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

2. 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.

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

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

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

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

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

8. 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)

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

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

11. 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.

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

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

14. 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.

15. 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
mg/dL – target for critically ill patient
<70 mg/dL – hypoglycemia
<40 mg/dL – severe hypoglycemia
Urine glucose
Not recommended
(continued)

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

17. 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

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

19. 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

20. 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

21. Lab Value

22. 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

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

24. 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

25. 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.

26. 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

27. 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 mg/dl q1h until it reaches 200

28. 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:

29. 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.

30. 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.

31. 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.

32. 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

33. 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.