Case Study DKA

 

Mrs. S is a 28-year-old patient, with a 12-year history of type I diabetes mellitus. Her husband states that she has had a “bad cold” for several days. Yesterday she stayed in bed and slept all day. She was “too ill” to check her blood sugar, and since she was not really eating, she did not take her insulin. This morning, she was not able to stand up and vomited twice. A Gram stain of Mrs. S’s blood contains gram-positive cocci in clusters. Her admission vital signs are: BP = 90/60; HR = 118 bpm (sinus tachycardia); RR = 32/min; T = 102.3° F; O2 sat via pulse oximetry = 96%. Her serum glucose is 398 mg/dl, and she is positive for serum ketones. She is admitted with a diagnosis of DKA.

Her baseline ABGs on 2 L of oxygen are: pH = 7.25; PCO2 = 28; HCO3 = 14; PaO2 = 92; O2 sat = 96%. Her respirations are deep, rapid, and labored. She has bronchial breath sounds in the right axillary area. There is bilateral chest expansion and no evidence of cyanosis.

A regular insulin bolus is given, and a regular insulin drip is initiated. Mrs. S’s IV fluids are infusing at 800 ml/hr. Her vital signs after 2 hours in the unit are: BP = 120/70; HR = 78 bpm (normal sinus rhythm); RR = 22/min; O2 sat = 100%. Her serum glucose is 250 mg/dl and serum potassium is 4.0 mEq/L. She is more alert and is feeling hungry.

What is insulin’s function in the body? What is the most significant basic defect in the development of DKA?
What is the cause of Ms. S experiencing DKA? Describe the pathophysiologic rationale for your answer.
List the classic signs and symptoms of DKA. Which signs and symptoms did Ms. S experience? What are the pathophysiologic causes of these signs and symptoms?
What is an anion gap? Why is the anion gap important to follow in the treatment of DKA?
What acid base disturbance is Ms. S experiencing? What compensatory mechanisms are in effect at this time?
What is the primary nursing diagnosis for Ms. S.? What are the goals for treatment (both independent and collaborative)? What interventions are imperative to initiate immediately? What interventions are important within the next 12-24 hours?
What are potential lab abnormalities for a patient in DKA?
What nursing considerations are important in planning Ms. S’s discharge?
Discuss the American Association of Critical Care Nurses (AACN) Synergy Model and how this concept would be important in this patient’s care.

 

Sample Solution

Insulin function

Insulin is a hormone produced by the beta cells of the pancreas. It is responsible for regulating blood sugar levels. Insulin allows glucose to enter cells from the bloodstream, where it can be used for energy or stored for later use.

Basic defect in DKA

The basic defect in DKA is a lack of insulin. This can be caused by type 1 diabetes mellitus, which is an autoimmune disease that destroys the beta cells of the pancreas. DKA can also be caused by other conditions, such as infections, stress, or certain medications.

Causes of DKA in Ms. S

Ms. S experienced DKA because she was not taking insulin and she had an infection. When the body does not have enough insulin, it breaks down fat for energy. This process produces ketones, which are acidic substances. The build-up of ketones in the blood and urine is called ketoacidosis.

Pathophysiology of DKA

The pathophysiology of DKA is complex and involves several different metabolic pathways. However, the basic process is as follows:

  1. Lack of insulin leads to hyperglycemia (high blood sugar).
  2. Hyperglycemia causes an osmotic diuresis, which leads to dehydration and electrolyte imbalances.
  3. Dehydration and electrolyte imbalances can lead to shock.
  4. Lack of insulin also leads to increased lipolysis (breakdown of fat).
  5. Increased lipolysis leads to production of ketones.
  6. Ketones are acidic substances, so their accumulation in the blood leads to metabolic acidosis.

Classic signs and symptoms of DKA

The classic signs and symptoms of DKA include:

  • Hyperglycemia
  • Ketonuria (ketones in the urine)
  • Dehydration
  • Electrolyte imbalances
  • Nausea and vomiting
  • Abdominal pain
  • Headache
  • Confusion
  • Lethargy
  • Rapid breathing
  • Kussmaul breathing (deep, rapid breathing)
  • Fruity breath odor

Signs and symptoms experienced by Ms. S

Ms. S experienced the following signs and symptoms of DKA:

  • Hyperglycemia (blood sugar of 398 mg/dl)
  • Ketonuria (serum ketones positive)
  • Dehydration (hypotension and tachycardia)
  • Electrolyte imbalances (hypokalemia)
  • Nausea and vomiting
  • Abdominal pain
  • Headache
  • Confusion
  • Lethargy
  • Rapid breathing
  • Fruity breath odor

Pathophysiologic causes of signs and symptoms

The pathophysiologic causes of the signs and symptoms of DKA are as follows:

  • Hyperglycemia: Hyperglycemia is caused by lack of insulin. Insulin allows glucose to enter cells from the bloodstream. Without insulin, glucose remains in the bloodstream, causing hyperglycemia.
  • Ketonuria: Ketonuria is caused by increased lipolysis (breakdown of fat). Increased lipolysis is caused by lack of insulin.
  • Dehydration: Dehydration is caused by osmotic diuresis. Osmotic diuresis is caused by hyperglycemia. When blood sugar is high, the kidneys try to excrete the excess sugar in the urine. This process also excretes water, leading to dehydration.
  • Electrolyte imbalances: Electrolyte imbalances are caused by dehydration and vomiting. Vomiting can lead to loss of important electrolytes, such as potassium and sodium.
  • Nausea and vomiting: Nausea and vomiting are caused by metabolic acidosis. Metabolic acidosis occurs when the body is unable to excrete enough acid. This can lead to a build-up of acid in the blood, which can cause nausea and vomiting.
  • Abdominal pain: Abdominal pain is caused by dehydration and vomiting.
  • Headache: Headache is caused by dehydration and metabolic acidosis.
  • Confusion: Confusion is caused by metabolic acidosis and dehydration.
  • Lethargy: Lethargy is caused by dehydration and metabolic acidosis.
  • Rapid breathing: Rapid breathing is caused by metabolic acidosis. The body tries to compensate for metabolic acidosis by increasing the rate of breathing. This helps to remove carbon dioxide from the blood, which is acidic.
  • Kussmaul breathing: Kussmaul breathing is a type of rapid breathing that is characterized by deep, rapid breaths. It is caused by metabolic acidosis.
  • Fruity breath odor: Fruity breath odor is caused by ketones. Ketones are acidic substances that are produced when the body breaks down fat for energy.

Anion gap

The anion gap is a measure of the difference between the measured positive ions (sodium and potassium) and the measured negative ions (chloride and bicarbonate) in the blood. A normal anion gap is between 10 and 16 mEq/L.

The anion gap is important to follow in the treatment of DKA because it can help to assess the severity of the acidosis and to identify any

 

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