Complications of Diabetes Mellitus

1
Complications of Diabetes Mellitus

• Dr Aidah Abu Elsoud Alkaissi
• An-Najah National University
• Faculty of Nursing

2
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.

3
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.

4
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.

5
Clinical Manifestations

• 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

6
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

7
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.

8
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.

9
DIABETIC KETOACIDOSIS
10
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

11
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.

12
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

13
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.

14
Pathophysiology

• In response to physical (and emotional)
  stressors, there is an increase in the level of
  stress hormonesglucagon, 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

15
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.

16
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 bodys
  attempt to decrease the acidosis, counteracting
  the effect of the ketone buildup.
• Patients may be alert, lethargic, or comatose.

17
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.

18
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.

19
REHYDRATION
Medical Management

• 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.

20
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.

21
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.

22
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.

23
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.

24
RESTORING ELECTROLYTES

• 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.

25
RESTORING ELECTROLYTES

• 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.

26
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.

27
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.

28
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.

29
HYPERGLYCEMIC HYPEROSMOLARNONKETOTIC SYNDROME
30
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 patients
  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.

31
HYPERGLYCEMIC HYPEROSMOLARNONKETOTIC SYNDROME

• 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.

32
HYPERGLYCEMIC HYPEROSMOLARNONKETOTIC SYNDROME

• 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.

33
Clinical Manifestations

• 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.

34
Assessment and Diagnostic Findings

• 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

35
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 patients sodium level and the
  severity of volume depletion.

36
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.

37
MACROVASCULAR COMPLICATIONS
38
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.

39
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

40
Diabetic Macrovascular Complications

• 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.

41
Diabetic Macrovascular Complications

• 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.

42
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

43
MICROVASCULAR COMPLICATIONS
44
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.

45
MICROVASCULAR COMPLICATIONSAND DIABETIC
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.

46
MICROVASCULAR COMPLICATIONSAND DIABETIC
RETINOPATHY

• 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).

47
MICROVASCULAR COMPLICATIONSAND DIABETIC
RETINOPATHY

• 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.

48
MICROVASCULAR COMPLICATIONSAND DIABETIC
RETINOPATHY

• 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.

49
Clinical Manifestations

• 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.

50
Assessment and Diagnostic Findings

• 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.

51
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.

52
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.

53
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.

54
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.

55
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

56
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

57
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.

58
laser therapy

• Diabetic foot ulcer beginning of low-level laser
  therapy (A), and in the end of treatment period
  (B).

59
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

60
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.

61
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.

62
The Scotchcast Boot
63
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
64
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.

65
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

66
The dressing for negative pressure wound therapy
is attached by tubing that provides
subatmospheric or negative pressure that can be
applied continuously or intermittently.