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Chapter 7 CARE OF THE PATIENT WITH ENDOCRINE DISORDERS 343

flushed, dry skin; sunken eyeballs; poor skin turgor taking more than 3 seconds
to return; parched lips; tachycardia; hypotension; variations in body tempera-
ture; and continued air hunger or Kussmaul’s respirations.
5 Interpreting Test Results DKA is rapidly confirmed through urine ketone test-
ing and fingerstick blood sugar analysis. Decreased arterial blood gas pH and
low bicarbonate levels are also evident with DKA. BUN, specific gravity, hema-
tocrit, and serum osmolality increase. Sodium and potassium levels decrease.
Emergency medical management is needed to reverse ketoacidosis. Insulin
and intravenous solutions are given to reduce hyperglycemia and restore fluid
volume and electrolyte balance. Gastric motility is affected with DKA and the
patient might require a nasogastric tube to decompress the stomach and relieve
the patient of gastric distention, abdominal pain, tenderness, vomiting, blood-
positive gastric contents, and paralytic ileus.
A Foley catheter needs to be inserted for accurate measurement of intake and
output to determine fluid volume status and renal functioning. Skin assessment for
moisture or dryness determines fluid volume distribution throughout the body.
Oral care is provided to moisten dry mucous membranes. Monitor vital signs
to assess cardiac responses to fluid replacement. Signs of circulatory fluid over-
load include moist lung sounds, dyspnea without exertion, and neck vein Downloaded by [ Faculty of Nursing, Chiangmai University 5.62.158.117] at [07/18/16]. Copyright © McGraw-Hill Global Education Holdings, LLC. Not to be redistributed or modified in any way without permission.
engorgement.

Prognosis
Mortality rates are less than 5% in cases of DKA if underlying causes are iden-
tified and prevented through appropriate patient education.

HHNS (Hyperosmolar Hyperglycemic Nonketotic Syndrome)
What Went Wrong? The primary difference in this syndrome is that the patient
with diabetes still has enough circulating insulin to prevent DKA, but not
enough to prevent severe hyperglycemia, osmotic diuresis, and severe dehydra-
tion. A deficit of insulin and an excess of glucagon exist. Extracellular fluid loss
can be as great as 9 L.
Hyperglycemic values can exceed 2,000 mg/dL, while hyperosmolality val-
ues can be as high as 350 mOsm/kg. The mortality rate with this syndrome
exceeds the mortality rate of DKA.
The patient develops lactic acidosis from poor tissue perfusion and not
ketoacidosis. An increase in hepatic glucose production occurs, dehydration
worsens, and confusion, lethargy, and seizures result due to CNS dysfunction.
Hemoconcentration of the blood can cause major organ infarctions and
thromboemboli.