Which of the following is NOT a hypertonic fluid?
A. 3% Saline
B. D5W
C. 10% Dextrose in Water (D10W)
D. 5% Dextrose in Lactated Ringer’s
B. D5W
What type of fluid would a patient with severe hyponatremia most likely be started on?
A. Hypotonic
B. Hypertonic
C. Isotonic
D. Colloid
B. Hypertonic
When administering a hypertonic solution the nurse should closely watch for?
A. Signs of dehydration
B. Pulmonary Edema
C. Fluid volume deficient
D. Increased Lactate level
B. Pulmonary Edema
A patient with cerebral edema would most likely be order what type of solution?
A. 3% Saline
B. 0.9% Normal Saline
C. Lactated Ringer’s
D. 0.225% Normal Saline
A: 3% Saline. A patient with cerebral edema would be ordered a HYPERTONIC solution to decrease brain swelling. The solution would remove water from the brain cells back into the intravascular system to be excreted. 3% Saline is the only hypertonic option.
_______ solutions cause cell dehydration and help increase fluid in the extracellular space.
A. Hypotonic
B. Osmosis
C. Isotonic
D. Hypertonic
D. Hypertonic
Which solution below is NOT a hypertonic solution?
A. 5% Dextrose in 0.9% Saline
B. 5% Saline
C. 5% Dextrose in Lactated Ringer’s
D. 0.33% saline (1/3 NS)
D. 0.33% saline (1/3 NS)
Which patient below would NOT be a candidate for a hypotonic solution?
A. Patient with increased intracranial pressure
B. Patient with Diabetic Ketoacidosis
C. Patient experiencing Hyperosmolar Hyperglycemia
D. All of the options are correct
A. Patient with increased intracranial pressure
Which condition below could lead to cell lysis, if not properly monitored?
A. Isotonicity
B. Hypertonicity
C. Hypotonicity
D. None of the options are correct
C. Hypotonicity
________ fluids remove water from the extracellular space into the intracellular space.
A. Hypotonic
B. Hypertonic
C. Isotonic
D. Colloids
A. Hypotonic
A patient is being admitted with dehydration due to nausea and vomiting. Which fluid would you expect the patient to be started on?
A. 5% Dextrose in 0.9% Saline
B. 0.33% saline
C. 0.225% saline
D. 0.9% Normal Saline
D. 0.9% Normal Saline
The doctor orders an isotonic fluid for a patient. Which of the following is not an isotonic fluid?
A. 0.9% Normal Saline
B. Lactated Ringer's
C. 0.45% Saline
D. 5% Dextrose in 0.225% saline
C. 0.45% Saline
What are the types of electrolytes?
Sodium
Potassium
Calcium
Magnesium
Chloride
Phosphate
What is third space fluid shift
fluid shifting of intracellular and goes into an area where it can't be used, results in decreased fluid in intracellular
When should 5% dextrose not be given?
Intracranial Pressure*
Diabetics(risk for HYPERglycemia)
What are Isotonic solutions?
Cell presents with the same concentration on the inside and outside with no shifting of fluids (HYDRATION)
Types of Isotonic solutions?
0.9% Saline
5% Dextrose *
5% Dextrose in 0.225 saline
Lactated Ringers (LR)
What are Hypertonic solutions?
Increase fluid in the extracellular space
Intracellulaer-> extracellular
DEHYDRATION(cell shrinks)
Types of hypertonic solutions?
3% saline
5% saline
10% Dextrose (fluid overload w/pulmonary edema)
5% Dextrose in 0.9 saline
5% Dextrose in 0.45 saline
5% Dextrose in LR
What are hypertonic solutions used for?
Hyponatremia (pulls sodium back into intravascular system)
Cerebral edema w/ swelling by remaining fluid off brain
What is Fluid Volume Deficit(HYPOVOLEMIA)
Loss of extracellular fluid exceeds intake ratio of water (DEHYDRATION)
Causes of Hypovolemia
-Abnormal fluid losses (vomiting,diarrhea,sweating,GI suction)
-Decreased intake(nausea, lack of access, anorexia)
-Third space fluid shifts(due to burns, ascites)
-Diabetes insipidus
-Adrenal insufficiency
-Hemorrhage
Clinical manifestations of Hypovolemia
-Weight loss
-↓ skin turgor,
-oliguria,
-concentrated urine,
- increased capillary filling time
- low CVP (central venous pressure), ↓ BP,
-flattened neck veins,
-dizziness, weakness, thirst
and confusion,
-↑ pulse,
muscle cramps, sunken
eyes, nausea, increased
temperature; cool, clammy,
pale skin
Labs indicate Hypovolemia
↑ hemoglobin and hematocrit,
↑ serum and urine osmolality and
specific gravity,
↓ urine sodium,
↑ BUN and creatinine,
↑ urine specific gravity and osmolality
Gerontologic considerations Hypovolemia
-cognition
-ambulation
-ADLs
-Gag reflex
Medical Management Hypovolemia
Oral route prefered
IV for acute or severe losses
Types of solutions
-Lactated Ringer’s solution or 0.9% sodium chloride first line choice for hypotensive pt with fvd
-Normotensive pt a hypotonic electrolyte solution (e.g., 0.45% sodium chloride) is used
-Pt severe FVD-fluid challenge test
Nursing management Hypovolemia
•I&O at least every 8 hours, sometimes hourly
•Daily weight
•Vital signs closely monitored
•Skin and tongue turgor, mucosa, urine output, mental status
•Measures to minimize fluid loss
•Administration of oral fluids
•Administration of parenteral fluids
What is fluid volume excess(Hypervolemia)
Expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ecf (secondary to increase total-body sodium content)
Causes of Hypervolemia
•fluid overload or diminished homeostatic mechanisms
•Heart failure, kidney injury, cirrhosis of liver
•Contributing factors: Consumption of excessive amounts of table salt or other sodium salts
•Excessive administration of sodium-containing fluids
Clinical manifestations of hypervolemia
-weight gain
•Edema(elevate legs)and ascites
•Distended jugular neck veins
•Crackles
-elevated CVP
-shortness of breath(oxygen), ↑ BP,
-bounding pulse and cough,
-↑ respiratory rate,
-↑ urine
output
Labs indicate hypervolemia
↓ hemoglobin and hematocrit, BUN
↓ serum and urine osmolality,
↓urine sodium and specific
gravity
Get chest x-ray
Medical management of hypervolemia
•Diuretics(Loop,Thiaside,Potassium)
•Dialysis (hemodialysis)
•Dietary restrictions of sodium
Nursing management of hypervolemia
•I&O AND DAILY WEIGHTS; ASSESS LUNG SOUNDS, EDEMA, OTHER SYMPTOMS
•MONITOR RESPONSES TO MEDICATIONS—DIURETICS AND PARENTERAL FLUIDS
•PROMOTE ADHERENCE TO FLUID RESTRICTIONS, PATIENT TEACHING RELATED TO SODIUM AND FLUID RESTRICTIONS
•MONITOR, AVOID SOURCES OF EXCESSIVE SODIUM
•PROMOTE REST
What is the normal sodium level
135-145
What does sodium do in the body?
regulate water in and out the cell
-muscle constriction and nerve impulses
Causes of hyponatremia
-Loss of sodium, as in use of diuretics(thiazides), loss of GI fluids, renal disease, and adrenal insufficiency.
-Gain of water, as in excessive administration of D5W and
water supplements for patients receiving hypotonic tube feedings; SIADH, such as head trauma and oat-cell lung tumor;
medications associated with water
retention (oxytocin and certain
tranquilizers); and psychogenic
polydipsia. Hyperglycemia and heart
failure cause a loss of sodium.
-hypotonic fluids
S&S of hyponatremia
anorexia, nausea and vomiting, headache, lethargy, dizziness,
confusion, muscle cramps and weakness, muscular twitching, seizures, papilledema, dry
skin/mucosa, decreased salivation
↑ pulse, ↓ BP,
weight gain, edema
labs indicate hyponatremia
↓ serum and urine sodium,
↓ urine specific gravity and osmolality
Medical and nursing management of hyponatremia
•Treat underlying condition
•Sodium replacement
•Water restriction
•Medication (AVP/ADH receptor antagonists)
•Assessment: I&O, daily weight, lab values, CNS changes
•Encourage dietary sodium
•Monitor fluid intake
•Effects of medications (diuretics, lithium)
Causes of hypernatremia
Fluid deprivation in patients who cannot respond to thirst,
hypertonic tube feedings without adequate water supplements,
diabetes insipidus, heatstroke,
hyperventilation, watery diarrhea, burns, and diaphoresis.
-Excess corticosteroid,
sodium bicarbonate, and sodium chloride administration, and saltwater nonfatal drowning victims.
S&S hypernatremia
Thirst, elevated body temperature, swollen dry tongue and sticky mucous membranes, hallucinations,
lethargy, restlessness,
irritability, increased DTR, pulmonary
edema, hyperreflexia,
twitching, nausea,
vomiting, anorexia,
↑pulse, and ↑ BP
Labs indicate hypernatremia
↑ serum sodium,
↓ urine sodium,
↑ urine specific gravity and osmolality(exceeds 300), ↓ CVP
Medial and nursing management of hypernatremia
•Gradual lowering of serum sodium level via infusion of hypotonic electrolyte solution (0.45% saline) or D5W(rare)
•Diuretics
•Assessment for abnormal loss of water and low water intake
•Assess for over-the-counter sources of sodium
•Monitor for CNS changes
Normal level of potassium
3.5-5
what does sodium do in the body
Found mainly in cell...... Na+ out... fluid balance and Na+ - K+ pumps
-opposite relationship with Na+
-Regulates muscle contractions
causes of hypokalemia
GI losses
corticosteroid administration,
hyperaldosteronism, recent ileostomy, tumor of intestine, alteration in acid base balance, laxative abuse
loop diuretics, too much insulin (k+ moves into cells) bulimia, osmotic diuresis, alkalosis, starvation, diuretics, and digoxin toxicity
S&S of hypokalemia
Fatigue, anorexia, nausea and
vomiting, muscle weakness,
polyuria, decreased bowel
motility, ventricular asystole or
fibrillation, paresthesias, leg
cramps, shallow respirations
↓ BP, ileus, abdominal
distention, hypoactive reflexes. (can cause death through cardiac or respiratory arrest)
ECG: flattened T waves,
prominent U waves, ST
depression, prolonged PR
interval
Metabolic alkalosis
medical and nursing management of hypokalemia
•Potassium replacement: Increased dietary potassium, oral potassium supplements or IV potassium for severe deficit (unless oliguria present)
•Monitor ECG for changes
•Monitor ABGs
•Monitor patients receiving digitalis for toxicity
•Monitor for early signs and symptoms
•Administer IV potassium only after adequate urine output has been established/ and after BUN and Creatinine
Eat foods with potassium-bannans, melons, potatoes, meat, whole grains, apricot
Causes of hyperkalemia
oliguric kidney injury, use of potassium- conserving diuretics in patients with renal insufficiency,
metabolic acidosis, Addison
disease, crush injury, burns,
rapid IV administration of
potassium, and certain
medications such as ACE
inhibitors, NSAIDs, cyclosporine
S&S of hyperkalemia
Muscle weakness, tachycardia →
bradycardia, arrhythmias,
flaccid paralysis, paresthesias,
intestinal colic, cramps,
abdominal distention,
irritability, anxiety, respiratory failure, slurred speech, confusion, metabolic/respiratory acidosis
ECG: tall
tented T waves, prolonged PR
interval and QRS duration,
absent P waves, ST depression
Medical and nursing management of hyperkalemia
•Monitor ECG, heart rate (apical pulse) and blood pressure, assess labs, monitor I&O
•Limitation of dietary potassium and dietary teaching
•Administration of cation exchange resins (sodium polystyrene sulfonate)
•Emergent care: IV calcium gluconate, IV sodium bicarbonate, IV regular insulin and hypertonic dextrose IV, beta-2 agonists(albuterol), dialysis
•Administer IV slowly and with an infusion pump
-loop diuretic-furosemide
-for very severe instances doctor may order K-excalate (pulls potassium out of body) anything over 6
Normal calcium level
8.8-10.4
What does calcium do?
Health of bones/teeth
-muscle/nerves, clotting
Hypocalcemia causes
Hypoparathyroidism (may follow
thyroid surgery or radical neck
dissection), malabsorption, osteoporosis, pancreatitis, alkalosis, vitamin D deficiency, massive subcutaneous infection, massive transfusion of citrated
blood, chronic diarrhea, decreased
parathyroid hormone, diuretic
phase of acute kidney injury,
fistulas, burns, alcoholism
S&S of hypocalcemia
Numbness, tingling of fingers,
toes, and circumoral region;
positive Trousseau sign and
Chvostek sign; seizures,
spasms, Tetnay
hyperactive dtr, irritability,
bronchospasm, anxiety,
impaired clotting time, laryngospasm
↓prothrombin, diarrhea, ↓ BP.
ECG: prolonged QT interval
and lengthened ST
Labs indicate: ↓ Mg++
Medical and nursing management of hypocalcemia
•IV of calcium gluconate for emergent situations (monitor for risk of extravasation)
•Seizure precautions
•Oral calcium and vitamin D supplements
•Exercises to decrease bone calcium loss
•Patient teaching related to diet and medications
Hypercalcemia causes
Hyperparathyroidism, malignant
neoplastic disease, prolonged
immobilization, overuse of
calcium supplements, vitamin D
excess, oliguric phase of acute
kidney injury acidosis,
corticosteroid therapy, thiazide
diuretic use(lithium), increased parathyroid
hormone, and digoxin toxicity
bone loss related to immobility
CANCER,
S&S of hypercalcemia
Muscular weakness,
constipation, anorexia,
nausea and vomiting,
polyuria and polydipsia,
dehydration, hypoactive dtr, lethargy,
deep bone pain, pathologic
fractures, flank pain, calcium
stones(abdominal distention), hypertension.
ECG:
shortened ST segment and
QT interval, bradycardia,
heart blocks
Medical and nurse management of hypercalcemia
•Treat underlying cause (Cancer)
•Administer IV fluids, furosemide, phosphates, calcitonin, bisphosphonates
•Increase mobility
•Encourage fluids
•Dietary teaching, fiber for constipation
•Ensure safety
Normal magnesium levels
1.8-2.6
What does magnesium do for the body?
Very important for the heart
Associated with hypokalemia and hypocalcemia
-nerve/muscle/vessels (relaxation BP
-competes with calcium binding site contraction
Hypomagnesium causes
alcoholism, GI losses,
hyperparathyroidism,
hyperaldosteronism, diuretic phase
of acute kidney injury,
malabsorptive disorders, diabetic
ketoacidosis, refeeding after
starvation, parenteral nutrition,
chronic laxative use, diarrhea, acute
MI,HF,decreased K+ and Ca++ and
certain pharmacologic agents (e.g.,
gentamicin, cisplatin, cyclosporine)
S&S Hypomagnesium
Neuromuscular irritability,
positive Trousseau sign
and Chvostek sign,
insomnia, apathy, anorexia,
vomiting, psychosis, weakness, increase DTR increased
tendon reflexes, and ↑
BP. Ca++ and K+ levels
ECG: PVCs, flat or
inverted T waves,
depressed ST segment,
prolonged PR interval,
and widened QRS
Medical and nurse management Hypomagnesium
•Magnesium sulfate IV is administered with an infusion pump; monitor vital signs and urine output
•Calcium gluconate or hypocalcemic tetany or hypermagnesemia
•Oral magnesium
•Monitor for dysphagia
•Seizure precautions
•Dietary teaching (green, leafy vegetables; beans, lentils, almonds, peanut butter)
Hypermagnesium causes
Flushing, hypotension,
muscle weakness,
drowsiness, hypoactive
reflexes, depressed
respirations, cardiac
arrest and coma,
diaphoresis.
ECG:
tachycardia →
bradycardia, prolonged
PR interval and QRS,
peaked T waves
Medical and nurse management of hypermagnesium
•IV calcium gluconate
•Ventilatory support for respiratory depression
•Hemodialysis
•Administration of loop diuretics, sodium chloride, and LR
•Avoid medications containing magnesium
•Patient teaching regarding magnesium-containing OTC medications
•Observe for DTRs and changes in LOC
Normal phosphate level
2.7-4.5
What does phosphate do for the body?
teeth/bone building, stored in bones
-absorbed in gut and excreted in kidneys
hypophoshatemia causes
Refeeding after starvation,alcoholism, DKA,respiratory and metabolic alkalosis ,↓magnesium &potassium,hyperparathyroidism, vomiting, diarrhea, hyperventilation, vitamin D
deficiency associated with
malabsorptive disorders, burns, acid–
base disorders, parenteral nutrition and diuretic and antacid use
S&S hypophosphatemia
Paresthesias, muscle weakness, bone pain and tenderness,chest pain,confusion,cardiomyopathy,respiratory failure,seizures, tissue hypoxia, and
increased susceptibility to infection, nystagmus
medical and nursing management hypophosphatemia
•Prevention is the goal
•Oral or IV phosphorus replacement (only for patients with serum phosphorus levels less than 1 mg/dL not to exceed 3 mmol/hr), Burosumab, correct underlying cause
•Monitor IV site for extravasation
•Monitor phosphorus, vitamin D and calcium levels
•Encourage foods high in phosphorus (milk, organ meats, beans nuts, fish, poultry), gradually introduce calories for malnourished patients receiving parenteral nutrition
causes of hyeprphosphatemia
Acute kidney injury and chronic kidney disease, excessive intake of
phosphorus, vitamin D excess,
respiratory and metabolic acidosis,
hypoparathyroidism, volume
depletion, leukemia/lymphoma
treated with cytotoxic agents,
increased tissue breakdown,
rhabdomyolysis, chemotherapy
S&S hyperphosphatemia
Tetany, tachycardia, anorexia, nausea and vomiting, muscle
weakness, signs and symptoms of
hypocalcemia; hyperactive reflexes;
soft tissue calcifications in lungs, heart, kidneys, and cornea
-trousseaus and chovesk
-soft tissue calcifications
medical and nurse management hyperphosphatemia
•TREAT UNDERLYING DISORDER
•VITAMIN D PREPARATIONS, CALCIUM-BINDING ANTACIDS, PHOSPHATE-BINDING GELS OR ANTACIDS, LOOP DIURETICS, IV FLUIDS (NORMAL SALINE), DIALYSIS
•MONITOR PHOSPHORUS AND CALCIUM LEVELS
•AVOID HIGH-PHOSPHORUS FOODS
•PATIENT TEACHING RELATED TO DIET, PHOSPHATE-CONTAINING SUBSTANCES, SIGNS OF HYPOCALCEMIA
Normal chloride levels
96-108
what does chloride do?
-acid-base balance
-digestion
-balance fluids w/Na+
Loss of sodium, loss of chloride
-Bicard has inverse relationship with chloride
Hypochloremia causes
Addison disease, reduced chloride intake, untreated DKA, chronic respiratory acidosis, excessive
sweating, vomiting, gastric suction,
diarrhea, sodium and potassium deficiency, metabolic alkalosis; loop, osmotic, or thiazide diuretic use; overuse of bicarbonate, rapid removal of ascitic fluid with a high sodium content, IV fluids that lack chloride (dextrose and water), draining
fistulas and ileostomies, heart failure, cystic fibrosis
S&S hypochloremia
Agitation, irritability,
tremors, muscle
cramps,
hyperactive deep
tendon reflexes,
hypertonicity,
tetany, slow
shallow
respirations,
seizures,
arrhythmias, coma
Labs indicate hypochloremia
↓serum chloride, ↓
serum sodium, ↑ pH, ↑ serum
bicarbonate, ↑ total carbon
dioxide content, ↓urine chloride
level, ↓ serum potassium
Medical and nursing management of hypochloremia
•Replace chloride-IV NS or 0.45% NS
•Ammonium chloride
•Monitor I&O, ABG values and electrolyte levels
•Assess for changes in LOC
Educate about foods high in chloride (tomato juice, bananas, eggs, cheese, milk) and avoid drinking free water (water without electrolytes)
hyperchloremia causes
Excessive sodium chloride infusions with water loss, head injury (sodium retention), hypernatremia, kidney injury, corticosteroid use, dehydration, severe diarrhea (loss of bicarbonate), respiratory alkalosis, administration of diuretics, overdose of salicylates and ammonium chloride use, hyperparathyroidism, metabolic acidosis
S&S hyperchloremia
Tachypnea, lethargy, weakness, deep
rapid respirations, decline in cognitive status, ↓cardiac output, dyspnea,
tachycardia, pitting edema, arrhythmias, coma
medical and nursing management hyperchloremia
•Correct the underlying cause and restore electrolyte and fluid balance
•Hypertonic IV solutions
•Lactated Ringers
•Sodium bicarbonate, diuretics
•Monitor I&O, ABG
•Focused assessments of respiratory, neurologic, and cardiac systems
•Patient teaching related to diet and hydration
ABG Normal levels
pH 7.35-7.45
PO2 (oxygen) 80-100%
PCO2(carbon dioxide) 35-45
HCO3(bicarb) 22-26
Metabolic Acidosis
Low pH (less than 7.35)
PCO2 normal
Bicarb low
-Hyperkalemia may occur
Metabolic acidosis causes
-Salicylate poisoning
-renal failure
-propylene glycol toxicity
-DKA
-starvation
Metabolic acidosis S&S
Headache, confusion, drowsiness, increased respiratory rate/depth
-low BP
-Low cardiac output/dysrhythmias
-shock
Metabolic acidosis medical/nurse management
•Correct underlying problem, correct metabolic imbalance
•Bicarbonate may be administered
•Monitor serum electrolytes
•Monitor potassium levels
•Hemodialysis
•Peritoneal dialysis
Metabolic Alkalosis
Increased pH and Bicarb
normal PCO2
Metabolic Alkalosis causes
Gi losses
-meds-longterm diuretic use
-hyperaldosteronism
-cushings syndrome
-hypokalemia
Metabolic Alkalosis S&S
symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia including tingling of toes, fingers, dizziness and tetany, ECG changes, decreased GI motility
Metabolic Alkalosis medical&nurse management
•Correct the underlying acid–base disorder
•Restore fluid volume with sodium chloride solutions
•Monitor I&O
•Monitor for ECG and neurologic changes
Respiratory Acidosis
Low pH
High CO2
Normal bicarb
Respiratory Acidosis causes
Pulmonary edema, overdose, atelectasis(collapsed lung), pneumothorax(trapped air in lung), severe obesity, pneumonia, COPD, muscular dystrophy, multiple sclerosis, myasthenia gravis
Respiratory Acidosis S&S
With chronic respiratory acidosis, , may be asymptomatic. With acute respiratory acidosis may see sudden increased pulse, respiratory rate, and BP; mental changes; feeling of fullness in head (intracranial pressure) and increased conjunctival vessels.
Respiratory Acidosis Medical/nurse management
•Improve ventilation
•Bronchodilators(albuterol), antibiotics, anticoagulants(heparin, warfarin)
•Pulmonary physiotherapy
•Adequate hydration
•Mechanical ventilation if necessary
•Monitor respiratory status, I&O
Respiratory Alkalosis
Increased pH
Decreased CO2
Bicarb normal
HYPERVENTILATION
Respiratory Alkalosis causes
Extreme anxiety, panic disorder, hypoxemia, salicylate intoxication, gram-negative sepsis, inappropriate ventilator settings
Respiratory Alkalosis S&S
Lightheadedness, inability to concentrate, numbness and tingling in extremities, tachycardia, and ventricular and atrial arrhythmias
Respiratory Alkalosis medical/nurse management
•Treat the underlying cause
•Antianxiety agent
•Have patient breathe into a bag
•Monitor anxiety and respiratory status
•Educate patient on techniques to decrease anxiety
Functional unit of the kidney
Nephron
Functions of the kidney
-Regulate BP
-urine formation
-excrete metabolic waste
-acid base regulation
-fluid and electrolyte regulation
-erythropoietine secretion
How is BP regulated in the kidneys
Hormone Rein is produced by the kidneys and elevates blood pressure.
What is the RAS system ?
When renin is secreted, it turns angiotensinogen into angiotensin l -->
Angiotensin l is then converted in the lungs into angiotensin ll-->
Angiotensin ll causes blood vessels to constrict, which raises BP
(Also causes kidneys to retain more sodium and water, this raises volume of blood)
What is the Antidiuretic Hormone ?
It is responsible for regulating the amount of water in the blood and is released from the pituitary gland based on signals from hypothalamus, which detects water levels of the blood
ADH LOW- kidneys excrete more water and urine output increased (diurese)
ADH HIGH- decreased urine output (retention)
Patients that retain fluid-
-heart disease
-kidney disease
-hyponatremia
-hypervolemic
Patients that don’t retain fluid-
-hypernatremia
-hypovolemia
What is aldosterone?
-Produced by adrenal gland
-acts in the kidneys to aid int he conservation of Na+, secretion of K+, water retention and to stabilize BP
Low aldosterone
AKA Hypoaldosteronism
-occurs as part of adrenal insufficiency -> dehydration, low BP, low blood sodium level, and high potassium level
High Aldosterone
AKA Hyperaldosteronism
-High BP
-Low blood levels of potassium
-abnormal increase in blood volume
What is Erythropoietin >
Is a glycoprotein cytokine secreted by the kidneys in response to cellular hypoxia- stimulates RBC production in the bone marrow
What kind of pt to monitor for kidney disorders ?
Dialysis
Cancer
Heart failure
Malnourishment
Enteral feeds(ng feeds)
Iv fluids
(F&E imbalance, weigh daily, I&O)
Relevant Labs
Blood:
Glomerular filtration Rate (GFR) >90
BUN
Hgb
Hct
Plasma osmality
Urine:
Specific gravity
Urinalysis, electrolytes
Creatinine clearance
More important ab values
Proteinuria/ Albuminuria
risk factors:
diabetes
hypertension
(Proteinuria is considered >300mg/day of albumin excreted)
Gerontologic Considerations kidney
•Older adults susceptible to kidney injury R/T renal structural and functional changes:
•Sclerosis of the glomerulus and renal vasculature
•Decreased blood flow
•Decreased GFR
•Altered tubal function and acid–base balance
•Incomplete emptying of bladder, urinary stasis, decreased nerve innervations
•Decreased drug clearance = increased drug–drug interactions
Causes of Acute Kidney Failure
•Hypovolemia
•Hypotension
•Reduced cardiac output and heart failure
•Obstruction of the kidney or lower urinary tract (kidney stones)
•Obstruction of renal arteries or veins
Phases of AKI
Onset
Oliguric
Diuretic
Recovery
Onset Phase
- Urine output
-HIGH BUN and creatinine
-Mild acidosis
-Diuretics will work
Oliguric Phase
-LESS than 400ml urine in 24hrs
-Electrolyte imbalances
-Acid-base imbalance
Diuretic Phase
-Fluid loss: 4-6 liters per day
-Maintain adequate fluid balance
-Correct electrolyte imbalances
(cycle)
Recovery Phase
•Prevention of further kidney injury
•May last 6 – 12 months
Acute Kidney Injury Patho
sudden loss of kidney function, typically within 24-48 hrs post-injury
AKI types
Pre-renal
Intra-renal
Post-renal
AKI Pre-renal patho
Damage due to the decreased perfusion to the kidneys
AKI Pre-renal S&S and treatment
Low urine output
Low GFR
High BUN/creatinine
Treatment:
-Treat underlying cause (nephrotic agents, sepsis, trauma, bleeding, poor cardiac output, anaphylaxis, burns, ileum)
-Fluid restriction
MAP(65)-when look at BP
AKI Intra-renal patho
Direct damage to kidney cells. (tubular necrosis, glomerulonephritis, interstitial nephritis)
AKI Inta-renal S&S and treatment
Low urine ouput
High BUN/Creatinine
Electrolyte imbalance
Acid-base imbalance
Treatment:
Fluid restriction
Dialysis
AKI Post-renal pathology/S&S and treatment
Obstruction in the flow of urine
S&S:
Abdominal pain, distention
Low urine output
Treatment:
Remove obstruction (kidney stones)
Surgery
Pre-renal Azotemia
when nitrogen water products such as creatinine and urea build up in body, these waste products acts a poison-> damage tissues and reduce organ function
Causes of Chronic Kidney Failure
•Diabetes mellitus
•Hypertension
•Chronic glomerulonephritis
•Pyelonephritis or other infections
•Obstruction of urinary tract
•Hereditary lesions
•Vascular disorders
•Medications or toxic agents
Chronic Kidney Disease Treatment
Renal replacement therapies: peritoneal dialysis, HD, CRRT
-Meds: diuretics, Bone marrow stimulants, erythropoietin, calcium reducer, vitamin supplements
-Diet restrictions: no protein or sodium
-Transplant
-Improve glucose control in diabetic pts
(Impaired immune response/ AVOID foleys)
Nursing Process: The Care of Patients With Chronic Kidney Disease and Acute Kidney Injury—Assessment
•Fluid status
•Nutritional status
•Patient knowledge
•Activity tolerance
•Self-esteem
Potential complications
Glomerular Diseases
•Acute nephritic syndrome
•Glomerulonephritis; chronic and acute
•Nephrotic syndrome
Diseases that destroy the glomerulus of the kidney are the third most common cause of stage 5 CKD
Acute Nephritic Syndrome
•Postinfectious glomerulonephritis, progressive glomerulonephritis, and membranous glomerulonephritis
•Manifestations: hematuria, edema, azotemia, proteinuria, and hypertension
•May be mild or may progress to acute kidney disease or death
•Medical management: supportive care and dietary modifications; treat cause if appropriate—antibiotics, corticosteroids, and immunosuppressants
Nursing Management: Acute Nephritic Syndrome
•Patient assessment
•Maintain fluid balance
•Fluid and dietary restrictions
•Patient education
•Follow-up care
Chronic Glomerulonephritis
•Repeated acute glomerular nephritis, hypertensive nephrosclerosis, hyperlipidemia, and other causes of glomerular damage
•Renal insufficiency or failure: asymptomatic for years as glomerular damage increases before signs and symptoms develop
•Abnormal laboratory test results: urine with fixed specific gravity, casts, proteinuria, electrolyte imbalances and hypoalbuminemia
•Medical management determined by symptoms
Nephrotic Syndrome
•Any condition that seriously damages the glomerular membrane and results in increased permeability to plasma proteins
•Results in hypoalbuminemia and edema
•Causes: chronic glomerulonephritis, diabetes mellitus with intercapillary glomerulosclerosis, amyloidosis, lupus erythematosus, multiple myeloma, and renal vein thrombosis
Medical management: drug and dietary therapy
Renal Replacement Therapy-Hemodialysis
•Hemodialysis: used when patient is acutely ill until kidneys resume function and for long-term replacement therapy in CKD and ESKD
•Objective is to extract toxic nitrogenous substances from the blood and to remove excess fluid:
–Diffusion, osmosis, and ultrafiltration
•Vascular access:
–Arteriovenous fistula
–Arteriovenous graft
Dialysis Concepts
Diffusion:
movement from higher to lower concentration
Convection:
Active movement of molecules across a semi-permeable membrane. Molecules are 'dragged'.
Osmosis:
Low to higher concentration
Ultrafiltration:
Fluid across a semipermeable membrane as a result of an artificially created pressure gradient. More efficient than osmosis in the removal of water
Hemodialysis
Shunting of patients blood from the body through a dialyzer in which diffusion and ultrafiltration occur and then back into the patients circulation.
-Helps restore F&E balance, control acid-base balance, and remove waste and toxic material from body.
Hemodialysis Access/ complications
Access:
Arteriovenous graft
Arteriovenous fistula
Femoral/ subclavian/ intrajugualr access
Complications:
-Rapid fluid shifts, hypotension
-Air embolus, infection
-Disequilibrium syndrome- Occurrence of neurological S&S, attributed to cerebral edema, during/after
-Arrhythmias
Hemodialysis Chronic Care Needs
-Patients require multiple meds
-Increased risk for other co-morbidities
-Multiple dietary and fluid restrictions
-Safety concerns: access sites: CLABSIs
Renal Replacement Therapy- Peritoneal Dialysis
•Goals are to remove toxic substances and metabolic wastes and to reestablish normal F&E balance
•Peritoneal membrane(under peritoneum above bowel) serves as semipermeable membrane
–Ultrafiltration
–Peritoneal catheter
•Acute intermittent, continuous ambulatory, continuous cyclic
•Complications: peritonitis, leakage, bleeding, electrolyte imbalance, adhesions, hernia, inadequate dialysis
(can become ineffective after several years)
Continuous Renal Replacement Therapy (CRRT)
Must have central access
Complications
-F&E imbalance
-Acid-base imbalance
-Hemorrhage
-Thrombosis
-Infection
Nursing Process: The Care of the Hospitalized Patient on Dialysis—Interventions
•Monitor all medications and medication dosages carefully
•Address pain and discomfort
•Stringent infection control measures
•Dietary considerations: sodium, potassium, protein, fluid, individual nutritional needs
•Skin care: pruritus, keep skin clean and well moisturized, trim nails, and avoid scratching
CAPD catheter care
Kidney Surgery
•Preoperative considerations
-CONSENT!!
•Perioperative concerns
•Postoperative management:
–Potential hemorrhage and shock
–Potential abdominal distention and paralytic ileus
–Potential infection
–Potential thromboembolism
-reaction Urine output(F&E)
-insentive spirometry (respiratory)
-monitor site for infection (drainage, bleeding thromboembolism, pneumonia- encourage movement)
Kidney Surgery Postoperative Interventions
•Pain relief measures, analgesic medications
•Promote airway clearance and effective breathing pattern, turn, cough, deep breathe, incentive spirometry, positioning
•Monitor UO and maintain potency of urinary drainage systems
•Use strict asepsis with catheter
•Monitor for signs and symptoms of bleeding
•Encourage leg exercises, early ambulation, and monitor for signs of DVT
Patient Education Kidney Surgery
•Instruct both patient and family
•Drainage system care
•Strategies to prevent complications
•Signs and symptoms
•Follow-up care
•Fluid intake
•Health promotion and health screening
Urinary Tract Infections
•Lower UTI
–Cystitis
–Prostatitis
–Urethritis
•Upper UTI
–Pyelonephritis: acute and chronic
–Interstitial nephritis
–Renal abscess and perirenal abscess
Factors Contributing to UTI
•Bacterial invasion of the urinary tract
•Pregnancy
•Urethrovesical reflux, ureterovesical reflux
•Menopause
•Uropathogenic bacteria
• sexual activity
•Shorter urethra in women
•chronic health condition
•BC
Nursing Process: The Care of the Patient With a UTI—Assessment
•Pain, burning upon urination, frequency, nocturia, incontinence, hematuria
•About half are asymptomatic
•Association of symptoms with sexual intercourse, contraceptive practices, and personal hygiene
•Gerontologic considerations
•Assessment of urine, urinalysis, and urine cultures
•Other diagnostic tests
Nursing Process: The Care of the Patient With a UTI—Diagnoses
•Acute pain related to infection
•Deficient knowledge about:
–Factors predisposing patient to infection and recurrence
–Detection and prevention of recurrence
–Pharmacologic therapy
(Cephalosporin,penicillin,fluroquinolone)
Factors That Contribute to Urinary Tract Infection in Older Adults
•Cognitive impairment
•Frequent use of antimicrobial agents
•High incidence of multiple chronic medical conditions
•Immunocompromise
•Immobility and incomplete emptying of bladder
•Obstructed flow of urine (e.g., urethral strictures, neoplasms, or a clogged indwelling catheter)
Collaborative Problems and Potential Complications UTI
•Sepsis (urosepsis)
•Acute kidney injury
Chronic kidney diseas
Interventions UTI
•Relieving pain
•Medications as prescribed: antibiotics, analgesics, and antispasmodics(flexerale)
•Application of heat to the perineum to relieve pain and spasm
•Increased fluid intake
•Avoidance of urinary tract irritants such as coffee, tea, citrus, spices, cola, and alcohol
•Frequent voiding
•Patient education
Hygiene
Urinary Incontinence
Types:
-Stress
-Urge
-functional
-iatrigenic (involuntary loss of fluid)
-Mixed incontinence
Patient Education Urinary Incontinence
•Urinary incontinence is not inevitable and is treatable
•Management takes time (provide encouragement and support)
•Education verbally and in writing
•Develop and use a voiding log or diary
•Behavioral interventions
•Medication education related to pharmacologic therapy
•Strategies for promoting continence
Urinary Retention
•Inability of the bladder to empty completely
•Residual urine: amount of urine left in the bladder after voiding
•Causes include:
–Adults 60 years and older may have 50 to 100 mL of residual urine remaining in the bladder after voiding
–Postoperative spasms
–Diabetes, prostatic enlargement, urethral pathology, trauma, pregnancy, neurologic disorder
–Medications
-Post-op pts
-BPH
-Pregnancy
-Spine injury
Urolithiasis and Nephrolithiasis
•Calculi (stones) in the urinary tract or kidney
•Causes: may be unknown
•Depends on location and presence of obstruction or infection
•Pain and hematuria
•Diagnosis: radiography, blood chemistries, and stone analysis; strain all urine and save stones
-Morphine given in IV fluids
Patient Education Urolithiasis and Nephrolithiasis
•Signs and symptoms to report
•Follow-up care
•Urine pH monitoring
•Measures to prevent recurrent stones
•Importance of fluid intake
•Dietary education
•Medication education as needed
Renal Cancers
•Bladder, kidney and renal pelvis, ureters, other structures such as prostrate
•Cancer of bladder:
–More common after age 55 years
–Leading cause of death
–Smoking increases risk 50%;
•S/S: visible painless hematuria; pelvic or back pain may indicate metastasis
•Diagnosis: ureteroscopy, excretory urography, CT, MRI, ultrasonography
Nursing management of Bladder Cancer
•Immediate post-op: monitor urine volume hourly
•Provide stoma and skin care
•Test urine and care for ostomy
•Encourage fluids and relieve anxiety
•Patient education about self-care: managing ostomy