Blood Pressure Control with Fenoldopam during Excision of a Pheochromocytoma 

A 64-yr-old woman experienced cardiorespiratory arrest and multisystem organ failure (subendocardial myocardial infarction, renal failure, hepatic dysfunction, quadraparesis, and pulmonary edema) after knee arthroscopy. While in the intensive care unit, a 6-cm left adrenal pheochromocytoma was diagnosed by ultrasound, computed tomographic scan, and plasma (epinephrine: 56,778 pgm/ml, normal: 10–200 pgm/ml; norepinephrine: 123,052 pgm/ml, normal: 80–520 pgm/ml) and urine catecholamine assays (vanillylmandelic acid: 82.9 mg/day, normal: 0–7 mg/day; metanephrine: 8.6 mg/day; normal <0.35 mg/day; normetanephrine: 5.4 mg/day, normal: <0.65 mg/day). After the diagnosis was established, therapy with phenoxybenzamine and metoprolol was started. She slowly recovered, but because of renal insufficiency (blood urea nitrogen-creatinine: peak, 98–5.3 mg/dl, discharge, 65–2.7 mg/dl) surgery was postponed for 3 months.

At the time of readmission for surgery, her blood pressure was well controlled with medication (phenoxybenzamine, 20 mg/day; metoprolol, 25 mg/day) and her renal function had improved (blood urea nitrogen-creatinine, 22–1.1 mg/dl). After sedation with fentanyl, invasive monitoring (arterial-pulmonary arterial catheterization) was established. General anesthesia was induced with thiopental and isoflurane, and paralysis was achieved using vecuronium. A transesophageal echocardiography transducer was placed for additional cardiac monitoring. During anesthesia, the patient's hemodynamic values were stable (mean arterial pressure [MAP], 80 mmHg; heart rate [HR], 70 beats/min) until the adrenal mass was manipulated (MAP, 108 mmHg; HR, 75 beats/min). A fenoldopam infusion was begun at 0.2 [micro sign]g [middle dot] kg^-1[middle dot] min^-1to control hypertension and titrated to 0.4 [micro sign]g [middle dot] kg^-1[middle dot] min^-1. After the tumor was removed, her MAP returned to 80 mmHg and HR increased to 80 beats/min and were stable for the rest of the operation. Fenoldopam was infused for a total of 50 min and was stopped just before tumor excision. No other antihypertensive agents were used. The patient was hydrated aggressively during the procedure with 11 5% albumin, 3 1 normal saline, and 1 unit packed erythrocytes to obviate hypotension after tumor removal. Her perioperative urine output was 100 ml/h, with no observed increase during the fenoldopam infusion. The patient's renal function remained normal after operation.

A 50-yr-old man with a 4-yr history of severe headaches and episodic hypertension and an 8-month history of hot flashes, sweating, and tachycardia had a blood pressure value of 170/90 mmHg. A computed tomography scan showed a 3 x 5 cm right adrenal mass and incidentally revealed a 5 x 5 cm mass in the left lower renal pole. The urine catecholamine assays (vanillylmandelic acid: 25.3 mg/day, normal: 2–10 mg/day; metanephrine: 7.2 mg/day, normal: <1.3 mg/day; normetanephrine: 6.4 mg/day, normal: < 0.9 mg/day) were consistent with a pheochromocytoma. The results of a workup for Von Hippel-Lindau syndrome were negative. A right adrenalectomy and left nephrectomy were performed after 6 weeks of treatment (phenoxybenzamine, 100 mg/day).

Anesthesia and monitoring for this patient were similar to those for case 1, with the addition of Dilaudid (Knoll Pharmaceuticals, Whippany, NJ) epidural anesthesia. Under anesthesia, the patient's hemodynamic values were controlled but varied (MAP, 55–85 mmHg; HR, 55–80 beats/min) until the adrenal mass was manipulated (MAP, 120 mmHg; HR, 68 beats/min). A fenoldopam infusion was begun at 0.2 [micro sign]g [middle dot] kg^-1[middle dot] min^-1and rapidly increased to 0.4 [micro sign]g [middle dot] kg^-1[middle dot] min^-1. Esmolol was titrated to 150 [micro sign]g [middle dot] kg^-1[middle dot] min^-1for HR control. During this time, transient hypertension occurred (MAP peaked transiently to 140 mmHg and HR increased to 103 beats/min with esmolol). The fenoldopam dose was increased to 0.8 [micro sign]g [middle dot] kg^-1[middle dot] min^-1and sodium nitroprusside was titrated to 0.8 [micro sign]g [middle dot] kg^-1[middle dot] min^-1. Good blood pressure control was achieved (MAP 85 mmHg) with a somewhat labile HR (95–135 beats/min) until the tumor was removed, when all three drugs were stopped. The nephrectomy was uncomplicated and hemodynamics were stable (MAP, 70–100 mmHg; HR, 90–110 beats/min). Fenoldopam was infused for a total of 100 min. The patient was hydrated aggressively during the procedure with 71 normal saline to prevent hypotension after tumor removal. The perioperative urine output was 100 ml/h, with no observed increase during the fenoldopam infusion. After operation, the patient's renal function deteriorated slightly, with a peak blood urea nitrogen-creatinine value of 15–2.8 mg/dl, but values returned to normal in 10 days.

Fenoldopam causes peripheral vasodilation via selective stimulation of dopamine 1 receptors. [1,2] It has been compared favorably with nitroprusside in several clinical studies of hypertensive patients. [3–5] The activity profile (onset and duration) of fenoldopam would place it well on the list of useful intravenous antihypertensive agents for intraoperative management (Table 1). [6] Its short duration of action makes it a desirable agent during pheochromocytoma resection because of the possibility of hypotension and shock after tumor removal. [7] Unlike sodium nitroprusside, fenoldopam also increases renal blood flow and can cause diuresis and natriuresis. [8,9] Although augmented renal blood flow is a desirable action of this agent, drug-induced diuresis would be undesirable in these patients, because volume expansion is an important part of their treatment. [10,11]

The adverse effects (flushing, hypotension, dizziness, headache, tachycardia) of fenoldopam are related directly to its hemodynamic actions. Compared with nitroprusside, which has toxic metabolites (cyanide, thiocyante), fenoldopam appears to be a safer drug; when used in combination with nitroprusside, it may help prevent the excessive infusion rates of nitroprusside associated with toxicity.

Our first patient needed only fenoldopam, whereas patient 2 also required sodium nitroprusside and esmolol for blood pressure and HR control. Both of these patients had epinephrine-secreting tumors, but patient 2 was not treated before operation with a beta-blocker. Using fenoldopam allowed us to decrease the amount of sodium nitroprusside needed to control blood pressure in this patient. These two case reports document the successful use of fenoldopam in patients with renal impairment during pheochromocytoma resection.