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Br J Anaesth. 2017 Nov 1;119(5):908-917. doi: 10.1093/bja/aex260.

Low end-tidal CO2 as a real-time severity marker of intra-anaesthetic acute hypersensitivity reactions.

Author information

1
Institut Pasteur, Department of Immunology, Unit of Antibodies in Therapy and Pathology, Paris, France.
2
INSERM, U1222, Paris, France.
3
Département d'Anesthésie-Réanimation, Hôpital Bichat, HUPNVS, APHP, Paris, France.
4
Département d'immunologie, UF Auto-immunité et Hypersensibilités, Hôpital Bichat, HUPNVS, APHP, Paris, France.
5
Inflammation Chimiokines et Immunopathologie, INSERM, Faculté de pharmacie, Université Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.
6
Département de médecine interne, Hôpital Foch, Suresnes, France.
7
Département de pneumologie. Hôpital Bichat, HUPNVS, APHP, DHU FIRE, Paris, France.
8
INSERM U1152, Université Paris Diderot Paris 7, Paris, France.

Abstract

Background:

Prompt diagnosis of intra-anaesthetic acute hypersensitivity reactions (AHR) is challenging because of the possible absence and/or difficulty in detecting the usual clinical signs and because of the higher prevalence of alternative diagnoses. Delayed epinephrine administration during AHR, because of incorrect/delayed diagnosis, can be associated with poor prognosis. Low end-tidal CO2 (etCO2) is known to be linked to low cardiac output. Yet, its clinical utility during suspected intra-anaesthetic AHR is not well documented.

Methods:

Clinical data from the 86 patients of the Neutrophil Activation in Systemic Anaphylaxis (NASA) multicentre study were analysed. Consenting patients with clinical signs consistent with intra-anaesthetic AHR to a neuromuscular blocking agent were included. Severe AHR was defined as a Grade 3-4 of the Ring and Messmer classification. Causes of AHR were explored following recommended guidelines.

Results:

Among the 86 patients, 50% had severe AHR and 69% had a confirmed/suspected IgE-mediated event. Occurrence and minimum values of arterial hypotension, hypocapnia and hypoxaemia increased significantly with the severity of AHR. Low etCO2 was the only factor able to distinguish mild [median 3.5 (3.2;3.9) kPa] from severe AHR [median 2.4 (1.6;3.0) kPa], without overlap in inter-quartile range values, with an area under the receiver operator characteristic curve of 0.92 [95% confidence interval: 0.79-1.00]. Among the 41% of patients who received epinephrine, only half received it as first-line therapy despite international guidelines.

Conclusions:

An etCO2 value below 2.6 kPa (20 mm Hg) could be useful for prompt diagnosis of severe intra-anaesthetic AHR, and could facilitate early treatment with titrated doses of epinephrine.

Clinical trial registration:

NCT01637220.

KEYWORDS:

anaesthesia; anaphylaxis; cardiac output; general; hypocapnia; neuromuscular blocking agents

PMID:
29040433
DOI:
10.1093/bja/aex260
[Indexed for MEDLINE]
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