Top 5 Takeaways from a lecture by Dr. Corrin Boyd
- The Pathophysiology of Canine Anaphylaxis Differs Significantly from the Human Model
The classic human paradigm of anaphylaxis as purely vasodilatory shock does not translate directly to dogs. Canine anaphylaxis presents a more complex cardiovascular picture that may include vasoconstrictive shock, mixed vasoconstriction and vasodilation, or hypotension without clear evidence of either. This variability stems from the concurrent effects of arterial vasodilation and decreased hepatic venous drainage, unique to this species. Additionally, dogs may present with either tachycardia or bradycardia, further complicating the clinical picture. Coagulation system dysfunction is also a recognised feature in canine anaphylaxis, with spontaneous haemorrhage – most commonly haemoperitoneum – contributing to the shock state. Recognition of these species-specific differences is essential for appropriate clinical assessment and treatment planning. - Diagnosis Remains a Clinical Exercise with Adjunctive Support
No single diagnostic test definitively confirms anaphylaxis. The diagnosis rests on the integration of history, exposure risk, and clinical signs. Classic presentations feature acute-onset dermatologic signs (angioedema, urticaria, erythema, pruritis) combined with involvement of at least one other organ system – such as cardiovascular, respiratory, or gastrointestinal. However, dermatologic manifestations are not universal; anaphylaxis should remain on the differential for acute severe cardiovascular or respiratory compromise even in the absence of skin changes, provided there is known or probable allergen exposure.
Point-of-care ultrasound offers a useful adjunct: the finding of the “halo sign” – representative of gallbladder wall oedema, may support the diagnosis, though careful exclusion of other causes (notably acute pericardial effusion) is mandatory.
Blood pressure measurement is critical, as hypotension may be the sole indicator of cardiovascular dysfunction.
Elevated ALT, coagulopathy, and lactic acidosis are consistent findings, while a normal C-reactive protein concentration can help differentiate anaphylaxis from other inflammatory conditions. - Adrenaline Is the Cornerstone of Acute Medical Management
Adrenaline (epinephrine) serves dual critical roles: preventing further release of inflammatory mediators from mast cells and basophils, and directly addressing both hypotension and bronchoconstriction. The recommended initial dose is 0.01 mg/kg administered intramuscularly. For patients with ongoing hypotension despite initial therapy, intravenous administration via continuous infusion at 0.005–1 mcg/kg/min should be initiated, titrated to achieve minimally acceptable normotension. The wide dose range reflects the significant individual variation in response.
Attention to catheter placement is essential: use a long catheter placed atraumatically and secured well to minimise extravasation risk, which can result in significant tissue injury. The intravenous route should be reserved for patients requiring ongoing cardiovascular support or those not responding to intramuscular administration. - Fluid Therapy and Coagulation Management Require Strategic Decision-Making
Intravenous fluid therapy is frequently necessary, particularly when a vasoconstrictive component is identified. Initial resuscitation should employ balanced isotonic crystalloids administered as boluses (10 mL/kg in dogs, 5-7 mL/kg in cats) over 10 minutes, with repeat administration as clinically indicated. Synthetic colloid fluids should be avoided due to their potential to exacerbate coagulopathy.
In cases complicated by significant haemorrhage, blood products become essential. Either whole blood or a combination of packed red blood cells and plasma should be administered to address volume deficits, oxygen-carrying capacity, and coagulation factor deficiencies simultaneously. Autotransfusion of peritoneal haemorrhage may be considered in appropriate cases.
Calcium should be monitored and supplemented as needed, as citrate can bind circulating calcium, causing hypocalcaemia. - Antihistamines and Glucocorticoids Play a Limited Role in Life-Threatening Anaphylaxis
While antihistamines and glucocorticoids remain part of the therapeutic armamentarium, their role is largely confined to resolving dermatologic manifestations. These agents have minimal impact on the life-threatening cardiovascular and respiratory dysfunction that defines anaphylaxis. Clinicians should avoid relying on them as primary therapy and instead prioritise adrenaline, fluid resuscitation, and oxygen therapy.
Gastrointestinal supportive care may be indicated for patients with vomiting, diarrhoea, or abdominal pain, but these measures are adjunctive to the core cardiovascular and respiratory support. This distinction is critical: the urgency of anaphylaxis management lies in addressing shock and airway compromise, not in modulating the allergic response itself through delayed-onset agents.
