Post operative apnoea

1. Post operative apnoea Ben Creagh-Brown SHO, UHL, November 2003

2. Overview • Causes and their associated management • Paediatric considerations • Controversies

3. Causes of postoperative hypoventilation / apnoea • Factors affecting airway • Factors affecting ventilatory drive • Factors affecting peripheral drive

4. Airway

5. Airway obstruction • Blood, clots, secretions: Recovery position / suction • Airway manoeuvres (jaw thrust, chin lift, head tilt) • Airways (OP / NP) • Intermittent: OSA • External airway compression (thyroid surgery)

6. Laryngospasm • Direct stimulation of cords or epiglottis by secretions/blood/FB/OP airway, LMA or following extubation • May be partial or complete • 100% O2, aspirate secretions, IPPV to ‘break’ spasm. Caution inflating stomach • If not improving consider deepening, Suxamethonium +/- reintubation • Rarely post thyroid surgery: recurrent laryngeal nerve palsy  cord palsy  obstruction

7. Bronchospasm • Irritable airways in smokers • Intrinsic asthma • Anaphylaxis • Effect of drug directly on bronchial muscle or via histamine release (thiopentone, morphine, mivacurium, atracurium) • Mx: O2 and bronchodilators, aminophylline, adrenaline.

8. Reduced ventilatory drive

9. Causes • Intracranial pathology (stroke, tumour, bleed) • Hypothermia • Hypocapnia (CSF lags Serum), severe hypercapnia • All induction and maintenance drugs (except ketamine) depress resp. drive. TIVA. • Opiates...

10. Opiates • Reduced vent. drive is obvious if RR or VT is low. • Can be subtle if moderate hypercapnia is undetected - causes hypertension and tachycardia, which may be mistaken for signs of pain and more opiates given • Elderly and children are particularly sensitive • Beware high spinals or SA epidurals • Naloxone as specific antidote. 400mcg in 1ml, dilute to 10ml and give in 40mcg boluses. T1/2 20-30mins (infusion 800mcg in 500ml saline over 6 hours or IM)

11. Benzodiazepines • Can be reversed with flumazenil • iv increments of 0.1mg to a maximum adult dose of 1mg. • However, Flumazenil is expensive, may cause arrhythmias, hypertension and convulsions. • It’s use is generally not indicated.

12. Blood glucose • Severe hypoglycaemia as a central cause for reduced ventilatory drive.

13. Peripheral factors

14. Causes • Muscle weakness • Pain • Abdominal distension • Obesity • Tight dressings • Pneumo/haemo thorax

15. Muscle weakness • Myasthenia gravis or other myopathies • Electrolyte disturbance • Residual neuromuscular blockade or inadequate reversal - uncoordinated jerky movements • VT measurement unreliable estimate of adequacy of reversal as normal VT with only 20% diaphragmatic power, poor coughing ability

16. Adequate reversal of NM blockade • Subjective • Grip strength • Adequate cough • TOF/DBS visualised • Objective • Sustained head lift 5s • Vital capacity of 10ml/kg • TOFR from accelerometer

17. Limiting NM blockade reversal • XS NM blocker • Too little time from blockade to reversal • Hypokalaemia, Hypermagnesaemia • Acidosis • Gentamicin • Local anaesthetics • Myopathy

18. NM monitoring • Variable individual response to muscle relaxants • Narrow therapeutic window. There is no detectable block until 75 to 85% of receptors are occupied and paralysis is complete at 90 to 95% receptor occupancy. • TOF: 4 supramaximal, square wave, pulses of 0.2s at 2Hz. 50mA. TOFR >70% best predicts adequate muscle power. • DBS: 2 short 50Hz bursts of 3 pulses, 750ms apart. Meant to be easier to visualise.

19. Limits to PNS • Testing TOF/DBS on forearm not same as testing diaphragm • Neostigmine inhibits metabolism of acetylcholione. 0.05-0.08mg/kg, peak effect 7 - 11m, duration 40m • Neostigmine up to 5mg total, in higher doses can worsen NM function.

20. Delayed elimination of NM blockers • Prolonged NM blockade as drugs persist can occur with all except atracurium and it’s derivative cis-atracurium • Renal or hepatic impairment • Atypical enzymes...

21. Cholinesterase • The enzyme which hydrolyses acetylcholine and other choline esters at a more rapid rate than noncholine esters • Specific cholinesterase - highly specific for acetylcholine and a few closely related esters • Nonspecific cholinesterase (serum cholinesterase = plasma cholinesterase = pseudocholinesterase = butyrylcholinesterase = S-type cholinesterase) • Normal range = 4000 – 12,000 IU/L

22. Atypical plasma cholinesterase • Prolonged NM block after suxamethonium or mivacurium • Either due to absent or faulty plasma cholinesterase • Sux apnoea lasts 20mins to 8 hrs. 2 commonest defective genes – 20 mins.

23. Genetics • Pseudocholinesterase deficiency is most common in people of European descent; it is rare in Asians. • The normal gene encoding for plasma cholinesterase is E1u (usual) • There are three abnormal genes: E1a (atypical), E1s (silent) and E1f (fluoride-resistant) 94% of the population are heterozygous for the usual gene (hence normal response to suxamethonium), E1a homozygotes occur in 0.03% of the population, E1s homozygotes in 0.001% and E1f homozygotes in 0.0003% of the population.

24. Aquired low cholinesterase levels • Liver disease • 3rd trimester pregnancy • Malnutrition • Severe anaemia • MI • Carcinomatosis • Hypothyroidism • Drugs: amethocaine, ketamine, pancuronium, oral contraceptives, propranolol, ecothiopate eye drops, cytotoxics, organophosphate insecticides or weedkillers.

25. Dangers of hypercapnia • Hypertension • Tachycardia • CO2 narcosis (>9kPa) • Unconsciousness, coma, respiratory arrest

26. Treatment • If reversible cause – treatFor Sux/Miva apnoea – consider FFP • Consider use of agent to increase ventilation… • If not immediately reversible and inadequate ventilation (severe hypercapnia / hypoxia / clinically deteriorating) then maintain artificial ventilation with minimal anaesthesia to prevent awareness

27. Other mechanical causes of hypoventilation • Obesity • Diaphragmatic splinting from abdo distension or tight dressings • Pain from thoracic or upper abdominal wounds • Intra pleural air/fluid/blood. NB Pneumothorax from IPPV in COPD / occasionally healthy young patients

28. To artificially increase ventilation • Controversial Doxapram • Produces respiratory stimulation mediated through the peripheral carotid chemoreceptors. As the dosage level is increased, the central respiratory centres in the medulla are stimulated with progressive stimulation of other parts of the brain and spinal cord. • The onset of respiratory stimulation following the recommended single intravenous injection of doxapram hydrochloride usually occurs in 20 to 40 seconds with peak effect at 1 to 2 minutes. The duration of effect may vary from 5 to 12 minutes. • Increased Vt and RR. CI: CAD, Epilepsy Aminophylline • 2mg/kg slow IV bolus. Can cause seizures, increases cerebral O2 requirements, arrhythmias

29. Paediatric considerations • Particularly sensitive to temperature • Can be extremely opiate sensitive • Prematures are highly susceptible to apnoea up to 60 weeks gestational age.

30. Thanks