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Approach to coma

NATESAN D

Consciousness

y Wakefulness / Arousal - (Sleep wave cycle) y Perception - Awareness of self and

environment ( Sensory System) y Reaction - Meaningful responsiveness (Motor system)

State of consciousness
Alert: Normal state of arousal Lethargy: responds-to verbal stimuli although slow and inappropriate. Stupor: the subject can be aroused only by vigorous and repeated noxious stimuli. Coma: unarousablely unresponsive.

Coma mimics

y Psychogenic unresponsiveness y Locked in syndrome y Akinetic mutism y Catatonia y Persistent vegetative state

Coma Pathophysiology

Coma Pathophysiology
y Coma implies dysfunction of:  Ascending Reticular Activating System or  Both hemi-cortices y Anatomically, this means  central brainstem structures (bilaterally) from caudal medulla to rostral midbrain  both hemispheres

The Comatose Patient

Classifications
y Supratentorial lesions cause coma by either widespread bilateral disease, increased intracranial pressure, or herniation. y Infratentorial lesions involve the RAS, usually with associated brainstem signs y Metabolic coma causes diffuse hemispheric involvement and depression of RAS, usually without focal findings y Psychogenic
Plum and Posner, 1982

Supratentorial Lesions
y Epidural or Subdural

Hematoma y Intraparenchymal haemorrhage y Large Ischemic Infarction y Tumour y Trauma y Abscess

Supratentorial Mass Lesions

Pathophysiology
y Altered consciousness is based on
Increased intracranial Herniation Diffuse bilateral

pressure

lesions

Herniation syndromes
1. 2. 3. 4. 5. 6.

Transtentorial Central Subfalcine Transcalvarial Upward Tonsillar

Herniation Syndromes
Central herniation Rostral caudal progression of respiratory, motor, and pupillary findings May not have other focal findings Uncal herniation Rostral caudal progression CN III dysfunction and contralateral motor findings

Transtentorial herniation and brainstem infarction in a patient with melanoma

Supratentorial Mass Lesions

Differential Characteristics
Initiating signs usually of focal cerebral dysfunction Signs of dysfunction progress rostral to caudal Neurologic signs at any given time point to one anatomic area diencephalon, midbrain, brainstem Motor signs are often asymmetrical
Plum and Posner, 1982

Rostral Caudal Progression

Breathing in coma
y Forebrain  Post hyperventilation apnea  Cheyne stoke respiration y Hypothalamus midbrain  Central neurogenic hyperventilation

Breathing in coma
y Lower pontine tegmentum  Apneustic breathing  Cluster breathing  Short cycle periodic breathing  Ataxic breathing y Medulla  Ataxic breathing  Slow regular respiration  Gasping (terminal)

Posture
y Cerebral


hemisphere
Decorticate posture Diagonal posture

y Diencephalon


supratentorial

y Upper brain stem  Decerebrate posture y Pontine  Abnormal ext arm  Weak flexion leg y Medullary  Flaccidity

Rostral Caudal Progression

Pupil size & Pupil reactivity

Rostral Caudal Progression

PUPIL
Diencephalic (metabolic) Midbrain tectal Midbrain nuclear 3rd nerve Pontine Opiate Organophosphorus Atropine

Small reactive Midsize,fixed Irregular pear shaped Fixed widely dilated Pinpoint reactive Pinpoint Small Wide dilated

The pupils usually are symmetrical in coma from toxic-metabolic causes. Patients with metabolic or toxic encephalopathies often have small pupils with preserved reactivity. Exceptions
- methyl alcohol poisoning: dilated and unreactive pupils - Late toxic or metabolic coma(terminal asphyxia) the pupils dilate initially and then become fixed at midposition within 30 minutes

y Pupillary reactivity is relatively resistant to

metabolic insult and usually is spared in coma from drug intoxication or metabolic causes, even when other brainstem reflexes are absent.
y Exceptions  Hypothermia may fix pupils  severe barbiturate intoxication may fix pupils  neuromuscular blocking agents produce midposition or small pupils  glutethimide and atropine dilate pupils

Infratentorial Lesions
y Cause coma by affecting reticular activating

system in pons y Brainstem nuclei and tracts usually involved with resultant focal brainstem findings

Infratentorial Lesions

Causes of Coma
y Basilar artery y

y y y

thrombosis Pontine or Cerebellar Hematoma Ischemic Cerebellar Infarction Tumour Abscess

Infratentorial Mass Lesions

Differential Characteristics
y History of preceding brainstem dysfunction or

sudden onset of coma y Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality y Cranial nerve palsies usually present y Bizarre respiratory patterns common, usually present at onset of coma
Plum and Posner, 1982

Ocular motility

Asymmetry in oculomotor function typically is a feature of structural lesions

Spontaneous and reflex eye movements


y Roving eye movements with full excursion are

most often indicative of metabolic or toxic abnormalities


y Reflex eye movements normally are intact in toxic-

metabolic coma
y Exceptions:  rarely in phenobarbital or phenytoin intoxication .

Eye movements: Examination


y Position at rest  Straight ahead  Dysconjugate  Conjugate deviation y Oculocephalic reflex  Positive Dolls eyes  Negative Dolls eyes y Oculovestibular reflex  Cold calorics

y Resting position  Midline


Deviation suggests

frontal/pontine damage


Conjugate
Dysconjugance suggests

CN abn.


Moving
Roving, dipping, bobbing

Eye movement

y Metabolic  Roving eye movement,  Oculocephalic,  Vestibuloocular y Supratentorial  Contralateral conjugate palsy y Thalamus  Upper turn down

Eye movements in Coma

y Midbrain  Ipsilateral 3rd cranial nerve paresis y Pontine  Ipsilateral 6th cranial nerve paresis  Ipsilateral gaze palsy  One and half syndrome  Bilateral gaze palsy  Ocular bobbing

Eye movements
y Oculocephalic reflex  Eye response to head turning  Proprioception from the neck triggers the pontine conjugate eye center

Eye movements
y Oculovestibular reflex  Eye response to cold water on the tympanic membrane  Horizontal semicircular canal stimulation triggers the pontine conjugate eye center

Caloric reflex
y Ensure TM integrity y Elevation of head to 30

y Watch for conjugance of

degrees (so that lateral semicircular canal is vertical) y Instillation of up to 10 ml of ice water


deviation y To test vertical eye movements




Awake: deviation toward,nystagmus away Comatose: deviation toward

Both ears, cold waterdownward gaze Both ears, warm waterupward gaze

y Wait 5 minutes, do other

ear

Metabolic Coma

Etiologies
y Respiratory
 

Hepatic

Hypoxia Hypercarbia Hypoglycemia Hyponatremia Hypercalcemia

y Electrolyte
  

encephalopathy Severe renal failure Infectious


Meningitis Encephalitis

Toxins,

drugs

Metabolic Coma

Differentiating Features
y Confusion and stupor commonly precede motor y y y y

signs Motor sings are usually symmetrical Pupillary reactions are usually preserved Asterixis, myoclonus, tremor, and seizures are common Acid-base imbalance with hyper- or hypoventilation is frequent
Plum and Posner, 1982

Differentiating Toxic-Metabolic Coma from Structural Coma


y History: the patient's underlying illnesses and

medications, or the setting in which they are found. y The response to initial emergency therapy may help differentiate metabolic or toxic causes of coma y Structural lesions have focal features or at least notable asymmetry on neurological examination. Toxic, metabolic, and psychiatric diseases are characterized by their symmetry

Differentiating Toxic-Metabolic Coma from Structural Coma


y Patients with metabolic problems often have

milder alterations in arousal, typically with waxing and waning of the behavioral state
y Patients with acute structural lesions tend to stay

at the same level of arousal or progressively deteriorate


y Toxins may also cause progressive decline in level

of arousal

Causes of Coma

More than half of all cases of coma are due to metabolic brain dysfunction (Almost half of these are drug poisonings)

Causes of Coma

y Plum and Posner 1982


500
101

consecutive cases of coma

supratentorial (44/101 ICH) 65 subtentorial lesions (40/65 brainstem infarcts) 326 diffuse or metabolic brain dysfunction
149

drug intoxication

Management of the Comatose Patient


o Airway, Breathing, Circulation with neck stabilization.

o Brief history & examination o I.V. line & sampling o Treat reversible causes of coma

supplemental oxygen intravenous thiamine (at least 100 mg) intravenous 50% dextrose in water (25 g) Naloxone hydrochloride intravenously, (0.4 to 2.0 mg) o Treatment of ICP until surgical intervention is possible. o Comprehensive history and secondary examination

Management of the Comatose Patient

Airway
y Intubate anyone who will let you y Any of the following are adequate criteria
o o o o o

GCS < 9 Airway not secure or open Breathing not adequate Any significant respiratory failure Uncertainty regarding direction or rate of mental status changes, particularly if constant observation not available (during CT scans, etc..)

Management of the Comatose Patient

Circulation
y Is patient in shock?
Check pulses, heart rate, blood pressure, perfusion Remember hypotension is late sign of shock Bradycardia and Hypertension can be sign of raised intracranial pressure.

Management of the Comatose Patient

Disability - Neurologic
y Glasgow coma scale  Provides easily reproducible  Allows rapid assessment and record of baseline neurologic status  Allows physician to track neurologic changes over time and multiple examiners

Glasgow Coma Scale


y Three components. Score derived by adding the

score for each component.


Eye opening (4

points) Verbal response (5 points) Best motor response (6 points)

Glasgow Coma Scale


y Eye opening

4 - spontaneous 3 - to speech 2 - to pain 1 - none

y Best Motor Response


6

y Verbal Response

5 - oriented 4 - confused conversation 3 - inappropriate words 2 - incomprehensible sounds 1 - none

- obeys 5 - localizes 4 - withdraws 3 - abnormal flexion 2 - abnormal extension 1 - none

Management of the Comatose Patient

Secondary Survey
y Do a quick general exam of the entire body to

identify acute life threatening conditions y Only very rarely is acute neurosurgical intervention appropriate before other acute life threatening injuries are stabilized

Neurologic Examination

Secondary Survey
Posner et al (2008), the key components of the
neurological examination of the comatose patient are:
y level of consciousness (GCS) y the pattern of breathing y size and reactivity of the pupils y eye movements and oculovestibular responses y motor responses (tone, reflexes and posturing)

LOCATION Bilateral hemispheric damage or dysfunction

ABNORMAL FINDINGS Symmetric tone and response (flexor or extensor) to pain Myoclonus (possible) Periodic cycling of breathing

Supratentorial mass Ipsilateral 3rd cranial nerve palsy with unilateral dilated compressing the fixed pupil and oculomotor paresis brain stem Contralateral homonymous hemianopia and absent blinking response to visual threat Contralateral hemiparesis Brain stem lesion Early abnormal pupillary and oculomotor signs Abnormal oculocephalic & oculovestibular reflex Asymmetrical motor responses Decorticate rigidity (usually due to an upper brain stem lesion) or decerebrate rigidity (usually due to a bilateral midbrain or pontine lesion) Hyperventilation (due to a midbrain or upper pontine lesion) Spontaneous, conjugate roving eye movements in mild coma Fixed eye position in deeper coma Abnormal oculovestibular reflex Decorticate and decerebrate rigidity or flaccidity

Toxic-metabolic dysfunction

Management and Evaluation of the Comatose Patient


y Does the patient have a rapidly

progressive intracranial lesion? y Assume yes, if:


   

1. Any evidence of brainstem abnormality 2. Any evidence of rostral caudal progression 3. Any focal deficits 4. Progression of motor exam from withdrawal to posturing

y If any factor is present, assume raised ICP,

herniation and irreversible damage imminent


    

Intubate Hyperventilate Mannitol CT scan neurosurgical intervention

y If none of the findings are present, surgical

lesion less likely than metabolic cause y Mass lesion still possible, though - CT scan y Urgency of intubation less but should consider


Will patient deteriorate, particularly while out of constant observation (CT scanner)? Can patient protect airway?

Coma mimics

y Psychogenic unresponsiveness y Locked in syndrome y Akinetic mutism y Catatonia y Persistent vegetative state

Persistent vegetative state


y Absent cognitive function . y Retained vegetative components y Extensive cortical grey or subcortical white matter

involvement with relative preservation of the brainstem.

Akinetic Mutism
y Silent, immobile but alert appearing y Usually due to lesion in bilateral mesial frontal lobes,

bilateral thalamic lesions or lesions in periaqueductal grey (brainstem)

Locked-In Syndrome
y Infarction of basis pontis (all descending motor

fibers to body and face) y May spare eye-movements y Often spares eye-opening and vertical movements y EEG is normal or shows alpha activity

Catatonia
y Symptom complex associated with severe

psychiatric disease with:


 

Mutism with marked decrease in motor activity can also be seen in organic brain disease: encephalitis, toxic and drug-induced psychosis

Thank you

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