1. Coma, head injury Judita Capkova, MD. PhD. Jozef Firment, MD. PhD. Department of Anaesthesiology & Intensive Care Medicine Šafárik University Faculty of Medicine, Košice

2. Firment 2 Coma Is a „state of unarousable unresposiviness“ (of unconsciousness from which the patient cannot be aroused) No evidence of arousal: no spontaneous eye opening, no speech, voluntary limb movement Unresponsive to external stimuli, although abnormal postures may be Involuntary movements (seizures) may occur GCS – level of consciousness, coma: GCS ≤ 8

3. Firment 3 GLASGOW COMA SCALE Decorticate posturing Decerebrate posturing

4. Firment 4 Causes of coma Metabolic Toxic Infection with or Structural lesions without Focal brainstem signs Lateralizing cerebral signs Meningeal irritation -toxic, metabolic causes usually do not produce focal signs - infections, structural lesions produce focal signs

5. Firment 5 Coma without focal/lateralizing neurological signs Anoxia/ hypoperfusion Metabolic: e.g. Hypo/-hyperglycaemia, acidosis/alkalosis, hepatic or renal failure Intoxications: e.g. alcohol, opiates, benzodiazepines,.. Endocrine : hypothyreoidism Hypo- or hyperthermia Epilepsy Hypertensive encephalopathy

6. Firment 6 Coma with focal/lateralizing neurological signs ( due to brainstem or cerebral dysfunction) Vascular : cerebral haemorrhage or infarction Supra or infratentorial space-occupying lesion: tumour, haematoma, abscess Coma with meningism Meningitis, encephalitis Subarachnoid haemorrhage

7. Firment 7 Immediate management 1. Stabilize the patient ABC Open the airway, breathing. give oxygen, stabilise the cervical spine as required OTI, ventilation ? (GCS ≤ 8) pO2, pCO2 Support the circulation: correct hypotension (colloids, inotropes), CVP? Treat seizures (diazepam, phenytoin) - Take blood for glucose, U+Es, calcium, liver enzymes, albumin, clotting screen, FBC, toxicology (+urine) CMRO2

8. Firment 8 2. Consider giving: thiamine (Wernickes encephalopathy) glucose (40 ml 40% glucose) naloxon (opiate intoxication) flumazenil (benzodiazepine intoxication) Hypoglycaemia

9. Firment 9 3. Examine patient: History General examination Core temperature, heart rate, rhythm, BP, respiratory pattern, breath, skin, heart, abdomen, fundi Is there meningism? – neck stiffness (inflammation, blood) Asses GCS Look for evidence of brainstem dysfunction Are there lateralizing signs?

10. Firment 10 Test brainstem dysfunction Pupillary response Corneal reflex Spontaneous eye movements Oculocephalic response/Doll’s head manoeuvre Oculovestibular response Swallowing reflex Respiratory pattern

11. Firment 11 Motor function: Decorticate posturing – lesions above the pons Decerebrate posturing – pontine damage Decorticate posturing Decerebrate posturing

12. Firment 12 4. Plan for further investigations: 1. Brainstem function intact: urgent CT head scan : - lesions (subdural haematoma,..), - normal – lumbar puncture, CSF analysis

13. Firment 13 4. Plan for further investigations: 1. Brainstem function intact: urgent CT head scan : - lesions (subdural haematoma,..), - normal – lumbar puncture, CSF analysis 2. Brainstem function not intact: Signs ICH (intracranial hypertension): - early: headache,vomiting,seizures, focal neurology, papilloedema - late: incr. BP, bradycardia, coma, Cheyne Stokes breathing, apnoe. - if herniation syndrome appears to be progressing rapidly - mannitol, hyperventilation, surgeon - if herniation syndrome appears to be progressing not so rapidly – mannitol and CT, surgeon

14. Firment 14 4. Plan for further investigations: 1. Brainstem function intact: urgent CT head scan : - lesions (subdural haematoma,..), - normal – lumbar puncture, CSF analysis 2. Brainstem function not intact: - if herniation syndrome appears to be progressing rapidly - mannitol, hyperventilation, surgeon - if herniation syndrome appears to be progressing not so rapidly – mannitol and CT Hyperventilation- hypocapnia- vasoconstriction of cerebral aa. – decrease of intracranial pressure

15. Firment 15 Head injury (HI) Primary brain injury : - brain lacerations, contusions, diffuse axonal injury due to accelaration or deceleration - the neurones lost at the time of HI are lost forever

16. Firment 16 Secondary injury: Due to raised intracranial pressure (ICP) and inadequate cerebral perfusion Causes of secondary brain injury : Systemic : Hypoxaemia Hypotension Hypercarbia Severe hypocapnia Pyrexia,.. Anaemia Hyper/hypoglycaemia Intracranial: Haematoma (extradural, subdural, intracerebral) Brain swelling/ oedema Cerebral ischemia (vasospasm, seizures) Inflammatory mediators

17. Firment 17 Prevention of secondary injury is the aim of the treatment. Prevention therapy may improve outcome.

18. Firment 18 INTRACRANIAL COMPENSATION FOR EXPANDING MASS

19. Firment 19 INTRACRANIAL PRESSURE (ICP) Up to 15 mmHg, above 40 malignant oedema Compensation Phase Transition phase De-compensation phase VOLUME PRESSURE [mmHg] 40 20 0

20. Firment 20 INCREASED ICP Normal ICP 0-10 mmHg ICP > 15-20 mmHg treatment is required Causes of raised ICP: -Increased extracellular fluid : cerebral oedema -Increased cerebral blood flow : hypoxia, hypercarbia,.. (vasodilatation) -Increased cerebral venous volume : venous obstruction in the neck, coughing,.. -Increased CSF volume : hydrocephalus,...

21. Firment 21 Patients with head injuries usually have a mixed type of oedema: vasogenic and cytotoxic.

22. Firment 22 Increased ICP >25 mmHg ICP peaks at 72 h Cerebral herniation Reduced CPP (cerebral perfusion pressure) MAP – ICP = CPP causing ischemia Therapy aim: CPP > 60 mmHg

23. Firment 23 Cerebral herniation Supratentorial herniation 1. Uncal 2. Central (transtentorial) 3. Cingulate (subfalcine) 4. Transcalvarial Infratentorial herniation 5. Upward (upward cerebellar or upward transtentorial) 6. Tonsillar (downward cerebellar)

24. Firment Normally CBF (cerebral blood flow) is maintained constant by autoregulation between a MAP 50- 140 mmHg (MAP = APd + 1/3 (APs-APd) mean AP = diastolic AP + 1/3 (systolic AP- diastolic AP) 24

25. Firment 25 Autoregulation is impaired : head injury, acidosis (hypoxia, hypercarbia ) CBF varies passively with CPP (ischemia!!)

26. Firment 26 Hypoxia and hypercapnia Dilates normal vessels and divert CBF away from damaged cerebral tissue CBV (cerebral blood volume) and ICP - CPP and CBF - aggravates ischaemia in damaged brain tissue

27. Firment 27 Hypocapnia Constricts normal vessels CBV and ICP CPP and CBF !! Severe hypocapnia – exccess vasoconstriction – ischaemia in normal tissue Recommended: normal P a CO 2 4,6 – 5,3 kPa (35-40mmHg)

28. Firment 28 Raised ICP: immediate management Open the airway, intubation, mechanical ventilation, keep P a CO 2 3,3 – 4,0 kPa (25-30mmHg) Correct hypotension: colloids, infusions of inotropes CPP < 70 mmHg is critical ! Spinal immobilisation- all pt Detect other injuries: 50% have potentially lethal thoracic or abdominal injuries Treat seizures (increase O 2 consumption) Sedation (paralysis) prevent ICP elevation in agitated pt Take blood for glucose, U+Es, calcium, liver enzymes, albumin, clotting screen,FBC

29. Firment 29 Radiographic evaluation: Immediate CT scan - in coma, GCS ≤ 8 - GCS 9-13 with skull fractures Intracranial hematoma is 10 x more common after skull fractures

30. Firment 30 Monitoring GCS is adequate in mild injuries ICP intracranial pressure – severe HI Cerebral oxygen saturation SjO 2 jugular venous bulb fibreopthic catheter SjO 2 < 55% inadequate (low) CBF

31. Firment 31 INTRACRANIAL PRESSURE Normal curve shape Low compliance

32. Firment 32 Management Prevention of secondary injury is the aim: optimise CBF: MAP – ICP = CPP MAP > 70 mmHg ICP 60 mmHg and oxygenation: SatO2 > 90%, S j O2 >55%

33. Firment 1. Reduce ICP: Hyperventilation : P a CO 2 3,3 – 4 kPa (25-30mmHg) not routinelly only if herniation appears Loop diuretics (furosemid 20-40 mg i.v. ), osmotic agents (mannitol 0,5-1 g/kg )- reduce ICP Improved venous drainage : midline haed position + 30°elevation, !! suctioning, PEEP, physiotherapy increase thoracic venous p. Ventriculostomy drainage/decompressive surgery – if other fails No corticosteroids 33

34. Firment 2. Reduce cerebral metabolism: Avoid hyperglycaemia (BS 4-7 mmol/l) hyperglycaemia increase cerebral lactate production Prophylactic anticonvulsants Adequate analgesia and sedation: benzodiazepines, propofol, thiopentone Antipyretics and cooling (33-34 °C maybe neuroprotective) 34

35. Firment 35 Treat complications: Hypotalamic injury :inappropriate ADH secretion – diabetes insipidus Meningitis – ATB Avoid nasogastic tubes in basilar skull fracture

36. Firment 36 TBI, maxillofaciálne poranenie, haemothorax Tracheostómia – UVP, PEG, drenáž hrudníka

37. Firment Thank you! 37 jcapkova@capko.sk

38. Firment 38 TRAUMATIC BRAIN INJURY Hypoxia and acidosisCerebral oedema

39. Firment 39 Immediate management 1.Stabilize the patient: ABC give oxygen, support circulation, treat seizures, stabilise the cervical spine as required 2.Consider giving thiamine, glucose (40 ml 40% glucose), naloxon, flumazenil 3.Examine patient 4.Plan for further investigations

40. Firment 40 ICP peaks at 72 h CPP (cerebral perfusion pressure ) = MAP - ICP MAP = APd + 1/3 (APs-APd) CPP is the effective pressure that results in blood flow to the brain.

41. Firment 41 CPP(cerebral perfusion pressure) = MAP - ICP CBF (cerebral blood flow) is maintained constant by autoregulation (between a MAP 50- 140 mmHg). Autoregulation is impaired : head injury, acidosis (hypoxia, hypercarbia ) CBF varies passively with CPP (ischemia!!) Therapy aim: CPP < 70 mmHg is critical !

42. Firment 42 5. Progress in monitoring Regular and frequent observations of vital signs and neurological state Emergency treatment of raised ICP (intracranial pressure) Signs ICH (intracranial hypertension): - early: headache,vomiting,seizures, focal neurology, papilloedema - late: incr. BP, bradycardia, coma, Cheyne Stokes breathing, apnoe.