Traumatic Brain Injury

Dr. Abimanyu Sakthivelu MDAssistant ProfessorDepartment of Accident, Emergency &

Critical care.Vinayaka Mission UniversitySalem, Tamil nadu, India

Cerebral Hemodynamics

Brain

Blood

Artery Arteriole Capillary

The blood-brain barrier (BBB) maintains the microenvironment of the brain tissue

Introduction

Movement across BBB regulates extracellular ion and neurotransmitter concentrations

Prolonged disruption of the BBB contributes to the development of post-traumatic vasogenic cerebral edema

The brain has an extremely high metabolic rate

Uses up to 20% of oxygen volume consumed by the body

The brain requires approximately 15% of the total cardiac output

Optimal regional CBF is maintained by altering cerebral vessel diameter in response to changing physiologic conditions

Cerebral Blood vessel

Cerebral vasoconstric

tion

Cerebral vasodilat

ion

Hypertension

AlkalosisHypocarbia

Hypotension

AcidosisHypercarbi

aHypoxia

IschemiaIncreased

ICP

Cerebral Perfusion Pressure

The cerebral perfusion pressure (CPP) is the pressure gradient required to perfuse the cerebral tissue

CPP is calculated as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP):

MAP – ICP = CPP

MAP = DBP + [(SBP – DBP)/3]

The local adjustment of cerebral blood flow within the brain microcirculation is termed autoregulation.

Cerebral autoregulation

Cerebral autoregulation is a homeostatic mechanism that minimizes deviations in cerebral blood flow (CBF) when cerebral perfusion pressure (CPP) changes.

CBF is 50 to 55 ml per 100g of brain tissue per minute

CBF is maintained at constant levelsMAP of 60 to 150 mm HgCPP of 50 to 160 mm Hg

Biomechanics of Head Trauma

Direct impactCompression

Energy applied

Cranium absorbs

Shock waves

Travel distant to the site of impact or compression

Distort and disrupt intracranial contents

Alter regional ICP

Prolonged application

Ability of the skull to absorb the force is overwhelmed

Multiple linear skull fractures

High-energy rapid compression force to a small area of the skull.

Depressed fractures

Compression

Cranial contents are set into vigorous motion

Bridging subdural vessels are strained

Indirect brain injury

DAI/Concussion

SDH

Differential acceleration – one brain region slides

past another

Shear and strain injuries results in diffuse injuries

Abrupt arrest of intracranial contents

Contrecoup contusions

Primary brain injury

It is mechanical irreversible damage that occurs at the time of head trauma and includes brain lacerations, hemorrhages, contusions, and tissue avulsions

Secondary brain injury

It results from intracellular and extracellular derangements that are probably initiated at the time of trauma by a massive depolarization of brain cells and subsequent ionic shifts

Hyperpyrexia (core body temperature >38.5 °C) – The mechanism involves stimulation of metabolism in injured areas of the brain, thus recruiting blood flow with a resultant increase in ICP

Anemia (hematocrit <30%) – reduces the oxygen-carrying capacity of the blood, thus reducing the amount of necessary substrate delivered to the injured brain tissue.

Secondary Systemic Insults

Secondary Systemic Insults

Hypoxia (Po2 less than 60 mm Hg) – cerebral vessels dilate to ensure adequate oxygen delivery to brain tissue

Brainstem compression or injury – transient or prolonged apnea

Partial airway obstructionChest wall injury interfering with expansion

Pulmonary injury reducing effective oxygenationIneffective airway management,

The overall mortality from severe head injury

may double or quadruple

Secondary Systemic Insults

Hypercarbia

Hyperthermia

Coagulopathy

Seizures

Pathophysiology

Increased Intracranial Pressure

It is defined as CSF pressure greater than 15 mm Hg (or 195 mm H2O) and is a frequent consequence of severe head injury.

ICP represents a balance of the pressures exerted by the contents of the cranial cavity.

This relationship is explained by the Monro-Kellie doctrine

Monro-Kellie doctrine

Total intra cranial volume remains constant as the cranial vault is a rigid non expansile container

Hayreh SS, Br J Ophthalmol, 1964;48:522–43.

FUNDOSCOPY

** CT BRAIN

Clinical signs

*ONSD or invasive monitoring

Traumatic mass lesion or edema increases ICP

CSF displaced from cranial vault to spinal canal

Compromise of compensatory mechanism

Accommodates volume

of 50 to 100 ml

Vasodilation, CSF obstruction, or small areas of focal edema

Compromise of CPP, vasoparalysis & Loss of autoregulation

Offsets increased blood or brain volume

Brain tissue compression compensates the increase in ICP

The CBF directly depends on systemic MAP

Loss of autoregulation cause massive cerebral vasodilation

Systemic pressure is transmitted to the capillaries

Outpouring of fluids into the extravascular space

Vasogenic edema further increase ICP

ICP rises to the level of the systemic arterial pressure, CBF ceases and brain death occurs

Cerebral edema

Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content.

On computed tomography scans

Bilateral compression of the ventricles

Loss of definition of the cortical sulci

Effacement of the basal cisterns

Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB

Cytotoxic edema is an intracellular process resulting from membrane pump failure when CBF ≤ 40% of baseline

Cushing's Reflex

Cerebral Herniation

New Orleans and Canadian CT Clinical Decision Rules

New Orleans Criteria—GCS 15* Canadian CT Head Rule—GCS 13–15*

Headache GCS <15 at 2 h

Vomiting Suspected open or depressed skull fracture

Age >60 y Any sign of basal skull fracture

Intoxication More than one episode of vomiting

Persistent antegrade amnesia Retrograde amnesia >30 min

Evidence of trauma above the clavicles Dangerous mechanism (fall >3 ft or struck as pedestrian)

Seizure Age 65 y

Identification of patients who have an intracranial lesion on CT

100% sensitive, 5% specific 83% sensitive, 38% specific

Identification of patients who will need neurosurgical intervention 

100% sensitive, 5% specific 100% sensitive, 37% specific

*Presence of any one finding indicates need for CT scan.

Limitations: Not applicable for children and patients on anticoagulation

Classification Of Head injury

Morphology

Severity

Mechanism

Mechanism

Blunt Penetrating

High Velocity Low velocity Gun shot

Automobile collision

Falls & assault

Stab wounds

Severity

Moderate - GCS 9-13Mild - GCS 14-15 Severe - GCS 3-8

Morphology

Skull fractures

Vault Basilar

Linear/stellateDepressed/non

depressedOpen/closed

±CSF leak ±7th -nerve palsy

Intracranial lesions

Epi Dural HematomaSub Dural

Hematoma Intra Cerebral

Hematoma

Focal Diffuse

Concussion Multiple contusion Hypoxic/ischemic

injury

Pre-Hospital Care

Airway

Airway interventions to prevent hypoxia

Unsuccessful attempts at field intubations delays IN – HOSPITAL CARE and increase the risk for aspiration or hypoxia

Unintentional hyperventilation of intubated patients

Outcome of Out – Of – Hospital Endotracheal intubations in TBI

Prehospital hyperventilation

Circulation

Compression of the brainstem and medulla have profound effects on the cardiovascular system - cardiac dysrhythmia

Establishing intravenous (IV) accessCardiac monitor during transport

Scalp lacerations should be secured with less bulky dressing and firm constant manual pressure should be applied to avoid excessive blood loss

Neurologic assessment

Should focus onGCS

Pupillary responsiveness and size

Level of consciousnessMotor strength and

symmetry

Determine the subsequent effectiveness of treatment

Need for sedation

Agitated patients Exacerbate physical injuryCause an increase in ICP

Interfere with appropriate stabilization and

management

Lorazepam

Diazepam

Midazolam

Haloperidol

Droperidol

Tripardol

Emergency Department management

Management Of Mild Head Injury (GCS14 -15)

History

General Examination to exclude systemic injuries

Limited Neurologic Examination

C-spine and other X-rays as indicated

Blood alcohol level and urine toxicology screening

CT scan is indicated if criteria for high or moderate risk of neurosurgical intervention are present

Observe or admit to hospital Discharge from hospital

Observe or admit to hospitalNo CT scanner available Abnormal CT scan All penetrating head injuriesH/O prolonged loss of consciousnessDeteriorating level of consciousness Moderate to severe headacheSignificant alcohol / drug intoxication

Skull fractureCSF leak – rhinorrhea or otorrheaSignificant associated injuriesNo reliable companion at homeAbnormal GCS score (<15)Focal neurological deficits

Discharge from hospital

Patient does not meet any of the criteria for admissionDiscuss need to return if any problems develop and issue

a “warning sheet”Schedule a follow – up visit

Management of moderate head injury (GCS 9-13)

Initial ExaminationSame as for mild head injury plus baseline blood workCT scan brain – obtained in all casesAdmit to a facility capable of definitive neurosurgical care

After AdmissionFrequent Neurologic ChecksFollow up CT if condition deteriorates or preferably before discharge

Improves (90%) Deteriorates (10%)

Discharge when appropriate

Follow up in clinic

If the patient stops following simple commands repeat CT scan

Manage as per severe head injury protocol

Management of severe head injury(3 - 8 )

ABCDEsPrimary Survey and ResuscitationSecondary Survey and ‘AMPLE’ historyAdmit to facility – neurosurgical care

Neurologic Re-evaluationEye openingMotor responseVerbal responsePupillary reaction

Therapeutic agents (administered after Neurosurgical consult) Mannitol Moderate hyperventilation (Pco2 ~ 35 mmHg)Anti convulsants

CT Brain

Airway

Attention must be given to the increased ICP that can potentially occur with any physical stimulation of the respiratory tractLidocaine (1.5–2 mg/kg IV push) Suppresses Cough reflexHypertensive responseIncreased ICP associated with intubation

Etomidate (0.3 mg/kg IV)

Short-acting sedative-hypnotic agentBeneficial effects on ICP by reducing CBF and metabolism.Has minimal adverse effects on blood pressure and cardiac output Fewer respiratory depressant effects than other agents.

Hypotension A cause other than the head injury should be

soughtScalp lacerations can cause hypovolemic hypotensionHemorrhage into an epidural or subgaleal hematoma (children)Neurogenic hypotension in concomitant high spinal cord injury

Fluids should never be withheld in the head trauma patient with hypovolemic hypotension for fear of increasing cerebral edema and ICP

Hyperventilation

Acute hyperventilation prevents or delays herniation in the patient with severe TBIGoal is to reduce the pco2 to the range of 30 to 35 mm hgThe onset of effect is within 30 seconds and peaks within 8 minutesHyperventilation lowers the ICP by 25%

Osmotic Agents

Mannitol is the mainstay for control of elevated ICP acute severe TBI.

Mannitol (0.25–1 g/kg)

Hypertonic saline (HTS)

Preclinical studies have demonstrated that HTS can significantly reduce ICP

Adverse events - Renal Failure, Central Pontine Myelinoysis, Rebound ICP elevation

Brain cell

VesselMannit

ol

Expands vessel

volume in hypovolemi

c shock

Decrease ICP (6 to 8

hrs) provides space for expansion

of hematoma

Reduces blood

viscosity & microcircula

tory resistance &

promotes CBF

Free radical

scavenger

In large doses Renal failure &

HypotensionInduce a paradoxical

effect

Crystalloids Vs Colloids

Role of Albumin in TBI

Mannitol Vs 7.45% Hypertonic Saline Solution (HSS)

Barbiturates

Reduce cerebral metabolic demands of the injured brain tissueAffect vascular tone and inhibit free radical-mediated cell membrane lipid peroxidation

Role of Barbiturates

Furosemide

To reduce ICT in conjunction with mannitol Dose 0.3 to 0.5 mg/kg Never use in Hypovolemia

Biomarkers for TBI

Admission serum albumin levels –Effective indicator of outcome of TBI

Role of Hypothermia TBI

Role of hyperglycemia in TBI

Seizure Prophylaxis

INDICATIONS FOR ACUTE SEIZURE PROPHYLAXIS IN SEVERE HEAD

TRAUMA

Depressed skull fracture

Paralyzed and intubated patient

Seizure at the time of injury

Seizure at emergency department presentation

Penetrating brain injury

Severe head injury (GCS score ≤8)

Acute subdural hematoma

Acute epidural hematoma

Acute intracranial hemorrhage

Prior history of seizures

Early seizures can cause hypoxia, hypercarbia, release of excitatory neurotransmitters, and increased ICP, which can worsen secondary brain injuryLorazepam (0.05–0.15 mg/kg IV over 2–5 minutes up to a total of 4 mg)Diazepam (0.1 mg/kg, up to 5 mg IV, every 10 minutes up to a total of 20 mg)Phenytoin (18–20 mg/kg IV) Fosphenytoin (15–18 phenytoin equivalents/kg) IV or IM can be given

Recombinant factor VIIa (rFVIIa)

Role of steroids in TBI

Cranial Decompression

Emergency trephination

Signs of herniationRefractory rise of ICPRapid detoriation

Blind invasive procedureChances of localizing the expanding lesions are uncertainMay temporarily reverse or arrest the herniation syndromeProvides time formal craniotomy

Specific indications for craniotomy

Clinical deterioration Size > 1cm thick extracerebral clot. Volume > 25 – 30 ml in

intracerebral hematomas. Midline shift > 5 mm. Enlargement of contralateral ventricle (temporal horn). Obliteration of basal cisterns or third ventricle. Raised or increasing ICP

EDH

Need surgical evacuation

Timing – Any patient with EDH in coma or Any EDH with >30cm3 irrespective of the GCS

Can wait

EDH<30cm3 <15mm thickness <5mm midline shift GCS> 8

Ref:-neurosurg-58,2006

When to operate in Acute SDH

Acute SDH >10mm or midline shift >5mm on CT regardless of GCS

If GCS is decreased in hospital from time of injury to Admission by >2, Anisocoria or ICP>20mmhg

Ref:-neurosurg-58,2006

Operations definitely indicated only if it is a compound (open) fracture (not over sagittal sinus) or if the fracture is so extensive that it causes mass effect.

Closed depressed skull fractures are usually treated conservatively, but operation may be appropriate in selected cases to reduce mass effect or correct defigurement.  

Role of probiotics and early entral nutrition in TBI

Researches and ongoing trials

ACHIEVE

To explore the efficacy of albumin as a neuroprotective agent for TBI in humans, a randomized controlled trial, Albumin for Intracerebral Hemorrhage Intervention (ACHIEVE), is currently underway

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