Endocrine Clinical Assessment and Diagnostic Procedures DKA

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Presentation transcript:

Endocrine Clinical Assessment and Diagnostic Procedures DKA Charnelle Lee, RN, MSN

Objectives Identify the components of an endocrine history. Describe clinical findings of a patient with pancreatic and posterior pituitary dysfunction. Explain the clinical significance of laboratory and diagnostic tests in pancreatic dysfunction. Explain the clinical significance of laboratory and diagnostic tests in posterior pituitary dysfunction.

Endocrine Function FIGURE 23-1 Location of endocrine glands with the hormones they produce, target cells or organs, and hormonal actions.

Endocrine Assessment Systematic process incorporating history and physical examination Endocrine glands inaccessible to clinical examination Assessment is indirect

Health History Endocrine System Current health status Description of current illness Medical history General endocrine status Family history

Pancreas Function Dysfunction usually presents as hyperglycemia Dx: Type I or Type II Nursing priorities: Hyperglycemia Hypoglycemia Provide information about pancreatic functioning

Diabetes Mellitus (DM) Type 1 Diabetes B cells no longer secrete insulin Autoimmune disease Insulin dependent diabetes Diabetic ketoacidosis (DKA) occurs without insulin

Diabetes Mellitus (DM) Type 2 Diabetes Majority of people are adults Body mass index > 30% Imbalance between insulin production and use Oral medications for most patients Complication of Type 2 diabetes is: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

Patient Compliance Only 40% with Type 1 Diabetes Monitor their blood glucose at least once a day.

Hyperglycemia Subjective Complaints Blurred vision, headache, weakness, fatigue, drowsiness, anorexia, nausea, abdominal pain

Knowledge check Three hours after surgery, the nurse note that the breath of the client who is a type 1 diabetic has a “fruity” odor. What is the nurse’s best first action? Document the finding as the only action. Increase the IV fluid flow rate. Call the physician for a arterial blood gas order Perform oral care.

Hyperglycemia Inspection FLUSHED SKIN POLYURIA POLYDIPSIA VOMITING Fluid volume ? Amb what defining characteristics. Osmotic Diuresis Occurs with Hyperglycemia Dehydration Tachycardia Hypotension Orthostatic Hypotension

Hyperglycemia Abdomen Subjective: Hunger then anorexia NV Abdominal Cramps Hypoactive Bowel sounds Palpation – Abdominal Tenderness

Lab Tests How Long Have I had Diabetes? Diabetic Control – Yes/No (4%-6%) Normal Value Provides information about the average amount of glucose present in the bloodstream over the past previous 3 to 4 months. Most accurate test about either new onset or patient’s level of control of their sugar Which of the following cells give us this laboratory test value Leukocytes Thrombocytes Erythrocytes Granulocytes Lymphyocytes Erythrocytes – During the 120 day life span of RBC the hemoglobin within each cell binds to the available blood glucose through a process know as glycosylation.

Glucose Laboratory Levels Laboratory Studies Fasting serum glucose (FSG) 70 to 100 mg/dL – normal 100 to 125 mg/dL – prediabetic >126 mg/dL – diagnostic of diabetes 140-180 mg/dL – target for critically ill patient <70 mg/dL – hypoglycemia <40 mg/dL – severe hypoglycemia Urine glucose Not recommended (continued)

Blood Ketones Blood ketones 2 to 4 mg/dL – normal Elevated in acute illness, fasting, type 1 diabetes with lack of insulin, illness, starvation

Urine Ketones Presence of urine ketones is an early warning sign before the onset of ketosis Should not be present in a healthy individual Exceptions- dieting, exercise, starvation and fasting Normally ketones are not present in the urine Elevated in diabetic ketoacidosis

Diabetes Mellitus Diabetic Ketoacidosis (DKA) 20% DKA newly diagnosed Type 1 diabetics 80% DKA in known Type 1 diabetics

Diabetes Mellitus Diabetic Ketoacidosis (DKA) Characteristics Hyperglycemia – blood glucose >250 mg/dl Ketosis – Acidemia- Arterial ph < 7.3 Bicarb level < 18 mEq/L Decreased insulin availability Role of counter-regulatory hormones

Major Cause of DKA Infection #1 Changes in Insulin dose, type Increased metabolic demand Growth spurts Surgery Trauma Eating disorders Early warning signs of DKA Polyuria Fatigue

Lab Value

Diabetic Ketoacidosis (DKA)Assessment Clinical Findings Headache Polyuria Malaise Polydipsia Nausea and vomiting CNS depression and decreased LOC, stupor Coma Dehydration Flushed dry skin Tachycardia Hypotension Kussmaul air hunger “Fruity” odor of acetone

DKA Diabetic Ketoacidosis (DKA) Assessment and Diagnosis Diagnosis Bedside finger stick Urine ketones ABG Serum osmolality Hematocrit Electrolyte panel BUN and Creatinine

Dka Diabetic Ketoacidosis (DKA) Collaborative Management Hydration Insulin Administration Intravenous Glucose Potassium and Phosphorus Administration Diabetic Ketoacidosis (DKA) Medical Management Goals Reverse dehydration Restore insulin-glucagon ratio Treat and prevent circulatory collapse Replenish electrolytes

Fluid Volume Deficit r/t osmotic diuresis Fluid deficit of up to 6liters can occur Isotonic saline 0.9% is infused immediately to reverse vascular deficits and hypotension. Fluids after this are based on serum osmolarity and serum sodium. Low sodium – 0.9% saline High sodium – 0.45% saline K+ is added after fluid volume deficit has been partially reversed and insulin has been started.

Hydration Assessment Assess Collaborate Intervene Reassess Report Body weight Hourly intake and output Patient complaint of thirst Pulse strength Blood pressure changes Gradual increase from subnormal to baseline Tachycardia to normocardia Condtion of mucous membranes

Colloborative DX: Hyperglycemia - Insulin Drip Patient is NPO IV bolus of ______ insulin 0.1 units/kg is administered. Continuous drip of 0.1 units per kg/hour is infused with other fluids. Goal is to decrease blood sugar by 50-70 mg/dl q1h until it reaches 200

Rationale for moderation in blood sugar decrease Cerebral edema can occur with too rapid of a reversal Notify physician of rapid drops as well as elevations in blood sugar. Symptoms of cerebral edema are:

Nursing – Administration Fluids/Insulin/Electrolytes Rapid IV infusion via pump NPO until the blood glucose is < 200 Blood sugar checks are hourly Sliding scale insulin is administered per drip Labs are drawn q2h in the initial 24 hours until the patient sugar stabilizes and acidosis resolves.

Regular Insulin Continued until acidosis, ketonuria, and fluid volume deficit have resolved. Call physician when blood glucose is at 200 – at that time D5NS will be started or D51/2 NS based on the sodium level of the patient at this time.

Potassium & phosphorus Will drop as sugar drops Administer IV potassium based on lab results Assess for s/s of potassium imbalance during acute states of DKA Monitor phosphorus as well, replace phosphorus if less than 1 mg/dl.

Knowledge Check A client with type 1 diabetes is found unresponsive in the morning by a family member and is admitted to the emergency department. On admission to the emergency department, the client is unresponsive to stimuli and has fruity, sweet breath with Kussmaul’s respirations. Laboratory results include arterial blood gases of pH 7.32, PCO2 34 mm Hg, and HCO3 11 mEq\L (11 mmol\L) and a plasma glucose of 518 mg\dl (28.8 mmol\L). The intervention that a nurse anticipates will be prescribed initially for the client is

Knowledge Check Describe the blood gas in this scenario? Fluid replacement therapy in the initial rehydration hours would be? What type of insulin would be given to this patient? Based on how fast the sugar should be decreased to prevent cerebral edema, the blood sugar measured in the next hour would be? A physician orders sodium bicarbonate for this patient. Nursing action would be: Which electrolytes would the nurse monitor closely in the first 4 hours of rehydration and insulin therapy.