TRAUMATIC BRAIN INJURY

& SPINAL INJURY

NAME –BIBASWAN CHAKRABARTY

DESIGNATION-1ST YEAR POST GRADUATE
TRAINEE
DEPT OF GENERAL SURGERY
UNIT 1
NBMCH
TRAUMATIC BRAIN INJURY
 DEFINITION:
Traumatic brain injury (TBI) is a nondegenerative,
noncongenital insult to the brain from an external mechanical
force, possibly leading to permanent or temporary impairment
of cognitive, physical, and psychosocial functions, with an
associated diminished or altered state of consciousness.
 PHYSIOLOGY:
CBF = 55 mL /min /100 gms of brain tissue.
Ischaemia <20 mL /min/100 gms
CPP= MAP-ICP.
CPP (75–105 mmHg) = MAP (90–110 mmHg) – ICP
(5–15 mmHg)
cerebral autoregulation.
THE MONRO KELLIE DOCTRINE:
 CLASSIFICATION OF HEAD INJURY

Mild
Moderate
Severe
Very severe
National Institute for Health and Care Excellence
discharge criteria in minor and mild head injury.
 GCS 15/15 with no focal deficits
 Normal CT brain
 Patient not under the influence of alcohol or drugs
Patient accompanied by a responsible adult
 Verbal and written head injury advice: seek medical
attention if: ● Persistent/worsening headache
despite analgesia ● Persistent vomiting ●
Drowsiness ● Visual disturbance ● Limb weakness
or numbness
 CONCUSSION:
Concussion is defined as alteration of
consciousness as a result of closed head
injury, but is generally used in describing mild
head injury without imaging abnormalities; loss
of consciousness (LOC) at the time of injury is
not a prerequisite.
Key features :
confusion and amnesia.
lethargic, easily distractable, forgetful, slow to
interact or emotionally labile. Gait disturbance
and incoordination
 MODERATE AND SEVERE
TRAUMATIC BRAIN INJURY
 MANAGEMENT:
 RESUSCITATION:
 HISTORY
● preinjury state (fits, alcohol, chest pain)
● mechanism and energy involved in the injury (speed
of vehicles, height fallen)
● conscious state and haemodynamic stability of the
patient after the accident
medication history ; anticoagulants and antiplatelet
agents
 PRIMARY SURVEY
● Ensure adequate oxygenation and
circulation
● Exclude hypoglycaemia
● Check pupil size and response and Glasgow
Coma Scale score as soon as possible
● Check for focal neurological deficits before
intubation, if possible
 SECONDARY SURVEY
● Battle’s sign, periorbital bruising and
blood in ears/nose/ mouth may point to
base of skull fracture
● Cervical spine fractures are common
and must be actively excluded
● Log-roll to check whole spine for steps
and tenderness, and for per rectum exam
 SURGICAL MANAGEMENT:
CLOSED LINEAR FRACTURE-
CONSERVATIVE

OPEN OR COMMINUTED-DEBRIDEMENT
AND BROAD SPECTRUM ANTIBIOTICS

DEPRESSED-EXPLORATION AND
ELEVATION
 FRACTURE SKULL BASE:
KEY FEATURES:
 OTORRHEA
 RHINORRHEA

 BRUISING AROUND EYE , BEHIND

EAR
 EXTRADURAL HAEMORRHAGE:
neurosurgical emergency.
 rupture of an artery, vein or venous sinus, in
association with a skull fracture
 Transient loss of consciousness is typical,
subsequent lucid interval with headache but
without any neurological deficit. contralateral
hemiparesis
 reduced conscious level
 ipsilateral pupillary dilatation
SUBDURAL HAEMORRHAGE
 HIGH ENERGY IMPACT
 RUPTURE OF CORTICAL SURFACE
VESSELS
 RAPIDLY EXPANDING HAEMATOMA
 NEED SURGICAL EVACUATAION
SUB ARACHNOID
HAEMORRHAGE
 COMMONEST CAUSE –TRAUMA
 C/F: THUNDERCLAP HEADACHE

NECK STIFFNESS
PHOTOPHOBIA
FEATURES OF RAISED ICP
 TREAMENT:CRANIOTOMY AND
PROCEED
THERAPEUTIC EMBOLISATION
NIMODIPINE-60 mg 4hrly x 21 days
 Cerebral contusions
found predominantly where brain is in
contact with the irregularly ridged inside
of the skull, i.e. at the inferior frontal
lobes and temporal poles.
heterogenous on CT
MEDICAL MANAGEMENT
 ICP CONTROL:
SEDATION OPTIMISATION
CORRECTION OF SERUM SODIUM
DIURETICS IN ICH
 ANTICONVULSANTS AND ANALGESICS

 ANTIEMETICS

 ENTERAL FEED <=72 hrs

 ANTIBIOTICS
 Key parameters to maintain in head-
injured patients in neurointensive care.
 pCO2 = 4.5–5.0 kPa
 pO2>11 kPa
 MAP = 80–90 mmHg
 ICP 60 mmHg
 [Na+ ] >140 mmol/L
 [K+ ] >4 mmol/L
TRAUMATIC SPINE INJURY
 ANATOMY:
MANAGEMENT
 PERTINENT HISTORY:
 mechanism and velocity of injury
 spinal pain
 onset and duration of neurological
symptoms
 SUSPICION OF SPINE INJURY?:
 ROAD TRAFFIC ACCIDENT
 HANGING
 PENETRATING INJURY
 BLUNT TRAUMA
 ANY UNRESPONSIVE TRAUMA PATIENT
 GUNSHOT WOUNDS
 SIGNS AND SYMPTOMS:
 RESPIRATORY DISTRESS
 PAIN WITH MOVEMENT
 TENDERNESS ALONG SPINE
 NUMBNESS, TINGLING , LOSS OF SENSATION
IN EXTREMITIES
 PARALYSIS OR PARAPLEGIA
 INCONTINENCE
 PHYSICAL EXAMINATION
 Initial assessment
• primary survey
• careful systems examination
• paying particular attention to the abdomen
and chest. Spinal cord injury may mask
signs of intra-abdominal injury.
 Spinal examination
• overlying entire spine must be
palpated. spinal log roll
• Significant swelling
• tenderness
• palpable steps/gaps
 A rectal examination
 Seatbelt marks on the abdomen and
chest must be noted
 Neurological examination
 DIAGNOSTIC IMAGING:
 PLAIN RADIOGRAPH
• anteroposterior and lateral radiographs
open mouth views.
• Clear visualisation of the cervicothoracic

 CT SCAN WITH 3D RECONSTRUCTION

 MRI
MANAGEMENT OF SPINAL AND
SPINAL CORD INJURIES
 ABCD
 SPINAL IMMOBILISATION
 CORTICOSTEROIDS:
• <3 hrs BOLUS 30mg/kg , INFUSION FOR
24 hrs @5.4 mg/kg/hr
• 3-8 hrs BOLUS + INFUSION FOR 48 hrs
• >8 hrs NO ROLE
 SURGERY-ONLY IF PROGRESSIVE
NEURODEFICIT
 Identification of shock
● Hypovolaemic shock. Hypotension with
tachycardia and cold clammy peripheries.
● Neurogenic shock. Hypotension, a
normal heart rate or bradycardia and
warm peripheries.
treated with inotropic support
● Spinal shock
paralysis, decreased tone and
hyporeflexia. Once it has resolved the
bulbocavernosus reflex returns.
 Complications associated with spinal
cord injury
• Pressure Sores
• Pain and spasticity
• Autonomic dysreflexia
• Thromboembolic events
• Osteoporosis, heterotopic ossification
and contractures
THANK YOU