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COMA

&

INTENSIVE CARE

Jozef Firment, MD. PhD.,

Judita Capkova, 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

• 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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• Metabolic

• Toxic

• Infection with or

• Structural lesions without

Causes of coma

• 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 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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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)

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1

2

Recovery position

3

4

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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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• Decorticate posturing –

lesions above the pons

• Decerebrate posturing –

pontine damage

Motor function:

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

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

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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.

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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,..

Intracranial:

•Haematoma (extradural, subdural,

intracerebral)

•Brain swelling/ oedema

•Raised ICP,...

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Prevention of secondary

injury is the aim of the

treatment.

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INTRACRANIAL COMPENSATION

FOR EXPANDING MASS

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PRESSURE [mmHg]

INTRACRANIAL PRESSURE

(ICP)

40

20

0

MAP – ICP = CPP

Compensation

Phase

De-compensation

phase

Transition

phase

VOLUME

Up to 15 mmHg, above 40 malignant oedema

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INTRACRANIAL PRESSURE

Normal curve shape

Low compliance

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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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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)

Cerebral herniation

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Head injury (HI)

• 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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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

• Detect other injuries: 50% have potentially lethal thoracic or

abdominal injuries

• Treat seizures (increase O 2 consumption)

• Sedation (paralysis)prevent ICP elevation

• Take blood for glucose, U+Es, calcium, liver enzymes, albumin,

clotting screen,FBC

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Monitoring

• GCS is adequate in mild injuries

• ICP – severe HI

• Cerebral oxygen saturation

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Management

• Prevention of secondary injury is

the aim:

optimise CBF:

MAP > 70 mmHg

ICP < 15 mmHg

CPP > 60 mmHg

and oxygenation:

SatO2 > 90%, S jO2 >55%

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• Elevate head of bed to 30° (-venous drainage)

• Mannitol 0,5-1 g/kg , furosemid 20-40

mg i.v.

• No corticosteroids

• Fluid restriction to 1,5-2 l/day

• Avoid hyperglycaemia (exacerbates ischaemia)

• Avoid inadequate analgesia, sedation

• Avoid pyrexia (increase c. metabolism)

• Avoid hyponatraemia (inappropriate ADH

secretion)

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TBI, maxillofaciaálne poranenie, haemothorax

Tracheostómia – UVP,

PEG,

drenáž hrudníka

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Brain death

• Is irreversible loss of the capacity for

consciousness combined with

irreversible loss of capacity to breathe

Preconditions

• No doubt that pt. has structural brain

damage which has been diagnosed

• Pt must be in apnoic coma (on

mechanical ventilator)

• No possibility of drug intoxication, no

significant metabolic, endocrine,

electrolyte disturbance

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Test for confirmation of

brain death

All brainstem reflexes must be absent

• Pupils fixed and unresponsive to bright light

• Absent cornel reflexes

• Absent vestibulo-ocular reflexes

• No motor response within the cranial nerve

distribution

• No reflex response to touching the pharynx,

nor to a suction catheter passed into the

trachea

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Apnoea – no respiratory movements when

the ventilator is disconnected and P aCO 2

reaches 6,6 kPa

Diagnosis should be made by 3 medical

practicioners (neurologist, anesthesiologists),

test must be performed on 2 occasions (after

2 hours)

No aditional tests are required in Slovakia

(Angiography of cerebral vessels – no

perfusion, EEG, brainstem evoked potentials)

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„Don´t take your

organs to heaven

..., heaven knows

we need them

here.“

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Cerebral oedema

• Signifies an increase in the brain water content.

There are three different types of cerebral oedema -

vasogenic, cytotoxic, and interstitial. Cerebral

oedema must be distinguished from brain swelling,

which is due to an increase in cerebral blood volume

(congestion).

Patients with head injuries usually have a mixed

type of oedema: vasogenic and cytotoxic.

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TRAUMATIC BRAIN INJURY

Hypoxia and acidosis Cerebral oedema

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