Overview of Coma and Impaired Consciousness

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:

Medical records should be reviewed if available.

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:

The neurologic examination Introduction to the Neurologic Examination The neurologic examination begins with careful observation of the patient entering the examination area and continues during history taking. The patient should be assisted as little as possible... read more 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 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 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.

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.

The following are evaluated:

Pupillary responses and extraocular movements provide information about brain stem function (see table Interpretation of Pupillary Response and Eye Movement Interpretation of Pupillary Response and Eye Movements ). 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 Etiology This photo shows anisocoria, which is a visible inequality in pupil diameter. In this case, the anisocoria is due to Horner's syndrome. In physiologic anisocoria, the most common cause of anisocoria... read more should be considered; they include past ocular trauma, certain headaches, and use of a scopolamine patch (if the drug comes in contact with the eyes).

The fundi should be examined. Papilledema Papilledema Papilledema is swelling of the optic disk due to increased intracranial pressure. Optic disk swelling resulting from causes that do not involve increased intracranial pressure (eg, malignant... read more 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 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.

Certain patterns of eye abnormalities and other findings may suggest brain herniation Brain Herniation Brain herniation occurs when increased intracranial pressure causes the abnormal protrusion of brain tissue through openings in rigid intracranial barriers (eg, tentorial notch). Because the... read more (see also figure Brain herniation Brain herniation and table Effects of Herniation Effects of Brain Herniation ).

The spontaneous respiratory rate and pattern should be documented unless emergency airway intervention is required. It may suggest a cause.

Initially, pulse oximetry, fingerstick plasma glucose measurements, and cardiac monitoring are done.

Blood tests should include a comprehensive metabolic panel (including at least serum electrolytes, blood urea nitrogen [BUN], creatinine, and calcium levels), complete blood count (CBC) with differential and platelets, liver tests, and ammonia level.

Arterial blood gases (ABGs) are measured, and if carbon monoxide toxicity is suspected, carboxyhemoglobin level is measured.

Blood and urine should be obtained for culture and routine toxicology screening; serum ethanol level is also measured. Other toxicology screening panels and additional toxicology tests (eg, serum drug levels) are done based on clinical suspicion.

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.

If coma is unexplained after MRI or CT and other tests, lumbar puncture Lumbar Puncture (Spinal Tap) Lumbar puncture is used to do the following: Evaluate intracranial pressure and cerebrospinal fluid (CSF) composition (see table Cerebrospinal Fluid Abnormalities in Various Disorders) Therapeutically... read more (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 Brain Herniation Brain herniation occurs when increased intracranial pressure causes the abnormal protrusion of brain tissue through openings in rigid intracranial barriers (eg, tentorial notch). Because the... read more ; 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 Intracranial Pressure (ICP) Monitoring Some monitoring of critical care patients depends on direct observation and physical examination and is intermittent, with the frequency depending on the patient’s illness. Other monitoring... read more is done continuously, and measures to decrease it Intracranial pressure control 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... read more 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).

Patients with any of the following require endotracheal intubation Tracheal Intubation Most patients requiring an artificial airway can be managed with tracheal intubation, which can be Orotracheal (tube inserted through the mouth) Nasotracheal (tube inserted through the nose)... read more to prevent aspiration and ensure adequate ventilation:

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.

To minimize the increase in ICP that may occur when the airway is manipulated, some clinicians recommend giving lidocaine 1.5 mg/kg IV 1 to 2 minutes before giving the paralytic. Patients are sedated before the paralytic is given. Etomidate is a good choice in hypotensive or trauma patients because it has minimal effects on blood pressure; IV dose is 0.3 mg/kg for adults (or 20 mg for an average-sized adult) and 0.2 to 0.3 mg/kg for children. Alternatively, if hypotension is absent and unlikely and if propofol is readily available, propofol 0.2 to 1.5 mg/kg may be used.

Succinylcholine 1.5 mg/kg or rocuronium 1 mg/kg IV is typically used as a paralytic. Paralytics should be used only when they are deemed necessary for intubation and needed to avoid further increases in ICP. Otherwise, paralytics should be avoided because rarely, drugs such as succinylcholine can lead to malignant hyperthermia and can mask neurologic findings and changes.

Pulse oximetry and ABGs (if possible, end-tidal CO2) should be used to assess adequacy of oxygenation and ventilation.

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:

If ICP continues to increase despite other measures to control it, the following may be used:

Patients require meticulous long-term care. Stimulants, sedatives, and opioids should be avoided.

Enteral feeding Enteral Tube Nutrition Enteral tube nutrition is indicated for patients who have a functioning gastrointestinal (GI) tract but cannot ingest enough nutrients orally because they are unable or unwilling to take oral... read more 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 Prevention Pressure injuries are areas of necrosis and often ulceration (also called pressure ulcers) where soft tissues are compressed between bony prominences and external hard surfaces. They are caused... read more . 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 Prevention Bacterial urinary tract infections (UTIs) can involve the urethra, prostate, bladder, or kidneys. Symptoms may be absent or include urinary frequency, urgency, dysuria, lower abdominal pain... read more and deep venous thrombosis Prevention Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions... read more .