Point-of-Care Ultrasound Techniques for the Small Animal Practitioner. Группа авторов

(see Figures 7.12, 36.8–36.12). In contrast, patients with pericardial effusion/tamponade and right‐sided congestive heart failure have a CVC that is expected to be “FAT” having a large maximum diameter with little respirophasic diametrical change because of the severe cardiac‐related hepatic venous congestion (see Figures 7.12, 36.8–36.12). The terms “flat” and “FAT” have been published as terms that similarly characterize the inferior vena cava (IVC) at the subxiphoid view in people (Ferrada et al. 2012a,b). Integration of other POCUS and FAST findings is imperative for accurate interpretation. More information regarding the CVC and its evaluation may be found in Chapters 19, 20, 26, 36, and 37.

       Canine AX‐Related Heparin‐Induced Hemoabdomen – Single Witnessed or Unwitnessed Hymenoptera sp. Envenomation

      Although we were the first group to describe the phenomenon in the veterinary literature (Lisciandro 2016b), all the credit goes to Dr Scott Johnson, of Austin, Texas. When Dr Johnson took our Global FAST course in 2010, he remarked that he had observed hemoabdomen in anaphylactic dogs, and that we should start looking during AFAST. We heeded his suggestion and have seen close to 100 canine anaphylactic dogs with positive fluid scores and dozens with confirmed hemoabdomen that responded to medical treatment (Lisciandro 2014a, 2016b; Hnatusko et al. 2019). Importantly, these are witnessed or unwitnessed events likely caused by a presumed single Hymenoptera species envenomation (not massive bee envenomation). The great majority of anaphylactic dogs have no obvious cutaneous signs (Lisciandro 2016b; Hnatusko et al. 2019).

      Heparin, a clinically tangible constituent of mast cells, likely plays a major role, thus the addition of “heparin‐induced” by the author to its descriptor (Lisciandro 2016b). The importance of recognizing this AX‐related heparin‐induced hemoabdomen is that these dogs are medically treated (Lisciandro 2014a, 2016b; Caldwell et al. 2018; Birkbeck et al. 2019; Hnatusko et al. 2019) and inadvertently taking these dogs to surgery will anecdotally result in a fatal outcome (Lisciandro 2014a, 2016b; Hnatusko et al. 2019). Interestingly, in a published case series of 432 dogs with hemoabdomen, 86 were operated, but only 83 were included in the study because the three that were excluded had no histopathological diagnosis (Lux et al. 2013). One has to wonder if these three dogs were AX‐related heparin‐induced hemoabdomen cases.

       Small‐Volume Bleeders/Effusions

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