A brief presentation on Traumatic brain injury and its management in the intensive care unit (ICU)

1. ICU MANAGEMENT OF
TRAUMATIC BRAIN INJURY
Dr. Opadotun O.A.
Resident doctor
Babcock University Teaching Hospital
8/2/2019 1

2. • Introduction
• Epidemiology
• Definition
• Pathophysiology
• Clinical features
• Management
• Sequelae
• References
8/2/2019 2

3. Introduction
• Every 21seconds, someone in US is affected by TBI.
• 60,000 TBI deaths annually: 44,000 occur at the scene or in E.R.:
16,000 occur afterwards.
• Traumatic brain injury (TBI) is a leading cause of death and disability.
In 2013, there were about 2.5 million (ED) visits, 282,000
hospitalizations, and 56,000 deaths related to TBI in USA. Many
survivors live with significant disabilities, resulting in major
socioeconomic burden as well.
• Challenge is to reduce mortality and improve outcome.
• Patients with severe head injury may frequently have other traumatic
injuries to internal organs, lungs, limbs, or the spinal cord
8/2/2019 3

4. Epidemiology
• Etiology of Head Injury (U.S.)
Falls
28%
Motor Vehicle Traffic
20%
Struck by/against
19%
Assault
11%
Pedal Cycle
(Non Motor Vehicle)
3%
Other Transport
2%
Suicide
1%
Other
7%
Unknown
9%
Falls Motor Vehicle Traffic Struck by/against
Assault Pedal Cycle (Non Motor Vehicle) Other Transport
Suicide Other Unknown
8/2/2019 4

5. Definition
•Traumatic Brain Injury has long been
recognized as a important medical entity
• Hippocrates first commented on mechanisms of
head injury and first described trephination as
modality to treat head injury.
• 16th century – French military surgeon Ambrose
Pare introduced term commotio cerebri to
describe mild injury to brain.
• Traumatic Brain Injury first came into use in 1996
after U.S. based Traumatic Brain Injury Act which
established federal funding for study of brain
injury
8/2/2019 5

6. Definition
•Traumatic Brain Injury
• Spectrum of Intracranial Injury
• Results from:
• Direct Forces = Object Striking or penetrating cranium
• Indirect Forces = Acceleration/Deceleration or
Rotational Mechanism
• Traumatic Brain Injury Scale
• Glasgow Coma Scale = 30 minutes after head injury
• Mild = 13-15, Moderate = 9-12, Severe < 9
• Dynamic Scale
• Over 25 different scales available
8/2/2019 6

7. Definition
• Concussion
• Concussion represents a subset of mild traumatic brain injury
• Derived from Latin term “Concutere” or to shake violently
• Historically, defined by the loss of consciousness
• 1965 Consensus Definition = Congress of Neurological Surgeons
• “ A clinical syndrome characterized by the immediate transient
post-traumatic impairment of neural function such as alteration of
consciousness, disturbance of vision or equilibrium due to
brainstem involvement.”
8/2/2019 7

8. Concussion
• American Academy of Neurology and the International Conference on
Concussion in Sport held in 2004 created a modified consensus
definition of concussion as “ a complex pathophysiological process
affecting the brain, induced by traumatic biomechanical forces that
typically includes:
• Concussion may be caused by either a direct blow to the head,
face, neck or elsewhere on the body with an “impulsive” force
transmitted to the head
• Concussion typically results in the rapid onset of short lived
impairment of neurologic function that resolves spontaneously
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9. • Concussion may result in neuropathologic changes but the acute
clinical symptoms largely represent a functional disturbance rather
than structural injury
• It results in a graded set of clinical syndromes that may or may not
involve loss of consciousness. Resolution of the clinical and
cognitive symptoms typically follows a sequential course.
• It is typically associated with grossly normal structural imaging
studies.”
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10. Normal Cerebral Autoregulation
• Brain is a semisolid organ that occupies 80% of cranial vault
• 20% of the body’s oxygen supply
• 15% of cardiac output
• Cranial Vault = Fixed in size by outer rigid skull
• Contains brain tissue, blood & vessels and CSF
• Monroe-Kelli Doctrine
• Defines the relationship between the volumes of the three
compartments
• The expansion of one compartment MUST be accompanied by
a compensatory reduction in the volumes of the other
compartments to maintain a stable intracranial pressure (ICP)
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11. Normal Cerebral Autoregulation
• CPP = CBF = MAP – ICP
• Cerebral Autoregulation
• Protective mechanism to maintain a tightly controlled
environment where fluctuations in systemic arterial
pressure or ICP do not have a large impact on cerebral
blood flow
• Maintained by intact blood brain barrier, a specialized set
of endothelial cells with tight junctions
• Disruption of the blood brain barrier by traumatic injury
may impair normal cerebral autoregulation
8/2/2019 11

12. Primary injury
• Head trauma is otherwise called traumatic brain injury ( TBI ) ,
occurs in two phases, Primary and Secondary brain injury.
• Primary injury : Results from the direct physical impact to the brain
parenchyma resulting in structural and shearing injury of neurons,
injury to vessels, and interruption of neurochemical processes.
• This leads to hemorrhage, edema, compression of intracranial
structures
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13. Pathophysiology
• Traumatic Brain Injury
• Primary Brain Injury
• Types of Primary Brain Tissue Injury
• Cellular Injury Mechanisms
• Secondary Brain Injury
• Systemic Insults
• Intracranial Insults
• Mechanisms of Traumatic Brain Injury
• Skull Fractures
• Extra-axial Fluid Collections
• Intraparenchymal Hemorrhage
• Subarachnoid Hemorrhage
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Advanced Emergency Trauma Course
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14. Primary Brain Injury
• Primary Brain Injury
• Direct or indirect force to brain tissue, resulting in
cellular injury
• Types of Primary Brain Injury
• Cortical Brain Contusion
• Shear Stress 2/2 Coup/Contracoup injury
• Focal injury at gray matter closest to the brain surface
generates localized brain edema and disruption of normal
neurological function
• Size of contusion defines extent of injury
• Diffuse Axonal Injury
• Rotational Mechanism –
• Widespread shearing strain at deep cerebral white matter
that disrupts normal axonal organization resulting in
disruption of axonal fibers and myelin sheaths
• Non-lateralizing neurological deficits
• Generalized edema occurs after injury, typically within 6
hours without any focal lesion on CT imaging
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15. Primary Brain Injury – Cellular Level
Primary Cellular Injury
“Neurotransmitter
Storm”
Massive Depolarization
of Brain Cells
Glutamate
Calcium
NMDA Disruption of normal cellular processes:
Protein Phosphorylation
Microtubule Construction
Enzyme Production
Membrane and
Cytoskeleton Breakdown
Cell Death
Oxygen Free Radical
Pathway Activation
Lipid Peroxidation
Cell Membrane Dysfunction
Cell Lysis
Nitric Oxide
Synthase
High Nitric Oxide
Levels
Intracellular Signaling
Processes8/2/2019 15

16. Secondary Brain Injury
• It is characterized by a cascade of events that starts within minutes of
the primary injury (actual trauma) and can last for hours to days. It
exercabate the brain injury and combine to worsen patient outcome.
• The injured brain has been shown to be intolerant of secondary
insults than the uninjured brain
• Categorized into:
• Systemic Insults
• Intracranial Insults
• Emergency Department Treatment is focused on limiting the extent of
secondary brain injury
8/2/2019 16

17. Secondary Brain Injury
•Systemic Insults
• Hypoxia (PaO2 < 60 mmHg, O2 Saturation <90% )
• Mortality of TBI pts with hypoxia doubles
• 40% of TBI ED patients exhibit hypoxia during course
• Hypertension (SBP > 160 mmHg or MAP > 110 mm Hg).
• Hypotension (SBP < 90 mmHg)
• Present in 33-35% of TBI patients
• Results from hemorrhagic shock, ↓CO due to cardiac
contusion or tamponade, tension pneumothorax, etc
• Hypotension → ↓Cerebral Perfusion→↑Cerebral Ischemia
→↑Doubles Mortality
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Advanced Emergency Trauma Course
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18. • Anemia: Hemoglobin [Hb] < 10 g/dL, or hematocrit [Ht] <
30%→ (↓Oxygen Carrying Capacity)
• Hypo/Hypercapnia
• Hypocapnia (PaCO2 < 35 mm Hg)
• Hypercapnia (PaCO2 > 45 mm Hg
• Hyperventilation → ↓pCO2 Levels → ↑Serum pH → Cerebral
Vasoconstriction → ↓Cerebral Blood Flow
• Previously was a mainstay of treatment esp of ↑ ICP and will
help to buffer an expanding hematoma in short-term, but will
ultimately decrease cerebral perfusion to penumbra region and
increase tissue death
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19. • Hyponatremia (serum sodium < 142 mEq/L).
• Hyperglycemia (blood sugar > 10 mmol/L).
• Hypoglycemia (blood sugar < 4.6 mmol/L).
• Hypo-osmolality (plasma osmolality [P Osm] < 290 mOsm/Kg H2O).
• Acid-base disorders (acidemia: pH < 7.35; alkalemia: pH > 7.45)
• Fever (temperature > 37.2°C)
• Hypothermia (temperature < 35.5°C)
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20. • Other Systemic Insults
• Seizures
• Electrolyte Abnormalities
• Coagulopathy
• Infection
• Iatrogenic (Under-resuscitation)
• Intracranial Insults
• Intracranial Hypertension
• Extra-axial Lesions
• Cerebral Edema (Peaks at 24-48 hrs post injury)
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21. Extra-axial Fluid Collections
• Epidural Hematoma
• Middle Meningeal Artery (36%)
• Head Injury w/ LOC + Lucid Interval followed
by deterioration
• Classic presentation In 47% of cases
• Lenticular Shape on CT
• Subdural Hematoma
• Injury to Bridging Veins
• Blood accumulation between dura mater and
pia arachinoid mater
• Increased risk in elderly and alcoholics due to
decreased brain volume/cerebral atrophy
• Hyperdense crescent shaped lesion
http://www.unipa.it/~
sparacia/rimg/caso1.
jpg
Wikipedia
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22. Intracerebral Hemorrhage
• Intraparenchymal Hemorrhage
• Subarachnoid Hemorrhage
• Disruption of subarachnoid vessels
• Common in moderate to severe
brain injury
• Worse prognosis
• Twice as likely as other head injured
patients to suffer from death, persistent
vegetative state or severe disability
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Advanced Emergency Trauma Course
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23. 8/2/2019 23

24. Clinical Features
• Hallmark Symptoms
• Confusion and amnesia w/ or w/o LOC
• Severe brain injury often characterized by decreased mental status and presence
of neurological deficits
• Patients may also deteriorate from mild to severe head injury during course of
evaluation.
• Amnesia
• May be anterograde or retrograde.
• Duration does correlate with severity and outcome of head injury
• Loss of Consciousness
• Results from rotational forces at the junction of the upper midbrain and thalamus
that results in disruption of reticular neuron function and inability to maintain
alertness
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25. Clinical Features
• Glasgow Coma Scale
• Developed by Teasdale and Jennett in 1974
• Originally designed to measure 6 hours after injury to provide long term
prognostic information about mortality and disability
• Now, standardized to measure 30 min after injury and repetitive
measurements throughout patient’s stay
• Should be performed after adequate resuscitation b/c scale is sensitive to
hypotension, hypoxia, intoxication and pharmacologic interventions
• Current Classification
• GCS = 13-15 = Mild Head Injury
• GCS = 9 – 12 = Moderate Head Injury
• GCS < 9 = Severe Head Injury
• Best prognostic indicator of outcome is CT Scan
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26. 8/2/2019
GCS Score Mortality(%)
3 65
4 45
5 35
6 24
7-13 10-15
26

27. Clinical Features
•Neurologic Exam
• Pupillary Size + Reactivity
• Fixed unilateral Dilated Pupil = Ipsilateral Intracranial
Hematoma resulting in uncal herniation
• Bilateral Fixed + Dilated = Poor Brain Perfusion, bilateral uncal
herniation or severe hypoxia
• Indicative of very poor neurological outcome
• Neurological Posturing
• Decorticate Posturing = Upper extremity flexion with lower
extremity extension
• Cortical Injury above the midbrain
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28. • Decerebrate Posturing = Arm extension and internal rotation
with wrist flexion
• Indicative of brainstem injury
• Very Poor predictor of outcome
• Full, Complete Neurological Exam
• Examine for subtle neurological deficits
• Look for specific injury patterns:
• Battle’s sign, CSF Otorrhea, CSF Rhinorrhea, Hemotympanum, peri-
orbital Ecchymosis is indicative of skull fracture and is concerning for
underlying brain injury
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29. 8/2/2019 29

30. Clinical Features
• Mild Head Injury
• Signs and symptoms (early/late)
Signs and Symptoms of Head Injury
Cognitive Somatic Affective
Confusion
Anterograde amnesia
Retrograde amnesia
Loss of consciousness
Disorientation
Feeling “zoned out”
Feeling “foggy”
Vacant stare
Inability to focus
Delayed verbal/motor response
Slurred or incoherent speech
Excessive Drowsiness
Headache
Fatigue
Disequilibrium
Dizziness
Nausea/vomiting
Visual disturbances
Photophobia
Phonophobia
Difficulty sleeping
Ringing of the ears
Emotional Lability
Irritability
Sadness
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31. Clinical Features
• Grading scale for mild head injury with GCS =between
13-15 and concussion syndrome
• Developed by Colorado Medical Society and American
Academy of Neurology
• Composite Grading System
• Grade 1 – Any head injury with transient confusion, no
LOC and symptoms that last less than 15 minutes
• Grade 2 – Transient confusion, no LOC, symptoms that
last longer than 15 minutes
• Grade 3 – All head injury with LOC
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32. Clinical Features
• Moderate
• GCS = 9-12
• Clinical presentation varies widely
• 10% of patients
• Specialized Subset = “Talk and Die Syndrome”
• Initially, talkative and without significant signs of external injury
• Within 48 hours of injury, rapidly deteriorate
• Epidural Hematoma is the cause in 78-80% of cases
• Patients with “talk and die syndrome” who present with a GCS > 9 but who
deteriorate have been shown to have a worse outcome than patients who
present with severe TBI at outset
• ? Delayed Diagnosis
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33. Severe Head Injury
• GCS < 9
• 10% of patients with TBI
• Early aggressive treatment is required with airway control,
resuscitation, admission to ICU setting
• 25% of this patient population will require neurosurgical
intervention
• Outcome is poor with mortality as high as 60%
• Typically with abnormal exam, often evidence of external
trauma, abnormal pupillary exam and neurological deficits
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34. • Cushing’s Triad = Acute entity seen in severely head injured patients
with significant increased intracranial pressure and impending
herniation
• Results from ischemia to hypothalamus with poor perfusion to the brain,
resulting in sympathetic stimulation of the heart to correct poor perfusion.
The sympathetic stimulation results in hypertension, but carotid
baroreceptors respond with parasympathetic stimulation resulting in
bradycardia
• Characterized by:
• Progressive Hypertension
• Bradycardia
• Irregular or impaired respiratory pattern
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35. Evaluation of the Head Injured Patient
• Sideline Evaluation
• Head Injury may not be recognized by an injured player or
non-medical personnel
• Multiple Standardized tools for evaluation of head injured
sports player
• Standardized Assessment of Concussion (SAC)
• Sport Concussion Assessment Tool (SCAT)
• E.D. Evaluation
• Neurological Exam
• Imaging
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36. Management in ICU
• Prior to arrival to the ICU, patients with severe TBI are usually
received, resuscitated and stabilized in emergency department or
operating room.
• Once the severely head-injured patient has been transferred to the
ICU, the management consists of the provision of high quality general
care and various strategies aimed at maintaining homeostasis which
includes
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37. • Stabilization of the patient, if still unstable .
• Prevention of intracranial hypertension.
• Maintenance of an adequate and stable cerebral perfusion pressure
(CPP).
• Avoidance of systemic, secondary brain insults (SBI).
• Optimization of cerebral hemodynamic and oxygenation
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38. General monitoring
• Electrocardiography (ECG monitoring)
• Arterial oxygen saturation (pulse oxymetry, SpO2),
• Capnography (endtidal CO2, PetCO2),
• Arterial blood pressure (arterial catheter)
• Central venous pressure (CVP)
• Systemic temperature
• Urine output
• Arterial blood gases
• Serum electrolytes and osmolality.
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39. INTRACRANIAL PRESSURE MONITORING
(ICPM)
8/2/2019
• Non invasive ICP monitoring
• Invasive ICP monitoring
39

40. Non invasive ICPM
• The patient should be evaluated for the following:
Headache, nausea, & vomiting(early morning
and projectile)
Degree of alertness or consciousness
(Glasgow coma score)
Language comprehension, repetition, fluency,
articulation
Pupillary reactivity (Pupillary asymmetry or
anisocoria of more than 2 mm should be noted.)
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41. • Extraocular movements and visual fields in all quadrants.
• Funduscopic examination (This also remains the criterion standard in
the evaluation of increased ICP.)
• Vital signs (Note particularly the absence or presence of Cushing
triad: respiratory depression, hypertension, bradycardia.)
• Optic nerve sheath diameter (ONSD)
Cutoff value 4.8-5.9mm for ICP estimation
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42. Imaging
• Noncontrast CT scanning of the head is a fast, cost-effective method
to evaluate for elevated ICP and associated pathology.
• Findings suggestive of elevated ICP are as follows:
Intracranial blood/bony fractures
Mass lesions
Obstructive hydrocephalus
Cerebral edema (both focal or diffuse)
Midline shift
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43. Invasive ICPM
• Intracranial pressure monitoring uses a device, placed inside the
head, which senses the pressure inside the skull and sends its
measurements to a recording device. Range 3-15 mmHg.
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44. indication
• Patient with GCS less than 8 after reversal of sedatives that were used
during intubation
• Patient with risk of raised ICP under general anesthesia
• Unilateral or bilateral motor posturing
• Close head injury
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45. Invasive techniques
• A- External ventricular drain placement (EVD) or ventriculostomy
• B- Intraparenchyma fiberoptic catheter placement
• EVD PLACEMENT:
An EVD is a highly accurate tool for monitoring ICP.
It requires placement of a catheter into the lateral ventricle at
the level of the foramen of Monro
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46. 8/2/2019 46

47. • Benefit:
In addition to monitoring, an EVD allows for therapeutic relief of
elevated ICP via CSF drainage.
• Disadvantages :
Parenchymal hematoma and infection/ventriculitis.
Obstruction of the drain requires replacement.
Continuous monitoring requires nursing staff to be educated on
management of the EVD.
8/2/2019 47

48. Critical Pathway for Treatment of Intracranial
Hypertension in the Severe Head Injury Patient
(Treatment Option)
*Threshold of 20-25 mmHg may be used. Other values may be substituted in individual conditions.
May Repeat Mannitol
if Serum Osmolarity
< 320 mOsm/L &
Pt euvolemic
High Dose
Barbiturate therapy
• Hyperventilation to PaCO2 < 30 mmHg
• Monitoring SjO2, AVDO2, and/orCBF
Recommended
Other Second
Tier Therapies
NO
YES NO
YES NO
YES NO
Carefully
Withdraw
ICP Treatment
Consider
Repeating
CT Scan
YES
Second Tier Therapy
Intracranial Hypertension?
Hyperventilation to PaCO2 30 - 35 mmHg
Intracranial Hypertension?
Mannitol (0.25 - 1.0 g/kg IV)
Intracranial Hypertension?
Ventricular Drainage (if available)
Intracranial Hypertension?*
Maintain CPP  70 mmHg
Insert ICP Monitor
8/2/2019 48

49. JUGULAR BULB VENOUS OXYGEN
SATURATION MONITORING
• The jugular venous oxygen saturation
(SjvO2) is an indicator and helps in
reflecting the ratio between cerebral
blood flow (CBF) and cerebral
metabolic rate of oxygen.
• A retrograde catheterization of the
internal jugular vein (IJV) is used for
SjvO2 monitoring. As the right IJV is
usually dominant
8/2/2019 49

50. • The normal average of the SjvO2, in a normal awake subject, is 62%
with a range of 55% to 71%.
• A sustained jugular venous desaturation of < 50% is the threshold of
cerebral ischemia and for treatment.
• SjvO2 monitoring can detect clinically occult episodes of cerebral
ischemia, allowing the prevention of these episodes by simple
adjustment of treatment
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51. Electrophysiological monitoring
• Electroencephalogram (EEG) is a clinically useful tool for monitoring
the depth of coma, detecting non-convulsive (sub-clinical) seizures or
seizures activity in pharmacologically paralyzed patients, and
diagnosing brain death
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52. Analgesia, sedation and paralysis
• In severe TBI patients, endotracheal intubation, mechanical
ventilation, trauma, surgical interventions (if any), nursing care and
ICU procedures are potential causes of pain.
• Narcotics, such as morphine, fentanyl and remifentanil, should be
considered first line therapy since they provide analgesia, mild
sedation and depression of airway reflexes (cough) which is required
in intubated and mechanically ventilated patients.
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53. • Administration of narcotics either as continuous infusions or as
intermittent boluses.
• Propofol is the hypnotic of choice in patients with an acute neurologic
insult, as it is easily titratable and rapidly reversible once
discontinued.
• However, propofol should be avoided in hypotensive or hypovolemic
patients because of its deleterious hemodynamic effects
• Benzodiazepines.
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54. Mechanical ventilation
• Patients with severe TBI are usually intubated and mechanically
ventilated.
• Hypoxia, defined as O2 saturation < 90%, or PaO2 < 60 mm Hg,
should be avoided.
• Prophylactic hyperventilation to a PaCO2 < 25 mm Hg is not
recommended
• Within the first 24 hours following severe TBI, hyperventilation should
be avoided, as it can further compromise an already critically reduced
cerebral perfusion.
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55. • Excessive and prolonged hyperventilation results in cerebral
vasoconstriction and ischemia. Thus, hyperventilation is
recommended only as a temporal measure to reduce an elevated ICP.
• A brief period (15-30 minutes) of hyperventilation, to a PaCO2 30-35
mm Hg is recommended to treat acute neurological deterioration
reflecting increased ICP.
• Longer periods of hyperventilation might be required for intracranial
hypertension refractory to all treatments including sedation,
paralytics, CSF drainage, hypertonic saline solutions (HSSs) and
osmotic diuretics.
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56. Hemodynamic support
• Hemodynamic instability is common in patients with TBI.
Hypotension is a frequent and detrimental secondary systemic
brain insult and has been reported to occur in up to 73% during
Intensive care.
Appropriately aggressive fluid administration to achieve adequate
intravascular volume is the first step in resuscitating a patient with
hypotension following TBI.
In patients who respond poorly to adequate volume expansion and
vasopressors, demonstrate hemodynamic instability, or have
underlying cardiovascular disease, a PICCO or pulmonary artery
catheter hemodynamic monitoring may be considered.
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57. • Dextrose containing IVF are to be avoided
• The injured brain tends to absorb free water disproportionately from
hypotonic solutions.
• Thus Isotonic fluids like Normal saline or Ringers lactate solution are
the fluid of choice for fluid resuscitation and volume replacement.
• Anemia is a common secondary systemic brain insult and should be
avoided, with a targeted hemoglobin ≥10 g/dL or hematocrit ≥0.30.
• Brain tissue is reach in thromboplastin and cerebral damage may
cause coagulopathy.
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58. 8/2/2019
• Coagulation abnormalities should be aggressively corrected with
blood products as appropriate.
• Hypertension is also a secondary systemic brain insult that can
aggravate vasogenic brain edema and intracranial hypertension.
However, hypertension may be a physiological response to a reduced
cerebral perfusion.
• Hypertension should not be treated unless a cause has been excluded
or treated, and SBP >180-200 mm Hg or MAP > 110-120 mm Hg.
58

59. Normothermia
• An increase in body and brain temperature is associated with an
increase in cerebral blood flow, cerebral metabolic oxygen
requirement and oxygen utilization, resulting in an increase in ICP and
further potential brain ischemia.
• Therefore, avoidance of hyperthermia should be one of the mainstays
of head-injury management; it may require the use of
pharmacological antipyretics and surface cooling measures.
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60. Cerebral perfusion pressure
• Cerebral ischemia is considered the single most important secondary event
affecting outcome following severe TBI.
• CPP, defined as the (CPP = MAP - ICP), below 50 mm Hg should be avoided.
• A low CPP may jeopardize regions of the brain with pre-existing ischemia,
and enhancement of CPP may help to avoid cerebral ischemia
• The CPP should be maintained at a minimum of 60 mm Hg in the absence
of cerebral ischemia, and at a minimum of 70 mm Hg in the presence
of cerebral ischemia
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61. Osmotic therapy
• Mannitol administration is an effective method to decrease raised ICP
after severe TBI.
• Mannitol creates a temporary osmotic gradient and it increases the
serum osmolarity to 310 to 320 mOsm/kg H2O.
• The effective dose is 0.25-1 g/kg, administered intravenously over a
period of 15 to 20 minutes.
• The regular administration of mannitol may lead to intravascular
dehydration, hypotension, pre-renal azotemia and hyperkalemia.
• Mannitol is contraindicated in patients with TBI and renal failure
because of the risk of pulmonary edema and heart failure
8/2/2019 61

62. • Hypertonic saline 5% (HTS) 250 ml over 20 min ,Can be used as
alternative to mannitol in
Hypernatremia
Hypovolemia
Hypotension
8/2/2019 62

63. Seizure prophylaxis
• Post-traumatic seizures are classified as early occurring within 7 days of
injury, or late occurring after 7 days following injury.
• Prophylactic therapy (phenytoin, carbamazepine, or phenobarbital) is not
recommended for preventing late post-traumatic seizures.
• Phenytoin is the recommended drug for the prophylaxis of early post-
traumatic seizures.
• A loading dose of 15 to 20 mg/kg administered intravenously (I.V.) over 30
minutes followed by 100 mg, I.V., every 8 hours, titrated to plasma level, for
7 days, is recommended.
• Patients receiving antiseizures prophylaxis should be monitored for
potential side effects
8/2/2019 63

64. DVT prophylaxis
• Severe TBI patients are at significantly high risk of developing venous
thrombo-embolic events (VTEs) including deep vein thrombosis (DVT)
and pulmonary embolism.
• Mechanical thromboprophylaxis, including graduated compression
stockings and sequential compression devices, are recommended
unless their use is prevented by lower extremity injuries.
• The use of such devices should be continued until patients are
ambulatory.
• In the absence of a contraindication, low molecular weight heparin
(LMWH) or low dose unfractionated heparin should be used in
combination with mechanical prophylaxis.
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65. Nutritional Support
• Severe TBI patients are usually in hypermetabolic, hypercatabolic and
hyperglycemic state, with altered gastro intestinal functions.
• There is evidence suggesting that malnutrition increases mortality
rate in TBI patients.
• Early enteral feeding is recommended than parenteral in patients with
severe TBI, as it is safe, cheap, cost-effective, and physiologic.
• The potential advantages of enteral feeding include stimulation of all
gastro-intestinal tract functions, preservation of the immunological
gut barrier function and intestinal mucosal integrity, and reduction of
infections and septic complications.
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66. General Intensive care
• Raising head of bed to 15° - 30°: that would reduce ICP and improves
CPP and lower the risk of ventilator-associated pneumonia (VAP).
• Keeping the head and neck of the patient in a neutral position: this
would improve cerebral venous drainage and reduce ICP.
• Avoiding compression of internal or external jugular veins with tight
cervical collar or tight tape fixation of the endotracheal tube that
would impede cerebral venous drainage and result in an increase in
the ICP.
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67. • Turning the patient regularly and frequently with careful observation
of the ICP.
• Providing eye care, mouth and skin hygiene.
• Administrating a bowel regimen to avoid constipation and increase of
intra-abdominal pressure and ICP.
• Performing physiotherapy.
• Peptic ulcer prophylaxis, Severe TBI is a well-recognized risk factor for
stress ulcers (Cushing’s ulcers) with an incidence of around 10%.
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68. Sequelae of Head Injury
• Usually depends on the extent of injury, age
• Post Concussive Syndrome
• Constellation of symptoms that develops within 4 weeks of the injury and
may persist for months (90% at 1 month, 25% at 1 year)
• Treatment is with analgesia, anti-depressants and anti-emetics
• Post-traumatic Epilepsy
• Seizure activity > 7 days from traumatic injury
• Head trauma is the cause of long term epilepsy in 3% of patients with epilepsy
• Incidence is highest in patients with compound skull fracture, intracranial
hemorrhage or presence of early acute symptomatic seizure (presence of all 3
factors increases risk by 50-80%)
• Cannot be prevented with prophylactic use of antiepileptics
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69. • Affective symptoms
• Amnesia
• Neurological deficits (paraparesis, paraplegia etc)
• Persistent Vegetative state
• Rare complication of severe head injury, first described in 1972 by
Jennett and Plum
• Disruption of cerebral cognitive function with sparing of brainstem
function
• No awareness of themselves or environment and cannot interact
with others but will maintain normal sleep-wake cycle
• Recovery is rare if symptoms persist for > 3 months, no recovery
documented after 12 months of symptoms
• Death
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70. Conclusion
• TBI is a devastating injury and often these patients would require
monitoring and treatment in intensive care unit.
• It is best prevented, so effort should be focused on preventing it
• Time is precious, so early intervention is the rule especially to reduce
secondary brain injury to the minimum.
• Management of TBI patients requires multidisciplinary approach,
frequent close monitoring and judicious use of multiple treatments to
lessen secondary brain injury and improve outcomes.
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71. References
• Guidelines for the Management of Severe Traumatic Brain Injury: A joint
initiative of: The Brain Trauma Foundation, The American Association of
Neurological Surgeons & The Joint Section on Neurotrauma and Critical
Care.
• Advanced Emergency Trauma Course (Head injury) by Patrick Carter, MD
• Haddad and Arabi: Critical care management of severe traumatic brain
injury in adults. Scandinavian Journal of Trauma, Resuscitation and
Emergency Medicine 2012 20:12.
• Traumatic brain injury: intensive care management by A. Helmy, M.
Vizcaychipi and A. K. Gupta British Journal of Anaesthesia 99 (1): 32–42
(2007).
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72. • Textbook of Critical Care 4th edition
• Acute Head Injuries in the Intensive Care Unit by Suzanne Gough
• Http://www.radiology.co.uk/srs-x/tutors/cttrauma/tutor2.htm
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