Coma and depressed sensorium


  • Coma is a state of unconsciousness with lack of awareness and loss of wakefulness.

  • A Glasgow Coma Scale score of less than 15 in children should be taken seriously.

  • Arousal may be depressed by either direct brainstem injury involving the reticular formation or bilateral cerebral hemispheric dysfunction.

  • The ABCs (airway, breathing, and circulation) should be prioritized during management of a comatose child. When in doubt, it is better to protect the airway in order to prevent hypoxemia and hypercarbia.

  • Early measurement of blood glucose is important during initial stabilization of a comatose child.

  • Abnormal pupillary reflexes and/or altered respirations may be signs of impending herniation.

  • The goal of therapy should be the prevention of secondary brain injury.

  • A combination of physical signs, electroencephalography, somatosensory evoked potentials, and magnetic resonance imaging can be helpful in predicting outcomes.

Coma refers to injury and impaired function of the brain due to structural central nervous system (CNS) and/or metabolic or systemic etiologies. Coma may result from traumatic or nontraumatic brain injury; it is a life-threatening medical emergency prompting immediate methodical evaluation and treatment. If not recognized and evaluated, secondary injury with resultant morbidity and mortality may occur. Conversely, rapid treatment may improve prognosis.


Consciousness is a spontaneous state of awareness of self and environment and wakefulness. Coma is a pathologic state of unconsciousness, with lack of awareness of self and environment and loss of wakefulness. Unlike states of transient unconsciousness, such as syncope and concussion, coma is a sustained state that requires the duration of unconsciousness to be at least 1 hour. Comatose patients present with their eyes closed; coma is distinct from normal sleep due to its deep unarousable state. ,

Coma may result in a spectrum of outcomes ranging from recovery to brain death. In between recovery and brain death are other disorders, including locked-in state, minimally conscious state, and the persistent vegetative state ( Table 62.1 ). As noted in these other states of disordered consciousness, awareness requires wakefulness, but wakefulness (with intact sleep-wake cycles) does not require awareness.

TABLE 62.1

Disorders of Consciousness and Other Conditions

Modified from Ashwal S. Medical aspects of the minimally conscious state in children. Brain Dev. 2003;25(8):535–545.

Condition Awareness Wakefulness Physical Exam Outcome
Brain death Absent Absent

  • No reflexes or only spinal reflexes

  • Absent respiratory function

No recovery
Coma Absent Absent

  • No purposeful movement

  • Variably depressed respiratory effort

Death, persistent vegetative state, or recovery by 4 wk
Persistent vegetative state Absent Intact

  • No purposeful movement

  • Normal respiratory effort

Dependent on etiology
Minimally conscious state Very limited Intact

  • Severe limitation of movement

  • Variably depressed respiratory effort

Recovery unknown
Locked-in syndrome Present Intact

  • Quadriplegia, pseudobulbar palsy; eye movements preserved

  • Normal to variably depressed respiratory effort

Recovery unlikely

Aside from these altered states of consciousness, other terms are used to describe alterations in mental status that reference states of heightened or reduced alertness. States of heightened alertness include delirium (see Chapter 134 ), delusions, and hallucinations; states of reduced alertness include lethargy, obtundation, and stupor. Lethargy refers to drowsiness or decreased wakefulness but with a preserved ability to communicate when appropriately stimulated. Obtundation refers to a deeper state of unresponsiveness, with loss of ability to respond to vigorous stimuli. Stupor refers to decreased responsiveness with arousability only to noxious stimuli. The subjective, examiner-dependent nature of these states and lack of uniformity in their definitions in the literature are problematic, rendering these terms less useful as specific descriptors of altered consciousness. , Rather, the use of validated coma scales to gauge level of consciousness (LOC) allows for improved objectivity and uniformity in describing states of altered consciousness. Ideally, these scales would have interrater reliability, ease of administration, applicability to both a wide range of ages and a variety of clinical scenarios resulting in altered consciousness, and an ability to differentiate levels of coma requiring intervention.

Among the available instruments, the Glasgow Coma Scale (GCS) score is the most commonly used and widely accepted ( Table 62.2 ). The GCS focuses on assessment of cortical function in three areas (motor response, verbal performance, and eye opening) and has been modified for use in children and infants. , , Total scores range from 3 to 15, with categorization of scores from 3 to 8, 9 to 12, and 13 to 15, reflecting severe, moderate, and mild injury, respectively.

TABLE 62.2

Glasgow Coma Scale Scoring With Modification for Infants and Children

Data from Kirkham FJ, Newton CR, Whitehouse W. Paediatric coma scales. Developmental Medicine & Child Neurology 2008;50:267–274; Wong CP, Tay EL. Childhood brain injury: a review. Neurol Asia. 2015;20:105–115.

Activity Infant Child Adult Score
Motor response

  • Moves spontaneously, purposely

  • Withdraws to touch

  • Withdraws to pain

  • Decorticate posturing to pain

  • Decerebrate posturing

  • None

  • Obeys commands, spontaneous movements

  • Localizes pain

  • Withdraws to pain

  • Flexion in response to pain

  • Extension in response to pain

  • None

  • Follows commands

  • Localizes pain

  • Withdraws to pain

  • Flexion in response to pain

  • Extension in response to pain

  • None

Verbal response

  • Coos and babbles

  • Irritable, cries

  • Cries in response to pain

  • Moans in response to pain

  • None

  • Age-appropriate, oriented, smiles

  • Confused, aware of environment

  • Irritable, inconsistently consolable

  • Inconsolable, unaware of environment, agitated

  • None

  • Oriented

  • Confused

  • Inappropriate words

  • Nonspecific sounds

  • None

Eye opening

  • Spontaneous

  • To sound

  • To pain

  • None

  • Spontaneous

  • To sound

  • To pain

  • None

  • Spontaneous

  • To sound

  • To pain

  • None



Estimating the incidence of pediatric coma is complicated by the fact that studies use different criteria for severity of brain injury. Typically, studies of traumatic brain injury (TBI) include patients with GCS scores less than 12, whereas studies of nontraumatic brain injury include patients with GCS scores less than 8. With these criteria in mind, the incidence of pediatric TBI (see Chapter 118 ) ranges from 765 per 100,000 children aged 0 to 15 years to 1188 per 100,000 children aged 0 to 4 years, but traumatic and nontraumatic coma appear to have approximately equal incidences of 30 per 100,000 children. , Notably, the incidence of nontraumatic pediatric coma is highest among infants, with 160 per 100,000 children age 0 to 1 years affected.


As a medical emergency, coma presents a challenge to intensivists because optimal care requires timely intervention. However, information is frequently limited during the initial evaluation. Assessment of LOC and knowledge of CNS anatomy and physiology may provide helpful clues in attempting to interpret patient history and physical findings and optimize care. A careful general physical examination with a focused neurologic examination can suggest the diagnosis, aid in the location of lesions, guide therapeutic intervention, and determine prognosis. Further adjunctive radiologic and laboratory evaluation may then confirm physical findings. A timely, methodical approach to the management of the comatose child may affect prognosis and long-term outcomes. Therefore, this chapter considers CNS anatomy, the pathophysiology of coma, historical and physical findings that aid in the localization of lesions and the etiology of coma, the emergent management and initial evaluation of patients with altered levels of consciousness, and the prognosis and outcomes of patients who present with coma.


Arousal is mediated by the ascending reticular activating system (ARAS). The ARAS is principally located in the brainstem in the paramedian tegmental gray matter immediately ventral to the pons ( Fig. 62.1 ). The ARAS is composed of two distinct anatomic pathways. The first pathway consists of cholinergic neurons originating in the pedunculopontine tegmental and laterodorsal tegmental nuclei of the mesopontine tegmentum. These cholinergic neurons send excitatory signals through the thalamus to the cortex. The second pathway consists of noradrenergic and serotonergic neurons originating in the upper brainstem and caudal hypothalamus. This second pathway bypasses the thalamus and activates neurons in the lateral hypothalamic area, basal forebrain, and cerebral cortex. This second pathway includes the locus coeruleus, the periaqueductal gray matter, and the raphe nuclei.

• Fig. 62.1

Ascending reticular activating system (ARAS). The ARAS is principally located in the brainstem and is composed of two distinct anatomic pathways. These pathways mediate arousal through projections to the thalamus and cortex.

Because the ARAS receives collaterals from and is stimulated by every major somatic and sensory pathway directly or indirectly, it is best regarded as a physiologic rather than an anatomic entity. This partly explains why patients with very large discrete lesions (e.g., brain tumors) may be entirely alert, whereas patients with anatomically undetectable but biochemically widespread lesions (e.g., hepatic encephalopathy) may be deeply comatose. Primarily, two types of lesions depress the level of arousal: direct brainstem–diencephalic injury involving the reticular formation and nuclei or bilateral cerebral hemisphere dysfunction. Consequently, conscious behavior depends on the interplay between the cerebral cortex and the ARAS because these neural components are required for arousal and to maintain awareness. ,


Coma is a nonspecific consequence of various CNS insults. Coma may present as part of the progression of a known illness, as an unpredictable consequence of a known systemic disease, or as a result of a totally unexpected event or illness. As discussed earlier, unilateral cortical lesions do not typically cause coma because the ARAS is widely distributed in the cortical region. However, a small brainstem lesion can cause immediate coma because of the close proximity to the ARAS. Lesions in the brainstem may be due to demyelinating diseases, vascular disease, neoplasm, or head trauma. Common etiologies of coma in the pediatric population include metabolic, toxic, structural, and intrinsic causes ( Box 62.1 ).

• BOX 62.1

Etiologies of Impaired Consciousness and Coma



  • Shock

  • Cardiac or pulmonary failure

  • Near drowning

  • Carbon monoxide poisoning

  • Strangulation

Metabolic disorders

  • Hypoglycemia

  • Acidosis

  • Diabetic ketoacidosis

  • Organic and aminoacidemias

  • Hyperammonemia

  • Hepatic encephalopathy

  • Reye syndrome

  • Urea cycle disorder

  • Disorders of fatty acid metabolism

  • Valproic acid encephalopathy

  • Uremia

Fluid and electrolyte imbalance

  • Dehydration

  • Hyponatremia

  • Calcium and magnesium imbalance

Endocrine disorders

  • Thyroid dysfunction

  • Adrenal insufficiency

  • Hypoparathyroidism

Hypertensive encephalopathy

Vitamin deficiency

  • Thiamine

  • Pyridoxine

  • Niacin

Mitochondrial disorders

Exogenous toxins and poisons

  • Narcotics, neuroleptics, antidepressants, antiepileptic drugs, stimulants

  • Over-the-counter drugs, acetaminophen, mushrooms

  • Industrial toxins (e.g., heavy metals, organic phosphate, cyanide, volatile hydrocarbons)

  • Substance abuse (e.g., alcohol, cocaine, heroin, amphetamine)

Poisoning, including in cases of munchausen by proxy


  • Bacterial

  • Viral

  • Rickettsial

Paroxysmal disorders

  • Epilepsy

  • Migraine



  • Concussion

  • Cerebral contusion

  • Epidural hematoma

  • Subdural hematoma/effusion

  • Intracerebral hematoma

  • Diffuse axonal injury


Vascular disease

  • Cerebral infarction

  • Thrombosis, embolism

  • Cerebral hemorrhage

  • Arteriovenous malformation

  • Aneurysm

  • Vasculitis

  • Trauma to carotid or vertebral artery in the neck

Focal infection

  • Cerebritis

  • Abscess


The differential diagnosis is age related ( Table 62.3 ). Hypoxemia and ischemia/reperfusion injury are important causes of coma in all ages of pediatric patients. These entities are thoroughly discussed in Chapter 62.

TABLE 62.3

Common Considerations of Altered Mental Status at Various Ages

Infant Child Adolescent
Infection Ingestion Ingestion
Inborn error of metabolism Infection Trauma
Metabolic Trauma, including inflicted Infection
Trauma, including inflicted Metabolic Psychological
Congenital abnormality Seizure Seizure
Hypoxic ischemic injury Hypoxic ischemic injury Hypoxic ischemic injury

Initial treatment of the comatose child

The approach to the comatose child necessitates immediate, ongoing resuscitation while simultaneously undertaking elements of the physical examination, seeking historical details, and initiating diagnostic evaluation.

Prehospital care

Survival and outcome depend on delivery of high-quality care as soon as possible after injury. Recommendations for prehospital trauma life support follow. ,

  • 1.

    Airway: Endotracheal intubation if GCS is 8 or less

  • 2.

    Breathing: Maintaining adequate oxygenation and normal ventilation

  • 3.

    Circulation: Control of external hemorrhage and intravenous fluid resuscitation to maintain systolic blood pressure appropriate for age

  • 4.

    Assessment of blood glucose levels

  • 5.

    Cervical spine precautions

  • 6.

    Recognition and treatment of increased intracranial pressure (ICP; see Chapter 63 )

  • 7.

    Treatment of seizures (see Chapter 64 )

  • 8.

    Safe transportation to a pediatric hospital with a high-level trauma center and neuroimaging and neurosurgical capacity if due to TBI

Initial stabilization

Upon arrival to the hospital setting, continued attention to airway, breathing, and circulation are paramount in the initial management and stabilization of the comatose child to ensure adequate oxygenation, ventilation, and tissue perfusion. Cervical spine injury and increased ICP should be suspected in comatose patients with TBI. Compared with other organs, metabolic activity in the brain is relatively high. The brain has little capacity to store glucose and accordingly depends on constant delivery of energy substrate and oxygen to maintain normal metabolic function. Early management of blood glucose and appropriate treatment of hypoglycemia is crucial to treatment and prevention of secondary injury. Comatose patients often are hypercapnic and hypoxemic. Thus, supplemental oxygen should be provided to the patient with hypoxia during the initial evaluation.


Upper airway obstruction as a result of decreased muscle tone of the pharyngeal soft tissue is a common problem in unresponsive patients, necessitating endotracheal intubation for airway protection. It also is common practice to endotracheally intubate patients with hemodynamic instability or neurologic instability. In most circumstances, it is safer to endotracheally intubate electively rather than emergently to protect an already compromised brain from further injury as a result of respiratory failure. Endotracheal intubation (if not already done prior to hospital arrival) should be performed if the GCS is 8 or less.

Hyperextension of the neck must be avoided during intubation. Rapid sequence intubation should be performed with careful selection of medications in order to avoid agents that may worsen intracranial hypertension and caution with the dosage of medication (e.g., benzodiazepines and barbiturates) to prevent compromise of mean arterial pressure and cerebral perfusion pressure. During endotracheal intubation, special precautions should be taken to protect cerebral circulation and prevent further increases in ICP. Pretreatment with lidocaine and thiopental may help to diminish elevation in ICP associated with airway manipulation and suctioning.

After intubation, careful attention to endotracheal tube position and suctioning of oropharyngeal secretions is warranted. Once the patient’s airway is secured, adequacy of oxygenation and ventilation must be maintained by choosing appropriate ventilator settings and evaluating respiratory effort, continuous pulse oximetry, and end-tidal carbon dioxide monitoring.


Hyperventilation may facilitate reduction in ICP or hypercarbia due to hypoventilation from altered mental status (e.g., in the setting of intoxication). However, it is also important to maintain Pa co 2 between 35 and 40 mm Hg in order to avoid rapid fluctuations in cerebral blood flow from cerebral vasoconstriction (seen with excessive hyperventilation) and exacerbation of secondary injury. An exception is in cases of brain herniation, where hyperventilation is often the most expeditious intervention. As noted in the patient’s initial stabilization, continued prevention of hypoxia is essential to maintaining normal metabolic function and prevention of secondary brain injury.


Rapid assessment of circulation and tissue perfusion—including evaluation of central and peripheral pulses, capillary refill, and blood pressure—is important. Hypotension must be corrected to reestablish adequate cerebral blood flow to ensure oxygen and substrate delivery. Once hypotension is corrected, some evidence indicates that blood pressure should be maintained higher than the 75th percentile for age to maintain adequate cerebral perfusion pressure pending placement of ICP monitoring equipment.

Vascular access may prove challenging—timely placement of intraosseous access must be considered. Aggressive fluid resuscitation with isotonic fluids to restore normal circulatory status may be necessary. Hypotonic fluids are not indicated and may exacerbate cerebral edema. Management of blood pressure depends on suspected etiology of the comatose state. On the one hand, maintenance of mean arterial pressure is necessary to ensure adequacy of cerebral perfusion pressure if increased ICP is suspected. On the other hand, in cases of hypertensive encephalopathy or intracranial hemorrhage, judicious correction and/or prevention of hypertension may be warranted.


Given the need to evaluate and treat the comatose child emergently, an abbreviated but targeted interview of the child’s parents or caregivers can provide insight into the etiology of the coma. Important elements to elicit from the history, which may elucidate the cause of the coma, include the following.

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 .

Jun 26, 2021 | Posted by in CRITICAL CARE | Comments Off on Coma and depressed sensorium
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