Hyperparathyroid Crisis: It's not All About Calcium!

Sir,

Primary hyperparathyroidism (PHPT) is characterized by excessive secretion of parathormone (PTH).[1] Hyperparathyroid crisis is a rare condition with rates ranging from 1.6% to 6% in patients having hyperparathyroidism.[1] Usually, the emphasis during the perioperative period revolves around the maintenance of normal serum calcium levels often overlooking serum magnesium, potassium, and phosphates levels. The presence of renal tubular acidosis (RTA) could further complicate the perioperative course.

We present a case of 35-year-old male diagnosed as a case of PHPT, nonresponsive to conservative management and listed for focused parathyroidectomy [Figure 1].

Figure 1

Focused parathyroidectomy

The biochemical analysis revealed serum calcium at 15.8 mg/dl, serum phosphates at 3.8 mg/dl, serum PTH levels at 350 pg/ml, serum creatinine at 1.8 mg/dl, and alkaline phosphatase at 2900 IU/ml.

Apart from routine monitoring, neuromuscular monitoring (NM), and invasive blood pressure monitoring were planned. Anesthesia was induced with intravenous fentanyl (50 μg), propofol (60 mg) and vecuronium (4 mg) and airway secured with 8.0 mm endotracheal tube. Anesthesia was maintained on propofol infusion (5 mg/min). Intermittent boluses of vecuronium were administered on the basis of NM monitoring.

Arterial blood gas analysis (ABG) performed intraoperatively showed metabolic acidosis with hypokalemia [Table 1 intraoperative-I]. Potassium supplementation showed no change in ABG [Table 1 intraoperative-II].

Table 1

Arterial blood gas analysis

At the completion of the procedure, NM showed inadequate recovery with only three twitches seen with train-of-four stimulation. The patient was shifted to postoperative Intensive Care Unit for mechanical ventilation and further management. With subsequent ABG showing no change [Table 1 postoperative-II] serum magnesium levels were checked which showed a value of 1.2 mg/dl. Subsequently, magnesium and potassium supplementation was started. The patient was mechanically ventilated for 24 h and with subsequent normal ABG analysis and adequate neuromuscular recovery, patient was weaned and extubated.

Hyperparathyroid crisis is defined as hyperparathyroidism with a marked elevation of PTH, serum calcium >15 mg/dl, and associated with acute onset of severe signs and symptoms such as dehydration, mental alteration, anorexia, vomiting, cardiac dysfunction, ventricular arrhythmia, and impaired renal function. Treatment modalities such as hydration, calcitonin, and bisphosphonates with or without furosemide have been used for treatment. Early surgical intervention (focused parathyroidectomy) in such cases (within 48–72 h of presentation) is recommended.[2]

The PTH inhibits proximal tubular bicarbonate reabsorption, thereby causing mild metabolic acidosis (proximal RTA).[3] Metabolic acidosis hampers binding of albumin with calcium resulting in increased ionized calcium levels. Calcium and magnesium seem to compete for transport in the thick ascending limb of the loop of Henle (TAL). The increased filtered calcium load in hypercalcemic states will deliver more calcium to the TAL; the ensuing rise in calcium reabsorption will diminish that of magnesium. As a consequence, some patients with PHPT can develop hypomagnesemia. Hypomagnesemia can also occur as part of the “hungrybone” syndrome, in which there is increased magnesium uptake by renewing bone after parathyroidectomy.[3]

Hypokalemia is a common event in hypomagnesemic patients, occurring in 40–60% of cases.[4] Hypokalemia in hypomagnesemia may be multifactorial. The occurrence of metabolic acidosis and hypokalemia suggests RTA or gastrointestinal loss of bicarbonate. There is also evidence of renal potassium wasting in hypomagnesemic patients that is likely due to an increased potassium secretion in the loop of Henle and perhaps the cortical collecting duct.[4]

The correction of hypokalemia in this setting requires correction of the magnesium deficit.

The assemblage of dyselectrolytemia (hypophosphatemia, hypomagnesemia, and hypokalemia) might manifest as cardiac failure, dysarrhythmias, and neuromuscular irritability.[1]

PHPT and ensuing hypercalcemia usually cause muscle weakness. Muscle weakness coupled with constellation of dyselectrolytemia and metabolic acidosis makes such patient highly unpredictable to the effects of neuromuscular blockers, thereby making weaning and extubation difficult.[5] General anesthesia in such patients is fraught with risks. Surgery under ultrasonography-guided bilateral superficial cervical plexus block is definitely better, but patient refusal made us resort to general anesthesia.

A preoperative ABG and serum magnesium levels would have certainly aided us in the perioperative management. The utility of perioperative magnesium supplementation and fluid management with balanced salt solution containing potassium and buffers such as acetate and gluconate can be a subject of future studies.

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Conflicts of interest

There are no conflicts of interest.