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Year : 2017  |  Volume : 50  |  Issue : 4  |  Page : 153-157

Severe rhabdomyolysis after head and neck surgery

Department of Surgical Critical Care Medicine, Changhua Christian Hospital, Changhua, Taiwan

Date of Submission26-Sep-2016
Date of Decision04-Dec-2016
Date of Acceptance23-Jan-2017
Date of Web Publication19-Jul-2017

Correspondence Address:
Man-Ling Kao
135 Nanhsiao Street, Changhua
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/fjs.fjs_48_17

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Rhabdomyolysis constitutes a severe medical emergency that requires immediate recognition and prompt treatment to prevent serious consequences. There are a variety of causes, but rhabdomyolysis after head and neck surgery is very rare. Here, we present a patient who underwent right parotidectomy and complicated with acute kidney injury secondary to severe postoperative rhabdomyolysis. Physicians require special attention for the high-risk patients to avoid severe complications.

Keywords: Acute kidney injury, creatine phosphokinase, rhabdomyolysis

How to cite this article:
Kao ML, Kao TL. Severe rhabdomyolysis after head and neck surgery. Formos J Surg 2017;50:153-7

How to cite this URL:
Kao ML, Kao TL. Severe rhabdomyolysis after head and neck surgery. Formos J Surg [serial online] 2017 [cited 2020 Sep 26];50:153-7. Available from: http://www.e-fjs.org/text.asp?2017/50/4/153/211087

  Introduction Top

Rhabdomyolysis is a potentially life-threatening, clinical, and biochemical syndrome that cause breakdown of striated muscle of any part of the human body, which results in extravasation of toxic intracellular contents from the myocytes into the circulatory system.[1],[2] Adenosine triphosphate (ATP) depletion, the end result of most causes of rhabdomyolysis, which results in Na/K-ATPase and Ca2+ ATPase pump dysfunction, thus, increased cellular permeability to sodium ions with increased in intracellular calcium concentration and increased the activity of intracellular proteolytic enzymes that degrade the muscle cell; then, large quantities of potassium, aldolase, phosphate, myoglobin, creatine kinase, lactate dehydrogenase, aspartate transaminase, and urate leak into the circulation.[2] There are many causes for rhabdomyolysis, such as exertion, trauma, infections, temperature extremes, drugs, toxins, myopathies, and connective tissue disorders.[3]

Postoperative rhabdomyolysis has been described. Rhabdomyolysis after head and neck surgery is very rare. To date, less than 10 prior cases have been published in contemporary English-language literature. We describe an uncommon case who had undergone head and neck surgery to treat benign tumor and had complicated with acute kidney injury secondary to severe postoperative rhabdomyolysis.

  Case Report Top

A 48 year-old male patient presented to the Department of ENT for the evaluation of swelling on the right side of his neck. He noted the mass for several months and its size became larger with swelling. There were no hoarseness, no dysphagia, and no body weight loss. He had a history of hypertension and diabetes mellitus Type-II, and he denied the history of smoking and alcoholic beverages use. His body mass index was 34 (1.73 m of height with 102 kg of body weight). Physical examination revealed a painless mass about 40 mm at the right infra-auricular region. All other systems examination was unremarkable. On follow-up magnetic resonance imaging of the neck, a mass measured 39.98 mm in the right parotid space and another one measured 17.25 mm in the left side, heterogeneously enhancing masses, were found [Figure 1]a and [Figure 1]b. After discussion with the patient and family, the patient underwent right parotidectomy.
Figure 1: Magnetic resonance imaging of the neck revealed a heterogeneously enhancing mass. (a) Right parotid mass, 39.98 mm. (b) Left parotid mass, 17.25 mm

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The patient was in supine position with the neck hyper-extended and head to the left side during the entire surgical procedure time. The surgical procedure time was 8.25 h with a total blood loss of 700 ml. Certainly, the blood pressure began to drop from 3 h after surgery; the lowest blood pressure was 75/38 mmHg with systolic blood pressure kept around 80–90 mmHg and diastolic blood pressure kept around 40–50 mmHg during the operative time. The intraoperative input/output was +2200 ml, and the blood pressure was 80/56 mmHg at the end of the operation. Due to his vital signs persisted unstable and the patient was noted very agitated, he was transferred to Surgical Intensive Care Unit (ICU) after operation. At ICU, fever up to 39.3°C, hypotension (80/56 mmHg) with darkly colored, and decreased urine output were found. His workup results showed hemoglobin 14.2 g/dL, white blood cells (WBCs) count 23.1 × 103/μL with neutrophil: 90%, and platelet count 207 × 103/μL; urine analysis was positive for proteinuria and pyuria (urine WBC: 164/μL). Sudden elevation of serum creatinine from preoperative level of 0.91 mg/dL to postoperative level of 2.79 mg/dL was found. Serum creatine phosphokinase (CPK) was elevated to 6226 U/L; a diagnosis of acute kidney injury secondary to rhabdomyolysis was done. Myoglobin levels were no assessed because it is less sensitive; the patient was treated with aggressive fluids resuscitation using 0.9% NaCl, vasopressor, and antimicrobials; because, in this obese diabetic patient, urosepsis cannot be ruled out completely (although his hemodynamic parameter looked less consistent with sepsis, rather similar to hypovolemia), empiric antibiotics for the possible urinary tract infection were administered initially at the same time. Furosemide bolus injection and alkalization of urine with sodium bicarbonate (NaHCO3) were administered. His urine output, urine pH, and arterial blood gas were monitored every 8 h. After a night in the ICU, his hemodynamic condition become stable and fever subsided, but the serum CPK continued to rise to a peak level of 31,710 U/L on the postoperative 1st day. His urine output has been maintained at more than two times the body weight. Serum CPK and renal functions were monitored daily, and the rest of the study was within normal limits. Fluids were titrated accordingly, and he did not require renal replacement therapy. The patient recovered well; his serum CPK, serum urea nitrogen, and serum creatinine levels were returned to normal range in a week [Figure 2] and [Figure 3]. He was extubated successfully and discharged to home. Follow-up at 1 month showed normal parameters with normal CPK level. On histological examination, the mass removed showed a picture of parotid gland with a well-circumscribed cystic tumor arranged in papillary growth lined by two-layered oncocytic columnar epithelia and composed of abundant lymphoid stroma, which revealed lymphoid follicle formation. Pathologic evaluation was consistent with Warthin's tumor of the parotid gland.
Figure 2: The levels of serum creatine phosphokinase (U/L) during Intensive Care Unit stay

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Figure 3: The levels of serum urea nitrogen and creatinine (mg/dL) before and during Intensive Care Unit stay

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  Discussion Top

The most common causes of rhabdomyolysis in adults are illicit drugs, alcohol abuse, medical drugs, muscle diseases, trauma, neuroleptic malignant syndrome (NMS), seizures, and immobility, whereas in pediatric patients, the most common causes are viral myositis, trauma, connective tissue disorders, exercise, and drug overdose. We review from different literature the following classification of causes:[2],[3]

Drugs and toxins

Drugs and toxins that cause rhabdomyolysis are alcohol, cocaine-barbiturates, benzodiazepines, and other sedative and hypnotics carbon monoxide (CO), hemlock herbs from quail, snake bites, spider venom (e.g., black widow spider), and massive honey bee envenomations. Salicylates, fibric acid derivatives (e.g., bezafibrate, clofibrate, fenofibrate, and gemfibrozil), neuroleptics, anesthetic and paralytic agents (malignant hyperthermia syndrome), quinine, corticosteroids, statins (e.g., atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, and cerivastatin), theophylline, cyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), aminocaproic acid, phenylpropanolamine, and propofol can lead to cause rhabdomyolysis.


Significant blunt trauma or crush injuries, high-voltage electrical injury (from lightning strikes or electrocution by high-voltage power supplies), and extensive third-degree burns cause rhabdomyolysis.

Excessive muscular activity

Strenuous exercise (e.g., marathons), status epilepticus, status asthmaticus, severe dystonia, acute psychosis, and military recruits in boot camp cause rhabdomyolysis.

Temperature extremes

Temperature extremes that cause rhabdomyolysis are heat stroke, NMS, and malignant hyperthermia syndrome. Exposure to cold with or without hypothermia can lead to rhabdomyolysis also, due to direct muscle injury.

Muscle ischemia

Compression of blood vessels (e.g., intraoperative use of tourniquets, tight dressings or casts, prolonged application of air splints or pneumatic antishock garments, and clamping of vessels during surgery), thrombosis, embolism, compartment syndrome, CO, and sickle cell trait; hypotension and shock states can cause rhabdomyolysis.

Prolonged immobilization

Anesthesia, coma, drug or alcohol-induced unconsciousness can cause rhabdomyolysis. The most common positions leading to rhabdomyolysis are the lateral decubitus, lithotomy, sitting, knee-to-chest, and prone position. The primary mechanism is reperfusion of damaged tissue after a period of ischemia, and the release of necrotic muscle material into the circulation after pressure is relieved. The risk factors for position-related rhabdomyolysis were identified as body weight more than 30% above ideal body weight, duration of surgery more than 5–6 h, extracellular volume depletion, preexisting azotemia, diabetes, and hypertension.


Infections that cause rhabdomyolysis are bacterial, viral, fungal, and protozoal.

Viral infections

Influenza Types A and B; HIV, coxsackievirus, Epstein–Barr virus, echovirus, cytomegalovirus, adenovirus, herpes simplex virus, parainfluenza, varicella zoster virus, and West Nile virus.

Bacterial infections

Legionella, Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus viridans, Salmonella species, Staphylococcus epidermidis, Francisella tularensis, Streptococcus faecalis, meningococci, Haemophilus influenzae, Escherichia coli, Pseudomonas, Klebsiella, Enterococcus faecalis, Bacteroides, Group B Streptococcus, Streptococcus pyogenes, Listeria species, Vibrio species, Leptospira species, Brucella species, Bacillus species, and Clostridium species.

Electrolyte and endocrine abnormalities

Hyponatremia, hypernatremia, hypokalemia, and hypophosphatemia are the electrolytic abnormalities that cause rhabdomyolysis. Hypothyroidism or hyperthyroidism, diabetic ketoacidosis, and nonketotic hyperosmolar diabetic coma are the endocrine abnormalities that cause rhabdomyolysis.


Toxins are CO, snake bites, spider venom, massive honey bee and wasps envenomation, and quail eating.

Genetic disorders

Enzyme deficiencies (of carbohydrate or lipid metabolism) and myopathies can cause rhabdomyolysis.

Connective tissue disorders

Polymyositis, dermatomyositis, and Sjögren's syndrome can cause rhabdomyolysis.

Fentanyl is a very commonly used opioid in the hospital setting, especially in the perioperative and procedural areas.[4] Fentanyl is a synthetic phenylpiperidine opioid that binds with receptors to provide analgesia. It is a 5-HT1A agonist, which augments serotonin release, and through weak serotonin reuptake inhibition, increases intrasynaptic serotonin levels. It requires the additive action of other serotonergic agents or use in combination with SSRIs. Oxycodone is a centrally acting synthetic morphine analog acting on κ and μ receptors to provide analgesia. It may cause increased serotonin-like activity at the synaptic level by direct action on postsynaptic membranes mimicking serotonin activity or may release serotonin through an unknown opioid-mediated release.[5]

Serotonin syndrome is a potentially life-threatening syndrome that often is misdiagnosing. It is precipitated by the use of serotonergic drugs and over-activation of both the peripheral and central postsynaptic 5HT-1A and most notably 5HT-2A receptors. This syndrome consists of a combination of mental status changes, neuromuscular hyperactivity, and autonomic hyperactivity.[6]

Many clinicians use five times the upper limit of normal CPK, approximately 850–1000 U/L.[7] A serum CPK five times the normal value is considered as a biochemical diagnosis of rhabdomyolysis. High values are pathognomonic for rhabdomyolysis because no other condition will lead to such extreme CPK elevation. The elevation in CPK levels is the most sensitive diagnostic evidence of muscle injury and is present in 100% of rhabdomyolysis cases.

Myoglobin levels were not assessed because the half-life of myoglobin is particularly short (2–3 h) since its clearance from the plasma is achieved rapidly through renal excretion or catabolism to bilirubin. In rhabdomyolysis, the level of myoglobin in the serum increases within 1–3 h, reaches its peak in 8–12 h, and then returns to normal within 24 h after the onset of the injury.[8]

Rhabdomyolysis constitutes a severe medical emergency that requires immediate recognition and prompt diagnosis to prevent late complications.[8] Fluid sequestration by the injured muscle cells causes volume depletion with subsequent prerenal azotemia. Acute renal failure (ARF) and hyperkalemia are the major complications that worsen the prognosis of rhabdomyolysis.[9] The risk factors for position-related rhabdomyolysis were identified as body weight more than 30% above ideal body weight, duration of surgery more than 5–6 h, extracellular volume depletion, preexisting azotemia, diabetes, and hypertension.[2]

The treatment of rhabdomyolysis is geared toward preserving renal function by preventing factors that can lead to ARF. Intravascular volume expansion with NaCl 0.9% is crucial for the prevention of myoglobinuric ARF (ARF is defined as a measurable increase in the serum creatinine concentration, usually relative increase of 50% or absolute increase by 0.5–1.0 mg/dL, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys.[10],[11] It may be associated with oliguria or normal urine output [12]). Moreover, the objective is to achieve at least 300 ml/h urine excretion. Alkalization of urine using intravenous administration of NaHCO3 with objective of reach a urine pH above 6.5 and a serum pH between 7.40 and 7.45 can be helpful. The alkaline pH of urine increases the solubility of myoglobin and uric acid and limits the formation of myoglobin casts and uric acid crystals. After hypovolemia is corrected, the patient should be subjected to forced diuresis, which is achieved through intravenous administration of mannitol and/or one of the Henle's loop diuretics, such as furosemide. Mannitol is an osmolar diuretic that improves renal perfusion and glomerular filtering and acts on the proximal convoluted tubules, contributing to the excretion of myoglobin. Furosemide prevents the accumulation of myoglobin in distal convoluted tubule. Other supportive treatment as treatment of electrolyte disorders and metabolic acidosis: hyperkalemia, hypocalcemia, and hyperphosphatemia; Hemodialysis in the case of severe hyperkalemia, persistent metabolic acidosis and ongoing ARF; In situ ation of compartment syndrome, when the intra-compartmental pressure exceeds 40 mm Hg, direct surgical decompression with fasciotomy is indicated.[9] CPK is the marker most commonly used to guide the diagnosis and therapy in daily clinical practice.[7]

Postoperative delirium is a form of delirium that manifests in patients who have undergone surgical procedures and anesthesia, usually peaking between 1 and 3 days after their operation. In diagnosing delirium, there are no definitive laboratory tests, and the differential diagnosis for acute abnormalities of cognition and attention is broad. A complete blood count, electrolyte panel, glucose measurement, arterial blood gas, urine analysis, and electrocardiography should be considered in all patients with acute confusion to rule out correctable conditions such as hypoxia, hypoglycemia, and electrolyte imbalance.[13]

In our patient, he meets with several causes or conditions that contribute to the occurrence of rhabdomyolysis such as diabetes, hypertension, obesity, intraoperative hypotension, hemodynamic complications, dehydration, and prolonged operative time. The diagnosis of rhabdomyolysis requires a high degree of clinical suspicion and attention by the surgeon as it can be asymptomatic. Rhabdomyolysis causing ARF is a rare but serious postoperative complication.[14] Prudential prevention in high-risk patients, prompt diagnosis, and intensive treatment with closely monitoring are the highlights of treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Ettinger J, Batista P, Azaro E. Post-operative rhabdomyolysis. In: Alvarez A, editor. Morbid Obesity. 2nd ed. Cambridge, CA: Cambridge University Press; 2010.  Back to cited text no. 1
Khan FY. Rhabdomyolysis: A review of the literature. Neth J Med 2009;67:272-83.  Back to cited text no. 2
Keltz E, Khan FY, Mann G. Rhabdomyolysis. The role of diagnostic and prognostic factors. Muscles Ligaments Tendons J 2014;3:303-12.  Back to cited text no. 3
Koury KM, Tsui B, Gulur P. Incidence of serotonin syndrome in patients treated with fentanyl on serotonergic agents. Pain Physician 2015;18:E27-30.  Back to cited text no. 4
Rastogi R, Swarm RA, Patel TA. Case scenario: Opioid association with serotonin syndrome: Implications to the practitioners. Anesthesiology 2011;115:1291-8.  Back to cited text no. 5
Volpi-Abadie J, Kaye AM, Kaye AD. Serotonin syndrome. Ochsner J 2013;13:533-40.  Back to cited text no. 6
El-Abdellati E, Eyselbergs M, Sirimsi H, Hoof VV, Wouters K, Verbrugghe W, et al. An observational study on rhabdomyolysis in the Intensive Care Unit. Exploring its risk factors and main complication: Acute kidney injury. Ann Intensive Care 2013;3:8.  Back to cited text no. 7
Giannoglou GD, Chatzizisis YS, Misirli G. The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. Eur J Intern Med 2007;18:90-100.  Back to cited text no. 8
Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome of rhabdomyolysis: Complications and treatment. Eur J Intern Med 2008;19:568-74.  Back to cited text no. 9
Kasper D, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J. Acute renal failure. Harrison's Manual of Medicine. 19thed., Ch. 138, McGraw-Hill Education; 2016.  Back to cited text no. 10
Waikar SS, Bonventre JV. Acute Kidney Injury. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J. Harrison's Principles of Internal Medicine 19th ed., Ch. 334. McGraw-Hill Education; 2015.  Back to cited text no. 11
Yaqub MS, Molitoris BA. Acute Kidney Injury. In: Lerma EV, Berns JS, Nissenson AR. CURRENT Diagnosis & Treatment: Nephrology & Hypertension. Ch. 9. McGraw-Hill Lange; 2009.  Back to cited text no. 12
Whitlock EL, Vannucci A, Avidan MS. Postoperative delirium. Minerva Anestesiol 2011;77:448-56.  Back to cited text no. 13
Dequanter D, Vercruysse N, Shahla M, Paulus P, Lothaire P. Rhabdomyolysis in head and neck surgery. Royal Belgian Soc Ear, Nose, Throat, Head & Neck Surgery 2014;10:171-3.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3]


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