Week 7; Acute Care Kidney Injury & Sexual Dysfunction Flashcards
AKI
Rapid reduction in kidney function; failure to maintain fluid and electrolyte balance and acid–base balance with accumulation of nitrogenous waste products in the blood. Evidenced by increased creatinine and BUN. Occurs over a few hours or days, causes systemic effects and complications, can result in death.
Glomerular filtration
First step in urine formation. Normal GFR averages 125 mL/min totaling 180 L day – this is included in reabsorption. Otherwise severe dehydration and death. Only about 1-3 L is excreted each day as urine.
GFR is controlled by BP and blood flow.
Kidneys self-regulate their own blood pressure and blood flow which keeps GFR constant
GFR decreases with age.
By age 65 the GFR is about 65mL/min (half of rate of a young adult) which increases risk of fluid overload.
Diabetes, HTN, or heart failure causes an even faster decline
The combination of reduced kidney mass, reduced blood flow, and a greater risk for drug reactions and kidney damage from drugs and contrast media in older adults.
AKI etiology
More likely in hospitalized adults with advanced age or pre-existing conditions, burns, third spacing depletes kidney of fluid, reduced cardiac output and fluid loss
3 Categories of Causes of AKI:
- Prerenal Causes – perfusion reduction, hypovolemia, low cardiac output
- Intrarenal Causes - Kidney damage, acute tubular necrosis, injury
- Postrenal Causes – Urine Flow Obstruction (Ureteral or Urethral)
Postrenal AKI causes
Ureteral obstruction from cancer, calculi, external obstruction, prostate enlargement, calculi, cancer, stricture, blood clot
Nursing priority with AKI
Preventing volume depletion and providing early intervention when volume depletion occurs are nursing PRIORITIES
Reduced perfusion is common cause of AKI
Reduced perfusion is a common cause of AKI; assess for:
Low urine output – oliguria begins within 1 day after a hypotensive event and can last 1-3 weeks
Decreasing BP
Decreasing pulse pressure
Orthostatic hypotension
Hypovolemic shock review
Abnormally decreased volume of circulating fluid causing peripheral circulatory failure
Endangers vital organs
Brain, heart, kidneys are particularly vulnerable
Tachycardia is an early sign of compensation for excessive blood loss
Tachycardia, tachypnea, BP normal initially, decrease or narrowing in pulse pressure (difference between systolic and diastolic)
elevated BP can occur initially until compensatory mechanisms fail
Acidosis with vasodilation and decreased BP, increased bleeding, decreased circulating volume, and subsequent organ death
Health promotion in the patient with AKI
Avoid dehydration by drinking 2 to 3 L of water daily, be aware of urine characteristic changes, such as sediment, hematuria (smoky or red color), foul odor, or any other worrisome changes, avoid nephrotoxic substances such as NSAIDS, antibiotics, organic solvents, chemicals like pesticides, heavy metals
Assessment of the patient with AKI
Urine characteristic changes or obstructive problems
Recent surgery or trauma
Drug history
Coexisting conditions
Acute illnesses (immunity-mediated AKI)
Anticipate AKI after hypotension or shock
Oliguria output-
<400 ml/24 hours
Anuria output-
<50 ml/day
Labs in pts with AKI
Creatinine, BUN
GFR (normal 90ml/min or higher)
Electrolyte values (K+, phosphorus, sodium)
Renal phosphate increases and calcium binds – so hyperphosphatemia with hypocalcemia
24 hour creatinine clearance
Treatment of AKI
Avoid hypotension, maintain fluid balance
Reduce exposure to nephrotoxic agents
Frequently monitor laboratory values
Closely watch I/O
Drug therapy – including diuretics to rid body of retained fluid, waste products (Lasix (furosemide), Mannitol)
Nutrition therapy
Kidney replacement therapy (intermittent versus continuous)
Why is nutrition therapy needed in AKI?
Patients with AKI often have high rate of catabolism (protein breakdown). Rate of protein breakdown correlates with the severity of uremia and azotemia (increase presence of nitrogenous wastes in blood). Parenteral nutrition may be indicated because patient is too ill.
Signs of uremia-
n/v, anorexia, headache, dizziness, coma, death
Nutrition needs in pts with AKI
Several kidney specific supplements that are lower in sodium, potassium and phosphorus but high in calories. Lower protein, carbs increased. Goal is to provide sufficient nutrients to maintain or improve nutrition status, preserve lean body mass, restore or maintain fluid balance and preserve kidney function
Azotemia –
build up of nitrogen based wastes
Uremia –
azotemia with symptoms
Key features of uremia
Metallic taste in mouth
Anorexia
N/V
Muscle cramps
Uremic “frost” on skin
Itching – caused by uremic frost, and excess phosphorus
Fatigue and lethargy
Hiccups
Edema
Dyspnea
Paresthesias
Albumin in the urine is a marker of __ __, whereas GFR reflects __ __.
kidney damage, kidney function
Teach patients with mild CKD:
carefully managing fluid volume, blood pressure, electrolytes, and other kidney damaging diseases by following prescribed drug and nutrition therapies can slow progression to end-stage kidney disease.
Stage 1 CKD
Patient may have normal GFR >90 but have abnormal urine findings, structural abnormalities or genetic traits that point to kidney disease
Patient is at increase risk for kidney damage from infection, pregnancy, dehydration, and hypotension
Careful management of conditions such as diabetes, hypertension, and hear failure can slow onset and progression
Stage 2 CKD
GFR reduced ranging between 60-89
Albuminuria may be present
Kidney nephron damage has occurred.
There may be slight elevations in BUN, serum creatinine, uric acid, and phosphorus
Stage 3 CKD
GFR reduction continue and ranges between 30-59
Albuminuria usually present
Nephron damage greater and azotemia reflecting poor waste elimination is present
Stage 4 CKD
Waste elimination poor
GFR 15-29
Manage complication
Educate about options for renal replacement therapy
Stage 5 CKD
End stage kidney disease (ESKD)
GFR <15
Kidneys cannot maintain homeostasis
Waste elimination poor and without kidney replacement therapy death will result
Systemic changes associated with CKD:
Metabolic changes
Electrolyte changes
Early stages hyponatremia, later stages hypernatremia
Hyperkalemia – late stage during diuresis - hypokalemia
As more nephrons are lost – METABOLIC ACIDOSIS
KUSSMAUL respirations – increases with worsening kidney disease
Respiratory system tries to adjust or compensate for increased blood hydrogen, acidosis or decreased pH by increasing rate and depth of breathing causing further acidosis, particularly severe in DKA
Systemic changes associated with CKD: cardiac changes
Hypertension
Hyperlipidemia (increased triglyceride, total cholesterol, and LDL)
Heart failure
Pericarditis
Hematologic/immunity changes
GI changes
Cognitive and functional changes
CKD incidence
African-Americans are nearly 3X as likely to develop kidney diseases than white populations. Kidney disease linked to HTN.
Health promotion and maintenance in pts with CKD
Control diseases that lead to CKD, dietary adjustments, weight maintenance, smoking cessation, exercise, limitation of alcohol
CKD teaching
Teach adults treated for an infection anywhere in the kidney/urinary system to take all antibiotics as prescribed. Urge adults to drink at least 2 L of water daily unless a health problem requires fluid restriction. Caution adults who use NSAIDs to use the lowest dose for the briefest time period because these drugs interfere with blood flow to the kidney. High-dose and long-term NSAID use reduces kidney function.
CKD assessment
Weight and height
Daily weights, use same scale, same time of day
Medical history, especially of kidney or urologic origin
Drug use
Dietary habits
GI and GU problems
Energy level
Physical assessment/signs and symptoms in CKD
Neurological and sensory changes
Fluid overload
Tachypnea and hyperpnea
Anemia, abnormal bleeding
Foul breath, mouth inflammation or ulceration
Osteodystrophy
Protein, sediment, or blood in urine
Skin discoloration or uremic frost
CKD assessment
Laboratory assessment
Various blood and urine tests
GFR estimated from serum creatinine, age, gender, race, and body size
Imaging assessment
x-ray findings
Kidney or CT scan
Patients with CKD are at risk for;
fluid overload, decreased cardiac function, and weight loss due to inability to ingest, digest, or absorb food and nutrients as a result of physiologic factors, potential for infection, injury, fatigue, anxiety, depression
Erthropoietin
EPO and reduced RBC production decreased. Risk for anemia
Patient may be prescribed Erythropoietin-Stimulating Agents such as:
Epoetin Alfa (Epogen or Procrit) injection
Signals bone marrow to make more RBCs
Monitor Hgb levels – do not give if over 13g/dL
Common drugs used in CKD
Loop Diuretics – Lasix
Vitamins and minerals
Combo bicarb, insulin, glucose if K+ rises too high
Folic acid, iron supplements
Erythropoietin Stimulating Agents – Epogen (anemia), decreases need for blood transfusion
Managing acidosis
Sodium bicarb or calcium carbonate to correct mild acidosis
Oral phosphorus binding agents to lower serum phosphate levels such as calcium carbonate or calcium acetate)
Aluminum hydroxide for acute hyperphosphatemia
Vit D supplements to improve calcium absorption
Kidney replacement therapy
Used for patients with loss of kidney function and inadequate waste elimination. Indications: uremia, persistent or rapidly rising high potassium levels (greater than 6.5), severe metabolic acidosis (ph less than 7.1), or fluid overload that inhibits tissue perfusion. If AKI occurs with drug or alcohol intoxication, KRT can also remove toxins
Hemodialysis
Most commonly done on intermittent basis. Can be done on inpatient, mostly done on outpatient in a dialysis center. Often done 2-3 times per week – takes approx. 4 hours. Most commonly, patient has a fistula for access. A dialysate and blood flow in opposite directions. The dialysate contains a balanced mix of electrolytes and water resembling human serum. Circulating process continues removing wastes. Blood clotting can occur during the procedure and anticoagulation, usually heparin is delivered into the blood circuit via a pump
