Transcript Coma - VCOMcc

Disorders of consciousness
Darlene Myles D.O.
2012



Define different levels of consciousness and coma
Know the Functional anatomy (structures involved in
levels of consciousness)
Know the Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Know the Emergency management for coma
Know the Possible etiologies
Know the Prognosis for Coma
Definitions


Consciousness
Consciousness may be defined as a state of awareness of
self and surroundings.
Alterations in consciousness are classified into two
types.
1) Affect arousal---Coma and encephalopathy ( focus of this
lecture)
2) Affect cognitive and affective mental function ( content of
mental function)-------Dementia, Delusion, psychiatric disorders.
State


Alert and awake
Lethargy

Stupor
with
environment,
stimuli other than pain
Obtunded

Comatose

Description of Patient
Normal state of arousal
fatigued with minimal difficulty
maintaining alertness
moderate reduction in alertness
decreased interest in
responsive to
unresponsiveness with arousal only
vigorous/painful stimulus, return to
unresponsiveness with removal of stimulus
unresponsive to noxious stimuli



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathies.
Prognosis for Coma
Consciousness Is Dependent on:
1)An Intact Ascending Reticular
Activating System (central
tegmental fasciculus)
2) Both Cerebral Hemispheres



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathies.
Prognosis for Coma
History





Onset
Recent complaints
Recent Injury
Prior Illness
Medications

A 57 year old female is brought in by EMS after
being found unresponsive.

What do you do first?

How do you get more history?

ABC’S

When do we intubate?

Why do we intubate?

Verbal responses






oriented speech
confused conversation
inappropriate speech
incomprehensible speech
no speech
Eye opening




spontaneous
verbal response
noxious response
none

Pupillary reactions



present
absent
Corneal responses
present
 absent



Spontaneous eye
movements




orienting
Roving
Miscellaneous
none




normal
full
minimal
none
Oculocephalic
responses

Oculovestibular
responses




Normal
Tonic conjugate
Dysconjugate
None

Respiratory pattern




regular
periodic
ataxic



Motor responses






obeys
localizes
withdrawals
abnormal flexion
abnormal extension
none
DTR’s


Normal
Increased
Decreased
Tone





Norm
Para
Flex
Ext
flaccid

The size, shape, reactivity, and centricity of the pupils is
extremely important in localizing the injury resulting in
coma.





Normal pupils strongly suggest the coma is not due to a
structural lesion of CNS.
Unilateral pupillary dilation is strongly suggestive of structural
injury.
Bilateral dilated pupils unresponsive to any light stimulus
(“fixed”) strongly suggests severe brain injury.
Bilateral midposition (6-8 mm) pupils unresponsive to light
indicates a midbrain lesion.
Pupils that are very small (“pinpoint”) strongly suggest a
medication effect (from opiates, benzodiazepine) or a lesion at
the pons.
Pupils in comatose patients
A patient’s response to pain is determined by
their level of arousal and any degree of CNS
injury. Possible responses include





Purposeful
Semi-purposeful
Random, non-purposeful
Decorticate (legs stiffly extended; arms flexed to
chest or neck)
Decerebrate (legs and arms stiffly extended)
A Glascow Coma Scale assessment often proves
valuable as a longitudinal measures of level of
consciousness, especially when the patient will be
examined serially in multiple settings.
This internationally standard scale rates purposeful
behavior on 3 axes: eye opening, verbal output, and
motor response to commend. The three axes have
maximum scores of 4, 5, and 6 respectively, for a
total score of 3-15.
Glasgow Coma Scale 3-15 *
Eye Opening
Never
To pain
To verbal
Spontaneous
Best Verbal Response
None
Sounds
Inapp words
disoriented
oriented
1
2
3
4
1
2
3
4
5
Best Motor Response
None
Extensor
Flexor Posture
Withdrawal
Localization
obeys
1
2
3
4
5
6



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathies.
Prognosis for Coma
Increased ICP/Herniation is a major life threatening
complication of coma, the following are the signs of
increased ICP/Herniation
 Pupils
Unilateral dilated pupil
Bilateral small poorly reactive pupils
 Eye movements
Third nerve palsy
Sixth nerve palsy
Can be assessed by cold caloric
 Fundoscopy
Signs of papilledema?
 Respiratory pattern?
Increased ICP Can be detected by a deterioration in
mental status, pupils, or motor exam
- Withdrawal to pain transitioning to
flexor withdrawal
- Flexor withdrawal to extensor posturing
Decortication-Flexor withdrawal-lesion above red
nucleus
Decerebration-Extensor posturing-lesion below
red nucleus
Compression of the midbrain from uncal herniation
causes loss of consciousness by damaging the
reticular activating system, pupil dilation and loss of
the light reflex by stretching of the third cranial
nerve and its associated parasympathetic fibers,
and abnormal posturing responses in the
contralateral arm and leg from damage to the
pyramidal fibers in the crus cerebri.

Uncal herniation
 Temporal lobe lesion protrudes through the tentorial
notch
 Structures impinged include the posterior cerebral
artery, the contralateral peduncle and the midbrain.
 Neurological findings may be unilateral dilated pupil
from ipsilateral CN III compression, oculomotor palsy,
homonymous hemianopia, contralateral hemiparesis

Central herniation


Midline tumor compresses basal ganglia, thalamus
and midbrain
Neurological findings may be small pupils,
lethargy, Cheyne-Stokes respirations

Tonsillar herniation
Posterior fossa tumors compress downward into the
foramen magnum
 Neurological findings may be posterior head ache,
cough induced syncope, vomiting, respiratory changes
 May be due to hemispheric lesions which cause
herniation of the cerebellar tonsils downward through
the foramen magnum. Compression of the medulla. This
can cause respiratory arrest and death.




Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathies.
Prognosis for Coma
Immediate assessment should focus on the
following reversible causes:
 R/O Neurosurgical Etiology- neoplasm, bleed
impending herniation
 R/O Infectious etiology
 R/O Epileptic Etiology
 R/O Metabolic Etiology (chratic is the most common)



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathies.
Prognosis for Coma


Ensure that the comatose patient’s basic metabolic parameters
are able to support brain function.
Remember to check
 Blood gases/Oxygen saturation (COPD)
 Hemoglobin and hematocrit (acute GI bleed)
 Sodium, potassium, calcium, BUN, glucose
 Liver enzymes




Management for Increased ICP
 Hyperventilation:
 Reduces ICP immediately, peak effect 1-2 hours
 NO BENEFIT TO drop PCo2 < 25, Ideal = 30
Mannitol:
 Onset in 30 minutes lasts 4-6 hours
Mannitol and lasix are synergistic.
 1 - 2 grams/kg bolus
 0.5 - 1 gram/kg every 6 hours
 Monitor sodium, osmolality, BUN
Hyperosmolality with 3% NaCl



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History and Physical examination
2. Life threatening complications.
3. Reversible causes of coma



Emergency management for coma
Possible etiologies and common encephalopathy.
Prognosis for Coma


Vascular
 Bilateral cerebral infarction
 Brainstem infarction
 Intracerebral hemorrhage
 Subarachnoid hemorrhage
Infections
 Bacterial/Tuberculous/Syphil
itic meningitis
 Viral encephalitis
 Postinfectious encephalitis
 Typhoid fever
 Malaria

Trauma





Subdural hematoma
Epidural hematoma
Diffuse axonal injury
Cerebral contusions
Toxic






Lead
Thallium
Cyanide
Methanol
Ethylene glycol
Carbon monoxide




Anoxic
Metabolic
 Hypoxia
 Hypercapnia
 Hypo/hypernatremia
 Lactic acidosis
 Hypermagnesemia
 Reye syndrome
 Aminoacidemia
 Wernicke's encephalopathy
 Porphyria *
 Hepatic encephalopathy *
 Uremia
Iatrogenic Disorders
Neoplasm

Drugs

Sedatives

Alcohol

Opiates

Salicylates

Tranquilizers

Anticholinergics

Lithium

Phencyclidine
Endocrine /Epilepsy/Emotional

Hypoglycemia

Hyperglycemic non-ketotic coma

Diabetic ketoacidosis

Myxedema coma/Thyroid storm

Addisonian crisis

Post-ictal state
Others

Shock

Fat embolism

Hypertensive encephalopathy

Hydrocephalus

Hypo/hyperthermia



A 65 year old white male presents via EMS
unresponsive. He has a long standing history
of COPD.
What is the probable cause of Coma?
What would you do First?
Several different states of impaired cognition or
consciousness may appear similar to coma or may be
confused with it.



Locked-in syndrome: Patient alert and aware, quadriplegic with
lower cranial nerve palsy. Lesion locates at bilateral ventral
pontine.
Persistent vegetative state: Absent cognitive function but
retained “vegetative” components. Extensive cortical gray or
subcortical white matter with relative preservation of
brainstem
Catatonia: Mute, with marked decrease in motor activity. It is
a psychiatric disease.



A 32 year female brings her 5 year old son to be
evaluated for a fever. While checking in she
collapses and is unresponsive. The child
reports that his mother was complaining of a
headache.
What do you do first?
What could it be?



Definitions of different levels of consciousness and coma
Functional anatomy ( structures involved in levels of
consciousness)
Emergency evaluation for coma
1. History
2, Physical examination



Emergency management for coma
Possible etiologies.( what is the lesion?)
Prognosis for Coma

In view of the current state of knowledge, outcome in any
comatose patient cannot be predicted with 100% certainty
unless that patient meets the criteria for brain death


Only about 15% of patients in non-traumatic coma make a
satisfactory recovery.
Functional recovery is related to the cause of coma.





Diseases causing structural damage, such as cerebrovascular disease including
subarachnoid hemorrhage, carry the worst prognosis
Coma from hypoxia-ischemia due to such causes as cardiac arrest has an
intermediate prognosis
Coma due to hepatic encephalopathy and other metabolic causes has the best
ultimate outcome.
Age does not appear to be predictive of recovery
The longer a coma lasts, the less likely the patient is to regain
independent functioning.

The prognosis for traumatic coma differs from that
for nontraumatic coma in many ways.
Many patients with head trauma are young.
 Prolonged coma of up to several months does not preclude a
satisfactory outcome in traumatic coma.
 In relationship to their initial degree of neurological abnormality,
traumatic coma patients do better than nontraumatic coma
patients.

Coma
Coma is a medical emergency that requires urgent
diagnosis and treatment.
Coma should be distinguished from related states such
as stupor, the persistent vegetative state, akinetic
mutism, locked-in-state, catatonia, and pseudocoma.
The clinical approach begins with treatment of
immediate life threatening complications followed
by a comprehensive evaluation for reversible causes
of coma.
The best prognosis is for patients with coma from
trauma, metabolic, toxic or infectious causes.