The document discusses traumatic brain injury (TBI). It summarizes a study of TBI patients in Uganda that found the majority were young males injured in road accidents or falls. TBI is a major cause of hospitalization and disability globally. It describes the pathophysiology of primary brain injury and outlines the Glasgow Coma Scale for assessing TBI severity. Clinical features, investigations, and acute management principles are outlined. Intracranial pressure monitoring and various medical and surgical treatments for raised ICP are discussed.

1. Traumatic Brain Injury
Julius kyomya
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2. Anatomy
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3. Epidemiology
• Prospective observational study at Mulago NRH – 15 months
• 3749 patients
• 69.7% were unintentional TBI and 30.3% were intentional TBI
• Main causes of unintentional TBI - road traffic injuries and falls.
• 73 deaths: 63 were patients with RTI and 10 had a fall
• Main causes of intentional TBI – assault and self harm
• 70% of patients between 19 and 45 years age group
• About 80% were males
• TBI an important cause of hospitalization, death and disability,
disproportionality affecting people in low/middle-income countries
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4. Pathophysiology of TBIs
• Primary injury involves the
external transfer of kinetic
energy to various structural
components of the brain
• Contact forces to the head
commonly result in skull
fractures, brain contusions,
and/or hemorrhages
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5. The Glasgow Coma Scale (GCS)
• Most widely used system to grade the arousal and functional capacity
of the cerebral cortex.
• Defines the level of consciousness according to eye opening, motor
response, and verbal response.
• A GCS score of 15 corresponds to a normal neurologic examination
• A GCS score of 3 to 8, 9 to 12, and 13 to 15 is consistent with severe,
moderate, and mild or minor brain injury, respectively
• Clinical variables predictive of poor outcomes
• Extremes of age, presence of hypotension, hypoxia and/or coagulopathy,
increased ICP, decreased GCS score (especially the motor score), and pupillary
changes
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6. The Glasgow Coma Scale (GCS)
• The possibility of ethanol or drug
intoxication, hypotension, hypoxia,
postictal state, hypoglycemia,
electrolyte imbalances, or
hypothermia should be considered
when administering this scale
• Opiates, sedatives, and
neuromuscular blockers affect the
neurologic examination, they
should not be administered until
the initial examination is complete
if at all possible.
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7. Clinical presentation
Generally level of consciousness on admission ranges from completely
unresponsive to awake and alert (ie, GCS 3-15)
• Symptoms
• Posttraumatic amnesia (eg, greater than 1 hour),
• Increasing dizziness
• Moderate-to-severe headache
• Nausea/vomiting
• Limb weakness
• Paresthesia.
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8. Clinical presentation
Signs
• Cerebrospinal fluid (CSF) otorrhea or rhinorrhea, seizures, or unequal
or unreactive pupils may indicate more severe injury.
• A rapid deterioration in mental status strongly suggests the presence
of an expanding lesion within the skull.
• Severe TBI may be accompanied by significant alterations or
instability in vital signs, including abnormal breathing patterns (eg,
apnea, Cheyne–Stokes respiration, tachypnea), hypertension, or
bradycardia.
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9. Laboratory tests
• Arterial blood gases (ABGs) indicating hypoxia (ie, decreased PaO2) or
hypercapnia (ie, increased PaCO2) may indicate compromised ventilation.
• A positive blood ethanol concentration and/or positive urine drug screen
indicates that drug intoxication may be affecting the patient’s mental status
in addition to the TBI.
• Electrolyte disturbances can cause alterations in mental status, and their
effects may interfere with assessment of the patient’s neurological status.
• Other Diagnostic Tests
• CT scan of the head is an important diagnostic tool for detecting the
presence of mass lesions and structural signs of edema (eg, midline shift,
compressed ventricles).
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10. Pharmacological measures
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11. Pharmacological measures
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12. Acute management of the patient with a TBI
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13. Acute management of the patient with a TBI
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14. Acute management of the patient with a TBI
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15. Initial Resuscitation
• The first priority - establishment of an airway that facilitates adequate
oxygenation and prevents aspiration
• Restoration and maintenance of SBP between 120 and 140 mm Hg
• More specifically correcting and preventing early hypotension (goal SBP
>100 mmHg for patients ages 50-69 years or >110 mmHg for patients ages
15-49 or over 70 years)
• Normal saline and lactated Ringer’s solution – initial resuscitation fluids of
choice in patients with TBI
• Hypertonic saline – not superior to isotonic solutions
• Vasopressors and inotropic agents- to maintain an adequate MAP if
hypotension persists after adequate restoration of intravascular volume
• Nonpharmacologic management of ICP includes raising the head of the bed
30°, and ventricular drainage if an extraventricular drain (EVD) is present.
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16. Post-resuscitative Care
• Following successful resuscitation, priorities shift toward diagnostic
evaluation of intracranial and extracranial injuries, and emergent
surgical intervention as needed.
• Evacuation of intracranial hematomas (ie, epidural, subdural, and
intracerebral hematomas) is essential to control ICP and improve
outcome.
• Elevation of depressed skull fractures and debridement of penetrating
wound tracts are other important emergent surgical procedures in
patients with TBI.
• Decompressive craniectomies with or without temporal or frontal
lobectomy may be considered in patients with increases in ICP
refractory to more conservative measures
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17. Post-resuscitative Care 2
• Continuous ICP monitoring (eg, EVD and/or intraparenchymal
fiberoptic catheter) has been the mainstay of ICP monitoring and
treatment
• Extraventricular drains have a therapeutic advantage over the
alternatives but
• Associated with a higher complication rate and can be difficult to place in the
setting of the swollen brain
• If continuous ICP monitoring is employed, the goal should be to treat
any ICP values > 22 mm Hg (2.9 kPa)
• Values above this level are associated with increased mortality
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18. Post-resuscitative Care 3
• Jugular venous oxygen saturation SjvO2 - detection of global cerebral
hypoxia
• Brain tissue oxygen (PbrO2) monitoring is an alternative to
SjvO2
• Another important monitoring parameter for patients with severe TBI
cerebral perfusion pressure (CPP)
• The difference between MAP and ICP (ie, CPP = MAP – ICP).
• Guidelines recommend maintaining a CPP range between 60 and 70
mm Hg (8.0 and 9.3 kPa).
• In order to achieve goal CPP the MAP may need to be increased
through the use of fluids and/or vasopressors, and by lowering
elevated ICP
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19. Treatment of intracranial pressure
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20. Treatment of intracranial pressure
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21. Treatment of intracranial pressure
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22. ICP Tx - Anesthetics, Analgesics, and Sedatives
• Role related to association of pain, agitation, excessive muscle movement,
and resisting mechanical ventilation with transient increases in ICP
• Their effect on ICP, CPP, and MAP are variable
• Morphine sulfate is the most commonly used analgesic and sedative
• Important to note that bolus doses of opiates may increase ICP by increasing CBF
• Continuous infusions of fentanyl and sufentanil are gaining in popularity,
their use also may be associated with mild elevations in ICP.
• Propofol - the sedative of choice in the treatment of patients with TBI
• ease of titration, rapidly reversible effects on discontinuation, and possible
neuroprotective effects
• Safety concerns with the use of propofol
• Propofol infusion syndrome (PRIS) characterized by hyperkalemia, hepatomegaly,
lipemia, metabolic acidosis, myocardial failure, rhabdomyolysis, renal failure, and
death in some cases
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23. ICP Tx - Anesthetics, Analgesics, and Sedatives
• Alternative sedatives
• Short-acting benzodiazepines (eg, midazolam), especially if there is a
reasonable suspicion of alcohol withdrawal as the underlying etiology of the
agitation
• Intermittent low-dose pentobarbital, ketamine, dexmedetomidine or
etomidate
• The potential for these agents to decrease MAP and CPP must be
monitored closely.
• Cumulative sedative effects of longer acting drugs, especially
benzodiazepines, must be taken into account
• Use of any sedative or paralytic agent also must be weighed against
its potential to obscure the neurologic examination of the patient.
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24. ICP Tx - Anesthetics, Analgesics, and Sedatives
• High-dose barbiturate therapy (ie, barbiturate coma) - used in the
management of increased ICP
• despite a lack of evidence on beneficial effects on patient morbidity and mortality.
• BTF/AANS and pediatric guidelines recommend that high-dose barbiturate
therapy be considered in
• hemodynamically stable patients with severe TBI refractory to maximal medical ICP-
lowering therapy and decompressive surgery.
• Prophylactic use of barbiturates is not advocated for.
• Prior to inducing a barbiturate coma, the patient with severe TBI must be
mechanically ventilated with continuous monitoring of arterial blood
pressure, electrocardiogram (ECG), and ICP.
• Pentobarbital - most commonly used, although thiopental - has been used
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25. Side effects - high-dose barbiturate therapy
• Hypotension caused by peripheral vasodilation may occur
• Necessitating decreasing the barbiturate dose or the administration of fluids
and vasopressors to maintain blood pressure.
• Gastrointestinal (GI) effects of barbiturates include
• Decreased GI muscular tone and decreased amplitude of contraction;
however, on emergence from coma, there may be a period of GI
hypermotility
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26. Corticosteroids
• Although corticosteroids are effective in preventing or reducing
cerebral edema in patients with nontraumatic conditions that
produce vasogenic edema, studies in patients with TBI have not
demonstrated their ability to lower ICP or improve outcomes.
• Specifically, use of corticosteroids following TBI has been associated
with increased mortality and complications including GI bleeding,
glucose intolerance, electrolyte abnormalities, and infection
• CRASH study
• higher risk of death within 2 weeks of enrollment (relative risk 1.18) in those
patients receiving corticosteroids compared with patients receiving placebo
• Based on this and other studies, high dose corticosteroid not be used
in patients with moderate-to-severe TBI
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27. Hypothermia
• Therapeutic hypothermia has been an attractive strategy for
attempting to minimize secondary brain injury after TBI for decades
• Early studies suggested promise for therapeutic hypothermia for
patient with TBI, as well as other patient populations with brain
ischemia (eg, cardiac arrest patients).
• Data from large clinical trials of prophylactic therapeutic hypothermia
in patients with TBI have not shown improved outcomes
• In addition, potential side effects of therapeutic hypothermia include
coagulation disturbances, infectious complications, and cardiac
arrhythmias.
• Prophylactic therapeutic hypothermia is not recommended as a
routine neuroprotective strategy in patients with TBI.
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28. Osmotic Agents
• A number of osmotic diuretics (eg, urea, glycerol) can be used to decrease
ICP, mannitol - most widely used.
• No clinical trial comparing mannitol effects against placebo.
• The mechanisms responsible for mannitol’s beneficial effects
• An immediate plasma-expanding effect that reduces blood viscosity and increases
CBF
• Establishment of an osmotic concentration gradient across an intact blood–brain
barrier that decreases ICP as water diffuses from the brain into the intravascular
compartment
• Recommended doses of mannitol typically range from 0.25 to 1 g/kg IV
every 2 to 4 hours
• To maximize benefit and minimize adverse events, mannitol be
administered as a bolus and not as a continuous infusion
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29. Osmotic agents
• Several adverse effects are associated with mannitol.
• Hypotension resulting from its diuretic effect
• Reversible acute renal dysfunction may occur in patients with previously
normal renal function after long-term, large-dose administration.
• Mannitol should be avoided in patients with AKI or CKD
• Acute exacerbation of underlying congestive heart failure and pulmonary
edema
• Hypertonic saline solutions have been used as a resuscitative fluid
following TBI
• Solutions ranging from concentrations of 2% to 23.4% have also been
used to acutely lower increased ICP
• Saline concentrations greater than 3% should be administered via a
central venous catheter
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30. Drug Dosing and Monitoring in Patients with TBI
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31. Treatment and Prophylaxis of Complications
Post-traumatic Seizures
• Adult patients who have experienced one or more seizures following
a moderate-to-severe TBI should receive anticonvulsant therapy
• Initial therapy should consist of incremental IV doses of
• Diazepam (5-40 mg adults, 0.1-0.5 mg/kg infants and children) or lorazepam
(2-8 mg adults, 0.03-0.1 mg/kg infants and children) to terminate any active
seizure activity,
• Followed by IV phenytoin to prevent seizure recurrence.
• Phenytoin dosing regimens for adults and pediatric patients
• IV loading dose of 15 to 20 mg/kg and 10 to 15 mg/kg, respectively,
• Maintenance dose of 5 mg/kg/day divided into two or three daily doses
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32. Post-traumatic Seizures
• The merits of preventive anticonvulsant therapy in patients who have
not had a seizure postinjury is controversial
• Risk factors for early posttraumatic seizures (< 7 days after injury)
• GCS score of less than 10, a cortical contusion, a depressed skull fracture, a
subdural hematoma, an epidural hematoma, an intracerebral hematoma, a
penetrating head wound, or a seizure within the first 24 hours of injury.
• The benefits of prophylactic anticonvulsants beyond 7 days have not
been demonstrated, and thus their use for this indication is not
recommended
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33. Evaluation of Therapeutic Outcomes
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34. Thank you for listening
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