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

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mH

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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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Thank you!

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jcapkova@capko.sk

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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.