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Coma

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The severity of coma is measured by comparing the intensity of an external ... posterior fossa lesions. medullary damage. overdoses of opiate and sedatives ... – PowerPoint PPT presentation

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Title: Coma


1
Coma
  • A state of unarousable psychologic
    unresponsive-ness in which the subjects lies with
    eyes closed
  • Coma vs. Consciousness
  • Consciousness wakefulness and responsiveness
  • The severity of coma is measured by comparing the
    intensity of an external stimulus and the
    complexity and purposefulness of the response

2
  • Hypersomnia
  • excessive drowsiness and excessive sleep
  • narcolepsy, hypothalamic disorders, drugs
  • Akinetic mutism
  • silent, alert, and awake appearance
  • regular sleep-wake cycles
  • no evidence of response to the environment,
    mental activities, or spontaneous movements

3
  • Locked-in syndrome
  • total paralysis of all somatic musculature
  • preserved consciousness and most sensory
    modalities
  • preserved vertical eye movements
  • ventral pontine infarct
  • Persistent vegetative state
  • preserved brainstem function, including breathing
  • spontaneous eye opening and regular sleep-wake
    cycles
  • no recognizable cognitive function

4
Three categories of Coma
  • Diffuse brain dysfunction
  • matabolic encephalopathy
  • drug intoxication
  • Primary brain stem disorders
  • brainstem stroke
  • brainstem neoplasm, absecess
  • Supratentorial mass lesions
  • causing secondary brain stem compression

5
Systemic evaluation of Coma
  • Is there systemic illness causing brain failure?
  • Is there evidence of diffuse or focal brain
    injury?
  • Is the patient improving or deteriorating?

6
Neurological examination in Coma
  • Response to external stimulation
  • Motor response
  • Size and reactivity of pupils
  • Eye movements and ocular reflexes
  • Pattern of breathing

7
Response to external stimulation
  • In order of verbal command, shouting, shaking,
    and noxious stimulation
  • Localizing pain
  • preserved brain stem function and intact
    connections to the appropriate cerebral
    hemisphere
  • Eye opening
  • preserved function of RAS

8
Motor responses
  • Absence of any motor response
  • severe brain stem damage
  • severe sedative drug ingestion
  • Decorticate, flexor posturing of the arms
  • bilateral cerebral hemisphere damage
  • toxic/metabolic encephalopathy
  • Decerebrate, extensor posturing of the arms
  • destructive lesions of the midbrain and upper
    pons
  • hepatic and anoxic-ischemic encephalopathy

9
Pupillary responses
  • Small, reactive pupils
  • metabolic
  • IICP with hypothalamic dysfunction
  • Very small pupils (pinpoint)
  • pontine lesion
  • narcotic (opioids) overdose
  • Bilateral dilated fixed pupils
  • seizure, anoxic encephalopathy
  • exogenous catecholamimes

10
Pupillary responses
  • Midposition and fixed pupils
  • midbrain dysfunction
  • brain death
  • Unilateral dilated pupil
  • damage to IIIrd nerve from trnastentorial
    herniation

11
Eye movements
  • Spontaneous roving, horizontal and conjugate eye
    movements
  • intact brain stem
  • diffuse or metabolic cortical dysfunction
  • Conjugate lateral deviation
  • massive hemispheric lesion (eyes toward lesion)
  • pontine lesion (eyes away from lesion)

12
Eye movements
  • Dolls eyes reflex
  • intact brainstem function with depressed cortical
    influences
  • normal sleep, coma, persistent vegetative state
  • Ice water caloric test
  • eyes toward the side of cold water
  • absence in brainstem lesion, inner ear disease,
    deep drug coma, and anticonvulsants overdose

13
Pattern of breathing
  • Cheyne-Stokes respiration
  • Central neurogenic hyperventilation
  • Apneustic breathing
  • Irregular periodic breathing
  • Ataxic breathing
  • Yawning

14
Cheyne-Stokes respiration
  • Periodic breathing, crescendo-decrescendo
  • The result of the loss of frontal lobe controls
  • Blood PCO2 drives brain stem respiratory center
  • Posthyperventilation apnea
  • Causes
  • Frontal lobe damage, unilateral or bilateral
  • Secondary to cardiac or respiratory failure

15
Central neurogenic hyperventilation
  • Sustained, rapid, deep hyperpnea
  • Not secondary to hypoxemia and acidemia
  • Causes
  • Upper brain stem lesion
  • Metabolic disorders, especially the early stages
    of hepatic coma

16
Apneustic breathing
  • Prolonged inspiratory gasp
  • Discrete lesions of the mid-to-lower pons
  • Need early intubation and ventilation
  • Causes
  • pontine infarct
  • hypoglycemia, anoxia, or severe meningitis

17
Ataxic and irregular periodic breathing
  • Completely irregular pattern
  • Slow and progressed to apnea
  • Respiratory center - dorsomedial medulla
  • Terminal states
  • Causes
  • posterior fossa lesions
  • medullary damage
  • overdoses of opiate and sedatives

18
Differential diagnosis of Coma
  • Metabolic and toxic causes
  • presence of pupillary light reflex
  • confusion and stupor precedes
  • symmetric motor signs
  • asterixis, myoclonus, tremor, seizures
    (generalized)
  • central hyperventilation

19
Differential diagnosis of Coma
  • Supratentorial mass lesions
  • focal neurologic sings
  • progresses in a rostral-caudal fasion
  • Subtentorial masses or destructive lesions
  • sudden onset of coma
  • history of brain stem dysfunction (the 6 Ds)
  • abnormal eye movements
  • cranial palsies
  • irregular respiration

20
Diagnostic procedures
  • Metabolic or toxic causes
  • blood, urine, gastric aspirates testing
  • EEG
  • Intracranial mass lesions, head injury
  • CT
  • Acute subarachnoid or intracerebral hemorrhage
  • CT
  • lumbar punctures
  • Meningitis or encephalitis
  • lumbar punctures

21
Treatment of Coma
  • Immediate treatment, even when the diagnosis is
    uncertain, to prevent further brain damage
  • Oxygenation and airway protection
  • ET tube
  • ventilation
  • Blood pressures maintain
  • volume replacement with isotonic solutions
  • hemodynamic monitoring
  • inotropic and vasopressor drugs

22
Treatment of Coma
  • Glucose (50 mL of 50 glucose)
  • Thiame (100 mg, with the glucose)
  • Seizures stop
  • Intracranial hypertension lower
  • Systemic infections control
  • Acid-base and electrolytes imbalances correct
  • Hyperthermia treat

23
Prognosis Hypoxic-ischemic encephalopathy
  • 1st day absence of pupillary responses predicts
    poor outcome
  • 2nd day no patients lack corneal reflex regained
    consciousness
  • After 3rd day lack or purposeful motor responses
    predict poor outcome

24
Persistent Vegetative State (PVS)
  • A form of eyes-open permanent unconsciousness.
  • Periods of wakefulness and physiologic sleep/wake
    cycles.
  • Unaware of self or environment.

25
Persistent Vegetative State (PVS)
  • No voluntary action or behavior. Only primitive
    reflexes and vegetative functions.
  • Careful and extended clinical observation,
    supported by laboratory studies.
  • In cases of hypoxic-ischemic encephalopathy,
    observation period of one to three months.
  • Prolonged survival.
  • No pain or suffering.

26
Neurological criteria for Death
  • The Uniform Determination of Death Acts
  • irreversible cessation of circulatory and
    respiratory functions, or
  • irreversible cessation of all functions of the
    entire brain, including the brain stem
  • The determination of death must be made in
    accordance with accepted medical standards

27
Diagnosis of Death by neurologic criteria
  • A clinical diagnosis, with preconditions and
    confirmatory tests
  • The core of the clinical diagnosis is to
    establish unresponsiveness and brain stem
    areflexia
  • The preconditions
  • the cause of coma be known
  • the cause be adequate to explain the coma

28
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32
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