Approach to unconscious patient

Level of consciousness:

• Fully conscious

• Drowsy – easily arousable by touch or noise, alertness persist for short period

• Stupor – arousable only by vigorous stimulation

• Coma – not arousable by any form of stimulus

Anatomy and physiology of coma:

• Reticular activating system (RAS) –

required to maintain alertness and

coherence of thought

• Causes of coma:

- lesion that damage RAS in upper midbrain

or its projections

- destruction of large portions of both

cerebral hemisphere

- suppression of reticulocerebral functions

by drugs, toxins or metabolic derangements

Causes of coma:1. Metabolic disturbance - drug / toxic - Diabetes mellitus – hypoglycemia - ketoacidosis - hyperosmolar coma - hyponatremia - uremia - hepatic failure - respiratory failure - hypothermia - hypothyroidism

2. Trauma - cerebral contusion - extradural hematoma - subdural hematoma

3. Cerebrovascular disease - subarachnoid hemorrhage - intracerebral hemorrhage - brain stem infarction/hemorrhage - cerebral venous sinus thrombosis

4. Infections - Meningitis - Encephalitis - Cerebral abscess - General sepsis

5. Others - Epilepsy - Brain tumor

Diabetic ketoacidosis• Complication of Type 1 DM• Precipitating factors:    Inadequate insulin administration    Infection (pneumonia/UTI/sepsis)    Drugs (cocaine)    Pregnancy

Symptoms:

-polyuria, thirst

-Abdominal pain

-Nausea, vomiting

-Shortness of breath

Signs:

-dehydration

-hypotension

-tachycardia

-Kussmaul breathing

-smell of acetone

-hypothermia

-confusion, drowsiness, coma (10%)

Hyperglycemic hyperosmolar non-ketotic diabetic coma

• complication of Type 2 DM

• due to sustained hyperglycemic diuresis

• prototypical patient is an elderly individual with type 2 DM,

with a several-week history of polyuria, weight loss, and diminished

oral intake that culminates in mental confusion, lethargy, or coma

• signs: dehydration, hypotension, tachycardia

• to differentiate from DKA:

i. evolution is over days

ii. No acetone odour on breath

iii. No Kussmaul respiration

iv. No abdominal pain

Hypoglycemia

• due to treatment with insulin and oral hypoglycemic drugs

• Symptoms:

i. Autonomic – sweating -hunger

- trembling -anxiety

- pounding heart

ii. Neuroglycopenic-confusion, drowsiness, convulsion, coma

-loss of fine motor skill, incoordination

Features Hypoglycemic coma DKA

History No food, too much insulin, unaccustomed exercise

Too little or no insulin, infection

Onset In good previous health ill health for several days

Symptoms Of hypoglycemia Of dehydration

Signs Full pulse Weak pulse

Normal or raised BP Low BP

Moist skin and tongue Dry skin and tongue

Shallow or normal breathing

Kussmaul breathing with acetone smell

Hepatic failure / hepatic encephalopathy

Liver fails nitrogenous waste(ammonia) builds up passes to brain

where astrocytes clear( glutamate to glutamine) excess glutamine

causes shift of fluid into cells cerebral edema

Grade:

I- altered mood, sleep disturbance

II- increasing drowsiness, confusion, slurred speech

III- stupor, restless

IV- coma

Other signs:

-Fetor hepaticus

-Asterixis

-Constructional apraxia

-signs of chronic liver failure if acute-on-chronic liver disease

Myxedema coma

• complication of hypothyroidism

• C/F: long standing history of hypothyroidism, usually elder patients

• precipitated by infections, hypoxia, hypercapnia, cardiac failure

• Looks of hypothyroid (pallor, coarse brittle diminished hair, puffy lids)

• hypothermia

• hyporeflexia

• convulsion

• may have episode of psychosis with delusions and hallucinations

‘myxedema madness’ before losing consciousness

• observe for goiter or any thyroidectomy scars

Drugs / poisons

OP poison – diarrhea, urinary incontinence, miosis, bradycardia, sweating,

emesis, lacrimation ; muscle twitching, fasciculations,

diminished respiratory effort; confusion, convulsion, coma

Opiates – miosis, bradycardia, hypothermia, respiratory depression, coma

Barbiturate, benzodiazepines – drowsiness, midposition/dilated pupil,

ataxia, nystagmus, minor hypotension,

respiratory depression, confusion, coma

Hypothermia

Causes:-Exposure-Alcoholic, barbiturate, sedative-Hypoglycemia-Peripheral circulatory failure-Extreme hypothyroidism

• Hypothermia itself causes coma only when temperature is <31℃

SeizuresGeneralized tonic-clonic seizures

-Altered consciousness at onset.

-Tonic phase:patient becomes cyanosed, does not breathe, heart rate changes

and may even stop, pupils dilated.

-Clonic phase: rhythmic jerks appear. Tongue may be bitten, urinary or

bowel incontinence may occur.

-In post ictal phase- patient may passed into coma also due to exhaustion

of energy reserves or locally toxic molecules by-product of seizures.

Not arousable, may be totally flaccid, plantar response extensor

Status epilepticus

-2 fits occur without recovery of consciousness in between

-A single fit last longer than 30 minutes with or without loss of

consciousness( some define as 5 minutes)

Epidural hematoma

-Etiology: head injury

-Typical lucid interval pattern: as ICP rises, patient will have increasing

headache, vomiting, confusion and comatose.

If bleeding continues, ipsilateral pupil dilates, coma deepens, bilateral

limb weakness

Breathing becomes deep, irregular (brainstem compression)

Subdural hematoma

-Etiology:

- Trauma (often forgotten)

- elderly (brain atrophy causing bridging vein atrophy)

- falls ( epileptics, alcoholics)

-Symptoms:

- fluctuating level of consciousness

- insidious physical or intellectual slowing

- headache

-Signs:

- of increased intracranial tension

Subarachnoid hemorrhage

Causes:-Aneurysm at circle of Willis-Arterio-venous malformation-Trauma-Mycotic aneurysm-Anticoagulant

C/F:

-Sudden onset of occipital headache, vomiting, seizures, stiff neck,

coma.

-Focal neurological deficits (may suggest site of aneurysm). Eg. 3rd nerve

palsy in posterior communicating artery aneurysm

Intracerebral hemorrhageCommonly occurs secondary to hypertension where penetratingbranches undergo degeneration.

Putamen is the most common site for hypertensive hemorrhage,

adjacent internal capsule is usually damaged Contralateral hemiparesis

When hemorrhages are large, signs of upper brainstem compression appear.

Coma ensues, accompanied by deep, irregular, or intermittent respiration,

a dilated and fixed ipsilateral pupil, and decerebrate rigidity

Pontine hemorrhages- deep coma with quadriplegia usually occurs

over a few minutes. Decerebrate rigidity and pinpoint pupils that react to light

Impairment of doll's-head reflex or by irrigation of the ears with ice water

Meningitis

-Pyogenic meningitis – headache, drowsiness, fever, vomiting, neck

stiffness, Kernig’s sign, Brudzinski’s sign

In severe case, may present in comatose condition.

-Viral meningitis usually benign in course unless associated with

encephalitis.

Encephalitis

-suspect encephalitis whenever patient presents with infectious prodrome:

- fever - lymphadenopathy

- rash - meningeal signs

together with encephalopathic behaviour:

- confusion

- disorientation

- poor coordination of movements

- focal neurological signs. Eg. Hemiparesis, aphasia

-Herpes simplex encephalitis – important to suspect as treatable

* Treat before exact cause is know

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