In September 2018, a 62-year-old man without underlying disease presented to the emergency department of E-Da Hospital, Kaohsiung, Taiwan, with right flank pain for 1 day. The patient reported sharp and persistent pain radiating to the right upper abdomen. On arrival at the emergency department, the patient had heart rate 120 beats per minute and blood pressure 85/54 mm Hg. Physical examination revealed right flank knocking tenderness. Laboratory test results, including blood test and urinary analysis, were unremarkable. Abdominal plain film radiograph revealed a large right renal mass displacing surrounding structures (Fig 1). Point-of-care ultrasound demonstrated a right renal mass with hyperechogenicity, which was surrounded by hypoechoic haematoma in the perinephric space (Fig 2). Subsequent abdominal computed tomography (CT) revealed rupture of right renal angiomyolipoma with pericapsular haematoma (Fig 3). Wunderlich syndrome complicated by hypovolaemic shock was diagnosed, and proper fluid resuscitation and blood transfusion were performed in the emergency department. The patient received partial nephrectomy of right kidney on the next day, and was discharged uneventfully from the hospital 2 weeks after admission.

Wunderlich syndrome, a rare but life-threatening entity, is defined as spontaneous nontraumatic renal haemorrhage confined to the subcapsular and perirenal space.1 Lenk’s triad, which consists of acute flank pain, palpable flank mass, and hypovolemic shock, is the classical clinical feature of Wunderlich syndrome.2 The aetiologies of Wunderlich syndrome are classified into neoplastic and non-neoplastic origins. Up to 60% of patients with Wunderlich syndrome are caused by neoplasm, including benign tumours such as angiomyolipoma and malignancies such as renal cell carcinoma.3 A variety of diseases account for non-neoplastic origins of Wunderlich syndrome, including vasculitis, renal artery aneurysm, arteriovenous malformation, renal vein thrombosis, nephritis, cystic renal disease, and coagulopathy.3 Angiomyolipoma, a benign neoplasm composed of smooth muscle, adipose tissue, and thick-walled blood vessels, is the most common cause of Wunderlich syndrome.3 The risk of tumour rupture leading to fatal internal haemorrhage increases when angiomyolipoma grows >40 mm in diameter.4 Aneurism formation due to poor elastic vascular structure might be the reason for angiomyolipoma rupture, especially during tumour growth.

For diagnosis of Wunderlich syndrome, contrast-enhanced CT scan is a standard medical imaging modality with 100% sensitivity in identifying perirenal haemorrhage.4 Computed tomography scan can present renal vascular structure, origins of tumours and pathological change in adjacent tissues. Furthermore, CT scan can also provide detailed vascular anatomy to provide a roadmap for superselective renal embolisation in management of perirenal haemorrhage. In contrast with CT scan, point-of-care ultrasound might be considered as a prompt tool to diagnose patients with Wunderlich syndrome. Point-of-care ultrasound can be used to screen the renal structure, quickly identify internal bleeding, and evaluate the hemodynamic condition by measuring the diameter of the inferior vena cava and assessing the cardiac preload and contractility. Ultrasound can also facilitate the initial differential diagnosis of patients with flank pain, such as renal colic, renal abscess or acute pyelonephritis. Initial treatments for Wunderlich syndrome include selective arterial embolisation and surgical intervention. However, clinical guidelines for management of Wunderlich syndrome are not yet well established.5 Selective arterial embolisation has the advantage of minimal invasiveness, renal preservation, and efficiency in treating acute renal haemorrhage. However, surgical intervention can provide a delicate strategy for tumour resection, especially if suspicious for malignancy, and prevent recurrent tumour bleeding.5 Since Wunderlich syndrome is a life-threatening condition, clinicians should be aware while approaching patients presenting with flank pain and in shock to facilitate timely emergency surgery or embolisation if needed.

All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

Concept and design of the study: HY Su.
Acquisition of data: YY Lin.
Analysis or interpretation of data: YY Lin.
Drafting of the article: HY Su.
Critical revision for important intellectual content: HM Li, CW Hsu.

All authors have disclosed no conflicts of interest.

This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

This study was conducted in accordance with the principles outlined in the Declaration of Helsinki.

1. Medda M, Picozzi SC, Bozzini G, Carmignani L. Wunderlich’s syndrome and hemorrhagic shock. J Emerg Trauma Shock 2009;2:203-5. Crossref

2. Simkins A, Maiti A, Cherian SV. Wunderlich syndrome. Am J Med 2017;130:e217-8. Crossref

3. Katabathina VS, Katre R, Prasad SR, Surabhi VR, Shanbhogue AK, Sunnapwar A. Wunderlich syndrome: cross-sectional imaging review. J Comput Assist Tomogr 2011;35:425-33. Crossref

4. Albi G, del Campo L, Tagarro D. Wünderlich’s syndrome: causes, diagnosis and radiological management. Clin Radiol 2002;57:840-5. Crossref

5. Flum AS, Hamoui N, Said MA, et al. Update on the diagnosis and management of renal angiomyolipoma. J Urol 2016;195(4 Pt 1):834-46. Crossref

In June 2017, a 58-year-old man, with no known cardiovascular risk factors, was admitted to a hospital in Singapore, presenting with a 1-week history of fever and progressively worsening epigastric pain. On the first day of his symptoms, he had visited the emergency department at another hospital where a computed tomography (CT) scan of the abdomen performed had not revealed significant pathology (Fig 1). He was treated symptomatically as for a viral infection, but he represented to our hospital a week later without significant symptomatic improvement. The patient had a known history of reaction to penicillin and a history of traumatic spinal injury more than 20 years ago requiring spinal instrumentation at the L4/5 level. On examination, the patient was febrile but haemodynamically stable. Abdominal examination revealed epigastric tenderness on deep palpation. Cardiorespiratory examination was unremarkable. The patient had leucocytosis of 15.37 × 10³/uL, raised C-reactive protein level of 109.2 mg/L, and erythrocyte sedimentation rate of 46 mm/h. Renal and liver function tests, and serum amylase and lipase levels were unremarkable. He was started empirically on intravenous ceftriaxone following blood cultures.

A new CT scan of the abdomen was performed, revealing an anterior pre- and para-vertebral soft tissue mass with focal hypodensities surrounding the aorta at the T12-L1 level (Fig 2). Blood culture results (which were received 3 days later) were positive for penicillin-sensitive Staphylococcus aureus. Magnetic resonance imaging of the thoracolumbar spine illustrated paravertebral soft tissue thickening at level of T12-L1 that appears multiloculated with rim enhancement, suggestive of an underlying paravertebral abscess without epidural extension. A transthoracic echocardiogram did not reveal any valvular lesions. The presence of an inflammatory collection around the aorta prompted concerns for an infectious aortitis.

Antimicrobial therapy was switched to intravenous cefazolin, which was continued for 6 weeks with symptomatic improvement. Repeated blood cultures did not show evidence of persistent S aureus bacteraemia. Monitoring of C-reactive protein level and erythrocyte sedimentation rate showed gradual improvement. A CT aortogram, after 6 weeks of parenteral antibiotics, showed interval improvement of the paravertebral collections and soft tissue thickening around the aorta, suggesting improving aortitis (Fig 3). Antibiotics were switched to oral trimethoprim and sulfamethoxazole. Another CT aortogram 8 months later showed complete resolution of aortitis and paravertebral abscess (Fig 4).

In the antibiotic era, infectious aortitis is a rare clinical entity. Gram-positive micro-organisms are most commonly implicated, in up to 60% of cases, with S aureus being the most frequently encountered micro-organism. Other micro-organisms commonly implicated include Enterococcus species, Streptococcus pneumoniae, Salmonella species, Mycobacterium tuberculosis, and in the more distant past, syphilis.1 Rare case reports have featured the radiological evolution of infectious aortitis while on conservative treatment, and these often illustrate peri-aortic soft tissue masses progressing to aneurysmal formation from S aureus or Salmonella species infection.1 2 3 4 5 Prompt antimicrobial therapy is crucial along with endovascular or surgical intervention.5 Our patient demonstrated radiological normality to pathology within a week of symptom onset and subsequent improvement while on conservative therapy alone, followed by full radiological resolution. We believe that his successful recovery is in part due to early appropriate and prolonged antimicrobial therapy.

The author designed the study, contributed to acquisition and analysis of data, drafted the article, and contributed to the critical revision for important intellectual content. The author had full access to the data, contributed to the study, approved the final version for publication, and takes responsibility for its accuracy and integrity.

The author has disclosed no conflicts of interest.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

This study was conducted in accordance with the principles outlined in the Declaration of Helsinki.

1. Cevasco M, Menard MT, Bafford R, McNamee CJ. Acute infectious pseudoaneurysm of the descending thoracic aorta and review of infectious aortitis. Vasc Endovascular Surg 2010;44:697-700. Crossref

2. Carreras M, Larena JA, Tabernero G, Langara E, Pena JM. Evolution of salmonella aortitis towards the formation of abdominal aneurysm. Eur Radiol 1997;7:54-6. Crossref

3. Rozenblit A, Bennett J, Suggs W. Evolution of the infected abdominal aortic aneurysm: CT observation of early aortitis. Abdom Imaging 1996;21:512-4. Crossref

4. Wein M, Bartel T, Kabatnik M, Sadony V, Dirsch Olaf, Erbel R. Rapid progression of bacterial aortitis to an ascending aortic mycotic aneurysm documented by transesophageal echocardiography. J Am Soc Echocardiogr 2001;14:646-9. Crossref

5. Kan CD, Lee HL, Yang YJ. Outcome after endovascular stent graft treatment for mycotic aortic aneurysm: a systematic review. J Vasc Surg 2007;46:906-12. Crossref

A 62-year-old woman with a long-standing history of type 1 diabetes mellitus presented to the breast clinic with a palpable breast lump. She had incidentally discovered a painless lump in her left breast that had increased in size over the last 3 months. She denied nipple discharge or overlying skin changes but reported a family history of one maternal aunt who had breast cancer diagnosed in her sixties.

Clinical examination revealed an irregular hard mass at the upper outer quadrant of the left breast with no evidence of axillary lymphadenopathy. The right breast was unremarkable.

Mammography showed heterogeneously dense breasts with asymmetrical density at the left upper breast, but no discrete mass or spiculations (Fig 1). There were also no suspicious microcalcifications or architectural distortion. Ultrasonography revealed an approximately 4-cm irregular hypoechoic lesion with strong posterior acoustic shadowing at the upper outer quadrant of the left breast and no increase in vascularity (Fig 2). Overall features were suspicious of malignancy.

Ultrasound-guided core biopsy was performed. Histological examination showed lymphocytic lobular mastitis associated with stromal fibrosis of the breast, findings compatible with diabetic mastopathy (Fig 3).

Diabetic mastopathy is a rare fibro-inflammatory disease of the breast. It is usually seen in association with type 1 diabetes mellitus,1 although rarely can also been with long-standing type 2 diabetes mellitus. It is typically found in premenopausal women. Many such patients are known to have other complications of diabetes mellitus such as retinopathy, nephropathy, and neuropathy.1 Its exact pathogenesis is not well understood but likely multifactorial, probably related to an inflammatory or immunological reaction.

Clinically, diabetic mastopathy often presents as a hard, painless, irregular breast mass that can also be multiple and bilateral (60% of the cases). The clinical findings are often suspicious of breast carcinoma and patients are thus referred for imaging.

On mammogram, diabetic mastopathy may appear as an ill-defined mass or asymmetric density, without associated calcifications or spiculations, corresponding to the site of presenting palpable abnormality, but very often obscured by dense breast tissue.2 On ultrasonogram, diabetic mastopathy appears as an irregular poorly defined hypoechoic mass of between 2 and 6 cm in size, with moderate to marked posterior shadowing and absence of vascularity on colour Doppler imaging.3

Clinical examination and imaging studies cannot differentiate diabetic mastopathy from breast carcinoma, and ultimately the diagnosis can only be made on histology from core or excisional biopsy.

Diabetic mastopathy is a benign entity without malignant potential4 5 and should therefore be treated conservatively. Surgery should be avoided as the recurrence rate following surgical excision has been reported to be rather high at around 32%, and usually within 5 years.6 Recurrences can be single or multiple, and can occur at the ipsilateral, contralateral, or bilateral breasts. Clinicians should be aware of this entity if a diabetic patient presents with a palpable breast lump, after eliminating the possibility of breast carcinoma. Once this benign condition is diagnosed, the patient should be advised to perform routine breast self-examination and have regular clinical breast examinations. If any changes are detected, they should be referred for imaging and core biopsy performed if necessary.

In summary, diabetic mastopathy is an uncommon but important benign entity that can mimic breast carcinoma clinically and radiologically. Ultrasound-guided core needle biopsy of the lesion is required to establish the diagnosis. Increasing awareness of this condition and careful correlation of radiological and pathological findings are essential to avoid unnecessary surgical intervention, reduce patient anxiety, and ensure optimal patient care.

All authors have made substantial contributions to the concept or design of the study, acquisition of data, analysis or interpretation of data, drafting of the manuscript, and critical revision for important intellectual content. All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

The authors have no conflicts of interest to disclose.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

This study was conducted in accordance with the principles outlined in the Declaration of Helsinki. The patient provided verbal informed consent.

1. Kudva YC, Reynolds C, O’Brien T, Powell C, Oberg AL, Crotty TB. “Diabetic mastopathy,” or sclerosing lymphocytic lobulitis, is strongly associated with type 1 diabetes. Diabetes Care 2002;25:121-6. Crossref

2. Wong KT, Tse GM, Yang WT. Ultrasound and MR imaging of diabetic mastopathy. Clin Radiol 2002;57:730-5. Crossref

3. Baratelli GM, Riva C. Diabetic fibrous mastopathy: sonographic-pathologic correlation. J Clin Ultrasound 2005;33:34-7. Crossref

4. Camuto PM, Zetrenne E, Ponn T. Diabetic mastopathy: a report of 5 cases and a review of the literature. Arch Surg 2000;135:1190-3. Crossref

5. Thorncroft K, Forsyth L, Desmond S, Audisio RA. The diagnosis and management of diabetic mastopathy. Breast J 2007;13:607-13. Crossref

6. Ely KA, Tse G, Simpson JF, Clarfeld R, Page DL. Diabetic mastopathy. A clinicopathologic review. Am J Clin Pathol 2000;113:541-5. Crossref

A computed tomography (CT) scan was performed in a 64-year-old man with a history of end-stage renal failure to evaluate recent acute-on-chronic graft failure. To conserve remnant renal function, no intravenous contrast was administered. There was no hydronephrosis but the balloon of the indwelling Foley catheter was seen adjacent to but exterior to the bladder (Fig 1). No evidence of pneumoperitoneum was seen. Free fluid was noted in the pelvis, compatible with the history of peritoneal dialysis. The suspicion of perforated urinary bladder was conveyed to the referring physicians, and the patient was admitted for further evaluation. No abdominal distension, tenderness or guarding was elicited on physical examination. Urine output via the indwelling catheter was within normal limits. The patient was haemodynamically stable with no leukocytosis.

Computed tomography cystography was performed: 20 mL of water-soluble contrast medium (Omnipaque 300) was diluted in 500 mL of normal saline. Transurethral perfusion of 250 mL of the prepared contrast medium was performed by free gravitational flow. Pre-instillation and post-instillation CT cystography (5 minutes and delayed 10 minutes) was performed. No intravenous contrast was administered.

Cross-sectional imaging revealed two large urinary bladder diverticula sited posteriorly, close to the native vesicoureteric junctions. The right diverticulum measured 3.8 × 4.6 cm with a 0.9-cm neck; the left diverticulum measured 4.5 × 5.8 cm with a 1.1-cm neck. On coronal images, a “Mickey-Mouse” appearance was noted, compatible with bilateral hutch diverticula. The inflated balloon of the urinary catheter was sited within the left diverticulum (Figs 2 3 4). The bladder contour was smooth. No evidence of intraperitoneal rupture was demonstrated. On pre-cystography images, the appearance had mimicked an externally sited catheter balloon due to the collapsed state of the bladder.

Spontaneous bladder perforation is rare but potentially fatal. Most such cases present with features of peritonitis. Some possible aetiologies include gonorrhoeal infection, radiation therapy, diabetes mellitus, neurogenic bladder, bladder diverticula, and indwelling urinary catheter.1 2 As our patient was largely pain-free with minimal abdominal symptoms, the overall clinical evidence did not favour bladder rupture even though the CT images were alarming.

Saline instillation and bedside ultrasound for rapid disposition of polytrauma patients and early diagnosis of bladder rupture has been described in the literature, with sensitivity reaching 90%.3 In cases with low clinical risk for perforation and when the patient is unfit for immediate CT, instillation of sterile saline to distend the bladder followed by ultrasound assessment provides a possible alternative to exclude bladder perforation. However, ultrasound results are highly operator-dependent and this procedure should be performed only in carefully selected patients. In experienced hands, following retrograde instillation of approximately 300 mL of sterile saline via the catheter, this imaging modality can be used to determine presence of ascites, evaluate the distension and configuration of the urinary bladder, look for bladder diverticula, and determine the position of the catheter balloon. This can be performed at the bedside for critically ill patients, involves no radiation and removes the risk of intravenous contrast-related anaphylaxis.

All authors contributed to the concept, image acquisition, image and data interpretation, manuscript drafting and critical revision for important intellectual content. All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

The authors have no conflicts of interest to disclose.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Relevant patient consent was obtained for the purpose of this case study.

1. Sawalmeh H, Al-Ozaibi L, Hussein A, Al-Badri F. Spontaneous rupture of the urinary bladder (SRUB); A case report and review of literature. Int J Surg Case Rep 2015;16:116-8. Crossref

2. Ogawa S, Date T, Muraki O. Intraperitoneal urinary bladder perforation observed in a patient with an indwelling urethral catheter. Case Rep Urol 2013;2013:765704. Crossref

3. Karim T, Topno M. Bedside sonography to diagnose bladder trauma in the emergency department. J Emerg Trauma Shock 2010;3;305. Crossref

Caesarean scar ectopic pregnancy is a rare pregnancy complication with an estimated incidence of 1/1800 to 1/2500 pregnancies.1 2 Complications include uterine rupture, massive haemorrhage, placenta accrete, and pregnancy loss.3 Ultrasound examination is usually the first-line investigation. Magnetic resonance imaging (MRI) serves as a powerful confirmation tool. With its inherent superior tissue contrast and mulitplanar capability, MRI depicts anatomical details with robust reproducibility.4 Caesarean scar ectopic pregnancy is associated with a high risk of uterine rupture and uncontrollable haemorrhage. Expectant management is possible but not advocated. Surgical treatment leads to quicker postoperative recovery but may be associated with major haemorrhage.5 Other treatment includes systemic methotrexate and uterine artery embolisation.3

A high index of suspicion is required to diagnose this condition so that timely treatment can be initiated and life-threatening complications from a ruptured ectopic pregnancy prevented.

A 34-year-old woman with a history of Caesarean section presented to the emergency department with per vaginal bleeding. Her pregnancy was 7 weeks of gestation by date.

On vaginal examination, the cervical os was closed and mildly blood-stained. She was haemodynamically stable with a normal haemoglobin of 12.9 g/dL and beta–human chorionic gonadotropin 15 877 mIU/mL. Transvaginal ultrasound revealed a single intrauterine gestational sac in the lower segment of the uterus, closely related to the myometrium (Fig 1). The fetal pole with positive fetal heart beat was identified. Crown to rump length was 11 mm, corresponding with 7 weeks and 1 day of gestation. The anterior uterine wall adjacent to the gestational sac was very thin with a thickness of only 4 mm (Fig 2). However, it was uncertain whether the placenta was directly implanted onto the Caesarean scar. A provisional diagnosis was made of pending abortion or Caesarean scar ectopic pregnancy. Magnetic resonance imaging of the pelvis was performed to determine whether the thin layer of soft tissue at the anterior uterine wall represented myometrium in the Caesarean scar with placental implantation elsewhere or if the placental tissue was implanted directly onto the scar.

Magnetic resonance imaging showed a 1.7-cm defect at the anterior lower segment of the myometrium, corresponding to the Caesarean section scar. It was distended by a gestational sac. A singleton pregnancy was identified with crown-rump length consistent with gestational age. Trophoblastic tissue was seen implanted onto the serosa of the uterus (Fig 3). Overall MRI findings were compatible with Caesarean scar ectopic pregnancy. There was no direct extension of trophoblastic tissue into adjacent organs such as the urinary bladder or sign of uterine rupture (Fig 4).

The superior contrast resolution in MRI for different soft tissues is advantageous in the differentiation of uterine serosa, myometrium, endometrium, and trophoblastic tissue. This helped confirm the diagnosis of Caesarean scar ectopic pregnancy in our patient and would have been difficult if only ultrasound findings were available.

The patient received intramuscular methotrexate therapy. Serial beta–human chorionic gonadotropin levels showed a decreasing trend. Subsequent definitive treatment with suction evacuation was performed. The patient made an uneventful recovery.

Concept and design of the study: All authors.
Acquisition of data: EMF Wong, W Shu.
Analysis and interpretation of data: EMF Wong, W Shu.
Drafting of the manuscript: JAWK Tang.
Critical revision for important intellectual content: JAWK Tang, EMF Wong.

All authors have disclosed no conflicts of interest. All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

1. Seow KM, Huang LW, Lin YH, Lin MY, Tsai YL, Hwang JL. Caesarean scar pregnancy: issues in management. Ultrasound Obstet Gynecol 2004;23:247-53. Crossref

2. Jurkovic D, Hillaby K, Woelfer B, Lawrence A, Salim R, Elson CJ. First-trimester diagnosis and management of pregnancies implanted into the lower uterine segment caesarean section scar. Ultrasound Obstet Gynecol 2003;21:220-7. Crossref

3. Michaels AY, Washburn EE, Pocius KD, Benson CB, Doubilet PM, Carusi DA. Outcome of cesarean scar pregnancies diagnosed sonographically in the first trimester. J Ultrasound Med 2015;34:595-9. Crossref

4. Kao LY, Scheinfeld MH, Chernyak V, Rozenblit AM, Oh S, Dym RJ. Beyond ultrasound: CT and MRI of ectopic pregnancy. AJR Am J Roentgenol 2014;202:904-11. Crossref

5. Alalade AO, Smith FJ, Kendall CE, Odejinmi F. Evidencebased management of non-tubal ectopic pregnancies. J Obstet Gynaecol 2017;37:982-91. Crossref