This dog came in with critical systemic hypertension. Humans with this condition are generally treated with intravenous administration of potent vasodilators such as nitroprusside. Since at least part of this dog’s systemic hypertension could be due to volume expansion, aggressive intravenous fluid therapy and mannitol could theoretically exacerbate the systemic hypertension. However, systemic hypertension secondary to renal failure in dogs is generally not responsive to diuretic administration or salt restriction. Consequently, it appears that systemic hypertension in dogs secondary to renal failure is primarily due to constriction of systemic arterioles and not due to volume expansion. However, one must be careful when administering intravenous fluids to these patients.
Drugs that dilate systemic arterioles are generally the most effective agents for treating systemic hypertension in dogs. Prazosin can be effective although it was not in this dog. Hydralazine and amlodipine are the next choices. The comments below are from when she was examined two days after her first discharge.
Follow-Up
Two Days Post Discharge
Hydralazine (7.5 mg or 1 mg/kg) was administered at 12:30 PM. Pressure at 1:30 PM was 105/67 with a mean of 86. Pressure at 4:30 PM was 138/106 with a mean of 126. The hypertension improved dramatically with hydralazine indicating that vasodilation improved the problem. However, hypertension is likely to be a continuing problem requiring continuous medication. Sent home with hydralazine 7.5 mg PO BID and reevaluated next morning.
Three Days Post Discharge
Blood pressure on 7.5 mg hydralazine: 147/111, mean 131. Still high but a dramatic improvement. Maintained on this dose. Recheck in five days.
Eight Days Post Discharge
BP: 116/84, mean 99. A little lower than desired. Hydralazine decreased to 5 mg PO BID. Recheck in 7–14 days.
Owner feels neurologic signs may be improving slightly. Suspect intracranial hemorrhage secondary to hypertension, cannot rule out neoplasia. Not a good anesthesia candidate for MRI/CSF tap. Owner elects to monitor at home.
Three Weeks Post Discharge
Hypermetric gait but does not run into walls (may have some vision). BP: 119/87, mean 101 — good. Continue hydralazine 5 mg BID. Phosphorus, creatinine, and BUN decreased — renal failure therapy working. Potassium still elevated, will monitor.
Four Months Later
Mitzie developed refractory glaucoma secondary to hyphema and presented for work-up prior to enucleation. Noted to have anemia and thrombocytopenia.
CBC: PCV = 16, thrombocytopenia of 97,000.
It is likely the hydralazine is the cause. In human medicine, hydralazine has been documented to cause blood dyscrasia. It has not yet been documented in dogs, however the reduction in two cell lines (RBC and platelets) supports it in this case.
P: Discontinue hydralazine. 24 hours later, start amlodipine 1.25 mg (0.15 mg/kg) PO SID and atenolol 12.5 mg (1.5 mg/kg) PO BID.
Bone marrow: megakaryocytic hyperplasia. No marrow suppression. Increased megakaryocytes with peripheral thrombocytopenia suggests a destructive process. Coombs test negative (does not rule out destruction). Most likely drug-induced.
Last Comment
Within two weeks, Mitzie’s PCV and platelet count increased while systemic hypertension remained controlled with amlodipine. This clinically confirmed the anemia and thrombocytopenia were secondary to hydralazine and that amlodipine was effective.
She lived for a little over a year after her initial presentation. During that time she successfully underwent anesthesia for an enucleation and developed a seizure disorder, presumably secondary to the CNS insult from her systemic hypertension. She was euthanized at the end because of worsening renal failure.
Hydralazine can induce a systemic lupus erythematosus–like reaction in humans. The exact mechanism of Mitzie’s abnormality is unknown but the fact that her problem resolved when the drug was discontinued certainly implicates hydralazine.