COMA

RELATED DISORDERS OF CONSCIOUSNESS

COMA

= suspension of consciousness a state of continuous awareness of one self and one environment

Consciousness depend by the integrity of reticular activating system of the upper brainstem = paramedian regions of the upper (rostral) pontine and midbrain tegmentum + thalamic nuclei (PM, parafascicular, medial portion of centromedian and intralaminar)

Receive collaterals of the direct spinothalamic pathways

whole cerebral cortex

modulates the incoming information via corticofugal projections to the reticular formation

Coma-producing alterations in the brain are of two main types

I one clearly morphologic

a) discrete paramedial lesions in the upper brainstem and lower diencephalon

b) widespread bilateral damage to the cortex and subcortical white matter

(traumatic damage, bilateral infarcts, hemorrhages,encephalitis, hypoxia)

II submicroscopic suppression of neuronal activity =metabolic, drugs , toxin

Mass lesion cause coma

a) Direct extension of the lesion into the diencephalon and midbrain

b) Lateral displacement of deep central structures, often with temporal lobe herniation compression, ischemia and secondary hemorrhages in the midbrain and subthalamic region

central syndrome with downward displacement and bilateral compression of the upper brainstem ! rostral-caudal deterioration of brainstem function apathy, confusion, drowsiness , coma

Miotic pupils

uncal syndrome with unilateral displacement and uncal gyrus herniation the Kernohan Woltman sign = compression of the opposite cerebral peduncle Babinski sign and hemiparesis controlateral to the original hemiparesis

! Differs mainly in that drowsiness in the early stages is accompanied or preceded by unilateral pupillary dilatatation (most often on the side of the mass)

3-5 mm drowsiness

5-8 mm stupor

8-9 mm coma

Diagnosis

A. Positive diagnosis -1) Anamnesis antecedents, circumstances in which the person was found, use of medications

2) Clinical exam - * general physical exam

* nuchal rigidity

* fundoscopy

**neurologic

3) Laboratory studies and imaging

B. Differential diagnosisC. Causes of coma= Aethiological diagnose

! Coma is not a disease per se but is always a symptomatic expression of an underlying disease.

When the comatose patient is first seen quickly make certain airway is clear

no bleeding

IV access

cervical stabilisation

Alterations in vital signs

A. TEMPERATURE - fever ! Intoxication with anticholinergic

hypothermia ! Alcohol,barbiturate, myxedema

B . RESPIRATION RATE slow breathing ! Barbiturate, opiate

rapid ! Diabetic and uremic acidosis (Kussmaul respiration)

C. PULSE RATE slow ! Cushing fen.

D. BLOOD PRESSURE HTA - ! Increased intracranial pressure

- hTA !!!

E. INSPECTION OF THE SKIN

F. ODOR OF THE BREATH

NEUROLOGIC EXAMINATION

A. Posture of the limbs and body

B. Presence or absence of spontaneous movements

- seizures

- multifocal myoclonus metabolic disorder (uremia, anoxia, drug intoxication)

- decorticate rigidity lesions at a more rostral level of the nervous system in the cerebral white matter or internal capsule and thalamus

- decerebrate rigidity damage to motor tracts in upper pons or midbrain = lesion below the level of the red nucleus

Reaction to noxious stimuli

NEUROLOGIC EXAMINATION
the brainstem reflexes = pupillary response to light, eye movements, corneal responses, respiratory pattern

D. Ocular movement resting position and spontaneous movements of the globes

- deviation of one eye

- conjugate deviation ! The eyes look toward a hemispheral lesion and away from a brainstem lesion

- ocular bobbing lesions in tegmentum of the midbrain and pons

// ocular dipping intoxications and anoxia

- oculocephalic reflexes = dolleye movement !Not present in a normal alert person // absence= damage within the brainstem

- oculovestibular or caloric response // absence = damage within the brainstem

absence of nystagmus despite conjugate deviation = cerebral hemispheres damage

NEUROLOGIC EXAMINATION

E. Pupillary reactions - pupil diameter ! Enlarged pupil > 5mm

- the pupillary reactions ! With coma due to drug intoxications and metabolic disorders, pupillary reactions are usually spared

F. Eyelids and Corneal response loss= deepening loss of consciousness

G. Respiratory pattern less localizing value

Kussmaul, Cheyne Stokes, apneustic breathing, agonal gasp

LEVELS OF CONSCIOUSNESS

CONSCIOUSNESS normalCONFUSED disoriented,impaired thinking and responsesDELIRIOUS disoriented, restlessness, hallucinations, sometimes delusions ! State I which hyperactivity is proeminent/ signs of the overactivity of the autonomic nervous system SOMNOLENT sleepyDROWSINESS inablity OBTUNDED decrease alertness, slowed psychomotor responsesSTUPOROUS sleep like state (not unconscious) little/no spontaneous activityCOMATOSE cannot be aroused; no response to stimuli

Other neurologic conditions that simulate coma

VEGETATIVE STATE= awake but nonresponsive state Yawning, coughing,swallowing and limb and head movements persist = awake coma. Respiratory and autonomic functions are retained.These people have emerged from coma after a period of days or weeksAKINETIC MUTISM = partially or fully awake state in which patient is immobile and muteLesions situated on the orbitofrontal surfacesLOCKED IN STATE = an awake patient has no means of producing speech or volitional movement, but retains vertical eye movements and lid elevation MORSE CODELesions that transect corticospinal and corticobulbar pathways infarcts or hemorrhage of the ventral pons , pontine myelinolisis, Guillain- Barre syndr., critical illness neuropathy ! PSYCHOGENIC COMA

Classification of Coma and Differential Diagnosis

I. Diseases that causes no focal or lateralizing neurologic signs, usually with normal brainstem functions,CT scan and cellular content of the CSF are normal.

A. Intoxication: alcohol, barbiturates and other sedative drugs, opiates, etc.

B. Metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic coma, hypoglycemia, addisonian crisis, profound nutritional deficiency.

C. Severe systemic infections:pneumonia, typhoid fever, malaria, septicemia, Waterhouse-Friderichsen syndrome.

D. Circulatory collapse from any cause.

E. Postseizure states.

F. Hypertensive encephalopathy and eclampsia.

G. Hyperthermia or hypothermia.

H. Concussion

I. Idiopathic recurring stupor and coma.

J. Acute hydrocephalus.

II. Disease that cause meningeal irritation with or without fever , with an excess of WBCs or RBCs in th CSF usually without focal or lateraliizng cerebral or brainstem signs. A. subarachnoid hemorrhage from rupture aneurism arteriovenous malformation,occasionally traumaB. acute bacterial meningitis C. some forms of viral encephalitisIII Disease that cause focal brainstem or laterally cerebral signs, with or without changes in the CSF. CT and MRI are usually abnormalA. hemispheral hemorrhages or infarctionB. brainstem infarction due to thrombosis or embolismC. brain abscess, subdural empyema.D. epidural and subdural hemorrhage and brain contusionE. brain tumorF. miscellaneous : cortical vein thrombosis, some of forms viral encephalitis , focal embolic encephalomalacia due to bacterial endocarditis, acute hemorrhage, leukoencephalitis, disseminated postinfection, encephalomyelitis, and others

TREATMENT

AIRWAY tracheal intubationIV ACCESS naloxone

+ dextrose

+ thiamine (avoid provoking Wernicke disease)

AETHIOLOGICAL TREATMENT

BRAIN DEATH - CRITERIA

Coma of a known causeAbsence of motor responsesAbsence of brainstem reflexes (pupillary, corneal, caloric, gag)Absence of coughing in response to tracheal suctionAbsence of respiratory drive at a PaCO2 60mmHg or 200mmHg above baseline= APNEA TESTInterval between exam usually 6hPerform confirmatory tests cerebral angiography EEG recording are obtained for at least 30min with a 16-18 channel TCD both MCA and AV nuclear imaging with technetium