HEAD TRAUMA INTENSIVE CARE Chanhung Lee MD, Ph'D Depatment of anesthesia and Perioperative Care Univ

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HEAD TRAUMA/INTENSIVE CAREChanhung Lee MD,
Ph.DDepatment of anesthesia and Perioperative
CareUniversity of California, San Francisco
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• Mechanism of injury
• Mode of injury
• 82 closed head injuries
• 18 gunshot wounds
• ----Traumatic coma data bank, 1991

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• Concept of secondary brain injury
• Initiated by the primary injury ischemia, brain
  edema, intracranial hemorrhage, intracranial
  hypertention, and herniation
• Aggregated by systemic factors
• Acute phase hypoxia, hypercarbia, hypotension,
  anemia, hyperglycemia
• Subacute phase seizures, infections/sepsis,
  hyperthermia, electrolyte disturbances,
  coagulation abnormalities

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• Pathology
• Skull fracture
• Intracranial lesions
• Subdural hematoma---a torn bridging vein between
  the cortex and the draining
  sinues.
• Epidural hematoma---torn dural vessels
• Intracerebral blood---hematoma or contusion
• Hemorrhagic contusions
• Diffuse brain injuries---concussion / diffuse
  axonal injury

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Severity of injury Glasgow coma scale Best
Eye Response. (4) 1.      No eye opening.
2.      Eye opening to pain. 3.      Eye
opening to verbal command. 4.      Eyes open
spontaneously. Best Verbal Response. (5)
1.      No verbal response 2.     
Incomprehensible sounds. 3.      Inappropriate
words. 4.      Confused 5.      Orientated
Best Motor Response. (6) 1.      No motor
response. 2.      Extension to pain. 3.     
Flexion to pain. 4.      Withdrawal from pain.
5.      Localizing pain. 6.      Obeys
Commands.
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• Glasgow coma scale
• level of consciousness
• GCS 3-15 severe 3-8, moderate 9-12, mild 13-15
• Pupillary response
• brain stem function
• Pupil reactivity bilateral reactive
  unilateral reactive bilateral unreactive
• Vegetative/death 9
  50 74
• ----Traumatic coma data bank, 1991

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• Secure the airway
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• Constraints
• elevated intracranial pressure
• uncertain cervical spine
• an uncertain airway (presence of blood,
  laryngeal-pharyngeal injury, skull base
  fracture)
• hypoxemia
• ---an uncooperative/combative patient
• ---uncertain volume status
• ---a full stomach

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Correct hypoxemia and stabilize the blood
pressure
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Hypoxemiaapnea---effect of acute elevation of
ICP on respiratory centerupper airway
obstruction---from unconsciousnessaspiration---fr
om depressed laryngeal/pharyngeal
reflexhypoxemia without airway
obstructionneurogenic pulmonary edema
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Hypoxemia without airway obstruction Increased
perfusion to hypoventilated alveoli i.e.
bronchoconstriction without compensatory hypoxic
vasoconstriction Mechanism ?elevated CSF
lactic acid, dysfunction of the
mid pontine structures
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• Neurogenic pulmonary edema
• rapid onset
• hypothalamic lesions
• attenuation by alpha-blockers and CNS depressants
  
• specific sequence of hemodynamic changes
• high protein in the edema fluids
• resemble to epinephrine-induced pulmonary edema
• Possible mechanism massive sympathetic discharge
  caused by intracranial hypertension affects the
  pulmonary vascular bed directly

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Blood pressure management Cerebral perfusion
(CPP) mean arterial pressure(MAP)
intracranial pressure(ICP)
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• Cerebral circulatory changes
• initial low CBF and defective autoregulation
• hyperemia after the first 24 hours post-injury
• vasospasm may occur 4 10 days post-injury with
  subarachnoid blood

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Resuscitation Fluids Crystalloids Hypotonic
versus Normal tonic versus Hypertonic
Crystalloids versus Colloids the debate is
not over, but there are some established
facts    
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Free water, decrease serum osmolality , cause
edema in both normal and abnormal brain. Lactated
Ringers when given in large volumes, causes
edema in normal brain. (Tommasino et al.
1988) ---mixture of lactated Ringers and normal
saline if large volumes of crystalloids needed
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a model of percussive head injury in rat has
demonstrated that aggravation of cerebral edema
is associated with a 50 reduction of colloid
oncotic pressure. (Drummond et al.,1998)---to
avoid profound reduction of colloid oncotic
pressure mixture of colloids and isotonic
crystalloids (NS).
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Hypertonic solutions are effective for volume
resuscitation and result in lesser degree of
cerebral edema. (Gunnar et al., 1988)---not
widely used due to uncertainty over the
physiological implications of high serum sodium
concentrations.
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• Intracranial hypertension
• Normal at rest 0-15 mm Hg
• Moderate intracranial hypertension 20-40 mm Hg
• Severe intracranial hypertension gt 40 mm Hg
• a reflection of the severity of the initial
  neurologic injury
• (develops in 50 of patients in coma caused by
  severe head injury)
• cause secondary injury to the brain through
  ischemia by
• reducing cerebral perfusion pressure
• distort and compress the brain stem

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ICP management pharmacological paralysis
(sedatives, muscle relaxant)hyperventilationC
SF drainagedehydration and diureticsbarbiturat
e
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• CO2 control
• Hyperventilation
• maintaining normal ICP,
• minimizing retractor pressure
• but potentially deleterious
• A clinical trail in patients with moderate head
  injury, comparing near-normocapnic group (35
  mmHg) and hypocapnic group (25 mmHg), examined
  outcome at 3 and 6 months following injury and
  observed a poor status in a subpopulation of the
  hyperventilation group.
• (Muizelaar et al., 1991)

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Choice of anesthetic agentsInhalational
agents versus i.v. anestheticsAvoid N2O in
settings of missile injury, compound skull
fracture, intracranial air
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• Posterior pituitary dysfunction
• antidiuretic hormone (ADH) deficiency
• Syndrome of inappropriate antidiuretic hormone
  secretion (SIDAH)

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• Syndrome of inappropriate antidiuretic hormone
  secretion (SIDAH)
• Head traumairritation to the hypothalamic-pituita
  ry axis limbic structures fail to inhibit ADH
  release. Begins 3-15 days after trama, last 10
  -15 days.
• Excessive water retention and renal sodium loss.
• Hyponatemia, serum hypoosmolarity (lt urine
  osmolarity), normal renal and adrenal function
• Treatment
• water restriction,
• hypertonic saline and diuretics to promote water
  loss for patients in coma or seizure

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• Antidiuretic hormone (ADH) deficiency
• Dabetes insipidus
• --hypoxic brain damage, hemorrhagic shock
  predispose necrosis of the posterior pituitary,
  fat embolization
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• polyuria gt2L/day, polydipsia, hypernatremia, high
  serum osmolarity 320 330 mOsm/kg, dilute urine,
  urine/serum osmolarity lt 1
• Dxfluid restriction with monitor of urine volume
  and osmolarity
• Treatment
• replace hourly urine output plus insensible loss
  with water
• vasopressin chlorpropamide (non-nephrogenic DI)
  thiazide diuretics

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Additional ICU issueshyperglycemiahyperthermia