Radiological imaging is now readily available in Hong Kong, in both the public and private sector. Imaging helps diagnose or screen for diseases, but can create noise or false alarms.1 Ophthalmology consultations are common in both in-patient and out-patient settings. Floaters, visual field defects, and abnormal incidental findings on computed tomography or magnetic resonance imaging (MRI) are all common reasons for consultations.2

In 2018, a 60-year-old man underwent an MRI scan for acoustic neuroma screening, which revealed an abnormal eyeball shape (Fig 1). Diligent consultation with an ophthalmologist was reassuring for both the physician and the patient. In December 2017, the patient had been referred to our eye department for visual disturbance and was diagnosed with right eye macula-on retinal detachment. He had no history of laser or other eye surgery, nor trauma to the eyes. The patient reported right eye floaters and loss of the inferior visual field. Fundus examinations found a large retinal U-shaped tear at the superior retina, with bullous retinal detachment over the right eye. There were also multiple small flat holes with lattice degeneration over the retina in the temporal and nasal aspect. Retinal detachment repair surgery with encircling band as scleral buckling, and intravitreal gas injection was done for the presence of multiple retinal holes.3 Given the patient’s older age, the presence of cataract, and perceived cataract progression with postoperative intravitreal gas,4 cataract extraction with intraocular lens insertion was also done in the same operation. These are all evidenced on the MRI scan contrasting the presence of a natural thickness lens over the left eye.

Retinal detachment surgery can be of external or internal approach to relieve the vitreous traction and flatten the retina. External approach can be localised or 360-degree encircling depending on the retinal status.

The formation of the pear-shaped eyeball was due to the buckling effect of the encircling band (Fig 2). With basic knowledge of normal organ shapes, all practitioners would be concerned by such a deformed organ on plain radiographs. Typically, intraocular tumours or eyeball ruptures are not regular nor symmetrical, except large ring melanoma of the ciliary body. The key to differentiating a genuine pathology from a congenital/postoperative variant lies heavily on clinical history.1 Operative implants usually appear regular, or even symmetrical on imaging.

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 or design: SCL Au.
Acquisition of data: SCL Au.
Analysis or interpretation of data: SCL Au.
Drafting of the manuscript: SCL Au.
Critical revision of the manuscript for important intellectual content: All authors.

All authors have disclosed no conflicts of interest.

This pictorial medicine paper 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. Relevant patient consent was obtained for the purpose of this case study.

1. Leslie A, Jones AJ, Goddard PR. The influence of clinical information on the reporting of CT by radiologists. Br J Radiol 2000;73:1052-5. Crossref

2. Carter K, Miller KM. Ophthalmology inpatient consultation. Ophthalmology 2001;108:1505-11. Crossref

3. Shanmugam PM, Ramanjulu R, Mishra KC, Sagar P. Novel techniques in scleral buckling. Indian J Ophthalmol 2018;66:909-15. Crossref

4. Thompson JT. The role of patient age and intraocular gases in cataract progression following vitrectomy for macular holes and epiretinal membranes. Trans Am Ophthalmol Soc 2003;101:485-98.

In January 2017, a 35-year-old woman was admitted to our hospital with insidious onset of upper abdominal pain. A computed tomography (CT) scan showed bilateral ovarian cysts with fat fluid level, calcifications, and Rokitansky protuberance, compatible with ovarian teratoma (Fig 1). Anti-dependent fatty pockets with soft tissue rim were found at the bilateral subphrenic space, likely representing reactive changes to spilt cyst content, which also explained the patient’s upper abdominal pain. The patient had stable vital signs and was therefore treated conservatively. Follow-up ultrasonography scan showed globular fatty locules on the liver surface, compatible with escaped fatty cyst content (Fig 2). Subsequently, the patient underwent bilateral ovarian cystectomy. Histology confirmed bilateral ovarian mature cystic teratoma. Intra-operatively, widespread flimsy adhesions and multiple sebum-like implants were seen in the peritoneal cavity, consistent with changes related to teratoma rupture. The peritoneal cavity was irrigated and her symptoms gradually subsided; however, follow-up CT showed mild interval enlargement of the fat-attenuated lesions (Fig 3).

Mature cystic teratomas (also known as dermoid cysts) are common ovarian germ cell neoplasms accounting up to 10% to 25% of all ovarian neoplasms.1 They are cystic tumours composed of well-differentiated derivations from at least two of the three germ cell layers. Tumours are bilateral in about 10% of cases. On ultrasonography, cystic teratoma commonly manifests as a cystic lesion with a densely echogenic tubercle projecting into the cystic lumen; or a diffusely or partially echogenic mass with posterior attenuation by sebaceous material and hair. Multiple thin echogenic bands caused by hair in cyst cavity can also been seen. Pure sebum within the cyst can be hypoechoic or anechoic, fluid-fluid level can result from sebum floating on aqueous fluid which appears more echogenic than the sebum layer. On CT, the diagnosis of mature cystic teratoma is rather straightforward; fat attenuation within a cyst is diagnostic of mature cystic teratoma. Teeth or other calcifications can be seen in 56% of cases.2

Spontaneous rupture is an uncommon complication of dermoid cysts owing to the presence of a thick capsule, and is only seen in 1% to 4% of cases.1 Acute peritonitis can result from sudden rupture of tumour contents as seen in the present case. Chronic granulomatous peritonitis is caused by chronically leaking teratoma and is characterised by multiple small white peritoneal implants and dense adhesions with variable ascites. Visualisation of fatty implants within the peritoneal cavity is diagnostic.3

The reported CT findings of granulomatous peritonitis or intraperitoneal rupture of teratoma are inconsistent.1 3 In one case, capsular fatty implants were seen in the dome of the liver, similar to the CT appearance in the present case. In other patients there can be a significant amount of intraperitoneal free fluid and an omental cake appearance mimicking peritoneal carcinomatosis.

Chronic granulomatous peritonitis is a potentially serious complication of ruptured dermoid cyst and can lead to bowel obstruction resulting from adhesion. Removal of cystic content and copious peritoneal lavage should be performed to prevent new adhesion and peritoneal granuloma, and can be a successful method for treating chemical peritonitis caused by ruptured ovarian teratoma.4 In the present case, progression of the right subphrenic fatty implant, possibly related to incomplete removal of the cystic content, resulted in chronic granulomatous peritonitis. The patient may have benefitted from further peritoneal lavage.

WL Wong contributed to acquisition of data. All authors contributed to concept or design, analysis or interpretation of data, drafting of the article, 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.

All authors have 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 approved by the Kowloon Central/Kowloon East Research Ethics Committee (Ref KC/KE-19-0158/ER-4). Informed consent was obtained from the patient.

1. Erbay G. Ruptured ovarian dermoid cyst mimicking peritoneal carcinomatosis: CT and MRI. J Clin Anal Med 2016;6:701-3.

2. Outwater EK, Siegelman ES, Hunt JL. Ovarian teratomas: tumor types and imaging characteristics. Radiographics 2001;21:475-90. Crossref

3. Fibus TF. Intraperitoneal rupture of a benign cystic ovarian teratoma: findings at CT and MR imaging. AJR Am J Roentgenol 2000;174:261-2. Crossref

4. Shamshirsaz AA, Shamshirsaz AA, Vibhaka JL, Broadwell C, Van Voorhis BJ. Laparoscopic management of chemical peritonitis caused by dermoid cyst spillage. JSLS 2011;15:403-5. Crossref

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