Point-of-Care Ultrasound Techniques for the Small Animal Practitioner. Группа авторов
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target="_blank" rel="nofollow" href="#ulink_c3c2daa2-9450-5d3f-84de-3ca02bedc2b7">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.
Large‐Volume Bleeders/Effusions
In lesser numbers of canine AX cases, “large‐volume bleeding,” AFS 3 and 4 (modified AFS system ≥3), occurs (Lisciandro 2014a, 2016b). When detected, the challenge is again not to overreact because in our experience, dogs with PT and aPTT times that range no more than 25% over upper reference often do not need replacement of clotting factors as long as standard therapy, including glucocorticoids and histamine‐2 receptor blockers (second‐line medications), is used upfront (without delay) in patient management (see Table 7.7). AFS 3 and 4 (modified AFS system ≥3) cases are often confirmed as AX‐related heparin‐induced hemoabdomen because the free intraabdominal fluid is safely accessible for abdominocentesis and fluid characterization. These cases require close monitoring and coagulation profile(s). In cases with initial or serial coagulation profiles of >25% of upper reference range, clotting factors should be replaced. However, PCV, vital signs, physical exams, and repeating AFAST with AFS (or Global FAST) can help monitor (track) the patient, whether coagulopathic or not. See Table 7.7 for suggested management guidelines.
Clinical Examples
Let's look at a couple of case scenarios of large‐volume canine AX‐related heparin‐induced bleeders. For example, if the high normal aPTT is 102 seconds, then an acceptable elevation not requiring FFP would be up to 129 seconds. The author has managed many cases with an AFS of 3 and 4 on admission that responded favorably to resuscitation with epinephrine, intravenous crystalloid fluid therapy, histamine‐1 and histamine‐2 receptor blockers, and glucocorticoids (see Table 7.7). These cases are continued on a short course of antiinflammatory glucocorticoids and histamine‐2 receptor blockers for the next several days with documented hemorrhagic effusion (and others highly suspected that fit the canine AX clinical profile). Often the AFS 3 and 4 is completely resolved (AFS 0) or nearly resolved (AFS 1) the following day on patient rounds. An excellent up‐to‐date anaphylaxis webinar and additional information regarding this unique and fascinating medically treated canine AX‐related complication is available free of charge at www.FASTVet.com
In uncommon to rare instances, packed red blood cells (pRBCs) are additionally needed. In the author's experience, some general guidelines for a clinical course and need for transfusion products would be that 1 in 5–7 AX‐hemoabdomen dogs (of any positive AFS) require replacement of clotting factors, 1 in 15 AX‐hemoabdomen dogs require a second round of FFP, and 1 in >25 AX‐hemoabdomen dogs require pRBCs treating as in Table 7.7, with the caveat that glucocorticoids and histamine‐2 receptor blockers are administered initially without delay. A recent case report documented a canine AX‐hemoabdomen without gallbladder wall edema, which in our experience is the vast exception rather than the rule (Caldwell et al. 2018;