Traumatic and Head Injury

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Traumatic Head Injury Toh C J

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No patient want to be this ........ No Neurosurgeon like to plant .......

Classification:

Classification Severity Anatomic findings

Classification:

Classification Severity Minimal : GCS 15, no LOC or amnesia Mild : GCS 14, or 15 + LOC or amnesia impaired alertness or memory Moderate : 9-13 or LOC ≥ 5 min or focal neurological deficit Severe : GCS 5 - 8 Critical : GCS 3 - 4

Classification:

Classification Anatomic findings Focal Diffuse Contusion Coup Countrecoup Gliding Fracture Hematoma Epidural Subdural Intraparenchymal Intermediary Concussion DAI

Marshall CT Grading of Brain Trauma:

Marshall CT Grading of Brain Trauma Diffuse Injury Grade CT appearance Mortality I Normal CT scan 9.6% II Cisterns present. Shift < 5mm 13.5% III Cisterns compressed/absent. Shift < 5mm. 34% IV Shift > 5mm 56.2%

Classification:

Classification Primary Secondary Injury sustained by the brain at the time of impact Examples: Brain laceration Brain contusion Injury sustained by the brain after the impact Causes: Hypoxia, Hypoperfusion Examples: cerebral edema, herniation

Prehospital management:

Prehospital management How to transfer head injury patient: Stabilize patient at trauma scene Do not move patient unnecessarily Maintain ABC, ABC, ABC, ABC Protect cervical spine Stop active bleeding Relay information to receiving doctors ABC status GCS & pupil size Suspected injuries Transfer patient only if it is SAFE

Head injury management in A&E room:

Head injury management in A&E room General aims Stabilization Prevention of secondary brain injury Specific aims Protect the airway & oxygenate Ventilate to normocapnia Correct hypovolaemia and hypotension CT Scan when appropriate Neurosurgery if indicated Intensive Care for further monitoring and management

Head injury management in A&E room:

Head injury management in A&E room Means of stabilization – RESUSCITATION Primary Survey & Resuscitation (ABC) To detect and treat immediately life-threatening conditions Idea: to keep the patient alive Secondary surgery To detect injury that can kill patient in few hours Idea: to keep the patient alive longer Definitive treatment Managing above injury urgently

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A B C D E

Secondary survey in trauma patients:

Secondary survey in trauma patients To detect life-threatening injury can kill in few hours if not treated Head-to-toe examination Injuries Intracranial hematomas Pneumo- or hemo-thorax Intra-abdominal organ injury Pelvic fracture Actively bleeding wound In head trauma Basically – to detect increased ICP

Secondary survey for head trauma:

Secondary survey for head trauma GCS Pupillary size Active bleeding scalp wound

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GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = incomprehensive sound 3 = inappropriate words 4 = confuse 5 = alert Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command

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GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries 3 = vocal sounds 4 = words 5 = orientated to face Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command Pediatric age 1- 5 yrs

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GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries 3 = vocal sounds 4 = words Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain Pediatric age upto 6 months

Pupillary response::

Pupillary response : Pupillary response can determine the level of nervous system dysfunction in a comatose patient.

Other NeuroExam:

Other NeuroExam Full exam Visual acuity in an alert patient Pupillary light reflexes, both direct and consensual Retinal detachment or hemorrhages or papilledema Spinal tenderness and, if the patient is cooperative, limb movements Motor weaknesses, if possible, and gross sensory deficits Reflexes, plantar response

Other NeuroExam:

Other NeuroExam Signs of Skull Base fracture Raccoon eyes Battle sign (after 8-12 h) CSF rhinorrhea or otorrhea Hemotympanum

Imaging of head injury:

Imaging of head injury Modalities Skull X-ray CT scan MRI Areas Skull, brain Cervical spine Chest Pelvis

Skull Fracture:

Skull Fracture Types Depressed / non-depressed Importance Non-depressed per se: minimal Depressed A/w low GCS Compound fractures Foreign body

Acute ExtraDural Hemorrhage:

Acute ExtraDural Hemorrhage Young patient Between skull & dura No direct injury to brain Blood clot – from torn blood vessel of dura (artery) Trauma – okay – slowly deteriorating – coma – death EDH patient should NOT die If patient die … we better die too

Acute SubDural Hemorrhage:

Acute SubDural Hemorrhage Young patient Clot – between dura & brain surface From damaged brain surface Brain laceration (otak koyak) Burst lobe (otak pecah) DIRECT brain injury Hematoma – usually thin Major problem – damaged brain Outcome – worse than EDH Usually need surgery, to remove Hematoma Skull bone (open the box)

Brain contusion (LEBAM):

Brain contusion (LEBAM) Young Direct brain injury Size: small  large If multiple – means severe diffuse brain injury Surgery if Large Easily accessible (senang buang) Prognosis: moderate

Diffuse brain injury:

Diffuse brain injury Young CT scan ‘normal’ Very small ‘white dots’ Acceleration – decerelation Shearing force “Poor GCS with ‘normal’ CT scan” Treatment – based on GCS, ICP & CPP Important to repeat CT after 24-48 hours Edema Delayed hematoma

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Management of TBI

Monro-Kellie hypothesis:

Monro-Kellie hypothesis The sum of the intracranial volumes of blood, brain, CSF is constant, and that an increase in any one of these must be offset by an equal decrease in another, or else pressure will rise.

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Management of TBI Detection & Monitor Treatment

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Detection & Monitor GCS Pupillary reflex ICP Monitor Symptoms & sign of herniation

Methods of monitoring intracranial pressure.:

Methods of monitoring intracranial pressure . Fiberoptic sensors (Camino), Microchips (internal strain-gauge devices)(Codman) Air pouch technologies (Spiegelberg)

Methods of monitoring intracranial pressure.:

Methods of monitoring intracranial pressure .

EVD, External Ventricular Drain:

EVD, External Ventricular Drain

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Primary injury Secondary injury Herniation Mass lesion ICP  ICP  ICP  ICP 

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Secondary injury Hypoxia Hypovolemia Cerebral edema

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How to manage raise ICP?

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Cerebral Protection ≠ Sedation

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Managing raise ICP General measure Medical management Surgical intervention

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General measure Head elevation Maintain normal temperature Neck vein compression? ? Chest Physio Hyperventilation Fluid management Glucose monitor Maintain normal Blod pressure

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Head elevation Head is raised 30 to 45 degrees above the level of the heart. This will enhance the venous drainage and thus reducing the intracranial blood volume and ICP.

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Neck vein compression? Neck in neutral position Collar is fixed properly Arm sling is not compressing the neck vein

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Maintain normal temperature Keep patient’s body temperature within normal limit

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? Chest Physio To give sedation during chest physiotherapy

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Hyperventilation NO HYPERVENTILATION !!!! Keep patient at the lower limit of normocapnia (32mmHg) Optimal Oxygenation !!! Increased CO2 = Vasoconstriction and Decreased ICP Decreased CO2 = Vasodilatation and Increased ICP

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Fluid management Fluid management should aim primarily at preventing hypotension while optimizing cerebral perfusion pressure.

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Glucose monitor Patient with injuries to the brain are often hyperglycaemic. High level of serum glucose levels may aggravate cerebral edema through an osmotic mechanism and may be responsible for increased anaerobic glycolysis leading to lactic acidosis.

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Medical management Sedation Muscle relaxant Barbiturate & Propofol analgesic antipyretic Mannitol & Frusemide Hypertonic saline antiepileptics Neuroprotective agent BP control

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Sedation analgesic Midazolam + Morphine

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Barbiturate & Propofol Barbiturates appear to exert their ICP-lowering effects through vasoconstriction, which results in a reduction in CBF and CBV secondary to the suppression of cerebral metabolism

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Muscle relaxant Increase incidence of aspiration pneumonia

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Mannitol & Frusemide The administration of mannitol has become the first choice for pharmacological ICP reduction , Mannitol has an immediate plasma-expanding effect that reduces haematocrit and blood viscosity and increases CBF and cerebral oxygenation delivery. Hyperosmotic agents remove more water from the brain than from other organs because the blood–brain barrier impedes the penetration of the osmotic agent into the brain maintaining an osmotic diffusion gradient. This osmotic effect of mannitol is delayed for 15–30 min. Mannitol consistently decreases ICP for 1–6 h.

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Mannitol & Frusemide An ultra-early single-shot administration of high-dose mannitol (1.4 g/kg) in the emergency room significantly improves the 6-month clinical outcome after head injury One risk of hyperosmotic agents is the rebound effect, which might increase ICP. To reduce this risk it is recommended that mannitol should be administrated as repeated boluses rather than continuously, only in patients with increased ICP and not longer than 3–4 days As mannitol is entirely excreted in the urine there is a risk of acute tubular necrosis, particularly if serum osmolarity exceeds 320 mOsmol/l

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Mannitol & Frusemide Although furosemide itself has only a minimal effect on ICP, in combination with mannitol it enhances the effects of mannitol on plasma osmolality, resulting in a greater reduction of brain water content

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Hypertonic saline Several studies have shown that hypertonic saline is equal or even superior to mannitol in reducing ICP. Vialet et al. suggested that hypertonic saline (2 ml/kg, 7.5%) is an effective and safe initial treatment for intracranial hypertension episodes in head trauma patients when osmotherapy is indicated. Even very high concentrated hypertonic saline solutions (23.5%) can be used and can reduce ICP in poor grade patients with subarachnoid haemorrhage.

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antipyretic antiepileptics Neuroprotective agent it is evident that hyperthermia should be avoided Is not for reduce ICP. But to prevent fit which will cause raise ICP Still under experimental stage

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Surgical intervention Removal of the pathological lesion CSF diversion procedure Open the cranium “craniectomy” Remove part of the non-eloquent brain “Lobectomy”

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Removal of the pathological lesion CSF diversion procedure Open the cranium “craniectomy” Remove part of the non-eloquent brain “Lobectomy”

Summary of TBI management:

Steps Rationale Respiratory support (intubation & ventilation) Comatose, unable to protect airways Elevate head 30-45° Facilitate venous drainage Straighten neck, no tape encircling the neck Facilitate venous drainage Avoid hypotension (SBP<90mmHg) Prevent hypoxia – edema Control hypertension Avoid transmission of pressure to ICP Avoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatation Control ventilation, aims PaCO2 35-40 mmHg Avoid vasoconstriction / -dilatation Adequate sedation To reduce brain metabolism Do CT brain Ascertain intracranial pathology rapidly Summary of TBI management

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Brain swelling

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Bleeding

Take Home Message::

CPP = MAP - ICP Take Home Message: ICP keep < 20 mmHg CPP keep 60 to 70 mmHg “Biar lambat asalkan selamat”

Summary::

Summary: Classification of TBI: Management: Prehospital. In Hospital: Primary survey & secondary survey. Imaging Monitor “cerebral protection” Surgical intervention.

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TQ

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