renal calculi

70

Upload: cerin-mathew-mathew

Post on 07-May-2015

11.237 views

Category:

Health & Medicine


3 download

TRANSCRIPT

Page 1: Renal calculi
Page 2: Renal calculi

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.

Page 3: Renal calculi
Page 4: Renal calculi
Page 5: Renal calculi
Page 6: Renal calculi

THE KIDNEY IS COMPOSED OF AN INNER MEDULLA AND AN OUTER CORTEX SURROUNDED BY A TOUGH FIBROUS CAPSULE.

Page 7: Renal calculi

The kidneys remove wastes, control the body's 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 form the renal pelvis.

Page 8: Renal calculi

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

Page 9: Renal calculi
Page 10: Renal calculi

INTRODUCTION

Page 11: Renal calculi
Page 12: Renal calculi
Page 13: Renal calculi

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

Page 14: Renal calculi

INCIDENCE

Urinary calculi are more common in men than in women.

Incidence of urinary calculi peaks between the 3rd and 5th decades of life.

Page 15: Renal calculi

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

Page 16: Renal calculi

CONTINUED………

There is seasonal variation with stone occurring more often in the summer months suspecting the role of dehydration in this process

Page 17: Renal calculi

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

Page 18: Renal calculi

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

Page 19: Renal calculi

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 phosphate.

Page 20: Renal calculi

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

Page 21: Renal calculi

Drug-Induced Stones (Indinavir and Nelfinavir Stones)

These agents are excreted as urinary crystals that may result in crystal deposition or stone formation

Page 22: Renal calculi

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 formation4. A combination of these conditions

Page 23: Renal calculi

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 demonstrate no apparent cause of hypercalciuria.

Page 24: Renal calculi

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 with this problem are often called "calcium wasters

Page 25: Renal calculi

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.

Page 26: Renal calculi

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

Page 27: Renal calculi

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.

Page 28: Renal calculi

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.

Page 29: Renal calculi

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.

Page 30: Renal calculi

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

Page 31: Renal calculi

CLINICAL MANIFESTATION

sharp, severe pain

Page 32: Renal calculi

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

Page 33: Renal calculi

CONTINUED……..

When the pain is severe, the client usually has nausea, vomiting, pallor, grunting respirations, elevated blood pressure and pulse, diaphoresis, and anxiety

Page 34: Renal calculi

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

Page 35: Renal calculi

DIAGNOSTIC EVALUATION 1. Assessment

Page 36: Renal calculi

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)

Page 37: Renal calculi

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.

Page 38: Renal calculi

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.

Page 39: Renal calculi

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 uropathy.

Page 40: Renal calculi

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.

Page 41: Renal calculi

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.

Page 42: Renal calculi

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

Page 43: Renal calculi

MANAGEMENT.

Page 44: Renal calculi

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.

Page 45: Renal calculi

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

Page 46: Renal calculi

URIC ACID STONES

Reduce urinary concentration of uric acid.

Alkalinize urine with potassium citrate. Administer allopurinol. Reduce dietary purines.

Page 47: Renal calculi

CYSTINE

Increase hydration.  Give alpha-penicillamine and tiopronin

to prevent cystin crystallization. Give potassium citrate to maintain

alkaline urine

Page 48: Renal calculi

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.

Page 49: Renal calculi

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.

Page 50: Renal calculi

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

Page 51: Renal calculi

SURGICAL MANAGEMENT

Page 52: Renal calculi

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.

Page 53: Renal calculi

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

Page 54: Renal calculi

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.

Page 55: Renal calculi

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

Page 56: Renal calculi

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

Page 57: Renal calculi
Page 58: Renal calculi

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

Page 59: Renal calculi

CONTINUED,……….

DELAYED Renal functional loss Hypertension Residual calculi Recurrent calculi

Page 60: Renal calculi

OPEN SURGICAL PROCEDURES

Page 61: Renal calculi

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

Page 62: Renal calculi

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

Page 63: Renal calculi

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

Page 64: Renal calculi

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 renal function after calculus removal.

Page 65: Renal calculi

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:

Page 66: Renal calculi

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 Milk and milk products

Page 67: Renal calculi

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

Page 68: Renal calculi

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,

Page 69: Renal calculi

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

Page 70: Renal calculi

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