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Head injury

Dr. B.Padmashini Department of Accident, Emergency & Critical Care Medicine. Vinayaka Mission Kirupananda Variyar Medical College & Hospital. Salem,Tamil Nadu

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Head Injury• Number One Killer in

Trauma • 25% of all trauma deaths• 50% of all deaths from MVC• 200,000 people in the world

live with the disability caused by these injuries

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Road Traffic Crashes

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Sports injuries

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Assaults(Sickle injuries)

Assaults(Sickle injuries)

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Basic Anatomy

• Scalp• Skull• Meninges

– Dura Mater– Arachnoid– Pia Mater

• Brain Tissue• CSF and Blood

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Skull

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Dura- mater

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Venous sinuses

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Arachnoid mater

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Pia- mater

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CSF

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Grey matter

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White matter

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Ventricles

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Intracranial Volume

• 80%

Brain Matter

• 10%

Blood

• 10%

CSF

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The MONROE KELLIE doctrine

Dictates that “the total volume of the intracranial contents MUST remain constant”

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Normal state- ICP normal

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Compensated state- ICP normal

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Uncompensated state- ICP Elevated

75 ml 75 ml

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Volume-Pressure Curve

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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”

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ROLE OF

INTRACRANIAL PRESSURE

• 10 mmHg - Normal

• > 20mmHg - Abnormal

• > 40mmHg - Severe

• ICP deteriorates brain function poor outcome

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Intracranial Pressure

• Cerebral Perfusion Pressure (CPP) can be determined by the following formula:

CPP = MAP - ICP

• Normal CPP range is 60 - 150 for autoregulation to work well!

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SYMPTOMS & SIGNS OF INCREASED ICP

• Diminishing level of consciousness

• Headache, vomiting, seizures

• Cushing’s Triad –

bradycardia

hypertension

abnormal respiration

• Pupillary changes

• Papilledema

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• Primary Injury• Mechanical irreversible damage - brain lacerations,

hemorrhages, contusions, and tissue avulsions,• Microscopy - primary injury causes permanent

mechanical cellular disruption and microvascular injury.

PATHOPHYSIOLOGY

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Secondary Injury • Neurologic outcome after head trauma - degree of secondary

brain injury.

• Common Secondary systemic insults –

Hypotension – SBP < 90

Hypoxia - Po2 less than 60

Anemia – reduces O2 Carrying capacity of the blood, to the injured brain tissue,

• Other causes - hypercarbia, hyperthermia, coagulopathy, and seizures.

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CLASSIFICATION

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MECHANISM

• BLUNT INJURY

High Velocity

Low Velocity

• PENETRATING INJURY

Gunshot

Sharp

instruments

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Severity -GLASGOW COMA SCALE

ASSESSMENT AREAS SCORE

Eye opening

Best Motor Response

Verbal Response

Total

4

6

5

15

Mild - GCS 13 - 15Moderate - GCS 9 - 12Severe - GCS 3 - 8

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MORPHOLOGY

• SCALP INJURY Cephal Hematoma Subgaleal Hematoma

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• SKULL FRACTURES

• Vault : linear/stellate depressed/non depressed open/closed

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

Battle sign Raccoon eyes CSF rhinorrhea

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INTRACRANIAL LESIONS

• Focal : epidural hematoma

subdural hematoma

intracerebral hematoma

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Epidural haematoma• Collection of blood & clot b/n dura matter and bones

of the skull• Source Middle Meningeal Artery

Dural Venous Sinuses • C/F Brief loss of consciousness,

headache,drowsiness,dizzy,nausea,vomitting• Rapid clinical deterioration• Talk & die

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EDH

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• Subdural hematomas• Most frequently from

tearing of a bridging vein between the cerebral cortex and a draining venous sinus.

• - acute - <24hrs

- subacute – 24hrs-2wks

- chronic - >2wks

SDH

Shape- Crescent

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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

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INTRACRANIAL LESIONS

Diffuse : concussion

multiple contusion

hypoxic/ischemic injury

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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

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DAI• Shearing forces disrupt

the axonal fibres in the white matter

• Shaken baby syndrome

• Blunt trauma

• Rapid rise in ICT.

• Prolonged or permanent.

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APPROACH TO A PATIENT WITH

HEAD INJURY

• History

• Initial Assessment

Primary Survey

Secondary Survey

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PRIMARY SURVEY

Airway maintenance with cervical spine protection

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• Breathing and ventilation : Intubation precautions

Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes prior to attempt

• Laryngoscopy produces an ICP Spike

Intubation with Cervical inline stabilization

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Circulation

• Maintain MAP >90mmhg- adequate

• Hematocrit >30%

• Cushing reflex

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• Isolated intracranial injuries do not cause hypotension

• LOOK FOR THE CAUSE OF HYPOTENSION

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Disability

• Pupil size

•GCS

Pupillary ChangesIrregular shapedEquality?Constricted?Dilated? Vision Problems?

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SECONDARY SURVEY

• AMPLE history

• Examination of Head to toe

• Glasgow Coma Scale

• Detailed Neurological Examination

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IMAGING STUDIES ONLY AFTER HEMODYNAMIC STABILIZATION

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MANAGEMENT OF

MILD HEAD INJURY(GCS13 -15)

• History

• General Examination

• Limited Neurologic Examination

• C-spine and other X-rays as indicated

• CT scan

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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

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INDICATIONS FOR CT SCAN

• Skull fracture

• Deteriorating GCS

• Neurologic deficit

• Amnesia, headache

• Seizure

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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 Deteriorates (10%)

• Discharge

• Follow up

• Repeat CT scan

• Manage as per severe head injury protocol

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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

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

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• Head end elevation – 30 deg• Intravenous fluids: • Maintain normovolemia• Hypotonic/glucose containing fluids

should not be used• Serum sodium levels monitored daily

MEDICAL THERAPIES FOR HEAD INJURY

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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.

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Furosemide

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

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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.

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Barbiturates

• Effective in reducing ICP – refactory to other measures

• Not used in presence of hypotension/hypovolemia

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• Anticonvulsants

Phenytoin-

Loading dose - 18 – 20 mg/kg

Maintenance dose - 100 mg q 8 hrly

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Surgical management

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

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Burr hole evacuation

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SUMMARY• Endotracheal intubation if GCS < 8

• Moderate hyperventilation

• Treat shock aggressively

• Resuscitate with normal saline or Ringer’sLactate solutions.

• Goal is to achieve a euvolemic state

contd..

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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

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