1. Coma in non neurological intensive
care units
Santiago ortega et al
University college of Wisconsin.
The Neurologist,Nov,2009.
2. Back ground
Increased survival among medical and
surgical ICU.
Increasing spectrum of illness secondary to
critical illness
1/3 of icu patients,55% mortality rate
Increase length of stay and disability
Systematic approach to identify potentially
reversible etiologies and prognostic factors
3. Clinical history
Physical examination
Degree of sedation
Neurologic examination
Herniation syndromes
Coma scales
4. Essential clinical history in patients
with loss of consciousness
History
Time course-abrupt
gradual
fluctuating
Preceding focal signs
Previous episodes
h/o recent illness
h/o recent fall
Altered behaviour
Drugs
Medical psychological history
Alcohol drug abuse
Possible causes
SAH, seizure, bleeding
Tumour, venous thrombosis
Metabolic,subdural hematoma.
Focal lesion
TIA, seizure
Infection, metabolic
Subdural, epidural bleed
Toxic, metabolic, infection
Toxic-metabolic.
Metabolic, psychiatric
Toxic-metabolic
11. Evaluation of comatose
Spontaneous activity, motor response, eye
position and movements, pupillary reflexes,
brainstem reflexes and asymmetry between
right and left responses.
Decorticate (flexor) posturing-lesion above
level of red nucleus.
Decerebrate posturing (extensor)-damage to
lower midbrain or upperpons, severe damage
and less chance of recovery.
Ciliospinal reflex
14. Abnormal pupillary responses in
coma
Bilateral small ,reactive
b/l dilated and unreactive
b/l dilation&reactive
Unilateral miosis
Metabolic encephalopathy, B/l
thalamic, pontine lesions,
hydrocephalus,narcotics,OP,barbitur
ates
Midbrain damage or compression
Seizure
Thalamus, sympathetic efferents
from posterior hypothalamus,
tegmentum, descending to the
cervical cord
15. Pupillary responses and coma
Unilateral, unreactive &
enlarged
-unilateral ptosis
-bilateral ptosis
Unilateral,small,reactive,
ipsilateral ptosis
-with face anhydrosis
-anhydrosis entire side of
body
-without anhydrosis
Compression of ipsilateral
III nerve
-Fascicular lesion
-Nuclear lesion
-Extracranial defect T1-T2
to carotid bifurcation
-Between hypothalamus
and spinal cord
-ICA vs cavernous sinus vs
SOF vs orbit
17. FOUR score scale
Eye response
4-eyelid open or opened, tracking or
blinking to command
3-eyelids open, not tracking
2-eyelids closed, open to loud voice, not
tracking
1-eyelids closed, open to pain, not tracking.
0-eyelids remain closed with pain
Motor response
4-thumbs up, fist, or peace sign to command
3-localizing to pain
2-flexion response to pain
1-extensor posturing
0-no response to pain or generalized
myoclonus/status
Brainstem reflexes
4-pupil & corneal reflex present
3-open pupil wide & fixed
2-pupil/corneal reflexes absent
1-pupil & corneal reflex absent
0-absent pupil, corneal & cough reflexes
Respiration
4-not intubated, regular breathing pattern
3-not intubated, cheyne-stokes breathing
pattern
2-not intubated, irregular breathing pattern
1-breathes above ventilator rate
0-breathes at ventilator rate
18. Cerebral herniation :clinical
syndromes
Uncal herniation Hemispheric/later
al middle fossa
Ipsilateral III
compression
Dilated ipsilateral
pupil with
preserved or
sluggish reaction
to light.
CnIII,ophthalmopl
egia,ipsilateral
hemipareis
Central herniation Supra tentorial
diffuse brain
edema,
haemorrage,
midline tumors
Initial obstruction
hydrocephalus,
thalamus,
hypothalamus
displacement
Decrease
consciousness,
small & reactive
pupils, normal
eye movements.
Fixed pupils,
cheyne stroke
respiration,
opthalmoplegia,
decorticate
posturing
19. Cerebral herniation clincal
syndromes
Midbrain
compression
Advanced stage
of central
herniation,
upward infra
tentorial lesions
Midbrain and
upper pons
Decerebrate
posturing,
midposition
pupils,
sometimes
irregular and loss
of pupillary,
oculocephalic
and oculo
vestibular
reflexes
Foramen
magnum
herniation
Infra tentorial
lesions
Medulla-lower
pons, cerebellar
tonsils
All brainstem
reflexes are lost,
flaccid paralysis,
ataxic respiration,
then ceasing
22. Major causes of organic coma-
infratentorial
Brainstem
pontine bleed
basilar artery
occlusion
central pontine
myelinolysis
brainstem contusion
Cerebellum
cerebellar infarct
cerebellar bleed
cerebellar abscess
cerebellar tumour
23. Medical ICU
Metabolic encephalopathy-28.6%
Seizures-28.1%
Hypoxic ischemic encephalopathy-23.5%
Stroke-22.1%
Sepsis is major cause of neurological
complication-38.8%
Bleck et al-2 yr period
24. Primary CNS processes
Acute stroke-1-4% in non neuro icu.
Angiographic studies
De clotting of Av shunts
Vascular line insertions
Air embolism
Cardioversion
Anticoagulation
Thrombolytic therapy
25. Primary CNS processes
Meningitis & encephalitis-change in
mental state with fever, csf analysis and
antibiotics.
Posterior reversible leuco
encephalopathy-acute hypertensive
crisis involving brain, vaso genic
edema, control with labetolol, nicardipine
etc.
27. Primary CNS processes
New onset seizure-0.8-4%,focal most
common.
Myoclonic seizures-metabolic, drugs,hypoxia.
Non convulsive status-10%(50%of TBI),
52% mortality in critically ill
Myoclonic status epilepticus-12hrs of cardiac
resuscitation, persists up to 48 hrs, poor
prognostic sign, unresponsive to medication.
30. Sodium disturbances
Hypo natremia-incidence of1%,prevalence of
2.5%.
Postoperative patients
Lethargy, confusion, coma ,seizures.
Central pontine myelinolysis
Hypernatremia-increase use for ICT.
Lethargy, obtundation, coma
Progressive shrinkage of brain leading to
cerebral vascular damage and sub dural
hamatoma
31. Calcium disturbance
Hyper calcemia- ionised calcium levels
and rate of rise.
Delirium, depression, coma.
Hypo calcemia-commonly associated
with sepsis.
Irritabilty, tremors and seizures
43. Tacrolimus/muromonab
Fine tremor, paresthesias, apraxia, aphasia,
akinetic mutism.
Cortical blindness, CIDP
Aseptic meningitis and toxic encephalopathy
Csf pleocytosis with neutrophil predominance,
mild protein elevation, normal glucose and
sterile cultures
Seizures, psychosis, visual loss
44. Offering prognosis
Etiology, severity, secondary CNS damage, age.
5-pont Glasgow outcome scale,6-point pediatric
cerebral performance category scale, GCS, FOUR
score-motor score, sphincter conrol, self care,
communication, pupillary reactivity
Children and young adults, toxic or metabolic
abnormalities-better
Absence of brainstem reflexes, low GCS, hypoxia
,hypotension-worst
MRI,MRS, DTI.
45. Anoxic coma
Pupils, corneal reflex, motor response to
pain ,myoclonic status, SSEP, serum neuron
specific enolase.
No response or extension to pain, EEG with
malignant characteristics, absent bilateral
ssep-poor prognosis
Elevated NSE at 24 and 48 hrs >33ng/ml
-poor prognosis
EEG with alternating high voltage slow waves
with low voltage irregular fast activity-good
prognosis
46. Brain death and organ donation
Irreversible loss of brain function including
brainstem
Traumatic brain injury and SAH
Prerequisites to diagnosis
Identify patients who are likely to progress to
brain death
Consent, ethical
Optimize and treat any physiological
disturbance associated with brain death to
protect organs for transplantation
47. hypothermia
To minimize secondary brain damage
Avoid hyperthermia-excito toxicity, free radical
generation, inflammation, apoptosis.
Therapeutic hypothermia-core body temp <33
c
Massive ischemic stroke, TBI, anoxia
External cooling devices, iv cold saline
infusions, iv cooling catheters.
Electrolyte abnormalities, cardiac
arrhythmia,infection.