Severe Multiple Organ Dysfunction and Gastrointestinal Hemorrhage After Accidental Paint Thinner Ingestion Managed With Multimodal Extracorporeal Therapies: A Case Report

Severe Multiple Organ Dysfunction and Gastrointestinal Hemorrhage After Accidental Paint Thinner Ingestion Managed With Multimodal Extracorporeal Therapies: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Severe Multiple Organ Dysfunction and Gastrointestinal Hemorrhage After Accidental Paint Thinner Ingestion Managed With Multimodal Extracorporeal Therapies: A Case Report An Wang, Feng Tao, Jingxing Zhang, Zhixiang Geng, Xiaoqian Zheng, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9370845/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Accidental ingestion of mixed organic solvents is uncommon but may rapidly lead to life-threatening multi-organ dysfunction, and no specific antidote is available. Case presentation: A 49-year-old Han Chinese man accidentally ingested “rosin water” a paint thinner–type organic solvent, and subsequently developed abdominal pain, vomiting, profuse watery diarrhea, hematochezia, and melena. On presentation to the emergency department, laboratory evaluation revealed severe acute liver injury, hyperbilirubinemia, acute kidney injury, marked coagulopathy, thrombocytopenia, and mild cardiopulmonary involvement. Repeat testing after intensive care unit (ICU) admission confirmed persistent multi-organ dysfunction. He received early hemoperfusion and continuous renal replacement therapy, followed later by repeated plasma exchange for progressive cholestatic hyperbilirubinemia. Because prolonged continuous therapy was not financially feasible, peritoneal dialysis was subsequently used for ongoing renal support. Additional management included acid suppression, inhibition of digestive secretions, blood product transfusion, hepatoprotective therapy, nutritional support, oxygen therapy, and adjunctive corticosteroids. Liver enzymes initially improved but later showed a transient rebound. Bilirubin, creatinine, coagulation abnormalities, and gastrointestinal bleeding gradually improved, and the patient was transferred to the general ward in stable condition for further recovery. Conclusion: Mixed lipophilic paint thinners may cause severe gastrointestinal, hepatic, renal, and coagulation abnormalities even in the absence of prominent central nervous system depression. This case suggests that delayed or rebound organ injury may occur during recovery. In selected patients, individualized multimodal supportive care, including extracorporeal therapies when clinically indicated, may be considered. Peritoneal dialysis may serve as a pragmatic option for ongoing renal support when prolonged continuous renal replacement therapy is not feasible. Paint thinner poisoning organic solvent intoxication multiple organ dysfunction acute kidney injury acute liver injury Figures Figure 1 Background Paint thinners are widely used as solvents for paints, inks, and adhesives, and also serve as cleaning agents in various industrial and household settings. These products often contain mixtures of organic solvents, such as toluene, xylene, acetone, hexane, benzene, and methyl isobutyl ketone. Most reported toxic exposures are associated with inhalation, whereas acute oral ingestion is relatively uncommon[1–3]. Clinical manifestations may include central nervous system depression, pulmonary toxicity, cardiovascular complications, rhabdomyolysis, metabolic disturbances, and hepatic and renal dysfunction[4–7]. We report a case of accidental paint thinner ingestion characterized predominantly by gastrointestinal hemorrhage, severe hepatic and renal dysfunction, and coagulopathy. The clinical course was notable for delayed or rebound organ injury after initial stabilization and for the use of peritoneal dialysis as a pragmatic option for continued renal support when prolonged continuous therapy was not feasible. Case presentation 2.1 Clinical presentation A 49-year-old Han Chinese male presented with abdominal pain 1 day after accidental ingestion of “rosin water,” an organic solvent used as a paint thinner. The pain was colicky in nature and was accompanied by non-projectile vomiting of gastric contents. He was initially treated at a local hospital, where gastric lavage, acid-suppressive therapy, hepatoprotective treatment, cardioprotective treatment, and mucosal repair therapy were administered. Despite these measures, he subsequently developed multiple episodes of foul-smelling watery diarrhea, followed by hematochezia that later progressed to melena. Because gastrointestinal bleeding was suspected, he was transferred to our hospital for further management. On arrival at the emergency department, his vital signs were as follows: temperature 36.5°C, respiratory rate 20 breaths/min, blood pressure 148/90 mmHg, and heart rate 120 beats/min. Initial laboratory tests obtained in the emergency department showed alanine aminotransferase (ALT) 1304 IU/L, total bilirubin 134.0 µmol/L, serum creatinine 195.6 µmol/L, lactate dehydrogenase (LDH) > 2000 U/L, and activated partial thromboplastin time (APTT) 81.3 s, suggesting significant multi-organ injury related to organic solvent poisoning. After admission to the intensive care unit (ICU), repeat laboratory testing demonstrated persistent and evolving organ dysfunction. Serum creatinine increased to 213.5 µmol/L, and coagulation testing showed a prothrombin time of 48.8 s, an activated partial thromboplastin time of 77.2 s, a thrombin time of 23.3 s, and a platelet count of 23 ×10^9/L. Liver injury remained prominent, with ALT 1334 IU/L and total bilirubin 117.8 µmol/L. These differences between emergency department and ICU values reflected serial measurements obtained at different time points during the early phase after poisoning.The clinical course and major therapeutic interventions are summarized in Fig. 1. [Insert Fig. 1 here] Figure 1.Clinical course after admission. (A) Standardized trajectories of alanine aminotransferase, serum creatinine, and total bilirubin. Each biomarker was normalized to its own peak value to facilitate comparison of temporal trends. Peak values were ALT 2420 IU/L on hospital day 2, creatinine 482 µmol/L on hospital day 5, and total bilirubin 625.0 µmol/L on hospital day 9. (B) Timeline of major extracorporeal interventions, including hemoperfusion (day 0), continuous venovenous hemofiltration (days 0–8), plasma exchange on hospital days 7, 9, and 10, and peritoneal dialysis from hospital day 12 to day 19. The vertical dashed line indicates transfer from the ICU to the general ward on hospital day 29. 2.2 Hospital Days 1–4: Early ICU Management After ICU admission, the patient was kept fasting and treated with proton pump inhibitors and octreotide for gastrointestinal bleeding, together with hepatoprotective and anti-jaundice therapy, transfusion of blood products, intravenous nutritional support, oxygen therapy, corticosteroids, and extracorporeal therapies including hemoperfusion and continuous renal replacement therapy (CRRT). Because the patient was oliguric and renal dysfunction was progressing, hemoperfusion and CRRT were initiated promptly. At the same time, plasma, cryoprecipitate, and platelet transfusions were administered for severe coagulopathy and thrombocytopenia. Magnesium isoglycyrrhizinate, ademetionine, and glutathione were also started for hepatic support. During the first several hospital days, the amount of hematochezia gradually decreased. By hospital day 4, no further overt gastrointestinal bleeding was observed, and bowel sounds were present on auscultation. Around the same time, the patient developed tachypnea with audible moist rales. Repeat chest computed tomography demonstrated bilateral dependent pneumonia and bilateral pleural effusions. Brain natriuretic peptide was markedly elevated (> 30,000 pg/mL), whereas cardiac troponin was only mildly elevated and electrocardiography showed no obvious abnormalities. Bedside echocardiography did not provide sufficient evidence for acute heart failure. Fluid removal during CRRT was performed, after which the patient’s respiratory symptoms improved and BNP levels decreased. 2.3 Hospital Days 5–10: Progressive Cholestatic Liver Injury and Plasma Exchange After an initial transient increase, ALT and AST began to decline from approximately hospital day 4 onward. However, total bilirubin continued to rise, predominantly in the direct bilirubin fraction, indicating progressive cholestatic liver injury. Initially, cholestasis secondary to dietary factors was considered, but bilirubin levels continued to increase despite intensified hepatoprotective and choleretic therapy. Therefore, plasma exchange was initiated on hospital day 7 and was subsequently performed on hospital days 7, 9, and 10. Adjunctive therapy included low-dose methylprednisolone, ursodeoxycholic acid, and alprostadil. Meanwhile, gastrointestinal bleeding remained controlled. Enteral nutrition was initiated on hospital day 6, after which the patient passed dark green stools that gradually turned into soft brown stools, indicating progressive recovery of gastrointestinal function. 2.4 Hospital Days 8–14: Renal Function Fluctuation and Transition to Peritoneal Dialysis Renal function showed dynamic changes during the early recovery phase. After early hemoperfusion and CRRT, urine output gradually increased, and by hospital day 8 the patient regained spontaneous urination, allowing discontinuation of CRRT. However, serum creatinine subsequently rose again, suggesting delayed or persistent renal injury. Because continued renal support was still required and the patient had financial constraints, peritoneal dialysis was initiated on hospital day 12. After the initiation of peritoneal dialysis, serum creatinine decreased. From hospital day 13, the patient began oral intake without obvious gastrointestinal symptoms. On hospital day 14, he entered a polyuric phase and developed electrolyte disturbances. Appropriate correction of electrolyte imbalance was performed while peritoneal dialysis was continued, resulting in stabilization of the internal milieu. During the same period, the patient also experienced a transient re-elevation of ALT, AST, and bilirubin, which gradually improved after continued hepatoprotective therapy. 2.5 Hospital Days 15–28: Progressive Recovery From approximately hospital day 15 onward, liver function, renal function, coagulation parameters, and gastrointestinal symptoms gradually improved. Bilirubin levels progressively declined, serum creatinine stabilized, and coagulation function returned toward normal. By hospital day 19, renal function had improved sufficiently to allow discontinuation of peritoneal dialysis. Thereafter, the patient’s respiratory status remained stable, no further gastrointestinal bleeding occurred, and vital signs remained stable. 2.6 Hospital Day 29: Transfer to the General Ward By hospital day 29, the patient’s overall condition had significantly improved, with stable vital signs, improved liver and renal function, and recovery of coagulation parameters. He was therefore transferred from the ICU to the general ward for further recovery and supportive care. Discussion Acute poisoning after oral ingestion of paint thinner is uncommon but can be life-threatening. In contrast to many previously reported fatal cases characterized by prominent central nervous system depression, our patient presented predominantly with gastrointestinal hemorrhage and severe hepatorenal dysfunction. Paint thinners often contain mixtures of lipophilic organic solvents, including toluene, xylene, acetone, and hexane. These compounds are mainly metabolized in the liver via cytochrome P450 enzymes, such as CYP2E1 in the case of toluene and xylene[8–10], and may generate reactive intermediates that contribute to oxidative stress and mitochondrial dysfunction[11, 12]. Among them, toluene and xylene, because of their high lipid solubility, may distribute into adipose-rich tissues such as the liver, kidneys, and central nervous system, which could partly account for delayed and prolonged hepatorenal toxicity[13–15]. In contrast, acetone is relatively more hydrophilic and may be eliminated more rapidly through the kidneys and lungs, potentially contributing less to persistent organ injury[16, 17]. However, because the exact chemical composition of the ingested product was not analytically confirmed in this case, these mechanisms should be interpreted with caution. A similar fatal case following paint thinner ingestion has been reported in an autopsy study. Multiple stress ulcers were observed in the gastric mucosa, and discoloration of the esophageal mucosa was also noted, possibly indicating acute corrosive injury to the gastrointestinal mucosa caused by the ingested thinner. In addition, paint thinner–related metabolites were detected in the liver, urine, and lungs, suggesting possible involvement of the hepatic, renal, and respiratory systems in the metabolism and/or elimination of these solvents[18]. Antonina Argo et al. also reported that, in patients who died after ingesting paint thinner, the most prominent toxicological effects were observed in lipid-rich tissues, including the heart, the brain, nervous system, liver, and kidneys[13]. This distribution may be related to the physicochemical properties of organic solvents, particularly their lipophilicity[19]. In addition, both studies detected only small amounts of organic compounds in the lungs. In our patient, pulmonary injury was also less pronounced than injury in other lipid-rich organs, such as the liver and kidneys, which might reflect differences in tissue distribution and retention of solvent components. The relatively large exchange surface of the lungs may also have facilitated partial volatilization and elimination of some compounds. In the absence of a specific antidote, extracorporeal therapies may play an important supportive role in the management of severe paint thinner poisoning. Hemoperfusion (HP) can enhance the removal of lipophilic toxins through adsorption, although its effectiveness may decrease once toxins redistribute into tissues[20]. Plasma exchange (PEX) primarily acts on the intravascular compartment; therefore, for toxins with a large volume of distribution or those predominantly sequestered in tissues, including intracellular compartments, its overall clearance may be limited[21–23]. In our case, the combination of early HP and repeated PEX was associated with an initial improvement in toxin-related biochemical abnormalities and coagulopathy[24, 25]. However, the transient re-elevation of liver enzymes suggests that these approaches alone may be insufficient to fully eliminate toxins or to prevent delayed tissue injury. Previous experimental studies have proposed that the liver may serve as a potential “toxin reservoir” for lipophilic solvents[26, 27]. For example, animal models of toluene exposure have shown persistent elevation of liver enzymes and histopathological abnormalities even after blood concentrations decline, suggesting prolonged retention in hepatocytes and adipose-rich tissues[28]. Although this mechanism cannot be confirmed in the present case, it may provide a possible explanation for the delayed peak in bilirubin and transaminases despite aggressive extracorporeal therapy. Following the acute phase, the patient developed recurrent renal dysfunction with rising creatinine. Because ongoing renal support was required and prolonged CRRT was not financially feasible, peritoneal dialysis (PD) was initiated[29, 30]. In this setting, PD served as a pragmatic and relatively low-cost alternative for continued renal support, particularly in a resource-constrained context[31]. Although there is limited evidence supporting PD specifically for solvent poisoning, current guidelines recognize PD as an acceptable option for acute kidney injury when CRRT is not feasible[30]. The use of low-dose methylprednisolone for progressive cholestatic hyperbilirubinemia in this patient was based on its potential anti-inflammatory and anti-edematous effects on the biliary system. Although corticosteroids are not routinely recommended for all cholestatic conditions, they were given adjunctively together with ursodeoxycholic acid and prostaglandin E1 (alprostadil) as part of a multimodal supportive strategy. Because this was a single case, the precise effect of these therapies on cholestatic recovery cannot be determined. Nevertheless, their use reflects the clinical need for individualized supportive management in patients with persistent cholestatic injury after lipophilic toxin exposure. In previously reported fatal cases of similar acute poisoning, central nervous system depression has been the most common cause of death[13, 32, 33]. In contrast, our patient mainly presented with gastrointestinal symptoms and marked hepatic and renal dysfunction, whereas central nervous system depression and pulmonary or cardiovascular/cerebrovascular involvement were relatively mild. However, the exact composition of the ingested product was not analytically confirmed, and no serial toxicological measurements were available; therefore, the proposed mechanisms and the contribution of individual therapies should be interpreted cautiously. Nevertheless, prompt gastric lavage and early extracorporeal support, including CRRT, hemoperfusion, and plasma exchange, may have been associated with attenuation of early systemic toxicity in this patient. Conclusion Unlike poisoning caused by a single solvent such as toluene, paint thinner ingestion may involve exposure to multiple organic solvents and therefore present with a more complex toxicological profile in the absence of a specific antidote. This case highlights that accidental ingestion of paint thinner can result in severe gastrointestinal, hepatic, renal, and coagulation abnormalities, with delayed or rebound organ injury during recovery. In such patients, close monitoring and individualized multimodal supportive care, including extracorporeal therapies when clinically indicated, may be considered. Peritoneal dialysis may serve as a pragmatic option for ongoing renal support when prolonged CRRT is not feasible. Declarations Status Ethical Approval And Consent to Participate This study is a single case report. According to the policy of our institutional ethics committee, ethical approval was waived for case reports. Written informed consent was obtained from the patient for the use of clinical data for research and publication. Consent for Publication Written consent for publication of this case report and any accompanying images was obtained from the patient and/or the legal guardian. Identifying information has been removed as far as possible to protect privacy. Availability of Supporting Data All data supporting the findings are included in this article. Additional details may be provided by the corresponding author upon reasonable request, subject to privacy and ethical restrictions. Competing Interests All authors declare that there are no competing interests in this study. No financial, commercial, or other interests that may affect the objectivity and fairness of the research are involved. Funding This study did not receive any external funding. All costs during the research process were borne by the authors' institutions or self - raised by the authors. Acknowledgements Thanks to all medical staff at The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University for their meticulous care and support during the patient's treatment. Authors’ contributions An Wang, Feng Tao, Jingxing Zhang, and Zhixiang Geng were involved in the diagnosis, treatment, and clinical management of the patient. Xiaoqian Zheng, Xiaowen Lin, and Yi Lin collected and organized the clinical data and performed the literature review. An Wang and Feng Tao drafted the manuscript. Xiaolong Zhang supervised the study and critically revised the manuscript for important intellectual content. All authors read and approved the final manuscript. References Some organic solvents, resin monomers and related compounds, pigments and occupational exposures in paint manufacture and painting. IARC Monogr Eval Carcinog Risks Hum, 1989. 47 : p. 1-442. Martínez-Alfaro, M., et al., Oxidative stress effects of thinner inhalation. Indian J Occup Environ Med, 2011. 15 (3): p. 87-92. Barzallo, T.P., et al., Spontaneous Pneumomediastinum in a 15-Year-Old Adolescent After Unintended Overexposure to Paint Diluent (Thinner) Fumes: First Reported Case. Ther Adv Pulm Crit Care Med, 2023. 18 : p. 11795484231201751. Zaidi, S.A., et al., Multi-organ toxicity and death following acute unintentional inhalation of paint thinner fumes. Clin Toxicol (Phila), 2007. 45 (3): p. 287-9. Dhibar, D.P., et al., Methemoglobinemia in a Case of Paint Thinner Intoxication, Treated Successfully with Vitamin C. J Emerg Med, 2018. 54 (2): p. 221-224. Sarıçopur, A., et al., Subacute myocardial infarction due to long-term paint thinner and ecstasy abuse. Anatol J Cardiol, 2015. 15 (2): p. 167-8. Latief, M., et al., Paint-thinner-induced Acute Kidney Injury: A Case Series and Review. Saudi J Kidney Dis Transpl, 2022. 33 (3): p. 487-491. Tassaneeyakul, W., et al., Human cytochrome P450 isoform specificity in the regioselective metabolism of toluene and o-, m- and p-xylene. J Pharmacol Exp Ther, 1996. 276 (1): p. 101-8. Gut, I., et al., Exposure to various benzene derivatives differently induces cytochromes P450 2B1 and P450 2E1 in rat liver. Arch Toxicol, 1993. 67 (4): p. 237-43. Iba, M.M., J. Fung, and F.J. Gonzalez, Functional Cyp2e1 is required for substantial in vivo formation of 2,5-hexanedione from n-hexane in the mouse. Arch Toxicol, 2000. 74 (10): p. 582-6. Mattia, C.J., S.F. Ali, and S.C. Bondy, Toluene-induced oxidative stress in several brain regions and other organs. Mol Chem Neuropathol, 1993. 18 (3): p. 313-28. Salimi, A., B.S. Talatappe, and J. Pourahmad, Xylene Induces Oxidative Stress and Mitochondria Damage in Isolated Human Lymphocytes. Toxicol Res, 2017. 33 (3): p. 233-238. Argo, A., et al., A fatal case of a paint thinner ingestion: comparison between toxicological and histological findings. Am J Forensic Med Pathol, 2010. 31 (2): p. 186-91. Engström, J. and V. Riihimäki, Distribution of m-xylene to subcutaneous adipose tissue in short-term experimental human exposure. Scand J Work Environ Health, 1979. 5 (2): p. 126-34. Pierce, C.H., et al., Interindividual differences in 2H8-toluene toxicokinetics assessed by semiempirical physiologically based model. Toxicol Appl Pharmacol, 1996. 139 (1): p. 49-61. Mörk, A.K. and G. Johanson, A human physiological model describing acetone kinetics in blood and breath during various levels of physical exercise. Toxicol Lett, 2006. 164 (1): p. 6-15. Slaughter, R.J., et al., Isopropanol poisoning. Clin Toxicol (Phila), 2014. 52 (5): p. 470-8. Collison, I. and W. Moorehead, Death by paint thinner. J Anal Toxicol, 2002. 26 (7): p. 532-6. Engelke, M., H. Tähti, and L. Vaalavirta, Perturbation of artificial and biological membranes by organic compounds of aliphatic, alicyclic and aromatic structure. Toxicol In Vitro, 1996. 10 (2): p. 111-5. Pond, S.M., Extracorporeal techniques in the treatment of poisoned patients. Med J Aust, 1991. 154 (9): p. 617-22. Iwai, H., et al., Removal of endotoxin and cytokines by plasma exchange in patients with acute hepatic failure. Crit Care Med, 1998. 26 (5): p. 873-6. Fauvelle, F., et al., Clinical pharmacokinetics during plasma exchange. Therapie, 2000. 55 (2): p. 269-75. Zdunek, M., A. Mitra, and M.H. Mokrzycki, Plasma exchange for the removal of digoxin-specific antibody fragments in renal failure: timing is important for maximizing clearance. Am J Kidney Dis, 2000. 36 (1): p. 177-83. Larsen, F.S., et al., High-volume plasma exchange in patients with acute liver failure: An open randomised controlled trial. J Hepatol, 2016. 64 (1): p. 69-78. Levi, M., et al., Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. Br J Haematol, 2009. 145 (1): p. 24-33. Pyykkö, K., H. Tähti, and H. Vapaatalo, Toluene concentrations in various tissues of rats after inhalation and oral administration. Arch Toxicol, 1977. 38 (3): p. 169-76. Bowen, S.E., J.H. Hannigan, and S. Irtenkauf, Maternal and fetal blood and organ toluene levels in rats following acute and repeated binge inhalation exposure. Reprod Toxicol, 2007. 24 (3-4): p. 343-52. Bergman, K., Application and results of whole-body autoradiography in distribution studies of organic solvents. Crit Rev Toxicol, 1983. 12 (1): p. 59-118. Kilonzo, K.G., H.F. Akrabi, and K.E. Yeates, Cost-effectiveness of acute peritoneal dialysis: Considerations from Africa. Clin Nephrol, 2020. 93 (1): p. 72-75. Cullis, B., et al., ISPD guidelines for peritoneal dialysis in acute kidney injury: 2020 update (adults). Perit Dial Int, 2021. 41 (1): p. 15-31. Leypoldt, J.K., Solute transport across the peritoneal membrane. J Am Soc Nephrol, 2002. 13 Suppl 1 : p. S84-91. Kurtzman, T.L., K.N. Otsuka, and R.A. Wahl, Inhalant abuse by adolescents. J Adolesc Health, 2001. 28 (3): p. 170-80. Ameno, K., et al., A fatal case of oral ingestion of toluene. Forensic Sci Int, 1989. 41 (3): p. 255-60. Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-9370845","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":633001003,"identity":"6cc763c7-3256-4b50-8878-bedcf47cf54a","order_by":0,"name":"An Wang","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"An","middleName":"","lastName":"Wang","suffix":""},{"id":633001006,"identity":"61b1e70a-6f58-47b5-8425-6870ab814c15","order_by":1,"name":"Feng Tao","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Feng","middleName":"","lastName":"Tao","suffix":""},{"id":633001007,"identity":"f94d261d-7db3-488c-9a20-aa3b0ff38e64","order_by":2,"name":"Jingxing Zhang","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Jingxing","middleName":"","lastName":"Zhang","suffix":""},{"id":633001008,"identity":"f857e3dd-1f90-439c-857b-33a637ebfdb0","order_by":3,"name":"Zhixiang Geng","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Zhixiang","middleName":"","lastName":"Geng","suffix":""},{"id":633001009,"identity":"f1ada390-f5ac-4ebd-aae9-e091f00bcd93","order_by":4,"name":"Xiaoqian Zheng","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Xiaoqian","middleName":"","lastName":"Zheng","suffix":""},{"id":633001010,"identity":"813d4f3c-cd4a-4bb5-b15e-2b058a05b352","order_by":5,"name":"Xiaowen Lin","email":"","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Xiaowen","middleName":"","lastName":"Lin","suffix":""},{"id":633001011,"identity":"1e79fe4f-644e-4bc8-b5bb-bc5c39123011","order_by":6,"name":"Yi Lin","email":"","orcid":"","institution":"Xiangshan County First People's Hospital","correspondingAuthor":false,"prefix":"","firstName":"Yi","middleName":"","lastName":"Lin","suffix":""},{"id":633001012,"identity":"07133a90-deda-47d4-afb6-1603afbea13e","order_by":7,"name":"Xiaolong Zhang","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAxUlEQVRIiWNgGAWjYFAC5uYHif9sIGwe4rQwthl8YEsjTUuD5Ay2wyRokZ+R2GDMw3M+ce2MBMYHb9sY5M0J2tFzsOExj8TtxG03EpgN57YxGO5sIKCFmb0RaIvB7VygFjZp3jaGBIMDBLSwMTM2SPMknANpYf9NlBYeoC2SMw4cANvCTJQWCZ6DbQYfG5Lrt5152Cw555yE4QZCWuRnJB9+kNhgZ2x2PPnghzdlNvIEbUECjA0gW4lXPwpGwSgYBaMANwAAdu5BK30YDo4AAAAASUVORK5CYII=","orcid":"","institution":"Second Affiliated Hospital \u0026 Yuying Children's Hospital of Wenzhou Medical University","correspondingAuthor":true,"prefix":"","firstName":"Xiaolong","middleName":"","lastName":"Zhang","suffix":""}],"badges":[],"createdAt":"2026-04-09 16:09:56","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9370845/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9370845/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":108978223,"identity":"b49f203c-5f99-4d5e-90ee-cce6ff9d0f7c","added_by":"auto","created_at":"2026-05-11 11:35:09","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":139442,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eClinical course after admission.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e(A) Standardized trajectories of alanine aminotransferase, serum creatinine, and total bilirubin. Each biomarker was normalized to its own peak value to facilitate comparison of temporal trends. Peak values were ALT 2420 IU/L on hospital day 2, creatinine 482 μmol/L on hospital day 5, and total bilirubin 625.0 μmol/L on hospital day 9.\u003c/p\u003e\n\u003cp\u003e(B) Timeline of major extracorporeal interventions, including hemoperfusion (day 0), continuous venovenous hemofiltration (days 0–8), plasma exchange on hospital days 7, 9, and 10, and peritoneal dialysis from hospital day 12 to day 19. The vertical dashed line indicates transfer from the ICU to the general ward on hospital day 29.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-9370845/v1/2cb985dd407dc5f47e026f0d.png"},{"id":108980017,"identity":"6ec1e04b-2966-4d74-a5c5-e53eb75b15f8","added_by":"auto","created_at":"2026-05-11 12:03:04","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":322465,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9370845/v1/19d44fe6-fb72-4c6d-933f-951c17cb75df.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Severe Multiple Organ Dysfunction and Gastrointestinal Hemorrhage After Accidental Paint Thinner Ingestion Managed With Multimodal Extracorporeal Therapies: A Case Report","fulltext":[{"header":"Background","content":"\u003cp\u003ePaint thinners are widely used as solvents for paints, inks, and adhesives, and also serve as cleaning agents in various industrial and household settings. These products often contain mixtures of organic solvents, such as toluene, xylene, acetone, hexane, benzene, and methyl isobutyl ketone. Most reported toxic exposures are associated with inhalation, whereas acute oral ingestion is relatively uncommon[1\u0026ndash;3]. Clinical manifestations may include central nervous system depression, pulmonary toxicity, cardiovascular complications, rhabdomyolysis, metabolic disturbances, and hepatic and renal dysfunction[4\u0026ndash;7].\u003c/p\u003e \u003cp\u003eWe report a case of accidental paint thinner ingestion characterized predominantly by gastrointestinal hemorrhage, severe hepatic and renal dysfunction, and coagulopathy. The clinical course was notable for delayed or rebound organ injury after initial stabilization and for the use of peritoneal dialysis as a pragmatic option for continued renal support when prolonged continuous therapy was not feasible.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003e2.1 Clinical presentation\u003c/h2\u003e \u003cp\u003eA 49-year-old Han Chinese male presented with abdominal pain 1 day after accidental ingestion of \u0026ldquo;rosin water,\u0026rdquo; an organic solvent used as a paint thinner. The pain was colicky in nature and was accompanied by non-projectile vomiting of gastric contents. He was initially treated at a local hospital, where gastric lavage, acid-suppressive therapy, hepatoprotective treatment, cardioprotective treatment, and mucosal repair therapy were administered. Despite these measures, he subsequently developed multiple episodes of foul-smelling watery diarrhea, followed by hematochezia that later progressed to melena. Because gastrointestinal bleeding was suspected, he was transferred to our hospital for further management.\u003c/p\u003e \u003cp\u003eOn arrival at the emergency department, his vital signs were as follows: temperature 36.5\u0026deg;C, respiratory rate 20 breaths/min, blood pressure 148/90 mmHg, and heart rate 120 beats/min. Initial laboratory tests obtained in the emergency department showed alanine aminotransferase (ALT) 1304 IU/L, total bilirubin 134.0 \u0026micro;mol/L, serum creatinine 195.6 \u0026micro;mol/L, lactate dehydrogenase (LDH)\u0026thinsp;\u0026gt;\u0026thinsp;2000 U/L, and activated partial thromboplastin time (APTT) 81.3 s, suggesting significant multi-organ injury related to organic solvent poisoning. After admission to the intensive care unit (ICU), repeat laboratory testing demonstrated persistent and evolving organ dysfunction. Serum creatinine increased to 213.5 \u0026micro;mol/L, and coagulation testing showed a prothrombin time of 48.8 s, an activated partial thromboplastin time of 77.2 s, a thrombin time of 23.3 s, and a platelet count of 23 \u0026times;10^9/L. Liver injury remained prominent, with ALT 1334 IU/L and total bilirubin 117.8 \u0026micro;mol/L. These differences between emergency department and ICU values reflected serial measurements obtained at different time points during the early phase after poisoning.The clinical course and major therapeutic interventions are summarized in Fig.\u0026nbsp;1.\u003c/p\u003e \u003cp\u003e[Insert Fig.\u0026nbsp;1 here]\u003c/p\u003e \u003cp\u003e \u003cb\u003eFigure\u0026nbsp;1.Clinical course after admission.\u003c/b\u003e \u003c/p\u003e \u003cp\u003e(A) Standardized trajectories of alanine aminotransferase, serum creatinine, and total bilirubin. Each biomarker was normalized to its own peak value to facilitate comparison of temporal trends. Peak values were ALT 2420 IU/L on hospital day 2, creatinine 482 \u0026micro;mol/L on hospital day 5, and total bilirubin 625.0 \u0026micro;mol/L on hospital day 9.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e(B) Timeline of major extracorporeal interventions, including hemoperfusion (day 0), continuous venovenous hemofiltration (days 0\u0026ndash;8), plasma exchange on hospital days 7, 9, and 10, and peritoneal dialysis from hospital day 12 to day 19. The vertical dashed line indicates transfer from the ICU to the general ward on hospital day 29.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003e2.2 Hospital Days 1\u0026ndash;4: Early ICU Management\u003c/h2\u003e \u003cp\u003eAfter ICU admission, the patient was kept fasting and treated with proton pump inhibitors and octreotide for gastrointestinal bleeding, together with hepatoprotective and anti-jaundice therapy, transfusion of blood products, intravenous nutritional support, oxygen therapy, corticosteroids, and extracorporeal therapies including hemoperfusion and continuous renal replacement therapy (CRRT). Because the patient was oliguric and renal dysfunction was progressing, hemoperfusion and CRRT were initiated promptly. At the same time, plasma, cryoprecipitate, and platelet transfusions were administered for severe coagulopathy and thrombocytopenia. Magnesium isoglycyrrhizinate, ademetionine, and glutathione were also started for hepatic support.\u003c/p\u003e \u003cp\u003eDuring the first several hospital days, the amount of hematochezia gradually decreased. By hospital day 4, no further overt gastrointestinal bleeding was observed, and bowel sounds were present on auscultation. Around the same time, the patient developed tachypnea with audible moist rales. Repeat chest computed tomography demonstrated bilateral dependent pneumonia and bilateral pleural effusions. Brain natriuretic peptide was markedly elevated (\u0026gt;\u0026thinsp;30,000 pg/mL), whereas cardiac troponin was only mildly elevated and electrocardiography showed no obvious abnormalities. Bedside echocardiography did not provide sufficient evidence for acute heart failure. Fluid removal during CRRT was performed, after which the patient\u0026rsquo;s respiratory symptoms improved and BNP levels decreased.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec5\" class=\"Section2\"\u003e \u003ch2\u003e2.3 Hospital Days 5\u0026ndash;10: Progressive Cholestatic Liver Injury and Plasma Exchange\u003c/h2\u003e \u003cp\u003eAfter an initial transient increase, ALT and AST began to decline from approximately hospital day 4 onward. However, total bilirubin continued to rise, predominantly in the direct bilirubin fraction, indicating progressive cholestatic liver injury. Initially, cholestasis secondary to dietary factors was considered, but bilirubin levels continued to increase despite intensified hepatoprotective and choleretic therapy. Therefore, plasma exchange was initiated on hospital day 7 and was subsequently performed on hospital days 7, 9, and 10. Adjunctive therapy included low-dose methylprednisolone, ursodeoxycholic acid, and alprostadil.\u003c/p\u003e \u003cp\u003eMeanwhile, gastrointestinal bleeding remained controlled. Enteral nutrition was initiated on hospital day 6, after which the patient passed dark green stools that gradually turned into soft brown stools, indicating progressive recovery of gastrointestinal function.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003e2.4 Hospital Days 8\u0026ndash;14: Renal Function Fluctuation and Transition to Peritoneal Dialysis\u003c/h2\u003e \u003cp\u003eRenal function showed dynamic changes during the early recovery phase. After early hemoperfusion and CRRT, urine output gradually increased, and by hospital day 8 the patient regained spontaneous urination, allowing discontinuation of CRRT. However, serum creatinine subsequently rose again, suggesting delayed or persistent renal injury. Because continued renal support was still required and the patient had financial constraints, peritoneal dialysis was initiated on hospital day 12. After the initiation of peritoneal dialysis, serum creatinine decreased.\u003c/p\u003e \u003cp\u003eFrom hospital day 13, the patient began oral intake without obvious gastrointestinal symptoms. On hospital day 14, he entered a polyuric phase and developed electrolyte disturbances. Appropriate correction of electrolyte imbalance was performed while peritoneal dialysis was continued, resulting in stabilization of the internal milieu. During the same period, the patient also experienced a transient re-elevation of ALT, AST, and bilirubin, which gradually improved after continued hepatoprotective therapy.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec7\" class=\"Section2\"\u003e \u003ch2\u003e2.5 Hospital Days 15\u0026ndash;28: Progressive Recovery\u003c/h2\u003e \u003cp\u003eFrom approximately hospital day 15 onward, liver function, renal function, coagulation parameters, and gastrointestinal symptoms gradually improved. Bilirubin levels progressively declined, serum creatinine stabilized, and coagulation function returned toward normal. By hospital day 19, renal function had improved sufficiently to allow discontinuation of peritoneal dialysis. Thereafter, the patient\u0026rsquo;s respiratory status remained stable, no further gastrointestinal bleeding occurred, and vital signs remained stable.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003e2.6 Hospital Day 29: Transfer to the General Ward\u003c/h2\u003e \u003cp\u003eBy hospital day 29, the patient\u0026rsquo;s overall condition had significantly improved, with stable vital signs, improved liver and renal function, and recovery of coagulation parameters. He was therefore transferred from the ICU to the general ward for further recovery and supportive care.\u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eAcute poisoning after oral ingestion of paint thinner is uncommon but can be life-threatening. In contrast to many previously reported fatal cases characterized by prominent central nervous system depression, our patient presented predominantly with gastrointestinal hemorrhage and severe hepatorenal dysfunction.\u003c/p\u003e \u003cp\u003ePaint thinners often contain mixtures of lipophilic organic solvents, including toluene, xylene, acetone, and hexane. These compounds are mainly metabolized in the liver via cytochrome P450 enzymes, such as CYP2E1 in the case of toluene and xylene[8\u0026ndash;10], and may generate reactive intermediates that contribute to oxidative stress and mitochondrial dysfunction[11, 12]. Among them, toluene and xylene, because of their high lipid solubility, may distribute into adipose-rich tissues such as the liver, kidneys, and central nervous system, which could partly account for delayed and prolonged hepatorenal toxicity[13\u0026ndash;15]. In contrast, acetone is relatively more hydrophilic and may be eliminated more rapidly through the kidneys and lungs, potentially contributing less to persistent organ injury[16, 17]. However, because the exact chemical composition of the ingested product was not analytically confirmed in this case, these mechanisms should be interpreted with caution.\u003c/p\u003e \u003cp\u003eA similar fatal case following paint thinner ingestion has been reported in an autopsy study. Multiple stress ulcers were observed in the gastric mucosa, and discoloration of the esophageal mucosa was also noted, possibly indicating acute corrosive injury to the gastrointestinal mucosa caused by the ingested thinner. In addition, paint thinner\u0026ndash;related metabolites were detected in the liver, urine, and lungs, suggesting possible involvement of the hepatic, renal, and respiratory systems in the metabolism and/or elimination of these solvents[18].\u003c/p\u003e \u003cp\u003eAntonina Argo et al. also reported that, in patients who died after ingesting paint thinner, the most prominent toxicological effects were observed in lipid-rich tissues, including the heart, the brain, nervous system, liver, and kidneys[13]. This distribution may be related to the physicochemical properties of organic solvents, particularly their lipophilicity[19]. In addition, both studies detected only small amounts of organic compounds in the lungs. In our patient, pulmonary injury was also less pronounced than injury in other lipid-rich organs, such as the liver and kidneys, which might reflect differences in tissue distribution and retention of solvent components. The relatively large exchange surface of the lungs may also have facilitated partial volatilization and elimination of some compounds.\u003c/p\u003e \u003cp\u003eIn the absence of a specific antidote, extracorporeal therapies may play an important supportive role in the management of severe paint thinner poisoning. Hemoperfusion (HP) can enhance the removal of lipophilic toxins through adsorption, although its effectiveness may decrease once toxins redistribute into tissues[20]. Plasma exchange (PEX) primarily acts on the intravascular compartment; therefore, for toxins with a large volume of distribution or those predominantly sequestered in tissues, including intracellular compartments, its overall clearance may be limited[21\u0026ndash;23]. In our case, the combination of early HP and repeated PEX was associated with an initial improvement in toxin-related biochemical abnormalities and coagulopathy[24, 25]. However, the transient re-elevation of liver enzymes suggests that these approaches alone may be insufficient to fully eliminate toxins or to prevent delayed tissue injury.\u003c/p\u003e \u003cp\u003ePrevious experimental studies have proposed that the liver may serve as a potential \u0026ldquo;toxin reservoir\u0026rdquo; for lipophilic solvents[26, 27]. For example, animal models of toluene exposure have shown persistent elevation of liver enzymes and histopathological abnormalities even after blood concentrations decline, suggesting prolonged retention in hepatocytes and adipose-rich tissues[28]. Although this mechanism cannot be confirmed in the present case, it may provide a possible explanation for the delayed peak in bilirubin and transaminases despite aggressive extracorporeal therapy.\u003c/p\u003e \u003cp\u003eFollowing the acute phase, the patient developed recurrent renal dysfunction with rising creatinine. Because ongoing renal support was required and prolonged CRRT was not financially feasible, peritoneal dialysis (PD) was initiated[29, 30]. In this setting, PD served as a pragmatic and relatively low-cost alternative for continued renal support, particularly in a resource-constrained context[31]. Although there is limited evidence supporting PD specifically for solvent poisoning, current guidelines recognize PD as an acceptable option for acute kidney injury when CRRT is not feasible[30].\u003c/p\u003e \u003cp\u003eThe use of low-dose methylprednisolone for progressive cholestatic hyperbilirubinemia in this patient was based on its potential anti-inflammatory and anti-edematous effects on the biliary system. Although corticosteroids are not routinely recommended for all cholestatic conditions, they were given adjunctively together with ursodeoxycholic acid and prostaglandin E1 (alprostadil) as part of a multimodal supportive strategy. Because this was a single case, the precise effect of these therapies on cholestatic recovery cannot be determined. Nevertheless, their use reflects the clinical need for individualized supportive management in patients with persistent cholestatic injury after lipophilic toxin exposure. In previously reported fatal cases of similar acute poisoning, central nervous system depression has been the most common cause of death[13, 32, 33]. In contrast, our patient mainly presented with gastrointestinal symptoms and marked hepatic and renal dysfunction, whereas central nervous system depression and pulmonary or cardiovascular/cerebrovascular involvement were relatively mild.\u003c/p\u003e \u003cp\u003eHowever, the exact composition of the ingested product was not analytically confirmed, and no serial toxicological measurements were available; therefore, the proposed mechanisms and the contribution of individual therapies should be interpreted cautiously. Nevertheless, prompt gastric lavage and early extracorporeal support, including CRRT, hemoperfusion, and plasma exchange, may have been associated with attenuation of early systemic toxicity in this patient.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eUnlike poisoning caused by a single solvent such as toluene, paint thinner ingestion may involve exposure to multiple organic solvents and therefore present with a more complex toxicological profile in the absence of a specific antidote. This case highlights that accidental ingestion of paint thinner can result in severe gastrointestinal, hepatic, renal, and coagulation abnormalities, with delayed or rebound organ injury during recovery. In such patients, close monitoring and individualized multimodal supportive care, including extracorporeal therapies when clinically indicated, may be considered. Peritoneal dialysis may serve as a pragmatic option for ongoing renal support when prolonged CRRT is not feasible.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eStatus\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical Approval And Consent to Participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study is a single case report. According to the policy of our institutional ethics committee, ethical approval was waived for case reports. Written informed consent was obtained from the patient for the use of clinical data for research and publication.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for Publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten consent for publication of this case report and any accompanying images was obtained from the patient and/or the legal guardian. Identifying information has been removed as far as possible to protect privacy.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of Supporting Data\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data supporting the findings are included in this article. Additional details may be provided by the corresponding author upon reasonable request, subject to privacy and ethical restrictions.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting Interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll authors declare that there are no competing interests in this study. No financial, commercial, or other interests that may affect the objectivity and fairness of the research are involved.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study did not receive any external funding. All costs during the research process were borne by the authors' institutions or self - raised by the authors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThanks to all medical staff at The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University for their meticulous care and support during the patient's treatment.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors’ contributions\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;An Wang, Feng Tao, Jingxing Zhang, and Zhixiang Geng were involved in the diagnosis, treatment, and clinical management of the patient. Xiaoqian Zheng, Xiaowen Lin, and Yi Lin collected and organized the clinical data and performed the literature review. An Wang and Feng Tao drafted the manuscript. Xiaolong Zhang supervised the study and critically revised the manuscript for important intellectual content. All authors read and approved the final manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003e\u003cem\u003eSome organic solvents, resin monomers and related compounds, pigments and occupational exposures in paint manufacture and painting.\u003c/em\u003e IARC Monogr Eval Carcinog Risks Hum, 1989. \u003cstrong\u003e47\u003c/strong\u003e: p. 1-442.\u003c/li\u003e\n \u003cli\u003eMart\u0026iacute;nez-Alfaro, M., et al., \u003cem\u003eOxidative stress effects of thinner inhalation.\u003c/em\u003e Indian J Occup Environ Med, 2011. \u003cstrong\u003e15\u003c/strong\u003e(3): p. 87-92.\u003c/li\u003e\n \u003cli\u003eBarzallo, T.P., et al., \u003cem\u003eSpontaneous Pneumomediastinum in a 15-Year-Old Adolescent After Unintended Overexposure to Paint Diluent (Thinner) Fumes: First Reported Case.\u003c/em\u003e Ther Adv Pulm Crit Care Med, 2023. \u003cstrong\u003e18\u003c/strong\u003e: p. 11795484231201751.\u003c/li\u003e\n \u003cli\u003eZaidi, S.A., et al., \u003cem\u003eMulti-organ toxicity and death following acute unintentional inhalation of paint thinner fumes.\u003c/em\u003e Clin Toxicol (Phila), 2007. \u003cstrong\u003e45\u003c/strong\u003e(3): p. 287-9.\u003c/li\u003e\n \u003cli\u003eDhibar, D.P., et al., \u003cem\u003eMethemoglobinemia in a Case of Paint Thinner Intoxication, Treated Successfully with Vitamin C.\u003c/em\u003e J Emerg Med, 2018. \u003cstrong\u003e54\u003c/strong\u003e(2): p. 221-224.\u003c/li\u003e\n \u003cli\u003eSarı\u0026ccedil;opur, A., et al., \u003cem\u003eSubacute myocardial infarction due to long-term paint thinner and ecstasy abuse.\u003c/em\u003e Anatol J Cardiol, 2015. \u003cstrong\u003e15\u003c/strong\u003e(2): p. 167-8.\u003c/li\u003e\n \u003cli\u003eLatief, M., et al., \u003cem\u003ePaint-thinner-induced Acute Kidney Injury: A Case Series and Review.\u003c/em\u003e Saudi J Kidney Dis Transpl, 2022. \u003cstrong\u003e33\u003c/strong\u003e(3): p. 487-491.\u003c/li\u003e\n \u003cli\u003eTassaneeyakul, W., et al., \u003cem\u003eHuman cytochrome P450 isoform specificity in the regioselective metabolism of toluene and o-, m- and p-xylene.\u003c/em\u003e J Pharmacol Exp Ther, 1996. \u003cstrong\u003e276\u003c/strong\u003e(1): p. 101-8.\u003c/li\u003e\n \u003cli\u003eGut, I., et al., \u003cem\u003eExposure to various benzene derivatives differently induces cytochromes P450 2B1 and P450 2E1 in rat liver.\u003c/em\u003e Arch Toxicol, 1993. \u003cstrong\u003e67\u003c/strong\u003e(4): p. 237-43.\u003c/li\u003e\n \u003cli\u003eIba, M.M., J. 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Mokrzycki, \u003cem\u003ePlasma exchange for the removal of digoxin-specific antibody fragments in renal failure: timing is important for maximizing clearance.\u003c/em\u003e Am J Kidney Dis, 2000. \u003cstrong\u003e36\u003c/strong\u003e(1): p. 177-83.\u003c/li\u003e\n \u003cli\u003eLarsen, F.S., et al., \u003cem\u003eHigh-volume plasma exchange in patients with acute liver failure: An open randomised controlled trial.\u003c/em\u003e J Hepatol, 2016. \u003cstrong\u003e64\u003c/strong\u003e(1): p. 69-78.\u003c/li\u003e\n \u003cli\u003eLevi, M., et al., \u003cem\u003eGuidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology.\u003c/em\u003e Br J Haematol, 2009. \u003cstrong\u003e145\u003c/strong\u003e(1): p. 24-33.\u003c/li\u003e\n \u003cli\u003ePyykk\u0026ouml;, K., H. T\u0026auml;hti, and H. Vapaatalo, \u003cem\u003eToluene concentrations in various tissues of rats after inhalation and oral administration.\u003c/em\u003e Arch Toxicol, 1977. \u003cstrong\u003e38\u003c/strong\u003e(3): p. 169-76.\u003c/li\u003e\n \u003cli\u003eBowen, S.E., J.H. Hannigan, and S. Irtenkauf, \u003cem\u003eMaternal and fetal blood and organ toluene levels in rats following acute and repeated binge inhalation exposure.\u003c/em\u003e Reprod Toxicol, 2007. \u003cstrong\u003e24\u003c/strong\u003e(3-4): p. 343-52.\u003c/li\u003e\n \u003cli\u003eBergman, K., \u003cem\u003eApplication and results of whole-body autoradiography in distribution studies of organic solvents.\u003c/em\u003e Crit Rev Toxicol, 1983. \u003cstrong\u003e12\u003c/strong\u003e(1): p. 59-118.\u003c/li\u003e\n \u003cli\u003eKilonzo, K.G., H.F. Akrabi, and K.E. Yeates, \u003cem\u003eCost-effectiveness of acute peritoneal dialysis: Considerations from Africa.\u003c/em\u003e Clin Nephrol, 2020. \u003cstrong\u003e93\u003c/strong\u003e(1): p. 72-75.\u003c/li\u003e\n \u003cli\u003eCullis, B., et al., \u003cem\u003eISPD guidelines for peritoneal dialysis in acute kidney injury: 2020 update (adults).\u003c/em\u003e Perit Dial Int, 2021. \u003cstrong\u003e41\u003c/strong\u003e(1): p. 15-31.\u003c/li\u003e\n \u003cli\u003eLeypoldt, J.K., \u003cem\u003eSolute transport across the peritoneal membrane.\u003c/em\u003e J Am Soc Nephrol, 2002. \u003cstrong\u003e13 Suppl 1\u003c/strong\u003e: p. S84-91.\u003c/li\u003e\n \u003cli\u003eKurtzman, T.L., K.N. Otsuka, and R.A. Wahl, \u003cem\u003eInhalant abuse by adolescents.\u003c/em\u003e J Adolesc Health, 2001. \u003cstrong\u003e28\u003c/strong\u003e(3): p. 170-80.\u003c/li\u003e\n \u003cli\u003eAmeno, K., et al., \u003cem\u003eA fatal case of oral ingestion of toluene.\u003c/em\u003e Forensic Sci Int, 1989. \u003cstrong\u003e41\u003c/strong\u003e(3): p. 255-60.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Paint thinner poisoning, organic solvent intoxication, multiple organ dysfunction, acute kidney injury, acute liver injury","lastPublishedDoi":"10.21203/rs.3.rs-9370845/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9370845/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: Accidental ingestion of mixed organic solvents is uncommon but may rapidly lead to life-threatening multi-organ dysfunction, and no specific antidote is available.\u003c/p\u003e\n\u003cp\u003eCase presentation: A 49-year-old Han Chinese man accidentally ingested “rosin water” a paint thinner–type organic solvent, and subsequently developed abdominal pain, vomiting, profuse watery diarrhea, hematochezia, and melena. On presentation to the emergency department, laboratory evaluation revealed severe acute liver injury, hyperbilirubinemia, acute kidney injury, marked coagulopathy, thrombocytopenia, and mild cardiopulmonary involvement. Repeat testing after intensive care unit (ICU) admission confirmed persistent multi-organ dysfunction. He received early hemoperfusion and continuous renal replacement therapy, followed later by repeated plasma exchange for progressive cholestatic hyperbilirubinemia. Because prolonged continuous therapy was not financially feasible, peritoneal dialysis was subsequently used for ongoing renal support. Additional management included acid suppression, inhibition of digestive secretions, blood product transfusion, hepatoprotective therapy, nutritional support, oxygen therapy, and adjunctive corticosteroids. Liver enzymes initially improved but later showed a transient rebound. Bilirubin, creatinine, coagulation abnormalities, and gastrointestinal bleeding gradually improved, and the patient was transferred to the general ward in stable condition for further recovery.\u003c/p\u003e\n\u003cp\u003eConclusion: Mixed lipophilic paint thinners may cause severe gastrointestinal, hepatic, renal, and coagulation abnormalities even in the absence of prominent central nervous system depression. This case suggests that delayed or rebound organ injury may occur during recovery. In selected patients, individualized multimodal supportive care, including extracorporeal therapies when clinically indicated, may be considered. Peritoneal dialysis may serve as a pragmatic option for ongoing renal support when prolonged continuous renal replacement therapy is not feasible.\u003c/p\u003e","manuscriptTitle":"Severe Multiple Organ Dysfunction and Gastrointestinal Hemorrhage After Accidental Paint Thinner Ingestion Managed With Multimodal Extracorporeal Therapies: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-05-11 10:54:15","doi":"10.21203/rs.3.rs-9370845/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"94808d02-f28c-4d38-a530-9588209adc3a","owner":[],"postedDate":"May 11th, 2026","published":true,"recentEditorialEvents":[{"type":"reviewersInvited","content":"6","date":"2026-05-01T14:07:57+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-04-30T11:30:57+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-04-30T06:20:47+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-05-11T10:54:15+00:00","versionOfRecord":[],"versionCreatedAt":"2026-05-11 10:54:15","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9370845","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9370845","identity":"rs-9370845","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}