Question

METI Diabetic Ketoacidosis Simulated Clinical Experience (SCETM) Overview Learning Objectives Location: Emergency Department 1. Formulates a nursing plan of care based on the pathophysiology of DKA (SYNTHESIS) History/Information: A 36-year-old man was admitted to the Emergency Department after his wite found him confused and agitated in their apartment. Apcording to his wite, he was diagnosed with Type 1 (Insulin-dependent diabates melitus 12 months ago. He was taking 48units of insulin daly: 12units of Humulin Regular plus 20units of Humulin NPH belore breakfast; Bunits of Humulin Regular before dinner; and Bunits of Humulin NPH at bedtime. She states he has had the for five days with vomiting and anorexia and stopped taking his insulin two days ago when he was unable to eat. There are no known allergies. The paramedics started a saline lock in the right forearm and administered 250mL of 0.9 % NS en route to the hospital 2. Designs an individualized plan of care for the nursing management of a patient in DKA (SYNTHESIS) 3. Prioritizes the implementation and approach to the nursing care of a patient in DKA (ANALYSIs) 4. Evaluates the patient's response to interventions and modifios the nursing care as appropriate for the patient in DKA (EVALUATION) Healthcare Provider's Orders Capilary glucose STAT Urine dipstiok for Ketones STAT CBC, Electrolytes, BUN, Creatinine, Glucose, Phospaste, Magnesium, Caloium, and Anion Gap STAT ABG STAT Urinalysis STAT Blood Cultures x2 now Unine Cuture and senaitivity now Portable Chest -ray STAT 12-lead ECO STAT Urinary catheter Continuous Sp0, monitoring Q, per nasal caniula at 21PM Maintain Spo, greater than 92% Continuous cardiac monitoring Vital signs and level of consciousness every one hour Intake and Output every one hour Electrolytes BUN Oreatinine Glucose, and Anion Gap every one hour N0% NS at rate of 1L/hour stan rNing Cunticuum etegation (PCP) Learner 1

Answer 1

Following are the detailed answers of first 4 Questions & short answers of remaining questions

Answer of 1: pathophysiologic changes in DKA

Condition of diabetic ketoacidosis(DKA) commonly occurs with Diabetes Mellitus Type 1(insulin dependent) but can also be occur in type 2 if not proper hypoglycemic medicine are not taken but rarely.

Insulin is needed in body for transporting Glucose into most cells of the body except Brain cells and hepatocytes. If patient do not take insulin blood glucose level rises inspite of decreased food intake. Because glucagon, epinephrin and glucocorticoids induce the gluconeogenesis. During infections and stress more glucocorticoids secreted so there are chances that glucose level raises inspite of low food intake. Low insuline level and high glucagon level induce gluconeogenesis in liver. Insulin prevent the mobilization of free fatty acids from adipocyte. So in the lack of insuline Free fatty acids mobilise and oxidised into acetyl CoA then converted to ketone bodies viz. Acetone, Acetoacetatic acid & Beta hydroxybutyric acid etc in the liver. In normal condition liver introduce this acetyl CoA in citric acid cycle but in low insuline synthesis ketone bodies. Out of these ketone bodies , acids are known as ketoacids. These ketone bodies are release into blood and utilise by body cells as fuel. Excessive of ketone bodies decrease the pH of blood and start to excrete in urine. Acetone is volatile and excreted by lung with expiration and result in acetone breath. This condition ia known as Diabetic ketoacidosis. Lack of insuline, decrease utilization of glucose and acidosis shift he pottasium out of cells. So initially hyperkalemia is occurs but soon This excess pottasium in blood is excreted in urine with ketoacids and glucose. Blood glucose level increased due to high glucose and ketone bodies level causes the osmotic diuresis. So the loss of fluid and potassium in urine result in dehydration and hypokalemia. Decrease total body potassium level and dehydration result in reduce nerve muscle excitibility so patient experience confusion, lethargy, disorientation etc. Low pH also stimulate respiratory center in medulla of brain so respiratory rate and depth increases(hyperventilation) which is characterise as kausmaul breathing. And this hyperventilation decrease the blood Partial pressure of Carbon-dioxide.

Answer of Question 2:

Blood glucose level : in uncontrolled diabetes mettitus type 1 with DKA show blood glucose level of more 270mg/dl or 15mmol/l . High glucose level does not cause DKA but the mechanism responsible for raising blood sugar level in uncontrolled diabetes is responsible for DKA that is low insulin level. The all is described above in answer 1.

Answer of Question 3

serum electrolyte imbalance: Dehydration, hyperkalemia then hypokalemia.

as stated in answer of question 1 , initially acidosis and low insuline result in extracellar shift of potassium. So the hyperkamemia(high potassium K+) but high glucose and ketone levels cause the osmotic diuressis. So high glucose and ketoacids filtered from glomerulus of nephrone can not be reabsorbed beyond Tm(Transport maximum) level of them. So high osmarity in tubular fluid attract more fluid so more urine formation. This excessive urination deplet the sodium, potassium, chloride and water from the body.

Sodium , chloride losses in propotional with water but intially high potassium in blood resulted in more potassium loss. So ultimately results in dehydration with hypokalemia.

Answer of Question 4: High Anion gap Metabolic Acidosis (pH <7.3)

as the name suggest it is Diabetic Ketoacidosis. Endogenous acid synthesis is raised. So it is metabolic acidosis. Acetoacetate and hydroxybutyrate are unmeasure anion, which reflect in anion gap,, are raised so it is high anion gap metabolic acidosis.

Answer of Question 5

a. serum electrolyte, Blood pressure and Urine output input analysis for fluid status.

b . by giving 0.9% NaCl solution atleast 2 to 3 L in first hr. Then repeat the lab tests to clear the picture of electrolyte imbalance and acid base balance.

c. By monitoring the blood pressure and using normal saline(0.9% NaCl).

d. Every hour using biochemical analizer.

e. By insulin infusion IV. Glucose is also given to keep the infusion rate constant.

f. It takes about 30 minutes. Insuline cause transport of glucose into cells.

g. Patassium. Because it start to shift into cell when insulin is given as well as its imbalance is more lethal than other electrolyte imbalance.

h. NaCl and KCl saline is given with regular serum electrolyte meausure and continous ECG recording.

ECG shows patassium imbalance.

I. By arterial Blood gas analysis and pH. Hourly

j. No need of special treatment if pH is not below 7.2

Just fluid and insulin treatment convert the ketoacids in bicarbonate which are alkaline. So acid base disturbance corrected.

Answer of Question 6:

Anion Gap: it is difference of serum Sodium concentration and serum chloride + serum bicarbonate. It shows the unmeasured anions such as phosphate, sulphate, acetate, butyrate or any other endogenous and exogenous anions.

serum Osmalarity: it is osmols in one liter of fluids.

One osmole reflect a undissociatable molecules. For example an avagrado numbers of Na+ or any other ion or compound is one osmole.

venous CO₂: it is partial pressure of CO₂ in venous blood. It reflect the pH changes.