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Anaphylactic dogs commonly have small‐volume effusions, AFS 1 and 2 (modified AFS system <3), that are not safely amenable to abdominocentesis (Lisciandro 2014a, 2016b). AFS 1 cases are most commonly positive at the AFAST DH view, with free fluid pocketing around the gallbladder, in between adjacent liver lobes, and between the liver and the diaphragm as an anechoic stripe generally with maximum dimensions of <0.5 to 1 cm (Lisciandro 2014a, 2016b). Often this free fluid is not safely accessible via abdominocentesis. AFS 2 cases are most often positive at the AFAST DH and CC views followed by AFS 2 cases being positive at the DH and HRU views (Lisciandro 2014a, 2016b; Hnatusko et al. 2019). It is important not to overreact, but rather acknowledge the complication is likely present in these AFS‐positive AX dogs and treat with standard AX therapy to prevent and/or mitigate the “second episode of AX” that likely causes the acquired and persistent coagulopathy prolonged even more without glucocorticoid and antihistamine‐2 receptor blockers (Table 7.7) (Simons et al. 2015). Most AFS 1 and 2 (modified AFS system <3) dogs that are appropriately treated do not become markedly coagulopathic and do not require replacement of clotting factors via transfusion products (Lisciandro 2014a, 2016b).

Figure 7.12. Integrating gallbladder wall edema with characterization of the caudal vena cava. The top row (A–C) shows a normal gallbladder wall (thin hyperechoic line) with variations of the caudal vena cava (CVC) as being (A) “fluid responsive” with a “bounce” or change to its respirophasic height, (B) “FAT” or distended and “fluid intolerant” with minimal change to its respirophasic height, and (C) “flat” or small sized due to hypovolemia and thus “fluid starved” with minimal change to its respirophasic height. The same images in rows (D–F) show gallbladder wall edema, which can occur with heart failure, as in (B), and referred to as a “cardiac gallbladder,” or with canine anaphylaxis as in (F) and referred to as an “anaphylactic gallbladder.” In right‐sided congestive heart failure the CVC is “FAT,” distended with a large maximum height, whereas in canine anaphylaxis with hypovolemic shock the CVC is “flat,” small with a small maximum height (see Table 7.6). Note also the distended hepatic veins associated with the “FAT” CVC, referred to as the “tree trunk sign” (Lisciandro 2014a,b) (see also Figure 36.8). There are other causes for gallbladder wall edema (Table 7.5).

Source: Reproduced with permission of Dr Gregory Lisciandro, Hill Country Veterinary Specialists and FASTVet.com, Spicewood, TX.

The manner in which the author recommends managing these cases is to get a baseline coagulation profile, when possible, as standard of care. In cases with coagulation profiles >25% of upper reference range, clotting factors should be replaced, that is, fresh frozen plasma (FFP). However, if a coagulation profile is not possible, AFS 1 and 2 (modified AFS system <3) dogs are “small‐volume effusions/bleeders” and, having an occult hemoabdomen until proven otherwise, do not have enough blood in their abdominal cavity to be life‐threatening. In fact, many AFS 3 and 4 (modified AFS system ≥3) will likewise resolve within 24–48 hours, if not excessively coagulopathic, with appropriate treatment (including initial treatment of glucocorticoids and histamine‐2 receptor blockers) to prevent the “second episode of anaphylaxis.” These treatment strategies are recommended in people (Simons et al. 2015).

Treat all AFS‐positive (AFS 1–4) AX dogs with standard resuscitative care including glucocorticoids and histamine‐2 receptor blockers to prevent histamine, heparin, bradykinin and other contributory inflammatory factors, prostacyclins, that contribute to the acquired coagulopathy (see Table 7.7). Monitor by performing serial Global FAST examination(s) that include AFAST and AFS. Expect the AFS to resolve to near 0 within 12–36 hours in dogs that are not continuing to bleed according to the “AFAST‐TFAST 48‐hour rule” (Lisciandro 2014a, 2016b). Packed cell volume is another inexpensive monitoring tool and is combined with patient AFS regarding blood loss (and the Global FAST approach for other complications and volume status assessment) versus drops in PCV and increases in AFS that become concerning, requiring additional intervention(s), such as coagulation profiles and administration of transfusion products, to maximum a successful patient outcome. For example, an increasing AFS to a 3 or 4 (modified AFS system, AFS ≥3) has become a “large‐volume bleeder” and with developing anemia warrants a change in treatment strategy with relevant testing (e.g., confirmatory abdominocentesis with fluid analysis and cytology and coagulation profile). In contrast, a static AFS 1 or 2 “small‐volume bleeder” with a stable, nonanemic PCV may be monitored using AFAST and an assigned AFS (or, better, Global FAST). The author always performs one more Global FAST four hours post admission and then on patient rounds every 12–24 hours in stable patients until the effusion has resolved (AFS 0), while also evaluating for any additional complications (TFAST and Vet BLUE). See Table 7.7 for suggested management guidelines.

Table 7.7. The author's treatment and monitoring guidelines for canine anaphylaxis (AX) in all AFAST fluid‐positive cases to prevent and treat AX‐related heparin‐induced hemoabdomen.

Source: Reproduced with permission of Dr Gregory Lisciandro, Hill Country Veterinary Specialists and FASTVet.com, Spicewood, TX.

	Intervention	Duration of activity	Comments
First line
Intravenous (IV) fluids	30–50 mL/kg IV repeated as needed	Short‐acting
Epinephrine (EPI)	Low dose 0.01 mg/kg, intramuscular (IM) or IV repeated as needed every 5–10 minutes; if this fails, injectable EPI then go to constant‐rate infusion (CRI)	Ultra short‐acting	Can use as a CRI starting at 0.05 μg/kg/min IV then increasing as needed based on blood pressure and taper off as soon as possible due to side effects
Second line
Dexamethasone Sodium phosphate(glucocorticoids)a	0.3 mg/kg IV	Long‐acting	Repeat 12 hours post admission at 0.15–mg/kg if not able to take PO prednisonea
Diphenhydramine(histamine‐1 receptor blocker)	2 mg/kg IM ONCE with maximum dose of 50 mg/dog	Intermediate	Avoid IV due to potential to initiate hypotension
Famotidine(histamine‐2 receptor blocker)	0.5 mg/kg IV or IM q12–24h (PO once appropriate)	Intermediate to long‐acting	Continue for 5–7 days while patient on steroids
Prednisonea	0.25 mg/kg q12h for 3 days then 0.25 mg/kg q24h for 3 days	Long‐acting	Tapering steroid regimen to prevent 2nd episode (wave) of inflammation that causes persistent coagulopathy
Fresh frozen plasma	Give if PT, aPTT greater than >25% over upper reference range and repeat as neededDelay if PT, aPTT less than <25% over upper reference range and recheck again in 4h and thereafter as needed depending on AFS and clinical course	Intermediate	Follow these cases with frequent PCV q2–4h plus serial AFAST and AFS until you are confident that the coagulopathy and hemoabdomen are resolving
Monitoring	AFAST	TFAST	Vet BLUE
Global FAST – combining AFAST and AFS and its target organ Approach, TFAST, and Vet BLUE	AFAST and AFS and its target organ approach – on admission and then 4h post admission if stable, sooner if unstable AFAST and AFS as part of daily patient rounds Expect dogs with resolved coagulopathy to have dramatic resolution of their AFS within 24h – AFS 1 or 0 (negative fluid score)	TFAST for pleural and pericardial effusion, volume status and cardiac status Left‐atrial to aortic (LA:Ao) ratio, fallback nonecho view Vet BLUE for left‐sided volume overload Right ventricular to left ventricular (RV:LV) ratio, fallback nonecho view of the caudal vena cava and hepatic veins for right‐sided volume overload	Vet BLUE for lung edema and other respiratory complications Expect lung to be dry in canine AX unless there are complications

^a Potent arachidonic acid inflammatory pathway blocker (inhibiting phospholipase A2), histamine blocker, and inhibitor of mast cell degranulation.