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Parathyroidectomy: Mgmt


In healthy patients, the parathyroid glands secrete parathyroid hormone (PTH) primarily in response to low serum ionized calcium (and to a lesser extent, mild hypomagnesemia). PTH release is chiefly inhibited by hypercalcemia but also by profound hypomagnesemia, calcitriol, and phosphate. PTH acts at three different locations to mobilize calcium stores to increase serum ionized calcium concentrations: bone, kidney, and intestine.

Excessive PTH secretion causes characteristic symptoms of hypercalcemia (abdominal pain, bone pain, confusion, depression, kidney stones and characteristic ECG changes, such as short QT interval and Osborn waves). Hyperparathyroidism is often categorized relative to the inciting derangement. Primary hyperparathyroidism occurs due to autonomous PTH secretion by the parathyroid glands. Secondary hyperparathyroidism occurs in the setting of normal physiology; it is the appropriate compensatory response to decreased serum ionized calcium. Tertiary hyperparathyroidism occurs in the setting of hypercalcemia as well, hence why presentation is similar to primary hyperparathyroidism. It can be viewed as a progressive stage of resolved secondary hyperparathyroidism and is often secondary to chronic kidney disease.


Though many patients presenting for elective parathyroidectomy are asymptomatic, patients may present with any number of hypercalcemia-related symptoms, such as dehydration, tachycardia, vomiting, and psychosis. If a patient presents on a more urgent/emergent basis, or if the anesthesiologist has any suspicion that the patient may be markedly hypercalcemic, checking an ionized calcium should help guide preoperative optimization. Emergent management of profound/symptomatic hypercalcemia may include normal saline infusion (2.5-3.0 mL/kg/hr), bisphosphonates (such as pamidronate 60 mg), loop diuretics, and/or IV phosphate.


Premedication, type of anesthesia, and airway management:

Patients nauseated with active vomiting secondary to hypercalcemia may benefit from administration of an H2 antagonist or sodium citrate at the appropriate time intervals prior to proceeding to the operating room. Though regional anesthesia may be attempted (superficial or deep cervical plexus blockade), inadequate anesthesia could prove catastrophic given the proximity of the surgical site to major blood vessels and nerves. General anesthesia with endotracheal intubation is usually the preferred modality of anesthesia, especially if the patient is presenting with symptomatic hypercalcemia. Symptomatic and urgent/emergent patients are usually higher risks for aspiration, particularly if they have ongoing nausea/vomiting or altered mental status. Rapid sequence induction is usually indicated for these symptomatic patients given the increased risk of aspiration.

These patients carry a higher risk for pathological fractures if they have been hypercalcemic for extended periods of time, making these patients higher risk for unstable cervical spine as a result of lytic lesions. Anesthesiologists should consider manual in-line traction of the neck and utilizing video laryngoscopy and/or fiberoptic bronchoscope to achieve tracheal intubation while minimizing cervical extension.

Monitors and Access:

Standard American Society of Anesthesiology monitors aside (oxygen saturation, capnography, heart rate, non-invasive blood pressure, and temperature), anesthesiologists should expect to monitor serum electrolytes closely during parathyroidectomies. Subsequently, anesthesiologists may opt for large intravenous access versus placement of an arterial catheter to best facilitate frequent blood sampling.

The gold standard of monitoring successful parathyroid removal involves close monitoring of serum parathyroid levels. A successful parathyroidectomy usually decreases serum PTH levels by greater than 50%. PTH has a short half life (3-5 minute) that allows anesthesiologists to frequently assess this integral parameter of successful removal. Significant variation exists between institutions, but generally speaking, PTH levels should be evaluated at multiple time point intervals (frequently pre-incision, pre-gland removal, and then at multiple intervals after gland removal).

Due to the high potential for recurrent laryngeal nerve injury (usually lies posterior to the parathyroid glands in close but highly variable proximity to the inferior thyroid artery), neuromonitoring is frequently requested by surgeons. This can be accomplished by utilizing short-acting neuromuscular blockers in combination with a neural integrity monitor endotracheal tube (NIM tube). The NIM tube converts laryngeal muscles action potentials into electromyography signals during periods of recurrent laryngeal nerve stimulation. Reductions in waveform amplitude and/or increases in waveform latency qualify as abnormal electromyography responses and indicate potential nerve injury, providing the surgeons valuable information throughout the delicate neck dissection.

Emergence and Analgesia

Due to the potential for vocal cord paralysis, as well as the effects of hypercalcemia, extubation should preferably occur in a fully awake state after complete reversal of neuromuscular blockade, establishing a regular breathing pattern with adequate tidal volumes, and hemodynamic stability. Complete neuromuscular blockade reversal should be accomplished prior to extubation; hypercalcemic patients are at higher risk for inadequate reversal with acetylcholinesterase inhibitors. Given the surgical location, every effort should be made to ensure a smooth extubation that minimizes bucking and coughing. Agents capable of blunting the laryngeal reflexes during extubation (opioids, alpha 2 agonists, and/or local anesthetics) should be considered prior to extubation.


Following parathyroidectomy, patients may manifest any number of characteristic complications. Early complications include bleeding (up to and including neck hematoma unto respiratory obstruction), electrolyte abnormalities (hypophosphatemia, hypomagnesemia, hypokalemia manifesting as cardiac failure, dysrhythmias, hemolysis, and/or platelet dysfunction), recurrent laryngeal nerve injury, and postoperative pain. Of particular interest is recurrent laryngeal nerve injury: unilateral nerve injury may only provoke hoarseness, while bilateral nerve injury would cause unopposed vocal cord adduction unto glottis closure and airway obstruction. Emergent re-intubation (and possibly tracheostomy) is required to manage bilateral laryngeal nerve injury.

Serum calcium is expected to decrease over the first 24 hours postoperatively. Patients with symptomatic and significant preoperative hyperparathyroidism may manifest “Hungry bone Syndrome” upon removal of the parathyroid glands, resulting in rapid and profound hypocalcemia secondary to rapid bone remineralization. Other symptoms of hypocalcemia may manifest as well, including tetany, laryngeal spasm, and seizures. EKG findings of hypocalcemia include prolonged QTc; rarely will atrial fibrillation or T-wave changes occur. Serum ionized calcium nadirs between three and seven days postoperatively, requiring patients to have frequent monitoring of their serum/ionized calcium as well as magnesium and phosphorus. Patients may require oral or IV calcium replacement during this time.


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