AMS: Delirium, Stupor and Coma

Delerium vs. Dementia-time course, autonomic involvement, and acuity

Delerium-think medications, esp. anti-ach also consider withdrawl

DTs-3 to 5 days, Withdrawl seizures-can start within 6 hours

If need to sedate use Haldol and Ativan combo

Pseudodementia-from depression in the elderly

Decreased LOC

Acute focal neurologic deficit

Decreased Level of Attention

Delirium

The term delirium stems from the Latin word “delirare.” In common usage it meant to be “crazy” and was derived from two other Latin words, “de” and “lira” (“the ridge between furrows”). The literal translation is “to go out of the furrow” while plowing.¹² In the first century AD, Celsus used the term delirium to distinguish a constellation of symptoms from that of hysteria, depression, and mania.¹³ It corresponded to “phrenitis” (English derivative—“frenzy”), which was known to Hippocrates (460-366 BC), who observed the appearance of cognitive and sleep disturbances and agitated behavior in patients with febrile illnesses.

DSM-IV include:¹

1. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention;

2. A change in cognition (e.g., memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not accounted for better by a pre-existing, established, or evolving dementia;

3. The disturbance develops during a short period (usually hours to days) and tends to fluctuate during the course of the day. There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by the direct physiologic consequences of a general medical condition, substance intoxication or side effect, substance withdrawal, multiple factors, or unidentified etiology. For substance intoxication, side effects, or withdrawal, there must be a temporal or etiologic relationship to the disturbance.

Quick Confusion Scale (QCS).

CAM

Differential DX

Drugs and withdrawal

Endocrine (thyroid, Addison's)

Lungs (hypercapnia, pneumonia)/Lytes (hypoglycemia)

Infection

Restraints, reduced mobility

Intracranial

Uremia/retention

Myocardial

CBC, LFTS, Lytes, Pulse Ox, ECG (Consider Enzymes), C-XR, UA, and ammonia levels

death after excited/agitated delerium  (AJEM 2001;19:187)

Coma and Depressed Level of Consciousness

Arousal takes place in the brainstem in the ascending reticular activating system (RAS) and the cerebellum

GCS-eyes 4 verbal 5 motor 6

Neuro Exam in the Comatose Patient

Triple flexion-flexion of the hip, knee, ankle.  Spinal cord reflex, does not imply any higher functioning.

Etiology of Coma

• Diffuse Brain Dysfunction

  • Neuronal damage caused by deprivation of oxygen, glucose, or metabolic cofactor

  • Hypoxia with an intact CBF, severe pulmonary disease, anemia

  • Decreased CBF (e.g., postcardiac arrest, cardiogenic and hypovolemic shock)

  • Cellular toxins: carbon monoxide, cyanide, hydrogen sulfide

  • Hypoglycemia

  • Thiamine deficiency (Wernicke-Korsakoff syndrome)

• Endogenous CNS toxins

  • Hyperammonemia (hepatic coma, postureterosigmoidostomy, prune belly syndrome)

  • Uremia

  • CO₂ narcosis

  • Hyperglycemia

• Exogenous CNS toxins

  • Alcohols: ethanol, isopropyl alcohol

  • Acid poisons (methanol, ethylene glycol, salicylates)

  • Sedatives and narcotics

  • Anticonvulsants

  • Psychotropics

  • Isoniazid

  • Heavy metals

• Endocrine disorders

  • Myxedema coma, thyrotoxicosis

  • Addison’s disease, Cushing’s disease, pheochromocytoma

• Abnormalities of ionic environment of CNS

  • Hyponatremia, hypernatremia

  • Hypocalcemia, hypercalcemia

  • Hypomagnesemia, hypermagnesemia

  • Hypophosphatemia

  • Acidosis, alkalosis

• Environmental disorders and disordered temperature regulation

  • Hypothermia

  • Heat stroke

  • Neuroleptic malignant syndrome

  • Malignant hyperthermia

• Intracranial hypertension

  • Hypertensive encephalopathy

  • Pseudotumor Cerebri

• CNS inflammation or infiltration

  • Meningitis

  • Encephalitis

  • Encephalopathy

  • Cerebral vasculitis

  • Subarachnoid hemorrhage

  • Carcinoid meningitis

  • Traumatic axonal shear injury

• Primary neuronal or glial disorders

  • Creutzfeldt-Jakob disease

  • Marchiafava-Bignami disease

  • Adrenoleukodystrophy

  • Gliomatosis cerebri

  • Progressive multifocal leukoencephalopathy

• Seizures and postictal state

• Focal Lesions of the CNS

  • Supratentorial lesions

    • Hemorrhage (traumatic and nontraumatic)

      • Intracerebral

      • Epidural

      • Subdural

    • Pituitary apoplexy

    • Infarction

      • Thrombotic arterial occlusion

      • Embolic arterial occlusion

      • Venous occlusion

    • Tumors

    • Abscess

  • Subtentorial lesions

    • Compressive

      • Cerebellar hemorrhage

      • Posterior fossa subdural or extradural hemorrhage

      • Cerebellar infarct

      • Cerebellar tumor

      • Cerebellar abscess

      • Basilar aneurysm

    • Destructive

      • Pontine hemorrhage

      • Brainstem infarct

      • Basilar migraine

      • Brainstem demyelination

The false-localizing ipsilateral hemiparesis, resulting from compression of the crus cerebri by the tentorium, likewise became known as the Kernohan–Woltman syndrome or Kernohan's notch phenomenon (Figure 1A). Although originally described in a patient with a primary brain tumour, the phenomenon may also occur with traumatic brain injury or with displacement of the cerebral peduncles

Figure 1: (A) Schematic coronal section of the brain showing large (supratentorial) right subdural hematoma causing ipsilateral transtentorial herniation, which has resulted in compression of the contralateral cerebral peduncle (broken, red arrow). This led to ipsilateral (right-sided) weakness. (B) Schematic coronal section of the brain showing (infratentorial) right meningioma (M) causing upward and leftward displacement of the midbrain and cerebral peduncles, which has resulted in compression of the left cerebral peduncle and corticospinal tracts against the tentorium cerebelli (open arrow), which contributed to the ipsilateral (right-side) weakness. In both figures, the solid arrows indicate the direction of shift due to the mass effect, either from the subdural hematoma or from the tumour.

Hyperammonemia

can be non-hepatic

(Postgrad Med J 2001;77:717)

can be from massive gi bleeding resulting in absorbtion of large amounts of nitrogen

Reversible Posterior Leukoencephalopathy Syndrome (RPLS)

encephalopathy

aka posterior reversible encephalopathy syndrome (PRES)

not always reversible or confined to posterior

vasogenic edema on MRI primarily in the posterior brain

presents c HA, confusion, visual sx, and seizures

Coma with Pinpoint Pupils

from life in the fast lane

The differential diagnosis of coma with small pupils includes:

Non-toxicological causes

• Pontine lesions (infarct or hemorrhage)
  classically involves sudden collapse with coma, pinpoint pupils and a spastic tetraparesis with brisk reflexes.
• Bilateral Horner’s syndrome*
  central (e.g. massive thalamic or supra-thalamic lesions, lateral brainstem lesions), pre-ganglionic (e.g Pancoast tumour), post-ganglionic (e.g. neck trauma, carotid artery dissection, cluster headaches)
• Senile miosis*
• Argyll-Robertson pupils*
  small, irregular, fixed pupil with little response to atropine and acts like a prostitute – accommodates but doesn’t react… to light.
  nearly pathognomonic of neurosyphillis
• Pseudo-Argyll Robinson pupils* (more likely to be mid-sized)
  diabetes mellitus
  any chronic lesion of the rostral midbrain (e.g. multiple sclerosis, encephalitis, Lyme disease, pinealoma, syringobulbia, chronic alcoholism)
• Holmes-Adie pupils* (constrictive phase)

Toxicological causes

• Sedatives

opioids
clonidine
barbiturates
chloral hydrate
GHB

• Antipsychotics

phenothiazines (eg. chlorpromazaine)
atypicals (olanzepine, quetiapine, clozapine)

• Cholinergic agents

acetylcholinesterase inhibitors

organophosphates
carbamates
nerve agents (e.g. sarin)

Alzheimers dementia agents* – e.g. donezepil, tacrine
Myasthenia gravis agents* – eostigmine, physostigmine, edrophonium

Acetylcholine agonists

muscarinic agents – pilocarpine (eye drops)*
nicotine
mushrooms

• Other drugs

valproate
phenoxybenzamine (alpha blocker)
beta blocker eye drops*

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