Traumatic brain injury

ANESTHESIA MANAGEMENT OF
TRAUMATIC BRAIN INJURY
-Dr. Richa Kumar

• Worldwide, Traumatic Brain Injury (TBI) is a leading cause of
morbidity and mortality
• Despite new medical advances in monitoring and treatment
strategies, outcomes after TBI remain poor.
• According to the Brain Trauma Foundation (BTF), the use of
evidence based protocols has reduced TBI mortality from 50%
to 25% over the last three decades

Pathophysiology of TBI
PRIMARY AND SECONDARY INJURIES
• The primary injury : initial injury( physical or mechanical ) on the
brain parenchyma and skull an inflammatory cascade including
cerebral edema, axonal injury, and decreased CPP
• Secondary injuries : consequence of the primary injury
electrolyte abnormalities, hypoxemia, glycemic imbalance,
hypotension, loss of autoregulation, increased ICP, and hyper or
hypocarbia.
• Patient outcomes correlate with the severity of the primary
injury. rapid and efficient TBI severity stratification and
management decreases effects of primary injuries and prevent
secondary injuries

• TBI may also be classified according to whether it is blunt or
penetrating.
• Penetrating injury may vary depending on site, depth, and
energy, but is generally fatal if it bilaterally traverses the
midbrain.
• Although initial mortality from penetrating injury is higher ,
outcome in survivors of both groups are similar.

• Vascular injury : superficial veins arterial blood vessels EDH rapidly
expanding quick neurological deterioration devastating if not treated
immediately

• Aceelaration-decelaration forces tear cortical bridging veins SDH may
manifest slowly without S/S

• Traumatic SAH (tSAH) : up to 60% of admissions for TBI
• Prolongation of the QTc interval is seen in 67% of patients with tSAH,
proportional to severity.
• Approximately 20% of patients with tSAH may also develop vasospasm, which
can lead to secondary ischemic insult.
• The diagnosis and management of the vasospasm are facilitated by the use of
transcranial Doppler monitoring

Evaluation of TBI Patients
• Focused history and physical examination
HISTORY TAKING SHOULD INCLUDE
• Neurological state (consciousness, pupillary response) and vital
parameters at the scene and during transport
• Estimated blood loss
• Nature of treatment at scene and in transit
• Use of airbags, seat-belts, crash-helmets
• Time, place, mechanism, vehicle speed (in relation to the accident)
• Past medical history
• Suspected influence of drugs or alcohol
• Possible medical reason for the accident (e.g. fit, heart attack,
spontaneous intracranial haemorrhage, stroke)
• Use of anticoagulants or antiplatelet therapy

• Physical examination:
• careful airway assessment
• thorough neurological examination (baseline sensation, motor
function, and the presence of new FND) degree of TBI & CSI
• During first assessment: recognize critical signs of other
trauma related injuries such as bleeding, pneumothorax,
cardiac tamponade, etc.

Determine the level of consciousness according to the Glasgow Coma
Scale
Repeated GCS measurement is indicated even when the initial GCS value is high. In
such case a decline of GCS is a useful guide for further CT and clinical decision making
e.g. as an indication for surgery or ICP monitoring.

Examine the pupils for size, symmetry, and reaction to light.

Cervical Spine Injury (CSI) after TBI
• Early assessment of cervical spine integrity is essential to rule out a hidden
cervical spine fracture, especially in the TBI patient.
• Studies show correlation between CSI and poor GCS
• Maintain a high degree of suspicion for CSI in a TBI patient especially with
a low GCS .
• O/E of the cervical spine look for
 tenderness along the spine,
 a “gap” or “step” deformity in the continuity of the spine,
 other mass effect due to edema, hematoma, or muscle spasm

• Imaging in CSI Patients
• Improves efficiency in treating TBI patients.
• There are two well established guidelines for obtaining cervical spine
radiographic imaging of TBI patients. The National Emergency X-Radiography
Utilization Study (NEXUS) and the Canadian C Spine Rule.
• The NEXUS study concluded that a patient was at low risk for CSI if none of
the following five clinical criteria are present:
• Low risk criteria for CSI (NEXUS) If following are absent:
1. Midline cervical tenderness
2. Focal neurological deficits
3. Altered mental status
4. Evidence of intoxication
5. Distracting injury present diverting attention from neck pain

IMMEDIATE ASSESSMENT AND TREATMENT
• Secure (or maintain) the patient’s airway. (A)
• Optimise oxygenation and ventilation. (B)
• Initiate haemodynamic resuscitation and fluid
administration. (C)
• Identify both intracranial and extracranial injuries.
• Prioritisation of injuries (see management algorithm).
• Collate information about the mechanism of the injury
and relevant past medical history.
• Continue to (re)assess level of consciousness

(A) Extracranial life-threatening haemorrhage. (Extremely rarely, intracranial
haemorrhage without
prior CT)
(B) Head. Extracranial as clinically indicated
(C) In selected patients only, particularly MRI of the spine in spinal injury patients
(D) Intracranial haematoma. Major extracranial injuries
(E) Indications for admission to ICU: coma with diffuse brain injury; post-neurosurgery;
altered
consciousness and requiring intubation; multi-injured/cardio-respiratory instability;
brain-stem death(?)

• Securing the Airway
• If radiographic study cannot be done (hemodynamic instability or
airway emergency) unstable cervical spine is assumed until
proven otherwise.
• Prevention of further neurological injury is critical.
• Maintaining spinal alignment, protecting the spinal cord, and
stabilizing the cervical spine.
• Cervical collar may stabilize the spine BUT, interferes with DL . So
removal of only anterior portion of the cervical collar is
recommended, leaving the posterior portion.

To maintain the patient’s cervical spine immobile during
laryngoscopy several techniques have been developed. The
most common is called Manual In-Line-Immobilization
(MILI)

• The use of MILI has less impact obtaining a view of the vocal cords during
direct laryngoscopy compared to immobilization with axial traction utilizing a
cervical collar, tape, or sandbag
• Historically, practitioners preferred nasotracheal intubation with flexible
bronchoscopy or a surgical airway due to the possibility of spinal injury during
oral intubation
Complications:
 Suspected basal skull fracture  endotracheal tube inserted blindly may find
path to the brain.
 Trauma to the nares and epistaxisimpair visualization of VC

• Therefore, OROTRACHEAL INTUBATION AFTER RAPID
SEQUENCE INDUCTION AND DIRECT LARYNGOSCOPY WITH
MILI IS SAFEST CHOICE .
• If airway management history or assessment reveals a
possible challenging intubation, an awake fiberoptic
intubation should be performed instead
• ADVANTAGES if done by experienced practitioner :maintains
the cervical spine in a neutral position & preserves airway
reflexes

• Ventilation in TBI
• Securing the airway by intubating our patient has three specific
goals:
 prevention of aspiration of gastric contents
 prevention of hypoxia and
 Prevention of hypercarbia.
• Hypoxia has direct correlation to poor outcomes in TBI patients
• A Level 3 recommendation by the BTF is to avoid PaO2 < 60
mmHg & maintain SPO2 >90%
release of catecholamines dilates
cerebral veins & increase ICP

• S/S elevated ICP:

 new onset of focal neurological deficits,
 decreased consciousness,
 inappropriate pupillary responses, vomiting,
 cardiac or respiratory arrest, or
 Cushing’s triad of hypertension bradycardia, and bradypnea,
 or signs of brain herniation

Preoperative Management
• The clinician should avoid hypercarbia related to the
administration of hypnotic agents or sedatives such as
benzodiacepines, narcotics, etc, prior to induction of
anesthesia

INTRAOPERATIVE MANAGEMENT
The patient will require to be anaesthetised, even when
consciousness is already
impaired, to minimise the risk of secondary brain damage due
to induced raised ICP
Rapid sequence induction and intubation is the
recommended technique using a combination of sedative with
low cardiopressant
effects (e.g. midazolam, ketamine), analgesic (fentanyl) and
muscle relaxant (e.g.
succinylcholine) agents

1. INTRAOPERATIVE MONITORING AND
INTRAVENOUS ACCESS:
• Besides standard ASA monitors, an arterial line and adequate intravenous
access are essential in the management of TBI patients.
• One very important consideration: placement of these lines should not delay
the start of the surgical intervention.
• Placement of two large bore (>/=18 gauge)
• If difficult IV central line, (the femoral vein is most appropriate in order to
avoid trendelenburg positioning )fail, then tibial or humeral intra-osseous
lines should be placed
• Temperature monitoring (lower esophageal= tympanic membrane)

• ICP monitoring can be done by placing intraparenchymal probe or
intraventricular catheter and ICP maintained <20mmHg
• Cerebral oxygenation can be measured by :
• Jugular venous O2 saturation , PET, near infrared spectroscopy
& direct brain tissue oxygenation.
• Currently, ICP/Pbo2 and ventriculostomy are frequently used in
the management of patients with severeTBI. (C/I:coagulopathy )
• NG tube especially in bad facial injuries ( caution in trauma of
base of skull)
Brain tissue hypoxia can be corrected by increasing FiO2,
blood tranfusion,
inotropic support and decreasing ICP

2. BLOOD PRESSURE MANAGEMENT:
• Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP)
- IntracranialPressure (ICP)
• If CPP decreases, brain parenchyma oxygenation can be further
compromised in TBI patients.
• Treatment should focus on keeping CPP within normal range and
also decreasing ICP
• The current recommendations are to maintain SBP> 90 mmHg &
CPP 50 and 70 mm Hg to avoid further brain ischemia

• Management of hypotension with vasopressor is common. The
choice of which vasopressor to use is unclear.
• FLUID RESUSCITATION IS MAINSTAY OF THERAPY (hypertonic
saline solutions optimal, no ideal IVF)
• The ideal medication for treatment of hypertension : easily
titratable and should not cause cerebral vasodilatation to avoid
further increase in ICP.
• Therefore the antihypertensive drugs recommended include
propranolol, esmolol,labetalol, and nicardipine
• Nitroglycerine, nitroprusside, and hydralazine should be avoided

3 . MANAGEMENT OF ICP
• The Brain Trauma Foundation states that ICP > 20 mmHg is associated
with increased mortality and worse outcomes .
• The fastest way to decrease ICP > 20 mmHg is to allow CSF drainage
from a CSF drain if present.
• elevate the patient’s head and maintain the neck in a neutral position,
to improve venous blood return.

• slow administration of 0.25-1 gm/kg of mannitol in stable
patients over fifteen minutes (not rapidly) ICP reduction, a
transient increase in oxygen transport, and increase in CBF
• monitor and replace urinary loses to prevent intravascular
volume depletion and hypotension when mannitol is
administered  otherwise adverse effect on kidney due to
hypoperfusion.
• Rebound increase in ICP due to worsening of vasogenic oedema
(damaged blood brain barrier)

• Hyperventilation can temporarily treat ICP but should be used with caution as
it can also decrease brain oxygenation leading to adverse outcomes. (maintain
PaCO2 near 35mmHg.. And not less than 20-25mmHg)
• It is recommended only for episode of increased ICP not corrected by other
modalities) Hyperventilation is a level 3 recommendation by the BTF as a
temporary measure to reduce ICP.
• (BE AWARE: excessive hyperventilation can lead to cerebral vasoconstriction
and oxygen deprivation)

• Hypertonic salineosmotic mobilization of water across the intact
BBBreduction in cerebral water contentdecrease the ICP and improve
blood flow to the brainbenefit of not causing hypotension as compared to
the use of mannitol
• Prevent hypernatremia (maintain not higher than 150-155 mEq/ml with a
blood osmolality of less than 320 mOsm/dl
• Hypotonic solutions are contraindicated because they add free water that
might lead to cerebral edema and worsened ICP in a TBI patient
• Therefore isotonic solutions should be used for fluid resuscitation in TBI
patients. 0.9% normal saline solutions are indicated because they are more
isotonic than Ringer’s lactate.
• Glucose containing solutions & albumin should be avoided, unless
hypoglycemia is present.

• Hypothermia may have a role in controlling ICP in patients with
TBI
• Oxygen consumption is decreased due to decreased metabolic
rate aprrox. 5-7% with per degree celsius of cooling.
• Corticosteroids had an adverse effect on mortality and
morbidity thus not recommended

4. COAGULOPATHY AND HEMOGLOBIN LEVEL
• TBI may produce coagulopathy through the systemic release of by-products
from neuronal death such as tissue factor and phospholipids  impairs
coagulation reactions, platelet function  disseminated intravascular
coagulation.
• Exaccerbated by colloid infusion
• Coagulation parameters should be measured immediately in acute TBI patients
• Any abnormal values should be identified and corrected.
• INR in TBI patients should be maintained less than or equal to 1.4
• Platelet count maintained above 75 k/uL .
• Hemoglobin levels should be maintained at or above 7 g/dl to avoid a decrease
in brain oxygen delivery

• TBI patients may also develop endogenous acute coagulopathy (EAC) due to
activation of the protein C pathway(25% of major trauma patients)
• EAC is characterised by anticoagulation derangement and hyperfibrinolysis 
not reflected by standard coagulation tests (aPTT and PT/INR).
• Therefore, once multiple injuries are found and the patient is unstable despite
crystalloid infusion, balanced transfusion of blood products should be
considered early, possibly without waiting for lab results.
• Balanced transfusion involves the use of plasma, platelets and packed red
blood cells (1:1:1), with the aim to effectively reconstitute whole blood.
• TEG or ROTEM, if accessible, should be performed during the first 72 hours
after trauma

5. GLYCEMIC CONTROL
• The presence of hyperglycemia might produce an increase in neuronal
metabolism and increase neuronal death after TBI.
• These events occur due to:
1. increased tissue acidosis through anaerobic metabolism,
2. creation of free radicals
3. increased blood brain barrier permeability.
• Ideal blood glucose level should range from 80-180 mg/dl

6 . THERMOREGULATION:
• it is important to remember that fever worsens the severity of brain injury by
increasing cerebral metabolic rate.
• early hyperthermia after TBI has been found to be a possible predictor of
paroxysmal sympathetic hyperactivity.
• The final BTF recommendation is to avoid hyperthermia and to maintain
normothermia with antipyretics and surface cooling devices
• Hypothermia still may have a role in controlling ICP in patients with TBI

7. OTHER ORGAN FAILURE:
• TAKOTSUBO CARDIOMYOPATHY may develop in severe TBI
• this is due to cathecholamine surge subendocardial ischemia biventricular
failure ( even in young previously healthy patients)
• This cycle may be exaccerbated in OR procedures.
• They may have an abnormal ECG, lactic acidaemia and a low pH.
• Arterial pressure may be elevated.
• Central venous saturation may be low.
• ECG shows prolonged ST segment elevation.
• Echocardiography shows transient left ventricular apical ballooning.
• This syndrome, previously named ‘neurogenic oedema’ or ‘stunned myocardium’
• With supportive management the condition often resolves within hours or days
but it ultimately requires a negative coronary angiogram for conclusive diagnosis.
• Beta blocking drugs may be protective in such a case

• Patients with Chest trauma, aspiration and massive
resuscitation after shock are at increased risk of ALI (ACUTE
LUNG INJURY)
• Earlier PEEP was C/I but now considered appropiate because
hypoxemia needs to be corrected
• With adequate intravascular resuscitation PEEP does not
increase ICP or decrease CPP and may infact increase CPP due
to correction of Hypoxemia and improved cerebral
oxygenation.
ALI AND CARDIAC INSUFFICIENCY AFTER TBI MAY LEAD TO
COMPROMISED OXYGENATION
AND THERFORE DECREASE CEREBRAL PERFUSION

Choice of Anesthetic Drugs
• Propofol is indicated as a sedative agent in the TBI patient with a
secure airway.
• Advantage : quick onset and offset of action that facilitates
neurologic assessment also decreases neuronal oxidative stres
• treatment of refractory status epilepticus with a recommended
starting loading dose of 1 mg/kg for more than 48 hour
• Caution: sympathetic blockade resulting in hypotension.
• Complication :propofol infusion syndrome(infusion>= 4 mg/kg/hr)

• Early studies concluded ketamine increased CBF and ICP
( based on small sample sizes with higher than recommended
induction doses)
• Recent studies do not show support this & instead prove
potential benefits : the blockade of reuptake of catecholamines
by ketamine prevent hypotensive episodes (maintain MAP &
CPP)
• Avoided in hypertensive patients

• Etomidate :
• D/A: causes dose dependent inhibition of 11-beta-hydroxylase
and 17-alpha-hydroxylase leading to adrenal suppression.
• This complication can occur after a single dose and may cause
maximal adrenal suppression 4 to 6 hours after its
administration.

Muscle relaxants:
• As RSI is commonly done in TBI  Succinylcholine is the neuromuscular
blocking agent of choice transient increase in ICP.
• Despite this potential side effect, the benefit of its rapid onset and duration of
action and the prevention of coughing during direct laryngoscopy greatly
outweighs its negative effect.
• This side effect can be prevented by administering defasciculating dose of a
non-depolarizing muscle relaxant or by using rocuronium 0.9-1.2mg/kg will
achieve same intubating conditions like succinylcholine at 60-90 seconds
however muscle paralysis might last for 30 to 40 minutes

• Opioids are used to suppress airway reflexes, decrease required dose of
induction agents and inhalation anesthetic maintenance as well as to blunt
the sympathetic response to direct laryngoscopy.
• Fentanyl, sufentanil, and remifentanil are commonly used in TBI patients.
• Careful opioid titration should be observed to avoid hypotension secondary
to a reduction in sympathetic tone and potential histamine release from
these agents

• MAINTENANCE OF ANESTHESIA
• Opioids do not further increase ICP, blunt the sympathetic response during
intubation and surgical stimulation and prevent hypertensive response that
would further increase ICP.
• Intravenous and inhalation anesthetics can be used safely
• Intravenous anesthetics such as sodium thiopental,etomidate, midazolam
and propofol decrease CBF,CBV,CMRO2 and ICP under controlled ventilation
conditions.
•
• They achieve these effects by producing cerebral vasoconstriction and acting
at the neurons’ GABA receptors to open chloride channels.

• Dexmedetomidine, alpha 2 receptor agonist, it exerts its effects in the
locus coeruleus.
• Despite its sedative and anxiolytic action it preserves adequate respiratory
function when compared with benzodiazepines or narcotics. This property
makes it an ideal agent in the non intubated TBI patient.
• In ICU setting dexemedetomidine has proved to decrease the incidence of
delirium.
• It suitable alternative to propofol for sedation purposes

• Inhalation Anesthetics (IAs) produce “uncoupling effect” that may lead to
increase ICP
• This effect can be avoided by titrating IAs to levels below 1 Minimal Alveolar
Concentration (MAC) .
• At a dose of 0.5 MAC, CMR suppression–induced reduction in CBF
predominates, and net CBF decreases in comparison with the awake state.
• At 1 MAC, CBF remains unchanged; CMR suppression and vasodilatory effect
are in balance.
• Beyond 1 MAC, the vasodilatory activity predominates, and CBF significantly
increases, even though the CMR is substantially reduced

• While nitrous oxide is the only inhalation anesthetic that produces an
increase in CMRO2, the rest, isoflurane, sevoflurane and desflurane decrease
CMRO2 (H>D>I>S)
• Therefore, the use of nitrous oxide should be avoided in TBI patients.
• The literature currently finds no difference in outcomes between theuse of
inhalation anesthetics and intravenous anesthetics or the combination of
both in the intraoperative and perioperative care of TBI patients
• there is no ideal anesthetic,
• BTF clinical guidelines should be followed while administering anesthesia to
this group of patients, especially avoiding hypoxemia,PaO2 below 60 mmHg,
oxygen saturation below 90%, hypercarbia and hypotension, (systolic blood
pressure below 90 mmHg)

Traumatic brain injury

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