"Emergency Anaesthesia for the Head Injured Patient for non head injury

procedures"

Dr. J. Balavenkat MD, DA

Consultant AnaesthesiologistGanga Hospital

Coimbatore

Man kills Man … On the Roads!.

Global Road Traffic Injury-Related Mortality

By 2050, India will have the greatest number of automobiles

on the planet, overtaking the United States

Before we coclude this two day meet about 500 people would have died and

more than 5000 injured in India

If you are between 15-45 years of age you have more chance of dying due to an accident than

any other disease

Statistics

• Nearly 1.5 to 2 million persons injured every year in India

• Road traffic injuries are the leading cause (60%) of TBIs followed by falls (20-25%) and violence (10%)

• Main cause of death for patients who survive >48 hours

• Initial Resuscitation and Investigation protocol?

• CT Scan : Timing in an unstable patient

Bleeding is a major cause of death in trauma*

MOF7%

Other4%

Unknown2% CNS

42%

Bleeding39%

Bleeding + CNS6%

Sauaia A et al. J Trauma 1995;38:185-93

N=289

* Patients dying in hospital within 48 hours

Contentious Issues…..

• Role of hyperventilation• Role of hypothermia• Role of Glucose level in the neurological

outcome• Best fluid to resuscitate• Cerebral protective strategies.

Pathophysiology of TBI is complex.But you do not need to know the details

Simple, early and focussed interventions are effective in preventing secondary injury

Basic pathophysiology of brain injury

• Primary insult: – Direct tissue damage at the time of impact

• What are causes of secondary brain injury?

– Tissue injury occurring after the initial injury due to multiple causes

– Raised ICP, hypotension, hypoxia, hypo and hypercarbia, hyperthermia,hypo and hyperglycaemia, seizures

– Treatment goal: limit or prevent these secondary insults

GLASGOW COMA SCALE SCORE

EYE OPENING 4 Spontaneous3 To speech2 To pain1 None

BEST VERBAL 5 Orientated4 Confused3 Inappropriate words2 Incomprehensible sounds1 None

BEST MOTOR 6 Obeys commands5 Localises to pain4 Withdraws to pain3 Abnormal flexion to pain2 Extension to pain 1 None

Key issue is prevention of secondary injury

• Attempt to maintain cerebral blood flow (CBF)

• Attempt to maintain cerebral oxygenation

• Applicable in all areas• Pre-hospital• ED• Peri-operative• Intensive Care

Immediate management • A, B, C approach

• Airway management must be with C-spine immobilisation and control

• If GCS ≤ 8 should be intubated and ventilated to low normocapnia [4-4.5 kPa, 30-35 mmHg]

• A rapid sequence induction/intubation is appropriate, but avoid ICP ↑

• Circulation must be supported with IV volume loading and a MAP of 90mmHg maintained

Intubation of the patient with Brain Injury

• Record GCS and pupils before RSI

• Rapid Sequence oro-tracheal intubation:

– In line stabilization of C-spine– Pre-oxygenation with 100% O2

– Induction agent?– NMB: suxamethonium or rocuronium?– OGT or NGT?

Actions after tracheal intubation?

• Confirm TT and gastric tube placement (clinical and CXR)

• Ventilate, aiming for PaCO2 4-4.5 kPa (30-35 mmHg)

• Oxygenate, using PEEP if necessary• PaO2 > 13 kPa (97 mmHg) SaO2 >94%

• Cardiovascular assessment and stabilization

• IV volume• MAP ≥ 70-90 mmHg

Circulation

Hypotensive bleeding patients• Early Vs Delayed Fluid Resuscitation• Large Vs Small Volume resuscitation• Crystalloids or colloids?• To Transfuse blood and blood products early

or late?

Circulation

CLASSIFICATION OF HYPOVOLEMIA

5 :1

Goals of Resuscitation before controlling haemorrhage in a head

injured• Systolic BP of 100 mmhg• Heart rate <120• Hb > 9.0 gms/dl• Urine output >0.5 ml\kg\hr• SpO2 > 96• Serum Lactate less than 2.2

mmol/lt

Third generation HES: Tetrastarch

• Positive effect on tissue oxygenation• Improves microcirculation• Less effect on coagulation• No effect on liver function• Even with 50ml/kg body wt renal parameters

not altered• Tissue accumulation less.

Acute extradural

midline shift

ventricle compression

Acute subdural

Compression and shift

What are indications for head CT?

• GCS less than 13 at any point since the injury. • GCS equal to 13 or 14 at two hours after the injury.

• Suspected open or depressed skull fracture.

• Signs of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid otorrhoea, Battle’s sign).

• Post traumatic seizure.

• Focal neurological deficit.

• More than one episode of vomiting • Amnesia for >30 minutes of events before impact

Transfer from secondary to tertiary care settings

• Prevent further injury during transfer to tertiary care

• Agree transfer guidelines between the referring hospital and the neurosurgical unit

• Resuscitate and stabilise the patient before transfer– beware the undiagnosed abdominal injury

• All patients with a GCS <9 (and maybe higher) requiring transfer to tertiary care should be intubated and ventilated

Basic Treatment

• A: Tracheal tube• B: Ventilate to pCO2 4-4.5 kPa (30-35 mmHg),

pO2 ≥ 13 kPa (95 mmHg)• C: MAP ≥ 70 mmHg (aim CPP 50-70 mmHg)

– IV volume – PEEP is allowed– Arterial and CVP lines– Vasopressors: noradrenaline initially

• D: Monitoring– Pupils– Blood glucose

Remember

• Hypoxia: 50% of patients with severe head injury have PaO2< 10 kPa (75 mmHg)

• Mortality is increased by 20% if hypoxia present on admission

• MAP < 90 mmHg = 30% increase in mortality

• Metabolic: Glucose > 10mmol/L (180mg%) = worse

Cerebral Perfusion Pressure

• CPP = MAP – ICP• Normal CPP = 70 – 100 mmHg• Normal ICP = 0 – 15 mmHg• Evidence supports favorable outcome

with CPP aim of 50-70 mmHg• Initially CPP is not known

– Maintain MAP >70 mmHg in an attempt to maximize CPP

Acute treatment of increased ICP

• Check A, B still OK– beware partially blocked ETT or chest wheeze

• Cautious, short-lived, hyper-ventilation• Maintenance of circulation and CPP• Osmotherapy• Neurosurgical interventions

– Decompression– CSF removal

Hyperventilation• Theory: ICP via constriction of cerebral vasculature and reduced brain

volume

• Change: 2- 4% in cerebral blood flow with every 1mmHg change in pCO2

• PaO2 below 60 mmHg (8 kPa) is the second most powerful predictor of poor outcome

• PaCO2 <4 kPa (30 mmHg) may increase ischaemic damage due to cerebral vasoconstriction

• Severe vasoconstriction with pCO2 < 25mmHg (3.5 kPa)

• Evidence suggest hyperventilation is harmful

Hyperventilation: Recommendations

• Brain Trauma Foundation: 1) Prophylactic hyperventilation is to be avoided

2) Hyperventilate for brief periods when there is acute neurologic deterioration3) Hyperventilate for ICP that is refractory to

sedation, paralysis, cerebral spinal fluid (CSF) drainage, and osmotic diuretics

Osmotherapy

• Mannitol

• Hypertonic saline

Mannitol

• Lowers ICP and Increases MAP

– 1) plasma expander: increases cerebral blood flow and cerebral oxygen delivery

– 2) Delayed effect (30 minute - 6 hour): osmotic agent

• Cardiovascular collapse if volume depleted

• May increase bleeding

• Renal failure: if serum osmolarity > 320 mOsm

• Concentrated in brain tissue with prolonged infusion

Mannitol: Recommendations

• Brain Trauma Foundation:1) No standard for mannitol2) Effective for control of ICP: intermittent boluses more

effective than continuous infusion. (dose: 0.25 g/kg to 1 g/kg)

3) Indications for mannitol prior to ICP monitoring: signs of transtentorial herniation or progressive neurological deterioration

4) Euvolemia should be maintained: fluid replacement

– No role for high dose

Intravenous Fluids: Hypertonic Saline

• Hypertonic Saline: 5% or 7.5% NaCl• Increases MAP and reduces ICP• Hypothesis: cerebral swelling may be prevented by

altering the osmolar load• Keep serum Na < 155 mmol/L [some centres will

accept ~ 170]• No central pontine myelinolysis reported as this is

not rapid correction of hyponatraemia

Intravenous Fluids

• 0.9% saline may be better than Ringers lactate• Hematocrit:

– Level of 30-33% believed optimal– < 30% exacerbates neurologic injury

• Glucose:– Hyperglycemia increases neurologic injury– Prevent hypoglycemia– Use of insulin improves outcome in lab animals– Goal: blood sugar 100 – 150 mg/dl (~5-8 mmol/l)

Barbiturates• ICP by suppressing cerebral metabolism

• No evidence that this is associated with reductions in mortality or disability.

• Occurrence of hypotension

• Significant fall in body temperature

Barbiturates: current recommendations

• Intractable ICP not responding to sedation

• Burst suppression on EEG

• Thiopentone drug of choice

• Caution: needs multimodality monitoring

Associated Injuries…..

• Spinal Cord Injury• Faciomaxillary Injury• Thoracic Injury• Abdominal Injury• Pelvic Injury• Musculoskeletal Injury

Spinal Cord Injury• Hypotension (neurogenic shock) –

characterized by bradycardia rather than tachycardia (due to loss of cardiac accelerator function and unopposed parasympathetic tone) may be difficult to distinguish from hypotension due to acute hemorrhage.

• The hypotensive trauma patient is always assumed to be bleeding, until this possibility is definitively ruled out.

Early Need for a Surgical Airway…..

• Head injury/coma

• Face or neck injury

• Cervical Spine injury

• Chest injury: rib fractures

• Haemo-pneumothorax

Rib Fractures

• Ribs 1-3 major force to break

:associated injuries

• Ribs 4-9 Lung contusions

: Haemothorax/pneumothorax

• Ribs 10-12 Intra-abdominal injuries

What are the causes of life threatening chest trauma?

Primary survey

• Airway obstruction

• Tension pneumothorax

• Open pneumothorax

• Massive haemothorax

• Flail chest

• Cardiac tamponade

Blunt Abdominal Trauma (BAT)

• Delicate organs in an expandable cavity with little bony protection

• May be the source of occult fatal exsanguination• Injury is sometimes obvious (evisceration) but

usually occult.• Clinical signs are unreliable and occur late

(expanding abdomen)

• Difficult to assess existence or extent of injury on clinical grounds alone.

• If suspicious, ORGAN INJURY MUST BE EXCLUDED.

FAST

• Laparotomy: splenic injury/ liver laceration splenectomy, packing abdomen, Temporary Closure with Vac dressing

Intra-abdominal Hypertension

Ivatury RR: Supranormal trauma resuscitation and abdominal compartment syndrome. Arch

Surg 2004; 139: 225.

Evidence-based…

Increase intra-abdominal pressure

Increase intrathoracic pressureIncrease intrathoracic pressure

Inhibit cerebro-venous outflow

Increase ICPCiterio G et al: Induced abdominal compartment syndrome increases ICP in neurotrauma patients: a prospective study. Crit Care Med 2001; 29: 1466.

Evidence-based…

“Multiple Compartment Syndrome”

Increased Intra-abdominal, Intra-thoracic and Intracranial Pressure

After Severe Brain Injury: Multiple

Compartment Syndrome

Thomas M. Scalea, Grant V. Bochicchio,

Nader Habashi, Maureen McCunn, Diane Shih, Karen McQuillan, Bizhan Aarabi

J Trauma 2007; 62: 647-656

ICP

CPP Administer fluids Sedation

(Unable to perform CPT)

Respiratory failure Ventilator supportIncreased intrathoracic

pressure

Increased intraabdominal pressure

“Multiple-compartment” Syndrome

Abdominal Trauma: Summary

• If appropriate mechanism or signs exist, intra-abdominal injury must be excluded.

• NOM requires strict criteria and intensive surveillance.

• Unstable = Damage Control Laparotomy• Penetration of deep fascia = Operation• A missed injury may be fatal.

Rt Int. Iliac artery injury

23 yr College student; RTA.Failure to stabilise with 2 lit replacement.

Musculoskeletal Trauma

• Common, may be life-threatening

• Often indicate major trauma and associated with others injuries

• Result in haemorrhage, compartment syndrome, rhabdomyolysis, and fat embolism are limb and life-threatening problems

Compartment Syndrome

Myoglobinuria

Rhabdomyolysis-Treatment

• Intravenous Fluids

• Mannitol

• Bicarbonate

• Acetazolamide

• Dialysis

How far to allow the surgeon to proceed?

Early Total Care

or Damage Control

Arterial Blood lactate Normal

Arterial pH > 7.35 OR

Base Deficit < 6mmol/L

Arterial Blood

lactate > 5mmol/L and/or

Arterial pH ≤ 7.35

OR Base Deficit

> 6mmol/L

Clinical Signs

Normotension

Normal Rate

Urine output.

Occult Hypo-perfusion

Resuscitated

Stable

Surgical strategy

Stable and Resuscitated

Stable but OHFailure to

stabilise

Needs Further resuscitation

Damage control

Surgeries

Surgery is safe

Damage Control is Selective

• Deliberate, calculated approach requiring mature surgical judgement.

• Make the decision early and do it.• Avoid the “dark angels” leading to fatal

coagulopathy– Hypothermia T< 35– Acidosis pH < 7.2– Massive transfusion > 6 units

Markers available

Procalcitonin

• • Pain relief strategies in head injured trauma

patient

Nociceptive Pain

Spinal CordSpinal Cord

BrainBrain

Pain-Pain-Autonomic ResponseAutonomic Response - Withdrawal Reflex- Withdrawal Reflex

Noxious Peripheral StimuliNoxious Peripheral Stimuli

Nociceptor Sensory Nociceptor Sensory NeuronNeuron

HeatHeat

ColdCold

IntenseIntenseMechanicalMechanical

ForceForce

ChemicalChemicalIrritantsIrritants

Woolf. Woolf. Ann Intern MedAnn Intern Med. 2004;140:441-451.. 2004;140:441-451.

Is responsive to NSAID’s, coxibs, paracetamol and opiates

Inflammatory Pain

Spinal CordSpinal Cord

BrainBrain

Spontaneous PainSpontaneous PainPain HypersensitivityPain Hypersensitivity -Allodynia -Allodynia -Hyperalgesia -Hyperalgesia

Nociceptor Sensory Nociceptor Sensory NeuronNeuron

MacrophageMacrophage

Tissue Tissue DamageDamage

InflammationInflammation

Mast CellMast Cell

NeutrophilNeutrophilGranulocyteGranulocyte

Woolf. Woolf. Ann Intern MedAnn Intern Med. 2004;140:441-451.. 2004;140:441-451.

Is responsive to NSAID’s,coxibs, paracetamol, and opiates

PerceptionPerception

ModulationModulation

TransductionTransduction

TransmissionTransmission

Reuben et al. J Bone Joint Surg. 2000;82:1754-1766.

Postoperative pain is nociceptive

Is responsive to NSAID’s,coxibs, paracetamol and opiates

Modes of action of analgesics1,2,3,4

1. D’Amours RH et al. JOSPT 1996;24(4):227-36. 2. Piguet V et al. Eur J Clin Pharmacol 1998;53:321-4.3. Pini LA et al. JPET 1997;280(2):934-40.4. Chandrasekharan NV et al. PNAS 2002;99(21):13926-31.

Opioids

Activation ofopioid receptors

Paracetamol

Inhibition of central Cox-3 (?)

(Inhibition of PG synthesis)

Paracetamol

Interaction withserotoninergic descending

inhibitory pathway

NSAIDs / Coxibs

Inhibition of peripheral and central Cox-1 / Cox-2

(Inhibition of PG synthesis)

Does paracetamol cross the blood-brain barrier?1

1. Bannwarth B et al. Br J Clin Pharmac 1992;34:79-81.

Open-label study

Patients with nerve-route compression pain requiring a diagnostic lumbar puncture

Plasma and CSF samples obtained between 20 minutes and 12 hours after dosing

N = 43 3-minutei.v. paracetamol 1g

infusion

Plasma and CSF paracetamol concentrationsfollowing a single i.v. dose of paracetamol

1g

1. Bannwarth B et al. Br J Clin Pharmac 1992;34:79-81.

(n= 43)Paracetamol rapidly crosses the blood-brain barrier

Dissolution

A unique manufacturing process evolved to enable bottling

pH adjustment

Volume adjustment

Filtration

Bottle filling

Stopping

Cap sealing

Terminal sterilisation

Secondary packaging

Vacuum

Perfalgan 1g dosage guidelines

•Minimal interval

•between infusions

1 g

100 ml of solution

4 g

4 hours

Dose per infusion

Daily dose

Adolescents& Adults > 50 kg

India Prescribing Information

CRASH 2 TRIAL: ROLE OF TRANEXAMIC ACID IN TRAUMA

A large randomised controlled trial among trauma patients with significant haemorrhage, of the

effects of antifibrinolytic treatment on death and transfusion requirement

TreatmentAmpoule

s

Dose (Tranexamic

Acid or placebo)Infusion rate

Loading 2 1 gram100 ml over 10 minutes

Maintenance

2 1 gram

120 mg/hr [60 ml/hr] for about 8 hours

Treatment

Head injury + Associated Injuries

Masking Symptoms is a concept invented by arm-chair academics with

Ivory tower induced myopia

DVT prophylaxis

• High risk: spinal injury, pelvic or lower limb fractures, brain injury.

• Use compression stockings early.• Institute medical prophylaxis once early

bleeding controlled and stable.• Encourage early mobilisation.• Also: Tetanus and post-splenectomy

immunisation in appropriate patients.

• Timing of tracheostomy in a head injured patient

• Nutrition in Head Injured patient : important tips

Case 1 :

• 23 year old male with polytrauma following RTA: GCS 8/15,Pulse 120/mt,

• Blood Pressure: 80/50, • Respiratory rate 20/mt, • Room air Oxygen saturation: 86%.• Primary survey shows open injury tibia and

closed fracture femur.• How to proceed?•

Team Work

Thank YouThank You