myths vs facts in head injury
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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.
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