Coma,
head injury
Judita Capkova, MD. PhD.
Jozef Firment, MD. PhD.
Department of
Anaesthesiology & Intensive Care Medicine
Šafárik University Faculty of Medicine, Košice
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
• GCS – level of consciousness,
coma: GCS ≤ 8
Firment
• Involuntary movements (seizures) may occur
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GLASGOW COMA SCALE
Firment
Decorticate posturing
Decerebrate posturing
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Causes of coma
Metabolic
Toxic
Infection
Structural lesions
with or
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
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•
•
•
Coma without focal/lateralizing
neurological signs
• Anoxia/ hypoperfusion
• Metabolic: e.g. Hypo/-hyperglycaemia, acidosis/alkalosis,
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Intoxications: e.g. alcohol, opiates, benzodiazepines,..
Endocrine : hypothyreoidism
Hypo- or hyperthermia
Epilepsy
Hypertensive encephalopathy
Firment
hepatic or renal failure
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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
• Meningitis, encephalitis
• Subarachnoid haemorrhage
Firment
Coma with meningism
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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,
•
Treat seizures (diazepam, phenytoin) - CMRO2
•
Take blood for glucose, U+Es, calcium, liver
enzymes, albumin, clotting screen, FBC, toxicology (+urine)
Firment
inotropes), CVP?
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2. Consider giving:
thiamine (Wernickes encephalopathy)
glucose (40 ml 40% glucose)
Hypoglycaemia
naloxon (opiate intoxication)
Firment
flumazenil (benzodiazepine intoxication)
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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,
Asses GCS
Look for evidence of brainstem dysfunction
Are there lateralizing signs?
Firment
blood)
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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
Firment
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•
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Motor function:
• Decerebrate posturing –
pontine damage
Decorticate posturing
Decerebrate posturing
Firment
• Decorticate posturing –
lesions above the pons
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4. Plan for further investigations:
Firment
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 - if herniation syndrome appears to be progressing not so
rapidly – mannitol and CT, surgeon
Firment
mannitol, hyperventilation, 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 - if herniation syndrome appears to be progressing not so
rapidly – mannitol
and CT vasoconstriction of cerebral
Hyperventilationhypocapniaaa. – decrease of intracranial pressure
Firment
mannitol, hyperventilation, surgeon
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Head injury (HI)
• Primary brain injury :
- brain lacerations, contusions,
diffuse axonal injury due to accelaration or
deceleration
Firment
- 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
•
Systemic :
Intracranial:
•Hypoxaemia
•Hypotension
•Hypercarbia
•Severe hypocapnia
•Pyrexia,..
•Anaemia
•Hyper/hypoglycaemia
•Haematoma (extradural, subdural,
intracerebral)
•Brain swelling/ oedema
•Cerebral ischemia (vasospasm,
seizures)
•Inflammatory mediators
Firment
• Causes of secondary brain injury :
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Prevention of secondary
injury is the aim of the
treatment.
Firment
Prevention therapy may
improve outcome.
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Firment
INTRACRANIAL COMPENSATION
FOR EXPANDING MASS
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PRESSURE [mmHg]
INTRACRANIAL PRESSURE
(ICP)
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De-compensation
phase
Compensation
Phase
Transition
phase
0
VOLUME
Up to 15 mmHg, above 40 malignant oedema
Firment
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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
-
Increased CSF volume
: hydrocephalus,...
Firment
: venous
obstruction in the neck, coughing,..
-
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Firment
• 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
Firment
• Reduced CPP (cerebral perfusion pressure)
MAP – ICP = CPP causing ischemia
Therapy aim: CPP > 60 mmHg
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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)
Firment
Cerebral herniation
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• Normally CBF (cerebral blood flow) is
maintained constant by autoregulation
Firment
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)
Firment
• 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
Firment
in damaged brain tissue
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Hypocapnia
• Constricts normal vessels
CBV and ICP
• !! Severe hypocapnia – exccess
vasoconstriction – ischaemia in normal tissue
Recommended: normal Pa CO2 4,6 – 5,3 kPa
(35-40mmHg)
Firment
CPP and CBF
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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
•
•
• Take blood for glucose, U+Es, calcium, liver enzymes, albumin,
Firment
•
•
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
clotting screen,FBC
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Radiographic evaluation:
Firment
• 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
Firment
• Cerebral oxygen saturation SjO2
jugular venous bulb fibreopthic catheter
SjO2 < 55% inadequate (low) CBF
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INTRACRANIAL PRESSURE
Low compliance
Firment
Normal curve shape
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Management
MAP > 70 mmHg
ICP < 15 mmHg
CPP > 60 mmHg
and oxygenation:
SatO2 > 90%, SjO2 >55%
Firment
• Prevention of secondary injury is
the aim:
optimise CBF: MAP – ICP = CPP
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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,
• Ventriculostomy drainage/decompressive
surgery – if other fails
• No corticosteroids
Firment
!! suctioning, PEEP, physiotherapy increase thoracic venous p.
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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
Firment
(33-34 °C maybe neuroprotective)
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Treat complications:
• Avoid nasogastic tubes in basilar
skull fracture
Firment
• Hypotalamic injury :inappropriate
ADH secretion – diabetes insipidus
• Meningitis – ATB
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Firment
TBI, maxillofaciálne poranenie, haemothorax
Tracheostómia – UVP,
PEG,
drenáž hrudníka
36
jcapkova@capko.sk
Firment
Thank you!
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TRAUMATIC BRAIN INJURY
Cerebral oedema
Firment
Hypoxia and acidosis
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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
Firment
Immediate management
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• ICP peaks at 72 h
• CPP(cerebral perfusion pressure) = MAP - ICP
• MAP = APd + 1/3 (APs-APd)
Firment
• 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 50140 mmHg).
Autoregulation is impaired : head injury,
acidosis (hypoxia, hypercarbia)
Firment
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)
headache,vomiting,seizures, focal neurology, papilloedema
- late: incr. BP, bradycardia, coma, Cheyne Stokes breathing,
apnoe.
Firment
Signs ICH (intracranial hypertension):
- early:
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