The anaesthetist in theatre put an axillary block using 20 ml of 1% lignocaine and 0.25% bupivacaine each. The patient received fentanyl 100 microgram and midazolam 2 mg to facilitate the block. The tracheostomy tube was replaced with size 7 laryngeal tube while patient was awake using 1% lignocaine spray. After confirming the stable haemodynamic status, general anaesthesia was induced with propofol 120 mg and atracurium 40 mg. Immediately on induction (within few seconds) patient desaturated to SpO2 of 50% on 100 oxygen, the chest became very wheezy and patient had a cardiac arrest. The laryngeal tube became blocked with yellow coloured sputum, so tube was changed to size 5 microlaryngeal tube.
Initially it was PEA arrest. Immediate CPR with adrenaline was administered, after which the rhythm changed to bradycardia and asystole. After third cycle of adrenaline and CPR the rhythm changed to VF. He was shocked with 150J which converted him to sinus tachycardia and the cardiac output was back. He needed metaraminol boluses and adrenaline infusion to maintain the good blood pressure. In theatre 50 ml of intralipid 20% was administered intravenously in an attempt to treat possible local anaesthetic toxicity. He also received doses of hydrocortisone and chlorphenyramine maleate.
Later the patient was transferred to intensive care for further management. After multidisciplinary discussion the probable causes for the cardiac arrest were thought to be-
1. Local anaesthetic toxicity- was unlikely due to the lower than maximum doses used for axillary block.
2. Troponin T of 1.1 microgram/l- might have been due to cardiac arrest or CPR, unlikely due to MI
3. Anaphylaxis to induction agents was questioned due to time of occurrence of arrest (within seconds of induction)
4. Probably airway obstruction from thick airway secretions was a possibility
The patient developed high white cell count of 30,000/cc and became dependent on high doses of ionotropes the next day.
Blood samples were sent to lab to measure local anaesthetic levels. Serum samples for tryptase levels were sent at 1, 6, 24 and 72 hours.
This patient remained on intensive care support for long period of time, remained very slow to wake up. He gradually improved consciousness wise and was transferred to rehabilitation unit for further care.
Discussion:
Many improvements have been seen in monitoring techniques, the widespread adoption of medical practice guidelines and patient care over the last two decades. So, many authors believe that the frequency of anaesthesia-related cardiac arrest and its mortality have declined over recent decades (1). Perioperative cardiac arrests were relatively higher in neonates, infants, elderly and in males with severe underlying disease and under emergency surgery. All anaesthesia-related cardiac arrests were related to airway management and medication administration which is important for prevention strategies (2).
Positive mast cell tryptase = lgE mediated reaction (i.e., anaphylaxis). Negative mast cell tryptase tests are only rarely associated with positive skin tests and antibody tests. While, if taken at the correct time, they usually mean anaphylaxis has not occurred. If tryptase is positive, the patient needs skin testing to identify the agent responsible. This needs to be done 4-6 weeks after the reaction (3).
Intravenous administration of adrenaline is hazardous and should be given in a dilution of at least 1:10 000 (never 1:1000). Intravenous injection of adrenaline must be reserved for patients with profound shock that is immediately life-threatening and for special indications, e.g. during anaesthesia. The injection should be given as slowly as seems reasonable while monitoring heart rate and the electrocardiogram (4).
An antihistaminic (chlorphenamine) should be administered as a secondary measure. Caution is needed to avoid "drug induced" hypotension: administer either by slow intravenous injection or by intramuscular injection. Its use may be helpful and is unlikely to be harmful. The dose for children and adults is determined by age as follows:
| | > 12 years : | 10 - 20 mg IM |
| | 6 - 12 years: | 5 - 10 mg IM |
| | 1 - 6 years: | 2.5 - 5 mg IM |
Hydrocortisone should be administered after severe attacks to help avert late sequelae. This is of particular importance for asthmatics (who are at increased risk of severe or fatal anaphylaxis) if they have been treated with corticosteroids previously. The dose of hydrocortisone should be given by slow intravenous or intramuscular injection - care being taken to avoid inducing further hypotension. The dose for adults and children is determined by age as follows:
| | > 12 years : | 100 to 500 mg IM |
| | 6 - 12 years: | 100 mg IM |
| | 1 - 6 years: | 50 mg IM |
If severe hypotension does not respond rapidly to drug treatment, fluid should be infused. A crystalloid may be safer than a colloid. A rapid infusion of 1-2 L may be needed. Children should receive 20 mls/kg rapidly, followed by another similar dose if there is no clinical response.
Patients with even moderately severe attacks should be warned of the possibility of an early recurrence of symptoms and in some circumstances should be kept under observation for up to 8 -24 hours.
In our case though the diagnosis was not clear to start with, we managed with standard resuscitation guidelines. We also looked at other possibilities of cardiac arrest under anaesthesia and managed on those lines.
References:
1. Keenan RL and Boyan CP. Decreasing frequency of anesthetic cardiac arrests. J Clin Anesth 1991; 3:354–7
2. British Journal of Anaesthesia 2006 96(5):569-575; doi:10.1093/bja/ael065
3. Australian Anaesthesia website- http://www.usyd.edu.au/anaes/austan/anaphylaxis.html#investigation
4. Resuscitation Council UK guidelines.
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