Transcript 2016 NUR 1021 Nursing Care of Patients with Diabetes Mellitus

Nursing Care of Patients
with Diabetes Mellitus
NUR 1021
Spring 2016
MTC
Diabetes Glossary
▪ Glucose: CHO as we take it in and use it for energy
▪ Glycogen: the storage form of glucose.
▪ Stored in liver and muscle.
▪ Storage is facilitated by insulin and cortisol.
▪ Glucagon: produced by alpha cells of pancreas.
▪ Increases BS levels by stimulating liver to convert glycogen
to glucose.
Glossary (continued)
▪ Glycogenesis: the process of
changing glucose into glycogen
for storage
▪ Insulin: TRANSPORTER!
REGULATOR! Produced by beta
cells of pancreas. Moves glucose
across the cell membrane.
Glossary(continued)
▪ Glycogenolysis: conversion of glycogen back into
glucose
▪ Gluconeogenesis: changing amino acids and fatty
acids into glucose
Diabetes Mellitus
▪ Diabetes is a group of chronic disorders resulting
in hyperglycemia.
▪ Type 1 DM
▪ Characterized by a total deficit of circulating
insulin
▪ Type 2 DM
▪ Characterized by insulin resistance
▪ One of the major roles of the nurse is that of
educator
Incidence and Prevalence
▪ 1.9 million new cases each year in U.S.
▪ Seventh leading cause of death due to widespread cardiovascular
effects
▪ Complications - common among diabetics with poor glycemic
control
▪ Acute myocardial infarction
▪ Stroke
▪ Renal failure
▪ Blindness
▪ Traumatic amputations
Demographics- Very Significant!
▪ Estimated - more than 25.8 million people in the United States have
diabetes
▪ Almost one third of these cases are undiagnosed
▪ In 2010, the number of people older than 20 years who were
newly diagnosed with diabetes increased by about 1.9 million
▪ Minority populations are disproportionately affected by diabetes.
▪ African Americans and members of other racial and ethnic groups
(Native Americans and persons of Hispanic origin)
▪ More likely to develop diabetes
▪ At greater risk for many of the complications
▪ Have higher death rates due to diabetes
What are the risk factors?
▪ Family history of diabetes
▪ Obesity
▪ Race, ethnicity
▪ Age >45 years
▪ Previously impaired fasting glucose
▪ Hypertension
▪ HDL cholesterol levels >35 or triglyceride level >250
▪ Gestational diabetes or birth of baby >9 #
Overview of Endocrine Pancreatic
Hormones and Glucose Homeostasis
▪ Hormones
▪ Glucagon
▪ Produced by alpha cells
▪ Glycogenolysis
▪ Gluconeogenesis
▪ Insulin
▪ Secreted by beta cells
▪ Somatostatin
▪ Produced by delta cells
Overview of Endocrine Pancreatic
Hormones and Glucose Homeostasis
▪ Blood glucose homeostasis
▪ Increased blood glucose
levels, amino acids, and fatty
acids
▪ Stimulate pancreatic beta
cells to produce insulin
▪ If blood glucose falls
▪ Glucagon released
▪ Raise hepatic glucose output
& raise glucose levels
Regulation (homeostasis) of blood glucose levels by
insulin and glucagon
High blood glucose is lowered by insulin release.
Regulation (homeostasis) of blood glucose levels by
insulin and glucagon
Low blood glucose is raised by glucagon release.
Pathophysiology of DM
▪ Four major types of DM
▪ Type 1 DM
▪ 5% to 10% of diagnosed cases
▪ Type 2 DM
▪ 90% to 95% of diagnosed cases
▪ Gestational DM
▪ 2% to 5% of all pregnancies
▪ Other specific types of DM
Pathophysiology of DM- What goes Wrong?
• Under normal conditions, when the body’s stores of
glycogen decrease, gluconeogenesis occurs
– Takes 8-12 hours without food to do this
• Diabetes: when there is no insulin to regulate the normal
processes, the end stages “go wild”
– Glycogen changes to glucose in large amounts because
there is no insulin to regulate it.
Another part of the pathophysiology
▪ Cells have receptor sites for insulin.
▪ These receptors bind with glucose
▪ This allows it to be transported across the cell membrane
(it’s a relatively large molecule that can’t get in alone)
▪ In Type II DM, cells are resistant to insulin
Review of Insulin Functions
▪ Transports glucose across cell membrane
▪ Promotes conversion of glucose to glycogen
▪ Regulates conversion of glycogen back into glucose
▪ Promotes storage of fats and proteins
▪ Inhibits the converting of fats and proteins into glucose.
The “See-Saw” Effect of glucagon and insulin
• When one goes up in the blood, the other goes down.
• Body secretes 40-60 units/day.
Other Hormones that Increase BS
▪ Growth hormone
▪ Epinephrine
▪ Thyroxin
▪ Glucocorticoids
Pathophysiology of DM
▪ Type 1 diabetes
▪ Immune-mediated
▪ Idiopathic
▪ Characterized by hyperglycemia and development of
ketosis
▪ Most often diagnosed in persons under age 30 years.
▪ Peak onset – ages 11 - 13
▪ Rate is 1.5 – 2 times higher in whites than nonwhites
Pathophysiology Of TYPE I DM
▪ Whatever the cause of Type I -destruction of beta cells occur &
results in:
▪ Decreased insulin production
▪ Unchecked glucose production by the liver
▪ Fasting hyperglycemia
▪ In addition, glucose derived from food cannot be stored in the liver
▪ Instead it remains in the bloodstream and contributes to
postprandial (after meals) hyperglycemia
There are even more problems with Type I DM!!!
▪ Glycosuria
▪ If level of glucose in the blood exceeds renal threshold
for glucose - usually 180 to 200 mg/dL
▪ Kidneys may not reabsorb all of the filtered glucose
▪ Glucose then appears in the urine (glycosuria)
▪ Osmotic diuresis occurs from the high level of glucose
in the urine
▪ When excess glucose is excreted in the urine it is
accompanied by excessive loss of fluids and
electrolytes
Guess what it – it gets worse
▪ Insulin normally inhibits glycogenolysis (breakdown of stored
glucose) and gluconeogenesis (production of new glucose from
amino acids)
▪ Type I DM- there is not insulin available
▪ Glycogenolysis & gluconeogenesis - occur unrestrained with
insulin deficiency & contribute further to hyperglycemia
▪ Also fat breakdown occurs
▪ Results in increased production of ketone bodies
▪ Ketones are highly acidic substances that form when the liver
breaks down free fatty acids in the absence of insulin
This really is the end of the road if not Rx
▪ Diabetic ketoacidosis (DKA)
▪ Occurs most commonly in persons with type 1 diabetes
▪ Results from a deficiency of insulin
▪ The highly acidic ketone bodies are formed and metabolic acidosis
occurs
▪ The three major metabolic derangements are hyperglycemia, ketosis,
and metabolic acidosis
▪ DKA is commonly preceded by a day or more of polyuria, polydipsia,
nausea, vomiting, & fatigue with eventual stupor and coma if not treated
▪ The breath has a characteristic fruity odor due to the presence of
ketoacids
Pathophysiologic
results of type 1 DM
Progression of Type I DM
• Progressive destruction of beta cells of pancreas from
autoimmune causes
• Unknown, possibly viral, & genetic predisposition
• The beta cells cannot produce insulin.
• The patient requires exogenous insulin
• Typically, rapid onset of symptoms
Pathophysiology of Type 1 DM
▪ Type 1 diabetes
▪ Manifestations
▪ Hyperglycemia
▪ Polyuria
▪ Glucosuria
▪ Polydipsia
▪ Polyphagia
▪ Weight loss, malaise, fatigue
Pathophysiology of Type 2 DM
▪ Type 2 diabetes
▪ Results from insulin resistance
▪ Occurs at any age
▪ Heredity plays an important role, along with
obesity
▪ Nonketotic
Type II DM- Some Function of the
pancreas yet!
▪ Pancreas produces some endogenous insulin.
▪ However, either not enough insulin produced or
is poorly utilized
▪ Insulin resistance – the glucose can’t get into the
cells
▪ Type 2 diabetes- insulin less effective at
stimulating glucose uptake by the tissues and
at regulating glucose release by the liver
The problems continue with Type 2
▪ The exact mechanisms that lead to insulin resistance and
impaired insulin secretion in type 2 diabetes are unknown
▪ Genetic factors are thought to play a role
▪ Hyperglycemia results
▪ There is enough insulin present to prevent the breakdown
of fat and production of ketones
▪ DKA does not typically occur in type 2 diabetes.
▪ However, uncontrolled type 2 diabetes may lead to another
acute problem—hyperglycemic hyperosmolar syndrome
(HHS) – will be discussed later with Complications
Pathophysiology of Type 2 DM
▪ Type 2 diabetes
▪ Manifestations
▪ Slow onset
▪ Hyperglycemia
▪ Polyuria
▪ Polydipsia
▪ Polyphagia
▪ Weight loss
Secondary Diabetes
▪ Occurs because of another medical condition or treatment
that causes abnormal blood glucose levels
▪ Conditions can include
▪ Cushing’s Syndrome, hyperthyroidism,parenteral nutrition, &
pancreatic diseases
▪ Medications that can induce DM in some people
▪ Corticosteroids, Dilantin, & some antipsychotics
Gestational diabetes
▪ Develops during pregnancy
▪ Occurs in about 4% of pregnancies in U.S.
▪ Higher risk of complications
▪ BS usually returns to normal within 6 weeks postpartum
▪ Mom’s risk for developing Type II DM within 5-10 years is
increased
Gestational DM in the U.S., per CDC
▪ “Immediately after pregnancy, 5% to 10% of
women with gestational diabetes are found to have
diabetes, usually Type 2.”
▪ “Women who have had gestational diabetes have
a 35% to 60% chance of developing diabetes
within the next 10-20 years.
DM in the Older Adult
▪ Type 2 more common
▪ Normal physiologic changes may mask manifestations.
▪ Classic symptoms of polyuria, thirst not necessarily
present
▪ Longer recovery period after surgery, serious illness
Prediabetes (previously classified as previous
abnormality of glucose tolerance)
▪ Previous history of hyperglycemia (e.g., during pregnancy or illness)
▪ Current normal glucose metabolism
▪ Impaired glucose tolerance or impaired fasting glucose screening
after age 40 years if there is a family history of diabetes
▪ Encourage ideal body weight-loss of 10–15 lb may improve
glycemic control
Metabolic Syndrome/Syndrome X
▪ Simultaneous presence of metabolic factors known to
increase risk for developing type 2 DM and cardiovascular
disease.
▪ Characterized by elevated insulin levels, high
triglycerides, decreased HDL, increased LDL, and HTN
▪ Risk factors include abdominal obesity, sedentary
lifestyle, polycystic ovary syndrome, family history,
gestational diabetes, and increased age
NCLEX Practice
▪ The client newly diagnosed with type 2 diabetes asks how diabetes type 1 and diabetes
type 2 are different. What is the nurse's best response?
▪ A.
“Diabetes type 1 develops in people younger than 40 years and diabetes type 2
develops only in older people.”
▪ B.
“Diabetes type 2 develops in people younger than 40 years and diabetes type 1
develops only in older people.”
▪ C.
“Patients with type 1 diabetes are at higher risk for obesity and heart disease,
whereas patients with type 2 diabetes are at higher risk for strokes.”
▪ D.
“Patients with type 1 diabetes produce no insulin and patients with type 2
diabetes produce insulin but their insulin receptors are not very sensitive to it.”
Prevention
▪ Type 2 diabetes can be prevented with appropriate changes in
lifestyle & preventative medication
▪ High risk type 2 diabetes – findings in group studies
▪ Intensive lifestyle recommendations changes- weight reduction of
greater than 7% of initial body weight physical activity of moderate
intensity
▪ 58 % reduction in incidence
▪ Use of metformin (Glucophage)- oral antidiabetic agent
▪ 31% reduction in incidence
Clinical Manifestations
▪ Hyperglycemia causes fluid and electrolyte imbalances
▪ Leads to e classic symptoms of diabetes: polyuria, polydipsia, and polyphagia.
▪ 3 “P”s - depend on level of hyperglycemia
▪ Polyuria - frequent and excessive urination
▪ Results from osmotic diuresis caused by excess glucose in the urine
▪ As a result of diuresis, sodium, chloride, and potassium are excreted in the
urine
▪ Water loss is severe
▪ Dehydration results
▪ Polydipsia (excessive thirst) occurs
Clinical Manifestations (cont)
▪ Polyphagia (excessive eating).
▪ This occurs because the cells receive no glucose
▪ Cell starvation occurs triggers polyphagia
▪ Despite eating vast amounts of food -starvation remains
until insulin is available to move glucose into the cells
Some more things happen then▪ Without insulin and glucose is not available for cell metabolism
▪ THEN fats break down
▪ This releases free fatty acids
▪ Free fatty acids convert to ketone bodies (small acids)
▪ This will provide a backup energy source
▪ HOWEVER -ketone bodies are abnormal breakdown products of
fatty acids
▪ Ketones collect in the blood when insulin is not available
▪ Will lead to metabolic acidosis.
A little more about Metabolic Acidosis
▪ Excess acids caused by absence of insulin will increase hydrogen
ion (H+) and carbon dioxide (CO2) levels in the blood
▪ This is the cause of metabolic acidosis
▪ These products trigger respiratory centers in the brain
▪ Increased rate and depth of respiration
▪ Body is trying to excrete more carbon dioxide and acid
▪ This breathing is known as Kussmaul respiration
▪ Acetone is exhaled, giving the breath a “fruity” odor
▪ When the lungs can no longer offset acidosis, blood pH drops
▪ Arterial blood gas studies = metabolic acidosis (decreased pH
with decreased arterial bicarbonate HCO3-)
NCLEX Practice
▪ In a patient with hyperglycemia, the respiratory center is triggered in an attempt to
excrete more carbon dioxide and acid, thus causing a rapid and deep respiratory
pattern. What is the term for this respiratory pattern?
▪ a.
Tachypnea
▪ b.
Cheyne-Stokes respiration
▪ c.
Kussmaul respiration
▪ d.
Biot respiration
NCLEX Practice
▪ Untreated hyperglycemia results in which condition?
▪ a.
Respiratory acidosis
▪ b.
Metabolic alkalosis
▪ c.
Respiratory alkalosis
▪ d.
Metabolic acidosis
Dehydration is also at work here
▪ Dehydration -if occurs with diabetes leads to the following:
▪ Hemoconcentration (an increased blood concentration)
▪ Hypovolemia (a decreased blood volume)
▪ Hyperviscosity (thick, concentrated blood)
▪ Poor tissue perfusion, and hypoxia (poor tissue oxygenation),
especially to the brain
▪ Hypoxic cells do not metabolize glucose efficiently
▪ Krebs’ cycle is blocked
▪ Lactic acid increases & this causes more acidosis
NCLEX Practice
▪ A patient with diabetes presents to the emergency department with a blood sugar
of 640 mg/dL and reports being constantly thirsty and having to urinate “all of the
time.” How does the nurse document this subjective finding?
▪ a.
Polydipsia and polyphagia
▪ b.
Polydipsia and polyuria
▪ c.
Polycoria and polyuria
▪ d.
Polyphagia and polyesthesia
Assessment - History
▪ Ask questions about risk factors and symptoms related to diabetes
▪ Age is important - type 2 diabetes mellitus (DM) more common in older patients
▪ Especially among African Americans and Mexican Americans
▪ Ask women how large their children were at birth
▪ Many women who develop type 2 DM had gestational diabetes or were glucose
intolerant during pregnancy.
▪ Often have given birth to infants weighing 9 pounds or more
Assessment – History (cont)
▪ Assessing weight and weight change
▪ Excess weight and obesity - risk factors for type 2 DM
▪ The patient with type 1 DM often has weight loss with increased appetite during
the weeks before diagnosis
▪ For both types of DM- patients usually have fatigue, polyuria, and polydipsia
▪ Ask about recent major or minor infections
▪ In particular, ask women about frequent vaginal yeast infections
▪ Ask all patients if they have had small skin injuries become infected more
easily or take longer to heal
▪ Assess for any changes in vision or sense of touch
Assessment – History (cont)
▪ Symptoms related to the diagnosis of diabetes
▪ Hyperglycemia
▪ Thirst & frequent urination
▪ Weight loss without trying
▪ Fatigue
▪ Diarrhea & constipation
▪ Cuts heal slowly
Assessment – History (cont)
▪ Hypoglycemia
▪
▪
▪
▪
▪
▪
▪
▪
▪
▪
▪
blurry vision
rapid heartbeat
diaphoresis
unexplained fatigue
pale skin
headache
hunger
shaking
sweating
trouble thinking clearly or concentrating
loss of consciousness
Assessment – History (cont)
▪ Results of blood glucose monitoring
▪ Status, symptoms, and management of chronic complications of diabetes:
▪ Eye
▪ Kidney
▪ Nerve
▪ Genitourinary
▪ Gastrointestinal
▪ Peripheral vascular-foot complications
▪ Adherence to/ability to follow prescribed dietary management plan
▪ Adherence to prescribed exercise regimen
▪ Adherence to/ability to follow prescribed pharmacologic treatment
(insulin or oral antidiabetic agents)
▪ Lifestyle, cultural, psychosocial, and economic factors that may
affect diabetes treatment
Laboratory Assessment for Diagnosis of Diabetes
TEST
NORMAL RANGE FOR
ADULTS
Fasting blood glucose test
<100 mg/dL-older adults:
Levels >126 mg/dL - on at least
Levels rise 1 mg/dL per decade two occasions are diagnostic of
of age
diabetes
Glucose tolerance test (2-hr post-load
result)
Glycosylated hemoglobin
(hemoglobin A1c [HbA1c]) test
<140 mg/dL
4%-6%
SIGNIFICANCE OF
ABNORMAL RESULTS
Levels >200 mg/dL -indicate
provisional diagnosis of
diabetes.
Levels >8% indicate poor
diabetic control and need for
adherence to regimen or
changes in therapy
What do these tests mean?
▪ Fasting Blood Glucose - education
▪ Fasting is defined as no caloric intake for at least 8 hr
before the test
▪ Do not eat any food or drink any liquid except water for
at least 8 hours before the test
What do these tests mean? (cont)
▪ Oral Glucose Tolerance Test
▪ Test is performed in the morning after a 10 to 12hour fast
▪ Fasting blood sample is obtained.
▪ Patient then drinks 300 mL of a flavored beverage containing 75 g
of glucose within 5 minutes of the fasting blood sample
▪ Blood samples drawn at 30-minute intervals for 2 hours
▪ During the test, should remain at rest and not smoke or drink liquids
What do these tests mean? (cont)
▪ Glycosylated hemoglobin - HbA1c
▪ Useful because blood glucose permanently attaches to
hemoglobin
▪ The higher the blood glucose level is over time, the more
glycosylated hemoglobin becomes
▪ Glycosylated HbA1c - good indicator of the average blood glucose
levels
▪ Measurement of A1c shows the average blood glucose level
during the previous 120 days—the life span of red blood cells
Glycosylated hemoglobin - HbA1c
▪ HbA1c testing is used to assess long-term glycemic control
▪ HbA1c test results - not altered by eating habits the day before the test
▪ Testing is performed at diagnosis and at specific intervals to evaluate the
treatment plan
▪ HbA1c testing-recommended at least twice yearly in patients who are
meeting expected treatment outcomes and have stable blood glucose
control
▪ Quarterly assessment is recommended for patients whose therapy has
changed or who are not meeting prescribed glycemic levels
NCLEX Practice
▪ According to the American Diabetes Association (ADA), which laboratory finding
is most indicative of DM?
▪ a.
Fasting blood glucose = 80 mg/dL
▪ b.
2-hour postprandial blood glucose = 110 mg/dL
▪ c.
1-hour glucose tolerance blood glucose = 110 mg/dL
▪ d.
2-hour glucose tolerance blood glucose = 210 mg/dL
Desired Outcomes
▪ The American Diabetes Association (ADA)
▪ Proposed treatment outcomes for glycosylated hemoglobin
(HbA1c) and blood glucose levels (ADA, 2010a):
▪ HbA1c levels are maintained at 7% or below
▪ Majority of premeal (preprandial) blood glucose levels are 70 to
130 mg/dL
▪ Peak after-meal (postprandial) blood glucose levels are less
than 180 mg/dL
Preventing Injury from Hyperglycemia
Expected Outcomes
▪ Diabetic patient- expected to manage DM and prevent disease progression by
maintaining blood glucose levels in the expected range
▪ Indicators that demonstrates these behaviors:
▪ Performs treatment regimen as prescribed
▪ Follows recommended diet
▪ Monitors blood glucose using correct testing procedures
▪ Manages symptoms of hyperglycemia
▪ Seeks health care if blood glucose levels fluctuate outside of recommended parameters
▪ Meets recommended activity levels
▪ Uses drugs as prescribed
▪ Maintains optimum weight
Acute Complications of Diabetes
▪ All three problems require emergency treatment and can be fatal if
treatment is delayed or incorrect
▪ Hypoglycemia
▪ DKA
▪ Hyperglycemic hyperosmolar syndrome (HHS)
Hypoglycemia
▪ Abnormally low blood glucose level (below 50–60 mg/dL); too much
insulin or oral hypoglycemic agents, excessive physical activity, and not
enough food
▪ Adrenergic symptoms: sweating, tremors, tachycardia, palpitations,
nervousness, hunger
▪ Central nervous system symptoms: inability to concentrate, headache,
confusion, memory lapses, slurred speech, drowsiness
▪ Severe hypoglycemia: disorientation, seizures, loss of consciousness,
death
Hypoglycemia
▪ Blood glucose level below 70 mg/dL alerts you to assess for
manifestations of hypoglycemia
▪ Monitor blood glucose levels
▪ before giving antidiabetic drugs
▪ before meals
▪ before bedtime
▪ when the patient is symptomatic
Most Common Causes of Hypoglycemia
▪ Too much insulin as it relates to food intake and physical activity
▪ Insulin injected at the wrong time relative to food intake and physical activity
▪ Wrong type of insulin injected at the wrong time
▪ Decreased food intake resulting from missed or delayed meals
▪ Delayed gastric emptying from gastroparesis
▪ Decrease liver glucose production after alcohol ingestion
▪ Increased insulin sensitivity as a result of regular exercise and weight loss
Patients at Risk for Hypoglycemia with DM
▪ Risk is increased:
▪ If elderly
▪ Liver or kidney impairment present
▪ Taking drugs that enhance the effects of antidiabetic drugs
▪ Hypoglycemia may be difficult to recognize if taking beta-blocking
drugs
▪ Symptoms less intense and less obvious
▪ Manifestations of hypoglycemia in older patients may be mistaken
for other conditions
Management of Hypoglycemia
▪ Give 15 g of fast-acting, concentrated carbohydrate
▪ Three or four glucose tablets
▪ 4 to 6 oz of juice or regular soda (not diet soda)
▪ Retest blood glucose in 15 minutes; retreat if >70 mg/dL or if
symptoms persist more than 10 to 15 minutes and testing is
not possible
▪ Provide a snack with protein and carbohydrate unless the
patient plans to eat a meal within 30 to 60 minutes
Emergency Measures
▪ If the patient cannot swallow or is unconscious:
▪ Subcutaneous or intramuscular glucagon (1 mg)
▪ 25 to 50 mL of 50% dextrose solution IV
▪ Notify the primary health care provider immediately
and follow instructions
Prevention Strategies
▪ Teach the patient to avoid the four common causes of hypoglycemia.
▪ Excess insulin-do not change insulin brands without medical supervision.
▪ Deficient intake or absorption of food-Teach importance of regular meal patterns
▪ Exercise- causes blood glucose levels to fall in a patient with type 1 DM
▪ Alcohol intake- inhibits liver glucose production and leads to hypoglycemia
Teaching for Prevention of Hypoglycemia
▪ Encourage the patient to wear a medical alert bracelet
▪ Emphasize that delaying a meal for more than 30 minutes raises the risk for
hypoglycemia when using some insulin regimens
▪ Instruct him or her to keep a carbohydrate source nearby at all times
▪ Teach the patient and family how to administer glucagon
▪ For the older patient with DM instruct to check blood glucose values if unsteady,
light-headed, poor concentration, trembling, or sweating occur
▪ Encourage a patient with a poor appetite to eat a small snack at bedtime to
prevent hypoglycemia during the night
Diabetic Ketoacidosis (DKA)
▪ Absence or inadequate amount of insulin resulting
in abnormal metabolism of carbohydrate, protein,
and fat
▪ Clinical features
▪ Hyperglycemia
▪ Dehydration
▪ Acidosis
The pathophysiologic mechanism of diabetic ketoacidosis (DKA)
Assessment of DKA
▪ Blood glucose levels >300 to 1,000
▪ Severity of DKA not only due to blood glucose level
▪ Ketoacidosis is reflected in low serum bicarbonate, low pH; low PCO2
reflects respiratory compensation (Kussmaul’s respirations)
▪ Ketone bodies in blood and urine
▪ Electrolytes vary according to degree of dehydration; increase in
creatinine, Hct, BUN
Symptoms of DKA
▪ Hyperglycemia leads to osmotic diuresis → dehydration & electrolyte loss
▪ Classic symptoms of DKA
▪ Polyuria, polydipsia, polyphagia
▪ Weight loss, vomiting, abdominal pain
▪ Dehydration, weakness
▪ Altered mental status
▪ Shock, coma
▪ Kussmaul respirations (rapid, deep respirations)
Risk Factors for DKA
▪ DKA occurs most often in patients with type 1 DM
▪ Can occur in type 2 DM - under severe stress (e.g.,
trauma, surgery, infection)
▪ Most common precipitating factor for development of
DKA-infection
▪ Death occurs in up to 10% of these cases even with
appropriate treatment.
Treatment of DKA
▪ Rehydration with IV fluid- careful monitoring of fluid volume status
▪ IV continuous infusion of regular insulin
▪ Subcutaneous insulin started when taking oral fluids and ketosis
has stopped
▪ Reverse acidosis and restore electrolyte balance
▪ Rehydration leads to increased plasma volume and along with
insulin therapy decreased K+ occurs- Need for replacement of
potassium
▪ Before giving IV potassium, make sure the patient produces at
least 30 mL/hr of urine
Patient and Family Education- DKA
▪ Sick-Day Rules
▪ Notify your health care provider that you are ill
▪ Monitor your blood glucose at least every 4 hours
▪ Test your urine for ketones if blood glucose level is greater than 240 mg/dL
▪ Continue to take insulin or oral antidiabetic agents
Sick –Day Rules - cont
▪ To prevent dehydration, drink 8 to 12 ounces of sugar-free liquids every hour that
you are awake
▪ If your blood glucose level is below your target range, drink fluids that contain
sugar
▪ Continue to eat meals at regular times
▪ If unable to tolerate solid food because of nausea, consume more easily tolerated
foods or liquids equal to the carbohydrate content of your usual meal
Sick –Day Rules – cont.
▪ Call your primary care provider for any of these danger signals:
▪ Persistent nausea and vomiting
▪ Moderate or large ketones
▪ Blood glucose elevation after two supplemental doses of insulin
▪ High (101.5° F [38.6° C]) temperature or increasing fever; fever for
more than 24 hours
▪ Treat symptoms (e.g., diarrhea, nausea, vomiting, fever) as directed
by your primary care provider
Hyperglycemic-hyperosmolar state (HHS)
▪ Formerly known as hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
▪ A hyperosmolar (increased blood osmolarity) state caused by hyperglycemia
▪ Both HHS and diabetic ketoacidosis (DKA) - caused by hyperglycemia and
dehydration.
▪ HHS differs from DKA
▪ Ketone levels are low or absent and blood glucose levels are much higher
▪ Blood glucose levels may exceed 600 mg/dL and blood osmolarity may exceed 320
mOsm/L
Kidneys are a major factor in HHS
▪ HHS is the end result of a sustained osmotic diuresis
▪ Kidney impairment in HHS
▪ Results in extremely high blood glucose levels
▪ Glucose impairs the concentrating ability of the kidney
▪ Normally, kidneys act as a safety valve to eliminate glucose above
levels around 180 mg/dL
▪ As serum concentrations of glucose exceed the renal threshold,
the kidney's capacity to reabsorb glucose is exceeded
Ongoing effects of HHS on Kidneys
▪ Decreased blood volume occurs caused by osmotic
diuresis
▪ Results in further deterioration of kidney function
▪ The decreased volume further reduces glomerular
filtration rate
▪ This causes the glucose level to increase
▪ Decreased kidney perfusion from hypovolemia further
impairs kidney function
The Concept of Osmotic Diuresis
▪ The “Happy Cell”
Osmotic Diuresis - continued
▪ “Unhappy” Cell
Pathophysiologic mechanism of hyperglycemic-hyperosmolar state
Hyperglycemic Hyperosmolar Syndrome
▪ Hyperosmolar hyperglycemia is caused by a lack of sufficient insulin
▪ Ketosis is minimal or absent
▪ Hyperglycemia causes osmotic diuresis
▪ Loss of water and electrolytes, hypernatremia, and increased osmolality
▪ Manifestations include hypotension, profound dehydration, tachycardia,
and variable neurologic signs caused by cerebral dehydration
▪ High mortality rate
Management of HHS
▪ Rehydration
▪ First priority for fluid replacement in HHS - increase blood volume
▪ If In shock or severe hypotension- give normal saline
▪ Otherwise- half-normal saline because it more rapidly corrects the water
deficit
▪ Monitor fluid volume and electrolyte status very closely
▪ Lack of improvement in level of consciousness may indicate inadequate
rates of fluid replacement
▪ Assess patient hourly for signs of cerebral edema—abrupt changes in
mental status, abnormal neurologic signs, and coma
Insulin administration- Rx HHS
▪ IV insulin is administered after adequate fluids have been replaced
▪ A reduction of blood glucose of 50 to 70 mg/dL per hour reasonable expected outcome
▪ Monitor the patient closely for indications of hypokalemia
▪ Potassium level may drop quickly when insulin therapy is started
▪ Potassium replacement - once urine output is adequate
Planning : Expected Outcomes
▪ The patient with DM is expected to have few episodes of
hyperglycemia and avoid HHS
▪ Indicators include that the patient consistently demonstrates these
behaviors:
▪ Maintains blood glucose levels within the target range
▪ Uses antidiabetic drugs appropriately
▪ Remains well hydrated
▪ Describes when to seek help from health care professionals
Making Healthy Choices…