Coma, head injury
Judita Capkova, MD. PhD.
Jozef Firment, MD. PhD.
Department ofAnaesthesiology & Intensive Care Medicine
Šafárik University Faculty of Medicine, Košice
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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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GLASGOW COMA SCALE
Decorticate posturing
Decerebrate posturing
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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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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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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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Immediate management1. 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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2. Consider giving:
thiamine (Wernickes encephalopathy)
glucose (40 ml 40% glucose)
naloxon (opiate intoxication)
flumazenil (benzodiazepine intoxication)
Hypoglycaemia
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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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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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Motor function:
• Decorticate posturing – lesions above the pons
• Decerebrate posturing – pontine damage
Decorticate posturing
Decerebrate posturing
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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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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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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 CTHyperventilation- hypocapnia- vasoconstriction of cerebral aa. – decrease of intracranial pressure
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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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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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Prevention of secondary injury is the aim of the
treatment.
Prevention therapy may improve outcome.
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INTRACRANIAL COMPENSATION FOR EXPANDING MASS
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INTRACRANIAL PRESSURE (ICP)
Up to 15 mmHg, above 40 malignant oedema
CompensationPhase
Transition phase
De-compensationphase
VOLUME
PR
ES
SU
RE
[m
mH
g]
40
20
0
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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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• Patients with head injuries usually have a mixed type of oedema: vasogenic and cytotoxic.
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Increased ICP >25 mmHg• ICP peaks at 72 h
• Cerebral herniation
• Reduced CPP (cerebral perfusion pressure)MAP – ICP = CPP causing ischemiaTherapy aim: CPP > 60 mmHg
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Cerebral herniationSupratentorial 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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• 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)
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• Autoregulation is impaired : head injury, acidosis (hypoxia, hypercarbia)
• CBF varies passively with CPP (ischemia!!)
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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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Hypocapnia
• Constricts normal vesselsCBV and ICP
CPP and CBF
• !! Severe hypocapnia – exccess vasoconstriction – ischaemia in normal tissueRecommended: normal Pa CO2 4,6 – 5,3 kPa
(35-40mmHg)
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Raised ICP: immediate management
• Open the airway, intubation, mechanical ventilation, keep Pa CO2 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 O2 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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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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Monitoring• GCS is adequate in mild injuries
• ICP intracranial pressure – severe HI
• Cerebral oxygen saturation SjO2
jugular venous bulb fibreopthic catheter SjO2 < 55% inadequate (low) CBF
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INTRACRANIAL PRESSURE
Normal curve shape
Low compliance
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Management
• Prevention of secondary injury is the aim:optimise CBF: MAP – ICP = CPP MAP > 70 mmHg ICP < 15 mmHgCPP > 60 mmHg
and oxygenation:SatO2 > 90%, SjO2 >55%
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1. Reduce ICP:• Hyperventilation :
PaCO2 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
•
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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)
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Treat complications:
•Hypotalamic injury :inappropriate ADH secretion – diabetes insipidus
•Meningitis – ATB
•Avoid nasogastic tubes in basilar skull fracture
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TBI, maxillofaciálne poranenie, haemothoraxTracheostómia – UVP, PEG, drenáž hrudníka
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TRAUMATIC BRAIN INJURYHypoxia and acidosis Cerebral oedema
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Immediate management
1. Stabilize the patient: ABCgive 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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• 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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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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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.