scholarly journals Euglycemic Diabetic Ketoacidosis in a Patient with Cocaine Intoxication

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Asma Abu-Abed Abdin ◽  
Muhammad Hamza ◽  
Muhammad S. Khan ◽  
Awab Ahmed

Diabetic ketoacidosis (DKA) is characterized by elevated anion gap metabolic acidosis, hyperglycemia, and elevated ketones in urine and blood. Hyperglycemia is a key component of DKA; however, a subset of DKA patients can present with near-normal blood glucose, an entity described as “euglycemic DKA.” This rare phenomenon is thought to be due to starvation and food restriction in insulin dependent diabetic patients. Cocaine abuse is considered a trigger for development of DKA. Cocaine also has anorexic effects. We describe an interesting case of euglycemic DKA in a middle-aged diabetic female presenting with elevated anion gap metabolic acidosis, with near-normal blood glucose, in the settings of noncompliance to insulin and cocaine abuse. We have postulated that cocaine abuse was implicated in the pathophysiology of euglycemic DKA in this case. This case highlights complex physiological interplay between type-1 diabetes, noncompliance to insulin, and cocaine abuse leading to DKA, with starvation physiology causing development of euglycemic DKA.

Author(s):  
Prashanth Rawla ◽  
Anantha R Vellipuram ◽  
Sathyajit S Bandaru ◽  
Jeffrey Pradeep Raj

Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Learning points: Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels.


2017 ◽  
Vol 9 (2) ◽  
pp. 106-115
Author(s):  
Md Zillur Rahman ◽  
Abdullah Al Shafi Majumder ◽  
Nazir Ahmed Chowdhury ◽  
Mesbauddin Ahmed

Background: Contrast induced nephropathy (CIN) is not an uncommon complication of percutaneous coronary intervention (PCI) and it is more in diabetic patients. But we do not know the incidence and consequences of CIN of patients with high blood sugar but not known diabetic. We planned to find the relationship between level of admission blood glucose and contrast induced nephropathy after PCI in Acute Coronary Syndrome (ACS) in non-diabetic patients.Methods: This prospective observational study was conducted in National Institute of Cardiovascular Diseases, Dhaka from January 2012 to June 2012. Total 120 patients were observed in two groups, group-I non-diabetic with normal blood glucose (?7.8 mmol/L) and group-II non-diabetic with high blood glucose (?7.8 mmol/L).Results: Results show increase in serum creatinine (0.1mg/dl vs. 0.3 mg/dl) and decrease in creatinine clearance rate (12.9 ml/min vs. 6.0ml/min) was more in hyperglycemic than normoglycemic. When most common definition of contrast induced nephropathy was used, the incidence of CIN was 24% in high blood glucose group and 4% in normal blood glucose group (p=0.004). The higher the admission blood glucose level there is more incidence of contrast induced nephropathy. Multivariate analysis of factors associated with CIN shows that patients with high blood glucose (>7.8 mmol/l) and > 150 ml of contrast exposure are independent predictors of contrast induced nephropathy. The patients subjected to PCI having high blood glucose were at 6 times higher risk of developing CIN than normal blood glucose and use of contrast >150 ml were more than 2 times higher risk of developing CIN.Conclusion: Patients with high blood sugar on admission of ACS patients have more chance of developing CIN after PCI.Cardiovasc. j. 2017; 9(2): 106-115


1986 ◽  
Vol 113 (3_Suppl) ◽  
pp. S74-S76 ◽  
Author(s):  
K. Fuhrmann

Abstract. The treatment of 620 insulin-dependent diabetic pregnant women is reported. The goal of treatment was to achieve a normal blood glucose concentration as soon as possibly during early, or even before pregnancy. When intensified conventional insulin therapy was started before conception, about 88% of the patients achieved normal blood glucose levels during the first weeks of pregnancy. In only about 20% of the pregnant diabetics without intensified preconceptional treatment a normal blood glucose level was obtained during their first hospitalization in pregnancy. The rate of congenital malformations was 1.1% in the former and 7.1% in the latter group.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A358-A358
Author(s):  
Kubra M Tuna ◽  
Randa Abdelmasih ◽  
Ramy Abdelmaseih ◽  
Mrhaf Alsamman ◽  
Joseph Robbins

Abstract Introduction: Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus (DM). In general, DKA characterized by blood sugar over 250 mg/dL, anion-gap metabolic acidosis, and increased plasma or urine ketones. Approximately 2–3% of DKA patients can present with normal blood glucose levels (less than 250 mg/dl) which called euglycemic DKA. Some of the etiologies of euglycemic DKA include recent use of insulin, low caloric intake, alcoholism, chronic liver disease, and pregnancy. Very rarely, SGLT2 inhibitor use may be responsible for euglycemic DKA. Case Presentation: Here we present a case of 44 years old female with a past medical history of DM type 2 who presented with acute onset of nausea and vomiting. Initial laboratory findings were remarkable for anion gap metabolic acidosis with a blood glucose level of 201 mg/dl. The patient was on long-acting insulin along with Canagliflozin and Metformin therapy over years and reported being compliant with medications. She was treated with intravenous insulin therapy which resolved acidosis as well as symptoms. The patient was discharged with recommendations of discontinuation of Canagliflozin. Discussion: SGLT2 inhibitors are the novel class of oral antidiabetic drugs which widely used due to their favorable cardiovascular and renal outcomes independent of glycemic control. However, their side effects remain a concern. DKA is a rare but serious side effect of SGLT2 inhibitors with an incidence rate of 9.4% in type 1 DM and less than 0.2% in type 2 DM. Patients typically present with euglycemia or low-grade hyperglycemia which results in a diagnostic challenge for treating physicians. SGLT2 inhibitors increase urinary glucose excretion with a subsequent decrease in circulating insulin and an increase in glucagon, rendering a metabolic shift from glucose to fatty acid utilization. During times of intercurrent illness (decreased oral intake, sepsis) or metabolic stress (surgery), decreased carbohydrate intake coupled with the aforementioned changes will result in decreased insulin secretion and increased counter-regulatory hormones including adrenaline and cortisol, promoting lipolysis, fatty acid oxidation, and ketone production by the liver which ultimately leading to euglycemic DKA. Conclusion: SGLT2 inhibitors induced euglycemic DKA treatment is identical to classic DKA with consideration of the lack of hyperglycemia. Appropriate patient counseling to ensure safe SGLT2 inhibitor therapy is crucial, including appropriate holding parameters during concomitant volume-depleting illnesses and decreased oral intake. Timely diagnosis of euglycemic DKA, and recognitions of other rare but lethal side effects to decrease overall morbidity and mortality.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Michael W Brands ◽  
Alexander Staruschenko ◽  
Bonnie L Blazer-Yost ◽  
Rabei Alaisami ◽  
Daniel Duggan

We reported that chronic intra-renal insulin infusion in diabetic dogs reversed the natriuresis and diuresis caused by 6 days of hyperglycemia. However, the sustained sodium-retaining action was not accompanied by hypertension. This study tested whether intra-renal insulin infusion would increase blood pressure in diabetic dogs with chronic angiotensin II (AngII) hypertension. Seven dogs were chronically instrumented and divided into D (diabetes) and Dir (D + intra-renal insulin) groups. Alloxan was administered to all 7 dogs, and continuous iv. insulin replacement therapy was used to maintain them at normal blood glucose. All dogs also were infused with AngII (3 ng/kg/min, iv) continuously. After 3 days of control measurements, with normal blood glucose, MAP averaged 135±3 and 129±3 mmHg in D and Dir dogs, respectively. Six days of hyperglycemia (diabetes) was induced in both groups by reducing the iv. insulin infusion dose. Intra-renal insulin at 0.3 mU/kg/min was initiated concurrently in the Dir dogs. MAP increased in the Dir group to an average of 141±4 mmHg by day 6 of diabetes. Moreover, Figure 1 shows the progressive separation in MAP compared to the D dogs, to an average difference of 19 mmHg by day 6 of diabetes. Renal blood flow (measured 24 hr/day along with MAP) increased in both groups, as did GFR. However, statistically significant differences were not achieved yet with these preliminary data. These results suggest that the chronic antinatriuretic effect of insulin in diabetes may have an AngII-dependent hypertensive action. The mechanism does not appear to be dependent on renal vasoconstriction, and may, therefore, be linked to effects on tubular sodium reabsorption.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Johnny F. Jaber ◽  
Matthew Standley ◽  
Raju Reddy

Diabetic ketoacidosis (DKA) in pregnancy is associated with high fetal mortality rates. A small percentage of DKA occurs in the absence of high glucose levels seen in traditional DKA. Prompt recognition and management is crucial. We report a case of a 30-year-old pregnant woman with type 1 diabetes mellitus admitted with euglycemic DKA (blood glucose <200 mg/dL). Initial laboratory testing revealed a severe anion gap acidosis with pH 7.11, anion gap 23, elevated β-hydroxybutyric acid of 9.60 mmol/L, and a blood glucose of 183 mg/dL—surprisingly low given her severe acidosis. The ketoacidosis persisted despite high doses of glucose and insulin infusions. Due to nonresolving acidosis, her hospital course was complicated by spontaneous intrauterine fetal demise. Euglycemia and severe acidosis continued to persist until delivery of fetus and placenta occurred. It was observed that the insulin sensitivity dramatically increased after delivery of fetus and placenta leading to rapid correction of ketoacidosis. This case highlights that severe ketonemia can occur despite the absence of severely elevated glucose levels. We discuss the mechanism that leads to this pathophysiologic state and summarize previously published case reports about euglycemic DKA in pregnancy.


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