ACUTE KIDNEY INJURY (ACUTE RENAL FAILURE)
Acute kidney injury, formerly known as acute renal failure, is the sudden interruption of renal function. Acute kidney injury can be caused by obstruction, poor circulation, or underlying kidney disease. It may be prerenal, intrarenal, or postrenal in origin; it usually passes through three distinct phases: oliguric, diuretic, and recovery.
Prerenal Kidney Injury
Arrhythmias, cardiac tamponade, cardiogenic shock, heart failure, and myocardial infarction
Burns, trauma, sepsis, and tumor
Dehydration and hypovolemic shock
Diuretic overuse and antihypertensive drugs
Hemorrhage, arterial embolism, arterial or venous thrombosis, and vasculitis
Disseminated intravascular coagulation
Eclampsia and malignant hypertension Intrarenal Kidney Injury
Poorly treated prerenal failure
Acute glomerulonephritis, acute interstitial nephritis, acute pyelonephritis, bilateral renal vein thrombosis, malignant nephrosclerosis, and papillary necrosis
Sickle cell disease
Systemic lupus erythematosus
Postrenal Kidney Injury
Bladder, ureteral, or urethral obstruction
Prerenal kidney injury is caused by a condition that diminishes blood flow to the kidneys, leading to hypoperfusion.
Hypoperfusion leads to hypoxemia, which can rapidly damage the kidney. The tubules are most susceptible to hypoxemia’s effect. The impaired blood flow results in decreased glomerular filtration rate (GFR) and increased tubular reabsorption of sodium and water. Life-threatening consequences include volume overload, hyperkalemia, and metabolic acidosis.
Intrarenal kidney injury, also called intrinsic or parenchymal renal failure, results from damage to the filtering structures of the kidneys. Nephrotoxicity or inflammation irreparably damages the delicate layer under the epithelium (basement membrane). Use of nephrotoxins also causes acute kidney injury because they accumulate in the renal cortex.
Postrenal kidney injury is a consequence of bilateral obstruction of urine outflow. The cause may be in the bladder, ureters, or urethra. Common causes include stones, blood clots, bladder tumors, pelvic malignancy, and prostatic hypertrophy.
Signs and Symptoms
Oliguria or anuria
Tachycardia and hypotension
Dry mucous membranes and flat neck veins
Cool, clammy skin
Seizures and coma
Hematuria, petechiae, and ecchymosis
Diagnostic Test Results
Blood studies show elevated blood urea nitrogen, serum creatinine, and potassium levels; decreased bicarbonate level, hematocrit, and hemoglobin levels; and low blood pH.
Urine studies show casts, cellular debris, and decreased specific gravity; in glomerular diseases, proteinuria and urine osmolality close to serum osmolality; urine sodium level less than 20 mEq/L if oliguria results from decreased perfusion and more than 40 mEq/L if the cause is intrarenal.
Creatinine clearance test measures GFR and reflects the number of remaining functioning nephrons.
Electrocardiogram (ECG) shows tall, peaked T waves, widening QRS complex, and disappearing P waves if hyperkalemia is present.
Ultrasonography, plain films of the abdomen, kidney-ureterbladder (KUB) radiography, excretory urography, renal scan, retrograde pyelography, computed tomography scans, and nephrotomography are used to investigate the cause of renal failure.
High-calorie diet low in protein, sodium, and potassium
Electrolyte imbalance: I.V. fluids and electrolytes; hemodialysis or peritoneal dialysis if needed; continuous renal replacement therapies
Edema: fluid restriction
Oliguria: diuretic therapy
With mild hyperkalemic symptoms (malaise, anorexia, muscle weakness): sodium polystyrene sulfonate by mouth or enema
With severe hyperkalemic symptoms (numbness and tingling and ECG changes): hypertonic glucose, insulin, and sodium bicarbonate I.V.
ACUTE TUBULAR NECROSIS
Acute tubular necrosis, also known as acute tubulointerstitial nephritis, accounts for about 75% of all cases of acute renal failure and is the most common cause of acute renal failure in hospitalized patients. Acute tubular necrosis injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Nonoliguric forms of acute tubular necrosis have a better prognosis.
Acute tubular necrosis results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill or those who have undergone extensive surgery.
Certain medications such as aminoglycosides
When ischemic injury occurs, the tubular cells of the kidney suffer from cellular energy depletion, intracellular accumulation of calcium, and damage to the cell membranes. Patch necrosis results at multiple points in the tubules, the basement membrane may be ruptured, and the tubular lumen may become occluded by casts and debris. The occlusion is worsened by the inflammatory cells that produce casts and debris, contributing further to the urinary occlusion. Obstructed urine flow causes an increase tubular intraluminal pressure in the nephron, resulting in a decrease GFR. If the basement membrane is not severely destroyed or if the episode of acute tubular necrosis is not fatal, regeneration eventually will completely reverse the damage.
When nephrotoxic injury occurs, hemoglobin or myoglobin precipitates in the urine. Tubular cells are destroyed by direct toxic effects, lysis of red blood cells (RBCs), activating the cascade of the inflammatory mediators, intravascular coagulation, occlusion of tubules, and tissue hypoxia. In this form of acute tubular necrosis, most necrosis occurs in the proximal tubules.
Signs and Symptoms
Early stages: effects of primary disease may mask symptoms of acute tubular necrosis
Decreased urine output may be first recognizable effect
Uremic syndrome, with oliguria (or, rarely, anuria) and confusion, which may progress to uremic coma
Heart failure and uremic pericarditis
Pulmonary edema and uremic lung
Poor wound healing
Diagnostic Test Results
Urine analysis shows sediment containing RBCs and casts, low specific gravity (1.010), osmolality less than 400 mOsm/kg, and high sodium level (40 to 60 mEq/L).
Blood studies reveal elevated blood urea nitrogen and creatinine levels, anemia, defects in platelet adherence, metabolic acidosis, and hyperkalemia.
ECG shows arrhythmias and, with hyperkalemia, widening QRS segment, disappearing P waves, and tall, peaked T waves.
Vigorous supportive measures until normal kidney function resumes; initial treatment may include:
I.V. fluids to flush tubules of cellular casts and debris and to replace fluid loss.
Give vasopressors and/or inotropes.
Long-Term Fluid Management
Daily replacement of projected and calculated losses (including insensible loss)
Other Measures to Control
Epoetin alfa to stimulate RBC production; packed RBCs for anemia
Stop all possible nephrotoxic drugs
Antibiotics for infection
Emergency I.V. administration of 50% glucose, regular insulin, and sodium bicarbonate for hyperkalemia
Sodium polystyrene sulfonate with sorbitol by mouth or by enema to reduce extracellular potassium levels
Continuous renal replacement therapies
Cancer of the bladder is the most common cancer of the urinary tract.
Workers in certain industries (rubber workers, weavers and leather finishers, aniline dye workers, hairdressers, petroleum workers, and spray painters) are at high risk for bladder cancer. The period between exposure to the carcinogen and development of symptoms is about 18 years.
Primary cause unknown
Smoking is most common causative factor
Transitional cell tumors — certain environmental carcinogens, including 2-naphthylamine, benzidine, tobacco, and nitrates
Squamous cell carcinoma of the bladder:
chronic bladder irritation or infection; for example, from kidney stones, indwelling urinary catheters, and cystitis from cyclophosphamide
Carcinogens are excreted in the urine, creating a medium for prolonged exposure to mucous membranes of the bladder. Bladder tumors can develop on the surface of the bladder wall (benign or malignant papillomas) or grow within the bladder wall (generally more virulent) and quickly invade underlying muscles. Ninety percent of bladder tumors are transitional cell carcinomas, arising from the transitional epithelium of mucous membranes. Less common are adenocarcinomas, epidermoid carcinomas, squamous cell carcinomas, sarcomas, tumors in bladder diverticula, and carcinoma in situ.
Signs and Symptoms
In early stages, no symptoms in approximately 25% of patients
First sign: gross, painless, intermittent hematuria (in many cases with clots in the urine)
Invasive lesions: suprapubic pain after voiding
Other signs and symptoms:
bladder irritability and urinary frequency
Diagnostic Test Results
Cystoscopy and biopsy confirm bladder cancer diagnosis.
Excretory urography identifies a large, early-stage tumor or an infiltrating tumor, delineates functional problems in the upper urinary tract, assesses hydronephrosis, and detects rigid deformity of the bladder wall.
Retrograde cystography evaluates bladder structure and integrity and also helps confirm bladder cancer diagnosis.
Bone scan detects metastases.
Computed tomography scan defines the thickness of the involved bladder wall and discloses enlarged retroperitoneal lymph nodes.
Ultrasonography finds metastases in tissues beyond the bladder and distinguishes a bladder cyst from a bladder tumor.
Complete blood count detects anemia.
Urinalysis detects blood in the urine.
Superficial Bladder Tumors
Transurethral cystoscopic resection and fulguration (electrical destruction); adequate when the tumor has not invaded the muscle
Intravesicular chemotherapy; useful for multiple tumors (especially those that occur in many sites) and to prevent tumor recurrence
Transurethral resection of the prostate (TURP) as adjunctive therapy
If additional tumors develop:
fulguration every 3 months
more radical therapy if tumors penetrate the muscle layer or recur frequently.
Segmental bladder resection to remove a full-thickness section of the bladder; only if tumor is not near the bladder neck or ureteral orifices
Instillation of thiotepa after transurethral resection
Infiltrating Bladder Tumors
Radical cystectomy — removal of the bladder with perivesical fat, lymph nodes, urethra, and prostate and seminal vesicles or uterus and adnexa
Possibly, preoperative external beam therapy to bladder
Urinary diversion, usually an ileal conduit (patient must then wear an external pouch continuously)
Possible later penile implant
Advanced Bladder Cancer
I.V. injection of a photosensitizing agent such as hematoporphyrin ether, which malignant cells readily absorb, followed by cystoscopic laser treatment to kill malignant cells
treatment also renders normal cells photosensitive (patient must totally avoid sunlight for about 30 days)
Intravesicular administration of interferon alfa and tumor necrosis factor
Cystitis and urethritis, the two forms of lower urinary tract infection (UTI), are nearly 10 times more common in women than in men and affect about 10% to 20% of all women at least once. Lower UTI is also a prevalent bacterial disease in children, most commonly in girls. Men are less vulnerable because their urethras are longer and their prostatic fluid serves as an antibacterial shield. In both men and women, infection usually ascends from the urethra to the bladder. UTIs generally respond readily to treatment, but recurrence and resistant bacterial flare-up during therapy are possible.
Ascending infection by a single, gram-negative, enteric species of bacteria, the most common being Escherichia (commonly Escherichia coli). Other less common organisms include Klebsiella, Proteus, Enterobacter, Pseudomonas, Staphylococcus saprophyticus, or Serratia.
Predisposition to infection by bacteria from vagina, perineum, rectum, or a sexual partner, a possible result of a short urethra
In Men and Children
Commonly related to anatomic or physiologic abnormalities
In 99% of patients, reinfection by the same organism or a new pathogen
Persistent infection — usually from renal calculi, chronic bacterial prostatitis, or a structural anomaly that harbors bacteria
Infection results from a breakdown in local defense mechanisms in the bladder that allow bacteria to invade the bladder mucosa and multiply. The antibacterial features in the urine that aid in the prevention of bacterial growth are pH less than 5.5, urea concentration, and presence of organic acids. These factors create an unfavorable medium for bacterial growth due to the acidity. When the local defenses are changed, bacteria quickly grows if present.
Normally, a small amount of urine remains in the bladder after emptying without incident if the natural defenses are present. In cases when the urine is more alkanine, bacteria is allowed to germinate.
Another defense is the unidirectional flow of the urine. If the urine flow is decreased, a catheter or other instrumentation is inserted, or post sexual intercourse, bacteria travels more readily into the bladder. Without the natural defense mechanisms, bacteria can flourish resulting in a local infection.
Signs and Symptoms
Urgency, frequency, and dysuria
Cramps or spasms of the bladder
Itching and feeling of warmth or burning during urination
Urethral discharge in males
Fever and chills
Other common features:
nausea and vomiting
low back pain and flank pain
abdominal pain and tenderness over the bladder area.
Diagnostic Test Results
Microscopic urinalysis is positive for pyuria, hematuria, or bacteriuria.
Bacterial count in clean-catch midstream urine specimen reveals more than 100,000 bacteria per milliliter.
Sensitivity testing determines the appropriate therapeutic antimicrobial agent.
Blood test or stained smear of the discharge rules out sexually transmitted disease.
Voiding cystoureterography or excretory urography detects congenital anomalies that predispose the patient to recurrent UTIs.
Premium Wordpress Themes by UFO Themes
Single-dose therapy with trimethoprim and sulfamethoxazole for 3 to 5 days or nitrofurantoin for 7 days may be effective in women with acute noncomplicated UTI.
If urine is not sterile after 3 days:
bacterial resistance likely
use of a different antimicrobial necessary.
Sitz baths or warm compresses
Increased fluid intake
Phenazopyridine hydrochloride (Pyridium) — a urinary analgesic
Infected renal calculi, chronic prostatitis, or structural abnormality — possible surgery
Prostatitis — long-term antibiotic therapy
In absence of predisposing conditions — long-term, lowdose antibiotic therapy
WordPress theme by UFO themes
%d bloggers like this: