Altered Level of Consciousness

Scope of the Problem
The term "coma" is broadly used to refer to any alteration in consciousness. Normal consciousness requires the integration of both wakefulness (or arousal) and awareness (or cognition).

• The ascending reticular activating system, located in the pons, is primarily responsible for arousal of the cerebral cortex.
• Impaired cognition is caused by total or near-total dysfunction of both hemispheres of the cerebral cortex.

  Etiology
  

  Traumatic	Subdural, epidural hematoma Axonal shear injury Hypovolemic shock
  Vascular	Hypertensive encephalopathy Subarachnoid hemorrhage (SAH), intracerebral hemorrhage Infarction Venous occlusion Basilar aneurysm, basilar migraine
  Infectious	Abscess, meningitis, encephalitis Septic shock
  Metabolic	Hypo-, hyperglycemia Wernicke’s encephalopathy Hypoxia, CO2 narcosis Hypo-, hypernatremia Hypo-, hypercalcemia Acidosis, alkalosis Uremia Hyperammonemia
  Environmental	Hypo-, hyperthermia
  Toxic	CO, cyanide, hydrogen sulfite poisoning Alcohols, narcotics, sedatives Anticonvulsants Psychotropics INH, heavy metals
  Endocrine	Hyper-, hypothyroidism Pheochromocytoma
  Hematologic	Anemia Porphyria
  Neurologic	Neurogenic shock Seizures, postictal state
  Neoplastic	CNS tumor Carcinoid meningitis
  Cardiac	Cardiogenic shock
  Autoimmune	Cerebral vasculitis
  Allergic	Anaphylactic shock

Diagnosis

• History
• The patient is usually unable to give a reliable history. Alternative sources of information include a purse or wallet, Medic-Alert bracelets or necklaces, prescription bottles, prehospital personnel, police, family, friends, and neighbors.
• When, and under what circumstances, did the patient lose consciousness? When was the last time the patient was observed in his usual state of health? Vascular events frequently evolve over seconds or minutes. Some metabolic processes develop over minutes to hours, while infectious and other metabolic disorders progress over hours to days. A CNS tumor, abscess, or chronic subdural hematoma may result in symptoms developing over days to weeks.
• Were there any preceding symptoms or events? A preceding state of confusion, without focal neurologic symptoms, usually suggests a metabolic etiology.
• What are the patient’s medications and allergies? Is there a history of drug or alcohol abuse?
• What is the patient’s medical history?
• Have there been any previous similar episodes?
• Vital Signs
• Rectal temperature is critical in patients with altered mental status. Hypothermia may be environmental, or accompany alcohol or sedative intoxication, hypoglycemia, sepsis, Wernicke’s or hepatic encephalopathy, or myxedema. Hyperthermia may be due to heat stroke, seizures, malignant hyperthermia, anticholinergic intoxication, pontine hemorrhage, sepsis or thyroid storm.
• The respiratory rate and character may vary but are only occasionally helpful in determining the pathology responsible for a patient’s alteration in consciousness. Some of the commonly described respiratory patterns are: (1) hyperventilation-resulting in reduced pCO2-associated with hypoxia, metabolic acidosis, brainstem herniation, salicylate overdose, and heptic encephalopathy; (2) hypoventilation-with CNS depressants, uremia, diabetic coma, and elevated ICP; (3) ataxic breathing-irregular rate and depth of inspirations and expirations-frequently precedes respiratory arrest; (4) Cheyne-Stokes-crescendo-decrescendo respiratory rate and depth, alternating with periods of apnea; and (5) apneustic breathing-bradypnea with a pause at end-inspiration.
• Blood pressure will vary depending upon etiology and may be very low, normal or elevated. Likewise, the pulse may also vary. Bradycardia and elevated blood pressure- referred to as Cushing’s reflex-is seen in patients with elevated ICP.
• Examination
• C-spine immobilization should be maintained in any patient with suspected trauma, and patients at risk for cervical injury with minor manipulation (e.g., rheumatoid arthritis).
• The initial exam should focus on the patient’s stability. Is the patient maintaining his airway? Is the patient’s breathing regular and effective? Does he have palpable pulses?
  Is there any external evidence of life-threatening pathology that needs to be addressed immediately (e.g., dilated pupil suggesting herniation)?
• General appearance: Note the patient’s posture. Patients with hemispheric dysfunction generally lie in normal positions. Brainstem lesions tend to be associated with abnormal postures. The patient’s breath may smell of acetone (in diabetic ketoacidosis) or alcohol. Completely undress, carefully inspect, and palpate the patient.
• HEENT: Check the scalp for signs of trauma, surgical scars, or a ventricular shunt.
  Look at the conjunctivae for icterus or pallor. The ears should be examined for hemotympanum. Is there a tongue laceration or dental trauma indicating seizure activity?
• Neck: Listen for bruits. Check range of motion (only if the cervical spine has been cleared). The absence of rigidity does not exclude the possibility of SAH or meningitis. Does the patient have a surgical scar, suggesting a thyroidectomy (and possible incidental removal of parathyroid glands)?
• Chest: Palpate for evidence of trauma. Listen for equal breath sounds throughout the chest. Is there any evidence of acute or chronic pulmonary disease?
• Cardiac: Is there evidence of cardiogenic shock (e.g., dysrhythmias, murmurs, extra heart sounds)?
• Abdomen: Palpate for intraperitoneal fluid, organomegaly, and pulsatile masses.
• Extremities: Does the patient have equal pulses bilaterally? Are there "track marks," indicating intravenous drug abuse? Range all joints to exclude injuries (e.g., posterior shoulder dislocation incurred during a seizure).
• Skin: Examination of the skin may reveal evidence of renal failure (uremic frost); hyperthyroidism (warm, moist, smooth skin); or hypothyroidism (cool, dry skin with a yellow tint).
• Neurologic: The neurologic exam is limited to the patient’s level of consciousness, eyes, spontaneous movements, and reflexes.
• The Glasgow Coma Scale was originally designed for use in accurately describing the best response of a patient who sustained head trauma. However, despite its limitations, it is widely used in nontrauma settings as well. Scores range from 3 (worst) to 15, with coma defined as a score less than 8 (unless the patient has spontaneous eye opening).

  Eyes	Verbal	Motor	Score
  No opening	No sounds	No movement	1
  Open to noxious stimulus	Unintelligible sounds	Extensor response	2
  Open to verbal stimulus	Nonsensical speech	Flexor response	3
  Open spontaneously	Confused	Flexion withdrawal	4
  	Oriented	Localizes noxious stimulus	5
  		Follows commands	6

• Examine the eyes at rest. Disconjugate gaze may localize the lesion to the pons or cerebellum (vertical, "skew" deviation), CN VI (persistent adduction of one eye), CN III (persistent abduction of one eye), or diffuse injury (conjugate upward gaze is seen in anoxic encephalopathy). Note pupil size, symmetry, and reactivity. Small pupils suggest an interruption of the sympathetic pathway, organophosphate poisoning, opiate overdose, or a pontine lesion. Dilated pupils indicate compression of CN III, anticholinergic overdose, or sympathomimetic intoxication. Pupils that are normal in size but unreactive are seen with brainstem (midbrain) lesions. Examination of the eyelids may reveal bilateral or unilateral ptosis. Bilateral ptosis occurs in midbrain lesions (e.g., basilar artery embolism); unilateral ptosis is seen with Horner’s syndrome and CN III palsy. Extraocular movements can be assessed by eliciting the oculocephalic or oculovestibular reflex. The oculocephalic (or doll’s eyes) maneuver should not be performed if the patient is at risk for cervical injury; instead, the more sensitive oculovestibular (or cold-water calorics) reflex should be tested. A normal response (i.e., conjugate, horizontal eye movements away from the direction of head movement, or toward the side of the cold-water irrigation) indicates an intact brainstem. Abnormal responses (e.g., no eye movement or downward deviation of the eyes) suggest brainstem involvement or sedative drug intoxication.
• Cranial nerves: The corneal reflex involves both the afferent limb of CN V and the efferent limb of CN VII. The presence or absence of a gag reflex (CN IX and X), although important for airway protection, has no localizing value.
• Motor: Observe the patient for spontaneous movements. Unilateral movement may suggest a focal neurologic deficit. The only evidence of nonconvulsive status epilepticus may be subtle movement. Observe the patient’s response to a noxious stimulus.
• Reflexes: Hyperreflexia and clonus suggest hemispheric dysfunction. Asymmetry of reflexes may localize the deficit.

Differential Diagnosis

• Locked-in syndrome: syndrome of intact consciousness, with voluntary movement restricted to opening and closing the eyes and moving the eyes in the vertical plane.
• Acute psychosis
• Psychogenic unresponsiveness
• Conversion reaction
• Malingering

Evaluation

• Pulse Oximetry
• Rapid assessment of the patient’s oxygenation status can be obtained with pulse oximetry.
• Labs
• Bedside glucose testing should be done to exclude hypoglycemia, an easily treated cause of altered mental status.
• An arterial blood gas will provide more information regarding the patient’s ventilatory (pCO2) and acid-base status (pH, HCO3, and base deficit). In addition, a low pO2 in the setting of a normal pulse oximetry value, as well as an elevated carboxyhemoglobin level, are indicative of carbon monoxide poisoning.
• Electrolytes (including calcium), BUN and creatinine are routinely ordered. Serum osmolarity, serum drug levels, ammonia, and TSH may be indicated based on the history and physical exam.
• Selective ordering of serum levels of ethanol and other toxic alcohols and toxicology screening may confirm or exclude intoxication. True coma is rarely caused by ethanol levels under 250 mg/dL; patients suspected of acute intoxication but with lower levels require further testing (e.g., head CT, LP) to search for another explanation for their symptoms.
• Urinalysis and pregnancy testing should routinely be performed.
• Consider blood, urine, and throat cultures in any case where sepsis is a concern.
• Lumbar puncture for analysis of cerebrospinal fluid (CSF) is indicated in any patient suspected of having a CNS infection or subarachnoid hemorrhage (after negative head CT). This procedure is deferred when there is clinical evidence of increased ICP.
• Electrocardiogram
• EKG may reveal a cardiac etiology (especially in the elderly) or evidence of other pathology: "cerebral" T waves in SAH, Osborne or "J" waves in hypothermia, or prolonged Q-T interval in hypocalcemia.
• EEG
• Although not readily available, bedside EEG may be useful in suspected nonconvulsive status epilepticus.
• Imaging
• Noncontrast head CT is the primary neuroimaging study and will identify intracranial hemorrhage and some abscesses, tumors, and noninfectious inflammatory disorders. Contrast-enhanced CT scans are more sensitive for abscess, tumor, and inflammatory processes; it will also identify infectious or neoplastic meningeal disease.
• Chest radiography is useful in suspected pulmonary infections and malignancy and is performed after endotracheal intubation for confirmation of adequate tube placement.
• MRI and CT are both insensitive in the first few hours after ischemic stroke.
  Diffusion-weighted MRI, however, will detect acute infarction.

Treatment

• Maintain an adequate oxygen saturation. Consider intubation for airway protection or maintenance of adequate ventilation.
• All patients with altered mental status of unknown etiology should receive thiamine 100 mg IV. Patients with hypoglycemia (also consider in patients with low-normal bedside results) should receive 25 g of 50% dextrose IV (pediatric dosing: 25% dextrose, 0.5 g/ kg). Although some references recommend empiric administration of naloxone, selective use guided by the history, vital signs, and physical exam is acceptable.
• Flumazenil is indicated only for acute benzodiazepine overdose. Indiscriminate use may cause seizures in patients with cocaine or tricyclic toxicity or cause withdrawal seizures in chronic benzodiazepine users.
• Hypotension should be treated with isotonic fluids and vasopressor agents, as needed. An appropriate target mean arterial pressure is 90 to 100 mm Hg.
• Determining the etiology of hypertension, malignant hypertension, ischemic stroke, or response to elevated ICP is crucial to guiding treatment (if any).
• Elevated intracranial pressure should be recognized early and managed with head-of-bed elevation to 30 degrees (when practical), hyperventilation (target CO2 30-35), mannitol 0.5 g/kg (20% solution) infused over 5-15 min, and furosemide 1 mg/kg IV. Use of medications will likely be in concert with neurosurgical consultation.

• Patients in true coma require admission to an ICU with neurologic emergencies or neurosurgical consultation, as appropriate. Patients with no clear etiology for their altered mental status should be admitted, even if all symptoms have resolved.
• Patients with hypoglycemia, unrelated to insulin use, should be admitted for evaluation to determine the cause of the episode (e.g., stroke, MI, sepsis in the elderly).
• Although admission is sometimes recommended for narcotic overdose (because of the long duration of action of most narcotics compared to that of naloxone), this is usually not practical. A period of observation in the ED (i.e., 4-6 h) is sufficient to prevent recurrence of symptoms
• Acute ethanol intoxication requires observation until the patient is able to "walk and talk." This allows reassessment for concomitant illness or injury and ensures that the patient is safe to leave.
• Patients with psychogenic "coma" may be discharged after resolution of symptoms.
  Psychiatric consultation is indicated prior to discharge.
• Patients who are discharged home should have follow-up with a primary physician within 24-48 h.