MedSurg II - DKA & HHS, SIADH & DI

olanjones's version from 2017-03-17 21:27


Question Answer
Diabetic Ketoacidosisprofound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, & dehydration. If not treated, pt will develop severe depletion of eletrolytes, hypovolemia, shock, renal failure->death
Precipitating factors for DKAillness & infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, & neglect
What are ketoneschemical produced when the body is using fat for energy. Diabetics make ketones because they don’t have enough insulin & can’t store glucose for energy
DKA S/SEarly: Dehydration, lethargy, & weakness
Severe dehydration: Abd pain, anorexia, N&V
Progresses to: Kussmaul respirations, ↓LOC, Acetone odor of breath
DKA Clinical s/s Hyperglycemia > 250 mg/dL, Ketonemia (ketone bodies in the blood), Ketonuria, Kussmaul respirations (deep/rapid), Metabolic Acidosis: pH < 7.30, Bicarb < 16 mEq/L
DKA CCthe initial goal of therapy is to establish IV access & begin F&E replacement (NaCL 0.45% or 0.9% at a rate to restore urine output to 30 to 60 mL/hr)
Hyperglycemic Hyperosmolar Syndrome (HHS)life-threatening, occurs in pt w/ DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, & extracellular fluid depletion
Precipitating factors for HHSUTI, pneumonia, sepsis, any acute illness, newly dx DM II; often r/t impaired thirst sensation/functional inability to replace fluids (usu a hx of inadequate fluid intake, ↑ mental depression, oliguria)
HHS Clinical s/sPlasma glu > 600 mg/dL, marked ↑serum osmolality; These factors produce more severe neurologic manifestations (somnolence, coma, seizures, hemiparesis, aphasia), can resemble a stroke
HSS CCIV insulin & NaCl (either 0.9% or 0.45%); HHS usually requires greater volumes of fluid replacement; HHS are commonly older and may have cardiac or renal compromise, requiring hemodynamic monitoring to avoid fluid overload during fluid replacement
Tx of DKA & HHS-IV fluid, IV Short-acting insulin (0.1 Unit insulin/kg/hr, 1 unit insulin/1 ml fluid), Electrolyte replacement
-Monitor: Mental status/I&O/central venous pressure/Labs (glucose, electrolytes, ketones)
-EKG, CV& Resp status
Why is it important to avoid rapid ↓glu dropmay lead to cerebral edema (reduce @ rate of 36 - 54 mg/dL/hr to avoid complications)
What should be done when glu falls to approx. 250 mg/dLIV fluids containing glucose are administered to prevent hypoglycemia (in both DKA & HHS)


Question Answer
SIADHsyndrome of inappropriate ADH, high ADH in absence of normal stimuli for release
Causes of SIADH-Malignant tumors
-CNS disorders (head inj/stroke/infection/disease)
-Drugs that stimulate production/potentiate existing ADH (anesthesia agents/opioids/thiazide diuretics/SSRIs/TCA/Chemo)
-Misc (hypothyroid/lung infection/COPD/HIV/adrenal insuf)
SIADH s/stachycardia, bounding pulse, HTN, ↓H&H, ↓sodium, ↓UO, weight gain
SIADH key featuresfluid retention, ↓serum osmolality, dilutional hyponatremia, ↓urine volume, normal urinary sodium
Dilutional hyponatremiaSerum sodium <134 mEq/L, serum osmolality < 280 mOsm/kg (280 mmol/kg), and a urine specific gravity >1.025
SIADH complicationswater intoxications, hyponatremia (s/s: personality change, HA, lethargy, N&V, diarrhea, ↓ tendon reflex, seizure/coma)
SIADH NI-Monitor: I&O/VS/heart & lung sounds; Signs of hyponatremia, inc seizures, N&V, muscle cramping, ↓neurologic function
-HOB flat (no more than 10 degrees) to enhance venous return to heart
-Frequent turning, ROM exercise to maintain skin integrity/joint mobility
-Frequent oral care & distractions (↓discomfort of fluid restriction)
SIADH TxFluid restriction (800 - 1000 mL/day); Diuretics (only if serum sodium is at least 125 mEq/L)
SIADH teachinguse ice chips/sugarless gum to decrease thirst; weigh daily; supplement diet w/ sodium & potassium (w/ food to help prevent GI irritation)
Diabetes insipidus (DI)↓ADH results in F&E imbalances caused by ↑UO & ↑plasma osmolality
Types of DIneurogenic (insufficent ADH from the brain); nephrogenic (inadequate response to ADH by the kidney); primary (excessive fluid intake d/t prob in thirst center/psychologic)
DI s/sweak pulse, HTN, polydipsia, may have fatigue & generalized weakness, s/s of dehydration (↑sodium, ↑H&H, dry skin/mucus membranes)
DI key featureshypernatremia, ↑serum osmolality (>295), polyuria (2 – 20 L/day), ↓urine specific gravity (<1.005), ↑urinary sodium
DI complicationsCV collapse, tissue hypoxia, seizures, encephalopathy
DI dx: Water deprivation testTest AM urine; Hold H2O 8-12 hrs (infant-4 hrs; child-7 hrs) then given desmopressin (DDAVP) sub-q or nasal; in central DI will ↑urine osmolality from 100 to 600 & ↓UO; in nephrogenic DI will not ↑urine osmolality >300
DI dx: ADHmeasure level of ADH after DDAVP is given; if central DI kidneys will respond by concentrating urine; if nephrogenic will not respond
Acute DIIV hypotonic saline or dextrose 5% in water (D5W) is given & titrated to replace urine output (BOLO hyperglycemia/glycosuria); Monitor: I&O, weight,VS/HR/UO & specific gravity (may be hourly)
DI teachingmaintenance of adequate hydration & F&E balance
DI medsADH replacement (DDAVP, vasopressin) – can be oral/nasal/IV/sub-q
Chlorproamide & carbamazepine to decrease thirst
In nephrogenic: ↓sodium diet (no more than 3 g/day) & thiazide diuretic; indomethacin may help ↑renal response to ADH

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