CH48 Diabetes Mellitus
DIABETES MELLITUS
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Chronic multisystem disease characterized by hyperglycemia r/t abnormal insulin production,
impaired insulin utilization or both
7th leading cause of death
Leading cause of adult blindness, end stage renal disease, and nontraumatic lower limb
amputations, as well as stoke & heart disease
Cause/Patho
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Genetic, autoimmune, environmental factors (virus or obesity)
Disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor
utilization of the insulin that is available
Normal Glucose and Insulin Pathology
o Insulin – hormone produced by the β-cell in the islet of Langerhans of the pancreas
 Constantly released into the blood stream in small increments, with increased
release when food is ingested
 Lowers blood glucose & facilitate stable, normal glucose range 70-110mg/dL
 Promotes glucose transport from the bloodstream across the cell membrane to
the cytoplasm of the cell
 Cells break down glucose to make energy, and liver and muscle cells store
excess glucose as glycogen
 Rise in plasma insulin after a meal inhibits gluconeogenesis, enhances fat
deposition of adipose tissue and increase protein synthesis
 Skeletal muscle and adipose tissue have specific receptors for insulin and are
considered insulin-dependent tissues
 Insulin requires to unlocked receptor sites, allowing transmission of glucose into
the cells to be used for energy
o Other hormones (glucagon, epinephrine, growth hormone, & cortisol) work to oppose
the effects of insulin referred to as counterregulatory hormones
 These hormones increase blood glucose levels by
 Stimulating glucose production and release by the liver
 Decreasing the movement of glucose into the cells
o Insulin and counterregulatory hormones maintain blood glucose levels within the
normal range during food intake & periods of fasting
Type 1 Diabetes – also known as juvenile onset diabetes or insulin dependent diabetes, affect
people under 40yrs of age.
o Cause/Patho
 Autoimmune disorder, body develops antibodies against insulin and/or the
pancreatic β-cells that produce insulin
o Onset of Disease
 Symptoms are usually rapid, pt seen with impending or actual ketoacidosis
 Polydipsia (excessive thirst), polyuria (frequent urination), polyphagia (excessive
hunger)
 Pt will require insulin from an outside source (exogenous insulin) to sustain life,
w/o insulin pt develops diabetic ketoacidosis
Type 2 Diabetes Mellitus – known as adult-onset diabetes or non-insulin dependent diabetes,
most prevalent
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Risk Factors: being overweight or obese, sedentary, being older, family hx of type 2
diabetes
o African Americans, Asian Americans, Hispanics, Native Hawaiians or Pacific Islanders and
Native Americans have higher rates
o Cause/Patho
 Combination of:
 Insulin resistance – body tissues do not respond to the action of insulin, insulin
receptors on muscles, fat & liver cells are unresponsive. Results in
hyperglycemia
 Pancreas responds to high glucose by producing greater amounts of
insulin, creates hyperinsulinemia along with hyperglycemia
 Inadequate insulin secretion - decrease in the ability of the pancreas to produce
insulin, in addition α-cells increase production of glucagon
 Inappropriate production of glucose by the liver – does not correspond to the
body’s need at the time
 Altered production of hormones & cytokines by adipose tissue (adipokines)
 Cause inflammation, a factor involved in insulin resistance, type 2
diabetes and cardiovascular disease
 Individual with metabolic syndrome are at increased risk for the development of
type 2 diabetes
 5 components: elevated glucose levels, abdominal obesity, elevated BP,
high levels of triglycerides & decreased levels of high density
lipoproteins
 3 out of 5 considered metabolic syndrome
o Onset of Disease
 Gradual, pt goes many years with undetected hyperglycemia with few
symptoms, many diagnosed on routine lab testing or when undergoing
treatment for other conditions
 Signs and symptoms develop when 50%-80% of β-cells are no longer secreting
insulin
Prediabetes
o Impaired glucose tolerance, impaired fasting glucose or both
o Intermediate stage b/w normal glucose homeostasis and diabetes
o Encourage pt to have their blood glucose and A1C checked regularly and monitor for
symptoms of diabetes; fatigue, frequent infections, or slow healing wounds
o Maintain healthy weight, exercise regularly and make healthy food choices
Gestational Diabetes
o Develops during pregnancy
o Increased risk for cesarean delivery, babies have increased risk for perinatal death, birth
injury & neonatal complication
o High Risk: obese women, advanced maternal age, or have family history of diabetes
Other Specific Types of Diabetes
o d/t medical condition or tx of a medical condition that causes abnormal blood glucose
levels
o Results from injury to, interference with or destruction of the β-cell function in the
pancreas
 Cushing syndrome, hyperthyroidism, recurrent pancreatitis, cystic fibrosis,
hemochromatosis & parenteral nutrition
o Commonly used meds that induce diabetes in some people
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Corticosteroids (prednisone), thiazides, phenytoin (Dilantin) and atypical
antipsychotics (clozapine [Clozaril])
Resolved when condition is treated or meds DC
Signs & Symptoms
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Type 1 Diabetes Mellitus
o Rapid onset, usually acute
o Polyuria, polydipsia, polyphagia
o Polyphagia d/t cellular malnourishment, weight loss occurs b/c body cannot get glucose
and turns to other energy sources such as fat & protein
 Weakness & fatigue results
o Ketoacidosis – a complication common to those with Type 1 Diabetes. Body needs
energy and starts to burn fats (ketones) for energy. Results in acid formation in the
blood.
Type 2 Diabetes Mellitus
o Nonspecific
o Similar to type 1; polyuria, polydipsia, polyphagia
o As well as fatigue, recurrent infections, recurrent vaginal yeast or candida infections,
prolonged wound healing & visual changes
Diagnostic Studies
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A1C of 6.5% or higher
o Measure the amount of glycosylated hemoglobin as a percentage of total hemoglobin
o Provides a measurement of blood glucose levels over the previous 2-3 months
o Greater convenience, no fasting required
Fasting plasma glucose (FPG) level greater than or equal to 126mg/dL (7.0mmol/L). No caloric
intake for 8hrs
Two-hour plasma glucose greater than or equal to 200mg/dL (11.1mmol/L) during an oral
glucose tolerance test (OGTT) using glucose load of 75g
In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight
loss) or hyperglycemic crisis, a random plasma glucose greater than or equal to 200mg/dL
(11.1mmol/L)
Fructosamine is another way to assess glucose levels
o Formed by chemical reaction of glucose with plasma protein, reflects glycemia in the
previous 1-3 weeks
Islet cell autoantibody testing is ordered to distinguish b/w autoimmune type 1 diabetes and
diabetes from other causes
Interprofessional Care
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Goal reduce symptoms, promote well being, prevent acute complications (r/t
hyper/hypoglycemia), prevent or delay onset or progression of long term complications
Drug Therapy: Insulin Type 1 diabetes require daily
exogenous insulin injections multiple times per day
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Type 2 diabetics only require insulin during
periods of severe stress illness or surgery
Types of Insulin
o Genetically modified from E. coil or
yeast
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Insulin Regimens
o Insulin regimen that most closely mimics endogenous insulin production is the basalbolus regimen, rapid or short acting (bolus) insulin before meals and intermediate or
long acting (basal) background insulin once or twice a day
o Intensive or physiologic insulin therapy – multiple daily insulin injections together with
frequent self-monitoring of blood glucose. Goal is to achieve blood glucose level of 80130 mg/dL before meals
Mealtime Insulin (Bolus)
o Rapid acting synthetic insulin analogs; lispro (Humalog), aspart (Novolog), and glulisine
(Apidra) have an onset of action approximately 15mins and should be injected w/in 15
mins of mealtime. Mimic natural insulin secretion in response to meal
o Short acting regular insulin has an onset of 30-60mins and is injected 30-45 mis before a
meal, ensure that onset of action coincides with meal absorption
Long- or Intermediate Acting (Basal) Background Insulin
o People with type 1 diabetes use to maintain blood glucose levels in-between meals and
overnight
o Glargine (Lantus, Toujeo), detemir (Levemir), degludec (Tresiba), released steadily and
continuously and for many people does not have a peak action
o Risk for hypoglycemia is greatly reduced. MUST NOT BE DILUTED OR MIXED WITH ANY
OTHER INSULIN OR SOLUTION IN THE SAME SYRINGE
o Intermediate acting insulin (NPH) basal insulin, duration of 12-18hrs. Has a peak ranging
from 4-12hrs which can result in hypoglycemia
o NPH, lispro protamine and aspart protamine are cloudy insulins b/c they contain
protamine – decreases solubility, must be gently agitated before administration
Combination Insulin Therapy
o 1-2 injections per day, mix of short or rapid acting insulin & intermediate acting insulin
in the same syringe
o Pt has both mealtime and basal coverage without having to administer two separate
injections
o Offer convenience, help those who lack visual, manual, or cognitive skills to mix insulin
themselves
o Limits the optimal blood glucose levels b/c less opportunity for flexible dosing based on
needs
Storage of Insulin
o Insulin vials & pens currently in use can be kept at room temp for up to 4 weeks, avoid
exposure to direct sunlight,
o Pt traveling in hot climate may store insulin in a thermos or cooler
o Unopened vials stored in the refrigerator
o Store in vertical position needle pointed up
o Before injections gently roll b/w palms for 10-20mins & resuspend particles
Administration of Insulin
o Admin subq route, regular insulin may be given IV route for immediate action
o Not given oral, inactivated by gastric fluids
o Teach pt to avoid IM d/t rapid & unpredictable absorption could result in hypoglycemia
o Insulin Injection
 Fastest absorption site abd, then arm, thigh, & buttock
 Caution pt about injecting site that is to be exercised ex. thigh when going
running (increases body heat and circulation which could increase rate of insulin
absorption and speed the onset of action = hypoglycemia
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 100U = 1mL
o Insulin Pump
 Delivers a continuous subq insulin infusion thru a small device worn on the belt,
pocket or under clothing
 Uses rapid acting insulin, loaded into cartridge and connected via plastic tubing
to a catheter inserted into the subq tissue
 Insulin increased or decreased based on carb intake, activity changes or illness
 At mealtime the user programs the pump to deliver a bolus infusion of insulin
based onto carb intake to correct blood glucose
 Infusion set change q2-3 days & placed in a new site to avoid infection and to
promote good insulin absorption
 Pump users check their blood glucose level at least 4 times per day
 Monitor 8 times or more per day is common
 Major advantage potential to keep blood glucose levels in a tighter range
 Pumps offer users more flexibility with meal and activity patterns
 Potential challenges = infection at insertion site, increased risk for DKA if insulin
is disrupted, increased cost of the pump & supplies
Problems With Insulin Therapy
o Allergic Reaction
 Local inflammatory reactions (itching, erythema, burning around injection site)
self limiting w/in 1-3 months may improve with low dose antihistamine
 True allergic reaction rare, systemic response with urticaria (hives) & possible
anaphylactic shock
 May be d/t zinc or protamine in insulin or latex or rubber stopper on vials
o Lipodystrophy
 Atrophy or hypertrophy of subq tissue, occur when same site used frequently
 Atrophy – wasting of subq tissue presents as indentation in injection site
 Hypertrophy – thickening of subq tissue, regress if pt doesn’t use the site for at
least 6 months
 Results in erratic insulin absorption
o Somogy Effect
 Hyperglycemia during the morning
 Occur when a high dose of insulin produces a decline in blood glucose levels
during night, counterregulatory hormones (glucagon, epinephrine, growth
hormone, cortisol) are released which stimulates lipolysis, gluconeogenesis and
glycogenolysis = rebound hyperglycemia
 If pt experiences morning hyperglycemia check blood glucose b/w 2-4am for
hypoglycemia to determine if it is Somogyi effect (SOMOGYI=SLEEPING=LOW)
 S/S: awaking with headache, night sweats or nightmares
 Give a bedtime snack, reduce insulin or both to help with Somogyi effect
o Dawn Phenomenon
 Hyperglycemia present on awaking
 Two counterregulatory hormones (growth hormone & cortisol)
 Affects majority of people with diabetes and tends to be most severe when
growth hormone is at its peak in adolescence and young adults
 Tx is increase in insulin or an adjustment in admin time
 Assessment must include insulin dose, injection site, and variability in the time
of meals or insulin admin
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Ask pt to measure and document bedtime, nighttime (b/w 2-4am) and morning
fasting blood glucose on several occasions
If predawn levels are less than 60mg/dL (3.3mmol/L) and signs and symptoms of
hypoglycemia are present, insulin dosage should be reduced
If 2-4am blood glucose id high, insulin dosage should be increased
Nutritional Therapy
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Counseling, education & ongoing monitoring, changing eating habits
Required coordinated team effort, take into account pt background, personal behavior, &
preferences
Goal: assist pt in making healthy nutritional choices, leads to maintaining safe & healthy blood
glucose levels
Type 1 Diabetes
o Based meal planning on usual food intake and preferences balanced with insulin and
exercise patterns
o Coordinates insulin dosing with eating habits and activity pattern
o Pt using rapid acting insulin adjust dose before each meal based on the current blood
glucose level & carb content of the meal
Type 2 Diabetes
o Emphasize achieving glucose , lipid & BP goals
o Weight loss recommended, may improve insulin resistance
o Nutritional meal, appropriate meal sizes, reduced saturated & trans fats and low carbs
can decrease caloric consumption
o Spacing meals throughout the day
o Weight loss of 5%-7% body weight lowers blood glucose levels
o Regular exercise
o Monitor blood glucose levels, A1C, lipids, and BP provides feedback on how well goals
are met
Food Composition
o Carbs – whole grains, fruits, vegetables, and low-fat dairy. No ideal number (about 50%
of diet)
o Fats – individualize saturated fats, less than 200mg/day of cholesterol, & limit trans fat
 Helps reduce risk of CVD. Consume healthy fats like, olives, nuts, & avocado
o Protein – individualize goal
o Alcohol – inhibits gluconeogenesis (breakdown of glycogen to glucose) by the liver,
causes severe hypoglycemia in pt on insulin or oral hypoglycemic meds that increase
insulin secretion
 Moderate alcohol intake if pt is monitoring blood glucose levels (one drink per
day for women & two for men
 Reduce risk of alcohol hypoglycemia by eating carbs when drinking, mixed
drinks = elevated blood glucose levels
 Sugar free mixed drinks and dry light wines
Patient Teaching Regarding Nutrition Therapy
o Carbohydrate counting – meal planning technique used to keep track of the amount of
carbohydrates eaten with each meal/per day
 Keep w/in healthy range, depends on weight, age, blood glucose levels, activity
level
 Adult usually 45-60g per meal
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Diabetes exchange list – pt chooses food from the exchange lists based on prescribed
meals
 Helps pt limit portion sizes & control food intake
Include family/care giver or whoever makes meals in nutrition education
Exercise
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Regular, consistent exercise is an essential part of diabetes and prediabetes management
At least 150mins/wk (30mins/5day/week) of moderate intensity aerobic physical activity
Resistance training 3 times/weeks
Decreases insulin resistance and can have a direct effect on lowering blood glucose levels
Contributes to weight loss, also decreases insulin resistance
Leads to decreased need for diabetes medication, reduce triglyceride and LDL levels, increase
HDL levels, reduce BP, & improve circulation
Pt starts slowly with gradual progression
Pt taking sulfonylureas or meglitinides are at increased risk for hypoglycemia, when physical
activity increased, especially at the time of peak drug action, or eat too little to maintain
adequate blood glucose
Pt taking meds that may cause hypoglycemia should schedule exercise 1hr after a meal or have
10-15g carb snack and check blood glucose before exercising
Eat small carb snacks every 30mins during exercise to prevent hypoglycemia
Pt at risk for hypoglycemia with meds should carry fast acting source of carb (glucose tabs, hard
candies) when exercising
Strenuous activity can be perceived by the body as stress and increase counterregulatory
hormones & elevate blood sugar
Pt who has type 1 diabetes and has hyperglycemia & ketones, exercise can worsen conditions
o Delay daily activity if blood glucose level if over 250mg/dL& ketones are present in the
urine
Exercise induced hypoglycemia may occur several hrs after exercise
Monitoring Blood Glucose
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Self monitoring blood glucose – allows pt to make decisions regarding food intake, activity
patterns, & medication dosages, produce accurate fluctuation of daily glucose
o Alerts pt to acute episodes of hypo/hyperglycemia
Recommended for all pt who use insulin to manage diabetes
Disposable lancet used to obtain small drop of capillary blood, placed on reagent strip, monitor
displays digital reading
Continuous glucose monitoring – system provides another route for monitoring glucose, insulin
pumps may have them
Values available every 1-5 mins, assist in identifying trends and patterns in glucose levels
Lab testing may be higher than home glucose monitor b/c home monitor tests while blood while
lab tests plasma reading
o Approximately 10-12% higher
Pt should monitor blood glucose whenever hypoglycemia suspected, to take immediate action
During illness check blood glucose at 4 different intervals to determine effect of illness on
glucose levels
Monitor blood glucose before/after exercise
Bariatric Surgery
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May be considered for pt w/ type 2 diabetes, especially if its related to comorbidities
Pt will need life long lifestyle support and monitoring
Pancreas Transplantation
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Treatment option for pt with type 1 diabetes, done for pt with end stage renal disease & have or
plan to have kidney transplant
Kidney & pancreas transplant often performed together, or pancreas after kidney
Only for pt who exhibit:
o Hx of frequent, acute, and severe metabolic complications
o Clinical & emotional problems w/ use of exogenous insulin therapy, severe causing
incapacitation
o Consistent failure of insulin based management to prevent acute complications
Can improve quality of life, eliminating need for exogenous insulin
Pt will require lifelong immunosuppressive therapy, which has complications
Pancreatic islet cell transplantation is another option, islets harvested from deceased organ
donor
Most require use of two or more pancreases, islets infused into catheter thru abd into portal
vein of the liver, procedure still experimental
Nursing Management
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Nursing Assessment – weight gain/loss, poor healing wounds, constipation/diarrhea, frequent
urination, frequent bladder infections, muscle weakness, fatigue, abd pain, headache, blurred
vision, numbness, tingling, ED, frequent vaginal infection
o Sunken eyeballs, dry warm, inelastic skin, rapid, deep resp (Kussmaul resp), low BP,
weak rapid pulse, dry mouth, vomiting, fruity breath
o Altered reflexes, restlessness, confusion
o Possible findings: serum electrolyte abnormalities, fasting blood glucose of ≥126mg/dL,
oral glucose tolerance test ≥200mg/dL, random glucose ≥200mg/dL, leukocytosis,
increase BUN, creatinine, triglyceride, cholesterol, LDL, VLDL, low HDL, A1C above 6.0%,
glycosuria, ketonuria, albuminuria. Acidosis
Nursing Diagnosis
o Ineffective health management
o Risk for unstable blood glucose levels r/t lack of following management plans
o Risk for injury r/t decreased tactile sensations, episodes of hypoglycemia
o Risk for peripheral neurovascular dysfunction r/t vascular effects of diabetes
o Goals:
 Engage in selfcare behavior, actively manage diabetes
 Experience few or no hyperglycemia or hypoglycemia emergencies
 Maintain blood glucose levels at normal or near normal levels
 Prevent/minimize chronic complications
 Adjust lifestyle to accommodate diabetes
Nursing Implementation
o Identify monitor and teach those at risk
o Routine screening for type 2 diabetes for overweight/obese
o Risk factors: age, ethnicity, (native American, Hispanic, African American, Asian, pacific
islander), obesity, having a baby weight over 9lb at birth
o Acute Illness and Surgery
 Emotional & physical stress can cause blood glucose to rise = hyperglycemia
 Acute illness, injury or surgery
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 Causes counterregulatory hormone response
 Acute ill pt with blood glucose greater than 240mg/dL should check urine for
ketones every 3-4hrs
 Teach pt to report to HCP when blood glucose above 300mg/dL twice in a row
of ketones levels moderate to high
 Type 1 diabetic may need to increase in insulin to avoid DKA
 Elevated blood glucose leads to poor would healing & infection
 Critically ill pt may start insulin if persistently greater than 180mg/dL
 Food intake important, if able to eat pt can continue with meal plan
 When illness causes pt to eat less than normal continue taking oral agents,
noninsulin injectable agents & insulin as prescribed w/ supplemental
carbohydrate containing fluids (low sodium soups, juices, & regular sugar
sweetened decaffeinated soft drinks
 Pt is given IV fluids & insulin (as needed) immediately before, during & after
surgery when there is no oral intake
 When caring for an unconscious surgical patient receiving insulin be alert for
signs of hypoglycemia (sweating, tachycardia, & tremors)
 Frequent monitoring can prevent severe hypoglycemia
Ambulatory Care
 Major goal enable the pt to reach an optimal level of independence in self care
activities
 Assess pt ability to perform SMBG & insulin injection
Insulin Therapy/Oral and Noninsulin Injectable Agents
 Proper administration & assessment of the patients response to insulin/OA
therapy
 Assess mental status, eating habits, home environment, attitude towards
diabetes & medication history
Personal Hygiene
 Potential for infection requires diligent skin & dental hygiene
 Avoid periodontal disease, encourage daily brushing, & flossing, have pt inform
dentist they are diabetic
 Regular bathing, foot care, inspect feet daily, avoid going barefoot, wear
comfortable/supportive shoes
 If cuts, scrapes, burns occur treat them promptly and monitor
 Wash area & apply nonabrasive or nonirritating antiseptic ointment
 Cover area with dry, sterile pads
 Notify HCP is injury doesn’t heal
Medical Identification and Travel
 Instruct pt to carry medical ID
 Being sedentary for a long time can increase blood glucose levels, encourage pt
to get up and walk every 2 hrs decrease risk of DVT
 Carry full set of diabetes care supplies (glucose monitor, insulin, noninsulin
injectable agents, oral meds & syringes
 Carry quick snack/quick acting carb for treating hypoglycemia
DIABETIC KETOACIDOSIS
Cause
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Deficiency of insulin, characterized by hyperglycemia, ketosis, acidosis & dehydration
Occur in pt with type 1 diabetes, may be seen in type 2 in severe illness, or stress when the
pancreas cannot meet demands for insulin
Precipitating factors: illness, infection, inadequate insulin dosage, undiagnosed type 1 diabetes,
poor self-management and neglect
Insufficient insulin supply, glucose can’t be used as energy, body compensate by breaking down
fat
Ketones are acidic by product of fat metabolism, cause serious problems in excessive amounts in
blood
o Ketosis alters pH balance, cause metabolic acidosis, ketonuria present
o Electrolytes depleted, cations eliminated (Excessive diuresis)
Insulin deficiency impairs protein synthesis causing protein degradation
o Causing nitrogen loss from tissues
o Stimulate glucose production from protein ↑ hyperglycemia
Signs and Symptoms
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Dehydration – poor skin turgor, dry mucous
membranes, tachycardia, orthostatic hypotension,
weakness, sunken eyes,
Abd pain, anorexia, nausea, vomiting
Kussmaul’s respirations (rapid, deep breathing,
dyspnea)
Acetone noted on breath – sweet, fruity odor
Blood glucose greater than or equal to 250mg/dL,
arterial pH less than 7.30, serum bicarb less than 16
and moderate to large ketones in urine or serum
Interprofessional Care
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Factors to consider when treating DKA, fever,
nausea, vomiting & diarrhea, altered mental status,
cause of ketoacidosis
Establish IV access and begin fluid and electrolyte
replacement
Infuse 0.45% or 0.9% NaCl to restore urine output
to 30-60ml/hr & raise BP
When blood glucose approaches 250mg/dL add 5%-10% dextrose to prevent hypoglycemia
Obtain serum potassium level before starting insulin
Insulin causes water and potassium to enter the cell along with glucose. This puts the patient at
risk for decr vascular volume and HYPOKALEMIA
IV insulin administration is directed towards correcting hyperglycemia & hyperketonemia
Ensure patent airway, administer O2 via nasal canula or nonrebreather mask
Started at 0.1U/kg/hr, I&O
Reduction of blood glucose by 36-54mg/dL/hr avoids complications
HYPEROSMOLAR HYPERGLYCEMIC SYNDROME
Cause
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Life threatening syndrome occurs in pts with diabetes who are just able to produce enough
insulin to prevent DKA
Occur in pt 60yrs of age with type 2 diabetes
Common cause UTI, pneumonia, sepsis, any acute illness, newly diagnosed type 2
Related to impaired thirst sensation & inability to replace fluids, increased mental depression &
polyuria
Pt usually has enough insulin to avoid ketoacidosis
Signs & Symptoms
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Causes severe neurologic manifestations
Somnolence, coma, seizures, hemiparesis & aphasia
Laboratory value of blood glucose greater than 600mg/dL, increase in serum osmolality
Ketones absent or minimal in urine & blood
Interprofessional Care
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Immediate administration of IV insulin and 0.9% or 0.45% NaCl
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Requires large volume of fluid replacement (slowly & carefully)
Hemodynamic monitoring (elderly pt with cardiac/renal problems) avoid fluid overload
When blood glucose falls to approximately 250mg/dL Iv fluids containing dextrose administered
to prevent hypoglycemia
Monitor electrolytes, assess vitals, I&O, lab values
Nursing Management for DKA & HHS
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Monitor blood glucose and urine for output and ketones
Monitor administration of IV fluids to correct dehydration, insulin therapy to reduce blood
glucose & serum ketone levels & electrolytes given to correct electrolyte imbalances
Assess renal & cardiopulmonary status
Monitor level of consciousness
Assess for signs of potassium imbalances from hyperinsulinemia & osmotic diuresis
o When insulin therapy is started potassium may decrease rapidly by moving into the cell
Cardiac monitoring – detect hyper/hypokalemia. LOW INSULIN=HIGH POTASSIUM
COMMON COMPLICATIONS- Fever, tachycardia, Kussmaul breathing, hypovolemia
HYPOGLYCEMIA
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Occur when there is too much insulin in proportion to available glucose
Blood glucose level drops below 70mg/dL
Counterregulatory hormones kick in (glucagon, epinephrine) which suppresses insulin
o Epinephrine causes shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, &
pallor
d/t the brain being deprived from glucose mental function is affected
o difficulty, speaking, visual disturbances, stupor, confusion, and coma
can progress to loss of consciousness, coma, seizures, & death
hypoglycemia unawareness – pt doesn’t experience warning signs or symptoms until glucose
levels reach critical point
o pt become incoherent & combative
o pt at risk: older patients, pts on β-adrenergic blockers
causes: mismatch in timing for food, & peak action of insulin or oral hypoglycemic agents, by
administering too much insulin, ingesting too little food, delay in eating, & unusual amount of
exercise
symptoms may occur when a high blood glucose falls too quickly
Nursing Management
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at first sign of hypoglycemia check blood glucose
less than 70mg/dL start tx
if greater than 70mg/dL investigate other signs & symptoms
follow “rule of 15”
o blood glucose less than 70mg/dL treated with 15g of simple (fast acting) carb such as 46oz of fruit juice, or regular soft drink, commercial products like gels or tablets with
glucose
recheck blood glucose 15 mins later, if it is still less than 70mg/dL ingest 15g more of carbs &
recheck blood glucose in 15 mins
if no changes occur after 2-3 tries contact HCP
after episode have pt consume a complex carb after recovery
avoid tx with carbs that contain fat (candy bar, cookies, whole milk & ice cream)
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o fat slows absorption of glucose and delay response to tx
avoid overtreatment with quick acting carbs
acute care setting pt treated with 20-50ml of 50% dextrose IV push
if pt is not alert enough and there is no IV access site give 1mg glucagon IM or subq
o deltoid makes glucose absorb more rapidly
o nausea common reaction after glucagon injection, turn pt to the side to avoid aspiration
o glucagon stimulates hepatic response to convert glycogen to glucose & makes glucose
rapidly available
o pt with minimal glycogen will not respond to glucagon
 pt with alcohol related hepatic disease, starvation, adrenal insufficiency
ANGIOPATHY
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Damage to blood vessels
leading cause of diabetes related death
Macrovascular – disease of large and medium size blood vessels that occur with greater
frequency
o Cerebrovascular, cardiovascular & peripheral vascular disease
o risk factors: obesity, smoking, HTN, high fat intake, sedentary lifestyle
o Treat HTN target BP less than 140/90
o Uses statin to decrease high lipids
o Recommended nutritional therapy, exercise, weight loss, & smoking cessation
Microvascular – thickening of the vessel membrane of the capillaries & arterioles
o Affect the eyes, kidneys & nerves
DIABETIC RETINOPATHY
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Microvascular damage to the retina as a result of chronic hyperglycemia, nephropathy & HTN
Common cause of blindness
Nonproliferative – partial occlusion of the small blood vessels in the retina cause
microaneurysms in the capillary walls. Fluid leaks out and causes retinal edema
Proliferative – retinal capillaries become occluded, body compensates by forming new blood
vessels to supply retina (neovascularization), new vessels are fragile & hemorrhage easily
causing vitreous contractions, prevents light from reaching retina pt sees black or red spots or
lines
Glaucoma – occlusions to outflow channels, difficult to treat results in blindness
Cataracts – progress more rapidly in diabetic pt
Dilated eye exam annually, type 1 has then Q5yrs
Prevent with good glucose maintenance
NEPHROPATHY
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Damage of small vessels that supply glomeruli of the kidneys
Leading cause of ESRD
Risk factor: HTN, genetic predisposition, smoking & chronic hyperglycemia
Screen annually with a radon spot urine collection, measure serum creatinine,
Pt with diabetes & albuminuria tx with ACE inhibitor (lisinopril, Prinivil, Zestril) angiotensin II
receptor antagonist (losartan, Cozaar)
Aggressive BP management to decrease progression of nephropathy
NEUROPATHY
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Nerve damage that occurs b/c of metabolic derangements associated with diabetes mellitus
Sensory neuropathy – loss of protective sensation in the lower extremities, screening daily by pt
and at every visit by HCP
o Loss of sensation, abnormal sensations, pain & paresthesias
o Pain – burning, cramping, crushing, tearing
o Paresthesia – tingling, burning, itching sensation
o Loss of sensitivity to touch & temperature
o Foot injury & ulcerations occur
o Capsaicin (Zostrix), tricyclic antidepressants (amitriptyline), selective serotonin and
norepinephrone reuptake inhibitor (deloxetine Cymbalta), antiseizure meds gabapentin
(neurontin), pregabalin (lyrica)
Persistent hyperglycemia leads to sorbitol & fructose in the nerves that cause damage, results in
reduced nerve conduction & demyelination , ischemic damage to blood vessels that supply
nerves
Autonomic neuropathy – affect all body systems, lead to hypoglycemia unawareness, bowel
incontinence, urinary retention, gastroparesis (delayed gastric emptying)
o which causes anorexia, nausea, vomiting, gastroesophageal reflux, persistent feeling of
fullness, trigger hypoglycemia by delaying food absorption
o Affect sex function ED
o Have pt urinary Q3H
o Cholinergic agonists – bethanechol (urecholine)
COMPLICATIONS OF FEET AND LOWER EXTREMITIES
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High risk for foot ulcers & lower extremity amputations
Sensory neuropathy & peripheral artery disease are risk factors, clotting abnormalities, impaired
immune function & autonomic neuropathy
Pt isn't aware of foot injury, & has decreased blood flow, wounds take longer to heal,
Pain at rest, cold feet, loss of hair, delayed cap refill
Pt must wear protective shoes, avoid injury to the feet, diligent skin care, nail care, inspect foot
daily, treat small problems promptly
Apply lanolin on feet to keep them dry, clean feet with soap & water, dry between toes
Mild powder of sweaty feet, wear clean absorbent cotton, exercise feet daily
INTEGUMENTARY COMPLICATIONS
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Dermopathy – lesions, reddish, brown, round or oval patches, scaly, flat, frequently on the shin,
also thighs, forearms, side of the foot & trunk
Acanthosis nigricans manifestation of insulin resistance, velvety light brown to black thickening
INFECTION
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More susceptible to infections d/t mobilization of white blood cells & impaired phagocytosis by
neutrophils & monocytes
Candida albicans, boils & furuncles lead HCP to suspect diabetes
Loss of sensation delay detection of infection
Persistent glycosuria predispose pt to UTI, especially pt with neurogenic bladder
Promote good hand hygiene, avoid exposure to individual with illnesses, get annual flu &
pneumonia vaccine