DM Last

Assessment and Management of
Patients With Diabetes Mellitus
Dr. Yazeed Gougazeh
Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Diabetes Mellitus
 Is a group of metabolic diseases characterized by hyperglycemia
related to:
 Absent or insufficient insulin production
 Impaired insulin utilization
 Or both
• Almost 1/3 of cases are undiagnosed, Prevalence is
increasing.

Pathophysiology:
Insulin produced by  cells of Islets of Langerhans
Released continuously into bloodstream in small
increments with larger amounts released after food intake.
When a person eats a meal; insulin secretion increases &
moves glucose from blood into muscle, liver & fat cells.

Insulin controls level of glucose in blood by regulating
production & storage of glucose.
In DM:
 Cells stop responding to insulin or
 Pancreas stop producing insulin
 Leading to hyperglycemia

Classifications of Diabetes
• Type 1 diabetes
• Type 2 diabetes
• Gestational diabetes: 24-28 weeks of pregnancy.
• DM associated with other conditions or syndromes
(e.g. HTN, Obesity, CAD, Renal)

Type 1 Diabetes
• “juvenile onset” or “insulin-dependent” diabetes
• Insulin producing beta cells in the pancreas are destroyed by an autoimmune
process
• Requires insulin, as little or no insulin is produced
• Onset is acute and usually before 30 years of age
• Etiology includes combined genetic, immunologic, and possibly
environmental (e.g., viral) factors are thought to contribute to beta-cell
destruction.
• Need exogenous insulin to preserve life
• Acute complication of hyperglycemia: DKA.

Type 2 Diabetes
• Decreased sensitivity to insulin (insulin resistance) &
impaired ß cell function results in decreased insulin
production.
• More common in persons over age 30 and in obese.
• Slow, progressive glucose intolerance
• Treated initially with drugs, diet & exercise
• Rx: Oral hypoglycemic agents & insulin may be used

Etiology and pathophysiology
- Type 2 DM is ch.ch. by a combination of inadequate

insulin secretion & insulin resistance.
-Pancreas usually makes some endogenous (self-made)
insulin. However, the body either does not make enough
insulin, does not use it effectively, or both.
-The presence of endogenous insulin is a major distinction
between type 1 and type 2 DM. In type 1 DM, there is an
absence of endogenous insulin.

Risk Factors
• Type 1:
Genetic predisposition combined with immunologic and
possibly environmental (viral) factors.
• Type 2:
Family history, obesity, race/ethnicity, age >45 years,
previous identified impaired fasting glucose or impaired
glucose tolerance, hypertension ≥ 140/90, HDL ≤ 35
and/or triglycerides ≥ 250, history of gestational diabetes
or babies over 9 pounds.

Clinical Manifestations
• “Three Ps”
– Polyuria
– Polydipsia
– Polyphagia
• Fatigue, weakness, vision changes, tingling or numbness
in hands or feet, dry skin, skin lesions or wounds that are
slow to heal, recurrent infections
• Type 1 may have sudden weight loss, nausea, vomiting,
& abdominal pain if DKA has developed.

Treatment goal is to normalize blood
glucose levels
• “ABCs of DM Management”:
(1) A1C, (2) B.P, & (3) Cholesterol.
• Intensive control dramatically decreases vascular
& neuropathic complications, through:
 Control blood glucose levels.
 Prevent acute complications.

 Prevent or delay long-term complications.
 develop self-care management skills.

5 components of diabetes management:
Diet / Nutritional therapy

Exercise
self-monitoring of blood glucose
Drug therapy
Health Education (patient and family)

Dietary Management Goals
• Provide optimal nutrition; all essential food constituents

• Meet energy needs
• Achieve & maintain a reasonable weight
• Prevent wide fluctuations of blood glucose levels
• Decrease serum lipids, if elevated

Role of the Nurse
• Be knowledgeable about dietary management

• Communicate important information to the dietician or
other management specialists
• Reinforce patient understanding
• Support dietary and lifestyle changes

Meal Planning
• Consider food preferences, lifestyle, usual eating times,
and cultural/ethnic background
• Review diet history & need for weight loss, gain, or
maintenance
• Caloric requirements & calorie distribution throughout the
day:
 Carbohydrates: 50–60% emphasize whole grains
 Fat: 20–30%
 Protein : 10% to 20%
 Fiber 14g/1000 kcal

Glycemic Index
• Describes how much a food increases blood glucose

• Combine starchy food with protein and fat containing
food slows absorption, and glycemic response
• Raw or whole foods tend to have lower response than
cooked, chopped, or pureed foods
• Eat whole fruits rather than juices; due to fiber-slowing
absorption.
• Adding food with sugars may produce lower response if
eaten with foods that are more slowly absorbed

Exercise
• Lowers blood sugar
• Helps in weight loss
• Lowers cardiovascular risk.
• Alter blood lipid concentrations, increasing levels of HDL &
decreasing total cholesterol & triglycerides.
• Improves insulin sensitivity & decrease need for insulin by
increasing insulin receptor sites
• Should be effective, not vigorous, enjoyable, preferable,
after meals
• Check blood glucose before & after.
• Planned or spontaneous.
Exercise Precautions
• Avoid exercise with elevated blood sugar levels (above

250 mg/dL) & ketones in urine = Insulin normally
decreases with exercise.
• Patients on exogenous insulin should eat a 15g
carbohydrate snack before moderate exercise to prevent
hypoglycemia.
• If exercising to control or reduce weight, insulin must be
adjusted.
• Potential post-exercise hypoglycemia
• Need to monitor blood glucose levels

Exercise Recommendations
• Encourage regular daily exercise

• Gradual, slow increase in exercise period is encouraged
• Modify exercise regimen to patient needs and presence of
diabetic complications or potential cardiovascular
problems.
• Exercise stress test for patients older than age 30 who
have 2 or more risk factors is recommended
• Gerontology considerations.

Insulin Therapy
Blood glucose monitoring:

KEY POINT
Insulin Storage:
not more than 30 degree, up to
4 weeks.
- Avoid direct sunlight
Inhaled is a rapid, 20 min

before meal, given in
combination with long
for type 1 DM.
Subcutaneous Injection Sites

Normal Pancreatic Insulin Release

Insulin Preparations
48
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Insulin Pump
Delivers a continuous SC insulin infusion through a small device worn on the belt,
in a pocket, or under clothing. It use rapid-acting insulin.

• The infusion set changed every 2 – 3 days, in a new site
to enhance the absorption.
• A major advantage: the potential for keeping glucose
levels in a tighter range with the goal of eliminating both
high and low glucose.
• It offer users more flexibility with meals and activities.
• Disadvantages:
- Risk for infection.
- Inconvenient
- Unexpected disruption of flow.
- Risk for DKA
Problems of insulin therapy
• Allergy (local or systematic)
• Lipo-dystrophy (changes in subcutaneous fatty tissue).
• Somogyi effect (hyperglycemia in morning)
• Dawn phenomenon (hyperglycemia on awakening).
• Hypoglycemia

Teaching Patients Insulin Self-
Management
Teach patient about:

•Use & action of insulin
• Symptoms & Required actions of hypoglycemia & hyperglycemia
•Blood glucose monitoring
•Self-injection of insulin
•Insulin pump use

Oral Anti-diabetic Agents
• Used for patients with type 2 diabetes who cannot be treated with
diet and exercise alone.
 Stimulate beta cells of pancreas to secrete insulin
 Improve binding between insulin & insulin receptors
 Increase number of insulin receptors
 Inhibit production of glucose by liver.
 Increase body tissues' sensitivity to insulin
 Delay absorption of complex carbohydrates.

• Combinations of oral drugs may be used
• Major side effect: Hypoglycemia
• Nursing interventions:
Monitor: glucose level, hypoglycemia and other potential side
effects, Patient teaching.

Acute DM complications
Diabetic Ketoacidosis (DKA)
 Cause: absence or markedly inadequate amount of

insulin
 Result in disorders in metabolism of carbohydrate,
protein, & fat.
 Most likely occurs in type 1
 Main clinical features of DKA
 Hyperglycemia
 Dehydration and electrolyte loss (polyurea)
 Ketosis
 Acidosis

Pathophysiology
Effects of hyperglycemia.
 Kidneys excrete glucose along with water and
electrolytes (e.g. sodium, potassium).
 Polyuria leads to dehydration and electrolyte loss.

 Breakdown of fat
 Free fatty acids converted into ketone bodies by liver.
 Excessive production of ketone bodies

 Precipitating factors for DKA
 Illness
 Infection
 Inadequate insulin dosage
 Undiagnosed type 1
 Poor self-management
 Errors in insulin dosage
 missed dose of insulin
 Neglect

Clinical Manifestations
 Polyuria
 Polydipsia
 Blurred vision, weakness, headache
 Hypotension
 Weak & rapid pulse.
 GI symptoms: anorexia, nausea, vomiting,
abdominal pain.
 Acetone breath
 Hyperventilation with very deep respirations:
body's attempt to decrease acidosis
 Mental status changes (alert, lethargic, or
comatose)
Assessment of DKA
• Blood glucose levels vary from 300–800 mg/dL

• Severity of DKA is not related to blood glucose level
• Ketoacidosis is reflected in low serum HCO3 and low pH;
low PCO2 reflects respiratory compensation
• Ketone bodies in blood & urine.
• Electrolytes vary according to water loss and level of
hydration.

Prevention
• “Sick day rules”:

• Testing glucose level, report high readings, take drugs,
take fluids, report N+V
• Assess for underlying causes
• Diagnosis and proper management of diabetes

Treatment of DKA
• Rehydration with IV fluid
• IV continuous infusion of regular insulin
• Reverse acidosis and restore electrolyte balance
• Note: rehydration leads to increased plasma
volume and decreased K+, insulin enhances the
movement of K+ from extracellular fluid into the
cells.
• Monitor
– Blood glucose & renal function/UO
– EKG and electrolyte levels—Potassium
– VS, lung assessments, signs of fluid overload
Hypoglycemia
• Abnormally low blood glucose level (below 50–60 mg/dL)
• Causes: too much insulin or oral hypoglycemic agents, too
little food, and excessive physical activity
• Manifestations:
– Adrenergic symptoms: sweating, tremors, tachycardia,
palpitations, nervousness, hunger
– CNS Symptoms: inability to concentrate, headache,
confusion, memory lapses, slurred speech, numbness of
lips & tongue, irrational or combative behavior, double
vision, drowsiness
– Severe hypoglycemia may cause disorientation, seizures,
and loss of consciousness, brain death.

Assessment
• Onset is abrupt and may be unexpected

• Symptoms vary from person to person
• Symptoms also vary related to the rapidly of decrease in
blood glucose and usual blood glucose range.

Management of Hypoglycemia
• Rx must be immediate
• Give 15 g of fast-acting, concentrated carbohydrate
– 3 or 4 glucose tablets
– 4–6 ounces of juice or regular soda
– 6–10 hard candies
– 2–3 teaspoons of honey
• Retest blood glucose in 15 minutes, retreat if <70 mg/dL
or if symptoms persist more than 10–15 minutes and
testing is not possible.
• Provide a snack with protein and carbohydrate unless the
patient plans to eat a meal within 30–60 minutes.
Emergency Measures
• If the patient cannot swallow or is unconscious:

– SQ or I.M Glucagon 1 mg
– 25–50 mL 50% dextrose solution IV

Hyperglycemic Hyperosmolar Non-ketotic
Syndrome (HHNS)
• Is a life-threatening complication of uncontrolled DM.

• Ch.ch by severe hyperglycemia, a marked increase in serum
osmolality, and clinical evidence of dehydration without
significant accumulation of ketoacids.
• Hyper osmolality & hyperglycemia occur due to lack of
effective insulin.
• Less common than DKA, occur in type 2 with age over 65y.
• Hyperglycemia causes osmotic diuresis with loss of water and
electrolytes; hypernatremia & increased osmolality.

• Manifestations:
hypotension, profound dehydration, poor skin turgor, tachycardia,
& variable neurologic signs due to cerebral dehydration
(seizures).
• Insulin level too low but enough to prevent breakdown of fats &
proteins = Ketosis is minimal or absent.
• Precipitating factors:
Treatment (dialysis), medications, acute illness.
• Patient may have a history of low fluid intake, high depression,
impaired cognition, polyuria.

Assessment & Diagnostic Findings
Blood glucose level: 600 to 1200 mg/dL,
 Osmolality exceeds 320 mOsm/kg.
 Electrolyte and BUN levels consistent with
clinical picture of severe dehydration.
 Absent/minimal ketone bodies
 Mental status changes.

Treatment of HHNS
• Rehydration
• Insulin administration
• Correct fluid volume & electrolyte status
• Prevention:
– Blood Sugar Monitoring
– Diagnosis & management of diabetes
– Assess & promote self-care management skills

Long-Term Complications of Diabetes
• Macro-vascular complications:
– Accelerated atherosclerotic changes
– CAD, cerebrovascular disease, & peripheral vascular
disease
• Micro-vascular complications:
– Diabetic retinopathy, nephropathy, dermopathy.
• Neuropathic changes:
– Peripheral neuropathy, autonomic neuropathies,
hypoglycemic unawareness, sexual dysfunction
Diabetic Retinopathy
• Refers to the micro-vascular damage to the retina because of
chronic hyperglycemia.
• Non-proliferative Retinopathy: most common, partial occlusion
of the small blood vessels in retina, causes micro-aneurysms in
the capillary walls. This causes capillary leak out causing retinal
edema, leading to mild to severe vision loss.
• Proliferative Retinopathy: When retinal capillaries become
occluded, the body compensates by forming new easily bleeding
blood vessels to supply the retina with blood.
• The patient sees black or red spots or lines
• Rx: laser therapy

Nephropathy
• Damage to the small blood vessels that supply the
glomeruli of the kidney leading to ESRD.
• Risk factors:
HTN, genetic predisposition, smoking, & chronic
hyperglycemia.

Neuropathy
Is nerve damage that occurs from the

metabolic imbalances associated with DM,
lead to the loss of sensation in the lower
Extremities.
Loss of sensation, abnormal sensations,

pain, and paresthesia.
Most commonly affects distal portions of
nerves (lower extremities).
It affects both sides of body symmetrically
Foot injury and ulcerations
Can cause atrophy of small muscles of
hands/feet.
Amputations.

• Infection:
• A person with DM is more susceptible to infections because of
a defect in the mobilization of WBCs & impaired phagocytosis
by neutrophils and monocytes.
• Loss of sensation (neuropathy) may delay the detection

of an infection.
• PSYCHOLOGIC CONSIDERATIONS
- Anxiety, stress, depression associated with diminished self-
care, Eating habit disorders.
• Skin complications:
- Dermopathy & skin lesions.

Nursing Process:
The Care of the Patient with DM:
Assessment
• Assess the primary presenting problem

• Assess needs related to diabetes
• Patient knowledge of diabetes & diabetes care skills
• Blood glucose levels
• Skin assessment
• Preventative health measures

Clinical Problems
• Altered blood glucose level
• Deficient knowledge
• Risk for injury
• Impaired endocrine function
• Neurologic problem

Planning
1. Engage in self-care behaviors to actively manage DM,
2. have few or no hyperglycemia or hypoglycemia emergencies,
3. maintain safe and healthy glucose levels,
4. reduce the risk for chronic complications,
5. adjust lifestyle to accommodate the DM plan with minimal
stress.

Implementation
• Health promotion
• Acute care
• Ambulatory care
• Drug therapy
• Personal hygiene

Teaching Patients Self-Care
• Assess knowledge and adherence to plan of care.
• Provide basic information about diabetes, its cause and
symptoms, and acute and chronic complications and their
treatment.
• Teach self-care activities to prevent long-term complications
including foot care, eye care, and risk-factor management.
• Include family in plan of care.
• Provide information, encourage health promotion activities,
and recommended health screenings.

DM Last

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DM Last

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Assessment and Management of

Patients With Diabetes Mellitus

Dr. Yazeed Gougazeh

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

- Type 2 DM is ch.ch. by a combination of inadequate

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Prevent acute complications.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Diet / Nutritional therapy

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Provide optimal nutrition; all essential food constituents

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Be knowledgeable about dietary management

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Describes how much a food increases blood glucose

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Avoid exercise with elevated blood sugar levels (above

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Encourage regular daily exercise

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Blood glucose monitoring:

Inhaled is a rapid, 20 min

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Teach patient about:

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Cause: absence or markedly inadequate amount of

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Polyuria leads to dehydration and electrolyte loss.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Inadequate insulin dosage

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Blood glucose levels vary from 300–800 mg/dL

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• “Sick day rules”:

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Onset is abrupt and may be unexpected

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• If the patient cannot swallow or is unconscious:

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• Is a life-threatening complication of uncontrolled DM.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Is nerve damage that occurs from the

Loss of sensation, abnormal sensations,