COMA & INTENSIVE CARE

Transcription

1 COMA & INTENSIVE CARE Jozef Firment, MD. PhD., Judita Capkova, MD. PhD. Department of Anaesthesiology & Intensive Care Medicine Šafárik University Faculty of Medicine, Košice

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 2

3 GLASGOW COMA SCALE Decorticate posturing Decerebrate posturing 3

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 4

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 5

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 6

7 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 7

8 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) 8

9 1 Recovery position

10 2. Consider giving: thiamine (Wernickes encephalopathy), glucose (40 ml 40% glucose), naloxon (opiate intoxication), Hypoglycaemia flumazenil (benzodiazepine intoxication) 10

11 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? 11

12 Test brainstem dysfunction Pupillary response Corneal reflex Spontaneous eye movements Oculocephalic response/doll s head manoeuvre Oculovestibular response Swallowing reflex Respiratory pattern 12

13 Motor function: Decorticate posturing lesions above the pons Decorticate posturing Decerebrate posturing pontine damage Decerebrate posturing 13

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 14

15 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. 15

16 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 16

17 Secondary injury: Due to raised intracranial pressure (ICP) and inadequate cerebral perfusion Causes of secondary brain injury : Systemic : Intracranial: Hypoxaemia Hypotension Hypercarbia Severe hypocapnia Pyrexia,.. Haematoma (extradural, subdural, intracerebral) Brain swelling/ oedema Raised ICP,... 17

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19 Prevention of secondary injury is the aim of the treatment. 19

20 INTRACRANIAL COMPENSATION FOR EXPANDING MASS 20

21 PRESSURE [mmhg] INTRACRANIAL PRESSURE (ICP) MAP ICP = CPP De-compensation phase Compensation Phase Transition phase 0 VOLUME Up to 15 mmhg, above 40 malignant oedema 21

22 INTRACRANIAL PRESSURE Normal curve shape Low compliance 22

23 INCREASED ICP Normal ICP 0-10 mmhg ICP > 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,... 23

24 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) 24

25 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. 25

26 CPP(cerebral perfusion pressure) = MAP - ICP CBF (cerebral blood flow) is maintained constant by autoregulation (between a MAP mmhg). Autoregulation is impaired : head injury, acidosis (hypoxia, hypercarbia) CBF varies passively with CPP (ischemia!!) Therapy aim: CPP < 70 mmhg is critical! 26

27 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 27

28 Monitoring GCS is adequate in mild injuries ICP severe HI Cerebral oxygen saturation 28

29 Management Prevention of secondary injury is the aim: optimise CBF: MAP > 70 mmhg ICP < 15 mmhg CPP > 60 mmhg and oxygenation: SatO2 > 90%, S j O2 >55% 29

30 Elevate head of bed to 30 (-venous drainage) Mannitol 0,5-1 g/kg, furosemid 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) 30

31 TBI, maxillofaciaálne poranenie, haemothorax Tracheostómia UVP, PEG, drenáž hrudníka Firment 31

32 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 32

33 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 33

34 Apnoea no respiratory movements when the ventilator is disconnected and P a CO 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) 34

35 Don t take your organs to heaven..., heaven knows we need them here. 35

36 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. 36

37 TRAUMATIC BRAIN INJURY Hypoxia and acidosis Cerebral oedema 37