Calculus Disease Renal Stones Radiology
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Calculus Disease Renal Stones Radiology



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    Calculus Disease Renal Stones Radiology Calculus Disease Renal Stones Radiology Presentation Transcript

    • Epidemiology  Most patients tend to present between 30-60 years of age.  Male : Female (3 : 1)  More common in Asians and whites than in Native Mediterranean Americans, Africans, African Americans.  Geography (stones are more common in hot and dry areas).  Diet and Hereditary also appears to be factor.
    • Etiology 1. Diet – Vitamin A deficiency causes desquamation of epithelium which acts as a nidus for stone formation. 2. Climate – In hot climate, urinary solutes will increase with decrease in colloids, which leads to chelation of solutes with calcium forming a nidus for stone. 3. Citrate level in urine (300-900 mg/24 hours) maintains the calcium phosphate and carbonate in soluble state. So any decrease in citrate level in urine causes stone formation. 4. Infection – Urea splitting organisms (E.coli, Staphylococcus, Proteus)
    • 5. Prolonged immobilization – causes decalcification of bones so hypercalciuria leading to stone formation. 6. Metabolic – Hyperparathyroidism causes hypercalciuria nephrocalcinosis B/L Hyperoxaluria – result of altered glycine metabolism. Hyperuricosuria (Gout) Renal tubular acidosis 7. Stasis/Slow urine flow – due to obstruction to urine flow (e.g. ureteral stricture).
    • Stages of stone formation 1. Super saturation 2. Nucleus formation 3. Crystallization 4. Aggregation 5. Matrix formation 6. Stone
    • Types of Stones
    • Calcium Oxalate Stones  80% of kidney stones contain calcium  General appearance: 1. White, hard, radiopaque 2. Calcium PO4: staghorn in renal pelvis (large) 3. Calcium oxalate: present in ureter (small) 4. Called Mulberry stone (brown) with sharp projections.
    • Phosphate Stones  10-15%  Either be Calcium phosphate (magnesium or ammonium)  Occurs in infection  Smooth and white color  In alkaline urine, it enlarges rapidly, filling renal calyces and taking their shape (STAGHORN CALCULUS).  Radiopaque
    • Uric Acid Stones  8% of renal stones contain uric acid  associated with hyperuricemia (with or without gout)  General appearance: 1. Small, friable, yellowish 2. May form staghorn 3. Radiolucent (plain x-rays cannot detect)
    • Cystine Stones  Occur in Cystinuria (defective resorption of cystine from renal tubules)  Autosomal Recessive  Form in acidic urine (soluble in alkaline urine)  Soft, yellow  Radiopaque (contains sulphur)
    • Xanthine Stones  Rare  Smooth, Brick Red  Deficiency of xanthine oxidase enzyme
    • Struvite Stones  Compound of magnesium, ammonium phosphate mixed with carbonate.  associated with chronic UTI  Occurs in presence of ammonia and urea splitting organisms in urine (e.g. Proteus, Klebsiella)  Radiopaque
    • Staghorn Calculus  Stone occupying the renal pelvis and calyces  Triple phosphate stone  White in color, soft, smooth occurs in pre-existing infection.  Unilateral/Bilateral
    • Clinical History  Classical features of renal colic (or ureteric colic) Sudden severe pain – caused by stones in the kidney, renal pelvis or ureter, causing dilatation, stretching and spasm of the ureter.  Pain starts at the level of the costovertebral angle (but sometimes lower) and moves to the groin, with tenderness of the loin or renal angle, sometimes with hematuria.  If the stone is high and distends the renal capsule then pain will be in the flank but as it moves down pain will move anteriorly and down towards the groin.  A stone that is moving is often more painful than a stone that is static.  The pain radiates down to the testis, scrotum, labia or anterior thigh.
    • D/D on basis of site of pain 1. Biliary colic. 2. Pyelonephritis: very high temperature. Pain is unlikely to radiate to the groin. 3. Acute pancreatitis. 4. Acute appendicitis. 5. Perforated peptic ulcer. 6. Epididymo-orchitis or torsion of testis: very tender testis. 7. Sinister causes of back pain: usually tender over vertebrae. 8. Drug addiction: There are reports of people with fictitious stories of renal colic, designed to obtain an injection of pethidine. 9. Münchhausen's syndrome.
    • D/D of Radiopaque Shadow  Calcified lumbar or mesenteric LN  Gallstone (10% radiopaque)  Concretion in appendix  Phleboliths  Ossified tip of 12th ribs  Chip fracture of transverse process of vertebra  Calcified renal tuberculosis  Calcified suprarenal gland  Foreign body in alimentary canal
    •  Caliceal calculi that are non-obstructing are usually asymptomatic. Patients with small caliceal calculi may still have gross or microscopic hematuria and may have colic symptoms despite the lack of imaging findings suggestive of obstruction.
    • Calculi causing Hydronephrosis  Hydronephrosis is dilatation of the renal pelvis and calyces.  It can be caused by obstruction of the ureters or bladder outlet. Hydronephrosis can also result from reflux (retrograde leakage of urine from the bladder up the ureters to the renal pelvis.
    • Grades of HN on IVU
    • Ureter  Ureter has 3 Constrictions: 1. Pelvic-ureteric junction 2. When it crosses external iliac vessel 3. Vesico-ureteric junction
    • Ureteric Calculus 1. Always of Renal Origin 2. Commonly of elongated shape 3. Can get impacted at 3 constrictions of ureter 4. Can cause: Obstruction Hydronephrosis Infection Ureteral Stricture 5. C/F: Colicky Pain (from loin to tip genitalia) along genitofemoral nerve. Hematuria, dysuria, frequency, strangury Tenderness in iliac fossa
    • Bladder Calculus 1. Primary vesical calculus: • occurs in sterile urine • Comes down from kidney through ureter and gets enlarged in bladder (usually oxalate stone). • Can irritate bladder mucosa causing hematuria 2. Secondary vesical calculus: • Occurs in presence of infection (commonest bladder stone) • Usually phosphate stone, occurs in bladder only
    • Etiology  Same as that of Renal Calculus  Others: 1. Diverticula bladder: which lead to stagnation of urine  superadded infection  stone formation 2. BPH 3. Urethral Stricture 4. Neurogenic Bladder 5. Schistosomiasis
    •  Bladder stones generally form in the bladder itself.  Causes: 1. bladder outflow obstruction (enlarged prostate) 2. neurogenic bladder (loss of bladder function due to spinal cord injury/disease). 3. Those with bladder wall abnormalities (ureterocele, diverticulum) or 4. those with recurrent urinary infections are also at higher risk of forming bladder stones.  When seen on an abdominal/pelvic X-ray they are often multiple and rounded.
    • Bladder Stone  Note that this stone has a faint longitudinal lucency which is the nidus around which the stone developed.
    • Jack Stone  Jackstone calculi resembles toy jacks.  composed of calcium oxalate dehydrate  dense central core and radiating spicules.  light brown with dark patches and are usually described to occur in the urinary bladder and rarely in the upper urinary tract.
    • Bladder Stone
    • Clinical Features  Frequency more during day than night, because during day, due to ambulation stone comes in contact with trigone of the bladder and irritates.  Pain – referred to tip of penis or labia.  Burning micturition and fever.
    • Investigation  Blood – ESR, Serum calcium, phosphate, creatinine, blood urea, uric acid, parathormone level.  Urine – Calcium, urate, cysteine if suspected only, pH.  X-Ray KUB  Intravenous Urethrogram  US Abdomen  CT
    • Kidney Ureter Bladder Kidney Transverse process of lumbar vertebrae (landmark for Ureter) Psoas shadow Bladder
    • Conditions mimicking calculi
    • Nephrocalcinosis  Refers to renal parenchymal calcification. The calcification may be dystrophic or metastatic. 1. With dystrophic calcification, there is deposition of calcium in necrotic tissue. This type of parenchymal calcification occurs in tumors, abscesses, and hematomas. 2. Metastatic nephrocalcinosis occurs most often with hypercalcemic states caused by hyperparathyroidism, renal tubular acidosis, and renal failure. Metastatic nephrocalcinosis can be  further categorized by the location of calcium deposition as cortical or
    • Causes of Nephrocalcinosis  Causes of cortical nephrocalcinosis include 1. acute cortical necrosis 2. chronic glomerulonephritis 3. chronic hypercalcemic states ethylene glycol poisoning, sickle cell disease, and rejected renal transplants  Causes of medullary nephrocalcinosis include 1. hyperparathyroidism (40%) 2. renal tubular acidosis (20%) 3. medullary sponge kidney bone metastases, chronic pyelonephritis, cushing’s syndrome, hyperthyroidism, malignancy, renal papillary necrosis, sarcoidosis, sickle cell disease, vitamin D excess, and Wilson’s disease.
    • Phleboliths  Calcification within venous structures.  Common in the pelvis where they may mimic ureteric calculi, and are also encountered frequently in venous malformations.  Round in shape (but not always) of a similar size that would correspond to the diameter of pelvic veins 1. look like a ring of bone 2. tend to occur laterally around the urinary bladder 3. appear as focal calcifications, often with radiolucent centers
    • Pancreatic calcification  retroperitoneal organs such as the pancreas which only become visible when calcified. Pancreatic calcification is a feature of chronic pancreatitis.
    • Adrenal Calcification  Adrenal (suprarenal) calcification is an uncommon finding and is usually incidental. Most often it is considered a result of previous haemorrhage or tuberculosis.
    • Dermoid cyst
    • Gallstones (10% radiopaque)  Radiopaque lucency in the RUQ and presents with typical laminated appearance  Note anterior location on lateral projection
    •  Gallstones have a variable position depending on the position of the gallbladder and may be mistaken for renal stones  Unlike renal stones they are often rounded and cluster together
    • Appendicolith  Small calcified stone within the appendix, and is seen in the right iliac fossa.
    • Vascular Calcification  Calcification of arteries seen on xrays is a sign of more generalised atherosclerosis.  Occasionally vascular calcification seen on an abdominal X-ray reveals an unexpected aneurysm
    •  Typical appearance of calcified abdominal aorta  Note the outward bulging of the anterior wall
    • Renal Tuberculosis  Genitourinary tract tuberculosis. Lobar calcification in a large destroyed right kidney in a patient with renal tuberculosis. Note the involvement of the right ureter
    • Miscellaneous X-Ray Abdomen Calcification
    • 1. Calcified vas deferens
    • The calcified arrowed structures are likely to be calcified injection sites.
    • Scrotoliths/Scrotal Pearls  The calcified lesions at the bottom of the image are scrotal calculi which are also known as a fibrinoid loose bodies or scrotal pearl.  Scrotoliths or scrotal pearls are benign incidental extra testicular macrocalcifcations within the scrotum. They frequently occupy the potential space of the tunica vaginalis or sinus of the epidydimis. They are usually of no clinical significance.  Causes micro trauma / repetitive trauma to scrotal region - e.g. mountain bikers prior torsion appendix of testis
    • CT Scan Renal Stone On CT almost all stones are opaque, but vary considerably in density. 1. calcium oxalate +/- calcium phosphate: 400600HU 2. struvite (triple phosphate): usually opaque but variable 3. uric acid: 100 - 200HU 4. cysteine: opaque 5. HIV medication related stones (indinavir) difficult to visualize
    •  Protocol 1. Collimation 5-7 mm 2. Pitch of 1.5-2 3. Slice reconstruction of 3 mm Advantages: 1. Avoidance of an injection of contrast medium 2. Rapid results 3. Sensitivity 94%, specificity 97% 4. Alternate diagnosis in patients with acute abdomen pain
    • Calculi on CT
    • Rx of Renal Stones
    • Conservative Rx  Flush Therapy – for low ureteric stones (drinking 2-3 litres of water/day)  IV Fluids  Inj. Frusemide 60-80 mg  Anti-spasmodic agents to relieve the pain.
    • Sx Most of the Stones can be removed without open Sx by:  ESWL - Extracorporeal shock wave lithotripsy (ESWL). This uses highenergy shock waves which are focused on to the stones from a machine outside the body to break up stones. You then pass out the tiny broken fragments when you pass urine.
    •  PCNL - Percutaneous nephrolithotomy (PCNL) is used for stones not suitable for ESWL. A nephroscope is passed through the skin and into the kidney. The stone is broken up and the fragments of stone are removed via the nephroscope. This procedure is usually done under general anaesthetic.
    •  URS - In this procedure, a thin ureteroscope is passed up into the ureter via the urethra and bladder. Once the stone is seen, a laser (or basket) is used to break up the stone.
    • Sx  Pyelolithotomy 1. For stones in extrarenal pelvis 2. Posterior subcostal incision 3. Renal pelvis is opened, stone is removed. 4. Drain is placed and wound is closed.  Extended Pyelolithotomy 1. Incision on hilum over renal sinus 2. To remove stones from pelvis and calyces
    •  Nephrolithotomy Incision behind the most convex surface (Brodel’s line) and stone is removed  Nephropyelolithotomy incision both over the kidney and pelvis. Often done for Staghorn Calculus.
    •  Partial Nephrectomy done when there are multiple calculi occupying a pole or when there’s damage to calyx  Bench Sx
    • Thank You  Abdominal images containing a pregnancy are rarely seen today.