Transcript Dr. Ahmed Aboelnaga MD pediatric and neonatal consultant

Alerted conscious
(coma)
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What is consciousness?
Consciousness is a state of wakefulness and
awareness of self and surroundings.
What is coma?
Coma is a state of altered consciousness with
loss of both wakefulness (arousal, vigilance)
and awareness.
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Consciousness means you see, talk, interact
with environment ,so ,it is controlled by many
centers in cerebral cortex(both),so to loss this
Consciousness you must had bilateral cerebral
cortex affection .
Cerebral cortex to work need activation from
reticular activating system in brain stem.
So to had coma lesion may be
A)diffuse cerebral cortex lesion(bilateral),or
B)brain stem injury.
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Trauma
Parenchymal injury
Intracranial hemorrhage
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intracerebral hematoma
Diffuse axonal injury
Nontraumatic causes
Toxic/metabolic
Hypoxic-ischemic encephalopathy
Shock
Cardiopulmonary arrest
Near-drowning
Carbon monoxide poisoning
Toxins
Medications: narcotics, sedatives, antiepileptics, antidepressants, analgesics, aspirin
Environmental toxins: organophosphates, heavy metals, cyanide, mushroom poisoning
Illicite substances: alcohol, heroin, amphetamines, cocaine
Systemic metabolic disorders
Substrate deficiencies
Hypoglycemia
Cofactors: thiamine, niacin, pyridoxine
Electrolyte and acid-base imbalance: sodium, magnesium, calcium
Diabetic ketoacidosis
Thyroid/adrenal/other endocrine disorders
Uremic coma
Hepatic coma
Reye syndrome
Inborn errors of metabolism
Urea cycle disorders
Amino acidopathies
Organic acidopathies
Mitochondrial disorders
Infections/postinfectious/inflammatory
Meningitis and encephalitis: Bacterial, viral, rickettsial, fungal
Acute demyelinating diseases
Acute disseminated encephalomyelitis
Multiple sclerosis
Inflammatory/autoimmune
Sarcoidosis
Sjögren disease
Lupus cerebritis
Mass lesions
Neoplasms
Abscess, granuloma
Hydrocephalus
Paroxysmal neurologic disorders
Seizures/SE
Acute confusional migraine
Vascular
Intracranial hemorrhage
Arterial infarcts
Venous sinus thromboses
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1)superatentorial
as hage,tumor,hematoma
Or metabolic,hypoxic-ischeamic,infection
2)infratentorial
hage,embolic,thrombetic,tumor
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Skull is closed box. So you need to know
A)there is increase in I.C.P.
B)there is herniation syndromes or not.
C)there is convulsion or not.
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Increase I.C.P. present in almost all
comatosed patient ,due to associated brain
oedema.
It may be mild undetected or may be sever
life therating.
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1)bulging anterior fontanel
2)neurologically:
-sluggish pupillary reaction
-increase tone
-hyper-reflexia
-hyperventilation with deep
inspiration and expiration.
3)Cushing respose:late,not constantly present
(hypertension,bradycardia,abnormal
respiration),=impending herniation
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Herniation syndromes
1)Central herniation
Increased pressure in both cerebral hemispheres, causing downward displacement of the diencephalon through the
tentorium, causing brainstem compression.
Diencephalic stage: withdraws to noxious stimuli, increased rigidity, or decorticate posturing; small, reactive pupils with
preserved oculocephalic and oculovestibular reflexes; yawns, sighs, or Cheyne-Stokes breathing.
Midbrain-upper pons stage: decerebrate posturing or no movement; mid-position pupils that may become irregular and
unreactive; abnormal or absent oculocephalic and oculovestibular reflexes; hyperventilation.
Lower pons-medullary stage: no spontaneous motor activity, but lower extremities may withdraw to plantar stimulation;
mid-position fixed pupils; absent oculocephalic and oculovestibular reflexes; ataxic respirations.
Medullary stage: generalized flaccidity; absent pupillary reflexes and ocular movements; slow irregular respirations, death.
2)Uncal herniation
Uncus of the temporal lobe is displaced medially over the free edge of the tentorium.
Ipsilateral third-nerve palsy (ptosis, pupil fixed and dilated, eye deviated down and out).
Ipsilateral hemiparesis from compression of the contralateral cerebral peduncle (Kernohan notch).
Other signs of brainstem dysfunction from ischemia secondary to compression of posterior cerebral artery.
3)Subfalcine (Cingulate) herniation
Increased pressure in one cerebral hemisphere leads to herniation of cingulated gyrus underneath falx cerebri.
Compression of anterior cerebral artery leads to paraparesis.
4)Tonsillar herniation
Increased pressure in the posterior fossa leads to brainstem compression.
Loss of consciousness from compression of reticular activating system.
Focal lower cranial nerve dysfunction.
Respiratory and cardiovascular function can be significantly affected early with relative preservation of upper brainstem
function, such as pupillary light reflexes and vertical eye movements.
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1)history
2)general examination
3)neurological examination
a)level of consciosness
b)respiratory pattern
c)motor response
d)eye examination
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1)level of consciousness
a-depressed consc.
lethergy:conscious but look sleepy
confusion:conscious but with
disorientation of the surroundings
b)unconsciousness(coma):4 stages
-stupor:can be aroused briefly(less than one
minute)then become uncosciosness
--light coma can not be aroused,respond by motor
---Deep coma no respose to painful stemuli
----Deep coma with apenea.
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Comatose patients with metabolic disease
– Confusion, stupor and coma precede motor
signs
– The motor signs are usually symmetrical
– The EEG is generally very slow
– Caloric stimulation elicits either tonic
deviation of the eyes or, if the patient
is deeply comatose, no response
– Seizures are common
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Abnormal focal motor signs (including focal seizures)
occur, which progress
rostrally to caudally, and are asymmetrical
– Neurological signs :point to one anatomical area
(mesencephalon, pons, medulla)
– Specific cognitive function disorders, such as
aphasia, acalculia, or agnosia,
appear out of proportion to a general overall
decrease in mental state
– The EEG may be slow, but in addition there is a
focal abnormality
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When present urgent C.T.and neurosurgical
consultation is life –saving.
1)asymmetric motor response
2)asymmetric brainstem reflexes.
3)uncal herniation.
4)focal convulsion
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Table 53.2 Initial evaluation of coma
Airway, breathing, and circulation assessment and stabilization
Ensure adequate ventilation and oxygenation.
Blood pressure management depends on considerations regarding underlying coma etiology. If hypertensive
encephalopathy or intracranial hemorrhage, lower blood pressure. If perfusion-dependent state, such as some strokes or
elevated intracranial pressure, reducing blood pressure may reduce cerebral perfusion.
Draw blood for glucose, electrolytes, ammonia, arterial blood gas, liver and renal function tests, complete blood count,
lactate, pyruvate, and toxicology screen.
Neurologic assessment
GCS score
Assess for evidence of raised intracranial pressure and herniation.
Assess for abnormalities that suggest focal neurologic disease.
Assess for history or signs of seizures.
Administer glucose IV (in an adult, thiamine should be given first)
If concern for infection delays lumbar puncture, broad-spectrum infection coverage should be provided (including bacterial,
viral, and possibly fungal).
Give specific antidotes if toxic exposures are known.
For opiate overdose, administer naloxone.
For benzodiazepine overdose, consider administering flumazenil.
For anticholinergic overdose, consider administering physostigmine.
Identify and treat critical elevations in intracranial pressure.
Neutral head position, elevated head by 20 degrees, sedation.
Hyperosmolar therapy with mannitol 0.25–1 g/kg or hypertonic saline.
Hyperventilation as temporary measure.
Consider intracranial monitoring.
Consider neurosurgical intervention.
Head CT (non-contrast)
Treat seizures with IV anticonvulsants. Consider prophylactic anticonvulsants.
Investigate source of fever and use antipyretics and/or cooling devices to reduce cerebral metabolic demands.
Detailed history and examination
Consider lumbar puncture, EEG or extended video EEG monitoring, MRI, metabolic testing (amino acids, organic acids,
acylcarnitine profile), autoimmune testing (ANA panel, antithyroid antibodies), thyroid testing (TSH, T3, T4).
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Skull is closed box so it is easy to develop,
1)increase I.C.P.
2)herniation syndroms
3)seizures
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Subclinical seizures in critically ill patients
may be an under-recognized phenomenon;
therefore, the index of suspicion in a
comatosed child shoud be high.
recent study of nonresponsive children in an
ICU demonstrated that 33% of children
manifested electrographic patterns
consistent with nonconvulsive status
epilepticus (NCSE).
Delayed diagnosis associated with high
mortality.