162. Altered Mental Status and Coma


Acute confusion state, impairment of attention and cognition. Confusion can fluctuate. 4 general causes: intracranial disease, systemic disease, exogenous toxins, drug withdrawal. Alertness is reduced by difficulty maintaining attention and concentration. Sometimes drowsy, but generally awake. Sleep-wake cycle affected, causing ‘sundowning.’ Agitation can be treated with Halidol 5-10mg PO, IM, IV, though in elderly, may just start with 1-2mg. Benzos such as lorazepam/Ativan 0.5-2mg PO, IM, IV. Atypical antipsychotics are usually withheld in elderly due to increased mortality.

Infectious: pneumonia, UTI, meningitis/encephalitis, sepsis. Metabolic/toxic: Hypoglycemia, alcohol ingestion, electrolyte abnormality, hepatic encephalopathy thyroid disorders, drug withdrawal. Neurologic: stroke/TIA, seizure/post-ictal state, SAH, ICH, CNS mass lesion, SDH. Cardiopulmonary: CHF, MI, PE, hypoxia/CO2 narcosis. Drug-related: anticholinergic, alcohol/drug withdrawal, sedative-hypnotic, narcotic analgesic, polypharmacy.


Impairment of memory, particularly recent. Preservation of motor and speech abilities. Early: memory loss, naming problems, forgetting items. Middle: loss of reading, decreased performance in social situations, loss of direction. Late: extreme disorientation, inabilty to perform self-care tasks, personality changes.

Alzheimer’s: most common, still unknown etiology, thought to be related to amyloid deposits.

Vascular Dementia: second most common, CV disease with multiple infarcts. Sometimes have specific dates of worsening. Usually within 3 months of CV event or abrupt deterioration in memory or cognitive abilities.

Huntingtons: autodominant dementia.

Parkinson’s: increased motor tone, extrapyramidal signs of rigidity or movement disorders.

Vitamin deficiencies: consider checking B12 or folate.

Normal Pressure Hydrocephalus: Large ventricles on CT. Wet (urinary incontinence), Wobbly (ataxia, gait disturbance), and Weird (dementia). Consider trial of LPs or VP shunt to help improve symptoms.


Patient cannot be aroused. Function of the brainstem or both hemispheres altered to cause coma.

Uncal Herniation: use to medial temporal lobe shift onto brainstem. Drowsiness leading to ipsilateral slugginess to dilated nonreactive pupil. Ipsilateral hemiparesis.

CPP: Cerebral Perfusion Pressure: MAP (Mean Arterial Pressure) – ICP (Intracranial Pressure). If ICP approaches MAP, cerebral blow flow decreases and ischemia occurs.

Cushing Reflex: Due to increased ICP causing coma, hypertension and bradycardia.

Nonconvulsive status epilepticus: occurs with patient that had generalized seizure and remains unresponsive 30 minutes after seizure. In state of electrical seizure.

References / Resources

Tintinalli, Chapter 162: Altered Mental Status and Coma


Unedited Notes:

Coma is the dysfunction of arousal and awareness. Its a spectrum from brain death to minimally responsive.

Coma: eyes closed; reflexive, nonpurposeful or absent responsiveness.

Primary survey: airway protection, possibility of spinal injury, fingerstick, naloxone.

Neuro Assessment: LOC, Brainstem exam, motor function, breath pattern.

LOC: Spontaneous eye opening, visual fixation or pursuit, spontaneous and purposeful movements.

Coma Scales

GCS vs FOUR score. FOUR score: Eye response (0-4), Motor Response (0-4), Brainstem reflexes (0-4), Respiration (0-4). – Came out around 2005. Trying to assess brainstem function unlike GCS.

Brainstem exam: pupillary light reflex, corneal reflex, visual threat reflex, oculocephalic reflex, gag/cough reflex.

Motor function: assess response to proximal stimuli before distal stimuli. Assess proximally to sort out flexing vs withdrawing.

Structural Causes: Traumatic (ICH, SDH), neurovascular, neoplastic, AIDS related).

Metabolic Causes: Anoxi-ischemic, seizures, metabolic alterations, endocrinopathies, infections, OD, intoxications.


Approach to the Comatose Patient, Wendy Chang, The Crashing Patient Conference 2015 – http://cloud.emedhome.com/cme/cme_45769_hi.mp4?iframe=true&width=920&height=470

Intracranial HTN does not equal herniation. Its a spectrum.

Uncal herniation: medial portion of temple lobe goes downward into tentorium: ipsalateral pupil dilation, contralateral limb weakness.

Subthalsine heration: contralateral lower extremity weakness. Decreased LOC as well.

Tonsillar hernation: cerebellar parenchyma pushingdown into forumen magnum. Most rapid decline.

GCS drop in 2 points + anisocoria + posturing: diagnosis of herniation until proven otherwise.

Pupillary dilation localizes herniation better than limb weakness.

Treatment: Reducing blood volume: avoid hyperemia, remove clot/mass. Reducing CSF Volume: shunts/drains; Reducing cerebral ischemia: analgesia/sedation, induce pharm coma, induce hypothermia.

Tier 0: elevated head of bed, avoid neck constriction, treat fever/pain/agitation.

Tier 1: CSF draingage via ventriculostomy, hyperosmolar therapy (mannitol vs hypertonic saline).

Tier 2: additonal hyperosmolar therapy, sedation with propofol.

Tier 3: induce pharma coma (barbituates), induce hypothermia.

Intracranial Hypertension and Herniation, Yemi Adebayo, The Crashing Patient Conference 2015.


162. Altered Mental Status and Coma

Leave a Reply

Your email address will not be published. Required fields are marked *