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The human case and these AX‐related factors are important to recognize for effective therapy. It is equally important to recognize that in people 4–5% (range ~2–20%) experience the “second episode of AX” in which inflammatory by‐products create a second wave of inflammation (Simons et al. 2015). The “second episode of AX” is countered therapeutically through the use of histamine‐2 receptor blockers (e.g., famotidine) and glucocorticoids, often continued over several days post AX. Histamine‐2 receptor blockers are readily available and help mitigate oozing of blood and plasma into the abdominal cavity. Glucocorticoids are important on several fronts, most importantly including: mitigating mast cell degranulation (stopping release of heparin and histamine), and indirectly attenuating the wind‐up of bradykinin (BK) through (a) blocking phospholipase A2 and the arachidonic acid pathway and (b) mitigating circulating heparin (Hnatusko et al. 2019) (see Table 7.7). Of note, maropitant and pantoprazole, commonly used drugs for gastrointestinal signs, do not treat AX and are ineffective for mitigating the “second episode of anaphylaxis” and treating the AX‐acquired coagulopathy.

In a recent case series of four dogs with AX‐hemoabdomen, three of the four dogs had small‐volume peritoneal effusion at the DH view and these three had short hospitalization courses (<48 hours). However, the fourth case had progression of the abdominal effusion and became unstable, requiring vasopressors and multiple units of FFP, surviving but hospitalized for five days. None of these four dogs received glucocorticoids or antihistamines to mitigate the “second episode of anaphylaxis.” The first three arguably got better on their own and were unlikely to progress no matter the treatment. However, the fourth dog arguably risked a poor outcome (death or euthanasia) and presumably had a large bill for its five days of intensive care with transfusion products and vasopressors (Birkbeck et al. 2019). One has to wonder if treating for the “second episode of AX” would have shortened the patient's course and curbed its complications and still would have been a low‐risk, high‐benefit, cost‐effective preventive therapy for the first three dogs. Moreover, performing a standardized AFAST and assigning an AFS would have provided more clinically relevant patient information rather than performing an unspecified POCUS abdominal exam using subjective descriptive terms for the ascites.

Pearl: Anaphylactic dogs commonly have AFAST‐positive fluid scores (AFS of 1 and 2, modified AFS system <3) with some developing large‐volume medically treated coagulopathic hemoabdomens (AFS 3 and 4, modified AFS system ≥3). Misdiagnosing and taking to surgery likely will be a fatal event.

Pearl: All canine AX‐hemoabdomen cases need to have as part of their work‐up a Global FAST and POCUS spleen evaluation to avoid “satisfaction of search error.” The combined evaluation will (1) semiquantitate volume of blood (AFS), (2) screen for gallbladder wall edema (AFAST), (3) screen for pericardial and pleural effusion (TFAST), (4) screen for right‐sided heart problems and dilated cardiomyopathy (TFAST), and (5) screen for a splenic mass (focused spleen). This combination of Global FAST and POCUS increases the probability of obtaining an accurate working diagnosis in the acutely collapsed or weak dog.