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REVIEW

Approach to a child with depressed level of consciousness and coma
Amit Sarnaik†, Nirmala B Bhaya & Prashant V Mahajan†Author for correspondenceDivision of Emergency Medicine, Carman and Ann Adams Department of Pediatrics, Children’s Hospital of Michigan, Wayne State University, 3901 Beaubien Blvd, Detroit, MI 4820, USATel.: +1 313 745 5260Fax: +1 313 993 [email protected]
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Keywords: brain impairment, coma, coma management, comatose child, neurological emergency

10.2217/14750708.5.4.435 © 2

Altered mental status and coma can be considered as an acute neurological emergency characterized by significant brain impairment, necessitating a rapid, methodical approach to evaluation and treatment. There are several, diverse causes of coma, which makes an exact diagnosis challenging. Regardless of the etiology, coma is suggestive of a primary insult to the brain, which, if left untreated, can rapidly progress to secondary injury, and thus result in substantial morbidity and even mortality. It is imperative to rapidly recognize this entity, institute appropriate treatments and improve prognosis. In this article, we review the pathophysiology of coma and its causes to get a basic understanding of this entity. We also discuss the various diagnostic and management approaches for timely recognition and treatment of this life-threatening emergency. In addition, we present some prognostic indicators in a comatose child.

Coma is a nonspecific manifestation of diffusebrain impairment and can result from a struc-tural or metabolic (or a combination of both)cause. Coma usually indicates a primary insult tothe brain, which, if left untreated, can rapidlyprogress to secondary injury, and thus result insubstantial morbidity and even mortality. It isimperative to rapidly recognize coma, instituteappropriate treatments and improve prognosis.

To better understand the etiology and manage-ment of coma, a brief overview of the physiologyof neurological processes that are responsible fornormal consciousness is necessary. The normalconscious state can be subdivided into a state ofarousal or wakefulness, and a state of the aware-ness of the self and environment. Arousal is theresult of sensory stimulation of ascending reticularactivating system (ARAS) in the brainstem, withsubsequent spread to the hypothalamus, thalamusand, eventually, the cerebral cortex. These, inturn, send numerous positive feedback signalsback to the same reticular nuclei to activate themfurther. Thus, there is self-sustenance secondaryto all the positive feedback activity. Therefore, itis clear that complex interplay of these path-ways, within themselves and the periphery, isresponsible for conscious awareness [1].

PathophysiologyFrom the above discussion it is clear that both ofthe components involved with arousal (i.e., thecerebral cortex as well as the ARAS) must be pre-served for normal consciousness. Principal causesof coma can therefore be owing to widespreaddamage in both cerebral hemispheres secondary

to ischemia, or trauma, or suppression of cerebralfunction by drugs, toxins, hypoxia or systemicmetabolic derangements, as in hypoglycemia,uremia or hepatic failure, and brainstem lesionsthat cause damage to ARAS.

DefinitionsComa is defined as a pathological state of deepand sustained (>1 h) unconsciousness, distin-guishable from normal sleep by the inability tobe aroused [2,3]. It can also be considered as astate of complete loss of arousal to any kind ofstimulation and complete loss of awareness ofthe self and the surrounding. While coma rep-resents the most severe case of altered senso-rium, the following are some of the termscommonly used to describe a patient’s alteredmental status with reduced alertness, in con-trast to hyper-alertness as exemplified by delir-ium, delusions and hallucinations [3]. The termlethargy indicates drowsiness or decreasedwakefulness, characterized by confusion and anability to communicate if an appropriate stimu-lus is applied [3]. The term stupor is used todescribe a state worse than lethargy and is char-acterized by significantly decreased responsive-ness, but arousability with noxious stimuli [3].The term obtundation is used to describe adeeper state of unresponsiveness, when thepatient is unable to respond to even vigorousstimulation [3]. Since these entities are very sub-jective and examiner-dependent, thereby ren-dering them obsolete, it therefore necessitatesthe use of validated measurement scores, suchas the Glasgow Coma Score (GCS), and its

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modification for the pediatric population toobjectively and accurately describe the level ofchange in the mental status of a patient.

Although certain chronic conditions mayresemble coma, there are distinct characteristicsthat allow a physician to differentiate them fromacute causes of altered mental states. Vegetativestate is characterized by complete loss of aware-ness of the surrounding; however, there may besome preservation of sleep–wake cycles andspontaneous eye opening. There may also beexhibition of reflex and nonpurposeful move-ments that are elicited by external stimulation.This state is considered to be permanent if it per-sists for more than 1 year in patients with a trau-matic brain injury or more than 3 months inpatients with nontraumatic brain injury [3]. Aminimally conscious state can be differentiatedfrom a vegetative state by the presence of pur-poseful, nonreflexive movements, the presence ofsome affective and emotional responses to thecontent of conversation, and the ability to par-tially fixate and follow visual stimuli [4]. Locked-in syndrome is characterized by presence of anintact consciousness, but inability of expressiondue to paralysis of voluntary muscles. Voluntaryeye movements and blinking may be retained.This condition is often seen in post-traumaticstates, pontine lesions and as a sequel of acuteneurologic conditions such as Guillain Barrésyndrome [5–9]. Akinetic mutism, a qualitativelydifferent condition, is characterized by very slowand delayed motor response, and is usually sec-ondary to lesions in the frontal lobe, responsiblefor initiating movements, but otherwise has thesame characteristics as locked-in syndrome.There is usually preservation of tone and reflexes.

It is important to recognize that all of theabovementioned chronic conditions, except veg-etative states and coma, are characterized bypreservation of pain perception, and thereforeadequate pain control should be an integral partof patient management. Brain death is the finalstage in the severity scale for altered mentalstates, and is characterized by severe coma, andirreversible loss and destruction of cortical andbrainstem functions, with no evidence of anyarousal, awareness or pain perception [10].

Causes of comaThere are many causes of coma and altered men-tal state (Boxes 1 & 2). These etiologies couldeither function alone or in combination to resultin altered mental states and coma. The impair-ment is, again, either primary, for example, due

to direct brain involvement, or secondary, forexample, brain involvement as a result of a sys-temic insult. The impairment can also be classi-fied as functional (absence of structural braindamage) or organic (presence of structural braindamage). Either mechanism can result in diffusecortical and brainstem depression. At the mole-cular level, these impairments are represented bynecrotic and apoptotic brain cell death [3]. Vari-ous mechanisms proposed to be involved withcell death are excessive release of excitatoryneurotransmitters, loss of ion homeostasis, ele-vated intracellular calcium and mitochondrialand inflammatory free radical production, DNAcleavage, proteolysis and lipid peroxidation [11].

The incidence of coma from various causes isapproximately 0.3%. Younger children are morelikely to have coma/altered mental states owingto nontraumatic etiologies as compared witholder children, where traumatic brain injury ismore likely. Among all the etiologies, traumaticbrain injury leading to coma deserves a specialmention, because head injuries in children areextremely common and account for a large per-centage of serious morbidity and mortality. Trau-matic brain injury accounts for over 80% offatalities recorded in the US National PediatricTrauma Registry [12].

Approach to managing a child with altered mental status & comaThe approach to a comatose patient has fourbroad components, consisting of:

• Initial stabilization, history, physical examina-tion and rapid neurologic assessment

• Use of reversal agents to treat certain metabolicand toxic derangements

• Determination of the level of CNS functionand the etiology of coma

• Institution of specific treatment

It is important to realize that these componentsare to be addressed simultaneously, rather than ina sequential manner. It is also important to under-stand some conceptual differences in the manage-ment of children versus adults. Children responddifferently to adults. Young children might not beable to describe symptoms or localize pain. Suchinability of communication leads to a challengingsituation, which may need significant experienceand patience on the part of the examiner. Ana-tomically, the head occupies a larger relative bodysurface area and mass than that of an adult. TheCNS of children younger than 3 years is in a stateof dynamic development. Increase in the head

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Box 1. Etiologic classification of coma and altered mental status .

Infection

• Viral: encephalitis• Bacterial: meningitis, brain abscess, emphysema, sepsis• Fungal: meningitis

Metabolic

• Hypoglycemia• Inborn errors of metabolism• Dyselectrolytemia: hypernatremia, hyponatremia• Mineral metabolic defect: hyper/hypocalcemia, hypomagnesemia, hypophosphatemia• Hyperammonemia• Hepatic failure: hyperammonemia• Renal failure: uremia• Endocrinopathies: hyper/hypothyroidism, adrenal insufficiency • Addison’s disease• Vitamin deficiency: nicotinic acid, pyridoxine, thiamine• Intussusception encephalopathy• Methhemoglobinemia• Porphyrias• Mitochondrial encephalopathy

Toxic/ingestions

• Alcohol• Anticholinergics• Antihistamines• Barbiturates• Benzodiazepines• Carbamazepine• Carbon monoxide• Cocaine• Cyanide • Heavy metals (lead)• Lysergic acid diethylamide (LSD)• Marijuana• Narcotics• Organophosphates• Phenothiazines• Salicylate• Hepatic failure secondary to toxins: amanita mushrooms, acetaminophen

Trauma

• Concussion• Cerebral contusion• Hematoma: subdural, epidural, subarachnoid• Diffuse axonal injury• Intraparenchymal hemorrhage• Intraventricular hemorrhage• Brainstem injury

Structural

• Hematoma: epidural, subdural• Brain abscess• Brain cyst• Brain tumor• Hydrocephalus• Hydrocephalus with shunt malfunction

Adapted from Tables 41–48 in [18].

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circumference in the first year reflects increasingbrain volume. The pediatric brain undergoes dou-bling of its weight by 6 months of life, and by 2years it is almost 80% of adult brain weight. Thisis also the time when there is active and ongoingmyelination, synapse formation, dendriticarborization and increasing neuronal plasticitytaking place, and therefore any injury to the brainat this time can lead to arrest of these processesand cause significant deficits [13,14]. As comparedwith adults, children also demonstrate exagger-ated cerebrovascular response to injury, and there-fore are more prone to develop diffuse brainswelling more readily [15]. The brain parenchymaof children is minimally compressible, contribut-ing minimally to an intracranial volume bufferingsystem, as compared with cerebrospinal fluid(CSF) and cerebral blood volume in situationsleading to increased intracranial pressure (ICP),and therefore a rapid recovery is often experiencedin children with no significant brain lesion, inwhom optimal cerebral perfusion pressure (CPP)is maintained throughout the disease process.

Prehospital careThe management of a child with a depressed levelof consciousness and coma should ideally beginin the prehospital setting. There has been signifi-cant research pertaining to prehospital manage-ment, especially concerning critically injuredpatients, whose best chance of survival is depen-dent upon receiving high-quality care from theearliest possible postinjury moment. This high-quality care is expected from the providers of

prehospital care. The recommendations made byprehospital trauma life support have shownfavorable results and provide guidelines for pre-hospital management of traumatic brain injury.These include the following [16]:

• The need for endotracheal intubation in a childor adult with GCS of equal to or less than 8;

• Maintenance of adequate oxygenation, assist-ing normoventilation at rates of 20/min forchildren, and 25/min for infants;

• Control of external hemorrhage;• Intravenous fluid resuscitation to maintain

systolic blood pressure greater than or equal to90 mmHg;

• Treatment of seizures with benzodiazepines• Assessment of blood glucose levels;• Recognition of the signs of increased ICP,

such as decrease in GCS by 2 points, fixed ornonreactive pupil, hemiparesis or hemiplegiaand Cushing’s triad (irregular breathing,bradycardia and hypertension);

• Initiation of corrective measures, such as con-sidering removal of cervical collar, sedationand paralysis of patient, osmotherapy andmild hyperventilation;

• Safe transportation of the patient to a traumacenter, with the availability of CT scan andneurosurgical services.

Initial stabilizationThe approach to the management of a comatosechild involves an immediate and rapid assess-ment of the ‘A, B, Cs’ – Airway, Breathing and

Vascular

• Embolism• Hemorrhage: subarachnoid, intraparenchymal• Vasculitis• Lupus• Hypertensive encephalopathy

Hypoxic

• Respiratory failure• Cardiac: dysrhythmia, arrest, cardiogenic shock• Toxins: carbon monoxide, cyanide• Near drowning

Epileptic

• Post-ictal states• Status epilepticus

Psychologic

• Conversion disorder, catatonia

Box 1. Etiologic classification of coma and altered mental status (cont.).

Adapted from Tables 41–48 in [18].




Box 2. Age-based e

Neonate• Congenital anomalies• Hypoxic ischemic inju• Hypoglycemia• Inborn errors of meta• Hypocalcemia• Seizures• Congenital infection• Sepsis• Intraventricular hemo

Infant

• Infection: meningitis/e• Trauma: accidental an• Shock: hypovolemic, c• Metabolic: hypo/hype

of metabolism• Ingestions: accidental• Seizures• Intussusception

Child

• Trauma• Infection: meningitis, • Ingestion• Metabolic: hypoglyce• Seizure

Adolescent

• Trauma• Infection: meningitis, • Ingestion • Seizure• Psychologic

Adapted from Tables 41–49

Circulation – to ensure adequacy of oxygen-ation, ventilation and tissue perfusion, respec-tively. Before determining specific etiologies,ordering specific tests or providing specific med-ications, care should be taken to ensure that thepatient’s airway is secure. If not secure, thepatient may require airway repositioning, sup-plemental oxygenation and suctioning oforopharyngeal secretions. Following this, theadequacy of breathing must be assessed. Patientsmay require support of their breathing byassisted ventilation in the form of a bag andmask, or even endotracheal intubation (oftencarried out with rapid sequence induction).Intubation should also be performed as an inter-vention to facilitate hyperventilation in anattempt to reduce intracranial hypertension, orin cases where the patient has significanthypoventilation, in instances of opioid intoxica-tion. The provider should recognize that use ofcertain medications that alter the intracranial

hemodynamics, especially ketamine (which isknown to cause an increase in ICP) or pentobar-bital (which is known to reduce systemic bloodpressure, thus potentially reducing CPP) may beharmful during rapid sequence induction for air-way control. Rapid assessment of the circulatorystatus (capillary refill and blood pressure) andaggressive efforts to restore normal circulatoryvolumes may be required. Interventions such asintraosseous needle placement should be encour-aged if immediate access to the vascular system isproblematic or considered time-consuming.Additionally, the possibility of a cervical spineinjury along with head injury should always beentertained in all children who present withaltered mental state, and patients should havetheir cervical spine stabilized by in-line traction.A rapid neurological evaluation should be per-formed to establish the patient’s level of con-sciousness, as well as papillary size and reaction.The AVPU method is a simple mnemonic todescribe the level of consciousness:

• A: Alert

• V: Responds to Vocal stimuli

• P: Responds only to Painful stimuli

• U: Unresponsive to all stimuli

A decreased level of consciousness may suggestdecreased cerebral oxygenation and/or perfusion,or may be owing to direct cerebral injury andindicate a need for immediate re-evaluation of apatient’s oxygenation, ventilation and perfusionstatus. The patient should also be completelyundressed to facilitate thorough examinationand assessment. Care must be taken to avoidhypothermia from undressing the patient.

History After initial stabilization is achieved, a brief inter-view with the child’s parents/care providers, alongwith circumstances leading to the alteration ofmental status, should be sought. Pertinent histor-ical details, such as rapidity of onset, specificsymptoms and signs (toxidromes) may providevaluable clues to the etiology and aid in subse-quent management of the patient. An acute pre-sentation in an otherwise normal individual maybe suggestive of etiologies such as acute trauma,metabolic disorders, cardiac dysarrhythmias orintoxication. Etiologies that cause progressive orgradual alteration of mental status over a periodof days often have limited scope for acute reversaltreatment, but still need comprehensive evalua-tion. Any knowledge of underlying pathology,such as pre-existing conditions (for example

tiologies of coma.

ry

bolism

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ncephalitisd nonaccidentalardiogenic and septicrnatremia, hypoglycemia, inborn errors

or nonaccidental (child abuse)

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diabetes mellitus, inborn errors of metabolism),in the patient could also prove to be a vital pieceof information for further analysis andtreatment [17]. The AMPLE history is a usefulmnemonic to obtain complete historical details:

• A: Allergies• M: Medications currently used• P: Past illnesses/Pregnancy• L: Last meal• E: Events/Environment related to the

patient’s status

Physical examinationEvery vital sign of the patient should be carefullyinspected and interpreted, as they may offerextremely valuable information to guide imme-diate treatment. For example, an elevated tem-perature could indicate systemic infection(bacteremia or septicemia), intracranial infection(meningitis, encephalitis or intracranial abscess),a post-ictal state or drug ingestions (anticholin-ergics), heat stroke or pontine hemorrhage.Hypothermia may suggest ingestions (alcohol,opiates), fulminant infections (septicemia, espe-cially in very young infants) and environmentalexposures (frost bite, submersion accidents).Bradycardia could suggest ingestions (β-blockers,calcium channel blockers) or can be a compo-nent of Cushing’s triad, suggestive of increasedICP. Tachycardia in a comatose child, on theother hand, can be secondary to pain, fever,dehydration, shock (hypovolemic, septic orcardiogenic), or ingestions (anticholinergics andsympathomimetics). Tachypnea could indicatecentral stimulation of the respiratory center withdrug intoxications such as salicylate, or as a com-pensatory mechanism for metabolic acidosis(e.g., Kussmaul’s breathing associated with dia-betic ketoacidosis). Hypoventilation, character-ized by slow, shallow breathing, may suggestintoxication with opiates or other agents thatdepress the CNS (alcohol, sedative hypnotics).Specific breathing patterns in regards to its rate,depth and cycling can suggest the presence ofcertain pathologies. Cheyne–Stokes respiration,characterized by periods of hyperpnea alternat-ing with apnea, is observed in bilateral hemi-spheric and diencephalic dysfunction, and mayherald the occurrence of transtentorial hernia-tion. Apneustic breathing, seen in lesions involv-ing the mid to lower pons, is characterized byprolonged pause at full inspiration. Low pontineand upper medullary lesions are associated withclusters of breath, alternating with periods of

apnea, also known as ataxic breathing, whichprogresses to agonal breathing with medullarylesions. Hypotension, suggestive of shock statesand intoxications such as accidental or inten-tional overdose of antihypertensives such asclonidine, β-blockers and calcium channelblocker medications, is a helpful parameter forinterpretation in combination with other vitalsigns, as is hypertension, which may occur sec-ondary to intoxications or as a feature ofCushing’s triad.

Other components of the physical examina-tion include inspection of the skin for color,lesions, rashes, pigmentation or needle tracks.These findings can suggest intoxications, infec-tions, illicit drug use and metabolic impairments.Skin erythema may suggest carbon monoxide ormercury poisoning. Cyanosis may be encoun-tered in patients with hypoxia, or due to the pres-ence of a congenital cyanotic heart lesion (whichpredisposes the patient to strokes and othercerebrovascular accidents) or ingestions thatcause altered sensorium and methhemoglobine-mia, which may result from toxic exposures suchas aniline or severe diarrheal illness in infancy.Petechia may be seen with infectious endocardi-tis, sepsis, disseminated intravascular coagulationor trauma (child abuse). An alteration in pigmen-tation (hyperpigmentation) could suggest Addi-son’s disease, and needle tracks suggestintravenous drug use. Breath odor can be used topinpoint etiologies such as diabetic ketoacidosis(fruity odor), alcoholic intoxication and cyanidepoisoning (bitter almonds). Examination of theeyes, ears and nose, with particular attention toany bruising around the eye and any drainagefrom the ears or nose, indicative of CSF otorrheaor rhinorrhea, can offer diagnostic clues for frac-tures and nonaccidental trauma. Fundoscopicevaluation is important to detect the presence ofpapilledema or retinal hemorrhages (seen in non-accidental trauma). Oral examination can revealtongue lacerations suggestive of injury secondaryto a seizure. Head examination, especially palpa-tion of the anterior fontanel, is often helpful todetermine raised ICP.

Role of reversal agentsWhile the evaluation is in progress, the physicianmust be vigilant regarding the possibility ofimmediately reversible causes of the coma, andhypoglycemia and opioid intoxication should beconsidered in the differential. Hypoglycemia canbe immediately reversed by administering a 25%dextrose solution (dose: 0.5–1 g/kg) as a rapid,




intravenous push. Opioid intoxication can bereversed, as well as detected, by administeringintravenous naloxone 0.1 mg/kg up to 20 kg forthose up to the age of 5 years and 2 mg for thoseover 5 years of age. Naloxone can also be adminis-tered subcutaneously and intramuscularly. Theadministration of flumazenil 0.2 mg intra-venously over 30 s can reverse benzodiazepineintoxication. The physician should be aware thatflumazenil can precipitate refractory seizures inpatients with chronic benzodiazepine exposure.Only in the presence of obvious etiology such astrauma is there a rationale for not using theseagents for immediate intervention. Intravenousaccess for these medications can also be utilized tosample blood for baseline yet broad-spectrumscreening laboratory investigations, such as acomplete blood count, serum electrolytes, bloodurea nitrogen, creatinine, glucose and calcium lev-els. At our institution we routinely collect bloodfor a rapid bedside glucose test, as well as capillaryblood gas evaluation for quick assessment ofacid–base status, while awaiting the laboratoryresults. Liver function tests, coagulation profile,serum ammonia, osmolality, carboxyhemoglobin,basic serum and urine toxicological screens canalso be obtained when specific etiologies areunder consideration.

Neurological examinationUpon stabilization of the patient, the physicianmust perform a detailed neurological evaluationto determine a specific etiology and depth ofalteration of sensorium, and also to guide furtherevaluation, specific laboratory workup and imag-ing modalities to determine the diagnosis. Thedetailed neurological examination (includingassessment of pupils, fundus, cranial nerves,motor and sensory evaluation) should be per-formed to help localize the site of the lesion inthe CNS.

The preservation of pupillary reflexes suggeststhe presence of metabolic encephalopathy, andtheir absence suggests structural pathologies, anexception being intoxication with atropine-likemedications, which results in fixed, dilatedpupils [18]. Pupillary size and response is depen-dent on the balance between sympathetic andparasympathetic stimulation. The sympatheticresponse dilates the pupil, whereas theparasympathetic response causes constriction.Parasympathetic fibers originate in theEdinger–Westphal nuclei in the midbrain andaccompany the oculomotor nerve along its longpath, whereas the sympathetic nerves originate

in the hypothalamus and traverse through thecervical spinal cord and cervical sympatheticchain to eventually innervate the pupillodilatormuscles of the eye, sweat gland of the face andthe Muller’s muscle of the eyelid. Lesion in theparasympathetic nuclei or fibers results in anipsilateral fixed, dilated pupil. Clinically, thisentity is suggestive of ipsilateral uncal herniation,and therefore should be treated as a surgicalemergency. Lesions anywhere along the pathwayof sympathetic input can result in ipsilateralpupillary constriction (miosis), ptosis with sec-ondary enophthalmos and anhydrosis, alsoknown as Horner’s syndrome. Unequal pupils(anisocoria) signify direct injury to the eye ordisruption of unilateral sympathetic or parasym-pathetic signals. Injury to nuclei in the midbrainaffects both autonomic pathways and may resultin neutral, fixed pupils. Lesions in the tectumand midbrain may cause slightly large, but fixedpupils. Due to preservation of accommodation,papillary size may vary, resulting in the clinicalentity called hippus. Pontine lesions disrupt thesympathetic pathways, resulting in pinpointpupils, which are classically seen in pontine hem-orrhage. Metabolic and toxic encephalopathiesare responsible for small and minimally reactivepupils. Symmetrically dilated and responsivepupils are seen with anticholinergic toxicity,whereas severe anoxic injuries result in dilatedand unresponsive pupils.

Assessment of extraocular movements is thenext important component of evaluation of acomatose child. The extraocular movements arefacilitated by complex interplay of several differ-ent neuronal pathways. The frontal lobes controlvoluntary eye movements, the rapid phase ofnystagmus and also influence brainstem reflexesthat determine eye movements. The oculomotornerve (third cranial nerve) and trochlear nerve(fourth cranial nerve), which originate in themidbrain, and abducens nerve (sixth cranialnerve), which originates in the pons, control theextraocular muscle movements. Conjugate eyemovements in the horizontal plane are coordi-nated between ipsilateral oculomotor nuclei andcontralateral abducens by the medial longitudi-nal bundle. Proprioceptive and vestibular inputsalso coordinate eye movements. Complex yetsmooth coordination between these pathwaysforms the basis for oculocephalic or ‘doll’s eye’reflex and the oculovestibular reflex testing.These influences are responsible for maintenanceof visual fixation despite movements of the head.In a comatose child, an oculocephalic reflex is



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considered abnormal if eyes do not move in theopposite direction of head movement, eitherfrom one side to the other or up and down. Ifthere is a concern for cervical spine injury, thistesting is absolutely contraindicated, and thesame pathways can be assessed by performing theoculovestibular reflex or caloric response test.Irrigation of one external ear canal with warm orcold water induces convection currents in theendolymph of the semicircular canals. In anawake person, nystagmus is elicited with a slowcomponent towards the ear irrigated with coldsaline and fast component away from the stimu-lus. The fast component response to cold orwarm stimulus is the basis of the mnemonic‘COWS’ (cold, fast component opposite, warm,fast component towards the ear tested). In apatient with a brainstem lesion with disruptioninvolving pathways between vestibular andabducens nuclei, both the oculovestibular andoculocephalic reflexes are absent. Conversely,presence of these reflexes in a comatose childindicates the intactness of the brainstem andmidbrain pathways.

Corneal reflexes test the integrity of pathwaysthat include the afferents carried by the tri-geminal nerve (fifth cranial nerve), and theresponse exhibited by upward movement of theeye mediated by the oculomotor nerve and,more importantly, closure of the eyelid mediatedby the facial nerve (seventh cranial nerve). Thepresence of this reflex is reflective of intact path-ways between the midbrain and the pons. Thisreflex loses its value in a sedated and paralyzedpatient, but is of significance by its absence in ametabolic disorder with profound coma. Intactgag reflex indicates integrity of glossopharyngealand vagal afferents.

The next step is examination of the motor sys-tem and starts with simple observation ofpatient’s posture, evidence of spontaneous activ-ity and response to various stimuli. Asymmetricalpostures may suggest hemiparesis or hemiplegiafrom contralateral structural lesions to the cor-tico-spinal tracts. Hypertonia may be suggestiveof acute brainstem injury at the level of midbrainand pons. Acute hypotonia or flaccid weakness isa hallmark of lower pontine, medullary or spinalcord lesions. Responses to noxious stimulation,such as purposeful withdrawal and vocalizationhelps the examiner to assess neurological status,and may also aid in the gradation of patients asregards to neurological assessment scales. Decor-ticate posturing characterized by flexion of armsand extension of legs indicates a bilateral lesion

between the midbrain and the cerebral cortex.On the other hand, decerebrate posturing char-acterized by hyperextension, with or withoutopisthotonus, is suggestive of lesion in the mid-brain pontine region or severe brainstem com-pression. Another important aspect of evaluationis to obtain assessment of a patient’s ICP andwhether there is evidence of any herniation. Mostherniation syndromes pose acute risk of braindeath and should be considered as dire emergen-cies, and emergent medical and surgical interven-tions should be instituted promptly. Uncalherniation is characterized by ipsilateral fixed anddilated pupil and ipsilateral ophthalmoplegia,and may also result in hemiparesis by compres-sion of cerebral peduncle. Central herniationsyndrome is secondary to a more generalized pro-cess such as cerebral edema, resulting in increasedICP, with compression of subcortical structuresand cerebellar herniation through the foramenmagnum. Clinically, physical findings evolve andvary as the severity and level of herniationprogresses. With herniation of midbrain andupper brainstem, the patient will exhibit decorti-cate posturing with small pupils. Brainstemreflexes may be preserved. These are the patientsthat exhibit the classic Cheyne Stokes respira-tions. As lower brainstem and pons start becom-ing compressed, the patient starts gettingdecerebrate posturing, with pupils becomingmore dilated, and generalized diminishedresponses accompanied by loss of brainstemreflexes. Cheyne Stokes respirations will bereplaced by more rapid and regular breathing.Once the lower pons and medulla are involved,there is complete loss of brainstem reflexes, withthe patient assuming a flaccid posture and respi-rations becoming very slow and irregular, beforeresulting in a complete cessation.

Motor responses, along with verbal and ocularresponses, are important cortically determinedaspects of consciousness, assessed by rating scalescores, such as the GCS, and its modification foruse in children (Table 1). These measures do nottake into account every aspect of neurologicalexamination, but its components have proven tohave descriptive and prognostic value.

Neurological examination in herniation syndromesLocalized mass lesions or increased ICP cancause several important cerebral herniation clini-cal syndromes. Uncal herniation is most oftenowing to a local mass lesion or swelling, whichpushes the uncus through the tentorial notch




Table 1. Glasgow Com

Activity GCS for adu

Eye opening

Spontaneous

To speech

To pain

None

Verbal response

Oriented

Confused

Inappropriate

Nonspecific so

None

Motor Follows comm

Localizes pain

Withdraws in r

Flexion in resp

Extension in re

None

Best total score = 15.Adapted from [3,43–45].GCS: Glasgow Coma Score.

and progressively compresses the ipsilateral ocu-lomotor nerve, initially affecting the parasympa-thetic pupillomotor fibers running along itssurface and resulting in a sluggishly reactive thenfixed and dilated pupil. Further compression ofthe oculomotor nerve causes partial ophthal-moplegia, with the affected eye turned outwardand downward owing to unopposed functioningof the lateral rectus and superior oblique muscles.Ipsilateral hemiparesis can also occur due to com-pression of the contralateral cerebral peduncle bythe tentorial notch.

Central herniation is most often due to diffusebrain edema or obstructive hydrocephalus, whichcauses increased ICP, with movement of the thal-amus and hypothalamus downward through thetentorial notch and of the cerebellar tonsilsthrough the foramen magnum. Compression andischemia of the diencephalon and brainstem canoccur in a slow rostrocaudal progression or canadvance abruptly to give signs of lower brainsteminjury. With a diencephalic-level injury, comatosepatients have decorticate posturing, Cheyne-Stokes respirations, and small pupils, but havepreserved brainstem reflexes and remain able tolocalize noxious stimuli. With involvement of themidbrain and upper pons, posturing becomesdecerebrate, pupils become midposition in sizeand sometimes irregular in shape, and there is aloss of pupillary, oculocephalic and oculovestibu-lar reflexes. Respirations may become regular and

rapid. With involvement of the lower pons andmedulla, all brainstem reflexes are lost, posturingis replaced with a flaccid paralysis and respira-tions become ataxic, irregular and slow, beforeeventually ceasing.

Investigating a comatose patientAs discussed earlier in the article, evaluation ofcoma requires significant multitasking withrespect to history, physical examination andsimultaneous attempt at determining the etiol-ogy of coma. Laboratory testing that can be uti-lized for evaluation of comatose patient can bedivided into three broad categories:

• Immediate bedside testing with a turnaroundtime of 1–2 min

• The second group of tests, being tests thathave a turnaround time of 30–45 min, whichis when the patient is being resuscitated

• Tests whose results may not be available forseveral hours to days, and very rarely impactacute resuscitation and stabilization measures

In the first set of laboratory investigations, themost widely utilized one is the bedside glucosemeasurement, which, if indicative of hypo-glycemia, can lead to reversal of coma by admin-istration of intravenous dextrose bolus. Mosthospitals, including the authors’, utilize capillaryblood gas with electrolyte measurement, which,apart from offering rapid valuable information

a Scale scoring and modification for children.

lts GCS modified for children GCS for infants Score

Spontaneous Spontaneous 4

To sound To sound 3

To pain To pain 2

None None 1

Age-appropriate oriented, smile Coos and babbles 5

Confused, aware of environment Irritable, cries 4

words Irritable, inconsistently consolable Cries in response to pain 3

unds Inconsolable, unaware of environment, agitation Moans in response to pain 2

None None 1

ands Obeys commands, spontaneous movements Moves spontaneously, purposely 6

Localizes pain Withdraws to touch 5

esponse to pain Withdraws in response to pain Withdraws to pain 4

onse to pain Flexion in response to pain Decorticate posturing to pain 3

sponse to pain Extension in response to pain Decerebrate posturing 2

None None 1



444

regarding acid–base status, is also capable ofmeasuring electrolytes, lactic acid, carboxyhemo-globin level and ionized calcium levels with fairaccuracy. The second set of laboratory investiga-tions include a complete blood count and ametabolic profile that includes serum electro-lytes, glucose, blood urea nitrogen and creati-nine, serum calcium, basic liver function tests,coagulation profiles, osmolality, serum ammoniaand lactate levels. The complete blood counts arehelpful in detecting leukocytosis, indicatinginfection or stress, anemia and thrombocyto-penia, indicating the possibility of intracranialbleeding, polycythemia and thrombocytosis,which could suggest stroke syndromes. Abnor-malities of electrolytes and renal and hepaticfunction can aid in detecting metabolic derange-ments, as well as uremia and hepatic injury fromconditions such as sepsis, shock or intoxications.High levels of ammonia and lactate can lead todiagnoses of inborn errors of metabolism,hepatic failure, and toxic and metabolicencephalopathy. The metabolic profile can alsoinclude screening for inborn errors of metabo-lism such as serum amino acids and urineorganic acids to screen for disorders of aminoacid metabolism and organic acidemias. Screen-ing for fatty acid metabolism can be performedby sending for levels of carnitine and acyl car-nitine. Abnormal neurohormonal states can bedetected by obtaining thyroid and cortisol levels.A toxicologic screening by obtaining urine andserum drug screens can detect the presence ofpotential toxicants, such as amphetamines, bar-biturates, cocaine, cannabinoids, phencyclidineand propoxyphene in the urine, and acetami-nophen, salicylates, tricyclic antidepressants,sympathomimetics and alcohol in the serum.The toxicologic screens are especially of value inacute presentations. The physician should beknowledgeable regarding his or her institutions’toxicologic panels, with regards to the agentsthat are screened therein. In cases with a veryhigh suspicion level for intoxication, a moreelaborate comprehensive toxicologic screeningmay be necessary. The physician must also becognizant of cross-reactivities of toxicologicscreens with routine over-the-counter medica-tions; for example, use of dextromethorphan, acommon ingredient of over-the-counter coughsyrup, may result in a positive immunoassayscreen for phencyclidine. Cultures from blood,urine and the CSF are obtained if there is suspi-cion for any acute infection. A spinal tap by

lumbar puncture can be deferred if there aresigns of increased ICP, impending cardiorespira-tory failure, bleeding disorders or local infec-tions. Administering broad-spectrum antibioticsshould not be deferred if a lumbar puncture cannot be performed and intracranial infections aresuspected. Neuroimaging with computed tomo-gram should preferably be performed prior tolumbar puncture. The physician must alwaysremember to screen for pregnancy in a reproduc-tive age-group female patient. The third groupof laboratory investigations is usually nonroutineand often obtained after consultation with spe-cialty services, and does not impact immediatemanagement. These investigations, as men-tioned earlier, are geared towards searching foran exact diagnosis to guide treatment furtherdown the line, exemplified by the ceruloplasminlevel for detection of Wilson’s disease.

A patient with a suspected structural or vascularlesion should undergo emergent computedtomography (CT) of the head. Even though thereare concerns of radiation exposure, CT has beenshown to be a very practical imaging modality,especially in an unstable patient, and has rapidturnaround times and acceptable sensitivity foracute intracranial lesions such as fractures, hemor-rhage, tumor and herniation syndromes. A nor-mal CT scan in a comatose patient may suggestmetabolic or toxic etiologies. Repeat CT scanningis indicated in patients with clinical deteriorationfor detection of edema, hemorrhage or herniation.MRI takes precedence over CT when the patientis reasonably stable and can afford to spend sometime in the MRI suite, as the average time foracquisition of accurate brain MRI is approxi-mately 30 min. However, it offers distinct advan-tages over CT in the detection of parenchymalabnormalities, with improved accuracy and morestructural detail such as gray–white matter differ-entiation or nondifferentiation as in axonopathiesand myelinolysis [19,20].

Electroencephalogram (EEG) testing isimportant in a comatose patient, especially todetect an entity known as nonconvulsive statusepilepticus [21], which is characterized by seizureactivity in the brain that is not clinically appar-ent in sedated and paralyzed patients and mayguide the physician to treat a patient with antie-pileptic medication. Certain EEG patterns, suchas temporal lobe seizure activity, can be an indi-cator in the diagnosis of herpes encephalitis.Serial EEGs may also prove to be of value forprognostication of the patient.




Box 3. Steps in the

1. Assure a stable airwa and circulation

2. Recognize and treat h

3. Consider specific anti

4. Monitor for, prevent a

5. Evaluate for and treat

6. Correct electrolyte an

7. Normalize body temp

Adapted from [3].

Electrocardiogram should be performed onall comatose patients to detect abnormalitiessuch as widened QRS, suggestive of tricyclicantidepressant exposure.

Management of comaAs discussed earlier, a coma state in a patient issuggestive of a primary injury to the brain,which, in the absence of prompt therapy, putsthe patient at risk for secondary injury, owing tovarious detrimental factors such as systemichypotension, hypoxia, respiratory failure andworsening cerebral edema and progressive herni-ation. Thus, secondary injury heralds a down-ward spiral for the patient and therefore has apoorer outcome. The management of comatakes into account mechanisms of cell injury,aims to preserve neurological function, preventsecondary injury and optimize regeneration andrecovery. The major components of manage-ment include normalization of circulation andrespiration, fluid management, maintenance ofoptimal CPP and treatment of seizures (Box 3).

Once the airway is secured and breathing isconfirmed to be effective, attention should nextbe focused upon management of intracranialhypertension and prevention of secondaryinjury. At this point, the patient should have atleast two large bore intravenous accesses, or anintraosseus approach if it is not possible toobtain intravenous access. The purpose of gen-erous intravenous or vascular access is to main-tain adequate cardiac output and tissueperfusion, more specifically, cerebral perfusion.Fluid resuscitation should be instituted to opti-mize end-organ perfusion, and if that alone doesnot achieve desired results, use of inotropicagents should be considered. The monitoring ofserum electrolytes and urine output serves as ahelpful guide in assessing circulatory status.

Fluid restriction has a role only if there is suspi-cion of syndrome of inappropriate secretion ofantidiuretic hormone.

Maintenance of a CPP at or above 50 mmHgis strongly correlated with survival after trau-matic brain injury [22]. Pediatric literature sug-gests that the goal of maintenance of CPP innontraumatic brain injury should be at or above40 mmHg in infants and toddlers, at or above50 mmHg for young children and at or above60–70 mmHg for older children and adoles-cents. Previous practice of maintaining patientsat risk for cerebral edema in a mild negative fluidbalance has shown to be of less benefit withrespect to outcome when compared with therapycomprising carefully titrated fluids and medica-tion to maintain optimum mean arterial pressureand CPP and, indirectly, the ICP [23]. The rela-tionship between these variables can be clearlydemonstrated by the following equation:

Reduction of intracranial hypertension formaintenance of optimum CPP forms the corner-stone of treatment of comatose patients at risk ofherniation from intracranial hypertension. Apatient suspected to be at risk for herniationshould have an emergent CT scan performed toevaluate for structural lesions that may beresponsible for increased ICP. If there is evidenceof swelling of the brain, monitoring of ICP isindicated. The goal is to maintain ICP below20 mmHg, and patients may benefit fromimmediate surgical decompression procedures.ICP monitoring is usually not initiated in theemergency department. Children in need of ICPmonitoring should be admitted to a pediatricintensive care unit. The first step in ensuringreduction of intracranial hypertension is secur-ing the airway by endotracheal intubation andmechanically hyperventilating the patient mildlyto maintain PaCO2 at 35 mmHg [24]. This inter-vention will result in just enough cerebral vaso-constriction to help relieve intracranialhypertension. Care should be taken to nothyperventilate excessively, as PaCO2 of25 mmHg is associated with severe cerebral vaso-constriction and may add insult to the injury bycausing severe cerebral vasoconstriction [25,26].There is also no role for ‘prophylactic’ hyper-ventilation for the same reason as mentionedabove. The risk of cerebral vasoconstriction canbe justified only in patients who have signs ofongoing herniation. Midline head positioning ofthe patient and head elevation by 30° helps

management of coma.

y, adequate oxygenation and ventilation,

ypoglycemia

dotes for medication overdose

nd treat increased intracranial pressure

seizures

d acid–base imbalance

erature

CPP Mean arterial pressure ICP–=



446

reduce hydrostatic pressures in the brain by facil-itating venous drainage and may contribute toreduction of ICP. As mentioned earlier, reduc-tion of intracranial hypertension can be achievedsurgically by removal of the offending structurallesion or placement of ventriculostomy drainage.

Medical therapy constitutes use of osmotic andloop diuretics. Mannitol is an osmotic diureticthat exerts its effect by causing a shift of fluid fromthe intracellular compartment of the brain intothe vascular compartment, thereby helping relieveintracranial hypertension. It can be used in dosesranging from 0.25 to 1 mg/kg, and requires fre-quent monitoring of the patient’s electrolytes andosmolality to watch for and prevent developmentof iatrogenic dehydration, which in turn mayreduce CPP. Recent literature suggests that use ofhypertonic saline (3% normal saline) may be ben-eficial in certain situations where elevated ICP isrefractory to conventional treatment. An addedbenefit is its inability to cause diuresis, therebydecreasing the risk of hypovolemia [27]. Diuretics,such as furosemide (acts on the loop of Henle)have been used in conjunction with mannitol tomaintain adequate CPP. Deep sedation, as well asparalysis, helps control intracranial hypertensionby preventing any ICP spikes secondary to patientmovements. Steroids for reduction of intracranialhypertension have been shown to be beneficial inspace-occupying lesions with localized edema, butdo not seem to have any benefit in the manage-ment of diffuse cerebral swelling. Barbituratecoma has been utilized to reduce ICP and cerebralmetabolism, but requires careful monitoring ofhemodynamic function in terms of cardiac outputand blood pressure.

Treatment of seizures forms an important com-ponent of therapy. Benzodiazepines are first-lineagents in controlling any initial seizure activityand are often successful in controlling acute sei-zures. Patients with status epilepticus (seizureactivity lasting for more than 30 min), can be ini-tially treated with benzodiazepines, which haverapid onset and short half-life, but need to be fol-lowed by longer-acting agents such as phenytoinand phenobarbitol. Phenytoin is nonsedating anddoes not affect subsequent neurological examina-tion. Phenobarbital, on the other hand, can causesedation and may affect subsequent neurologicalexamination. Phenobarbital offers a distinctadvantage in controlling diffuse seizure activity,such as toxic seizures, over phenytoin, which ismore effective in controlling focal seizures. If sei-zures persist after administration of these anti-epileptic agents, they are considered refractory

and warrant institution of repeated dosing of phe-nobarbital to achieve very high levels for completecessation of seizure activity. As mentioned earlier,the physician should bear in mind the possibilityof nonconvulsive seizure activity in patients whoare sedated and paralyzed, and must take care totreat them appropriately. An urgent EEG shouldbe requested in all such cases. Prophylactic treat-ment with anticonvulsants reduces the risk ofearly post-traumatic seizures, as well as improvingoutcomes among children with traumatic braininjury [28–31]. The general consensus amongexperts is to institute anticonvulsant therapy dur-ing the first week following severe traumatic braininjury [32].

Other management components includetreatment with broad-spectrum antibiotics inany patient suspected to have systemic or intra-cranial infection. Frequent electrolyte andacid–base monitoring is important to rule outany imbalances as a result of altered patient phys-iology and treatment measures. Frequent moni-toring of electrolytes and urine output also helpsclinicians to detect conditions such as syndromeof inappropriate antidiuretic hormone or diabe-tes insipidus. The wide fluctuations in fluidintake and losses that these conditions may causecan put the patient at severe risk for secondarybrain injury.

Studies on the use of controlled therapeutichypothermia in a select group of patients haveshown some promise, and need to be exploredfurther [33]. There is, however, no question thatany increase in the temperature must be aggres-sively treated to prevent increased cerebralmetabolism and demand [34].

Some other supportive components includeearly nutritional support by hyperalimentation,which have been shown to accelerate neuro-logical recovery [35]. Care should be taken to pre-vent development of deep-vein thrombosis andsecondary pulmonary embolism by using variousmodalities such as heparin and compressionstockings. Early involvement of physical therapyhas demonstrated significant improvements inneurological outcome.

Generally, specific management can be facili-tated once the presumptive diagnosis is con-firmed, with initiation of definitive therapy inthe emergency department. Any patient notresponding to therapeutic interventions orrequiring ongoing monitoring or critical care, orwhose diagnosis is still in question after theinitial management, needs to be transferred to apediatric intensive care unit.




Box 4. Glasgow Out

1. Death

2. Persistent vegetative

3. Severe disability: cons

4. Moderate disability: d

5. Good recovery

Adapted from [3].

Box 5. Pediatric Cer

1. Normal: normal at agregular school

2. Mild disability: conscilevel, school-age child’s neurological deficit

3. Moderate disability: cage-appropriate indepeneducation class. May ha

4. Severe disability: cons

5. Coma or vegetative sawake in appearance. Ccortical function

6. Brain death: apnea oron electroencephalogra

Adapted from [3].

Outcome of comaInstitution of prompt treatment helps to modifythe outcome favorably. The prognosis of coma islargely dependent on etiology, with good prog-nosis for uncomplicated drug intoxications andpoor prognosis for hypoxic ischemic encephalo-pathy. There are scales that measure the out-comes based on recovery and functionalindependence, as exemplified by Glasgow Out-come Scale (Box 4) [36], whereas other measures,such as the Pediatric Cerebral Performance Cate-gory Scale (Box 5), have more age-appropriatefunctional performance measures that help toquantify outcomes more accurately [37]. Thereare also a number of scales that gauge social andemotional responses as additional dimensions formeasurement of outcomes. Most survivingpatients should undergo serial neuropsychologi-cal testing to accurately measure various aspectsof neurological recovery.

Literature on recovery after cerebral eventsleading to altered mental states/coma suggeststhat the recovery of motor skills is better whencompared with recovery of cognitive skills. Thismay be related to the fact that children havedynamic neuronal networks and more suscepti-bility of the neuronal pathways that controlcognition as compared with motor skills [38,39].

There is also abundant literature on outcomeprediction by means of clinical, radiological andelectrophysiological measurements. Patients withan initial GCS of 3 have mortality rates between50 and 60% after traumatic brain injury, withsignificant outcome variation depending on thedegree and severity of secondary brain injury.Children with a GCS of 4–8 have a significantlyhigher likelihood of survival [40,41]. A studyinvolving children with nontraumatic braininjury suggested that younger children withlower GCS scores, absent brainstem reflexes,poor motor responses, or hypothermia orhypotension at presentation tend to have pooreroutcomes [42]. There have been large numbers ofstudies that now conclusively prove that themortality rate is extremely high for children whopresent to the emergency room in cardiac arrest,regardless of the precipitating event.

ConclusionComa in a pediatric patient is a medical emer-gency that requires rapid and organized inter-vention. Evaluation of a comatose child consistsof initial stabilization of basic life-supportneeds, airway, breathing and circulation, andsimultaneous conduction of effective historyand accurate physical examination. Regardlessof etiology, there are general principles for themanagement of coma, which the physician mustbe familiar with in order to achieve optimalresults and outcomes.

Financial & competing interests disclosure The authors have no relevant affiliations or financialinvolvement with any organization or entity with a finan-cial interest in or financial conflict with the subject matteror materials discussed in the manuscript. This includesemployment, consultancies, honoraria, stock ownership oroptions, expert testimony, grants or patents received orpending or royalties.

No writing assistance was utilized in the production ofthis manuscript.

come Scale.

state

cious but disabled

isabled but independent

ebral Performance Category Scale.

e-appropriate level, school-age child attends

ous, alert and able to interact at age-appropriate grades may not be appropriate for age, mild

onscious, sufficient cerebral function for dent activities. School-age child attending special

ve learning disability

cious. Dependent on others for daily activities

tate: any degree of coma, unawareness even if erebral unresponsiveness. No evidence of

areflexia or absence of brain activity m



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Executive summary

• Coma is suggestive of a primary insult to the brain, which, if left untreated, can rapidly progress to secondary injury, and thus result in substantial morbidity and even mortality.

• It is imperative to rapidly recognize this entity, institute rapid and appropriate treatment and improve outcome.

Approach to coma

• It is important to understand the basic pathophysiology of coma.• It is important to be aware of other clinical states and subjective terminologies that exist to define states of altered mental status.• The etiologies of coma are numerous and diverse, resulting in either a direct or indirect brain injury.• Early management includes initial evaluation and treatment, which includes initial stabilization, rapid assessment, use of reversal

agents to treat certain metabolic and toxic etiologies, and diagnostic studies, followed by detailed history and physical examination, inclusive of a detailed and specific neurological examination.

• The subsequent management goal is to prevent and treat increased intracranial pressure by judicious use of medications, as well as surgical intervention depending upon the specific etiology.

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