Transcript COMA
COMA
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Coma= State of deep sleep
Coma is a profound state of unconsciousness.
A person in a coma cannot be awakened
Fails to respond normally to pain, light or sound
Does not have sleep-wake cycles, and
Does not take voluntary actions.
A person in a state of coma can be described as
comatose.
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Unconsciousness
Syncope
Brain death
Locked-in syndrome
Vegetative state
• All persons in coma are unconscious, but all
who are unconscious are not in coma
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• Unconsciousness/ loss of consciousness or
lack of consciousness, is an alteration of
mental state that involves complete or nearcomplete lack of responsiveness to people and
other environmental stimuli.
– Being in a comatose state or coma is an
illustration of unconsciousness.
– Fainting due to a drop in blood pressure and a
decrease of the oxygen supply to the brain is an
illustration of a temporary loss of consciousness.
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• Syncope is the medical term for fainting, a
sudden, usually temporary, loss of
consciousness
• Generally caused by insufficient oxygen in the
brain either by
– Cerebral hypoxia
– Hypotension
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• Brain death is the irreversible state when
there is no brain activity (including involuntary
activity necessary to sustain life) due to total
necrosis of the cerebral neurons following loss
of brain oxygenation
• Reflexes in brain death
• Pupillary response – none (fixed pupils)
• Oculocephalic reflex- none
• Corneal reflex- None
• Response to the caloric reflex test- none
• Spontaneous respirations- None
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• Locked-in syndrome is a condition in which a
patient is aware and awake but cannot move
or communicate verbally due to complete
paralysis of nearly all voluntary muscles in the
body except for the eyes.
– It is the result of a brain stem lesion in which the
ventral (anterior) part of the pons is damaged
– Also k/a cerebromedullospinal disconnection, deefferented state, pseudocoma, and ventral
pontine syndrome
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• A vegetative state is a condition of patients
with severe brain damage who were in a
coma, but progressed to a state of partial
awareness.
• After four weeks in a Vegetative State (VS),
the patient is classified as in a Persistent
Vegetative State.
• This diagnosis is classified as a Permanent
Vegetative State (PVS) after approximately 1
year of being in a Persistent Vegetative State.
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COMA contd..
• Patients in the deepest level of coma:
– Do not respond with any body movement to pain,
– Do not have any speech, and
– Do not open their eyes
• Comas typically last for no more than a few
weeks.
• However, if the coma continues, the patient is
usually considered to be in a persistent vegetative
state
• Very less chance of awakening after remaining in
that state for one year.
• Level of consciousness can be measured by GCS
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Glasgow Coma Scale (GCS)
Eye Opening (E)
Verbal Response (V)
Spontaneous
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Oriented
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To loud voice
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Confused, Disoriented
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To pain
2
Inappropriate words
3
None
1
Incomprehensible words
2
None
1
Motor Response (M)
Obeys commands
6
Localizes pain
5
Withdraws from pain
4
Abnormal flexion
posturing
3
Extensor posturing
2
None
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Level of consciousness
E+M+V
Lowest score = 3 (Deep coma)
Highest score = 15 (Fully awake or aware)
Spontaneous Eye Opening +
Obeys command+
Oriented +
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CAUSES OF COMA
• Vascular
• Infectious
• Neoplastic
• Degenerative
• Inflammatory-immunologic
• Congenital-developmental
• Autoimmune
• Toxic/ traumatic
• Endocrine/ metabolic
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Causes of COMA
1. Metabolic disturbances
Diabetes- Hypoglycemia/ DKA/ HONK
Toxins-> Hepatic Failure (Ammonia)/
Respiratory failure (CO2)
Hypothermia/ Hyponatraemia/ Uremia
Drug Overdose/ Alcohol
4. Infections
Meningitis
Encephalitis
Cerebral abscess
2. Trauma
Cerebral Contusions
Extradural/ Subdural hemorrhages
hemorrhages
5. Others
Epilepsy-> Status Epilepticus
Tumor
Thiamine deficiency
3. Cerebrovascular diseases
SAH/ ICH
Brain stem infarction thrombosis
Cerebral venous sinus thrombosis
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History
1. Events from attendance/ visitors focusing on
probable causes
– Trauma, Drug ingestion, Alcohol
– Rapidity with which neurologic symptoms
developed
– Preceding medical/Neurologic symptoms (Fever,
Headache, Vomiting, Seizures, dizziness,
Diplopia)
– Medical diseases:
Hepatic/Renal/cardiac/Respiratory
– Past history: TIA, Stroke
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When approaching a patient with a neurologic
disorder look for:
Location of the lesion
Cerebrum
Cerebellum
Brainstem
Spinal cord
Nerve root
Peripheral nerve
Neuromuscular junction
Muscle
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General physical examination:
1. Vitals: Pulse, BP, Temperature, Respiratory
rate and pattern of breathing
2. Oxygen saturation
3. Skin rash
4. Bleeding manifestation
5. Odor
6. Anemia/ Jaundice/ Cyanosis
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Pattern of Breathing:
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Cheyne-stokes breathing Periods of apnea
alternate with periods of hyperapnea seen in Brain
damage (bihemispheral damage)due to cerebral
hemorrhage or trauma
Kussmaul’s respiration Deep and rapid
respiration due to stimulation of respiratory center
seen in Metabolic acidosis due to Ketoacidosis or
Uremia
Hyperventilation Rapid and shallow breathing
resulting in alkalosis and tetany
Ataxic breathing Irregular in time and depth
seen in Brain stem damage.
Shallow,slow,regular Metabolic/Drug related
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Neurologic assessment:
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First observe the patient without intervention
Assess the level of arousal/Elicited movements
Glasgow coma scale
Response to noxious stimuli
Pupillary light reflex:
Normal reactive mid size pupil Excludes mid brain
lesion
One unreactive and dilated pupil Compression of
third cranial nerve
Bilateral dilated and unreactive pupil Severe mid
brain damage
Reactive but bilateral small pupil Metabolic
encephalopathy, Deep hemispheric lesion
Bilateral pin point pupil Pontine hemorrhage,
Barbiturate/ Opoid overdose
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6.Ocular movements:
• Note resting eye position
• Look for rectus palsy
• Roving movements
• Nystigmus
7.Oculocephalic reflex:
• Elicited by moving head from side to side
• Doll’s eye reflex
8.Oculovestibular reflex:
• Caloric stimulation:
• Irrigating external auditory canal with either cold or warm
water Observe for the tonic deviation of the eyes
Remember“COWS”
9.Corneal reflex
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10.Other Neurologic examination in detail
• Cranial nerve
• Motor
• Meningeal signs
• Skull and Spine
SYSTEMIC EXAMINATION:
• Cardiac
• Respiratory
• Hepatic
• Renal
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Investigation:
1. Blood:
• TC, DC, Hb
• Glucose, Electrolytes, Calcium, Urea, Creatinine,
ABG, NH3
• Toxicological screening
2. CSF analysis
3. Neuroimaging
• CT scan head
• MRI head
4. EEG
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Contraindications of investigations:
• Signs and symptoms of raised ICP (Papilloedema,
decreased LOC, progressive deficit, headache)
due to mass lesion
• Do CT first and then proceed to lumbar puncture
(LP) if there is no neurologic findings suggestive
of localized mass lesion
• Obstructive hydrocephalus, or evidence of blood
infection at LP site
• Coagulopathy (e.g. anticoagulant drugs) or
thrombocytopenia
• Developmental abnormality (i.e. tethered spinal
cord)
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Diagnostic Tests with CSF:
• Opening pressure
• Protein
• Glucose
• Cell counts
• Color
• VDRL
• Viral PCR
• IgG levels
• Oligoclonal bands
• Fungal antigens
• Microbiological stains (Gram, ZN, fungal)
• Bacterial culture and PCR
Correlate with typical CSF Findings in CNS Infections
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Management:
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Immediate goal: to prevent further brain damage
ABC
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Oropharyngeal airway
Tracheal intubation
Correction of Hypotension
Securing IV access/Drawing blood samples
Hypo/Hyperthermia
3. Treat the metabolic cause:
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Glucose, Electrolytes, Acid Base imbalance
4. Antidotes:
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Naloxone (For morphine/ heroin)
5. Assess for head injury/ Cervical spine injury
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Control of Raised ICP
Head end elevation:15-30 ̊
Hyperventilation to decrease PaCo2
Osmotic agent: Mannitol, Furosemide, Glycerol
Control of seizures
Treatment of underlying cause
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• Advanced Life Support (ALS)
– Emergency medical care for sustaining life, including
defibrillation, airway management, and drugs and
medications
• The Basic Life Support (BLS)
– Provide a wide variety of healthcare professionals
the ability to recognize several life-threatening
emergencies, provide CPR, use an Automated
External Defibrillator (AED), and relieve choking in a
safe, timely and effective manner
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DNR (Do Not Resuscitate)
• A do not resuscitate
document, often called a
living will, is a binding
legal document that states
resuscitation should not
be attempted if a person
suffers cardiac or
respiratory arrest.
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• Intracranial pressure (ICP) is the pressure inside
the skull [Brain tissue and cerebrospinal fluid
(CSF)].
• CSF pressure can be influenced by abrupt
changes in intrathoracic pressure during coughing
(intraabdominal pressure), valsalva
(Queckenstedt's maneuver).
• ICP is measured in millimeters of mercury
(mmHg)
– At rest, is normally 7–15 mmHg for a supine adult
– −10 mmHg in the vertical position
• At 20–25 mm Hg (The upper limit of normal)
treatment to reduce ICP is needed.
• Measured by intracranial transducers
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• Causes of increased intracranial
pressure
• Increase in venous pressure
– Venous sinus thrombosis
– Heart failure
– Obstruction of superior
mediastinal or jugular veins.
• Causes are classified by the
mechanism in which ICP is
increased:
• Mass effect
– Brain tumor
– Infarction with oedema
– Contusions, subdural or epidural
hematoma, or abscess
• Obstruction to CSF flow
and/or absorption
• Generalized brain swelling
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Ischemic-anoxia states
Acute liver failure
Hypertensive encephalopathy
Pseudotumor cerebri
Hypercarbia
These conditions tend to decrease
the cerebral perfusion pressure
but with minimal tissue shifts.
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– Hydrocephalus (blockage in
ventricles or subarachnoid
space at base of brain, e.g., by
Arnold-Chiari malformation)
– Extensive meningeal disease
(e.g., infectious,
carcinomatous, granulomatous,
or hemorrhagic)
– Obstruction in cerebral
convexities and superior
sagittal sinus (decreased
absorption).
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Signs and Symptoms
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Headache
Vomiting without nausea
Ocular palsies
Altered level of consciousness
Back pain
Papilloedema
Pupillary dilatation
Cushing's triad
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Increased systolic blood pressure
Widened pulse pressure
Bradycardia
Abnormal respiratory pattern.
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Treatment
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Adequate Airway
Breathing
Oxygenation
Maintain circulation
Mannitol
Treatment of cause
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