Coma in the infant/child

Pediatric Coma

Related Conditions

Altered mental status, neurologic depression, stupor, lethargy, drowsiness, obtundation

1. Description of the problem

What every clinician needs to know

Coma in children can occur commonly and from a number of etiologies. Focus in care should be on rapidly treating the ABCs of the patient while thinking through etiologic possibilities, ordering appropriate additional testing and determining other specfic directed therapy. Determining whether the condition is acute, subacute or chronic is also essential to management.

Clinical features

Coma can be defined in many ways, but a standard definition is: any decrease in level of consciousness, where consciousness represents a state of awareness of self and the environment. Further subdividing levels of consciousness is problematic and may not affect management. The Glasgow coma scale (GCS) is also used in children, with score ranges from 3-15 as in adults. Components include eye (1-4), verbal (1-5) and motor (1-6).

GCS was devised for initial assessment in first 24 hours for adults with head trauma. It has been revised for children and often used after 24 hours. While not able to be used for predictive value at that point, it does provide a shorthand for characterization of level of consciousness. A GCS of less than 8 is considered an alternate definition of coma.

Modified pediatric GCS (child/infant)

Eye

1 No opening

2 Opens in response to pain only

3 Opens in response to voice

4 Opens spontaneously

Verbal

1 No response

2 Incomprehensible words/moans in response to pain

3 Inappropriate words/cries in response to pain

4 Confused/Irritable cries

5 Oriented, appropriate/coos and babbles

Motor

1 No response

2 Responds to pain with extension/responds to pain with decorticate posturing

3 Responds to pain with flexion/responds to pain with decerebrate posturing

4 Withdraws in response to pain

5 Localizes painful stimulus/responds to touch

6 Obeys commands/movesspontaneously and purposefully

Key management points

Management should address acute stabilization, directed testing and more specific therapy based on underlying cause.

2. Emergency Management

Key management steps

Acute management includes:

• Airway: provision of a patent airway is of utmost importance. Simple positioning maneuvers can often provide marked improvement in the obtunded patient. Intubation should be performed in the child who appears to be unable to protect his or her airway and is an aspiration risk. Generally a GCS of 8 or less is considered a high risk and an indication for endotracheal intubation.

• Breathing: Adequate respiratory effort and assuring normocarbia is vital. Avoiding excess carbon dioxide concentration is important in elevated ICP settings, although prophylactic hyperventilation is not recommended.

• Circulation: assuring adequate cerebral perfusion is critical. Maintaining both perfusion and mean arterial pressure is key. Use of fluid boluses must be balanced against concern for worsening of cerebral edema. Vasopressor support can be used somewhat earlier than might be normally considered to insure adequate cerebral perfusion pressure (MAP-CPP). Treat malignant hypertension cautiously to avoid excessive drop in blood pressure.

• Da Brain:

• Both assessment and intervention occur at this point.

• Computerized tomography (CT) of the head provides the most rapid radiographic assessment.

• Administer IV glucose.

• If considering infection, consider LP but do not delay braod-spectrum antibiotic therapy.

• Treat suspected seizures with anticonvulsants.

• Give specfic antidotes if suspected ingestion: opiates-naloxone, benzodiazepines-flumazenil, anticholinergics-physostigmine.

• Elevation of head of bed to 30-40 degrees with the head midline is a simple but effective maneuver to improve cerebral venous return.

• Hypertonic saline (3%) has become increasingly used as an osmotic of choice (dose 3-5 ml/kg as needed) for suspected or actual increased intracranial pressure compared to longstanding approaches of mannitol (0.5-1 gram/kg).

• Hypertonic saline infusions may be used to maintain osmotic control with close sodium monitoring.

• Hyperventilation may be transiently provided for acute elevations in ICP but not maintained prophylactically.

Greek proverb: Act quickly, think slowly. Treat the A,B,C,Ds even as you are undertaking diagnostic workup.

Hypertonic (3%) saline: 3-5 ml/kg IV over 15-20 minutes for actual or suspected increased intracranial pressure, symptomatic cerebral edema

Mannitol: 0.5-1 mg/kg IV push for increased intracranial pressure

Serum sodium concentrations, urine output should be monitored closely.

3. Diagnosis

Differential diagnosis

The differential diagnosis of pediatric coma is broad and deep. General categories are metabolic, toxic and structural. Two approaches can be taken. One classic differential is described by the acronym AEIOUTIPs (vowel-TIPs) modified for the infant/child:

Acidosis (lactic, DKA)/alcohol ingestion.

Epilepsy/exposure (heat, cold)/endocrine-hypo, hyperglycemia, hypothyroid.

Infection/intussesception/inborn error of metabolism.

Overdose/oxygen deficit (hypoxemia, near droowning, apnea).

Uremia.

Trauma/iumor.

Psychosis/poisoning (carbon monoxide).

Stroke/intracranial lesions: vasculitis, hydrocephalus.

Causative mechanisms of coma also define etiology as below.

Specific diagnosis is established by directed laboratory assessment based on prioritizing likely diagnoses.

Targeted laboratory and radiologic diagnosis is coupled with rapid neurological exam to determine level of neurologic lesion:

General assessment of responsiveness to sensory, auditory stimuli.

Respiratory pattern – abnormal patterns associated with central lesions include: Cheyne-Stokes breathing (alternating hyperpnea and apnea suggesting extensive bilateral dysfunction), central neurogenic hyperventilation (pontine or tegmental lesion), apneustic breathing (pontine lesions), ataxic breathing (medulla).

Pupillary changes–can give clues to site and source:

• Small, reactive: metabolic

• Small, reactive: hypothalamic

• Large, nonreactive, hippus: tectal

• Pinpoint: pontine

• Mid-position, fixed: midbrain

• Ipsilateral pupil fixed, dilated: oculomotor nerve, uncal herniation

• Bilateral fixed, dilated: severe hypoxic-ischemic encephalopathy

• Dilated and fixed, with SLUDGE symptoms: anticholinergic poisoning

• Pinpoint pupils: opiate poisoning

Posture – can define source of AMS

• Kernig’s, Brudzinski signs: meningitis

• Decorticate posturing: supratentorial lesion

• Decerebrate posturing: brainstem dysfunction

• Arm extension with leg flexion: pontine lesion

• Flaccidity: brainstem damage below pontomedullary level

Lab and radiologic tests

Laboratory and radiologic testig should be directed at most likely etiologies, with prioritization on tests with the most rapid turnaround and tests associated with an etiology amenable to treatment. Potential lab studies include: Arterial blood gas.

• Serum toxin levels, urine drug screen, serum ethanol levels

• Liver function tests

• Serum ammonia level

• Electrolytes to include glucose

• Complete blood count with differential to assess for evidence of infection

• Urine organic acids and serum amino acids

• Blood culture

• CSF examination

• Carnitine levels

• Urine, serum osmolarity

• Anticonvulsant levels

Potential testing methods:

• CT scan, head

• EEG

• Chest radiograph

• Skeletal survey

• MRI scan

Pertinent laboratory findings: laboratory findings can help isolate etiology of coma as above.

Pathophysiology

Pathophysiologic mechanisms of coma are related to the cause.

Traumatic (direct and indirect injury):

Concussive syndrome

Epidural hematoma

Subdural hematoma

Diffuse axonal injury (shear)

Intracerebral hemorrhage

Carotid artery trauma

Structural:

Neoplasms

Vascular disease

Cerebral infarct-thrombosis, embolism

Cerebral hemorrhage-AVM, aneurysm

Vasculitis

Hydrocephalus

Infectious:

Meningitis

Abscess

Cerebritis

Meningoencephalitis

Subdural empyema

Metabolic:

Hypoglycemia

Hyperglycemia (DKA)

Acidosis

Hyperammonemia

Thyroid dysfunction, adrenal insuficiency

Uremia

Toxic:

Ingestions-accidental/intentional: multiple types-EX: sedatives, analgesics, antidepressants, clonidine

Recreational drugs

Alcohol

Cyanide

Hypoxic-Ischemic:

Shock

Near drowning

Carbon monoxide poisoning

Strangulation

Epidemiology

Most common etiologies of coma/altered mental status by age include:

Infant

Infection

Inborn error of metabolism

Metabolic

Abuse

Trauma

Seizure

Child

Ingestion

Infection

Seizure

Trauma

Abuse

Intussusception

Adolescent

Ingestion

Intentional

Trauma

Drug/alcohol overdose

Prognosis

Prognosis is dependent on etiology of coma, level of depression and rapidity of recovery of neurologic signs. MRI of brain at after 24 hours with watershed or basal ganglia injury or brainstem injury has 100% positive predictive value for unfavorable outcome.

Special considerations for nursing and allied health professionals.

N/A

What's the evidence?

Plum, F, Posner, J. The diagnosis of stupor and coma. 1980. (The classic text on altered mental status.)

Pearson-Shaver, A, Mehta, R, Fuhrman and Zimmerman. “Coma and Depressed Sensorium”. Pediatric Critical Care. 2006. pp. 855-64.

Abend, N, Kessler, S, Nichols. “Evaluation of the comatose child”. Rogers Textbook of Pediatric Intensive Care. 2008. pp. 846-61.

Ashwal, S. “Medical aspects of the minimally conscious state in children”. Brain Dev. vol. 25. 2003. pp. 535-45.

Michelson, D, Ashwal, S, Wheeler, Wong, Shanley. “Evaluation of coma”. Pediatric Critcal Care Medicine. 2006. pp. 924-34.

Christophe, C. “Value of MR imaging of the brain in children with hypoxic coma”. AJNR Am J Neuroradiol. vol. 23. 2002. pp. 716-23. (Good reference on MR findings and outcome.)

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