AKI and Male Reproductive Disorders Flashcards
Chronic Kidney Disease (CKD)
○ Progressive, irreversible loss of kidney function
○ Hypertension - chronically uncontrolled
Acute Kidney Injury (AKI):
A potentially reversible, abrupt decline in kidney function leading to increased creatinine, decreased urine output, or both.
Usually associated with other life-threatening conditions
***Follows severe, prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent (gentamycin, CT contrast - flush with fluids)
Develops over hours - days
High mortality rate
Most common people with AKI
■ Sepsis patients
■ Hypovolemic shock
■ Burn patients
■ Fractures - blood loss
■ Athletes - diaphoresis, not replacing fluids
Manifestations of AKI
Mildly elevated serum creatinine –> anuric renal failure
Prerenal and postrenal AKI correctible – ADDRESS THE CAUSE
Untreated prerenal and postrenal causes +/ or intrarenal causes ATN
Causes leading to AKI
Prerenal
- External to the kidneys (ie hypovolemia or meds)
- Usually, reversible
Infrarenal
- Conditions that cause direct damage to renal tissue (parenchyma) impaired nephron function (ie ATN due to ischemia, nephrotoxins, or sepsis)
- Due to prolonged ischemia OR the presence of nephrotoxins (ie gentamycin or CT contrast dye), Hgb from hemolyzed RBC’s (ie sickle cell disease) or myoglobin released from necrotic muscle cells
Postrenal
- Mechanical obstruction of urine outflow (ie BPH, Prostate Ca, renal calculi, tumors).
- Usually reversible if identified before permanent kidney damage occurs
What are the three phases of AKI
Initiation
Maintenance
Recovery
what happens if people do not recover from AKI?
CKD develops
Initiation phase of AKI
Characterized by:
serum creatinine + BUN
urine output
Maintenance phase of AKI
Days to weeks
May be anuric, oliguric, or nonoliguric
Nonoliguric
dilute urine but uremic toxins present (low specific gravity)
Oliguric
lasts 10-14 days usually. The longer it is prolonged, the poorer the outcome
Oliguric means the patient produces LESS THAN 400mL/day or 20mL/ hr
Manifestations include:
- Changes in urinary output
- Fluid and electrolyte abnormalities
- Uremia
Anuric
Anuric means the patient produces NO URINE
Oliguric changes in maintenance phase
Urinary Changes: U/O decreased to <400mL/24h
Fluid volume excess: JVD, edema, hypertension - pulmonary edema, pericardial and/ or pleural effusions
Metabolic acidosis: Kussmaul’s resps (deep rapid) to increase blowing off CO2 - lethargy/ stupor (if prolonged)
Sodium Balance: Hyponatremia
Potassium Excess: Hyperkalemia - tall, peaked T waves (ECG)
Hematological Disorders: Anemia, increased bleeding,, decreased WBCs.
Calcium and Phosphate: Hypocalemia + hyperphosphatemia
Waste Product Accumulation: increased creatinine, increased BUN, decreased eGFR
Neurological Disorders: Fatigue/ difficulty concentrating - seizures, stupor, coma
Metabolic acidosis
Kidneys can’t synthesize ammonia, which is needed for hydrogen ion excretion or to excrete acid products of metabolism. Serum bicarb level decreases b/c bicarb is used up buffering H+ ions.
Sodium Balance
Damaged tubules cannot conserve sodium, therefore, the urinary excretion of sodium may increase resulting in hyponatremia.
Hematological Conditions
Anemia r/t impaired erythropoietin production. Uremia reduces platelet adhesiveness, leading to bleeding. WBC’s are altered leading to immune deficiency. Infection in association with AKI is associated with double the mortality rate.
Potassium Excess
Occurs b/c the normal ability of the kidneys to regulate an dexcrete potassium is impaired. May be precipitated by a number of causes: massive tissue trauma; bleeding and blood transfusions may cause cellular destruction; acidosis worsens hyperkalemia a hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid. Prompt treatment is essential
Calcium and PO4
Activated Vit D must be present for GI absorption of calcium. Only functioning kidneys can activate Vitamin D, therefore, in damaged kidneys, serum calcium decreases. In response, the parathyroid gland releases PTH, stimulating bone demineralization. Phosphate is released as well, leading to hyperphosphatemia, worsened by the reduced excretion of PO4 by the kidneys. Metabolic acidosis also causes more calcium to be in its ionized state (vs bound to protein). An ionized calcium level that decreases significantly can lead to tetany
Waste Product Accumulation
Kidneys are the primary excretors for urea, the end product of protein metabolism and creatinine, and end product of endogenous muscle metabolism. BUN results have to be interpreted with caution b/c dehydration, corticosteroid use, catabolism d/t infection, severe injury, and GI bleeding can also increase BUN. creatinine and BUN. BUN non-specific. Clinically, the recommended method to evaluate kidney function is with an eGFR.
Neurological Disorders
related to accumulation of nitrogenous waste products in the brain and nervous tissue.
Recovery phase
Marked by return of BUN, Creatinine and GFR towards normal states
Diuresis –> fluid & electrolyte abnormalities
- Begins 1-3 L/ 24h –> 3-5 L/ 24h
- Pts must be monitored for hyponatremia, hypokalemia and dehydration
- May last 1-3 weeks
Patient’s acid-base, electrolyte and waste product values begin to normalize
Renal function may take up to 12 mos to stabilize.
Diuresis
The high urine output occurs d/t osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine.
AKI dx studies
Urinalysis
- Sediment WITH casts, cells or proteins - intrarenal disorders
Urine specific gravity, sodium content, osmolality - helps differentiate different types of AKI
Renal ultrasound: anatomy and function
Renal CT: can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk
MRI and MRA are NOT recommended
Care of AKI
GOALS of CARE:
Eliminate the cause(s)
Manage signs and symptoms
Prevent complications
Care of AKI
Is there sufficient Intravascular volume and cardiac output to perfuse the kidneys?
Diuretic Therapy
- Loop diuretics (ie Lasix)
- Osmotic diuretic (ie mannitol)
Fluid Restriction: 600mL (insensible losses) + previous 24h losses
Treatment of Electrolyte imbalances
Renal Replacement Therapy (RRT) – Usually, hemodialysis (HD)
If AKI is already established, fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications.
Nutrition therapy of AKI
Main challenge - Balancing adequate calories to prevent catabolism despite restrictions required to prevent electrolyte and fluid disorders
Energy from fat and carb sources prioritized to prevent ketosis
25-35kCal/kg
Electrolyte replacement in accordance with serum levels
- Sodium is restricted
- Hyperphosphatemia, hypermagnesemia and hypocalcemia
Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)
Health promotion of AKI
ID high-risk populations for AKI
Control nephrotoxic drugs (ie IV contrast)
Prevent prolonged episodes of hypovolemia or hypotension
AKI prevention
essential d/t high mortality rates associated with AKI
For patients with ANY level of renal insufficiency (esp those with diabetes or older adults), special attention must be given to prevent nephrotoxic events secondary to contrast dye. ADEQUATE HYDRATION before and after the test is critical.
Preventing prolonged episodes of hypovolemia INCLUDES monitoring output (esp when pts receiving ++ diuretic therapy, or in with excessive diarrhea/ NG/ vomiting.
