NSG 320 – Adult Concepts 1
Week 9: Exam 3
Diabetes
Diabetes Mellitus
• Chronic hyperglycemia that results from issues with glucose regulation
o Reduced insulin secretion to NO insulin secretion
o Reduced insulin function
DM Background
• Over 37.3 million people in USA have diabetes, about 11.3% (2022)
o 28.7 million diagnosed
o 8.5 million undiagnosed
• 1.6 of those have T1DM
• Majority have T2DM
• 96 million people with Prediabetes (38% of the US population)
• 7th leading cause of death in the USA
Pathophysiology
• Exocrine function in the pancreas à acinar cells
• Within the organ of the pancreas, there are islet
cells à where the endocrine function comes
from in the pancreas
o Includes:
§ Alpha Cells à release glucagon
§ Beta Cells à secrete insulin
§ Delta Cells
Insulin
• Glucose requires insulin to move into cells
o Insulin is the “key” that allows glucose into the cell
o Insulin connects to a receptor that is the “lock”
o Allows the cell to be more permeable to glucose
o Without insulin, the glucose cannot get into the cell
o Without glucose, the cell has no energy
• Insulin is vital to life à need it in order to allow the glucose to get into our cells and maintain life with
energy
• Insulin is released in 2 different ways:
o Basal Secretion
§ Low level secretion during fasting
§ Blood glucose releases in the body; insulin follows the glucose
§ We have a constant basal supply that we’re getting of glucose
§ Glucose and Insulin increase during meals
• Insulin covers the glucose to get it into the cells
§ Body is constantly releasing glucose to keep us at the metabolic state
§ Insulin follows the same natural flow throughout time
§ Constantly getting a basal secretion of insulin to cover us as our basal metabolic rate
§ Covering what we use
o Prandial Secretion
§ Insulin is secreted in a two-phase release after eating, followed by an increasing
release that lasts until the blood glucose level returns to normal
Insulin Function vs. Liver Function
• Insulin Function
o Binds to receptors on cells so that cells are more permeable, allowing glucose in (for energy,
metabolism)
o Works with liver to store or release glucose
o High levels (during meals) promote storage of glucose
o Low levels (during fasting periods) promote production of glucose
• Liver Function
o Glucose reservoir
o Manufactures glucose from glycogen/carbohydrates à glycogenolysis
o Manufactures glucose from amino acids, waste products, and fat byproducts à
gluconeogenesis
• Insulin and liver keep blood glucose levels where they need to be
• Insulin works with liver to store and release glucose
Counter-Regulatory Hormones
• Glucagon
o Counteracts insulin
o Triggers conversion of glycogen to glucose in liver and muscle
o If you have really high levels of insulin, you would see some glucagon released as well
o Prevents blood glucose from getting too low (aka: hypoglycemia)
• Other hormones that assist in keeping glucose at adequate levels
o They are released whenever a blood glucose is getting low (d/t to high insulin levels) and
sometimes when they’re high
o They are meant to counteract insulin à helping to increase glucose levels (catecholamines)
§ Epinephrine & Norepinephrine
• Shaky
• Increased HR
• Diaphoretic/Sweaty
• AKA: “Cold and clammy…need some candy” à HYPOGLYCEMIA
• Whenever blood sugar is low, people release E & NE
• They are responsible for all of the S/S of hypoglycemia
§ Cortisol
• Optimal Blood Glucose Levels à FASTING Blood Glucose: 80-110mg/dL
What
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Happens When You Don’t Have INSULIN?
Remember: insulin is the key that unlocks the receptors to get glucose into all the cells
Cells cannot use glucose à glucose builds up in blood
Cells have no fuel à breakdown of fat and protein (Lipolysis & Proteolysis)
o Lipolysis gets concerning because it causes ketogenesis
§ Ketogenesis à development of ketones
• Increased ketogenesis
• Increased release of counter-regulatory hormones (when insulin is really low)
o Cause an increased release in glucose (esp. cortisol)
o Cortisol à Body needs a lot of energy for “Fight or Flight” (also with epinephrine)
Too Much Glucose = HYPERGLYCEMIA
• Results in symptoms of diabetes
o 3 P’s:
§ Polyuria
• Osmotic diuresis à peeing out all of the water
• Loss of glucose in urine
o Glucose gets into our kidneys, and water follows glucose (bully!)
• Loss of electrolytes à specifically Potassium (becomes critically important to
nursing interventions for treating elevated glucose)
• Loss of water à dehydrated
§ Polydipsia
• Initiates thirst
§ Polyphagia
• Starving Cells à pt’s are hungry and eat a lot
• Dehydration
o Pt becomes hypovolemia à causes a bunch of tissue to not get any O2 (hypoxia)
§ AKA: impaired perfusion
o Hypoxia à ischemic tissue (anaerobic metabolism) à lactic acid production
o Lactic Acid drives our pH DOWN, so we become acidotic à Metabolic Acidosis
o Metabolic Acidosis
• Ketogenesis
o Because cells aren’t getting enough fuel, so the body starts breaking down fat and protein
o Fat is most concerning because in the process it produces ketones
o Conversion of fat to ketone bodies
§ Acetone, Acetoacetate, B-Hydroxybutyrate à all fatty acids
§ Development furthers the metabolic acidosis
§ When pt’s become really acidotic, they become very obtunded and unresponsive
• Acid-Base Imbalance
o Metabolic Acidosis yields an attempt by the lungs to correct the acidosis
o Respiratory Alkalosis occurs in response by:
§ Blowing off CO2 and Acid
• Increased breathing rate
• Increased depth of breathing
• AKA: Kussmaul Breathing
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Kussmaul Breathing
o Hallmark Sign of Acidosis related to HYPERglycemia
o Increased rate/depth of breathing
o Smells like sweet acetone/rotten citrus fruit/fruity alcohol smell (very distinct)
Electrolytes
o In general, people who are hyperglycemic are HYPOkalemic à “peeing out potassium”
o During acidosis, potassium moves OUT of cells INTO the blood à HYPERkalemia
§ Replacing hydrogen that is moving into cells because the blood is so acidotic, and the
potassium goes out of the cells
§ Potassium serum tends to be high in acidotic people because it’s leaked out of the cells
§ In reality, this person is not (as a whole) hyperkalemic because they’re losing
potassium through urine
o When we correct the acidosis, potassium moves back into the CELLS à low normal or
HYPOkalemia
§ Hydrogen comes out of the cells and goes back into the blood
§ Potassium level becomes more reflective of what is usually is
o Lose electrolytes when blood glucose is getting really high
o Ex) Pt came to ED and was obtunded/confused. She was in moderate DKA, had sepsis and
severe dehydration. The nurse set up fluids and insulin, and accidentally ran the fluid at the
insulin rate (ie. 3-5mL/hr – not a lot of fluid), and the insulin at the fluid rate (ie. 150mL/hr). It
corrected the hypoglycemia too fast and fixed the acidosis so quickly, that the pt’s potassium
went from 5.5 to 2.9 in less than an hour. Pt didn’t code (fortunately), but easily could have.
Pt was sent to ICU.
o Want to fix acidosis VERY SLOWLY so we have time to monitor the potassium and fix it if we
need to
§ Fix it by:
• Fluids
• Decrease blood sugar à IV insulin
§ Done slowly to ensure it’s not a rapid drop
o We expect the see the potassium to decrease
T1DM vs. T2DM
• T1DM
o Autoimmune pathology causing destruction of beta cells in pancreas
§ Body develops antibodies that attack the beta cells
o No insulin production/Insulin dependent
§ Results in an elimination of insulin
o Onset at young age
§ Used to be called “Juvenile Diabetes” (but not anymore)
• T2DM
o Insulin resistance
§ Person can manufacture insulin, but the cells have insulin resistance and no longer
respond to the insulin trying to “unlock the door”
§ Lifestyle issues à obesity, sedentary lifestyle
o Strong genetic component
o Insulin production/majority do not require insulin
o Majority of T2DM are obese à related to lifestyle (Metabolic Syndrome)
§ Insulin resistance is a primary characteristic of Metabolic Syndrome
o Onset in 50’s à becoming more common in youth (linked to the increase in obesity)
o Gestational diabetes more likely to develop T2DM later
T2DM
• Insulin Resistance à cells become less sensitive to insulin
o Caused by risk factors: aging (50+), obesity, smoking, inactivity/sedentary lifestyle
• Pancreas responds by developing more insulin
o Eventually, the beta-cells can no longer produce as much insulin
o Results in LESS insulin production
o Overtime, a pt with T2DM will require insulin if left unmanaged
• Can eventually lose ability to produce insulin
Metabolic Syndrome
• Co-Existing cardiovascular disease and other risk factors for
T2DM development
o Abdominal/Truncal Obesity
o Hyperglycemia
o HTN
o Hyperlipidemia
• Increased risk of cardiovascular events, stroke, and mortality
• Need to get these things managed
• Insulin resistance is the biggest factor related to this
• Anti-Psychotics cause metabolic syndrome
o Newer ones à if pt’s are on chronically, they can develop metabolic syndrome
o It increases their risk of cardiovascular disease
Assessment
• Hx
• Fatigue
o T1DM, T2DM
• Weight
o T1DM – tend to lose weight at onset
o T2DM – obesity is associated with development of T2DM
• 3 P’s:
o Polyuria à excessive urination
o Polydipsia à excessive thirst
o Polyphagia à excessive hunger
o *Most important symptoms of HYPERglycemia*
• Wounds and delayed healing time
o When blood sugars are super high
o r/t hyperglycemia à immune system doesn’t function well
o Glucose contributes to infection frequency
• Frequent infections
o At increased risk of infection
o Bacterial Infections are significantly higher
• Changes in vision
o Hyperglycemia
o Develop retinopathy
o Damages the micro-vessels à causes fluid leakage à causes blurry vision
Diagnostics
*Commit to memory and be able to understand why we’d use one over another*
• Blood Glucose Level Testing
o Fasting Blood Glucose
§ < 100 mg/dL = Normal
§ >126 on more than 2 occasions = Indicative of Diabetes
o Glucose Tolerance *don’t really need to memorize this other than we use it for pregnancy*
§ Used for pregnant women typically
§ Pregnant women drink sugary drink à wait a couple of hours à check CBG
§ Determines gestational diabetes, but also other forms of diabetes
§ <140 = Normal
§ >200 = Indicative of Diabetes
o Serum Blood Test: HgbA1C
§ Looking at how Hgb binds to glucose over time
§ The more glucose there is, the more binding there will be
§ Provides a good understanding of what glucose is over time (~90 days/3 mos)
§ The amount of glucose bound to Hgb is reflective of how high the Hgb has been for
the last 3 months
§ Great to know if this patient is actually diabetic, or if they’re in a stressful state
§ 4-6% = Normal Glycosylated Hg (A1C)
§ A1C > 6.5% is indicative of diabetes (indicates they’ve had high glucose for 3 mos)
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Urine
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Urine
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§ A1C > 8% is indicative of poor diabetes control for pt’s dx’ed
§ 5.7-6.4% = increased risk of developing diabetes (indicative of pre-diabetes)
Ketones (with blood glucose level)
T1DM checks urine ketones often
Development of ketones à a sign that cells are not getting enough glucose and they’re
breaking down fat for fuel, which is leading to the development of fatty acids
T2DM à does not develop ketones
§ T2DM do not go into DKA
Albumin
30-299 mg/24 hours = Early-Stage Diabetic Nephropathy
Indicative that a pt is passing protein in their urine
Indicative of Kidney Damage from excess glucose
Helpful to track overtime for pt’s with DM to know if they’re possibly developing kidney
disease
*DM is the leading cause of Kidney Disease
Interventions
• Very complex disease, requiring high level of self-management
• Patient Education is ongoing à there is no end point
• Important to assess where a person is and continue to work with them in order to best manage
their diabetes
• Nutrition
• Exercise
• Weight
• Blood Glucose monitoring and responding appropriately
• Recognizing S/S of problems/complications
• Medication
• *Reduce complications from DM*
Monitoring and Maintaining Healthy Blood Glucose Levels
• Goals for pt’s with DM:
o Majority of pre-meal levels should be 70-130 mg/dL
o Post-Meal Levels < 180 mg/dL
o A1C Goal < 7%
• Goals may be more or less stringent depending on patient
• This is where we meet people where they are, and help strengthen their glucose control
• There are also times when pt’s can’t meet these goals as good as others
o Ex) Mother with T1DM with four children under 5-years-old à A1C is higher than 7% à
Doctor agreed that her A1C has to be higher because she can’t risk becoming hypoglycemic
with young children at home (ie. Can’t risk losing consciousness)
• When/How often to check blood glucose:
o S/S of hypo/hyperglycemia
o Times of stress/illness (blood glucose rises)
§ Stress response to illness causes hyperglycemia
o Exercise
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§ Can cause both hyper/hypoglycemia
§ People need to know how they respond to exercise
§ Check before exercise
New meds/new doses of medications
During Pregnancy
T1DM à check at a minimum of 4x/day and as frequently as 10x/day
T2DM à check at a minimum of 1x/day and more often if necessary
Home Glucose Meter
• Can use finger or alternate site (earlobe)
o Finger à most common place; preferred site
o Warn patients with hypoglycemic unawareness
• User Error is more likely than machine error
o Great place for education
• Infection control
o People do reuse lancets à not preferred (but they are expensive)
o As long as they understand it increases their risk of infection
Continuous Glucose Monitoring
• Before a pt starts using continuous glucose monitoring, it’s important they understand:
o Intended to supplement capillary blood glucose (CBG) readings à NOT replace them
o They should still be checking their CBG
o Continuous glucose monitors need to be calibrated for accuracy
• Parts:
o Transmitter à on outside of skin; transmits CBG to receiver
o Sensory à beneath the adhesive that is in the interstitial space and subcutaneous tissue
§ Gets a glucose reading that goes to the transmitter, which communicates with a
receiver
o Receiver à can be kept in an app on cell phone
• Provides glucose readings every 1-5 minutes
• Requires capillary glucose (CBG) readings for calibration (accuracy)
o Needs to be calibrated daily
• Lag time between capillary glucose and sensor readings (interstitial fluid)
o Interstitial Fluid is behind what you’d see on a CBG
o If pt is feeling S/S of hypo/hyperglycemia, do NOT depend on continuous glucose monitor à
it might be incorrect because of the lag time
• Use capillary readings to verify extreme values
o Ex) If pt has really high or low values on continuous glucose monitor, they need to double
check with a CBG
• Helpful as far as getting pt into “tight” glucose control
Insulin Administration
• Basal Coverage Insulin à long-acting insulin
o Don’t check CBG before dose à check the previous 24 hours of CBG’s if they got the same
amount the day before
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Meal Coverage Insulin à rapid-acting insulin
o Always check CBG before administration
Traditional Injections via various insulin regimens
o Rotate Sites
§ Should stay in the same area (abdomen or back of upper arm) but rotate site within
that area
o Appropriate Timing
§ Ensure they’re taking insulin at the correct times (ie. Meal times, AM for basal doses
of insulin)
o 90 vs. 45 degree
§ 90 à subcutaneous tissue
§ 45 à pt’s who don’t have a lot of subcutaneous tissue (skinny people)
• Use if you CAN’T “pinch an inch”
Injection devices
o Pens
o Syringe/Needles
Continuous SQ Infusion
o Best way to administer insulin to mimic the body
o Helps pt get into the “tightest” control of glucose
o Continuous flow of Basal Insulin
o Increases at Mealtime
o Very Effective
o Insulin Pump à should be adjusted/managed based on glucose sensor/readings
o Usually matched with the continuous glucose monitor
o Pt has to be able to manage their diabetes the traditional way before they can qualify for
the continuous infusion method
Nutrition
• Important aspect of education for pt’s with DM
• Every pt with DM needs a nutritional intervention
• Individualized meal plan that is flexible and realistic
• Take into account the preferences, cultural, financial, and lifestyle of the patient
• Should assist in achieving optimal:
o Blood glucose levels
o Lipids
o Blood Pressure
o Weight loss (if needed)
Medical Nutrition Therapy
• Recommended for all adults with DM
• Referral to a Dietician
• Goal à Reduced caloric intake if weight loss is needed
• Dietary recommendations are based on patient’s:
o Normal diet
o Weight management expectations (if needed)
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o Lipid profile
o Glucose patterns
Requires consistency on eating times
o Helpful education regarding coordinating eating times with insulin action
Coordinate eating times with insulin action
Nutrition
• Nutrition-Dense Foods
o Avoid empty calories
o Most nutritionally dense junk food à pizza
§ Has more nutrition per calories that you’re eating
• Goal à 25g of Fiber/day
• Avoid beverages with sugar
• Monosaturated Fats = GOOD
o Pistachios
o Cashews
o Peanuts
o Almonds
o Avocados
o Olive Oil
o Walnuts
o Olives
o Chocolate
o Hazelnut
o Sunflower Seeds
o Pumpkin Seeds
o Canola Oil
• AVOID:
o Saturated Fats
o Trans Fats
o Cholesterol
• Moderate alcohol intake
o Educate pt’s with DM:
§ Know how you respond to alcohol
§ Know how your blood sugar responds to alcohol
§ If you’re going to drink, be sure to keep it limited to occasion and/or 1-2 drinks
Nutrition: CHO Counting
• Not every diabetic needs to count carbs
• Helps to determine insulin coverage needed
• Pt is provided with a ratio (from physician) of how many units of insulin they would get for a certain
amount of carbs
o Ex) 1 unit of insulin per 15g of CHO (1:15)
o Varies from person to person, and can change for a person over time
• Calculate CHO’s
•
o Toast (12g) + apple (25g) = 37 g
Calculate Insulin Dose
o 37 g CHO = 2 units of insulin for that particular meal (toast and apple)
Exercise
• Can either cause a pt’s blood glucose to increase or decrease à people need to know how their
glucose responds to exercise
• Ultimately leads to better control of glucose (both T1DM and T2DM)
• T2DM à exercise helps:
o Insulin-resistance piece
o Cells uptake the glucose
o Insulin work better à can help pt stay off medications and avoid overproduction of insulin
that wears pancreas out
• Educate pt’s to exercise AND manage blood glucose closely when they do exercise
• Decreases:
o Risk of cardiovascular disease
o LDL’s
o Triglycerides
• Increases:
o HDL’s
• Preference:
o 150 minutes/week of moderate-to-intensive exercise
…or…
o 75 minutes/week of vigorous exercise
o At least 3 days/week
o Add-on Resistance exercise at least 2 days/week
• People trying to control hyper/hypoglycemia need to either:
o Reduce Insulin OR Increase Food Intake for exercise
o Also need to know what glucose is in the first place
• Can lead to HYPERglycemia or HYPOglycemia
o Glucose < 100mg/dL (hypo)
o Glucose > 250mg/dL (hyper)
o WANT glucose to be BETWEEN 100-250
§ If it’s less than 100, they need to increase their food intake before exercising
§ If it’s higher than 250, they need to take some insulin
§ If it’s T1DM and higher than 250, they need to check their ketones prior to exercising
(pee stick)
o Check blood glucose more often that day they exercise
• Before pt exercises, they need to make sure they don’t have ketones in their urine à BAD sign that
fats are breaking down
• Prior to exercising, pt’s need to:
o Avoid extreme temperatures
o Stay hydrated
o Wear suitable footwear à d/t lack of sensation in feet
o Eat a CHO snack
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o Bring candy/juice in case of hypoglycemia during exercise (esp. rigorous or exercise
they’ve never engaged in)
o Check blood glucose
After exercising, pt’s need to:
o Examine feet
o Check blood glucose
Avoid exercise during PEAK insulin action
Exercise: Retinopathy
• Diabetics with proliferative or severe retinopathy should AVOID:
o High intensity CV (cardiovascular) exercise
o Resistance weight training
o Anything that initiates the Valsalva Maneuver (can worsen retinopathy)
§ Close your mouth and pinch your nose shut and try to exhale
o Anything that adds pressure behind their eyes
• At risk for:
o Retinal detachment
o Vitreous bleeding
o Skin breakdown/injury
T2DM
• Encourage Weight Loss
o Reduced caloric intake
o Increased exercise
§ Also helps cells uptake insulin…they become less resistant
§ Keeps pt’s off insulin
• Rest
• Smoking Cessation
Complications of Diabetes: Hypoglycemia vs. Hyperglycemia
• People taking insulin are at risk of hypoglycemia
o Need to educate them about what this looks like
• Patients need to know when they’re at risk of being hypo/hyperglycemic and S/S of both
• Also need to check blood sugars when they may be hyper/hypoglycemic
• Hypoglycemia
o CBG < 70 mg/dL
o Irritable, Anxious à nonresponsive
o Tremor
o Fatigue
o Muscle weakness
o Cool, Diaphoretic à “Cold and Clammy…need some candy”
o Hunger
o Nausea
o HA
o Clumsiness
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o Not every person with DM experiences all the S/S of hypoglycemia à some people develop
an unawareness over time
o DANGEROUS à brain isn’t getting glucose and within 5 mins will start causing major
problems
§ Coma can occur quickly
o Counter-Regulatory Hormones are causing all these problems
Hyperglycemia
o CBG > 250mg/dL
o Impaired concentration à nonresponsive
o Fatigue
o Warm, Dry à “Hot and dry…sugar is high”
o Hunger
o N/V
o Headache
o Blurred Vision
o Rapid, Deep Breathing à they’re becoming acidotic
If Your Patient Has HYPERglycemia…
• It may NOT be diabetes
o Not every person that has high blood sugar has diabetes
• If pt has high glucose, but is not diabetic, it could be linked to worse outcomes:
o Increased risk for infection
o Longer length of hospital stay
o Increased risk of higher acuity
§ Tend to have more complications
o Increased mortality
• Sepsis is more likely to cause hyperglycemia in non-diabetics
• If this is your patient, it’s okay to ask the physician:
o “Do we need to get their blood glucose under control?”
o “Do they need some insulin so that they get better faster?”
• Getting blood glucose under control for non-diabetic patient lends to faster healing for that patient
Hospital Care of Pt’s with HYPERglycemia
• Monitor Blood Glucose
• Goals:
o < 140 mg/dL à BEFORE meals
o < 180 mg/dL à at random
o 140-180 mg/dL à critically ill patients
• Ask physician to review/reset insulin orders if blood glucose is really high or really low
Hyperglycemia Interventions (In-Patient)
• Insulin
o IV Insulin
§ Given if pt is hyperglycemic but are NOT diabetic (don’t give PO medications)
Does come with complications (ie. Hypoglycemic) à need to make sure pt is aware of
what s/s of hypoglycemia are
§ Tends to be for higher acuity patients à IV drip
o SQ Insulin
§ Basal Coverage
• Not everyone needs this
§ Meal Coverage
§ Correction
If pt comes into hospital and are regularly on PO diabetic medications à we will take them off their
regular diabetes PO medications
o Managed with insulin while they’re inpatient
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DKA vs. HHS
• Extreme high blood glucose can lead to either DKA or HHS
• DKA à Diabetic Ketoacidosis (T1DM)
o Hyperglycemia + Metabolic Acidosis + Ketones
o Severe hypoglycemia for T1DM
o Development of ketones contributes to acidosis
• HHS à Hyperglycemia w/Hyperosmolarity (T2DM)
o Hyperglycemia + Hyperosmolarity
o NO Ketones
o Do not see the same development of acidosis
o Still very serious à have a higher mortality rate than a pt with DKA
• DKA Characteristics:
o Diabetic Ketoacidosis (>300 mg/dL)
o T1DM
o Often triggered by infection or insufficient insulin
§ See it a lot when people stop taking their insulin
o Rapid Onset
o 5-10% mortality rate
o Dehydration
o Electrolyte Imbalance
§ Concerned with shifting of potassium that occurs d/t acidosis component
o Urine Ketones
o Acidosis < 7.3
§ Try to avoid intubation
§ Kussmaul breathing is helpful and don’t want to negate with ventilation
o 3 P’s (Polyphagia, polyuria, polydipsia)
§ This is what is causing the problem
§ Pt has become really dehydrated d/t the high blood glucose
o Abdominal Pain, N/V
o Kussmaul Breathing
o Confusion à Coma à Death
• HHS Characteristics:
o Hyperglycemic-Hyperosmolar State (>600 mg/dL)
T2DM
Often triggered by infection, dehydration
Gradual Onset
15-20% mortality rate
Profound dehydration
§ 1st thing we need to do is start fluids for this patient
o Electrolyte Imbalance
o Osmolarity > 320
o 3 P’s (Polyphagia, polyuria, polydipsia)
§ This is what is causing the problem
§ Pt has become really dehydrated d/t the high blood glucose
o NO Urine Ketones
o NO Acidosis (pH > 7.4)
o Confusion/Coma < 20%
o THINK: pt’s in nursing homes
Not a big difference in how DKA vs. HHS patients are managed
o The 2 previous protocols have been combined
o Providers choose a different fluid based on pt’s presentation and whether they’re acidotic
or not
DKA Interventions:
o Tx SLOWLY à d/t potassium (need to monitor potassium; don’t want pt’s to code)
o ABC
§ Concern bc patients are comatose
§ Tend to breathe fine even though they’re comatose
§ Circulation is an issue because pt’s are dehydrated
o Monitor/Assess
§ Frequent Serum Glucose, Electrolytes, ABG’s
• Difficult to manage
• Can’t use a CBG machine, because up to a certain point it won’t read properly,
will need serum glucose levels (draw blood)
§ Telemetry
§ Fluid Overload/Respiratory (because we give them so much fluid)
o Hydrate
§ Usually do boluses
• *ONLY give boluses of isotonic fluids (ie. NS, LR)
§ NS
§ D5 w/K+
• Add when we get blood glucose to a certain level (usually around 250)
• Don’t necessarily give K+ at first à depends on their K level
o Blood Glucose à Continuous IV Insulin
§ Do NOT give SQ à not helpful in this situation
o Electrolyte Management
§ By giving fluid + insulin = correcting acidosis
§ When correcting acidosis, need to remember that we’re going to cause the potassium
to shift back into the cell à will see a DROP in potassium (HYPOkalemia)
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HHS Interventions:
o Tx slowly
o ABC
§ Concern bc patients are comatose
§ Tend to breathe fine even though they’re comatose
§ Circulation is an issue because pt’s are dehydrated
o Monitor/Assess
§ Serum Glucose, Electrolytes, ABG’s
§ Neuro Status
§ Telemetry
o Hydrate
§ Typically will receive a bolus of NS, then switch over the 1/2NS
• *ONLY give boluses of isotonic fluids (ie. NS, LR)
§ NS
§ 1/2 NS
o Blood Glucose à Continuous IV Insulin
§ Do NOT give SQ à not helpful in this situation
o Electrolyte Management
Hypoglycemia Causes
• Quicker onset than hyperglycemia
• Too much insulin
• Inadequate food intake
• Wrong type of insulin
• Insulin and meal timing mismatch
o *Don’t draw up insulin until food trays are passed out*
o Occurs in hospitals whenever nurses give insulin too early and/or trays are late
o Read the orders carefully
§ Ie) some meal-time doses don’t have anything to do with food
• Alcohol intake
• Exercise
• Kidney Failure à decreased insulin clearance (insulin can get too high)
o Have a higher likelihood of being hypoglycemic
Hypoglycemia
• Prevention
• Brain à stores enough glycogen for a few minutes; unable to produce glucose
• Without glucose, brain tissue dies within a few minutes
o Ie) 5 mins
• Neuroglycopenia à confusion, paralysis, seizures, coma
o Important to teach pt’s about this
o Occurs very quickly
• Initial symptoms à warning sign before the brain’s glucose begins to drop <70 (tachycardia,
diaphoresis)
o T1DM à can lose these early warning signs à HYPOGLYCEMIC UNAWARENESS
These people should be
checking blood sugars more
often
o Beta-Blockers block/mask these
symptoms d/t blocking the SNS à
another warning sign
§ These people should be
checking blood sugars more
often
§
Treating Hypoglycemia
• CHO tx
o 15-20g Glucose (<70 CBG)
o 30g Glucose (<50 CBG)
o Liquid Preferred (juice, soda)
§ 8oz juice = 25-30g glucose
o Tell pt’s:
§ After the juice, have something else like a PB cracker or another snack
o If pt is unable to swallow (ie. Coma, or confused and it’s unsafe to swallow):
§ SQ/IM Glucagon
§ IV D50 (50% dextrose)
§ There are very specific protocols for hypoglycemia in the hospital
o Repeat blood glucose measurement in 15 minutes, then again in 1 hour once it’s at a normal
state
When to HOLD Insulin
• What to do when your patient is NPO?
o Typically do NOT hold à long-acting insulin
§ Also don’t need to check a CBG when giving a long-acting insulin in that moment
§ Need to look at CBG’s for 24 hours before because that long-acting insulin is about
providing BASAL COVERAGE
§ Ex) If pt’s CBG’s in the past 24 hours were in the 70s, 65s à that dose of longacting insulin is too high à call provider and ask to reduce dose
§ Ex) If pt’s CBG in the past 24 hours were 250, 280, 290 à that dose of long-acting
insulin is too little à call provider
o Typically HOLD à fast-acting insulin/meal-time insulin
§ Especially if patient is NPO
§ Read Orders
o IV Insulin
Long-Term Complications
• Microvascular Disease
o Nephropathy
o Neuropathy
o Retinopathy
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Cardiovascular Disease
Cerebrovascular Disease
Immunity
Microvascular Disease
• Hyperglycemia damages small vessels à changes in vessels à poor tissue perfusion à cell death
• Includes:
o Nephropathy
o Neuropathy
o Retinopathy
• 1% DECREASE in A1C = 25-30% decrease in kidney and eye complications
Peripheral Neuropathy
• Nerve Damage
• Results in loss of sensation, pain, and weakness
• Can result in system-wide problems
o Foot injury (late complication)
o Skin à more likely to have wounds
o GI à can slow down mobility
o Neurogenic bladder
o Erectile Dysfunction
Feet
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Most common complication of DM that leads to hospitalizations
Foot ulcers often lead to loss of limb
Delayed healing (neuropathy)
Foot deformities
o Charcot Foot à overtime the bones in the foot get weak, and they collapse d/t the
neuropathy
§ The area of your foot where you’re not stepping on it, it will protrude out
§ Will get wounds in this area
§ Wounds are almost impossible to heal
§ Very debilitating
§ Can still ambulate/walk
Numbness
Dry, thinning skin
Foot Care
• *BIG DEAL*
• Wear appropriate shoes à Podiatrist
• Avoid injury from heat sources
o Don’t soak feet in hot water
o No lotion between the toes à causes skin breakdown between the toes
• Inspect feet DAILY
• Report Injuries
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Assess protective sensation often
o Semmes-Weinstein Monofilaments
Nephropathy
• Kidneys lose ability to filter urine over time à kidney failure
• DM is leading cause of kidney failure in USA
• Preventable with:
o Optimal glucose control
o Kidney protective medications (ie. ACE Inhibitors)
o BP control
• Annual urine albumin test
o 30-299 mg/24 hours = early nephropathy
o T1DM > 5 years
o T2DM yearly
• Once albuminuria is present:
o Focus on preventing progression through:
§ BP control
§ Glucose control
§ Avoiding nephrotoxic agents
Retinopathy
• Characterized by:
o Blocked vessels à leaky blood vessels à retinal hypoxia
• Blindness is 25x more likely for diabetics
• Higher risk for:
o Glaucoma
o Cataracts
• Largely dependent on duration of diabetes
o > 20 years, all patients have some degree of retinopathy
• Asymptomatic until vision loss occurs
• Prevention:
o BP control
o Hyperglycemia control
o Lipid Control
o Annual eye exams
Management of Vision Loss
• Vision Support
o Ophthalmologist
o Optometrist
• Functional Vision Assessment
o Technician
o Diabetes educator
Interventions for Diabetic Patients with Visual Impairment
• Coding objects with bright colors (ie. Insulin vial)
• Adjust lighting
• Large print
• No pre-filled insulin pens
• Insulin syringe devices designed for those with visual loss
• Appropriate selection of glucose monitor
• Hospital:
o Assess and report vision loss
o Use vision support when patient is awake
o Keep things off the floor
o Keep objects within reach
Macrovascular Disease
• At risk of:
o Cardiovascular Disease
§ Reduce modifiable risks
o Cerebrovascular Disease (ie. Stroke)
o Reduced Immunity
Education
• Patients really need to be aware of the pathophysiology of diabetes
o Can keep it simple
• Self-Management is key to preventing complications
o #1 reason related to amputations = diabetes
• Family/Support System Education
• Requires interdisciplinary approach
o Provider
o Dietitian
o Nutritionist
• This process is ongoing