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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.

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.

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

Coma and Depressed Level of Consciousness

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

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

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

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 signs	CVA: 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 cancer Immunosuppression	CT
Meningism	Meningitis or menigoencephalitis	Fever Meningococcal rash	LP CT
	Sub-arachnoid haemorrhage	‘Worst headache ever’ Subhyaloid hemorrhages SAH risk factors	LP CT
No focal signs or meningism (MESOT)	Metabolic causes: Hypoxia Hypercapnoea Hyponatraemia Hyperglycaemia Hypoglycaemia Hypo/hyperthermia Hypo/hyperosmolarity	History essential	SO2 ABG ETCO2 UEC BSL Temperature ketones
	Endocrine: Adrenal insufficiency Hypopituitarism Hypothyroidism Diabetic coma	Time course Steroid medications Phenotype	TFT free T3/4 Temperature BSL UEC Ca, PTH Cortisol
	Seizures (including eclampsia)	?witnessed ?post-ictal ?non-convulsive epilepsy	EEG CT for SOL
	Organ Failure Renal: uraemia Liver: PSE	Urine output History/exam findings of liver disease ? paracetamol OD	EUC LFTs, NH3 INR
	Toxins/drugs, especially: Sedatives Narcotics Alcohol Psychotropics Carbon monoxide Many other poisons!	Toxicology risk assessment	ABG analysis Specific drug levels Osmolality ECG
	Pseudocoma	history of mental illness history 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 Syndrome Local pathology/ trauma	Sympathetic paralysis Damage to sympathetics
Bilateral	Pontine lesion Thalamic haemorrhage Metabolic encephalopathy Senile miosis Argyll-Robertson pupils Holmes-Adie pupils Drug ingestion, eg. Organophosphate Barbiturate Narcotics	Sympathetic paralysis Mechanisms: Cholinesterase inhibition Central effects
Mydriasis (>5mm)
Unilateral	Uncal herniation Midbrain lesion	CN3 stretched on petroclinoid ligament CN3 nucleus damage
Bilateral fixed pupils	Bilat uncal herniation Massive midbrain bleed Hypoxic injuryDrugs: Atropine Tricyclics Sympathomimetics	Brain herniation Bilateral 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.

Hyperammonemia

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

AMS: Delirium, Stupor and Coma

Delirium

Coma and Depressed Level of Consciousness

Neuro Exam in the Comatose Patient

Etiology of Coma

Hyperammonemia

Reversible Posterior Leukoencephalopathy Syndrome (RPLS)

Coma with Pinpoint Pupils