postoperative apnoea

1. Post operative apnoea
HOSSAM M ATEF
SUEZ CANAL UNIVERSITY

2. Causes of postoperative
hypoventilation / apnoea
Factors affecting airway
Factors affecting ventilatory drive
Factors affecting peripheral drive

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

4. 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

5. 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.

6. Reduced ventilatory drive

7. Causes
 Intracranial pathology (stroke, tumour, bleed)
 Hypothermia
 Hypocapnia, severe hypercapnia
 All induction and maintenance drugs (except
ketamine) depress resp. drive. TIVA.
 Opiates...

8. Opiates
 Reduced vent. drive is obvious if RR or VT is low.
 Elderly and children are particularly sensitive
 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)

9. 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.

10. Blood glucose
 Severe hypoglycaemia as a central
cause for reduced ventilatory drive.

11. Peripheral causes
 Muscle weakness
 Pain
 Abdominal distension
 Obesity
 Tight dressings
 Pneumo/haemo thorax
 P E

12. 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

13. 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

14. Limiting NM blockade reversal
 NM blocker
 Too little time from blockade to reversal
 Hypokalaemia, Hypermagnesaemia
 Acidosis
 Gentamicin
 Local anaesthetics
 Myopathy

15. 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.

16.  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.

17. 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.

18. 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...

19. 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 = S-
type cholinesterase)
 Normal range = 4000 – 12,000 IU/L

20. Atypical plasma cholinesterase
 Prolonged NM block after
suxamethonium or mivacurium
 Either due to absent or faulty plasma
cholinesterase
 Sux apnoea lasts 30mins to 8 hrs. 2
commonest defective genes – 30 mins.

21. Genetics
 Pseudocholinesterase deficiency is
most common in people of European ;
rare in Asians.
 The normal gene encoding for plasma
cholinesterase is E1u (usual)

22.  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 0.003% and E1f
homozygotes in 0.0003% of the
population.

23.  Suxamethonium is broken down by pCE
 Inherited abnormal genetic variant of
pCE (autosomal recessive)
 Prolonged apnoea after a standard dose
of suxamethonium
 Several variations:
 normal pCE enzyme gene = E1U.
 E1a (a = abnormal)

24.  (E1uE1a) recovery time from
suxamethonium < 30 minutes
 (E1aE1a) recovery time from
suxamethonium >2 hours
 3. E1f(the fluoride pCE)
 4. E1s(silent) → little pCE activity
→recovery from suxamethonium
 can take >> 3 hours.

25. Acquired low cholinesterase
levels
 Liver disease
 3rd
trimester pregnancy
 Malnutrition
 Severe anaemia
 MI ; plasmapheresis
 Carcinomatosis
 Hypothyroidism
 Drugs: amethocaine, ketamine, pancuronium, oral
contraceptives, propranolol, ecothiopate eye drops,
cytotoxics, organophosphate insecticides .

26.  Dibucaine is a local anaesthetic that
inhibits the activity of pCE.
 The normal gene is inhibited by 80%
(dibucaine number = 80%), atypical gene
by 20% (dibucaine number = 20%) and
heterozygous gene by 40-60%
(dibucaine number = 40-60%).
 In the same way a fluoride number can
be determined

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

28. Treatment
 If reversible cause – treat
For Sux/Miva apnoea – consider FFP
 If not immediately reversible and inadequate
ventilation (severe hypercapnia / hypoxia /
clinically deteriorating) then maintain artificial
ventilation with minimal anaesthesia to prevent
awareness

29. 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

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

31. Thanks