The urinary tract includes the kidneys, ureters, bladder and urethra. Within each kidney, urine flows from the outer cortex to the inner medulla. The renal pelvis is the funnel through which urine exits the kidney and enters the ureter.
THE KIDNEY IS COMPOSED OF AN INNERMEDULLA AND AN OUTER CORTEXSURROUNDED BY A TOUGH FIBROUS CAPSULE.
The kidneys remove wastes, control the bodys fluid balance, and regulate the balance of electrolytes The medulla is composed of a series of conical masses called the renal pyramids. The apex of these pyramids form a papilla which projects into the lumen of the minor calyces. The cortex extends between these medullary pyramids as the renal columns The minor calyces are cup shaped tubes which surround the renal papilla. These converge to form the major calyces, which in turn unite to
Malignant hypertension caused by renovascular disease. The renal artery is narrowed by atherosclerotic plaque causing an elevation in blood pressure. The increased pressure damages the walls of the small arterioles and glomerular capillaries in the cortex. The vessels rupture causing hemorrhage and infarction (scarring). The granular surface of the kidney indicates atrophy and fibrosis of the cortex due to the destruction of the small blood vessels
DEFINITION The stones are solid concretions or calculi (crystal aggregations) formed in the kidneys from dissolved urinary minerals Stones are formed in the urinary tract when urinary concentrations of substances such as calcium oxalate, calcium phosphate, and uric acid increase
INCIDENCE Urinary calculi are more common in men than in women. Incidence of urinary calculi peaks between the 3rd and 5th decades of life.
CONTINUED…………….. The incidence of upper urinary tract stones is greater in industrial countries, such as the United States and countries of Europe, than in developing nations. 50% re-occurrence with in 5-10 years Between 70 and 80 percent of stones are made up primarily of calcium oxalate crystals; the rest contain calcium phosphate salts, struvite (magnesium, ammonium, and phosphate), uric acid, or cystine (an amino acid) India-each year 5-7 million cases are diagnosed 1/1000 need hospitalisation
CONTINUED……… There is seasonal variation with stone occurring more often in the summer months suspecting the role of dehydration in this process
ETIOLOGY AND RISK FACTORS Metabolic Abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid or citric acid. Climate Warm climates that cause increased fluid loss. Low urine volume and increased solute concentration in urine
CONTINUED…………….. DIET Large intake of dietary proteins that increases uric acid excretion. Excessive amounts of tea or fruit juices that elevate urinary oxalate level. Large intake of calcium and oxalate. Low fluid intake that increases urinary concentration
CONTINUED…………….. Genetic factors• Family history of stones formation, cystinuria, gout or renal acidosis. Lifestyle• Sedentary occupation and immobility. A major pre-disposing factor is the presence of UTI. Infection increases the presence of organic matter around which minerals can precipitate and increases the alkalinity of the urine by the production of ammonia. This results in precipitation of calcium phosphate and magnesium-ammonium
CONTINUED…………….. Stasis of urine also permits precipitation of organic matter and minerals. Other factors associated with the development of stones include long-term use of antacids, vitamin D, large doses of vitamin C and calcium carbonate. Any foreign body in the bladder serves as a nidus for infection and calculi formation
Drug-Induced Stones (Indinavir and Nelfinavir Stones) These agents are excreted as urinary crystals that may result in crystal deposition or stone formation
PATHOPHYSIOLOGY Many theories have been proposed to explain the formation of stones in the urinary tract. No single theory can account for stone formation in all cases. Crystallization appears to be the primary factor in calculus development from:1. Supersaturation of urine with increased solutes2. Matrix formation caused when mucoproteins bind to the mass of the stone3. Lack of inhibitors caused by increased or absent protectors against stone formation
TYPES OF CALCULI Calcium Calcium is the most common substance and is found in up to 90% of stones. Calcium stones are usually composed of calcium phosphate or calcium oxalate. They may range from very small particles, often called "sand" or "gravel," to giant staghorn calculi, which may fill the entire renal pelvis and extend up into the calyces. About 35% of all clients with calcium stones do not have high serum levels of calcium and
There are two variants of hypercalciuria The primary abnormality is increased intestinal absorption of calcium or increased bone reabsorption. The resulting higher serum calcium level triggers increased renal filtration of calcium and parathyroid hormone (PTH) suppression. This in turn decreases tubular reabsorption, thereby increasing the concen-tration of calcium in the urine. "Renal leak" of calcium, the other abnormality, is caused by a tubular defect. The resulting hypocalcemia stimulates PTH production, which increases intestinal absorption of calcium. Clients
2.OXALATE The second most frequent stone is oxalate, which is relatively insoluble in urine. Its solubility is affected only slightly by changes in urinary pH. The mechanism of oxalate availability is unclear but may be closely related to diet. The disease is most common in areas where cereals are a major dietary component and least common in dairy-farming regions.
An increased incidence of oxalate stones may be related to: Hyperabsorption of oxalate, seen with inflammatory bowel disease Postileal resection or small-bowel bypass surgery Overdose of ascorbic acid (vitamin C), which metabo-lizes to oxalate Familial oxaluria (oxalate in the urine) Concurrent fat malabsorption, which may cause calcium binding, thus freeing oxalate for absorption
3.STRUVITE Struvite stones, also called triple phosphate, are composed of carbonate apatite and magnesium ammonium phosphate. Their cause is certain bacteria, usually Proteus, which contain the enzyme urease. This enzyme splits urea into two ammonia molecules, which raises the urine pH. Phosphate precipitates in alkaline urine. Stones formed in this manner are staghorn calculi .Abscess formation is common. Struvite stones are difficult to eliminate because the hard stone forms around a nucleus of bacteria, protecting them from antibiotic therapy. Any small fragment left after surgical removal of the stone begins the cycle again.
4. URIC ACID STONE Uric acid stones are caused by increased urate excretion, fluid depletion, and a low urinary pH. Hyperuricuria is the result of either increased uric acid production or the administration of uricosuric agents. Approximately 25% of people with primary gout and about 50% of persons with secondary gout develop uric acid stones.
A high dietary intake of food rich in purine (a protein) may predispose clients to uric acid stone formation. Also, treating neoplastic disease with agents that cause rapid cell destruction may increase the urinary uric acid concentration. It is hypothesized that uric acid crystals absorb some of the crystal inhibitors normally found in urine.
5.CYSTINE Cystinuria is the result of a congenital metabolic error inherited as an autosomal recessive disorder. Cystine stones typically appear during childhood and adolescence; development in adults is very rare
CLINICAL MANIFESTATION sharp, severe pain
most characteristic manifestation of renal or ureteral calculi caused by movement of the calculus and consequent irritation Renal colic originates deep in the lumbar region and radiates around the side and down toward the testicle in the male and the bladder in the female Ureteral colic radiates toward the genitalia and thigh
CONTINUED…….. When the pain is severe, the client usually has nausea, vomiting, pallor, grunting respirations, elevated blood pressure and pulse, diaphoresis, and anxiety
Urinary tract infection Other manifestations of calculi include infection with an elevated temperature and white blood cell (WBC) count and urine obstruction that causes hydroureter, hy-dronephrosis, or both Haematuria Pain resulting from the passage of a calculus down the ureter is intense and collicky. The patient may be in mild shock with cool, moist skin
DIAGNOSTIC EVALUATION 1. Assessment
1.HISTORY Prior stone formation Renal or bladder colic type pain without objective evidence of calculi formation Risk factors Location, character, and duration of current pain Current and previous radiation patterns (indicates possible location and movement of calculus through the urinary system)
2. PHYSICAL EXAMINATION Vital signs include increased pulse, respirations, and blood pressure associated with colicky pain; fever indicates serious infection. Hyperactive bowel sounds occur with nausea and vomiting; hypoactive or absent bowel sounds occur with ileus.
2.DIAGNOSTIC STUDIES Urinalysis, urine culture, and sensitivity testing determine the presence of urinary tract infection, hematuria, or urine crystals. Radiographic studies Ninety percent of calculi are visible on radio-graphic images. Calcium phosphate stones are brightest on radio-graph; uric stones are least visible (radiolucent). KUB using plain abdominal film detects larger, radiopaque stones.
Intravenous urography (IVU) locates radiopaque stones, allowing evaluation of associated obstructive uropathy and crude eval-uation of renal function (i.e., the ability to concen-trate and excrete contrast material). it is a standard method for examining the urinary tract for obstruction in cases of renal colic Tomograms locate stones in the pericaliceal sys-tem. They are performed in combination with IVP. Renal and bladder ultrasound locates stone, creates hypoechogenic "shadow”and gives some indication of associated obstructive
Computed tomography scan locates radiopaque stones. Radionuclide study is an alternative technique tor locating calculi among patients allergic to contrast materials or in a nonfunctioning kidney Among endoscopic procedures, cystoscopy is performed for bladder stone, ureteroscopy for ureteral calculus, and nephroscopy for stone in the pericaliceal system.
D. LABORATORY STUDIES Serum chemistry tests identify calcium, phosphate, oxalate, cystine metabolism, and renal function (creatinine, BUN) abnormalities. Complete blood count detects systemic infection Twenty-four-hour urine collection measures ex-cretion of phosphorous, calcium, uric acid, and creatinine levels. Stone analysis determines the composition of the calculus and assists in designing a preventive pro-gram.
COMPLICATIONS Obstructive uropathy compromises the function of the affected kidney. Microscopic or gross hematuria is rarely associated with significant hemorrhage. Urosepsis is infection that may cause shock or death without prompt intervention. Ileus may occur
CALCIUM OXALATE: Increase hydration. Reduce dietary oxalate. Give thiazide diuretics. Give cellulose phosphate to cholate calcium and pre-vent GI absorption. Give potassium citrate to maintain alkaline urine. Give cholestyramine to bind oxalate. Give calcium lactate to precipitate oxalate in GI tract.
CALCIUM PHOSPHATE Treat underlying causes and other stones Administer antimicrobial agents, acetohydroxamic acid and antibiotics. Use surgical intervention to remove stone. Take measure to acidify urine
URIC ACID STONES Reduce urinary concentration of uric acid. Alkalinize urine with potassium citrate. Administer allopurinol. Reduce dietary purines.
CYSTINEIncrease hydration. Give alpha-penicillamine and tiopronin to prevent cystin crystallization. Give potassium citrate to maintain alkaline urine
STRUVITE STONES Complete removal of the stone with subsequent sterilization of the urinary tract is the treatment of choice for patients who can tolerate the procedures. Percutaneous nephrolithotomy is the preferred surgical approach for most patients. At times, extracorporeal lithotripsy may be used in combination with a percutaneous approach. Open surgery is rarely required.
CONTINUED………. Irrigation of the renal pelvis and calyces with hemiacidrin, a solution that dissolves struvite, can reduce recurrence after surgery. Stone-free rates of 50–90% have been reported after surgical intervention. Antimicrobial treatment is best reserved for dealing with acute infection and for maintenance of a sterile urine after surgery.
CONTINUED……………. Urine cultures and culture of stone fragments removed at surgery should guide the choice of antibiotic. For patients who are not candidates for surgical removal of stone, acetohydroxamic acid, an inhibitor of urease, can be used. side effects-headache, tremor,and thrombophlebitis, that limit its use
1. URETEROSCOPY- involves first visualizing the stone and then destroying it. Access to the stone is accomplished by inserting a ureteroscope into the ureter and then inserting a laser, electrohydraulic lithotriptor, or ultrasound device through the ureteroscope to fragment and remove the stones. A stent may be inserted and left in place for 48 hours or more after the procedure to keep the ureter patent. Hospital stays are generally brief, and some patients can be treated as outpatients.
LITHOTRIPSY LASER LITHOTRIPSY. A newer treatment for calculi is laser lithotripsy. Lasers are used together with a uretero-scope to remove or loosen impacted stones. Constant wa-ter irrigation of the ureter is required to dissipate the heat
EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL) ESWL is a noninvasive procedure used to break up stones in the calyx of the kidney. In ESWL, a high-energy amplitude of pressure, or shock wave, is generated by the abrupt release of energy and transmitted through water and soft tissues. When the shock wave encounters a substance of different intensity (a renal stone), a compression wave causes the surface of the stone to fragment. Repeated shock waves focused on the stone eventually reduce it to many small pieces.
CONTINUED…………. These small pieces are excreted inthe urine, usually without difficulty.the fragments may be passed upto 3 months after the procedure Stone size should be 1.5-2 cm
PERCUTANEOUS LITHOTRIPSY Percutaneous litho-tripsy involves the insertion of a guide percutaneously (through the skin) under fluoroscopy near the area of the stone. An ultrasonic wave is aimed at the stone to break it into fragments. stone size should be >2.5 cm
POST OPERATIVE COMPLICATIONS IMMEDIATE Pain Urinary infection Obstructive uropathy Haematuria Urinoma-URINOMA HAPPENS AS A RESULT OF URETERAL TEAR WHICH ALLOWS THE ENTRY OF FREE FLUID INTO THE RETROPERITONEUM Renal and perirenal haematoma Surrounding organ injury
OPEN SURGICAL PROCEDURES If the stone is too large or if endourologic and lithotripsy procedures fail to remove it, an open surgical procedure is performed ureterolithotomy is the surgical removal of a stone from the ureter through a flank incision for higher stones or an abdominal incision for lower ones. A Penrose drain and ureteral catheter are usually placed postoperatively for healing and drainage of urine
CONTINUED……………. Cystolithotomy, removal of bladder calculi through a suprapubic incision, is used only when stones cannot be crushed and removed transurethrally. Stricture (abnormal narrowing) is the most common postoperative complica-tion. A stone is removed from the renal pelvis by pyelo-lithotomy and from the renal calyx by a nephrolithotomy
MEDICATIONS Lortab (500) mg one tab by mouth every 6 hours as needed for pain Percocet (325) mg one tab by mouth every 6 hours as needed for pain Pyridium (100, 200) mg one tab per mouth every 8 hours for dysuria (burning) Cipro (250, 500) mg one tab per mouth twice a day
PROGNOSIS Despite advances in the treatment of urinary calculi, it is often impossible to remove all stone fragments com-pletely. From 5 to 30 percent of patients have residual stone burden requiring ongoing treatment. Recurrence rate is approximately 30 percent within years. Extracorporeal shock wave lithotripsy and endoscopic stone removal techniques have significantly improved long term prognosis of rena function after calculus removal.
NURSING INTERVENTION adequate hydration, dietary sodium restrictions, dietary agrees, and the use of above-stated medication minimise stone formation High fluid intake at least 3000 ml per day is recommended. Dietary intervention may be important in the management of formation urolithiasis. nutritional management should include limiting oxalate- foods and thereby reducing oxalate excretion. Foods high in , calcium or oxalate contents are as follows:
RICH SOURCES OF CALCIUM Cereals such as ragi, whole bengal, gram(chana), moth beans(matki),Rajmah, soyabeans, horsegram All green leafy vegetables Oilseeds such as dry coconut, gingelly seeds (til), mustard seeds Figs and all dry fruits such as cashewnuts, almonds, dried figs All kinds of fish. Snail, mutton muscle
RICH SOURCES OF PHOSPHORUS Cereals such as bajra, barley, millet, jowar, dry maize, ragi, oatmeal Soya bean. Moderate sources of phosphorus are bengal gram (chana),Cowpea (chawli), rajmah Dry fishes Milk powder, milk
RICH SOURCES OF OXALIC ACID Horsegram (kuleeth), kesari dalAlmonds, cashewnuts, gingelly seeds, ripe chillies, amla, woodapple. Cocoa, coffee, tea Green leafy vegetables such as amaranth, curry leaves, drumstick leaves, mustard leaves, neem leaves,
FOODS CONTAINING PURINE Foods with high Purine content.Organ meats such as kidney, liver, pancreas, brain. Sweet breads. Sardines. Meat extracts. Foods with moderate amounts of Purine Meat, Fish, Shell fish, Alcohol ,Chickoo, apple Foods with small amounts of Purine Asparagus, Mushrooms, Cauliflower, Spinach, Peas, Dry beans ,Pulses, Coffee, Tea
NURSING DIAGNOSIS ACUTE PAIN R/T OBSTRUCTING URINARY CALCULUS ALTERED URINARY ELIMINATION RELATED TO PRESENCE OF URINARY CALCULI RISK TOR INFECTION R/T OBSTRUCTING URINARY CALCULUS ALTERED RENAL PERIPHERAL TISSUE PERFUSION R/T POSTRENAL OBSTRUCTION