Head injury and role of anaesthesiologist in management

1. Head injury and role of anaesthesiologist in management Moderator-Dr. Mohan Presenters-Dr. Jitendra Dr. Mritunjay www.anaesthesia.co.inanaesthesia.co.in@gmail.com

2. Important physiology • Human brain receives ~ 15% of the resting cardiac output • 20% of the body’s oxygen consumption • Mean cerebral blood flow ~ 50 ml/100g/min • CMRO2- 3.2 ml/100g/min • Glucose- main substrate (60 mg/100g/min) • CPP= MAP- ICP- VP • Normal ICP - 0-15 mm Hg in adults; in children 10 mm Hg • Regulation of cerebral blood flow • Auto regulation- 60-160 mm Hg • Flow-metabolism coupling • CO2 & O2 reactivity

3. Monro-Kellie doctrine • The total ICV is fixed because of inelastic nature of the skull & only small increases in its volume can be tolerated before pressure within the compartment rises dramatically

4. Primary The initial, “irreversible” mechanical injury: Lacerations Intracerebral haemorrhage Contusions Avulsion DAI Secondary- Further insults that ultimately lead to ischemia: systemic Hypotension Hypoxemia Excessive hypocapnia Anaemia Hyperthermia Hyper or hypoglycemia Sepsis & coagulopathy Hypertension Pathophysiology of Head injury

6. Intracranial causes of secondary brain injury • Factors causing elevation of ICP • Hypercapnia • Hypoxemia • Jugular venous obstruction • Increase in central venous pressure • Cerebral edema • Cerebral vasospasm • Intracranial infection • Cerebral hypoxemia • Posttraumatic epilepsy

7. Systemic effects of Head injury • Impaired gas exchange • Associated chest & abdominal injuries • Impaired reflexes aspiration ARDS • Fat embolism syndrome • Cerebral hemisphere or basal ganglia damage apnea & hypoventilation; cheyne stoke, apneustic breathing • Neurogenic alterations in FRC & V/Q matching • Acute neurogenic pulmonary edema • Severe hypertension • Cardiac dysrhythmias or M.I. & ECG abnormalities

8. Systemic effects of Head injury • Hypotension in young children due to blood loss • Coagulation disturbances- due to release of tissue thromboplastin, hypothermia & large blood transfusion • Electrolyte abnormalities • Hypokalemia- stress induced B adrenergic stimulation, respiratory alkalosis from hyperventilation & diuretic therapy • Hyponatremia- SIADH • Hypernatremia- Diabetes insipidus, repeated administration of mannitol

9. Prehospital management • Prehospital management & faster transport and admission – important keys to survival J. Neurosurgery 71:202-207, 1989 • Primary survey • Airway management • Breathing • Circulation and Control of haemorrhage • Disablilty – AVPU, GCS, Cervical spine injury • Exposure and Environmentcontrol • Others – Foley catheter, Gastric tube

10. Airway management • Open airway-clear the mouth of vomitus etc; look for foreign bodies, soft tissue swellings • A jaw thrust is used instead of a head tilt– chin lift to open the airway • Manual in line axial stabilization/ rigid collar for C-spine • Observe for hypoxemia as or when possible and give O2 supplementation when required

11. Indications for intubation and ventilation • Immediately • Coma (GCS<9) • Loss of protective airway reflexes • Hypoxemia (PaO2<13 kPa), Hyperventilation(PaCO2<3.5 kPa) • Respiratory arrhythmias • Uncontrolled seizures • Before transfer • Deteriorating level of consciousness (decrease in GCS>2, and not due to drugs) • Bilaterally fractured mandible • Copious bleeding into mouth (e.g.- from a basal skull fracture) • Seizures

12. Endotracheal intubation • Nasotracheal tube in the spontaneously breathing patient, and orotracheal intubation in the apnoeic patient. • Nasal intubation best avoided in the basal skull fracture- risk passing the ETT through the skull defect & infection • Rapid sequence induction • Suppression of intubation response- lignocaine 1 mg/kg • Ketamine contraindicated; propofol with caution; Thiopentone, etomidate ideal • Succinylcholine can be used – hyperkalemia is a consideration in >48 h after injury not in acute settings • Precurarization

13. Circulation • Look for breathing, movement, level of consciousness, skin colour and pulse • External haemorrhage should be identified and controlled with manual pressure • Hypotension is the most important predictor of the outcome • Hypotension is defined as < 90 mm of Hg in adults and less than the 5th percentile for the younger age group • Pneumatic splint can be used • At least two large bore lines for fluid resuscitation • Keep the patient warm

14. Fluid resuscitation • Isotonic fluid- Ringer lactate OR normal saline • Uncrossmatched O negative PRBC should be available for early use in patients with significant blood loss • The use of glucose containing solutions is discouraged unless hypoglycemia is suspected • Judicial use of fluids – cerebral edema & haemodilution to be avoided- ATLS instructor’s manual: American College of surgeons, Chicago 1996 • Adequacy of resuscitation reflected by the serum lactate levels- Scalea etal Crit Care Med:22;1610-1615,1994 • Hypertonic saline/ dextran infusion@ 4 ml/kg as a 10-20 minutes improves microcirculation and cerebral perfusion • Crystalloid versus colloids - debated • The ideal pre-hospital fluid regimen may be a combination of an initial hypertonic solution, followed by crystalloids and, in some cases, artificial colloids Injury2005 Sep;36(9):1001-10. Epub 2005 Apr 19

15. Glasgow coma scale

16. Glasgow coma scale • Patients who are intubated are unable to speak are evaluated only with eye opening and motor scores, and the suffix T is added to the their score to indicate that the patient is intubated. In intubated patients, the maximal GCS score is 10T and the minimum score is 2T • If eyes closed by swelling – suffix C • GCS 13-15- mild head injury; 9-12- moderate head injury, < 8- severe head injury.

17. Secondary survey • History AMPLE -Allergies, Medications, Past medical history/ Pregnancy, Last meal, Events relating to the injury • Examination – • Head- palpation for fractures and lacerations • Eyes- visual acuity, pupillary size & reactivity, ocular motility & haemorrhage and to remove contact lens • Face- ecchymosis or leakage of CSF from ears/ nose • Neck- midline trachea, edema, JVP distension • Spine- pain or a step off through the entire column • Chest, Abdomen, Pelvis & perineum • Detailed neurological examination – repeat GCS, pupils, gross examination of sensation and movement

18. Pupillary examination • Should be performed after resuscitation & before administration of sedatives or paralytics • Pupil reactivity to light - positive reaction - > 1mm constriction • Pupil asymmetry - > 1mm difference • Fixed/Dilated Pupils - >4mm and react < 1mm

19. Indications of CT scan • GCS less than 13 at any point since the injury • GCS equal to 13 or 14 at 2 hours after the injury • Suspected open or depressed skull fracture • Any sign of basal skull fracture • Post-traumatic seizure • Focal neurological deficit • More than one episode of vomiting • Amnesia for greater than 30 minutes of events before impact • If LOC in patients older then 65 years, coagulopathy or dangerous mechanism of injury

20. Indications for referral to neurosurgeon • Persistent coma (GCS<8) after initial resuscitation • Unexplained confusion persisting for more than 4 hours • Deterioration in GCS after admission • A seizure without full recovery • Progressive focal neurological signs • Definite or suspected penetrating injury • CSF leak • Tense fontanelle in a child • Patient fulfills criteria for CT but can’t be done in 4 hrs • Abnormal CT scan • CT normal but patient’s progress unsatisfactory

21. Transfer • Key to a successful and safe transfer • Adequate resuscitation & stabilization of the patient prior to transfer • Adequate monitoring, apt. resuscitation equipment & drugs • Accompanied by experienced, skilled doctor/paramedics • Good communication b/w referring & receiving centres and efficient handover • What the receiving centre need to know – • Patient’s age and medical history, if known • Neurological status • Cardiorespiratory state • Injuries and imaging findings • Management and care given

22. Intensive care after Head injury

23. Early indicators of prognosis • Glasgow coma scale score • Glasgow outcome scale • Age - >60 years • Pupillary diameter & light reflex • Hypotension • CT scan features

24. Glasgow outcome scale 1= Dead 2= persistent vegetative state 3= Severe Disability 4= Moderate disability 5= Good recovery Extended Glasgow outcome scale 1= Dead 2= persistent vegetative state 3= Lower severe disability 4= Upper severe disability 5= Lower moderate Disability 6= Upper moderate Disability 7= Lower good recovery 8= Upper good recovery Glasgow outcome scale

25. Marshall classification

27. SDH EDH SAH

28. Monitoring • Monitoring systemic physiology- • Direct arterial blood pressure • CVP line • Continuous pulse oximetry • Core temperature monitoring • Regular measurement of blood sugar • Global CNS monitoring • Transcranial Doppler Ultrasound - for non invasive estimation of CBF • Jugular venous monitoring • Monitoring of brain electrical activity - EEG , MLAEP

29. Jugular venous oximetry • As long as haemoglobin and arterial saturation remain constant, the SjVO2 is an indicator of cerebral oxygen demand • Based on Fick’s principle- CMRO2=CBFx(SaO2-SjvO2) • Retrograde cannulation of the internal jugular vein in the cephaloid direction • Serial sampling or fibreoptic catheters for continuous monitoring • Normal value – 55- 71% • Useful in monitoring interventions such as hyperventilation therapy • Newer techniques for brain oximetry-NIRS, direct tissue oximetry, cerebral micro dialysis

30. Brain targeted therapy • PaO2 >60 mm Hg or Oxygen saturation >90% • PaCO2 35-40 mm Hg • MAP>90 mm Hg • ICP treatment at upper threshold of 20-25 mm Hg • CPP >60 mm Hg* • SjVO2 >55% • Blood sugar- 70-130 mg/dl • Avoid & correct electrolyte imbalance • Temperature < 37o c • Seizure control • Surgical evacuation *In the absence of cerebral ischemia, aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors should be avoided because of the risk of adult respiratory distress syndrome.

32. Hyperventilation • Chronic prolonged hyperventilation (PaCO2 < 25 mmHg ) should be avoided in absence of increased ICP • Prophylactic hyperventilation (PaCO2 < 35 mm Hg ) during first 24 hours of injury to be avoided • May be needed for brief period when there is acute neurological deterioration • For longer period in intracranial hypertension refractory to sedation, CSF drainage & osmotic diuretics

33. Sedation • Aim – to decrease CBF, cerebral metabolism & ICP while preserving pressure autoregulation and the cerebrovascular response to CO2 • Propofol – good agent, but risk of hypotension and CPP Continuous infusion- lipid overload, should be taken into account for daily caloric intake • Midazolam + opioids • Fentanyl, sufentanil & alfentanil can increase ICP in patients with head injury due to changes in PaCO2 (in spontaneously breathing pts) and reflex cerebral vasodilatation

34. Neuromuscular blockade • Used to synchronise ventilation, manipulate PaCO2 and minimise increases in ICP caused by coughing and bucking over the ETT • Atracurium– commonly used, tolerated well hemodynamically Laudanosine– epileptogenic, not a clinical problem in humans • Pancuronium boluses or Vecuronium infusion also used • Long term use associated with continued paralysis after drug discontinuation & acute myopathy specially with steroid based agents

35. Fluid therapy • Guided by clinical and lab assessment & by invasive haemodynamic monitoring • Target serum osmolality 290-300 mOsm • Hypotonic fluids and dextrose containing solutions are avoided • Hypertonic saline – small volume resuscitation • Albumin or plasma can be used for maintenance of plasma oncotic pressure –Lund protocol • Pentastarch may be effective in reducing the cerebral edema associated with cerebral ischemic and reperfusion injury

36. Nutrition • Metabolic rate ~140% of resting metabolic rate • Increase largely abolished by neuromuscular blockade or barbiturate coma • 15% Of calories - protein • Negative nitrogen balance for approximately first 3 weeks after injury • Early (<7 days) establishment of full feeding associated with lower mortality • Same neurological outcome with parenteral or enteral feeding but fewer infectious complications with enteral feeding

37. General Measures • Head position – 15-30oc elevation of the head of the bed • Prophylaxis • Thomboembolism • Stress ulcer • Antibiotics Treatment of coagulopthies • Physiotherapy • Moderate Hypothermia (32-33oc) improves outcome by reducing – • CMRO2, • Neurotransmission • Frequency of energy depleting ischemic depolarizations • Free radical production • Intracranial hypertension

38. Osmotic therapy • Mannitol is effective for control of ICP • Effective dose- 0.25 mg/kg -1 mg/kg body weight • Also used in case of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes • Serum osmolality to be kept <320 mOsm because of concern of renal failure • Euvolemia – adequate fluid replacement. Foley’s • Should be discontinued if doesn’t cause diuresis • Intermittent boluses more effective than continuous infusion • Can accumulate in injured brain • Frusemide acts synergistically with mannitol • Hypertonic saline is equally effective -Neurocrit Care. 2004;1(2):219-33

39. Antiepileptic therapy • Early- <7 days, late >7days • Factors associated with increased risk: • GCS <10 • Presence of cortical contusion, depressed skull #, SDH, EDH, intracerebral haematoma • Penetrating head wound • Seizure within 24h of injury • Effective in preventing early post-traumatic seizure • Not recommended for late post-traumatic seizure • Phenytoin, Carbmazepine, Valproate are used • Initial dose Maintenance can be tapered in 1 week if no Early post-traumatic seizures • MgSO4 & NMDA antagonists are being investigated for the prevention of late post-traumatic seizures

40. Cerebral metabolic suppressants • Decrease ICP • High dose barbiturate (Barbiturate coma) in haemodynamically stable patients with refractory intracranial hypertension • Titrate dose to achieve EEG burst suppression • Propofol, etomidate, ketamine, opioids can also be used • S/E – prolonged recovery, increased chest infections

41. Novel neuroprotective intervention • Anaesthetic agents - High dose barbiturate (Barbiturate coma), Propofol, etomidate, ketamine, opioids • Excitatory amino acid antagonist – dizoclipine • Calcium channel blockers – Nimodipine • Antioxidants – pegorgetin, tirilazad • Steroids – not useful in TBI Lancet 2004:364;1321-29 • Sodium channel blockers – phenytoin, lamotrigine, lubelozole, riluzole • NSAIDS - indomethecin

42. No Head injury is so serious that it should be despaired or not so trivial that it can be ignored -Hippocrates Thank you ! www.anaesthesia.co.inanaesthesia.co.in@gmail.com