Care of Acute Head Injury

Dr Ben ManionCAPT 2HSB ARESNeurosurgical registrarGold Coast Hospital

My background

My background

Scope

Immediate triage and treatmentLogistics and definitive point of careDifficulty in accurately predicting the course of a brain injury

Relevance

Up to 25% of battlefield injuries are head and spine 115000 traumatic brain injuries US army 2002-2005 Prevention, diagnosis and treatment of traumatic brain

injury is currently a high profile topic in the US military Up to 62% of Iraqi veterans have screened positive for

acquired brain injury We may miss up to 40% of brain injuries in the field Recent Australian ArmySAFE initiative Prompt and rational treatment makes a significant

difference to outcome

Trimodal death distribution

Primary brain injury

Events at time of trauma Immediate and complete Irreversible, prevention is the only intervention Begins a cascade of events which can cause

further damage Occurs in up to 25% of combat injuries Blast effects currently are the predominant

cause

Cascade of blast effects Direct concussive Blunt or

penetrating injury Contre coup

Physiology of brain injury

Monroe Kellie Doctrine Rigid skull with deformable contents CPP = MAP – ICP Autoregulation fails below 50 or above

160 Normal ICP 0-15

CSF

Arterial Inflow Venous outflow

Capillary blood

Brain Parenchyma

Rigid Skull

Monroe Kellie Doctrine

Physiology of brain injury

Intracranial pressure Monroe Kellie

Doctrine Cerebral perfusion

pressure Critical point of

herniation

Point of herniation 60mmHg

Secondary Brain Injury Hypoxia Hypotension Ischaemia Oedema Haemorrhage Metabolic derangement – hypercapnia, acidosis,

infection Neurotoxic cascades - excitatory amino acids,

endogenous peptides, apoptosis and calcium influx Increased ICP – cerebral oedema, hydrocephalus, brain

herniation

Assessment Patient factors – age, time of injury, GCS, pupils Mechanism – Concurrent fatalities, nature of forces involved,

helmet sensors, care with C-spine Primary Survey (ABC)

A: Hypoxia C: Hypotension Associated injuries

Must examine prior to sedatives/strong analgesics/paralytics Repeat Survey – Changes over time are most important feature of

progression of injury Keep accurate records, standard scoring

Classification of acute head injury

Mechanism Blunt Penetrating Mixed

Morphology Skull fracture Intracranial lesion

Severity mild (14-15) moderate (9-13) severe (3-8)

Mild head injury

GCS 14-15 Awake, amnesic, may be confused Vulnerable to C-spine injury Remove from field CT head if available Multiple scanning tools to assess for concussion

being developed (MACE, ANAM) May have sequelae

Moderate head injury

GCS 9-13 Confused, somnolent or aggressive, focal

neurologic deficits Protect airway Cardiopulmonary stability as priority Remove from field with medical support and

airway capabilities CT head in all cases No role for IV antibiotics in closed head injury

Severe head injury

GCS 3-8 Follow EMST ABCD primary survey protocol Early intubation, 100% oxygen C-spine protection with hard collar Ventilate to pCO2 35 Rapid stabilisation of cardiopulmonary axis

Systolic >100mm Hg Minimal volume isotonic resusc fluids, aim for euvolaemia Hypotension rarely due to primary head injury

Early evac with full medical support

urther managementAirway secured, supplemental oxygen/CPAP PRN. Ventilator as needed to maintain pCO2. End tidal CO2, pulse oximetry.Monitor haemodynamics. Fluids and pressors. Aim for euvolaemia.CP assessment

30% head up to facilitate venous drainageMaintain other parameters Glucose, body temp, sodium Antiemetics, bowel care, maintain nutrition with feeding tube or PEG.

Minimal sedation to facilitate neurological examination and assessment of progress.

ther Management

Mannitol or hypertonic saline to reduce ICP. Can aggravate hypovolaemia. Use in signs of herniation. +/-rusemide (unproven) depending on clinical picture. Steroids not routinely usedAnticonvulsants if high risk (early seizures, depressed skull fracture, intracranial haematoma, epilepsy). Seizures create very high ICPMonitor sodiumMagnesium currently under investigation, may combat calcium influx and cellular damage.

urgical management

ntracranial pressure monitorsExternal ventricular drains

Kochers Point3cm from midline11cm from nasion

xternal ventricular drain entriculostomy)nvasive procedure with moderate risksAllows CSF sampling, ICP monitoring and rapid and ongoing treatment of hydrocephalusCommonly inserted at Kochers point to place EVD in frontal hornLess than 5-7cm depthnsert perpendicular to all planes

urgical management

ntracranial pressure monitorsDecompressive ventricular drainsScalp woundsDepressed skull fracturesntracranial mass lesionsMost GCS <8 do not have intracranial haematomas Burr holes are not often a good solution in an acute

traumatic haematoma, but they may be lifesaving Decompressive craniotomy if facilities permit

xploratory burr ole placementn order of placement

Extend from burrhole with bone nibblers if haematoma foundHighly invasiveMay cause bleeding and brain trauma

ecompressive craniectomyBifrontal

decompressive craniectomy performed

day 8 post injury

ummary

Rapid assessmentTreat and repeat ABCD Avoid hypoxia, hypotensionEarly retrieval as warrantedMedical and nursing managementSurgical options can aid management

eferencesPrevention of secondary brain injury: targeting technology. Littlejohns L, Bader MK. Department of Clinical Development, Integra NeuroSciences, Plainsboro, NJ, USA.ATLS course manual 1997Prevention of secondary brain injury following Head Trauma; Cowley and da Silva Trauma.2008; 10: 35-42 Emedicine - Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology; Segun T DawoduCalcium in cell injury and death; Zheng Dong,1 Pothana Saikumar,2 Joel M. Weinberg,3 and Manjeri A. Venkatachalam Annual Review of Pathology: Mechanisms of DiseaseVol. 1: 405-434 Secondary Brain Injury: Prevention and Intensive Care Management; TVSP Murthy MD, Parmeet Bhatia MBBS, K Sandhu MD; T Prabhakar MD, R LGogna MD; Department of Anesthesia and Intensive care; Army Hospital R&R), Delhi Cantt; Indian Journal of Neurotrauma (IJNT) 2005, Vol. 2, No.

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