The Other DKA: A Case Report
AAPA ePoster library. Hricz C. 05/17/17; 180502; 112
Craig Hricz
Craig Hricz
Login now to access Regular content available to all registered users.
Abstract
Rate & Comment (0)
TITLE: The 'Other' DKA: A Case Report PURPOSE Diabetic ketoalkalosis is an uncommon complication of Type 1 diabetes mellitus (T1DM) that presents as a mixed acid-base disorder consisting of diabetic ketoacidosis (DKA) and metabolic alkalosis. Diabetic ketoacidosis, characterized by a high anion gap acidosis, is a consequence of hyperglycemic induced ketonemia. Metabolic alkalosis, characterized by base excess, can be a consequence of acid-loss associated with vomiting. A common etiology of diabetic ketoalkalosis is contraction alkalosis secondary to frequent vomiting or diuretic use. Gastroparesis, a common complication of T1DM, is a risk factor for recurrent vomiting leading to a diabetic ketoalkalotic state. The purpose of this case report is to bring to light a relatively rare occurrence of co-existing DKA and metabolic alkalosis in a patient with T1DM. METHODOLOGY This case report describes a 27-year-old male who presented to the emergency department with diabetic ketoalkalosis after 5 days of vomiting secondary to gastroparesis. Initial evaluation revealed an average sized man in no acute distress with vital signs remarkable for hypertension and tachycardia. His oral mucosal membranes appeared dry and with the exception of a mild-moderate regular tachycardia, the rest of his exam was unremarkable. There were no signs or symptoms consistent with an infectious process. Significant laboratory results included the following: Glucose 335; BUN 69; Creatinine 3.51; CO2 35; pH 7.48; pCO2 47; pHCO3 35; Base excess 11.5; Anion Gap 15; Serum Ketones 2.6. Admitting Diagnoses: Metabolic Alkalosis, Diabetic Ketoacidosis, Acute on Chronic Kidney Injury 20 hypovolemia, Vomiting 20 Diabetic Gastroparesis, hyperphosphatemia RESULTS Hospital Course: The patient received aggressive IV hydration for his significant hypovolemia as well as an insulin infusion for his DKA. He was eventually transitioned to subcutaneous insulin. Upon discharge his vital signs had returned to normal and he was noted to have the following pertinent laboratory results: Glucose 73; CO2 25; BUN 57; Creatinine 2.80 (baseline for this patient was 2.2); normalized anion gap. CONCLUSIONS Metabolic alkalosis in this patient can be attributed to vomiting and volume contraction. Vomiting produced direct loss of acid and fluid. Hypovolemia stimulated the angiotensin/aldosterone system to promote renal bicarbonate absorption and hydrogen/potassium secretion. Hyponatremia fu...
TITLE: The 'Other' DKA: A Case Report PURPOSE Diabetic ketoalkalosis is an uncommon complication of Type 1 diabetes mellitus (T1DM) that presents as a mixed acid-base disorder consisting of diabetic ketoacidosis (DKA) and metabolic alkalosis. Diabetic ketoacidosis, characterized by a high anion gap acidosis, is a consequence of hyperglycemic induced ketonemia. Metabolic alkalosis, characterized by base excess, can be a consequence of acid-loss associated with vomiting. A common etiology of diabetic ketoalkalosis is contraction alkalosis secondary to frequent vomiting or diuretic use. Gastroparesis, a common complication of T1DM, is a risk factor for recurrent vomiting leading to a diabetic ketoalkalotic state. The purpose of this case report is to bring to light a relatively rare occurrence of co-existing DKA and metabolic alkalosis in a patient with T1DM. METHODOLOGY This case report describes a 27-year-old male who presented to the emergency department with diabetic ketoalkalosis after 5 days of vomiting secondary to gastroparesis. Initial evaluation revealed an average sized man in no acute distress with vital signs remarkable for hypertension and tachycardia. His oral mucosal membranes appeared dry and with the exception of a mild-moderate regular tachycardia, the rest of his exam was unremarkable. There were no signs or symptoms consistent with an infectious process. Significant laboratory results included the following: Glucose 335; BUN 69; Creatinine 3.51; CO2 35; pH 7.48; pCO2 47; pHCO3 35; Base excess 11.5; Anion Gap 15; Serum Ketones 2.6. Admitting Diagnoses: Metabolic Alkalosis, Diabetic Ketoacidosis, Acute on Chronic Kidney Injury 20 hypovolemia, Vomiting 20 Diabetic Gastroparesis, hyperphosphatemia RESULTS Hospital Course: The patient received aggressive IV hydration for his significant hypovolemia as well as an insulin infusion for his DKA. He was eventually transitioned to subcutaneous insulin. Upon discharge his vital signs had returned to normal and he was noted to have the following pertinent laboratory results: Glucose 73; CO2 25; BUN 57; Creatinine 2.80 (baseline for this patient was 2.2); normalized anion gap. CONCLUSIONS Metabolic alkalosis in this patient can be attributed to vomiting and volume contraction. Vomiting produced direct loss of acid and fluid. Hypovolemia stimulated the angiotensin/aldosterone system to promote renal bicarbonate absorption and hydrogen/potassium secretion. Hyponatremia fu...
    This eLearning portal is powered by:
    This eLearning portal is powered by MULTIEPORTAL
Anonymous User Privacy Preferences

Strictly Necessary Cookies (Always Active)

MULTILEARNING platforms and tools hereinafter referred as “MLG SOFTWARE” are provided to you as pure educational platforms/services requiring cookies to operate. In the case of the MLG SOFTWARE, cookies are essential for the Platform to function properly for the provision of education. If these cookies are disabled, a large subset of the functionality provided by the Platform will either be unavailable or cease to work as expected. The MLG SOFTWARE do not capture non-essential activities such as menu items and listings you click on or pages viewed.


Performance Cookies

Performance cookies are used to analyse how visitors use a website in order to provide a better user experience.


Save Settings