Olgu Sunumu: Nadir bir nedenden dolayı rabdomiyoliz gelişen ileri yaşta bir kadın hasta sunuyoruz: intrakraniyal kitle lezyonlarıyla ilişkili beyin ödemine bağlı akut kuadripareze sekonder rabdomiyoliz.

Sonuç: Rabdomiyoliz nörolojik patolojiler sonucu gelişen akut kuadripareziye bağlı nadir görülen bir komplikasyon olabilir. Rabdomiyoliz hayatı tehdit edebilecek sonuçlar doğurabileceği için klinisyenlerce erken tanı ve tedavisi önemlidir.

In this article, we present a case in which rhabdomyolysis occurs due to an uncommon cause: Rhabdomyolysis secondary to acute quadriparesis due to brain edema associated with intracranial mass lesions.

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Table 1: Laboratory values of the patient.

The patient was hospitalized in the Nephrology service with a pre-diagnosis of rhabdomyolysis and hydration treatment was started. The patient’s CK enzyme level started to decrease. However because of decreased muscle strength, impaired consciousness, not being able to recognize his relatives and having meaningless speech, she was consulted with the neurology department. Brain computed tomography and diffusion MR images revealed multiple intracranial mass lesions and brain edema due to these lesions (Figure 1). During 3 days, 1000 mg/day intravenous methylprednisolone treatment was administered. Partial improvement was observed in the confusion and, in the light of clinical and radiological diagnosis, biopsy was planned for pathologic diagnosis. In this case; there was no traumatic, pharmacologic, toxic, infectious factor and electrolyte disorder that may cause rhabdomyolysis other than quadriparesis due to brain edema associated with intracranial mass lesions. This is an exceptional state that causes rhabdomyolysis in the light of the literature.

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Figure 1: The T2 flair axial and sagittal post-contrast T1 weighted brain MRI image demonstrates multiple intracranial mass lesions and brain edema

The most common causes of rhabdomyolysis are drug or alcohol abuse, drug use, trauma, excessive exercise, infections, electrolyte imbalances, neuromuscular causes, and inactivity. Rhabdomyolysis may also be caused by tightening of the muscles and being in the same position for a long time. The pathogenesis of rhabdomyolysis is related to direct sarcolemic injury or depletion of ATP in myocytes and leads to irregular leakage of calcium ions into cells ⁴. Sarcoplasmic calcium is strictly regulated by energy-dependent ion pumps such as Na+/ K+ATPase and Ca+2 ATPase in sarcolemma. These pumps keep calcium levels in resting muscle low, but allow actin-myosin binding and increase in calcium levels when muscle contraction is required. Regardless of the underlying mechanism, muscle injury increases sarcoplasmic calcium and causes persistent contraction. Finally, there is muscle fiber necrosis after activation of the cell protease. Then, potassium, phosphate, myoglobin, CK and uric acid are released out of the cell into the systemic circulation ⁵. Rhabdomyolysis is clinically characterized by myalgia, red-brown urine due to myoglobinuria, and increased serum muscle enzymes ⁶.

Taştekin et al. ^7, presented two rhabdomyolysis cases with rare etiologic factors. One developed acute renal failure associated with rhabdomyolysis after epileptic seizure and other developed acute renal failure associated with rhabdomyolysis after swimming. With these rare cases, they emphasized that epileptic seizures and excessive exercise such as swimming can cause rhabdomyolysis.

Statins are well decsribed and frequent cause of drug- induced rhabdomyolysis ⁸.

On the other hand systemic diseases such as Henoch- Schonlein purpura may be a rare and surprising cause of rhabdomyolysis. In their report, Turan MI et al ^9, treated HSP caused rhabdomyolysis case successfully with appropriate fluid and steroid treatment.

In the present rhabdomyolysis case we represent here, all other causes of etiologic factors excluded, and it was caused by a very exceptional etiology due to quadriparesis caused by brain edema associated with intracranial mass lesions.

1) Sauret JM, Marinides G, Wang GK. Rhabdomyolysis. Am Fam Physician 2002; 65: 907-912.

2) Huerta-Alard ́ın AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis - an overview for clinicians. Crit Care 2005; 9: 158-169.

3) Lima RS, da Silva Junior GB, Liborio AB. Acute kidney injury due to rhabdomyolysis. Saudi J Kidney Dis Transpl 2008; 19: 721-729.

4) Giannoglou GD, Chatzizisis YS, Misirli G. The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. European Journal of Internal Medicine 2007;18: 90-100.

5) Khan. FY. Rhabdomyolysis: A review of the literature. Neth J Med 2009; 67: 272-283.

6) Akbaş EM, Özlü C, Ünver E (Editörler). Gürel A. Rabdomiyoliz. Dahili Aciller. 1. Baskı, İstanbul: Akademisyen Kitabevi, 2020.

7) Taştekin F, Sırmatel P, Şahin G. Rabdomiyolizin nadir sebepleri; Epileptik nöbet ve yüzmeden sonra rabdomiyoliz. Turk Neph Dial Transpl 2018; 27: 93-95.

8) Yıldırım T, Ede H, Özdemir ZT, Börekçi E. Statine bağlı rabdomiyoliz: Olgu sunumu. Bozok Tıp Derg 2015; 5: 75-79.

9) Turan Mı, Cayir A. Henoch-Schönlein Purpurasına Bağlı Şiddetli Rabdomiyoliz: Bir vaka takdimi. Medicine Science 2014; 3: 1525-1529.