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Describe the intraoperative management goals.
After adequate preoperative peripheral vasodilatation and replacement of intravascular volume, the primary intraoperative goal is to prevent and treat sympathetic activity. Manipulations such as establishment of invasive monitoring, induction of anesthesia, endotracheal intuba-tion, positioning, and surgical stimulus increase sympathetic outflow. Invasive arterial pressure monitoring is important due to frequent and dramatic fluctuations in blood pres-sure. The requirement for other invasive monitoring is based on the patient’s pre-existing medical condition. Placement of invasive monitors is accomplished under heavy sedation to minimize anxiety, which predisposes patients to sympathetic activity.
Combined epidural and general techniques provide partial protection from sympathetic outflow and are advocated by some, but they have drawbacks. Epidurals can complicate fluid management and judgment of anesthetic depth. Preoperative placement of epidural catheters can cause dramatic increases in sympathetic activity, even with sedation.
Most of the large published series of pheochromo-cytoma management are of open adrenal resections. Laparoscopic adrenalectomy has become the surgical standard of care. Benefits of laparoscopy are a shorter post-operative course and less postoperative pain compared with open procedures. However, recent studies show this minimally invasive technique is no more hemodynamically stable than open surgery. Pneumoperitoneum with carbon dioxide (CO2) is a potent sympathetic stimulus, and causes an exaggerated response in patients with pheochromo-cytoma. Manipulation of the tumor in laparoscopy causes as much release of catecholamines from the tumor as in open surgery. Management of these stimuli is similar to the management in open procedures, with short-acting vasodilation and β-blockade.
Vancomycin and histamine releasers, such as curare, atracurium, and morphine, are best avoided. Episodes of hypotension often result in severe rebound hypertension from sympathetic compensation. Similarly, droperidol, an α-adrenergic blocker, must be used with caution. Succinylcholine fasciculations might cause catecholamine release from a pheochromocytoma through mechanical effects. Sympathomimetics, such as ephedrine, and vagolytics, such as atropine, also predispose to tachycardia and hypertension.
Tumor manipulation frequently results in catecholamine release causing hypertension and tachycardia. This reaction should be anticipated and treated. A short-acting agent such as phentolamine or sodium nitroprusside, with or without β-blockade, is a good choice.
Following ligation of the tumor’s venous drainage, the emphasis switches from protecting against hypertension to treating hypotension. The patient is catecholamine-depleted because the contralateral adrenal has been chron-ically suppressed by the pheochromocytoma. The sudden absence of endogenous catecholamines and the general sympathetic depression caused by anesthesia result in passive vasodilatation with the potential for hypotension. Persistent chemical sympathectomy from regional tech-niques can exacerbate hypotensive episodes. Hypotension is treated with reduction of anesthetic depth, intravascular volume infusion, and peripheral vasoconstriction with nor-epinephrine or phenylephrine. Hypotension improves upon emergence from anesthesia, when sympathetic tone returns.
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