Post operative apnoea
Dr. Shailendra V.L
Anaesthesia specialist
Al Bukeriya general hospital
Overview
 Causes and their associated
management
 Paediatric considerations
 Controversies
Causes of postoperative
hypoventilation / apnoea
Factors affecting airway
Factors affecting ventilatory drive
Factors 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.
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 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.
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 – 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
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, Epilepsy
Aminophylline
 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

Post-operative apnoea

  • 1.
    Post operative apnoea Dr.Shailendra V.L Anaesthesia specialist Al Bukeriya general hospital
  • 2.
    Overview  Causes andtheir associated management  Paediatric considerations  Controversies
  • 3.
    Causes of postoperative hypoventilation/ apnoea Factors affecting airway Factors affecting ventilatory drive Factors affecting peripheral drive
  • 4.
  • 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 stimulationof 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 airwaysin 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.
  • 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 bereversed 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  Severehypoglycaemia as a central cause for reduced ventilatory drive.
  • 13.
  • 14.
    Causes  Muscle weakness Pain  Abdominal distension  Obesity  Tight dressings  Pneumo/haemo thorax
  • 15.
    Muscle weakness  Myastheniagravis 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 ofNM 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 blockadereversal  XS NM blocker  Too little time from blockade to reversal  Hypokalaemia, Hypermagnesaemia  Acidosis  Gentamicin  Local anaesthetics  Myopathy
  • 18.
    NM monitoring 1. Variableindividual 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 ofNM 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 enzymewhich 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 deficiencyis 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 reversiblecause – 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 causesof 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  Particularlysensitive to temperature  Can be extremely opiate sensitive  Prematures are highly susceptible to apnoea up to 60 weeks gestational age.
  • 30.

Editor's Notes

  • #7 Why is complete paralysis of the cords better than partial? Unilateral neuropraxia not uncommon and results in voice change and slight stridor (abductor fibres more at risk Bilateral palsy rare: 1/30,000 flaccid cords are drawn together by the Bernouli effect during inspiration causes complete obstruction requiring reintubation and tracheostomy it used to be taught to extubate the patient deep to allow evaluation of vocal cord movement by direct laryngoscopy but this is becoming less popular Vocal cord paralysis is usually secondary to injury of the recurrent laryngeal nerve resulting in unopposed superior laryngeal nerve mediated adduction of the vocal cords. Such an injury can occur with neck surgery (especially thyroidectomy) [48], thoracic surgery [49,50], internal jugular line placement [51], and endotracheal intubation
  • #8 How much aminophylline? How much adrenaline? 1 in 10,000, take 1 ml and dilute into 10ml. Each ml is 10mcg of adrenaline. expect a response when given 0.5mcg/kg
  • #11 All mu receptor opioid agonists, including morphine, fentanyl, sufentanil, and alfentanil, produce dose-dependent depression of ventilation, primarily through a direct action on the medullary respiratory center The first signs of high spinal block are hypotension, bradycardia and difficulty in breathing. Before hypotension is detected, the patient often complains of nausea or “not feeling well”. Tingling in the fingers indicates a high block at the level of T1 Respiratory difficulty is caused by loss of chest wall sensation caused by paralysis of the intercostal muscles. Patients often describe their breathing as feeling abnormal, but can demonstrate a good inspiration and can cough and speak normally. When a total spinal occurs the nerve supply to the diaphragm (cervical roots 3-5) is blocked and respiratory failure develops rapidly. Early warning signs include poor respiratory effort, whispering and an inability to cough. Sudden respiratory arrest is usually caused by hypoperfusion of the respiratory centres in the brainstem
  • #16 Myotonic dystrophy (esp. sensitive to thiopentone) Duchenne’s, Becker’s Central core disease
  • #18 Gentamicin or high Mg can be treated with Calcium Chloride 10ml of 10%