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Diabetes Mellitus

Type 1 Diabetes Mellitus

Type 2 Diabetes Mellitus

Diabetes Mellitus
An endocrine disorder in which there is insufficient amount or lack of insulin
secretion to metabolize carbohydrates.
It is characterized by hyperglycemia, glycosuria and ketonuria.
Maintenance of blood glucose levels. (A) Normal physiology: Foods (especially
carbohydrates) are broken down into glucose, which is absorbed into the
bloodstream for transport to the cells. Insulin, produced by the beta cells of the
islets of Langerhans in the pancreas, is needed to open the door to the cells,
allowing the glucose to enter. (B) In type 1 diabetes mellitus, the pancreas does not
produce insulin. Because glucose is unable to enter the cells, it builds up in the
bloodstream, causing hyper- glycemia. (C) In type 2 diabetes mellitus, insulin
production is reduced and/or cells are resistant to insulin. Less glucose enters the
cell, and hyperglycemia results.

Diabetes mellitus (or simply diabetes) is a condition when: the organism


begins to malfunction metabolic disorder
levels of the hormone insulin in the blood become insufficient
the body cells fail to respond to the insulin that is produced, or both.
as a result, blood sugar levels grow abnormally high (hyperglycaemia)
This is Diabetes and is not curative

The characteristic symptoms are


excessive urine production (polyuria) due to high blood glucose levels,
excessive thirst and increased fluid intake (polydipsia) attempting to
compensate for increased urination,
blurred vision due to high blood glucose effects on the eye's optics,
unexplained weight loss, and lethargy

How Genes Trigger Diabetes


Type 1 diabetes is triggered
by some (mainly viral) infections,
by stress or environmental exposure (such as
exposure to certain chemicals or drugs).
Type 2 diabetes - a stronger inheritance pattern.
If first relatives have type 2 diabetes
risk of developing type 2 diabetes is much
higher.

This risk increases with increase in number of


relatives with diabetes.

Diabetic Emergencies

Laboratory Studies Laboratory studies to evaluate glucose regulation


include the following:
Fasting blood glucose level.
In critically ill patients, measuring glucose levels from blood samples drawn from
venous lines, central lines, or arterial lines is preferred over fingerstick glucose
testing.
Fingerstick testing requires adequate tissue perfusion for accuracy and in many
critically ill patients, tissue perfusion is impaired

Blood glucose levels are measured at least 8 hours after the last food intake to
evaluate carbohydrate metabolism.
Two hour postprandial glucose testing is helpful as well, especially in people with
known diabetes mellitus.
Glycosylated hemoglobin (HbA1c or A1C) testing offers information about the
average amount of glucose present in the patients bloodstream for the past 3 to 4
months, by measuring the amount of glucose attached to hemoglobin in the
erythrocytes. (The average lifespan of an erythrocyte is 100 to 120 days.)
Insulin level. This test measures the amount of circulating serum insulin in the
fasting state.
C-peptide level. C-peptide is a byproduct of insulin production. Low values (or no
insulin C-peptide) indicate that the persons pancreas is producing little or no
insulin, as in type 1 diabetes.2
Glucagon level.
Glucagon, a hormone produced in the -cells in the islets of Langerhans, controls
the production, storage, and release of glucose. Normally, insulin opposes the action
of glucagon. A deficiency of glucagon occurs when pancreatic tissue is lost because
of chronic pancreatitis or pancreatic tumors. Increased glucagon levels occur in
diabetes, acute pancreatitis, chronic renal failure, cirrhosis, and in the presence of
catechol- amine secretion (as occurs with infection, high stress levels, or
pheochromocytoma).
Serum ketones.
Elevated serum ketone levels suggest that the body is metabolizing fat for energy
in lieu of dietary carbohydrates, a condition seen in critically ill patients with type 1
diabetes.
Urine ketones. Ketones are not normally found in the urine; when they are, they
are associated with diabetes and other disorders of altered carbohydrate
metabolism.
Acute, life-threatening complications that can occur in patients with diabetes
mellitus include
1. diabetic ketoacidosis (DKA),
2. hyperosmolar hyperglycemic syndrome (HHS),
3. hypoglycemia.
Patients with type 1 diabetes are most likely to experience DKA and patients with
type 2 diabetes HHS.
Diabetic Ketoacidosis
DKA is a critical illness resulting from severe insulin deficiency that leads to the
disordered metabolism of proteins, carbohydrates, and fats.
Clinical manifestations include
1. severe hyperglycemia and hyperosmolality,
2. metabolic acidosis,
3. fluid and electrolyte imbalances.
DKA seldom occurs in patients with type 2 diabetes because these patients still
secrete just enough insulin to avoid ketoacidosis; however, it is possible for patients
with type 2 diabetes to manifest DKA as a result of catabolic stress associated with
severe critical illness.
1. The most common precipitating cause of DKA is infection (especially urinary tract
infection and pneumonia).
2 Other precipitating factors include severe illness (eg, stroke, myocardial infarction,
pancreatitis); alcohol or drug abuse; trauma; or discontinuation of insulin therapy

(eg, due to lack of knowledge or lack of financial resources). DKA is associated with
a 2% to 5% mortality rate.
3 The cause of death is rarely a direct result of the metabolic acidosis or the
hyperglycemia; instead, death is more often related to the underlying illness that
precipitated the metabolic decompensation.
Pathophysiology
Three major physiological disturbances exist in DKA:
(1) hyperosmolality due to hyperglycemia,
(2) metabolic acidosis due to accumulation of ketoacids, and
(3) volume depletion due to osmotic diuresis
Hyperglycemia and Hyperosmolality
The first major consequence of DKA is hyperosmolality due to hyperglycemia. As the
serum glucose increases, the serum osmolality increases incre- mentally. The
hyperglycemia seen in DKA is the result of insulin deficiency and excessive hepatic
(gluconeogenesis) and renal (glycogenolysis) glucose production, as well as reduced
glucose utilization in peripheral tissues. When the blood glucose level exceeds the
normal threshold of about 180 mg/dL, glucose begins to escape into the urine
(glycosuria) because the reabsorption capacity of the tubules is exceeded.
Glycosuria promotes an osmotic diuresis that leads to hypovolemia and a decreased
glomerular filtration rate (GFR), which in turn reduces glucose losses and permits
the blood glucose level to rise even higher. This serum hyper- osmolality and
dehydration accounts for the lethargy, stupor, and ultimately, coma that occurs as
DKA worsens.
Ketoacidosis
The second major consequence of severe insulin deciency is uncontrolled
ketogenesis. Lipase causes the breakdown of triglycerides into glycerol and free
fatty acids; free fatty acids are released as precursors of ketoacids.
In the liver, they are oxidized to form ketones. Insulin normally controls the
ketones, but in cases of insulin deficiency, ketones accumulate, causing
ketoacidosis. The anion gap is frequently measured to deter- mine the presence of
ketones, which are unmeasured anions. The anion gap is determined by subtracting
the total measured anions (chloride plus bicarbonate) from the total measured
cations (sodium plus potassium). The normal value is 12 to 15 mEq/L. A high anion
gap indicates metabolic acidosis and is used as an indirect measure of the ketoacids
present.
As the ketoacids continue to accumulate, the anion gap increases. As the
ketoacidosis is corrected with insulin administration, the anion gap will decrease
until it reaches a normal level. Lactic acidosis, resulting from poor tissue per- fusion
and hypovolemia, also contributes to the metabolic acidosis seen in DKA. The
excess carbon dioxide and ketones are removed by hyperventilation
Kussmauls respirations (deep, rapid breathing) associated with fruity-smelling
breath are characteristic physical findings in DKA that are the result of the bodys
attempt to eliminate ketones and correct the metabolic acidosis.
Volume Depletion
As described earlier, glycosuria promotes an osmotic diuresis. Additionally, high
ketone levels cause osmotic diuresis because ketoacids are excreted in the urine
largely as sodium, potassium, and ammonium salts. This osmotic diuresis can result
in the loss of 5 to 8 L of fluid (15% of total body water in begins with fluid and
insulin, the potassium levels decrease quickly and will need to be replaced. Other
consequences of diminished vascular volume include decreased tissue perfusion,
hypotension, and the development of shock and acute renal failure.
Assessment
Initial assessment includes an immediate bedside determination of glucose level,
followed by laboratory analysis of a blood sample to confirm the diagnosis. A more
complete assessment follows, which includes a detailed history and physical

examination, a search for precipitating causes, and more complete laboratory tests
(eg, blood glucose, blood chemitries, osmolality, anion gap, pH, ABGs, urine
acetone, urine glucose).
Clinical Manifestations of Diabetic Ketoacidosis (DKA)
Polyuria and polydipsia
Hyperventilation (Kussmauls respirations) and fruity breath
Lethargy, stupor, coma
Abdominal cramping, anorexia, nausea and vomiting
Acute weight loss
Hyperglycemia
Glycosuria
Volume depletion
Hyperosmolality
Increased anion gap (greater than 15 mEq/L)
Decreased bicarbonate (less than 10 mEq/L)
Decreased pH (less than 7.45)
Management Treatment goals include the following:
1. Improve circulatory volume and tissue perfusion
2. Correct electrolyte imbalances
3. Decrease serum glucose and serum osmolality levels
4. Correct ketoacidosis
5. Determine precipitating events
Fluid Replacement
The immediate threat to life in a critically ill ketoacidotic patient is volume
depletion. The goal is to reverse the severity of the extracellular volume depletion
and restore renal perfusion as soon as pos- sible. The fi rst liter of 0.9% (normal)
saline may be infused in 1 hour in patients with normal cardiac function. This
replaces only a fraction of the extra- cellular loss in the average patient, which can
range from 6 to 8 L. Volume losses continue throughout the fi rst hours of treatment
until the glycosuria and osmotic diuresis are controlled. Fluid replacement continues at roughly 1 L/h until hemodynamic stability is attained. Hypotonic solutions
(eg, 0.45% normal saline) can be administered at a rate of 150 to 250 mL/h after
the intravascular volume has been restored, or if the serum sodium level is greater
than 155 mg/dL. Other plasma expanders, such as albu- min and plasma
concentrates, may be necessary if low blood pressure and other clinical signs of
vascu- lar collapse do not respond to saline alone.
RED FLAG! Rapid infusion of saline in a patient with DKA can lower serum
osmolality, which lowers the osmotic pressure of the plasma. This allows fluid to
leak out of the vascular space, contributing to the development of pulmonary or
cerebral edema, particularly in older adults. Patients must be observed carefully
during the first 24 to 36 hours for signs of pulmonary or cerebral edema.
Insulin Therapy Insulin is the cornerstone of management of DKA. It decreases the
ketones and manages ketoacidosis, inhibits hepatic gluconeogenesis, restores
cellular

The body perceives the urinary loss of large quantities of sodium and water as a
serious threat to the maintenance of circulation, and a variety of compensatory
mechanisms are called into play to prevent vascular collapse and shock. One such
compensatory mechanism is a shift of body fluids into the vascular space from the
extravascular compartments.
The higher the blood glucose level, the more water is drawn out of the cells and into
the vascular space.
Hyperosmolality provides a temporary mechanism for preventing vascular collapse;
however, vascular volume continues to decrease as DKA progresses. As vascular
volume decreases, glomerular filtration also decreases. The excretion of potassium
by the kidney occurs through the exchange of potassium for sodium. Adequate
sodium must be present at the exchange site in the kidney for the rate of potassium

excretion to keep pace with the need for excretion. When renal perfusion decreases,
sodium levels may not be adequate for this exchange. As a result, despite a totalbody depletion of potassium, the serum potassium level may initially be above
normal, even to dangerously high levels. Once treatment
C O L L A B O R AT I V E C A R E G U I D E for the Patient With Diabetic Ketoacidosis
(DKA)
OUTCOMES INTERVENTIONS
Oxygenation/Ventilation
ABGs are maintained within normal limits.
Provide chest physiotherapy, turning and deep breathing, coughing,
incentive spirometry q4h and PRN.
There is no evidence of acute respiratory failure.
Continuously monitor patients respiratory rate, depth, and pattern.
Observe for Kussmauls respirations, rapid and shallow breathing, and other
signs of respiratory distress.
Monitor ABGs, pulse oximetry and, if intubated, end tidal CO2.
Provide supplemental oxygen.
Prepare for intubation and mechanical ventilation.
The patients lungs are clear.
Auscultate breath sounds q2h and PRN.
There is no evidence of atelectasis or pneumonia.
Take daily chest x-ray.
Provide chest physiotherapy q4h.
Mobilize out of bed as soon as patient is stabilized.
Circulation/Perfusion
Blood pressure and heart rate are within normal limits. If PA catheter is in place,
hemodynamic parameters are within normal limits.
Monitor vital signs q1h and PRN.
Assess for dehydration/hypovolemia: tachycardia, decreased CVP and
PAOP.
Assess for hypervolemia: neck vein distention, pulmonary crackles and
edema, increased CVP and PAOP.
Administer vasopressor agents if hypotension is related to vasodilation.
Patient is free of dysrhythmias.
Monitor ECG continuously.
Evaluate and treat the cause of dysrhythmias (eg, acidosis, hypoxia,
hypokalemia/ hyperkalemia).
Fluids/Electrolytes
There is evidence of rehydration without complications:
balanced intake and output
normal skin turgor
hemodynamic stability
intact sensorium
Infuse normal saline or lactated Ringers, then 0.45% normal saline.
Monitor serum osmolality, urine output, neurological status, and vital signs
closely during rehydration. Observe for complications of DKA (eg, shock, renal
failure, decreased LOC, and seizures).
Assess BUN, creatinine, urine for glucose and ketones.
Serum electrolyte levels and acidbase balance are normal.
Assess and replace electrolytes as indicated.
Closely monitor potassium fluctuations as serum glucose is decreased and
acidosis reversed.
Assess arterial pH and bicarbonate level q24h during rehydration and
insulin administration.
Serum glucose returns to normal range.
Monitor serum glucose q3060min, then q14h after level <300 mg/dL.
Administer IV insulin bolus then continuous low dose infusion.
Infuse D51/2 normal saline or D5W after glucose is <250 mg/dL.
Mobility/Safety
The patient is free of injury related to altered sensorium or seizures.
Place on seizure and fall precautions.
Assess neurological status q1h, then q24h after initial rehydration phase.
The patient maintains muscle tone and joint range of motion.
Provide range-of-motion exercises q4h.
Reposition in bed q2h.
Mobilize to chair when condition stable.

Consult physical therapist.


Skin Integrity
Patient is without evidence of skin breakdown.
Assess risk for skin breakdown using the Braden Scale.
Initially assess skin and circulation q12h for 12 h.
If risk for skin breakdown low, assess skin q8h and each time patient is
repositioned.
Turn q2h.
Consider pressure relief/reduction mattress if at risk for skin breakdown.
Nutrition
Nutritional intake meets calculated metabolic need (eg, basal energy expenditure
equation).
Provide parenteral feeding if patient is NPO.
Provide clear, then full, liquid diet, and assess patient response. Progress
to diabetic diet (ADA).
Consult dietitian or nutritional support service regarding special nutritional
needs.
There is no evidence of metabolic dysfunction.
Monitor albumin, prealbumin, transferrin, cholesterol, triglycerides, glucose,
and protein levels.
Comfort/Pain
Control Patient is as comfortable as possible (as evidenced by stable vital signs or
cooperation with treatments or procedures).
Document pain assessment, using numerical pain rating or similar scale
when possible.
If analgesics are needed, administer cautiously due to risk of respiratory
and neurological complications.
Consider nonpharmacological pain management techniques (eg,
distraction, touch).
The patient experiences relief from nausea, vomiting, and abdominal pain or
tenderness.
Maintain nasogastric tube patency.
Assess bowel sounds q12h.
Administer antiemetic as ordered
.
Provide ice chips and frequent oral hygiene.
Psychosocial Patient demonstrates decreased anxiety.
Provide nonjudgmental atmosphere in which patient can discuss concerns
and fears.
Provide patients who are intubated with a method to communicate.
Provide patients with decreased LOC with sensory input.
Provide for adequate rest and sleep.
Teaching/Discharge Planning
Patient and family understand the tests needed for treatment.
Prepare patient and family for procedures such as EEG, ECG, and multiple
laboratory studies.
Patient and family understand the severity of the illness, ask appropriate questions,
and anticipate potential complications.
Explain the widespread effects of diabetes and the potential for
complications of DKA such as seizures, renal failure, or vascular collapse.
Encourage patient and family to ask questions related to complications,
pathophysiology, monitoring, treatments, and so on.
Patient and family are prepared for home care.
Teach information needed to manage diabetes: diabetic diet, skin care,
glucose monitoring, insulin administration, signs and symptoms of
hypoglycemia and hyperglycemia, and appropriate actions.
Discuss sick-day management and factors that can precipitate DKA.
Initiate contacts with diabetic support groups, social services, and home
health agency..

Comparison of Signs and Symptoms of Diabetic Ketoacidosis (DKA) and


Hyperglycemic Hyperosmolar Syndrome (HHS)

Onset

DKA
Gradual or sudden, usually

HHS
Gradual, usually more than

less than 2 d

Type of diabetes
mellitus
Age of patient
Mortality risk
Drug history

Type 1

Physical signs

Polydipsia, polyuria,
dehydration, Kussmauls
respirations, mental status
changes, fruity breath,
febrile at times, ketoacidosis,
nausea and vomiting
Mean, 600 mg/dL

Glucose level

Ketones
Osmolality
Bicarbonate

Usually younger than 40 y


1%15%
Insulin

Present
(mean) 320 mOsm/L 400
mOsm/L Arterial pH
Markedly low (less than 10
mEq/L)
Greater than 12 mEq/L

5 d Previous history of
diabetes mellitus 85% (15%
have new onset) 60%
Type 2
Usually older than 60 y
20%40%
Steroids, thiazides, oral
agents
Dehydration, obtundation,
hypothermia, toxic
appearance, nonketotic

Mean, 1100 mg/dL Range,


2501200 mg/dL Range,
4004000 mg/dL
Absent
(mean) 7.07 7.26

Normal or greater than 15


mEq/L
Anion gap
Less than 12 mEq/L,
variable
Adapted from American Diabetes Association: Position statement:
Hyperglycemic crisis in patients with diabetes mellitus.

Hyperosmolar Hyperglycemic Syndrome HHS,

characterized by marked hyperglycemia and hyperosmolalitwithout


ketoacidosis, may develop in patients with type 2 diabetes when they
become critically ill
HHS has a higher mortality rate than any other complication of diabetes (20%
to 40%), a result of the high serum osmolality levels and the comorbidities
that often accompany the disorder.
The Older Patient. Frail elderly people are at high risk for developing HHS;
acute illness increases their risk even more.
Pathophysiology
compares HHS and DKA. It is speculated that patients who develop HHS may have
just enough insulin to prevent ketosis but not enough to control the glucose level.
Pathophysiologically, the mechanisms of disease are the same as for DKAa
reduction in circulating insulin or insulin resistance occurs, coupled with
hyperglycemia and the extreme hyperosmolar syndrome. However, because insulin
is still being produced, excessive ketone production does not occur. The acidosis
that patients with HHS may develop is attributed to lactic acidosis from poor tissue
perfusion, rather than ketoacidosis. HHS develops slowly over days to weeks, and
patients often experience polydipsia, polyuria, and progressive decline in level of
consciousness. Marked dehydration occurs with the typical fluid loss associated with
HHS (about 9 L). As dehydration worsens, serum glucose and serum osmolality
increase, and a life-threatening cycle of hyperglycemia, hyperosmolality, osmotic
diuresis, and profound dehydration ensues. Worsening dehydration leads to CNS
dysfunction, manifested as confusion and lethargy.

Factors that can precipitate HHS include


Infection (30% to 60% of patients; urinary tract infections and pneumonia
are most common) Acute illness (eg, stroke, myocardial infarction,
pancreatitis) with stress response
Excessive carbohydrate intake or exposure (eg, through dietary
supplements, total enteral support with tube feedings, peritoneal dialysis)
Medications (corticosteroids, thiazide diuretics, sedatives,
sympathomimetics)

The Older Patient. The possibility of HHS should be considered when an older
patient with diabetes presents with the new onset of an acute, serious infection or
illness (eg, myocardial infarction, pancreatitis, pneumonia).
Assessment Often family members or long-term care personnel report that the
patient has become a bit drowsy, taken in less food and fluid over several days, and
slept more until he or she became difficult to awaken. The clinical manifestations of
HHS are reviewed in Table 27-3, as are the laboratory values, which differ from
those of DKA in terms of glucose and osmolality levels, presence of ketones, and
serum pH.
Management Therapy for HHS is directed at correcting the volume depletion,
controlling hyperglycemia, and identifying the underlying cause of the HHS and
treating it. The amount of volume depletion is usually greater in HHS than in DKA.
Rapid rehydration is more cautiously carried out in an elderly patient with
comorbidities. Isotonic saline is administered initially to correct the fluid imbalance,
and some patients may require as many as 9 to 12 L of fluid overall. The nurse must
be vigilant for signs of fluid overload during rehydration; critically ill patients
(especially those who are elderly and have cardiac or renal disease) may require
hemodynamic monitoring during fluid resuscitation. The nurse also monitors fluid
intake, urine output, blood pressure, central pressures, pulse, breath sounds, n
eurological status, and laboratory test results.
The Older Patient. Older patients who develop HHS are at risk for
intravascular thrombosis and focal seizures because of the hemoconcentration of
the blood and the hyperosmolar state. Use of seizure precautions is necessary at all
times.
Patients receive low doses of insulin along with the fluid replacement. It is
necessary to give low-dose insulin by continuous infusion (0.1 U/kg/h) because
these patients are vulnerable to the sudden loss of circulating blood volume that
occurs with higher doses of insulin and a rapid blood sugar reduction. As the
glucose level returns close to normal (250 to300 mg/dL), the insulin infusion is
decreased and dextrose is added to the IV fluids to prevent a sudden drop in the
blood glucose level. At this point, insulin therapy can be changed to the
subcutaneous route. Investigation of the underlying cause of HHS is warranted, and
treatment, if possible, is necessary. Removal of exogenous sources of glucose (tube
feedings, medications) is appropriate while treating patients in the hyperglycemic
state. Critical care management continues until the patients hyperglycemic state
has stabilized, his or her neurological condition and vital signs return to normal, and
the precipitating cause has resolved.
Hypoglycemia
Insulin-induced hypoglycemia, the most common diabetes-related
emergency, is a well-recognized complication among patients with type 1 diabetes.
Mild hypoglycemia causes unpleasant symptoms and discomfort; however,
severe hypoglycemia can lead to serious complications (eg, seizures, coma)
and death if not reversed. The more profound the hypoglycemia and the longer it
lasts, the greater the chance of transient or even permanent cerebral damage after
blood glucose levels are restored.
Pathophysiology
Because the neurons in the brain cannot store glucose, the brain depends on the
glucose supplied by the circulation for energy.
The term neuroglycopenia refers to hypoglycemia sufficient to cause brain
dysfunction that results in personality changes and intellectual deterioration. The
brain recognizes an energy deficiency when the serum glucose level falls abruptly
to about 45 mg/dL; however, the exact level at which symptoms occur varies widely
from person to person, and it is not uncommon for levels as low as 30 to 35 mg/dL
to occur (eg, during glucose tolerance tests) without causing symptoms in people
with long-term diabetes. As the blood glucose level falls below normal, impairment
of higher cerebral functions (eg, trouble thinking or concentrating) is followed by the
release of epinephrine by the autonomic nervous system, producing symptoms such
as tachycardia and sweating. As hypoglycemia persists and worsens, consciousness
is progressively impaired, leading to stupor, seizure, or coma.
Assessment

Clinical Manifestations of Hypoglycemia


Personality and behavioral changes
Difficulties with motor function (eg, trouble walking, slurred speech)
Cortical changes (eg, aphasia, vertigo, localized weakness, focal seizures)
Autonomic neurological responses (eg, tachycardia, pallor, sweating, anxiety,
tremor, headache)
Impaired consciousness (eg, stupor, seizure, coma)
Blood glucose measurement, before the administration of glucose if possible,
verifies the diagnosis.
A major focus of assessment is determining the precipitating cause of the
hypoglycemic reaction so that measures can be taken to prevent future reactions.
Common Causes of Hypoglycemia
Insulin shock
Insulinoma
Inborn errors of metabolism
Stress
Weight loss
Postgastrectomy status
Alcohol
Glucocorticoid defi ciency
Fasting hypoglycemia
Profound malnutrition
Prolonged exercise
Severe liver disease
Severe sepsis
Drug effects
Ethanol
Salicylates
Quinine
Haloperidol
Insulin
Sulfonylureas
Sulfonamides
Allopurinol
Clofi brate
-Adrenergic blockers
Frequently, the precipitating event is clear (eg, a skipped meal or an unusually
strenuous bout of exercise). Problems with insulin dosage or administration may
also be an issue. The nurse investigates every detail of insulin therapy thoroughly,
especially any recent change in any part of the regimen. Prescription errors,
mismatched syringe and insulin units, use of new injection sites, or an atypical (eg,
early or late) response to insulin therapy may emerge as the cause of the reaction.
Oral hypoglycemic agents can also produce severe and long-lasting hypoglycemia,
especially in patients who are older and undernourished, with impaired renal or
hepatic function. Finally, the administration or withdrawal of other medications must
also be considered as the precipitating event for recurrent insulin reactions.
Management
Treatment of insulin reactions is always glucose.

The amount of glucose needed to reverse an insulin reaction acutely is not


large. In an average-sized adult, less than 15 g (3 tsp) of glucose can raise
the blood glucose level from 20 to 120 mg/dL.

If the patient can swallow, the most convenient form of delivery is a glucoseor sucrose-containing drink because it is absorbed into the intestines.

If the patient is too groggy, stuporous, or uncooperative to drink, the glucose


is administered as an IV bolus (25 g of 50% dextrose given over several
minutes)

If this route or dosage is unavailable, 1 mg of glucagon is given


subcutaneously or intramuscularly. The response to oral glucose takes 5 to 15
minutes, whereas the response to IV glucose should occur within 1 or 2
minutes at most.

Adrenal Crisis
Adrenal crisis (acute adrenal insufficiency) is a life- threatening complication
that can develop in critically ill patients when the additional stress of injury or illness
quickly depletes cortisol stores or causes cortisol resistance, rendering the body
unable to meet metabolic needs. Adrenal crisis can also result from worsening of
primary or secondary adrenal insufficiency or bilateral adrenal hemorrhage.
Assessment
Because adrenal insufficiency affects both glucocorticoids and
mineralocorticoids, many body functions are affected, including glucose
metabolism,fluid and electrolyte balance, cognitive state, and cardiopulmonary
status.
Laboratory values in acute adrenal insufficiency show hyponatremia,
hyperkalemia, decreased serum bicarbonate levels, hypoglycemia, anemia,
leukocytosis, and elevated blood urea nitro- gen (BUN). Metabolic acidosis may
occur because of the dehydration.
Management
The immediate goal= to administer the needed corticosteroid replacement
and restore fluid and electrolyte balance.
The corticosteroid of choice for critically ill patients is hydrocortisone (50 mg
every 6 to 8 hours) because it most resembles endogenous cortisol.
Fluid resuscitation is started with normal saline. The rate of fluid and
electrolyte replacement is dictated by the degree of volume depletion, serum
electrolyte levels, and clinical response to therapy. Associated medical or surgical
problems may indicate the need for invasive blood pressure and hemodynamic
monitoring.