Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
2. Definition of Coma
Coma is a state of complete behavioral
unresponsiveness to external stimulation
3. Anatomy of consciousness
Ascending reticular activating system (ARAS)
Activating systems of upper brainstem, hypothalamus, thalamus
Determines the level of arousal
Cerebral hemispheres and interaction between functional areas in
cerebral hemispheres
Determines the intellectual and emotional functioning
Interaction between cerebral hemispheres and activating systems
4. Ascending RAS
The ascending RAS, from the lower border of the pons to the
ventromedial thalamus
The cells of origin of this system occupy a paramedian area in the
brainstem
5. Levels of arousal (consciousness)
Conscious: alert, attentive and cooperative, awareness of self
and environment
Confused: conscious but talks irrelevantly
Drowsy: sleepy but can be aroused easily by external stimulus
Stupor: Deep sleep, can only be aroused by painful stimulus
Coma: unconsious, no response to external stimuli
6. AVPU scale
Alert: The patient is awake
Verbal: The patient responds to verbal stimulation
Pain: The patient responds to painful stimulation
Unresponsive: The patient is completely unresponsive
EMS crews may begin with AVPU assesment, to be
followed by GCS if the score is below "A."
7. Glasgow Coma Scale (GCS)
Best eye
response (E)
Best verbal
response (V)
Best motor
response (M)
4 Eyes opening
spontaneously
5 Oriented 6 Obeys commands
3 Eye opening to
speech
4 Confused 5 Localizes to pain
2 Eye opening in
response to pain
3 Inappropriate words 4 Withdraws from pain
1 No eye opening 2 Incomprehensible
sounds
3 Flexion in response to
pain
1 None 2 Extension to pain
1 No motor response
8. Glasgow coma scale
Individual elements as well as the sum of the score are important.
Hence, the score is expressed in the form "GCS 9 = E2 V4 M3
Generally, comas are classified as:
Severe, with GCS ≤ 8
Moderate, GCS 9 - 12
Minor, GCS ≥ 13.
10. Differential Diagnosis of Coma
1. No focal neurologic signs, CT scan and cellular
content of the CSF are normal
2. Focal neurological signs, with or without changes in
the CSF; CT and MRI are abnormal
3. Meningitis syndromes, with an excess of WBCs in the
CSF, usually without focal signs; CT or MRI shows no
mass lesion
11. Diseases without focal neurological signs
Diseases that cause no focal or lateralizing neurologic signs,
usually with normal brainstem functions; CT scan and cellular
content of the CSF are normal
a. Intoxications: alcohol, sedative drugs, opiates, etc.
b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia,
hypercalcemia, diabetic ketoacidosis, hypoglycemia, uremia,
hepatic coma, hypercarbia, Addisonian crisis
c. Severe systemic infections: septicemia, typhoid fever, malaria
d. Shock from any cause
e. Postseizure states, status epilepticus, nonconvulsive status
epilepticus
f. Hypertensive encephalopathy, eclampsia
g. Severe hyperthermia, hypothermia
12. Diseases with focal neurological signs
Diseases that cause focal brainstem or lateralizing cerebral
signs, with or without changes in the CSF; CT and MRI are
abnormal
a. CNS hemorrhage or infarction
b. Brain abscess, subdural empyema
c. Brain tumor with surrounding edema
d. Brain trauma: Epidural and subdural hemorrhage, brain
contusion
e. Metabolic coma (see above) with preexisting focal damage
f. Miscellaneous: Cortical vein thrombosis, herpes simplex
encephalitis, septic emboli due to bacterial endocarditis, acute
disseminated encephalomyelitis, thrombotic thrombocytopenic
purpura, cerebral vasculitis
13. Meningitis syndromes
Diseases that cause meningeal irritation with or without fever,
and with an excess of WBCs or RBCs in the CSF, usually without
focal or lateralizing cerebral or brainstem signs; CT or MRI shows
no mass lesion
a. Subarachnoid hemorrhage from ruptured aneurysm,
arteriovenous malformation, trauma
b. Acute bacterial meningitis
c. Viral encephalitis
d. Miscellaneous: fat embolism, cholesterol embolism,
carcinomatous and lymphomatous meningitis
15. Approach to Coma
General examination: On arrival to ER immediate attention to:
Airway
Breathing
Circulation
establishing IV access
Blood should be withdrawn: estimation of glucose # other
biochemical parameters # drug screening
16. Approach…
Attention is then directed towards:
Assessment of the patient
Severity of the coma
Diagnostic evaluation
All possible information from:
Relatives
Paramedics
Ambulance personnel
Bystanders particularly about the mode of onset
17. History
1. The circumstances and rapidity with which neurologic
symptoms developed
2. The antecedent symptoms (confusion, weakness,
headache, fever, seizures, dizziness, double vision, or
vomiting)
3. The use of medications, drugs, or alcohol
4. Chronic liver, kidney, lung, heart, or other medical
disease
18. Approach…
Clues obtained from the patient's
Clothing or
Handbag
Careful examination for
Trauma requires complete exposure and ‘log roll’ to
examine the back
Needle marks
19. Approach…
If head trauma is suspected, the examination must await adequate
stabilization of the neck.
Glasgow Coma Scale: the severity of coma is essential for
subsequent management.
Following this, particular attention should be paid to brainstem
and motor function.
22. General exam…
Temperature
Fever in sepsis, meningitis, encephalitis, heat stroke,
anticholinergic drug intoxication
Hypothermia in alcohol, barbiturate, sedative intoxication;
hypoglycemia, peripheral circulatory failure
Respiratory rate
Tachypnea in acidosis or pneumonia
Aberrant respiratory patterns in brainstem disorders
23. General exam…
Skin
Injuries, Bruises: traumatic causes
Dry Skin: DKA, Atropine
Moist skin: Hypoglycemic coma
Cherry-red: CO poisoning
Needle marks: drug addiction
Rashes: meningitis, endocarditis
24. General exam…
Odour of breath
Acetone: DKA
Fetor Hepaticus: in hepatic coma
Urineferous odour: in uremic coma
Alcohol odour: in alcohol intoxication
25. Level of Arousal
Tickling the nostrils with a cotton wisp is a moderate
stimulus to arousal
Pressure on the knuckles or bony prominences and
pinprick stimulation are humane forms of noxious
stimuli
Pinching skin causes unsightly ecchymoses and is
generally not necessary but may be useful in eliciting
abduction withdrawal movements of the limbs
26. Posturing
Decorticate rigidity
Flexion of the elbows and wrists and supination
of the arm
Bilateral damage rostral to midbrain
Decerebrate rigidity
Extension of the elbows and wrists with
pronation
Damage to motor tracts in the midbrain or
caudal diencephalon
28. Brainstem Reflexes
The brainstem reflexes that are examined are
1. Pupillary reflex
2. Ocular movements
3. Corneal reflex
4. Respiratory pattern
As a rule, coma due to bilateral hemispheral
disease preserves these brainstem activities
29. Pupils
Pupils
Size, inequality, reaction to a bright light.
An important general rule: most metabolic encephalopathies give
small pupils with preserved light reflex.
Atropine, and cerebral anoxia tend to dilate the pupils, and
opiates will constrict them.
31. Pupils
Structural lesions are more commonly associated with pupillary
asymmetry and with loss of light reflex.
Midbrain lesions : round, regular, medium-sized pupils, do not
react to light
Cranial nerve III distal to the nucleus: Ipsilateral fixed, dilated
pupil
Pontine lesions: bilaterally small pupils, {in pontine hge, may be
pinpoint, although reactive}
32. Pupils
Lateral medullary lesion: ipsilateral Horner's syndrome.
Occluded carotid artery causing cerebral infarction: Pupil on that
side is often small
34. Ocular movements
The position of the eyes at rest
Presence of spontaneous eye movement
The reflex responses to oculocephalic and oculovestibular
maneuvers
The eyes look toward a hemispheral lesion and away from a
brainstem lesion.
35. The oculocephalic reflex
The oculocephalic reflexes, elicited by moving the head from side
to side or vertically and observing eye movements in the direction
opposite to the head movement
If the eyes move conjugately in the opposite direction to that of
head movement, the response is positive and indicates an intact
pons mediating a normal vestibulo-ocular reflex
The “doll’s eyes” refers to the reflex elevation of the eyelids with
flexion of the neck
These reflexes are normally suppressed in the awake patient
37. The oculovestibular reflex
These are tested by the installation of ice-cold water into the
external auditory meatus, having confirmed that there is no
tympanic rupture.
A normal response in a conscious patient is the development of
nystagmus with the quick phase away from the stimulated side
This requires intact cerebropontine connections
39. Respiration
Cheyne–Stokes respiration: (hyperpnoea alternates with apneas)
is commonly found in comatose patients, often with cerebral
disease, but is relatively non-specific.
Rapid, regular respiration is also common in comatose patients
and is often found with pneumonia or acidosis.
40. Respiration
Central neurogenic hyperventilation
Brainstem tegmentum (mostly tumors):
↑ PO2, ↓ PCO2, and
Respiratory alkalosis in the absence of any evidence of
pulmonary disease
Sometimes complicates hepatic encephalopathy
41. Respiration
Apneustic breathing
Brainstem lesions Pons may also give with a pause at full
inspiration
Ataxic:
Medullary lesions: irregular respiration with random deep and
shallow breaths
43. Abnormal breathing patterns in
coma
Midbrain
Pons
Medulla
ARAS
Cheynes - Stokes
Ataxic
Apneustic
Central Neurogenic
44. Motor function
Particular attention should be directed towards asymmetry of tone
or movement.
The plantar responses are usually extensor, but asymmetry is again
important.
The tendon reflexes are less useful.
The motor response to painful stimuli should be assessed carefully
(part of GCS)
45. Motor function
Painful stimuli: supraorbital nerve pressure and nail-bed pressure.
Rubbing of the sternum should be avoided (bruising and distress
to the relatives)
Patients may localize or exhibit a variety of responses, asymmetry
is important
46. Motor function
Flexion of the upper limb
with extension of the lower
limb (decorticate response)
and extension of the upper
and lower limb (decerebrate
response) indicate a more
severe disturbance and
prognosis.
47. Signs of lateralization
Unequal pupils
Deviation of the eyes to one side
Facial asymmetry
Turning of the head to one side
Unilateral hypo-hypertonia
Asymmetric deep reflexes
Unilateral extensor plantar response (Babinski)
Unilateral focal or Jacksonian fits
50. Head and Neck
Head and neck
The head
Evidence of injury
Skull should be palpated for depressed fractures.
The ears and nose: haemorrhage and leakage of CSF
The fundi: papilloedema or subhyaloid or retinal haemorrhages
52. Laboratories
Obtain ABG, serum electrolytes, glucose, creatinine,
complete blood count, liver functions and urinalysis
Drug levels ordered if appropriate
Toxicology screen of blood and urine if suspected
53. Imaging
A head CT should be obtained to evaluate for structural
abnormalities
Brain MRI can be useful if head CT is nondiagnostic and
there is suspicion for an ischemic or parenchymal
lesion (especially of the posterior fossa)
55. Cerebrospinal fluid (CSF) examination
Lumbar puncture (LP) considered in patients with fever
and/or new headache
A fundus examination and/or head imaging prior to LP
to assess risk of herniation
Basic cerebrospinal fluid (CSF) studies (e.g. protein,
glucose, cell count, Gram stain, and aerobic culture)
obtained with additional studies depending on the
possible etiology
59. Treatment of Elevated ICP
Insert ICP monitor—ventriculostomy versus
parenchymal device
General goals: maintain ICP <20 mmHg and
CPP ≥60 mmHg
60. Treatment of Elevated ICP
1. Elevate head of the bed; midline head position
2. Drain CSF via ventriculostomy (if in place)
3. Osmotherapy—mannitol or hypertonic saline
4. Glucocorticoids—for vasogenic edema from tumor,
abscess
5. Hyperventilation—to PaCO2 30–35 mmHg
6. Pressor therapy— dopamine or norepinephrine to
maintain adequate MAP to ensure CPP ≥60 mmHg
7. Second-tier therapies for refractory elevated ICP
a. Decompressive craniectomy
b. High-dose barbiturate therapy (“pentobarb coma”)
c. Hypothermia to 33°C
62. Prognosis in coma
In general, coma carries a serious prognosis
This is dependent to a large extent on the underlying cause
Coma due to depressant drugs carries an excellent prognosis
provided that resuscitative and supportive measures are available
and no anoxia has been sustained
Metabolic causes, apart from anoxia, carry a better prognosis than
structural lesions and head injury
63. Prognosis in coma
Length of coma and increasing age are of poor prognostic
significance.
Brainstem reflexes early in the coma are an important predictor of
outcome