Post operative apnoea

Ben Creagh-Brown

SHO, UHL, November 2003

Overview

Causes and their associated management

Paediatric considerations Controversies

Causes of postoperative hypoventilation / apnoea

Factors affecting airwayFactors affecting ventilatory driveFactors affecting peripheral drive

Airway

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)

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

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.

Reduced ventilatory drive

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...

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)

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.

Blood glucose

Severe hypoglycaemia as a central cause for reduced ventilatory drive.

Peripheral factors

Causes

Muscle weakness Pain Abdominal distension Obesity Tight dressings Pneumo/haemo thorax

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

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

Limiting NM blockade reversal

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

NM monitoring

1. Variable individual response to muscle relaxants2. 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.

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.

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...

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

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.

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.

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.

Dangers of hypercapnia

Hypertension Tachycardia CO2 narcosis (>9kPa) Unconsciousness, coma, respiratory

arrest

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

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

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, EpilepsyAminophylline 2mg/kg slow IV bolus. Can cause seizures, increases cerebral O2

requirements, arrhythmias

Paediatric considerations

Particularly sensitive to temperature Can be extremely opiate sensitive Prematures are highly susceptible to

apnoea up to 60 weeks gestational age.

Thanks