{"paper_id":"1f020829-5cdd-4e47-9f32-c62f92f642f5","body_text":"A Case of Life-Threatening Metformin-Induced Lactic Acidosis Associated With Euglycemic Ketoacidosis and Acute Multiorgan Dysfunction: 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 A Case of Life-Threatening Metformin-Induced Lactic Acidosis Associated With Euglycemic Ketoacidosis and Acute Multiorgan Dysfunction: A Case Report karim hussein This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6353603/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 Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of metformin therapy. We present a case of a 63-year-old female with type 2 diabetes mellitus (on metformin and insulin) who developed severe lactic acidosis, euglycemic diabetic ketoacidosis (DKA), and acute kidney injury (AKI) following a three-day history of gastrointestinal symptoms. Despite initial stabilization efforts, the patient deteriorated into refractory shock and cardiac arrest, requiring intensive care unit (ICU) admission, continuous venovenous hemodiafiltration (CVVHD), vasopressor support, and mechanical ventilation. Serial arterial blood gas (ABG) analyses demonstrated profound metabolic acidosis (pH 6.77, lactate 20 mmol/L) with gradual normalization following CVVHD. The patient recovered fully, highlighting the importance of early recognition and aggressive management of MALA, including renal replacement therapy (RRT), in critically ill patients. diabetic ketoacidosis lactic acidosis metabolic acidosis acute renal failure post cardiac arrest Figures Figure 1 Figure 2 Figure 3 Figure 4 Introduction Metformin, a cornerstone therapy for type 2 diabetes mellitus, is widely regarded as safe, yet it carries a rare but life-threatening risk of lactic acidosis. Studies like the UK Diabetes Study [ 1 ] and insights from Peters et al. highlight the contentious nature of managing metformin-associated lactic acidosis (MALA). Treatment options range from supportive care and activated charcoal to bicarbonate infusions, hemodialysis, or continuous venovenous hemofiltration. Peters and colleagues previously reported in Critical Care that mortality rates in MALA patients admitted to the ICU were comparable between those who received dialysis and those who did not. However, dialysis was often reserved for the sickest patients-those with acute and chronic comorbidities-suggesting it may have mitigated an otherwise higher mortality risk. In rare instances, metformin toxicity can spiral into multiorgan failure, driven by renal impairment and lactic acidosis, as illustrated in this case. Case Presentation A 63-year-old woman with a history of hypothyroidism (managed with levothyroxine), hypertension (controlled with medication), morbid obesity, and type 2 diabetes (treated with insulin and metformin) arrived at the emergency department (ED) after three days of fatigue, nausea, vomiting, diarrhea, and profound weakness. Paramedics found her hypoglycemic (glucose 17 mg/dL) and administered glucose en route. She reported severe abdominal pain, distention, and polyuria over the prior two days but denied fever, chest pain, respiratory issues, or headache. Notably, she had skipped her medications on the day of admission. Presentation Upon arrival in the ED, the patient appeared lethargic yet remained fully alert, with a Glasgow Coma Scale score of 15/15, and showed clear signs of severe dehydration. Despite normalization of her blood glucose levels, she was hypotensive and exhibited alarming metabolic abnormalities, including elevated ketones, severe metabolic and lactic acidosis, acute kidney injury (AKI), and anuria. Thyroid function tests were normal, while septic markers showed only mild elevation. Management and Progression Resuscitation began immediately with intravenous fluids, vasopressors, sodium bicarbonate, and a diabetic ketoacidosis (DKA) protocol. Despite these aggressive measures, her condition deteriorated into refractory shock, requiring dual vasopressor support. She experienced a cardiac arrest in the ED but was successfully revived after two cycles of CPR and intubation. Imaging studies, including CT of the brain, abdomen, and pelvis, as well as a chest X-ray, were performed to identify potential causes of her decline. Suspecting metformin toxicity due to persistent lactate levels above 20 mmol/L and severe acidosis-despite negative cultures-she was transferred to the ICU for urgent continuous venovenous hemodiafiltration (CVVHD). Imaging revealed several findings. The CT of the abdomen and pelvis with contrast showed a normal liver, gallbladder, spleen, and pancreas, with no evidence of focal lesions or ductal abnormalities. The kidneys appeared normal in size and enhancement, without hydronephrosis or lesions, while diffuse colonic wall thickening with uncomplicated diverticula suggested an infectious process. The left adrenal gland was bulky, though the right adrenal was unremarkable, and no pneumoperitoneum, ascites, or intra-abdominal adenopathy was observed. Atheromatous calcification was noted in the aorta and its branches, and left basal consolidation and cardiomegaly were also evident. The chest X-ray revealed that the endotracheal tube was positioned low in the right main bronchus, necessitating adjustment, while the left costophrenic angle was obscured by the cardiac shadow. No airspace opacities or pneumothorax were identified. In the ICU, CVVHD was initiated alongside ventilatory support and triple vasopressor therapy to stabilize her hemodynamics. Within 24 hours, her ketones normalized, urine output exceeded 1 mL/kg/hour, and lactate levels began to decline, reaching normal by day three. Serial arterial blood gas (ABG) and lactate measurements tracked her progress, as shown in Table 1 . Table 1 Serial ABGs with Lactate Levels from Admission to Pre-Extubation Parameter Reference Range On Admission 12 Hours 24 Hours 36 Hours 48 Hours 72 Hours pH 7.35–7.45 6.77 7.05 7.19 7.25 7.38 7.46 pO2 (kPa) 10–13.3 (75–100 mmHg) 16.7 15.4 14.2 12.4 9.2 10 pCO2 (kPa) 4.7–6.0 (35–45 mmHg) 2.17 2.19 2.8 3.1 3.6 3.9 HCO3 (mmol/L) 22–26 5 5.2 8.4 14.0 18.8 28.6 Base Excess (BE) -2 to + 2 -27.9 -27.7 -24.5 -21.2 -4.2 -2.3 Lactate (mmol/L) 0.5–2.0 20 12.5 9 6.1 3.2 2.6 Outcome By day four in the ICU, the patient was weaned off vasopressors and ventilatory support, becoming fully awake and communicative. Her renal function improved steadily, eliminating the need for further CVVHD. After one additional day of observation in the ICU, she was transferred to the medical ward under nephrology care and was discharged home after 13 days in the hospital. Notable Observations During her hospital stay, her hemoglobin dropped from 13 g/dL to 9.5 g/dL over seven days without evidence of bleeding, but it spontaneously recovered to 12 g/dL within weeks. Additionally, mildly elevated amylase and lipase levels were noted on admission, though no clear cause was identified. This case underscores the urgency of recognizing and treating euglycemic DKA and metformin toxicity in vulnerable patients with severe metabolic compromise. Pancreas is normal in size with normal shape No active intestinal ischemia No intestinal ischemia The chest X-ray revealed that the endotracheal tube was positioned low in the right main bronchus, necessitating adjustment, while the left costophrenic angle was obscured by the cardiac shadow. No airspace opacities or pneumothorax were identified. Discussion Metformin-associated lactic acidosis (MALA) is a rare but potentially lethal complication of a drug otherwise celebrated for its efficacy and safety in type 2 diabetes management. The diagnostic criteria for MALA hinge on a history of metformin exposure coupled with lactic acidosis, defined here as a lactate concentration ≥ 5 mmol/L and bicarbonate < 22 mmol/L at or before ICU admission. While plasma metformin levels can confirm toxicity, their routine measurement is neither widely available nor clinically essential, as metformin exerts its toxic effects intracellularly. Even at therapeutic concentrations (0.5-1 mg/L fasting, 1–2 mg/L postprandial), metformin can disrupt lactate metabolism by inhibiting pyruvate carboxylase, reducing glucose utilization, and increasing hepatocyte lactate production [ 2 ]. This case exemplifies how such metabolic derangements, compounded by acute stressors like gastroenteritis and dehydration, can precipitate a cascade of renal failure, acidosis, and multiorgan dysfunction. The patient’s presentation with euglycemic diabetic ketoacidosis (DKA)-a state of ketosis without hyperglycemia-further complicates the diagnostic landscape. Euglycemic DKA is an underrecognized entity, often linked to factors like reduced carbohydrate intake, vomiting, or, as in this case, metformin’s interference with glucose metabolism. Her severe gastroenteritis likely exacerbated metformin accumulation by causing hypovolemia and acute kidney injury (AKI), impairing the drug’s primary route of elimination-renal excretion. This synergy of factors underscores the importance of considering MALA in any metformin-treated patient presenting with unexplained acidosis, even in the absence of overt hyperglycemia. Therapeutic approaches to MALA remain debated, as highlighted by Finkle [ 1 ]. Options include gastrointestinal decontamination (e.g., activated charcoal), sodium bicarbonate to correct acidosis, and renal replacement therapies like hemodialysis or continuous venovenous hemodiafiltration (CVVHD). In this case, CVVHD proved pivotal, rapidly clearing lactate and stabilizing the patient’s hemodynamics despite initial refractory shock and cardiac arrest. The cardiac toxicity of uncorrected acidosis, as noted by Lebaco et al., stems from reduced myocardial contractility-a risk that timely renal replacement therapy can mitigate. Notably, the patient’s negative cultures ruled out sepsis as a primary driver, reinforcing metformin toxicity as the central etiology. The broader literature offers conflicting insights into MALA’s prognosis. Peters et al. observed similar mortality rates between dialyzed and non-dialyzed patients, yet dialysis was disproportionately used in sicker individuals, suggesting a survival benefit in severe cases [ 1 ]. In our patient, the combination of CVVHD, ventilatory support, and vasopressors reversed a dire trajectory, with lactate normalizing within 72 hours and renal function recovering without further intervention. This aligns with reports that early, aggressive management can avert fatal outcomes, particularly when multiorgan failure looms. Additional observations, such as the transient hemoglobin drop (13 g/dL to 9.5 g/dL) without bleeding, warrant consideration. While metformin-induced hemolytic anemia has been documented [ 2 , 3 ], the spontaneous recovery here suggests hemodilution or stress-related marrow suppression rather than a direct drug effect. In contrast, diagnostic tools like the direct antiglobulin (Coombs’) test, used to detect immune-mediated hemolysis in newborns [ 4 ], are less relevant in this adult context, where no evidence of hemolysis (e.g., schistocytes, elevated bilirubin) emerged. Similarly, the mild elevation in amylase and lipase, without imaging evidence of pancreatitis, may reflect a nonspecific stress response or subtle metformin-related gastrointestinal injury [ 5 ]. These findings highlight the multisystem impact of MALA and the need for comprehensive monitoring beyond acid-base status. This case also raises questions about risk stratification and prevention. Metformin’s excellent enteral bioavailability and renal clearance make it vulnerable to accumulation in settings of dehydration, renal impairment, or overdose. Clinicians must remain vigilant for prodromal symptoms like gastroenteritis, which can tip a stable patient into crisis. Patient education on medication adherence and prompt reporting of such symptoms could further reduce MALA’s incidence, though its rarity complicates broad screening efforts. Conclusions This case of a 63-year-old woman with euglycemic DKA, severe lactic acidosis, acute renal shutdown, and multiorgan dysfunction-precipitated by long-term metformin use and a prodrome of gastrointestinal symptoms-serves as a stark reminder of metformin’s rare but devastating potential. The constellation of high lactate, metabolic acidosis, and renal failure in a diabetic patient on metformin should prompt suspicion of MALA, with or without overt DKA. Here, the patient’s rapid deterioration into shock and cardiac arrest, followed by recovery with CVVHD and supportive care, illustrates both the gravity of this condition and the efficacy of timely intervention. Prognostic factors in MALA are complex. Admission for shock, as seen here, portends a higher mortality risk than isolated renal failure or intentional overdose. Yet, the degree of lactic acidosis itself does not reliably predict outcome, suggesting that systemic effects-such as liver function (reflected by prothrombin time)-and the speed of therapeutic response are critical determinants. The interplay of gastroenteritis, dehydration, and AKI in this case likely amplified metformin toxicity, a scenario that may be underappreciated in clinical practice. The rarity of metformin poisoning presenting with severe gastroenteritis, lactic acidosis, renal failure, and multiorgan dysfunction in a single patient makes this report noteworthy. It adds to the literature by emphasizing the need for heightened awareness among critical care providers. Early recognition of MALA’s atypical presentations-particularly in euglycemic states-coupled with swift initiation of CVVHD and supportive measures, can avert catastrophic outcomes like refractory shock or death. Moreover, this case underscores the importance of a multidisciplinary approach, integrating nephrology, critical care, and endocrinology to optimize outcomes in such complex scenarios. Beyond acute management, this report calls for reflection on preventive strategies. Patients on metformin should be counseled about the risks of dehydration and gastrointestinal illness, with clear guidance to seek care if symptoms persist. While routine metformin level testing remains impractical, future research could explore biomarkers or risk scores to identify vulnerable patients before toxicity ensues. For now, this case reinforces a fundamental lesson: even a familiar drug can harbor rare dangers, and vigilance paired with decisive action can be lifesaving. Declarations Consent to publish was obtained. References Finkle SN (2009) Should dialysis be offered in all cases of metformin-associated lactic acidosis? Crit Care 13:110. 10.1186/cc7161 Hyap AS, Kashyap S (2000) Hemolytic anemia due to metformin. Postgrad Med J 76:125–126. 10.1136/pmj.76.892.125 Meir A, Kleinman Y, Rund D, Da’as N (2003) Metformin-induced hemolytic anemia in a patient with glucose-6-phosphate dehydrogenase deficiency. Diabetes Care 26:956–957. 10.2337/diacare.26.3.956 Herschel M, Karrison T, Wen M, Caldarelli L, Baron B (2002) Evaluation of the direct antiglobulin (Coombs’) test for identifying newborns at risk for hemolysis as determined by end-tidal carbon monoxide concentration (ETCOc); and comparison of the Coombs’ test with ETCOc for detecting significant jaundice. J Perinatol 22:341–347. 10.1038/sj.jp.7210702 Audia P, Feinfeld DA, Dubrow A, Winchester JF (2008) Metformin-induced lactic acidosis and acute pancreatitis precipitated by diuretic, celecoxib, and candesartan-associated acute kidney dysfunction. Clin Toxicol (Philadelphia 46:164–166. 10.1080/15563650701355314 Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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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-6353603\",\"acceptedTermsAndConditions\":true,\"allowDirectSubmit\":true,\"archivedVersions\":[],\"articleType\":\"Case Report\",\"associatedPublications\":[],\"authors\":[{\"id\":436917934,\"identity\":\"a991e113-c9ae-4232-919a-8e5e5fd9bba6\",\"order_by\":0,\"name\":\"karim 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Report\\u003c/p\\u003e\",\"fulltext\":[{\"header\":\"Introduction\",\"content\":\"\\u003cp\\u003eMetformin, a cornerstone therapy for type 2 diabetes mellitus, is widely regarded as safe, yet it carries a rare but life-threatening risk of lactic acidosis. Studies like the UK Diabetes Study [\\u003cspan citationid=\\\"CR1\\\" class=\\\"CitationRef\\\"\\u003e1\\u003c/span\\u003e] and insights from Peters et al. highlight the contentious nature of managing metformin-associated lactic acidosis (MALA). Treatment options range from supportive care and activated charcoal to bicarbonate infusions, hemodialysis, or continuous venovenous hemofiltration. Peters and colleagues previously reported in Critical Care that mortality rates in MALA patients admitted to the ICU were comparable between those who received dialysis and those who did not. However, dialysis was often reserved for the sickest patients-those with acute and chronic comorbidities-suggesting it may have mitigated an otherwise higher mortality risk. In rare instances, metformin toxicity can spiral into multiorgan failure, driven by renal impairment and lactic acidosis, as illustrated in this case.\\u003c/p\\u003e \"},{\"header\":\"Case Presentation\",\"content\":\"\\u003cp\\u003eA 63-year-old woman with a history of hypothyroidism (managed with levothyroxine), hypertension (controlled with medication), morbid obesity, and type 2 diabetes (treated with insulin and metformin) arrived at the emergency department (ED) after three days of fatigue, nausea, vomiting, diarrhea, and profound weakness. Paramedics found her hypoglycemic (glucose 17 mg/dL) and administered glucose en route. She reported severe abdominal pain, distention, and polyuria over the prior two days but denied fever, chest pain, respiratory issues, or headache. Notably, she had skipped her medications on the day of admission.\\u003c/p\\u003e\\n\\u003ch3\\u003ePresentation\\u003c/h3\\u003e\\n\\u003cp\\u003eUpon arrival in the ED, the patient appeared lethargic yet remained fully alert, with a Glasgow Coma Scale score of 15/15, and showed clear signs of severe dehydration. Despite normalization of her blood glucose levels, she was hypotensive and exhibited alarming metabolic abnormalities, including elevated ketones, severe metabolic and lactic acidosis, acute kidney injury (AKI), and anuria. Thyroid function tests were normal, while septic markers showed only mild elevation.\\u003c/p\\u003e \\u003cdiv id=\\\"Sec3\\\" class=\\\"Section2\\\"\\u003e \\u003ch2\\u003eManagement and Progression\\u003c/h2\\u003e \\u003cp\\u003eResuscitation began immediately with intravenous fluids, vasopressors, sodium bicarbonate, and a diabetic ketoacidosis (DKA) protocol. Despite these aggressive measures, her condition deteriorated into refractory shock, requiring dual vasopressor support. She experienced a cardiac arrest in the ED but was successfully revived after two cycles of CPR and intubation. Imaging studies, including CT of the brain, abdomen, and pelvis, as well as a chest X-ray, were performed to identify potential causes of her decline. Suspecting metformin toxicity due to persistent lactate levels above 20 mmol/L and severe acidosis-despite negative cultures-she was transferred to the ICU for urgent continuous venovenous hemodiafiltration (CVVHD).\\u003c/p\\u003e \\u003cp\\u003eImaging revealed several findings. The CT of the abdomen and pelvis with contrast showed a normal liver, gallbladder, spleen, and pancreas, with no evidence of focal lesions or ductal abnormalities. The kidneys appeared normal in size and enhancement, without hydronephrosis or lesions, while diffuse colonic wall thickening with uncomplicated diverticula suggested an infectious process. The left adrenal gland was bulky, though the right adrenal was unremarkable, and no pneumoperitoneum, ascites, or intra-abdominal adenopathy was observed. Atheromatous calcification was noted in the aorta and its branches, and left basal consolidation and cardiomegaly were also evident. The chest X-ray revealed that the endotracheal tube was positioned low in the right main bronchus, necessitating adjustment, while the left costophrenic angle was obscured by the cardiac shadow. No airspace opacities or pneumothorax were identified.\\u003c/p\\u003e \\u003cp\\u003eIn the ICU, CVVHD was initiated alongside ventilatory support and triple vasopressor therapy to stabilize her hemodynamics. Within 24 hours, her ketones normalized, urine output exceeded 1 mL/kg/hour, and lactate levels began to decline, reaching normal by day three. Serial arterial blood gas (ABG) and lactate measurements tracked her progress, as shown in Table\\u0026nbsp;\\u003cspan refid=\\\"Tab1\\\" class=\\\"InternalRef\\\"\\u003e1\\u003c/span\\u003e.\\u003c/p\\u003e \\u003cp\\u003e \\u003cdiv class=\\\"gridtable\\\"\\u003e\\u003ctable float=\\\"Yes\\\" id=\\\"Tab1\\\" border=\\\"1\\\"\\u003e \\u003ccaption language=\\\"En\\\"\\u003e \\u003cdiv class=\\\"CaptionNumber\\\"\\u003eTable 1\\u003c/div\\u003e \\u003cdiv class=\\\"CaptionContent\\\"\\u003e \\u003cp\\u003eSerial ABGs with Lactate Levels from Admission to Pre-Extubation\\u003c/p\\u003e \\u003c/div\\u003e \\u003c/caption\\u003e \\u003ccolgroup cols=\\\"8\\\"\\u003e \\u003cdiv align=\\\"left\\\" class=\\\"colspec\\\" colname=\\\"c1\\\" colnum=\\\"1\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"left\\\" class=\\\"colspec\\\" colname=\\\"c2\\\" colnum=\\\"2\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"left\\\" class=\\\"colspec\\\" colname=\\\"c3\\\" colnum=\\\"3\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"char\\\" char=\\\".\\\" class=\\\"colspec\\\" colname=\\\"c4\\\" colnum=\\\"4\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"left\\\" class=\\\"colspec\\\" colname=\\\"c5\\\" colnum=\\\"5\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"char\\\" char=\\\".\\\" class=\\\"colspec\\\" colname=\\\"c6\\\" colnum=\\\"6\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"char\\\" char=\\\".\\\" class=\\\"colspec\\\" colname=\\\"c7\\\" colnum=\\\"7\\\"\\u003e\\u003c/div\\u003e \\u003cdiv align=\\\"left\\\" class=\\\"colspec\\\" colname=\\\"c8\\\" colnum=\\\"8\\\"\\u003e\\u003c/div\\u003e \\u003cthead\\u003e \\u003ctr\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003eParameter\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003eReference Range\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003eOn Admission\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e12 Hours\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e24 Hours\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e36 Hours\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e48 Hours\\u003c/p\\u003e \\u003c/th\\u003e \\u003cth align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e72 Hours\\u003c/p\\u003e \\u003c/th\\u003e \\u003c/tr\\u003e \\u003c/thead\\u003e \\u003ctbody\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003epH\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e7.35\\u0026ndash;7.45\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e6.77\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e7.05\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e7.19\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e7.25\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e7.38\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e7.46\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003epO2 (kPa)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e10\\u0026ndash;13.3 (75\\u0026ndash;100 mmHg)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e16.7\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e15.4\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e14.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e12.4\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e9.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e10\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003epCO2 (kPa)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e4.7\\u0026ndash;6.0 (35\\u0026ndash;45 mmHg)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e2.17\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e2.19\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e2.8\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e3.1\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e3.6\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e3.9\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003eHCO3 (mmol/L)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e22\\u0026ndash;26\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e5\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e5.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e8.4\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e14.0\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e18.8\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e28.6\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003eBase Excess (BE)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e-2 to +\\u0026thinsp;2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e-27.9\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e-27.7\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e-24.5\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e-21.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e-4.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e-2.3\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003ctr\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c1\\\"\\u003e \\u003cp\\u003eLactate (mmol/L)\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c2\\\"\\u003e \\u003cp\\u003e0.5\\u0026ndash;2.0\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c3\\\"\\u003e \\u003cp\\u003e20\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c4\\\"\\u003e \\u003cp\\u003e12.5\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c5\\\"\\u003e \\u003cp\\u003e9\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c6\\\"\\u003e \\u003cp\\u003e6.1\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"char\\\" char=\\\".\\\" colname=\\\"c7\\\"\\u003e \\u003cp\\u003e3.2\\u003c/p\\u003e \\u003c/td\\u003e \\u003ctd align=\\\"left\\\" colname=\\\"c8\\\"\\u003e \\u003cp\\u003e2.6\\u003c/p\\u003e \\u003c/td\\u003e \\u003c/tr\\u003e \\u003c/tbody\\u003e \\u003c/colgroup\\u003e \\u003c/table\\u003e\\u003c/div\\u003e \\u003c/p\\u003e \\u003c/div\\u003e\\n\\u003ch3\\u003eOutcome\\u003c/h3\\u003e\\n\\u003cp\\u003eBy day four in the ICU, the patient was weaned off vasopressors and ventilatory support, becoming fully awake and communicative. Her renal function improved steadily, eliminating the need for further CVVHD. After one additional day of observation in the ICU, she was transferred to the medical ward under nephrology care and was discharged home after 13 days in the hospital.\\u003c/p\\u003e\\n\\u003cp\\u003e\\u003cstrong\\u003eNotable Observations\\u003c/strong\\u003e\\u003c/p\\u003e\\n\\u003cp\\u003eDuring her hospital stay, her hemoglobin dropped from 13 g/dL to 9.5 g/dL over seven days without evidence of bleeding, but it spontaneously recovered to 12 g/dL within weeks. Additionally, mildly elevated amylase and lipase levels were noted on admission, though no clear cause was identified. This case underscores the urgency of recognizing and treating euglycemic DKA and metformin toxicity in vulnerable patients with severe metabolic compromise.\\u003c/p\\u003e\\n\\u003cp\\u003ePancreas is normal in size with normal shape\\u003c/p\\u003e\\n\\u003cp\\u003eNo active intestinal ischemia\\u0026nbsp;\\u003c/p\\u003e\\n\\u003cp\\u003eNo intestinal ischemia\\u0026nbsp;\\u003c/p\\u003e\\n\\u003cp\\u003eThe chest X-ray revealed that the endotracheal tube was positioned low in the right main bronchus, necessitating adjustment, while the left costophrenic angle was obscured by the cardiac shadow. No airspace opacities or pneumothorax were identified.\\u003c/p\\u003e\"},{\"header\":\"Discussion\",\"content\":\"\\u003cp\\u003eMetformin-associated lactic acidosis (MALA) is a rare but potentially lethal complication of a drug otherwise celebrated for its efficacy and safety in type 2 diabetes management. The diagnostic criteria for MALA hinge on a history of metformin exposure coupled with lactic acidosis, defined here as a lactate concentration\\u0026thinsp;\\u0026ge;\\u0026thinsp;5 mmol/L and bicarbonate\\u0026thinsp;\\u0026lt;\\u0026thinsp;22 mmol/L at or before ICU admission. While plasma metformin levels can confirm toxicity, their routine measurement is neither widely available nor clinically essential, as metformin exerts its toxic effects intracellularly. Even at therapeutic concentrations (0.5-1 mg/L fasting, 1\\u0026ndash;2 mg/L postprandial), metformin can disrupt lactate metabolism by inhibiting pyruvate carboxylase, reducing glucose utilization, and increasing hepatocyte lactate production [\\u003cspan citationid=\\\"CR2\\\" class=\\\"CitationRef\\\"\\u003e2\\u003c/span\\u003e]. This case exemplifies how such metabolic derangements, compounded by acute stressors like gastroenteritis and dehydration, can precipitate a cascade of renal failure, acidosis, and multiorgan dysfunction.\\u003c/p\\u003e \\u003cp\\u003eThe patient\\u0026rsquo;s presentation with euglycemic diabetic ketoacidosis (DKA)-a state of ketosis without hyperglycemia-further complicates the diagnostic landscape. Euglycemic DKA is an underrecognized entity, often linked to factors like reduced carbohydrate intake, vomiting, or, as in this case, metformin\\u0026rsquo;s interference with glucose metabolism. Her severe gastroenteritis likely exacerbated metformin accumulation by causing hypovolemia and acute kidney injury (AKI), impairing the drug\\u0026rsquo;s primary route of elimination-renal excretion. This synergy of factors underscores the importance of considering MALA in any metformin-treated patient presenting with unexplained acidosis, even in the absence of overt hyperglycemia.\\u003c/p\\u003e \\u003cp\\u003eTherapeutic approaches to MALA remain debated, as highlighted by Finkle [\\u003cspan citationid=\\\"CR1\\\" class=\\\"CitationRef\\\"\\u003e1\\u003c/span\\u003e]. Options include gastrointestinal decontamination (e.g., activated charcoal), sodium bicarbonate to correct acidosis, and renal replacement therapies like hemodialysis or continuous venovenous hemodiafiltration (CVVHD). In this case, CVVHD proved pivotal, rapidly clearing lactate and stabilizing the patient\\u0026rsquo;s hemodynamics despite initial refractory shock and cardiac arrest. The cardiac toxicity of uncorrected acidosis, as noted by Lebaco et al., stems from reduced myocardial contractility-a risk that timely renal replacement therapy can mitigate. Notably, the patient\\u0026rsquo;s negative cultures ruled out sepsis as a primary driver, reinforcing metformin toxicity as the central etiology.\\u003c/p\\u003e \\u003cp\\u003eThe broader literature offers conflicting insights into MALA\\u0026rsquo;s prognosis. Peters et al. observed similar mortality rates between dialyzed and non-dialyzed patients, yet dialysis was disproportionately used in sicker individuals, suggesting a survival benefit in severe cases [\\u003cspan citationid=\\\"CR1\\\" class=\\\"CitationRef\\\"\\u003e1\\u003c/span\\u003e]. In our patient, the combination of CVVHD, ventilatory support, and vasopressors reversed a dire trajectory, with lactate normalizing within 72 hours and renal function recovering without further intervention. This aligns with reports that early, aggressive management can avert fatal outcomes, particularly when multiorgan failure looms.\\u003c/p\\u003e \\u003cp\\u003eAdditional observations, such as the transient hemoglobin drop (13 g/dL to 9.5 g/dL) without bleeding, warrant consideration. While metformin-induced hemolytic anemia has been documented [\\u003cspan citationid=\\\"CR2\\\" class=\\\"CitationRef\\\"\\u003e2\\u003c/span\\u003e, \\u003cspan citationid=\\\"CR3\\\" class=\\\"CitationRef\\\"\\u003e3\\u003c/span\\u003e], the spontaneous recovery here suggests hemodilution or stress-related marrow suppression rather than a direct drug effect. In contrast, diagnostic tools like the direct antiglobulin (Coombs\\u0026rsquo;) test, used to detect immune-mediated hemolysis in newborns [\\u003cspan citationid=\\\"CR4\\\" class=\\\"CitationRef\\\"\\u003e4\\u003c/span\\u003e], are less relevant in this adult context, where no evidence of hemolysis (e.g., schistocytes, elevated bilirubin) emerged. Similarly, the mild elevation in amylase and lipase, without imaging evidence of pancreatitis, may reflect a nonspecific stress response or subtle metformin-related gastrointestinal injury [\\u003cspan citationid=\\\"CR5\\\" class=\\\"CitationRef\\\"\\u003e5\\u003c/span\\u003e]. These findings highlight the multisystem impact of MALA and the need for comprehensive monitoring beyond acid-base status.\\u003c/p\\u003e \\u003cp\\u003eThis case also raises questions about risk stratification and prevention. Metformin\\u0026rsquo;s excellent enteral bioavailability and renal clearance make it vulnerable to accumulation in settings of dehydration, renal impairment, or overdose. Clinicians must remain vigilant for prodromal symptoms like gastroenteritis, which can tip a stable patient into crisis. Patient education on medication adherence and prompt reporting of such symptoms could further reduce MALA\\u0026rsquo;s incidence, though its rarity complicates broad screening efforts.\\u003c/p\\u003e\"},{\"header\":\"Conclusions\",\"content\":\"\\u003cp\\u003eThis case of a 63-year-old woman with euglycemic DKA, severe lactic acidosis, acute renal shutdown, and multiorgan dysfunction-precipitated by long-term metformin use and a prodrome of gastrointestinal symptoms-serves as a stark reminder of metformin\\u0026rsquo;s rare but devastating potential. The constellation of high lactate, metabolic acidosis, and renal failure in a diabetic patient on metformin should prompt suspicion of MALA, with or without overt DKA. Here, the patient\\u0026rsquo;s rapid deterioration into shock and cardiac arrest, followed by recovery with CVVHD and supportive care, illustrates both the gravity of this condition and the efficacy of timely intervention. Prognostic factors in MALA are complex. Admission for shock, as seen here, portends a higher mortality risk than isolated renal failure or intentional overdose. Yet, the degree of lactic acidosis itself does not reliably predict outcome, suggesting that systemic effects-such as liver function (reflected by prothrombin time)-and the speed of therapeutic response are critical determinants. The interplay of gastroenteritis, dehydration, and AKI in this case likely amplified metformin toxicity, a scenario that may be underappreciated in clinical practice.\\u003c/p\\u003e \\u003cp\\u003eThe rarity of metformin poisoning presenting with severe gastroenteritis, lactic acidosis, renal failure, and multiorgan dysfunction in a single patient makes this report noteworthy. It adds to the literature by emphasizing the need for heightened awareness among critical care providers. Early recognition of MALA\\u0026rsquo;s atypical presentations-particularly in euglycemic states-coupled with swift initiation of CVVHD and supportive measures, can avert catastrophic outcomes like refractory shock or death. Moreover, this case underscores the importance of a multidisciplinary approach, integrating nephrology, critical care, and endocrinology to optimize outcomes in such complex scenarios. Beyond acute management, this report calls for reflection on preventive strategies. Patients on metformin should be counseled about the risks of dehydration and gastrointestinal illness, with clear guidance to seek care if symptoms persist. While routine metformin level testing remains impractical, future research could explore biomarkers or risk scores to identify vulnerable patients before toxicity ensues. For now, this case reinforces a fundamental lesson: even a familiar drug can harbor rare dangers, and vigilance paired with decisive action can be lifesaving.\\u003c/p\\u003e\"},{\"header\":\"Declarations\",\"content\":\"\\u003cp\\u003eConsent to publish was obtained.\\u003c/p\\u003e\"},{\"header\":\"References\",\"content\":\"\\u003col\\u003e\\u003cli\\u003e\\u003cspan\\u003eFinkle SN (2009) Should dialysis be offered in all cases of metformin-associated lactic acidosis? Crit Care 13:110. \\u003cspan class=\\\"ExternalRef\\\"\\u003e\\u003cspan class=\\\"RefSource\\\"\\u003e10.1186/cc7161\\u003c/span\\u003e\\u003cspan address=\\\"10.1186/cc7161\\\" targettype=\\\"DOI\\\" class=\\\"RefTarget\\\"\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/li\\u003e \\u003cli\\u003e\\u003cspan\\u003eHyap AS, Kashyap S (2000) Hemolytic anemia due to metformin. Postgrad Med J 76:125\\u0026ndash;126. \\u003cspan class=\\\"ExternalRef\\\"\\u003e\\u003cspan class=\\\"RefSource\\\"\\u003e10.1136/pmj.76.892.125\\u003c/span\\u003e\\u003cspan address=\\\"10.1136/pmj.76.892.125\\\" targettype=\\\"DOI\\\" class=\\\"RefTarget\\\"\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/li\\u003e \\u003cli\\u003e\\u003cspan\\u003eMeir A, Kleinman Y, Rund D, Da\\u0026rsquo;as N (2003) Metformin-induced hemolytic anemia in a patient with glucose-6-phosphate dehydrogenase deficiency. Diabetes Care 26:956\\u0026ndash;957. \\u003cspan class=\\\"ExternalRef\\\"\\u003e\\u003cspan class=\\\"RefSource\\\"\\u003e10.2337/diacare.26.3.956\\u003c/span\\u003e\\u003cspan address=\\\"10.2337/diacare.26.3.956\\\" targettype=\\\"DOI\\\" class=\\\"RefTarget\\\"\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/li\\u003e \\u003cli\\u003e\\u003cspan\\u003eHerschel M, Karrison T, Wen M, Caldarelli L, Baron B (2002) Evaluation of the direct antiglobulin (Coombs\\u0026rsquo;) test for identifying newborns at risk for hemolysis as determined by end-tidal carbon monoxide concentration (ETCOc); and comparison of the Coombs\\u0026rsquo; test with ETCOc for detecting significant jaundice. J Perinatol 22:341\\u0026ndash;347. \\u003cspan class=\\\"ExternalRef\\\"\\u003e\\u003cspan class=\\\"RefSource\\\"\\u003e10.1038/sj.jp.7210702\\u003c/span\\u003e\\u003cspan address=\\\"10.1038/sj.jp.7210702\\\" targettype=\\\"DOI\\\" class=\\\"RefTarget\\\"\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/li\\u003e \\u003cli\\u003e\\u003cspan\\u003eAudia P, Feinfeld DA, Dubrow A, Winchester JF (2008) Metformin-induced lactic acidosis and acute pancreatitis precipitated by diuretic, celecoxib, and candesartan-associated acute kidney dysfunction. Clin Toxicol (Philadelphia 46:164\\u0026ndash;166. \\u003cspan class=\\\"ExternalRef\\\"\\u003e\\u003cspan class=\\\"RefSource\\\"\\u003e10.1080/15563650701355314\\u003c/span\\u003e\\u003cspan address=\\\"10.1080/15563650701355314\\\" targettype=\\\"DOI\\\" class=\\\"RefTarget\\\"\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/span\\u003e\\u003c/li\\u003e\\u003c/ol\\u003e\"}],\"fulltextSource\":\"\",\"fullText\":\"\",\"funders\":[],\"hasAdminPriorityOnWorkflow\":false,\"hasManuscriptDocX\":true,\"hasOptedInToPreprint\":true,\"hasPassedJournalQc\":\"\",\"hasAnyPriority\":true,\"hideJournal\":true,\"highlight\":\"\",\"institution\":\"Dubai Hospital\",\"isAcceptedByJournal\":false,\"isAuthorSuppliedPdf\":false,\"isDeskRejected\":\"\",\"isHiddenFromSearch\":false,\"isInQc\":false,\"isInWorkflow\":false,\"isPdf\":false,\"isPdfUpToDate\":true,\"isWithdrawnOrRetracted\":false,\"journal\":{\"display\":true,\"email\":\"info@researchsquare.com\",\"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\":\"diabetic ketoacidosis, lactic acidosis, metabolic acidosis, acute renal failure, post cardiac arrest\",\"lastPublishedDoi\":\"10.21203/rs.3.rs-6353603/v1\",\"lastPublishedDoiUrl\":\"https://doi.org/10.21203/rs.3.rs-6353603/v1\",\"license\":{\"name\":\"CC BY 4.0\",\"url\":\"https://creativecommons.org/licenses/by/4.0/\"},\"manuscriptAbstract\":\"\\u003cp\\u003eMetformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of metformin therapy. We present a case of a 63-year-old female with type 2 diabetes mellitus (on metformin and insulin) who developed severe lactic acidosis, euglycemic diabetic ketoacidosis (DKA), and acute kidney injury (AKI) following a three-day history of gastrointestinal symptoms. Despite initial stabilization efforts, the patient deteriorated into refractory shock and cardiac arrest, requiring intensive care unit (ICU) admission, continuous venovenous hemodiafiltration (CVVHD), vasopressor support, and mechanical ventilation. Serial arterial blood gas (ABG) analyses demonstrated profound metabolic acidosis (pH 6.77, lactate 20 mmol/L) with gradual normalization following CVVHD. The patient recovered fully, highlighting the importance of early recognition and aggressive management of MALA, including renal replacement therapy (RRT), in critically ill patients.\\u003c/p\\u003e \\u003cp\\u003e \\u003c/p\\u003e \\u003cp\\u003e \\u003c/p\\u003e\",\"manuscriptTitle\":\"A Case of Life-Threatening Metformin-Induced Lactic Acidosis Associated With Euglycemic Ketoacidosis and Acute Multiorgan Dysfunction: A Case Report\",\"msid\":\"\",\"msnumber\":\"\",\"nonDraftVersions\":[{\"code\":1,\"date\":\"2025-04-10 06:59:16\",\"doi\":\"10.21203/rs.3.rs-6353603/v1\",\"editorialEvents\":[{\"type\":\"communityComments\",\"content\":0}],\"status\":\"published\",\"journal\":{\"display\":true,\"email\":\"info@researchsquare.com\",\"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\":\"3771b1be-88ac-464d-8fa5-f46666da002e\",\"owner\":[],\"postedDate\":\"April 10th, 2025\",\"published\":true,\"recentEditorialEvents\":[],\"rejectedJournal\":[],\"revision\":\"\",\"amendment\":\"\",\"status\":\"posted\",\"subjectAreas\":[],\"tags\":[],\"updatedAt\":\"2025-04-10T06:59:16+00:00\",\"versionOfRecord\":[],\"versionCreatedAt\":\"2025-04-10 06:59:16\",\"video\":\"\",\"vorDoi\":\"\",\"vorDoiUrl\":\"\",\"workflowStages\":[]},\"version\":\"v1\",\"identity\":\"rs-6353603\",\"journalConfig\":\"researchsquare\"},\"__N_SSP\":true},\"page\":\"/article/[identity]/[[...version]]\",\"query\":{\"redirect\":\"/article/rs-6353603\",\"identity\":\"rs-6353603\",\"version\":[\"v1\"]},\"buildId\":\"XKTyCvWXoU3ODBz1xrDgd\",\"isFallback\":false,\"isExperimentalCompile\":false,\"dynamicIds\":[84888],\"gssp\":true,\"scriptLoader\":[]}","source_license":"CC-BY-4.0","license_restricted":false}