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• W2769704049 abstract "The term ‘acute scrotum’ applies to patients presenting with scrotal pain, swelling and/or redness. It comprises a wide list of differential diagnoses, of which torsion of the spermatic cord (testicular torsion) is the most urgent to treat. The acute scrotum represents 0.3% of all paediatric emergency presentations.1 This article examines acute scrotal presentations and their differential diagnoses. Its intent is to arm clinicians with a pragmatic set of guidelines and an approach to diagnosis that will minimise the risk of missing a patient with testicular torsion. The classic presentation of testicular torsion is sudden onset severe unilateral pain, associated with nausea and vomiting, often with referred pain to the ipsilateral iliac fossa. Hallmark features on examination are: a high riding testis with an abnormal transverse lie; a thickened spermatic cord; an absent cremasteric reflex; as well as erythema, tenderness and swelling. The pain is often so severe the patient will involuntarily push the examiner's hand away.2-5 Patients with testicular torsion tend to present earlier than those with other scrotal pathologies. Just over a third (36–39%) will present within 6 h, and 49–69% within 12 h.6, 7 Only 3–10% with testicular appendage (TA) torsion will present this early.8, 9 Sudden onset of pain is classical of testicular torsion; however, 69% of torted appendage patients also report this feature.10, 11 Paradoxically, the longer the symptoms persist the less likely is testicular torsion a diagnosis. In several studies, no patient with testicular torsion had symptoms lasting longer than 72 h.1, 12 Similar past symptoms occur in 7–8% of patients with testicular torsion, suggesting previous torsion and spontaneous detorsion events.7, 11 Nausea and/or vomiting occurs in 31–43% of patients with testicular torsion, less commonly (<5%) in patients with a torted appendage.7, 12 Abdominal pain is an associated complaint in up to 28% of patients with testicular torsion12; however, this is also common with other differential diagnoses.8 In 5–12% of patients with testicular torsion, there is no testicular pain on history.2, 12, 13 Patients may be reluctant to volunteer a history of testicular pain, so this must be specifically sought in all males presenting with lower abdominal pain. These clues in a careful history point to testicular torsion, but no one feature is pathognomonic.14 Similarly with examination, a diagnostic picture is constructed from multiple clues. Early descriptions reported an absent cremasteric reflex was diagnostic of testicular torsion.15 This reflex is absent in up to 30% of normal testes.16 Up to 25% patients with a torted appendage, and 16% with epididymitis, will have an absent cremasteric reflex and patients with testicular torsion can have a preserved reflex.10, 15, 17 Once inflammation has developed from each pathology, it may be very difficult to elicit the cremasteric reflex. Erythema is more a feature of epididymitis than testicular torsion. Up to two-thirds of patients with epididymitis have erythema, compared to 32–55% of patients with a torted appendage, and up to 37% in testicular torsion.2, 8, 9 Swelling occurs in 75–98% of testicular torsions, and up to 100% with epididymitis. Swelling is a variable feature in patients with a torted appendage.6, 9, 12, 13 The ‘blue dot sign’ arises from haemorrhagic infarction of a TA, and is reported in 22–32% of those with that diagnosis.7, 10, 13, 18 It is seen in up to 17% of patients with testicular torsion.9 Isolated superior pole tenderness can be a reliable feature of those with TA torsion7; however, others report it more frequently in epididymitis.9 Fever occurs more frequently in patients with epididymitis than other diagnoses (100% vs. 76% with testicular torsion).9 Pyuria (83% vs. 11% in testicular torsion) is also more common.10 Testicular torsion can be missed if pyuria leads to an incorrect diagnosis.19 Other differential diagnoses such as hernia/hydrocele, idiopathic scrotal oedema (ISO) and testicular tumours constitute <10% of acute scrotal diagnoses.12, 20 Mandating operations on every acute scrotum has 100% sensitivity for testicular torsion, but leads to many unnecessary scrotal explorations. A more selective approach – using history, examination and clinical acumen to minimise unnecessary surgery – risks missing testicular torsion.21 False negative diagnoses occur in up to 12.5%, most commonly due to an incorrect diagnosis of appendage (rather than testicular) torsion.9, 12 Various attempts at scoring systems have been made, but validation studies have found testicular torsion even in the lowest-scoring patients.22-24 It is not enough to decide the patient does not have testicular torsion; an alternative diagnosis must be determined otherwise the clinician has not explained the pathology. Testicular torsion is statistically not the most likely cause of an acute scrotum. In cohorts with universal or near-universal exploration policies, the risk of a torted TA is 35–57%, testicular torsion is 25–45% and epididymitis is 11–17%.6, 9, 13 Less than 10% of cases have unusual abnormalities (such as fat necrosis or ISO), or have no anomaly detected. Aspects of the major differentials are discussed below. Torsion of TAs is the most common cause of acute scrotal pain in many paediatric series of scrotal explorations (Figs 1,2).2, 9, 13, 26 Patients are typically younger, with a peak incidence around 10–11 years. The pain is often more gradual in onset, and tenderness is initially confined to the upper pole of the testis. A blue dot sign may not always be present or visible, and does not on its own secure the diagnosis. When a confident diagnosis of TA torsion has been made, a non-operative approach can be considered. While there are few studies, anecdotal experience suggests such an approach will be successful in the majority of patients.27 In patients booked for exploration, there is no unanimity among surgeons regarding exploration of the index side only, versus bilateral exploration and fixation after removal of appendages. The risk of metachronous contralateral appendage torsion is estimated to be 2.6–5.3%.28, 29 Epididymitis or epididymo-orchitis is rare in children, and is often only diagnosed following scrotal exploration.30, 31 Only 14–25% patients complain of dysuria.7, 32 An abnormal urine analysis is only present in up to 50% of cases tested, and symptoms and signs can be variable, mimicking those of testicular torsion and TA torsion.8, 9, 11, 12 Many centres adopting a non-operative approach for the acute scrotum report a higher incidence of epididymitis if they rely on ultrasound in their diagnostic workup; 71 versus 11% in centres where exploration is the norm.7, 13 An erroneous diagnosis of epididymitis is made sonographically due to inflammation caused by a torted TA.32 In infants undergoing further investigations for epididymitis up to 18% can have an associated urologic abnormality such as vesicoureteric reflux, neurogenic bladder or renal anomalies.11, 25 The most common organism grown in urine cultures is Escherichia coli. Other organisms isolated include Klebsiella, Enterococcus and Enterobacter.8, 11, 12, 20, 25 ISO was first described in 1956 (Fig. 3).33 It represents up to 12% of all acute scrotal presentations below 20 years of age.34 Intestinal worm infestation has been shown as an association, though a direct link remains unproven.35 Other theories ascribe ISO to insect bites, or to an atopic phenotype. Atopy is, if anything, less common in patients with ISO than in age-matched controls.34 ISO approximates a normal distribution about a mode of 7–8 years, skewed to younger ages. The cardinal signs are scrotal redness and swelling. The majority are unilateral, more commonly left-sided. Pain or tenderness, mostly mild, is reported in 60% – though the severity of tenderness in ISO is less than in other acute scrotal conditions. There is almost never an identified precipitating event. Erythema and oedema are limited to the scrotum in 28% of cases. In the majority (72%) redness and swelling also involves the perineum, groin or penis.34 Erythema and swelling beyond the scrotum – typically a red flare into the perineum – effectively excludes pathology confined to the tunica vaginalis, such as torsion. Blood tests are not necessary, as they are usually normal save for an eosinophilia in 20%.34 Antibiotics, antihistamines and non-steroidal anti-inflammatory medications are all commonly prescribed. There is no evidence for their efficacy, and ISO generally resolves in 2–3 days, regardless of treatment. There are no reported cases lasting more than 7 days, but the condition can recur in up to 10% of patients.34 An otherwise well child, with erythema and oedema extending beyond the scrotum, who is not particularly sore or tender, may well have ISO. If so, reassurance only is required. Mumps orchitis is exceedingly rare in prepubertal children..36, 37 The tunica albuginea of the testis limits the swelling associated with inflammation, but leads to a rise in intratesticular pressure and subsequent necrosis of seminiferous tubules. Of testes affected, 30–50% show a degree of testicular atrophy. Mumps vaccination was introduced to Australia in 1982 and New Zealand in 1990.36 37 Second doses were recommended from shortly thereafter, but were not introduced systematically and there were a variety of ‘catch-up’ campaigns in both countries. The net result is that there is a cohort of adults born in the late 20th century who may not have had two doses of the vaccine and are therefore at risk of mumps orchitis.38, 39 They may not have been exposed to mumps due to higher vaccination rates in their younger contemporaries. Outbreaks of mumps continue to occur, particularly in this adult cohort. The risk of orchitis is significantly lower (30.3 vs. 6.4%; P < 0.001) in vaccinated children compared to their unvaccinated counterparts.40 Approximately 10% of all testicular torsion occurs in the perinatal period, a significant percentage (up to 50%) antenatally. Presentation is often delayed, even in cases of post-natal torsion. The hallmarks of hemiscrotal pain, tenderness and swelling are the same as for pubertal torsion but may not be noticed initially (Fig. 5). Non-tender perinatal torsion indicates the testis torted some time ago and is infarcted. Inflammation has resolved, and with it pain and tenderness. In that scenario, there is no chance of salvaging the testis. The issue is what to do with the contralateral testis. Many surgeons would advocate elective fixation of a single testis, since torsion of that sole testis will render the patient anorchic. The chance of perinatal torsion falls with age, so the risk of a contralateral torsion is highest on the day the patient is seen. In patients with non-tender perinatal torsion and a normal contralateral testis, it would seem most pragmatic and prudent to electively fix the contralateral side at the earliest opportunity. If the testis is tender then a decision for emergent (non-fasted) surgery can be considered, with a chance of testicular salvage. Success rates for emergent exploration are lower than for pubertal torsion, but may be up to 21.7% for emergency operations. The contralateral side should be pexed to mitigate against anorchia. Metachronous contralateral torsion while on a waiting list for surgery has been reported, as have bilateral torsions with only unilateral signs.43 Amongst Australasian paediatric surgeons, sonography is not recommended. Imaging is operator dependent, and delays treatment. Many studies have an unacceptably high false negative rate.3, 13, 44 In Gaither's series of missed testicular torsions leading to lawsuits, 16 of 25 (64%) had blood flow demonstrated to the testis on sonography. Sonography overcalls epididymitis and undercalls torsion of the TA, probably because the torted appendage leads to inflammation of the epididymal head.32, 41 There is no role for sonography as a single tool to exclude testicular torsion, or as a substitute for surgical review. The risk of testicular loss increases the longer blood flow is interrupted: time since the onset of torsion, possibly modified by the severity (tightness) of torsion, and by torsion/detorsion events allowing some blood flow for periods of time. Salvage rates are often placed into time bands, reflective of the degree of uncertainty surrounding the time since the onset of torsion (Fig. 6). In most series ‘salvage’ really means the testis was left in situ, rather than being removed (orchidopexy, not orchidectomy). Delayed atrophy post-orchidopexy in this setting exceeds 50% in some series.13, 47 Fertility is difficult to assess following testicular torsion, since studies on this subject frequently conflate alleged paternity with actual paternity. Misattributed paternity rates vary between studies, from 0.8 to 30% (median 3.7%).48 Early rat studies appeared to demonstrate impairments in fertility proportional to the number of twists in the cord and to length of time torted.49, 50 More recent rat studies show no effects on fertility following testicular torsion and orchidectomy, when compared with sham operated controls.51 If there are changes in the exocrine function of the testis following torsion, it is unclear whether these might be due to a reperfusion injury to the testis, or to the formation of antisperm antibodies (ASA) following disruption of the blood:testis barrier. The ASA rates are 0–2% in the normal adult male population, compared to 7–25% in infertile men.52 Some studies have shown that ASA levels are not significantly higher in men who have had a testicular torsion when compared to controls.53 In prepubertal boys genital tract anomalies (including hypospadias, cryptorchidism, malignant testicular infiltration and testicular torsion) are all risk factors for the development of ASA.54 Whatever laboratory studies may suggest, the ultimate proof of fertility is fatherhood. Recent studies show no decrease in hormone levels, pregnancy rates, or increase in the interval to pregnancy over the expected rates for the general population. These results were independent of whether the torsion had resulted in orchidopexy or orchidectomy.55, 56 While ASA may result from testicular damage, this is not universally the case and their titres may not be high enough to impair fertility. In patients with acute scrotal pain, a careful history and examination, paying attention to the discriminating questions and features of examination, is the best way of reducing the risk of an incorrect diagnosis. Failure to exclude torsion and/or failure to provide an alternative diagnosis mandates a surgical referral or operative exploration. The diagnosis is clinical, and laboratory or radiological tests add little. Time is of the essence, with testicular salvage rates decreasing with time since symptom onset. Fertility does not seem to be compromised by torsion and/or the loss of one testis. There are identifiable patterns related to missed testicular torsions. A cursory and unquestioning approach is a common theme, along with over-reliance on single aspects of history or examination rather than an inclusive approach." @default.
• W2769704049 created "2017-12-04" @default.
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• W2769704049 date "2017-11-01" @default.
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• W2769704049 title "Acutely painful scrotum: Tips, traps, tricks and truths" @default.
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