Severe Canine Anaphylaxis Prognostic Information and Mortality Rate | VETgirl Veterinary Continuing Education Podcasts

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In this VETgirl online veterinary CE podcast, we review canine anaphylaxis. These cases present to our veterinary facilities with varying clinical signs, but one thing they have in common is their urgency which requires rapid thinking, sometimes rushed discussions with owners, and quick medical intervention. The condition we call anaphylaxis can sometimes be confused in name with an allergic reaction. But with anaphylaxis, we are talking about the more severe clinical signs beyond hives and puffy faces. In anaphylaxis, we often see gastrointestinal side effects like vomiting or diarrhea, cardiovascular impairment such as cardiovascular decompensation and shock, and respiratory failure, on top of cutaneous signs like urticaria. Unfortunately, there is no direct test to give us a diagnosis of anaphylaxis, so we are left with things like patient history, and clinical signs to help us come to this diagnosis.

So, what’s the prognosis for canine anaphylaxis and what’s the data say? Studies have previously reported overall mortality rate ranges from 13% (in cats) to a 0% mortality rate in dogs. This latter canine study likely missed some of our more severe cases of canine anaphylaxis, and although we don’t often lose these patients, I can’t say my personal experience is a 0% mortality rate. So, Smith et al wanted to evaluate severe cases of anaphylaxis inn a study entitled Mortality rate and prognostic factors for dogs with severe anaphylaxis: 67 cases (2016–2018) to determine if there’s any prognostic factors in this subset of severe canine anaphylaxis and what the mortality rates are like for this particular group. The purpose of this retrospective study was to evaluate this subset of severe canine anaphylaxis to determine a representative mortality rate for this subset and to look for any prognostic indicators that can help us with case management and client communications for this condition.

Clinical signs commonly seen with anaphylaxis are the result of disruptions within 4 main body systems: cutaneous, cardiovascular, gastrointestinal, and respiratory. Disruptions in these body systems stem from the hallmark hepatic arterial vasodilation and concurrent hepatic venous outflow obstruction in anaphylaxis that is caused by release of vasoactive mediators- the most well-known being histamine. So by increasing blood flow to the liver but preventing outflow of blood from the liver, the result is liver damage in the form of hepatocellular necrosis, portal hypertension, cardiovascular collapse and multiorgan dysfunction.

Medical records from private specialty hospitals and a university teaching hospital were retrospectively reviewed to evaluate cases of canine anaphylaxis, anaphylactic shock, and allergic reactions. The authors only included records in this study that documented a peracute onset of clinical signs, involvement of two of the four body systems we described earlier, and other diagnostic findings supportive of anaphylaxis such as ultrasonographic finding of gallbladder wall edema or abdominal effusion. Since there are no cookie cutter, classic signs of anaphylaxis present in all cases, we need to be aware of some of the polar-opposite differences in clinical signs that we can be presented with. Patients can present with either bradycardia (described in this study as heart rate less than 60 bpm) or tachycardia (described in this study as heart rate greater than 150 bpm). And, likewise, respiratory rates could present as tachypneic or bradypneic (described in this study as greater than 35 breaths per minute or less than 10 breaths per minutes respectively). Authors assigned severity grades to cases of canine anaphylaxis as “grade zero” if only cutaneous signs were seen, “grade 1” if there were cutaneous signs and abdominal signs (like vomiting or diarrhea, or both), “grade 2” if there were cutaneous signs with persistent GI signs and/or evidence of cardiovascular dysfunction or respiratory compromise, and “grade 3” if there were signs of cardiovascular decompensation or respiratory failure. Authors then selected only the “grade 3” cases for review in this study. Additional inclusion criteria included patients being admitted within 12 hours of clinical signs and patients receiving biochemical analysis and HCT results at hospital admission. If patients were found to have any other concurrent health conditions that could contribute or explain the clinical signs being attributed to anaphylaxis, these cases were excluded from this study. Included cases were then grouped as “non-survivors” and “survivors,” and reviewed in greater detail for any differences between those that survived and those that did not. “Non-survivors” were patients that either died of natural causes or were euthanized due to progression of disease. It’s important to note that the authors excluded any cases where euthanasia was related to extraneous non-health circumstances (I’m assuming this means things such as financial constraints). This makes their data more representative of the disease.

67 dogs were included in this study: 29 males and 38 females with a mean age of about four years. Signalment, age, and sex did not appear to have any correlation with survival. All patients exhibited clinical signs of cardiac compromise, 94% of patients showed GI signs, 67.2% of patients exhibited respiratory signs, and 26.9% of patients had cutaneous signs. Authors found a correlation between body temperature and survival with lower body temperatures carrying a poorer prognosis. Lower body temperatures are thought to occur from histamine’s peripheral vasodilatory affects, and eventual cardiac decompensation (shock). The median temperature in the non-survivor group was 97.5°F (36.3°C), and median body temperature in the survivor group was 99.9°F (37.7°C). Across survivors and non survivors, the authors found the occurrence of hypotension to be 66.7%, normotension to be 27.3%, and hypertension to be 6%. Blood pressure, and time from onset of clinical signs to hospital admission did not appear to have any correlation with survival.

White blood cell count, hematocrit, and platelet levels were not found to be correlated to survival. There were some biochemical abnormalities noted to have correlation with survival including blood sugar and phosphorus levels. Across both groups, most dogs (94%) had elevated ALT activity, but ALT levels didn’t show a correlation with survivability. Serum phosphorus was found to be higher in the non-survivor group with a mean of 10.1 mg/dL compared to mean of 5.9 mg/dL in the survivor group. Proposed mechanisms of hyperphosphatemia in anaphylaxis include release of intracellular components from hepatocellular necrosis and/or from rhabdomyolysis (CK levels were not evaluated thoroughly in this study, but suggested to have a correlation). The authors concluded that patients with serum phosphorus concentrations greater than 12 mg/dL were almost 80X more likely to die as patients with lower values in serum phosphorus concentrations.

Hypoglycemia, defined in this article as a value less than 80 mg/dL, had a significant association with mortality, but only if the hypoglycemia was refractory to glucose supplementation. So when a patient required dextrose supplementation (the trigger point was a BG less than or equal to 68 mg/dL), this was significantly associated with eventual mortality. Hypoglycemic patients that responded to glucose boluses and CRI’s, and eventually normalized, had a better survival rate than those that remained refractory to supplementation. Mechanisms behind hypoglycemia in anaphylaxis are poorly understood, but plausible reasons can include impaired hepatic production, impaired mobilization, bacterial translocation from compromised GI mucosal barriers, or increased cellular utilization.

Lastly, authors looked at the coagulation panel for correlation with mortality. Although most patients in both groups had some degree of elevation in PT or PTT or both, the only factor that was correlated to mortality was a PT value >50% above the reference range. The authors concluded that patients were 11X as likely to die if their PT values were greater than 50% above the reference range limit. This finding highlights the importance of quantifying our PT and PTT elevations and not just reporting them as abnormal or outside reference intervals. A common way to quantify PT/PTT elevations is to take your patient’s value, subtract the high end of the test’s reference range value, divide this resulting number by the high end of the test reference range value, and then multiply this number by 100 to produce your percentage increase above normal.

Gallbladder wall edema, also known as the gall bladder “halo sign,” is a common finding in anaphylaxis and is thought to be the result of either hepatic venous congestion and portal hypertension, or inflammation from cytokine release – the exact mechanism is still not yet understood. This study found that of the patients that received abdominal ultrasound at hospital admission, 84.5% were found to have gallbladder edema and 65.5% had abdominal effusion. The effusions were most commonly a hemorrhagic effusion (84.2%) or a modified transudate with hemorrhage. Development of abdominal effusion may occur through vascular leakage due to massive cytokine release, or could be associated with coagulopathy or leakage from portal hypertension. Neither gallbladder appearance nor the presence of abdominal effusion proved to carry any prognostic value.

So, what about treatment? Epinephrine is the vital medical treatment for anaphylaxis to help counteract the extreme vasodilatory effects of vasoactive mediator release (histamine). All patients treated with epinephrine first received a bolus of 0.1-0.2 mg/kg IM or IV, and then were treated with either repeat boluses as needed or with a CRI ranging from 0.05 – 0.1 mcg/kg/min. No prognostic information was provided regarding overall doses of epinephrine required and correlation to survival.

This study found the overall mortality rate for dogs with severe anaphylaxis to be 14.9% (10/67), compared to a prior study that had reported a 100% survival rate for dogs presenting with anaphylaxis. However, that study only included cases that resolved within 72 hours after admission, which may have selected for a less severely afflicted population. Since anaphylaxis can present with such critical and rapidly changing body system derangements, it is important for the clinician to be able to advise pet owners on how to proceed with medical care, including information such as length of hospitalization and monetary investments weighed against the chance for survival. We can now say that odds are fairly good for severe anaphylaxis cases to survive with appropriate and immediate medical treatments. This study didn’t report on how long cases were hospitalized for, and this may open the door for a follow-on study.

The biggest limitation of this study is that there is not definitive test to confirm a diagnosis of anaphylaxis. We rely so heavily on patient history as opposed to specific directed testing which leaves room for error – both with underreporting and over-reporting this condition. Another limitation is the use of euthanasia as an end point for the study. There are client factors that can influence the decision to euthanize that may not be reflective of the disease progression. However, it was good to see in the study that the authors excluded causes for euthanasia that were known to be from reasons outside of disease progression, so the effect of client influence on euthanasia is likely minimal.

In conclusion, dogs with severe anaphylaxis were found to have an 85.1% survival rate. Coagulopathy, gallbladder wall edema, and abdominal effusions are a relatively common occurrence in canine anaphylaxis. Serum phosphorus levels greater than 12 mg/dL, refractory hypoglycemia, and PT prolongation greater than 50% are correlated with a decreased chance of survival.


Smith MR, Wurlod VA, Ralph AG, et al. Mortality rate and prognostic factors for dogs with severe anaphylaxis: 67 cases (2016–2018). J Am Vet Med Assoc. 2020 May 15;256(10):1137-1144.

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