1. Anaesthesia management of
head trauma patients in OT &
ICU

2. 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.

3. Pathophysiology of raised ICP

4. Intracranial Pressure Volume relation

5. Factors affecting ICP
Pathophysiology Causes
Focal brain oedema (localized mass lesion) Traumatic hematomas (extradural, subdural, intracerebral)
Neoplasms (gliomas, meningiomas, metastasis)
Ischemic or hemorrhagic stroke, abscess
Diffuse brain oedema Encephalitis, meningitis, diffuse head injury, seizures,
encephalopathy (hepatic, toxic, uremic or septic),
hypoxemic ischemic encephalopathy, water intoxication,
Reye's syndrome
Disturbance of CSF circulation Obstructive hydrocephalus
Communicating hydrocephalus
Subarachnoid hemorrhage
Obstruction to major venous sinuses Depressed fractures overlying major venous sinuses.
Cerebral venous thrombosis
Vascular malformations Arteriovenous malformation
Idiopathic Benign intracranial hypertension

6. S/S elevated ICP:
Headache
Nausea and vomiting
Systolic hypertension
Bradycardia Cushing's triad
Irregular respiration, Cheyne-stokes respiration
Decreased mental abilities
Confusion
Double vision
Pupils not reacting to light and unequal pupils
Loss of consciousness and finally coma as the pressure
worsens.

7. Management of raised ICP
Increased ICP aggravates secondary brain injury.
Detrimental processes are cerebral ischemia, cerebral edema and
neurochemical interplay of excitatory neurotransmitters, free
radicals’ formation, and increased levels of calcium and potassium
intracellularly.
Most commonly the interventions are aimed at decreasing the
cerebral blood volume and the fluid component of the brain tissue.
Drainage of CSF or surgical removal of brain tissue are done in
selected cases.

8. GENERAL MANAGEMENT/TIER ZERO
Airway - Proper and prompt management of airway, breathing and
circulation prevents hypoxia, hypercapnia and hypotension.
Ventilation - Hypercarbia is a potent cerebral vasodilator causing
increase in cerebral blood volume and ICP.
Blood Pressure - Hypotension will decrease the cerebral perfusion
pressure in a brain with impaired autoregulation, maintain CPP between
60-70 mm hg.
Fluids - Saline vs. Albumin Fluid Evaluation (SAFE) study found that
mortality was higher in patients resuscitated with albumin compared
with saline, avoid hypotonic solutions as well to prevent brain edema.

9. Sedation and Analgesia -
Sedative Advantages Cautions Literature
Propofol Recommended for the control of ICP (level IIb) High dose or prolonged infusion: Propofol infusion syndrome First line sedative
15
Midazolam Safe in rICP lowest incidence of spreading depolarizations, a
potentially modifiable secondary injury mechanism
Tachyphylaxis First line sedative
15
-Robin et al.: iv bolus of midazolam prior to suctioning significant
reduction in ICP
16
Ketamine NMDA receptor antagonist neuroprotective effect inconclusive
Used as an adjunct with other sedatives: has shown to decrease
ICP
17
Early case reports concluded that it increases CSF secretion
increases ICP
Intraoperative administration of ketamine for craniotomy: 1 mg/kg
Ketamine reduced ICP
18
Further RCTs required
Barbiturates Only for elevated ICP refractory to maximum standard medical and
surgical treatment.
Prophylactic use against the development of raised ICP: not
recommended.
Hemodynamic stability is essential
Brain Trauma Foundation guidelines
9
Dexmedetomidine Sedation and analgesia without respiratory depression
Patient is arousable, facilitates neurological assessment
Rapid distribution and elimination properties
Hypotension, bradycardia, Agitation
Further studies to establish its dose and duration
Aryan et al., neurosurgical patients: safe and effective, mean ICP
decreased.
19
avoid loading dose, higher maintenance doses to
ensure adequate sedation
Inhaled sedatives: sevoflurane and isoflurane Emerging as sedative agent Flow metabolism uncoupling action
Acute cerebrovascular disease: sevoflurane was associated with a
significant increase in ICP
20
Subarachnoid hemorrhage without rICP: 0.8 % isoflurane
significantly improved regional CBF with modest effect on ICP
when compared with propofol

10. Cerebral Venous Drainage - Head end of the bed should be kept
elevated at 15–30 degrees with the head in a neutral position to
enhance cerebral venous drainage and to promote the circulation of
CSF from intracranial to spinal compartment.
Fever Control - Fever increases metabolic rate by 10% to 13% per
degree Celsius and is a potent vasodilator. It increases ICP.
Glucocorticoids - Steroids are contraindicated in treating raised ICP
or for improving outcome secondary to TBI or spontaneous
hemorrhage (Level I Evidence)

11. Tier 1 Specific Therapy
Osmotic Therapy - Hyperosmolar agents help to decrease ICP by
effectively reducing brain water,
Mannitol is effective for control of raised ICP at doses of 0.25–1 g/kg
body weight. Doses > 200g/day may cause ARF. The serum
osmolarity should be monitored and kept below 320 mOsm/kg.
Onset starts within 1-5 minutes , peaks in 40 minutes, stays for 1.5-
6 hrs.
Hypertonic saline (HTS) - Bolus dosing 3%: 2.5–5 mL/kg over 5–20
minutes.
CVP line access is recommended.

12. Tier 2 management
Resection of Mass Lesions - definitive therapy for the lesions.
CSF Drainage - by external ventricular drain (EVD) lowers ICP
immediately by reducing intracranial volume.
Decompressive Craniectomy - removal of a portion of the skull vault,
large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm
diameter) is recommended over a small frontotemporoparietal DC for
reduced mortality and improved neurologic outcomes in patients with
severe TBI.
Hyperventilation - temporizing measure for the reduction of ICP in the
setting of refractory hypertension and for brief periods (<2 hours) in
cases of cerebral herniation or acute neurologic deterioration

13. Antiseizure Therapy - Seizure will increase CMR and CBF. Latest BTF
guidelines have recommended phenytoin to decrease the incidence
of early posttraumatic seizures (PTS), within 7 days of injury.

14. Tier 3 management: Most aggressive with most side effects
Barbiturate coma: The mechanism of ICP reduction by barbiturates is
probably the result of a coupled reduction in CBF and CMR. Thiopentone
is given in a loading dose of 5mg/kg over 30 minutes followed by infusion
of 1-5 mg/kg hour until the electroencephalogram shows a burst
suppression pattern. Complications of barbiturate coma include
hypotension, hypokalemia, respiratory depression, infections due to
immune suppression, and hepatic and renal dysfunction.
Therapeutic Hypothermia - reduces the CMR in a similar way as
pentobarbital coma. It also reduces the basal component of cellular
metabolism along with suppression of electrical activity of brain.37 The
evidence for benefit is stronger for post-cardiac arrest patients and for
neonatal hypoxic ischemia.

15. Tight Brain Checklist

16. If above checklist does not resolve the issue, follow
methods of rapid reduction of ICP and BV.
1. Further reduction of PaCO2 (but not less than 25 mm Hg)
2. CSF drainage ( ventriculostomy, brain needle)
3. Diuretics ( usually mannitol)
4. CMR suppression ( barbiturates, propofol)
5. MAP reduction (if dysregulated)
6. Surgical Control ( lobectomy, removal of bone flap )

17. 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.

18. Manual In Line Stabilization (MILS)

20. The use of MILS 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.

21. Ventilation in TBI
Securing the airway by intubating our patient has three specific goals:
1. prevention of aspiration of gastric contents
2. prevention of hypoxia and
3. prevention of hypercarbia.
Release of catecholamines→ dilates cerebral veins & increase ICP
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%

22. Preoperative Management
The clinician should avoid hypercarbia related to the administration of
hypnotic agents or sedatives such as benzodiazepines, narcotics, etc,
prior to induction of anesthesia.
Blood group cross matching to be done and blood products to be
available SOS.
ICP management.

23. Monitoring
General: Invasive arterial pressures, GCS and pupils, Arterial blood
gases, ECG, Pulse Oximetry, Temperature, Blood sugar, Endtidal Co2.
Specific: Intracranial pressure, Transcranial doppler, Jugular saturation,
Brain oximetry, Microdialysis, Imaging

24. Which patients need ICP monitoring?
1. GCS 3-8 and abnormal CT scan
2. GCS 3-8 with normal CT and two or more of the following:
Age > 40 years.
Motor posturing
Systolic blood pressure (SBP) <90 mmHg
3. GCS 9-15 and CT scan
Mass lesion (extra-axial > 1 cm thick temporal contusion, intracranial hemorrhage, or ICH, > 3cm)
Effaced cisterns.
Shift > 5 mm.
4. Following craniotomy
5. Neurological examination cannot be followed (i.e., requires another surgical procedure,
sedation).

25. INTRAOPERATIVE MANAGEMENT
The patient will require to be anesthetized, even when consciousness is
already impaired, to minimize 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 cardio-pressant
effects (e.g. midazolam, ketamine), analgesic (fentanyl) and muscle
relaxant (e.g. succinylcholine) agents.

26. 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)

27. 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.
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

28. BLOOD PRESSURE MANAGEMENT:
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) –
Intracranial Pressure (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> 100-110 mmHg &
CPP 60 and 70 mm Hg to avoid further brain ischemia.

30. Management of hypotension with vasopressor is common. The choice of
vasopressor is usually norepinephrine.
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.

31. 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.
Exacerbated 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

32. TBI patients may also develop endogenous acute coagulopathy (EAC) due to
activation of the protein C pathway (25% of major trauma patients)
EAC is characterized 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

33. 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

34. 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

35. Patients with Chest trauma, aspiration and massive resuscitation after
shock are at increased risk of ALI (ACUTE LUNG INJURY)
PEEP can be considered for correcting hypoxemia.
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

36. 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 stress.
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.

37. Barbiturates: causes
(1) hypnosis,
(2) depression of CMR,
(3) reduction of CBF due to increased cerebral vascular resistance, and
(4) anticonvulsant activity.
(5) absorption of CSF.
Hence barbiturates are highly effective in lowering ICP.
Their anticonvulsant properties are also advantageous in neurosurgical
patients who are at increased risk of seizures.

38. Ketamine
Only IV anesthetic that dilates the cerebral vasculature and increases CBF
(50–60%).
Ketamine may also impede the absorption of CSF without affecting
formation.
Increases in CBF, cerebral blood volume, and CSF volume can potentially
increase ICP.
Ketamine’s blockade of the NMDA receptor during periods of increased
glutamate concentrations, as occurs during brain injury, may be protective
against neuronal cell death.

39. Etomidate :
To be avoided in patients with known history of seizures, because of
increased frequent incidence of myoclonic movements.
Decreases the CMR, CBF, and ICP.
Decreases production and enhances absorption of CSF.

40. Muscle relaxants:
As RSI is commonly done in TBI → Succinylcholine is the neuromuscular
blocking agent of choice, but 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 will last for 30 to 40
minutes.

41. 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

42. 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.
Intravenous anesthetics such as sodium thiopental, etomidate,
midazolam and propofol decrease CBF, CBV, CMRO2 and ICP under
controlled ventilation conditions.

43. Dexmedetomidine, alpha 2 receptor agonist, it exerts its effects in the
locus coeruleus. It reduces both CBF and CMR.
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 dexmedetomidine has proved to decrease the incidence
of delirium.
It suitable alternative to propofol for sedation purposes

45. 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)
>With IV agents, NO has minimal effects on CBF, CMR, and ICP.
>With VAs , NO further increase CBF.
>NO alone causes cerebral vasodilation and can potentially increase ICP.
Therefore, the use of nitrous oxide should be avoided in TBI patients.
The literature currently finds no difference in outcomes between the use of
inhalation anesthetics and intravenous anesthetics or the combination of
both in the intraoperative and perioperative care of TBI patients.

46. EDH surgical management

47. SDH surgical management

48. Post-op care:
For only EDH evacuation, pt. can be extubated once wide awake.
For other injuries like DAI, SDH, prolonged mechanical ventilation
required.
Peak brain edema takes 24-48 hrs to ensue.
Therefore post operative care mainly revolves around preventing
secondary brain injuries due to brain edema, hypoxia, hypotension etc.
Continued brain insults will cause altered brain consciousness, focal
neuro deficits, unequal pupillary response.

49. Mechanical thromboprophylaxis using graduated stockings or sequential calf
compression device are recommended.
Avoid use of UFH or LMWH to prevent I/C hematoma expansion.
Prophylaxis for seizures with phenytoin or CBZ initiated early after injury to reduces
the incidence of traumatic seizures (for 7 days).
General ICU care like, 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.

50. 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.
NUTRITIONAL SUPPORT
Severe TBI patients are usually in hypermetabolic, hypercatabolic and
hyperglycemic state, with altered G.I.T Functions, hence early enteral
feeding is recommended over parenteral feed.

51. Brain Trauma Foundation summary for TBI,
2016
1. Decompressive craniectomy (DC)
A large frontotemporoparietal (FTP) DC (not less than 12 × 15 cm or 15
cm diameter) is recommended.
2. Prophylactic hypothermia
Early (within 2.5 hours), short term (48 hours postinjury) prophylactic
hypothermia is not recommended to improve outcomes in patients
with diffuse injury.

52. 3. Hyperosmolar therapy
Although hyperosmolar therapy may lower ICP, there is insufficient
evidence about effects on clinical outcomes to support a specific
recommendation, or to support use of any specific hyperosmolar
agent, for patients with severe TBI.
4. Cerebrospinal fluid (CSF) drainage
An external ventricular drainage (EVD) system zeroed at the midbrain
with continuous drainage of CSF may be considered to lower ICP
burden more effectively than intermittent use. Use of CSF drainage to
lower ICP in patients with an initial Glasgow Coma Scale (GCS)

53. 5. Ventilation therapies
Prolonged prophylactic hyper ventilation with partial pressure of carbon
dioxide in arterial blood (PaCO2) o f 25 mmHg or less is not recommended.
6. Anesthetics, analgesics, and sedatives
Administration of barbiturates to induce burst suppression measured by EEG
as prophylaxis against the development of intracranial hypertension is not
recommended. High-dose barbiturate administration is recommended to
control elevated ICP refractory to maximum standard medical and surgical
treatment. Hemodynamic stability is essential before and during barbiturate
therapy. Although propofol is recommended for the control of ICP, it is not
recommended for improvement in mortality or 6-month outcomes. Caution
is required as high-dose propofol can produce significant morbidity.

54. 7. Steroids
The use of steroids is not recommended for improving outcome or
reducing ICP. In patients with severe TBI, high dose methylprednisolone
is associated with increased mortality and is contraindicated.
8. Nutrition
Feeding patients to attain basal caloric replacement at least by the fifth
day and, at most, by the seventh day postinjury is recommended to
decrease mortality. Transgastric jejunal feeding is recommended to
reduce the incidence of ventilator-associated pneumonia (VAP)

55. 9. Infection prophylaxis
Early tracheostomy is recommended to reduce mechanical ventilation
days when the overall benefit is felt to out weigh the complications
associated with such a procedure. However, there is no evidence that
early tracheostomy reduces mortality or the rate of nosocomial
pneumonia. The use of povidone-iodine (PI) oral care is not
recommended to reduce VAP.
10. Deep-vein thrombosis (DVT) prophylaxis
LMWH or low-dose UFH may be used in combination with mechanical
prophylaxis. However, there is an increased risk for expansion of
intracranial hemorrhage.

56. 11. Seizure prophylaxis
Prophylactic use of phenytoin or valproate is not recommended for
preventing late post-traumatic seizure (PTS). Phenytoin is
recommended to decrease the incidence of early PTS (within 7 days of
injury), when the overall benefit is felt to outweigh the complications
associated with such treatment. However, early PTS has not been
associated with worse outcomes.

57. Monitoring recommendations:
1. ICP monitoring
Management ofsevere TBIpatients using information from ICP
monitoring is recommended to reduce in-hospital and 2-week,
postinjury mortality.
2. Cerebral perfusion pressure (CPP) monitoring
Management of severe TBI patients using guidelines-based
recommendations for CPP monitoring is recommended to decrease 2-
week mortality.

58. 3. Advanced cerebral monitoring
Jugular bulb monitoring of arterio venous oxygen content difference
(AVDO2), as a source of information for management decisions, may be
considered to reduce mortality and improve outcomes at 3 and 6
months postinjury.

59. Thresholds recommendations:
1. Blood pressure thresholds
Maintaining SBP at ≥100 mmHg for patients 50–69 years old or at ≥110
mmHg or above for patients 15–49 or over 70 years old may be
considered to decrease mortality and improve outcomes.
2. ICP thresholds
Treating ICP above 22 mmHg is recommended because values above
this level are associated with increased mortality. Combination of ICP
values and clinical and brain CT findings may be used to make
management decisions.

60. 3. CPP thresholds
The recommended target CPP value for survival and favorable
outcomes is between 60 and 70 mmHg. Whether 60 or 70 mmHg is the
minimum optimal CPP threshold is unclear and may depend upon the
patient’s autoregulatory status. Avoiding aggressive attempts to
maintain CPP above 70 mmHg with fluids and pressors may be
considered because of the risk of adult respiratory failure.
4. Advanced cerebral monitoring thresholds
Jugular venous saturation of < 50% to be avoided to reduce mortality.