Point-of-Care Ultrasound Techniques for the Small Animal Practitioner. Группа авторов
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sonographic striation could have been missed (Caldwell et al. 2018; Lisciandro and Lisciandro 2019) (see Figure 7.11B).
Lastly, nearly all of our canine AX cases (100+) have had Global FAST performed and we have found a couple more important observations: pericardial and pleural hemorrhage has not been documented as a complication of the acquired AX‐related heparin‐induced hemoabdomen coagulopathy, and lung has always been “dry” with “absent B‐lines All (Vet BLUE) views (ABAV)” initially and on serial Global FAST examinations (Lisciandro et al. 2016; Hnatusko et al. 2019), in contrast to a single case report in the literature of massive bee envenomation accompanied by marked pulmonary edema (Walker et al. 2005). Importantly, these AX cases are single witnessed or witnessed Hymenoptera sp. envenomation and not massive bee envenomations, a much different subset of dogs. Anecdotally, AX‐related hemabdomen has occurred with vaccine‐induced AX.
Speculated Pathogenesis
There is only a single report of which we are aware in the human literature of an AX‐related hemoabdomen (Borahay et al. 2011). The case involved a near‐term pregnancy in a woman, interestingly from Galveston, Texas, with previous AX to contrast agents. She was anemic and received a blood transfusion prior to a scheduled C‐section and tubal ligation. During the procedure, she was given a cephalosporin antibiotic and complained of pruritus and had cutaneous and vital signs supporting a diagnosis of AX. She was started on epinephrine as a constant‐rate infusion. Postoperatively she became hypotensive and bedside point‐of‐care ultrasound was performed and she was positive for free fluid. Coagulation profile supported an acquired coagulopathy and disseminated intravascular coagulopathy (DIC) was diagnosed. She was reoperated after receiving histamine‐1 and histamine‐2 receptor blockers and glucocorticoids. At surgery, no discrete bleeding was found but only generalized oozing; topical hemostatic agents were placed intraoperatively and FFP was administered. She survived and her coagulopathy corrected within 24 hours (Borahay et al. 2011).
The case is interesting because likely the acquired coagulopathy in these dogs is complex and multifactorial and variable depending on what factor(s) is the major player in each case. However, heparin must play a role because some dogs have obvious discordance in coagulation times with a much higher aPTT than PT time (consistent with heparinization). Mast cell granules contain heparin. Additional factors likely playing a role include histamine, bradykinin, tryptase, platelet‐activating factor, and others (Lisciandro 2016b; Caldwell et al. 2018; Hnatusko et al. 2019).
Therapy for Canine Anaphylaxis
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.
AFAST DH View for Pericardial Effusion
Anatomy and Advantages over TFAST Transthoracic Views
The premise is simple – always, always, always look cranial to the diaphragm at the FAST DH view (Figure 7.13; see also Figures 6.8 and 6.9) (Lisciandro 2016a, 2019). The use of the DH view for pericardial effusion (PCE) avoids air interference (ultrasound cannot transit through air) from lung at transthoracic views, especially since dogs and cats (and people) often have respiratory distress as their chief complaint. In fact, the subcostal FAST view in human medicine is the number 1 view for PCE that may be used a single view because the heart is so well imaged through the acoustic window provided by the liver and gallbladder into the thorax. In dogs and cats, the observation of the “racetrack sign” is essentially pathognomonic for PCE (Lisciandro 2014a, 2016a) (see Figure 7.13).
The best way to comprehend the relevant anatomy at the DH view is to look at an inverted canine (and feline) lateral thoracic radiograph (TXR). The TXR helps in learning the relative locations of the major structures, including the location of the muscular apex of the heart, called the “cardiac bump,” the expected positioning of heart chambers relative to the diaphragm, location of the CVC, and the expected location of the canine and feline gallbladder (Figure 7.14; see also Figures 6.11 and 6.12). The “cardiac bump” is the descriptor used for the observation of the beating heart and its muscular apex immediately against and, in dogs, often indenting the surface of the diaphragm where the heart and diaphragm come into contact (see Figures 7.14, 6.11,