Dr. Shailendra D. Anjankar

“No head injury is so trivial that it can be ignored, and none so serious that the life must be despaired of”

~ Hippocrates

Sri Ganeshaya namaha!

Myth # 1.

Head Injury patient

have poor prognosis

and most of them die

Prognosis of patient is dependent on:1. Initial GCS

2. Age of the Patient

3. Pupils size and reaction to light

4. Hypotension, Hypoxia and Anemia

5. Individual CT characteristicsa. Status of basal cisterns

b. Traumatic SAH

c. Presence and degree of midline shift

d. Presence and type of intracranial lesions

GCS GOS 1 (Death)

3 65%

4 45%

5 35%

6 24%

7-13 10-15%

Fearnside et al in 315 pt

Reference : 1. Fearnside MR, Cook RJ, McDougall P, et al.: The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical, and CT variables. Br J Neurosurg 7:267-279, 1993. 2. Braakman R, Gelpke GJ, Habbema JD, et al.: Systematic selection of prognostic features in patients with severe head injury. Neurosurg 6:362-370, 1980.

GCS GOS 1 (Death)

3 100%

4 80%

5 68%

6 51%

7 27%

8 22%

9-15 15%

Braakman et al in 305 pt

Mortality in patients and its correlation with Admission GCS.

Mortality in patients and Age of Patient correlation

Prognosis of patients and its correlation with Pupils size and reactivity to light

Reference : Chesnut RM, Marshall SB, Piek J, et al.: Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochirurgica (Suppl) 59:121-5, 1993

Reference :Miller JD, Becker DP: Secondary insults to the injured brain. J Royal Coll Surg (Edinburgh) 27:292-298, 1982

Prognosis of patients with Hypoxia & Hypotension

References: 1. Marshall LF, Gantille T, Klauber MR, et al.: The outcome of severe closed head injury. J Neurosurg (Suppl) 75: 28-36, 1991. 2. Van Dongen KJ, Braakman R , Gelpke GJ: The prognostic value of computerized tomography in comatose head injured patients. J Neurosurg 59:951-957, 1983.3. Kakarieka A: Traumatic subarachnoid hemorrhage. Springer-Verlag, Berlin, 1997.

Prognosis of patients with CT characteristics

Marshall et al. Traumatic Coma Data Bank (TCDB).

Presence of mass lesions carries a PPV of 78% to unfavorable outcome.

Mortality is higher in acute subdural hematoma than in extradural hematoma.

Reference: Marshall LF, Gautille T, Klauber MR, et al.: The outcome of severe closed head injury. J Neurosurg (Suppl) 75:28-36, 1991.

If we cant CURE the patient; but definitely can CARE for the patient.

CARECURE

Myth # 2.

Managing head injury

patient is difficult.

Managing a Head Injury patient is simple if proper monitoring and timely interventions are undertaken.

ICP should be vigilantly monitored and kept under normal limit by specific interventions.

Need to have Good Neurointensive care units and strict adherence to protocols.

First and Foremost…. ABC’s

AirwayBreathingCirculation (C - is not CT scan Brain)

DisabilityExposure

EMERGENCY MANAGEMENT:

AIRWAYHandle Neck With Caution: Assume C-spine Injury

Use Jaw Thrust

Avoid Obstruction of Venous Drainage

Intubate If GCS < 8

May Need to Protect Airway Due to Seizures or Trauma

Intubation Should Be Oral

Even a Small Rise in PaCO2 Causes a Significant Rise in ICP

“Adequate” Breathing may not be enough- Aim for PaCO2 of 35-40 mmHg

Hyperventilation Is the Quickest Way to Lower ICP if there are signs of Herniation

EMERGENCY MANAGEMENT:

BREATHING

Blood Pressure Must Be Optimized to Help Maintain Adequate CPP

Only Use Isotonic Fluids for Volume Expansion

May Need Inotropic or Pressor Support

Control Bleeding

EMERGENCY MANAGEMENT:

CIRCULATION

Primary Brain Injury – Cellular LevelPrimary Cellular

Injury

“Neurotransmitter Storm”

Massive Depolarization of Brain Cells

Glutamate

Calcium

NMDADisruption of normal cellular

processes:Protein Phosphorylation

Microtubule ConstructionEnzyme Production

Membrane and Cytoskeleton Breakdown

Cell Death

Oxygen Free Radical Pathway

Activation

Lipid PeroxidationCell Membrane

DysfunctionCell Lysis

Nitric Oxide Synthase

High Nitric Oxide Levels

Intracellular Signaling Processes

Systemic Insults

Hypoxia (PaO2 < 60 mmHg)

Hypotension (SBP < 90 mmHg)

Anemia +/- Blood Loss (↓Oxygen Carrying Capacity)

Hypo/Hypercapnia

Secondary Brain Injury

Our Aim is to prevent this Secondary injury

Myth # 3.

Surgery “to do or not to

do” for head injury

patient depends on

Neurosurgeons wish.

Indications for surgery

1. Penetrating injuries or blunt injuries with breach of the calvarium/skull

2. Presence of expanding intracranial hematomaa) Epidural Hematoma

b) Subdural Hematoma

3. Malignant cerebral edemaDecompressive Craniotomy - Decreases ICP, improves cerebral perfusion, prevents ischemia

Epidural Hematoma

• Middle Meningeal Artery (36%)• Head Injury without LOC + Lucid Interval followed by deterioration

(Classic presentation = 47% of cases)• Lenticular Shape on CT• Surgery is Indicated – If volume > 30 cm3

EDH

Subdural Hematoma

• Injury to Bridging Veins• Blood accumulation between dura mater and pia arachinoid mater• Increased risk in elderly and alcoholics due to decreased brain volume• Hyperdense crescent shaped lesion on CT• Surgery is Indicated – If size > 10 mm on CT or if 5 mm shift

SDH

Myth # 4.

Surgery should be done

only after pupils start

dilating.

* Reactive: ICP increasing

* Nonreactive (altered LOC): increased ICP

* Nonreactive (normal LOC): not from head injury

Pupils

Both dilated

* Nonreactive: brainstem

* Reactive: often reversible

Unilaterally dilated

Myth # 5.

Right side bleed will

only cause left

hemiparesis

Myth # 6.

Patient with E2 (eye

opening to pain) response

can be M6 (following

commands).

There are few combinations with are possible and some which are not.

E2 is compatible with M1, M2, M3, M4, M5 (pain response)

E3 or E4 patient should be M6 (command response)

V1, V2, V3 cannot be with M6

Neurological Posturing

Decorticate Posturing (M3) = Upper extremity flexion with lower extremity extension(Cortical Injury above the midbrain)

Decerebrate Posturing (M2) = Arm extension and internal rotation with wrist flexion(Indicative of brainstem injury, Very Poor predictor of outcome)

Myth # 7.

All trauma patient

requires CT scan Head.

New Orleans CriteriaCT imaging is required for patients with minor head injury with any one of the following findings. The Criteria only apply to patients who have a GCS of 15.1.Headache2.Vomiting3.Age > 60 years4.Drug or Alcohol Intoxication5.Persistent anterograde amnesia6.Visible trauma above the clavicle7.Seizure

Canadian CT Head RuleCT Imaging is only required for patients with minor head injury with any one of the following findings. The criteria apply to patients with minor head injury who present with GCS of 13-15 after witnessed LOC, amnesia or confusion.High Risk for Neurosurgical Intervention1.GCS < 15 at two hours after injury2.Suspected open or depressed skull fracture3.Any sign of basilar skull fracture (Hemotympanum, Peri-orbital Eccymosis, Otorrhea or Rhinorrhea, Battle sign)4.Two or more episodes of vomiting5.Age > 65 yearsMedium risk for Brain Injury Detection by CT Imaging6.Amnesia before impact of 30 or more minutes7.Dangerous mechanism (E.g. Pedestrican vs. Motor vehicle, Ejection from motor vehicle or fall from an elevation of 3 or more feet or 5 stairs)

Head CT Clinical Rules

New Orleans Criteria Sensitivity and Specificity of detecting a clinically significant CT

finding Sensitivity = 100% Specificity = 24.5 % Estimated to decrease CT imaging by 23%

Canadian Head CT Rule Sensitivity and Specificity for need for neurosurgical intervention

and clinically significant finding on CT imaging Sensitivity = 100% Specificity = 68% Proposed to reduce CT scanning by 46%

Myth # 8.

Sub arachnoid

hemorrhage in brain

means aneurysmal bleed.

Trauma is leading cause. Rx – maintain intravascular volume

to prevent ischemia from vasospasm.

Mortality 39% { national traumatic coma databank}

Myth # 9.

Patient with poly

trauma, head injury is

always a priority.

We have to treat a patient as a whole, and not only a specific organ.

PRIMARY BRAIN INJURY DOES NOT CAUSE SHOCK, BUT

SHOCK DOES CAUSE SECONDARY BRAIN INJURY

*THE BRAIN NEEDS OXYGEN

*OXYGEN IS CARRIED IN BLOOD

NO BLOOD, NO OXYGEN, ……BRAIN CELLS DIE

Principles of Trauma Management

1. Organized team approach 2. Assumption of most serious injury 3. Treatment along with diagnosis 4. Thorough examination 5. Frequent assessment

Myth # 10.

Head injury patient

having hypotension.

Vital Sign Change with Increasing ICP

Respiration Increase, decrease, irregular

Pulse Decrease

BP Increase, widening pulse pressure

• Cushing’s response

classically explained as –

- Hypertension- Bradycardia- Altered Respiratory pattern

in a setting of Increased ICP

Myth # 11.

Neurosurgery clearance

required for operating

on poly trauma patient

with associated head

injury.

“Clearance given” is itself a myth.

No one can guarantee further deterioration if patient is stable at that point.

Only, few precautions can be taken to avoid aggravation of the problem-

Example- 1.Avoid Nitous oxide during anestheisa in pneumocephalus.

2. Avoid Spinal anesthesia/ Lumbar puncture in patient with intracranial mass lesion

Myth # 12.

Patient with altered

sensorium and poly

trauma, should always

have concomitant Head

injury.

A – AlcoholE – Endocrine/ ElectrolyteI – Insulin O – Opiate/OxygenU – Uremia

T – Toxin/Trauma/TempratureI – Infections P – Psychiatric/ porphyriaS – SAH, Stroke, SOL,

Shock,

E- Endocrine/Electrolyte• Hypothyroidism/ Hyperthyroidism• Hyperparathyroidism• Adrenal Hypofunction• Diabetes Mellitus• Hyponatremia (<120Meq/dL)• Hepatic coma• Serum Osmollity (<240, >330mOsm/l)• Hypercalcemia (>19mg/dL)

“AEIOU TIPS” – for altered sensorium

Myth # 13.

If SpO2 is maintained,

intubation can be

avoided in severe head

injury patient in

emergency.

Indications for intubation in traumatic brain injury

1. GCS <8

2. Loss of airway reflexes or presence of signs/ symptoms of an airway injury

3. Ventilatory insufficiency (PaO2 < 80 mmHg on room air or a PaCO2 > 50mmHg)

4. Severe facial injuries (La Forte fracture, mandibular fracture)

5. Seizures

Severe head injury patient or the patient in altered sensorium who have risk of aspiration and hypoxia, it is advisable to intubate the patient to protect airway and maintain blood oxygen saturation.

Myth # 14.

No Loss of

consciousness means

no Head injury.

*The diagnosis of a Mild Traumatic Brain Injury does not require a LOC.

*The most famous and striking example of a severe TBI with no LOC is the case of Phineas Gage, in 1848.

*Phineas Gage never lost consciousness. He was reported to be sitting up and talking with the iron bar protruding from his left temporal and frontal lobes

Post Traumatic Amnesia (PTA)  

*Amnesia for even a few minutes after a blow to the head is evidence of diffuse brain damage.

*PTA continues to be “the primary and most specific diagnostic indicator of injury”.

Reference: Brown AW et al., “Predictive utility of weekly post-traumatic amnesia assessments after brain injury: a multicentre analysis” (2010) 24:3 Brain Injury 472-478.

Less than 5 minutes very mild5 to 60 minutes mild1 to 24 hours moderate1 to 7 days severe

1 to 4 weeks very severeMore than 4 weeks extremely severe

Myth # 15.

Mild head injury patient,

with normal scan

recovers completely.

Post Concussive Syndrome

• Constellation of symptoms that develops within 4 weeks of the injury and may persist for months

• Treatment is with analgesia, anti-depressents and anti-emetics

Concussion (Latin “Concutere” = shake violently)(In technical language – its SOFTWARE not a HARDWARE problem.)

Another concussion during this period can lead to irreparable damage to Brain tissue.

Myth # 16.

Mean arterial pressure

monitoring not

required if ICP is

normal in head injury

patient.

Maintenance of Cerebral perfusion pressure is more important in treating increased ICP patients.

*Our Goal to maintain CPP by

1) Reducing ICP, +/-

2) Increasing MAP

Management aimed at maintaining CPP (70 mmHg) improves outcomes.

(Formulas)

CPP = MAP- ICP

MAP = 2xDP+SP/3

Reference: Rosner et al. (1995) Journal of Neurosurgery, 83(6)

Outside of the limits of autoregulation,

raising MAP raises CPP and

raising ICP lowers CPP.

Myth # 17.

Mannitol should be

given in all patients

with head injury.

MannitolOsmotic agent

Mechanism of action – works as osmotic diuretic extract extra and intra cellular edema fluid from brain

Free radical scavenger

Reduces ICP within 30 minutes, last 6-8 hours

Dosage0.25-1 gm/kg bolus

Additional mechanismReduces blood viscosity ( by hemodilution) and improves Rheology Increases CBF vasoconstriction decreases volume reduces ICP.

Risks 1. Repeated dose reduced osmotic gradient 2. Hyperosmolar state ( serum osm>320 mOsm) renal

failure, rhabdomyolysis, hemolysis3. Increase size of EDH

Myth # 18.

ICP and cerebral edema

can not be decreased by

measures except Mannitol

or surgery.

ICP can be decreased by

1. Head elevation to 30 degree

2. Medication – Furosemide, Acetazolamide, 3% saline, Glycerol

3. Hypothermia – by decreasing cerebral metabolism

4. CSF drainage

5. Barbiturate coma

Keep neck mid-line and elevate head of bed …. To what degree?

Reference: Feldman et al. (1992) Journal of Neurosurgery, 76

Head Elevation

*Decreased CSF formation

*Decreased systemic and cerebral blood volume (impairs sodium and water movement across blood brain barrier)

*May have best affect in conjunction with mannitol

Loop Diuretic - Furosemide:

Reference: Pollay et al. (1983) Journal of Neurosurgery, 59.

Hypertonic saline

Causes – reduction in mean ICP, is effective within 12 hours of continuous infusion of 3% saline solution.

Little continued benefit after 72 hours of treatment

Reference: Qureshi et al. (1998) Critical Care Medicine, 26(3)

Reference: Qureshi et al. (1998) Critical Care Medicine, 26(3)

Goal:

Sodium 145-155 mmol/L

Hyperosmolar Therapy

• Sodium: square

• ICP: circle

*32.5 degree C body temp., reduced cerebral metabolic rate for oxygen (CMRO2) by 45% without change in CBF

*Also, the intracranial pressure decreased significantl (p < 0.01)

*Side-effects:• Potassium flux• Coagulopathy• Shivering• Skin Breakdown

Hypothermia

Reference: Metz et al. (1996) Journal of Neurosurgery, 85(4)

CSF drainage-

* It is effective and safe.

*Provides gradient for bulk flow of edema fluid from parenchyma of brain to ventricles.

*Ex- Continuous (EVD) or Intermittent (tapping) can be done.

Barbiturate Coma

*Lowers ICP, cerebral metabolic O2 demand

*Not indicated in the Emergency

Myth # 19.

Hyperventilation can be

increased if ICP is not

decreasing.

Cerebral Blood FlowRegulation of Cerebral Vascular Resistance

PaCo2 (mmHg)

Normal 30 - 50 mmHg

Ref: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651

Hyperventilation*Not recommended as

prophylactic intervention

*Never lower than 25 mm Hg

*Reduces ICP by vasoconstriction, may lead to cerebral ischemia

*Used as a last resort measure

*Aim is to - Maintain PaCO2 at 30-35 mm Hg

Myth # 20.

Routine Nursing

activities have no effect

on ICP.

0

2

4

6

8

10

12

14

16

18

20

Before During After

TurningSuctioningBathing

Nursing Activities and ICP

Reference: Rising (1993) Journal of Neuroscience Nursing, 25(5)

ICP

Myth # 21.

Relatives should not

touch the Severe Head

Injury patient in ICU.

Family Contact and ICP

Reference: Treolar (1991) Journal of Neuroscience Nursing, 23(5)

Presence, touch and voice of family / significant others has been demonstrated to decrease ICP

Note: Visitors requires education and preparation before spending time at bedside !

Similarly, music therapy is also known for better recovery. It stimulate brain function controlling movement, cognition, speech, emotions and the senses.

Reference: Bradt, J. et al. Music therapy for acquired brain injury. Cochrane Database of Systematic Reviews 2010 Jul 7;(7)

Healing Hand –Doctors

Relatives

Treating patient with Head Injury is a TEAM WORK!

Myth # 22.

Neuroprotective drugs

are fool proof in

preventing further

brain damage

Market is full of Hundreds of Neuroprotective drugs!

And the evidence available for its efficacy are done by either pharmaceutical company or in their collaboration.

So, how effective they are, is the matter of debate and doctors personal discretion.

Myth # 23.

Anticonvulsants

prevents post traumatic

seizures.

Prophylactic phenytoin reduces the incidence of seizure in the first week after injury but not thereafter in moderate to severe head injury.

Brain Injury Foundation recommends anti-epileptic medications be administered to high risk patients for first 7 days post-injury

*There are insufficient data to recommend routine PTS prophylaxis in patients with mild TBI.

Myth # 24.

Children recover better

than adult after severe

head injury.

*The developing brain may be at more risk. It will take longer to see the effects of the brain injury.

*Even though a young child's brain has more plasticity and a greater ability for other neurons to take on new function, the brain is less developed overall.

*Our data of 509 patient of head injury in pediatric population showed bad outcome for severe head injury

Myth # 25.

Sedation and

paralysing medication

can be continued for

long time for head

injury if patient on

ventilator.

*Dictum “Weaning process should start just after Intubation”.

Ventilators are for respiratory support, not substitute!

*Neuromuscular blockade is indicated for intubation; but long acting blocking agents should be avoided because they limit serial examinations

*Longer term use can cause myopathy and dependence on ventilator.

Myth # 26.

“Recovery will take

about a year”.

When a person has a brain injury, the concept of recovery may be misleading.

For a person with a brain injury, although they may look the same the changes are most likely long-lasting and adjustment is an ongoing process.

For Brain Injury, PREVENTION is always better than CURE;

WEAR HELMET , if you are riding a bike, or sitting at rear.

Myth # 27.

Hyponatremia in Head

injury is only due to

SIADH.

Myth # 28.

Head injury have no

effect on heart.

The pathophysiology of cardiovascular complications after brain injury.

Refernce: Gregory T , and Smith M Contin Educ Anaesth Crit Care Pain 2011

Typical ECG changes after SAH showing deep T wave inversion and prolongation of the QTc interval.

Myth # 29.

Delayed quadriplegia in

head injury patient is

because of missed cervical

spine injury.

Critical illness polyneuropathy (CIP) and myopathy (CIM)

* are complications of critical illness that present with muscle weakness simulating quadriplegia.

*Functional changes can cause electrical inexcitability of nerves and muscles with reversible muscle weakness.

*Mechanism- Microvascular changes and cytopathic hypoxia might disrupt energy supply and use. An acquired sodium channelopathy causing reduced muscle membrane and nerve excitability is underlying cause of CIP and CIM.

Reference: Latronico N et al. Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis. Lancet Neurol. 2011 Oct;10(10):931-41.

Myth # 30.

Your questions..

Fact is more stranger than fiction!

Thank you.