Metformin-Associated Nonketotic Metabolic Acidosis

1997 ◽  
Vol 31 (1) ◽  
pp. 53-55 ◽  
Author(s):  
Mark R Jurovich ◽  
John D Wooldridge ◽  
Rex W Force
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Early Recognition ◽  
Normal Serum ◽  
Anion Gap ◽  
Diabetic Patients ◽  
Strict Adherence ◽  
Arterial Blood

OBJECTIVE: To document a case of anion gap, nonketotic metabolic acidosis occurring in a patient with acute renal failure who was receiving metformin. CASE SUMMARY: A 67-year-old white man presented with a 9-day history of weakness, nausea, dizziness, and difficulty moving; he had also not eaten during the previous 2 days. The patient had numerous abnormalities on his serum chemistry panel and arterial blood gases, including a pH of 7.1 and an anion gap of 21 mEq/L. No ketones were detected in the urine. The patient was treated with intravenous fluids, sodium bicarbonate, insulin, and hemodialysis. All medications were discontinued. The acidosis resolved shortly after hemodialysis. The hospital course was complicated by the onset of atrial fibrillation occurring on day 2 that did not respond to chemical cardioversion. On day 6 the patient was discharged home with resolving acute renal failure and normal serum pH. CONCLUSIONS: The mortality rate of biguanide-induced lactic acidosis is approximately 50%; thus, early recognition and treatment are essential. Suspicion of lactic acidosis should be high when diabetic patients who are taking a biguanide present with acidosis. The majority of cases of metformin-induced lactic acidosis have occurred in patients with contraindications to the drug (i.e., renal dysfunction). Thus, it is important to maintain strict adherence to these contraindications and monitor patients for deteriorating renal function.

A teenager presenting with anuric acute renal failure and metabolic acidosis with a high anion gap: Questions

2020 ◽  
Vol 35 (12) ◽  
pp. 2253-2255
Author(s):  
Çağla Serpil Doğan ◽  
Gülşah Kaya Aksoy ◽  
Kadir Aras Demircan ◽  
Şenay Yıldırım
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Anion Gap

A teenager presenting with anuric acute renal failure and metabolic acidosis with a high anion gap: Answers

2020 ◽  
Vol 35 (12) ◽  
pp. 2257-2258
Author(s):  
Çağla Serpil Doğan ◽  
Gülşah Kaya Aksoy ◽  
Kadir Aras Demircan ◽  
Şenay Yıldırım
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Anion Gap

High anion gap metabolic acidosis induced by cumulation of ketones, L- and D-lactate, 5-oxoproline and acute renal failure

2017 ◽  
Vol 73 (4) ◽  
pp. 313-316 ◽  
Author(s):  
Laura Heireman ◽  
Boris Mahieu ◽  
Mark Helbert ◽  
Wim Uyttenbroeck ◽  
Jan Stroobants ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Anion Gap

scholarly journals Euglycemic DKA Associated With SGLT2 Inhibitors

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A382-A382
Author(s):  
Asieh TakallooBakhtiari ◽  
Julio Piedra Butina ◽  
Sheri A Gillis Funderburk ◽  
Hari V Brundavanam
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Level ◽  
Urine Analysis ◽  
Oral Intake ◽  
Sglt2 Inhibitors ◽  
Anion Gap ◽  
Diabetic Patients ◽  
Care Providers ◽  
Glucose Levels ◽  
Arterial Blood

Abstract Background: DKA associated with SGLT2 inhibitors also known as Euglycemic DKA (EDKA) is a rare condition characterized by milder degrees of hyperglycemia with a blood glucose level < 200 mg/dl. Unfortunately, this unusual feature can often lead to missed or delayed diagnosis with potential life-threatening outcomes. Clinical Case: The patient is a 53-year-old Caucasian male with PMH of type 2 diabetes mellitus treating with Metformin and Empagliflozin. He presented to the emergency room with shortness of breath, flu-like symptoms, and decreased oral intake for a couple of days. Vital signs at presentation were: Temperature 98.2 °F, pulse rate 108 beats/min, respiratory rate 28 breaths/min, and blood pressure 134/72 mmHg. He was alert but ill-looking, moderately dehydrated with dry mucus membranes. The rest of the physical examination was unremarkable at the time of admission. In the initial blood work, sugar was found to be mildly elevated (163mg/dl), and hemoconcentration besides mild pre-renal acute kidney injury was detected. He was also found infected by the COVID-19 virus without hypoxemia or signs of pneumonia. Arterial blood gases showed metabolic acidosis with an elevated anion gap (PH 7.21, CO2 39.93mmHg, HCO3− 10mEq/L, anion gap 21mEq/L). Urine analysis was positive for ketones and glucose. After ruling out other causes of metabolic acidosis by screening for alcohols, salicylates, acetaminophen, lactic acid, and urine toxicology; the diagnosis of EDKA was made. He was treated with a 3L bolus of IV normal saline and an insulin drip with dextrose solution started as per the protocol based on his glucose levels and promptly admitted to the intensive care unit (ICU). Serial blood tests showed gradual resolution of ketoacidosis and anion gap normalized after 36 hours when insulin drip was stopped and replaced by subcutaneous insulin therapy. Conclusion: SGLT2 inhibitors increase the urinary excretion rate of glucose and subsequent fall in plasma glucose level. Thus, In the absence of exogenous insulin use, increase glucagon release resulting in upregulation of lipolysis and activation of the ketogenesis. Factors such as low oral intake, concurrent infection, and alcohol use can also exacerbate the process. Timely diagnosis of EDKA can be a challenge for physicians unfamiliar with this class of medications, additionally, ketone studies and blood gas analyses are not part of the routine workup for diabetic patients in the emergency department. We recommend all first-line care providers to consider ketosis in ill patients with diabetes and metabolic acidosis, despite the normal or near-normal serum glucose levels. EDKA is mainly a diagnosis of exclusion, but treatment is not different from DKA; correcting dehydration by using intravenous fluids and then, initiating insulin drip along with dextrose-containing solutions, and frequent monitoring of serum anion gap.

Alcohol Related Non-traumatic Rhabdomyolysis and Compartment Syndrome

2007 ◽  
Vol 6 (1) ◽  
pp. 33-34
Author(s):  
JPL Ong ◽  
◽  
LA Thomas ◽  
Keyword(s):  
Skeletal Muscle ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Lower Extremity ◽  
Compartment Syndrome ◽  
Early Recognition ◽  
Clinical Entity ◽  
Threatening Condition ◽  
Life Threatening ◽  
Renal Support

Rhabdomyolysis is a serious and life-threatening condition in which skeletal muscle is damaged, commonly resulting in acute renal failure. The causes of this clinical entity can be traumatic and non-traumatic. In the latter group, alcohol is the commonest cause. This report describes the case of a 25 year old man who presented with rhabdomyolysis leading to acute renal failure after an alcohol binge. He presented with painful legs and lower extremity compartment syndrome. The patient recovered with surgical fasciotomy and renal support. This case illustrates the importance of early recognition and treatment of alcohol related non-traumatic rhabdomyolysis and compartment syndrome.

Acute Tubular Necrosis: Diagnosis, Treatment, and Nursing Implications

1992 ◽  
Vol 3 (3) ◽  
pp. 688-697
Author(s):  
Sara Douglas
Keyword(s):  
At Risk ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Critical Care ◽  
Acute Tubular Necrosis ◽  
Early Recognition ◽  
Recovery Phase ◽  
Vital Role ◽  
Laboratory Findings ◽  
Tubular Necrosis

Acute tubular necrosis (ATN) is the most common cause of acute renal failure. Early recognition of patients who are at risk for ATN can prevent or improve the course of ATN. Acute renal failure is classified as prerenal, intrinsic, or postrenal disease. ATN is classified as a type of intrinsic renal disease. The clinical course of ATN is divided into the renal failure phase, diuretic phase, and recovery phase, with each phase having distinct symptoms and laboratory findings. Diagnosis of ATN often is complicated and confusing; understanding of laboratory findings can facilitate the critical care nurse’s ability to assess those at risk for ATN. The care and treatment of the patient with ATN is complicated, and specific treatments are discussed in detail. The critical care nurse can play a vital role in identifying the patient at risk, preventing the development of ATN in those at risk, and providing appropriate care for those who develop ATN

scholarly journals Therapeutic approach in patients undergoing percutaneous coronary interventions

2009 ◽  
Vol 62 (7-8) ◽  
pp. 331-336 ◽  
Author(s):  
Zdravko Mijailovic ◽  
Zoran Stajic ◽  
Miodrag Jevtic ◽  
Srdjan Aleksandric ◽  
Radomir Matunovic ◽  
...  
Keyword(s):  
Renal Failure ◽  
Primary Care Physicians ◽  
Coronary Revascularization ◽  
Coronary Intervention ◽  
Normal Serum ◽  
Diabetic Patients ◽  
Percutaneous Coronary Interventions ◽  
Coronary Interventions ◽  
Iodinated Contrast ◽  
Percutaneous Coronary

While the performance of percutaneous coronary interventions remains the domain of interventional cardiologists, the management of these patients before, during, and after the procedure is in the domain of general cardiologists, internists and primary care physicians. Therefore, for optimal patient care it is crucial that all engaged physicians should understand the procedural risks, complications and optimal treatment strategy before, during and after the procedure. Before a percutaenous coronary intervention, patients with known allergies to iodinated contrast dye should be pretreated with oral corticosteroids and H1-receptor blockers. Diabetic patients as well as patients with renal failure need special care. Hydration is crucial for patients with renal insufficiency in order to minimise the risk of contrast nephropathy. Metformin therapy should be discontinued before the procedure in patients with renal failure in order to avoid lactic acidosis, and it should be reinstituted after the procedure only when normal serum creatine level is confirmed. Double antiplatelet therapy (aspirin plus clopidogrel) should be initiated at least six hours before the procedure. While aspirin therapy after the procedure is life long, the duration of clopidogrel therapy depends on the type of implanted stent (in patients with bare stents implanted clopidogrel should be taken at least 3 - 4 weeks post procedural, and in patients with drug-eluting stents implanted clopidogrel should be taken at least 6 - 12 months after the procedure due to in-stent restenosis prevention). Patients who experience typical anginal pain in a period of one to eight month after percutaneous coronary revascularization are likely to have restenosis, and they should be reevaluated with stress echocardiography and/or repeated coronary angiography.

Phosphatemic Control during Acute Renal Failure: Intermittent Hemodialysis versus Continuous Hemodiafiltration

2001 ◽  
Vol 24 (4) ◽  
pp. 186-191 ◽  
Author(s):  
H.K. Tan ◽  
R. Bellomo ◽  
D.A. M'Pisi ◽  
C. Ronco
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Normal Serum ◽  
Serum Phosphate ◽  
Phosphate Concentration ◽  
Intermittent Hemodialysis ◽  
Normal Range ◽  
Continuous Hemodiafiltration ◽  
Intensive Care Patients ◽  
Blood Tests

Background Achieving “adequacy of dialysis” includes the maintenance of normal serum phosphate concentrations and is an important therapeutic goal in the treatment of acute renal failure (ARF). It is unknown whether this goal is best achieved with intermittent or continuous renal replacement therapy. Methods We compared the effects of continuous veno-venous hemodiafiltration (CVVHDF) and intermittent hemodialysis (IHD) on serum phosphate concentrations using daily morning blood tests in 88 consecutive intensive care patients half of which were treated with IHD and half with CRRT. Results Mean patient age was 54 ± 14 years for IHD and 60 ± 14 years for CVVHDF (NS). However, patients who received CVVHDF were more critically ill (mean APACHE II scores: 24.4 ± 5.1 for IHD vs. 29.2 ± 5.7 for CVVHDF, p<0.003). Before treatment, the serum phosphate concentration was 2.04 ± 0.16 mmoll L for IHD and 1.96 ± 0.17 mmoll L for CVVHDF (NS), with abnormal values in 79.4% of IHD patients and in 64.8% of CVVHDF patients (NS). During treatment, CVVHDF induced a greater reduction in serum phosphate (p=0.02) during the first 48 hours and conferred superior subsequent control of hyperphosphatemia (achieved in 64.6% of observations during CVVHDF vs. 41.8% during IHD; p<0.0001). The serum phosphate concentration was also more likely to be within the normal range during CVVHDF (55.3% vs.36.2%; p<0.0001). There was a trend toward more frequent hypophosphatemia (9.3% vs. 5.6%; P<0.1) during CVVHDF. Conclusions Abnormal serum phosphate concentrations are frequent in ARF patients before and during renal replacement, however, normalization of phosphatemia is achieved more frequently with CVVHDF.

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