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21 Parathyroidectomy: Surgical Techniques
Fig. 21.32 Incision was
made on the chosen site
Fig. 21.33 Identifying the
lesion with the probe
309
and an in vivo to background ratio >150% is strongly suggestive of parathyroid
adenoma (Figs.21.34, 21.35, and 21.36).
The excised tissue is reassessed with a probe away from the patient. Higher
activity of more than 20% of background activity is suggestive of parathyroid adenoma (Fig.21.37).
The probe is further inserted to search for additional incidental lesions. A second
lesion may fail to light up when a more active lesion is in situ. The probe is used to
search for a second hyperfunctioning gland while waiting for post-excision PTH
values (Fig.21.38).
Frozen section biopsy is not always necessary but helpful to conrm the diagnosis. But the result will not guarantee the completeness of excision when the multiglandular disease is suspected.
The incision is closed when the IOPTH assay is supportive of the complete
removal of hyperfunctioning glands.
310
Fig. 21.34 The lesion
identied with the probe
Fig. 21.35 The lesion
being removed
C. G. Nair and R. Ramachandran
Fig. 21.36 Ensuring high
radioactivity before
removing the lesion
21 Parathyroidectomy: Surgical Techniques
Fig. 21.37 Ensuring the
high radioactivity on the
removed lesion
Fig. 21.38 Looking for
residual lesion
311
21.4.5 Mini-parathyroidectomy
Focused parathyroidectomy can be done through an incision of 3–4cm exactly over
the lesion when concordance in two different imaging is available. The widely practiced protocol is to perform parathyroid scintigraphy followed by ultrasound for
anatomical localization. Scintigraphy coupled with SPECT is a good alternative but
hindered by a lack of universal availability. The procedure is done only when ably
supported by intraoperative PTH assay to ensure completeness of the procedure.
312
y
C. G. Nair and R. Ramachandran
a
d
Fig. 21.39 Mini parathyroidectomy
b
e
c
A,B,C,D,E
Steps of
Mini
parathyroidectom
The steps of the surgical procedure do not differ but need good precision in all
movements (Fig.21.39a–e). Parathyroid lesions in symptomatic diseases are generally larger in size and so require precise and gentle handling of tissues.
21.4.6 Postoperative Management
Many patients develop transient hypocalcemia following parathyroidectomy lasting
for <4 days. Usually, this is corrected with oral calcium supplementation along with
dihydroxy vitamin D.
21.4.7 Hungry Bone Syndrome
The term “hungry bone syndrome” (HBS) may be dened as prolonged hypocalcemia following parathyroidectomy. Serum corrected calcium remains below 8.4mg/
dl after the 4th postoperative day necessitating prolonged calcium supplementation.
HBS is often encountered following parathyroidectomy for symptomatic PHPT.The
prevalence among Indians seems to be high (21–87%) [8, 9].
HBS is related to the correction of dysregulation in bone formation and bone
resorption induced by uncontrolled PTH secretion. Bone undergoes the cyclical
process of osteoclastic bone resorption and remodeling with new bone formation by
osteoblastic activity. PTH favors excess osteoclastic activity changing the rhythm in
the cyclical activity. Successful parathyroidectomy curbs the osteoclastic activity
and decreases the remodeling space. For the resultant gain in bone mass, more minerals such as calcium and magnesium are needed. This phenomenon is believed to
cause a marked fall in serum calcium, phosphate, and magnesium levels which parallels the normalization of bone turnover.
21 Parathyroidectomy: Surgical Techniques
313
Old age (>70), 25 OHD deciency, preoperative high serum alkaline phosphatase levels (reect the state of bone turnover), and evidence of bone disease such as
osteitis brosa cystica are predictors of HBS.Large volume hyperactive parathyroid
gland(s) are likely to be associated with HBS [10].
The hallmark of the condition is lasting hypocalcemia which may be mild
(>7.62mg/dl) or severe when serum total calcium level has gone below 7.62mg/dl.
The mild form is usually asymptomatic or with mild disturbances. Severe hypocalcemia is always symptomatic and may be associated with life-threatening
manifestations.
Treatment of the HBS is aimed at replenishing the circulating calcium decit,
and in the longer term, at normalizing bone turnover leading to stable mineralization of the skeleton.
Mild hypocalcemia (>7.62mg/dl (1.9 mmol/L). Mild hypocalcemia is treated
with oral supplementation calcium and an active form of vitamin D.Two widely
used calcium preparations are calcium carbonate (40% elemental calcium) and calcium citrate (21% elemental calcium). Calcium carbonate preparations (1000 g)
twice daily before food and calcitriol 0.5μg daily is recommended. The patient has
to be reviewed in 4–7 days for monitoring the serum levels and the dose of supplementation is adjusted to achieve normalcy [11].
Acute severe symptomatic hypocalcemia (with seizure, laryngospasm, and tetany)
is a medical emergency. The patient has to be monitored since rapid correction of
hypocalcemia may cause hypotension and dysrhythmias. These patients require an
intravenous infusion of calcium for quick response. One ampule (10ml of 10% calcium gluconate) delivers 93mg of elemental calcium. Intravenous rapid infusion of
10–20ml of 10% calcium gluconate diluted in 100 ml of 5% dextrose is infused in
20min. The rapid infusion may be repeated after 10–60min when symptoms persist.
After controlling symptoms, a patient is given a dose-adjusted maintenance infusion.
Based on serum levels, calcium load in infusion is calculated (as 0.5–2mg/kg/h).
Quick intravenous infusion of calcium could result in arrhythmias and so patients
should be carefully monitored. Oral supplementation is initiated after acute symptoms
have subsided [11].
Infusion of calcium preparations containing >200mg/100ml through peripheral
veins may cause vein wall damage and thrombophlebitis. Calcium infusion in large
volume uid causes uid overload in patients with secondary hyperparathyroidism
and in elderly patients with compromised cardiac function. Calcium phosphate
deposition in the lungs, kidney, or other soft tissue may occur in patients receiving
intravenous calcium especially in the presence of high serum phosphate levels.
Magnesium is an important electrolyte having a direct inuence on various
other electrolytes such as calcium and potassium. Normal serum magnesium level
(1.46 and 2.68mg/dl) is essential since it is the cofactor of many of the body’s
biochemical reactions. Decreased levels of magnesium impair the magnesiumdependent adenyl cyclase pathway and decrease the release of parathyroid hormone (PTH) which in turn decreases serum calcium. There is an increased uptake
of magnesium for renewing bone following parathyroidectomy and so hypomagnesemia is a common accompaniment of hungry bone syndrome. Hypomagnesemia
314
C. G. Nair and R. Ramachandran
is found in 50–60% of intensive care patients. Hypomagnesemia is common following starvation and alcohol abuse and is associated with liver and kidney diseases [12].
Hypomagnesemia can induce or potentiate neuromuscular symptoms such as
tremors, tetany (including positive Trousseau and Chvostek signs, muscle spasms,
muscle cramps), and seizures. Cardiovascular manifestations include atrial and ventricular arrhythmias, cardiac ischemia, and ECG changes (widening of the QRS
complex, peaked T waves, prolongation of the PR interval).
Correction of hypomagnesemia in a hemodynamically unstable patient is done
as the emergent rapid infusion of 1–2g of magnesium sulphate (in 100ml of 5%
dextrose) in about 15min. In a symptomatic stable patient, an infusion is given
slowly over 2h. The serum magnesium level repletes quickly but the intracellular
magnesium takes a longer duration to normalize. So, in patients with normal renal
function supplementation is continued for 2 days more. But patients with compromised renal function (eGFR<30ml/min/1.73m2) dose adjustment is necessary to
avoid hypermagnesemia [12].
Maintenance therapy may require oral administration of Mg2+ oxide
(400mg twice daily or three times daily)-400mg (equivalent to 240mg elemental magnesium) or magnesium gluconate 400mg daily (270mg elemental
magnesium).
The doses of calcium and active vitamin D preparations required and the duration of treatment is guided by serum calcium and bone turnover marker levels. The
duration may sometimes last in excess of 12 months after successful surgery. HBS
patients require periodic evaluation of serum calcium, phosphate, and ALP levels
for monitoring supplementation. Vitamin D deciency is a common accompaniment and corrective supplementation is concurrently done.
Preoperative bisphosphonates and correction of vitamin D deciency were
thought to reduce the severity and duration of postoperative hypocalcemia.
Further prospective studies are needed to optimize pre-and post-operative treatment strategies in patients with PHPT and skeletal manifestations at high risk for
HBS [10].
Hungry bone syndrome following parathyroidectomy for secondary HPT is
found in about 27% of patients. Risk factors included younger age, higher body
weight, higher preoperative serum alkaline phosphatase, lower preoperative serum
calcium level, and lower postoperative serum calcium. Calcium and magnesium
correction is recommended as routine but requires careful adjustment to avoid uid
overload.
21.5 Complications
Complications following parathyroidectomy for PHPT are found in <2% of patients.
Surgical site infection is rare and routine perioperative antibiotic therapy is not necessary. Other surgical site-related complications such as bleeding, hematoma, and
seroma are found occasionally. Careful hemostasis should be ensured prior to
wound closure.
21 Parathyroidectomy: Surgical Techniques
315
Recurrent laryngeal nerve palsy is a potential complication but frequency shall
be minimized by careful dissection. Occasional patients who have lesions with
adhesions to soft tissue secondary to malignant inltration or inammation are candidates for nerve palsy.
The postoperative mortality (30 days) after parathyroidectomy for renal HPT is
reported to range between 1% and 3% [13]. The single most preventable cause of
postoperative death is hyperkalemia. Alkaline phosphatase is re-emerging as a better predictor of high/low bone turnover, and it has a more linear association with
mortality in patients on dialysis than PTH [14].
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