1. SBH M&M Angioneurotic oedema and ACE inhibitors
Peter Sherren

2. NOT EVERY SWOLLEN FACE IS ANAPHYLAXIS
Airway scenario
NOT EVERY SWOLLEN FACE IS ANAPHYLAXIS

3. Introduction
In 1990, the Association of Anaesthetists of Great Britain and Ireland (AAGBI) published its first report on suspected anaphylactic reactions associated with anaesthesia.
The reported suspected that, between , anaphylactic reactions related to anaesthesia in the UK averaged 55 per year, compared with 319 for all drugs1.
10% of anaesthetic reports were of fatalities compared with 3.7% for all drugs reported1.
The understandable concentration on anaphylaxis within anaesthesia means that the knowledge of differential diagnoses and therapeutic options may be limited.

4. Clinical History MP V? 66 yr-old Afro-Caribbean lady
Htn, DM, IHD and PPM
05.00 Sudden onset tongue swelling and DIB
Called to DGH ED 06.15
Dramatic angioedema+, drooling++, stridor, poor vocalisation, agitated, SpO2 ~92% FiO FM. CVS stable

5. Incident Unexpected complication of treatment.
Unresponsive to steroids/anti-histamines/adrenaline.
ODP transported difficult airway trolley to resus.
Surgical Spr not happy/competent to perform emergency awake trache.
18g cannula cricothyroidotomy performed pre-induction uneventfully.
RSI, Grade III/IV (oedematous, distorted anatomy) view with McCoy.
GEB sited 3rd pass.
Unable to pass 7.0 coett, 6.0 passed with difficulty, minimal leak with no cuff deflated.
No issues ventilating.
Progression of angioedema post intubation.
10 day ICU admission, discharged to ward neurologically intact with trache insitu.

6. Good practice points
Out of hours communication/mobilisation of staff and equipment outside of theatres.
Familiarity with, and applied use of equipment on a well-stocked (theatre) difficult airway trolley.
Flexible use of DAS algorithm.

7. Management problems Inadequate difficult airway trolley in ED.
Rail-roading size 6.0 coett over 15F bougie is fiddly. Any smaller would have required a CHANGE of bougie for a 10F.
Retrospectively, the needle cricothyroidotomy was unnecessary, exposing already difficult airway to potential trauma.
General surgical training inadequate?

8. Learning points Causes of angioneurotic oedema
Idiopathic- large proportion.
Mast cell related/anaphylaxis.
Hereditory (HAE) I and II- C1 inhibitor deficiency or dysfunction.
Acquired- immunosuppression and lymphoproliferative disorders.
Drug related- Aspirin/NSAIDS, ACE, opiates, abx.
ACE inhibitors related angioneurotic oedema2,3:
Now most common exogenous cause of angioedema seen.
Can occur any time from initiation through to 10 years into treatment.
% of those receiving the drug.
Usually has no associated urticaria.
Due to increased bradykinin levels because kinin degradation is inhibited.
Can cause dramatic swelling of tongue, pharynx, or larynx- Secure airway early.
Deaths related to AIRWAY, no reported deaths from primary CVS collapse.
Some response to Adrenaline and minimal to steroids and anti-histamines.
HAE-Chromosome 11 deletion, use of FFP and C1 inhibitor concentrate
Vs standard treatment Steroids/antihistamines/adrenaline

10. Recommendations In angioneurotic oedema (like burns):
Use of size 10F bougie
Use of uncut COETT
Range of sizes of COETT ready for use
Potential unique use of the Melker vs other large bore cricothyroidotomy kit
Improvement/standardisation of difficult airway trolley in ED

11. Discussion Choice of large bore cricothyroidotomy kit?
CUFFED seldinger vs PCK vs Quicktrach II
Place for selected pre-emptive cannula cricothyroidotomy and later use of Melker?

12. References
AAGBI Working party. SUSPECTED ANAPHYLACTIC REACTIONS ASSOCIATED WITH ANAESTHESIA. AAGBI Revised Edition
Adebayo PB, Alebiosu OC. ACE-I induced angioedema: a case report and review of literature. Cases J Jul 27;2:7181.
Cupido C, Rayner B. Life-threatening angio-oedema and death associated with the ACE inhibitor enalapril. S Afr Med J Apr;97(4):244-5