Diabetes Pt 5 - Acute Complications Flashcards
Diabetic Ketoacidosis (DKA)
- Caused by profound deficiency of insulin
- Most likely to occur in Type 1 DM
Characterized by: hyperglycemia, ketosis, acidosis, & dehydration
Precipitating factors
- Illness
- Infection
- Inadequate insulin dosage
- Undiagnosed type 1 diabetes
- Poor self-management
- Neglect
- When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel
- Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop
- Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations or are eliminated along w/the anionic ketones in an attempt to maintain electrical neutrality
- Insulin deficiency impairs protein synthesis & causes excessive protein degradation. This results in nitrogen losses from the tissues
- Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver & leads to further hyperglycemia
- B/c there’s a deficiency of insulin, the addl glucose cannot be used & the BG lvl rises further, adding to the osmotic diuresis
- If not treated, the pt will develop severe depletion of sodium, potassium, chloride, magnesium, & phosphate
- Vomiting c/b the acidosis results in more F&E losses
- Eventually, hypovolemia will ensue & be followed by shock
- Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones & glucose, & the acidosis progresses
- Untreated, the pt becomes comatose as a result of dehydration, electrolyte balance, & acidosis. If the condition is not treated, death is inevitable
DKA - Clinical Manifestations
Dehydration
- Poor skin turgor
- Dry mucous membranes
- Tachycardia
- Orthostatic hypotension
- Lethargy & weakness early
- Skin dry & loose; eyes soft & sunken
- Abdominal pain, anorexia, n/v
- Kussmaul respirations
- Sweet, fruity breath odor
- Blood glucose lvl of 250 mg/dL or higher
- Blood pH lower than 7.30
- Serum bicarbonate lvl lower than 16 mEq/L
- Moderate to high ketone lvls in urine or serum
- Less severe form may be treated on outpatient basis
- Hospitalize for severe F&E imbalance, fever, n/v, diarrhea, AMS
- Also if communication w/HCP is lacking
- Pts w/DKA who have an illness such as PNA or a UTI are usually admitted to the hospital
- Ensure patent airway; administer O2 via NC or non-rebreather mask
- B/c F&E balance is potentially life-threatening, the initial goal of therapy is to establish IV access & begin F&E replacement
- 0.45% or 0.9% NaCl to restore u/o to 30-60 mL/hr & to raise BP
- Add 5% to 10% dextrose when BG lvl approaches 250 mg/dL (to prevent hypoglycemia as well as sudden drop in glucose that can be assoc w/cerebral edema)
- Continuous regular insulin drip, 0.1 U/kg/hr
- Potassium replacement as needed
Hyperosmolar Hyperglycemic Syndrome (HHS)
- Life-threatening syndrome
- Occurs w/type 2 DM
> Precipitating factors
- UTIs, PNA, sepsis
- Acute illness
- Newly dx’d type 2 DM
- Often r/t impaired thirst sensation and/or functional inability to replace fluids
- Enough circulating insulin to prevent ketoacidosis
- Fewer sx’s lead to higher glucose lvls (>600 mg/dL)
- More severe neurologic manifestations because of ↑ serum osmolality
- somnolence, coma, seizures, hemiparesis, & aphasia
- Ketones absent or minimal in blood & urine
! Medical emergency; high mortality rate
- Therapy similar to that for DKA
- IV insulin & NaCl (0.45% or 0.9%) infusions
- More fluid replacement needed
- Monitor serum potassium & replace as needed (hypokalemia not as significant in HHS as it is in DKA)
- Correct underlying precipitating cause
DKA/HHS Nursing Management
Monitor
- Admin of IV fluids to correct dehydration
- Insulin therapy to reduce BG & serum acetone lvls
- Electrolytes given to correct electrolyte imbalance
Assess
- Renal, cardiopulmonary status
- LOC
- For signs of potassium imbalance resulting from hypoinsulinemia & osmotic diuresis
* When treatment w/insulin begins, serum potassium lvls may decrease rapidly as potassium moves into the cells once insulin becomes avail. This movement of potassium into & out of ECF influences cardiac functioning
- Cardiac monitoring
- Assess VS often to determine presence of fever, hypovolemic shock, tachycardia, & Kussmaul respirations
?
- Too much insulin in proportion to glucose in the blood
- BG lvl <70 mg/dL
- Neuroendocrine hormones released
- ANS activated
Hypoglycemia
Hypoglycemia - Common manifestations (d/t epinephrine release) [these can mimic alcohol intoxication]
- Shakiness
- Palpitations
- Nervousness
- Diaphoresis
- Anxiety
- Hunger
- Pallor
- Altered mental functioning
- Difficulty speaking
- Visual disturbances
- Stupor
- Confusion
- Coma
! Untreated hypoglycemia can progress to LOC, seizures, coma, & death
Hypoglycemic unawareness
- No warning s/s until glucose lvl critically low
- R/t autonomic neuropathy & lack of counter-regulatory hormones
- Pts @ risk (those who’ve had repeated eps of hypoglycemia; older pts; & pts who use β-adrenergic blockers) should keep BG lvls somewhat higher
Hypoglycemia - Causes
- Too much insulin or oral hypoglycemic agents
- Too little food
- Delaying time of eating
- Too much exercise
- Sx’s can also occur when high glucose lvl falls too rapidly
> Check BG lvl
- If <70 mg/dL, begin treatment
- If more than 70 mg/dL, investigate further cause of s/s
- If monitoring equipment not available, treatment should be initiated
Hypoglycemia - Treatment: Rule of 15
Consume 15g of a simple (fast-acting) CHO
- fruit juice or regular soft drink, 4-6 oz
Recheck glucose lvl in 15 min
- Repeat if still less than 70 mg/dL
! Avoid foods w/carbs that contain fat which decrease absorption of sugar & avoid over-treatment w/large quantities of quick-acting carbs so that a rapid flux to hyperglycemia doesn’t happen
15 grams of simple carbohydrates
- glucose tablets & gel tube (follow package instructions)
- 2 tbsp raisins
- 4 oz (1/2 cup) of juice or regular soda (not diet)
- 1 tbsp sugar, honey, or corn syrup
- 8 oz nonfat or 1% milk
- hard candies, jellybeans, or gumdrops (see package on how many to have)
Treatment
* In acute care settings
- 50% dextrose, 20-50 mL, IV push
- Patient not alert enough to swallow or no IV access
- Glucagon, 1 mg, IM or SC
- Explore reason why occurred
- Glucagon stimulates a strong hepatic response to convert glycogen to glucose & therefore makes glucose rapidly avail
- Nausea is a common rxn >inj
