Diabetic Ketoacidosis Discussion

Diabetic Ketoacidosis Discussion
Diabetic Ketoacidosis Discussion
Ms. Blake is an older adult with diabetes and has been too ill to get out of bed for 2 days. She has had a severe cough and has been unable to eat or drink during this time. She has a history of Type I diabetes. On admission her laboratory values show:
Sodium (Na+) 156 mEq/L
Potassium (K+) 4.0 mEq/L
Chloride (Cl–) 115 mEq/L
Arterial blood gases (ABGs) pH- 7.30; Pco2-40; Po2-70; HCO3-20
Normal values
Sodium (Na+) 136-146 mEq/L
Potassium (K+) 3.5-5.1 mEq/L
Chloride (Cl–) 98-106 mEq/L
Arterial blood gases (ABGs) pH- 7.35-7.45
Pco2- 35-45 mmHg
Po2-80-100 mmHg
HCO3–22-28 mEq/L
Ms. Blake is an older adult with diabetes and has been too ill to get out of bed for 2 days
What is the etiology of Diabetic Ketoacidosis?
Describe the pathophysiological process of Diabetic Ketoacidosis.
Identify the hallmark symptoms of Diabetic Ketoacidosis.
Identify any abnormal lab results provided in the case and explain why these would be abnormal given the patient’s condition.
What teaching would you provide this patient to avoid Diabetic Ketoacidosis symptoms?
In addition to the textbook, utilize at least one peer-reviewed, evidence based resource to develop your post.
Ms. Blake is an older adult with diabetes and has been too ill to get out of bed for 2 days
abnormal given the patient’s condition.
Sodium (Na+) 156 mEq/L elevated normal range 136-146 mEq/L. The American Diabetes Association criteria for the diagnosis of DKA are: (1) a serum glucose level >250 mg/dl, (2) a serum bicarbonate level <18 mg/dl, (3) a serum pH <7.30, (4) the presence of an anion gap, and (5) the presence of urine and serum ketones. Arterial blood gases (ABGs) Pco2-40; Po2-70; HCO3-20. Metabolic acidosis confirmed by arterial blood gas (ABG) analysis is one of the diagnostic criteria for diabetic ketoacidosis (DKA). Given the direct relationship between end-tidal carbon dioxide (ETCO2), arterial carbon dioxide (PaCO2), and metabolic acidosis, measuring ETCO2 may serve as a surrogate for ABG in the assessment of possible DKA. (Soeimanpour et al., 2013). These labs are abnormal because the body is compensating for the high level of glucose in the renal system and the loss of glucose in the urine. Ms. Blake has not been eating and probably has been taken her insulin as she was before she got sick. When you have diabetes and don’t get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes Ketones. Lots of ketones in your blood turn it acidic. People who drink much alcohol for a long time and don’t eat also enough build up ketones. It can happen when you aren’t eating at all, too. This condition can all lead to or be a predictor of existing Ketoacidosis. Diabetic ketoacidosis (DKA) is a condition that occurs when insulin levels are insufficient to support the body’s basic metabolic needs. It is most common in people with type 1 diabetes. In a small percentage of people, DKA is the first symptom of type 1 diabetes. Insulin deficit can be total (as in interruptions in exogenous insulin treatment) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). DKA can be triggered by a variety of physiological stressors. Infection that is severe (particularly pneumonia and urinary tract infection) Myocardial infarction (MI) is a type of heart attack that occurs when the Stroke sPancreatitis sPregnancy sTrauma DKA has been linked to a number of medicines. Corticosteroids Thiazide diuretics are a type of diuretic. Sympathomimetics Inhibitors of the sodium-glucose co-transporter 2 (SGLT-2) DKA is less common in people with type 2 diabetes, but it can happen in the presence of exceptional physiologic stress. Ketosis-prone type 2 diabetes is a kind of type 2 diabetes that affects obese persons, most of whom are of African (including African-American and Afro-Caribbean) heritage. Patients with ketosis-prone diabetes (also known as Flatbush diabetes) may experience substantial beta cell dysfunction as a result of hyperglycemia, and are hence more susceptible to suffer DKA when significant hyperglycemia develops. In both type 1 and type 2 diabetes, SGLT-2 inhibitors have been linked to DKA. DKA may develop at lower blood glucose levels in pregnant women and those on SGLT2 inhibitors than in other types of DKA. DKA Pathophysiology When the body doesn’t have enough insulin, it turns to triglycerides and amino acids for energy instead of glucose. Glycerol and free fatty acids levels in the blood rise due to unrestricted lipolysis, while alanine levels rise due to muscle catabolism. Glycerol and alanine are substrates for hepatic gluconeogenesis, which is aided by the excess glucagon produced when insulin shortage is present. Glucagon also promotes the conversion of free fatty acids to ketones in the mitochondria. Insulin generally prevents the transfer of free fatty acid derivatives into the mitochondrial matrix, but ketogenesis can occur even when insulin is absent. Acetoacetic acid and beta-hydroxybutyric acid, the two main ketoacids generated, are powerful organic acids that cause metabolic acidosis. Acetone is produced through the metabolism of acetoacetic acid and accumulates in the bloodstream before being exhaled slowly. Diabetic Ketoacidosis Discussion Hyperglycemia owing to insulin shortage induces osmotic diuresis, which results in significant water and electrolyte losses in the urine. Ketone excretion in the urine necessitates increased salt and potassium losses. Natriuresis causes a drop in serum sodium, while excretion of significant amounts of free water causes an increase. Potassium is also lost in high amounts, up to 300 mEq/24 hours (> 300 mmol/24 hours) in some cases.
Despite a large total body potassium deficit, the extracellular migration of potassium in response to acidosis causes initial serum potassium to be normal or high.
Insulin therapy drives potassium into cells, thus potassium levels fall even more during treatment.
Hypokalemia, which can be fatal, can develop if serum potassium is not checked and replenished as needed.
DKA Symptoms and Signs
Symptoms and indicators of diabetic ketoacidosis include hyperglycemia as well as nausea, vomiting, and abdominal pain, especially in youngsters.
More severe decompensation is characterized by lethargy and somnolence.
Due to dehydration and acidity, patients may be hypotensive and tachycardic, and they may breathe fast and deeply to compensate for the acidemia (Kussmaul respirations).
Exhaled acetone may cause them to have a fruity breath.
Fever is not an indication of DKA in and of itself, but it does indicate an underlying infection if it is present.
DKA can escalate to coma and death if not treated promptly.
Acute cerebral edema is a condition that affects roughly 1% of DKA patients and is more common in children than adolescents and young adults.
In some individuals, headache and a variable state of awareness signal this consequence, although respiratory arrest is the first symptom in others.
The etiology is unknown, but it could be linked to too-rapid drops in serum osmolality or cerebral ischemia.
When DKA is the first symptom of diabetes mellitus, it is most likely to develop in children under the age of five.
At presentation, children with the highest BUN (blood urea nitrogen) levels and the lowest PaCO2 appear to be at the greatest danger.
Additional risk factors include hyponatremia correction delays and the use of bicarbonate during DKA treatment.