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Maria V DeVita

Publications and source records attributed to Maria V DeVita.

2 recordsLinked to original sources

Refractory hypotension and edema caused by right atrial compression in a woman with polycystic kidney disease.

We present the case of a 60-year-old woman with a history of autosomal dominant polycystic kidney disease and long-standing hypertension who developed persistent hypotension. While in the hospital for the treatment of bacteriemia, the patient had low systolic blood pressures (90 to 100 mm Hg), which was thought to be the consequence of infection. After the infection was adequately controlled and the blood pressure did not improve, an echocardiogram was done to further elucidate her hypotension. It was nondiagnostic and revealed an ejection fraction of 70% with left ventricular hypertrophy. Shortly after discharge, she developed significant lower extremity edema and her blood pressure remained low. Due to the low blood pressure it was not possible to mobilize the fluid with her dialysis treatments. A repeat transthoracic echocardiogram at that time revealed that the right atrium was partially compressed throughout the cardiac cycle by polycystic hepatic tissue. This tissue invaginated up through the right hemidiaphragm. A partial liver resection was considered for the patient. Instead, right nephrectomy was performed and the blood pressure improved.

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Failure of intravenous fluid therapies to decrease serum sodium levels in elderly hospitalized patients.

Elderly patients may have a tendency to develop hyponatremia due to sensitivity to stimuli that release ADH as well as an impaired ability to excrete a water load. We evaluated changes in serum sodium in elderly hospitalized patients who received various forms of intravenous fluid therapies. All patients were required to have a baseline serum sodium of 136-145 meq/L. Fourteen patients were enrolled in the study. The mean age was 82.9 +/- 6.8 years (mean +/- SEM). Thirty-six % were nursing home residents. Seventy-nine % were females. Seventy-two % received half normal saline and the remainder received normal saline as intravenous fluid therapy. The patients received a mean of 1098 +/- 145 mL of intravenous fluid per day, in addition to oral fluids. Mean follow up period was 5.9 days (3-10 days). Mean baseline serum sodium was 140.2 +/- 0.7 meq/L andmean follow up serum sodium was 141.4 +/- 0.9 meq/L. The m ean baseline BUN was 25 +/- 3.6 mg/dL and mean follow u BUN was 19.6 +/- 3.4 mg/dL. The mean baseline serum creatinine was 0.9 +/- 0.1 mg/dL and mean follow up creatinine was 0.9 +/- 0.1 mg/dL. The postintravenous fluid therapy serum sodium in the group receiving half normal saline was 141.7 +/- 0.7 meq/L and 140.8 +/- 3 meq/L in the normal saline group. No significant difference was observed between the pre and post fluid therapy for any of these paramenters (p > 0.05). Mean baseline plasma renin activity was 1.6 +/- 0.7 ng/ml/hour and fifty-seven % had PRA of less than 1 ng/ml/hour. Mean plasma aldosterone was 8.5 +/- 1.8 ng/mL and forty-two % were less than 5.5 ng/mL. Plasma ADH and ANP was 5.7 +/- 3.4 pg/mL and 83.6 +/- 26.9 pg/mL, respectively. Mean serum and urine osmolalities were 290 +/- 3.1 mOsm/kg and 471 +/- 57.7 mOsm/kg, respectively. No patient developed hyponatremia and 7 of the 14 patients experienced an increase in serum sodium during the follow up period. We conclude that many elderly patients hospitalized for acute medical illnesses either maintain a stable serum sodium or experience an increase in serum sodium. This occurs because total fluids administered to these patients are generally insufficient.

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