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neurosurgical managment of traumatic brain injury copy

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Neurosurgical management of
traumatic brain injury
(TBI)
Dr. Mohammed Muneam
M.B CH.B A.B.H.S Neurosurgery
Introduction:
6–60% of patients with GCS score ≤ 8 have 1 or more other organ
system injured.1 25% have “surgical” lesions. There is a 4–5%
incidence of associated spine fractures with significant head
injury (mostly C1 to C3).
When a detailed history is unavailable, remember: the loss of
consciousness may have preceded (and possibly have caused) the
trauma. Therefore, maintain an index of suspicion for e.g.:
aneurysmal SAH, hypoglycemia, etc. in the differential diagnosis
of the causes of trauma and associated coma.
Brain injury from trauma results from two distinct
processes:
1. primary brain injury: occurs at time of trauma (cortical
contusions, lacerations, bone fragmentation, diffuse
axonal injury, and brainstem contusion).
2. secondary injury: develops subsequent to the initial
injury. Includes injuries from intracranial hematomas,
edema, hypoxemia, ischemia (primarily due to elevated
intracranial pressure (ICP) and/or shock), vasospasm
(OUR focus should be on reducing secondary injuries).
Classification Of Head Trauma
A simple system based only on GCS score is as follows:
1-Minimal: GCS 15
2-Mild: GCS 14
3-Moderate: GCS 9-13
4-Sever: 5-8
5-Critical: 3-4
Intracranial hypertension (IC-HTN)
The critical parameter for brain function and survival is
not actually ICP, rather it is adequate cerebral blood flow
(CBF) to meet CMRO2 demands. CBF depends on cerebral
perfusion pressure (CPP), which is related to ICP.
cerebral perfusion pressure = mean arterial pressure intracranial pressure
CPP= MAP- ICP
Cerebral autoregulation is a mechanism whereby over a
wide range, large changes in systemic BP produce only
small changes in CBF. Due to autoregulation, CPP would
have to drop below 40 in a normal brain before CBF would
be impaired.
Normal Intracranial Constituents
brain parenchyma & ECF :1400 ml
cerebral blood volume (CBV): 150 ml
cerebrospinal fluid (CSF): 150 ml
Traumatic Intracranial hypertension
cerebral edema
hyperemia
traumatically induced masses
hydrocephalus
hypoventilation (causing hypercarbia
→ vasodilatation)
systemic hypertension (HTN)
venous sinus thrombosis
increased muscle tone
sustained posttraumatic seizures
(status epilepticus)
cerebral vasospasm
hyponatremia
Management of TBI
A-Rapid primary survey
The primary survey is performed simultaneously
with resuscitation and includes the “A, B, C, D, Es”
of trauma care.in accordance with Advanced
Trauma Life Support (ATLS) principles (American
College of Surgeons, The Committee on Trauma).
A: Airway maintenance (while taking care to protect the cervical spine)
B: Breathing and ventilation
C: Circulation and control of hemorrhage
D: Disability assessment including a brief evaluation of neurologic status (ask
the patient to move his/her extremities, ask if he/she can feel?) and Glasgow Coma
Scale (GCS)
E: Exposure and environmental control, which includes fully exposing the
patient and measures to prevent hypothermia.
B-Resuscitation & stabilization (with
primary survey)
Major goals
 avoid hypoxia (pO2 < 60 mm Hg)
 avoid hypotension (SBP ≤ 90 mm Hg): 67% positivepredictive value (PPV) for poor outcome (79% PPV when
combined with hypoxia)
 SPINAL PRECAUTIONS
1-positioning:
elevate HOB 30–45° & keep head midline
2- Hypotension (shock)
monitor BP and avoid hypotension (SBP < 90 mm Hg), hypotension in
TBI can occurs in
● in terminal stages
● in infancy, where enough blood can be lost intracranially or into
the subgaleal space to cause shock
● scalp wounds
Important notes
 IVF of choice is isotonic (NS + 20 mEq KCl/L)
 avoid hypotonic solutions (lactated ringers)
 if mannitol is required, patient should be maintained at
euvolemia
 also exercise caution with fluids in CSW & SIADH
 pressors (dopamine) are preferable to IV fluid boluses in head
injury
 arterial line for BP monitoring and frequent ABGs
 CVP line if high doses of mannitol are needed (goal: keep
patient euvolemic
3-oxygenation
avoid hypoxia (PaO2 < 60 mm Hg or O2 saturation < 90%).
Intubate if:
1. depressed level of consciousness
2. need for hyperventilation
3. severe maxillofacial trauma:
4. need for pharmacologic paralysis for evaluation or
management
(What is the risk of intubation in TBI?)= pneumonia , basal skull
fracture , GCS
4-paralytics and sedatives
1- intracranial hypertension
2-for intubation.
3-or where use is necessary for transport or to permit evaluation
of the patient (to get a combative patient to hold still for a CT
scan).
5-Early prophylactic hyperventilation (risks?)
avoid hyperventilation: keep PaCO2 at the low end of eucapnia
(35 mm Hg) (USE IT LATER ON IN DOCUMENTED IC-HTN)
6-Mannitol in E/R: indicated in
 evidence of intracranial hypertension
 evidence of mass effect (focal deficit, e.g., hemiparesis)
 sudden deterioration prior to CT (including pupillary
dilatation)
 after CT, if a lesion that is associated with increased ICP is
identified
 after CT, if going to O.R.
 to assess “salvageability
Contraindications:




hypotension
hypovolemia.
mannitol may slightly impede normal coagulation
CHF.
7-Prophylactic antiepileptic drugs AED
8-Anti-ulcer medication
9- indwelling (Foley) catheter:
to prevent distension from urinary retention
10-Biochemical investigation:
11- temperature regulation: aggressive control of fever (fever is
a potent stimulus to increase CBF, and may also increase plateau
waves)
12-Analgesics.
13-Aggressive management of hyperglycemia
prevent hyperglycemia: (aggravates cerebral edema) usually
present in head injury (steroids)
C-Secondary Survey
1-History:
 allergies, medications, illnesses, pregnancy, last
meal.
 mechanism of injury, time of injury
 presence and location of pain in conscious patient
 loss of consciousness, vomiting, seizures
 occurrences of transient or persistent neurologic
symptoms
 hx of congenital malformation, IC pathology,
previous operations
2-General physical examination:
1. visual inspection of cranium
 Evidence of basal skull fracture
 check for facial fractures
 periorbital edema, proptosis
2-cranio-cervical auscultation
3-physical signs of trauma to spine
4-evidence of seizure: single, multiple, or continuing (status
epilepticus)
3-Neurologic exam:
GCS, Cranial nerves, Motor, sensory, reflexes
Important note: look for signs of intracranial
hypertension:
1. pupillary dilatation (unilateral or bilateral)
2. asymmetric pupillary reaction to light
3. decerebrate or decorticate posturing (usually contralateral
to blown pupil)
4. progressive deterioration of the neurologic exam not
attributable to extracranial factors
4-Radiological investigations:
CT:
An unenhanced (i.e., non-contrast) CT scan of the head
usually suffices for patients seen in the emergency
department presenting after trauma or with a new
neurologic deficit. Enhanced CT or MRI may be
appropriate after the unenhanced CT in some
circumstances, but are not usually required emergently.
Skull X-rays:
significant ICI can occur with a normal skull X-ray, SXRs affect
management of only 0.4–2% of patients in most reports.
MRI scans in trauma:
Usually not appropriate for acute head injuries.
Arteriogram in trauma:
useful with non-missile penetrating trauma.
D-Initiation of definitive management
1- ICP monitoring:
For salvageable patients with severe traumatic brain injury GCS ≤
8 after cardiopulmonary resuscitation), treatment for IC-HTN
should be initiated for ICP > 22 mm Hg.
keep ICP ≤ 22 mm Hg & keep CPP ≥ 50 mm Hg.
(TYPES OF ICP MONITORS)
2- Initiate treatment if ICP > 22 mm Hg. See below table
3- second tire therapy:
1. high dose barbiturate therapy
2. hyperventilate to PaCO2 = 25–30
3. hypothermia
4. decompressive surgery:
5. lumbar drainage
6. hypertensive therapy
4- surgical Indication in TBI:
1- traumatic intracranial masses
2- decompressive craniectomy may be considered for IC-HTN that
cannot be controlled medically
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