Printer Friendly

Protracted hypocalcemia following post-thyroidectomy lumbar rhabdomyolysis secondary to evolving hypoparathyroidism.


Rhabdomyolysis is characterized by skeletal muscle breakdown. It is a potential cause of serious electrolyte and metabolic disturbances, acute kidney insufficiency, and death. Recently, rhabdomyolysis has been increasingly recognized following certain surgical procedures. We discuss the case of a morbidly obese 51 -year-old woman who developed postoperative rhabdomyolysis of the lumbar muscles following a prolonged thyroidectomy for a large goiter. We discuss how her morbid obesity, the supine surgical position, the duration of surgery (including prolonged exposure to anesthetic agents), and postoperative immobility contributed to the development of rhabdomyolysis. Immediately after surgery, the patient developed hypocalcemia, which was likely due to rhabdomyolysis since her serum parathyroid hormone level was normal. Later, however, persistent hypocalcemia despite resolution of the rhabdomyolysis raised a suspicion of iatrogenic hypoparathyroidism, which was confirmed by a suppressed parathyroid hormone level several days after surgery. In post-thyroidectomy patients with risk factors for rhabdomyolysis, maintaining a high degree of clinical suspicion and measuring serum creatine kinase and parathyroid hormone levels can allow for an accurate interpretation of hypocalcemia.


Rhabdomyolysis (RML) can cause serious electrolyte imbalances such as hyperkalemia, hyperphosphatemia, and hypocalcemia, as well as metabolic derangements such as hyperuricemia and metabolic acidosis. Acute kidney insufficiency (AKI) can occur secondary to myoglobinuria and to hypovolemia, which occurs as a result of fluid shifts into the affected muscles. (1) Common causes of RML include trauma, ischemia, electrolyte derangement, strenuous exertion, seizures, burns, and various infections. (2,3) In addition, a wide range of medications such as HMG-CoA reductase inhibitors, ethanol, antihistamines, salicylates, benzodiazepines, anesthetics/paralytics, and opiates have been associated with nontraumatic forms of RML. (4) In more than 60% of cases of RML, the etiology is multifactorial. (5)

RML is diagnosed when the serum creatine kinase (CK) level reaches 5 to 10 times the upper limit of normal in a patient with symptoms of or risk factors for RML. (6) The mainstays of management are treatment of the underlying etiology, aggressive fluid resuscitation, and judicious use of loop diuretics to ensure a urine output of at least 1.5 ml/kg/hr. (7) Complications include AKI, compartment syndrome, disseminated intravascular coagulation, liver failure, and death.

Postoperative RML (PORML) has been associated with various surgeries. We report a case of post-thyroidectomy RML in which hypocalcemia initially occurred secondary to RML and persisted long after the resolution of RML as a result of evolving hypoparathyroidism.

Case report

A morbidly obese 51-year-old woman was hospitalized for thyroidectomy. She had a 6-month history of compressive symptoms secondary to a massive goiter with substernal extension. She also had hypertension, diet-controlled diabetes, peripheral neuropathy, and hypothyroidism. Her medications included lisinopril, metoprolol, furosemide, gabapentin, and levothyroxine. Her body mass index was 56 kg/[m.sup.2] and she was clinically euthyroid. She had normal complete blood counts and a normal basic metabolic panel. Her serum creatinine (SCr) level was 1.1 mg/dl (normal: 0.7 to 1.4), her thyroid-stimulating hormone concentration was 1.69 [micro]U/ ml (normal: 0.34 to 5.6), and her free thyroxine level was 7.8 [micro]g/dl (6.1 to 12.2).

A total thyroidectomy and parathyroid autotransplantation were performed. Surgery was conducted with the patient in the supine position with adequate cushioning and padding. General anesthesia was attained with succinylcholine, propofol, and sevoflurane. The patient also received a total of 500 [micro]g of fentanyl during the procedure. The operation lasted significantly longer (7 hours, 53 minutes) than the length of a routine procedure (2 to 3 hours) because of the size of the gland and detection of extensive fibrosis.

Postoperatively, the patient complained of severe low back pain. On physical examination, paraspinal muscle spasms and severe tenderness were noted in the lumbar region. The patient was afebrile. Her laboratory data showed an SCr level of 1.8 mg/dl, a phosphorous level of 7.4 mg/dl (normal: 2.5 to 4.9), an ionized calcium level of 0.99 mmol/L (1.12 to 1.32), and a magnesium level of 1.7 mg/dl (1.6 to 2.6). Calcium gluconate, vitamin D, and magnesium sulfate were started, and the levothyroxine was continued.

Intravenous morphine, cyclobenzaprine, and metaxalone were administered to treat the patients excruciating back pain and spasms, and IV hydration was started. However, despite the administration of up to 64 mg/day of IV morphine, the patient continued to experience significant pain over the next 2 days, which severely restricted her mobility. Because of her morbid obesity, prolonged surgery, and intractable lower back pain with lumbar tenderness, we suspected RML of the lumbar muscles.

On postoperative day 2, blood testing revealed the following:

* CK: 30,216 IU/L (0 to 220);

* myoglobin: 9,121 IU/L (0 to 70);

* aspartate transaminase: 588 IU/L (0 to 41);

* alanine transaminase: 162 IU/L (0 to 45);

* lactate dehydrogenase: 776 IU/L (90 to 200);

* ionized calcium: 1.03 mmol/L (1.12 to 1.32); and

* intact parathyroid hormone (PTH): 7 pg/ml (11 to 54).

We made a diagnosis of PORML. To determine the time of its onset, we analyzed a sample of the patient's blood that had been collected and stored in the laboratory immediately after surgery. It revealed that the serum CK level was 18,000 IU/L and the PTH level was 33 pg/ ml. Computed tomography of the lumbar area demonstrated paraspinal muscle edema and a loss of normal fatty striations. An urgent evaluation by the orthopedic service ruled out a compartment syndrome based on a normal compartment pressure.

With aggressive hydration and diuresis, the patient's AKI resolved over the next 48 hours, and within a week her pain abated and her serum CK level returned to normal (figure 1). However, her ionized calcium level remained low (0.94 mmol/L) which, in conjunction with suppressed PTH, reflected the development of iatrogenic hypoparathyroidism. The patient was discharged home on postoperative day 7 on long-term calcium and vitamin D supplementation.


PORML has been increasingly recognized as a complication of various bariatric, urogynecologic, orthopedic, cardiothoracic, and abdominal surgeries. Risk factors for PORML include obesity, prolonged surgery, diabetes, and high-risk operative positions:

* Obese patients are at increased risk for PORML because they have a higher risk of traumatic compression and because their surgical procedures are likely to last an unusually long time. (8-11)

* A diabetes-associated hyperosmolar state has been linked with both subclinical elevations in serum CK levels and the clinical syndrome of RML. (12)

* The surgical positions that are considered to carry the highest risk for the development of PORML include the knee-chest and lithotomy positions; the seated, prone, and supine positions have also been associated with it. (8) Involvement of specific muscle groups in PORML is dependent on the specific operative position; however, gluteal compartment muscles are the most commonly involved.

The perioperative use of several medications, including anesthetic agents, has been associated with PORML, and a longer duration of surgery would obviously mean prolonged exposure to anesthesia. Succinylcholine, commonly used for neuromuscular blockade, can cause PORML with or without features of malignant hyperthermia. (13) The exact pathogenesis is poorly understood, but it is believed to involve potassium efflux from muscles. (14) Propofol, another commonly used anesthetic agent, has been associated with PORML possibly via mitochondrial respiratory chain dysfunction. (15) Sevoflurane has also been implicated in PORML, although the exact mechanism is unlcear. (16) The perioperative use of HMG-CoA reductase inhibitors has also been associated with an increased risk of PORML. (17)

Lumbar PORML is a rare complication of surgeries performed while the patient is in the supine position. Bertrand et al observed that patients who develop lumbar PORML tend to report severe back pain, which can limit their early ambulation and worsen RML. (8) In such patients, effective analgesia can facilitate early ambulation. On the other hand, escalating doses of opiates can cause drowsiness and thus further restrict mobility.

To the best of our knowledge, post-thyroidectomy lumbar RML has not been previously reported. In 2005, Toprak et al published the case of a 24-year-old woman who developed hypocalcemia, convulsions, RML, and AKI 3 weeks post-thyroidectomy. (18) The authors concluded that the RML in that case was caused by hypocalcemia-induced convulsions.

Hypocalcemia caused by iatrogenic hypoparathyroidism complicates 5.4% of all thyroidectomies. (19) Hypocalcemia is also seen in RML as a result of hyperphosphatemia and AKI. In a post-thyroidectomy patient with RML, it is important to distinguish between the two etiologies of hypocalcemia. In RML associated with AKI, calcium metabolism follows a characteristic biphasic pattern.

During the early oliguric phase, hypocalcemia occurs as a result of hyperphosphatemia and decreased synthesis of calcitriol. During the recovery (early polyuric) phase, hypercalcemia occurs as a result of elevated calcitriol and PTH levels and the resolution of AKI. This is generally followed by normalization of calcium and PTH dynamics in the late polyuric phase. (20) In a post-thyroidectomy patient with RML, the onset of hypoparathyroidism during the recovery phase of RML can interfere with the expected normalization of calcium and PTH dynamics, leading to protracted hypocalcemia.

Our patient developed AKI and hypocalcemia immediately after surgery. We initially thought the AKI had been caused by fluid shifts during the prolonged surgery and that iatrogenic hypoparathyroidism had caused the hypocalcemia. However, considering the patient's risk factors and intractable backpain, we suspected PORML, which was confirmed by the presence of elevated serum CK, myoglobin, and phosphate levels.

A retrospective review of intact PTH, CK, phosphate, and calcium levels in stored blood that had been collected immediately after surgery showed an elevated CK, a high phosphate, a low calcium, and a normal PTH level. Therefore, it became clear that our patient had developed early hypocalcemia secondary to RML on the day of surgery, since her initial PTH level was normal. Iatrogenic hypoparathyroidism then developed over the course of the next 48 hours, which was evident by persistent hypocalcemia despite the resolution of the RML and AKI and by inappropriately suppressed PTH level (figure 2).

In conclusion, a high degree of clinical suspicion for PORML canhelp prevent life-threatening complications. Obesity, high-risk operative positions, extended duration of surgery with prolonged exposure to anesthetic agents, and postoperative immobility are all important risk factors to consider. Preoperative risk stratification; dedicated cushioning, padding, and frequent turning during surgery; judicious use of opiates; early ambulation; and prompt institution of therapy can prevent significant morbidity and potential mortality.

Interpretation of post-thyroidectomy hypocalcemia in patients with suspected PORML is tricky but vital. Measurements of serum CK and PTH levels and renal indices can help make an early distinction between hypocalcemia caused by RML and that caused by iatrogenic hypoparathyroidism. Hypoparathyroidism should be suspected if serum calcium and PTH levels fail to follow the characteristic biphasic pattern seen during the evolution and recovery phases of RML.


We thank Romesh Khardori, MD, of the Department of Endocrinology at the Southern Illinois University School of Medicine (SIU), and Ashraf Tamizuddin, MD, FACP, MRCP(UK) of the Department of Nephrology at SIU, for reviewing this article and providing valuable suggestions.


(1.) Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.

(2.) Fernandez WG, Hung O, Bruno GR, et al. Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med 2005;23(l):l-7.

(3.) Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: An evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005;84(6):377-85.

(4.) Cervellin G, Comelli I, Lippi G. Rhabdomyolysis: Historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med 2010;48(6):749-56.

(5.) Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore) 1982;61(3): 141-52.

(6.) Lappalainen H, Tiula E, Uotila L, Manttari M. Elimination kinetics of myoglobin and creatine kinase in rhabdomyolysis: Implications for follow-up. Crit Care Med 2002;30(10):2212-15.

(7.) Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990;322(12):825-9.

(8.) Bertrand M, Godet G, Fleron M, et al. Lumbar muscle rhabdomyolysis after abdominal aortic surgery. Anesth Analg 1997;85(1):11-15.

(9.) Youssef T, Abd-Elaal I, Zakaria G, Hasheesh M. Bariatric surgery: Rhabdomyolysis after open Roux-en-Y gastric bypass: A prospective study. Int J Surg 2010;8(6):484-8.

(10.) Szewczyk D, Ovadia P, Abdullah F, Rabinovici R. Pressure-induced rhabdomyolysis and acute renal failure. J Trauma 1998;44(2):384-8.

(11.) de Menezes Ettinger JE, dos Santos Filho PV, Azaro E, et al. Prevention of rhabdomyolysis in bariatric surgery. Obes Surg 2005;15(6):874-9.

(12.) Singhal PC, Abramovici M, Venkatesan J. Rhabdomyolysis in the hyperosmolal state. Am J Med 1990;88(1):9-12.

(13.) Escudero A, Castillo RM, Ibanez-Esteve C, et al. Rhabdomyolysis after succinylcholine administration [letter; in Spanish], Rev Esp Anestesiol Reanim 2005;52(3): 184-5.

(14.) Yentis SM. Suxamethonium and hyperkalemia. Anaesth Intensive Care 1990;18(1):92-101.

(15.) Laquay N, Prieur S, Greff B, et al. Propofol infusion syndrome [in French], Ann Fr Anesth Reanim 2010;29(5):377-86.

(16.) Takamatsu F, Taoda M, Uchihashi Y, Satoh T. Rhabdomyolysis induced by succinylcholine chloride and sevoflurane in an elderly man [in Japanese]. Masui 1996;45(11): 1406-9.

(17.) Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: Prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005;366(9493):1267-78.

(18.) Toprak O, Uzum A, Ersoy R, Cirit M. Hypocalcemia induced rhabdomyolysis and acute renal failure after thyroidectomy: A case report. European Journal of General Medicine 2005;2(2):76-9.

(19.) Pattou F, Combemale F, Fabre S, et al. Hypocalcemia following thyroid surgery: Incidence and prediction of outcome. World J Surg 1998;22(7):718-24.

(20.) Llach F, Felsenfeld AJ, Haussler MR. The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. N Engl J Med 1981;305(3):117-23.
COPYRIGHT 2015 Vendome Group LLC
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2015 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Cheema, Usman Y.; Vogler, Carrie N.; Thompson, Joshua; Sattovia, Stacy L.; Vallurupalli, Srikanth
Publication:Ear, Nose and Throat Journal
Article Type:Report
Geographic Code:1USA
Date:Mar 1, 2015
Previous Article:Common carotid artery dissection: A rare cause of acute neck swelling.
Next Article:A case of solitary fibrous tumor arising from the palatine tonsil.

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters