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APPROACH TO COMA
Dr Abdullah Ansari
Definition of Coma
Coma is a state of complete behavioral
unresponsiveness to external stimulation
Anatomy of consciousness
ī‚¨ Ascending reticular activating system (ARAS)
ī‚¤ Activating systems of upper brainstem, hypothalamus, thalamus
ī‚¤ Determines the level of arousal
ī‚¨ Cerebral hemispheres and interaction between functional areas in
cerebral hemispheres
ī‚¤ Determines the intellectual and emotional functioning
ī‚¨ Interaction between cerebral hemispheres and activating systems
Ascending RAS
ī‚¨ The ascending RAS, from the lower border of the pons to the
ventromedial thalamus
ī‚¨ The cells of origin of this system occupy a paramedian area in the
brainstem
Levels of arousal (consciousness)
ī‚¨ Conscious: alert, attentive and cooperative, awareness of self
and environment
ī‚¨ Confused: conscious but talks irrelevantly
ī‚¨ Drowsy: sleepy but can be aroused easily by external stimulus
ī‚¨ Stupor: Deep sleep, can only be aroused by painful stimulus
ī‚¨ Coma: unconsious, no response to external stimuli
AVPU scale
ī‚¨ Alert: The patient is awake
ī‚¨ Verbal: The patient responds to verbal stimulation
ī‚¨ Pain: The patient responds to painful stimulation
ī‚¨ Unresponsive: The patient is completely unresponsive
EMS crews may begin with AVPU assesment, to be
followed by GCS if the score is below "A."
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
Glasgow coma scale
ī‚¨ Individual elements as well as the sum of the score are important.
ī‚¨ Hence, the score is expressed in the form "GCS 9 = E2 V4 M3
ī‚¨ Generally, comas are classified as:
ī‚¤ Severe, with GCS ≤ 8
ī‚¤ Moderate, GCS 9 - 12
ī‚¤ Minor, GCS â‰Ĩ 13.
Differential Diagnosis of Coma
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
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
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
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
Approach to Coma
Approach to Coma
ī‚¨ General examination: On arrival to ER immediate attention to:
ī‚¤ Airway
ī‚¤ Breathing
ī‚¤ Circulation
ī‚¤ establishing IV access
ī‚¤ Blood should be withdrawn: estimation of glucose # other
biochemical parameters # drug screening
Approachâ€Ļ
ī‚¨ Attention is then directed towards:
ī‚¤ Assessment of the patient
ī‚¤ Severity of the coma
ī‚¤ Diagnostic evaluation
ī‚¨ All possible information from:
ī‚¤ Relatives
ī‚¤ Paramedics
ī‚¤ Ambulance personnel
ī‚¤ Bystanders particularly about the mode of onset
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
Approachâ€Ļ
ī‚¨ Clues obtained from the patient's
īŽ Clothing or
īŽ Handbag
ī‚¨ Careful examination for
īŽ Trauma requires complete exposure and ‘log roll’ to
examine the back
īŽ Needle marks
Approachâ€Ļ
ī‚¨ If head trauma is suspected, the examination must await adequate
stabilization of the neck.
ī‚¨ Glasgow Coma Scale: the severity of coma is essential for
subsequent management.
ī‚¨ Following this, particular attention should be paid to brainstem
and motor function.
Examination of Comatose
General examâ€Ļ
Pulse
ī‚¨ Bradycardia: brain tumors, opiates, ICT, myxedema
ī‚¨ Tachycardia: sepsis, hyperthyroidism, uremia
Blood Pressure
ī‚¨ High: hypertensive encephalopathy
ī‚¨ Low: Addisonian crisis, alcohol, barbiturate, MI, sepsis
General examâ€Ļ
Temperature
ī‚¨ Fever in sepsis, meningitis, encephalitis, heat stroke,
anticholinergic drug intoxication
ī‚¨ Hypothermia in alcohol, barbiturate, sedative intoxication;
hypoglycemia, peripheral circulatory failure
Respiratory rate
ī‚¨ Tachypnea in acidosis or pneumonia
ī‚¨ Aberrant respiratory patterns in brainstem disorders
General examâ€Ļ
Skin
ī‚¨ Injuries, Bruises: traumatic causes
ī‚¨ Dry Skin: DKA, Atropine
ī‚¨ Moist skin: Hypoglycemic coma
ī‚¨ Cherry-red: CO poisoning
ī‚¨ Needle marks: drug addiction
ī‚¨ Rashes: meningitis, endocarditis
General examâ€Ļ
Odour of breath
ī‚¨ Acetone: DKA
ī‚¨ Fetor Hepaticus: in hepatic coma
ī‚¨ Urineferous odour: in uremic coma
ī‚¨ Alcohol odour: in alcohol intoxication
Level of Arousal
ī‚¨ Tickling the nostrils with a cotton wisp is a moderate
stimulus to arousal
ī‚¨ Pressure on the knuckles or bony prominences and
pinprick stimulation are humane forms of noxious
stimuli
ī‚¨ Pinching skin causes unsightly ecchymoses and is
generally not necessary but may be useful in eliciting
abduction withdrawal movements of the limbs
Posturing
Decorticate rigidity
ī‚¨ Flexion of the elbows and wrists and supination
of the arm
ī‚¨ Bilateral damage rostral to midbrain
Decerebrate rigidity
ī‚¨ Extension of the elbows and wrists with
pronation
ī‚¨ Damage to motor tracts in the midbrain or
caudal diencephalon
Posturing
Brainstem Reflexes
The brainstem reflexes that are examined are
1. Pupillary reflex
2. Ocular movements
3. Corneal reflex
4. Respiratory pattern
ī‚¨ As a rule, coma due to bilateral hemispheral
disease preserves these brainstem activities
Pupils
Pupils
ī‚¨ Size, inequality, reaction to a bright light.
ī‚¨ An important general rule: most metabolic encephalopathies give
small pupils with preserved light reflex.
ī‚¨ Atropine, and cerebral anoxia tend to dilate the pupils, and
opiates will constrict them.
Pupils
Reactive and round pupils of midsize (2.5–5 mm)
essentially exclude midbrain damage
Pupils
Structural lesions are more commonly associated with pupillary
asymmetry and with loss of light reflex.
ī‚¨ Midbrain lesions : round, regular, medium-sized pupils, do not
react to light
ī‚¨ Cranial nerve III distal to the nucleus: Ipsilateral fixed, dilated
pupil
ī‚¨ Pontine lesions: bilaterally small pupils, {in pontine hge, may be
pinpoint, although reactive}
Pupils
ī‚¨ Lateral medullary lesion: ipsilateral Horner's syndrome.
ī‚¨ Occluded carotid artery causing cerebral infarction: Pupil on that
side is often small
Small, reactive
Diencephalons
Dilated, Fixed
small, pinpoint
In hge reactive
Pons
Midbrain
Ipsilateral dilated,
Fixed
Medium-sized, fixed
.
Ocular movements
ī‚¨ The position of the eyes at rest
ī‚¨ Presence of spontaneous eye movement
ī‚¨ The reflex responses to oculocephalic and oculovestibular
maneuvers
ī‚¨ The eyes look toward a hemispheral lesion and away from a
brainstem lesion.
The oculocephalic reflex
ī‚¨ 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
ī‚¨ 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
ī‚¨ The “doll’s eyes” refers to the reflex elevation of the eyelids with
flexion of the neck
ī‚¨ These reflexes are normally suppressed in the awake patient
The oculocephalic reflex
The oculovestibular reflex
ī‚¨ These are tested by the installation of ice-cold water into the
external auditory meatus, having confirmed that there is no
tympanic rupture.
ī‚¨ 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
The oculovestibular reflex
Respiration
ī‚¨ Cheyne–Stokes respiration: (hyperpnoea alternates with apneas)
is commonly found in comatose patients, often with cerebral
disease, but is relatively non-specific.
ī‚¨ Rapid, regular respiration is also common in comatose patients
and is often found with pneumonia or acidosis.
Respiration
ī‚¨ Central neurogenic hyperventilation
ī‚¨ Brainstem tegmentum (mostly tumors):
ī‚¤ ↑ PO2, ↓ PCO2, and
ī‚¤ Respiratory alkalosis in the absence of any evidence of
pulmonary disease
ī‚¨ Sometimes complicates hepatic encephalopathy
Respiration
ī‚¨ Apneustic breathing
ī‚¤ Brainstem lesions Pons may also give with a pause at full
inspiration
ī‚¨ Ataxic:
ī‚¤ Medullary lesions: irregular respiration with random deep and
shallow breaths
Cheyne-Stocks
Ataxic
Apneustic
Central Neurogenic Hyperventilation
Cluster
Abnormal breathing patterns in
coma
Midbrain
Pons
Medulla
ARAS
Cheynes - Stokes
Ataxic
Apneustic
Central Neurogenic
Motor function
ī‚¨ Particular attention should be directed towards asymmetry of tone
or movement.
ī‚¨ The plantar responses are usually extensor, but asymmetry is again
important.
ī‚¨ The tendon reflexes are less useful.
ī‚¨ The motor response to painful stimuli should be assessed carefully
(part of GCS)
Motor function
ī‚¨ Painful stimuli: supraorbital nerve pressure and nail-bed pressure.
Rubbing of the sternum should be avoided (bruising and distress
to the relatives)
ī‚¨ Patients may localize or exhibit a variety of responses, asymmetry
is important
Motor function
ī‚¨ 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.
Signs of lateralization
ī‚¨ Unequal pupils
ī‚¨ Deviation of the eyes to one side
ī‚¨ Facial asymmetry
ī‚¨ Turning of the head to one side
ī‚¨ Unilateral hypo-hypertonia
ī‚¨ Asymmetric deep reflexes
ī‚¨ Unilateral extensor plantar response (Babinski)
ī‚¨ Unilateral focal or Jacksonian fits
Meningeal irritation signs
1. Neck rigidity
2. Kernig’s sign
3. Brudzinski’s sign
Head and Neck
Head and neck
ī‚¨ The head
ī‚¤ Evidence of injury
ī‚¤ Skull should be palpated for depressed fractures.
ī‚¨ The ears and nose: haemorrhage and leakage of CSF
ī‚¨ The fundi: papilloedema or subhyaloid or retinal haemorrhages
Diagnostic Testing
Laboratories
ī‚¨ Obtain ABG, serum electrolytes, glucose, creatinine,
complete blood count, liver functions and urinalysis
ī‚¨ Drug levels ordered if appropriate
ī‚¨ Toxicology screen of blood and urine if suspected
Imaging
ī‚¨ A head CT should be obtained to evaluate for structural
abnormalities
ī‚¨ 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)
Diagnostic Procedures
Cerebrospinal fluid (CSF) examination
ī‚¨ Lumbar puncture (LP) considered in patients with fever
and/or new headache
ī‚¨ A fundus examination and/or head imaging prior to LP
to assess risk of herniation
ī‚¨ 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
Electroencephalography (EEG)
ī‚¨ Electroencephalography (EEG) to rule out seizures
ī‚¨ Nonconvulsive status epilepticus is a common cause of
unexplained encephalopathy in the critically ills
Elevated Intracranial Pressure
Treatment of Elevated ICP
ī‚¨ Insert ICP monitor—ventriculostomy versus
parenchymal device
ī‚¨ General goals: maintain ICP <20 mmHg and
CPP â‰Ĩ60 mmHg
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 â‰Ĩ60 mmHg
7. Second-tier therapies for refractory elevated ICP
a. Decompressive craniectomy
b. High-dose barbiturate therapy (“pentobarb coma”)
c. Hypothermia to 33°C
Prognosis
Prognosis in coma
ī‚¨ In general, coma carries a serious prognosis
ī‚¨ This is dependent to a large extent on the underlying cause
ī‚¨ Coma due to depressant drugs carries an excellent prognosis
provided that resuscitative and supportive measures are available
and no anoxia has been sustained
ī‚¨ Metabolic causes, apart from anoxia, carry a better prognosis than
structural lesions and head injury
Prognosis in coma
ī‚¨ Length of coma and increasing age are of poor prognostic
significance.
ī‚¨ Brainstem reflexes early in the coma are an important predictor of
outcome
Approach to the Comatose patient
Approach to the Comatose patient

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Approach to the Comatose patient

  • 1. APPROACH TO COMA Dr Abdullah Ansari
  • 2. Definition of Coma Coma is a state of complete behavioral unresponsiveness to external stimulation
  • 3. Anatomy of consciousness ī‚¨ Ascending reticular activating system (ARAS) ī‚¤ Activating systems of upper brainstem, hypothalamus, thalamus ī‚¤ Determines the level of arousal ī‚¨ Cerebral hemispheres and interaction between functional areas in cerebral hemispheres ī‚¤ Determines the intellectual and emotional functioning ī‚¨ Interaction between cerebral hemispheres and activating systems
  • 4. Ascending RAS ī‚¨ The ascending RAS, from the lower border of the pons to the ventromedial thalamus ī‚¨ The cells of origin of this system occupy a paramedian area in the brainstem
  • 5. Levels of arousal (consciousness) ī‚¨ Conscious: alert, attentive and cooperative, awareness of self and environment ī‚¨ Confused: conscious but talks irrelevantly ī‚¨ Drowsy: sleepy but can be aroused easily by external stimulus ī‚¨ Stupor: Deep sleep, can only be aroused by painful stimulus ī‚¨ Coma: unconsious, no response to external stimuli
  • 6. AVPU scale ī‚¨ Alert: The patient is awake ī‚¨ Verbal: The patient responds to verbal stimulation ī‚¨ Pain: The patient responds to painful stimulation ī‚¨ 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 ī‚¨ Individual elements as well as the sum of the score are important. ī‚¨ Hence, the score is expressed in the form "GCS 9 = E2 V4 M3 ī‚¨ Generally, comas are classified as: ī‚¤ Severe, with GCS ≤ 8 ī‚¤ Moderate, GCS 9 - 12 ī‚¤ Minor, GCS â‰Ĩ 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 ī‚¨ General examination: On arrival to ER immediate attention to: ī‚¤ Airway ī‚¤ Breathing ī‚¤ Circulation ī‚¤ establishing IV access ī‚¤ Blood should be withdrawn: estimation of glucose # other biochemical parameters # drug screening
  • 16. Approachâ€Ļ ī‚¨ Attention is then directed towards: ī‚¤ Assessment of the patient ī‚¤ Severity of the coma ī‚¤ Diagnostic evaluation ī‚¨ All possible information from: ī‚¤ Relatives ī‚¤ Paramedics ī‚¤ Ambulance personnel ī‚¤ 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. Approachâ€Ļ ī‚¨ Clues obtained from the patient's īŽ Clothing or īŽ Handbag ī‚¨ Careful examination for īŽ Trauma requires complete exposure and ‘log roll’ to examine the back īŽ Needle marks
  • 19. Approachâ€Ļ ī‚¨ If head trauma is suspected, the examination must await adequate stabilization of the neck. ī‚¨ Glasgow Coma Scale: the severity of coma is essential for subsequent management. ī‚¨ Following this, particular attention should be paid to brainstem and motor function.
  • 21. General examâ€Ļ Pulse ī‚¨ Bradycardia: brain tumors, opiates, ICT, myxedema ī‚¨ Tachycardia: sepsis, hyperthyroidism, uremia Blood Pressure ī‚¨ High: hypertensive encephalopathy ī‚¨ Low: Addisonian crisis, alcohol, barbiturate, MI, sepsis
  • 22. General examâ€Ļ Temperature ī‚¨ Fever in sepsis, meningitis, encephalitis, heat stroke, anticholinergic drug intoxication ī‚¨ Hypothermia in alcohol, barbiturate, sedative intoxication; hypoglycemia, peripheral circulatory failure Respiratory rate ī‚¨ Tachypnea in acidosis or pneumonia ī‚¨ Aberrant respiratory patterns in brainstem disorders
  • 23. General examâ€Ļ Skin ī‚¨ Injuries, Bruises: traumatic causes ī‚¨ Dry Skin: DKA, Atropine ī‚¨ Moist skin: Hypoglycemic coma ī‚¨ Cherry-red: CO poisoning ī‚¨ Needle marks: drug addiction ī‚¨ Rashes: meningitis, endocarditis
  • 24. General examâ€Ļ Odour of breath ī‚¨ Acetone: DKA ī‚¨ Fetor Hepaticus: in hepatic coma ī‚¨ Urineferous odour: in uremic coma ī‚¨ Alcohol odour: in alcohol intoxication
  • 25. Level of Arousal ī‚¨ Tickling the nostrils with a cotton wisp is a moderate stimulus to arousal ī‚¨ Pressure on the knuckles or bony prominences and pinprick stimulation are humane forms of noxious stimuli ī‚¨ 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 ī‚¨ Flexion of the elbows and wrists and supination of the arm ī‚¨ Bilateral damage rostral to midbrain Decerebrate rigidity ī‚¨ Extension of the elbows and wrists with pronation ī‚¨ 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 ī‚¨ As a rule, coma due to bilateral hemispheral disease preserves these brainstem activities
  • 29. Pupils Pupils ī‚¨ Size, inequality, reaction to a bright light. ī‚¨ An important general rule: most metabolic encephalopathies give small pupils with preserved light reflex. ī‚¨ Atropine, and cerebral anoxia tend to dilate the pupils, and opiates will constrict them.
  • 30. Pupils Reactive and round pupils of midsize (2.5–5 mm) essentially exclude midbrain damage
  • 31. Pupils Structural lesions are more commonly associated with pupillary asymmetry and with loss of light reflex. ī‚¨ Midbrain lesions : round, regular, medium-sized pupils, do not react to light ī‚¨ Cranial nerve III distal to the nucleus: Ipsilateral fixed, dilated pupil ī‚¨ Pontine lesions: bilaterally small pupils, {in pontine hge, may be pinpoint, although reactive}
  • 32. Pupils ī‚¨ Lateral medullary lesion: ipsilateral Horner's syndrome. ī‚¨ Occluded carotid artery causing cerebral infarction: Pupil on that side is often small
  • 33. Small, reactive Diencephalons Dilated, Fixed small, pinpoint In hge reactive Pons Midbrain Ipsilateral dilated, Fixed Medium-sized, fixed .
  • 34. Ocular movements ī‚¨ The position of the eyes at rest ī‚¨ Presence of spontaneous eye movement ī‚¨ The reflex responses to oculocephalic and oculovestibular maneuvers ī‚¨ The eyes look toward a hemispheral lesion and away from a brainstem lesion.
  • 35. The oculocephalic reflex ī‚¨ 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 ī‚¨ 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 ī‚¨ The “doll’s eyes” refers to the reflex elevation of the eyelids with flexion of the neck ī‚¨ These reflexes are normally suppressed in the awake patient
  • 37. The oculovestibular reflex ī‚¨ These are tested by the installation of ice-cold water into the external auditory meatus, having confirmed that there is no tympanic rupture. ī‚¨ 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 ī‚¨ Cheyne–Stokes respiration: (hyperpnoea alternates with apneas) is commonly found in comatose patients, often with cerebral disease, but is relatively non-specific. ī‚¨ Rapid, regular respiration is also common in comatose patients and is often found with pneumonia or acidosis.
  • 40. Respiration ī‚¨ Central neurogenic hyperventilation ī‚¨ Brainstem tegmentum (mostly tumors): ī‚¤ ↑ PO2, ↓ PCO2, and ī‚¤ Respiratory alkalosis in the absence of any evidence of pulmonary disease ī‚¨ Sometimes complicates hepatic encephalopathy
  • 41. Respiration ī‚¨ Apneustic breathing ī‚¤ Brainstem lesions Pons may also give with a pause at full inspiration ī‚¨ Ataxic: ī‚¤ 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 ī‚¨ Particular attention should be directed towards asymmetry of tone or movement. ī‚¨ The plantar responses are usually extensor, but asymmetry is again important. ī‚¨ The tendon reflexes are less useful. ī‚¨ The motor response to painful stimuli should be assessed carefully (part of GCS)
  • 45. Motor function ī‚¨ Painful stimuli: supraorbital nerve pressure and nail-bed pressure. Rubbing of the sternum should be avoided (bruising and distress to the relatives) ī‚¨ Patients may localize or exhibit a variety of responses, asymmetry is important
  • 46. Motor function ī‚¨ 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 ī‚¨ Unequal pupils ī‚¨ Deviation of the eyes to one side ī‚¨ Facial asymmetry ī‚¨ Turning of the head to one side ī‚¨ Unilateral hypo-hypertonia ī‚¨ Asymmetric deep reflexes ī‚¨ Unilateral extensor plantar response (Babinski) ī‚¨ Unilateral focal or Jacksonian fits
  • 48. Meningeal irritation signs 1. Neck rigidity 2. Kernig’s sign 3. Brudzinski’s sign
  • 49.
  • 50. Head and Neck Head and neck ī‚¨ The head ī‚¤ Evidence of injury ī‚¤ Skull should be palpated for depressed fractures. ī‚¨ The ears and nose: haemorrhage and leakage of CSF ī‚¨ The fundi: papilloedema or subhyaloid or retinal haemorrhages
  • 52. Laboratories ī‚¨ Obtain ABG, serum electrolytes, glucose, creatinine, complete blood count, liver functions and urinalysis ī‚¨ Drug levels ordered if appropriate ī‚¨ Toxicology screen of blood and urine if suspected
  • 53. Imaging ī‚¨ A head CT should be obtained to evaluate for structural abnormalities ī‚¨ 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 ī‚¨ Lumbar puncture (LP) considered in patients with fever and/or new headache ī‚¨ A fundus examination and/or head imaging prior to LP to assess risk of herniation ī‚¨ 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
  • 56. Electroencephalography (EEG) ī‚¨ Electroencephalography (EEG) to rule out seizures ī‚¨ Nonconvulsive status epilepticus is a common cause of unexplained encephalopathy in the critically ills
  • 57.
  • 59. Treatment of Elevated ICP ī‚¨ Insert ICP monitor—ventriculostomy versus parenchymal device ī‚¨ General goals: maintain ICP <20 mmHg and CPP â‰Ĩ60 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 â‰Ĩ60 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 ī‚¨ In general, coma carries a serious prognosis ī‚¨ This is dependent to a large extent on the underlying cause ī‚¨ Coma due to depressant drugs carries an excellent prognosis provided that resuscitative and supportive measures are available and no anoxia has been sustained ī‚¨ Metabolic causes, apart from anoxia, carry a better prognosis than structural lesions and head injury
  • 63. Prognosis in coma ī‚¨ Length of coma and increasing age are of poor prognostic significance. ī‚¨ Brainstem reflexes early in the coma are an important predictor of outcome