General Clinical Practice

Diabetes Mellitus Review

Meg Blair

D
iabetes mellitus is a
group of physiological
dysfunctions charac-
terized by hypergly-
© 2016 Society of Urologic Nurses and Associates
Blair, M. (2016). Diabetes mellitus review. Urologic Nursing, 36(1), 27-36.
doi:10.7257/1053-816X.2016.36.1.27

Diabetes mellitus is a group of physiological dysfunctions characterized by hyper-

cemia resulting directly from
glycemia resulting directly from insulin resistance, inadequate insulin secretion,
insulin resistance, inadequate
or excessive glucagon secretion. Type 1 diabetes (T1D) is an autoimmune disor-
insulin secretion, or excessive
der leading to the destruction of pancreatic beta-cells. Type 2 diabetes (T2D),
which is much more common, is primarily a problem of progressively impaired
glucagon secretion (Ignatavicius

glucose regulation due to a combination of dysfunctional pancreatic beta cells

& Workman, 2016; Lewis,

and insulin resistance. The purpose of this article is to review the basic science
Dirksen, Heitkemper, & Butcher,

of type 2 diabetes and its complications, and to discuss the most recent treatment
2014). There are two main types

of diabetes. Type 1 diabetes
(T1D) is an autoimmune disorder
leading to the destruction of pan-
Key Words: Diabetes mellitus, insulin, hyperglycemia, glucose regulation.
creatic beta-cells. Type 2 diabetes
(T2D), which is much more com-
mon, is primarily a problem of
progressively impaired glucose
regulation due to a combination
of dysfunctional pancreatic beta
cells and insulin resistance
(Ignatavicius & Workman, 2016;
Lewis et al., 2014). T2D is specif-
ically defined by the American
Diabetes Association (ADA)
(2014a) as “a condition character-
ized by hyperglycemia resulting
from the body’s inability to use
blood glucose for energy…either
the pancreas does not make
enough insulin or the body is
unable to use insulin correctly.”
Currently, there are approximate-
ly 26 million people in the
United States (U.S.) diagnosed
with diabetes and another 79
million people with prediabetes,
resulting in nearly one-third of
the population being affected by
the disease (Ignatavicius &
Workman, 2016; Lewis et al.,
2014). The purpose of this article
is to review the basic science of
type 2 diabetes and its complica-
tions, and to discuss the most
recent treatment guidelines.
Meg Blair, PhD, MSN, RN, CEN, is a
Professor, NE Methodist College, Omaha,
NE.
guidelines.
Pathophysiology, Etiology,
And Manifestations
T2D generally develops in
people with known risk factors
and genetic predisposition, and
may be related to environmental
causes, such as viruses (Ignata-
vicius & Workman, 2016; Lewis et
al., 2014; McCance, Huether,
Brashers, & Rote, 2014; Seggelke &
Everhart, 2012). The major risk
factor for T2D is obesity, with
abdominal obesity conferring the
highest risk. Obesity is often asso-
ciated with the consumption of
high fat/carbohydrate diets and
lack of physical activity. Obesity
can also lead to insulin resistance.
Other predisposing risk factors
include low levels of HDL (“good
cholesterol”), sedentary lifestyle,
and polycystic ovary disease.
There is also some data in the lit-
erature suggesting that people
with depression have higher rates
of diabetes and should be
screened. A worrisome develop-
ment is the increase in T2D in
children, most likely related to
obesity. Age, ethnicity, and hered-
ity are non-modifiable risk factors
(Ignatavicius & Workman, 2016;
Lewis et al., 2014; McCance et al.,
2014; Seggelke & Everhart, 2012).
While the person with T2D
may have the classic signs relat-
ed to hyperglycemia more often
seen in T1D (polyuria, polydip-
sia, and polyphagia), signs and
symptoms of T2D are often more
vague and may include fatigue,
possible weight gain, frequent
infections, sores that heal slowly,
and frequent vaginal yeast infec-
tions in women. Visual changes
and alterations in sensation rep-
resent later signs and symptoms
that occasionally drive people to
seek health care (Ignatavicius &
Workman, 2016; Lewis et al.,
2014; McCance et al., 2014;
Seggelke & Everhart, 2012).
Diagnostic Studies
Diagnostic studies for T2D
usually include measures of both
short-term and long-term glucose
levels. Short-term measurements
include a fasting blood glucose or
a two-hour blood glucose drawn
during an oral glucose tolerance
test (OGGT). A random blood glu-
cose can be useful in a patient
with the classic symptoms of

UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1 27

 Table 1.
Tests to Determine Diabetes Mellitus
Test Results Patient Preparation
Fasting blood Normal: 70 to 110 mg/dL* Patient must fast for 8 hours
glucose Impaired glucose tolerance: 110 to 125 Critical values: < 50 mg/dL or > 450 mg/dL
mg/dL Several factors may cause elevated glucose: stress, illness
Diagnostic: >126 mg/dL or infection, some medications, caffeine, myocardial
Critical values: < 50, > 450 mg/dL infarction.
Adults over 50 may have some age-related increase.
2-hour < 50, < 140 mg/dL Not usually used as a primary diagnostic measure but can
postprandial > 50, < 150 mg/dL be used to determine need for other testing.
Known diabetic target: < 140 mg/dL Several factors may cause elevated glucose: stress, illness
> 200 mg/dL may be considered or infection, some medications, caffeine, myocardial
diagnostic infarction.
Adults over 50 may have some age-related increase.

Oral glucose Diagnostic: Two-hour blood glucose Patient must fast for 12 hours prior to the test, but must eat
tolerance test level > 200 mg/dL after receiving adequate meals for three days before testing.
75 g of carbohydrate Smoking or exercising during the test will elevate results.
Several factors may cause elevated glucose: stress, illness
or infection, some medications, caffeine, myocardial
infarction.
Adults over 50 may have some age-related increase.

Random blood Diagnostic: > 200 mg/dL None; check patient for symptoms of hyperglycemia if
glucose test greater than 200 mg/dL.
Also called “casual” blood glucose test.
Several factors may cause elevated glucose: stress, illness
or infection, some medications, caffeine, myocardial
infarction.
Adults over 50 may have some age-related increase.

A1C Normal: < 5.7% None.

Prediabetes: 5.7% to 6.4%
Diagnostic: > 6.5%
Correlates with mean plasma glucose (MPG) through a
mathematical formula (MPG = [35.6xMPG] – 77.3).
Inaccurate after blood transfusions or in conditions where
RBC turnover is abnormally high (hemolytic anemia),
splenectomy (causes longer RBC lifespan).
Several factors may cause elevated glucose: stress, illness
or infection, some medications, caffeine, myocardial
infarction.
Adults over 50 may have some age-related increase.

*Some sources state 70 to 100 mg/dL (NIH) or less than 100 (ADA).
*Before diagnosing a patient with diabetes, the abnormal test should be repeated or a different test should be completed.

Sources: American Diabetes Association, 2013, 2014b; Ignatavicius & Workman, 2016; Lewis, Dirksen, Heitkemper, &
Butcher, 2014; Pagana & Pagana, 2014.

hyperglycemia. Long-term glucose
measurement is combined with
the hemoglobin A1C. (see Table 1).
A diagnostic value obtained via
fasting blood glucose, OGGT, or
random blood glucose must be
confirmed by a second test, prefer-
ably with the same test (ADA,
2013 2014b; Ignatavicius &
Workman, 2016; Lewis et al.,
2014; Pagana & Pagana, 2014).
The hemoglobin A1C meas-
ures the amount of glycosylated
hemoglobin as a percent of the
patient’s total hemoglobin over a
period of two to three months, so
it is particularly valuable for
determining long-term control of
disease in individuals with dia-
betes (Ignatavicius & Workman,
2016; Lewis et al., 2014; Pagana &
Pagana, 2014). The hemoglobin
A1C is a tiny part of normal
hemoglobin. As red blood cells
circulate through the body, some
of the glucose that is also present
in the bloodstream attaches to
the A1C portion. The more glu-
cose that is present, the more
often this happens. Because the
average lifespan of a red blood
cell is 90 to 120 days, the meas-
ured A1C reflects the amount of
glucose in the blood over the last
approximately 120 days (ADA,
2014b; Pagana & Pagana, 2014).
Readings are expressed as a
percentage. The higher the per-
cent, the higher the glucose level
over time. A hemoglobin A1C of
5% means that 5% of the hemo-
globin is saturated with glucose.
For the person without diabetes,
a normal reading is 4% to 5.9%.
Good diabetic control is indicat-

28 UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1

ed when readings are less than
7%. Fair control is considered to
be 8% to 9%, and poor control is
anything over 9%. There is a dis-
crepancy between recommended
readings by the ADA (good con-
trol: A1C less than 7%) and the
American College of Endocrin-
ologists (good control less than
6.5%). The reading is not affect-
ed by fasting and can be taken at
any time (ADA, 2013; Pagana &
Pagana, 2014).
For those with known dia-
betes, other screening and diag-
nostic testing should be per-
formed. These include annual fun-
doscopic eye examination, annual
urine screen for creatinine (indica-
tive for microalbuminuria and
possible kidney involvement), vi-
sual examination of the feet at
every visit to a health care pro-
vider, annual comprehensive foot
examination (including microfila-
ment testing for sensation), and at
least annual assessments for car-
diovascular risks. Routine moni-
toring can prevent complications
related to diabetes or at least catch
them in time for early treatment
(Ignatavicius & Workman, 2016;
Lewis et al., 2014).
Complications
Diabetes complications can
be separated into two categories:
microvascular and macrovscular
(World Health Organization,
2013). Microvascular complica-
tions are due to damage of small
blood vessels. Macrovascular
complications are due to damage
to larger blood vessels. Micro-
vascular complications involve
damage to the kidneys (nephro-
pathy), leading to renal failure;
eyes (retinopathy), leading to
blindness; and the nerves (neu-
ropathy), causing impotence and
diabetic foot disorders that can
result in infections and amputa-
tions. Macrovascular complica-
tions include cardiovascular dis-
eases, such as strokes, heart
attacks, and blood flow insuffi-
ciency to the legs. According to
the literature, lower limb ampu-
tations are approximately 10
times greater in people with dia-
betes than in individuals without
UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1
diabetes in developed countries
(Ignatavicius & Workman, 2016;
Lewis et al., 2014).
There are more macrovascular
complications among individuals
with diabetes that present at an
earlier age (ADA, 2014a, c, 2015a;
Ignatavicius & Workman, 2016;
Lewis et al., 2014). Controlling
blood pressure (target less than
130/80 mmHg) is vital to prevent
or slow the onset of these condi-
tions. The ADA recently revised
its diastolic blood pressure stan-
dard to less than or equal to 90
mmHg. Managing lipid abnormal-
ities is also vital to preventing
and/or managing complications.
The ADA targets are total choles-
terol less than 200 mg/dL, low-
density lipoproteins (LDL) less
than 100 mg/dL, triglycerides less
than 150 mg/dL, and high-density
lipoproteins (HDL) cholesterol
greater than 40 mg/dL in men and
50 mg/dL in women (ADA, 2014a,
c, 2015a; Ignatavicius & Workman,
2016; Lewis et al., 2014).
Microvascular complications
are unique and common to dia-
betics (micro = small; seen in the
smaller population of diabetics
as compared with the larger gen-
eral [non-diabetic] population).
They result from exposure to
high glucose that causes thicken-
ing of blood vessels. The end-tar-
get organs are affected by these
complications, which include
diabetic retinopathy, neuropathy,
and nephropathy. Dermopathies
also exist, but typically cause
only mild discomfort and cos-
metic dysfunction, and are not
discussed here (Ignatavicius &
Workman, 2016; Lewis et al.,
2014).
Visual Complications
Diabetes is the leading cause
of blindness in adults (Ignata-
vicius, & Workman, 2016; Lewis et
al., 2014; Shotliff & Balasanthiran,
2009). The types of retinopathy
include nonproliferative (most
common) and proliferative. Non-
proliferative retinopathy occurs
when small blood vessels be-
come partly occluded, leading to
microaneurysms and leaking of
capillary fluid. Vision is affected
if the macula is involved. Pro-
liferative retinopathy occurs
when retinal capillaries become
occluded and the body forms
new capillaries in response.
These new vessels are abnormal
and fragile, which leads to hem-
orrhage. The new vessels can
pull the retina out of place, lead-
ing to tears. Blindness results if
the macula is involved. Indi-
viduals with diabetes tend to
develop glaucoma and cataracts
more frequently and at an earlier
age than the general population
(Ignatavicius, & Workman, 2016;
Lewis et al., 2014; Shotliff &
Balasanthiran, 2009). Dilated eye
examinations are recommended
annually to detect these condi-
tions. Prevention is best obtained
through tight control of blood
glucose and blood pressure.
Current treatments include pho-
tocoagulation and vitrectomy
(Ignatavicius & Workman, 2016;
Lewis et al., 2014; Shotliff &
Balasanthiran, 2009). In photoco-
agulation, lasers seal the leaking
blood vessels in the eye with heat
(“Laser Photocoagulation for
Diabetic Retinopathy,” 2015).
Vitrectomy removes the vitreous
gel from the eye (“Diabetic
Retinopathy – Surgery,” 2014).
Diabetic Neuropathy
Diabetic neuropathy affects
nearly two-thirds of all individu-
als with diabetes, and is probably
the result of chronic high blood
glucose that damages the nerves
and blood vessels. Other risk fac-
tors include increasing age, obe-
sity, and having concurrent peri-
pheral vascular disease (Benbow,
2012; Sharp & Clark, 2011; Turns,
2011; Woo, Santos, & Gamba,
2013; Ziegler & Fonesca, 2015).
Peripheral neuropathy involves
altered sensations and ischemia,
which usually occurs in the bilat-
eral extremities starting first in
the lower extremities and gradu-
ally moving upward. Individuals
with diabetes can have a total
lack of sensation, paresthesias,
numbness, and loss of tempera-
ture sensation. This leads to com-
plications, such as ulcers, ampu-
tations, atrophy of muscles, and
loss of fine movements. The most
common presentation is the “dia-
29
betic foot,” where an infected
ulcer started with an injury the
patient was unaware of due to
loss of sensation (Benbow, 2012;
Turns, 2011; Sharp & Clark, 2011;
Woo et al., 2013; Ziegler &
Fonesca, 2015).
Prevention is the best meth-
od of management; tight gly-
cemic control and daily foot
inspections are crucial. Un-
fortunately, this works best in
patients with T1D. The paresthe-
sias can be managed with med-
ications, such as topical creams,
tricyclic antidepressants, anti-
seizure medications, selective
serotonin reuptake inhibitors, or
selective norepinephrine reup-
take inhibitors (Benbow, 2012;
Turns, 2011; Sharp & Clark, 2011;
Woo et al., 2013; Ziegler &
Fonesca, 2015). The FDA has
only approved two drugs for the
treatment of diabetic neuropathy:
pregabalin ([Lyrica®], an anticon-
vulsant; and duloxetine [Cym-
balta®], a serotonin-norepineph-
rine reuptake inhibitor) (Ziegler
& Fonesca, 2015).
Although peripheral neu-
ropathy is best known, autonom-
ic neuropathy also affects many
individuals with diabetes. This
group of disorders includes dia-
betic gastroparesis, urinary reten-
tion, sexual dysfunction in men
and women, bowel incontinence
and/or diarrhea, postural hypo-
tension, tachycardia at rest, angi-
na-free myocardial infarction,
and hypoglycemic unawareness
(Ignatavicius, & Workman, 2016;
Lewis et al., 2014.
Diabetic Nephropathy
Diabetic nephropathy is due
to damage to small vessels in the
glomeruli of the kidneys and
affects up to 40% of individuals
with diabetes (Thomas & Kodack,
2011). Diabetic nephropathy is
commonly defined by abnormally
high albumin levels in urine in a
patient without known renal dis-
ease. The earliest indicator is
microalbuminuria, defined as
albumin excretion of less than 30
mg/day or a urinary albumin/cre-
atinine ratio of greater than 3.0
mg/mmol (Bennett & Aditya,
2015). It is the leading cause of
30
end stage renal disease and is
more common among individuals
with diabetes who smoke, and
who have uncontrolled hyperten-
sion and chronically high blood
glucose (Bakris & Weir, 2002;
Bennett & Aditya, 2015; Thomas,
& Kodack, 2011; Williams,
Manias, Walker, & Gorelik, 2012).
Despite the use of therapy to pro-
tect the kidneys of individuals
with diabetes, end stage renal dis-
ease is increasing in the diabetic
population at the rate of about 9%
a year (Joint Committee on Dia-
betic Nephropathy, 2015; Kazawa
& Moriyama, 2013; Krolewski,
2015).
The treatment of choice for
diabetic nephropathy is either an
angiotensin-converting enzyme
inhibitor (ACEI) such as lisinopril
[Zestril®] or an angiotensin recep-
tor blocker (ARB) such as losartan
[Cozaar®]. These drugs have a
dual effect of controlling hyper-
tension and slowing the progres-
sion of kidney damage and dys-
function. For patients with nor-
mal blood pressure and normal
kidney function, this form of
treatment may not be necessary.
Patients who spill albumin in
their urine should be treated with
one of the described drugs.
Providers should monitor these
patients’ creatinine, potassium,
and urine albumin excretion rou-
tinely. These laboratory values
help assess the patient’s therapeu-
tic response and monitor disease
progression. However, relying on
creatinine alone may lead to renal
impairment being missed. If the
glomerular filtration rate (GFR)
meets the criteria for chronic kid-
ney disease (< 60 mL/min/1.73 m2
for three months or more), the
patient should be referred to a
specialist for further management.
Albumin concentration is a strong
independent predictor of renal
prognosis, but the severity of the
albumin concentration does not
always correlate closely with
renal function. Renal impairment
also increases the risk of hypo-
glycemia in the patient with dia-
betes. This is often multifactorial
in etiology but is often the result
of impaired gluconeogenesis seen
in kidney disease (Andresdottir et
UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1
al., 2014; Bakris & Weir, 2002;
Bennett & Aditya, 2015; Thomas
& Kodack, 2011; Williams et al.,
2012).
A recent Cochrane review of
26 studies showed that the use of
an ACEI decreased the number of
diabetics who went on to develop
chronic kidney disease (CKD)
compared to other types of antihy-
pertensive medications (Jicheng
et al., 2013). The ACEIs signifi-
cantly reduced the risk of new
onset for both micro- and macro-
albuminuria. ARBs did not show
the same benefit; however, a sub-
group analysis showed benefits in
using ARBs in high-risk patients.
There were only two published
studies regarding the combination
of ACEI and ARB (Jicheng et al,
2013). Of these two studies, only
one demonstrated a benefit of
using combined drugs. The cur-
rent recommendation remains
that ACEIs are the drug of choice
to prevent CKD in patients with
diabetes (Fried et al., 2015;
Jicheng et al., 2013).
ACE inhibitors and ARBs
inhibit the renin-angiotensin sys-
tem, which leads to lowered
blood pressure. This, in turn,
reduces both cardiovascular and
renal risk, both of which are sig-
nificant contributors to morbidi-
ty in the diabetic population, par-
ticularly in the older adult sub-
set. However, research has
shown that ACEIs and ARBs are
vastly under-utilized in this pop-
ulation due mainly to concerns
of providers about potential side
effects. The ADA (2014a) recom-
mends them as first-line treat-
ment for patients with hyperten-
sion with or without albuminuria
or other signs of renal insuffi-
ciency, no matter what age.
Diuretics can also be considered
in conjunction with this therapy.
Appropriate labs (serum creati-
nine, potassium) should be mon-
itored when using these drugs
(Bennett & Aditya, 2015; Fried et
al., 2015; Pagana & Pagana, 2015;
Pappoe, & Winkelmayer, 2010).
Krolewski (2015) has pro-
posed a “new paradigm” for dia-
betic nephropathy that does not
use albuminuria as the marker of
impaired renal function. After 25
years of research, Krolewski pro-
poses monitoring the decline of
GFR as a more accurate indicator
of renal involvement in diabet-
ics. Specifically in this model,
the loss of greater than 3.5
mL/min/year of GFR indicates
progressive renal decline. The
decline in GFR precedes the
onset of albuminuria, and un-
checked, this process can lead to
end stage kidney disease. Al-
though the exact mechanism of
this process is unclear, Krolewski
claims that by using this model,
one can separate patients into
groups with rapid, moderate, or
minimal rates of progression
which can lead to better targeted
therapies (Krolewski, 2015).
Lower urinary tract compli-
cations can also occur in patients
with diabetes. Dysfunction can
occur at the level of the bladder
and the sphincter leading to prob-
lems of both storage and empty-
ing. Bladder contractility is espe-
cially affected in patients with
diabetes, often leading to hypo-
contractility, which worsens the
longer the disease lasts. Urinary
incontinence is a frequent finding
that may not be related to age.
Urinary retention, nocturia, weak
urine stream, urinary tract infec-
tions (UTIs), and frequency are
other complications. Erectile dys-
function (ED) can also occur.
These seem to be related to in-
creased responsiveness to para-
sympathetic input and decreased
responsiveness to adrenergic
input (autonomic neuropathy)
(Kempler et al., 2011; Lee et al.,
2015; Lemack, 2007; Pop-Busui et
al., 2015; Vinik, Maser, Mitchell,
& Freeman, 2003; Yilmaz et al,,
2014).
Bladder dysfunction occurs
in 25% of patients with T2D.
There is a high correlation
between bladder disturbances
and peripheral neuropathy. Pa-
tients often complain of symp-
toms, such as frequency and
urgency, often leading to inconti-
nence, nocturia, and the sensa-
tion of incomplete bladder emp-
tying. Men may complain of
symptoms confused with benign
prostatic hyperplasia (BPH):
weak urinary stream, dribbling,
UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1
and interrupted urinary stream.
The pathophysiology of this dys-
function appears to be a combi-
nation of alteration in detrusor
smooth muscle, dysfunction of
neurons, and urothelial dysfunc-
tion, all related to chronically
high blood glucose (Kempler et
al., 2011; Pop-Busui et al., 2015;
Yilmaz et al., 2014).
Providers should screen pa-
tients complaining of these symp-
toms with a validated tool assess-
ing incontinence and lower uri-
nary tract symptoms (LUTS). A
urinalysis with culture should be
obtained to rule out UTI because
patients with diabetes are so
prone to infection and because
UTI can lead to these symptoms.
Urodynamic testing may be valu-
able for bladder dysfunction
assessment. Post-void residual
should be assessed. For patients
who have severe bladder dys-
function, intermittent cathe-
terization is the treatment of
choice. Bladder training, includ-
ing timed voiding and double-
voiding, is used for incontinence.
(Kempler et al., 2011; Nazarko,
2015; Pop-Busui et al., 2015).
Many medications used to treat
bladder dysfunction (cholinergic
and anti-cholinergic drugs) are
inappropriate for older adults.
Sacral neuromodulation, a surgi-
cal procedure, has good success
with patients with diabetes
(66.7%); however, infected de-
vices had to be removed in
37.5% of diabetic recipients, lim-
iting their practical usefulness
(Nazarko, 2015).
ED is estimated to affect up
to 90% of men with diabetes.
Although many providers and
patients are embarrassed to
broach this topic, it is important
to recognize and assess for it. ED
is a well-established risk factor
and independent predictor of
serious cardiovascular events
and coronary artery disease in
men with diabetes. The patho-
physiology relates mainly to
decreased ability of the smooth
muscle of the corpus cavernosum
to relax and to impaired nitric
oxide function. Neuropathy may
also be implicated leading to
decreased sensation in the glans
penis, further compounding the
ED. Providers should use validat-
ed tools to assess for the presence
and impact of ED (Kempler et al.,
2011; Moussa, Hill, Claydon, &
Klufio, 2015; Pop-Busui et al.,
2015). Women can also suffer
from diabetes-induced impair-
ment of sexual function, such as
decreased desire, diminished
lubrication, and decreased ability
to achieve an orgasm (Yilmaz et
al., 2014).
Management of ED includes
sexual counseling (including the
patient’s partner), good glycemic
control, and medications, such as
sildenafil (Viagra®), vardenafil
(Levitra®), and tadalafil (Cialis®).
Other treatments can include
intracavernous injections, intrau-
rethral alprostadil (Caverject®),
constriction devices, or prosthetic
implants (Kempler et al., 2011). A
challenge in treating these pa-
tients is the relationship to coro-
nary artery disease. Many of these
men are on nitrate preparations,
which preclude the use of phos-
phodiesterase inhibitors, such as
sildenafil. Patients should be
encouraged to discuss this matter
with their cardiologists; a “nitrate
holiday” may make limited use of
these types of drugs possible
(Ignatavicius & Workman, 2016;
Lewis et al., 2014).
Perioperative Complications
Individuals with diabetes
present special challenges dur-
ing the perioperative period. The
hospital stay of the post-opera-
tive patient with diabetes is
longer, with the patient experi-
encing more complications, in-
cluding a 50% higher risk of
mortality than patients without
diabetes. Specific complications
include wound infection (2 to 3
times higher), poor wound heal-
ing, hyperglycemia (including
diabetic ketoacidosis), hypo-
glycemia, joint infection, and
thrombotic events. Complica-
tions from other co-morbid con-
ditions are also a possible prob-
lem (Dhinsa, Khan, & Puri, 2010;
Levasque, 2013; Munoz, Lowry,
& Smith, 2012; Sharp, & Clark,
2011; Wallace, 2012).
31
 Good glycemic control is
vital in the perioperative patient
with diabetes, although there is
disagreement on specific proto-
cols. Tight control may decrease
the incidence of wound infec-
tion. In fact, for elective surgery,
reducing the A1C to 7% or less is
ideal because patients in this
range have an overall lower rate
of wound infection. Control is
complicated by the body’s re-
sponse to surgery; stress increas-
es the release of catabolic hor-
mones and pro-inflammatory
mediators, while at the same
time decreases the release of
insulin. This tends to lead to
hyperglycemia. Overly aggres-
sive glucose control, combined
with hypoglycemic unawareness
(common in older patients) can
lead to hypoglycemia. Patients
are best managed with a specific
and detailed protocol using
insulin during the operative and
immediate post-operative period
while the patient is still not eat-
ing. Typically, oral medications
can be started once the patient is
eating well. See the discussion
on medications below for more
detail (Dhinsa et al., 2010;
Levasque, 2013; Munoz et al.,
2012; Wallace, 2012).
Medications
Medications to treat T2D
include insulins and several dif-
ferent classes of oral medica-
tions. Insulin replaces the pa-
tient’s own endogenous insulin
and is required in patients with
T1D. Patients with T2D may
need exogenous insulin to man-
age blood glucose levels during
periods of acute stress (i.e., sur-
gery or serious illness) or may
use insulin to supplement their
oral medications for tighter con-
trol (Ignatavicius & Workman,
2016; Lewis et al., 2014).
Insulins
Insulins come in rapid-act-
ing, short-acting, intermediate-
acting, long-acting, and combina-
tion formulas (see Table 2).
Regimes can include taking in-
jections once, twice, or three
times a day, or can involve a
32
basal-bolus routine in which the
patient takes a long-acting in-
sulin once a day and supple-
ments with rapid acting insulin
at mealtimes. This allows greater
flexibility in working with food
intake (Cleary, 2013; Vallerand, &
Sanoski, 2013).
Oral and Non-Insulin
Injectable Medications
Several classifications of oral
medications are available, with
new drugs being developed at a
rapid pace. Patients may be on
mono- or dual therapy. When
desired results are not achieved
on single drug therapy, it is more
beneficial to add a medication
from a different class instead of
switching drugs altogether (ADA,
2015c). Hospitalized patients,
unless very stable, should have
oral medications discontinued
and their blood glucose values
managed with insulin. See Table
3 for a discussion of oral and non-
insulin injectable medications
(ADA, 2015b; D’Arrigo, 2015;
Ignatavicious & Workman, 2016;
Vallerand & Sanoski, 2013).
Medication Use in the
Hospitalized Patient
With Diabetes Mellitus
The hospitalized patient (un-
less quite stable) should be taken
off oral medications and switched
to insulin. Most hospital policy
calls for fasting and preprandial
testing with sliding scale insulin
based on the patient’s blood glu-
cose readings. However, this does
not take into account the upcom-
ing meal with its carbohydrate
load. The 2009 consensus state-
ment from the ADA and the
American Association of Clinical
Endocrinologists discourages the
use of this standard protocol.
There is no scientific evidence to
support this approach, and its use
can be dangerous to patients.
Rather, the consensus statement
recommends scheduled subcuta-
neous insulin (for non-critical
patients) using “basal, nutritional,
and correctional components”
(Kubacker, 2014, p. 33). The cor-
rectional component factors in the
patient’s sensitivity to insulin and
is calculated using available for-
UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1
mulas (DeYoung, Bauer, Brady, &
Eley, 2011). Poor glycemic control
in the hospitalized patient can
lead to several adverse outcomes,
including increased morbidity
and mortality, length of stay, num-
ber of admissions, and cost
(Crawford, 2013; DeYoung et al.,
2011; Kubacka, 2014; Seggelke &
Everhart, 2012).
Other Care Measures
It is important that diabetics
have an in-depth knowledge of
certain self-care measures. They
need to have a good understand-
ing about appropriate nutrition,
physical activity, sick day man-
agement, and self-monitoring of
blood glucose (SMBG). It is the
role of the health care provider to
provide this education. To effi-
ciently accomplish this, health
care providers must remain cur-
rent in these topics.
Nutrition
Nutrition is a cornerstone of
care for all patients with dia-
betes. Nutritional modifications
can be challenging for many
patients, and the ADA recom-
mends a registered dietician with
knowledge and expertise in dia-
betes as part of the care team. A
healthy diet for a diabetic can
incorporate the same foods typi-
cally eaten by non-diabetics. The
dietary goal is to eat in a way that
promotes tight glycemic control
and helps limit complications
(i.e., cardiovascular). For the
majority of individuals with dia-
betes, this includes eating 45
grams of carbohydrates at each of
three meals and 15 grams of car-
bohydrates each of two to three
daily snacks. As part of the total
carbohydrate intake, 25 to 30
grams should be fiber. Protein
should be 20% to 30% of total
intake, with the rest being com-
posed of healthy fats. Alcohol is
allowed but should be used in
moderation and with food to
avoid hypoglycemia accompa-
nied by unawareness because the
effects of alcohol blunt the body’s
response to hypoglycemia (Ignat-
avicious & Workman, 2016;
Lewis et al., 2014).
 Table 2.
Insulin Types

Type of Insulin Examples Pharmacodynamics Nursing Considerations

Rapid acting Lispro (Humalog®) Onset: 10 to 30 minutes Community-dwelling patients should be instructed
Aspart (NovoLog®) Peak: 30 minutes to 3 hours to eat within 5 minutes of taking insulin;
Duration: 3 to 5 hours hospitalized patients should not be given this
insulin until the food tray has arrived.
Short acting Regular (Humulin®, Onset: 30 minutes to 1 hour Ensure patient has food within 30 minutes.
Novolin®) Peak: 2 to 4 hours
Duration: 5 to 8 hours
Intermediate NPH (Novolin® N) Onset: 1 to 3 hours Appears cloudy.
acting Peak: 6 to 8 hours Do not confuse with NovoLog.
Duration: 12 to 18 hours
Long acting Glargine (Lantus®) Onset: 1 to 4 hours Patient may use additional bolus injections with
Detemir (Levemir®) Peak: None meals.
Duration: 24 to 26 hours Caution: “Sound alike drug” – Lovenox®.
Combination NPH/Regular 70% NPH, 30% regular; All types appear cloudy.
Insulins 70/30 (Humulin® need to know onset/peak/ Do not confuse Humulin with Humalog.
70/30) duration for both
Assess patient for hypoglycemia at both peak
Lispro® protamine/ 50/50 mix of rapid and times.
Lispro® 50/50 intermediate acting
(Humalog® Mix
50/50)
Inhaled insulin Insulin human Onset: 15 to 30 minutes Taken at the beginning of a meal.
(Afrezza®) Peak: 12 to 15 minutes Patients still require long-term insulin or oral
Duration: 3 hours medications for long-term control.
Not recommended for patients with lung disease.
• Insulin doses may need to be decreased with renal impairment.
• Insulin is a “high alert” drug and has been implicated in patient harm and death.
• Insulin doses should be checked by a second nurse.
• Use of corticosteroids may increase insulin needs.
• Pre-filled pens are available for many types of insulins and may be easier for patient to use.
• Carefully check type of insulin before use.
• Administration is most consistent when insulin is injected into the abdomen.
• Teach patients to rotate injection sites within one body area (i.e., throughout the abdomen) and not area-to-area (i.e.,
not abdomen to arm to leg).

Sources: Hazard & Sanoski, 2013; Ignatavicius & Workman, 2016; Ledet, Graves, Bostanian, & Mandal, 2015; Lewis, Dirksen,
Heitkemper, & Butcher, 2014; Meetoo & Allen, 2010; Vallerand & Sanoski, 2013.

Physical Activity
The ADA (2014a) recom-
mends that individuals with dia-
betes get at least 150 minutes of
exercise a week, which is an aver-
age of 30 minutes five days a
week. Exercise has many benefits,
both for glycemic control and
reducing risk factors and co-mor-
bidities, such as cardiovascular
disease. The decrease in insulin
resistance seen with exercise can
last up to 48 hours. The ADA also
recommends that diabetics not be
sedentary for more than 90 min-
utes at a time (ADA, 2014a;
Ignatavicious & Workman, 2016;
Lewis et al., 2014).
Blood Glucose Monitoring
Blood glucose is considered a
fifth vital sign for patients with dia-
betes. However, timing of testing is
somewhat controversial. There are
multiple potential times during the
day to test: fasting, before each of
three meals, after each of three
meals, before and/or after exercis-
ing, and at bedtime (Ignatavicious,
& Workman, 2016; Lewis et al.,
2014; Schrott, 2004). Patients with
type 2 diabetes tend towards fast-
ing and 2-hour postprandial test-
ing, which evaluates the effect of a
carbohydrate load on blood glu-
cose (Ignatavicious, & Workman,
2016; Lewis et al., 2014; Schrott,
2004). This allows the patient with
diabetes to make decisions regard-
ing meal composition and the tim-
ing of exercise toward fasting and
2-hour postprandial testing, which
evaluates the effect of a carbohy-
drate load based on their individ-
ual responses. Even with normal
fasting levels and “controlled”
A1C readings, a large percentage of
patients with diabetes will have
higher than desired postprandial
levels less than or equal to 140
mg/dL (Ignatavicious & Workman,
2016; Lewis et al., 2014; Schrott,
2004). Over the years, some studies
have demonstrated better glycemic
control in specific patient popula-

UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1 33

 Table 3.
Oral and Non-Insulin Injectable Medications
Dose Adjustment
Mechanism Nursing in Renal
Classification Examples of Action Considerations Impairment
Oral Medications
Biguinides Metformin Decreases glucose First line therapy unless Yes; lower dose in
(Glucophage®) production by the liver. contraindicated. renal impairment;
Makes muscle tissue Usually does not cause contraindicated in
more sensitive to hypoglycemia (can be used for renal failure.
insulin. other conditions such as polycystic
ovary disease).
Withhold for contrast dye studies
and for at least 48 hours afterward.
Sulfonylureas Chlorpropamide Simulate beta cells to Be careful with look-alike, sound- Most can be used
(Diabenase®) release more insulin. alike drugs. with caution if patient
Glipizide May cause blood dyscrasias; has mild renal
(Glucotrol®) monitor complete blood count impairment and no
Lyburide routinely. liver disease.
(Micronase®)
Meglitinides Repaglinide Stimulate beta cells to Contraindicated in lactating Decreased dose only
(Prandin®) release more insulin. women. needed for severe
Nateglinide renal impairment.
(Starlix®)
Thiazolidinediones Rosiglitazone Reduces production of Monitor liver function closely. No adjustment
(Avadia®) glucose by liver. May increase risk of heart failure. needed for renal
Pioglitazone Improves insulin action impairment.
(ACTOS®) in muscle and fat.
DPP-4 inhibitors Sitagliptin Prevents breakdown of Stiagliptin may cause pancreatitis Most in this category
(Januvia®) a compound that or Stevens-Johnson syndrome. need dose adjustment
Saxagliptin reduces blood sugar; for renal impairment;
(Onglyza®) this compound is linagliptin (Tradjenta®)
normally broken down does not.
rapidly.
SGLT-2 inhibitors Canagliflozin Causes excess glucose May cause urinary tract infection Reduce dose in
(Invokana®) to be excreted in the and genital yeast infections. mild to moderate
Dapagliflozin urine. impairment; avoid in
(Farxiga®) severe impairment.
Alpha-glucosidase Acarbose Blocks the breakdown May cause gas. Avoid in moderate
inhibitors (Precose®) of starches in the Monitor liver function. to severe renal
Miglitol (Glyset®) intestine and may slow impairment.
the breakdown of other
sugars.
Injectable Non-Insulin Medications
Incretin mimetic Albiglutide Encourages insulin Possible link to thyroid cancer. Contraindicated in
agents (Tanzeum®) release from pancreas, May cause pancreatitis. severe renal
Exenatide limits glucagon impairment.
(Byetta®) production, slows Dulaglutide is injected weekly.
Liraglutide digestion. Taken with other oral medications
(Victoza®) or insulin.
Dulaglutide
(Trulicity®)

Amlyn analogue Pramlintide Slows digestion which Taken with insulin or oral agent. None.
(Symlin®) slows release of
glucose into
bloodstream.
Decreases appetite.

Sources: Bennett & Aditya, 2015; Hazard & Sanoski, 2013; Ignatavicius & Workman, 2016; Lewis, Dirksen, Heitkemper, &
Butcher, 2014; Meetoo & Allen, 2010; Vallerand & Sanoski, 2013.

34 UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1

tions who test after meals versus
before (de Vegiana et al., 1995;
Muhamad, Kadir, & Mohamed,
2012). However, a testing plan
should ideally be developed in
conjunction with the patient’s
goals and willingness to partici-
pate in active care. Postprandial
testing appears to be more highly
correlated to reducing cardiovas-
cular risk, which is an added ben-
efit (Schrott, 2004) and is better
correlated to tighter long-term
control. Patients with T1D often
test fasting and before meals; how-
ever, this is also controversial,
especially in hospitalized patients
(Ignatavicious & Workman, 2016;
Lewis et al., 2014).
Sick Day Management
Sick day management should
be planned in advance. The
patient and provider should dis-
cuss and agree on a plan for
when the patient is ill and not
eating. The patient should be
advised to check blood sugars
more frequently, have food and
beverage on hand that can be tol-
erated and that provide some car-
bohydrates, and continue at least
a partial dose of his or her med-
ication. Diabetic ketoacidosis is
often caused by individuals with
diabetes who discontinue their
medications not realizing that
their blood glucose continues to
rise even though they may not be
eating. Patients with diabetes
should also know when to seek
health care (Ignatavicious &
Workman, 2016; Lewis et al.,
2014).
Conclusion
Diabetes mellitus is a grow-
ing health care problem with
ramifications affecting individu-
als’ health, the health care sys-
tem, and the economy of the
United States and the world
(Ignatavicious & Workman, 2016;
Lewis et al., 2014). Nurses in
every setting will encounter
patients/clients with diabetes. It
is the role of all nurses to be
properly educated about diabetes
and the most current recom-
mended treatments. It is also
important to involve patients in
UROLOGIC NURSING / January-February 2016 / Volume 36 Number 1
the active management of their
condition. These important roles
could have a great impact on the
prevention and management of
this disease that has such high
morbidity and mortality rates.
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