Post-operative apnoea fortunately rare can catch the anaesthetist off guard. A through knowledge is needed to make a quick differential diagnosis to correct the problem leading to prolonged apnoea

1. Post operative apnoea
Dr. Shailendra V.L
Anaesthesia specialist
Al Bukeriya general hospital

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.

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
1. Variable individual response to muscle relaxants
2. 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 – treat
For 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