Ch 67

Diabetes Mellitus (DM)

 Chronic metabolic disease that requires lifelong behavioral and lifestyle changes
 Complications:
o Hypertension
o Hyperlipidemia (high blood lipid levels) Nursing priority  helping pt achieve and maintain
o Can be greatly reduced with glycemic (blood glucose) control lifestyle changes that prevent long-term
complications by keeping blood glucose levels and
along with management of hypertension and hyperlipidemia
cholesterol levels as close to normal as possible
 Leading cause of:
o Blindness
o End stage kidney disease
o Foot/ leg amputations

Diabetes can lead to

 Amputations
 Macrovascular Diseases
 Microvascular Disease
 Kidney damage (microalbuminurea)
PATHOPHYSIOLOGY
Classification  chronic hyperglycemia (high blood glucose level)

 Results from problems with insulin secretion, insulin action, or both

 Failure to synthesize and utilize insulin (cannot use insulin or make insulin) – may be a block

The Endocrine Pancreas

Pancreas

 Exocrine functions  related to digestion

 Endocrine functions  related to blood glucose control
o Islets of Langerhans – approx. 1 million small glands
 Alpha Cells  secrete glucagon
 Beta Cells  produce insulin and amylin

Glucagon

“counter-regulatory” hormone

 Glucagon  Stored in the liver

 Maintains blood sugar levels
 Targets liver to perform glycogenolysis. – Glycogen converted to glucose
 Can give as an IM injection (to prevent hypoglycemia)
 Prevents Hypoglycemia Bcuz it forces liver to release glucose into bloodstream
 Actions opposite of insulin
 Prevents hypoglycemia (low blood sugar) – by triggering the release of glucose from cell
storage sits

Insulin

 Prevents hyperglycemia - by allowing body cells to take up, use, and store carbs, fat, and
protein
 Secreted at low levels during fasting (basal insulin secretion)
 Secreted at increased levels after eating (prandial)

Glucose Homeostasis

 Glucose  main fuel for CNS cells

 Brain cannot produce or store much glucose, needs a continuous supply from circulation to
prevent neuronal dysfunction and cell death
 Glucose – stored in cells as glycogen in liver and muscles
o Free fatty acids stored as triglycerides in fat cells (fat = most efficient means of storing
energy)
 Several organs and hormones play a role in maintaining glucose homeostasis
o Fasting state
 Stomach empty – BG 60-150
 Insulin is like a “key” that opens “locked” membranes to glucose
o Allows glucose in blood to move into cells to generate energy
  Insulin
o Exerts many effects on metabolism and cellular processes in diff body tissues/organs
o Main metabolic function  stimulate glucose uptake in skeletal muscle and heart
muscle to suppress liver production of glucose, and very-low-density lipoprotein (VLDL)

(read more) pg 1412

Absence of Insulin

 Insulin – needed to move glucse into most body tissues

 Lack of insulin prevents somecells from using glucose for energy
o Lack of production or problem with insulin use at its cell receptor
o Prevents cells from using glucose for energy
 Without insulin, glucose builds up in blood  Hyperglycemia
 Hyperglycemia – causes fluid and electrolyte imbalances, leading to classic symtpoms of
diabetes
 1. Polyuria
 2. Polydipsia
 3. Polyphagia
 Polyuria  frequent and excessive urination
o Results from osmotic diuresis caused by excess glucose in urine.
o Diuresis causes:
 Sodium, Potassium, and Chloride – excreted
in urine and water loss is severe
 Dehydration results from this – become
excessively thirsty (Polydipsia)
o When dehydration occurs:
 Hemoconcentration (increased blood
concentration)
 Hypovolemia (decreased blood volume)
 Hyperviscosity (thick, concentrated blood)
 Poor tissue perfusion
 Hypoxia (poor tissue oxygenation) – esp to brain
 Polydipsia  excessive thirst
o Cells do not receive glucose
o Cell starvation triggers excessive eating (polyphagia)
 Polyphagia  excessive eating
o Despite eating vast amts of food, person remains in starvation until insulin is available to
move glucose into cells
o Metabolic Acidosis may occur
 Insulin deficiency - fats break down, release free fatty acids
 Conversion of fatty acids to ketone bodies (small acids) – provide backup energy
  Ketone bodies are abnormal breakdown products of fatty acids - collect in blood
when insulin is not available  Metabolic acidosis
 Excess acids caused by absence of insulin – increase hydrogen ion and carbon dioxide levels in
blood, causing metabolic acidosis
o “Kaussmaul Breathing” occurs  These products trigger resp. centers of brain –
increase rate and depth of resp. in attempt to excrete more carbon dioxide and acid
 Acetone is exhaled  “fruity” odor
o When lungs can no longer offset acidosis – blood ph drops
o Arterial blood gas studies show metabolic acidosis (decreased ph and decreased arterial
bicarbonate) and compensatory respiratory alkalosis (decreased partial pressure of
arterial carbon dioxide)
 Insulin lack initially causes potassium depletion
o Increased fluid loss from hyperglycemia – excessive potassium excreted into urine –
leads to low serum K+ levels
o High serum K+ levels may occur in acidosis (bcuz of shift of K+ from inside the cells to
the blood)
o Serum K+ levels in DM:
 May be low (hypokalemia)
 May be high (hyperkalemia)
 Or normal
*depends on hydration, severity of acidosis, pts response to treatment

Acute Complications of Diabetes

3 glucose related emergencys

1. Diabetic ketoacidosis (DKA)  caused by lack of insulin and ketosis (muscle breakdown)
2. Hyperglycemic-hyperosmolar state (HHS)  caused by
All 3 problems require emergency
insulin deficiency and profound dehydration
treatment and can be fatal if treatment is
3. Hypoglycemia  from too much insulin or too little glucose
delayed or incorrect
Chronic complications of diabetes

 Macrovascular Complications changes in large blood vessels in tissues and organs

o Coronary heart disease
o Cerebrovascular disease “CVA” (stroke) Complications result from poor tissue
o Peripheral vascular disease circulation and cell death

 Microvascular Complications  changes in small

blood vessels in tissues and organs
o Nephropathy (kidney dysfunction)
o Neuropathy (nerve dysfunction)
Main cause  Chronic high blood glucose
o Retinopathy (vision problems) levels

Additional RF

 Smoking
 Physical inactivity
Many can be modified
 Increased body weight
 Hypertension
 Excessive cholesterol and other fats
Macrovascular Complications Macro –
Cardiovascular Disease
1. Cardiovascular disease Increased risk of
MI/Stroke
a. Largely a result of cardiovascular disease (CVD)
b. Most pts die as a result of a thrombotic event – usually MI
i. Albuminuria (albumin in urine)  increased risk for coronary heart disease and
mortality from MI
c. Women effected more than men
d. Ethnicity
e. Rf
i. Obesity
ii. Hypertension Best Way to prevent any
complications  Control
iii. Dyslipidemia
Glycemic Index / Blood
iv. Sedentary lifestyle Sugar
v. Cigarrete smoking
vi. Family history
f. Reduce risk
i. Management of hyperglycemia, hypertension, hyperlipidemia
ii. BP <130/80 mmHg
iii. LDL <100mg/dL (if no manifestations of CVD)
iv. LDL <70mg/dL (with manifestations)
1. Diet low in sat fat
v. Lifestyle modifications to improve lipid profile
1. Reduce sat fat, trans fat, cholesterol intake
2. Increase omega-3 fatty acids
3. Fiber
4. Plant sterols
5. Weight loss (if indicated)
6. Increased physical activity

Priority Nursing actions  reduce modifiable Risk Factors associated with CVD

 Smoking cessation
 Diet & exercise
Cigarette smoking and family history –
 Blood pressure control great risk for CV
 Maintenance of prescribed aspirin use
 Maintenance of prescribed lipid-lowering drug therapy

2. Cerebrovascular Disease “CVD” (stroke)

a. 2-4x high risk of stroke for ppl with DM
b. DM – at risk for severe carotid atherosclerosis
c. Risk factors for CVD
i. hypertension
ii. hyperlipidemia Chronic hyperglycemia with microvascular disease
may contribute to:
iii. nephropathy
 Neuronal damage
 Brain atrophy
 Cognitive impairment
 iv. peripheral vascular disease (PVD)
v. alcohol and tobacco
d. stroke outcomes
i. irreversible brain damage with carotid emboli
ii. brain injury and higher mortality if glucose level is high at time of attack

Microvascular Complications

1. Eye and Vision Complications

a. Legal blindness (25x more common in diabetes)
b. Diabetic retinopathy (DR)
i. After 20yrs of DM – retinopathy usually occurs
2. Diabetic Neuropathy
a. Progressive deterioration of nerves that results in loss of nerve function
b. Damage to sensory nerve fibers – pain or loss of ssenation
c. Damage to motor nerve fibers – muscle weakness
d. Damage to autonomic nerve fibers –dysfunction in every part of body
e. Diffuse neuropathies  Most common neuropathy
i. Widespread nerve function loss
ii. Slow onset
iii. Affect both sides of body
iv. Motor and sensory nerves affected
v. Permanent
vi. Complications : foot ulcers and deformitites
f. Focal neuropathies
i. Single nerve
ii. Acute ischemic event or nerve trapping
iii. Begin suddenly
iv. One side of body
v. Most commonly effects eye muscles – double vision
vi. Resolves in 2-3 months
g. Cardiovascular autonomic neuropathy (CAN)  affects sympathetic / parasympathetic
nerves of heart / blood vessels
i. s/s – orthostatic hypertension, syncope (brief loss of consciousness on standing)
ii. increase risk for falls
h. autonomic neuropathy
i. affect entire GI system
1. gastroesophageal reflex
2. delayed gastric empting
3. gastric retention
4. early satiety
5. heartburn
6. nasusea
7. vomiting
8. anorexia
 9. gastroparesis –delay in gastric emptying) – caused by hypoglycemia
3. Diabetic Nephropathy
a. Pathologic change in kidney that reduces kidney function and leads to kidney failure
b. Diabetes is leading cause of end-stage kidney disease (ESKD) and kidney failure
c. Risk factors
i. 10-15yrs of DM
ii. Diabetic retinopathy
iii. Poor blood glucose control
iv. Uncontrolled hypertension
v. Genetic predisposition
d. Prevention – delay by maintain optimum blood glucose control, BP control, drug therapy
to protect kidneys
i. Drugs  Angiotensin-Converting Enzyme (ACE) inhibitors / Angiotensin
receptor blockers (ARBs)
e. Microalbuminuria (small amts of albumin in the urine)  Earliest manifestation of
nephropathy
i. Indicates kidneys are damaged (Bad!!)
4. Male Erectile Dysfunction
Etiology and Genetic Risk

Type 1 Diabetes

 Autoimmune disorder
 Beta cells destroyed
 Immune system fails to recognize normal body cells as “self”
 Immune system cells, mediators, and antibodies  attack and destroy insulin-secreting cells in
the islets
o Islet cell antibodies (ICAs)
o Insulin autoantibodies (IAAs)
o Glutamic acid decarboxylase antibodies (GAD)
o Tyrosine phosphates autoantibodies
 No interventions are successful in preventing type 1
o Health promotion  controlling hyperglycemia to reduce its long term complications

Type 2 Diabetes

 Progressive disorder in which the person has a combination of insulin resistance and decreased
secretion of insulin by pancreateic beta cells
 Insulin resistance develosp from obesity and physical inactivity in a genetically susceptible
person
 Often accompanied by CV risk factors:
o Hyperlipidemia
o Hypertension
o Increased clot formation
 Most type 2 patients are obese
 Heredity – plays a major role in development of type 2 Diabetes
o Offspring – 15% risk of inheritance / 30% risk of impaired glucose tolerance
 Metabolic Syndrome “Syndrome X”  metabolic RF for Type 2 and CV disease
o Abdominal obesity
o Hyperglycemia
o Hypertension (130/85 or higher)
o Hyperlipidemia (triglycerides >150mg/dL / HDL less than 40 (men) or 50 (women)
*Any of these increase rate of atherosclerosis and risk for stoke, Coronary Heart
Disease, and early death
o Lifestyle changes:
 Reduce weight BMI <25
 Drug therapy for BP and cholesterol
Incidence / Prevalence

 Prediabetes  impaired fasting glucose / impaired glucose tolerance

o 5 fold to 15 fold high risk for type 2
o Associated with obesity (esp abdominal or central), dyslipidemia with high triglycerides,
low HDL cholesterol, hypertension
 90% of diabetes is type 2
 Increased risk for Type 2
o Middle aged / older adults
o African Americans
o Mexican Americans
o Higher for men than women
o Obesity / increased BMI
 Reduced risk
o Physical activity and Eating habits (reduced calories from fat) that result in weight loss
 Diabetes  7th leading cause of death in United States

S/S (type 1 and 2)

 Fatigue
 Polyuria
 polydipsia
 HEALTH PROMOTION AND MAINTENANCE

Type 1

No interventions are successful in preventing type 1 DM

Health promotion  controlling hyperglycemia to reduce its long term complications

Type 2

 Low calorie diet that results it weight loss

 Increasing physical activity – improves metabolic and cardiac factors
o Reduces HTN
o Increase heart rate variability betwn resting rate and exercise rate
o Lowering triglyceride levels
Reduces risk of Type 2 diabetes by
o Increasing HDL (“good cholesterol”)
58%
o Reducing LDL (“bad cholesterol”)

Both types

 Tight control of blood glucose levels can prevent many complications

 Regular follow ups with health care provider or endocrinologist
 Eyes and vision tested yearly
 Urine microalbumin levels tested yearly
Cultural Awareness

 AA
 American Indians
 Mexican Americans
 Microvascular complications of eyes, nerves, and kidneys  more common in AA and American
Indians with diabetes than in non-Hispanic white with diabetes
 Patient Centered Collaborative Care

Assessment/History

Ask about risk factors and symptoms

 Gestational diabetes - Ask women how large their children were at rbirth (type 2 – babys 9lbs or
more)
 Weight changes
o Type 1 - weight loss with increased appetite
o Type 2 - excess weight and obesity
 Both types – Assess for:
o Fatigue
o Polyuria
o Polydipsia
o Ask about infections
o Ask women about frequent vaginal yeast infection
o Small skin injuries becoming infected easier?
o Changes in vision / sense of tough

Laboratory Assessment

Diagnosis of Diabetes
Unlike fasting blood glucose test, HbA1c is
Diagnosis  Assess blood glucose levels not altered by eating habits the day
before the test
1. Glycosylated Hemoglobin A1C (HbA1c)  measures how much
glucose permanently attaches to a specific area of hemoglobin
molecule
a. Not affected by eating habits the day before the test
b. This is how the doctor knows if pt is cheating on meals. Tells you what the blood sugar
was for last 120 days.
c. Keep below 7. (5 is good)
2. Fasting plasma glucose (FPG)  diagnose diabetes in nonpregnant adults
a. No caloric intake for at least 8 hrs (water permitted)
b. No insulin / oran antidiabetic agents taken
c. Diagnosis made with 2 separate test results ( greater than 126)
d. Random or casual plasma glucose (greater than 200)  for pts with severe classic
hyperglycemia or hyperglycemic crisis
3. Oral Glucose Tolerance Testing (OGTT)
a. Most sensitive tset for diagnosis of diabetes
b. Not routinely used - inconvenient, costly, time consuming
c. Used for diagnosis of gestational diabetes
d. Drink glucose load beverage – blood samples collected at hourly intervals
 4. Other blood tests
a. Help determine between type 1 and type 2
b. Type 1 – autoimmune with presence of autoantibodies to proteins
c. Presence of islet cell antibodies – indicator for type 1

Blood Glucose Testing

Screening for Diabetes

 Type 1 – measurement of islet cell antibodies Tests – Hemoglobin A1C / fasting

 Prediabetes & Type 2 – pts older than 45 / obese (BMI glucose
>25)

Ongoing Assessment: Pg 1420

Urine Tests

Ketone Bodies (product of fat metabolism)

KetoAcidosis  Muscles are breaking
 Measure ketones in urine to detect Ketoacidosis (muscle off
breakdown)
 Newly diagnosed with diabetes – measure ketones in urine
with a dipstick.
 Hyperketonuria  presence of ketones in urine
o Indicates severe lack of insulin
o With hyperglycemia  medical emergency
 When to do the test:
o In the Morning before breakfast
o Acute illness or stress
o Consistently high Blood glucose levels (over 300) (may be spilling in the urine)
o Pregnancy
o Ketoacidosis symptoms present
o Diabetes pt trying to lose weight
Test for kidney function

 Diabetes can damage kidneys

 Check for Microalbuminuria – protein in the urine (albumin excretions of 20-200mg/min)
o May indicate kidney damage from diabetes
 Presence of urine protein without kidney symptoms  microvascular changes in kidney (kidney
damage)
 Minor elevations of albumin are associated with increased mortality
 May need dialysis –many pts on dialysis is because of kidney damage from diabetes

Urine glucose testing

 Less precise than blood glucose testing

 Fluid intake, urine elimination patterns, drugs – affect the results
 Should not be used for monitoring diabetes

ANALYSIS

Priority problems for pts with diabetes

 Injury (related to hyperglycemia and neuropathy, retinopathy)

 Impaired wound healing (endocrine and vacular effects)
 Pain (related to neuropathy)
 Kidney disease (impaired renal circulation)
 Hypoglycemia
 Diabetic ketoacidosis
 Hyperglycemic-hyperosmolar state and coma
 NON – SURGICAL MANAGEMENT FOR DIABETES

Drug therapy

Nutrition therapy

Exercise therapy

Blood Glucose Control in Hospitals

 PLANNING AND IMPLEMENTATION

Preventing Injury from Hyperglycemia

Most important  Manage blood glucose
Planning  Maintain blood glucose levels
levels!!
Interventions – Nonsurgical Management

 Type 1 – insulin therapy

 Type 2 – when diet, exercise, and stress management do not work

Drugs – start at lowest effective dose and increase every 1-2 wks or until reached maximum levels

 If max is reached with no help, then second agent may be added **Antidiabetic drugs are not a substitute
 Type 2- insulin therapy may be used in 2 or 3 diff Antidiabetic agents for dietary modification and exercise!!
cannot control blood glucose

Short acting drugs (e.g. Glizapizide)

 Older pts
 Irregular eating schedules
 Liver, kidney, cardiac function problems

Long Acting Drugs (e.g. Glyburide, Glimepiride)

 Once daily dosing – better for adherence

 Type2 – beta cell function often declines over time, reducing effectiveness of some rugs. Treatment for
type 2 may eventually reqire insulin therapy alone or with drugs
 Drug Therapy: Antidiabetic Drugs

*when dietary control doesn’t work

Some are oral, some are sub1 injections

1. Insulin Secretagogues
a. Stimulate pancreatic beta cells – for pts who can still produce insulin
2. Sulfonylurea Agents
a. Oral
b. E.g. Glipizide (Glucotrol)
c. Lower fasting plasma glucose – triggers insulin from beta cells
d. At risk for hypoglycemia
e. Side effects: weight gain, hypoglycemia (esp. older adults with CV, liver, kidney impairment)
3. Meglitinide Analogs
a. Classification – insulin secretagogues
b. Actions/adverse effects – similar to sulfonylureas
c. Lower by 1.5% pts
d. E.g. Repaglinide (Prandin)
i. Take before meals
ii. Rapid onset
iii. Limited duration of action
iv. Used to both treat fasting & after meal hyperglycemia
v. Adverse effects:
1. Hypoglycemia
2. GI disturbances
3. Upper resp injections
4. Joint and back pain
5. headache
e. Nateglinide (Starlix)
i. Rapidly absorbed
ii. Stimulates insulin secretion within 20 min
iii. Taken before meals to control mealtime hyperglycemia
iv. Improves overall glycemic control in pts with Type 2
v. Adverse effect  Hypoglycemia
vi. Pts who skip meals – skip scheduled dose (hypoglycemia risk)
f. Rapidly absorbed / short duration of action
g. Lower HBa1c levels
4. Insulin Sensitizers
a. Biguanidies
i. Not at risk for hypoglycemia if taken
alone. If mixed with sulfonylureas –
pt will be at risk for hypoglycemia
ii. Metformin (Glucophage)
iii. Does not increase insulin secretion
 iv. Decreases liver glucose production, thereby reducing fasting plasma glucose release,
and improves insulin receptor sensitivity
v. Initial therapy for type 2 DM – does not induce weight gain or hypoglycemia,
relatively low cost, few adverse effects
vi. Pt not at risk for hyp0glycemia – unless medication is mixed with sulfonylurea
vii. Contraindicated with persons with kidney disease, elevated blood creatinine levels,
viii. Withhold drug for 48 hrs. before and after using contrast material / surgical
produces requiring anesthesia
ix. Lowers HbA1c levels by 1.5% pts
x. Take with meals to reduce GI effects
xi. Side effects
1. Abdominal discomfort and diarrhea  most common
2. Lactic acidosis – pts with kidney problems
3. Increased risk for lactic acidosis
a. hypoxemia,
b. dehydration,
c. sepsis
d. alcohol
4. Report if: fatigue, unusual muscle pain, difficulty breathing, unusual /
unexpected stomach discomfort, dizziness, lightheadedness, irregular
heartbeats
5. Do not use with conditions that decrease drug clearance
a. Liver disease
b. Alcoholism
c. Severe congestive heart failure
d. Older than 80yo
b. Thiazolidinediones (TZDs)
i. Pioglitazone (Actos)
ii. Rosiglitazone (Avandia)
1. Increase risk for hear
related deaths, bone
fracture, macular edema
2. Contraindicated in pts with symptomatic heart failure
3. Black bod warning
4. Causes / exacerbates congestive heart failure in some pts
a. Monitor for s/s of heart failure (excessive rapid weight gain, diff
breathing, swelling)
b. Discontinue if s/s and manage heart Black box warning – gov designation indicating the
failure drug has at least one serious side effect

iii. Reduce blood lipid levels

iv. Side effects
1. Increase in adipose tissue and fluid retention
2. Weight gain
3. Edema with development of congestive heart failure (rare)
 v. Do periodic liver function studies – potential for liver damage
vi. Increase in fracture of upper arms, hands, feet in women
vii. Lower HbA1c by 0.5 – 1.4% pts
viii. bind to regulatory proteins that regulate glucose and fat metabolism
ix. increase cellular utilation of glucose which lowers blood glucose levels
5. Alpha Glucosidase Inhibitors
a. Prevent after meal hyperglycemia
b. Delay absorption of carbohydrates from small intestines
c. Prevents sudden glucose surge after meals
d. Lower HbA1c levels by 0.5-0.8% pts
e. Do not cause hypoglycemia unless given with sulfonylureas or insulin
f. Pt teaching : use oral glucose tablets, glucose gel, or low fat milk to mange hypoglycemia
g. s/e:
i. flatulence
ii. diarrhea
iii. abdominal discomfort
h. Acarbose (Precose)
i. Delays rather than prevents glucose absorption
ii. Does not cause weight loss
iii. Start at low dose and increase slowly
iv.
i. Miglitool (Glyset)
i. Take 3x/day with first bite of each main meal
6. Incretin Mimetics
7. DPP-4 Inhibitors
8. Amylin Analogs
9. Combination Agents
 Insulin Therapy

Insulin  small protein that is quickly

*used for type 1 digested and inactive in GI tract, it
*May also be needed for type 2 must be administered as an injection
or by another route that bypasses the
Patient teaching  Rotate sites, store insulin in GI tract
refrigerator, roll it in your hands to warm it up. Teach pt
to change needle every time.

1. Types on insulin

Lipodystrophy – spongy then become

2. Factors influencing insulin absorption
hard??
a. Injection site
i. Rotate injection sites to prevent:
1. Lipohypertrophy (increased fat deposits in the skin)
2. LipoAtrohpy (loss of fatty tissue, leaving an uneven appearance)
ii. Rotation within one anatomic site is preferred
iii. Preferred spot  Abdomen
1. Avoid 2 inch radius around naval (umbilicus)
b. Absorption rate
i. Increase insulin absorption with increased blood flow
1. Local heat application
2. Massage area
3. Exercise injected area
ii. Scarred sites – less painful but less absorption
iii. Longer duration of action – unpredictable absorption
 c. Injection depth
i. Subq injection. Grasp forld of skin and inject at 90degree angle. Aspiration for
blood not needed (subq). Thin pt – pinch skin and inject at 45degree angle to
avoid accidental IM injection
d. Timing of injection
i. GET FROM DONIKAS NOTES
e. Mixing insulin’s
i. When rapid acting (Humalog or Novolog) or short acting (regular) insulin is mixed
with a longer acting insulin, draw the shorter acting dose in to the syringe first
1. Prevents contamination of shorter acting insulin vial with the longer
acting insulin
2. Short acting and NPH insulins may be used immediately after mixed or
stored away
3. Mixing clouds the solution and makes the onset of action and peak
effect time less predictable
3. Complications of insulin therapy
a. Dawn Phenomenon  results from nighttime release of growth hormone that causes
blood glucose elevations at about 5-6am
i. Managed by providing more insulin for overnight period (e.g. giving evening
dose of intermediate acting insulin at 10pm)
b. Somogyi Phenomenon  morning hyperglycemia from the counter regulatory
response to night time hypoglycemia
i. Managed by ensuring adequate dietary intake at bedtime and evaluating the
insulin dose and exercise programs to prevent conditions that lead to
hypoglycemia
c. *both problems are diagnosed by blood glucose monitoring during the night
4. Alternative methods of insulin administration
a. Continuous subcutaneous infusion
i. More effectivie then
ii. Externally worn pump continaing a syringe and reservoir with rapid acting
insulin – connected to pt by infusion set
iii. Adjust the amt of insulin based on data from blood glucose monitoring
iv. Problems : risk for skin infection
1. Ketoacidosis – inexperience in pump use
2. Hypo/hyperglycemia
b. Injection devices
i. Needless system (ultra thin illiquid stream of insulin forced through skin under
high pressure)
ii. Pen-type injector
Pt education: Drugs

a. Insulin storage
iii. Varies by use
iv. Teach pt to refrigerate insulin that is not in use to maintain potency, prevent exposure to
sunlight, and inhibit bacterial growth.
v. Insulin in use – may be kept at room temp up to 28 days (reduces irritation caused by cold
insulin)
1. Insulin glargine (Lantus) should be stored in a refrigerator even when in use.
Discard any unusued insulin after 28 days
vi. To prevent loss of potency
1. Avoid temps below 36F or above 86F, avoid excessive shaking, and protect insulin
from direct heat and light. Do not allow insulin to freeze.
2. Roll prefilled syringes between hands before using
b. Dose preparation
vii. Inspect insulin for changes  may indicate loss of potency
1. Clumping, frosting, precipitation, change in clarity or color
viii. Rapid acting, short acting, Glargine insulins (Lantus)  should be clear
ix. All other types  uniformly cloudy after gently rolling between hands
c. Syringes
x. Disposable needles - use 1x only
1. Reusing needles  compromise insulin sterility / diabetes pts – at risk for
infection
xi. Do no reuse smaller needle (30-31gauge) -needle tip may become bent to form a hook,
which can lacerate tissue or break off and leave fragments in skin

Pt education – blood glucose monitoring – 1437-1438

c. Accuracy of blood glucose monitor

d. Frequency of testing
e. Target goals
f. Infection control
g. Alternate site tesing
h. Ciontinuous blood glucose monitoring
 Nutrition therapy

 Nutrition Goals
o Maintain Blood glucose
o Blood lipid profile
o Blood pressure
o Prevent/slow rate of development of chronic complications
 Principles of Nutrition in Diabetes
o Carbohydrates  at least 130g/ day
 Fruits, vegetables, whole grains, legumes, low fat milk
 Amt of carbs consumed have the greatest impact on after meal (postprandial) blood
glucose levels
o Fat / Cholesterol 
 Sat fat < 7% total calories Trans fat increase LDL and decrease HDL (CV
 Minimize trans fat disease risk)
 Cholesterol <200mg/day e.g. margarine, fried food in hydrogenate oils
 2 or more servings of fish / week
o Protein  15-20% calories
 Microalbuminuria – reduce to 10%
o Fiber  25g/day
 Improves carbohydrate metabolism / lowers cholesterol levels
 Legumes, fiber-rich cereals, fruits, Veggies, whole grain products
 Adding fiber – may reduce abdominal cramping, loose stools, flatulence
o Sweeteners  does not need to be restricted (e.g. sucrose)
o Alcohol  effects blood glucose levels
 Moderate is okay
 2 more men / 1 for women

*because of potential for alcohol-induced hypoglycemia, instruct pt with diabetes to ingest alcohol only
with or shortly after meals

Special considerations for Type 1

 develop insulin regimens that conform to pts preferred meal routines, preferences, and exercise
patterns
 Monitor before and 2 hours after meals to determine if insulin to carbohydrate ratio is correct
 Physical Exercise
o Physical exercise can cause hypoglycemia if insulin is not decreased before activity
o Planned exercise – reduce insulin dosage
o Unplanned exercise – additional intake of CHO usually needed

Special Considerations for Type 2

  Focus on lifestyle changes
 Many are overweight and insulin resistant
 Lifestyle changes that reduce calories eaten and increase calories expended through physical
activity
 Moderate caloric restriction & increase in physical activity  improve diabetic control and
weight control

 Exercise Therapy

 Exercise does not result in hyper or hypoglycemia

 Type 1 – pt cannot make hormonal changes needed to maintain stable blood glucose levels during
exercise
 Exercise can cause hypoglycemia because of increased muscle glucose uptake and inhibited glucose
release from liver
o Can offur during exercise and up to 24hrs

Benefits of Exercise

Type 1

 Results in better regulation of BG levels and lowering of insulin requirements

 Decreases risks for CV disease
 Decreases lipid levels and increases HDLs
 Decreased BP and improves CV function

Type 2

 Regular vigorous activity prevents/delays type 2 by reducing body weight, insulin resistance,
glucose tolerance

Adjustments for Diabetes Complications

 Vigorous exercise contraindicated in

o proliferative retinopathy
o Severe non-proliferative retinopathy
 Retinopathy
o Avoid activities that increase BP
 E.g. “Valsalva maneuverer” (holding breath while bearing down)
o At risk for vitreous hemorrhage / retinal detachment:
 Heavy lifting, rapid head motion, jarring activates
 Peripheral neuropathy
o Decreased pain sensation – increased risk for skin breakdown/injection/ joint
destruction
 Pt teaching : if foot injury or open sore 0 engage in non-weight bearing activities
(e.g. swimming, bicycling, arm exercises)
 Autonomic neuropathy  increased risk for:
o Exercise induced injury from impaired temp control
o Postural hypotension
o Impaired thirst – risk for dehydration
 Physical activity may increase urine protein excretion
 Start with short periods of low intensity exercise and increase slowly

Safety Assessment
  Exercise increases risk musculoskeletal injury and life-threatening cardiovascular events – screen
before exercise
 Benefits of exercise are short term
 Type 2 – resistance exercise 3x/wk
 No more than 2 consecutive days missed
 Exercise guidelines based on glucose and ketone levels
o Test glucose levels before, during, and after working out
o When urine ketones are present – no exercise
 Eat carbs before exercises to raise glucose levels above 100mg/dL
o Type 1 – vigorous exercise only if:
 glucose 100-250mg/dL
 no ketones present

Patient Education: Exercise Promotion

 wear shoes with good traction and cushioning

 examine feet daily and after exercise
 no exercise in extreme heat/hold
 no exercise during periods of poor blood
glucose control
 stay hydrated esp during and after exercise in
warm environment
 no exercise within 1 hr of insulin injection /
peak time of insulin action
o exercise increases absorption of insulin
 risk for hypoglycemia when exercising
injected body part
 Prevent hypoglycemia
 Wear identification

Preventing Hypoglycemia

 Snacks containing rapidly absorbable carbs before and during exercise (1hr before if not eaten yet)
 Eat snacks 1 hr before exercise and during exercise
 Need glucose to be at least 100mg/dL
 Extra carbs for 24 hrs after exercise
 Decrease insulin dosage before exercise
 Additional 15-30g carbs for every 30-60min exercise
o E.g. fruit, fruit juice, bread, whole milk
 Simple sugar (e.g. hard candy)
Blood Glucose Control in Hospitalized Patients

 Causes of hyperglycemia
o “Stress hyperglycemia” Hypoglycemia  <40mg/dL
o Illness
Hyperglyceima >198?
o Decreased physical activity
o Withholding antidiabetic drugs
o Drugs that cause hyperglycemia (e.g. corticosteroids)
o Inititain of tube feeds
o Parenteral nutrition
 At risk for
o Infection
o Longer hospital stays
o Increased need for Intensive care
o Greater mortality
o Glucose greater than 200 after cardiothoracic surgery  increased risk for wound
infection
o Glucose greater than 198  greater risk for mortality and complications
 Hypoglycemia - @ risk for mortality
 Maintain blood glucose
o Critically ill pts  140-180mg/dL
o Premeal  less than 140mg
o Random  less than 180
o Prevent hypoglycemia
 Examine insulin regimen if under 100mg/dL
 Modify if under 70mg/dL
 Hypoglycemia in Hospitals
o Causes:
 Inappropriate insulin type
 Mismatch btwn insulin type/ timing of nutritional intake
 Altered nutritional intake without insulin dosage
o Treatment
 Provide carb replacement if pt is alert and can swallow
 administer 50%dextrose IV (D50)
 glucagon Subq (if cannot swallow)
o If pt is NPO
 Give Basal insulin  treats baseline glucose levels
 No rapid/short acting insulin, amylin, or incretin mimetics  causes
hypoglycemia
 No insulin mixtures – may contain short or long acting insulin – causes
hypoglycemia
 Surgical Management

a. Whole Pancreas Transplantation

b. Islet Cell Transplantation

Surgical treatment  Pancreas Transplant

 Can elimate acuate complications, but only partially successful in reversing longterm
diabetes complications
 Pancreas transplant is successful when pt no longer needs inulin therapy and all blood
measures of glucose are normal
 Requires lifelong drug therapy to prevent graft rejection
o Toxic side effects (some raise blood glucose levels)
 Pancreas –alone transplant (PTA) Considered for:
o Severe metabolic complications
o Clinical and emotional problems with insulin
 Pancreas transplant considered for:
o Consistant failure of insulin-based therapy to prevent acute complications
o Pts with diabetes and end-stage kidney disease who have had / plan to have kidney
transplant

Whole Pancreas Transplantation

3 ways:

- Pancreas alone (PTA)

- Pancreas after kidney transplant (PAK)
- Simultaneous pancereas and kidney transplant (SPK) – (ideal procedure for pts with DM and
uremia)

a. Operative procedure
a. Recipants pancreas left in plance
b. Donated pancreas placed in pelvis
b. Rejection management
a. Combination of drugs and antibodes used to revese rejection
b. In most cases of rejection – kidney problems occur before pancreatic problems
c. Increase in serum creatinine  Indicates rejection of both the transplanted kidney and
pancreas
d. Pts with bladder drainage of pancreatic hormones 0- decrease in urine amylase level by
25%  indication to treat rejection
e. High blood glucose levels  late marker of rejection
i. Usually indicates irreversible graft failure
c. Long Term Effects
a. Long term antirejection therapy risks:
 i. Increased risk for infection, cancer, and atherosclerosis
d. Complications
a. Common in pts with long term rejection meds
b. Monitor
i. Lab values
ii. Fluid and electrolyte status
iii. Physical changes
iv. Changes in vital signs
c. Prevent infection
i. Early removal of IV and intra-arterial lines
ii. Sterile technique with dressing changes
iii. Catheter irrigations
iv. Strict hand washing
v. Good pulmonary hygiene
d. Complications immediately after surgery:
i. Thrombosis (30% of pts)
ii. Pancreatitis
iii. Anastomosis lead with infection
iv. Rejection of transplanted pancreas
e. Report:
i. Sudden drop in urine amylase levels
Pancreatitis – occurs to some degree
ii. Rapid increases in blood glucose
in all pts after surgery
iii. Gross hematuria (bloody urine)
iv. Tenderness/pain in graft area (iliac fossa) Report elevation in serum amylase
f. Most serious complication of enteric-drained pancreas that persist after 48-96hrs
transplant  leading and intra-abdominal abscess
i. Resport elevated temp, abdominal
discomfort, elevated WBCf count
ii. Bladder drained pancreas- lower rate of abscess formation
g. Acute Rejection , decreased kidney function indicated by:
i. Increased serum creatinine
ii. Decreased urine output
iii. Hypertenstion
iv. Increased weight
v. Graft tenderness
vi. Fever
h. Chronic graft rejection
i. First indication  proteinuria
1. Check for increased blood amylase, lipase, or glucose
2. Decreased urina amylase
3. Graft tenderness
4. Hyperglycemia
5. Fever
 *it is esp important to assess signs off infection and start appropriate therapy., fever can
indicate both infection and rejection.

i. Side effects of anti-rejection drugs

i. Cyclosporine (neural) – toxic to kidney
1. s/s: elevated creatinine / decreased urine output
ii. azathioprine (Imuran) – may suppress bone marrow function
1. monitor WBC counts daily
iii. Predisone - Elevated blood glucose
iv. Tacrolimus (Prograf)
1. Hypertension
2. Kidney toxicity
3. Neurotoxicity
4. GI toxicity
5. Glucose intolerance
*may need insulin injections for hyperglycemia caused by antirejection drugs

Islet Cell Transplantation

- Eliminates need for insulin

- Protects against complications of diabetes
- Type 1 diabetes
o May successfully restore long term endogenous insulin production and glycemic control
- Most pts have progressive loss of islet cell function over time
- Very few islet cell transplant recipients have remained insulin free for over 4 yrs
 Enhancing Surgical Recovery

a. Planning: Expected Outcomes

a. Wound healing
b. No infection
c. Maintain glucose levels
d. Discharge rediness
b. Interventions
a. Preop care
i. Admitted 2-3 days before surgery \
ii. Second generation sulfonylureas discontinued 1 day before surgery
iii. Metformin (Glucophage) stopped 48hrs before surgery – restarted after kidney
function is normal
iv. All other drugs – stopped day of surgery
v. Long acting insulin pts - switch to intermediate acting 1-2 days before surgery
vi. Blood glucose levels – 200mg/dL
1. High levels – may cause neutrophil dysfunction, increased infection
rates, and impair wound healing
vii. Plan ahead for pain control
1. Pain (stressor) – triggers release of counter-regulatory hormones,
increasing glucose levels and insulin needs
2. Opioid analgesics- slow GI motility , alter glucose levels
a. Older pts – at risk for confusion, paralytic ileus, hypoventilation,
hypotension, urinary retention
b. Pt controlled analgesia (PCA) – reduce resp complications and
confusion
b. Intraop care
i. Standard therapy:
1. Iv infusion of insulin, glucose, potassium
2. Keeps glucose btwn 140-180
a. Under 180 – reduces risk for wound infection
ii. Monitor temp
c. Postopcare
i. Hyperglycemia – increased risk for motality/morbidity
ii. Maintain btwn 140-180 for critically ill pts
iii. Short term insulin teraphy may be needed for pts who usually take oral agents
iv.
c. Monitoring
 Beta blockers for HTN mask s/s for hypoglycemia
 Azotemia (increased protein/nitrogen in blood) – may have fluid management problems
o Check central venous pressure/pulmonary artery pressure
 Hyperglycemia can occur before a fever
a. Cardiovascular monitoring
i. ECG – for type 1 diabetes pts / heart disease pts
ii. DM pts – higher risk for MI after surgery w/ higher mortality rate
 iii. Changes in ECG or K+ levels  may indicate silent MI
b. Kidney monitoring
i. Diagnosis of Kidney impairment – use of xray studies using dye
1. May be nephrotoxic (may need nephrotoxic antibodies)
2. Ensure adequate hydration
ii. observe fluid and electrolyte balance for impending kidney failure
d. Nutritional Care
a. Clear/full liquid diets
i. Need 200g of carbs daily
ii. Liquids should not be sugar free
b. Tube feeding pts
i. Standard formula (50%carbohydrate), or
ii. Lower-carbohydrate formula (33-40%carbs)
c. Food intake initiated asap after surgery
i. Pts need at least 150-200g Carbs daily to prevent hypoglycemia
d. TPN – may cause severe metabolic changes
i. Hyperglycemia will occur with TPn therapy
ii. Monitor glucose often – may need short acting insulin
 Preventing Injury from Peripheral Neuropathy – pg 1445-1448

Planning: Expected Outcomes

 Follow preventative foot care, inspects feet daily, proper shoes, no bare feet, trims toenails
properly, resport non-healing breaks in skin

Interventions: common complication is food injury. Need teacking. Amputations are preceded and
extension. Claw toe: toes hyperextended. Thinning fat pad leads to decreased cushinioning and
increased pressure areas. CHorcot foot: hallux valgus (inverted toe), warm, wollen, painful,m rocker
bottom shape

*loss of skin temp regulation and normal weating = dry tin skin. Cracks are risk for infection. Numb and
reduced sensation-doesn’t notice injury. Reduced blood flow = risk for ulcer, reduced healing. Infection
impairs glucose control=higher glucose level and reduced immunity=increased risk of infection

Prevention: keep glucose levels normal. Stop smoking. Evaluate feet annually

Foot exam: test monofilament against cheek so they know what to expect, test site, use smooth not
jabbing motion at right angle, 1-2 seconds each. Don’t test ulcer, callus, scar or reapeat contact

Don’t wear shoes for longer than 2 hrs at a time, avoid extreme temps, test water temp when doing
dishes, use potholeders, don’t eat “steaming hot” food – allow to cool, foods high in fiber, drink 2-3L of
water, sit if dizzy, look at feet/ground when walking, avoid rugs, use hand rails

Footwear: should be ½-5/8” longer than longest toe. Heels less than 2”. Ight shoes damage tissue in
4hrs. change shoes midday and at night. Socks:” soft, no seams, holes. Avoid constricting bands. Buy
custom shoes with high, wide toe bodes and extra depth. Charcot feet need molded shoes. Need
frequent inspection for irrituation or blistering. Trim with nail clippers and emery board, don’t use
adhesive tape, don’t treat blister at home, never use heating pads to warm feet, don’t go barefoot,
don’t use really hot or really cold water, don’t wear sandals, don’t cross legs or wear tight stockings,
don’t soak your feet.

Footcare: teach to inspect feet daily, between toes. Wash with lukewarm water, dry thoroughly. Apply
moisturizer but not between toes. Blean cotton socks daily. Don’t wear same pair of shoes 2 days in a
row- made breatheable material. Check shoes for foreign objects, cracks. Buy shoes later in the day
when feet normally larger, keep feet warm.

Wound care: if ulcers; moist environment, debridement, and elimination of pressure. Antiseptics:
providone iodine, hydrogen peroxide, chlorhexidine interfere with healing. Don’t wear shoes on affected
food. Use custom-molded shoe inserts. Offloading redistributes force away from ulcers. Total contact
casts redistribute, reducing vertical force. Removed 24-48hrs and reapplied weekly until ulcer is healed.
Growth factor also applied to wound.

Teach that ulcers will recur unless weight is permanently redistributed

Managing Pain

 Outcome: Pain relief. Using preventative measures, resources to increase comfort, reports pain
controlled
 Interventions : symptoms: burning, cramping, stabbing pain, metatarsalgia (walking on
marbles), hyperalgesia (painful response), tingling, numbness
 Maintain glucose levels to prevent neuropathic pain
 Give anticonvulsants: gabapentin and pregablin and serotonin-norepinephrine reuptake
inhibitor Duloxetine
 Antidepressants not approved
 Burning respond to capsaicin cream
 Teach to apply 4x/day
 Pain worsens before it improves
 Avoid abrupt discontinuation, must wean off
 Use bed cradle to lift linenet off hypersensitive skin
Preventing Injury from Reduced Vision

 Planning: Expected outcomes: no further reduction of vision fields, no double vision

 Interventions
o Blood glucose control
o Regular eye exams
o Assess remaining vision
o Get proper prescription
o Can get magnifiers, talking calculators, adjust lighting. Place dark equipment against
light background. Code vials with bright colors. Bring insulin lancet closer to eye to see
better. Use large or bold type for reading. Prefilled insulin pens not recommended
unless have magnifiers. Use count a dose insulin mearing device: draws insulin by using
thumb wheel w clicks heart and felt
o Must differentiate fast and slow acting bottles with rubber band around fast acting

Reducing Risk for Kidney Disease

 Planning: Expected Outcomes :urine protein WNL, 24hr intake-output balance, BUN and
creatinine WNL, electrolytes WNL
 Interventions:
o Prevention – ESRD can be delayed with normal bp, correcting hyperlipidemia, restricting
protein
o GFT and creatinine measured annually
o Excreting 30-299 mg of albumin daily = kidney disease. To screen: random collection
(recommended), 24hr collection, timed collection
o Teach that bp and glucose levels affect kidney function
o Smoking accelerates deterioration
o For UTIs teach to take antibiotics for entire course of treatment
o Need follow up cultures for maintenance, avoid indwelling catheters
o Avoid nephrotoxic agents: Ibuprofen (advil) or naproxen (aleve). Monitor IV hydration
pre and psot contrast administration
 Drug therapy ACE & ARB’s  reduce progression but do not prevent. Monitor for hyperK+
 Nutrition therapy  restrict protein to 0.8g/kg of weight daily./ once GFR declines, reducing
protein helps slow progression
 Fluid and electrolyte management  avoid dehydration0diuretics is most common cause.
Assess fluid balance. Teach to report edema and orthostatic hypotension. Dosage of insulin
adjusted when starting dialysis
Preventing Hypoglycemia

 Hytpoglycemia aka Whipples triad  manifestations of low blood glucose, low plasma glucose
concentration, resolution of manifestation when glucose raise.d if glucose below 70mg/dL:
(early) peripheral symtpoms of sweating, irritability, tremors, anxiety, tachycardia, hunger occur
before(late) neuro symtpoms of consiion, paralysis, seizure, coma, occur. Longstanding DM pts
develop “hypoglycemic unawareness” – no longer get warning symptoms
 Outcomes: remain AAOx3
 Interventions
o Blood glucose management
 Monitor glucose before giving antidiabetics, before meals or bedtime
 Symtpoms in those taking beta blockers harder to detect. Pts taking long acting
insulin metformimn – at risk for hypoglycemia
o Nutrition therapy  Start carb replacement : 15-20mg of glucose. Repear q15min if not
improving. Concentrated, sweet fluids (juice w/ sugar, soft drinks) slow absorption.
Adding protein not helpful. Adding fats slow absorption.
o Drug therapy  glucagon subq or IM and 50% dextrose IV if pt cannot swallow
 Glucagon causes vomiting, watch for aspiration. After no longer nauseous give
simple sugar and small snack. If sulfonylurea induced hypoglycemia: give
diazoxide and sandostatin)
 If sulfonylurea induced hypoglycemia  give Diazoxide and sandostatin
 Evaluate every few hours
o Prevention strategies  avoid common causes
 Excess insulin – don’t give insulien brands without speaking to pmd
 Deficient intake/absorption of food – teach importance of regularly in timing
and quantity of food
 Exercise – glucose levels cal fall 0 must monitor glucose and carb consumption
before and during exercise
 Alcohol – inhibits liver glucose. Drink only with or right after eating. No ecxcess
at bedtime
o Education  wear medical bracelet. Teach that delaying meal more than 30 min puts pt
at risk for hypoglycemia
o Keep carb sources nearby at all times. Major risk if engaging in exercise programs. May
get nightmares of headaches from exercise and hypoglycemia

Preventing Diabetic Ketoacidosis

- Hyperglycemia leads to osmotic diuresis with dehydration and electrolyte loss

 Outcomes: few epsodes of hyperglycemia and DKA
 Interventions
o Blood glucose management  check BP, pulse, respiration q15min until stable. Record
urine output, temp, mental status hously. Once stable, q4hrs
o Fluid and electrolyte management  assess for fluid retention/ overload, dehydration,
acidosis, temp may be elevated, abd girth, jvd,. Restore fluids: 15-20lm/kg/hr in first
 hour. Then hypotonic fluids after 4-14ml/kg. When glucose is at 250 – give 5% dextrose
and 45% NS. Monitor fluid replacement through BP and Input and Output
o Drug therapy  blood insulin effective when bolus given before infusion (conctinuous
because of half life and slow onset) subq insulin started when keosis stops. Resolution of
DKA  glucose under 200, bicards over 18, ph over 7.3, ion gap under 12. Assess hourly
o Acidosis management  normal anion gap – 7-9mEq/L. if over 100  metabolic
acidosis
 Insulin therapy, acidosis correction, and volume expansion decreases hyperK
 If hypoK, need replacements
 Check ECG for changes
 Bicarbs given only for severe acidosis : if given too fast worsens mental staus
 Bicarbs only if pH below 7
 Acidosis corrected with fluid replacement and insulin
 After imbalance corrected then determine cause of DKA
o Education  check glucose q4-6hrs if nausa, vomiting, anorexia present
 Check urine ketones if glucose over 300
 Reduce dehydration risk: drink 3L daily; increase when infection present
 When nausea - drink Gatorade
 When glucose normal/high – calorie and caffeine free 8-12oz hourly
 Eat 150g to prevent ketosis
 Contact pmd if glucose over 250, ketonuria more than 24hrs, cant eat or drink,
sick for more than 2 days

Preventing Hyperglycemic-Hyperosmolar State

- HHS differs from DKA – ketone levels absent, glucose levels higher. End result of sustained
osmotic diuresis. Pt secretes enough insulin to prevent keotosis but not enough to prevent
hyperglycemia
 Outcomes  avoid HHS
 Interventions: Monitoring
o Fluid therapy  rehydrate, resotre glucose 36-72hrs. fluid replacement – if in deficit
replated in 12hrs the rest over next 36hrs (rate of infusion based on wt, urine output,
kidney function, pulmonary congestion, jvd). Assess hourly for cerebral edema. If no
improvement in LOC – fluid not enough/ for HHS – immediately report change sin LOC,
pupil size, shape or reaction, seizures
o Continuing therapy  IV insulin. Monitor for hypoK because may drop fast with insulin.
K+ replacement started when output adequate. Electrolytes q2hrs and ECG.

COMMUNITY BASED CARE

-no energy to learn if glucose fluctuating. Pace teachings

Must be able to state when, where insulin is to be injected or stored

Should be able to say the action of insulin and effects of deficiency