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Address reprint requests and correspondence: Brian D. Saunders, MD, FACS, Department of Surgery, Penn State College of Medicine, Penn State Milton S. Hershey Medical Center, 500 University Dr, Mail Code H149, Hershey, PA 17033-0850.
Secondary hyperparathyroidism is a systemic metabolic derangement that leads to massive expansion of parathyroid tissue and overproduction of parathyroid hormone. Accurate biochemical diagnosis is crucial to establishing a plan of care for these patients. Indications and timing of surgical intervention once refractory to medical management are best established through multidisciplinary care including an expert parathyroid surgeon. Principles of careful parathyroid surgery including identification of all parathyroid tissue in a bloodless field allow for the appropriate management of parathyroid excision. Subtotal resection of parathyroid tissue and total parathyroidectomy with immediate parathyroid autotransplantation are equivalent options. Hypocalcemia is the most common postoperative occurrence and should be anticipated and managed aggressively.
Homeostatic control of calcium level is centered in the parathyroid glands. In the normal state, 4 small glands, totaling 200 mg of tissue and residing in the central neck, are responsible for regulating calcium level in the blood in response to stimuli such as serum calcium level, serum phosphorous level, and serum vitamin D level.
This careful balance allows total and ionized calcium levels to remain in a rather tight concentration range, and thus bodily functions such as nerve conduction, muscle action potentials, bone metabolism, and coagulation, to name just a few, proceed in a normal fashion.
Overactivity of the parathyroid glands can either be driven from autonomy of the parathyroid cells or from stimulation from a dysregulation in calcium, phosphorous, or vitamin D. Parathyroid autonomy, in the form of single or multiple gland neoplasms, may be sporadic or driven by an inherited genetic mutation. This is known as primary hyperparathyroidism.
This is to be distinguished from the physiologically appropriate, though possibly exuberant, response of the parathyroid glands to alterations in the controlling factors of parathyroid hormone gene transcription and translation. The latter is termed secondary hyperparathyroidism. That is, the generation of hyperparathormonemia in response to altered systemic levels of determinants of parathyroid hormone production.
Secondary hyperparathyroidism may result from any number of causes of low serum calcium. Renal tubular handling of calcium and phosphorous may become dysregulated such that there is a leak of calcium into the urine, or a retention of phosphorous. Either of these circumstances may secondarily increase circulating levels of parathyroid hormone. Finally, decreased bodily stores of vitamin D, either through malabsorptive states, decreased integumentary exposure to ultraviolet light, or decreased liver and especially renal production of metabolically active analogues of vitamin D can lead to higher levels of parathyroid hormone synthesis and secretion.
Many pathophysiologic states leading to a secondary hyperparathyroidism are transient or remediable without the need for surgery. The prototypical example is vitamin D3 supplementation to remedy hypovitaminosis D–induced secondary hyperparathyroidism. Renal failure in contrast, however, may often not be correctable. The physiologic parameters seen with kidney dysfunction, such as hypocalcemia, hyperphosphatemia, and hypovitaminosis D, lead to, sometimes severe, secondary hyperparathyroidism. Those clinicians managing renal failure, most notably nephrologists, possibly in combination with endocrinologists, would often try multiple pharmaceutical agents in an attempt to bring down the secondary overproduction of parathyroid hormone. These drugs include vitamin D supplements (cholecalciferol and calcitriol), phosphate binders, and calcimimetic agents. It is often necessary, however, to perform a parathyroid resection as temporizing or permanent therapy for renal failure–induced secondary hyperparathyroidism.
Preoperative Diagnosis and Operative Indications
The initial consideration of parathyroid surgery for secondary hyperparathyroidism must commence with confirmation of the biochemical diagnosis. Parathyroid disorders are a diagnosis confirmed with laboratory data rather than imaging findings. Secondary hyperparathyroidism is diagnosed with an elevated parathyroid hormone in the setting of normal or low total serum or ionized calcium. The phosphorous levels are often elevated, and the vitamin D levels are low. It is not at all uncommon for the parathyroid hormone levels to be 10-80 times the upper limit of normal. In fact, in the absence of severe hypercalcemia, which could indicate a parathyroid carcinoma, only renal failure–induced secondary hyperparathyroidism produces parathyroid hormone levels of that magnitude.
Once the diagnosis of secondary hyperparathyroidism has been secured, a multidisciplinary discussion among the parathyroid surgeon, the nephrologist, and the endocrinologist most often yields the optimal patient care planning. Need for and timing of parathyroidectomy may be influenced by the possibility of renal transplantation. Further, while the sheer magnitude of parathyroid elevation itself may not drive indications for operation, it is unlikely that a parathyroid hormone level much beyond 10 times the upper limit of normal would respond favorably to medical intervention.
Other indications (Table 1) for parathyroidectomy as therapy for secondary hyperparathyroidism include evidence of progressive bone mineral density loss, metastatic vascular calcium-phosphate deposition leading to ischemic ulcers (calciphylaxis), bone fractures or tendon tears, severe myalgias or arthralgias, and severe uremic pruritus.
Preoperative cardiopulmonary risk assessment is necessary for all patients planned for parathyroidectomy for renal failure–related secondary hyperparathyroidism. Comorbid conditions are prevalent in this patient population, and medical optimization may allow avoidance of perioperative complications. Perioperative volume status must be carefully planned with dialysis timing in the preoperative setting mapped out in advance. Calcitriol supplementation, if not already on it, for at least 2 days before operation can potentially mitigate some of the anticipated postoperative hypocalcemia. Discussion, too, with the individual patient about potential prolonged hospitalization after operation is imperative given the significant possibility of severe hypocalcemia in the near term following the operation.
Imaging and Preoperative Localization
Secondary hyperparathyroidism is by its pathophysiologic nature a multiglandular parathyroid dysfunction. In this setting, then, minimally invasive operations that identify less than all 4 parathyroid glands play no role.
Regardless of the extent of resection planned (to be discussed below), a bilateral neck exploration must be undertaken. High-resolution cervical ultrasonography may be performed by surgeon or radiologist in an attempt to identify the parathyroid glands preoperatively, though sidedness and conduct of the operation are not going to be significantly altered by the sonogram.
Ectopic or supernumerary parathyroid glands are unlikely to be identified with ultrasound given the limitations of the technique.
Nuclear medicine parathyroid scanning may be employed to identify the multiple parathyroid tumors, though this modality suffers decreased performance in a multiglandular setting.
A distinct advantage of nuclear medicine parathyroid scans is the ability to identify ectopic or supernumerary glands, of which preoperative knowledge can minimize the chances of operative failure or early disease recurrence.
Surgical Management
Parathyroidectomy is a functional surgical procedure to remove overactive parathyroid tissue. The extent of resection is dependent upon the specific parathyroid disease process. Secondary hyperparathyroidism is uniformly characterized by hyperplasia of all endogenous parathyroid tissue.
Therefore, the aim of any surgical approach for secondary hyperparathyroidism is to render the patient nearly euhormonal, ideally with a parathyroid mass equivalent to one normal gland (50 mg). National management guidelines exist for the target parathyroid hormone level for each stage of chronic kidney disease.
This metric of operative success can be met with the subtotal removal of all parathyroid tissue, leaving a portion of 1 parathyroid gland in situ, supplied by its native vasculature. An alternative is the complete removal of all parathyroid tissue with the immediate autotransplantation of a small amount of parathyroid tissue into a heterotopic location. These 2 operative approaches have been widely practiced, and have repeatedly achieved similar outcomes with respect to disease recurrence and postoperative hypoparathyroidism.
Comparison between subtotal parathyroidectomy and total parathyroidectomy with autotransplantation for secondary hyperparathyroidism in patients with chronic renal failure: A meta-analysis.
Often it is left to the preference and experience of the parathyroid surgeon, in consultation with the primary treating nephrologist, as to which operation to perform. In those patients for whom a parathyroid transplant is intended, preoperative discussion of handedness and a thorough understanding of present and future dialysis access plans should be reviewed. Immediate parathyroid autotransplants are often placed into a muscle bed in the nondominant forearm.
Great care should be taken to avoid injuring a functional dialysis fistula or graft, or disturbing the bed of a soon-to-be constructed fistula.
Surgery for secondary hyperparathyroidism should be planned for an inpatient procedure given the likelihood of adequate debulking of parathyroid tissue, regardless of specific operation performed, and of postoperative hypocalcemia requiring monitoring and parenteral administration of calcium. This is an operation that is often done under a general anesthetic, though can, in the properly selected patient, be completed with local anesthetic alone.
The wound classification for parathyroid surgery is clean, and therefore rarely requires the administration of preoperative parenteral antibiotics. Individual patient characteristics, of course, should be considered in the decision to prescribe antibiotics. Owing to the procedural risk of cervical hematoma, as well as the comorbid uremic platelet dysfunction, pharmacologic thromboembolic prophylaxis is often not used. Meticulous dissection in a bloodless field is paramount for the success of parathyroid surgery in removing the appropriate amount of parathyroid tissue while avoiding central neck morbidity such as laryngeal nerve injuries. One must be particularly cautious on the side of the neck ipsilateral to any functional dialysis fistula, as the increased venous pressure can lead to multiple small and large unnamed venous collaterals. Operative loupes are often helpful to the operating surgeon.
Once in the operating theater, the patient is laid supine on the operating room table. After successful induction of either general anesthesia or locoregional block accompanied by intravenous sedation, the patient׳s arms are tucked either at the side or lying naturally across the lower abdomen. Alternatively, and if a parathyroid autotransplant is planned, the nondominant arm may be kept out and prepped sterilely into the field. The patient׳s neck is extended, often aided with a towel or gel roll posterior to the shoulders. The patient is then positioned in the semi-Fowler position, with the head of the bed elevated, the feet down, and the operating table as a whole placed in the Trendelenburg position. Depending on personal preference, the operating table can be rotated 90- or 180-degrees away from the anesthesia machine to allow for more full access by the surgical team to the patient׳s head and neck.
The skin incision is made in the line of a skin crease roughly 1-2 cm caudal to the cricoid cartilage, or 1-2 fingerbreadths cephalad to the sternal notch (Figure 1). An incision length of 3-5 cm is usually sufficient to access and extirpate the parathyroids, while also viewing all critical structures. Ensuring that the incision is parallel to the skin lines of neck is vital for long-term cosmesis. Dissection is deepened through the subcutaneous tissues and through the platysma muscle. Subplatysmal myocutaneous flaps are created with electrocautery. These extend to the thyroid cartilage superiorly and to the sternal notch inferiorly. Care must be taken to avoid injury to the anterior jugular veins (Figure 2).
Figure 1Planned incision for a parathyroidectomy in relation to anatomical landmarks.
Figure 2Subplatysmal myocutaneous flaps are raised to expose the central neck, and underlying sternohyoid and sternothyroid muscles, which will be separated in the midline to reveal the thyroid and parathyroids.
Entry into the deeper space of the central neck is accomplished by separating the lower neck strap muscles. The avascular raphe between the left and the right sternohyoid and sternothyroid muscles can be opened with electrocautery. This exposes the thyroid isthmus. The 2 strap muscles are then elevated off the thyroid lobe. The space between these 2 muscle layers may be developed for additional lateral retraction as well as to access the carotid sheath laterally, for phlebotomy of the internal jugular vein for intraoperative rapid measurements of parathyroid hormone. Retraction of the muscles may be accomplished with either a self-retaining retractor or with handheld retractors depending upon surgeon׳s preference and availability of operative assistance. It is almost never necessary to transversely divide these strap muscles to achieve adequate exposure.
Surgery for secondary hyperparathyroidism requires identification of all 4 parathyroid glands as an obligate part of the operative procedure. As such, commencing the exploration on either the right or the left side is dependent upon surgeon preference and proceeds in essentially an identical fashion. Hence, it would be described here without laterality indicated. With lateral retraction of the strap musculature and carotid sheath, the thyroid lobe can be pulled medially. Dissection in the loose areolar tissue between the thyroid lobe and the common carotid artery would allow for progression back to the prevertebral space. It is crucial to extend the dissection back this far posteriorly to minimize the chance of missing parathyroid glands deep in the tracheoesophageal groove or in the retroesophageal or retrotracheal position. This exposure would often allow for identification and ligation of the middle thyroid vein. With this space fully exposed, it is often possible to identify the recurrent laryngeal nerve in the tracheoesophageal groove. Identification of this important structure helps in injury prevention as well as parathyroid localization. Superior parathyroid glands originate posterior to the recurrent laryngeal nerve, whereas the inferior parathyroids often lie anterior to this nerve (Figure 3).
Figure 3Wide exposure of the central neck to explore both the eutopic and ectopic locations for parathyroid glands is obtained with anteromedial rotational retraction of the ipsilateral thyroid lobe and lateral retraction of the carotid sheath and overlying strap muscles. This allows for identification of the recurrent laryngeal nerve as it traverses cephalad in the tracheoesophageal groove.
The superior parathyroid glands are positioned behind the superior pole of the thyroid lobe. A finger or a Kittner dissector may be used to roll the superior pole anteromedially. If necessary, the blood supply to the superior pole can be divided to allow for elevation of this portion of thyroid. The eutopic superior parathyroid gland would be posterior to the recurrent laryngeal nerve as it passes underneath the tubercle of Zuckerkandl, and just posterolateral to the ligament of Berry. The superior parathyroid glands are more constant in position relative to the inferior parathyroid glands. Difficulty in identifying a superior parathyroid gland may be ameliorated by locating the contralateral superior parathyroid gland.
Owing to relatively limited space for enlargement and subtle fascial layers in the neck, enlarged superior parathyroid glands may grow caudally in the tracheoesophageal groove. With the blood supply in the normal anatomical position, these low-lying superior parathyroid glands have attained acquired ectopia and are termed pseudoectopic. Care must be taken in dissecting them free as the recurrent laryngeal nerve may be draped over top of the lesion. Gentle digital pressure on the tracheoesophageal groove and spreading of tissue is often more revealing than unnecessary division of crossing structures. Truly ectopic positions for superior parathyroid glands include low in the tracheoesophageal groove, retroesophageal, retrotracheal, intrathyroidal, and inside the carotid sheath. Each of these locations should be examined for a missing superior parathyroid gland. Care should be taken when exploring the carotid sheath to look for a well-circumscribed, brownish nodule usually anterior to the common carotid artery. The vagus nerve and sympathetic ganglia lie posterior in the carotid sheath and should not be accidentally removed. Intrathyroidal parathyroids may be identified with the aid of intraoperative ultrasound and by incising the capsule of the thyroid gland.
Once identified, the superior parathyroid gland should be dissected back to its vascular pedicle and left until all other parathyroid glands have been identified. Great care should be taken when dissecting on or around parathyroid glands to avoid violation of the gland׳s capsule. Such entry into the gland risks seeding of parathyroid tissue and the development of parathyromatosis, a particularly difficult-to-treat cause for disease persistence or recurrence.
Though often quite enlarged and evident as parathyroid tissue, confirmation of tissue identification can be obtained with either frozen section pathology or a gland aspirate sent for parathyroid hormone measurement.
The inferior parathyroid glands have a more variable position than the superior glands, though there is often again symmetry between the 2 sides of the neck. The typical location for the parathyroid glands is just caudal to the tip of the lower pole of the thyroid lobe. The parathyroid gland may be up against the thyroid lobe, or slightly away, in the perithyroidal fat tissue, or formally in the thyrothymic ligament. Enlargement of the inferior parathyroid glands would often lead to a globular-shaped lesion that may descend because of gravity into the anterior, superior mediastinum. These can easily be extracted from the cervical incision given that their vascular pedicle originated from the inferior thyroid artery.
Ectopic inferior parathyroid glands may lie anywhere in the thyrothymic ligament, in the intrathoracic thymus, undescended in the carotid sheath anterior the carotid bifurcation, or within the thyroid parenchyma. Tissue identification of the inferior parathyroids may again be obtained by a small sliver being sent for intraoperative frozen section or a gland aspirate analyzed for parathyroid hormone level.
Once identified, the inferior parathyroid gland should be dissected back to its vascular pedicle while all the other parathyroid glands are identified.
Transcervical Thymectomy
The cervical horns of the thymus should be removed during operation for secondary hyperparathyroidism regardless of the specific operative plans with regard to parathyroid resection.
The thymus gland and the inferior parathyroid glands share a common embryologic origin, and rest of the parathyroid tissue may be present within the thymus. In the physiologic state, these tiny bits of parathyroid tissue may function normally. However, in the chronically stimulated state of secondary hyperparathyroidism, these foci of parathyroid tissue can expand greatly.
The cervical portion of the thymus can easily be approached through the same cervical incision and exposure done for identification of parathyroid glands. Inferior to the lower pole of the thyroid lobe, and posterior to the clavicular head, one can identify the thymic horn as it emanates from the anterior-superior mediastinum. This tongue of thymus often has a canary yellow color. It is invested by a thin capsule that needs to be dissected through to be able to gently pull the thymic tissue cephalad into the neck. Careful, hand-over-hand, gentle upward traction would allow the thymus to be delivered into the field (Figure 4). The cervical portion of the thymus would often thin out, exposing draining blood vessels that should be ligated with suture or metallic clips. This dissection is done separately on each side of the neck. Back table inspection of the removed thymus tissue is helpful to identify any grossly evident parathyroid tissue.
Figure 4A transcervical thymectomy is a necessary component to any operation for secondary hyperparathyroidism. The thymic remnant is gently grasped and pulled up from the mediastinum and into the cervical incision.
Subtotal Parathyroidectomy and Total Parathyroidectomy with Immediate Autotransplantation
A total of 2 functionally equivalent operations are available to the parathyroid surgeon for secondary hyperparathyroidism. First, the surgeon may resect all but a small, vascularized portion of one of the parathyroid glands. This is termed a subtotal parathyroidectomy. The advantage of this approach is to reduce the burden of parathyroid tissue, but leave an amount equivalent to a normal parathyroid gland in place and able to function immediately. Although the patient may still develop postoperative hypocalcemia, this is usually transient. Recurrent disease, however, requires revision operation in the neck and the inherent risks to vital structures such as the laryngeal nerves. The alternate operation is the total or complete removal of parathyroid tissue from the neck and immediate transplantation of a small amount of parathyroid tissue into a well-vascularized muscle bed. This approach reduces risks of recurrence, and moves a potential repeat operation away from the neck. However, the patient has an obligate period of dense hypoparathyroidism while the transplant tissue engrafts.
The subtotal parathyroidectomy centers upon dividing one of the parathyroid glands and leaving a portion of gland on a viable blood supply. The choice of parathyroid gland to divide and leave in place depends on several factors. The most important, however, is the appearance of the gland and the predicted ease of gland division without risking the arterial supply to the remnant. If all else is equal, an inferior gland remnant is preferable owing to the more anterior location of the inferior glands, and the ease of reoperation without having to traverse posterior to the recurrent laryngeal nerve. The overall morphology of the parathyroid glands also needs to be considered, as the easiest gland to divide is often the most normal, and least nodular, appearing gland. The divided gland is the first to be tackled in a subtotal parathyroidectomy, and the viability of the remnant needs to be checked before each sequential gland resection. The nonvascular pole of the chosen parathyroid gland can be divided sharply with scissors or a scalpel blade, or after application of a medium titanium clip (Figure 5). Careful recording of the position of the remnant parathyroid gland in the medical record is vitally important to the patient׳s future care. The remnant gland can be sutured to the thyroid capsule, or marked with a metallic clip or a colored, permanent suture tag. Once the parathyroid gland to be subtotally resected has been chosen and divided, the remaining 3 parathyroid glands can be removed with division of the respective vascular pedicle with a clip or a ligature.
Figure 5Diagram showing the right side of a completed subtotal parathyroidectomy, leaving a right lower parathyroid gland remnant on its native blood supply off the inferior thyroid artery, and marked with a titanium clip.
A total parathyroidectomy requires removal of each of the parathyroid glands. This is accomplished by dividing the vascular pedicle of each gland with a metallic clip or a suture ligature. Once all parathyroid tissue has been removed, a portion of one of the glands is chosen and prepared for immediate heterotopic autotransplantation. This portion of the operation should proceed without any delay to decrease the warm ischemic time of the parathyroid transplant. The transplant site is usually a muscle bed away from the neck. Most often, the brachioradialis muscle of the nondominant forearm is used. The arm can be sterilely prepped at this point, and a longitudinal incision is fashioned over the muscle. Dissection is deepened through all of the subcutaneous tissues and overlying muscle fascia. Hemostasis is vitally important as hematoma can lead to loss of parathyroid transplant viability. The portion of parathyroid tissue to be transplanted should equate to approximately 50 mg of tissue, divided in 1 × 1 × 1 mm3 fragments (Figure 6). In general, roughly 10-20 fragments are individually placed into tiny muscle pockets, and the pocket is sealed with either a clip or an absorbable suture.
Figure 6Roughly 50 mg of parathyroid tissue is minced with a scalpel into 1 mm3 fragments for autotransplantation into individual pockets in the brachioradialis muscle. Each pocket is individually closed. Care should be taken to perform this in the nondominant forearm and away from the current or future location of any dialysis access.
With removal of all parathyroid tissue and immediate heterotopic parathyroid autotransplantation, one should consider cryopreserving some small amount of parathyroid tissue for a possible later second attempt at autotransplantation in the event the first graft fails.
The procedures for preparing the tissue for preservation are institution-specific and should be investigated in the preoperative setting. Cryopreserved tissue can be thawed, prepared, and sterilely transplanted in a second operative procedure done under local anesthesia should profound hypoparathyroidism persist beyond 6 months after index operation. Cryopreserved tissue does lose viability with prolonged storage time, and rarely has success with more than 2 years of freezing.
The cervical incision needs to be inspected for excellent hemostasis before closure. Compressive cervical hematoma is a rare, but is a devastating complication in the early postoperative period. Valsalva maneuvers can be employed to ensure hemostasis. Hemostatic agents may be placed in the bilateral tracheoesophageal grooves. Routine placement of closed-suction drains is not required. The midline strap musculature is reapproximated with interrupted absorbable sutures. The platysma muscle is reapproximated with interrupted, absorbable sutures. The skin edges may be reapproximated with sutures or skin adhesive.
Intraoperative Parathyroid Hormone Monitoring
The diagnosis of hyperparathyroidism is dependent upon the demonstration of inappropriately normal or frankly elevated parathyroid hormone levels with respect to the serum calcium level. Conversely, the documentation of disease resolution or adequate debulking of overactive parathyroid tissue too comes with measurement of parathyroid hormone. The utility, reliability, and percent decline from baseline of parathyroid hormone levels in the setting of operation for multiglandular diseases such as secondary hyperparathyroidism remain unsettled. Long-term eucalcemia and cure of primary hyperparathyroidism can be prognosticated with a decline by 50% in parathyroid hormone as measured in a rapid fashion during operation. Many investigators would add the criteria of decline of parathyroid hormone into the normal reference range to the definition of operative cure.
Literature supports adequacy of resection or even operative cure for multiglandular parathyroid disease as determined by a drop in the intraoperative rapid parathyroid hormone measurement of 75%-90%.
Caution must be taken, however, with renal failure–induced secondary hyperparathyroidism, as too low a parathyroid hormone may be deleterious to the patient. Further, as parathyroid hormone is largely renally cleared, the kinetics of parathyroid hormone decay is altered in cases of renal failure–induced secondary hyperparathyroidism, and what is a normal level at the completion of operation could be frankly low by postoperative day number 1, heralding a prolonged period of severe hypocalcemia.
Parathyroid hormone sampling during the operation may be from a number of vascular sources. Phlebotomy from the internal jugular vein is convenient with the operative exposure obtained for parathyroidectomy (Figure 7). An acceptable alternative is a peripheral blood draw, often facilitated by a peripherally placed intravenous catheter. Finally, the anesthesiologist may elect to place an arterial line to facilitate hemodynamic monitoring throughout the operation. If this is the case, sampling from the arterial side of the circulation would also provide reliable hormone monitoring. Peripheral sampling, vs central venous sampling, may allow for an earlier time point of blood draw (eg, 10 minutes post resection vs 15 minutes post resection) because of the kinetics of parathyroid hormone decline and the distance from the immediate venous effluent of the parathyroid glands.
Figure 7Intraoperative measurement of parathyroid hormone is considered essential to ensure adequate resection of overactive parathyroid tissue. Blood can be sampled from a multitude of sites, though access to the bilateral internal jugular veins is made easy to the surgeon by the dissection performed for the operation. Furthermore, 3-4 mL of blood needs to be drawn up for a rapid parathyroid hormone assay that can result in as little as 10-15 minutes.
After operation, these patients should be admitted to the hospital for observation for the development of a cervical hematoma and for monitoring of serum calcium levels. Ideally, total- or ionized calcium levels are monitored every 6 to 8 hours for at least 2 days after the operation. The parathyroid hormone level should be documented 1 day postoperatively. Any calcimimetic medication should be discontinued. An aggressive oral calcium and calcitriol regimen should be started. One example is 1,500 mg of calcium orally thrice daily and 1 mg of calcitriol orally twice daily. Intermittent intravenous calcium gluconate may be needed. A continuous calcium infusion may also be needed. Dialysis against a high calcium bathe can aid in the prevention of or treatment of hypocalcemia. Hospital discharge can be considered once calcium levels have stabilized on an oral regimen of medication.
Conclusion
Parathyroid surgery for secondary hyperparathyroidism is a technically delicate procedure for which outcomes are determined by careful preoperative and intraoperative decision-making. Multidisciplinary care of these patients would allow for the optimal timing of operative intervention and prevention of postsurgical metabolic complications. Critical intraoperative steps include mandatory identification of all parathyroid glands and maintenance of a sufficient amount of viable parathyroid tissue in either the native position or a transplanted site. Surgical adjuncts including parathyroid localizing studies and intraoperative parathyroid hormone monitoring may play an important role.
Disclosure
The author (B.D.S.) has no relevant financial disclosure.
Comparison between subtotal parathyroidectomy and total parathyroidectomy with autotransplantation for secondary hyperparathyroidism in patients with chronic renal failure: A meta-analysis.
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