35 Anaesthetic emergencies

Adult Basic Life Support (BLS) 910

Adult Advanced Life Support (ALS) 912

Severe bradycardia 916

Narrow complex tachycardia 918

Broad complex tachycardia 920

Severe hypotension in theatre 922

Severe hypertension in theatre 924

Severe hypoxia in theatre 926

Severe laryngospasm 930

Air/gas embolism 932

Aspiration 934

Status asthmaticus 936

Pulmonary oedema 938

Failed intubation 940

Can't intubate, can't ventilate 942

Malignant hyperthermia 946

Anaphylaxis 948

Intra-arterial injection 950

Unsuccessful reversal of neuromuscular blockade 952

Paediatric emergencies: Advanced Life Support 954

Paediatric emergencies: ventricular fibrillation or pulseless VT 956

Paediatric emergencies: neonatal resuscitation 958

Paediatric emergencies: collapsed septic child 960

Paediatric emergencies: major trauma 962

Paediatric emergencies: acute severe asthma 964

Paediatric emergencies: anaphylaxis 966

Paediatric doses and equipment 968

See also:

No matter whatever or whoever ‘caused’ the crisis, use objective and non-judgmental comments. Insults tend to provoke an aggressive or withdrawal response from the recipient and inhibit team function.

To communicate effectively, your messages or commands must be: ADDRESSED–ask specifically named individuals to perform tasks. HEARD–reduce background noise and distractions by turning off the radio, etc. UNDERSTOOD–if you make a complex request, ask the recipient to repeat it back to you.

If the cause of the problem is unknown, say so. Say what you don't know as well as what you do know. Encourage others to contribute.

Reappraise the situation regularly. Update the rest of the team with new information. If you are still unsure about what to do, send for help—a second person with a fresh approach may pick up on missed clues.

A good team leader is able to step back from the situation to consider the whole picture. This can only be achieved by delegation of responsibility for tasks to other members of the team.

A repeated and systematic ABC approach helps render the patient ‘safe’, buys thinking time, and increases the likelihood of detecting signs that may lead to a definitive diagnosis.

Most members of an impromptu emergency team will need to adopt the role of ‘team players’. A good team player is adaptable, assumes complete responsibility for delegated problems, and feels comfortable enough to advocate an opinion or feed back information to the rest of the team.

Help summoned quickly by telephone.

CPR to be started immediately using airway adjuncts.

If indicated, defibrillation attempted rapidly (within 3min at most).

Optimise the airway and remove any visible obstruction.

Look, listen, and feel for signs of life. Put your ear by the patient's mouth whilst observing for chest/abdominal movements and feeling for a carotid pulse. Take no more than 10s.

Occasional gasps or slow laboured breathing are indicative of actual or impending cardiac arrest.

Rate of delivery = 100/min.

Finding the right place: don't waste time. Ideally, locate the middle of the lower half of the sternum. Place the heel of one hand there, with the other hand on top of the first. Interlock the fingers of both hands and lift them to ensure that pressure is not applied over the patient's ribs. Do not apply any pressure over the upper abdomen or bottom tip of the sternum.

Aim to depress the sternum approximately 4–5cm (or one-third of the chest depth) and apply only enough pressure to achieve this.

The pressure should be firm, controlled, and applied vertically. Erratic or violent action is dangerous.

About the same time should be spent in the compression phase as in the released phase.

Use an inspiratory time of 1s and sufficient volume to make the chest rise.

Add supplemental oxygen as soon as it is available.

Once the airway is secured give uninterrupted compressions at 100/min and simultaneously ventilate the lungs at a rate of 10 breaths/min.

Apply self-adhesive defibrillation pads over the sternum and vertically in the mid-axillary line.

Don't interrupt chest compressions until you are ready to assess the rhythm.

Defibrillation is indicated for VF/VT.

Potential secondary damage will be minimised by in-line immobilisation of the C-spine.

Try to use a jaw thrust and/or a Guedel airway to open the airway rather than tilting the neck.

Avoid placing the patient in the recovery position.

Consider a single precordial thump.

If a defibrillator is immediately available, give a single 360J shock.

Start CPR immediately after delivery of the shock without pausing to assess pulse or heart rhythm.

Give 100% oxygen, obtain IV access, and establish ECG, SpO₂, BP, RR, and temperature monitoring.

Look for correctable pathophysiology/biochemistry and establish higher dependency care.

For biphasic defibrillators, follow the manufacturer's recommendations. If in any doubt, use 200J initially.

Electrode polarity is unimportant. Use defibrillation pads to improve electrical contact. One pad is placed to the right of the sternum below the clavicle, the other over the lower left ribs in the mid-axillary line (level with the V6 ECG electrode), avoiding placement over the breast tissue in females. Put the long axis of this pad vertical and make sure it is lateral to the cardiac apex.

Don't attempt to reposition pads that have already been stuck on the chest—it is more important to deliver the shock quickly.

Remove transdermal patches to prevent arcing, and place defibrillator pads/paddles 12–15cm away from implanted pacemakers.

For safety reasons, charge the defibrillator only when the paddles are in contact with the patient. Hold the oxygen mask away from the patient during actual defibrillation, but leave bag connected to ETT.

Recheck rhythm trace on monitor immediately prior to shock delivery.

It is the responsibility of the defib operator to visually check that everyone is clear and to state STAND CLEAR prior to delivery of each shock.

VT and pulseless VT are the commonest causes of reversible cardiac arrest in adults. These are the most 'recoverable' rhythms and it is therefore always worthwhile persisting with CPR whilst they are present. However, successful resuscitation does depend on early defibrillation. BLS, IV access, and airway control should not delay delivery of shocks.

Resume CPR IMMEDIATELY after delivering a shock. Delay pulse/rhythm checks for 2min.

A pause in chest compressions allows coronary perfusion pressure to fall substantially and is followed with a delay before the original perfusion pressure is restored after ECM is recommenced.

Consider calcium chloride 10ml 10% slow IV if PEA is thought to be caused by hyperkalaemia, hypocalcaemia, overdose of Ca channel blockers, or magnesium.

Consider lidocaine 1mg/kg as an ALTERNATIVE treatment.

Give magnesium sulphate 8mmol (4ml 50% solution) for refractory VF if patient has hypomagnesaemia (e.g. diuretic induced), or torsade de pointes, or digoxin toxicity.

Bretylium is no longer recommended.

Remember that HCO₃^– + H⁺ n H₂O + CO₂, therefore bicarbonate administration requires an increase in minute ventilation. Check ABGs before repeating the dose.

Reverse any biochemical abnormalities.

Unless the period of arrest has been very brief (less than 3min), the patient should remain intubated and be transferred to ICU.

Consider inducing mild hypothermia (32–34°C).

Third-degree atrioventricular block and second-degree Möbitz type II AV block will result in significant bradycardia, haemodynamic instability, and the possibility of asystole. Other significant risk factors for asystole include a recent episode of asystole and ventricular pauses of >3s.

Indications for referral for preoperative pacing:

Narrow complex tachycardia in an unstable patient [reduced conscious level, and/or chest pain (if awake), LVF, systolic BP <90mmHg; VR >150bpm; ischaemia] requires urgent synchronised DC shock.

Differentiating narrow from broad complex tachycardia can be difficult, especially at high ventricular rates. Vagal manoeuvres or adenosine should slow A-V conduction of an SVT but not a VT.

Theophylline interacts with adenosine and tends to block its effect.

Dipyridamole and carbimazole potentiate the effects of adenosine.

Adenosine should be used with caution in WPW syndrome and should be avoided in asthmatics.

Atrial fibrillation may require anticoagulation of the patient prior to cardioversion.

Verapamil should not be administered in the presence of β-blockade.

Serum therapeutic range for digoxin = 0.8–2.0µg/l.

Secondary treatment is aimed at stabilising sinus rhythm and preventing recurrence (antiarrhythmics and electrolyte correction).

Torsade de pointes is a polymorphic form of VT characterised by beat-to-beat variation, a constantly changing axis, and a prolonged QT interval. Treat with magnesium 2g IV and correct any electrolyte abnormalities such as hypokalaemia.

If the patient is not adversely affected by the tachyarrhythmia, correct electrolytes whilst giving antiarrhythmics.

Mediastinal/hepatic/renal surgery (blood loss and caval compression).

Pre-existing myocardial disease/dysrhythmia.

Multiple trauma.

Sepsis.

Carcinoid syndrome (bradykinin).

Check peripheral perfusion: warm peripheries suggest excessive anaesthesia (GA/regional) or sepsis.

Suspect tension pneumothorax (particularly following central line insertion) if IPPV and trachea shifted away from a hyper-resonant lung field with diminished breath sounds. Neck veins may be engorged. Treat immediately by decompressing the pleural cavity with an open cannula placed in the 2nd intercostal space in the mid-clavicular line.

Suspect hypovolaemia if the patient has HR >100bpm, RR >20bpm, capillary return >2s, cool peripheries, collapsed veins, a narrow and peaked arterial line trace, or marked respiratory swing to either CVP or arterial line trace. Dehydration if the patient is thirsty, has a dry tongue, is producing dark concentrated urine, and has globally elevated blood cell, urea, creatinine, and electrolyte values.

Suspect cardiac failure if the patient has HR >100bpm, RR >20bpm, engorged central veins, capillary return >2s, cool peripheries, pulmonary oedema, or worsening SpO₂ with fluid challenge.

Suspect air or gas embolus if the patient had a pre-existing low CVP and open venous bed. Signs are variable but may include sudden ↓ETCO₂, ↓SpO₂, loss of palpable pulse, PEA, and rise in CVP.

Suspect fat embolus or cement reaction in the presence of multiple bony injuries or long bone intramedullary surgery.

Iatrogenic drug response: histamine release or wrong dilution.

High central neural blockade may be heralded by Horner's syndrome (small pupil, ptosis, stuffy nose, anhydrosis).

Anaphylaxis—cardiovascular collapse 88%, erythema 45%, bronchospasm 36%, angio-oedema 24%, rash 13%, urticaria 8.5%.

‘Optimise preload’ (check initial CVP if already sited, change in CVP is more informative than actual CVP). Lifting the legs returns blood into the central venous compartment and also increases afterload. Fluid challenge of 10ml/kg crystalloid/colloid using a pressure infusor. Assess response (BP/HR/CVP) and repeat if appropriate.

Increase contractility: ephedrine 6mg IV (mixed direct and indirect action); adrenaline 10µg IV (β_1,2 and α activity); consider calcium slowly IV (up to 10ml 10% calcium chloride).

Systemic vasoconstriction (NB A-agonists increase perfusion pressure but may reduce cardiac output). Metaraminol 1–2mg IV; phenylephrine 0.25–0.5mg IV; adrenaline 10µg IV.

Maintenance infusion of vasoconstrictor (e.g. adrenaline or noradrenaline) or inotrope (e.g. dobutamine) if required.

Patients taking β-blockers may not demonstrate a tachycardia despite significant hypovolaemia.

Aortic surgery (cross-clamp may ↑↑SVR).

Drugs: MAOIs (+pethidine); ketamine; ergometrine.

Family history of multiple endocrine neoplasia (type 2) syndrome, medullary thyroid carcinoma, Conn's syndrome.

Acute head injury.

Inadequate depth of anaesthesia: check volatile agent concentration; sniff test (smell gases); check TIVA pump, line, and IV cannula.

Inadequate analgesia: if in doubt administer alfentanil 10–20µg/kg and observe effect.

Measurement error: palpate the distal pulse manually whilst repeating an NIBP; check when pulsation returns against the monitor deflation figure. Invasive BP—check the transducer height.

Iatrogenic drug response: cocaine, wrong drug such as ephedrine, adrenaline, or wrong dilution (remember surgical drugs, e.g. adrenaline with LA, Moffet's solution, phenylephrine).

Pre-eclampsia: if over 20wk pregnant, check for proteinuria, platelet count ± clotting studies, and LFTs.

Thyroid storm causing elevated T₄ and T₃ levels.

Phaeochromocytoma causing elevated plasma noradrenaline levels. Adrenaline will also cause tachydysrhythmias.

Cushing response = hypertension and reflex bradycardia (baroreceptor mediated). This intracranially mediated response maintains cerebral perfusion in the presence of ↑ICP (see below).

Vasodilators (may cause tachycardia): ↑ isoflurane concentration—this is most rapidly achieved by simultaneously increasing fresh gas flow. Hydralazine 5mg slow IV every 15min. GTN (50mg/50ml, start at 3ml/hr and titrate to BP) or SNP. Magnesium sulphate 2–4g slow IV (8–16mmol) over 10min, followed by infusion of 1g/hr.

β-blockade (particularly in the presence of ↑HR or dysrhythmias): Esmolol 25–100mg, then 50–200µg/kg/min. (Note that esmolol is supplied as 10mg/ml and 250mg/ml solutions.) Labetalol 5–10mg IV prn (1–2ml increments from a 100mg/20ml ampoule). β:α block ratio = 7:1.

α-blockade (particularly in the presence of normal or ↓HR): phentolamine 1mg IV prn (10mg ampoule made up to 10ml, in 1ml increments).

Check for myocardial damage with an ECG, serial cardiac enzymes including CKMB, and/or troponins.

Thyroid function tests, 24hr urine collection for noradrenaline, adrenaline, and dopamine excretion.

Failure to preoxygenate exacerbates any airway difficulties at induction.

Laryngospasm can result in negative pressure pulmonary oedema.

Head and neck surgery (shared access to the airway) increases the risk of undetected disconnection.

History of congenital heart disease or detection of a heart murmur (left to right communication).

Chronic lung disease.

Sickle cell disease.

Methaemoglobinaemia (interpreted as deoxyhaemoglobin by pulse oximeters).

Ventilation: cross-check rise and fall of chest with auscultation over stomach and in both axillae, capnograph trace, measured expired tidal volume, and airway pressure.

Measurement error: does patient appear cyanosed? Beware in anaemia when 5g/dl deoxyhaemoglobin may not be visible.

Aspiration/airway secretions: auscultate and aspirate using tracheal suction catheter ± litmus paper.

Suspect tension pneumothorax (particularly following central line insertion) if IPPV and trachea shifted away from a hyperresonant lung field with diminished breath sounds. Neck veins may be engorged. Treat immediately by decompressing the pleural cavity with an open cannula placed in the 2nd intercostal space in the mid-clavicular line.

Suspect hypovolaemia if patient has HR >100bpm, RR >20bpm, capillary return >2s, cool peripheries, collapsed veins, a narrow and peaked arterial line trace, or marked respiratory swing to either CVP or arterial line trace.

Suspect cardiac failure if patient has HR >100bpm, RR >20bpm, engorged central veins, capillary return >2s, cool peripheries, pulmonary oedema, or worsening SpO₂ with fluid challenge.

Suspect air or gas embolus if patient had a pre-existing low CVP and open venous bed. Signs are variable but may include sudden ↓ ETCO₂, ↓ SpO₂, loss of palpable pulse, PEA/EMD, and subsequent rise in CVP.

Suspect fat embolus or cement reaction in the presence of multiple bony injuries or long bone intramedullary surgery.

Malignant hyperthermia: especially if accompanied by ↑ ETCO₂, ↑ RR, ↑ HR, ↑ ectopics.

Anaphylaxis—cardiovascular collapse 88%, erythema 45%, bronchospasm 36%, angio-oedema 24%, rash 13%, urticaria 8.5%.

Confirm FiO₂: if there is any doubt about inspired oxygen concentration from the anaesthetic machine, use a separate cylinder supply (as a last resort use room air via a self-inflating bag = 21% O₂).

Misplaced ETT—cross-check rise and fall of chest with auscultation over stomach and in both axillae and the capnograph trace.

Ventilation problem: simplify the breathing system until the problem is removed, i.e. switch to bag rather than the ventilator, use a Bain circuit instead of the circle system, try a self-inflating bag, + mask rather than ETT, etc.

Diagnosis of the source of a leak or obstruction: is not as important initially as oxygenation of the patient. Make the patient safe first then use a systematic approach. The fastest way to isolate the problem is probably by division. For instance, does breaking the circuit at the ETT connector leave the problem on the patient side or the anaesthetic machine side?

Severe right to left shunt: severe hypoxia occurs when blood starts flowing through a congenital heart defect in the presence of low SVR, thus bypassing the pulmonary circulation. The resultant hypoxaemia then exacerbates the problem by causing hypoxic pulmonary vasoconstriction which increases PVR and increases the tendency for blood to shunt across the cardiac defect. Treatment is therefore twofold: 1) Increase SVR—by lifting the legs and giving adrenaline and IV fluid, especially in sepsis. 2) Minimise PVR—by removing PEEP, avoid high intrathoracic pressure, and maximise FiO₂.

Bronchospasm: eliminate ETT obstruction by sounding ETT with a gum elastic bougie. Treat by increasing volatile agent concentration, IV salbutamol (250µg)—see Status asthmaticus ( p. 936).

The foramen ovale remains patent in 20–30% of patients but is normally kept closed because left atrial pressure is usually higher than right atrial pressure. IPPV, PEEP, breath holding, CCF, thoracic surgery, and PE can reverse the pressure gradient and result in shunt.

Always check SpO₂ probe is well positioned and has a good trace.

Intense surgical stimulation: anal stretch; cervical dilatation; incision and drainage of abscesses.

Extubation of a soiled airway.

Thyroid surgery.

Hypocalcaemia (neuromuscular irritability).

Multiple crowns (inhaled foreign body).

Check that the airway is clear of obstruction or potential irritants.

Give high concentration oxygen with the expiratory valve of the circuit closed and maintain a close seal by mask with two hands if necessary to maintain CPAP. The degree of CPAP can be controlled by intermittently relaxing the airway seal at the level of the mask.

If the laryngospasm has occurred at induction, it may be relieved by deepening anaesthesia using further increments of propofol (disadvantage = potential ventilatory depression) or by increasing the volatile agent concentration (disadvantage = irritation of the airway, less so with sevoflurane, more with isoflurane). Don't use nitrous oxide, as it will decrease oxygen reserves.

If the laryngospasm fails to improve, remove any airways that may be stimulating the pharynx.

Suxamethonium 0.25–0.5mg/kg will relieve laryngospasm. If IV access is impossible, consider giving 2–4mg/kg IM or SL.

CPAP may have inflated the stomach with gas so decompress it with an orogastric tube and recover the patient in the lateral position.

Unilateral recurrent laryngeal nerve trauma results in paralysis of one vocal cord and causes hoarseness, ineffective cough, and potential to aspirate. Bilateral vocal cord paralysis is more serious, leading to stridor on extubation—this may mimic laryngospasm but doesn't get better with standard airway manoeuvres. The patient will require reintubation and possibly tracheostomy.

Tracheomalacia is likely to cause more stridor with marked negative inspiratory pressure so treat initially with CPAP. Reconstructive surgery may be necessary.

Anaesthesia: hypovolaemia; any open vascular access point; operation site higher than heart; pressurised infusions.

Orthopaedic surgery: multiple trauma; long bone surgery—especially intramedullary nailing; hip surgery.

General surgery: laparoscopic procedures; hysterectomy; neck surgery; vascular surgery.

ENT surgery: middle ear procedures.

Neurosurgery: posterior fossa operations in the sitting position (almost historical).

Awake patients complain of severe chest pain.

Heart rate may rise.

Sudden rise in CVP due to a fall in cardiac output and rise in PVR.

Classically a ‘millwheel’ murmur can supposedly be heard.

Doppler ultrasound is an extremely sensitive (0.25ml air!) but possibly unavailable diagnostic tool.

PEA/EMD arrest may occur. ECG may show signs of acute ischaemia, e.g. ST segment depression >1mm.

It is claimed that symptoms/signs of air embolus appear following 0.5ml/kg/min of intravascular gas.

Prevent further gas/air from entering the circulation. Get the surgeon to apply compression to major drainage vessels and flood the wound with irrigation fluid or cover with damp pack, stop reaming, etc.

Decompress any gas-pressurised system/cavity, e.g abdomen during laparoscopy.

Lower the operation site to below heart level.

Turn off N₂O (because it will expand any intravascular gas volume).

Increase venous pressure with rapid IV infusion of fluids ± vasopressors.

If PEA/EMD arrest occurs, start chest compressions and adopt ALS protocol for non-VF/VT cardiac arrest.

Aspirate CV line. Classic teaching is to tip patient head down in left lateral position to keep the bubble in the right atrium or apex of the right ventricle until it dissolves or can be aspirated via a central line advanced into the right atrium. In practice, if there is not already a CVP line in situ aspiration is likely to be difficult.

Moderate CPAP has been advocated as a means of rapidly increasing intrathoracic and therefore CVP in the event of gas embolus. Whilst this manoeuvre may limit the extent and progress of an air embolus, it must be borne in mind that 10% of patients may have a patent foramen ovale. Sustained rise in right atrial pressure may then lead to a right-to-left shunt and paradoxical air embolism to the cerebral circulation.

Correct any pre-existing hypovolaemia.

Avoid nitrous oxide for the remainder of the anaesthetic, and maintain a high FiO₂.

Perform a 12-lead ECG to look for ischaemia. Air in coronary arteries is suggestive of paradoxical air embolism.

Consider hyperbaric therapy if available. ↑ Ambient pressure (3–6 bar) will ↓ volume of gas emboli.

Known reflux.

Raised intragastric pressure (intestinal obstruction, pregnancy, laparoscopic surgery).

Recent trauma.

Perioperative opioids.

Diabetes mellitus.

Topically anaesthetised airway.

CXR: diffuse infiltrative pattern especially in right lower lobe distribution (but often not acutely).

Administer 100% oxygen and minimise the risk of further aspirate contaminating the airway.

If the patient is awake or nearly awake, suction the oro-/nasopharynx and place in the recovery position.

If the patient is unconscious but breathing spontaneously, apply cricoid pressure. Avoid cricoid pressure if the patient is actively vomiting (risk of oesophageal rupture) and place patient in a left lateral head-down position. Intubate if tracheal suction and ventilation indicated.

If the patient is unconscious and apnoeic, intubate immediately and commence ventilation.

Treat as an inhaled foreign body: minimise positive pressure ventilation until the ETT and airway have been suctioned and all aspirates are clear.

Monitor respiratory function and arrange a CXR. Look for evidence of oedema, collapse, or consolidation.

If SpO₂ remains 90–95%, atelectasis can be improved with CPAP (10cmH₂O) and chest physiotherapy.

If SpO₂ remains <90% despite 100% oxygen, there may be solid food material obstructing part of the bronchial tree. If the patient is intubated, consider using fibreoptic/rigid bronchoscopy or bronchial lavage using saline to remove any large foreign bodies or semi-solid material from the airway. Refer to ICU postoperatively.

Prophylactic antibiotics are not generally given routinely (unless infected material aspirated) but may be required to treat subsequent secondary infections.

If gastric aspirate has been buffered to pH =7, the resulting aspiration pneumonitis is less severe, volume for volume, than if it is highly acidic. However, solid food material can produce prolonged inflammation, even if the overall pH is neutral.

Blood, although undesirable, is generally well tolerated in the airway.

Intercurrent respiratory tract infection.

Carinal irritation by ETT.

Central trachea with bilaterally hyperexpanded and resonant lung fields ± expiratory wheeze (absent if severe).

Severe bronchospasm is a diagnosis of exclusion. The quickest method of ascertaining the source of increased airway resistance is to break the breathing circuit distal to all connectors/filters and to try ventilating directly with a self-inflating bag. If the inflation pressure still feels too high the problem is due to airway/ETT obstruction or reduced compliance.

Eliminate ETT obstruction by ‘sounding’ the ETT with a graduated gum elastic bougie (note the distance it can be inserted down the ETT and compare it with the external tube markings).

Increase volatile agent concentration—sevoflurane is the least irritant and is less likely to precipitate dysrhythmias in the presence of hypercapnia (halothane is most likely).

Salbutamol 250µg IV or 2.5mg by nebuliser up to 5mg every 15min. Alternatively (as an immediate measure) administer 2–6 puffs of β-agonist inhaler into the airway by placing the device in the barrel of a 50ml syringe. Attach the syringe by Luer lock to a 15cm length of fine-bore infusion/capnograph tubing, which can then be fed directly down the ETT. The inhaler can be discharged by pressure applied via the syringe plunger. Use of the fine-bore tubing decreases deposition of the drug on the ETT.

Aminophylline 250mg by slow IV injection (up to 5mg/kg).

Hydrocortisone 200mg IV.

Check the drug chart and notes for possible drug allergies to agents already administered.

Arrange CXR—check for pneumothorax and ETT tip position (withdraw if carinal).

Check ABGs and electrolytes (prolonged use of β₂ agonists causes hypokalaemia).

Refer to ICU.

Gas trapping: raised mean intrathoracic pressure may result from IPPV in the presence of severe bronchospasm. If pulse pressure falls and neck veins appear distended, consider obstructed venous return and a dependent fall in cardiac output. Intermittently disconnect the ETT from the circuit and observe the (connected) capnograph trace for evidence of prolonged expiration and return of pulse pressure.

Ventilator setting advice during this phase: 100% oxygen, initially by hand, may need high pressures, slow rate, prolonged expiration, do not worry about CO₂ levels providing SpO₂ is adequate. May be necessary to accept reduced ventilatory rate to allow adequate expiration to occur (permissive hypercapnia).¹

Drugs/toxins (fluid overload—especially in renal failure and the elderly, drug reaction, myocardial depression).

Aspiration (chemical pneumonitis).

Pre-existing lung disease or infection (increased capillary permeability).

Malnutrition (low oncotic pressure)—rare.

Acute head injury or intracranial pathology (neurogenic).

Severe laryngospasm or airway obstruction (negative intrathoracic pressure).

Severe hypertension; LVF; mitral stenosis (high pulmonary vascular hydrostatic pressure).

Lateral decubitus position (unilateral).

Impairment of lymphatic drainage (e.g. malignancy).

Rapid lung expansion (e.g. re-expansion of a pneumothorax).

Following pneumonectomy.

Monitors: ↑ HR; ↑ RR; ↓ SpO₂; ↑ airway pressure; ↑ CVP; ↓ PCWP (greater than 25–30mmHg).

CXR: basal shadowing; upper lobe diversion; ‘bat's wing’ or ‘stag horn’ appearance; hilar haze; bronchial cuffing; Kerley B lines; pleural effusions; septal/interlobar fluid lines.

ECG: evidence of right heart strain; evidence of MI.

If awake and breathing spontaneously: sit up to offload the pulmonary vasculature and improve FRC; high-flow 100% oxygen via mask with reservoir bag; furosemide 50mg IV; diamorphine 5mg IV; consider using CPAP 5–10mmHg, and a vasodilator if hypertensive (e.g. GTN 0.5–1.5mg SL, or 10mg transcutaneous patch. Beware of IV GTN administration in the absence of invasive BP monitoring).

If anaesthetised and intubated: commence IPPV with PEEP (5–10cmH₂O) in a 15 head-up position to reduce atelectasis and improve FRC; aspirate free fluid from the trachea intermittently; drug therapy as above.

Consider inotropic support with a β-agonist (e.g. dobutamine) or venesection (500ml) if filling pressures remain high or signs of inadequate circulation persist.

Suspect oesophageal placement if you cannot confirm: normal breath sounds in both axillae and absent sounds over the stomach; rise AND fall of chest; normal ETCO₂ trace; normal airway pressure cycle.

The trachea is a rigid structure, the oesophagus is not. If negative pressure is applied to the ETT, failure to aspirate air (e.g. with a bladder syringe directly attached to the ETT) suggests oesophageal placement.

Confirm ETT placement with fibrescope.

Remember—if in doubt, pull it out and apply bag and mask ventilation.

Attempt oxygenation even if it appears futile. Insert both an oral AND a nasopharyngeal airway. Emergency oxygen flush. Apply a close-fitting facemask with two hands and lift/dislocate the mandible firmly forwards (jaw thrust). Although an assistant may help by bag squeezing, it may be easiest to attempt ventilation by allowing an intermittent leak around the mask.

Consider using a conventional LMA, intubating LMA, ProSeal LMA, or Combitube. No single airway adjunct has clear advantages over others. This is not a time to experiment with unfamiliar devices so stick to whatever you feel comfortable with and abandon them early if they prove to be of no benefit.

If the patient is making spontaneous effort and respiratory noise, maintain CPAP and 100% oxygen until they awake.

Options are surgical cricothyroidotomy and needle cricothyroidotomy.

Needle cricothyroidotory: Extend the neck. You may find access easier if someone else does this for you and simultaneously fixes the skin by applying slight traction bilaterally to the soft tissues of the neck.

Find the cricothyroid membrane (lies between the superiorly notched thyroid cartilage and the cricoid cartilage) —see figure 35.7.

Attach a 20ml syringe containing 10ml saline to a large-bore needle or cannula (14–16G). Advance through the cricothyroid membrane in a slightly caudally inclined direction aspirating until air bubbles freely into the syringe.

If you have used a needle, hold it firmly in place. If you have used a cannula guard against kinking.

There are several ways of connecting a needle/cannula to a standard breathing circuit:

Transtracheal oxygenation by needle/cannula is a temporary emergency measure. Fully effective ventilation will not be possible, but there should be flow of oxygen down the bronchial tree to the alveoli.

If there is significant oxygen leakage upwards, occlude the mouth and nose during the inspiratory phase of ventilation.

Call urgently for an ENT surgeon to perform an emergency tracheostomy. If possible, improve transtracheal access with a 'Minitrach' or similar device. There are several easy-to-use commercial kits that exist based around a Seldinger method of insertion. If the patient remains paralysed, attempt fibreoptic/blind nasal intubation.

Consider transtracheal jet ventilation but stop ventilating immediately if surgical emphysema forms in the neck.

Surgical cricothyroidotomy requires a scalpel, tracheal hook/forceps/clamp, and a small tube (6–7mm).

If the problem is an inability to achieve a seal due to the presence of a beard, quickly apply a large transparent self-adhesive dressing over the whole of the lower face. Make a large hole in it for the mouth and nostrils, and re-apply the mask ± an airway.

If the problem is an inability to pass a small enough ETT tube down a narrowed trachea (either ETT too short or size unavailable) consider passing an airway exchange catheter. This is a robust guide that resembles a yellow but hollow gum elastic bougie. It comes with either a Luer lock or 15mm connector allowing oxygen to be passed through it into the distal airway whilst a more definitive airway is established either by railroading a larger tube over it or by surgical tracheostomy.

Commercially available trans-tracheal needles and injectors are now widely available.

Check that your theatres have a well-stocked difficult/failed intubation trolley available at all times.

www.youtube.com has some good examples of different techniques of cricothyroidotomy.

Exposure to suxamethonium or volatile agents (even if previous exposures were uneventful).

Exertional heat stroke. Exercise-induced rhabdomyolysis, central core disease, scoliosis, hernias, strabismus surgery.

Unexplained tachycardia together with an unexpected rise in end-tidal CO₂ (IPPV) or minute volume (SV).

Falling SpO₂ despite increased FiO₂.

Cardiovascular instability, dysrhythmias especially multiple ventricular ectopics, peaked T waves on ECG.

Generalised rigidity.

Core temperature rise of 2^oC per hour.

Hyperventilate with 100% oxygen using a high fresh gas flow to flush out volatile agent and expired CO_2.

Tell the rest of the theatre team what the problem is. Ask for more help and obtain dantrolene immediately.

Use a fresh breathing circuit +/− a ‘vapour-free’ machine if it is easy to do so, but not if it results in rebreathing of expired CO₂, a low FiO₂, or delays administration of dantrolene.

When available, give dantrolene 2–3mg/kg IV (it comes in 20mg ampoules so about four are required). Usually about 2.5mg/kg is required in total, but up to 10mg/kg may be given.

Stop surgery if feasible, otherwise maintain anaesthesia with TIVA (propofol).

Reduce core temperature by: evaporation; ice to groin and axillae; cold fluids into IV lines, the bladder via urinary catheter, stomach via NGT, or peritoneal cavity if open.

Check ABGs and K⁺, especially if dysrhythmias occur, and correct acidosis/ hyperkalaemia where appropriate.

Surgical team—call for senior help to conclude the operation as quickly as is safely possible.

Send a clotting screen for DIC, and serum CK assay (up to 1000 times normal).

Send a urine sample for myoglobin estimation secondary to muscle breakdown.

Monitor for acute renal failure and promote a diuresis with fluids and mannitol.

Refer to the MH Investigation Unit for in vitro muscle contracture tests (IVCTs).

Emptying several ampoules into a sterile dish and adding a large volume of sterile water may help mix dantrolene more rapidly.

Follow up involves muscle biopsy under LA and in vitro halothane, caffeine, ryanodine, and chlorocresol contracture tests.

Beware of using bicarbonate to correct acidosis since the reaction with hydrogen ions produces an increased CO₂ load.

Note that cross-sensitivities with NSAIDs and muscle relaxants mean that previous exposure is not always necessary.

True penicillin allergy is a reaction to the basic common structure present in most penicillins (β-lactam ring).

Erythema          45%

Bronchospasm      36%

Angio-oedema      24%

Rash           13%

Urticaria         8.5%

Call for help.

Maintain the airway and give 100% oxygen.

Lay the patient flat with the legs elevated.

Give adrenaline in 50µg IV increments (0.5ml 1:10 000 solution) at a rate of 100µg/min until pulse pressure or bronchospasm improves. Alternatively give adrenaline 0.5–1mg IM (repeated after 10min if necessary).

Give IV fluid (colloid or suitable crystalloid).

Corticosteroids: give hydrocortisone 100–300mg IV.

Catecholamine infusion as CVS instability may last several hours: Adrenaline 0.05–0.1µg/kg/min (= 4ml/hr of 1:10 000 or 5mg/50ml saline—70kg adult). Noradrenaline 0.05–0.1µg/kg/min (= 4ml/hr of 4mg/40ml 5% glucose—70kg adult).

Check ABGs for acidosis and consider bicarbonate 0.5–1.0mmol/kg (8.4% solution = 1mmol/ml).

Check for the presence of airway oedema by letting down the ETT cuff and confirming a leak prior to extubating.

Consider bronchodilators (see ‘Status asthmaticus’ p. 936) for persistent bronchospasm.

The anaesthetist should follow up the investigation, report reactions to the CSM, and arrange testing with an immunologist (see p. 1006).

Radial aspect of wrist: inadvertent cannulation of superficial branch of radial artery.

Arterial injection is more likely to cause damage with stronger drug concentration (e.g. 5% thiopental).

A cannula that has been inserted previously and only been flushed with saline (not painful) may present later.

Blanching of the skin.

Blistering.

Within 2hr: oedema; hyperaesthesia; motor weakness.

Later: signs of arterial thrombosis ± gangrene.

Principles of treatment are to dilute the irritant, reverse vasospasm, and prevent thrombosis.

Keep the cannula in situ—you will need access to reverse local vasoconstriction within the distal arteriolar tree.

If the drug administered was highly irritant, flush the vessel with isotonic saline or Hepsal®.

Administer LA via the cannula to reduce vasospasm and reduce pain (e.g. 5ml 1% lidocaine).

Administer a vasodilator (e.g. papaverine 40mg).

Once the immediate reaction has subsided, if the hand is well perfused and pink, remove the cannula and apply sufficient pressure to the puncture site to minimise local haematoma formation.

Renal and hepatic impairment causing delayed elimination of relaxant in long cases (except atracurium).

Perioperative administration of magnesium (especially above the therapeutic range 1.25–2.5mmol/l).

Hypothermia.

Acidosis and electrolyte imbalance.

Co-administration of aminoglycoside antibiotics.

Myasthenia gravis (reduced number of receptors).

Low levels of plasma cholinesterase (pregnancy, renal and liver disorders, hypothyroidism) or competition with drugs also metabolised by plasma cholinesterase (etomidate, ester LAs, and methotrexate).

Abnormal plasma cholinesterase (suxamethonium apnoea).

Ecothiopate eyedrops for glaucoma (historical—now not available on general prescription).

Train of four is classically measured as adductor pollicis twitches in response to supramaximal stimulation via two electrodes placed over the ulnar nerve—see pp. 1057–1059.

Double burst stimulation is said to be more accurate as a means of quantifying train of four ratio—see pp. 1057–1059.

Post-tetanic count is used to monitor deep relaxation, when the train of four will not show any twitches. Firstly establish that the peripheral nerve stimulator is actually working and has adequate battery charge. A 50Hz tetanic stimulus is applied for 5s followed by single stimuli at 1Hz. Post tetanic facilitation in the presence of non-depolarising blockade allows a number of twitches to be seen. Reversal with an anticholinesterase should be possible with a count of >10.

If you have already given a dose of neostigmine ensure it was adequate (0.05mg/kg) and that it did actually enter the circulation (check the IV line for backflow and the site of cannulation for swelling).

If you have used an aminosteroid muscle relaxant (rocuronium, vecuronium, or pancuronium) consider administering sugammadex (a selective relaxant binding agent) at a dose of 2–4 mg/kg.

Hypothermia, electrolyte imbalance, and acidosis will impair reversal and should be corrected.

Aminoglycoside or Mg²⁺-induced poor reversal may improve with calcium gluconate (10ml 10%) titrated IV.

Suspected myasthenia gravis should be confirmed postoperatively with a Tensilon® test.

If the patient has suffered a period of awareness whilst paralysed, admit it, explain it, apologise, and ensure that the patient has access to professional counselling if required.

Approach with care.

Free the patient from immediate danger.

Evaluate the patient's ABC.

Chest compressions should be started if a central pulse cannot be palpated or the child has a pulse rate <60bpm with poor perfusion.

Where no vascular access is present, immediate intraosseous access is recommended.

Once the airway has been secured, chest compressions should be continued at 100/min uninterrupted, with breaths administered at a rate of 10/min.

When circulation has been restored, ventilate the child at 12–20 breaths/min to normalise PCO₂.

Purpose-made paediatric pads are recommended for children aged between 1 and 8yr, but an unmodified adult AED may be used for children older than 1yr.

Adrenaline 10 µg/kg = 0.1ml/kg of 1:10 000 solution.

Consider hypokalaemia, hypothermia, and poisoning.

Antiarrhythmic agents:

Prolonged delivery; instrumental delivery; shoulder dystocia; multiple births.

Maternal drugs: opioids, general anaesthesia for Caesarean section.

Preterm delivery (survival is very poor if gestation <23wk and resuscitation is not recommended).

A baby requiring resuscitation is floppy, silent, blue or pale, has a heart rate <100bpm, and gasping, diminished, or absent respiratory effort.

Open and clear airway but keep the neck in a neutral position.

Give FIVE effective inflation breaths (2–3s at 30cmH₂O) of air or oxygen.

Heart rate should increase; if so, continue ventilating until spontaneous effort is adequate.

If heart rate remains <60bpm commence chest compressions with thumbs around chest at a compression rate of 120/min and a ratio of 3:1 breaths.

Reassess heart rate every 30s.