4 Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome Nursing Care Plans

Deficient Fluid Volume

Without insulin, the amount of glucose entering the cells is reduced, and the production and release of glucose by the liver are increased, leading to hyperglycemia. In an attempt to rid the body of excess glucose, the kidneys excrete the glucose along with water and electrolytes. This osmotic diuresis, which is characterized by excessive urination, leads to dehydration and marked electrolyte loss.

Nursing Diagnosis

• Deficient Fluid Volume

May be related to

• Decreased intake of fluids due to diminished thirst sensation or functional inability to drink fluids.
• Excessive gastric losses due to nausea and vomiting.
• Hyperglycemia-induced osmotic diuresis.

Possibly evidenced by

• Polyuria
• Diluted urine
• Sudden weight loss
• Weakness
• Dry skin and mucous membranes, poor skin turgor
• Hypotension, tachycardia
• Delayed capillary refill

Desired Outcomes

• The client will remain normovolemic as evidenced by urinary output greater than 30 ml/hr, normal skin turgor, good capillary refill, normal blood pressure, palpable peripheral pulses, and blood glucose levels between 70-200 mg/dL.
• The client will display normal electrolyte levels and stable vital signs.

Nursing Assessment and Rationales

1. Assess precipitating factors such as other illnesses, new-onset diabetes, or poor compliance with the treatment regimen.
These will provide baseline data for education once with resolved hyperglycemia. Urinary tract infection and pneumonia are the most common infections causing DKA among older clients. Poor compliance with insulin through the omission of insulin injections occurs due to a lack of client or guardian education, or as a result of psychological stress, particularly in adolescents (Hamdy & Khardori, 2021).

2. Assess skin turgor, mucous membranes, and thirst.
This provides baseline data for further comparison. Skin turgor will decrease and tenting may occur. This occurs because the skin relies on hydration to maintain its elasticity and suppleness. The oral mucous membranes will become dry, and the client may experience extreme thirst.

3. Monitor hourly intake and output.
Oliguria or anuria results from reduced glomerular filtration and renal blood flow. Hyperglycemia usually exceeds the renal threshold of glucose absorption and results in significant glucosuria. Glucosuria leads to osmotic diuresis, dehydration, and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function (Hamdy & Khardori, 2021).

4. Monitor vital signs, especially for orthostatic hypotension and Kussmaul’s respirations.
Decreased blood volume may be manifested by a drop in systolic blood pressure and orthostatic hypotension. Acetone breath is due to the breakdown of acetoacetic acid. Kussmaul’s respiration (rapid and shallow breathing) represents a compensatory mechanism by the respiratory buffering system to raise arterial pH by exhaling more carbon dioxide. Fever with flushed, dry skin may indicate dehydration. Compensatory mechanism results in peripheral vasoconstriction with a weak, thready pulse that is easily obliterated.

5. Assess neurological status every two hours.
Decreased level of consciousness results from blood volume depletion, elevated or decreased glucose level, hypoxia, or electrolyte imbalances. Altered consciousness in the form of mild disorientation or confusion can occur. Although frank coma is uncommon, it may occur when the condition is neglected or if dehydration or acidosis is severe (Hamdy & Khardori, 2021).

6. Weigh the client daily.
This provides baseline data on the current fluid status and adequacy of fluid replacement. A weight loss of 2.2 lbs (1 kg) over 24 hours indicates a liter of fluid loss. Typical free water loss in DKA is approximately six liters or nearly 100 mL/kg of body weight. The initial half of this amount is derived from intracellular fluid and precedes signs of dehydration, while the other half is from the extracellular fluid and is responsible for signs of dehydration (Hamdy & Khardori, 2021).

7. Assess for the presence of nausea and vomiting.
Nausea and vomiting usually occur and may be associated with diffuse abdominal pain, decreased appetite, and anorexia. Ketones, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA.

Nursing Interventions and Rationales

1. Maintain a fluid intake of at least 2500 liters/day within cardiac tolerance when oral intake is resumed.
This maintains hydration and adequacy of circulating volume. Hydration causes a decline in counter-regulatory hormones, enhances renal glucose clearance following improved renal perfusion, and augments insulin sensitivity. This, in turn, causes a significant reduction in hyperglycemia, hypertonicity, and acidemia. Hydration alone (intravenous and oral) has been shown to reduce glucose concentration by 17 to 80% over a duration of 12 to 15 hours (Javashree et al., 2019).

2. Be alert to indicators of fluid overload, particularly among older adults or clients with a history of heart or renal failure.
Indicators of fluid overload, such as jugular vein distention, dyspnea, crackles, or CVP of more than 12 mm Hg, can occur with rapid infusion of fluids. Be extremely cautious to avoid cerebral edema and pulmonary edema. Although initial aggressive fluid replacement is necessary in all clients, particular care must be taken in those with comorbidities such as renal failure or congestive heart failure (Hamdy & Khardori, 2021). 

3. Monitor laboratory studies such as blood glucose levels, serum ketones, potassium, sodium, creatinine, and blood urea nitrogen (BUN).
DKA occurs when the blood glucose level is greater than 250 mg/dL. Elevated ketones are associated with DKA. Initially, hyperkalemia occurs in response to metabolic acidosis. As the fluid volume deficit progresses, the potassium level decreases. Both DKA result in hypokalemia. Increased blood sugar causes water to shift from intracellular into extracellular, resulting in serum sodium depletion. Elevated BUN and creatinine indicate cellular breakdown from dehydration or a sign of acute renal failure.

4. Monitor ABG for metabolic acidosis.
In clients diagnosed with DKA, ABGs frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH of less than 7.3. Venous pH may be used for repeat pH measurements. When monitoring the response to treatment, guidelines recommend the use of venous blood rather than arterial blood in blood gas analyzers, except where respiratory problems preclude using arterial blood (Hamdy & Khardori, 2021).

5. Insert indwelling urinary catheter as indicated.
This provides accurate measurement of urinary output, especially if autonomic neuropathies result in neurogenic bladder with urinary retention and overflow incontinence. The catheter may be removed when the client is stable to reduce the risk of infection.

6. Administer isotonic solutions (0.9% NaCl) initially.
The initial goal of therapy is to correct circulatory fluid volume deficit. Isotonic normal saline will rapidly expand extracellular fluid volume without causing a rapid fall in plasma osmolality. Clients typically need one to three liters within the first two hours of treatment. A liter is administered every four hours following the first two hours, depending on the degree of dehydration and central venous pressure readings (Hamdy & Khardori, 2021).

7. Administer succeeding IV therapy with a hypotonic solution such as 0.45% normal saline.
Continuation of IV administration depends on the degree of fluid deficit, urinary output, and serum electrolyte values. After initial stabilization with isotonic saline, switch to half-normal saline at 200 to 1000 mL/hour. Half-normal saline matches losses due to osmotic diuresis (Hamdy & Khardori, 2021).

8. Add dextrose to IV fluid when serum blood glucose level is less than 180 mg/dL in DKA.
When blood sugar decreases to less than 180 mg/dL, isotonic sodium chloride solution is replaced with 5 to 10% dextrose with half isotonic sodium chloride solution (Hamdy & Khardori, 2021). Dextrose is added to prevent the occurrence of hypoglycemia and an excessive decline in plasma osmolality that can result in cerebral edema.

9. Administer IV potassium and other electrolytes as indicated.
If the potassium level is greater than 6 mEq/L, do not administer a potassium supplement. Instead, monitor until potassium levels are 4,5 to 6 mEq/L, then administer 10 mEq/hour of potassium chloride. The administration of insulin to lower blood glucose promotes the movement of potassium intracellularly. The infusion must be stopped if the potassium level is greater than 5 mEq/L (Hamdy & Khardori, 2021).

10. Administer bicarbonate as indicated.
Sodium bicarbonate is only infused if decompensated acidosis starts to threaten the client’s life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100 to 150 mL of 1.4% concentration is infused initially. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis (Hamdy & Khardori, 2021).

11. Administer IV insulin by continuous infusion using an infusion pump.
Regular insulin has a rapid onset and therefore immediately helps move glucose intracellularly. A low-dose insulin regimen has the advantage of not inducing the severe hypoglycemia or hypokalemia that may be observed with a high-dose insulin regimen.  The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available. The incidence of DKA was reduced with the introduction of pumps equipped with sensitive electronic alarm systems that alert users when the infusion catheter is blocked (Hamdy & Khardori, 2021).

12. Before initiating treatment, flush the tubing with at least 30 mL of the insulin-containing IV solution.
When added to IV solutions, insulin may be absorbed by the container and plastic tubing. Flushing the tubing ensures that maximum adsorption of the insulin by the container and tubing has occurred before it is delivered to the client.