Desmopressin acetate, known as DDVAP (1-deamino-8-d-arginine vasopressin), increases factors VIII and vWF, shortens activated partial thrombin time and bleeding time. Desmopressin is the best treatment in emergency situation, increases the release of the von Willebrand factor from the endothelium in uremic bleeding.1 Potential side effects of desmopressin include headache, nausea, malaise, hypotension, facial flushing, tachycardia, dizziness and hyponatremia.2 However hypertension weren’t defined before, we present two cases of hypertensive pulmonary edema after the infusion of desmopressin prior to ultrasound (USG) guided percutaneous kidney biopsy.
A 49 year-old female with end-stage renal failure secondary to unknown etiology received a living-donor transplant 3 years ago, was scheduled to have a transplant biopsy due to deteriorating graft function. Blood pressure was 160/90mmHg, pulse was 72beats/min, and respiratory rate was 14breaths/min.
She was given an infusion of 15μg of intravenous DDAVP over 20min in preparation for biopsy. Biopsy performed without complications. After 40min from the infusion; the patient suffers from dyspnea. Her blood pressure elevated to 220/140mmHg. On examination there was crepitation on the both lungs on every area. SPO2 was 70 on the pulse oximeter.
Respiratory rate was elevated to 40. Immediately she was given furosemide and nitroglycerin infusion with oxygen. Her SPO2 levels elevated after the treatment. She was monitoring all day and her blood pressure fall to 140/80 after 8h.
A 42 year-old male with crescentic IgA nephropathy, who was diagnosed 7 months ago, was treated with pulse steroid and cyclophosphamide for induction. On examination, the patient was relieve, body temperature was 36.6C, blood pressure was 150/90mmHg, pulse was 72beats/min, and respiratory rate was 14 breaths/min.
He was given an infusion of 15μg of intravenous DDAVP over 20min in preparation for biopsy. Biopsy performed without complications. After 2h from the infusion; the patient suffers from dyspnea. His blood pressure elevated to 230/120mmHg. He was treated with oxygen, furosemide and nitroglycerin. His blood pressure was 150/90mmHg after 8h of intense therapy. His oxygen saturation had risen to 98 from 75 on room air.
Both of cases didn’t have any history of coronary heart disease or heart failure but they have hypervolemia due to renal failure.
Hergesell et al. reported that risks in order to minimize, to adopt adequate biopsy technique is not only important, but also high-risk patients, especially uncontrolled blood pressure, with a clotting disorder, or has emphasized that it is necessary to exclude those unwilling to cooperate.3 Mannucci et al. reported that prohibited for use in who have arterial disease. DDAVP related myocardial infarction and cerebrovascular disease has been reported to case presentations, can’t be used in patients with known cardiovascular disease.4
DDAVP was an analog of vasopressin, may provoke symptomatic hyponatremia because of water retention. According to the U.S. Food and Drug Administration Agency, the half-life of DDAVP in patients with severe renal impairment can be extend by 9h. Therefore, patients should be advised to restrict fluid intake from 1h before to 9h after administration of DDAVP. Blood sodium control is proposed following use in hyponatremic patient.5,6
There are no publications that specify the use of DDAVP in hypervolemic patient. In our cases DDAVP effected like vasopressin and increased water retention in the hypervolemic patients. In patients without structural heart disease DDAVP may have a role that could lead to hypertensive pulmonary edema. In our patients; increased blood pressure responded diuretic and vasodilator treatment.
Hypertension is not a limiting factor to evaluate the use of DDAVP because of falsely elevated blood pressure due to anxiety. We recommend careful use of DDAVP in hypertensive patients due to a hypervolemia without structural heart disease, and we think this situation could lead role in the hypertensive pulmonary edema.
