NCM 116A (Problems in Nutrition, Gastro-Intestinal, Metabolism, and Endocrine, and

Perception and Coordination (Acute and Chronic)

MODULE 4D: “DISTURBANCES IN NUTRITIONAL-METABOLIC PATTERNS /

RESPONSESTO ENDOCRINE FUNCTIONS”

DIABETES MELLITUS

COMPLICATIONS OF INSULIN THERAPY

1. LOCAL ALLERGIC REACTIONS

a) Redness, swelling, tenderness, and induration or a wheal at the site of injection may
occur 1to 2 hours after administration.
b) Reactions usually occur during the early stages of insulin therapy.
c) Instruct the client to cleanse the skin with alcohol before injection.

2. INSULIN LIPODYSTROPHY
a) Lipoatrophy is loss of subcutaneous fat and appears as slight dimpling or more serious
pitting of subcutaneous fat; the use of human insulin helps prevent this complication
b) Lipohypertrophy is the development of fibrous fatty masses at the injection site and is
caused by repeated use of an injection site
c) Instruct the client to avoid injecting insulin into affected sites.
d) Instruct the client about the importance of rotating insulin injection sites.

3. INSULIN RESISTANCE
a) The client receiving insulin develops immune antibodies that bind the insulin, thereby
decreasing the insulin available for use in the body.
b) Treatment consists of administering a purer insulin preparation.
c) Insulin resistance is also the term used for lack of tissue sensitivity to the insulin from the
body, which results in hyperglycemia.

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4. DAWN PHENOMENON
a) Dawn phenomenon results from reduced tissue sensitivity to insulin, and usually
develops between 5 and 8 AM (prebreakfast hyperglycemia occurs); it may be caused
by nocturnal release of growth hormone.
b) Treatment includes administering an evening dose (or increasing the amount of a current
dose) of intermediate-acting insulin at about 10 PM.

5. SOMOGYI PHENOMENON
a) Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at
about 2 to 3 AM, which causes an increase in the production of counterregulatory
hormones.
b) By about 7 AM, in response to the counterregulatory hormones, the blood glucose
rebounds significantly to the hyperglycemic range.
c) Treatment includes decreasing the evening (predinner or bedtime) dose of intermediate-
acting insulin or increasing the bedtime snack.

Insulin injection sites

a) The main areas for injections are the abdomen, arms (posterior surface), thighs (anterior
surface), and hips (Fig. 55-1).
b) Insulin injected into the abdomen may absorb more evenly and rapidly than at other sites.
c) Systematic rotation within one anatomical area is recommended to prevent lipodystrophy;
client should be instructed not to use the same site more than once in a 2- to 3-week
period.
d) Injections should be 11⁄2 inches apart within the anatomical area.
e) Heat, massage, and exercise of the injected area can increase absorption rates and may
result in hypoglycemia.
f) Injection into scar tissue may delay absorption of insulin.

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 Administering insulin
 Insulin glargine (Lantus) cannot be mixed with any other types of insulin.

a) To prevent dosage errors, be certain that there is a match between the insulin
concentration noted on the vial and the calibration of units on the insulin syringe; the
usual concentration of insulin is U 100 (100 units/mL).
b) Most insulin syringes have a 27- to 29-gauge needle that is about 1⁄2-inch long.
c) Before use, swirl the insulin vial gently or rotate between the palms to ensure that the
insulin and ingredients are mixed well; otherwise, an inaccurate dose will be drawn;
vigorously shaking the bottle will cause bubbles to form.
d) Premixed insulins (NPH and regular insulin; insulin aspart protamine and insulin aspart)
are available as 70/30 (most commonly used) and premixed insulin lispro protamine and
insulin lispro 75/25 and 50/50 are also available.
e) Inject air into the insulin bottle (a vacuum makes it difficult to draw up the insulin).
f) When mixing insulins, draw up the shortest-acting insulin first (Fig. 55-2).

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Prepared by: Asso. Prof. Frissida Asid-Daud, RN, MAN Page 4 of 21
 g) Short-acting (i.e., regular, lispro, aspart, and glulisine) insulin may be mixed with NPH.
h) Lispro insulin may be mixed with Humulin N.
i) Insulin aspart protamine may be mixed with NPH insulin only.
j) Administer a mixed dose of insulin within 5 to 15 minutes of preparation; after this time,
the short-acting insulin binds with the NPH insulin and its action is reduced.
k) Aspiration after insertion of the needle generally is not recommended with self-injection
of insulin.
l) Administer insulin at a 45- to 90-degree angle in clients with normal subcutaneous mass
and at a 45- to 60-degree angle in thin persons or those with a decreased amount of
subcutaneous mass.

 RAPID AND SHORT-ACTING INSULINS are the only types of insulin that can be
administered intravenously.

MANAGEMENT OF METABOLIC EMERGENCIES

There are three major acute complications of diabetes related to short-term

imbalances in blood glucose levels: hypoglycemia, diabetic ketoacidosis (DKA), and
hyperglycemic hyperosmolar nonketotic syndrome (HHNS), which is also called
hyperglycemic hyperosmolar syndrome or state (HHS).

I. HYPOGLYCEMIA (INSULIN REACTIONS)

 Hypoglycemia (abnormally low blood glucose level) occurs when the blood glucose falls to
less than 50 to 60 mg/dL (2.7 to 3.3 mmol/L). It can be caused by:
 too much insulin or oral hypoglycemic agents,
 too little food, or
 excessive physical activity.

 Hypoglycemia may occur at any time of the day or night. It often occurs before meals,
especially if meals are delayed or snacks are omitted.

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 For example, midmorning hypoglycemia may occur when the morning regular insulin is
peaking, whereas hypoglycemia that occurs in the late afternoon coincides with the peak of
the morning NPH or Lente insulin. Middle-of-the-night hypoglycemia may occur because of
peaking evening or predinner NPH or Lente insulins, especially in patients who have not
eaten a bedtime snack.

CLINICAL MANIFESTATIONS:
 The clinical manifestations of hypoglycemia may be grouped into two categories:
1. adrenergic symptoms and
2. central nervous system (CNS) symptoms.

 In mild hypoglycemia, as the blood glucose level falls, the sympathetic nervous system is
stimulated, resulting in a surge of epinephrine and norepinephrine. This causes
symptoms such as: (STTPNH)
1. sweating
2. tremor,
3. tachycardia,
4. palpitation,
5. nervousness, and
6. hunger

 In moderate hypoglycemia, the fall in blood glucose level deprives the brain cells of
needed fuel for functioning. Signs of impaired function of the CNS may include :
1. inability to concentrate,
2. headache,
3. lightheadedness,
4. confusion,
5. memory lapses,
6. numbness of the lips and tongue,
7. slurred speech, impaired coordination,
8. emotional changes,

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 9. irrational or combative behavior,
10. double vision, and drowsiness

 In severe hypoglycemia, CNS function is so impaired that the patient needs the
assistance of another person for treatment of hypoglycemia. Symptoms may include: DSDL
1. disoriented behavior,
2. seizures,
3. difficulty arousing from sleep, or
4. loss of consciousness

Assessment and Diagnostic Findings

 Symptoms of hypoglycemia may occur suddenly and unexpectedly and vary considerably
from person to person.
 Decreased hormonal (adrenergic) response to hypoglycemia may also contribute to lack of
symptoms of hypoglycemia. This occurs in some patients who have had diabetes for many
years.
 It may be related to autonomic neuropathy, a chronic diabetic complication. As the blood
glucose level falls, the normal surge in adrenalin does not occur, and the usual adrenergic
symptoms, such as sweating and shakiness, do not take place.
 The hypoglycemia may not be detected until moderate or severe CNS impairment occurs.
 Affected patients must perform SMBG on a frequent regular basis, especially before driving
or engaging in other potentially dangerous activities.

Management
 Immediate treatment must be given when hypoglycemia occurs. The usual recommendation
is for 15 g of a fast-acting concentrated source of carbohydrate such as the following,
given orally:
 Three or four commercially prepared glucose tablets
 4 to 6 oz of fruit juice or regular soda
 6 to 10 hard candies
 2 to 3 teaspoons of sugar or honey

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 The blood glucose level should be retested in 15 minutes and retreated if it is less than 70 to
75 mg/dL (3.8 to 4 mmol/L).
 If the symptoms persist for longer than 10 to 15 minutes after initial treatment, the treatment
is repeated even if blood glucose testing is not possible.
 Once the symptoms resolve, a snack containing protein and starch (eg, milk or cheese
and crackers) is recommended unless the patient plans to eat a regular meal or snack within
30 to 60 minutes.

Teaching Patients
 It is important that patients with diabetes, especially those receiving insulin, learn to carry
some form of simple sugar with them at all times (ADA, 2004k).

 Patients are advised to refrain from eating high-calorie, high-fat dessert foods (eg,
cookies, cakes, doughnuts, ice cream) to treat hypoglycemia).

 Patients who feel unduly restricted by their meal plan may view hypoglycemic episodes
as a time to reward themselves with desserts. It may be more prudent to teach these
patients to incorporate occasional desserts into the meal plan.

INITIATING EMERGENCY MEASURES:

 In emergency situations, for adult patients who are unconscious and cannot swallow, an
injection of glucagon 1 mg can be administered either subcutaneously or
intramuscularly.

 Glucagon is a hormone produced by the alpha cells of the pancreas that stimulates the
liver to release glucose (through the breakdown of glycogen, the stored glucose).
Injectable glucagon is packaged as a powder in 1-mg vials and must be mixed with a
diluent before being injected. After injection of glucagon, the patient may take as long
as 20 minutes to regain consciousness.

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  A concentrated source of carbohydrate followed by a snack should be given to the
patient on awakening to prevent recurrence of hypoglycemia (because the duration of
the action of 1 mg of glucagon is brief—its onset is 8 to 10 minutes, and its action lasts
12 to 27 minutes) and to replenish liver stores of glucose.

 Some patients experience nausea after the administration of glucagon. If this occurs, the
patient should be turned to the side to prevent aspiration in case the patient vomits.

IN HOSPITALS AND EMERGENCY DEPARTMENTS

 for patients who are unconscious or cannot swallow:
 25 to 50 mL of 50% dextrose in water (D50W) may be administered IV.
 The effect is usually seen within minutes.
 The patient may complain of a headache and of pain at the injection site.
 Assuring patency of the IV line used for injection of 50% dextrose is essential, because
hypertonic solutions such as 50% dextrose are very irritating to veins.

Teaching Patients Self-Care

 Hypoglycemia is prevented by a consistent pattern of
a) Eating,
b) Administering insulin, and
c) Exercising.

 Between-meal and bedtime snacks may be needed to counteract the maximum insulin
effect. In general, the patient should cover the time of peak activity of insulin by eating a
snack and by taking additional food when physical activity is increased. Routine blood
glucose tests are performed so that changing insulin requirements may be anticipated and
the dosage adjusted.

 Because unexpected hypoglycemia may occur, all patients treated with insulin should
wear an identification bracelet or tag stating that they have diabetes.

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  Patients and family members must be instructed about the symptoms of hypoglycemia.

 Some patients who have autonomic neuropathy or who are taking beta-blockers such as
propranolol to treat hypertension or cardiac dysrhythmias may not experience the typical
symptoms of hypoglycemia. It is very important that these patients perform blood
glucose tests on a frequent and regular basis. Patients who have type 2 diabetes and
who take oral sulfonylurea agents may also develop hypoglycemia, which can be
prolonged and severe; this is a particular risk for elderly patients.

II. DIABETIC KETOACIDOSIS (DKA)

 DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in
available insulin results in disorders in the metabolism of carbohydrate, protein, and fat.

 The three main clinical features of DKA are: H-D-A

 1. Hyperglycemia
 2. Dehydration and electrolyte loss
 3. Acidosis

Pathophysiology
 Without insulin, the amount of glucose entering the cells is reduced, and production and
release of glucose by the liver is increased. Both factors lead to hyperglycemia.

 In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along
with water and electrolytes (eg, sodium, potassium). This osmotic diuresis, which is
characterized by excessive urination (polyuria), leads to dehydration and marked
electrolyte loss.

 Patients with severe DKA may lose up to 6.5 L of water and up to 400 to 500 mEq each
of sodium, potassium, and chloride over a 24-hour period.

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  Another effect of insulin deficiency or deficit is the breakdown of fat (lipolysis) into free
fatty acids and glycerol.

 The free fatty acids are converted into ketone bodies by the liver. In DKA, there is
excessive production of ketone bodies because of the lack of insulin that would
normally prevent this from occurring. Ketone bodies are acids; their accumulation in
the circulation leads to metabolic acidosis.

 Three main causes of DKA are:

1. Decreased or missed dose of insulin,
2. Illness or Infection
 associated with insulin resistance: “STRESS hormones  Counteracting effect of
insulin; and
3. Undiagnosed and Untreated Diabetes
 DKA may be the initial manifestation of diabetes).

Clinical Manifestations
 The hyperglycemia of DKA leads to:
1. polyuria and
2. polydipsia (increased thirst)
3. blurred vision,
4. weakness, and
5. headache
6. orthostatic hypotension/ frank hypotension with a weak, rapid pulse.
7. GIT symptoms:
a. A-N-V
b. Abdominal Pain (The abdominal pain and physical findings on examination can be so
severe that they resemble an acute abdominal disorder that requires surgery. )
c. Acetone Breath (a fruity odor) with elevated ketone levels
d. Hyperventilation

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  With very deep, but not labored, respirations  Kussmaul R. ) may occur
counteracting the effect of the ketone buildup).
e. Mental Status vary widely
 The patient may be alert, lethargic, or comatose, most likely depending on the plasma
osmolarity).

Abnormal metabolism that causes signs and symptoms of DKA

Assessment and Diagnostic Findings

1. Blood glucose levels may vary between 300 and 800 mg/dL (16.6 to 44.4 mmol/L).
 Some patients have lower glucose values, and others have values of 1000 mg/dL (55.5
mmol/L) or higher (usually depending on the degree of dehydration).
 The severity of DKA is not necessarily related to the blood glucose level.

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  Some patients have severe acidosis with modestly elevated blood glucose levels, whereas
others have no evidence of DKA despite blood glucose levels of 400 to 500 mg/dL (22.2
to 27.7 mmol/L).

2. Evidence of ketoacidosis is reflected in low serum bicarbonate (0 to 15 mEq/L) and low

pH (6.8 to 7.3) values. A low PCO2 (10 to 30 mm Hg) reflects respiratory compensation
(Kussmaul respirations) for the metabolic acidosis.

3. Accumulation of ketone bodies (which precipitates the acidosis) is reflected in blood and
urine ketone measurements.

4. Sodium and potassium concentrations may be low, normal, or high, depending on the
amount of water loss (dehydration).

5. Increased levels of creatinine, blood urea nitrogen (BUN), and hematocrit may also be seen
with dehydration. After rehydration, continued elevation in the serum creatinine and
BUN levels is present in patients with underlying renal insufficiency.

Prevention
 The most important concept to teach patients is not to eliminate insulin doses when
nausea and vomiting occur.
 Consume frequent small portions of carbohydrates (including foods usually avoided, such
as juices, regular sodas, and gelatin).
 If cannot follow usual meal plan, substitute soft foods (eg, 1/3 cup regular gelatin, 1 cup
cream soup, ½ cup custard, 3 squares graham crackers) six to eight times per day.
 If vomiting, diarrhea, or fever persists, take liquids (eg, ½ cup regular cola or orange
juice, ½ cup broth, 1 cup Gatorade) every ½ to 1 hour to prevent dehydration and to
provide calories.
 Drinking fluids every hour is important to prevent dehydration.
 Blood glucose and urine ketones must be assessed every 3 to 4 hours.

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  After the acute phase of DKA has resolved, the nurse should assess for underlying
causes of DKA. If there are psychological reasons for the patient's deliberately missing
insulin doses, the patient and family may be referred for evaluation and counseling or
therapy.

Medical Management (FEI)

 In addition to treating hyperglycemia, management of DKA is aimed at correcting
dehydration, electrolyte loss, and acidosis.

1. REHYDRATION
 In dehydrated patients, rehydration is important for maintaining tissue perfusion. In
addition, fluid replacement enhances the excretion of excessive glucose by the kidneys.
 6 to 10 L of IV fluid to replace fluid losses caused by polyuria, hyperventilation,
diarrhea, and vomiting.
 Initially, 0.9% sodium chloride (normal saline) solution is administered at a rapid rate,
usually 0.5 to 1 L/hour for 2 to 3 hours.

 Half-strength normal saline (0.45%) solution (also known as hypotonic saline

solution) may be used for patients with hypertension or hypernatremia and those at
risk for heart failure.

 After the first few hours, half-strength normal saline solution is the fluid of choice
for continued rehydration, provided the blood pressure is stable and the sodium
level is not low.

 Moderate to high rates of infusion (200 to 500 mL/hour) may continue for several more
hours.

 When the blood glucose level reaches 300 mg/dL (16.6 mmol/L) or less, the IV solution
may be changed to dextrose 5% in water (D5W) to prevent a precipitous decline in the
blood glucose level

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  Monitoring of fluid volume status involves frequent measurements of vital signs
(including monitoring for orthostatic changes in blood pressure and heart rate), lung
assessment, and monitoring of intake and output. Initial urine output lags behind IV fluid
intake as dehydration is corrected.

 Plasma expanders may be necessary to correct severe hypotension that does not respond
to IV fluid treatment.

 Monitoring for signs of fluid overload is especially important for patients who are older,
have renal impairment, or are at risk for heart failure.

2. RESTORING ELECTROLYTES
 The major electrolyte of concern during treatment of DKA is POTASSIUM.
 Although the initial plasma concentration of potassium may be low, normal, or even high,
there is a major loss of potassium from body stores and an intracellular-to-
extracellular shift of potassium.

 Some of the factors related to treating DKA that reduce the serum potassium
concentration include:
 Rehydration, which leads to increased plasma volume and subsequent decreases in the
concentration of serum potassium. Rehydration also leads to increased urinary
excretion of potassium.

 Insulin administration, which enhances the movement of potassium from the

extracellular fluid into the cells.

 Cautious but timely potassium replacement is vital to avoid dysrhythmias that may
occur with hypokalemia. As much as 40 mEq/hour may be needed for several hours.
Because extracellular potassium levels decrease during DKA treatment, potassium must
be infused even if the plasma potassium level is normal.

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  Frequent (every 2 to 4 hours initially) ECGs and laboratory measurements of potassium
are necessary during the first 8 hours of treatment. Potassium replacement is withheld
only if hyperkalemia is present or if the patient is not urinating.

3. REVERSING ACIDOSIS
 The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown,
thereby stopping acid buildup.

 Insulin is usually infused intravenously at a slow, continuous rate (eg, 5 units/hour).

Hourly blood glucose values must be measured.

 IV fluid solutions with higher concentrations of glucose, such as normal saline (NS)
solution (eg, D5NS, D5.45NS), are administered when blood glucose levels reach 250 to
300 mg/dL (13.8 to 16.6 mmol/L), to avoid too rapid a drop in the blood glucose level (ie,
hypoglycemia) during treatment.

 Regular insulin, the only type of insulin approved for IV use, may be added to IV
solutions. The nurse must convert hourly rates of insulin infusion (frequently prescribed
as “units per hour”) to IV drip rates. (For example, if 100 units of regular insulin are
mixed into 500 mL of 0.9% NS, then 1 unit of insulin equals 5 mL; therefore, an initial
insulin infusion rate of 5 units/hour would equal 25 mL/hour.

 The insulin is often infused separately from the rehydration solutions to allow frequent
changes in the rate and content of the latter.)

 Insulin must be infused continuously until subcutaneous administration of insulin

can be resumed. Any interruption in administration may result in the
reaccumulation of ketone bodies and worsening acidosis.
 Even if blood glucose levels are decreasing and returning to normal, the insulin drip
must not be stopped until subcutaneous insulin therapy has been started. Rather, the

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 rate or concentration of the dextrose infusion should be increased. Blood glucose
levels are usually corrected before the acidosis is corrected. Therefore, IV insulin may
be continued for 12 to 24 hours, until the serum bicarbonate level improves (to at
least 15 to 18 mEq/L) and until the patient can eat.

 In general, bicarbonate infusion to correct severe acidosis is avoided during treatment

of DKA because it precipitates further, sudden (and potentially fatal) decreases in
serum potassium levels.

 Continuous insulin infusion is usually sufficient for reversal of DKA.

Nursing Alert  When mixing the insulin drip, it is important to flush the insulin solution
through the entire IV infusion set and to discard the first 50 mL of fluid. Insulin molecules
adhere to the inner surface of IV infusion sets; therefore, the initial fluid may contain a
decreased concentration of insulin.

Nursing Management focuses on:

1. Monitoring fluid, electrolyte, and hydration status as well as blood glucose levels;
2. Administering fluids, insulin, and other medications;
3. Preventing other complications such as fluid overload.
4. Urine output is monitored to ensure adequate renal function before potassium is
administered to prevent hyperkalemia
5. ECG is monitored for dysrhythmias indicating abnormal potassium levels
6. Vital signs (especially blood pressure and pulse), arterial blood gases, breath sounds, and
mental status are assessed every hour and recorded on a flow sheet.
7. Documenting the patient's laboratory values and the frequent changes in fluids and
medications that are prescribed and monitors the patient's responses.

As DKA resolves and the potassium replacement rate is decreased, the nurse makes
sure that:
 There are no signs of hyperkalemia on the ECG (tall, peaked or tented T waves)

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  Laboratory values of potassium are normal or approaching normal
 The patient is urinating (ie, no renal shutdown).

III. HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME

 HHNS is a serious condition in which hyperosmolarity and hyperglycemia predominate,

with alterations of the sensorium (sense of awareness).
 At the same time, ketosis is usually minimal or absent.
 The basic biochemical defect is lack of effective insulin (ie, insulin resistance).

 Persistent hyperglycemia causes osmotic diuresis, which results in losses of water and
electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid
space to the extracellular fluid space.
 With glycosuria and dehydration, hypernatremia and increased osmolarity occur
(compares DKA and HHNS.)
 What distinguishes HHNS from DKA is that ketosis and acidosis generally do not occur
in HHNS, partly because of differences in insulin levels.

 In DKA, no insulin is present, and this promotes the breakdown of stored glucose,
protein, and fat, which leads to the production of ketone bodies and ketoacidosis.

 In HHNS, the insulin level is too low to prevent hyperglycemia (and subsequent
osmotic diuresis), but it is high enough to prevent fat breakdown.

 Patients with HHNS do not have the ketosis-related gastrointestinal symptoms that lead
them to seek medical attention.
 Instead, they may tolerate polyuria and polydipsia until neurologic changes or an
underlying illness (or family members or others) prompts them to seek treatment.

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  Because of possible delays in therapy, hyperglycemia, dehydration, and
hyperosmolarity may be more severe in HHNS.

Clinical Manifestations
 The clinical picture of HHNS:
1. hypotension,
2. profound dehydration (dry mucous membranes, poor skin turgor),
3. tachycardia, and
4. variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis).
 The mortality rate ranges from 10% to 40%, usually related to an underlying illness, the
vulnerability of the elderly patient, and the severity of HHNS.

Assessment and Diagnostic Findings

1. blood glucose,
2. electrolytes, BUN,
3. complete blood count,
4. serum osmolality, and
5. arterial blood gas analysis
 Electrolyte and BUN levels are consistent with the clinical picture of severe dehydration.
 Mental status changes, focal neurologic deficits, and hallucinations are common secondary
to the cerebral dehydration that results from extreme hyperosmolality.
 Postural hypotension accompanies the dehydration (ADA, 2004h).

Medical Management
 The overall approach to the treatment of HHNS is similar to that of DKA.
1. Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient's sodium
level and the severity of volume depletion.
 Central venous or hemodynamic pressure monitoring guides fluid replacement.

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 2. Potassium is added to IV fluids when urinary output is adequate and is guided by
continuous ECG monitoring and frequent laboratory determinations of potassium.
Extremely elevated blood glucose concentrations decrease as the patient is rehydrated.

 Insulin plays a less important role in the treatment of HHNS because it is not needed
for reversal of acidosis, as in DKA. It is usually administered at a continuous low rate
to treat hyperglycemia.

 Replacement IV fluids with dextrose are administered (as in DKA) after the glucose
level has decreased to the range of 250 to 300 mg/dL (13.8 to 16.6 mmol/L) (ADA,
2004h).

 Other therapeutic modalities are determined by the underlying illness and the results of
continuing clinical and laboratory evaluation.

 It may take 3 to 5 days for neurologic symptoms to clear, and treatment of HHNS
usually continues well after metabolic abnormalities have resolved.
.
Nursing Management
1. Nursing care of patients with HHNS includes close monitoring of vital signs, fluid status,
and laboratory values.
2. Strategies are implemented to maintain safety and prevent injury related to changes in the
sensorium secondary to HHNS.
3. Fluid status and urine output are closely monitored because of the high risk of renal failure
secondary to severe dehydration.
4. The nurse must direct nursing care to the condition that may have precipitated the onset of
HHNS.

5. Because HHNS tends to occur in older patients, the physiologic changes that occur with
aging should be noted.

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  Careful assessment of cardiovascular, pulmonary, and renal function throughout
the acute and recovery phases of HHNS is important.

Comparison of DKA and Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

Characteristics DKA HHNS

 Patients most commonly  Can occur in type 1 or type 2  Can occur in type 1 or type 2 diabetes;
affected diabetes; more common in more common in type 2 diabetes,
type 1 diabetes especially elderly patients (50-70 y.o)
with type 2 diabetes
 Precipitating event  Omission of insulin;  Physiologic stress (infection, surgery,
physiologic stress (infection, CVA, MI)
surgery, CVA, MI)
 Onset  Rapid (<24 h)  Slower (over several days)
 Blood glucose levels  Usually >250 mg/dL (>13.9  Usually >600 mg/dL (>33.3 mmol/L)
mmol/L)
 Arterial pH level  <7.3  Normal
 Serum and U. ketones  Present  Absent
 Serum osmolality  300–350 mOsm/L  >350 mOsm/L
 Plasma bicarbonate level  <15 mEq/L  Normal
 BUN and Cr. Levels  Elevated  Elevated
 Mortality rate  <5%  10–40%

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