Featured case study:
9-year-old neutered male
Australian shepherd, Bailey
Submitted by
David Judy, DVM, Judy Veterinary Clinic, El Cajon, CA
Physical examination
Bailey was collapsed on presentation.
He had pale mucous membranes, severe lethargy, rapid and weak femoral pulses, tachypnea and
palpable abdominal fluid. There was a green discoloration/staining of all his paws. His
temperature was 97.8° F, pulse 90 bpm and blood pressure 64/40 mmHg. He was determined to be in
hypovolemic shock. Further inquiry regarding the green substance on Bailey’s paws raised the
possibility of exposure to rodenticide. The owners thought that Bailey hadn’t been exposed, but a
call to their son at home revealed that one of the rodent bait stations set behind a log pile had
been pulled out and pellets were widely scattered. The pellets contained a second generation
rodenticide containing 0.01% diphacinone.
Differential diagnoses
Signs of hypovolemic shock combined
with palpable fluid in the abdomen is a potential sign of serious disease often carrying a poor
prognosis. Abdominal fluid can be a result of any number of pathologic processes including
transudates associated with hypoalbuminemia, exudates associated with active inflammatory disease,
chylous effusions associated with lymphatic obstruction/destruction or even neoplastic effusions.
Hemorrhage into the abdominal cavity is possible also and is most commonly secondary to trauma
(unknown origin), a ruptured benign or neoplastic mass (splenic, hepatic, vascular) or a primary
or secondary hemostatic disorder. A primary hemostatic disorder is less likely in this case as
there was no mucosal surface bleeding, petechiae or ecchymoses. A secondary hemostatic disorder
(coagulopathy) is much more likely if the abdominal fluid is hemorrhagic. A partial differential
list for coagulopathy includes acquired or inherited clotting factor deficiency, hepatic
disease/failure and rodenticide or other toxicity. Due to the probability of diphacinone
ingestion, rodenticide toxicity was high on the differential list for this patient.
Diagnostic plan
A complete blood count (CBC), chemistry
profile with electrolytes, and prothrombin time (PT) and activated partial thromboplastin time
(aPTT) tests were performed patient-side to screen for problems related to primary or secondary
hemostasis and/or primary and secondary organ involvement or dysfunction. Abdominal radiographs
and abdominocentesis were also performed to further evaluate the abdominal fluid palpated on the
physical examination.
Laboratory data
Erythron—All parameters were within reference interval limits
except for the MCHC which was elevated. Elevation of MCHC (above the analyzer reportable range)
may be due to the presence of cell-free hemoglobin due to in vitro or in vivo hemolysis or a
combination of both.
Leukon—Although all parameters were within reference interval
limits, the very low normal lymphocyte count is supportive of an underlying glucocorticoid
influence (“stress”), which would be very understandable with Bailey’s clinical presentation.
Evaluation revealed no significant morphology abnormalities including the presence of immature
neutrophils or toxic neutrophil forms; therefore, no obvious inflammatory component is present.
Thrombon—A platelet count within the reference interval limit
eliminated thrombocytopenia as a contributor to abdominal bleeding if it were present. Other
primary hemostatic disorders due to thrombocytopathy, such as von Willebrand’s disease, would be
uncommon given the history and signalment of the patient, but would be possible.
Clinical chemistry
Renal panel—The minimally increased BUN and creatinine
indicate slight decreased glomerular filtration, which was likely secondary to hypovolemia,
although a primary or secondary renal component was considered due to the critical status of the
patient. A urinalysis to help characterize the azotemia (concentrated urine for hypovolemia and
decreased perfusion—prerenal azotemia; nonconcentrated urine for primary or secondary renal
component—renal azotemia) could not be obtained at this time due to the compromised status of the
patient.
Electrolyte panel—Although the sodium and chloride are within
reference interval limits, the chloride is slightly low relative to the sodium supporting a
potential metabolic alkalosis associated with chloride loss or sequestration. Since no vomiting
was reported in the clinical presentation, sequestration should be considered. The potassium was
mildly decreased below the reference interval. If a significant alkalemia is present there could
be a extracellular to intracellular shift of potassium associated with hydrogen ions moving out
of the cells during alkalemia. All changes are extremely mild, but the pattern of mild changes
are compatible with one another and further investigation, such as a complete acid-base
characterization (Na, K, Cl, TCO2 and anion gap) and potential blood gas analysis, should be
considered.
Glucose—The observed hyperglycemia was likely due to an
endogenous glucocorticoid influence (“stress”) although possible diabetes mellitus would still
have to be considered. An absence of glucose in the urine would be additional support for
glucocorticoid affect; however, as is noted above, due to the compromised status of the animal,
a urine sample could not be obtained.
Additional diagnostics
Thoracic radiographs—the presence of mild microcardia and
hypoperfused lungs supports hypovolemia.
Abdominal radiographs—the loss of abdominal detail suggested
abdominal effusion, such as hemorrhage. The urinary bladder appeared intact, indicating that
uroperitoneum was unlikely.
Abdominocentesis—Frank blood was aspirated from the abdomen
confirming the presence of abdominal hemorrhage.
Coagulation profile
A citrated PT and aPTT were prolonged
beyond the analyzer reference interval limits indicating a problem with secondary hemostasis. (The
reference interval limits for the citrated PT are 11–17 seconds and for the citrated aPTT are 72–102 seconds.) This profile
can be seen with various conditions including consumptive coagulopathy (disseminated intravascular
coagulopathy or DIC), selective factor deficiency in the common coagulation pathway as well as
vitamin K antagonism (warfarin and diphacinone toxicosis).
Diagnostic summary
From the history, rodenticide toxicity
was the primary differential for this patient, but there is always the question as to whether or
not the animal actually ingested any rodenticide and whether the clinical signs are related
specifically to rodenticide ingestion. Based on signalment, physical examination findings and
laboratory data including identification of a lack of a thrombocytopenia, rodenticide toxicosis
remained the primary differential. Bleeding into the abdominal cavity was more supportive of a
secondary (coagulation) rather than primary (platelet or vascular related) hemostasis abnormality.
Performing PT and aPTT tests
patient-side together with other laboratory data allowed for thorough
evaluation of primary and secondary hemostasis. The lack of a severe or overwhelming inflammation
as well as the lack of or no evidence of systemic illness or major organ dysfunction or injury
strongly speaks against conditions like consumptive coagulopathy (DIC) as the cause of the
coagulation profile abnormalities seen in this case. These findings are all supportive of
rodenticide toxicosis.
Therapeutic plan
Bailey was treated with aggressive
therapy for hypovolemic shock secondary to likely rodenticide toxicosis. Vitamin K1 was
administered at 60 mg SC. His blood pressure was improved one hour after initiating shock therapy
(97/80 mmHg) and his HCT and RBC were 31% and 4.79 M/µL respectively. He showed good clinical
improvement to initial therapy and was referred to a local emergency clinic for continued
overnight monitoring and treatment. Bailey was discharged from the emergency clinic in stable
condition. The owners were instructed to keep him quiet and monitor him closely for any signs of
bleeding, including hematoma formation and melena. They were further instructed to return to this
hospital in three days for reevaluation and monitoring of the CBC and PT and aPTT (sooner if his
status deteriorated). Vitamin K1 was dispensed at 2.5 mg/kg PO divided BID.
Clinical case outcome
Bailey was doing very well
clinically at the time of his recheck. His CBC values were improved and a citrated PT and aPTT
returned to within the reference interval limits (13 and 73 seconds respectively). Unfortunately,
his owners did not return for reevaluation upon completion of the two-week course of vitamin K1
therapy as directed.
It was recommended that the PT be measured 48 hours after the last dose of
vitamin K1 therapy. If Bailey were doing well clinically and the PT were normal, no further
treatment would have been required. If the PT were prolonged, the recommendation would have been to continue vitamin
K1 therapy for another two weeks then recheck the PT.
References:
- Cote E. Clinical Veterinary Advisor: Dogs and Cats. St Louis, Mo: Mosby; 2007:84–85.
- Duncan JR et al. Veterinary Laboratory Medicine: Clinical Pathology, 4th ed. Ames,
Iowa: Iowa State University Press; 2003.
- Stockham SL et al. Fundamentals of Veterinary Clinical Pathology, 1st ed. Ames, Iowa:
Iowa State University Press; 2008.
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