Week 6: Homeostasis: DKA & HHS, Adrenal

GLUCOSE REGULATION

• Insulin – does what

• Glucagon – does what

Diabetes mellitus review: what is it?

Interrelated concepts:

• Nutrition

• Tissue Integrity

• Sensory Perception

• Perfusion

• Immunity

• Fluid and electrolyte Balance

• Acid–Base Balance

Think about the process with each

QUICK REVIEW

• type 1 dibetes

• type 2 diabetes

• DX:

QUICK REVIEW

• blood sugar levels normal, prediabetic, diabetic

DKA
- why does it happen

Hallmark s/s: (5)

• Results from a shortage of insulin + an increase in counterregulatory (rise in hormones that increase blood sugar) hormones = hallmark signs of DKA

• Anion gap

• Metabolic acidosis

• Hyperglycemia

• Elevated serum ketones

• Fruity breath

counterregulatory hormones (4)

• Glucagon

• Catecholamines: Epinephrine/norepinephrine

• Cortisol

• Growth Hormone

DKA Risk Factors

• (7)

• What type of diabetes is at higher risk?

• medications (4)

• Infection

• Discontinuation of/or inadequate insulin therapy

• Trauma

• Pancreatitis

• Stroke

• AMI

• New-onset Type 1 that is undiagnosed

• Some medications – corticosteroids, thiazide diuretics,

antipsychotic agents, pentamidie

DKA: Recognize Cues

• s/s (8)

• Laboratory findings (3)

• Most common precipitating factor: (2)

• Uncontrolled hyperglycemia, metabolic acidosis, and increased ketone production

• Kussmaul respirations (deep, rapid breathing)

- Dyspnea

• Signs of dehydration

- Polyuria

- N/V –abdominal pain

• Hypovolemic shock

- Potential hypotension and tachycardia

• Altered level of consciousness

• Tachycardia, fever (if infection present)

• Laboratory findings: glucose elevation, serum ketones, metabolic acidosis

• Most common precipitating factor: infection or illness

DKA Analyze Cues

• The process of DKA

• What complicates DKA? (1)

• Insulin deficiency leads to breakdown of fats, proteins,

and glycogen

• The body then metabolizes triglycerides and amino acids

instead of glucose

• This results in ketone body formation and metabolic

acidosis

• This can cause Osmotic diuresis (an increase in urine production caused by unabsorbed solutes) causes dehydration and electrolyte

imbalances

• Potassium shifts complicate the clinical picture

DKA Prioritize Hypotheses

• what are we worrying about in patients in DKA (4)

• Life-threatening fluid and electrolyte imbalance

• Metabolic acidosis

• Severe hyperglycemia and ketoacidosis

• Potential for cardiac dysrhythmias (potassium imbalance)

• Risk for cerebral edema with rapid glucose correction

Metabolic acidosis

• Why is there acidosis? Why do we call it ketoacidosis? (1)

• Why do ketones increase in the blood? Why do we see ketones in the urine? (3)

• How does the body compensate for the decreasing pH, (acidosis state)? (2)

Osmotic diuresis

• What is osmotic diuresis

• Why does this happen in DKA

• What are the results of osmotic diuresis for the patient (3)

• Osmotic diuresis: an increase in urine production caused by unabsorbed solutes, drawing water into the renal tubules through osmosis.

It happens in DKA due to:

• Elevated glucose levels increase intravascular osmotic pressure

• Fluids are pulled into the intravascular compartment

• Kidneys increase excretion of glucose and urine

Results of osmotic diuresis:

• electrolyte loss

• hemoconcentration - (an increased concentration of red blood cells and other solids in the blood caused by a drop in liquid plasma volume)

• dehydration

DKA Compensatory

• How does the body compensate? (4)

How does the body compensate?

• Activation of the renin-angiotensin-aldosterone system

• Antidiuretic hormone secreted

• Compensatory vasoconstriction

• Autonomic nervous system to secrete catecholamines (epinephrine, NE), and glucocorticoids (cortisol) (Raises blood sugar)

DKA Decompensation

• when/why does it happen (3)

• Compensatory mechanisms exhausted

• Loss of consciousness, decrease in blood pressure and pulse

• Catecholamine supply exhausted

DKA Anion Gap

• What does an anion gap blood test for?

• When does an anion gap occur?

• It’s a cause of what? (1)

• How to calculate anion gap?

• Nomral range?

An anion gap blood test calculates the difference between positively and negatively charged electrolytes in your blood to help detect acid-base imbalances

1. A cause of metabolic acidosis

2. Anions are negatively charged particles

3. Cations are positively charged particles

4. In homeostasis, anions and cations are in balance

5. A gap results when anion excess exists in the body

1. Anion gap = (Na+ + K+) – (Cl- + HCO3-)

2. Normal 10-16 mEq/L

High Anion Gap: Acidosis

• defined as a anion gap greater than what?

• potential causes (3)

• how urgent?

• Anion gap greater than 17 mEq/L

• Needs immediate attention

Potential causes

• Starvation

• Lactic acidosis

• Diabetic ketoacidosis

DKA Generate Solutions and Take Action (6)

• what do do immediately (1)

• restore what, How? (2)

• Lower what, How, how fast? (3)

• correct what, especially (1)

• monitor what (2)

• Resolve what? (1)

• patient education

DKA: Fluid Replacement

• Goal (2)

• What assessments should we do on this patient while infusing fluids? (5)

• example protocol

Goals:

• Keep adequate perfusion to all vital organs and tissues

• Intravascular volume expansion

Assessments:

• Monitor for edema (legs, lungs, cerebral edema)

• SOB

• Neurologic status (headache, LOC, confusion)

• Vital signs

• Electrolyte imbalances

Insulin (KNOW)

• Regular insulin (IV) – onset, peak, duration?

• Follow agency protocol

• Initial bolus – _______?

• IV maintenance infusion – ______ equals ____

• Goal?

• Assess what?

• Maintain serum glucose _______ until acidosis is reversed

• Regular insulin (IV) – onset, peak, duration?

• Follow agency protocol

• Initial bolus – 0.1 units/kg

• IV maintenance infusion – 0.1 units/kg/h (equals 5-10 units/h)

• Goal – decrease serum glucose 50-75 mg/dL and assess glucose hourly

• Maintain serum glucose 150-200 until acidosis is reversed

Potassium (3.5-5)

• What happens to potassium in DKA?

• Insulin causes what?

• Risk of what, which can cause what?

• Interventions (1)

• establish what?,How? (3)

• what is rare in DKA on presentation?

• If potassium is < 3.5, what do you do? (2)

• DKA – K shifts from ICF (inside of cells) to ECF (outside of cells)

• Insulin increases Na/K ATPase pump activity and

facilitates K entry back into the cells  leading to a decrease in serum K

• Risk of hypokalemia – dysrhythmias

• Obtain serum K prior to insulin administration

• Establish adequate renal perfusion (how?) (IV fluids, correcting electrolyte imbalances, and having a urine output of around 50ml/hr.

• Hypokalemia on presentation in DKA is rare

• If < 3.5 mEq/L hold insulin and administer potassium 10-20 mEq/L per hour until > 3.5

If IV Potassium Is Needed

• what do we never do with potassium?

• concentrated or diluted and why?

• never give more then ____ mEq/h IV piggy back in peripheral vein

• central line: may give ___ mEq/h but must be on what?

• IV potassium can cause what (1)

• Assess regularly for what (2)

• Normal range for potassium?

• Consider ________ mEq K added to each liter of IV fluid to keep between 4-5 mEq/L

• if K 5. mEq/L mEq/L – check K how often

• Labs to monitor (3)

• Monitor electrolytes how often

• Monitor serum creatinine and BUN how often

• Never give IV potassium bolus or push

• Always diluted (it can burn)

• Never give > 10 mEq/h IVPB in a peripheral vein

• Central line – may give 20 mEq/h but must be on cardiac monitor

• IV potassium can cause Vein irritation (peripheral veins)

-Assess regularly for phlebitis and infiltration (tissue necrosis

K 3.5 – 5. mEq/L

• Consider 20 – 30 mEq K added to each liter of IV fluid to keep between 4-5 mEq/L

K - 5. mEq/L – check K every 2 hours

Monitor electrolytes every 2 – 4 hours

Monitor serum creatinine and BUN every 2 – 4 hours

FOLLOW AGENCY GUIDELINES

Magnesium

hypomagnesemia can lead to what (1)

what is magnesium needed for (1)

maintain magnesium > ___ mEq/L

• Hypomagnesemia can lead to hypokalemia

• Needed for normal cardiac function

• Maintain > 2 mEq/L

DKA: Evaluate Outcomes

• what are we evaluating (1) (4)

• education

• plans for discharge and home management

Return to homeostasis

• Blood glucose <200 mg/dL (normal 70-99)

• Serum bicarbonate >18 mEq/L (normal 22-28)

• Venous pH >7.30 (normal 7.35-7.45)

• Calculated anion gap <12 mEq/ (normal 10-16)

Education

Plan for discharge and home management

HHS: HYPERGLYCEMIC HYPEROSMOLAR STATE

• results from (2)

• At risk populations (3)

HHS

• does type 2 diabetic produce any insulin?

• HHS process

Does the Type 2 diabetic produce any insulin?

• Yes…but in moderate levels

Pathophysiology:

• Fluids accumulate in extracellular spaces in response

to the glucose elevations

• Progressive increase in osmolality

• Increased osmotic diuresis

• Increasing dehydration

HHS: Recognize Cues

• s/s (5)

• often presents in what population

• may resemble what

Extremely high blood glucose levels (often >600 mg/dL)

Blood osmolarity >320 mOsm/L

Severe neurologic manifestations: somnolence, coma, seizures, hemiparesis, aphasia

Signs of profound dehydration

Ketone bodies absent or minimal in blood and urine

Often presents in older adults

May resemble stroke symptoms (BE FAST)

HHS: Analyze Cues

process

• Decreased insulin leads to hyperglycemia from decreased glucose uptake and glycogen breakdown

• Little to no breakdown of fats, so minimal ketone formation

• Sustained osmotic diuresis causes severe extracellular dehydration

• Intracellular dehydration leads to severe hyperosmolarity

• Can progress to shock, tissue hypoxia, kidney impairment, and coma

• Enough circulating insulin to prevent ketoacidosis

HHS: PRIORITIZE HYPOTHESES (5)

What matters most

Priority concerns (5)

HHS: GENERATE SOLUTIONS

What can we do? (5)

HHS: TAKE ACTION

• immediate action (1)

• for shock/severe hypotension (2) (Initial rate, when to reduce)