Diabetic ketoacidosis (DKA) is a life-threatening emergency caused by a relative or absolute deficiency of insulin. This deficiency in available insulin results in disorders in the metabolism of carbohydrate, fat, and protein. Main clinical features of DKA are hyperglycemia, acidosis, dehydration, and electrolyte losses such as hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, and hypophosphatemia.
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) is a condition characterized by the presence of hyperglycemia, hyperosmolarity, and dehydration. There is enough production of insulin to reduce ketosis but not to control hyperglycemia. Persistent hyperglycemia causes osmotic diuresis, which results in the fluid and electrolyte imbalances. The clients with HHNS may present with symptoms of hypotension, tachycardia, marked dehydration, and neurological manifestation such as seizures, hemiparesis, and alterations in the sensorium).
Nursing Care Plans
The nursing care plan for clients with Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome includes provision of information about disease process/prognosis, self-care, and treatment needs, monitoring and assistance of cardiovascular, pulmonary, renal, and central nervous system (CNS) function, avoiding dehydration, and correcting hyperglycemia and hyperglycemia complications.
- Risk For Fluid Volume Deficit
- Risk For Infection
- Deficient Knowledge
- Imbalanced Nutrition: Less Than Body Requirements
Risk For Fluid Volume Deficit
- Risk for Fluid Volume Deficit
- 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
- [not applicable].
- 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.
|Assess precipitating factors such as other illnesses, new-onset diabetes, or poor compliance with 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 and HHNS among older clients.|
|Assess skin turgor, mucous membranes, and thirst.||To provide baseline data for further comparison. Skin turgor will decrease and tenting may occur. The oral mucous membranes will become dry, and the client may experience extreme thirst.|
|Monitor hourly intake and output.||Oliguria or anuria results from reduced glomerular filtration and renal blood flow.|
|Monitor vital signs:|
||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) represent 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.|
||Decreased level of consciousness results from blood volume depletion, elevated or decreased glucose level, hypoxia or electrolyte imbalances.|
|Weigh client daily.||Provides baseline data of current fluid status and adequacy of fluid replacement. A weight loss of 2.2 lbs over 24 hours indicates a 1 liter of fluid loss.|
|Monitor laboratory studies:|
DKA: blood glucose level greater than 250 mg/dL.
HHNS: blood glucose level greater than 600 mg/dL with serum osmolality >320 mOsm/kg.
||Elevated ketones is associated with DKA.|
||Initially, hyperkalemia occurs in response to metabolic acidosis. As the fluid volume deficit progresses, potassium level decreases. Both DKA and HHNS 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 an acute renal failure.|
|Monitor ABG for metabolic acidosis.||Clients with DKA have metabolic acidosis with arterial a bicarbonate level less than 18 mEq/L, and a pH less than 7.30.|
|Insert indwelling urinary catheter as indicated.||To provide accurate measurement of urinary output especially for clients with neurogenic bladder.|
|Administer fluid as indicated: Isotonic solution (0.9% NaCl).||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 2 to 3 liters within the first 2 hours of treatment.|
|Administer succeeding IV therapy: 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.|
|Add dextrose to IV fluid when serum blood glucose level is less than 250 mg/dL in DKA or less than 300 mg/dL in HHNS.||Dextrose is added to prevent the occurrence of hypoglycemia and an excessive decline in plasma osmolality that can result in cerebral edema.|
|Administer IV potassium and other electrolytes as indicated.||Potaasium is added to the IV once serum potassium drops below 5.5 mEq/L to prevent hypokalemia. The administration of insulin to lower blood glucose promotes the movement of potassium intracellularly.|
|Administer bicarbonate as indicated.||This is given in clients with a severe hyperkalemia and severe acidosis with pH of less than 7.1.|
|Administer an IV bolus dose of regular insulin, followed by a continuous infusion of regular insulin.||Regular insulin has a rapid onset and therefore immediately helps move glucose intracellularly. IV route is the initial route because subcutaneous injection of insulin may be absorbed unpredictably. While a continuous infusion is an optimal way to consistently administer insulin to prevent hypoglycemia.|
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