Department of Anaesthesia

University of Cape Town

Complications in Anaesthesia
Modern anaesthesia in a first world environment, administered by a trained anaesthesiologist, is
remarkably safe. In South Africa relatively untrained medical officers are often required to
anaesthetise patients in rural areas. Knowledge of potential complications of anaesthesia is important
as the majority can be avoided by a good pre-operative assessment and adequate planning.
Complications may be divided into minor (non life threatening) and major (life threatening).

Minor complications
Although minor complications are not life threatening, they may be very important to the patient and
some may have the potential for litigation.

1) Airway injuries
Injuries to the mouth, throat and teeth can be caused by placement of a laryngoscope blade,
oropharyngeal airway, laryngeal mask airway (LMA) or endotracheal tube (ETT). A patient’s dentition
must always be examined pre-operatively and precautions taken if risks are high, e.g. expensive
bridge work or loose teeth. A gum guard may be used and laryngoscopy should be performed with
extra care. The correct size ETT and careful placement will prevent damage to vocal cords. Avoid
over-inflating the cuff as this may cause oedema and postoperative intubation stridor; and in the long
term, tracheal stenosis. The use of cuffed ETTs is controversial in children under the age of 8 years.
Select the correct size of oropharyngeal airway and LMA to avoid trauma to the pharynx.

2) Eye injuries
Facemasks should fit properly and avoid pressure on the eyes. Anaesthesia obtunds the corneal
reflex and paralysed patients are unable to blink. Corneal ulceration will occur if eyes are not taped
closed during anaesthesia. In the prone position, eyes should be checked regularly to ensure that
they are free from pressure. Eyes should be padded before taped shut for head and neck surgery.

3) Positional injuries
Improper positioning of patients allowing pressure on peripheral nerves can lead to nerve damage;
particularly those nerves passing over bony prominences. Nerves at risk include the radial nerve
(Saturday night palsy); ulnar nerve; brachial plexus from hyper-extending the arm beyond 90 degrees;
the lateral popliteal nerve in the lithotomy position (foot drop), and the femoral nerve during surgery in
the Lloyd-Davis (extended lithotomy) position. During long procedures, pressure points should be
padded to avoid the development of pressure sores and the limbs moved from time to time by the
anaesthetist, if possible.

4) Complications of regional anaesthesia

Spinal and epidural anaesthesia are not without risk. Without meticulous attention to asepsis and
proper technique, several complications can occur – Epidural abscess, meningitis, epidural
haematoma, and nerve injuries may follow. These are fortunately very rare, but catastrophic if they do
occur. Postspinal headache is a common complication and can be reduced by using a “pencil point”
needle, e.g. Whitacre or Sprotte, and a smaller gauge (25 G versus 22 G). Neuraxial anaesthesia
often causes hypotension that is easily managed. However it may also lead to profound hypotension
if the volume of local anaesthetic was too high or the patient volume depleted. A high spinal is a risk
for respiratory depression and cardiovascular collapse, and possibly an anaesthesia-related death!

5) Complications of central venous cannulation

Early complications Late complications
Technical Infection
Pneumothorax Sepsis
Haemothorax Endocarditis
Nerve damage
Dysrhythmias (from guide wire) Thrombosis
Air embolism (patient should be head down) Tamponade
 Complications in anaesthesia

6) Postoperative nausea and vomiting (PONV)

PONV is common, second only to pain. Some patients with a history of severe PONV fear this
complication more than the postoperative pain. Do not confuse the risks for and treatment of PONV
with the risks of a full stomach and resultant aspiration. These are two very different complications.
There are patient, surgical and anaesthetic factors that increase the likelihood of PONV.

Risk factors for PONV

Patient factors
Children, females, history of motion sickness, previous PONV, obesity.
Anaesthetic factors
Prolonged pre-operative starvation.
Hypotension with spinals or epidurals.
Emetic drugs: Opiates, etomidate, ketamine, N2O and all volatile anaesthetic agents.
Surgical factors
Ear and eye surgery, especially strabismus (squint) surgery; intra-abdominal surgery,
particularly laparoscopy & gynaecological, and orchidopexy.
Post op factors
Pain, opiates, hypotension and forcing oral fluids too soon postoperatively.

Prevent or reduce the incidence of PONV by avoiding emetic drugs, e.g. etomidate, ketamine, N2O,
opiates and volatile anaesthetic agents. Regional anaesthesia is an option, if appropriate, as it avoids
most of these drugs; and propofol total intravenous anaesthesia (TIVA) is a good method for providing
general anaesthesia. Propofol has intrinsic anti-emetic properties.
Pharmacological management includes the administration of commonly used anti-emetic drugs in
theatre: e.g. Droperidol (Inapsin®), a butyrophenone; prochlorperazine (Stemetil®), a phenothiazine;
ondansetron (Zofran®), a serotonin-3 antagonist, and dexamethasone or betamethasone, steroids.
Metoclopramide (Maxolon®), a dopamine agonist, is also commonly used postoperatively; however, it
only has a moderate anti-emetic effect and is really a prokinetic agent, better used to promote gastric
emptying in patients with a full stomach.
Routine pharmacological prophylaxis is not indicated and should be reserved for high-risk patients. In
high-risk patients, prophylaxis with dexa- / beta- methasone and droperidol is a good combination.
Dexa- / beta- methasone is a prophylactic measure and will not be effective if given postoperatively for
the treatment of vomiting. Ondansetron and the other serotonin-3 antagonists, or prochlorperazine
are used postoperatively.
Non-pharmacological management includes keeping the patient well hydrated with intravenous
fluids; and several complementary and alternative therapies including the use of acupuncture point
bracelets and ginger. Interestingly, smoking is protective against PONV!

7) Awareness
Awareness under anaesthesia is the ability to recall events occurring during general anaesthesia.
Hearing is the last sense to disappear under anaesthesia. Anaesthetists rely on clinical observation of
motor movement and sympathetic nervous system stimulation (hypertension, tachycardia, sweating or
lacrimation) to assess the depth of anaesthesia. Motor movement will be masked by muscle relaxants
and sympathetic signs modified by β-blockers and opiates. Objective methods to measure awareness
using processed electro-encephalogram (EEG) data have been developed, but are not always
available. Examples of this are the Bispectral Index (BIS® - Aspect) and Entropy (Datex-Ohmeda).
Causes of awareness include faulty equipment and light anaesthesia. Awareness due to inadequate
volatile agent is reduced by the use of an anaesthetic agent analyser to measure the concentration of
the anaesthetic agent in the breathing circuit. Benzodiazepines are also extremely useful due to their
ability to cause anterograde amnesia.
Awareness is an extremely uncommon event and the incidence ranges from 1 in 10 000 for conscious
awareness with pain; to 1 in 1 000 people being able to report some awareness in the postoperative
interview, although not in any way distressing. The first type where the patient is fully aware while
being paralysed and feels pain is the worst scenario and can lead to the patient developing post-
traumatic stress disorder. These patients should be followed up regularly, and referred for psychiatric
help if necessary.

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8) Hypothermia
Hypothermia is a core temperature below 35° C. It is quite common under both general and regional
anaesthesia. The temperature should be monitored for any case longer than 15 minutes.
Heat loss occurs due to the cool ambient theatre temperature (18 - 22° C) and exposure during the
surgery. Cold irrigation fluids and IV fluids can contribute to cooling. The anaesthetic agents interfere
with normal homeostatic thermal control. Most anaesthetic agents also result in vasodilatation and
increase the heat loss from the core. Compounding this is that while under anaesthesia, you are
unable to move and ‘get warmer’ as you would usually do when awake.
There are many pathophysiological effects of hypothermia that are deleterious during the peri-
operative period. It may lead to increased bleeding with platelet dysfunction and inactivate clotting
factors at < 35° C; delayed emergence from general anaesthesia; poor ventilatory efforts;
dysrhythmias (ventricular fibrillation at < 32° C); slowed drug metabolism due to inactive phase I and
phase II enzymes at lower temperatures; and shivering postoperatively causing pain and more
importantly increased O2 consumption by 200 %.
Prevent heat loss by covering exposed areas with a forced-air warming blanket (Bair-hugger®) or
warming under-blankets. Space blankets (metallic foil) have no role in warming the patient in theatre.
Warm all IV and irrigating fluids. Warm the gases the patient is inhaling. A heat moisture exchange
filter (HMEF) will help humidify, warm and filter gases. Warm the theatre temperature if necessary. If
these non-invasive methods are ineffective, you may require more aggressive and invasive methods
of warming such as intra-thoracic and / or peritoneal lavage, or even cardiopulmonary bypass
(extracorporeal circulation) to warm the patient.
Hypothermia, if severe, can be a cause of major and life threatening complications.

Major (life threatening) complications

The most feared complications of anaesthesia are brain damage and death. The incidence of death
attributable to anaesthesia in first world hospitals is approximately 1 : 40 000 anaesthetics. In rural
environments, with poorly trained anaesthetists, the rate is much higher and may approach 1 : 280.
Adverse outcomes following surgery and anaesthesia can be due to patient, anaesthetic or surgical
factors. Only anaesthetic factors will be considered here. Most major complications can be prevented
through early recognition and correct management.

1) Endotracheal intubation
Failure to intubate is a major cause of anaesthetic related mortality, especially with caesarean section.
Patients with a difficult airway should be identified at the pre-operative assessment and a
management strategy planned. Possible strategies to avoid a difficult intubation include regional /
local anaesthesia or a laryngeal mask airway (LMA). If intubation is mandatory the most senior
anaesthetist should be present. Pre-oxygenate the patient for 3 - 5 minutes with 80 - 100 % oxygen to
increase the safety margin. Consider an inhalational induction and avoid muscle relaxants until a
good view of the larynx is established. In more extreme cases, awake fibre-optic intubation or an
awake tracheostomy must be performed. All operating theatres should have a difficult intubation
trolley. See attached ‘difficult airway algorithm’ for a complete management strategy.
Intra-operatively several problems may arise with the endotracheal tube (ETT). It can dislodge and
come out, or migrate too deep and result in endobronchial intubation. The ETT can kink, especially
once warm; or if there is a surgeon leaning on it. The weight of the breathing system pulling on the
tube due to gravity can also cause the ETT to kink or dislodge. Obstruction of the ETT with a foreign
body or secretions will make ventilation difficult or impossible. Often the first sign of kinking,
obstruction or endobronchial intubation is a rising airway pressure. Dislodgement of the ETT out the
trachea may result in a leak and a reduced end-tidal CO2. Careful strapping of the ETT, consideration
of patient position and the surgeon’s position in proximity to your tube, and lastly the positioning of the
breathing system, can avoid disaster. Always check the patient and tube first whenever ventilatory or
oxygenation problems occur, and then work your way systematically back to the anaesthetic machine
looking for the problem.

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2) Aspiration
This topic is thoroughly dealt with in the Emergency Anaesthesia chapter. Peri-operative aspiration of
gastric contents can cause a chemical pneumonitis (Mendelson’s syndrome), and result in the
potentially fatal acute respiratory distress syndrome (ARDS).
Patients at risk include those with a:
Full stomach Pregnancy
Gastric outlet obstruction (very high risk!) Obesity
Ileus Hiatus hernia
Acute abdomen Trauma
Patients should be starved of food for 6 hours and of clear fluid for at least 2 hours prior to elective
surgery. Trauma may delay gastric emptying for many hours.
Strategies to reduce the risk of aspiration include:
– Raising gastric pH with: A non-particulate antacid, e.g. sodium citrate 30 ml
An H2-receptor antagonists, e.g. ranitidine 300 mg (Zantac®),
A proton-pump inhibitor (PPI), e.g. omeprazole 40 mg (Losec®)
– Increase gastric emptying and increase lower oesophageal sphincter tone with metoclopramide,
– Reduce gastric volume via suction with a nasogastric tube.
All patients at risk of aspiration should be intubated using a rapid sequence induction (RSI) with pre-
oxygenation and cricoid pressure. After surgery, such patients should remain intubated until
consciousness has been regained and airway reflexes returned.

3) Respiratory complications
Once again, these can be due to patient, anaesthetic or surgical factors. A brief overview will be
\

given, also refer to the chapter on Anaesthesia for Respiratory Disease. The majority of these
complications end in one final common pathway – Hypoxia.

a) Laryngospasm
 Causes
o Insertion of an ETT, LMA or oral airway while still in a light plane of anaesthesia
o Inhalation of irritating anaesthetic volatile agents (desflurane, isoflurane and enflurane)
o Secretions on the vocal cords
o Surgical stimulus, e.g. dilatation of the cervix or anal sphincter
o Surgical stimulus during light level of anaesthesia
 Management
o Avoid manipulation of the airway whilst in a light plane of anaesthesia
o Stop the causative stimulus
o 80 - 100 % O2 with facemask and positive pressure ventilation is often all that is needed
o A small bolus of propofol (10 - 50 mg) is very helpful
o Consider spraying cords with 2 % lignocaine using the MacIntosh sprayer
o If fast control is needed, give suxamethonium 1 mg kg-1 and intubate.
If the laryngospasm occurs during emergence, then give only one quarter of the usual
dose of suxamethonium and support the airway or intubate if not able to

b) Bronchospasm
 Causes
Same causes as for laryngospasm, plus the following:
o Pushing the ETT too deep with carinal stimulation can precipitate bronchospasm
o Asthmatics, chronic bronchitis or recent chest infection
o Histamine release from certain drugs, e.g. suxamethonium, some non-depolarising
muscle relaxants (atracurium and rocuronium) and rarely morphine or thiopentone
o Anaphylactic reaction
 Management
o Avoid elective surgery if underlying respiratory conditions are not optimised
o Consider regional techniques in high risk patients
o Stop the precipitating cause. Give 100 % oxygen
o Deepen anaesthesia with a non-irritating inhalational agent
o Inhaled or intravenous β2-stimulant, e.g. salbutamol
o Once again a small dose of propofol is very useful
o In resistant cases IV aminophylline (toxic!) and ketamine may be considered

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c) Obstruction
 Causes
o In the ventilatory circuit, including the endotracheal tube
o In the airway from the oropharynx to the bronchi, e.g. a mucous plug or foreign body
o During spontaneous ventilation with a facemask, the tongue may obstruct the oropharynx
when loss of tone occurs with anaesthesia
 Management
o Jaw-thrust and chin-lift during facemask anaesthesia
o Check all tubing for kinking, compression and / or foreign bodies
o Examine the ETT for the same, as well as cuff herniation
o Pass suction catheter down the ETT to check patency and suction out secretions
o Ensure that the throat pack, blood or vomitus are cleared from the pharynx at the end
o Insert an oropharyngeal (Guedel) airway to prevent the patient biting down on the ETT at
the end of the procedure as well as postextubation, if level of consciousness still low

d) Postoperative respiratory depression and hypoventilation

 Causes
o Residual anaesthetic agents, e.g. opioids or inhalational anaesthetic agent
o Incomplete reversal of muscle relaxants
o Partial airway obstruction
o Severe pain after abdominal surgery or abdominal distension
o Hypoglycaemia and / or electrolyte disturbances
o High blockade after epidural or spinal anaesthesia
o Central depression due to neurological damage, e.g. stroke (rare)
 Management
o Jaw-thrust and chin-lift
o Exclude and treat above causes
o N.B. Be careful of just giving a patient facemask O2: A good SaO2 on the pulse oximeter
is not indicative of adequate ventilation, and may mask dangerous hypercarbia (↑↑ CO2)!
o Assist ventilation until patient is making adequate breathing efforts

e) Pneumothorax
 Causes
o Pre-existing due to trauma
o Attempts at central venous cannulation
o Surgery involving the diaphragm or thoracic cavity
o Volutrauma due to excessive positive end-expiratory pressure (PEEP) or airway
pressures during assisted ventilation
o Spontaneous rupture especially in patients with bullous lung disease
 Management
o Use normal / low ventilatory volumes or spontaneous ventilation in high risk patients
o Have high index of suspicion
o Insert intercostal drain if needed

4) Cardiovascular complications
a) Hypotension
Most anaesthetic agents tend to lower blood pressure (except ketamine). In healthy patients, a
decline of 20 - 30 % from the pre-operative blood pressure is acceptable. If the BP falls more than
this, cerebral and myocardial oxygenation become compromised. In patients with compromised
circulations, e.g. ischaemic heart disease, more meticulous pressure control is needed.
 Causes
o Overdose of drugs, e.g. premedication, induction agents, opioids or inhalational agents
o Spinal and epidural anaesthesia through vasodilatation due to sympathetic block
o Hypovolaemia due to bleeding, starvation, evaporation and third space losses from
surgical field, and pre-operative diuretic use
o Pre-operative β-blocker therapy compounds the drop in pressure due to other causes
o Intermittent positive pressure ventilation (PPV) – Increased intrathoracic pressure
decreases the venous return and thus the cardiac output
o Septic shock
o Anaphylactic reactions

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 Management
o Evaluate the clinical scenario and treat the cause
o Elevate the legs if appropriate and possible during the surgery; or tilt the whole table
head down; improving the venous return
o Decrease anaesthetic agent administration
o Volume load appropriately with crystalloids or colloids
o Vasopressor therapy, e.g. ephedrine, phenylephrine or inotropes where appropriate

b) Hypertension
 Causes
o Sympathetic stimulation during laryngoscopy and intubation, especially in a known
hypertensive patient
o Hypercarbia due to hypoventilation
o Insufficient analgesia or anaesthetic agent
o Essential hypertension
o Hyperthyroidism
o Phaeochromocytoma
o Drug administration error, e.g. ephedrine or adrenaline instead of another drug.
Always check your ampoules carefully for name, dose and expiry date
 Management
o Treat cause
o Increase depth of anaesthesia
o Analgesia if needed
o Antihypertensives where indicated, e.g. β-blockers (labetalol, esmolol), nitrates, MgSO4

c) Dysrhythmias and cardiac arrest

Dyshythmias occur in 1 % of all anaesthetics and are mostly benign. It is important to
recognise life-threatening dysrhythmias and treat them appropriately.
 Causes
o Drugs, e.g. halothane, may increase the sensitivity of the cardiac conduction system to
catecholamines. Halothane is the most dysrhythmogenic volatile
o Electrolyte abnormalities, especially hyperkalaemia
o Sympathetic or parasympathetic stimulation, e.g. intubation, peritoneal stretching
o Underlying heart disease
 Management
o Identify high risk patients pre-operatively and review the need for a pacemaker
o Treat the cause
o Use appropriate anti-dysrhythmic drugs
o Check and know how to operate a defibrillator. Follow the advanced life support (ALS)
guidelines for life-threatening dysrhythmias and cardiac arrest.
Refer to the lecture on CPR and the algorithms at the back of the book

d) Myocardial infarction
These factors have been shown to increase the likelihood of peri-operative myocardial infarction.
 Patient factors
o Cardiac disease
o Peripheral vascular disease
o Hypovolaemia
o Acute coronary syndrome
o Decompensated congestive cardiac failure (CCF)
o Dysrhythmias
o Severe valvular heart disease
 Anaesthetic factors
o Hypotension
o Hypertension
o Tachycardia
o Hypoxia

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 Surgical factors: Types of surgery

o Intrathoracic surgery
o Abdominal surgery
o Vascular surgery
o Emergency surgery
 Management
o Identify high risk patients pre-operatively and order appropriate special investigations,
e.g. stress test, angiography where indicated
o Postpone elective surgery until patient optimised
o Postpone elective surgery for 6 months after an acute coronary event
o Optimise O2 supply : Demand ratio by optimising Hb, O2 administration, HR and BP
o Keep HR controlled with pre-operative β-blocker therapy, an anxiolytic premed, adequate
analgesia and / or fluid therapy
o Reduce the afterload with analgesia, inhalational agents and nitrates where appropriate

5) Equipment failure
The anaesthetic machine, ventilator, tubing, vaporisers, intubation equipment, cabling and monitors
can all malfunction. Faulty equipment or lack of essential equipment can lead to disastrous outcomes
such as failure to ventilate, hypoxia, awareness, electrical shock and burns. All equipment must be
checked prior to an anaesthetic. Warning alarms should be in place such as an oxygen failure alarm
and oxygen analyser. Monitoring alarms should be set to detect any adverse clinical parameters and
abnormal ventilatory pressures. A self-inflating emergency resuscitator, e.g. Ambu® bag, and an
oxygen cylinder should be available in case of ventilator failure. Equipment must be serviced and
calibrated at appropriate intervals.

6) Anaphylaxis
Anaphylactic reactions are a potential hazard of any anaesthetic. Anaphylaxis is a type I
hypersensitivity reaction. The Ig E molecules on the mast cells and basophils recognise the allergen
(antigen) and become cross-linked by this antigen. The final common pathway is degranulation of
mast cells or basophils and the release of potent preformed substances such as histamine, and newly
formed substances such as arachadonic acid metabolites.
Clinical presentation is the classic triad of skin reactions, respiratory and cardiovascular effects.
Skin signs include a wheal and flare reaction with urticaria
Respiratory symptoms include angio-oedema (upper-airway swelling), bronchospasm and hypoxia
Cardiovascular symptoms range from hypotension and tachycardia, to cardiovascular collapse
and, in severe cases, cardio-respiratory arrest.
Not all anaphylactic reactions present with all three of the triad; and there is great variation in severity,
from the very mild to severe with a cardiac arrest unresponsive to resuscitation.
Anaesthetists frequently administer a number of drugs intravenously within a short space of time.
The drugs most likely to cause anaphylactic reactions are the antibiotics and muscle relaxants
(especially suxamethonium, the benzylisoquinoliniums and rocuronium). Other potential antigens
include the opiates, local anaesthetics (esters more than amides), colloids (not crystalloids), blood,
latex and rarely the induction agents (thiopentone, propofol).
Volatiles do not cause anaphylaxis.
Emergency management involves the A B Cs, calling for help and the administration of adrenaline.
The dose depends on the severity of the presentation. In an arrest, follow the Resuscitation Council of
South Africa (RCSA) guidelines for anaphylaxis attached and give Adrenaline 0,5 mg IV / IM
(6 - 12 yrs = 0,3 mg, < 6 yrs = 0,15 mg) and start CPR.
If the BP is low, titrate smaller doses of adrenaline to effect – Dilute 1 mg (1 amp) of adrenaline into
20 ml and give ½ - 1 ml (25 - 50 µg) at a time. The RCSA guidelines suggest the intramuscular (IM)
administration of adrenaline; but with a cardiovascular collapse, the IM dose of adrenaline will not be
effective quickly due to peripheral shutdown. There will be IV access in theatre and will be the
superior route of administration.
Further management includes aggressive IV fluid replacement with crystalloid or colloid (if a colloid
precipitated the reaction, use a different colloid). Steroid (hydrocortisone 100 mg IV) and a
bronchodilator will help with bronchospasm, but these will take some time to work and they are
second-line treatment. Do not delay administration of adrenaline. Airway oedema may be significant
and there may be a need for prolonged ventilation. Do not extubate if uncertain. If the patient is
unstable and requires ongoing ventilatory and inotropic support they should be admitted to the ICU.
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The diagnosis of an anaphylactic reaction can be confirmed by the presence of mast cell tryptase in
serial blood samples. Patients should be referred to an allergy clinic to determine the drug that
caused the anaphylactic reaction, a Medic-Alert bracelet issued and the patient’s GP informed.

7) Pharmacogenetic diseases
Pharmacogenetic diseases are genetic diseases that are unmasked by exposure to specific drugs.
Several of these have particular relevance to anaesthesia.

a) Malignant hyperthermia (Malignant hyperpyrexia - MH)

 Definition
A rare inherited syndrome characterised by a life-threatening acute hyper-metabolic state triggered
by exposure to a triggering agent – all volatile anaesthetic agents and / or suxamethonium.
It is caused by a defect in a receptor on the sarcoplasmic reticulum called the ryanodine receptor.
This is a calcium channel receptor. Once exposed to the trigger agent, the receptor stays open
and floods the cell with calcium with a resultant persistent contractile state. Hyperthermia is
defined as a core temperature above 38° C, although this is a late sign with MH.
 Clinical features (in order of presentation):
o Tachycardia
o Tachypnoea if breathing spontaneously
o Increased O2 consumption, and eventually cyanosis
o Hypercapnia with PETCO2 rising to > 3 x normal and the baseline rises as soda-lime is
overwhelmed
o Masseter muscle spasm and whole body skeletal muscle rigidity
o Dysrhythmias and cardiovascular collapse
o Metabolic and respiratory acidosis
o Hyperkalaemia
o High temperature is a late sign. The term malignant hyperthermia is a misnomer
o Myoglobinuria
o Untreated, it is likely to progress to acute renal failure, hepatic failure, coagulopathy,
cerebral oedema and death. If diagnosed early however, it is fully treatable

MALIGNANT HYPERTHERMIA MANAGEMENT PROTOCOL

 Discontinue volatile anaesthetic and suxamethonium
 Call for help!!
 Hyperventilate with 100 % oxygen at high flows
 Mix dantrolene sodium with sterile water and administer 2,5 mg kg-1 IV ASAP
 Institute cooling measures
 Treat complications such as dysrhythmias, hyperkalaemia, and acidosis
 Administer additional doses of dantrolene if needed.
(Dantrolene is a type of centrally acting muscle relaxant, and once administered
the patient will have weakness and must therefore be ventilated)
 Transfer to ICU – Recurrence is not uncommon

 Diagnosis
Definitive diagnosis can be made after the event with a muscle biopsy. This is now rarely
performed as it is difficult to do. If the patient has a family history of malignant hyperthermia then
a diagnosis is presumed and a MH-safe anaesthetic is performed. The test is not currently
available in South Africa.
 MH-safe anaesthesia
o Avoid general anaesthesia (GA) entirely and choose a regional technique
o If GA is needed:
Patient should be first on the list
Use an anaesthetic machine that has no vaporisers on it to prevent inadvertent
administration of volatile. The machine should be flushed with high flow O2 for 20
minutes prior to the anaesthetic
A propofol TIVA technique is ideal
For muscle relaxation: Non-depolarising muscle relaxants are safe
Know where the dantrolene is kept in your hospital – Usually locked up

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b) Halothane hepatitis
In 1 : 35 000 anaesthetics, metabolites of halothane can trigger a fatal fulminant hepatitis via an
immune mediated mechanism (type 2 hypersensitivity reaction). This rare condition is more
common after repeat exposure to halothane within 6 months. For this reason repeat halothane
anaesthetics should not be administered within 6 months of a previous halothane anaesthetic.
Additional risk factors include middle age, females, obesity, and existing hepatic diseases.
Hepatitis is more likely to occur with halothane than with other volatile gents as it undergoes 20 %
metabolism and the others much less so. Isoflurane and desflurane have been implicated in
causing fulminant hepatitis, although much less frequently, presumably because of the lower
metabolism in the body.

c) Scoline apnoea
Susceptible individuals have an abnormal or absent pseudocholinesterase (buturylcholinesterase)
enzyme resulting in prolonged paralysis after a single dose of suxamethonium (Scoline /
succinylcholine). Homozygous patients for the condition will need to be sedated and ventilated for
several hours after administration of suxamethonium. Although the missing enzyme is found in the
plasma, the use of fresh frozen plasma (FFP) to speed up recovery is not recommended; unless
there are inadequate facilities for ventilation. FFP is a blood product and it does have the same
risks as a blood transfusion. You will have to weigh up the risks versus the benefits.
Ventilation and sedation is the treatment of choice.
Always check for recovery from suxamethonium before administering a non-depolarising muscle
relaxant. The patient should show return of twitches on the nerve stimulator or signs of breathing.
If you don’t do this, at the end of the case when the patient remains paralysed with no twitches on
the nerves stimulator, you will not know whether it is due to the suxamethonium or the non-
depolarising muscle relaxant.
On discharge the patient should be fully informed and be given a Medic-Alert bracelet.

d) Porphyria
A pharmacogenetic disease involving porphyrin metabolism in which certain drugs such as
barbiturates (thiopentone) can precipitate an acute attack resulting in paralysis, abdominal pain and
even death. South Africa has a relatively high incidence of the variegata form, especially in
patients of Dutch / Afrikaner descent (but not unknown in the English speaking population). The
acute Swedish type is also found in our population. Most patients are aware of the presence of the
disease in their family and this must be ascertained at the pre-operative assessment.
If confronted with a patient at risk of having the disease, consult one of the safe / use with caution /
unsafe drug lists, and plan accordingly.

Documentation
Documentation is of the utmost importance whenever a complication or critical incident has occurred.
Document clinical parameters as well as management. Precaution to prevent complications should
also be documented on the anaesthetic chart such as: Eyes checked / taped, pressure points padded
and protected and special dentition noted. Patients should be notified postoperatively of complications
that can recur with a subsequent anaesthetic.
Please remember to practise medicine with medical insurance.

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