Journal of The Korean Society of Clinical Toxicology

Rhabdomyolysis induced by venomous snake bite: Lee Jungho, Moon Jeongmi, Chun Byeongjo; J Korean Soc Clin Toxicol. 2022;20(2):51-57. Published online December 31, 2022; DOI: https://doi.org/10.22537/jksct.2022.20.2.51

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Abstract PDF: Purpose: Despite previous studies reporting the development of rhabdomyolysis (RM), this affliction tends to be neglected as an envenomation sign in South Korea. The current retrospective study investigates the prevalence and prognosis of RM after a snakebite. We further searched for predictors of snakebite-induced RM, which can be observed at presentation. Methods: This study included 231 patients who presented to the ED within 24 hours after a snakebite. The patients were classified according to the severity of RM, and the data, comprising baseline characteristics and clinical course including the level of creatine kinase (CK), were collected and compared according to the severity of RM. Results: The prevalence of RM and severe RM were determined to be 39% and 18.5%, respectively. Compared to the group without RM or with mild RM, the group with severe RM had a higher grade of local swelling, a higher frequency of acute kidney injury and neurotoxicity, and a greater need for renal replacement therapy and vasopressor administration. However, the incidence of acute renal injury in the RM group was 7.7%, with two patients needing renal replacement therapy. No mortalities were reported at discharge. Results of the multinomial logistic regression model revealed that the WBC levels are significantly associated with the risk of severe RM. Conclusion: RM should be considered the primary clinical sign of snake envenomation in South Korea, although it does not seem to worsen the clinical course. In particular, physicians should pay attention to patients who present with leukocytosis after a snakebite, which indicates the risk of developing RM, regardless of the CK level at presentation.

Delayed death after chlorfenapyr poisoning: Jang Young Lee; J Korean Soc Clin Toxicol. 2021;19(1):51-54. Published online June 30, 2021; DOI: https://doi.org/10.22537/jksct.2021.19.1.51

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Chlorfenapyr is a widely used insecticide, that is very lethal if ingested. It exhibits delayed toxicity in which there are few symptoms at first which suddenly worsen after a few days. A 66-year-old female patient ingested about 90 mL of chlorfenapyr liquid hydrating agent (Chlofenapyr 10%) and showed stable vital signs with no specific symptoms and findings other than a mild fever, vomiting, and nausea. From the 3rd day of ingestion, creatine kinase was high, and rhabdomyolysis was suspected. From the 4th day of ingestion, pancreatic enzymes began to gradually increase. A diffusion-weighted image showed a multifocal high signal intensity in the white matter and corpus callosum area. On the 8th day after ingestion, she suffered a high fever and a heart attack and died. Thus, if a patient is suspected of taking chlorfenapyr, he/she needs active treatment and monitoring even if he/she does not exhibit any symptoms.

Citations

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Toxicological Review of an Uncoupler, Chlorfenapyr
Sun Cheun Kim
Korean Journal of Legal Medicine.2025; 49(2): 35. CrossRef
A Fatal Case of Chlorfenapyr Poisoning and the Therapeutic Implications of Serum Chlorfenapyr and Tralopyril Levels
Ming-Jin Chung, Yan-Chiao Mao, Chia-Tien Hsu, Mu-Chi Chung, Tsai-Jung Wang, Tung-Min Yu, Po-Yu Liu, Pin-Kuei Fu, Chia-Ming Hsieh
Medicina.2022; 58(11): 1630. CrossRef

Motor Peripheral Neuropathy Involved Bilateral Lower Extremities Following Acute Carbon Monoxide Poisoning: A Case Report: Jae-Hyung Choi, Hoon Lim; J Korean Soc Clin Toxicol. 2015;13(1):46-49. Published online June 30, 2015

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Abstract PDF: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

The Predictive Factors of the Serum Creatine Kinase Level Normalization Time in Patients with Rhabdomyolysis due to Doxylamine Ingestion: Min-Chul Shin, Oh-Young Kwon, Jong-Suk Lee, Han-Sung Choi, Hoon-Pyo Hong, Young-Gwan Ko; J Korean Soc Clin Toxicol. 2009;7(2):156-163. Published online December 31, 2009

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Abstract PDF: Purpose: Doxylamine succinate (DS) is frequently used to treat insomnia and it may induce rhabdomyolysis in the overdose cases. The purpose of this study is to evaluate the factors that can predict the serum creatine kinase (CK) level normalization time for patients with rhabdomyolysis due to DS ingestion. Methods: This study was conducted on 71 patients who were admitted with rhabdomyolysis after DS ingestion during the period from January 2000 to July 2009. Rhabdomyolysis was defined as a serum CK level over 1,000 U/L. The collected data included the general characteristics, the anticholinergic symptoms, the ingested dose, the peak serum CK level, the time interval (TI) from the event to the peak CK level and the TI from the event to a CK level below 1,000 U/L. We evaluated the correlation between the patients' variables and the TI from the event to the peak CK level time and the time for a CK level below 1,000 U/L. Results: The mean ingested dose per body weight (BW) was $30.86{pm}18.63;mg/kg$ and the mean TI from the event to treatment was $4.04{pm}3.67$ hours. The TI from the event to the peak CK level was longer for the patients with a larger ingestion dose per BW (r=0.587, p<0.05). The CK normalization time was longer for the patients with a larger ingested dose per BW (r=0.446, p<0.05) and a higher peak CK level (r=0.634, p<0.05). Conclusion: The ingested dose per BW was correlated with the TI from the event to the peak CK level, and the ingested dose per BW and the peak CK level have significant correlations with the CK normalization time. These factors may be used to determine the discharge period of patients who had rhabdomyolysis following a OS overdose.

Rhabdomyolysis after Lamotrigine Poisoning: A Case report: Gun-Bea Kim, Hong-Du Gu; J Korean Soc Clin Toxicol. 2008;6(2):142-145. Published online December 31, 2008

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Abstract PDF: Lamotrigine is a newer anti-epileptic drug for adjunctive treatment of refractory epilepsy, partial seizures, generalized tonic-clonic seizures, and bipolar disorder. Lamotrigine overdose causes serious central nervous and cardiovascular problems, but reports are uncommon. Few lamotrigine overdoses have been described because anti-epileptic drug use is limited and usually used with combination of other anti-epileptic drugs. In addition, most patients visit emergency departments with multi-drug overdoses, so few cases of lamotrigine poisoning alone exist. We had a female patient visit our emergency department a couple of hours after a lamotrigine overdose treated with intravenous hydration and urine alkalization by NaHCO3. She recovered successfully without any evidence of renal injury. However, she developed profound rhabdomyolysis, a previously unreported complication of this medication. We suggest that serial creatine kinase levels should be measured after lamotrigine poisoning.

A Case of Rhabdomyolysis after Alprazolam Overdose: Sung-Ho Ki, Hyun-Joo Park, Woong-Gil Choi, Hyung-Keun Roh; J Korean Soc Clin Toxicol. 2004;2(2):151-153. Published online December 31, 2004

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Abstract PDF: Causes of rhabdomyolysis can be divided into traumatic and nontraumatic, Among the nontraumatic rhabdomyolysis, it is known that ingestion of drugs is one of the common causes. However, there have been few reports that benzodiazepine overdose causes rhabdomyolysis, moreover there was no report about rhabdomyolysis after alprazolam overdose. We experienced a case of rhabdomyolysis after alprazolam overdose. A 51-year-old woman was brought to the emergency room 11 hours after ingestion of 30 tablets (15 mg) of alprazolam in a suicidal attempt. On admission she was comatose and her CK level was 8,290 lUlL. The CK level increased up to 25,598 IU/L 10 hours after admission, but she became alert on the third day. Subsequently the CK level decreased gradually with supportive care without renal impairment and she discharged from the hospital on the $10^{th}$ day. Although a pressure effect on the dependent portion of the body due to mental alteration before admission might have caused the rhabdomyolysis, the alprazolam, per se, cannat be ruled out for the cause.

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