The Comatose Child



The Comatose Child


James Owens

Daniel G. Glaze



DEFINITION AND PATHOPHYSIOLOGY

Coma is not a specific disorder, but a sign of central nervous system (CNS) dysfunction. It may be caused by either a primary or a systemic condition affecting the CNS. A patient in a coma is unresponsive to any environmental stimuli. Coma is a medical emergency and represents a life-threatening situation; it requires prompt supportive therapy to prevent hypoxia and rapid etiologic diagnosis to ensure that proper specific therapy is initiated.

The term coma often is used inappropriately to describe virtually any state of altered consciousness. The terms used in this chapter to describe altered states of consciousness are defined here. The correct use of these terms in clinical practice and in publications is recommended (Box 404.1).


The standardized Glasgow Coma Scale (GCS) is used widely in evaluating a patient’s responsiveness after traumatic coma and, more recently, nontraumatic coma (Table 404.1). This scale, which depends only on a clinical examination performed at the bedside, allows staging by serial examinations of the patient and has permitted comparative study of patients in different centers. Its usefulness in young children is limited somewhat, however, because some of the parameters depend on the patient’s understanding and responding to language.

In general, the underlying pathophysiology of coma is accounted for by two types of lesions or processes: those that affect the reticular formation of the brainstem (which also may involve centers maintaining respiratory and circulatory integrity) and those that affect the brain diffusely (bilateral hemispheric dysfunction). The latter category includes CNS lesions, systemic infections, and toxic or metabolic disturbances. These disturbances also may be associated with brain edema and prolonged seizures, which in themselves may cause brain damage.


EVALUATION AND TREATMENT


Short-Term Treatment

The evaluation and treatment of the comatose child fall into two phases. During the immediate phase, treatment precedes establishment of a diagnosis, and its most important aspects include stabilizing the child and protecting him or her from sustaining further brain damage. An evaluation of etiologic possibilities for the coma follows. After providing immediate treatment to the comatose child, the physician must be prepared to manage the potential complications of a prolonged altered state of consciousness. Knowledge of the probable prognosis for recovery or long-term impairment will facilitate provision of patient care and will improve communication with the child’s parents.

During the initial phase of treatment, the physician must ensure that the patient’s brain is receiving adequate substrate for energy production. The airway must be maintained, and sufficient oxygen and ventilation must be provided; a child with inadequate respiratory effort needs intubation and respirator assistance. The patient’s cardiac output must be evaluated, and cardiac dysrhythmias and hypotension must be treated appropriately. Treatment also should include control of body temperature, especially in children with hyperthermia (greater than 42°C), to prevent irreversible damage to the CNS. The possibility of reversible hypoglycemic encephalopathy being present should be considered, and immediate treatment of the patient (after blood is obtained for determination of the serum glucose level) should include the administration of 1 mg/kg of concentrated glucose solution (50% dextrose).

Recurrent or prolonged seizures can produce brain damage; iatrogenic paralysis and ventilation do not protect against this damage. Therefore, status epilepticus requires emergency treatment (see Chapter 402).








TABLE 404.1. MODIFIED GLASGOW COMA SCALE
























< Response Older than 5 Years Old Younger than 5 Years Old Score
Eye opening Spontaneous
To speech
To pain
None
Spontaneous
To speech
To pain
None
4
3
2
1
Verbal Oriented
Confused
Inappropriate words
Incomprehensible sounds
None
Alert, normal sounds
Less than normal, irritable
Cries to pain
Moans to pain
No response
5
4
3
2
1
Best motor Obeys commands
Localizes pain
Withdraws
Abnormal flexion
Extension response
None
Normal spontaneous movements
Localizes pain (>9 months)
Withdraws
Abnormal flexion
Extension response
None
6
5
4
3
2
1
Modified from Kirkham, F. Non-traumatic coma in children. Arch Dis Child 2001;85:303.


During the initial treatment period, a rapid physical examination should be performed to search for signs of trauma that could necessitate performing immediate laboratory testing and surgical or neurosurgical intervention. The child should be evaluated for signs of increased intracranial pressure (ICP), keeping in mind that papilledema may not be apparent for hours after the onset of ICP. Loss of venous pulsations may be helpful in the early identification of ICP. If intracranial hypertension is present, immediate therapy, including hyperventilation to reduce the partial pressure of carbon dioxide to 25 to 30 mm Hg and elevation of the head, should be initiated. (For further therapeutic measures for intracranial hypertension, see Chapter 399.)

After immediate assessment and treatment have been performed, further historical information should be obtained. The diagnostic workup should include measurement of serum electrolyte, arterial blood gas, and serum calcium levels, along with liver and renal function tests and a complete white blood cell count. Lumbar puncture should be considered in the presence of signs of meningeal irritation, such as nuchal rigidity, to evaluate for such possibilities as meningitis or subarachnoid hemorrhage. Signs of meningeal irritation may be absent in young children or infants. When the history is suggestive or the cause of coma is not clear, blood and urine evaluations for toxicologic studies should be performed.


Physical Examination

The general physical examination can provide clues to the cause of coma. Of particular importance are signs of trauma and vital signs, including respiratory pattern, heart rate and rhythm, and blood pressure. The neurologic examination must include particular attention given to pupillary size and reactivity, ocular motility, respiratory rate and pattern, and motor response to pain.


Pupils

Metabolic coma or early-stage rostral-caudal herniation with interruption of descending sympathetic pathways is associated with small but reactive pupils; involvement of the midbrain is associated with nonreactive, midposition, or mildly dilated (5 to 7 mm) pupils; intoxication or poisoning by organophosphates, phenothiazines, or opiates is associated with miosis (pupils less than 2 mm in diameter). Less frequently, small pupils may be seen with pontine lesions.


Extraocular Motility

In a comatose child, intact brainstem function is suggested by full-reflex eye movements in response to the doll’s eye maneuver, which is performed by holding the patient’s eyes open and rocking the head from side to side multiple times. If the eyes remain in the primary position or straight ahead during this maneuver, function of the brainstem is compromised. Caloric stimulation is a more sensitive test that may be performed after the tympanic membrane is determined to be intact. The head is positioned in the midline and is raised 30% from the horizontal. Then, 50 mL of ice water is instilled into the external auditory canal against the intact tympanic membrane. Tonic deviation of the eyes to the side in which the ice water was instilled indicates an intact brainstem; any asymmetry or absence of eye deviation implies a structural or metabolic brainstem lesion.


Respiration

Bilateral cortical damage may result in Cheyne-Stokes respiration, which is characterized by periodically alternating episodes of hyperventilation and apnea. Metabolic disturbances, such as respiratory alkalosis or metabolic acidosis, or a midbrain lesion may cause central neurogenic hyperventilation characterized by rapid regular breathing.

True neurogenic hyperventilation is a rare finding; the tachypneic hypocapnia that is observed commonly in unconscious individuals probably is the result of stimulation by pulmonary congestion of afferent peripheral reflexes arising in the lung and chest wall. Pontomedullary damage may be associated with an atactic or irregular respiratory pattern.


Motor Response

The quality of the patient’s motor response may be assessed after the administration of a painful stimulus such as supraorbital ridge compression. Purposeful movement with localization of the stimulus by the patient suggests a high level of intact brain function. Lesions compressing the brain at the thalamic level may be associated with decorticate posturing, which is characterized by flexion of the upper extremities at the elbow and extension with internal rotation of the lower extremities.
Midbrain lesions may be associated with decerebrate posturing, which is characterized by extension and internal rotation of both the upper and lower extremities. Pontomedullary lesions frequently are associated with no response to pain.


Etiologic Factors

Once the child’s condition has been stabilized, a more exhaustive search for a cause of the coma may be necessary. In general, the causes of coma can be divided into two major categories: traumatic and nontraumatic.

Blunt trauma to the head is a common occurrence in childhood. Alteration of consciousness that lasts less than 24 hours after blunt trauma is termed concussion. The neuropathologic implication of concussion is that no microscopic or gross change in the brain has resulted. If the period of unresponsiveness lasts longer than 24 hours, the clinical diagnosis is contusion of the brain. The neuropathologic changes associated with contusion include focal hemorrhage and necrosis of brain tissue. The magnitude of alteration caused in brain function after blunt trauma depends on several variables, including the amount of force exerted on the skull, the area of the skull involved, the direction of force against the skull, the relative mobility of the skull, and the angular velocity of the brain after the trauma. The frontal, temporal, and occipital lobes are especially prone to injury caused by rotational acceleration forces when rotation and flexion of the skull on the neck have occurred. Flexion and rotational acceleration may cause brainstem injury.

Radiologic evaluation of pediatric head trauma should begin with a noncontrast computed tomography (CT) scan, followed by a magnetic resonance imaging (MRI) scan if significant neurologic deficits are found on examination. Even in children with only mild alteration in consciousness (GCS score of 13 to 14), the incidence of intracerebral hemorrhage was shown in one study to be approximately 19% (30 of 135 patients). Depressed skull fractures may be associated with laceration of the brain and dura, and they should be identified and evaluated quickly. Fractures across the middle meningeal artery groove may be associated with tearing of the meningeal artery and subsequent epidural hemorrhage. Epidural hematoma frequently is associated with a biphasic clinical presentation: an initial episode of coma occurring immediately after the injury, followed by a lucid interval, after which loss of consciousness ensues as the hematoma enlarges. Periorbital ecchymosis, cerebrospinal fluid (CSF) rhinorrhea, and hemorrhage behind the tympanic membrane are signs of basilar skull fracture. Acute subdural hematoma may develop after laceration of the dura associated with depressed skull fracture occurs.

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Jul 24, 2016 | Posted by in ORTHOPEDIC | Comments Off on The Comatose Child
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