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Coma, head injury Judita Capkova, MD. PhD. Jozef Firment, MD. PhD. Department of Anaesthesiology & Intensive Care Medicine Šafárik University Faculty of Medicine, Košice
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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
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Firment 3 GLASGOW COMA SCALE Decorticate posturing Decerebrate posturing
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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
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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
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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
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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
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Firment 8 2. Consider giving: thiamine (Wernickes encephalopathy) glucose (40 ml 40% glucose) naloxon (opiate intoxication) flumazenil (benzodiazepine intoxication) Hypoglycaemia
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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?
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Firment 10 Test brainstem dysfunction Pupillary response Corneal reflex Spontaneous eye movements Oculocephalic response/Doll’s head manoeuvre Oculovestibular response Swallowing reflex Respiratory pattern
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Firment 11 Motor function: Decorticate posturing – lesions above the pons Decerebrate posturing – pontine damage Decorticate posturing Decerebrate posturing
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Firment 12 4. Plan for further investigations: 1. Brainstem function intact: urgent CT head scan : - lesions (subdural haematoma,..), - normal – lumbar puncture, CSF analysis
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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
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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
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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
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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
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Firment 17 Prevention of secondary injury is the aim of the treatment. Prevention therapy may improve outcome.
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Firment 18 INTRACRANIAL COMPENSATION FOR EXPANDING MASS
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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
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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,...
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Firment 21 Patients with head injuries usually have a mixed type of oedema: vasogenic and cytotoxic.
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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
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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)
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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
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Firment 25 Autoregulation is impaired : head injury, acidosis (hypoxia, hypercarbia ) CBF varies passively with CPP (ischemia!!)
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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
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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)
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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
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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
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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
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Firment 31 INTRACRANIAL PRESSURE Normal curve shape Low compliance
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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%
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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
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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
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Firment 35 Treat complications: Hypotalamic injury :inappropriate ADH secretion – diabetes insipidus Meningitis – ATB Avoid nasogastic tubes in basilar skull fracture
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Firment 36 TBI, maxillofaciálne poranenie, haemothorax Tracheostómia – UVP, PEG, drenáž hrudníka
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Firment Thank you! 37 jcapkova@capko.sk
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Firment 38 TRAUMATIC BRAIN INJURY Hypoxia and acidosisCerebral oedema
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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
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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.
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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 !
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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.
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