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.
Purpose: A high anion gap (AG) is known to be a significant risk factor for serious acid-base imbalances and death in acute poisoning cases. The strong ion difference (SID), or strong ion gap (SIG), has recently been used to predict in-hospital mortality or acute kidney injury (AKI) in patients with systemic inflammatory response syndrome. This study presents a comprehensive acid-base analysis in order to identify the predictive value of the SIG for disease severity in severe poisoning. Methods: A cross-sectional observational study was conducted on acute poisoning patients treated in the emergency intensive care unit (ICU) between December 2015 and November 2020. Initial serum electrolytes, base deficit (BD), AG, SIG, and laboratory parameters were concurrently measured upon hospital arrival and were subsequently used along with Stewart's approach to acid-base analysis to predict AKI development and in-hospital death. The area under the receiver operating characteristic curve (AUC) and logistic regression analysis were used as statistical tests. Results: Overall, 343 patients who were treated in the intensive care unit were enrolled. The initial levels of lactate, AG, and BD were significantly higher in the AKI group (n=62). Both effective SID [SIDe] (20.3 vs. 26.4 mEq/L, p<0.001) and SIG (20.2 vs. 16.5 mEq/L, p<0.001) were significantly higher in the AKI group; however, the AUC of serum SIDe was 0.842 (95% confidence interval [CI]=0.799-0.879). Serum SIDe had a higher predictive capacity for AKI than initial creatinine (AUC=0.796, 95% CI=0.749-0.837), BD (AUC=0.761, 95% CI=0.712-0.805), and AG (AUC=0.660, 95% CI=0.607-0.711). Multivariate logistic regression analyses revealed that diabetes, lactic acidosis, high SIG, and low SIDe were significant risk factors for in-hospital mortality. Conclusion: Initial SIDe and SIG were identified as useful predictors of AKI and in-hospital mortality in intoxicated patients who were critically ill. Further research is necessary to evaluate the physiological nature of the toxicant or unmeasured anions in such patients.
Copper sulfate is widely used as a fungicide and pesticide. Acute copper sulfate poisoning is rare but potentially lethal in severe cases. Copper sulfate can lead to cellular damage of red blood cells, hepatocytes, and myocytes. Toxic effects include intravascular hemolysis, acute tubular necrosis and, rhabdomyolysis. A 76-year-old man presented with vomiting and epigastric pain. He had ingested a copper-containing fungicide (about 13.5 g of copper sulfate) while attempting suicide 2 hours prior to presentation. From day 3 at the hospital, laboratory findings suggesting intravascular hemolysis were noted with increased serum creatinine level. He was treated with a chelating agent, dimercaptosuccinic acid (succimer). His anemia and acute kidney injury gradually resolved with a 19-day regimen of succimer. Our case suggests that succimer can be used for copper sulfate poisoning when other chelating agents are not available.
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Acute poisoning of copper sulfate: a case report and review literature Samaneh Hajimohammadi, Somayeh Gharibi, Vahid Pourbarkhordar, Seyed Reza Mousavi, Hanieh Salmani Izadi The Egyptian Journal of Internal Medicine.2022;[Epub] CrossRef
Hyung Hun Park, Kyu Ill Choi, Je Won Lee, Jung Min Park, Jinwook Park, Sang Moon Noh, Jaekyung Cho, Daero Lee, Jae Chul Cho, Dong Chan Park, Yang Hun Kim, Joo Hwan Lee
J Korean Soc Clin Toxicol. 2020;18(2):110-115. Published online December 31, 2020
Purpose: Acute kidney injury (AKI) in patients with glyphosate poisoning has a poor prognosis. This study aimed to predict the risk factors for AKI in patients with glyphosate poisoning at the emergency department (ED). Methods: Clinical data on glyphosate poisoning patients at ED who were older than 18 years were collected retrospectively between January 2013 and December 2019. The clinical characteristics and clinical outcomes of the AKI group in patients with glyphosate poisoning were compared with the non-AKI (NAKI) group. Results: Of 63 glyphosate poisoning patients, AKI was observed in 15 (23.8%). The AKI patients group showed the following: old age (p=0.038), low systolic blood pressure (p=0.021), large amount of ingestion (p=0.026), delayed hospital visits (p=0.009), high white blood cells (WBC) (p<0.001), high neutrophil counts (p<0.001), high neutrophil-lymphocyte (LN) ratios (p<0.001), high serum potassium (p=0.005), low arterial blood pH (p=0.015), and low pO2 (p=0.021), low bicarbonate (p=0.009), and high Poisoning Severity Score (PSS) (p<0.001). AKI patients required hemodialysis, ventilator care (p<0.001, p=0.002), and inotropics (p<0.001). They also showed more intensive care unit admission (p<0.001), longer hospitalization (p<0.001), and high mortality (p<0.001). Logistic multivariate regression analysis showed that high WBCs (OR, 1.223) and increased LN ratios (OR, 1.414) were independently associated with the occurrence of AKI. Conclusion: In patients with glyphosate poisoning at ED, high WBCs and increased LN ratios can help predict the occurrence of AKI.
Dioscorea tokoro has long been used in Korean traditional medicine as a pain killer and anti-inflammatory agent. A 53-year-old male who consumed water that had been boiled with raw tubers of D. tokoro as tea presented with numbness and spasm of both hands and feet. Laboratory results showed hypocalcemia, hypoparathyroidism, and vitamin D insufficiency. During his hospital stay, colitis, acute kidney injury, and toxic encephalopathy developed. The patient received calcium gluconate intravenous infusion and oral calcium carbonate with alfacalcidol. His symptoms improved gradually, but hypocalcemia persisted despite the calcium supplementation. We suggest that ingestion of inappropriately prepared D. tokoro can cause symptomatic hypocalcemia in patients with unbalanced calcium homeostasis.
Drug abuse and its related problems are increasing continuously in Korea. One of the most frequently abused drugs is methamphetamine, but there are few medical report in Korea. This is the first report of the identification of methamphetamine in the blood of a patient who had a return of spontaneous circulation after cardiac arrest and survived discharge. A 33-year-old male arrived at the emergency department presenting with chest pain and dyspnea. He had ingested methamphetamine and alcohol approximately 7 hours before arrival. One hour after arrival, he had seizure followed by cardiac arrest. Spontaneous circulation was recovered after 4 minutes of CPR. An analysis of the National Forensic Service identified plasma methamphetamine with an estimated average concentration of plasma methamphetamine at the time of arrival of 0.6 mg/L, a lethal dose. He had rhabdomyolysis and acute kidney injury but survived after continuous renal replacement therapy. Since then, he has suffered chronic kidney disease, and he is being followed up at the out-patient department. In Korea, although drug abuse is still uncommon, it is on the increase. Therefore, emergency physicians should be aware of the clinical characteristics of methamphetamine poisoning.
Chronic silica nephropathy has been associated with tubulointerstitial disease, immune-mediated multisystem disease, chronic kidney disease, and end-stage renal disease. On the other hand, acute intentional exposure is extremely rare. The authors' experienced a 44-year-old man who took rapid cement hardener (sodium silicate) in a suicide attempt whilst in a drunken state. He visited the emergency department approximately 1 hour after ingestion. Information on the material was obtained after 3 L gastric lavage. The patient complained of a sore throat, epigastric pain, and swollen to blood tinged vomitus. Proton pump inhibitors, hemostats, steroid, and fluids were administered. Nine hours after ingestion, he was administered 200 mL hematochezia. Immediately after, a gas-troenterologist performed an endoscopic procedure that revealed diffuse hyperemic mucosa with a color change and variable sized ulceration in the esophagus, whole stomach, and duodenal $2^{nd}$ portion. Approximately 35 hours later, persistent oligouria and progressive worsening of the renal function parameters (BUN/Cr from 12.2/1.2 to 67.5/6.6 mg/dL) occurred requiring hemodialysis. The patient underwent 8 sessions of hemodialysis for 1 month and the BUN/Cr level increased to 143.2/11.2 mg/dL and decreased to 7.6/1.5 mg/dL. He was discharged safely from the hospital. Follow up endoscopy revealed a severe esophageal stricture and he underwent endoscopic bougie dilatation. Acute cement hardener (sodium silicate) intoxication can cause renal failure and strong caustic mucosal injury. Therefore, it is important to consider early hemodialysis and treatment to prevent gastrointestinal injury and remote esophageal stricture.
Purpose: To evaluate the effects of low-dose intravenous N-acetylcysteine on the prevention of contrast-induced nephropathy (CIN) in patients undergoing computed tomography (CT). Methods: All patients presenting to our emergency department and undergoing CT with intravenous contrast media between August 2014 and April 2016 were retrospectively enrolled. We included hospitalized patients with renal dysfunction [estimated glomerular filtration rate (GFR) between 30 and $89mL/min/1.73m^2$]. A 600-mg injection of N-acetylcysteine was given to patients once before and once immediately after CT, depending on the preference of physician. The primary outcome was CIN defined as an increase in creatinine level of ${geq}25%$ or ${geq}0.5mg/dL$ from the baseline within 48 to 72 hours after CT. A trained person blindly reviewed all medical records. Results: Of the 1903 admitted patients, CIN occurred in 9.8% of patients who received 1200 mg intravenous N-acetylcysteine (24/244) and 6.8% of patients who did not (113/1659, p=0.090). In a multivariable regression analysis, N-acetylcystine was not relevant to the prevention of CIN (odds ratio=1.42 [95% CI, 0.90-2.26]). Even in the stratified analysis using the propensity score matching, N-acetylcysteine was irrelevant (GFR 30-59: odds ratio=1.06 [95% CI, 0.43-2.60]; GFR 60-89: odds ratio=1.76 [95% CI, 0.75-4.14]). After adjustment, crystalloids were significantly associated with the reduction in CIN compared with dextrose water (odds ratio=0.60 [95% CI, 0.37-0.97]). Conclusion: No effect was found when low-dose intravenous N-acetylcysteine was used to prevent CIN. However, there seems to be an association between crystalloids and reduction in CIN.
Dabigatran is the first oral direct thrombin inhibitor approved by the US Food and Drug Administration (FDA) for prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Because dabigatran is excreted mainly by the kidneys, serum levels of dabigatran can be elevated to a supratherapeutic range in patients with renal failure, predisposing to emergent bleeding. We describe the case of a 66-year-old man taking dabigatran 150 mg twice daily for atrial fibrillation and cerebral infarction who presented with hematochezia and disseminated intravascular coagulation. Laboratory evaluation showed a hemoglobin level of 6.3 g/dL, platelets of $138,000/mm^3$, activated partial thromboplastin time (aPTT) of 10 s, and an international normalized ratio (INR) of 8.17. Colonoscopy showed a bleeding anal fissure. Hemostasis was provided by hemoclips and packed red blood cells and fresh frozen plasma were transfused. Since then, there was no further hematochezia, however, bleeding including oral mucosal bleeding, hematuria, and intravenous site bleeding persisted. At presentation, his serum creatinine was 4.96 mg/dL (baseline creatinine, 0.9 mg/dL). Dabigatran toxicity secondary to acute kidney injury was presumed. Because acute kidney injury of unknown cause was progressing after admission, he was treated with hemodialysis. Fresh frozen plasma transfusion was provided with hemodialysis. At 15 days from admission, there was no further bleeding, and laboratory values, including hemoglobin, partial thromboplastin time, and prothrombin time were normalized. He was discharged without bleeding. After 2 months, he undergoes dialysis three times per week and no recurrence of bleeding has been observed.