Coma is unresponsiveness from which the patient cannot be aroused and in which the patient's eyes remain closed. Impaired consciousness refers to similar, less severe disturbances of consciousness; these disturbances are not considered coma. The mechanism for coma or impaired consciousness involves dysfunction of both cerebral hemispheres or of the reticular activating system (also known as the ascending arousal system). Causes may be structural or nonstructural (eg, toxic or metabolic disturbances). Damage may be focal or diffuse. Diagnosis is clinical; identification of cause requires laboratory tests and neuroimaging. Treatment is immediate stabilization and specific management of the cause. For long-term coma, adjunctive treatment includes passive range-of-motion exercises, enteral feedings, and measures to prevent pressure ulcers.
Decreased or impaired consciousness or alertness refers to decreased responsiveness to external stimuli. Severe impairment includes
Coma: The patient cannot be aroused, and the eyes are closed and do not open in response to any stimulation.
Stupor: The patient can be awakened only by vigorous physical stimulation.
Less severely impaired levels of consciousness are often labeled as lethargy or, if more severe, obtundation. Lethargy usually involves fatigue and a lack of energy. Obtundation is a reduced level of alertness or consciousness. However, differentiation between less severely impaired levels is often imprecise; the label is less important than a precise clinical description (eg, “the best level of response is partial limb withdrawal to nail bed pressure”).
Delirium differs because cognitive disturbances (in attention, cognition, and level of consciousness) fluctuate more; also, delirium is usually reversible. Delirium is considered an acute loss of prior mental function. Patients with delirium may have periods of appropriate attention and cognition alternating with periods of impaired attention and cognition.
Pathophysiology
Maintaining alertness requires intact function of the cerebral hemispheres and preservation of arousal mechanisms in the reticular activating system (RAS—also known as the ascending arousal system)—an extensive network of nuclei and interconnecting fibers in the upper pons, midbrain, and posterior diencephalon. Therefore, the mechanism of impaired consciousness must involve both cerebral hemispheres or dysfunction of the RAS.
To impair consciousness, cerebral dysfunction must be bilateral; unilateral cerebral hemisphere disorders are not sufficient, although they may cause severe neurologic deficits. However, rarely, a unilateral massive hemispheric focal lesion (eg, left middle cerebral artery stroke) impairs consciousness if the contralateral hemisphere is already compromised or if it results in compression of the contralateral hemisphere (eg, by causing edema).
RAS dysfunction can result from a condition that has diffuse effects, such as toxic or metabolic disturbances (eg, hypoglycemia, hypoxia, uremia, drug overdose). RAS dysfunction can also be caused by focal ischemia (eg, certain upper brain stem infarcts), hemorrhage, or direct, mechanical disruption.
Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion pressure, resulting in secondary brain ischemia. Secondary brain ischemia may affect the RAS or both cerebral hemispheres, impairing consciousness.
When brain damage is extensive, brain herniation (see also figure Brain herniation and table Effects of Herniation) may occur; it contributes to neurologic deterioration because it does the following:
Directly compresses brain tissue
Blocks the blood supply to areas of the brain
Increases ICP
May lead to hydrocephalus by obstructing the cerebral ventricular system
Results in neuronal and vascular cell dysfunction
May shift brain structures from one side of the brain to the other side
In addition to the direct effects of increased ICP on neuronal and vascular cells, cellular pathways of apoptosis and autophagy (which are forms of programmed cell death or destruction) can become activated. Apoptosis has early and late phases that ultimately lead to the destruction of deoxyribonucleic acid (DNA) in cells. In autophagy, components of cell cytoplasm are recycled in an attempt to remove nonfunctional organelles and can sometimes lead to neuronal and vascular cell injury (1). Additional pathways that are tied to apoptosis and autophagy have been newly discovered; these pathways involve circadian clock genes that can oversee daily cellular function (2).
Impaired consciousness may progress to coma and ultimately to brain death.
Pathophysiology references
1. Maiese K, Chong ZZ, Shang YC, Wang S: Targeting disease through novel pathways of apoptosis and autophagy. Expert Opin Ther Targets 16 (12):1203–1214, 2012. doi: 10.1517/14728222.2012.719499 Epub 2012 Aug 27.
2. Maiese K: Cognitive impairment and dementia: Gaining insight through circadian clock gene pathways. Biomolecules 11 (7):1002, 2021. doi: 10.3390/biom11071002
Etiology
Coma or impaired consciousness may result from structural disorders, which typically cause focal damage, or nonstructural disorders, which most often cause diffuse damage (see table Common Causes of Coma or Impaired Consciousness).
Older age increases the risk of impaired consciousness (see Geriatrics Essentials: Coma and Impaired Consciousness)
Psychiatric disorders (eg, psychogenic unresponsiveness) can mimic impaired consciousness, are volitional, and can be distinguished from true impaired consciousness by neurologic examination.
Symptoms and Signs
Consciousness is decreased to varying degrees. Repeated stimuli arouse patients only briefly or not at all.
Depending on the cause, other symptoms develop (see table Findings by Location):
Eye abnormalities: Pupils may be dilated, pinpoint, or unequal. One or both pupils may be fixed in midposition. Eye movement may be dysconjugate or absent (oculomotor paresis) or involve unusual patterns (eg, ocular bobbing, ocular dipping, opsoclonus). Homonymous hemianopia may be present. Other abnormalities include absence of blinking in response to visual threat (almost touching the eye), as well as loss of the oculocephalic reflex (the eyes do not move in response to head rotation), the oculovestibular reflex (the eyes do not move in response to caloric stimulation), and corneal reflexes.
Autonomic dysfunction: Patients may have abnormal breathing patterns (Cheyne-Stokes or Biot respirations), sometimes with hypertension and bradycardia (Cushing reflex). Abrupt respiratory and cardiac arrest may occur. However, hypotension may occur if impaired consciousness is caused by severe infection, severe dehydration, major blood loss, or cardiac arrest.
Motor dysfunction: Abnormalities include flaccidity, hemiparesis, asterixis, multifocal myoclonus, decorticate posturing (elbow flexion and shoulder adduction with leg extension), and decerebrate posturing (limb extension and internal shoulder rotation).
Other symptoms: If the brain stem is compromised, nausea, vomiting, meningismus, occipital headache, ataxia, and increasing somnolence can occur.
Diagnosis
History
General physical examination
Neurologic examination, including eye examination
Laboratory tests (eg, pulse oximetry, bedside glucose measurement, blood and urine tests)
Immediate neuroimaging
Sometimes measurement of ICP
If diagnosis is unclear, lumbar puncture or electroencephalography (EEG)
Impaired consciousness is diagnosed if repeated stimuli arouse patients only briefly or not at all. If stimulation triggers primitive reflex movements (eg, decerebrate or decorticate posturing), impaired consciousness may be deepening into coma.
Diagnosis and initial stabilization (airway, breathing, and circulation) should occur simultaneously. Temperature is measured to check for hypothermia or hyperthermia; if either is present, treatment is started immediately. Glucose levels must be measured at bedside to identify low levels, which should also be corrected immediately. If trauma is involved, the neck is immobilized until clinical history, physical examination, or imaging tests exclude an unstable injury and damage to the cervical spine.
History
Medical identification bracelets or the contents of a wallet or purse (eg, hospital identification card, drugs) may provide clues to the cause. Relatives, paramedics, police officers, and any witnesses should be questioned about the circumstances and environment in which the patient was found; containers that may have held food, alcohol, drugs, or poisons should be examined and saved for identification (eg, drug identification aided by a poison center) and possible chemical analysis.
Relatives should be asked about the following:
The onset and time course of the problem (eg, whether seizure, headache, vomiting, head trauma, or drug ingestion was observed; how quickly symptoms appeared; whether the course has been progressive or waxing and waning)
Baseline mental status
Recent infections and possible exposure to infections
Recent travel
Ingestions of unusual meals
Psychiatric problems and symptoms
Prescription drug history
Use of alcohol and other recreational drugs (eg, anesthetics, stimulants, depressants)
Previous and concurrent systemic illnesses, including new-onset heart failure, arrhythmias, respiratory disorders, infections, and metabolic, liver, or kidney disorders
The last time the patient was normal
Any hunches they may have about what might be the cause (eg, possible occult overdose, possible occult head trauma due to recent intoxication)
Medical records should be reviewed if available.
General physical examination
Physical examination should be focused and efficient and should include thorough examination of the head and face, skin, and extremities. Examination of the heart and lungs is important to assess blood flow and oxygenation to the brain.
Signs of head trauma include periorbital ecchymosis (raccoon eyes), ecchymosis behind the ear (Battle sign), hemotympanum, instability of the maxilla, and cerebrospinal fluid (CSF) rhinorrhea and otorrhea. Scalp contusions and small bullet holes can be missed unless the head is carefully inspected.
If unstable injury and cervical spine damage have been excluded, passive neck flexion is done; stiffness suggests subarachnoid hemorrhage or meningitis.
Findings may suggest a cause:
Hypothermia: Environmental exposure, near-drowning, sedative overdose, severe hypothyroidism, Wernicke encephalopathy, or, in older people, sepsis
Hyperthermia: Heatstroke, infection, stimulant drug overdose, or neuroleptic malignant syndrome
Fever, petechial or purpuric rash, hypotension, or severe extremity infections (eg, gangrene of one or more toes): Sepsis or central nervous system (CNS) infection
A bitten tongue: Seizure
Breath odor: Alcohol, other drug intoxication, or diabetic ketoacidosis
Hypotension or pulse abnormalities: Cardiac dysfunction with hypoperfusion
Difficulty breathing: Acute respiratory dysfunction from bacterial or viral illness
Neurologic examination
The neurologic examination determines whether the brain stem is intact and where the lesion is located within the CNS. The examination focuses on the following:
Level of consciousness
Eyes
Motor function
Deep tendon reflexes
Level of consciousness is evaluated by attempting to wake patients first with verbal commands, then with nonnoxious stimuli, and finally with noxious stimuli (eg, pressure to the supraorbital ridge, nail bed, or sternum).
The Glasgow Coma Scale (see table Glasgow Coma Scale) was developed to assess patients with head trauma. For head trauma, the score assigned by the scale is valuable prognostically. For coma or impaired consciousness of any cause, the scale is used because it is a relatively reliable, objective measure of the severity of unresponsiveness and can be used serially for monitoring. The scale assigns points based on responses to stimuli.
Eye opening, facial grimacing, and purposeful withdrawal of limbs from a noxious stimulus indicate that consciousness is not greatly impaired. Asymmetric motor responses to pain or deep tendon reflexes may indicate a focal hemispheric lesion.
As impaired consciousness deepens into coma, noxious stimuli may trigger stereotypic reflex posturing.
Decorticate posturing can occur in structural or metabolic disorders and indicates hemispheric damage with preservation of motor centers in the upper portion of the brain stem (eg, rubrospinal tract).
Decerebrate posturing indicates that the upper brain stem motor centers, which facilitate flexion, have been structurally damaged and that only the lower brain stem centers (eg, vestibulospinal tract, reticulospinal tract), which facilitate extension, are responding to sensory stimuli.
Decerebrate posturing may also occur, although less often, in diffuse disorders such as anoxic encephalopathy.
Flaccidity without movement indicates that the lower brain stem is not affecting movement, regardless of whether the spinal cord is damaged. It is the worst possible motor response.
Asterixis and multifocal myoclonus suggest metabolic disorders such as uremia, hepatic encephalopathy, hypoxic encephalopathy, and drug toxicity.
Psychogenic unresponsiveness can be differentiated from physiologically impaired consciousness by finding that although voluntary motor response is typically absent, muscle tone and deep tendon reflexes remain normal, and all brain stem reflexes are preserved. Vital signs are usually not affected.
Eye examination
The following are evaluated:
Pupillary responses
Extraocular movements
Fundi
Other neuro-ophthalmic reflexes
Pupillary responses and extraocular movements provide information about brain stem function (see table Interpretation of Pupillary Response and Eye Movement). One or both pupils usually become fixed early in coma due to structural lesions, but pupillary responses are often preserved until very late when coma is due to diffuse metabolic disorders (called toxic-metabolic encephalopathy), although responses may be sluggish. If one pupil is dilated, other causes of anisocoria
The fundi should be examined. Papilledema may indicate increased ICP but may take many hours to appear; papilledema is usually bilateral. Increased ICP can cause earlier changes in the fundi, such as loss of retinal venous pulsations, disk hypermia, dilated capillaries, blurring of the medial disk margins, and sometimes hemorrhages. Subhyaloid hemorrhage may indicate subarachnoid hemorrhage.
The oculocephalic reflex is tested by the doll’s-eye maneuver in unresponsive patients: The eyes are observed while the head is passively rotated from side to side or flexed and extended. This maneuver should not be attempted if cervical spine instability is suspected.
If the reflex is present, the maneuver causes the eyes to move in the opposite direction of head rotation, flexion, or extension, indicating that the oculovestibular pathways in the brain stem are intact. Thus, in a supine patient, the eyes continue to look straight up when the head is turned side to side.
If the reflex is absent, the eyes do not move and thus point in whatever direction the head is turned, indicating the oculovestibular pathways are disrupted. The reflex is also absent in most patients with psychogenic unresponsiveness because visual fixation is conscious.
If the patient is unconscious and the oculocephalic reflex is absent or the neck is immobilized, oculovestibular (cold caloric) testing is done. After integrity of the tympanic membrane is confirmed, the patient’s head is elevated 30°, and with a syringe connected to a flexible catheter, the examiner irrigates the external auditory canal with 50 mL of ice water over a 30-second period.
If both eyes deviate toward the irrigated ear, the brain stem reflex is functioning normally, suggesting mildly impaired consciousness.
If nystagmus away from the irrigated ear also occurs, the patient is conscious and psychogenic unresponsiveness is likely. In conscious patients, 1 mL of ice water is often enough to induce ocular deviation and nystagmus. Thus, if psychogenic unresponsiveness is suspected, a small amount of water should be used (or caloric testing should not be done) because cold caloric testing can induce severe vertigo, nausea, and vomiting in conscious patients.
If the eyes do not move or movement is dysconjugate after irrigation, the integrity of the brain stem is uncertain and the coma is deeper. Prognosis may be less favorable.
Pearls & Pitfalls
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Certain patterns of eye abnormalities and other findings may suggest brain herniation (see also figure Brain herniation and table Effects of Herniation).
Respiratory patterns
The spontaneous respiratory rate and pattern should be documented unless emergency airway intervention is required. It may suggest a cause.
Periodic cycling of breathing (Cheyne-Stokes or Biot respiration) may indicate dysfunction of both hemispheres or of the diencephalon.
Hyperventilation (central neurogenic hyperventilation) with respiratory rates of > 25 breaths/minute may indicate midbrain or upper pontine dysfunction.
An inspiratory gasp with respiratory pauses of about 3 seconds after full inspiration (apneustic breathing) typically indicates pontine or medullary lesions; this type of breathing often progresses to respiratory arrest.
Testing
Initially, pulse oximetry, fingerstick plasma glucose measurements, and cardiac monitoring are done.
Arterial blood gases (ABGs) are measured, and if carbon monoxide toxicity is suspected, carboxyhemoglobin level is measured.
ECG (12-lead) is also done to check for myocardial infarction and new arrhythmias.
Chest x-ray should be done to check for new lung disease that may affect brain oxygenation.
If the cause is not immediately apparent, noncontrast head CT should be done as soon as possible to check for masses, hemorrhage, edema, evidence of bone trauma, and hydrocephalus. Initially, noncontrast CT rather than contrast CT is preferred to rule out brain hemorrhage; CT detects cerebral bleeding and bone injuries (eg, skull fractures) best within 72 hours of injury. MRI can be done instead if immediately available, but it is not as quick as newer-generation CT scanners and may not be as sensitive for traumatic bone injuries ; however, MRI is now as sensitive as CT for detecting blood early as well as late. If noncontrast CT is not diagnostic, MRI or contrast CT can then be done; either of them may detect isodense subdural hematomas, multiple metastases, sagittal sinus thrombosis, herpes encephalitis, or other causes missed by noncontrast CT. MRI provides greater detail than CT when done > 72 hours after symptom onset but is more difficult logistically than CT if the patient is intubated.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
© 2017 Elliot K. Fishman, MD.
If coma is unexplained after MRI or CT and other tests, lumbar puncture (spinal tap) is done to check opening pressure and to exclude infection, subarachnoid hemorrhage, and other abnormalities. However, MRI or CT images should first be reviewed for intracranial masses, obstructive hydrocephalus, and other abnormalities that could obstruct CSF flow or the ventricular system and thus significantly increase ICP. Such abnormalities contraindicate lumbar puncture. Suddenly lowering CSF pressure, as can occur during lumbar puncture, in patients with increased ICP could trigger brain herniation; however, this outcome is uncommon.
CSF analysis includes cell and differential counts, protein, glucose, Gram staining, cultures, and sometimes, based on clinical suspicion, specific tests (eg, cryptococcal antigen test, cytology, measurement of tumor markers, Venereal Disease Research Laboratory [VDRL] tests, polymerase chain reaction [PCR] for herpes simplex, visual or spectrophotometric analysis for xanthochromia).
If increased ICP is suspected, CSF pressure is measured. If ICP is increased, ICP monitoring is done continuously, and measures to decrease it are taken.
If seizures may be the cause of coma, particularly if nonconvulsive status epilepticus (recurrent seizures without prominent motor symptoms) is being considered, or if the diagnosis remains uncertain, EEG may be done. In most comatose patients, EEG shows slowing and reductions in wave amplitude that are nonspecific but often occur in toxic-metabolic encephalopathy. In some patients with nonconvulsive status epilepticus, the EEG shows spikes, sharp waves, or spike and slow complexes. If psychogenic unresponsiveness or seizure activity (pseudoseizure) that results from a behavior disorder is possible, video EEG monitoring is required.
Depending on the destination, recent travel should prompt testing for bacterial, viral, and parasitic infections that may lead to coma.
Clinicians can consider evoked potentials such as brain stem auditory evoked potentials to assess brain stem function or somatosensory evoked potentials to assess the cortex, thalamic, brain stem, and spinal cord pathways (eg after cardiac arrest).
Prognosis
Prognosis for patients with impaired consciousness depends on the cause, duration, and depth of the impairment of consciousness. For example, absent brain stem reflexes indicates a poor prognosis after cardiac arrest, but not always after a sedative overdose. In general, if unresponsiveness lasts < 6 hours, prognosis is more favorable.
After coma, the following prognostic signs are considered favorable:
Early return of speech (even if incomprehensible)
Spontaneous eye movements that can track objects
Normal resting muscle tone
Ability to follow commands
If the cause is a reversible condition (eg, sedative overdose, some metabolic disorders such as uremia), patients may lose all brain stem reflexes and all motor response and yet recover fully. After trauma, a Glasgow Coma Scale score of 3 to 5 may indicate fatal brain damage, especially if pupils are fixed or oculovestibular reflexes are absent.
After cardiac arrest, clinicians must exclude major confounders of coma, including sedatives, neuromuscular blockade, hypothermia, metabolic derangements, and severe liver or kidney failure. If brain stem reflexes are absent at day 1 or lost later, testing for brain death is indicated. Prognosis is poor if patients have any of the following:
Myoclonic status epilepticus (bilaterally synchronous twitching of axial structures, often with eye opening and upward deviation of the eyes) that occurs within 24 to 48 hours after cardiac arrest
No pupillary light reflexes 24 to 72 hours after cardiac arrest
No corneal reflexes 72 hours after cardiac arrest
Extensor posturing or no response elicited by painful stimuli 72 hours after cardiac arrest
No response 20 milliseconds (N20) after stimulation of somatosensory evoked potential (SEP)
Serum neuron-specific enolase level of > 33 mcg/L
Preexisting disorders such as coronary artery disease, hypertension, and diabetes mellitus
If patients who are unresponsive after cardiac arrest have been treated with hypothermia (often for about 24 hours after arrest), 72 hours should be added to the above times because hypothermia slows recovery of brain metabolism. If any of the above criteria is met, outcome is usually (but not always) poor; thus, whether to withdraw life support may be a difficult decision.
Patients may also have other neurologic and nonneurologic complications, depending on the cause and duration of impaired consciousness. For example, a drug or disorder causing metabolic coma may also cause hypotension, arrhythmias, myocardial infarction, or pulmonary edema. Prolonged hospitalization in an ICU may also result in polyneuropathy, myopathy, and other complications (eg, pulmonary embolism, pressure ulcers, urinary tract infection).
Treatment
Immediate stabilization (airway, breathing, circulation, or ABCs)
Admission to an intensive care unit (ICU)
Supportive measures, including, when necessary, control of ICP
Treatment of underlying disorder
Airway, breathing, and circulation must be ensured immediately. Hypotension must be corrected. Patients with impaired consciousness are admitted to the ICU so that respiratory and neurologic status can be monitored. If hypertension is present, blood pressure should be reduced carefully; lowering blood pressure below the patient's usual level can lead to brain ischemia.
Because some patients in coma are undernourished and susceptible to Wernicke encephalopathy
If a recent (within about 1 hour) overdose of certain drugs is possible, gastric lavage (with airway protection) can be done through a large-bore orogastric tube (eg, ≥ 32 Fr) after endotracheal intubation.
Coexisting disorders and abnormalities are treated as indicated. For example, metabolic abnormalities are corrected. Core body temperature may need to be corrected (eg, cooling for severe hyperthermia, warming for hypothermia).
Endotracheal intubation
Patients with any of the following require endotracheal intubation to prevent aspiration and ensure adequate ventilation:
Infrequent, shallow, or stertorous respirations
Low oxygen saturation (determined by pulse oximetry or ABG measurements)
Impaired airway reflexes
Severe unresponsiveness (including most patients with a Glasgow Coma Scale score ≤ 8)
If increased ICP is suspected, intubation should be done via rapid-sequence oral intubation (using a paralytic drug) rather than via nasotracheal intubation; nasotracheal intubation in a patient who is breathing spontaneously causes more coughing and gagging, thus increasing ICP, which is already increased because of intracranial abnormalities.
Pulse oximetry and ABGs (if possible, end-tidal CO2) should be used to assess adequacy of oxygenation and ventilation.
Intracranial pressure control
If intracranial pressure (ICP) is increased, clinicians should monitor intracranial and cerebral perfusion pressure, and pressures should be controlled. The goal is to maintain ICP at ≤ 20 mm Hg and cerebral perfusion pressure at 50 to 70 mm Hg. ICP is usually lower in children than in adults. In neonates, ICP can be below the atmospheric pressure. Thus, children are evaluated independently from adult guidelines.
Control of increased ICP involves several strategies:
Sedation:
Hyperventilation: Hyperventilation causes hypocapnia, which causes vasoconstriction, thus decreasing cerebral blood flow globally. Reduction in PCO2 from 40 mm Hg to 30 mm Hg can reduce ICP about 30%. Hyperventilation that reduces PCO2 to 28 to 33 mm Hg decreases ICP for only about 30 minutes and is used by some clinicians as a temporary measure until other treatments take effect. Aggressive hyperventilation to < 25 mm Hg should be avoided because it may reduce cerebral blood flow excessively and result in cerebral ischemia. Other measures to control increased ICP may be used.
Hydration:
Diuretics:
Blood pressure (BP) control: Systemic antihypertensives are needed only when hypertension is severe (>
Corticosteroids:
Removal of cerebrospinal fluid (CSF): CSF can be slowly removed through a shunt inserted into the ventricles to help lower increased ICP. CSF is removed at a rate of 1 to 2 mL/minute for 2 to 3 minutes. Continuous drainage of CSF (eg, through a lumbar drain) should be avoided because it may lead to brain herniation.
Position: Positioning the patient to maximize venous outflow from the head can help minimize increases in ICP. The head of the bed can be elevated to 30° (with the head above the heart) as long as cerebral perfusion pressure remains at the desired range. The patient’s head should be kept in a midline position, and neck rotation and flexion should be minimized. Tracheal suctioning, which can increase ICP, should be limited.
If ICP continues to increase despite other measures to control it, the following may be used:
Titrated hypothermia: When ICP is increased after head trauma or cardiac arrest, hypothermia in the range of 32 to 35° C has been used to reduce ICP to < 20 mm Hg. However, use of hypothermia to lower ICP is controversial; some evidence suggests that this treatment may not effectively lower ICP in adults or children and may have adverse effects (1).
Decompressive craniotomy: Craniotomy with duraplasty can be done to provide room for brain swelling. This procedure can prevent deaths, but overall functional outcome may not improve much, and it may lead to complications such as hydrocephalus in some patients (2). It may be most useful for large cerebral infarcts with impending herniation, particularly in patients < 50 years.
Long-term care
Patients require meticulous long-term care. Stimulants, sedatives, and opioids should be avoided.
Enteral feeding is started with precautions to prevent aspiration (eg, elevation of the head of the bed); a percutaneous endoscopic jejunostomy tube is placed if necessary.
Early, vigilant attention to skin care, including checking for breakdown especially at pressure points, is required to prevent pressure ulcers. Patients require frequent turning and position changes to prevent pressure ulcers, but the head should be kept elevated. Special air mattresses may help manage pressure ulcers.
Topical ointments to prevent desiccation of the eyes are beneficial.
Passive range-of-motion exercises done by physical therapists and taping or dynamic flexion splitting of the extremities may prevent contractures. Initiating physical therapy early can improve functional outcome in patients with polyneuropathy and myopathy.
Measures are also taken to prevent urinary tract infections and deep venous thrombosis.
Treatment references
1. Moler FW, Silverstein FS, Holubkov R, et al: Therapeutic hypothermia after in-hospital cardiac arrest in children. N Engl J Med 376 (4):318-329, 2017. doi: 10.1056/NEJMoa1610493
2. Su TM, Lan CM, Lee TH, et al: Risk factors for the development of posttraumatic hydrocephalus after unilateral decompressive craniectomy in patients with traumatic brain injury. J Clin Neurosci 63:62–67, 2019. doi: 10.1016/j.jocn.2019.02.006 Epub 2019 Mar 1.
Geriatrics Essentials: Coma and Impaired Consciousness
Older patients may be more susceptible to coma, altered consciousness, and delirium because of many factors, including the following:
Less cognitive reserve due to age-related brain effects and/or preexisting brain disorders
Higher risk of drug interactions affecting the brain due to polypharmacy
Higher risk of drug accumulation and drug effects on the brain due to age-related decreased function of organs responsible for drug metabolism and elimination
Higher risk of incorrect drug dosing due to polypharmacy with complex dosing regimens
Presence of comorbid disorders (eg, diabetes mellitus, hypertension, renal disease)
Higher risk of subdural hematoma due to traumatic rupture of veins crossing the growing subdural space between the dura and surface of the aging atrophic brain
Relatively minor problems, such as dehydration and urinary tract infections, can alter consciousness in older people.
In older patients, mental status and communications skills may be compromised, making lethargy and obtundation harder to recognize.
Age-related decreases in cognitive reserve and neuroplasticity can impair recovery from brain injury.
Key Points
Coma and impaired consciousness require dysfunction of both cerebral hemispheres or dysfunction of the reticular activating system.
Manifestations include abnormalities of the eyes (eg, abnormal conjugate gaze, pupillary responses, and/or oculocephalic or oculovestibular reflexes), vital signs (eg, abnormal respirations), and motor function (eg, flaccidity, hemiparesis, asterixis, multifocal myoclonus, decorticate or decerebrate posturing).
Taking a complete history of prior events is critical; ask witnesses and relatives about the time course for the change in mental status and about possible causes (eg, recent travel, ingestion of unusual meals, exposure to possible infections, drug or alcohol use, possible trauma).
Do a general physical examination, including thorough examination of the head and face, skin, and extremities and a complete neurologic examination (focusing on level of consciousness, the eyes, motor function, and deep tendon reflexes), followed by appropriate blood and urine tests, toxicology screening, and fingerstick plasma glucose measurements.
As soon as the patient has been stabilized, do noncontrast CT or, if immediately available, MRI to check for masses, hemorrhage, edema, hydrocephalus, or evidence of bone trauma (particularly on a CT scan); overall, MRI provides greater detail for diagnostic purposes when it is done 72 hours or more after symptom onset.
Ensure adequate airway, breathing, and circulation.
Control ICP using various strategies, which may include sedatives (as needed) to control agitation, temporary hyperventilation, fluids and diuretics to maintain euvolemia, and antihypertensives to control BP.
Treat the cause.
