Kembara Xta - Medicine - Diabetes Ketoacidosis ( DKA) Introduction euglycemic DKA is a rare medical emergency in diabetics that can happen without hyperglycemia during pregnancy and in people taking sodium-glucose cotransporter-2 inhibitors. It most frequently affects people with type 1 diabetes and is characterized by a biochemical triad of hyperglycemia, ketosis, and high anion gap metabolic acidosis. Neurology, endocrine/metabolic system(s) affected Incidence and prevalence in Epidemiology Incidence Age groups with the highest incidence were 1 to 17 (10.1%), 18 to 44 (53.3%), 45 to 64 (27.1%), 65 to 84 (8.7%), and 85 and over (0.8%). Pathophysiology and Etiology Impaired glucose uptake as a result of insulin insufficiency, which activates counter-regulatory mechanisms (gluconeogenesis, glycogenolysis, and proteolysis) that raise blood sugar levels and cause the generation of ketone bodies. Ketoacidosis and hyperglycemia that result cause osmotic diuresis, electrolyte abnormalities, dehydration, and acidosis. Infection and noncompliance with medicine are major contributing factors. Other triggering factors include: - Myocardial infarction (MI); cerebrovascular accident (CVA); - First presentation of DM - Drugs (SGLT2 inhibitors, sympathomimetics, atypical antipsychotics, and corticosteroids) - Alcohol and cocaine; illicit substances - Surgery; trauma - Comorbidities in mental health and emotional stress - Maternity Type 1 diabetes and type 2 diabetes (Hispanic and African American ancestry, G6PD deficiency) are risk factors. Prevention Follow the "sick day" management advice and closely check your blood sugar levels while you are under stress, ill, or experiencing trauma. Careful insulin management, consistent blood glucose monitoring, and instruction in symptom recognition More than 30% of patients exhibit symptoms of both hyperosmolar hyperglycemia syndrome (HHS) and DKA. Diagnostic standards for a diagnosis[C] - Hyperglycemia, which is quickly determined by fingerstick glucose testing and validated by serum chemistry (normally 250–800 mg/dL). Low HCO3 levels (typically 18 mEq/L) - The presence of metabolic acidosis on arterial blood gases (pH 7.3) Positive B-hydroxybutyrate (B-OHB) in serum is extremely sensitive and specific. Anion gap = serum sodium (serum chloride + bicarbonate); >10 mmol. The severity of a diagnosis can be divided into three categories. You should take note of the wide range, from euglycemia to severe hyperglycemia with acidosis, dehydration, and coma. It is necessary to tailor treatment based on clinical and laboratory evaluation (1). History, recent illnesses, accidents, or surgeries, as well as dietary or pharmaceutical changes. Polyuria, polydipsia, polyphagia, weight loss, generalized weakness, malaise, fatigue, sluggishness, nausea, vomiting, abdominal pain, missed insulin doses or disobedience, anorexia or increased appetite clinical assessment Tachypnea, hyperpnea, Kussmaul respirations, acetone-smelling breath, abdominal tenderness, decreased bowel sounds, dry mucous membranes, poor skin turgor, dehydration, decreased reflexes, altered mental status, coma, and vital signs such as hypotension, tachycardia, fever, or hypothermia. Differential Diagnosis: Alcoholic ketoacidosis, starving ketosis, and lactic acidosis; Hyperosmolar Hyperglycemic State; Toxic Ingestions (Salicylates, Methanol, Ethylene Glycol); Uremia/Chronic Renal Failure Acute pancreatitis Sepsis Initial test results from the laboratory and imaging Essential labs The main ketone generated, -hydroxybutyrate (-HOB), is favoured over serum ketone levels. When HB is greater than 3 mg/dL, it is abnormal and needs to be reduced to 1.5 mg/dL within 12 to 24 hours. - Venous blood gases (VBG) or an ABG for determining pH: VBG pH is 0.03 lower than ABG pH, on average. - Ketoneuria and glycosuria in urine tests. - Creatinine and BUN: Significantly elevated serum ketones may react with one another and lead to an unnaturally high serum creatinine. - Derangements in the electrolytes, including hypophosphatemia, hypomagnesemia, and base deficit with a significant anion gap - Lower K+ levels throughout the body: Severe acidosis artificially raises K+ levels. For every 100 mg/dL increase in serum glucose above 100 mg/dL, it is currently recognized to add 2.4 mmol/L to measured Na+ in order to rectify pseudohyponatremia related to hyperglycemia or hypertriglyceridemia. - Determine the serum osmolality. If the result is less than 320 mOsm/kg, especially in individuals with disturbed mental status, explore other etiologies to diabetic ketoacidosis (DKA). - Glycosylated hemoglobin (HbA1c) is used to evaluate the long-term history of diabetes management. -CBC: Compare infections versus leukocytosis associated to DKA. Additional tests: Clinical suspicion of infection may lead to the following tests: - Blood and urine cultures, chest x-rays, and lumbar punctures - ECG: this test frequently reveals sinus tachycardia (nonspecific), alterations consistent with electrolyte problems, and/or ischemic changes with MI as a precipitating factor. - Troponin - Head CT scan if suspected of having a CVA or cerebral edema Tests in the Future & Special Considerations The diagnosis of pancreatitis in DKA may not be accurate with elevated lipase and amylase levels. Fluid resuscitation, resolution of anion gap acidosis, and ketosis, correction of electrolytes, identification and treatment of precipitating cause(s), insulin therapy to normalize serum glucose. General Actions An ICU setting is necessary for severe DKA. Start with an isotonic crystalloid solution, such as a lactated Ringer bolus or 0.9% saline. Check serum electrolytes, BUN, creatinine, venous pH, and glucose every hour for the first two to four hours until stable. First Line of Medicine A top priority is intravenous fluid (IVF). – In the first hour, the ADA advises giving patients 1,000 to 1,500 mL of normal saline. – In patients who do not have cardiac, renal, or hepatic impairment, the IVF infusion rate should be adjusted after the first hour based on hemodynamics and electrolytes (often 250 to 500 mL/hr). – After initial fluid resuscitation, there is no evidence to support or reject the use of 0.45% NaCl in patients with normal to high corrected Na+ concentration; nonetheless, the risk of hyperchloremic metabolic acidosis with continuous 0.9% NaCl should be taken into account. – To prevent hypoglycemia, switch to 5% dextrose with 0.45% NaCl at the same rate when blood sugar reaches 200 mg/dL. ○ A new fluid management technique known as the "two bag method" involves running two bags of 0.45% NaCl, one with and one without dextrose 10%. To maintain a total infusion rate of 250 mL/hr, infusion rates are modified based on hourly glucose levels. Comparing this procedure to traditional fluid replacement, acidosis has been shown to be corrected earlier. After initial IVF resuscitation and correction of hypokalemia (3.3 mg/dL), insulin should be started intravenously (1)[C],(3)[C]. - Optional 0.1 U/kg IV first bolus followed by 0.1 U/kg/hr continuous infusion (Do not use initial insulin bolus in youngsters). - 0.14 U/kg/hr continuous infusion is advised if bolus is not administered (1). - Aim for a drop in blood glucose of 50 to 75 mg/dL/hr in the first hour; after that, adjust the rate of infusion every hour until a consistent decline is seen. – The ADA advises lowering the infusion rate to 0.02 to 0.05 U/kg/hr IV in order to keep the blood glucose between 150 and 200 mg/dL up until the acidosis is corrected. – Use of basal insulin (glargine 0.25 U/kg SC) within 12 hours of beginning treatment may shorten hospital stays, reduce rebound hyperglycemia, and reduce time to gap closure. – After SC insulin infusion starts, overlap and continue IV insulin infusion for 1 to 2 hours. In 1 L IVFs, start potassium replacement with 20 to 30 mEq/L of K+ when serum K+ is below 5.2 mg/dL and if urine output is sufficient. – Give IV potassium at a rate of 20 to 30 mEq/hr with fluids until K+ is >3.3 mg/dL to prevent cardiac arrhythmia and hold insulin if K+ is 3.3 mg/dL. Serum K+ will alter by around 0.6 mEq in the opposite direction for every 0.1 unit change in pH. Phosphorus: Routine replacement is not advised because it can cause hypocalcemia; if levels are extremely low (1.0 mg/dL), administer 20 to 30 mEq/L of K-Phos in liquids. The evidence currently available does not support the use of sodium bicarbonate in patients with pH values of 6.9 or above (1),(3). Patients with pH 6.9 or hyperkalemia that is life-threatening are more likely to have a negative outcome; as a result, the ADA advises delayed administration of 100 mEq NaCHO over a 2-hour period in these circumstances. Use of NaCHO3 may make people more susceptible to cerebral edema, particularly children. Magnesium: If the patient has symptoms and the magnesium level is below 1.2 mg/dL or 1.8 mg/dL, magnesium therapy should be explored. Take precautions by turning off the insulin pump. – Give regular insulin 0.14 U/kg IV bolus and then continuous infusion at prior rate if blood sugar does not decrease by 10% in the first hour. – If using sodium bicarbonate, mix 400 mL of isotonic solution with 20 mEq KCL >200 mL/hr for two hours, or until the venous pH is >7.0, and then cease the infusion (4). Next Line Patients who are awake, accept oral intake, have blood bicarbonate levels greater than 10 mEq/L, and have a pH greater than 7.0 may benefit from rapid-acting subcutaneous insulin. Load with 0.3 U/kg SC, then 0.1 to 0.2 U/kg every one to two hours. Reduce dose to 0.05 to 0.1 U/kg q1-2h until ketoacidosis resolves once glucose is below 200 mg/dL. Child Safety Considerations It is advised to start with initial insulin infusion rates between 0.05 and 0.1 U/kg/h. Cerebral edema has a death rate of 20–50% while being an uncommon condition (1%): – repeat your neurological assessment. Neuroimaging should not be used as an excuse to put off treatment if it is suspected, as determined by clinical examination. pregnant women's issues DKA by itself is not a sign of an emergency birth; it is crucial to stabilize the mother first. Tocolytics and corticosteroids can cause euglycemic DKA. Death during pregnancy: 9–35% Additional Referral Questions For diabetics with poor control, the ADA 2021 Diabetes Care Guidelines advise outpatient follow-up within a month or every one to two weeks. CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING Ketones in urine and an ICU setting for severe DKA are required by the ADA as admission criteria (6). Child Safety Considerations discharge when the DKA has subsided, anion gap 12, glucose 200 mg/dL, pH >7.3, and bicarbonate >18 mEq/L. Patient must be capable of continuing home medication regimen and able to tolerate PO intake. NPO at first, then advance eating when nausea and vomiting are under control. Avoid foods with a high glycemic index, such as fruit juice, white bread, soft drinks, and added sugar. Glucose self-monitoring, glucose targets, and when to contact a PCP Detecting and avoiding hypoglycemia Nutritious food options Managing sick days Appropriate usage of insulin syringes and/or needles The prognosis is worse at the oldest and youngest ages and when coma and hypotension are present. Overall DKA mortality ranges from 0.5 to 2%. The most frequent cause of death in children with DKA is cerebral edema, along with pulmonary edema, respiratory failure, and myocardial infarction. Complications Vascular thrombosis, hyperkalemia, hypophosphatemia, and hypokalemia Acute renal failure, cardiac dysrhythmia (related to hypokalemia or acidosis), and Late hypoglycemia (a result of therapy) An infection
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