Coma and Confusion

Introduction

• Disorders of consciousness
  • Arousal
    • Wakefulness and alertness centred in RAS
  • Content of consciousness
    • Self-awareness, language, reasoning, spatial awareness, emotions centred in cerebral cortex
• Dementia = Impairment of content with preserved arousal
• Coma = Failure of both arousal and content
• Psychiatric disorders and altered mental states may share features such as delusions or hallucinations

Definitions

• Confusion – Inability to think with normal speed and clarity, associated with inattentiveness, reduced awareness and disorientation
• Delirium – Confusion with agitation and hallucination
• Stupor – Unresponsiveness without deep and repeated stimuli
• Coma – Unarousable unresponsiveness
• Locked-in syndrome – Total paralysis below third cranial nerve nuclei with normal or impaired mental function
• Persistent vegetative state – Prolonged coma >1 month
• Akinetic mutism – Prolonged coma with apparent alertness and flaccid motor tone
• Minimally conscious state – Preserved wakefulness, awareness and brainstem reflexes but poorly responsive

Delirium, dementia, psychiatric

Delirium

• Transient disorder of attention and cognition
• 10-25% of elderly hospitalised patients have delirium at some point
• ¼ of ED patients >70yo have impaired mental status or delirium and routine evaluation will miss many of these
• Pathophysiology
  • Primary intracranial disease
  • Systemic diseases secondarily affecting the CNS
  • Exogenous toxins
  • Drug withdrawal
• Clinical features
  • Usually develops over days
  • Alertness reduced as manifest by impaired attention and focusing concentration
  • May appear quite awake but attention is impaired
  • Activity levels may be increased or decreased and can fluctuate rapidly
  • Symptoms can be intermittent
  • Sleep-wake cycles often disrupted
  • Tremor, asterixis, tachycardia, sweating, hypertension and emotional outbursts can all occur
  • Hallucinations tend to be visual
• Diagnosis
  • Collateral from caregivers is crucial
  • Acute onset of attention deficit and cognitive impairment fluctuating throughout day and worse at night = pathognomonic of delirium
• Ix
  • Directed at underlying cause as per four major differentials
  • FBC, Chem20, Urinalysis, CXR, head CT +- LP
  • Always consider drugs, OTC, intoxications and withdrawal
• MMSE useful to assess aspects of cognition not routinely tested in ED during course of hx and examination
  • Does not identify mild cognitive impairments
  • Affected by intellignce and chronic cognitive impairment
• Quick Confusion Scale takes <3 minutes, correlates well to MMSE results
  • What year is it?
  • What month is it?
  • Repeat memory phrase
  • About what time is it?
  • Count backwards from 20
  • Say the months in reverse
  • Repeat memory phrase again
• Differential (massive)
  • Infectious: Pneumonia, UTI, meningitis, encephalitis, sepsis
  • Metabolic/toxic: Hypoglycaemia, alcohol, electrolyte disturbance, hepatic encephalopathy, thyroid disorders, alcohol/drug withdrawal
  • Neurological: Stroke, TIA, seizure/post-ictal, subarachnoid, ICH, CNS mass lesion, subdural
  • Cardiopulmonary: CCF, MI, PE, hypoxia or CO2 narcosis
  • Drug-related: Anticholinergic, alcohol/drug withdrawal, sedative-hypnotics, narcosis, SSRI/SNRI, polypharmacy, digoxin
• Treatment
  • Airway/breathing: Consider and treat hypoxia/hypercapnoea
  • Circulation: Correct poor perfusion
  • Disability: Identify and treat pain, consider underlying neurological pathology e.g. SDH
  • Drugs:
    • Review medications
    • Consider ceasing anticholinergic agents
    • Haloperidol 0.5mg is first line but use should be sparing and only if necessary
      • Lorazepam 0.5mg is better alternative in Lewy body dementia, prolonged QT or parkinsonism
  • Exposure: Examine for urinary retention/incontinence/constipation
  • Fluids/electrolytes: Check fluid balance, treat dehydration, correct electrolytes
  • Glucose: Seek and treat hypoglycaemia
  • Infection: Full septic screen including skin/pressure areas
  • General: Regular reorientation, speak calmly and politely, suitable lighting, hearing aids/spectacles, promote sleep

Coma

• State of reduced alertness and responsiveness from which patient cannot be aroused
• GCS
  • Does not acknowledge hemiparesis or other focal motor signs and does not test higher cognitive functions
• Differentiated into systemic and primary CNS causes
  • Systemic causes typically affect entire CNS with no localising signs
  • Primary CNS causes may result from brainstem disorders or bilateral cortical dysfunction and may show localising signs

Coma

• Normal LOC depends on interaction between rostral RAS and cerebral hemispheres
• Anatomical bilateral hemispheric lesions or brainstem lesions can alter consciousness
• Large unilateral hemispheric lesions may cause upper brainstem compression and alter consciousness in this manner

Coma – With Focal signs

• Trauma – Extradural, subdural, parenchymal haemorrhage, concussion
  • Signs of trauma on exam. Exclude coexistant ingestions
• Vascular – Intracerebral haemorrhage
  • Sudden onset. Consider secondary causes of HTN
• Vascular – Thromboembolic
  • Sudden onset, risk factors, AF, endocarditis, bruits
• Brain abscess 
  • Consider IE, suppurative lung disease, dental and ENT sources

Coma – Without focal signs but with meningeal irritation

• Meningoencephalitis
  • Hours to days onset. Consider underlying immunosuppression
• Subarachnoid haemorrhage
  • Consider polycystic kidney disease

Coma – Without focal signs or meningeal irritation

• Metabolic
  • HypoNa, hypoglycaemia, hyperglycaemia, hypoxia, hypercapnoea, hypo- or hyperthermia, hypo- or hyperosmolar states
• Endocrine
  • Myxoedema, adrenal insufficiency, hypopituitarism
  • Clues: Abnormal electrolyte profile, hypoglycaemia
• Seizure disorders
• Organ failure
  • Heparic, renal
• Toxic/drug
  • Sedatives, narcotics, alcohol, psychotropic
• CO poisoning
• Behavioural

DDx of coma

• Systemic causes
  • Encephalopathy: Hypoxic, metabolic, hypertensive
  • Hypoglycaemia
  • HHS
  • Electrolytes (Na, Ca)
  • Hepatic or uraemic encephalopathy
  • Endocrine: Addison’s, Hypothyroid
  • Hypoxia
  • CO2 narcosis
  • Toxins
  • Drug reactions e.g. NMS, serotonin syndrome, anticholinergic
  • Environmental e.g. hyper/hypothermia
  • Wernicke’s encephalopathy, B12 deficiency
  • Sepsis

DDx of coma

• Primary CNS causes
  • Direct CNS trauma e.g. DAI, subdural, epidural
  • Vascular e.g. Intraparenchymal haemorrhage
  • SAH
  • Infarction (specifically brainstem)
  • CNS infection
  • Neoplasm
  • Seizures i.e. NCSE or post-ictal

Coma – Clinical features

• Toxic-metabolic coma
  • Lack of focal neurological findings
  • Pupillary response usually preserved (small but reactive)
  • If EOM are present, usually symmetrical
  • Notable exception is barbiturates with bilateral dilated fixed pupils, absent EOM, flaccid muscles and apnoea (mimicing braindeath)
• Coma from supratentorial lesions
  • Progressive hemiparesis or asymmetric muscle tone and reflexes
  • May suspect hemiparesis based on asymmetric responses to stimuli or posturing
  • Coma without lateralising signs may occur with reduced cerebral perfusion due to raised ICP
    • May get reflex changes in BP and HR in this setting

Coma– Clinical features

• Coma from infratentorial lesions
  • Abrupt cerebellar lesion may cause coma, abnormal extensor posturing, loss of pupillary reflexes and loss of extraocular movements
  • Early brainstem compression with loss of brainstem reflexes can occur rapidly
  • Pontine haemorrhage can present with acute coma and pinpoint pupils (unique in this respect – presents like opioid narcosis)
• Pseudocoma
  • Manual eye opening (should be minimal or no resistance in true coma)
  • Extraocular movements – specifically if avoidance of gaze is seen consistently
  • If caloric vestibular testing remains intact, strong evidence for feigned unresponsiveness

Coma – Diagnosis

• Liberal use of CT is advised due to exceptions to clinical diagnoses
• Abrupt onset – Seizure, stroke
• Slowly progressive – Progressive CNS lesion e.g. tumor or subdural or metabolic/toxic
• Signs of trauma or intoxication
• CNS – Pupils, posturing, tone, corneal reflexes, oculovestibular reflexes may all help suggest focal lesion
• Abnormal extensor or flexor posturing are non-specific but suggest profound CNS dysfunction
• Need to rapidly determine if diffuse impairment or focal lesion (perhaps surgically remediable)
• Early CT is key followed by LP if CNS infection or SAH suspected
• Suspect basilar artery thrombosis in patient with normal CT and comatose
  • May only see hyperdense basilar artery
  • CTA then required

Eye signs in ALOC

• Doll’s eye reflex intact = Median longitudinal fasciculus and brainstem intact
• Response to caloric testing
  • Bilateral nystagmus
    • Suggests intact cerebrum, MLF and brainstem
  • Bilateral conjugate deviation towards stimulus
    • Suggests metabolic dysfunction of cerebrum
  • No response
    • Suggests structural or metabolic dysfunction of brainstem
  • Ipsilateral dysconjugate deviation
    • Suggests structural dysfunction of brainstem

Eye signs in coma

• Horizontal eye movements to the contralateral side are initiated in the ipsilateral frontal lobe and coordinated by the contralateral pons
  • In paralytic frontal lobe lesion, eyes deviate to ipsilateral side
  • In paralytic pontine lesion, eyes deviate to contralateral side
• Conjugate eye movements are organised by the median longitudinal fasciculus
• Vertical eye movements are under bilateral cortical and upper midbrain control
• Spontaneous roving eye movements rules out brainstem pathology

Temperature in coma

• Hypothermia
  • Alcohol or barbiturate intoxication
  • Sepsis with shock
  • Drowning
  • Hypoglycaemia
  • Myxoedema
  • Coma
  • Exposure to cold
• Hyperthermia
  • Pontine haemorrhage
  • Intracranial infection
  • Stroke
  • Anticholinergic drug toxicity

Pupillary responses

• Miosis (<2mm)
  • Unilateral – Horner’s, local trauma to sympathetics
  • Bilateral – Pontine lesions, thalamic haemorrhage, metabolic encephalopathy, drug ingestion, organophosphate poisoning, barbiturates, narcotics
• Mydriasis (>5mm)
  • Unilateral fixed dilated – Midbrain (3^rd nerve nucleus), uncal herniation (3^rd nerve)
  • Bilateral fixed dilated – Massive midbrain haemorrhage (bilateral 3^rd nerve), hypoxic cerebral injury, atropine, tricyclics, sympathomimetics

Brain herniation

• Central herniation
  • Upper brainstem compression
  • Progressive obtundation, Cheyne-Stokes respiration, small pupils then extensor posturing and medium-sized fixed dilated pupils
• Uncal herniation
  • Early pupil dilatation due to third nerve compression

Patterns of dysfunction

Last Updated on June 25, 2021 by Andrew Crofton