CHAPTER 3:

COMA, INCREASED INTRACRANIAL PRESSURE AND BRAIN DEATH

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ALTERED STATES OF CONSCIOUSNESS The neurologic examination of the child with altered state of consciousness is not that difficult. When confronted with a child with altered state of consciousness, history taking, physical/neurological examination, and implementation of emergency measures should be concurrently performed. The initial examination may not be exhaustive. We can always repeat the examination of the patient once he is stabilized.

PATHOPHYSIOLOGY OF CONSCIOUSNESS AND UNCONSCIOUSNESS A person must be conscious in order to be able to perform symbolic verbal communication, abstract concept formation, and extensive cognition. Consciousness in its simplest definition is awareness of self and the environment. Human conscious behavior requires the interplay between the cerebral cortex and the subcortical structures. All of these properties (conscious behavior) reside in the cortical gray matter. These areas are connected multisynaptically to various regions of the nervous system. The system resides in a poorly delineated anatomical structure called the ascending reticular activating system (ARAS) that constitutes the central core of the brainstem from the caudal medulla to the rostral pons. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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The ARAS receives information from all sensory pathways, while it gives information to the cerebral cortex. We all expect to be conscious while awake although at times we may be staring blankly at something

(daydreaming) when preoccupied with other thoughts. But this does not mean that we are unconscious. We can snap out of this state instantly. In contrast, unconsciousness is most perturbing. The only physiologic unconscious state is sleep. Pathological unconsciousness and sleep have many similarities: yawning, closing of the eyes, roving eye movements, diminished muscle tone, loss of reflexes, and even urinary incontinence. The greatest difference, however, is that a sleeping person can be aroused with ease and can resume full consciousness. Altered states of consciousness (ASC) be it in the child or in the adult are caused by a variety of disease processes. All of these lead to decreased responsiveness to any form of stimulation. The exact mechanism at which the various diseases produce ASC is not known. Altered state of consciousness is not an “all or none” phenomenon. There are distinct gradations from diminished alertness to unconsciousness. The

need for medical decisiveness requires that the extent of altered mental state be precisely and sequentially recorded. It is best to describe in detail the patient’s reaction to various sensory stimulations and to distinguish changes over the course of time. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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To alter consciousness, there should be diffuse bilateral destruction or dysfunction of the cerebral cortices, or compressions and/or destruction of the ARAS in the brainstem, or a metabolic failure

affecting the cerebral cortices or the brainstem, or a combination of these factors. A unilateral cerebral lesion alters consciousness only if an independent process involving the other hemisphere is present or if there is increased intracranial pressure (ICP), which compromises the contralateral hemisphere’s integrity. Neurologic signs like aphasia, apraxia, and agnosia, which may be seen in unilateral cerebral pathology, may mimic one of the various states of altered consciousness.

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DEFINITIONS The earliest manifestation of alteration of consciousness is lethargy. This means that there is reduced wakefulness where one cannot sustain attention. The individual becomes easily distracted, misjudges sensory perceptions, has

a faulty memory, but is able to communicate verbally or by gestures. In this state, drowsiness is prominent. When the individual’s alertness becomes more blunted, he is said to be obtunded. In this state there is lessened interest in or response to the environment, although communication is partially preserved. If the individual appears to be sleeping, and can only be aroused through repeated and vigorous stimulation with very minimal or communication, such person is said to be in stupor. The deepest form of ASC is coma. In this state, the individual is unarousable. His eyes are closed and he has no spontaneous movements. Speech is absent and his response to noxious stimuli may be purposeful withdrawal but cannot localize pain with discrete or defensive movements or posturing. Delirium is a state characterized by disorientation, irritability, delusions, and hallucinations. In this state, the patient is often agitated, assaultive, and combative. Delirium is often associated with toxic, metabolic, infectious, or traumatic encephalopathies. Delirious patients may proceed to stupor and coma if left unattended. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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EVALUATION OF THE PATIENT The neurologic examination in a patient with ASC should be quick and simple. The initial assessment has 3 goals: (1)

To confirm the diagnostic impression

(2)

To localize the level of neurologic dysfunction

(3)

To serve as a basis for comparison of future examinations

There are five pathophysiologic variables in the evaluation of the unconscious child which ascertain the nature of the lesion affecting the brain, the functional level of involvement, and the extent of the disease process. These are: (1) mental status; (2) respiratory patterns; (3) pupillary sizes and reactivity; (4) oculo-cephalic (doll’s eyes) and oculo-vestibular (iced water caloric) responses; and (5) motor responses.

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MENTAL STATUS The use of the terms lethargy, obtundation, stupor, coma, etc., does not really give much clinical significance. More so, it is very frustrating for anyone caring for the patient to see progress records of patients that show these words day by day. They do not provide a basis for comparison as to whether the patient is improving or worsening. It is perhaps best to describe the patient’s response to various stimuli (e.g., ordinary voice, loud voice, tactile, or painful stimuli, etc.). Attempts to test for higher cortical functions should be performed such as language capabilities, degree of orientation, and memory. A patient who reacts appropriately by having coherent words and is able to follow commands indicates well-functioning cerebral cortices; whereas a

patient who mumbles incoherently or moans and groans indicates a more diffuse and severe cerebral dysfunction. A non-verbal patient who requires deeper forms of stimuli generally indicates a more serious state.

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RESPIRATORY PATTERNS Metabolic control of breathing resides in the respiratory centers in the lower

pons and in the medulla. These are modulated by the cortical centers mainly in the forebrain. Clinically, various respiratory patterns may be seen, and each represents a certain level in the neuraxis. Among the more commonly encountered breathing patterns are: Cheyne-Stokes respirations: These are characterized by a crescendodecrescendo hyperventilation alternating with apnea occurring in a regular pattern. This type of breathing usually indicates bilateral cerebral dysfunction or upper diencephalic dysfunction. Most of the disorders that produce this breathing abnormality are reversible so that a vigorous search for its underlying etiology and measures to counteract it should be employed. Central neurogenic hyperventilation: This is characterized by a continuous rapid inspiration and expiration of the same amplitude. It indicates midbrain dysfunction. Such breathing pattern can be aggravated when accompanied by hypoglycemia.

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RESPIRATORY PATTERNS Apneusis or Apneustic breathing: This is characterized by periodically

occurring apnea after each prolonged inspiration and expiration. It indicates pontine dysfunction. Apneusis signifies an extensive, usually irreversible damage. Ataxic breathing: This is characterized by a breathing that is chaotic and follows no pattern. It indicates medullary dysfunction. Such respiratory abnormality usually indicates a terminal event. What we have learned in Physical Diagnosis as Biot’s breathing, though similar to ataxic breathing is specifically applied to the terminal breathing events in tuberculous meningitis. Ineffectual breathing: It is characterized by very shallow respiratory excursion and generally indicates depression of the respiratory centers and is usually secondary to toxic states, thus some are reversible when appropriate ventilatory assistance is provided.

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PUPILLARY SIZES AND REACTIVITY The pupillary sizes are controlled by the autonomic nervous system (ANS) and are an invaluable aid in the diagnosis of unconsciousness. Their sizes and reactivity – are perhaps one of the better distinguishing features of metabolic coma (also in narcotic and barbiturate intoxication) whereby the pupils, although small remain reactive to light. A magnifying glass may be needed to verify this especially in very small pupils. The pupils are generally equal in size and should react briskly to light, both directly and consensually. We should also remember that the pupils are greatly influenced by pharmacologic agents as well as alterations of the visual pathways. Hemispheric lesions in general do not affect the pupils. Hypothalamic pathology produces small pupils, which may be asymmetric with a Horner syndrome in the constricted side. A unilaterally dilated pupil that is non-reactive to bright light indicates III nerve compression, generally signifying uncal herniation on the same side. Midbrain lesions produce midpositioned fixed pupils. Pontine lesions produce pinpoint pupils. Opiates and derivatives also produce pinpoint pupils. Pupils that are bilaterally dilated and non-reactive indicate medullary dysfunction. Because of the importance of the pupillary responses, the use of mydriatics in unconscious patients should be avoided.

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OCULO-CEPHALIC (DOLL’S EYES) AND OCULOVESTIBULAR (ICE WATER CALORICS) RESPONSES These procedures test the status of the brainstem. The doll’s eyes maneuver is done by briskly turning the head to one side, keeping both eyes open (make certain that there is no cervical spine pathology as in trauma cases). In an intact brainstem there is tonic conjugate deviation of the eyes toward the side opposite the direction of the face. The maneuver should be repeated on the

other side. If there is no response, ice water caloric test is performed. The ice water caloric test consists of elevating the patient’s head by 30 degrees, and the external auditory canals are examined and freed of wax. The tympanic members must be intact. Thirty to fifty ml. of ice water is slowly instilled into the canal. Keeping both eyes open, the movements of the eyes are observed. In a functioning brainstem, there is tonic conjugate deviation of both eyes towards the stimulated side. If there is a fast jerk nystagmus toward the opposite side, then hemispheric functions are present. The same procedure is done to the other ear after an interval of >5 minutes. If there is

no lateral movement of the eye on the stimulated side (i.e., no abduction) but there is adduction of the other eye indicates a lateral rectus palsy, which is commonly seen in raised ICP.

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OCULO-CEPHALIC (DOLL’S EYES) AND OCULOVESTIBULAR (ICE WATER CALORICS) RESPONSES If there is abduction of the eye on the stimulated side and there is no movement (no adduction) of the other eye, then there is involvement of the medial longitudinal fasciculus (internal ophthalmoplegia). It indicates brainstem dysfunction, usually at the level of the pons. The absence of ice water caloric response indicates a poor prognosis, but does not proclaim total irreversibility.

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MOTOR RESPONSES Many patients with altered states of consciousness trash about and move all limbs. Such observation indicates that there is no paralysis. Asymmetric movements indicate motor weakness (e.g., hemiparesis). The patient may be able to move in response to commands depending upon his level of consciousness. Appropriate responses may be observed such as the patient’s attempts to remove a noxious stimulus (e.g., pinching). More serious states are manifested by various postures. In decortication, both lower extremities are adducted and extended, while the upper limbs assume shoulder adduction, elbow flexion, forearm supination, and hand fisting. This posture indicates a dysfunction at the diencephalic level or bilateral cerebral lesions. In decerebration, the lower limbs are also adducted and extended, while the upper extremities are adducted, extended and internally rotated with fisted hands. This posture indicates a midbrain transaction and carries poor prognosis. Both postures are exaggerated during stimulation. The application of painful stimuli should only be to “socially” acceptable sites. Examples of these maneuvers are: pressure on the supraorbital ridges or sternum, pinching of the Achilles tendon, pressure on the fingernails, etc. The muscle tone is increased in both postures reflecting the involvement of the upper motor neurons. However in drug intoxications, spasticity is practically

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The deep tendon reflexes (DTRs) are elicited the usual manner and symmetries compared. Brisk and asymmetric reflexes generally indicate a more serious lesion on the contralateral side. When intravenous lines, splints, and casts cover the patient’s limbs so that the DTRs cannot be tested, elicitation of the shoulder jerks (pectorals) should be done and is sufficient for comparison. The shoulder jerk is elicited by tapping a finger applied to the pectoralis major tendon at the anterior border of the axilla. Plantar responses are elicited the usual way and are almost always

extensor in these instances. In lighter stages of altered states of consciousness, the primitive reflexes (i.e., sucking, rooting, pout, palmar, and plantar grasps) may be present. They generally indicate the release of inhibitory influences of the higher (frontal) centers. A simple method of evaluating the level of consciousness is through the use of the Glasgow Coma Scale (GCS). The scale essentially consists of an assessment of a motor score ranging from obeying commands to flaccidity; eye opening from spontaneous to none; and verbal response from fully oriented to one. A normal person has a score of 15; while a brain-dead patient has a score of 3. Although the classic description of the scale was made for adults, modifications have been made for its application to children. Table 3-I enumerates the CGS; for adults and children Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Table 3-I. Glasgow Coma Scale for Adults and Children FUNCTION

ADULTS

CHILDREN

SCORE

Eye Opening

Spontaneous

Spontaneous

4

To command

To sound

3

To pain

To pain

2

None

None

1

Oriented

Appropriate for age, flexes

5

Verbalization

and follows, social smile

Motor

Disoriented

Inconsolable cry

4

Inappropriate

Persistently irritable

3

Incomprehensible Restless, lethargic

2

None

None

1

Obeys commands Spontaneous movements

6

Localizes pain

Localizes pain

5

Withdraws

Withdraws

4

Reflex flexion

Reflex flexion

3

Reflex extension

Reflex extension

2

None

None

1

Total

15

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ETIOLOGY Based on the aforementioned principles (bilateral cerebral lesions or diffuse cerebral dysfunction or brainstem dysfunction), there are three major causes

of altered states of consciousness. These are supratentorial mass lesions with contralateral displacement; infratentorial mass or destructive lesions; and metabolic and/or diffuse cerebral disorders. Psychogenic states like catatonia and hysteria may be mistaken for “unconsciousness.” Supratentorial mass lesions present initially with focal neurologic signs, which are asymmetric. Cranial nerve palsies are not present until late. Characteristically, it follows a rostro-caudal progression (i.e., affects various levels of the neuraxis from cortex to brainstem in a neuroanatomically orderly manner). Infratentorial mass or destructive lesions present with cranial nerve palsies and contralateral long tract signs. Abnormalities of pupillary light reflex and ocular movements are common. Coma occurs abruptly and is associated with early respiratory abnormalities. There may also be neck stiffness especially with increased ICP. In metabolic encephalopathies, altered states of consciousness precede motor signs.

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There are usually no focal neurologic findings. Respiratory abnormalities are common. The pupils remain reactive. Asterixis and myoclonus are frequently

seen. Seizures are common. In addition, there may be peculiar breath odors. Table 3-II enumerates the more commonly encountered causes of altered states of consciousness. Among the more common supratentorial mass lesions are brain tumors, subdural, epidural, and intracerebral hematomas, brain abscesses, and cerebral infarcts with associated edema. Infratentorial lesions include tumors and hemorrhages involving the brainstem and cerebellum. Metabolic and diffuse cerebral disorders account for most of the causes of coma. These include anoxia from various reasons, concussion syndromes, seizures, and post-ictal states. Infections particularly meningitis

and encephalitis, subarachnoid hemorrhage (post-traumatic or spontaneous), exogenous toxins (intentional or accidental ingestion) and endogenous toxins such as diabetic coma, uremia, hepatic coma, hypertensive encephalopathy, and heat stroke are also included in the diffuse cerebral disorders category.

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TABLE 3-II: COMMON CAUSES OF ALTERED STATES OF CONSCIOUSNESS I.

Infectious and Parainfectious Disorders A. Meningitis (various etiologies) B. Encephalitis (various etiologies) C. Brain abscess D. Post-infectious encephalitis II. Trauma A. Concussion syndrome B. Cerebral contusion and edema C. Epidural, subdural, intraventricular, intracerebral hematoma D. Subarachnoid hemorrhage III. Physical Factors A. Electrocution B. Drowning C. Heat Stroke D. Hypothermia IV. Neoplasms A. Primary supratentorial tumors B. Primary infratentorial tumors C. Metastatic tumor V. Metabolic disorders A. Acid-base disturbances B. Hypoglycemia C. Hypoxia D. Diabetes mellitus E. Uremia F. Dehydration (shock) G. Hyperosmolar states H. Hyper and hyponatremia I. Inborn errors of metabolism VI. Poisons A. Overdose of drugs (e.g., sedatives, stimulants, other illicit drugs, alcohol, etc.), deliberate or accidental VII. Vascular disorders A. Hypertensive encephalopathy B. Cerebral-vascular disorders (strokes) C. Spontaneous subarachnoid hemorrhage (arterio-venous malformations, aneurysms) D. Cardiac dysrhythmias E. Hypotension VIII. CNS Paroxysmal disorders A. Seizures B. Post-ictal states IX. Raised Intracranial Pressure from any cause PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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MANAGEMENT Many patients are brought to the hospital by an ambulance, the police, a babysitter, a maid, a friend, a member of the family, or a complete stranger who just happened to pass by. The informant should be thoroughly questioned especially on the circumstances how the patient was found. External evidence of trauma may be obvious or occult and has to be inspected. If the family is available, elicit the history of previous illnesses, names of currently taken prescribed and non-prescribed medications, possible exposure to toxins and infectious diseases, his emotional and

psychiatric states (possible drug overdose), and the name of his physician to contact. Inquire also about the drugs or medications at home as well as history of recent travel. The CAB (Circulation-Airway-Breathing) of life must be applied. Apply the principles of basic life support (i.e., cardiac massage first followed by airway and breathing). An airway should be inserted (an endotracheal tube is ideal when the expertise is available). Airway patency and vital signs (blood pressure, pulse, and respirations) should be checked immediately and frequently. Draw blood for culture (in a febrile patient), complete blood count (CBC), electrolytes, sugar, BUN, creatinine, serum osmolality, blood pH, blood gases, ammonia, toxic drug screen, liver function tests, coagulation profile, and antiepileptic drug (AED) levels (when appropriate). Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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An intravenous (IV) line should be inserted making certain that adequate fluid is administered. If Dextrostix is available, do one and if there is hypoglycemia, infuse 2 mL/kg body weight of a 25% dextrose solution. If Dextrostix is not available, you still have to infuse the recommended amount of dextrose solution in the preceding sentence. It is almost a routine to limit IV fluids in these patients for fear of aggravating coexisting increased ICP (cerebral edema). This is to be done with caution because many of these patients are initially dehydrated or in shock. Vasopressor agents may have to be given in cases of hypotension and shock. Of prime importance is maintenance of a normal blood pressure. Hypotonic solutions may actually aggravate cerebral edema. Isotonic fluid solutions given in full maintenance have been found to be beneficial and do not further compromise cerebral edema. Insert an indwelling Foley catheter and perform a urinalysis including urine osmolality. Carefully examine the skin and mucous membranes for trauma, exanthems, needle tracts, and signs to suggest a systemic disease. Palpate the scalp for possible trauma and the anterior fontanel if still patent; auscultate the head (for bruits); and check for possible cerebrospinal fluid (CSF) leaks in the nose and ears. Carefully examine the neck for fractures, dislocation, and for meningeal signs. Perform a fundoscopic examination and a complete physical examination after the patient has been stabilized. If CNS infection is strongly suspected, do an LP and have the CSF analyzed. Obtain a head CT scan after stabilization (this may have to be performed prior to doing an LP especially those with unequivocal signs of raised ICP). Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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The management of coma depends on its etiology. Specific measures are to be applied. Rapidly expanding supratentorial or infratentorial lesions call for immediate neurosurgical intervention. Metabolic derangements, infections, seizures, and trauma are discussed in their respective chapters. Most of the other causes (metabolic) of coma are not within the scope of pediatric neurology. The reader is advised to refer to a pediatric text for a more thorough discussion and management of specific disorders. If the facilities are available, the patient should be admitted to the ICU where he could be carefully monitored and managed. He should be positioned in a semiprone or lateral decubitus to prevent aspiration of oral secretions. Frequent but gentle oro-nasal suctioning should be done. Because of respiratory abnormalities, frequent determinations of blood gases are indicated. Oxygen administration and ventilatory assistance are also done, especially on those with respiratory irregularities (intubate patient if comatose). Acid-base balance should be carefully monitored. Absolute intake and output should be measured and charted. Daily weight measurements have remained one of the best indices of water retention and should be performed. Frequent determination of serum electrolytes and serum and urinary osmolality are ideal. Co-existing increased ICP has to be dealt with (see next section). Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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INCREASED INTRACRANIAL PRESSURE Intracranial hypertension is not a disease but a symptom of varied etiologies ranging from congenital lesions, neoplastic diseases, metabolic disorders, toxic conditions, infectious diseases, and trauma. It is a

neurologic emergency that requires prompt recognition and control to avert serious sequelae and death. We must be cautious in applying to children the concepts of intracranial hypertension derived from experience with adults. Although many of the clinical manifestations are similar in both age groups, distinct differences exist. For example, children may harbor an intracranial mass for sometime without overt signs of increased intracranial pressure (ICP), only to deteriorate rapidly and dramatically to a non-salvageable state. Often, intracranial masses in children may be accompanied by phenomena not

encountered in adults, such as failure to reach developmental milestones, or progressive enlargement of the head. Unique properties of the immature brain and its container affect the brain’s response to changes in ICP. The discussion that follows aims to briefly review the basic mechanisms at which intracranial pressure is maintained; mention the more common signs and symptoms of increased ICP; and the management of intracranial Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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hypertension. Intracranial pressure monitoring is performed by a variety of ways, most of which are invasive. These monitoring techniques are excellently reviewed in neurology and neurosurgery texts and the reader is referred to these books for details.

NORMAL INTRACRANIAL PRESSURE The upper limits of normal ICP in adults and older children is usually given as 15

mm Hg. Transient changes resulting from coughing, sneezing, or straining often produce pressures exceeding 30 mm to 55 mm Hg but ICP returns rapidly to baseline levels. Measurements of ICP in younger children and infants by spinal puncture using manometers may not be that reliable because of poor cooperation of the child and the displacement of fluid in the manometer device. Given these practical difficulties the published norms of ICP for children range from 3 mm to 7.5 mm Hg and from 1.5 mm to 6 mm Hg for young infants. While it has been traditional to refer the ICP in mm of saline or water, practically all of the current literature expresses these figures in mm of Hg. A conversion formula as was previously mentioned in the chapter on Neurodiagnostic Procedures is 1 mm of Hg is rough 13.6 mm of saline or water. All reported values for ICP of younger children are lower than those reported for adults but are probably reasonable approximations of the actual level of the ICP. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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The low levels reported for children may be explained by comparing them with adults. In adults, the ability to perfuse the brain effectively depends on the maintenance of a cerebral perfusion pressure (CPP) of >50 mm Hg. The critical CPP of the immature brain has not been determined. Since the mean

arterial pressure (MAP) of infants and children is considerably lower than that of adults, a lower normal ICP may be the mechanism for maintaining adequate CPP. In the physiologic steady state, baseline ICP remains constant despite a variety of transient perturbations. Since ICP depends on relative constancy of volume, any change in the volume of one of the normal intracranial contents must occur at the expense of the other. This can be remembered by the following equation: V intracranial (constant) = V CSF + V Blood + V CSF (+V Others) The explanation of this interaction between volume (V) and pressure is based on the Monro-Kellie doctrine, which states that for the ICP to remain normal, intracranial volume must remain nearly constant because the skull, after closure of the fontanels and sutures, form a rigid container. The

presence of abnormal components such as tumor or hematoma demands reciprocal changes in the volumes of brain, blood, or CSF to maintain ICP at physiologic levels Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Even the physiologic state is far from static. Constant changes induced by the heartbeat as well as systemic blood pressure, fluid status, and intrathoracic pressure requires dynamic changes within the intracranial compartment to maintain the steady state.

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SIGNS AND SYMPTOMS The classic Cushing triad (systemic hypertension, bradycardia, and irregular respirations) reported in intracranial hypertension may not be appreciated in children especially with chronic increase in ICP. This may,

however, be seen in acute rises of ICP. Some signs and symptoms of increased ICP are common in both infants and older children. It is therefore helpful to see how each group is like to present clinically with a mass lesion and elevated ICP. Common to both are the nonspecific signs of lethargy, vomiting, VI and III nerve palsies. In the infant, however, the signs may not be as localized as they are in the older child. The infant is irritable. The anterior fontanel is full, tense, and bulging. Vital signs may be altered and the patient may fail to thrive. In addition, the head is big with distended scalp veins. A cracked pot sound

(Macewen sign) is appreciated on percussion and a setting sun sign (see chapter on Big, Small, and Odd-Shaped Heads) may be present. The older child is more likely to present with headache, double vision, localizing signs such as hemiparesis, cranial nerve palsies, and personality changes (mood swings, memory loss, irritability, lethargy, poor academic performance, and depression). Papilledema appears to be the most reliable objective sign of increased ICP. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Papilledema rarely occurs in young infants with open sutures and fontanels. Visual acuity is normal in papilledema unless optic atrophy has set in (end-effect). Progression of increased ICP produces varying degrees of altered states of consciousness and may lead to brain herniation. Two types of brain herniation are seen in association with increased ICP. In

transtentorial or central herniation, the diencephalon is displaced through the tentorium cerebelli notch into the posterior fossa. It results from increases in ICP that involve both cerebral hemispheres to a similar degree (e.g., cerebral edema, posttraumatic edema or hemorrhage, toxic or metabolic encephalopathy, and bilateral or unilateral [late] cerebral hemispheric mass lesions). Typically, transtentorial herniation presents with rostro-caudal progression of symptoms. Uncal herniation results from an expanding lesion that occupies the middle cranial fossa or the parenchyma of the temporal lobe. Ipsilateral III nerve dysfunction (mydriasis, ptosis, and external ophthalmoplegia) and contralateral hemiparesis characterize uncal herniation.

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EVALUATION The evaluation of the child with increased ICP also includes stabilization of the patient. As in the preceding section (altered states of consciousness), the CABs of life should be instituted. Whenever possible, the child should be intubated. A precise history and physical examination are carried out. The neurologic examination especially on patients with altered states of consciousness, need not be exhaustive (see the preceding section) and GCS is applied.

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MANAGEMENT The treatment for intracranial hypertension should be directed to the underlying cause whenever possible. The previously mentioned equation provides a conceptual framework for examining the components of the intracranial volume responsible for non-steady state situations and allows treatment to be directed in a focused manner. When hydrocephalus causes intracranial hypertension and its etiology cannot be eradicated, a temporary or permanent CSF diversion may be necessary. When obstruction of the CSF pathways is by a space occupying lesion (e.g., tumor), it is usually possible – and preferable – to surgically remove the lesion, which relieves the obstruction. If CSF diversion is required, options exist which permit either a temporary external drainage (ventriculostomy), or a permanent internal drainage (ventriculo-peritoneal shunt). Personally, I am not much in favor of temporary external drainage because of the possibility of infection. When mechanical methods of CSF diversion are impossible at that particular moment, adjunctive therapy using drugs like acetazolamide (Diamox®), furosemide (Lasix®), and corticosteroids can transiently decrease CSF production. Acetazolamide, however, has a cerebral vasodilator effect, and this may transiently worsen intracranial hypertension, therefore its use is contraindicated in patients with close head injury. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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The second component of intracranial volume is blood, which is contained within the cerebral vasculature. While most of the cerebral blood volume (CBV) resides within the pial blood vessels, it is the precapillary arterioles that

controls cerebral blood flow (CBF). Although some success has been reported with drug therapy for increased CBV, hyperventilation (HV) and elevation of the head can best accomplish clinical treatment. Hyperventilation causes respiratory alkalosis consequently producing vasoconstriction of the pial vessels. This will limit cerebral blood flow. The potential advantage may only last about 24 hours and can be offset by extreme HV, which can cause excessive vasoconstriction sufficient to produce cerebral ischemia. Since CBF monitoring is not available in many clinical settings, less stringent criteria for use of HV must be used. Effective control of increased ICP in children has been achieved with HV to lower PaCO2 below 20 mm Hg. At this level, cerebral ischemia induced by HV may not be present since metabolites accumulate as CBF decreases producing vasodilatation. Most clinical observations indicate that sustained reduction of ICP can be maintained for several days by using HV. When HV is discontinued, it should be tapered over

24 to 48 hours. Abrupt discontinuation can cause vasodilatation as extracellular pH falls resulting in ICP elevations. Elevation of the head by 30 degrees decreases ICP by encouraging venous return. This degree of head elevation does not alter cerebral perfusion pressure. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Transmission of elevated intrathoracic pressure to the intracranial veins can be avoided by sedating the patient and limiting the inspiratory phase of the ventilator. Since systemic hypertension may be observed in raised ICP, the

inexperienced might attempt to decrease CBF by reducing systemic blood pressure. This should not be done abruptly because it leads to lowering CPP and results in arterioral vasodilatation, which subsequently increases both CBV and ICP. This effect is seen in systemic hypertension, in which CBF is reduced but CBV and ICP are increased because of vasodilatation related to hypercapnea, anoxia, and acidosis. The third intracranial component is the volume occupied by brain tissue. Increases in brain weight occur most frequently as a result of cerebral edema, which is a nonspecific reaction to a variety of processes. Cerebral

edema is defined as an increase in water content of the brain and be broadly categorized as vasogenic and cytotoxic. Vasogenic edema refers to leakage of protein-rich fluid across the capillary membrane into the extracellular spaces of the white matter. Vasogenic edema can produce local or generalized mass effects, which results in increased ICP. This type of edema usually occurs in neoplasms, infections, and trauma. Cytotoxic edema is caused by expansion of the intracellular fluid compartment due to cellular toxins or injury. This occurs in metabolic, toxic, and hypoxic-ischemic disorders. Cytotoxic edema also contributes to injury by impairing cellular pump mechanisms. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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The first goal in the treatment for increased ICP due to brain edema is directed toward removing the cause of the edema, controlling its propagation, and enhancing its clearance. Further efforts to decrease formation of

vasogenic edema include prevention of cerebrovascular hypertension, preservation of an adequate CPP, and appropriate choice of fluid resuscitation. Control of systemic and cerebrovascular hypertension is especially important when intracranial hypertension exists or when cerebral autoregulation is impaired. The choice of antihypertensive drugs in patients with increased ICP is important. Agents like nifedipine (Adalat®, Calcibloc®, etc.), chlorpromazine (Thorazine®) and reserpine all decrease MAP and increase ICP, thereby reducing CPP. These findings are more pronounced when ICP exceeds 40 mm

Hg. Propranolol (Inderal®) has been shown to be superior to hydralazine (Apresoline®) for control of hypertension in head-injured patients because propranolol decreases both cardiac demands and serum levels of epinephrine and norepinephrine. The choice of IV fluids for resuscitation is also important because 10% to 15% of head-injured patients are hypotensive due to associated injuries. Aggressive correction of shock improves the survival and clinical outcome. Isotonic fluids (e.g., D5 ½ normal saline, normal saline, and lactated Ringer) Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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all acceptable, but hypotonic solutions like D5W, which lower serum osmolality will increase cerebral edema. In cytotoxic injury, efforts to decrease formation of edema center on the correction of the etiology of disordered cell function.

With toxins, this would involve treatment directed toward the causative agent. When anoxia and ischemia exist, reversal of causative factors may bring improvement if the duration of anoxia and ischemia has not been prolonged. The second goal in the treatment of cerebral edema is to improve neuronal and axonal function. Although a variety of agents have been tried to improve the function, steroids and barbiturates are the most employed drugs for the treatment of both vasogenic and cytotoxic edema. Corticosteroids are of unquestionable value in the treatment of patients with brain tumors, but no definite benefits have been shown when used in head-injured patients.

Corticosteroids have been shown to inhibit membrane lipid hydrolysis and decrease free radical-induced lipid peroxidation, the principal molecular basis for posttraumatic neuronal degeneration. Among the commonly used corticosteroids, methylprednisolone (Solu-Medrol®) has the highest lipid antioxidant capacity whereas prednisolone is efficacious in vitro but only half as potent. Even in high doses, hydrocortisone (Solu-Cortef®) has no antioxidant activity; dexamethasone (Decadron®) is slightly less effective than methylprednisolone and prednisolone. Interestingly, excessive doses of corticosteroids may possibly be deleterious and exacerbate lipid peroxidation. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Dexamethasone (0.4 to 1 mg/kg/day) in divided doses) is especially effective in patients with tumors. In older and larger children, the usual adult dose of 4 mg administered every 6 hours may be used. The use of steroids in

subarachnoid hemorrhage has no proven benefit. In cases of cerebral ischemia, steroids worsen the outcome either by means of direct glucocorticoid toxicity or as a consequence of elevated serum glucose levels, which exacerbate ischemic lactic acidosis. Barbiturates are the second group of agents used to improve neuronal and axonal function in the presence of edema. Their benefit appears to accrue from reducing ICP (thus improving CPP), reducing CBF (lowering end-capillary pressure and limiting edema formation) and decreasing cerebral metabolic requirement of oxygen [CMRO2] (permitting

tolerance of a degree of ischemia/anoxia not otherwise acceptable on the cellular level). Pentobarbital has proved most effective at controlling ICP than phenobarbital or thiopental sodium. Barbiturates are effective in reducing ICP but do not improve outcome in many studies. Even prophylactic use of barbiturates has not improved outcome or led to easier control of ICP. Considering the risks of high-dose barbiturates, their application is more appropriate for patients in whom conventional measures to control ICP have failed. Usually a bolus of pentobarbital (5 to 10 mg/kg) is administered over Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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30 minutes followed by a continuous hourly maintenance of 1 to 5 mg/kg to achieve a serum concentration of 3.5 to 4.5 mg/100 ml or a “burst suppression” pattern is attained by bedside EEG monitoring. Barbiturate

coma should only be used in an intensive care setting. Despite maintenance of normal blood volume and cardiac output, hypotension occurs in 50% of cases and is probably due to decreased peripheral vascular resistance. Volume expansion in addition to dopamine or levarterenol may be necessary to restore systemic blood pressure. Other potential complications related to high-dose barbiturates include hyponatremia, pneumonia, and cardiac depression. Fortunately, these problems often respond to dobutamine. Increasing the clearance of edema can further reduce brain volume. Both osmotic and loop diuretics are widely used and can treat both vasogenic and

cytotoxic edema. Osmotic agents increase serum osmolality and create an osmotic gradient between the brain and serum. The effect draws free water from the brain into the intravascular compartment along the osmotic gradient. The drugs used most commonly for increasing intravascular osmolality are mannitol, urea, and glycerol. Mannitol (20 % solution) is most often used and is considered by many as the agent of choice. Osmotic agents transiently increase CBF independent of their effect on ICP, and so their use in the presence of hyperemia and increased CBV may be contraindicated. Since Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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Since some head-injured children exhibit hyperemia, lack of responsiveness to mannitol may prompt the use of barbiturates earlier in the treatment of severe intracranial hypertension.

The dose of mannitol is 500 mg to 1000 mg/kg, and this can be given as a repeated bolus or in smaller doses as a continuous infusion. Complications with osmotic therapy are dehydration, electrolyte imbalance, and with extreme hyperosmolality – renal failure. Fluid replacement is aimed at preserving isovolemia while increasing serum osmolality. Osmolality should not exceed 320 mOs/L because the renal tubule can be injured as osmolality exceeds this level. Maintenance of high serum mannitol levels can lead to penetration of mannitol into the injured brain, reversing the blood-brain osmotic gradient and causing rebound intracranial hypertension. Loop diuretics such as furosemide can be used in conjunction with mannitol to control ICP associated with brain edema. Furosemide works synergistically with mannitol to remove free water and is most appropriate for patients with fluid overload. The addition of furosemide increases the likelihood of dehydration and loss of potassium. Although furosemide decreases CSF production, this effect probably does not contribute greatly to lowering ICP in an acute setting

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The most effective treatment for increased ICP consists of removing volumes not normally found within the intracranial compartments; these include tumors, abscesses, and hematomas. When a definable abnormal mass is responsible for intracranial hypertension, the mass should be removed. The modalities discussed above should be considered adjunctive and supportive therapy in these settings.

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BRAIN DEATH The many advances in emergency and resuscitative medicine have made the traditional definition of death no longer tenable. Ventilators and drugs like vasopressors and antibiotics can prolong “life.” Physicians have been entrusted the grave task to determine whether or not certain patients have the potential to recover. The Ad Hoc Committee on Brain Death from the Children’s Hospital of Boston (MA, USA) has defined brain death as the state “when cerebral and brainstem

functions are irreversibly absent. Absent cerebral function is recognized clinically as the lack of receptivity; that is, no autonomic or somatic response to any sort of external stimulation, mediated through the brainstem. Absent brainstem functions is recognized clinically when pupillary and respiratory reflexes are irreversibly absent… Particularly in children, peripheral nervous system activity, including spinal cord reflexes may persist after brain death; however decorticate or decerebrate posturing is inconsistent with brain death.” Brain death has to be differentiated from cerebral death, which in itself (brain death) means irreversible coma. In cerebral death, brain damage is extensive,

and the patient is incapable of maintaining external homeostasis (return of intellectual functions and full consciousness does not happen). But he has the integrity to maintain internal homeostasis (able to maintain vegetative functions). Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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All surviving comatose patients “wake up,” irrespective of the severity after a period of 1 to 2 weeks. Full consciousness may not be recovered as these patients assume a state of wakefulness or arousal but will no longer appropriately react with themselves or the environment. They are those who are severely brain-damaged and are in a chronic vegetative state. There are many ethical, moral, legal, and medical implications in the declaration of brain death. Despite these issues, it is important in today’s

practice of medicine to make a decision of brain death for the following reasons: (1)

Advances in medicine have taken a giant leap in that many lives have

been saved through organ transplantation. The viability of the donor organ depends upon adequate perfusion, so that it is most desirable to “donate” these organs prior to cardiovascular failure. (2)

The bed in the intensive care unit is “wasted,” as it could be offered

to someone else who may be in need. (3)

The operating costs of such maintenance are prohibitively expensive.

(4)

It prolongs the emotional and physical strains not only of the family

but the medical and paramedical personnel as well.

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While there are been many modifications for the criteria of brain death, the following are essential components: (1)

Pupillary reactions: The pupils must be non-reactive. The previous

use of topical mydriatics or parenteral agents like atropine invalidates these findings. Widely dilated and fixed pupils remain a strong sign of brainstem failure. Persistently mid-positioned fixed pupils as seen in cadavers together with the absence of other brainstem functions are just as good indicators of brainstem failure as those which are maximally dilated. (2)

Oculo-cephalic and Oculo-vestibular responses: The absence of

oculo-cephalic and oculo-vestibular responses is also strongly indicative of brainstem failure. However, one must be absolutely certain that the auditory canal is clear and that the water has reached the tympanic membranes. (3)

Motor responses: No facial grimacing on supraorbital or sternal

pressure. Posturing and other movements are absent. A movement of an arm or leg following or during noxious stimulation is not unusual. It is a withdrawal reflex on a spinal level and should not be regarded as a sign of cerebral activity. The presence of deep tendon reflex(es) alone also cannot be regarded as evidence of cerebral activity. (4)

Other reflexes: Corneals, gag, etc., must be absent.

(5)

Systemic circulation: Must be intact. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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(6) Documentation of apnea: It is vital to prevent hypoxemia when performing this procedure. The administration of 100% oxygen for 10 minutes is recommended prior to withdrawal of ventilatory support. A catheter is inserted into the endotracheal tube and oxygen is delivered at 6 L/minute. This amount has been found to be sufficient in maintaining a normal paO2 through passive alveolar diffusion. Thus, adequate oxygen is provided even in the deeply comatose and completely apneic patient. Before disconnecting the patient from the ventilator, draw arterial blood for blood gas analysis. Ensure that the paCO2 is >25 Torr. Disconnect the ventilator for 10 minutes. During this period, respiratory excursions should be observed. At the end of the procedure, draw arterial blood for repeat blood gas analysis. The paCO2 should rise to almost 60 Torr. At this level, the respiratory center should be stimulated. The absence of respiratory movements is a strong indication of medullary failure. This test is one of the most important parameters in the diagnosis of brain death and must be performed appropriately. (7) Ancillary tests: Laboratory investigations in the diagnosis of brain death are not absolutely essential. However because of the heavy legal implications, they are desirable. An isoelectric EEG, when properly performed (at normal and maximum gains) is contributory of the diagnosis of brain death. EEG activity is seen in some brain-dead children. EEGs are no longer required for the declaration of brain dead children except in very young infants (see Table 3-IV). Studies that delineate cerebral blood flow are more confirmatory evidence of brain death. In brain death, evidence of cerebral circulation is absent. The simplest of these is radionuclide scanning. Pebenito. (2011). Easy and Practical Child Neurology (2nd ed.) PROPERTY OF THE DEPARTMENT OF NEUROSCIENCE AND BEHAVIORAL MEDICINE

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(8)

Duration of observation: Following the initial examination, the patient

should again be examined with an interval or at least 6 or more hours (see Table 3-IV for recommendation of duration of observations). During the interim period, the patient should show no change, and clinical and laboratory findings are the same as the first examination. It is important to know the cause of coma, since many cases without evidence of injury or history of having had underlying medical or neurological illness

may be due to drug overdose. Drug-overdosed patients may mimic signs of brain death including an isoelectric EEG. All efforts must be made to rule out this possibility. Extreme hypothermia, hypoxia, and other intoxications particularly to barbiturate can also mimic brain death.

Tables 3-III and 3-IV enumerate the guidelines of the Task Force for the Determination of Brain Death in Children and the duration of observation for the examination according to the age of the child

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TABLE 3-III. GUIDELINES FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN (GUIDELINES FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN. TASK FORCE FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN. ARCH NEUROL. 1987;44:587-8 HISTORY DETERMINATION OF CAUSE OF DEATH IS NECESSARY TO ENSURE THE ABSENCE OF TREATABLE OR REVERSIBLE CONDITIONS (I.E., TOXIC OR METABOLIC DISORDERS, HYPOTHERMIA, HYPOTENSION, OR SURGICALLY REMEDIABLE CONDITIONS)

Physical Examination •

Coexistent coma and apnea

•

Loss of consciousness and volitional activity

•

Absent brainstem function

•

Fixed and dilated or midpositioned pupils

•

Absent spontaneous and oculo-caloric/oculo-vestibular eye movements

•

Absent movement of facial or oropharyngeal muscles

•

Absent corneal, gag, cough, sucking, and rooting reflexes

•

Spinal cord reflex withdrawal not included

•

Consistent examination throughout the observation period

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TABLE 3-IV: AGE-DEPENDENT OBSERVATION PERIOD (TASK FORCE FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN): GUIDELINES FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN. TASK FORCE FOR THE DETERMINATION OF BRAIN DEATH IN CHILDREN. ARCH NEUROL. 1987;44587-8

Age

Hours between 2

Recommended

examinations

number of EEGs

48

2

2 months to 1 year 24

2

>1 year

Not needed

7 days to 2 months

12

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CHAPTER 3:

COMA, INCREASED INTRACRANIAL PRESSURE AND BRAIN DEATH

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