RENAL CALCULI PRESENTATION FINAL COPY.pptx

Renal calculi

1. RENAL CALCULI/STONES A PRESENTATION BY MICHAEL BANDA AND MPASO BVULANI MODERATOR: PROF K.BOWA ROTATION:UROLOGY UNIVERSITY OF LUSAKA 5 TH YEAR AUG 2023

2. INTRODUCTION Definitions; Nephrolithiasis refers to renal stone disease. Urolithiasis refers to the presence of stones in the urinary system. Stones, or calculi, are formed in the urinary tract anywhere from the kidney through to the ureters and bladder by the crystallization of substances excreted in the urine.

3. LEARNING OBJECTIVES DEFINE THE TERM RENAL CALCULI. DESCRIBE THE ETIOLOGY OF RENAL CALCULI. DISCUSS THE PATHOGENESIS INVOLVED IN THE DISEASE PROCESS. LIST THE TYPES OF RENAL CALCULI. EXAMINE THE CLINICAL FEATURES CLOSELY. DIFFERENTIATE THE VARIOUS DIAGNOSTIC MEASURES. EXPLAIN THE MEDICAL AND NON-OPERATIVE TREATMENT. IDENTIFY AND EXPLAIN THE OPERATIVE TREATMENT OF RENAL CALCULI.

4. EPIDEMIOLOGY Urolithiasis occurs in all parts of the world: A lifetime risk: 2-5% for Asia 8-15% for the West 20% for the Kingdom of Saudi Arabia Hot Climate Dietary habits Hereditary factors The lower the economic status, the lower the likelihood of renal stones. Most at 20-49 years Peak incidence at 35-45 years Male-to-female ratio of 3:1

5. RISK FACTOR S HIGH MINERAL CONTENT IN DRINKING WATER. DIETARY INTAKE ( vit d, meat consumption) UTI(protease and klebsiela are ureas predisposing factors) & H/O FEMALE GENITAL MUTILATION. PROLONGED INDWELLING CATHETERISATION ( bacteria attach )

6. IMMOBILITY ( predisposes to bone demineralization, hypercalciuria ) SEDENTARY LIFE STYLE. DEHYDRATION ( causes supersaturation ) METABOLIC DISTURBANCES. HISTORY OF RENAL CALCULI.

7. DRUGS ( corticorsteroids ; increase enteric calcium absorption, chemotherapeutric agents) OTHERS; IBD, GOUT

8. STONE FORMATION : Urinary concentration :the less the urinary solvent( less water in urine ), the higher the levels of urinary saturation of solutes ( oxalate, calcium, phosphates). this leads to crystallization ( stones formation). Urinary saturation occurs when there is excess solutes like calcium and oxalate. Urine has the ability to hold more solutes than pure water due to inhibitors of crystallization ( e.g. citrate). Citrate forms a soluble complex with calcium, which prevents calcium from combining with oxalate or phosphate. Other inhibitors are : magnesium, glycosaminoglycans and tamm horse fall- protein. phases of stone formation: (a). Nucleation : formation of nucleus in kidneys. (b) growth . ( c ) aggregation .

9. Etio -pathogenesis Infection : Organisms such as Proteus, Pseudomonas, Klebsiella produce recurrent UTI. These organisms produce the enzyme urease which splits urea into ammonium and carbon dioxide. The ammonium renders the urine alkaline which facilitates precipitation of phosphates. Triple phosphate stones (also called struvite stones) are formed in this manner. Nucleus of the stone may harbor these bacteria. Hot climate causes dehydration resulting in production of highly concentrated urine laden with precipitable solutes, namely calcium and oxalate which leads to formation of calcium oxalate stones. Dietary factors • Diet rich in red meat, fish, eggs can give rise to aciduria (purine rich diet causes uric acid stones). • Diet rich in calcium—tomatoes, milk, spinach, rhubarb produce calcium oxalate stones. • Diet lacking in vitamin A causes desquamation of urothelium and the cellular debris resulting as a consequence there of provides a nidus for crystal aggregation around it.

10. Metabolic causes Hyperparathyroidism increases serum calcium levels by parat-harmone induced bone resorption leading to hypercalciuria which by complexing with oxalate crystals forms renal stones. Gout increases uric acid levels and causes multiple uric acid stones. Any cause of hyperuricemia (increased uric acid levels in the serum) can lead to aggregation of uric acid crystals to form uric acid stones. Common cause of hyperuricemia are dietary excess, gout and increased cellular destruction as in chemotherapy . Immobilization : Immobilization, as in bedridden patients (due to any cause, example— paraplegia), leads to extensive bone demineralization. This in turn causes hypercalciuria culminating in increased risk of stone formation. Such stones are called “recumbency stones”. Decreased urinary citrate : Citric acid (300–900 mg/ 24 hours) keeps the urinary pH low . When citric acid levels decrease, it promotes precipitation of urinary calcium. Citrate excretion is under hormonal control. Citrate is a naturally occurring stone inhibitor substance. Urinary PH : alkaline pH , favors the formation of calcium and phospahate containing stones. Acidic ph promotes the formation uric acid and cystine stones.

11. Urinary stasis : Urinary stasis due to resistance to urinary flow as in anomalous kidneys (Example: Horseshoe kidney, ectopic kidneys, congenital pelvi -ureteric junction obstruction, congenital vesico -ureteric junction obstruction) increases the risk of infections and stone formation. Randall’s plaques : Randall’s observation of submucosal whitish-yellow precipitations of crystalline substances at the tips of renal papillae—well known as Randall’s plaques supports “fixed particle theory” of litho-genesis. The fixed plaque initiates nucleation, the first step in stone formation. Nucleation can be induced by variety of substances—noteworthy among these are free crystals (free particle theory), proteinaceous matrix, foreign bodies (suture material), crystals in clogged lymphatics ( Carr’s hypothesis) and particulate tissue.

12. CLASSIFICATION- BY CHEMICAL COMPOSITION Calcium salts Uric acid Mg ammonium PO4 Cystine Other (xanthine, etc.)

13. CLASSIFICATION ACCORDING TO PH

14. Radio-opaque Calcium Salt Stones Cystine stones (Faint) Struvite Radiolucent • Uric Acid Stones CLASSIFICATION ACCORDING TO X-RAY FINDINGS:

15. CLASSIFICATION- BY LOCATION Urinary stones are typically classified by their location in the; kidney (nephrolithiasis), ureter (ureterolithiasis), bladder (cystolithiasis),

16. Common sites of stones : 1. pelvic ureteric junction(PUJ);where renal pelvis meets the ureter. 2. crossing the pelvic brim 3. vesicoureteric junction(VUJ);where ureter enters the bladder

17. CHEMICAL TYPES Four main chemical types: Calcium stones 85 % Struvite (magnesium ammonium phosphate) stones, common in infection 2-20% Uric acid stones 5-10 % Cystine stones 1 %

18. CALCIUM STONES calcium oxalate account for 85% of Urolithiasis. Commonest variety among urinary calculi . Radio-opaque Two subtypes : Relatively friable calcium oxalate dihydrate ( Weddelite ) and harder calcium oxalate monohydrate ( Wewellite ) They are called mulberry stones as they resemble the mulberry fruit. Their thorny surface can abrade the urothelium causing hematuria which in time imparts a brownish hue to these stones (formation of acid hematin by breakdown of hemoglobin in acidic urine). Small spiky stones are intensely symptomatic especially when they travel down the ureters. In infected urine they exist as mixed stones (calcium oxalate and calcium phosphate). Citrate deficiency

19. 50 % of patients with calcium stones have hypercalciuria, and there are three types : 1. absorptive; increased intestinal absorption of calcium. 2. renal; renal leak( a defect in calcium reabsorption from renal tubules which causes excessive urine loss). 3. resorptive; increased bone demineralization ( hyperparathyroidism)

20. CALCIUM STONE ETIOLOGIES Incidental Hyperparathyroidism hypercalcemia Hyperoxaluria , can be due to: 1).increased renal leak of oxalate, 2).increased oxalate production in short bowel syndrome. Renal phosphate leak Hyperuricosuria ( high urinary uric acid levels) Hypocitraturia ( low urinary citrate excretion)

21. CALCIUM STONE

22. STRUVITE (MAGNESIUM AMMONIUM PHOSPHATE) STONES Account for 15% of renal calculi Infectious stones. Gram-negative rods ( urease producing bacteria ) capable of splitting urea into ammonium, which combines with phosphate and magnesium. More common in females. Urine pH is typically greater than 7.

23. STRUVITE (MAGNESIUM AMMONIUM PHOSPHATE) STONES Stag horn stones are non obstructive thus painless. Slowly growing. Discovered incidentally.

24. URIC ACID STONES Account for 6% of renal calculi. Human urine is supersaturated with insoluble uric acid. Urine pH less than 5.5. uric acid is insoluble in acidic urine Hence ; saturation of uric acid and low ph lead to formation High purine intake eg. organ meats(RED MEATS). Legumes. Malignancy . 25% of patients have gout.

25. URIC ACID STONES

26. CYSTINE STONES 2% of renal calculi. only occurs in patients with cystinuria an inherited autosomal recessive trait. Intrinsic metabolic defect resulting in failure of renal tubular reabsorption of: Cystine, Ornithine,Lysine , Arginine. Urine becomes supersaturated with cystine, with resultant crystal deposition. Radio-faint.

27. HISTORY The presentation is variable. Patients with urinary calculi may report . Pain. Infection. Hematuria. Asymptomatic.

28. CLINICAL FEATURES • Renal pain : Dull aching to pricking type of pain posteriorly in the renal angle formed by the sacro -spinalis and 12th rib. Pain is the most common symptom and it is not related to the size of the stone. Murphy’s kidney punch test demonstrates tender-ness at renal angle. The same pain may some times be felt anteriorly in the costal margin. Hence, it is described as costovertebral pain. Nausea and vomiting is due to intense sympathetic stimulation caused by stretching of renal capsule mediated by coeliac plexus. • Ureteric colic : When the stone is impacted in the pelvi -ureteric junction or anywhere in the ureter, it results in severe colicky pain originating at the loin and radiating to the groin, testicles, vulva and medial side of the thigh. This may be associated with strangury. The referred pain is due to irritation of the genitofemoral, ilioinguinal and ilio-hypogastric nerves.

29. • Haematuria is common with renal stone because majority of stones are oxalate stones. The quantity of blood lost is small but it is fresh blood . • Recurrent UTI : Fever with chills and rigors, burning micturition, pyuria may occur, along with increased frequency of micturition . • Guarding and rigidity of the back and abdominal muscles during severe attack of pain.

30. COMPLICATIONS Calculous hydronephrosis occurs due to back pressure producing renal enlargement. Stretching of the renal capsule results in pain. In such cases, an associated palpable kidney mass suggests hydronephrosis. Calculous pyelonephrosis : Infected hydronephrosis wherein the kidney is converted into a bag of pus. Renal failure: Bilateral staghorn stones may not be symptomatic until they present with uremia and renal failure. Squamous cell carcinoma: Long-standing stones increase the risk of carcinoma.

31. INVESTIGATIONS Blood urea and creatinine to rule out renal failure . Plain X-ray KUB. To diagnose stones. 90% of the renal stones are radio-opaque. Enlarged renal shadow can be seen. USG Presence of the stone can be diagnosed Exact size and location of the stone can be evaluated . Non-contrast CT scan It is the gold standard investigation .

32. Intravenous urogram (IVU) To locate the stone accurately within the collecting system of the kidney (pelvicalyceal system and the ureter) and to assess renal function. A nonradiopaque stone can be seen as a filling defect. Hydronephrosis and hydronephroureterosis can also be seen. Presently, noncontrast CT scan and contrast CT scan are used for more accurate detection of causes of abdominal colic . Urine for culture and sensitivity . Metabolic workup is done in young patients with stones, recurrent stones, nephrocalcinosis and struvite stones—serum uric acid, ionized calcium ,etc.

33. TREATMENT Medical management Analgesic Spasmotic eg Buscopan NSAIDs eg Steroid Maintain I/O charting Provide rest

34. TREATMENT NON-OPERATIVE TREATMENT Conservative: Small stones less than 5 mm in size, stones in the lower ureter, pass off with intake of copious amount of fluids and at times forced diuresis. Intravenous hydration followed by intravenous frusemide may help pass the stones spontaneously. Extracorporeal shock wave lithotripsy (ESWL ): It is indicated when stone is <2 cm in size. The treatment modality of achieving stone fragmentation by focusing externally generated shock waves on the target, i.e. the stone within the renal collecting system through intact skin and across the body wall is called extra corporeal shockwave lithotripsy (ESWL or SWL).Hard stones like cystine and Calcium Oxalate Monohydrate are refractory to treatment by ESWL.

35. II. Operative Treatment ENDOSCOPIC PROCEDURES. OPEN SURGICAL PROCEDURES. Endoscopic Procedures Percutaneous nephrolithotomy (PCNL): It is indicated for stones more than 2 cm in size. Retrograde pyelography (RGP) is done when the stone is located in the pelvis of the kidney. With a small 1 cm incision in the loin, the PCN needle is passed into the pelvis of the kidney and is confirmed by fluoroscopy. A guide wire is passed through the needle into the pelvis of the kidney. The needle is withdrawn, with the guide wire left within the pelvis. Dilators are passed over the guide wire and a working sheath is introduced into the pelvis.

36. A nephroscope is passed into the pelvis and if the stone is small, it can be taken out. If it is big, it may have to be crushed using ultrasound probes and the fragments are removed. Ultrasound or pneumatic energy is used for fragmenting. Holmium- Yag laser can also be used to fragment the stones. Laser fiber can be introduced through the operating nephroscope to achieve this. The method of fragmenting renal stones using different energies introduced through endoscopes is called intracorporeal lithotripsy. Complications of PCNL • Injury to the colon/sepsis. • Injury to the blood vessels. • Urinary leak may persist for a few days.

37. OPEN SURGICAL PROCEDURES Depending upon the location of the stone, various types of procedures are done. They are as follows: Pyelolithotomy : When there is extrarenal pelvis. Nephrolithotomy : When there is intrarenal pelvis, the stone has to be removed by incising through the kidney parenchyma. Extended pyelolithotomy : By retracting the kidney parenchyma off the collecting system, the incision over the pelvis can be extended over to the calyx and the stone can be extracted from the calyx. Even a large staghorn calculus can thus be removed.

38. OPEN SURGICAL PROCEDURES con .. Pyelo -nephrolithotomy : Stone is extracted through an incision in the pelvis as well as the renal parenchyma. Partial nephrectomy : When the stone is impacted in polar calyces and has caused segmental atrophy (polar scarring). Nephrectomy : Significant functional loss (poorly functioning kidney) which is not expected to recover even after stone removal. This is done in patients with recurrent infections.

39. SPECIAL SITUATIONS Bilateral renal stones : Dealing with bilateral stone disease is a matter of clinical judgment. In most instances, the time interval between interventions for two sides is 1–2 weeks. Hence, the symptomatic or obstructed side is dealt first. If both the kidneys are obstructed or are causing symptoms, any one side is destoned (rendered stone free) in the first phase with concurrent institution of a drainage procedure (DJ stenting or percutaneous nephrostomy) for the other side which will be dealt with in about 1–2 weeks. In bilateral disease, if the patient is uremic, urgent bilateral drainage either by DJ stent deployment or nephrostomy is undertaken. Definitive intervention is done once the functional recovery takes place. Kidney with better function has to be operated first. 1–2 weeks later, the opposite side can be operated.

40. If there is pyelonephrosis with high grade fever, pain and tenderness, nephrostomy is done percutaneously under ultrasound guidance in which tube drain is placed in the pelvis of the kidney for drainage of pus and urine. This is called percutaneous nephrostomy or PCN. Once the pus clears, fresh assessment of renal function is done. If the kidney is nonfunctioning, nephrectomy is done. If the kidney is functioning.

41. REFERENCES Skolarikos , A., et al. Metabolic evaluation and recurrence prevention for urinary stone patients: EAU guidelines. Eur Urol , 2015. 67: 750. https://pubmed.ncbi.nlm.nih.gov/25454613/. Turk, C., et al. EAU Guidelines on Diagnosis and Conservative Management of Urolithiasis. Eur Urol , 2016. 69: 468. https://pubmed.ncbi.nlm.nih.gov/26318710/. Turk, C., et al. EAU Guidelines on Interventional Treatment for Urolithiasis. Eur Urol , 2016. 69: 475. https://pubmed.ncbi.nlm.nih.gov/26344917/. Davis, N.F., et al. Treatment outcomes of bladder stones in children with intact bladders in developing countries: A systematic review of >1000 cases on behalf of the European Association of Urology Bladder Stones Guideline panel. J Pediatr Urol , 2022. 18: 132. https://pubmed.ncbi.nlm.nih.gov/35148953/.