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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.
Renal calculi
Renal calculi
Renal calculi
THE KIDNEY IS COMPOSED OF AN INNER
MEDULLA AND AN OUTER CORTEX
SURROUNDED BY A TOUGH FIBROUS CAPSULE.
 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
 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
Renal calculi
INTRODUCTION
Renal calculi
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
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 solutes

2. Matrix formation caused when mucoproteins bind
   to the mass of the stone
3. 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
MANAGEMENT.
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.
CYSTINE

Increase 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
SURGICAL MANAGEMENT
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
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
CONTINUED,……….

 DELAYED
 Renal functional loss

 Hypertension

 Residual calculi

 Recurrent calculi
OPEN SURGICAL PROCEDURES
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

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Renal calculi

  • 2.  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.
  • 6. THE KIDNEY IS COMPOSED OF AN INNER MEDULLA AND AN OUTER CORTEX SURROUNDED BY A TOUGH FIBROUS CAPSULE.
  • 7.  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
  • 8.  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
  • 13. 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
  • 14. INCIDENCE  Urinary calculi are more common in men than in women.  Incidence of urinary calculi peaks between the 3rd and 5th decades of life.
  • 15. 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
  • 16. CONTINUED………  There is seasonal variation with stone occurring more often in the summer months suspecting the role of dehydration in this process
  • 17. 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
  • 18. 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
  • 19. 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
  • 20. 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
  • 21.  Drug-Induced Stones (Indinavir and Nelfinavir Stones)  These agents are excreted as urinary crystals that may result in crystal deposition or stone formation
  • 22. 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 solutes 2. Matrix formation caused when mucoproteins bind to the mass of the stone 3. Lack of inhibitors caused by increased or absent protectors against stone formation
  • 23. 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
  • 24.  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
  • 25. 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.
  • 26.  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
  • 27. 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.
  • 28. 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.
  • 29.  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.
  • 30. 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
  • 31. CLINICAL MANIFESTATION  sharp, severe pain
  • 32.  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
  • 33. CONTINUED……..  When the pain is severe, the client usually has nausea, vomiting, pallor, grunting respirations, elevated blood pressure and pulse, diaphoresis, and anxiety
  • 34.  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
  • 35. DIAGNOSTIC EVALUATION  1. Assessment
  • 36. 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)
  • 37. 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.
  • 38. 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.
  • 39.  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
  • 40.  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.
  • 41. 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.
  • 42. 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
  • 44. 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.
  • 45. 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
  • 46. URIC ACID STONES  Reduce urinary concentration of uric acid.  Alkalinize urine with potassium citrate.  Administer allopurinol.  Reduce dietary purines.
  • 47. CYSTINE Increase hydration.  Give alpha-penicillamine and tiopronin to prevent cystin crystallization.  Give potassium citrate to maintain alkaline urine
  • 48. 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.
  • 49. 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.
  • 50. 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
  • 52. 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.
  • 53. 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
  • 54. 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.
  • 55. 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
  • 56. 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
  • 58. 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
  • 59. CONTINUED,……….  DELAYED  Renal functional loss  Hypertension  Residual calculi  Recurrent calculi
  • 61. 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
  • 62. 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
  • 63. 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
  • 64. 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.
  • 65. 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:
  • 66. 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
  • 67. 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
  • 68. 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,
  • 69. 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
  • 70. 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