complications of diabetes mellitus dr aidah abu elsoud alkaissi an-najah national university faculty...

Complications of Diabetes Mellitus

Dr Aidah Abu Elsoud Alkaissi

An-Najah National University

Faculty of Nursing

Acute Complications of Diabetes

There are three major acute complications of diabetes related to short-term imbalances in blood glucose levels: Hypoglycemia. Diabetes Ketoacidosis (DKA). HHNS, which is also called hyperglycemic

hyperosmolar nonketotic coma or hyperglycemic hyperosmolar syndrome.

HYPOGLYCEMIA (INSULIN REACTIONS)

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.

It often occurs before meals, especially if meals are

delayed or snacks are omitted.

Clinical Manifestations

The clinical manifestations of hypoglycemia may be grouped into two categories: adrenergic symptoms central nervous system (CNS) symptoms.

In mild hypoglycemia, as the blood glucose level falls, the sympathetic nervous system is stimulated, resulting in a rise of epinephrine an norepinephrine.

This causes symptoms such as sweating, tremor,

tachycardia, palpitation, nervousness, and 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 inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behavior, double vision, and drowsiness.

In severe hypoglycemia, CNS function is so impaired. Symptoms may include disoriented behavior, seizures, difficulty arousing from sleep, or loss of consciousness

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 Life Savers or other hard candies 2 to 3 teaspoons of sugar or honey

INITIATING EMERGENCY MEASURES

For 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).

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.

INITIATING EMERGENCY MEASURES

In the emergency department, patients who are unconscious or cannot swallow may be treated with 25 to 50 mL 50% dextrose in water (D50W) administered intravenously.

Assuring patency of the intravenous (IV) line used for injection of 50% dextrose is essential because hypertonic solutions such as 50% dextrose are very irritating to the vein.

DIABETIC KETOACIDOSIS

DIABETIC KETOACIDOSIS

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: Hyperglycemia Dehydration and electrolyte loss Acidosis

Pathophysiology Without insulin, the amount of glucose entering the cells is reduced

and the liver increases glucose production. 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 and 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 liters of water and up to 400 to 500 mEq each of sodium, potassium, and chloride over a 24-hour period.

Pathophysiology

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.

Ketone bodies are acids; their accumulation in the circulation leads to metabolic acidosis

Pathophysiology

Causes of DKA are decreased or missed dose of insulin, illness or infection, and undiagnosed and untreated diabetes (DKA may be the initial manifestation of diabetes).

Errors in insulin dosage may be made by patients who are ill and who assume that if they are eating less or if they are vomiting, they must decrease their insulin doses.

Pathophysiology

In response to physical (and emotional) stressors, there is an increase in the level of “stress” hormones—glucagon, epinephrine, norepinephrine, cortisol, and growth hormone.

These hormones promote glucose production by the liver and interfere with glucose utilization by muscle and fat tissue, counteracting the effect of insulin.

If insulin levels are not increased during times of illness and infection, hyperglycemia may progress to DKA

Clinical Manifestations Polyuria and polydipsia.

Patients may experience blurred vision, weakness, and headache.

Patients with marked intravascular volume depletion may have orthostatic hypotension

Volume depletion may also lead to hypotension with a weak, rapid pulse.

Clinical Manifestations The ketosis and acidosis of DKA lead to GI symptoms such as

anorexia, nausea, vomiting, and abdominal pain. Patients may have acetone breath (a fruity odor), which occurs with

elevated ketone levels. Hyperventilation (with very deep respirations) may occur.

These Kussmaul respirations represent the body’s attempt to decrease the acidosis, counteracting the effect of the ketone buildup.

Patients may be alert, lethargic, or comatose.

Assessment and Diagnostic Findings Blood glucose levels may vary from 300 to 800 mg/dL

(16.6 to 44.4 mmol/L).

Evidence of ketoacidosis is reflected in low serum

bicarbonate (0 to 15 mEq/L) and low pH (6.8 to 7.3) values.

Assessment and Diagnostic Findings

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

Accumulation of ketone bodies (which precipitates the acidosis) is

reflected in blood and urine ketone measurements.

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

Elevated levels of creatinine, blood urea nitrogen (BUN), hemoglobin, and hematocrit may also be seen with dehydration.

REHYDRATION In dehydrated patients, rehydration is important for

maintaining tissue perfusion. In addition, fluid replacement enhances the excretion of

excessive glucose by the kidneys.

Patients may need up to 6 to 10 liters of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting.

Medical Management

REHYDRATION

Initially, 0.9% sodium chloride solution is administered at a rapid rate, usually 0.5 to 1 L per 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 or those at risk for heart failure.

After the first few hours, half-normal saline solution is the fluid of choice for continued rehydration.

REHYDRATION

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

When the blood glucose level reaches 300 mg/dL

(16.6 mmol/L) or less, the IV fluid may be changed to

dextrose 5% in water (D5W) to prevent a precipitous

decline in the blood glucose level.

REHYDRATION

Initial urine output will fall 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 older patients, those with renal impairment, or those at risk for heart failure.

RESTORING ELECTROLYTES

The major electrolyte of concern during treatment of DKA is potassium.

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.

The serum level of potassium drops during the course of

treatment of DKA as potassium re-enters the cells; therefore, it must be monitored frequently.


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. Up to 40 mEq per hour may be needed for several hours.

Because extracellular potassium levels drop during DKA treatment, potassium must be infused even if the plasma potassium level is normal.

Frequent (every 2 to 4 hours initially electrocardiograms and laboratory measurements of potassium are necessary during the first 8 hours of treatment.

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 per hour). Hourly blood glucose values must be measured.

IV fluid solutions with higher concentrations of glucose, such as normal saline (NS) solution (eg, D5NS or D50.45NS), 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.

REVERSING ACIDOSIS

Various IV mixtures of regular insulin may be used. The nurse must convert hourly rates of insulin infusion (frequently prescribed as “units per hour”) to IV drip rates.

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

REVERSING ACIDOSIS

Blood glucose levels are usually corrected before the acidosis is corrected.

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.

HYPERGLYCEMIC HYPEROSMOLAR

NONKETOTIC SYNDROME

HYPERGLYCEMIC HYPEROSMOLARNONKETOTIC SYNDROME

Hyperglycemia predominate, with alterations of the sensorium (sense of awareness). At the same time, ketosis is minimal or absent.

The basic biochemical defect is lack of effective insulin (ie, insulin

resistance). The patient’s persistent hyperglycemia causes osmotic diuresis, resulting in losses of water and electrolytes.

To maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space.

With glucosuria and dehydration, hypernatremia and increased

osmolarity occur.


This condition occurs most often in older people (ages 50 to 70) with no known history of diabetes or with mild type 2 diabetes.

HHNS can be traced to a precipitating event such as an acute illness (eg, pneumonia or stroke), medications that exacerbate hyperglycemia (thiazides), or treatments, such as dialysis.

The history includes days to weeks of polyuria with adequate fluid intake.


What distinguishes HHNS from DKA is that ketosis and acidosis do not occur in HHNS partly because of differences in insulin levels.

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 may tolerate polyuria and polydipsia until neurologic changes or an underlying illness (or family members or others) prompts them to seek treatment.

Because of possible delays in therapy, hyperglycemia, dehydration,

and hyperosmolarity may be more severe in HHNS.


The clinical picture of HHNS is one of hypotension, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis).

The mortality rate ranges from 10% to 40%, usually related to an underlying illness.


The blood glucose level is usually 600 to 1,200 mg/dL, and the osmolality exceeds 350 mOsm/kg. 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

Medical Management

The overall approach to the treatment of HHNS is: fluid replacement, correction of electrolyte imbalances, and insulin administration.

Because of the older age of the typical patient with HHNS, close monitoring of volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias.

Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient’s sodium level and the severity of volume depletion.

Medical Management

Potassium is added to IV fluids when urinary output is adequate and is guided by continuous electrocardiographic monitoring and frequent laboratory determinations of potassium.

Extremely elevated blood glucose levels drop 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.

Insulin is usually administered at a continuous low rate to treat hyperglycemia, and replacement IV fluids with dextrose are administered when the glucose level is decreased to the range of 250 to 300 mg/dL.

MACROVASCULAR COMPLICATIONS

Diabetic Macrovascular Complications

Diabetic macrovascular complications result from changes in the medium to large blood vessels.

Blood vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls. Eventually, blood flow is blocked.

Coronary artery disease, cerebrovascular disease, and peripheral

vascular disease are the three main types of macrovascular complications that occur more frequently in the diabetic population.

Diabetic macrovascular complications

Myocardial infarction is twice as common in diabetic men and three times as common in diabetic women. Coronary artery disease may account for 50- 60% of all deaths in patients with diabetes.

Patients may not experience the early warning signs of decreased coronary blood flow and may have “silent” myocardial infarctions.

These silent myocardial infarctions may be discovered only as changes on the electrocardiogram. This lack of ischemic symptoms may be secondary to autonomic neuropathy


Cerebral blood vessels are similarly affected by accelerated atherosclerosis.Occlusive changes or the formation of an embolus elsewhere in the vasculature that lodges in a cerebral blood vessel can lead to transient ischemic attacks and strokes.

People with diabetes have twice the risk of developing

cerebrovascular disease, and studies suggest there may be a greater likelihood of death from cerebrovascular disease in patients with diabetes.


Signs and symptoms of peripheral vascular disease include diminished peripheral pulses and intermittent claudication (pain in the buttock, thigh, or calf during walking).

The severe form of arterial occlusive disease in the lower extremities is largely responsible for the increased incidence of gangrene and subsequent amputation in diabetic patients.

Management Diet and exercise are important in managing obesity, hypertension,

and hyperlipidemia. The use of medications to control hypertension and hyperlipidemia

may be indicated.

Smoking cessation is essential. Control of blood glucose levels may reduce triglyceride levels and can

significantly reduce the incidence of complications.

In addition, patients may require increased amounts of insulin or may need to switch from oral antidiabetic agents to insulin during illnesses

MICROVASCULAR COMPLICATIONS

MICROVASCULAR COMPLICATIONSAND DIABETIC RETINOPATHY

The eye pathology referred to as diabetic retinopathy is caused by changes in the small blood vessels in the retina, the area of the eye that receives images and sends information about the images to the brain.

It is richly supplied with blood vessels of all kinds: small arteries and veins, arterioles, venules, and capillaries.

There are three main stages of retinopathy: nonproliferative (background )retinopathy, preproliferative retinopathy, and proliferative retinopathy.


Nearly all patients with type 1 diabetes and more than 60% of patients with type 2 diabetes have some degree of retinopathy after 20 years

Changes in the microvasculature include microaneurysms, intraretinal hemorrhage, hard exudates, and focal capillary closure.

A complication of nonproliferative retinopathy, macular

edema, occurs in approximately 10% of people with type 1 and type 2 diabetes and may lead to visual distortion and loss of central vision.


An advanced form of background retinopathy, preproliferative retinopathy, is considered a precursor to the more serious proliferative retinopathy.

In preproliferative retinopathy, there are more widespread vascular changes and loss of nerve fibers.

10- 50% of patients with preproliferative retinopathy will develop proliferative retinopathy within a short time (possibly as little as 1 year).


Proliferative retinopathy is characterized by the proliferation of new blood vessels growing from the retina into the vitreous.

These new vessels are prone to bleeding. The visual loss associated with proliferative retinopathy is caused by this vitreous hemorrhage and/or retinal detachment.


The vitreous is normally clear, allowing light to be transmitted to the retina. When there is a hemorrhage, the vitreous becomes clouded and cannot transmit light, resulting in loss of vision.

Another consequence of vitreous hemorrhage is that resorption of the blood in the vitreous leads to the formation of fibrous scar tissue. This scar tissue may place traction on the retina, resulting in retinal detachment and subsequent visual loss.


Retinopathy is a painless process.

In nonproliferative and preproliferative

retinopathy, blurry vision secondary to macular

edema occurs in some patients.

Symptoms indicative of hemorrhaging include floaters or cobwebs

(spider like) in the visual field, or sudden visual changes including spotty or hazy vision, or complete loss of vision.


Diagnosis is by direct visualization with an ophthalmoscope or with a technique known as fluorescein angiography.

Dye is injected into an arm vein and is carried to various parts of the body through the blood, but especially through the vessels of the retina of the eye.

This technique allows the ophthalmologist, using special

instruments, to see the retinal vessels in bright detail and gives useful information that cannot be obtained with just an ophthalmoscope.

Medical Management

For advanced cases, the main treatment of diabetic retinopathy is argon laser photocoagulation.

The laser treatment destroys leaking blood vessels and areas

of neovascularization.

For patients at increased risk for hemorrhaging, panretinal photocoagulation may significantly reduce the rate of progression to blindness.

Diabetic Foot Foot ulcers are one of the main complications of DM,

with a 15% lifetime risk for foot ulcers in all diabetic patients.

With damage to the nervous system, a person with diabetes may not be able to feel his or her feet properly.

Normal sweat secretion and oil production that lubricates the skin of the foot is impaired.

Diabetic Foot

These factors together can lead to abnormal pressure on the skin, bones, and joints of the foot during walking and can lead to breakdown of the skin of the foot.

Sores may develop.

Diabetic Foot Damage to blood vessels and

impairment of the immune system from diabetes make it difficult to heal these wounds.

Bacterial infection of the skin, connective tissues, muscles, and bones can then occur.

These infections can develop into gangrene.

Risk factors The development of a foot ulcer has traditionally been

considered to result from a combination of:

peripheral neuropathy (PNP)

peripheral vascular disease (PVD)

infection

Low-level laser therapy for diabetic foot wound healing

Increases the speed, quality and tensile strength of tissue repair, and also resolves inflammation and provides pain relief.

Improves wound epithelialisation and increases cellular content, granulation tissue, collagen deposition and microcirculation.

Stimulates the immune system, and decreases free

radical oxidation processes

Laser therapy

Many studies observed a regeneration of microcirculation in the ulcer and a regeneration of lymphatic circulation.

The laser irradiation method produces a sterilizing effect from bacteria that over-infect the diabetic ulcer.

Attempts have been made to use helium neon, CO2, and KTP lasers in encouraging wound healing in diabetics.

laser therapy Diabetic foot ulcer; beginning of low-level laser therapy

(A), and in the end of treatment period (B).

Topical Hyperbaric Oxygen

Topical hyperbaric oxygen (Limb chambers are occasionally used for wound healing) alone or in combination with a low power laser are valuable adjuvants to conventional therapy for diabetic foot ulcers.

Hyperbaric oxygen therapy enhances wound healing by increasing local delivery of oxygen to ischemic tissues. Studies suggest that hyperbaric oxygen therapy may stimulate angiogenesis

Effectiveness of Bilayered Cellular Matrix (BCM) (OrCel®), in Healing of Neuropathic Diabetic Foot Ulcers

Diabetic neuropathic foot ulcers treated with BCM showed a faster rate of wound healing than those treated with standard care alone (moist saline gauze).

Is made of human dermal cells cultured in bovine collagen sponge. The absorbable matrix is used as a wound dressing.

The collagen framework provide strength to the skin and contains no cells that can cause rejection or irritation.

The Effect of the Scotchcast Boot and the Aircast Device on Foot Pressures of the Contralateral Foot

Offloading the diabetic foot ulcer is a key element to successful wound healing.

The offloading devices do not seem to alter foot pressures on

the contralateral foot, monitoring the contralateral foot is of paramount importance.

Asymmetric gait pattern and/or difficulties with balance are essential factors to keep in mind when describing offloading devices to patients with peripheral neuropathy.

The Scotchcast Boot

massage the injured area, milking away edema and reducing swelling. Because the Aircast Duplex™ aircell it provides consistent, uninterrupted compression without space between compartments where edema can collect

The Use of Negative Pressure Wound Therapy on Diabetic Foot Ulcers

Negative pressure wound therapy (NPWT) was developed to promote healing of open wounds.

Increase of local blood flow, formation of granulation tissue, and decrease of bacterial colonization

The diabetic foot ulcers were surgically debrided prior to initiation of NPWT or moist gauze dressing.

In the treatment of diabetic ulcer wounds, NPWT provided a faster wound resolution compared to saline-moistened gauze.

Combination of Subatmospheric Pressure Dressing and Gravity Feed Antibiotic Instillation in the Treatment of Post-Surgical Diabetic Foot Wounds

A new negative pressure wound therapy (NPWT) device with solution instillation capability (V.A.C.® Instill?, KCI, San Antonio, Tex)

The healing mechanism probably involves providing a moist wound healing environment and exudate management as well as a decrease in bacterial load, an increase in wound temperature, and cellular stimulation

Historical delivery methods for local antibiotic levels directly to the post-surgical field are antibiotic-laced beads, instillation catheters, and closed suction irrigation.

Combining instillation therapy with the existing negative pressure dressings should help assist in decreasing overall wound fluid viscosity, removing infectious materials, and lowering the bioburden to convert an infected or critically colonized wound to a clean or contaminated wound

The dressing for negative pressure wound therapy is attached by tubing that provides subatmospheric or negative pressure that can be applied continuously or intermittently.

complications of diabetes mellitus dr aidah abu elsoud alkaissi an-najah national university faculty...

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