Dr.

Sireesh, Associate Professor General Surgery

HEAD INJURIES

HEAD INJURES
INTRODUCTION CAUSES PHYSIOLOGY & PATHOPHYSIOLOGY CLASSIFICATION ASSESSMENT MANAGEMENT

INTRODUCTION
Number

One Killer in Trauma 25% of all trauma deaths 50% of all deaths from RTA 200,000 people in the world live with the disability caused by these injuries

CAUSES OF HEAD INJURY

Road Traffic Crashes

Sports injuries

Assaults (Sickle injuries)

Head Injury & Traumatic Brain Injury(TBI)

Head

injury associated with traumatic brain injury (TBI) occurs with an incidence of 2040 cases per 100 000 population per year. It is the most common cause of death in young adults (age 1524 years) and is more common in males than females.

Head Injury - Normal Physiology

Brain

consumes 20% of total O2 Receives 15% of Cardiac Output Brain tissue perfusion - Normal cerebral blood flow is approximately 55 ml /100 g/min maintained by Autoregulation despite variation in MAP between 50150 mm Hg.

Intracranial Volume

80%
Blood

Brain Matter

10%

10%

CSF

Intracranial Pressure

The pressure of the brain contents within the skull is intracranial pressure (ICP) The pressure of the blood flowing through the brain is referred to as the cerebral perfusion pressure (CPP)

The pressure of the blood in the body is the mean arterial pressure (MAP) CEREBRAL BLOOD FLOW Normal CBF 50ml/100gm of brain/min AUTOREGULATION

ROLE OF INTRACRANIAL PRESSURE

8 - 12 mmHg > 20mmHg > 40mmHg

- Normal - Abnormal - Severe

ICP deteriorates brain function poor outcome

Cerebral Perfusion Pressure

Cerebral Perfusion Pressure (CPP) = MAP ICP Cerebral perfusion pressure should be maintained at > 65 mmHg in severely head-injured patients. This is an independent prognostic factor in neurological outcome. Normal CPP - 60 - 150 for autoregulation to work well.

Normal state- ICP normal

HEAD INJURY MASS EFFECT Compensated state- ICP normal

MASS Effect - Uncompensated state- ICP Elevated - Brain herniation Rapid clinical deterioraion

Brain herniations
(1) Subfalcine herniation associated with midline shift (2) (3) Herniation of the uncus of the temporal lobe is associated with compression of the ipsilateral third nerve. (4) Central herniation and (5) Tonsillar herniation are associated with compression of brainstem structures.

SYMPTOMS & SIGNS OF INCREASED ICP

Diminishing level of consciousness Headache, vomiting, seizures Cushings Triad bradycardia hypertension abnormal respiration Pupillary changes Papilledema

Vicious cycle in head injuries

Head Injury Pathophysiology

Primary

injury

Irreversible cellular injury as a direct result

of the injury occurs at the time of impact Includes injuries such as brainstem and hemispheric contusions, diffuse axonal injury and cortical lacerations.
Prevent

the event

Head Injury-Pathophysiology

Secondary injury
Damage to cells that are not initially injured Occurs hours to weeks after injury

Causes of secondary brain injury

Hypoxia: PO2 < 8 kPa Hypotension: systolic blood pressure (SBP) < 90 mmHg Raised intracranial pressure (ICP): ICP > 20 mmHg Low cerebral perfusion pressure (CPP): CPP < 65 mmHg Pyrexia Seizures Metabolic disturbance
Hypoxemia, Hypotension ,Anemia, Hyperglycemia,

Prevent Secondary Brain Injury

Evacuation of mass

CLASSIFICATION OF HEAD INJURIES

MECHANISM

FALL FROM HEIGHT BLUNT INJURY

RTA

High Velocity Low Velocity

PENETRATING INJURY Gunshot Sharp instruments

Severity -GLASGOW COMA SCALE

ASSESSMENT AREAS Eye opening Best Motor Response Verbal Response Total SCORE 4 6 5 15

minor head injury: GCS 15 with no loss of consciousness (LOC); mild head injury: GCS 14 or 15 with LOC; moderate head injury: GCS 913; severe head injury: GCS 38.

MORPHOLOGY

SCALP INJURY Cephal Hematoma Subgaleal Hematoma

SKULL FRACTURES Vault : linear/stellate depressed/non depressed open/closed

Basilar : with/with out CSF leak with/with out seventh-nerve palsy

Battle sign

Raccoon eyes

CSF rhinorrhea

INTRACRANIAL LESIONS

Focal : epidural hematoma subdural hematoma intracerebral hematoma

Epidural haematoma
Is a neurosurgical emergency Collection of blood & clot b/n dura matter and bone of the skull Nearly always associated with a skull fracture - temporal, frontal or the posterior fossa Source Middle Meningeal Artery Dural Venous Sinuses

 The

classical presentation - initial injury followed by a lucid interval (headache but fully alert and orientated with no focal deficit). After minutes or hours a rapid deterioration occurs, with contralateral hemiparesis, reduced conscious level and ipsilateral pupillary dilatation as a result of brain compression and herniation.

EDH
EDH on a CT scan lentiform (lens shaped or biconvex) hyperdense lesion between the skull and brain An associated mass effect on the underlying brain, with or without a midline shift.

EDH- TREATMENT
immediate The

surgical evacuation

overall mortality for all cases of EDH is about 18% but for isolated EDH it is about 2%.

SDH

Subdural hematomas - in the space between the dura and the arachnoid. Most frequently - tearing of a bridging vein between the cerebral cortex and a draining venous sinus or brain laceration. - acute - <24hrs - subacute 24hrs2wks - chronic - >2wks

Shape Crescent concave appearance

SDH- TREATMENT

Small haematomas with little mass effect may be managed conservatively in neurosurgical centres

Acute SDH evacuation via a craniotomy. Mortality rate from Acute SDH 40 %

Chronic SDH and most acute-on-chronic SDH evacuation via burr hole(s) rather than craniotomy.

Intra Cerebral Heamatoma

Formed within brain tissue & caused by shearing or tensile forces that mechanically stretch and tear deep small caliber arterioles Most common in temporal and frontal regions C/F depend on site involved

SUBARACHANOID HAEMORRHAGE
Trauma

is by far the commonest cause of subarachnoid haemorrhage overall, Aneurysms are the most common cause of spontaneous subarachnoid haemorrhage. Traumatic subarachnoid haemorrhage is managed conservatively.

INTRACRANIAL LESIONS
Diffuse : concussion multiple contusion hypoxic/ischemic injury

Concussion

Temporary & brief interruption of neurological function after minor head injury Due to shearing / stretching of white matter fibres at the time of impact or temporary neuronal dysfunction C/o headache, confusion, amnesia CT/MRI cannot detect

DAI

Shearing forces disrupt the axonal fibres in the white matter Shaken baby syndrome Blunt trauma Rapid rise in ICT. Prolonged or permanent.

APPROACH TO A PATIENT WITH HEAD INJURY

Taking a history in head injury Mechanism of injury Loss of consciousness or amnesia Level of consciousness at scene and on transfer Evidence of seizures Probable hypoxia or hypotension Pre-existing medical conditions Medications (especially anticoagulants) Illicit drugs and alcohol Initial Assessment Primary Survey Secondary Survey

PRIMARY SURVEY
ABCDE of trauma care A Airway maintenance and cervical spine protection B Breathing and ventilation C Circulation with haemorrhage control D Disability: neurological status E Exposure: completely undress the patient and assess for other injuries

PRIMARY SURVEY Airway maintenance with cervical spine

protection A definitive airway is required in cases of severe head injury for patients in traumatic coma is unable to protect their airway and is at risk of aspiration; gas exchange may be impaired; the safe interhospital transfer of a patient with an impaired conscious level . Hypoxia and hypercapnia avoidedPevent secondary brain injury

Intubation with Cervical inline stabilization

Breathing and ventilation : Intubation precautions Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes prior to attempt Laryngoscopy produces an ICP Spike

Circulation

Maintain MAP >90mmhg- adequate Hematocrit >30% Cushing reflex bradycardia, wide pulse irregular respiration

pressure &

Isolated intracranial injuries do not cause hypotension LOOK FOR THE CAUSE OF HYPOTENSION
USG ABDOMEN

PELVIC COMPRESSION TEST

Disability
Pupil size Pupillary Changes Irregular shaped Equality? Constricted? Dilated? Vision Problems? GCS

Assessment Findings

Constricted?
narcotics?

Sluggish/dilated?
mid brain ICP

Unilateral dilation?
pressure on CNIII

Fixed and Dilated?

herniation

Adjuncts to the primary survey

Blood

FBC, urea and electrolytes, clotting screen, glucose, toxicology, cross-match ECG Two wide-bore cannulae for intravenous fluids Urinary and gastric catheters Radiographs of the cervical spine and chest

SECONDARY SURVEY

Review of patients history (AMPLE) Allergy Medication including tetanus status Past medical history Last meal Events of the incident Examination of Head to toe Glasgow Coma Scale Detailed Neurological Examination

IMAGING STUDIES ONLY AFTER HEMODYNAMIC STABILIZATION

MANAGEMENT OF MILD HEAD INJURY(GCS13 -15)

History General Examination Limited Neurologic Examination C-spine and other X-rays as indicated CT scan

CRITERIA FOR ADMISSION

No CT scanner available Abnormal CT scan findings All penetrating head injuries Skull fractures CSF leak Deteriorating level of consciousness Moderate to severe headache Significant alcohol / drug intoxication Significant associated injuries

INDICATIONS FOR CT SCAN

Glasgow Coma Score (GCS) < 13 at any point GCS 13 or 14 at 2 hours Focal neurological deficit Suspected open, depressed or basal skull fracture Seizure Vomiting > one episode

Urgent

CT head scan if none of the above but:

Age > 65 Coagulopathy (e.g. on warfarin) Dangerous mechanism of injury (CT within 8 hours) Antegrade amnesia > 30 min (CT within 8 hours

MANAGEMENT OF MODERATE HEAD INJURY(GCS 9-12)

Initial Examination - Same as for mild head injury - CT scan brain obtained in all cases - Admission for observation After Admission

Frequent Neurologic Checks

Improved Discharge Follow up

Deteriorates (10%)
Repeat CT scan Manage as per severe head injury protocol

MANAGEMENT OF SEVERE HEAD INJURY(3 - 8 )

Primary Survey and Resuscitation Secondary Survey and AMPLE history Admit to facility neurosurgical care Neurologic Re-evaluation Eye opening Motor response Verbal response Pupillary reaction

CT scan only after hemodynamic stabilization Medical therapy for raised ICP Immediate neurosurgeon opinion If needed surgical management

MEDICAL THERAPIES FOR HEAD INJURY

Head end elevation 30 deg Intravenous fluids: Maintain normovolemia Hypotonic/glucose containing fluids should not be used Serum sodium levels monitored daily

Mannitol

0.25-1g/kg Osmotic agent- dec ICP, maintains CBF,CPP and brain metabolism Dec ICP within 6 hrs. Expands volume, O2 carrying capacity. Diuretic effect- net intravascular volume is reduced.

Furosemide

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

HYPERVENTILATION

No role as prophylaxis in 24 hrs. Reducing PaCO2 cerebral vasoconstriction Maintain PaCo2 25 35 mmhg Last resort for reducing ICP TEMPORARY MEASURE ONLY.

Barbiturates

Effective in reducing ICP refactory to other measures Not used in presence of hypotension/hypovolemia

Anticonvulsants PhenytoinLoading dose Maintenance dose - 18 20 mg/kg 100 mg q 8 hrly

Surgical management

Scalp wounds cleaning & debridemant Elevation of depressed Fractures Craniotomy & evacuation of Haematoma Cranial decompression for reduction of ICT

Burr hole evacuation

SUMMARY

Endotracheal intubation if GCS < 8 Moderate hyperventilation Treat shock aggressively Resuscitate with normal saline or RingersLactate solutions. Goal is to achieve a euvolemic state contd..

SUMMARY

Frequent neurological assessment Exclude cervical spine injuries Transfer all moderate to severe head injured patients if neuro surgeon is not available at your facility

THANK YOU