Complications of Diabetes Mellitus, type 1

Complications can be acute or chronic.

Acute complications include the following:

o Hypoglycemia
o Local allergic reactions
o DKA

Chronic complications are further subdivided into macrovascular,

microvascular, and miscellaneous.
o Macrovascular complications

Atherosclerosis

Cerebrovascular disease

Ischemic heart disease

Ischemia of lower limb (ie, gangrene)

o Microvascular complications

Peripheral neuropathy

Peripheral neuropathy with trophic ulceration

Diabetic retinopathy, cataract, glaucoma

Diabetic nephropathy

o Miscellaneous complications

Skin infections

Necrobiosis lipoidica

A more detailed discussion of some of the possible complications is as

follows:

Hypoglycemia
o This may be due to change in insulin dose, a small or missed
meal, or strenuous exercise. Common symptoms are lightheadedness, dizziness, confusion, shakiness, sweating, and
headache.
o Patients should be educated about symptoms of hypoglycemia
and to respond rapidly with sugar intake. These patients
should be advised to carry candy or sugar cubes. Family
members can be taught to administer a subcutaneous
injection of glucagon. In emergency, initial treatment is a
bolus injection of 25 mL of 50% glucose solution followed by a
continuous glucose infusion.
o The dawn phenomenon is the normal tendency of the blood
glucose to rise in the early morning before breakfast. This rise
in glucose, which may be due to the nocturnal spikes in
growth hormone causing insulin resistance, is probably
enhanced by increased hepatic gluconeogenesis secondary to
the diurnal rise in serum cortisol. However, in some patients,
nocturnal hypoglycemia may be followed by a marked
increase in fasting plasma glucose with an increase in plasma
ketones (Somogyi phenomenon). Thus, both the dawn and
Somogyi

phenomena

are

characterized

by

morning

hyperglycemia, but the latter is due to rebound (counterregulation) hyperglycemia. In cases of dawn phenomenon, the
patient should check blood glucose levels at 2-4 am. The dawn

and

Somogyi

phenomena

can

be

ameliorated

by

administering intermediate insulin at bedtime.

Local allergic reactions

o Local allergic reactions can occur at the site of insulin
injections and can cause pain, burning, local erythema,
pruritus,

and

induration.

These

complications

are

less

common with human insulin than observed previously with

animal insulins.
o These reactions usually resolve spontaneously without any
intervention.
o Generalized
immediately

insulin
after

allergy
the

is

injection

rare.
and

Symptoms
include

occur

urticaria,

angioedema, pruritus, bronchospasm, and, rarely, circulatory

shock. It may be treated with antihistamines. Some cases may
require epinephrine and IV steroids.

Diabetic ketoacidosis
o DKA is acute metabolic changes in the body due to lack of
insulin or poor response to insulin due to stress or illness. It is
characterized by hyperglycemia, ketosis, and acidosis, leading
to osmotic diuresis and dehydration.
o The key to treatment of DKA is volume repletion, insulin
therapy, and specific metabolic corrections.

Macrovascular

complications

(ie,

atherosclerosis):

People

with

diabetes experience accelerated atherosclerosis. It affects small

arterioles with the following predominant effects:

o Heart: Coronary atherosclerosis often occurs earlier and is

more severe and extensive than in those without diabetes,
increasing the risk of ischemic heart disease.
o Brain:

Atherosclerosis

of

the

internal

carotid

and

vertebrobasilar arteries and their branches predisposes to

cerebral ischemia.
o Lower extremity: Severe atherosclerosis of the iliofemoral and
smaller arteries of the lower legs predisposes to gangrene.
Ischemia of a single toe or ischemic areas on the heel are
characteristic of diabetic peripheral vascular disease. This is
due to the involvement of much smaller and more peripheral
arteries.
o Kidneys: Atherosclerosis of the main renal arteries and their
intrarenal branches causes chronic nephron ischemia. It is a
significant component of multiple renal lesions in diabetes.
Nephropathy is a significant life-threatening complication and
is due to the adverse effects of glucose-induced preglomerular
vasodilation on glomerular hemodynamics. Glomerulosclerosis
is initiated early in the course of diabetic nephropathy by
exacerbated expression of cytokines like tumor growth factor
beta 1. However, not all people with type 1 DM are at risk of
nephropathy because of some polymorphisms in the various
factors involved in its pathogenesis, which can modulate the
course of this disease from one person to the other. Although
end-stage renal disease (ESRD) is one of the most severe
complications of type 1 DM, the incidence of ESRD has been
very low, 2.2% at 20 years after diagnosis and 7.8% at 30
years after diagnosis.1

Microvascular disease

o This is a significant feature of diabetes and causes multiple

pathological

complications.

Hyaline

arteriosclerosis,

characteristic pattern of wall thickening of small arterioles and

capillaries is wide- spread and is responsible for ischemic
changes in the kidney, retina, brain, and peripheral nerves.
o In

the

kidneys,

nephropathy,

this

which

wall
is

thickening
characterized

leads
by

to

diabetic

proteinuria,

glomerular hyalinization (Kimmelstiel-Wilson), and chronic

renal failure.

In the retina, this condition causes diabetic retinopathy. It is the

leading cause of blindness in the United States in people younger
than 60 years and affects the eyes in the following different ways:
o Background retinopathy: This complication is due to retinal
small

vessel

abnormality

leading

to

hard

exudates,

hemorrhages, and microaneurysms. It does not affect acuity.

o Proliferative retinopathy: This is due to extensive proliferation
of new retinal small blood vessels. A sudden loss of vision can
occur due to vitreous hemorrhage from proliferating new
vessels or retinal detachment.
o Maculopathy: This complication is due to edema and hard
exudate or retinal ischemia. It causes a marked reduction of
acuity.
o Cataract: This is frequent in people with diabetes.
o Glaucoma: This condition relates to the neovascularization of
the iris, rubeosis iridis.

In the brain, the condition causes lacunar infarction and ischemic

white matter degeneration.

In the peripheral nerves, diabetes causes peripheral neuropathy.

Four types of diabetic neuropathies develop, including (1) peripheral
distal symmetrical polyneuropathy, predominantly sensory; (2)
autonomic neuropathy; (3) proximal painful motor neuropathy; and
(4) cranial mononeuropathy (ie, III, IV, VI). Sensory and autonomic
neuropathy

are

due

to

axonal

degeneration

and

segmental

demyelination. Motor neuropathy and cranial mononeuropathy are

due to vascular disease in blood vessels supplying nerves.

Infections: People with diabetes are susceptible to various types of

infections. The most common sites affected are the skin and urinary
tract system. Increased risk

of staphylococcal follicular skin

infections, superficial fungal infections, cellulitis, erysipelas, and oral

or genital candidal infections exists. These patients develop
frequent lower urinary tract infections and are at increased risk of
acute pyelonephritis.

Necrobiosis lipoidica: Local fat atrophy or hypertrophy at injection

sites is not unusual and usually improves by switching to human
insulin and injecting it directly into the affected area. Patients do not
require any specific treatment of local fat hypertrophy, but injection
sites should be rotated.

Charcot joint is a type of arthropathy observed in people with

diabetes. It is a progressive deterioration of foot joints caused by
underlying neuropathy. Tarsometatarsal and midtarsal joints are
affected most commonly. Other neuromuscular foot deformities also
may be present. Early diagnosis and treatment is important to
prevent further joint degeneration.

Controlling blood glucose, Hb A1c, lipids, blood pressure, and weight are
important prognostic factors and predict the development of long-term
macrovascular and microvascular complications. More than 60% of
patients with type 1 DM fare reasonably well over the long term. Many of

the rest develop blindness, end-stage renal disease, and, in some cases,
early death. If a patient with type 1 DM survives the period 10-20 years
after onset of disease without fulminant complications, he or she has a
high probability of reasonably good health. Other factors affecting longterm outcomes are the patients education, awareness, motivation, and
intelligence level.

Education is the most important aspect of diabetes management.

The physician or the health care provider should educate the patient
and, in the case of children, the parents about the disease process,
management, goals, and long-term complications. They should be
made aware of the signs and symptoms of hypoglycemia and ways
to manage it.

A dietitian should provide specific diet control education to the

patient and family.

A nurse should educate the patient about selfinsulin injection and

performing finger sticks for blood glucose level monitoring.