|Year : 2009 | Volume
| Issue : 4 | Page : 492-495
Patients with Symptomatic Primary Hyperparathyroidism: An Anaesthetic Challenge
Puneet Chopra1, Sukanya Mitra2
1 Senior Resident, Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Chandigarh, India
2 Professor, Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Chandigarh, India
|Date of Web Publication||3-Mar-2010|
203-B,New Type-VFlats, Sector 24-A, Chandigarh 160023
Source of Support: None, Conflict of Interest: None
Primary hyperparathyroidism is a disease characterized by hyperealeaemia attributable to autonomous overproduction of parathormone. Many patients with primary hyperparathyroidism are asymptomatic. Osteoporosis and nephrolithiasis are some of the major sequelae seen in the symptomatic patients. Parathyroidectomy is the only curative therapy. However anaesthetic management of such patients may be problematic with associated cardiac arrhythmias and skeletal muscle weakness. Low serum albumin and alteration in the acid base status in the perioperative period can affect the serum calcium level and thus adds to the existing problem. We present the successful anaesthetic management of a patient with primary hyperparathyroidism who initially presented with pathological fractures, and discuss the anaesthetic issues involved.
Keywords: Hyperparathyroidism, Calciu in, Anaesthesia
|How to cite this article:|
Chopra P, Mitra S. Patients with Symptomatic Primary Hyperparathyroidism: An Anaesthetic Challenge. Indian J Anaesth 2009;53:492-5
|How to cite this URL:|
Chopra P, Mitra S. Patients with Symptomatic Primary Hyperparathyroidism: An Anaesthetic Challenge. Indian J Anaesth [serial online] 2009 [cited 2021 Jan 19];53:492-5. Available from: https://www.ijaweb.org/text.asp?2009/53/4/492/60325
| Introduction|| |
Calcium plays a central role in a large number of physiological actions that are essential for life. Of particular relevance to the anaesthetist are the effects of calcium on the myocardium, vascular smooth muscle and blood coagulation. The estimated incidence of hypercalcaemia is 1:1000 cases in males and 2-3:1000 cases in females, with primary hyperparathyroidism beingthe most common etiology. Primary hyperparathyroidism is the most common cause of hypercalcaemiain the outpatient setting with many patients being asymptomatic. Leftundiagnosed, it can lead to severe complications of hyperparathyroidism such as osteitis fibrosa cystica and nephrocalcinosis. We describe the successful anaesthetic management ofa patient with primary hyperparathyroidism who initially presented with pathological fractures.
| Case Report|| |
A 17-year-old female patient with a body weight of 40 kg presented with pain in lefthip jointwhile walking forthe last 6-8 months. There was no history of trauma. She was diagnosed with pathological fracture of left sided neckof femur with healed fracture right neck of femur, forwhich she was put on bilateral skin traction. The patient was investigated forpatho logical fractures which revealed following results: serum calcium 11.8 mg/dl, serum parathormone 302.90 pg/ml (normal value 15.0-68.30pgr'ml), and alkaline phosphatase 2869 IU/l. Hersemm electrolytes, blood urea, serum creatinine, albumin levels and electrocardiogram were within normal limits. Adiagnosis ofprimary hypeiparathyroidism was made onthe basis of hypercalcaernia with increased parathormone levels. Ultrasound neck revealed presence ofa hypo echoic mass of 3Xl.lxl.2cm size just below the posteroinferioraspect of left lobe of thyroid. Technetium-99-m sestamibi parathyroid scan localized increased tracer uptake to posterior margin of left lobe of thyroid suggestive of left inferior parathyroid adenoma.
Once the diagnosis was confirmed, the patient was started on medical management with intravenous (IV) fluids and furosemide at dose of 40 mg IV 12 hourly. Subsequently her serum calcium came down to 8.2 mg/dl. Her hydration status and serum electrolytes were monitored duringthis forced saline diuresis therapy. The patient was then placed for left parathymidectomy. Preoperatively, the patientwas kept nil per orally after 10 pm. Premeditation included ranitidine 150 mg, alprazolam 0.25mg orally night before and at 6 a.m. on the morning of surgery. In the operating room, intravenous access was securedthe patientwas connected to multichannelmonitor (S/5 Datex Ohmeda, Finland) and monitored for electrocardiogram (ECG), non-invasive blood pressure (NIBP), oxygen saturation, end tidal carbon dioxide (EtCO2) and neuromuscular function. The patient was pre-oxygenated for 3 minutes, and anaesthesia was induced with IV morphine 4.5 mg and IV thiopentone sodium 250 mg. Vecuronium bromide 5 mg IV was administered to facilitate tracheal intubation. Anaesthesia was maintained with 66% nitrous oxide in oxygen and isoflumne 0.51%. Patient's ECG was continuously monitored to detect any change in cardiac rhythm due to altered calcium metabolism. Further boluses of vecuronium bromide were given on the basis of neuromuscular monitoring. Patient's heart rate and blood pressure were stable throughout the period of surgery. End tidal CO 2 was maintained between 32 and 36 mmHg. The surgery lasted for 90 minutes during which she received 1.5 L of crystallo ids. After completion of surgery, the residual paralysis was reversed with neostigmine and glycopyrrolate in dosages of 2 mg and 0.4 mg respectively, with the guidance of neuromuscular monitor. During extubation the position of vocal cords was checked to assess any damage to recurrent laryngeal nerve. Intravenous calcium gluconate infusion was started slowly as a prophylactic measure and continued for 24 hours.
Postoperatively, the patient was kept in post anaesthesia care unit and was closely observed for signs and symptoms ofhypocalcaemia. Serum calcium levels were checked regularly. On the second postoperative day, the patient was started on oral calcium. She received injectable p aracetamol and tramadol for postoperative pain control Her postoperative course was uneventful For the pathological fracture, the patient was continued on skin traction and was discharged home with regular follow up at orthopaedics outpatient department.
| Discussion|| |
Calcium is essentialfor many biologicalprocesses including cardiac automaticity, excitation contraction coupling, blood coagulation, neuronalconduction, synaptic transmission, hormone secretion and mitotic division.  Extracellularcalcium occurs in three forms: as nonionized protein bound (approximately 50%), as calcium-anion complexes (5%) and as ionized divalent cations (approximately 45%). It is the free (ionized) extracellularcalcium concentration that mediates all the physiological effects, maintenance of which is affected by three main calciotropic hormones: parathyroid hormone (PTH), vitamin D and calcitonin.  Most patients have single parathyroid adenoma (80%). Multiple gland hyperplasia is found in 10-20% of patients and parathyroid carcinoma is rare (1%).
Many patients with primary hyperparathyroidism are asymptomatic. In symptomatic patients common findings include renal calculi, bone pains, pathological fractures, skeletal muscle weakness or non-specific symptoms such as depression, lethargy, vague aches and pains. Cardiac manifestations include prolonged PR interval, short QTinterval and systemic hypertension.  The diagnosis of primary hyper parathyroidism is demonstrated by persistent hypercalc aemia in the presence of normal or elevated parathyroid hormone concentration. ,
In ourcase, the patient presented with pathological fractures and bone pains. The patient was investigated for pathological fractures which subsequently demonstrated hyp ercalcaemia with primary hyperparathyroidism.
Preoperative localization ofhypersecretingparathyro id gland has been attempted by many techniques. The most sensitive appears to be ultrasonography (which is operator dependant) and technetium-99m sestamibi tomographic nuclear scanning.  In our case technetium-99 m sestamibi scan localized increased tracer activity in the left inferior parathyroid gland.
Primary hypeiparathyroidism and the associated hypercalcaemiaare treated initially by medical means followed by definitive surgical removal of the diseased orabnormalportions of parathyroid glands. Parathyroidectomy is the only curative treatment for primary hypeiparathyroidism and is associated with 95% cure rate with minimal morbidity in the hands of an experienced endocrine surgeon.  Intravenous fluids are the initial therapy for severe hypercalcaemia. Diuretic therapy should not be initiated until euvolemia is achieved. Loop diuretics depress the proximal tubular reabsorption of calcium and can increase the urinary calcium excretion by 200-250 mEq/day. Thiazide diuretics are avoided as these drugs may enhance renal tubular reabsorption of calcium. The risks of forced diuresis include cardiac decompensation, hypophosphataemia, hypokalaemia and hypomagnesaemia. Other treatment modalities include antiresorptive agents such as bisphosphonates, calcitonin and dialysis, which are reserved forthe patients with renal failure. , In ourcase, normocalcaemiawas achieved with hydration and furosemide therapy.
Although there are no specific guidelines for the conduct of anaesthesia in patients with primary hyperparathyroidism, anaesthesia for hyperparathym idism is not without problems. One needs to be vigilant about various factor that might alter serum calcium levels. It is importantto correct malnutrition and low albumin levels in the preoperative period. Preexisting hypertension, which is more common inprimary hypetparathyroidism, should be controlled ifpresent. In the intraoperative period, special focus needs to be made on the acid base status and transfusion of large amounts of citrated blood, lest life threatening hypocalcaemia may ensue.  Continuous ECG monitoring in these patients is imperative as hyper calcaemiamay be associated with disturbance in cardiac rhythm, although there is evidence that QT interval may not be a reliable index of changes in serum calcium concentrations during anaesthesia.  Coexisting skeletal muscle weakness may decrease the requirement of muscle relaxant inthis group of patients. A reduction in the duration of action of rocuronium has been reported in a patient with normocalcaemic hyperparathyroidism, hence neuro - muscular monitoring is mandatory, if available, in this group.  Our patient was also monitored for neuromuscularb to ckade, although there was no alteration in the duration of action of muscle relaxant. Acidosis decreases calcium bindingto albumin thus increasing the levels of ionized calcium, which can cause life threatening hypercalcaemia, hence it is important to maintain normocarbia. Our patient had severe osteoporosis and pathological fractures. This is apoint ofconcem while managing patients with hypercalcaemia. Positioning in the operating table thus needs special care in these patients. One of the serious complications in these patients is recurrent latyngealnerve injury. Hence assessment of vocal cord movement during extubation is imperative. Other severe problems encountered during surgery are bleeding and permanenthypoparathyroidism. Postoperative hypoparathyroidism needs to be monitored carefully. Ahigh index of suspicion may avert life threatening respiratory failure and concomitant ECG changes. Serum calcium level usually normalizes by 3 rd - 4 th day and thus needs to be checked at regularpostoperative intervals. ,, Patients with primary hyperparathymidism usually develop less severe hypo calcaemiathat is amenable to calcium therapy and itshould be routinely initiated following subtotal parathyroidectomy.  Our patient received IV calcium gluconate infusion forthe first 24 hours. Subsequently oral calcium therapy was instituted. Further, in the postoperative period, non-steroidal anti-inflammatory drugs should be avoided for pain control in case there is renal function impairment. 
In conclusion, it may be worth ermphasizingthat successful anaesthetic management of a patient with hyperparathyroidism requires vigilance for several factors that might potentiate adverse effects of hypo- and hypercalcaemia. These factors and their anaesthetic implications are summarized in [Table 1]. Adequate preoperative assessment and preparation, close monitoring of the signs and symptoms of hypo- and hypercalcaemia, restoration and keeping ionized calcium within nonnallimits duringperioperative period can go along way in the successful anaesthetic management of patients with abnormal calcium metabolism.
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