk of reperfusion injury during the early post-resuscitation period.

Indications – We suggest ATC in all pediatric patients who do not have purposeful movements or responses on neurologic examination following cardiac arrest.

Target temperature – We suggest maintaining core body temperature ≤37.5°C (99.5°F). Based upon the available evidence and international resuscitation guidelines for comatose infants and children after cardiac arrest, it is reasonable to use one of two temperature targets [10,11,21,22]:

Normothermia (temperature 36 to 37.5°C [96.8 to 99.5°F]) for a duration of three to five days or per institutional guidelines.

Or

Therapeutic hypothermia (targeted temperature range 32 to 34°C [89.6 to 93.2°F]) for two days followed by three days of normothermia. Patients who receive therapeutic hypothermia are at increased risk of shivering, coagulopathy with bleeding, hyperglycemia, arrhythmias, myocardial dysfunction, and cold diuresis that can cause hypovolemia and electrolyte imbalance [1,23-25].

The authors maintain normothermia with strict avoidance of fever for most patients during post-cardiac arrest care because of fewer adverse effects and similar benefit when compared to hypothermia. When targeting normothermia, many experts maintain children at 35°C to provide a buffer that avoids fever because temperature elevation can occur rapidly in these patients. However, this approach has not been studied or compared to either normothermia or therapeutic hypothermia.

Timing and duration – ATC should be started as soon as is feasible (within minutes to hours after achieving ROSC). It is typically continued for three to five days. When targeting normothermia, the same temperature target is used for the entire duration. When using therapeutic hypothermia, the lower temperature is maintained for 48 hours, followed by a period of slow rewarming and then one to three days of targeted normothermia.

Cooling devices – ATC is administered using cooling devices that have automated feedback mechanisms to maintain the temperature in the target range. Various cooling devices are commercially available. The most common approach is a surface method such as a water-circulating gel-coated pad or water and/or air-circulating blanket. Additional details are provided separately. (See "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Devices'.)

Monitoring – Accurate monitoring of core body temperature requires the use of a low-reading thermometer and is best obtained with a flexible temperature probe. Sites of measurement include the bladder, rectum, esophagus, nasopharynx, and central vein. Rectal temperature probes are commonly used for this purpose; however, clinicians should be aware that the rectal temperature may lag behind the true core temperature.

During active temperature control, frequent monitoring of the following laboratory studies is also warranted:

White blood cell count

Blood glucose

Electrolytes and calcium

PT/INR and aPTT

The frequency of monitoring of these studies is determined by whether the target is therapeutic hypothermia (more frequent) or normothermia (less frequent) as well as the presence of derangements soon after ROSC.

Adverse effects – Shivering is common among patients receiving ATC, particularly when targeting lower temperatures. Sedation is generally required, and some patients may require neuromuscular blockade for management of shivering. (See 'Sedation, analgesia, and neuromuscular blockade' below.)

Other adverse effects that can occur in patients receiving therapeutic hypothermia include [1,23-25]:

Coagulopathy and bleeding – The risk increases with decreasing temperature; major bleeding is uncommon at the temperatures used for therapeutic hypothermia

Hyperglycemia

Cardiovascular effects (bradycardia, arrhythmias, ventricular dysfunction, hypotension)

Cold diuresis

Electrolyte derangements (eg, hypokalemia, hyperkalemia, and hypocalcemia)

Supporting evidence – The evidence supporting ATC after cardiac arrest in pediatric patients comes from two multicenter clinical trials and several observational studies [23,26-28]. Additional indirect evidence comes from studies in neonates and adult patients, which are discussed separately. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy", section on 'Therapeutic hypothermia' and "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Efficacy'.)

Trials comparing therapeutic hypothermia versus targeted normothermia – The available clinical trial data suggest that clinical outcomes are similar for patients managed with therapeutic hypothermia (32 to 34°C [89.6 to 93.2°F]) or targeted normothermia (36 to 37.5°C [96.8 to 99.5°F]) [23,26,27]. This question was addressed in two randomized controlled trials, one involving 260 children who were resuscitated from an out-of-hospital cardiac arrest (THAPCA-OH [Therapeutic Hypothermia after Pediatric Cardiac Arrest Out of Hospital trial]) and the other involving 329 children resuscitated from in-hospital cardiac arrest (THAPCA-IH) [26,27]. In an individual patient-level meta-analysis of both trials, patients who were assigned to therapeutic hypothermia had similar one-year survival compared with those assigned to targeted normothermia (44 versus 38 percent; RR 1.15, 95% CI 0.95-1.38) [23]. Rates of moderate or greater neurologic disability at one year were also similar in both groups (17 versus 11 percent).

Studies comparing ATC versus no ATC – The THAPCA trials do not address the question of whether ATC improves outcomes relative to standard post-resuscitation care without ATC because all patients enrolled in these trials received ATC (albeit targeting different temperatures). The evidence addressing this question is limited to retrospective observational studies evaluating outcomes in patients who received ATC (mostly in the form of mild therapeutic hypothermia) compared with patients who were managed without ATC [28]. These studies have reached variable conclusions, with some finding no association between ATC and survival or neurologic outcome [25,29-32], whereas others reported that ATC was associated with improved survival and/or favorable neurologic outcome [33,34].

Important uncertainties remain, including the optimal temperature range and duration for ATC and the optimal methods for cooling and rewarming. An ongoing clinical trial is addressing some of these questions [35].

Increased intracranial pressure (ICP) — Patients with significant anoxic brain injury are presumed to have cerebral edema and increased intracranial pressure during the first 48 hours after cardiac arrest. For this reason, in patients with stable blood pressure and without signs of shock, general measures to mitigate increased ICP are appropriate:

Elevation of the head of the bed 15 to 30 degrees with head maintained in midline

Active temperature control as described above (see 'Active temperature control' above)

In intubated patients, sedation, analgesia, and neuromuscular blockade (see 'Sedation, analgesia, and neuromuscular blockade' below)

However, unless the patient has severe traumatic brain injury, placement of an intracranial pressure monitor is not indicated. Furthermore, osmotic therapy for intracranial hypertension with hypertonic saline or mannitol is typically reserved for patients with clinical signs of acute brain herniation.

Seizures — Infants and children who remain comatose after cardiac arrest should have electroencephalogram (EEG) evaluation and continuous EEG monitoring for the presence of seizures. EEG evidence of seizure activity requires prompt antiseizure therapy to reduce the risk of worsening neurologic injury. However, prophylactic administration of antiseizure medications has not been shown to improve outcomes and is not recommended [1,2]. The management of convulsive status epilepticus in children is provided in the algorithm (algorithm 8) and along with nonconvulsive status is discussed separately. (See "Management of convulsive status epilepticus in children" and "Nonconvulsive status epilepticus: Treatment and prognosis".)

Based upon small observational studies, seizures are common following resuscitation from pediatric cardiac arrest occurring in approximately 33 to 50 percent of patients [36-38]. Non-convulsive status epilepticus has also been described and may affect a significant proportion of patients. As an example, non-convulsive status epilepticus was found after cardiac arrest in 6 of 19 children in one series [36].

Sedation, analgesia, and neuromuscular blockade — During post-cardiac arrest care, children frequently require sedation and analgesia to control pain and to prevent or manage shivering. Dosing, type of administration (intermittent or continuous), and specific agent depends upon a variety of factors that include the patient's age, underlying comorbidities, degree of neurologic injury, hemodynamic status, and time since arrest. Agents used for sedation and analgesia can cause hypotension and complicate neurologic assessment. Thus, the minimally effective dose should be used.

Our typical approach consists of sedation with a continuous infusion of dexmedetomidine combined with fentanyl or morphine for analgesia. For patients with seizures, we use a continuous infusion of midazolam instead of dexmedetomidine. We also use midazolam in single doses to supplement dexmedetomidine sedation as needed.

Some patients may also require neuromuscular blockade (eg, intermittent dosing of vecuronium or rocuronium) to achieve oxygen saturation or paCO2 targets and to avoid asynchrony between the patient's breathing and mechanical ventilation. Patients receiving active temperature control may also require neuromuscular blockade to counteract shivering.

Sedation and neuromuscular blockade conceal neurologic examination and impair the ability to detect clinical seizures, determine adequacy of analgesia, and assess prognosis [1]. Thus, children receiving neuromuscular blockade should also have continuous EEG monitoring, if not already established, to identify seizures. In addition, neuromuscular blockade should be permitted to wear off on a scheduled basis to permit regular evaluation of neurologic status and discomfort.

Glucose homeostasis — The clinician should monitor blood glucose levels and promptly treat hypoglycemia. (See "Approach to hypoglycemia in infants and children", section on 'Immediate management'.)

In addition, sustained hyperglycemia (blood glucose >180 mg/dL [10 mmol/L]) is associated with higher mortality in critically ill children and should be avoided [39,40]. Evidence indicates that blood glucose should be maintained below this threshold, but the role of "tight control" that uses insulin to achieve a specified blood glucose range is of uncertain value in children after cardiac arrest [41]. If performed, tight glucose control requires close monitoring of blood glucose and avoidance of hypoglycemia. Intensive insulin therapy in adults to maintain a blood glucose range of 80 to 110 mg/dL (4.4 to 6.1 mmol/L) increases the risk of hypoglycemia without benefit. (See "Glycemic control in critically ill adult and pediatric patients", section on 'Our approach'.)

Electrolyte abnormalities — Hypokalemia, hyperkalemia, and hypocalcemia are common electrolyte abnormalities encountered in post-cardiac arrest care and can cause cardiac arrhythmias with recurrent cardiac arrest. For this reason, serum electrolytes and ionized calcium should be evaluated frequently (eg, at minimum every four to six hours and more frequently in patients who have abnormal values). The treatment of specific electrolyte abnormalities is discussed in detail separately:

Hyperkalemia (algorithm 9) (see "Management of hyperkalemia in children")

Hypokalemia (see "Hypokalemia in children", section on 'Potassium supplementation')

Hypocalcemia (see "Primary drugs in pediatric resuscitation", section on 'Calcium')

Patients with hypokalemia should also have serum magnesium measured for detection and treatment of hypomagnesemia, as hypokalemia may not correct until magnesium is repleted. (See "Primary drugs in pediatric resuscitation", section on 'Magnesium sulfate'.)

Acute kidney injury — Approximately 30 to 40 percent children who survive cardiac arrest develop acute kidney injury (AKI) during post-cardiac arrest care [42]. Rarely, patients with severe AKI may require renal replacement therapy within the first 48 hours after ROSC [42]. For this reason, ongoing assessment of urine output and serial measurement of blood urea nitrogen and serum creatinine (eg, every 12 hours) are necessary to assess kidney function. In addition, frequent measurement of serum electrolytes, calcium, and phosphate (eg, every 4 to 6 hours) is required to identify and treat related electrolyte abnormalities such as hyperkalemia (algorithm 9), metabolic acidosis, and hyperphosphatemia with hypocalcemia. (See "Prevention and management of acute kidney injury (acute renal failure) in children", section on 'Management of acute kidney injury'.)

Maintaining adequate blood pressure while avoiding fluid overload are important priorities to decrease the likelihood of AKI in these patients. Avoid nephrotoxic medications in the immediate post-cardiac arrest period. For children with significant AKI, renal adjustment of medication dosing is best accomplished in consultation with trained pharmacy teams and nephrologists with pediatric expertise, as described separately. (See "Prevention and management of acute kidney injury (acute renal failure) in children".)

The primary indications for renal replacement therapy during post-cardiac arrest care include fluid overload unresponsive to pharmacologic therapy such as diuretics, hyperkalemia (serum or plasma potassium >6.5 mEq/L), and uremia (BUN >80 to 100 mg/dL). (See "Pediatric acute kidney injury: Indications, timing, and choice of modality for kidney replacement therapy".)

PROGNOSIS — Neuroprognostication for children during post-cardiac arrest care should be performed by pediatric neurologists or physicians with similar expertise. Many factors impact the prognosis for neurologic recovery after cardiac arrest in children. The ability to predict outcomes within the first 24 to 48 hours of arrest is generally poor, especially when the physical examination is altered by sedation and/or the use of therapeutic hypothermia. In particular, lack of motor function and pupillary response should not be used as reasons to withdraw care soon after return of spontaneous circulation (ROSC) in children [1]. (See "Treatment and prognosis of coma in children", section on 'Prognostic factors in hypoxic-ischemic and traumatic brain injury'.)

Serial electroencephalograms, evoked potentials, and magnetic resonance imaging (MRI) are all studies that can be used to assess cerebral function but have limitations as well, especially soon after cardiac arrest. Thus, they should not be used in isolation to make clinical decisions regarding withdrawal of care [2,3]. In particular, MRI performed for prognostic purposes is typically performed between three and seven days post-arrest.

COMMUNICATION WITH FAMILY — During post-cardiac arrest care, parents/primary caregivers require accurate and empathetic communication of their child's condition, current level of support and treatments, and next steps in care. Soon after return of spontaneous circulation, the clinician should emphasize that outcomes are difficult to predict and that multiple clinical findings must be considered by a physician with the appropriate expertise. The clinician should avoid premature predictions of clinical outcomes. Given the dynamic nature of post-arrest physiology, it is generally our practice to provide a broad overview during initial communication without focusing on speculative details. It is often helpful for families to anticipate at least several days of critical care; for comatose patients, the prognosis may remain unknown for at least three to five days.

SUMMARY AND RECOMMENDATIONS

Stabilization – During post-cardiac arrest care in children, important interventions to prevent recurrent arrest soon after return of circulation (ROSC) include:

Oxygenation – Provide supplemental oxygen, as needed, to maintain pulse oximetry 94 to 99 percent or, if the child has cyanotic congenital heart disease, the baseline value appropriate for the child's condition; avoid hyperoxia (pulse oximetry 100 percent). Both hypoxemia and hyperoxemia are harmful after a cardiac arrest. (See 'Oxygenation (pulse oximetry target)' above.)

Airway – Assess airway and maintain C-spine motion restriction in patients with trauma. (See 'Airway (C-spine motion restriction)' above.)

Most children with altered mental status, respiratory distress, or shock after ROSC require endotracheal intubation. For unintubated children, perform endotracheal intubation as indicated. Modify sedation for rapid sequence intubation, as needed, to avoid hypotension. (See 'Unintubated' above and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

For intubated children, ensure correct endotracheal tube positioning clinically and with chest radiography; place a gastric tube to prevent gastric distension and vomiting. (See 'Intubated' above.)

Breathing – For intubated children, correlate continuous quantitative end-tidal capnography with an initial arterial blood gas measurement to monitor PaCO2. Target mechanical ventilation to maintain normocapnia (eg, PaCO2 35 to 45 mm Hg) or, in patients with chronic lung disease with hypercapnia, near their baseline PaCO2. (See 'Ventilation (PaCO2 target)' above.)

Circulation – After ROSC, provide support to achieve a near-normal blood pressure (table 5 and table 6 and table 7) that is well above the 5th percentile threshold for shock and address any contributing factors to hemodynamic instability, as shown in the table (table 1).

Treat shock with a rapid infusion of isotonic fluid (lactated Ringer's or normal saline). The typical volume and rate is 10 to 20 mL/kg over 10 to 20 minutes with the lower volume used for patients with suspected or confirmed myocardial dysfunction. In patients with ongoing shock despite fluid administration, start a vasoactive infusion, typically epinephrine. (See 'Maintain blood pressure and treat shock' above and "Shock in children in resource-abundant settings: Initial management".)

Treat recurrent arrest (algorithm 3 and algorithm 4) and arrhythmias (algorithm 5 and algorithm 6) per Pediatric Advanced Life Support guidelines. (See 'Treat arrythmias' above.)

Obtain ancillary studies as described above. (See 'Ancillary studies' above.)

Disability – Minimize the risk of secondary brain injury:

-Dextrose – Measure rapid blood glucose and treat hypoglycemia (table 8), as needed.

-Elevate head of bed – For hemodynamically stable patients, elevate the head of the bed 15 to 30 degrees and keep the head midline. (See 'Increased intracranial pressure (ICP)' above.)

-Active temperature control, as discussed below.

-Electroencephalogram (EEG) monitoring – Initiate continuous EEG monitoring; promptly treat convulsive (algorithm 8) and non-convulsive seizures. (See "Management of convulsive status epilepticus in children" and "Nonconvulsive status epilepticus: Treatment and prognosis".)

Active temperature control (targeted temperature management) – For children who do not have purposeful movements or responses on neurologic examination after cardiac arrest, we suggest active temperature control to maintain core body temperature ≤37.5°C (99.5°F) (Grade 2C). It is reasonable to use one of two temperature targets (see 'Active temperature control' above):

-Normothermia (temperature 36 to 37.5°C [96.8 to 99.5°F]) for a duration of three to five days or per institutional guidelines. When targeting normothermia, many experts maintain children at 35°C to provide a buffer that avoids fever because temperature elevation can occur rapidly in these patients. However, evidence is lacking for this approach.

Or

-Therapeutic hypothermia (targeted temperature range 32 to 34°C [89.6 to 93.2°F]) for two days followed by three days of normothermia.

Definitive care – After ROSC, stabilize the child, consult with a pediatric critical care specialist, and rapidly transfer to a pediatric intensive care unit for ongoing management. (See 'Transfer to definitive care' above.)

Post-cardiac arrest care (PCAC) priorities – Priorities in PCAC in children and ongoing management are provided in the table (table 1). In addition, to continuing interventions established during stabilization as above, important actions include (see 'Ongoing management' above):

Treat reversible causes – Continue to evaluate and treat reversible and underlying causes of the cardiac arrest.

Sedation, analgesia, and neuromuscular blockade – Provide sedation and analgesia using the minimally effective dose to avoid hypotension. For most patients, we suggest a continuous infusion of dexmedetomidine plus fentanyl or morphine rather than other sedations regimens (Grade 2C). An exception is the patient with seizures, for whom we use a continuous infusion of midazolam instead of dexmedetomidine. (See 'Sedation, analgesia, and neuromuscular blockade' above.)

We suggest neuromuscular blockade (eg, intermittent dosing of vecuronium or rocuronium) for patients with any of the following (Grade 2C):

-Inability to achieve oxygen saturation or PaCO2 targets despite optimizing ventilator settings and sedation

-Asynchrony with the ventilator

-Shivering in the setting of active temperature control (ATC) that is refractory to sedation

Maintain glucose homeostasis – Continue to monitor blood glucose. Promptly treat hypoglycemia. Avoid sustained hyperglycemia (blood glucose >180 mg/dL [10 mmol/L]) as described separately. (See "Glycemic control in critically ill adult and pediatric patients", section on 'Our approach'.)

Anticipate and manage cardiovascular dysfunction – Impaired cardiac contractility and derangements in vascular tone commonly occur during the first 24 hours of PCAC. Management consists of fluid resuscitation with isotonic fluids (eg, lactated Ringer's or normal saline) to maintain central venous pressure, titration of vasoactive infusions (eg, epinephrine, milrinone, or both), and correction of hypocalcemia, hypoglycemia, and severe metabolic acidosis, as indicated.

Family communication and prognosis – Soon after ROSC, emphasize to the parents/primary caregivers that outcomes are difficult to predict and avoid speculating about the chance of survival or recovery. Consult pediatric neurologists or physicians with similar expertise to provide neuroprognostication. (See 'Prognosis' above and "Treatment and prognosis of coma in children", section on 'Prognostic factors in hypoxic-ischemic and traumatic brain injury'.)

  1. Topjian AA, de Caen A, Wainwright MS, et al. Pediatric Post-Cardiac Arrest Care: A Scientific Statement From the American Heart Association. Circulation 2019; 140:e194.
  2. Topjian AA, Raymond TT, Atkins D, et al. Part 4: Pediatric Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2020; 142:S469.
  3. Maconochie IK, Aickin R, Hazinski MF, et al. Pediatric Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation 2020; 156:A120.
  4. Ferguson LP, Durward A, Tibby SM. Relationship between arterial partial oxygen pressure after resuscitation from cardiac arrest and mortality in children. Circulation 2012; 126:335.
  5. Holton C, Lee BR, Escobar H, et al. Admission Pa o2 and Mortality Among PICU Patients and Select Diagnostic Subgroups. Pediatr Crit Care Med 2023; 24:e362.
  6. Del Castillo J, López-Herce J, Matamoros M, et al. Hyperoxia, hypocapnia and hypercapnia as outcome factors after cardiac arrest in children. Resuscitation 2012; 83:1456.
  7. Guerra-Wallace MM, Casey FL 3rd, Bell MJ, et al. Hyperoxia and hypoxia in children resuscitated from cardiac arrest. Pediatr Crit Care Med 2013; 14:e143.
  8. Bennett KS, Clark AE, Meert KL, et al. Early oxygenation and ventilation measurements after pediatric cardiac arrest: lack of association with outcome. Crit Care Med 2013; 41:1534.
  9. Barreto JA, Weiss NS, Nielsen KR, et al. Hyperoxia after pediatric cardiac arrest: Association with survival and neurological outcomes. Resuscitation 2022; 171:8.
  10. American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary and Emergency Cardiovascular Care - Part 12. Pediatric advanced life support. https://eccguidelines.heart.org/index.php/circulation/cpr-ecc-guidelines-2/part-12-pediatric-advanced-life-support/ (Accessed on November 10, 2015).
  11. de Caen AR, Berg MD, Chameides L, et al. Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132:S526.
  12. Maconochie IK, de Caen AR, Aickin R, et al. Part 6: Pediatric basic life support and pediatric advanced life support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015; 95:e147.
  13. Gardner MM, Hehir DA, Reeder RW, et al. Identification of post-cardiac arrest blood pressure thresholds associated with outcomes in children: an ICU-Resuscitation study. Crit Care 2023; 27:388.
  14. Topjian AA, French B, Sutton RM, et al. Early postresuscitation hypotension is associated with increased mortality following pediatric cardiac arrest. Crit Care Med 2014; 42:1518.
  15. Lin YR, Li CJ, Wu TK, et al. Post-resuscitative clinical features in the first hour after achieving sustained ROSC predict the duration of survival in children with non-traumatic out-of-hospital cardiac arrest. Resuscitation 2010; 81:410.
  16. Lin YR, Wu HP, Chen WL, et al. Predictors of survival and neurologic outcomes in children with traumatic out-of-hospital cardiac arrest during the early postresuscitative period. J Trauma Acute Care Surg 2013; 75:439.
  17. Topjian AA, Telford R, Holubkov R, et al. Association of Early Postresuscitation Hypotension With Survival to Discharge After Targeted Temperature Management for Pediatric Out-of-Hospital Cardiac Arrest: Secondary Analysis of a Randomized Clinical Trial. JAMA Pediatr 2018; 172:143.
  18. Laverriere EK, Polansky M, French B, et al. Association of Duration of Hypotension With Survival After Pediatric Cardiac Arrest. Pediatr Crit Care Med 2020; 21:143.
  19. Post-cardiac arrest care. In: Pediatric Advanced Life Support Provider Manual, Kadlec KD, McBride ME, Meeks R, et al (Eds), American Heart Association, Dallas 2020. p.261.
  20. Bembea MM, Nadkarni VM, Diener-West M, et al. Temperature patterns in the early postresuscitation period after pediatric inhospital cardiac arrest. Pediatr Crit Care Med 2010; 11:723.
  21. Duff JP, Topjian AA, Berg MD, et al. 2019 American Heart Association Focused Update on Pediatric Advanced Life Support: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics 2020; 145.
  22. Wyckoff MH, Greif R, Morley PT, et al. 2022 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Pediatric Life Support; Neonatal Life Support; Education, Implementation, and Teams; and First Aid Task Forces. Circulation 2022; 146:e483.
  23. Scholefield BR, Silverstein FS, Telford R, et al. Therapeutic hypothermia after paediatric cardiac arrest: Pooled randomized controlled trials. Resuscitation 2018; 133:101.
  24. Topjian A, Hutchins L, DiLiberto MA, et al. Induction and maintenance of therapeutic hypothermia after pediatric cardiac arrest: efficacy of a surface cooling protocol. Pediatr Crit Care Med 2011; 12:e127.
  25. Fink EL, Clark RS, Kochanek PM, et al. A tertiary care center's experience with therapeutic hypothermia after pediatric cardiac arrest. Pediatr Crit Care Med 2010; 11:66.
  26. Moler FW, Silverstein FS, Holubkov R, et al. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Engl J Med 2015; 372:1898.
  27. Moler FW, Silverstein FS, Holubkov R, et al. Therapeutic Hypothermia after In-Hospital Cardiac Arrest in Children. N Engl J Med 2017; 376:318.
  28. Buick JE, Wallner C, Aickin R, et al. Paediatric targeted temperature management post cardiac arrest: A systematic review and meta-analysis. Resuscitation 2019; 139:65.
  29. Scholefield BR, Morris KP, Duncan HP, et al. Evolution, safety and efficacy of targeted temperature management after pediatric cardiac arrest. Resuscitation 2015; 92:19.
  30. Doherty DR, Parshuram CS, Gaboury I, et al. Hypothermia therapy after pediatric cardiac arrest. Circulation 2009; 119:1492.
  31. Cheng HH, Rajagopal SK, Sansevere AJ, et al. Post-arrest therapeutic hypothermia in pediatric patients with congenital heart disease. Resuscitation 2018; 126:83.
  32. Matsui S, Hirayama A, Kitamura T, et al. Target Temperature Management and Survival with Favorable Neurological Outcome After Out-of-Hospital Cardiac Arrest in Children: A Nationwide Multicenter Prospective Study in Japan. Ther Hypothermia Temp Manag 2022; 12:16.
  33. Lin JJ, Hsia SH, Wang HS, et al. Therapeutic hypothermia associated with increased survival after resuscitation in children. Pediatr Neurol 2013; 48:285.
  34. Lin JJ, Lin CY, Hsia SH, et al. 72-h therapeutic hypothermia improves neurological outcomes in paediatric asphyxial out-of-hospital cardiac arrest-An exploratory investigation. Resuscitation 2018; 133:180.
  35. Study record details for the Pediatric Influence of Cooling Duration on Efficacy in Cardiac Arrest Patients (P-ICECAP) trial. Available at: https://clinicaltrials.gov/study/NCT05376267.
  36. Abend NS, Topjian A, Ichord R, et al. Electroencephalographic monitoring during hypothermia after pediatric cardiac arrest. Neurology 2009; 72:1931.
  37. Kirkham F. Cardiac arrest and post resuscitation of the brain. Eur J Paediatr Neurol 2011; 15:379.
  38. Constantinou JE, Gillis J, Ouvrier RA, Rahilly PM. Hypoxic-ischaemic encephalopathy after near miss sudden infant death syndrome. Arch Dis Child 1989; 64:703.
  39. Srinivasan V, Spinella PC, Drott HR, et al. Association of timing, duration, and intensity of hyperglycemia with intensive care unit mortality in critically ill children. Pediatr Crit Care Med 2004; 5:329.
  40. Kong MY, Alten J, Tofil N. Is hyperglycemia really harmful? A critical appraisal of "Persistent hyperglycemia in critically ill children" by Faustino and Apkon (J Pediatr 2005; 146:30-34). Pediatr Crit Care Med 2007; 8:482.
  41. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:S876.
  42. Neumayr TM, Gill J, Fitzgerald JC, et al. Identifying Risk for Acute Kidney Injury in Infants and Children Following Cardiac Arrest. Pediatr Crit Care Med 2017; 18:e446.
Topic 140197 Version 3.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟