Rhabdomyolysis, Acute Renal Failure, and Multiple Focal

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with bullous formation, with the symptoms having first been noted .... of myoglobinuric renal failure following a centipede bite ... syndrome after an alcohol binge.
RENAL FAILURE Vol. 26, No. 1, pp. 93–97, 2004

CASE REPORT

Rhabdomyolysis, Acute Renal Failure, and Multiple Focal Neuropathies After Drinking Alcohol Soaked with Centipede I-Kuan Wang,1 Shih-Pin Hsu,2 Ching-Chi Chi,3 Kam-Fai Lee,4 Paul Yann Lin,4 Hsueh-Wen Chang,5 and Feng-Rong Chuang1,* 1

Division of Nephrology, 2Neurology, 3Dermatology, and 4Pathology, Chang Gung Memorial Hospital at Chiayi, Taiwan 5 Department of Biology, National Sun Yat-Sen University, Kaohsiung, Taiwan

ABSTRACT Many Chinese like to drink alcohol soaked with creatures for promoting health. This study reports a 49-year-old male who presented with multiple focal neuropathies of the upper limbs, coagulopathy, erythematous swelling of the bilateral upper extremities and trunk with bullous skin lesions, and rhabdomyolysis associated with acute renal failure after drinking alcohol soaked with centipede. Soaking a centipede, Scolopendra subspinipes mutilans, in 53% alcohol, produced the wine. Supportive treatment was administered, and the skin lesions and renal failure improved with subsequent neurologic deficit during the week following initial presentation. Alcohol binge or immobilization was the likely cause of neuropathy, bullous skin lesions and rhabdomyolysis in the patient. However, there is a possibility that centipede venom also contributed to the illness in this patient. Key Words:

Neuropathy; Rhabdomyolysis; Centipede.

circulatory system. Massive rhabdomyolysis can cause life-threatening disseminated intravascular coagulation, hyperkalemia, myoglobinuric renal failure and various other complications.[1 – 3] Animal venoms have been identified as causes of rhabdomyolysis.[1 – 4] Many

INTRODUCTION Rhabdomyolysis refers to the disintegration of striated muscle, which causes the release of muscular cell constituents into the extracellular fluid and the

*Correspondence: Feng-Rong Chuang, Division of Nephrology, Chang Gung Memorial Hospital, Chiayi, 6 West Chia-Pu Road, Putz, Chiayi, Taiwan; Fax: 886-5-3623002; E-mail: [email protected]. 93 DOI: 10.1081/JDI-120028562 Copyright D 2004 by Marcel Dekker, Inc.

0886-022X (Print); 1525-6049 (Online) www.dekker.com

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Chinese like to drink alcohol soaked with creatures for promoting health. This study reports a 49-year-old male who developed multiple focal neuropathies, bullous skin lesions, and myoglobinuric renal failure after drinking 53% alcohol infused with a centipede, Scolopendra subspinipes mutilans.

CASE REPORT A 49-year-old male patient was admitted to our hospital with the chief complaint of erythematous swelling of the bilateral upper extremities and trunk, with bullous formation, with the symptoms having first been noted upon waking that morning. The patient, a chronic alcoholic, had drunk 600 mL strong wine over the two days prior to admission. The wine was produced by soaking a centipede, Scolopendra subspinipes mutilans, measuring 14 cm, in 53% alcohol (Figure 1). On the night before admission the patient got drunk and slept on the floor, and was squeezed in a narrow space. The next morning, the patient developed erythematous swelling of the bilateral upper extremities with bullous formation, along with several discrete small vesicles over the bilateral thighs. Moreover, the patient also developed dropping of the right hand, impaired left hand grasping, and paresthesic sensation of bilateral hands. Accordingly, the patient was ad-

Figure 2. (A) Erythematous swelling of the left upper extremity with several bullous eruptions is seen. (B) Erythematous swelling of the trunk with blisters is seen. (View this art in color at www.dekker.com.)

Figure 1. The wine was made from soaking a centipede, Scolopendra subspinipes mutilans, in 53% alcohol. (View this art in color at www.dekker.com.)

mitted for treatment. The patient’s past medical history included hypertension for 10 years and gout for 5 years, both untreated. On arrival, the patient had a body temperature of 36.8°C, pulse of 128 per minute, respiratory rate of 20 per minute, and blood pressure of 123/61 mmHg. Physical examination revealed erythematous swelling of the left upper extremity, right forearm, and trunk with bullous formation (Figures 1 and 2). Several discrete vesicles were also noted over the bilateral thighs. Furthermore, the patient exhibited dropping in his right hand, inability to grasp in his left hand, and paresthesic sensation in both hands. Laboratory examination (Table 1) revealed a white blood count of 21500/mm3 with a differential count of

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Complications After Drinking Alcohol Soaked with Centipede Table 1.

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Summary of laboratory data. Day after admission

Normal value White blood cells Hemoglobin Platelets Prothrombin time Activated partial thromboplastin time Urea Creatinine Creatinine phosphokinase Aspartate aminotransferase Bilirubin Alkaline phosphatase Myoglobin Uric acid Sodium Potassium Calcium Phosphate

1 3

3.9 – 10.6K/mm 13.5 – 17.5 g/dL 150 – 400K/mm3 11.0 seconds 29.1 seconds

21500 14.0 301 23.4 > 100

6 – 21 mg/dL 0.4 – 1.4 mg/dL 15 – 130 U/L 0 – 34 U/L 0 – 1.3 mg/dL 28 – 94 U/L < 80 mg/L < 8.0 mg/dL 134 – 148 meq/L 3.0 – 4.8 meq/L 7.9 – 9.9 meq/dL 2.4 – 4.7 meq/dL

23 2.0 75257 433 1.3

87% segments, 0.5% bands, 8% lymphocytes, and 3.5% monocytes. Laboratory examination also found hemoglobin 14.0 g/dL, prothrombin time 23.4 seconds with a control of 11.0 seconds and activated partial thromboplastin time of over 100 seconds with a control of 29.1 seconds. Urinalysis showed protein 75 mg/dL, 4 +

5

7

9

25 2.2 1092

18 1.7

147 2.5

142 2.7

9.9 22.5 40 4.2 10862

54 23543.64 135 3.8

10.0 141 2.7 7.4 3.9

occult blood test, and 5– 8 red blood cells per high power field. Moreover, blood chemistry tests revealed urea nitrogen 23 mg/dL, creatinine 2.0 mg/dL, aspartate aminotransferase 433 U/L, sodium 135 meq/L, potassium 3.8 meq/dL, myoglobin 23543.64 mg/L and creatinine phosphokinase 75257 U/L. Arterial blood gas

Figure 3. There is ischemic necrosis of epidermis, sweat glands and mild leukocytoclastic vasculitis. (Hematoxylin and eosin strain; original magnification, *100). (View this art in color at www.dekker.com.)

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under room air showed PH 7.336; PaCO2 15.7 mmHg; PaO2 93.2 mmHg; HCO3 8.2 mmol/L. Furthermore, renal sonography displayed slight enlargement of bilateral kidneys without parenchymal defect. Pathology of skin biopsy (Figure 3) demonstrated ischemic necrosis of epidermis, sweat glands and intravascular thrombus formation. Mild leukocytoclastic vasculitis was also observed. Immunofluorescence study of skin biopsy was negative. Under the diagnosis of acute renal failure owing to rhabdomyolysis, the patient was treated with intravenous isotonic saline. Additionally, hydrocortisone, 100 mg intravenous every 8 hours for 1 week was prescribed for bullous skin lesions. Renal replacement therapy was not performed because of the lack of uremic symptoms and signs. Renal function and skin lesions gradually improved during the subsequent week. On the 9th hospitalization day, blood chemistry tests revealed urea nitrogen of 18 mg/dL and creatinine of 1.7 mg/dL. However, neurologic deficits of bilateral hands with paresthesia still persisted. Finally, nerve conduction study revealed multiple sensory and focal motor neuropathies with conduction block at the forearm level on the left median nerve, left ulnar nerve, and right radial nerve. The patient was discharged and underwent rehabilitation in the outpatient department.

DISCUSSION In English medical literature, myoglobinuric renal failure was first noted among victims of crush injuries during the wartime bombing of London.[5] Since then, additional etiologies of rhabdomyolysis have been identified, including infections, electrolyte imbalances, hereditary enzyme deficiencies, excessive exertion, seizures, drugs, and toxins.[1 – 3] Drugs and toxins can cause rhabdomyolysis by inducing coma leading to limb compression, excessive muscular activity, hyperthermia, vasoconstriction with resultant muscle ischemia, impaired ATP formation, hypokalemia and hypophosphatemia, myositis secondary to hypersensitivity reaction and direct toxic effects.[2,3] Alcohol is the leading cause of nontraumatic rhabdomyolysis. One study found that alcohol was involved in 67% of 87 episodes of rhabdomyolysis.[1] Notably, among patients with acute or chronic alcohol intoxication, muscular dysfunction can be attributed to a combination of immobilization, hypokalemia, hypophosphatemia, agitation, and/or direct myotoxicity.[2,3] Envenomation following bites or stings by various venomous creatures, including bees, spiders, hornets, centipedes, and various snakes, or following the inges-

tion of quails and certain fish species (Haff disease) has been reported to cause rhabdomyolysis.[2 – 4] Centipedes are segmented arthropods found in both tropical and subtropical regions. Centipedes are nocturnal, fast moving, and use their venom to paralyze other insects or even small animals before eating them. Despite being poisonous, centipedes are still used as an ingredient in traditional Chinese medicine. Most cases of centipede envenomation result from centipede bites.[4,6 – 8] Centipede bites typically result in local reactions such as immediate localized burning pain, erythema, bullae, superficial skin necrosis, rashes, edema, numbness, and paresis.[6 – 8] In India, systemic reactions of centipede bites include nausea and vomiting (5.8%), dizziness (5.8%), headache (8.1%), restlessness (5.8%), sweating (2.3%), lymphangitis and adenopathy (4.7%), tachycardia (12%) and fever (9.3%).[8] Only one case of poisoning from centipede ingestion has been reported.[9] This case involved the ingestion of a Scutigera morpho centipede by a 6-month-old, causing lethargy and a pale, floppy child.[9] No skin lesion was noted in this case. Centipede venom has been reported to contain histamine and serotonin.[10] Mohamed et al. reported that the venom extracted from centipedes Scolopendra morsitans contained phospholipids, cholesterol, free fatty acids, triglycerides, cholesterol esters, squalene, the enzyme esterase, alkaline phosphatases, amino acid naphthylamidase, and acid phosphatase.[11] Anticoagulation and coagulant components have also been identified.[12] Absorption from the stomach occurs if the venom is acid stable, but the PH stability of centipede venom has not been studied. To date, no antitoxin exists. The treatment of centipede envenomation is symptomatic and supportive. The patient reported here developed myoglobinuric renal failure, erythematous swelling of the bilateral upper extremities and trunk with bullous lesions, neurologic deficits of bilateral hands, and coagulopathy after drinking alcohol soaked with centipede. Only one case of myoglobinuric renal failure following a centipede bite has been reported, and this case occurred following the bite of the giant desert centipede, Scolopendra heros.[4] Possible causes of rhabdomyolysis in the present case included alcohol and toxic effects of centipede, and compartment syndrome following limb compression. Additionally, possible etiologies of the neurologic deficits in the present case included compartment syndrome following rhabdomyolysis,[13,14] direct toxic effects of alcohol, toxic effects of centipede, or limb compression after alcohol binge. After supportive and symptomatic treatment, both renal function and skin lesions recovered in the present patient. However, the recovery of neurological deficits remained incomplete.

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In conclusion, alcohol is a common cause of rhabdomyolysis. Alcohol binge or immobilization was the likely cause of neuropathy, bullous skin lesions and rhabdomyolysis in the patient. However, there is a possibility that centipede venom also contributed to the illness in this patient. Further investigation should be conducted to assess the toxicity of alcohol soaked with centipede.

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Gabow, P.A.; Kaehny, W.D.; Kelleher, S.P. The spectrum of rhabdomyolysis. Medicine 1982, 61, 141 – 152. Curry, S.C.; Chang, D.; Connor, D. Drug- and toxin-induced rhabdomyolysis. Ann. Emerg. Med. 1989, 18, 1068 –1084. Vanholder, R.; Sever, M.S.; Erek, E.; Lameire, N. Rhabdomyolysis. J. Am. Soc. Nephrol. 2000, 11, 1553– 1561. Logan, J.L.; Ogden, D.A. Rhabdomyolysis and acute renal failure following the bite of the giant desert centipede Scolopendra heros. West. J. Med. 1985, 142, 549 –550. Bywaters, E.G.L.; Beall, D. Crush injuries with impairment of renal function. Br. Med. J. 1941, 1, 427 – 432. Lin, T.J.; Yang, C.C.; Yang, G.Y.; Ger, J.; Tsai, W.J.; Deng, J.F. Features of centipede bites in Taiwan. Trop. Geogr. Med. 1995, 47, 300– 302.

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Mohri, S.; Sugiyama, A.; Saito, K.; Nakajima, H. Centipedes bites in Japan. Cutis 1991, 47, 189– 190. Uppal, S.S.; Agnihotri, V.; Ganguly, S.; Badhwar, S.; Shetty, K.J. Clinical aspects of centipede bite in the Andamans. J. Assoc. Phys. India 1990, 38, 163– 164. Barnett, P.L.J. Centipede ingestion by a six-monthold infant: toxic side effects. Pediatr. Emerg. Care 1991, 7, 229– 230. Gomes, A.; Datta, A.; Sarangi, B.; Kar, P.K.; Lahiri, S.C. Occurrence of histamine and histamine release by centipede venom. Indian J. Med. Res. 1982, 76, 888– 891. Mohamed, A.H.; Abu-Sinna, G.; El-Shabaka, H.A.; El-Aal, A.A. Proteins, lipids, lipoproteins and some enzyme characterizations of the venom extract from the centipede Scolopendra morsitans. Toxicon 1983, 21, 371 –377. Jangi, B.S. Centipede venoms and poisoning. In Handbook of Natural Toxins Vol. 2, Insect Poisons, Allergens, and Other Invertebrate Venoms; Tu, A., Ed.; Marcel Dekker: New York, 1984; 333. Sofat, N.; Bell, S.; Turner, J.; Warrens, A.N. A case of acute renal failure and compartment syndrome after an alcohol binge. J. Accid. Emerg. Med. 1999, 16, 296– 298. Maddison, P. Acute rhabdomyolysis and brachial plexopathy following alcohol ingestion. Muscle Nerve 2002, 25, 283 –285.

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