12 Ettinger B, Pak CY, Citron JT, Thomas C, Adams-Huet B, Vangessel A (1997) Potassium magn esium citrate is an effective prophylaxis against recurrent calcium oxalate nephrolithiasis . J Urol 158:2069 \200\22373. 13 Barcelo P, Wuhl O, Servitge E, Rousaud A, Pak CY (1993) Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis. J Urol 150:1761 \200\2234. 14 Pearle MS, Roehrborn CG, Pak CY (1999) Meta-analysis of randomized trials for medical pr evention of calcium oxalate nephrolithiasis. J Endourol 13:679. 15 Ettinger B, Tang A, Citron JT, Livermore B, Williams T (1986) Randomized trial of allopu rinol in th eprevention of calcium oxalate calculi. N Engl J Med 315:1386-9. CHAPTER 9 Stone disease 486 Bladder stones Composition Struvite (i.e. they are infection stones) or uric acid (in non-i nfected urine). Adults Bladder calculi are predominantly a disease of men aged >50 and with BOO due to BPE. They also occur in the chronically catheterized patient (e.g. SCI patients), where the cha nce of developing a bladder stone is 25% over 5y (similar risk whether urethral or suprapub ic location of the stone).1 Children Bladder stones are still common in Thailand, Indonesia, North Africa, the Middle E ast, and Burma. In these endemic areas, they are usually com- posed of a combination of amm onium urate and calcium oxalate. A low phosphate diet in these areas (a diet of breast milk and polished rice or millet) results in high peaks of ammonia excretion in the urine. Symptoms May be symptomless (incidental \201 nding on KUB X-ray or bladder USS or on cyst oscopy) \200\224the common presentation in spinal patients who have limited or no bladder s ensation). In the neurologically intact patient \200\224 suprapubic or perineal pain, haema turia, urgency, and/or urge inconti- nence, recurrent UTI, LUTS (hesitancy, poor \202 ow) . Diagnosis If you suspect a bladder stone, they will be visible on KUB X-ray or renal USS (F ig. 9.15). Treatment Most stones are small enough to be removed cystoscopically (endoscopic cystolitho lapaxy), using stone-fragmenting forceps for stones that can be engaged by the jaws of the forceps and EHL or pneumatic lithotripsy for those that cannot. Large stones (Fig. 9.15) ca n be removed by open sur- gery (open cystolitholapaxy).1 1 Ord J (2003) Bladder management and risk of bladder stone formation in spinal cord injure d patients. J Urol 170:1734 \200\2237. BLADDER STONES 487 Fig. 9.15 A bladder stone. CHAPTER 9 Stone disease 488 Management of ureteric stones in pregnancy While hypercalciuria and uric acid excretion inc reases in pregnancy (pre- disposing to stone formation), so too do urinary citrate and magn esium levels (protecting against stone formation). The \200\230net \200\231 effect \200 \224incidence of ureteric colic is the same as in non-pregnant women.1 Ureteric stones occu r in 1 in 1500 \200\2232500 pregnancies, mostly during second and third tri- mesters. They are associated with a signi \201 cant risk of preterm labor2 and the pain caused by ureter ic stones can be dif \201 cult to distinguish from other causes. Differential diagnosis of \202 ank pain in pregnancy Ureteric stone, placental abruption, appendicitis, pyelonephritis, and all the other (many) causes of \202 ank pain in non-pr egnant women. Diagnostic imaging studies in pregnancy Exposure of the fetus to ionizing radiation can cau se fetal malformations, intrauterine growth retardation, malignancies in later life (leukem ia), and mutagenic effects (damage to genes, causing inherited disease in the off- spring o f the fetus). The fetus is most at risk during organogenesis (weeks 4 \200\22310 of gestati on). Fetal radiation doses during various procedures are shown in Table 9.8. Radiation dose s of <100mGy are reported as unlikely to have an adverse effect on the fetus.3 In USA, the National Council on Radiation Protection has stated that \200\230fetal risk is considered to be negligible at <50mGy when compared to the other risks of pregnancy and the risk of ma lformations is signi \201 cantly increased above control levels at doses >150mGy \200\231. 4 The American College of Obstetricians and Gynecologists has stated that \200\230X-ray ex posure to <50mGy has not been associated with an increase in fetal anomalies or pregnancy l oss \200\231.5 However, every effort should be made to limit exposure of the fetus to radia tion. Table 9.8 Fetal radiation dose after various radiological investigations (note lcGy is equi valent to 10mGy) Risk of inducing cancer (up to age 15y) Procedure Fetal dose (mGy) KUB X-ray 1.4 1 in 24 000 IVU 6 shot 1.7 1 in 10 000 IVU 3 shot \200\223 \200\223 CT: abdominal 8 1 in 4000 CT: pelvic 25 1 in 1300 Fluoroscopy for JJ stent insertion 0.4 1 in 42 000 Adapted from the Joint Guidance from the National Radiographic protection Board, College of Radiographeres Royal College of Radiologists, 1998. MANAGEMENT OF URETERIC STONES IN PREGNANCY 489 Plain radiography and IVU Limited usefulness (fetal skeleton and the enlarged uterus obscur e ureteric stones; delayed excretion of contrast limits opaci \201 cation of ureter; theo- retical risk of fetal toxicity from the contrast material). Recommendations are for a limi ted IVU (e.g. control \201 lm followed by a 30min \201 lm) with fetal shielding. CT-KUB Very accurate method for detecting ureteric stones, but most radiologists and urolog ists are unhappy to recommend this form of imaging in preg- nant women due to increased fet al radiation exposure. Low and ultra-low dose CT protocols are being developed. MRU The American College of Obstetricians and Gynecologists and the US National Council on Radiation Protection state that \200\230although there is no evidence to suggest that the embryo is sensitive to magnetic and radio- frequency at the intensities encountered in MRI, it might be prudent to exclude pregnant women during the \201 rst trimester \200\231.5,6 MRU can, therefore, potentially be used during the second and third trimesters, but not du r- ing the \201 rst trimester. Involves no ionizing radiation. Very accurate (100% sensit ivity for detecting ureteric stones)7, but expensive and not readily available in most hosp itals, particularly out of hours. Management Most (70 \200\22380%) will pass spontaneously.3 - Pain relief premature closure of the ductus arteriosus by blocking prostaglandin synthesis) . Indications for intervention pain refractory to analgesics, suspected urinary infection ( high fever, high WBC), high-grade obstruction, and obstruction in a solitary kidney). : opiate-based analgesics; avoid NSAIDs (can cause : the same as in non-pregnant patients \200\224 Options for intervention Depend on the stage of pregnancy and on local facilities and exper tise: - 4 requires regular changing (approximately JJ stent urinary diversion: 6 \200\2238 weeks to avoid encrustation). Nephrostomy urinary d iversion. Ureteroscopic stone removal with laser fragmentation. Aim to minimize radiation exposure to the fetus and to minimize the risk of miscarriage and preterm labor. General anesthesia can precipitate preterm labor and many urologists and ob stetricians will err on the side of temporizing options such as nephrostomy tube drainage o r JJ stent placement, rather than on operative treatment in the form of uretero- scopic sto ne removal. Avoid PCNL; ESWL is contraindicated. CHAPTER 9 Stone disease 490 1 Coe FL, Parks JH, Lindhermer MD (1978) Nephrolithiasis during pregnancy. N Engl J Med 298 :324 \200\2236. 2 Hendricks SK (1991) An algorithm for diagnosis and therapy of urolithiasis during pregnan cy Surg Gynecol Obst 172:49 \200\22354. 3 Hellawell GO, Cowan NC, Holt SJ, Mutch SJ (2002) A radiation perspective for treating loi n pain in pregnancy by double-pigtail stents. BJU Int 90:801 \200\2238. 4 National Council on Radiation Protection and Measurement (1997) Medical radiation exposur e of pregnant and potentially pregnant women. NCRP Report no. 54. Bethesda, MD: NCRPM. 5 American College of Obstetricians and Gynecologists Committee on Obstetric Practice (1995 ) Guidelines for Diagnostic Imaging During Pregnancy. ACOG Committee Opinion no. 158. Washi ngton DC: ACOG. 6 Roy C (1996) Assessment of painful ureterohydronephrosis during pregnancy by MR urogra- p hy. Eur Radiol 6:334 \200\2238. 7 Watterson JD, Girvan AR, Beiko DT, et al. (2002) Ureteroscopy and holmium: an emerging de \201 nitive management strategy for symptomatic ureteral calculi in pregnancy. Urology 60 :383 \200\2237. 8 Sharp C, Shrimpton JA, Bury RF (1998) Joint Guidance from National Radiological Protectio n Board, College of Radiographers and Royal College of Radiologists. Advice on Exposure to Ionizing Radiation during Pregnancy. Produced by the National Radiological Protection Board , Chilton, Didcot [online]. Available from: M http://www.nrpb.org. 491 Chapter 10 Upper tract obstruction, loin pain, hydronephrosis Hydronephrosis 492 Management of ureteric strictures (other than PUJO) 496 Pathophysiology of urinary tract obstruction 498 Physiology of urine \202 ow from kidneys to bladder 499 Ureter innervation 500 Retroperitoneal \201 brosis 502 CHAPTER 10 Upper tract obstruction 492 Hydronephrosis Dilatation of the renal pelvis and calyces (Fig. 10.1). When combined with d ilatation of the ureters, known as hydroureteronephrosis. Obstructive nephropathy is damage to the renal parenchyma, result- ing from an obstruction to the \202 ow of urine anywhere along the urinary tract. Dilatation of the renal pelvis and calyces can occur without obstruction and therefore, hyd ronephrosis should not be taken to necessarily imply the presence of obstructive uropathy. Ultrasound - False negative (i.e. obstruction present, no hydronephrosis): onset of obstruction; in the presence of an intrarenal collecting system; with dehydration; misdiagnosis of dilatation o f the calyces as renal cortical cysts (in acute ureteric colic, ultrasonography fails to de tect hydronephrosis in up to 35% of patients with proven acute obstruction on IVU). False p ositive (i.e. hydronephrosis, no obstruction): extrarenal pelvis; parapelvic cysts; VUR; hi gh urine \202 ow. acute capacious Diagnostic approach to the patient with hydronephrosis Patients with hydronephrosis may pre sent either as an incidental \201 nding of hydronephrosis on USS or CT done because of no n-speci \201 c symptoms or it may be identi \201 ed in a patient with a raised creatinine or presenting with loin pain. Symptoms, if present, will depend on the rapidity of onset o f obstruction of the kidney (if that is the cause of the hydronephrosis), whether the obstr uction is complete or partial, unilateral or bilateral, and whether the obstruction to the ureter is extrinsic to the ureter or is within its lumen. History - Severe \202 ank pain suggests a more acute onset of obstruction and if very sudden in ons et, a ureteric stone may well be the cause. Pain induced by a diuresis (e.g. following cons umption of alcohol) suggests a possible PUJO. Anuria (the symptom of bilateral ureteric obs truction or complete obstruction of a solitary kidney). If renal function is impaired, symp toms of renal failure may be present (e.g. nausea, lethargy, anorexia). Extrinsic causes of obstruction (e.g. compression of the ureters by retroperitoneal malignancy) usually have a more insidious onset whereas intrinsic obstruction (ureteric stone) is often present with severe pain of very sudden onset. An increase in urine output may be reported by the patien t due to poor renal concentrating ability. Obstruction in the presence of bacterial pyelone phritis ( \202 ank pain and tenderness, fever) or sepsis. UTI \200\224signs and symptoms of HYDRONEPHROSIS 493 Fig. 10.1 Hydronephrosis as seen on renal ultrasonography. Examination - Measure BP: overload). Bilateral oedema (due to \202 uid overload). Abdominal examination : DRE (? cervical cancer). Check serum creatinine to determine the functional effect of the hydronephrosis. Renal ultrasonography (if not already done). elevated in HPCR due to BPO (caused by \202 uid - percuss and palpate for an enlarged bladder. (? prostate or rectal cancer) and, in women, v aginal examination IVU \201 ndings in renal obstruction - - - - - An obstructive (dense) nephrogram. A delay in \201 lling of the collecting system with co ntrast material. Dilatation of the collecting system. An increase in renal size. Rupture of fornices (junction between renal papilla and its calyx) with urinary extravasation. Ureter ic dilatation and tortuosity. A standing column of contrast material in the ureter. Unilateral hydronephrosis KUB X-ray (a ureteric stone may be seen); CTU (or IVU) if stone s uspected. - If no stone seen, but hydronephrosis is con \201 rmed and ureter is non-dilated, the obstr uction must be at the PUJ. In the absence of a ureteric stone visible on CTU, the diagnosis must be PUJO. If no stone seen and the ureter is dilated as well as the kidney, ureteric T CC is likely. Arrange retrograde ureterography to identify site of obstruction and ureteros copy/ureteric biopsy. CHAPTER 10 Upper tract obstruction 494 Bilateral hydronephrosis - If the patient is in retention or has a substantial post-void residual urine volume, pass a catheter. If the elevated creatinine falls (and the hydronephrosis improves), the diagnosi s is BOO due, for example, to BPH, prostate cancer, urethral stricture, DSD. If the creatin ine remains elevated, the obstruction affecting both ureters is higher \200\230upstream \200\231. TRUS CT scan looking for malignant bilateral ureteric obstruction, AAA. and prostatic biopsy if prostate cancer suspected on DRE, HYDRONEPHROSIS 495 Causes of hydronephrosis Unilateral - - - - - Obstructing ureteric stone. PUJO. Obstructing clot in ureter. Obstructing ureteric TCC. (An y of the causes listed below where the pathologic process has not yet extended to involve b oth ureters). Bilateral - BOO . - BPH. - Prostate cancer. - Urethral stricture. - DSD. - Posterior urethr al valve. Bilateral ureteric obstruction at their level of entry into the bladder. - Locall y advanced cervical cancer. - Locally advanced prostate cancer. - Locally advanced rectal c ancer. - Poor bladder compliance (often combined with DSD): neuropathic bladder (spinal cord injury, spina bi \201 da), post-pelvic radiotherapy. Periureteric in \202 ammation. - From adjacent bowel involved with in \202 ammatory bowel disease (e.g. Crohn \200\231s, ulcerative colitis) or diverticular disease. Retroperitoneal \201 brosis. - Idiopathic (diagnosed following exclusion of other causes) . - Periarteritis \200\224aortic aneurysm, iliac artery aneurysm. - Post-irradiation. - Dru gs \200\224methysergide, hydralazine, haloperidol, LSD, methyldopa, beta blockers, phenacetin, amphetamines. Malignant \200\224retroperitoneal malignancy (lymphoma, metastatic disease from, e.g. breast cancer), post-chemotherapy. Chemicals \200\224talcum powder. - Infection \200\224TB, syphilis, gonorrhea, chronic UTI. - Sarcoidosis. Bilateral Hydronephrosis of pregnancy (partly due to smooth muscle relaxant effect of progesterone, partly obstruction of ureters by fetus). Hydronephrosis in associat ion with an ileal conduit (a substantial proportion of patients with ileal conduit urinary diversion has bilateral hydronephrosis in the absence of obstruction). Bilateral ureteric s tones (rare). PUJO (uncommon). CHAPTER 10 Upper tract obstruction 496 Management of ureteric strictures (other than PUJO) De \201 nition A normal ureter undergo es peristalsis and therefore, at any one moment, at least one area of the ureter will be ph ysiologically narrowed. A ureteric stricture is a segment of ureter that is narrowed and re mains so on several images (i.e. it is a length of ureter that is constantly narrow). Causes Most ureteric strictures are benign and iatrogenic. Some follow the impac- tion of u reteric stone for a prolonged period; malignant strictures \200\224within wall of ureter (e .g. TCC ureter), extrinsic compression from outside wall of ureter (e.g. lymphoma, malignan t retroperitoneal lymphadenopathy); retroperitoneal \201 brosis (RPF) which may be benign (idiopathic, aortic an- eurysm, post-irradiation, analgesic abuse) or malignant (retroperi toneal malignancy, post-chemotherapy). Mechanism of iatrogenic ureteric stricture formation Normally ischaemic: - Usually injury at time of open or endoscopic surgery (e.g. damage to ureteric blood supply or direct damage to the ureter at time of colorectal resection, AAA graft, hysterectomy); a t ureteroscopy \200\224 mucosal trauma (from ureteroscope or electrohydraulic lithotripsy), perforation of ureter (urine extravasation, leading to \201 brosis). Radiotherapy in the vicinity of the ureter. Stricture of ureteroneocystostomy of renal transplant. Investigations The stricture may be diagnosed following investigation for symptoms (loin pa in, upper tract infection) or may be an incidental \201 nding on an investigation done fo r some other reason. The stricture may be diagnosed on renal USS (hydronephrosis), IVU, or CTU. A MAG3 renogram will con- \201 rm the presence of obstruction (some minor strictures may cause no renal obstruction) and establish split renal function. Where ureteric TCC is possible, proceed with ureteroscopy and biopsy. \200\230Treatment \200\231 options - Nothing (symptomless stricture in an old patient with signi \201 cant comorbidity or <25% function in an otherwise healthy patient with a normally functioning contralateral kidney). Permanent JJ stent or nephrostomy, changed at regular intervals (symptomatic stricture in an old patient with signi \201 cant comorbidity or <25% function in affected kidney with c ompromised overall renal function). Dilatation (balloon or graduated dilator) (Figs. 10.2 a nd 10.3). Incision + balloon dilatation (endoureterotomy by Acucise ureteroscopy or nephros tomy and incision, e.g. by laser). Leave a 12 Ch stent for 4 weeks. Excision of stricture a nd repair of ureter (open or laparoscopic approach). Nephrectomy. balloon; MANAGEMENT OF URETERIC STRICTURES (OTHER THAN PUJO) 497 Fig. 10.2 Balloon dilatation of a lower ureteric stricture. Fig. 10.3 The catheter used for balloon dilatation. Factors associated with reduced likelihood of a good outcome after endoureterotomy - - - - <25% function in kidney. Stricture length >1cm. Ischaemic stricture. Midureteric stricture (compared with upper and lower) \200\224tenuous blood supply. JJ stent size <12 Ch. Ureteroenteric strictures (ileal conduits, ureteric implantation into neobladder) These are due to ischaemia and/or periureteral urine leak in the imme- diate post-operative period, which leads to \201 brosis in the tissues around the ureter. In ileal conduits, the left ureter is affected more than the right because greater mobilization is required to bring it to the right side and it may be compressed under the sigmoid mesocolon, both of which impa ir blood \202 ow to the distal end of the ureter. CHAPTER 10 Upper tract obstruction 498 Pathophysiology of urinary tract obstruction Effects of obstruction on renal blood \202 o w and ureteric pressure Acute unilateral ureteric obstruction (UUO) Leads to a triphasic re lationship between renal blood \202 ow (RBF) and ureteric pressure. - (up to 1.5h post-obstruction): ureteric pressure rises, Phase 1 RBF rises (afferent arteriole dilatation). Phase 2 rise, RBF falls (efferent arteri ole vasoconstriction). Phase 3 (afferent arteriole vasoconstriction). (from 1.5 \200\2235h post-obstruction): ureteric pressure continues to (beyond 5h): ureteric pressure falls, RBF continues to fall Acute bilateral ureteric obstruction (BUO) or obstruction of a solitary kidney - Phase 1 RBF rises (afferent arteriole dilatation). Phase 2 rise, RBF is signi \201 cantly lower than that during UUO. Phase 3 (beyond 5h): ureteric pressure remains elevated (in con trast to UUO). By 24h, RBF has declined to the same level for both UUO and BUO. (up to 1.5h post-obstruction): ureteric pressure rises, (from 1.5 \200\2235h post-obstruction): ureteric pressure continues to In UUO, the decrease in urine \202 ow through the nephron results in a greater degree of Na absorption so Na excretion falls. Water loss from the obstructed kidney increases. Release of BUO is followed by a marked natriuresis, increased K excre- tion, and a diuresis (a solute diuresis).This is due to: - An appropriate (physiological) natriuresis to excrete excessive Na which is a consequence o f BUO. A solute diuresis from the accumulation of urea in A diminution of the corticomedull ary concentration gradient, which is normally established by the countercurrent mechanism o f the Loop of Henle, and is dependent on maintenance of \202 ow through the nephron \200 \224reduction of \202 ow, as occurs in BUO, reduces the ef \201 ciency of the countercur rent mechanism (effectively, the corticomedullary concentration gradient is \200\230washed out \200\231). ECF. There may also be accumulation of natriuretic peptides (e.g. ANP) during BUO, which contrib utes to the natriuresis following release of the obstruction. Likelihood of recovery of renal function after release of obstruction In dogs with complete ly obstructed kidneys, full recovery of renal function after 7 days of UUO occurs within 2 weeks of relief of obstruction. A total of 14 days of obstruction leads to a permanent redu ction in renal function to 70% of control levels (recovery to this level taking 3 \200\2236 months after re- versal of obstruction). There is some recovery of function after 4 weeks of obstruction, but after 6 weeks of complete obstruction, there is no recov- ery. In human s, there is no clear relationship between the duration of BUO and the degree of recovery of renal function after relief of obstruction. PHYSIOLOGY OF URINE FLOW FROM KIDNEYS TO BLADDER 499 Physiology of urine \202 ow from kidneys to bladder Urine production by the kidneys is a continuous process. Its transportation from the kidneys down the ureter and into the bladde r occurs intermit- tently by waves of peristaltic contraction of the renal pelvis and urete r (peristalsis = wave-like contractions and relaxations). The renal pelvis delivers urine t o the proximal ureter. As the proximal ureter receives a bolus of urine, it is stretched an d this stimulates it to contract while the segment of ureter just distal to the bolus of ur ine relaxes. Thus, the bolus of urine is projected distally. The origin of the peristaltic wave is from collections of pacemaker cells in the proximal m ost regions of the renal calyces. In species with multiple calyces such as humans, there ar e multiple pacemaker sites in the proxi- mal calyces. The frequency of contraction of the c alyces is independent of urine \202 ow rate (it is the same at high and low \202 ow rat es) and it occurs at a higher rate than that of the renal pelvis. Precisely how the frequen cy of contraction of each calyx is integrated into a single contraction of the renal pelvis is not known. All areas of the ureter are capable of acting as a pacemaker. Stimulation of the ureter at any site produces a contraction wave that propagates proximally and distally from the site of stimulation, but under normal conditions, electrical activity arises prox imally and is conducted distally from one muscle cell to another (the proximal most pacemak ers are dominant over these latent pacemakers). Peristalsis persists after renal transplantation and denervation and does not, therefore, a ppear to require innervation. The ureter does, however, receive both parasympathetic and sy mpathetic innervation and stimulation of these systems can in \202 uence the frequency of peristalsis and the volume of urine bolus transmitted. At normal urine \202 ow, the frequency of calyceal and renal pelvic contrac- tions is gre ater than that in the upper ureter and there is a relative block of electrical activity at the PUJ. The renal pelvis \201 lls; the ureter below it is collapsed and empty. As renal pelvic pressure rises, urine is extruded into the upper ureter. The ureteric contractile pr essures that move the bolus of urine are higher than renal pelvic pressures. A closed PUJ m ay prevent back-pressure on the kidney. At higher urine \202 ow rates, every pacemaker- i nduced renal pelvic contraction is transmitted to the ureter. To propel a bolus of urine, the walls of the ureter must coapt (touch). Resting ureteric pr essure is 0 \200\2235cmH2O and ureteric contraction pressures range from 20 to 80cmH2O. Ure teric peristaltic waves occur 2 \200\2236 times per min. The VUJ acts as a one-way valve un der normal condi- tions, allowing urine transportation into the bladder and preventing re \202 ux back into the ureter. CHAPTER 10 Upper tract obstruction 500 Ureter innervation Autonomic: the ureter has a rich autonomic innervation. - Sympathetic: post-ganglionic \201 bres arise from the coeliac, aorticorenal, mesenteric, superior, and inferior hypogastric (pelvic) autonomic plexuses. Parasympathetic: S2 \200 \2234 to lower ureter. preganglionic \201 bres from spinal segments T10 \200\223L2; vagal \201 bres via coeliac to upper ureter; \201 bres from The role of ureteric autonomic innervation is unclear. It is not required for ureteric peri stalsis (though it may modulate this). Peristaltic waves origi- nate from intrinsic smooth muscle pacemakers located in minor calyces of the renal collecting system. Afferent Upper ureter \200\224afferents pass (alongside sympathetic nerves) to T10 \200\223 L2; lower ureter \200\224afferents pass (alongside sympathetic nerves and by way of the pel vic plexus) to S2 \200\2234. Afferents subserve stretch sensation from the renal capsule, c ollecting system of kidney (renal pelvis and calyces), and ureter. Stimulation of the mucos a of the renal pelvis, calcyes, and ureter also stimulates nociceptors, the pain so felt be ing referred in a somatic distri- bution to T8 \200\223L2 (kidney T8 \200\223L1, ureter T10 \200\223L2), in the distribution of the subcostal, iliohypogastric, ilioinguinal, or genit ofemoral nerves. Thus, ure- teric pain can be felt in the \202 ank, groin, scrotum or lab ia, and upper thigh, depending on the precise site in the ureter from which the pain arises . This page intentionally left blank CHAPTER 10 Upper tract obstruction 502 Retroperitoneal \201 brosis Retroperitoneal \201 brosis (RPF) was \201 rst clearly de scribed by the French urologist Albarran in 1905. Further cases were described by Ormond in 1948. Benign causes - Autoimmune: Idiopathic RPF (periaortitis) comprises two-thirds of cases. Considered to be a response to an insoluble lipid called ceroid that has leaked through a thinned arterial wa ll from atheromatous plaques, a \201 brous plaque extends laterally and downwards from th e renal arteries encasing the aorta, inferior vena cava and ureters, but rarely extends int o the pelvis. The central portion of the plaque consists of woody scar tissue, while the gr owing margins have the histological appearance of chronic in \202 ammation. It may be asso ciated with abdominal aortic aneurysm (AAA), intra-arterial stents, and angioplasty; medias tinal, mesenteric, or bile-duct \201 brosis. Drugs including methysergide, beta-blockers, hydralazine, haloperidol, amphetamines, and LSD; methyl methacrylate cement used for joint replacement. Chronic urinary infection including TB. In \202 ammatory conditions such as Crohn \200\231s disease, Reidel \200\231s thyroiditis, or sarcoidosis. Amyloidosis and periaortic haematoma may mimic RPF. Malignant causes - - Lymphoma is the most common cause, also sarcoma. Metastatic or locally in \201 ltratative carcinoma of the breast, stomach, pancreas, colon, bladder, prostate, and carcinoid tumors. Radiotherapy may cause RPF, although rare in recent years with precise \201 eld localiza tion. Chemotherapy, especially following treatment of metastatic testicular tumors, may lea ve \201 brous masses encasing the ureters. These may or may not contain residual tumor. Presentation - Idiopathic retroperitoneal \201 brosis classically occurs in the \201 fth or sixth deca de of life. Men are affected twice as commonly as women. In the early stage, symptoms are r elatively non-speci \201 c, including loss of appetite and weight, low-grade fever, sweati ng, and malaise. Lower limb swelling may develop. Dull, non-colicky abdominal or back pain is described in up to 90% of patients. Later, the major complication of the disease develop s: bilateral ureteric obstruction, causing anuria and renal failure. Examination may reveal hypertension in up to 60% of patients and an underlying cause such as an abdominal aortic aneurysm. Investigations - In \202 ammatory serum markers are elevated in idiopathic RPF (60 \200\22390% elevated ESR ). RETROPERITONEAL FIBROSIS 503 - Pyuria or bacteriuria are common. Ultrasound will demonstrate uni- or bilateral hydronephro sis. CT, IVU, or ureterography reveal tapering medial displacement of the mid-ureters with proximal dilatation and will exclude calculus disease. Up to one third of patients will hav e a non-functioning kidney at the time of presentation due to long standing obstruction. CT -guided \201 ne needle biopsy of the mass may con \201 rm the presence of malignant dise ase or infection. A negative result does not exclude malignancy. Management - Emergency management of a patient presenting with established renal failure requires relief of the obstruction by percutaneous nephrostomy or ureteric stenting. Replacement of \202 uid and electrolyte losses following relief of bilateral ureteric obstruction is vital due to the frequent post-obstructive diuresis. Assess with daily weighing and measurement of b lood pressure lying and standing. Steroids may decrease the oedema often associated with re troperitoneal \201 brosis and in this way help reduce the obstruction. If used, they are usually discontinued when in \202 ammatory markers return to normal. Azathioprine, tamoxif en, and cyclophosphamide have been used successfully in some patients. Surgical ureterolysi s with omental wrap is often necessary to free and insulate the ureters from the encasing \201 brous tissue. Monitor for recurrent disease with serum creatinine and ultrasound 3 \200\2236 monthly or annual DMSA renography for 5y. This page intentionally left blank 505 Chapter 11 Trauma to the urinary tract and other urological emergencies Initial resuscitation of the traumatized patient 506 Renal trauma: classi \201 cation, mec hanism, grading 508 Renal trauma: clinical and radiological assessment 512 Renal trauma: tr eatment 516 Ureteric injuries: mechanisms and diagnosis 520 Ureteric injuries: management 5 22 Pelvic fractures: bladder and ureteric injuries 526 Bladder injuries 532 Posterior ureth ral injuries in males and urethral injuries in females 535 Anterior urethral injuries 536 Testicular injuries 540 Penile injuries 542 Torsion of the t estis and testicular appendages 544 Paraphimosis 545 Malignant ureteric obstruction 546 Spi nal cord and cauda equina compression 548 CHAPTER 11 Trauma to the urinary tract 506 Initial resuscitation of the traumatized patient The resuscitation of the traumatized patie nt is usually initiated in the \201 eld by the paramedic team and is continued systematic ally once the patient reaches the emergency department by a rapid multidisciplinary priorit y- based approach. Goals of resuscitation: Restoration of cardiac, pulmonary, and neurological function. Diagn osis of immediate life-threatening conditions. Prevention of complications from multisystem injuries. - The initial resuscitation process can be divided into three phases \200\224the primary surv ey, the secondary survey, the de \201 nitive survey. Primary survey ABC: assess the patient \200\231s Airway, Breathing, and Circulation. Airway and Breathing - - Establish a secure airway. Ventilate by oxygen mask or endotracheal intubation and mechanic al ventilation. Immobilize the cervical spine. Circulation Assess circulatory function by pulse rate and BP. The commonest cause of hypotension in the polytraumatized patient is hypovolaemia secondary to hemorrhage. With hypovolaemic shock, an immediate bolus of intravenous isotonic crystal loid solution should be given and the patient \200\231s response (pulse rate, BP) is assess ed. Radiological imaging Determined by local facilities. Increasingly, in the severely traumati zed pa- tient, CT of chest, abdomen, and pelvis is used to identify signi \201 cant chest, abdominal, and pelvic injuries. If not available, arrange supine chest, abdo- men, and pel vic X-rays to identify the presence of rib and pelvic fractures and to identify the presenc e of signi \201 cant quantities of blood in the chest, abdomen, and pelvis and in patients with persistent hypotension from pre- sumed bleeding, search for occult hemorrhage using a diagnostic perito- neal lavage or focused abdominal USS. Hypovolaemic shock is not always associated with hypotension. In young patients, compensato ry mechanisms, e.g. rapid vasoconstriction can compensate for as much as a 35% volume loss without signi \201 cant decreases in BP. Remember non-hypovolaemic causes of hypotension: Tension pneumothorax. Cardiac tamponade. M yocardial infarction. Neurogenic ( - - SCI). INITIAL RESUSCITATION OF THE TRAUMATIZED PATIENT 507 Urinalysis Routinely performed in every trauma patient because it provides valuable informa tion regarding the likelihood of injuries to the upper and lower urinary tract. The absence of haematuria, however, does not exclude a urinary tract injury (e.g. haematuria may be ab sent in acceleration/deceler- ation renal injuries (see b p. 508)). As life-threatening injuries are found during the primary survey, resus- citation efforts a re initiated concurrently (e.g. chest drain for pneumotho- rax). The decision to transfer a patient from the emergency room to either the operating room or angiography suite is made during the primary survey. Secondary survey Performed after completion of the primary survey. Take a completehis- tory and perform a physical examination from head to toe. Arrange selec- tive skeletal X-rays a ccording to physical \201 ndings. De \201 nitive survey During this phase, focus attention on identifying speci \201 c orga n injuries using clinical and radiographic means. Genitourinary injuries are usually recogn ized during the de \201 nitive survey. During all phases of the initial resuscitation, assess vital signs (BP, respi- ratory rate, blood gasses, urinary output, and body temperature) continu- ally. Vascular pressure monit oring, using central venous and pulmonary arterial catheters, can be performed selectively. Frequent re-evaluation should be performed to detect changes in the patient \200\231s cond ition and the appropriate actions taken. CHAPTER 11 Trauma to the urinary tract 508 Renal trauma: classi \201 cation, mechanism, grading Classi \201 cation Two categories \200\224blunt and penetrating. See Table 11.1. Proportion of all renal injuries that are bl unt \200\224Europe 97%, United States 90%, South Africa 25 \200\22385%. Proportion depends on whether urban or non-urban community. This classi \201 cation is useful because it predicts the likely need for surgical explora tion to control bleeding. Experience from large series shows that 95% of blunt injuries can be managed conservatively whereas 50% of stab injuries and 75% of gunshot wounds require e xploration. Blunt injures - - - Direct blow to the kidney. Rapid acceleration or rapid deceleration. A combination of the a bove. Rapid deceleration frequently causes renal pedicle injuries (renal artery and vein tears or thrombosis, PUJ disruption) because the renal pedicle is the site of attachment of the kid ney to other \201 xed retroperitoneal structures. Most common cause \200\224motor vehicle accidents (e.g. pedestrian hit by a car, direct blo w combined with rapid acceleration and then deceleration). Seemingly trivial injuries (e.g. fall from a ladder), direct falls onto the \202 ank, or sporting injuries can lead to si gni \201 cant renal injuries. Penetrating injuries Stab or gunshot injuries to the \202 ank, lower chest, and anterior abdominal area may in \202 ict renal damage. Fifty percent of patients with penetrating tr auma and haematuria have grade III, IV, or V renal injuries. Penetrating injuries anterior to the anterior axillary line are more likely to injure the renal vessels and renal pelvis, compared with injuries posterior to this line where less serious parenchymal injuries are more likely. Thus, renal inju- ries from stab wounds to the \202 ank (i.e. posterior to t he anterior axillary line) can often be managed non-operatively. Wound pro \201 le of a low-velocity gunshot wound is similar to that of a stab wound. High -velocity gunshot wounds (>350m/s) cause greater tissue damage due to stretching of surroun ding tissues ( \200\230temporary cavity \200\231). Mechanism The kidneys are retroperitoneal structures surrounded by perirenal fat, the verte bral column and spinal muscles, the lower ribs, and abdominal contents. They are, therefore , relatively protected from injury and a con- siderable degree of force is usually required to injure them (only 1.5 \200\2233% of trauma patients have renal injuries). Associated in juries are, therefore, common (e.g. spleen, liver, mesentery of bowel). Renal injuries may not initially be obvious, hidden as they are by other structures. To con \201 rm or exclud e a renal injury, imaging studies are required. In children, there is proportionately less perirenal fat to cushion the kidneys against injury and thus, renal injuries occur with les ser degrees of trauma. RENAL TRAUMA: CLASSIFICATION, MECHANISM, GRADING 509 Staging of the renal injury Using CT, renal injuries can be staged according to the America nAssociation for the Surgery of Trauma (AAST) Organ Injury Severity Scale. Higher inju- ry severity scales are associated with poorer outcomes. Grade I Contusion (normal CT) or subca psular haematoma with no parenchymal laceration. Grade II <1cm deep parenchymal laceration of cortex, no extravasa- tion of urine (i.e. collecting system intact). Grade III >1cm deep parenchymal laceration of cortex, no extravasa- tion of urine (i.e. collecting system intact). Grade IV Parenchymal laceration, involving cortex, medulla and collect- ing system OR renal artery or renal vein injury with contained hemorrhage. Grade V Completely shattered kidney OR avulsion of renal hilum. Pediatric renal injuries The kidneys are said to be more prone to injury in children becaus e of the relatively greater size of the kidneys in children, the smaller protective muscle mass and cushion of perirenal fat, and the more pliable rib cage. CHAPTER 11 Trauma to the urinary tract 510 Table 11.1 Summary of mechanisms, causes, grading, and treatment of renal disease Mechanisms and cause Blunt: direct blow or acceleration/deceleration (RTAs, falls from a height, fall onto \202 ank) Penetrating: knives, gunshots, iatrogenic (e.g. PCNL) Imaging and grading CT: accurate, rapid, images other intra-abdominal struc-tures Staging: AAST Organ Injury Severity Scale: I: contusion or subcapsular haematoma II: <1cm laceration without urinary extravasation III: >1cm laceration without urinary extravasation