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760 SECTION VI Pediatric Critical Care Neurologic Timing of the Onset of Symptoms Sudden, acute onset may suggest trauma, intoxication, specific metabolic derangements, intracranial hemorrhage, seizur[.]

760 S E C T I O N V I   Pediatric Critical Care: Neurologic Timing of the Onset of Symptoms Sudden, acute onset may suggest trauma, intoxication, specific metabolic derangements, intracranial hemorrhage, seizure, or cardiac arrhythmia Progressive, gradual onset leads to a broader differential diagnosis, including indolent infection, mass lesion, hydrocephalus, or metabolic derangements Antecedent Events History of fever and travel history may indicate a potential infectious etiology Questions about known or suspected trauma, most recent oral intake, and known or suspected ingestion—together with direct inquiry about access to household medications and toxic substances—are indicated Associated Signs or Symptoms Specific questions about signs or symptoms may also narrow the differential diagnosis For example, changes in head circumference or headache with positional changes suggest evidence of increased ICP Neck stiffness or rigidity suggests meningitis or encephalitis Alterations in speech, vision, or motor function may raise the possibility of stroke or seizure Incontinence of bowel or bladder function may also raise the suspicion of seizure A murmur, gallop, or dysrhythmia may suggest congenital heart disease or endocarditis, which may be associated with stroke or intracranial abscess formation Preexisting Conditions and Comorbidities A history of medication use, seizures, underlying neurologic disease, structural brain abnormalities, inborn errors of metabolism, diabetes mellitus, autoimmune disease, hepatic or renal failure, history of congenital heart disease or dysrhythmia, or psychiatric disease can provide further clues into the etiology of coma as well Patients presenting with an altered LOC and underlying illnesses—such as systemic lupus erythematosus, sickle cell disease, nephrotic syndrome, or coagulation disorders—are at risk for cerebral infarction resulting from a vascular obstruction Physical Examination Once the patient’s airway, breathing, and hemodynamics are stabilized, a complete general examination and specific neurologic examination should be performed and any signs of trauma should be noted Cervical immobilization should be maintained until trauma has been excluded, and the cervical spine has been cleared by radiographic and physical examinations The physical examination should start with careful vital sign determination, as abnormalities may direct immediate treatment Elevated temperature may indicate infection or ingestion (e.g., anticholinergics or serotonin syndrome) Hypothermia may indicate either infection, especially in infants, or environmental exposure Tachycardia may be due to fever, hypovolemia, or arrhythmia Bradycardia may be due to increased ICP or toxic ingestions Hypotension could be due to shock or toxic ingestion Hypertension could be due to renal failure or toxic ingestion, or it could be indicative of a response to increased ICP Changes in respiratory rate and pattern are covered in more detail later The patient should be completely exposed to allow a visual appraisal of swelling, lacerations, bruises, and other obvious signs of trauma Blood or clear fluid noted in the nose or ears suggests a basilar skull fracture Injuries with characteristic patterns, characteristic shapes, and characteristic locations suggest child abuse (see Chapter 121) Focused Neurologic Examination A focused neurologic examination is key to documenting the baseline neurologic status and helps to locate lesions and determine prognosis in patients with a diminished LOC The neurologic examination of a comatose patient differs from that of an awake, communicative subject It involves respiratory pattern; a detailed cranial nerve examination, including pupillary response; and stimuli required to elicit a motor response Respiratory Pattern Changes in respiratory rate, depth, or regularity are associated with coma Abnormalities in the respiratory pattern may provide important clues in localizing a lesion Respiratory patterns and associated anatomic areas of injury are found in Table 62.4 and Fig 62.2 Eye Examination Specific eye findings can help localize the level of lesions and establish prognosis Pupillary changes due to structural lesions depend on the site of the primary lesion and secondarily on the effects of increased ICP as described in Table 62.5 and presented in Fig 62.3 Because pupillary pathways are relatively resistant to metabolic insults, the pupillary light reflex is the single most important physical sign differentiating metabolic from structural coma.2 TABLE 62.4 Respiratory Patterns in Patients With Depressed Sensorium Pattern Description Localization Posthyperventilation apnea Apnea for 10 s after deep breaths Bilateral hemispheric dysfunction Cheyne-Stokes respiration Rhythmic waxing and waning of respiratory amplitude Bilateral hemispheric dysfunction Central neurogenic hyperventilation Continuous deep breathing Bilateral hemispheric dysfunction, lower midbrain, upper pons Apneustic respiration Prolonged pause at full inspiration Pons Ataxic or cluster respiration Irregular, gasping respirations Lower pons or upper medulla Ondine curse Failure of involuntary respiration with retained voluntary respiration Medulla Apnea No respiration Medulla down to C4: peripheral nerves, neuromuscular junction CHAPTER 62  Coma and Depressed Sensorium 761 A B C D E A B C D E • Fig 62.2  ​Respiratory patterns and associated levels of injury (A) Cheyne-Stokes respiration is seen with metabolic injury and lesions in the forebrain and diencephalon (B) Central neurogenic hyperventilation is most commonly seen with metabolic encephalopathies (C) Apneustic breathing (inspiratory pauses) is seen in patients with bilateral pontine lesions (D) Cluster breathing and ataxic breathing are seen in lesions at the pontine medullary junction (E) Apnea occurs when the medullary ventral respiratory nuclei are​ injured Pupillary size is the result of a balance in tone between two opposing muscle groups of the iris: the dilator pupillae and the sphincter pupillae muscles The dilator pupillae is responsible for dilation of the pupils (mydriasis) under the control of sympathetic nerve fibers The sphincter pupillae muscle is responsible for constriction of the pupils (miosis) under control of parasympathetic nerve fibers Pupillary size is regulated by reflex mechanisms that occur as a result of ambient light and is further affected by age, emotional state, state of arousal, and intraocular pressure The pupillary light reflex requires a four-neuron pathway Light information from retinal ganglion cells travels through the optic nerves, optic chiasm (where the nasal fibers decussate), and optic tracts, and synapse in the pretectal nuclei of the dorsal midbrain Pretectal nuclei receive input from both eyes and send axons to bilateral parasympathetic Edinger-Westphal nuclei Pupillary constriction occurs as a result of parasympathetic activity The contralateral innervation of the Edinger-Westphal nuclei is the anatomic basis for the consensual light response Parasympathetic nerve fibers travel along the third cranial nerve to the ipsilateral ciliary ganglion within the orbit The pupillary sphincter muscle (and ciliary muscle for lens accommodation) is innervated by the postganglionic parasympathetic fibers Pupillary dilation is mediated through the three-neuron sympathetic (adrenergic) pathways Sympathetic fibers originate in the hypothalamus and descend caudally to synapse in the cervical spinal cord between levels C8 and T2 at the area of the ciliospinal center of Budge Neurons then travel from the cervical spinal synapse through the brachial plexus, over the lung apex, and ascend to the superior cervical ganglion near the angle of the mandible at the bifurcation of the common carotid artery Postganglionic fibers then ascend within the adventitia of the internal carotid artery through the cavernous sinus in close relation to the sixth cranial nerve Finally, the oculosympathetic pathway joins the ophthalmic division of the trigeminal nerve and innervates the dilator pupillae, Müller muscle (a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction), and the sweat glands of the face Defects in this sympathetic pathway cause Horner syndrome (miosis, ptosis, and anhidrosis of the face) 762 S E C T I O N V I   Pediatric Critical Care: Neurologic TABLE Clinical Findings With Different Levels of Central Nervous System Dysfunction 62.5 Structure Response to Noxious Stimuli Pupils Eye Position and Movements Breathing Motor Findings for Structural Lesions Supratentorial: Initial Focal Signs, Retrocaudal Progression, Asymmetric Examination Early Both cortices Withdrawal Small, reactive Extraocular movements can be elicited Ipsilateral deviation in frontal lobe lesion Posthyperventilation apnea or CheyneStokes respiration Contralateral hemiparesis Thalamus Decorticate posturing Equal and small unless there is damage to optic tract Eyes deviated down and in toward the side of the lesion Posthyperventilation apnea or CheyneStokes respiration Contralateral hemiparesis Infratentorial: Sudden Onset of Coma, Cranial Nerve Abnormality, and Respiratory Pattern Often Observed Midbrain Decorticate or decerebrate posturing Midposition Fixed to light Spontaneous fluctuation Nystagmus may be present Absent vertical movement Retained horizontal movements Loss of ability to adduct Both eyes may be deviated laterally and down in third cranial nerve damage Post hyperventilation apnea or CheyneStokes respiration Possible central reflex hyperpnea Hemiplegia with contralateral third cranial nerve palsy Pons Decerebrate posturing Bilateral pinpoint pupils Reactive to light, especially with midline pontine hemorrhage Horner syndrome with lateral lesions Ocular bobbing Absent conjugate horizontal movements with retained vertical movements and accommodation Eyes are often deviated medially, seventh cranial nerve damage May exhibit central reflex hyperpnea, cluster breathing, or apneustic breathing Hemiplegia with contralateral sixth or seventh cranial nerve palsy Medulla Weak or absent leg flexion Nonreactive Normal size Small Horner syndrome with lateral lesions Usually no effect on spontaneous eye movements May interfere with reflex responses Nystagmus Rarely ataxic respiration Apnea if respiratory centers involved Flaccid weakness with difficulty swallowing, phonating, and incoordination None Normal reaction Abnormal response if brainstem affected Normal Normal Flaccid weakness Loss of bladder and bowel control Other Spinal cord Toxic, Metabolic, or Infectious Processes: Confusion/Stupor Often Precedes Signs, Symmetric Examination Normal Small, reactive Anisocoria is indicative of a lesion in the efferent fibers supplying the pupillary sphincter muscles A lesion in the afferent limb of the pupillary reflex should not produce anisocoria Afferent pupillary defects are noted when the direct and consensual responses to light are different When anisocoria is noted, it is important to try to identify the abnormal pupil When the pupils are more asymmetric in bright light, the larger pupil is pathologic owing to an abnormality of the parasympathetic pathway or the oculomotor nerve When the pupils are more asymmetric in darkness, the smaller pupil is pathologic owing to an abnormality in the sympathetic pathway These findings may direct further investigation to localize the lesion Fundi should be examined to assess the presence of papilledema and retinal hemorrhages Papilledema is a late sign of increased ICP, and its absence does not rule out raised ICP Signs of papilledema Altered Cheyne-Stokes include blurring of the margins of the optic disc and a decrease in venous pulsations Retinal hemorrhages are most commonly associated with abusive head trauma, although they may be seen following severe coagulopathy or acute intracranial hemorrhage.18 Cranial Nerve Examination Even without patient cooperation, a careful cranial nerve examination provides information about the function of the brainstem Third nerve palsy is the result of lesions anywhere between the oculomotor nucleus and the extraocular muscles The oculomotor nerve originates in the midbrain It innervates the levator muscle of the eyelid, four of the six ipsilateral extraocular muscles (the medial rectus, superior rectus, inferior rectus, and inferior oblique), and the sphincter pupillae (parasympathetic fibers) The CHAPTER 62  Coma and Depressed Sensorium Metabolic small reactive Diencephalic small reactive Tectal large fixed, hippus Pons pinpoint III nerve (uncal) dilated, fixed Midbrain midposition, fixed •  Fig 62.3  ​Pupils in comatose patients Pupillary changes due to structural lesions depend on the site of the primary lesion remaining extraocular muscles, the superior oblique muscle and lateral rectus muscle, are innervated by the fourth and sixth cranial nerves, respectively Third nerve palsies present with ptosis, gaze abnormalities, and varying degrees of pupillary dysfunction Classically, the affected eye is dilated and unresponsive to light, and the eye is directed laterally and inferiorly The oculocephalic—or “doll’s eye”—reflex and the oculovestibular or cold caloric reflex are useful to assess brainstem function These tests assess the function of the midbrain and pons in addition to cranial nerves III, IV, VI, and VIII The oculocephalic reflex should not be tested in patients with suspected cervical spine injury Cranial nerves V and VII are tested by the corneal reflex Cranial nerves IX and X are tested by the cough and gag reflexes Motor Examination Motor examination may reveal focal or generalized neurologic deficits If a single anatomic lesion can explain all of the signs, then 763 the differential diagnosis shortens to structural CNS causes of coma If there is neuroanatomic inconsistency, toxic and metabolic causes of coma are most common Physical examination findings and their expected anatomic correlates are presented in Table 62.5 Decorticate posturing (i.e., tonic flexion of upper extremities and tonic extension, adduction, and internal rotation of lower extremities) reflects a lesion above the red nucleus in the midbrain Decerebrate posturing (i.e., tonic extension of upper extremities as well tonic extension, adduction, and internal rotation of lower extremities) is elicited in response to noxious stimuli in patients with lesions below the red nucleus These findings and their associated anatomic locations are shown in Fig 62.4 Diffuse flaccid weakness occurs with lesions below the pontinemedullary junction It should be noted that acute lesions often cause decerebrate posturing regardless of anatomic location, and both decorticate and decerebrate posturing may occur in combination These facts render posturing less reliable for exact localization of CNS lesions Although not always reliable for localization, posturing suggests that cortical control centers are not functioning Herniation Syndromes Expanding mass lesions develop at the expense of one of the CNS compartments (brain, blood, or cerebrospinal fluid [CSF]) Herniation occurs when the brain is subjected to pressure gradients that cause portions of it to extrude from one intracranial compartment to another (Fig 62.5) Central herniation occurs when diffuse brain swelling or a centrally located mass causes the diencephalon to move caudally through the tentorial notch Dysfunction of the ARAS and cerebral hypoperfusion cause the alteration of consciousness Patients initially become less alert and later progress to coma Diencephalic dysfunction initially produces small reactive pupils because sympathetic output from the hypothalamus is lost At this stage, decorticate posturing may be spontaneous or elicited by noxious stimuli, and Cheyne-Stokes respiration is noted (see Fig 62.2) It is important to recognize this constellation of symptoms because herniation at this stage is reversible As rostral-caudal progression of central herniation continues into the midbrain and pons, the likelihood of reversibility markedly decreases As the midbrain begins to fail, pupils enlarge to midposition, and decerebrate A B • Fig 62.4  ​Stereotypic posturing (A) Decorticate posturing reflects a lesion above the red nucleus in the midbrain (B) Decerebrate posturing reflects a lesion below the red nucleus 764 S E C T I O N V I   Pediatric Critical Care: Neurologic Trans-calvarial herniation gradient across the foramen magnum increases, cerebellar tonsils may be pushed through the foramen and also can compress the upper cervical spinal cord Increased pressure on the brainstem can result in dysfunction of brain centers responsible for controlling respiratory (and cardiac) function, which may result in apnea Patients with cerebellar tonsillar herniation may complain of neck pain before losing consciousness Upward transtentorial herniation occurs when contents of the posterior fossa herniate into the diencephalic region This syndrome can be seen in patients who have ventricular drains placed for relief of hydrocephalus or with posterior fossa mass lesions If a low to high pressure differential is created between the supratentorial and subtentorial regions, respectively, upward transtentorial herniation may occur Mass Diagnostic Evaluation Laboratory Tests Sub-falcine herniation Central herniation Tonsillar herniation Uncal herniation • Fig 62.5  ​Herniation syndromes posturing is noted Attempts to elicit horizontal eye movements with either oculocephalic reflex or oculovestibular reflex fail, and the respiratory rhythm becomes irregular The patient becomes overtly comatose Further progression affects the medullary respiratory centers Virtually all brainstem reflexes are absent, and death becomes imminent The initial cardiovascular response to diminished brainstem perfusion is hypertension, which leads to reflex bradycardia Classic cushingoid reflex responses (i.e., hypertension, bradycardia, and abnormal respirations) are seen mostly after the development of herniation syndromes and are a poor prognostic sign Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles Uncal herniation occurs when a lateral expanding cerebral mass pushes the uncus and hippocampal gyrus over the lateral edges of the tentorium, putting pressure on the brainstem, especially the midbrain A unilateral dilated pupil that is first to appear, often without severe impairment of consciousness, and contralateral hemiparesis are the hallmark findings of uncal herniation (see Fig 62.3) Cranial arteries may be compressed during herniation Once present, changes in brainstem function, ipsilateral hemiplegia, and altered oculocephalic reflexes may progress rapidly In some patients, bilateral pupillary dilation develops, presumably because of distortion of third cranial nerve anatomy and midbrain ischemia At this point, uncal herniation begins to affect the midbrain and upper pons, producing fixed pupils and extensor posturing, bradycardia, and respiratory abnormalities Further progression is indistinguishable from central herniation Subfalcine herniation occurs when a lateral mass or unilateral hemispheric swelling displaces the frontal lobe beneath the falx cerebri This causes compression of the anterior cerebral artery against the falx and can present with contralateral leg weakness Cerebellar tonsillar herniation is seen in patients with posterior fossa masses that cause compression of the brainstem, cranial nerve dysfunction, and obstructive hydrocephalus As the pressure Diagnostic tests that may facilitate supportive management and/ or elucidate the etiology of coma may be obtained in a stepwise manner1 (Table 62.6) Immediate tests that can be performed at the bedside include blood glucose and blood gas with electrolytes; these results are typically obtained within a few minutes If present, treating hypoglycemia with intravenous administration of dextrose bolus can lead to reversal of coma Blood gas analysis can provide information on acid-base abnormalities as well as electrolyte derangements that may also elucidate the etiology of the comatose state The second tier of laboratory tests typically requires additional time for turnaround of results and should be obtained during ongoing resuscitation of the comatose patient The third tier of tests does not affect immediate management and may be obtained as indicated after further consultation with other subspecialty services in an attempt to elucidate the exact etiology of the comatose state Imaging and Other Studies In addition to these laboratory tests, prompt computed tomography (CT) of the head is indicated when the patient is appropriately resuscitated CT may be rapidly obtained (typically in less than minutes of scanning time) and can reveal trauma/fracture, intracranial hemorrhage (subdural, epidural, intraparenchymal), tumor, abscess, calcifications, hydrocephalus, edema, or herniation Absence of CT findings may suggest a metabolic or toxic etiology Notably, CT should be obtained prior to lumbar puncture, but a normal CT does not definitively indicate normal ICP Clinical examination findings must be considered If airway and hemodynamic stability permit lengthier imaging (,30 minutes of scanning time), a magnetic resonance imaging (MRI) scan may elucidate other etiologies of the comatose state, including parenchymal abnormalities, infarction, sinus venous thrombosis, diffuse axonal injury, gray-white matter changes, encephalitis, demyelination, and more Electroencephalography (EEG) is warranted, as it may indicate the presence of subclinical status epilepticus, particularly in a patient who is receiving sedation and/or neuromuscular blockade The EEG may reveal characteristic patterns indicative of diagnoses such as metabolic encephalopathies or herpes encephalitis Additional studies, such as electrocardiography, may reveal the presence of conduction abnormalities particular to toxic drug levels Chest radiography and a skeletal survey may indicate ... with metabolic encephalopathies (C) Apneustic breathing (inspiratory pauses) is seen in patients with bilateral pontine lesions (D) Cluster breathing and ataxic breathing are seen in lesions... consensual light response Parasympathetic nerve fibers travel along the third cranial nerve to the ipsilateral ciliary ganglion within the orbit The pupillary sphincter muscle (and ciliary muscle for... laterally and down in third cranial nerve damage Post hyperventilation apnea or CheyneStokes respiration Possible central reflex hyperpnea Hemiplegia with contralateral third cranial nerve palsy

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