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Altered Mental Status – Delirium, Stupor and Coma

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

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

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)

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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

 

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FOUR Score

(Critical Care Medicine Issue: Volume 40(9), September 2012, p 2671–2676)

four-score

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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

Q1. What’s the differential for the decreased level of consciousness? (From LitFL Blog)

Answer and interpretation

There are many ways to break this down into a logical sieve. This is a modified version of  the apporach described by Bala Venkatesh in Oh’s Intensive Care Manual:

Differential Diagnosis of Coma

Category Specific Disorder Clinical features Key investigation Focal signsCVA:

  • Ischemic
  • Haemorrhagic

Risk factors for CVA CT Trauma Look signs of base-of-skull fracture CT Space occupying lesion:

  • Infective
  • non-infective

Look for ENT and dental sources of infection Past history of cancerImmunosuppression CT Meningism Meningitis ormenigoencephalitis FeverMeningococcal rash LPCT Sub-arachnoid haemorrhage ‘Worst headache ever’Subhyaloid hemorrhages SAH risk factors LPCT No focal signs or meningism

(MESOT)

Metabolic causes:

  • Hypoxia
  • Hypercapnoea
  • Hyponatraemia
  • Hyperglycaemia
  • Hypoglycaemia
  • Hypo/hyperthermia
  • Hypo/hyperosmolarity

History essential SO2ABGETCO2UECBSLTemperature ketones Endocrine:

  • Adrenal insufficiency
  • Hypopituitarism
  • Hypothyroidism
  • Diabetic coma

Time courseSteroid medicationsPhenotype TFTfree T3/4TemperatureBSLUEC Ca, PTHCortisol Seizures (including eclampsia) ?witnessed?post-ictal?non-convulsive epilepsy EEGCT for SOL Organ Failure

  • Renal: uraemia
  • Liver: PSE

Urine outputHistory/exam findings of liver disease? paracetamol OD EUCLFTs, NH3INR Toxins/drugs, especially:

  • Sedatives
  • Narcotics
  • Alcohol
  • Psychotropics
  • Carbon monoxide
  • Many other poisons!

Toxicology risk assessment ABG analysisSpecific drug levelsOsmolality ECG Pseudocoma history of mental illnesshistory of sleep disorder Diagnosis of exclusion

This, of course, is a very generic approach. Immediately post op, you can also think of causes as being:

  • Related to the anaesthetic
  • Related to the surgery
  • Related to post-operative events

 

Again, an approach modified from that of Bala Venkatesh in Oh’s Intensive Care Manual is shown::

Pupillary abnormality Cause Pathology Miosis (<2mm)Unilateral Horner’s SyndromeLocal pathology/ trauma Sympathetic paralysisDamage to sympathetics Bilateral Pontine lesionThalamic haemorrhageMetabolic encephalopathySenile miosisArgyll-Robertson pupils Holmes-Adie pupilsDrug ingestion, eg.

  • Organophosphate
  • Barbiturate
  • Narcotics

Sympathetic paralysis

Mechanisms:

  • Cholinesterase inhibition
  • Central effects

Mydriasis (>5mm)Unilateral Uncal herniationMidbrain lesion CN3 stretched on petroclinoid ligamentCN3 nucleus damage Bilateral fixed pupils Bilat uncal herniationMassive midbrain bleed Hypoxic injuryDrugs:

  • Atropine
  • Tricyclics
  • Sympathomimetics

Brain herniationBilateral CN3 damage Mesencephalic damageMechanisms:

  • Parasympathetic paralysis
  • TCA’s pevent reuptake of catecholamines by nerve endings
  • Sympathetic stimulation

For further review read Neurological Mind-boggler 002 on the causes of coma with small pupils, and Ophthalmological Befuddler 001 for the causes of a dilated pupil.

 

 

 

 

 

 

 

 

 

 

 

 

The false-localizing ipsilateral hemiparesis,resulting from compression of the crus cerebri by the tentorium,likewise became known as the Kernohan–Woltman syndromeor Kernohan’s notch phenomenon (Figure 1A). Although originallydescribed in a patient with a primary brain tumour, the phenomenonmay also occur with traumatic brain injury or with displacementof 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.

 

 

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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

 

 

Causes of non-hepatic hyperammonaemia

Inherited defects of the urea cycle enzymes   Portosystemic shunts    Transport defects of intermediates in the urea cycle   Urinary   Organic acidurias    Urinary diversion for example, ureterosigmoidostomy and ileal conduit   Other metabolic causes    Urinary tract infections    Hyperinsulinaemic hypoglycaemia    Subureteric injection for vesicoureteric reflux    Distal renal tubular acidosis   Haematological    Primary carnitine deficiency    Following allogenic peripheral blood progenitor cell transplantation    Fatty acid oxidation defects    Multiple myeloma   Drugs    Acute myeloblastic leukaemia, chronic myelocytic leukaemia    Chemotherapyfor example, 5-fluorouracil, asparaginase   Other    Sodium valproate    Parenteral nutrition    Anaesthetic agentsfor example, halothane, enflurane    Muscular origin   Reye’s syndrome*    Idiopathic * Need to exclude inborn errors of metabolism as possible causefor example, medium chain acyl-CoA deficiency. With normal liver function, as distinct from portosystemic shunts occurring in the context of chronic liver disease where resultant hyperammonaemia may be termed hepatic hyperammonaemia

 

 

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Reversible Posterior Leukoencephalopathy Syndrome (RPLS) or (PRES)

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

PRES Review

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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 mellitusany 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

opioidsclonidinebarbiturateschloral hydrateGHB

  • Antipsychotics

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

  • Cholinergic agents

acetylcholinesterase inhibitors organophosphatescarbamatesnerve agents (e.g. sarin) Alzheimers dementia agents* – e.g. donezepil, tacrineMyasthenia gravis agents* – eostigmine, physostigmine, edrophonium Acetylcholine agonists muscarinic agents – pilocarpine (eye drops)*nicotinemushrooms

  • Other drugs

valproatephenoxybenzamine (alpha blocker) beta blocker eye drops*

 

 

 

 

 

 

 

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