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Treatment and prognosis of coma in children

Treatment and prognosis of coma in children
Literature review current through: Jan 2024.
This topic last updated: Oct 16, 2019.

INTRODUCTION — Coma is an alteration of consciousness in which a person appears to be asleep, cannot be aroused, and shows no awareness of the environment [1]. Coma is therefore the most profound degree to which the two components of consciousness, arousal and awareness, can be diminished. Less profound states of impaired consciousness (stupor, lethargy, obtundation) preserve one or more of these components to some degree.

This topic will discuss issues related to the acute management of a child presenting with altered arousal. The differential diagnosis and evaluation of stupor and coma in children and the evaluation, treatment, and prognosis of stupor and coma in adults are presented separately. (See "Evaluation of stupor and coma in children" and "Stupor and coma in adults".)

TREATMENT — Early treatment of coma is generally supportive until a definitive diagnosis is made. An important goal of early treatment is to limit brain injury.

Although discussed separately, the assessment and management of children in coma are performed jointly in practice (table 1). The primacy of ABCs (airway, breathing, circulation) applies to coma as to other medical emergencies.

Airway — Establishing a secure airway and providing adequate ventilation may be lifesaving and also may limit neurologic injury. Establishing a secure airway in a patient with coma may be attained by repositioning the child to open the airway, but often requires intubation to ensure adequate ventilation and to prevent aspiration of secretions or gastric contents. (See "Technique of emergency endotracheal intubation in children".)

Patients with Glasgow Coma Scale (GCS) <8 (table 2) are usually unable to adequately protect their airway and should be intubated. If trauma is suspected, the cervical spine should be stabilized with a collar while securing the airway. Approaches to minimize the impact of intubation on potentially elevated intracranial pressure (ICP) should be considered. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis".)

Breathing — Oxygen saturation should be continuously monitored and supplemental oxygen provided (see "Continuous oxygen delivery systems for the acute care of infants, children, and adults"). Adequacy of ventilation should be assessed by examination, end-tidal carbon dioxide monitoring, and/or blood gases.

For most patients, the goal of assisted ventilation is to maintain normal carbon dioxide levels (ie, PaCO2 35 to 40 mmHg); hypo- and hyperventilation should be avoided since both can contribute to secondary brain injury. Hyperventilation is reserved only for patients with acute or impending herniation. In this setting it is provided as a temporary measure while awaiting more definitive intervention. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Therapeutic hyperventilation'.)

Circulation — Hypotension can contribute to secondary brain injury and should be treated aggressively [2-4]. Effective circulation through intravenous (IV) isotonic fluid administration (normal saline or lactated Ringers) and vasoactive medications, if necessary, is essential to maintain adequate cerebral perfusion. (See "Shock in children in resource-abundant settings: Initial management".)

For patients with hypertensive encephalopathy, the blood pressure should be lowered slowly to avoid superimposing an ischemic insult. Short-acting IV medications are preferred to longer-acting agents for closer control of blood pressure. (See "Approach to hypertensive emergencies and urgencies in children", section on 'Treat hypertensive emergency or urgency'.)

Hypertensive encephalopathy has an excellent prognosis for recovery if ischemia can be avoided [5]. (See "Acute toxic-metabolic encephalopathy in children", section on 'Hypertensive encephalopathy and reversible posterior leukoencephalopathy'.)

Glucose — Fingerstick blood sugar and a serum glucose should be checked immediately in the evaluation of a comatose child. Hypoglycemia may be a cause or complication of coma. In either case, hypoglycemia should be treated immediately (2.5 mL/kg of 10 percent dextrose solution). Ongoing monitoring and treatment may be needed. (See "Approach to hypoglycemia in infants and children".)

Intracranial pressure — When increased ICP is suspected based on computed tomography (CT) findings, papilledema, split sutures, or a herniation syndrome, emergent treatment is recommended. Increased ICP is assumed when there is coma after head injury.

Early interventions to reduce ICP include treating fever, elevating the head of the bed to 30 degrees above horizontal, and administering hyperosmolar therapy (eg, mannitol or hypertonic saline). Neurosurgery should be consulted. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Ongoing Management' and "Elevated intracranial pressure (ICP) in children: Management", section on 'Treatment of elevated ICP'.)

Seizures — Ongoing seizures (status epilepticus) are treated as an emergency; typically, lorazepam 0.1 mg/kg IV up to a maximum of 4 mg is administered. (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment'.)

If seizures have occurred but are not ongoing, antiseizure medications (eg, fosphenytoin, 15 to 20 mg/kg phenytoin equivalent IV) should be administered to prevent recurrence. (See "Seizures and epilepsy in children: Initial treatment and monitoring".)

Recurrent seizures or status epilepticus may increase ICP and may be associated with secondary brain injury and worse neurologic outcome. Prolonged seizures have been associated with adverse outcomes in meningitis, encephalitis, and other central nervous system (CNS) infections [6-10]. (See "Management of convulsive status epilepticus in children".)

Nonconvulsive status epilepticus should be considered as a diagnosis even when there are no obvious seizure movements. Nonconvulsive seizures can cause coma and also complicate other etiologies of coma, including infection and metabolic disease. If nonconvulsive seizures are suspected and an electroencephalogram (EEG) is not available, a therapeutic trial of fosphenytoin or lorazepam (0.1 mg/kg IV) is reasonable. (See "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis".)

Infection — Empiric antibiotic and antiviral therapy are recommended if bacterial meningitis (eg, ceftriaxone 100 mg/kg per day in one or two divided doses, maximum dose 4 g per day, plus vancomycin 60 mg/kg per day in four divided doses) or viral encephalitis (acyclovir 30 to 60 mg/kg per day, in three divided doses) are among the suspected entities [11,12]. Blood cultures should be obtained prior to starting antibiotics. Since lumbar puncture is generally deferred until neuroimaging is obtained, initiation of therapy should not be delayed for lumbar puncture. Therapy should be continued until these conditions have been excluded (table 3). (See "Bacterial meningitis in children older than one month: Treatment and prognosis", section on 'Empiric therapy' and "Viral meningitis in children: Management, prognosis, and prevention" and "Viral meningitis in children: Clinical features and diagnosis", section on 'Clinical features' and "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical features'.)

Temperature control — Fever should be treated aggressively with antipyretics and/or cooling blankets. Hyperthermia (>38.5°C) can contribute to brain damage in cases of ischemia. Fever also increases cerebral metabolism and blood flow [13]. This can cause worsening intracranial hypertension in patients with elevated ICP and can contribute to secondary brain injury following acute traumatic or anoxic brain injury. Shivering also can contribute to elevated ICP and should be avoided.

While induced hypothermia has been suggested as a second-tier therapy for refractory increased ICP in children with traumatic brain injury (TBI), it is currently not recommended for the treatment of severe TBI in children. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Temperature control'.)

The use of targeted temperature management (ie, active control of temperature in a predefined range) for children after resuscitation after an out-of-hospital cardiac arrest is discussed separately. (See "Pediatric advanced life support (PALS)", section on 'Active temperature control'.)

Acid-base and electrolyte imbalance — Electrolyte imbalance and acidosis may cause or be a complication of coma, and may increase the risk of neurologic injury. Electrolyte abnormalities and acidosis should generally be corrected and monitored serially. (See "Acute toxic-metabolic encephalopathy in children", section on 'Electrolyte derangements' and "Approach to the child with metabolic acidosis".)

An exception to this is mild to moderate hypernatremia. Intervention is generally not necessary to correct mild to moderate hypernatremia in the management of children with severe traumatic or hypoxic-ischemic brain injury. Hypernatremia commonly occurs in patients treated with hypertonic saline for management of intracranial hypertension; moderate hypernatremia is a goal of therapy in this setting. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Hypertonic saline'.)

By contrast, hyponatremia can exacerbate cerebral edema and should be corrected while a search for the cause is underway. (See "Hyponatremia in children: Etiology and clinical manifestations".)

Antidotes — Antidote use is recommended only in the setting of known or strongly suspected drug overdose [14]. Naloxone (0.1 mg/kg IV in patients up to 20 kg or ≤5 years; maximum 2 mg) is a relatively safe and effective treatment and should be considered when the history suggests possible opiate ingestion.

While flumazenil is an effective antidote for benzodiazepine overdose, such overdoses alone are rarely life-threatening and may be managed with supportive airway measures. However, if comprehensive management of the pediatric airway is not available, then reversal should be considered. Flumazenil will also render benzodiazepines ineffective in the event of a seizure, another reason to limit its use.

The management of toxic ingestions is discussed separately. (See "Approach to the child with occult toxic exposure" and "Opioid intoxication in children and adolescents".)

Agitation — Sedative agents should be administered only when the benefits of relieving agitation outweigh the need for close neurologic monitoring by exam. Agitation may increase ICP, interfere with respiratory support, and increase the risk of injury. However, oversedation may obscure the neurologic exam and can contribute to hypotension and hypoventilation. During the acute postinjury period (ie, first 24 to 48 hours), short-acting sedative agents may be preferred to allow intermittent lifting of sedation for serial assessments of neurologic examination.

PROGNOSIS — Coma is a transient state, usually lasting no more than two to four weeks [15]. Children recover, die, or evolve into a persistent vegetative or minimally conscious state. The features of persistent vegetative and minimally conscious states are described separately. (See "Evaluation of stupor and coma in children", section on 'Definitions'.)

A vegetative state is considered permanent, with little chance of improvement, if it lasts longer than 12 months after traumatic injury or longer than three months after nontraumatic injury. There are fewer studies regarding minimally conscious patients, but the prognosis is probably less dire. Accurate differentiation of minimally conscious patients from vegetative patients requires repeated assessments by an experienced multidisciplinary team [15]. Functional magnetic resonance imaging (MRI) and positron emission tomography (PET) studies hold promise for better classification of these patients [16].

Etiology — The prognosis in coma is largely specific to the etiology. For children presenting with stupor or coma due to poisoning or overdose (accidental or intentional), the prognosis is generally good. With appropriate supportive care, most children make a full recovery. (See "Prevention of poisoning in children", section on 'Fatalities'.)

By contrast, for children with acute hypoxic-ischemic injury (eg, following cardiac arrest or drowning), outcomes are generally poor. (See 'Prognostic factors in hypoxic-ischemic and traumatic brain injury' below.)

In a study of 278 previously healthy children, mortality rates varied considerably according to etiology [17]:

Drowning – 84 percent

Infection (predominantly Neisseria meningitis) – 60 percent

Metabolic causes – 27 percent

Intoxication (accidental and intentional) – 3.4 percent

The prognosis of specific etiologies of coma are discussed separately:

Bacterial meningitis (see "Bacterial meningitis in children: Neurologic complications")

Encephalitis (see "Acute viral encephalitis in children: Treatment and prevention", section on 'Prognosis')

Drowning (see "Drowning (submersion injuries)", section on 'Outcome')

Brain tumors (see "Overview of the management of central nervous system tumors in children", section on 'Prognosis')

Intracranial hemorrhage (see "Hemorrhagic stroke in children", section on 'Prognosis')

Prognostic factors in hypoxic-ischemic and traumatic brain injury — Prognosis for coma recovery in children has been most studied for hypoxic-ischemic encephalopathy (HIE) and traumatic brain injury (TBI). As a general rule, the potential for neurologic recovery is greater with TBI compared with HIE. Studies of outcome in these conditions are not applicable to other etiologies.

In general, more severe injury is associated with worse prognosis for neurologic recovery, and many of the individual factors described below are surrogates for injury severity [18]. While these factors have been shown to be associated with prognosis, none have sufficient predictive power alone for clinical decision-making.

Combinations of factors are likely more predictive than any single test. As an example, in one study of severely brain-injured children, when performed >24 hours after the event, pupillary response, motor response, and bilateral somatosensory evoked potential (SEP) testing together reached a specificity of 100 percent for both favorable and unfavorable outcomes [19]. Other studies also confirm the superior ability of combined assessments to predict outcome [18].

Similarly, serial assessments are more informative than a single assessment. The ability to predict outcomes at 24 to 48 hours following brain injury is generally poor. However, prognostic accuracy improves as additional clinical data become available [20].

In most studies, age is not an independent predictor of neurologic outcome among pediatric patients [21].

Initial postinjury period — The details of the clinical presentation and initial postinjury period (eg, first 24 to 48 hours) are important to consider; however, these factors alone do not reliably predict outcome.

Duration of CPR – In children who have suffered cardiac arrest, duration of cardiopulmonary resuscitation (CPR) prior to return of spontaneous circulation is an important predictor of outcome [22,23]. In a prospective, multicenter registry of 3419 children who suffered in-hospital cardiac arrest, the probability of a favorable neurologic outcome fell linearly in the first 15 minutes of CPR and decreased by 1.2 percent for each additional minute of CPR [23]. The likelihood of survival with favorable neurologic outcome was 31 percent among those with CPR duration ≤15 minutes compared with 12 percent and 10 percent in those with CPR duration 16 to 35 minutes and >35 minutes, respectively. Outcomes following out-of-hospital cardiac arrest are generally worse than for in-hospital arrest [24].

Early complications – Hypotension, hypoxia, and/or seizures are associated with worse outcome [2,25-29]. Their presence may reflect a more severe primary insult; in addition, they may contribute to secondary brain injury and worse outcome on that basis. In a study of 93 children with severe TBI, hypotension in the field and/or emergency department was associated with poor neurologic outcome [2].

In children who have suffered cardiac arrest or global hypoxic-ischemic insult, high levels of lactic acidosis and other organ failures (eg, acute kidney injury, hepatic injury) are early indicators of the extent of injury and correlate with risk of death or poor neurologic outcome [29,30]. Similarly, in patients with TBI, initial hyperglycemia, increased intracranial pressure (ICP), and the need for mechanical hyperventilation correlate with a poor neurologic outcome [31].

Injury type — Children with TBI due to nonaccidental (abusive) trauma appear to have increased morbidity and mortality compared with those with TBI due to accidental mechanism; this may be related to delays in seeking care or preexisting neurologic injury [32]. (See "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children".)

Patients who present after drowning may have a better prognosis than patients with hypoxic-ischemic injury secondary to another cause of cardiac arrest. This may be due to neuroprotective effects of hypothermia. (See "Drowning (submersion injuries)", section on 'Outcome'.)

Examination findings — Examination findings correlate with the severity of brain injury and can be useful prognostic indicators, particularly as deficits persist past the initial few days. However, the use of sedative medications and the presence of secondary complications can also confound the neurologic examination and suggest a worse prognosis than is warranted.

A low Glasgow Coma Scale (GCS) score (table 2) at 24 hours is associated with poor prognosis in both HIE and TBI [21,33-38]. In a study of 57 children with HIE, GCS <5, and absent spontaneous breathing at 24 hours, each had a positive predictive value of 100 percent for severe disability or death [33]. However, these exam findings did not capture all children who later progressed to severe disability or death, with a sensitivity of approximately 50 percent [33]. In patients with HIE after cold-water submersion, a low-admission GCS may be less predictive of poor outcome [39].

The use of the GCS in an intubated patient may be limited as verbal responses are not possible; in this setting, we find purposeful or pain-localizing movements (eg, reaching for the endotracheal tube) reassuring.

Other assessments — Assessments such as electroencephalogram (EEG), evoked potentials (EPs), neuroimaging, and serum biomarkers play a role in assessing prognosis, particularly when the neurologic examination is affected by sedation [18,29].

Electroencephalogram — EEG has been studied as a predictor of outcome in coma of certain etiologies. Limiting factors include its sensitivity to electrical noise, common in an emergency department or intensive care unit. Sedative drugs cause EEG abnormalities and make interpretation difficult, particularly for prognosis. (See "Electroencephalography (EEG) in the diagnosis of seizures and epilepsy", section on 'Routine EEG technique'.)

Studies using EEG for prognosis in comatose children are limited. Serial EEGs appear to be more useful than a single study [39,40]. In a meta-analysis including patients older than 10 years of age with HIE, EEG findings of an isoelectric baseline or a burst suppression pattern during the first week after coma were 100 percent specific for poor outcome [41]. This finding, however, is not predictive of a poor outcome in other toxic metabolic encephalopathies. Other EEG patterns (eg, periodic epileptiform discharges, nonreactive rhythms) have been associated with poor outcome, but have poor sensitivity and specificity [33,39,42].

EEG may have additional benefit of identifying nonconvulsive status epilepticus, which can both cause coma and complicate other etiologies of coma, including infection and metabolic disease. In one study of children with TBI who were monitored with EEG, 16 percent had subclinical seizures and 13 percent had subclinical status epilepticus [43]. (See "Evaluation of stupor and coma in children", section on 'Electroencephalogram'.)

Evoked potentials — EPs are measured responses in electrical signals of the brain after a sensory stimulus. Compared with EEG, EPs are less affected by sedative medication and are insensitive to electrical noise. The test is technically more demanding to perform, however [44]. Also, patients with focal brain lesions, subdural hemorrhage, or craniotomy may have an absent (false-positive) EP response; data should be interpreted with caution in these patients. EP should be performed more than 24 hours after the onset of coma and reconfirmed 24 hours after the initial examination in order to maximize specificity [45].

SEPs have high specificity and are more useful than EEG in predicting poor outcome in both children and adults in coma, especially due to HIE [39,41,46,47]. As an example, in one study of 57 children with HIE, SEPs, when bilaterally absent at 24 hours, had a positive predictive value for poor outcome of 100 percent and a sensitivity of 63 percent [33].

False-positive SEP results may be more problematic in other conditions. In one series of 53 children with coma from a variety of etiologies and bilaterally absent SEPs, the overall prognosis was very poor; 38 died and 11 survived with persistent vegetative state or severe neurologic deficits [25]. However, four, all with TBI, did survive with mild to moderate neurologic deficits. A systematic review of SEPs for prognosis in coma in patients of all ages, published before this report, found an overall false-positive rate of <0.5 percent; however, it noted that most of the false positives were children and cases of TBI [45]. Another systematic review included an independent analysis of 10 studies done in children in coma. It found an overall false-positive rate of 7 percent for absent SEPs in children who awakened from coma [48].

While associated with poor outcome, absent visual EP and brainstem auditory EP do not have adequate predictive ability for outcome in childhood coma [47,49,50].

Magnetic resonance imaging — MRI often shows a greater extent of injury than can be appreciated on computed tomography (CT); this can be helpful in making qualitative assessments regarding prognosis [51,52].

In one study of 40 children with HIE, MRIs were scored based on findings of brain edema, herniation, or structural changes in "watershed areas" or basal ganglia [53]. A high score had a sensitivity of 96 percent and specificity of 50 percent for moderate to severe disability. The presence and extent of brain edema, brainstem injury, and diffuse axonal injury on MRI have also been associated with poorer prognosis in patients with TBI [21,54-57].

Other neuroimaging modalities, magnetic resonance spectroscopy, functional MRI, and PET are not useful in the evaluation of coma prognosis [58]. Studies, awaiting validation, suggest that these tools may help discriminate between persistent vegetative state, minimally conscious state, and other states of impaired consciousness [59].

Serum biomarkers — A number of serum biomarkers have been studied in children with HIE and TBI, but are not used in routine clinical practice [60-63]. S100B and neuron-specific enolase (NSE) have been investigated the most; neither is used routinely in clinical practice. Studies evaluating the prognostic value of these markers have been limited by small sample size, inconsistencies in outcomes measured (some reports evaluated only the correlation with neuroimaging findings), and, in some cases, conflicting results. Further studies are needed to clarify the role of these tests in predicting outcome in pediatric coma.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Coma (The Basics)")

SUMMARY AND RECOMMENDATIONS — Stupor and coma are alterations in arousal; these are neurologic emergencies.

Evaluation and early therapeutic interventions should proceed promptly, even simultaneously. A protocol for urgent evaluation and management is outlined in the table (table 1). (See 'Treatment' above.)

The prognosis for neurologic recovery depends in large part on etiology, with good prognosis for uncomplicated drug intoxications, and a poor prognosis for hypoxic-ischemic encephalopathy (HIE). (See 'Prognosis' above.)

Examination findings, clinical course, electrophysiologic tests, and magnetic resonance imaging (MRI) all provide information that is helpful in gauging neurologic prognosis. (See 'Prognosis' above.)

However, uniformly reliable tools that accurately predict outcome in most clinical situations are lacking. In cases of HIE, which are not associated with cold-water drowning, a Glasgow Coma Scale (GCS) score <5 and bilaterally absent somatosensory evoked potentials (SEPs) appear to have the best established predictive ability for poor neurologic outcome. (See 'Examination findings' above and 'Evoked potentials' above.)

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Topic 6164 Version 13.0

References

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