We report a case of a 66-year-old Filipino male patient. Informed consent was obtained for publication. He is an ex-smoker and nondrinker. The patient had a previous history of thyroid nodular hyperplasia treated with total thyroidectomy, prostate cancer treated with robotic prostatectomy and external beam radiotherapy 5 years previously, cholecystectomy for cholecystitis, diabetes mellitus, and hyperlipidemia. He was also incidentally found to be positive for hepatitis B core antigen but had never received treatment for hepatitis B.
He had previously been imaged using fluorine-18 (18F)-choline PET/CT for follow-up of his prostate cancer. The last scan done 11 months previously had shown an indeterminate hypodensity in segment VII but was not significantly choline-avid to be considered suspicious []. However, given the history of prostate cancer and that prostate cancer may metastasize to the liver, albeit rarely, the patient then underwent MRI of the liver with Primovist for further characterization. This showed a T2-hyperintense nodule with signal drop out on the out of phase sequence and suggestive of arterial enhancement and delayed washout corresponding to the lesion seen on PET/CT, with differentials of hepatic adenoma, HCC, and angiomyolipoma [Figures -]. Follow-up MRI scans done over the next 10 months showed that the lesion remained stable and did not show any restricted diffusion, leading to the impression of a benign lesion. Interestingly, the patient's prostate-specific antigen (PSA) and alpha-fetoprotein (AFP) both remained within normal limits throughout the period of follow-up. The final MRI scan then showed an increase in size from 1.0 to 1.5 cm []. We therefore performed a whole body PET/CT using an integrated scanner (GE 690) 60 min after intravenous injection of 140.6 MBq of 68Ga-labeled Glu-urea-Lys(Ahx)-HBED-CC (68 Ga-PSMA). The scan showed an intensely tracer-avid nodule corresponding to the lesion seen on MRI [Figures and ], without any suspicious lesion seen elsewhere in the body, particularly the prostate bed [].
Given the history of hepatitis B and prostate cancer as well as the absence of other suspicious lesions, the patient then underwent a robotic-assisted laparoscopic resection of the segment VII lesion.
Microscopic examination of the specimen showed a cirrhotic liver with a well-circumscribed, unencapsulated hepatocellular lesion [] which showed macrovesicular steatosis []. Portal tract invasion was noted near the edges of the lesion on hematoxylin and eosin stained sections. Immunohistochemical (IHC) staining for CD34 showed capillarization of the sinusoids in the lesion. There was also focal positivity on IHC staining for glypican-3 and a raised Ki-67 index in the lesion. Overall, the features were consistent with a well-differentiated HCC.
The patient recovered well from the operation and was discharged on the 3rd day postoperation.


A 5-year-old male child patient was referred to the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Cairo University with a complaint of an asymptomatic slowly growing swelling in the left mandibular area of 8 months duration. The medical and family histories were unremarkable, as were the results of the physical examination.
Extraoral examination revealed facial asymmetry, with swelling present on the left side of the mandible. Intraoral examination revealed a non-tender bony hard swelling causing obliteration of the vestibule of the left side of the mandible, extending from the right deciduous lateral incisor to the left deciduous second molar region, measuring approximately approximately 7 × 4 cm in size. The swelling caused buccal and lingual cortical expansion and the buccal plate was perforated in some areas ().
The CT revealed a well-defined multilocular radiolucent lesion extending from the lower right deciduous lateral incisor to the left deciduous second molar region causing bucco-lingual expansion and thinning of the buccal plate. The lesion also showed small calcified areas and multiple impacted permanent teeth (). Based on the clinical and radiographic findings, a presumptive preoperative diagnosis of odontogenic tumour was made with differential diagnosis of AFO, calcifying epithelial odontogenic tumour and calcifying odontogenic cyst.
Incisional biopsy was performed and the specimen was sent to the oral and maxillofacial pathology department for histopathological analysis. Macroscopically, the specimen was white in colour, measured 3 × 2.3 × 2 cm in greatest dimension and was firm in consistency with irregular surface.
Microscopically, the lesion showed multiple follicles of proliferating odontogenic epithelium. The odontogenic epithelium showed peripheral tall columnar cells exhibiting nuclear palisading, hyperchromatism, and reversed polarity. The central cells were loosely arranged and angular to spindle in shape (). The surrounding primitive ectomesenchyme showed increased cellularity simulating the dental papillae with areas showing dentin formation (). Extensive areas with cartilage formation were also observed, showing hypercellularity and some binucleated cells. The cartilaginous areas exhibited increased maturation as they progressed further away from the epithelial follicles (, ). Immunohistochemical examination revealed that all epithelial components showed strong diffuse reactivity for cytokeratin (). The chondroid tissue also showed cytokeratin expression (). Vimentin expression was detected in both the stromal ectomesenchymal component () and in the chondroid tissue (). S-100 protein showed negative expression in all components (, ).
The lesion was treated by complete surgical excision and the excisional biopsy was examined confirming the diagnosis. The patient was followed-up for 6 months without any signs of recurrence.


28-years-old, nulligravid and sexually inactive woman admitted to our hospital emergency department with severe abdominopelvic pain. She described an abdominal pain ongoing approximately two weeks, but her pain has increased to intolerable state one day ago . She also complained about the reduction of appetite but no nausea and vomiting. She also reported that she had previously normal bowel movements. Her last menstrual period was 13 days before. She was also suffering from malodorous vaginal discharge. She had no urinary symptoms such as dysuria or frequency and no gastrointestinal symptoms such as constipation or blockage of colonic gas passage. She had no medical illness history, no surgical history, no allergies, and no remarkable family medical history. Her vital signs at admittance were as follows; systolic blood pressure: 90 mmHg, diastolic blood pressure: 60 mmHg, heart rate: 110 beat/minute, body temperature: 38.2 °C. Laboratory tests showed increased white cell count (WBC 16.1 × 10/L and neutrophils 14.1 × 10/L) and C-reactive protein (33 ng/L). Hemoglobin level, renal and liver function tests were normal.
The abdominal palpation of the patient revealed abdominal tenderness with defense and rebound positivity indicating acute abdomen. On abdominopelvic ultrasound imaging; uterus size was normal with homogeneous myometrium, endometrial thickness was 9 mm, right ovary was normal. But left tuba uterina and left ovary could not be visualized with abdominal ultrasonographic examination. On left adnexa there was a complex cystic and solid pelvic mass sized with 6x7cm extending towards cul de sac. Then abdominopelvic computed tomography scan was performed and it was showed that there was a complex adnexal mass sized 5x5 cm on left adnexa with conspicuous air-fluid levels supporting tubo-ovarian abscess. The sigmoid colon wall was edematous due to inflammation and beside it in the mesenteric area there was a solid mass measured 41x23mm including air-fluid levels (). Our initial diagnosis before operation was ruptured tuboovarian abscess.
Due to acute abdomen, we performed urgent laparatomy with midline incision. On inspection, abdominal cavity was contaminated with spread, purulent and malodorous fluid. It was observed that culde sac was obliterated with intestines and omentum. Interestingly uterus and bilaterally fallopian tubes and ovaries was normal. The culde sac obliteration was eliminated with gentle dissection. After mobilization of pelvic mass from culde sac, it was seen that there was a huge perforation area on sigmoid colon with omental reaction (). Resection of sigmoid colon and colostomy were performed. The postoperative period was uneventful. The final diagnosis was adenocarcinoma of familial adenomatous polyposis (FAP) of the sigmoid colon.


A 51-year-old man (158 cm, 68 kg) with mitral regurgitation (MR) was scheduled for elective, minimally invasive mitral valve repair. Preoperative TEE showed severe MR due to prominent prolapse of the middle scallop of the posterior leaflet (P2) with torn chordae. The left atrium was dilated (left atrial diameter 36 mm). Left ventricular ejection fraction was 63%.
General anesthesia was induced with 5 mg of midazolam, 100 μg of fentanyl, 50 mg of rocuronium, and 0.2 μg/kg/min of remifentanil intravenously. A left-sided 35-Fr double-lumen tube was intubated, and the proper position was confirmed by bronchoscopy. After intubation, a TEE probe was inserted.
We placed a central venous catheter and pulmonary artery through the left internal jugular vein and a 16-Fr venous cannula through the right internal jugular vein for the superior vena cava drainage. Anesthesia was maintained with 1%–1.5% sevoflurane in oxygen and air and continuous infusions of remifentanil at 0.2–0.5 μg/kg/min and propofol at 3–4 mg/kg/h.
Right thoracotomy was made at the level of the fourth intercostal space in the left semi-lateral position. The femoral arteries were cannulated with a 20-Fr arterial cannula. Another 24-Fr venous cannula was placed inferior vena cava. The vent tube was inserted through the right superior pulmonary vein into the left ventricle. We confirmed that the tip of 24-Fr venous cannula and the vent tube was proper potion on TEE.
After establishing CPB, an antegrade cardioplegia cannula was inserted into the ascending aorta, and a flexible cross-clamp was subsequently applied. Myocardial protection was provided using mild systemic hypothermia (34°C), and antegrade cold blood cardioplegia was provided at 30-min intervals throughout the procedure.
After transseptal atrial approach, the plication of the posterior leaflet (P2) and reinforcement mitral annuloplasty with a 30-mm MEMO 3D mitral ring (Sorin Biomedica Cardio S.r.L., Saluggia, Italy) were performed. After declamping the aorta, dopamine infusion was started at 3 μg/kg/min. De-airing was performed by standard maneuver including manual cardiac agitation and conventional aspiration of the aortic root vent and left ventricular vent. During de-airing, TEE revealed a hyperechoic mass in the left atrium, which seemed to be adhering to the mitral ring, suggestive of atrial thrombus []. However, during CPB, activated coagulation time was maintained over 500 s and atrial thrombus seemed unlikely to have arisen under such conditions. Weaning from CPB was attempted, and as left atrial pressure increased, the hyperechoic mass disappeared from TEE []. We thus finally diagnosed this structure as an inverted LAA. Weaning from CPB was very smooth. After weaning, TEE showed no abnormal mass in the left atrium. The postoperative course has been uneventful, and the patient was discharged 7 days after surgery.


A 13-year-old male patient [] reported to the Outpatient Department of Sharad Pawar Dental College and Hospital, Sawangi (Meghe), Wardha, with a chief complaint of swelling with pain for 1 month. The patient was apparently alright 1 month back when he noticed a swelling on the left side of the face which was initially small in size and has gradually increased to present size of 6 cm × 4 cm. The lesion was firm, ill-defined, tender, nonmobile and was associated with pain which was pricking in nature. No history of fever, trauma and bleeding or pus discharge had been reported for the patient. Medical and dental history was not contributory. On inspection, the face was bilaterally asymmetrical due to diffuse swelling on the left side of size 6 cm × 4 cm approximately, roughly oval in shape, smooth in surface, color same as adjacent skin with ill-defined margins. The swelling was extending anterior posteriorly (A/P) from the left corner of mouth to left preauricular region, superior inferiorly (S/I) from infraorbital region to level of the left corner of the mouth. Temperature was not raised; tenderness present, consistency was soft to firm. Intraorally, a single-diffuse swelling seen in upper left palatal region of the jaw of size 4 cm × 3 cm approximately, roughly oval in shape, surface was ulcerated, color was same as that of adjacent mucosa, the swelling was extending A/P – from upper left 1–7 region, S/I – from mid-palatal region to depth of vestibule with ill-defined borders [].
Orthopantomogram did not show any relevant findings []. On further examination, the patient was found to be systemically fit with all the blood count values to be in normal range. Biopsy was performed under local anesthesia which led to the diagnosis of round cell malignancy.
Under microscopic examination, low-power view showed sheets of uniform, monotonous round cells separated by thin connective tissue septa at places []. The round cells are diffusely arranged throughout []. Numerous endothelial lined blood vessels of varying shape and sizes are seen with intravasated red blood cell counts. The neoplastic round cells are seen invading into muscle tissue suggestive of muscle invasion. Under high-power view, the round cells showed hyperchromatic nuclei occupying the entire cell with a thin rim of eosinophilic cytoplasm. At places, cells show nuclear pleomorphism []. With these features, a diagnosis of round cell malignancy was made.
Round cells can be seen in Ewing's sarcoma family tumors, rhabdomyosarcoma, osteosarcoma and lymphoma. To rule out Ewing's sarcoma, Periodic acid–Schiff stain was performed which came out negative. Immunohistochemistry was performed to rule out other small round cell tumor. Leukocyte common antigen/CD45 came out positive suggesting the diagnosis of lymphoma []. For further typing, CD3 and CD20 markers were applied for T-cell and B-cell lymphoma, respectively. CD3 came out positivity suggesting the final diagnosis of T-cell lymphoma [].


A 61-year-old man presented with blue-colored papuloplaques on his left temple that had been present for over 1 year. Over the previous 2 months, the lesions had grown rapidly, without any symptoms. Physical examination revealed a large ill-defined dark blue patch studded with pinhead to bean sized cobblestone surfaced papulonodules and satellite papules (). Punch biopsies were performed in the center and at the periphery of the plaque. Microscopic examination of the central specimen revealed compact sheet-like proliferation of heavily pigmented epithelioid and, occasionally, short spindle cells in the entire dermis and subcutaneous fat layer, without junctional activity. One focus of tumor necrosis was found. The tumor cells showed mild to moderate nuclear enlargement and inconspicuous nucleoli. The mitotic count was up to 4 per 10 high power fields with deep and mid-dermal mitotic cells. The Breslow thickness was 4.53 mm. In the periphery of the lesion, the overall pattern of tumor cell infiltrates was similar to that of the center. However, many of the tumor cells had small pyknotic nuclei and the lesser remainders showed mild to (rarely) moderate nuclear enlargement, vesicular nuclei, and small nucleoli. There were rare exceptions of overtly atypical cells showing hyperchromatic enlarged nuclei, and bizarre giant cells. Due to these atypical cells, albeit rare, the histologic findings of peripheral lesion are not compatible with those of other benign dermal melanocytic lesions, i.e., common or cellular blue nevus and Ota nevus. Furthermore, there was no necrosis or mitosis in the dermis (). The tumor cells of both lesions were positive to HMB45, Melan-A and S-100 protein immunohistochemical staining. MIB-1 labelling index was 22%. Considering the clinicohistopathological findings, we diagnosed both lesions as BNLM.
Following the punch biopsy, a fluorodeoxyglucose-positron emission tomography scan revealed multiple lymph node and bone metastases, but no remarkable findings in the urinary tract. The patient was admitted for chemotherapy with dacarbazine 407 mg/day (250 mg/m2 body surface area). During the admission, hematuria of unknown duration was detected. Catheterized urine cytology on SurePath liquid-based preparation was performed. This demonstrated many singly scattered, pigmented cells admixed with red blood cells and occasional necrotic cells. The cells were oval to spindle-shaped with blunt ends and showed a moderate degree of variation in shape and size. Although difficult to recognize nuclear details due to heavy melanin pigment in many of the cells, most cells had small nuclei; only a few cells had nuclei showing mild to moderate nuclear enlargement and nuclear hyperchromasia. Most of the cells on the smear were positive for HMB45 and Melan-A; hence, they were determined to be metastatic BN-like melanoma cells (). However, some histiocytes and urothelial cells were negative for both stains. Subsequent abdominopelvic computed tomography revealed possible liver, spleen, and right kidney metastases, and suggested potential metastases in the bladder dome and lungs. Owing to the patient's poor general condition, cystoscopy with biopsy was not performed. The patient died from pneumonia 3 months after the initial diagnosis.


A 35-year-old male farmer was referred to our hospital with mild dyspnea, hemoptysis, abdominal pain, and intermittent cough. He denied both weight loss and fever. He had no medical history. Physical examination revealed tenderness on the right upper quadrant. All blood investigations were normal except for total counts (15,600 cells/cum), presence of anti-hydatid cyst antibody (measured by ELISA), and blood eosinophilia (>5%). The radiography of the chest was normal. The abdominal ultrasound (US) revealed a hepatic cyst with multiple daughter cysts in the right lobe of the liver and multiple cystic structures in the inferior vena cava (IVC) secondary to the spread of the liver hydatid disease (figures and ). The CT scan confirmed multiple cystic structures within the IVC and pulmonary artery embolism. The diagnosis was an infected hydatid cyst associated with partial thrombosis of the IVC. The patient was given an anticoagulant with a curative dose; a medical treatment (albendazole) was prescribed.
The indication for surgery was retained for the hydatid cyst of the infected liver, which ruptured in the IVC. During his hospitalization, a fatal hydatid pulmonary embolism occurred and the patient was quickly intubated. Death occurred on the second day of hospitalization.


A 30-year-old male butcher was admitted to our department for dyspnea, cough, and severe right upper quadrant pain. He had no medical history. Physical examination revealed tenderness on the right upper quadrant. The laboratory findings were normal except for an elevated liver function (alkaline phosphate 432, U/L gamma glutamyl transpeptidase 252 U/L) and the presence of anti-hydatid cyst antibody (measured by ELISA). The abdominal ultrasonography (US) showed a hydatid cyst lesion in the liver, compressing the portal and hepatic veins. On Doppler US, a germinal membrane of the cyst was found to be extending into the inferior vena cava. A contrast-enhanced CT of the abdomen and chest was performed to delineate the extension of the germinal membrane of the cyst. It confirmed the findings of the ultrasound, and showed more enhancement defects of the segmental and subsections segmental pulmonary arteries filled with the material corresponding to hydatid embolism. The hydatid cyst was opened in the retrohepatic vena cava and remained only passing sluices enhancing after injection (figures and ). There was no hydatid cyst in the lung parenchyma.
During hospitalization, curative doses of anticoagulation were prescribed. After confirming the diagnosis, a surgery was indicated but was refused by the patient. Therefore, a medical treatment was initiated (albendazole) and taken for 9 months. A CT scan was performed after 9 months and showed no regression in the hydatid cyst size.


A 28-year-old female presented to an outside hospital in 2007 with fainting spells that were suspicious for seizures by family's report. A magnetic resonance imaging (MRI) was obtained and revealed a right occipital tumor. The patient underwent a right occipital craniotomy and image-guided resection of the lesion. It was noted that there were three areas which were concerning for tumor invasion of the surrounding parenchyma due to its general discoloration. Frozen biopsies were sent for evaluation. The pathology report came back negative for marginal tumor infiltration. The patient was incorrectly told that the tumor was meningioma due to an incorrect preliminary read and that no further treatment was necessary; however, the final pathological diagnosis revealed a WHO grade III anaplastic ependymoma. Unfortunately, the revised diagnosis was not made known to the patient, nor her future physicians. She did not undergo chemotherapy or radiation at that time.
In 2012, the patient presented to our hospital with severe (8/10) headaches, nausea, and photophobia. Computed tomography (CT) and MRI of the brain did not show any acute pathology or evidence of tumor recurrence. The patient was given a diagnosis of migraine headaches and treated medically.
The patient re-presented in 2014 with relapse of her headaches and fainting spells. An MRI of the brain was obtained, revealing a recurrent 4.1 cm enhancing mass in the right occipital lobe with surrounding edema (without evidence of drop metastasis or other enhancing lesions on spinal MRI []). In light of the rather rapid interval growth of the lesion, despite no new onset focal deficits, and concern for malignant transformation to a WHO grade IV glioma, the neurosurgical team recommended re-resection of the tumor. The patient underwent subsequently re-do craniotomy, and did well clinically postoperatively as she remained neurologically intact and showed improvement in her headaches. The postoperative MRI demonstrated a gross total resection and she subsequently underwent adjuvant radiotherapy.
Two years after her second resection, the patient presented to her primary care physician with a cough lasting for several weeks. A chest X-ray was performed, which revealed multiple, bilateral pulmonary nodules. The largest lesion was seen in the left lower lobe, measuring 4.5 × 3.4 × 3.9 cm []. The second largest lesion was in the left upper lobe, in close proximity to the major fissure. Additional pleural-based masses were seen. A CT-guided biopsy of the mass was performed, confirming the diagnosis of grade III anaplastic ependymoma.
An MRI of the brain was obtained at the same time, which revealed the interval development of several new right-sided intracranial frontal extraaxial masses side, but without any evidence of tumor recurrence in the right occipital lobe tumor resection bed [Figure –]. The largest mass measured at 4.7 × 4.4 × 3.0 cm and was located along the right temporal–frontal convexity. Imaging displayed heterogeneous hyper-intense T2- and hypo-intense T1-signal characteristics and some foci of restricted diffusion. There was diffuse heterogeneous enhancement on postcontrast imaging. The lesion exerted significant mass effect upon the adjacent right temporal lobe gyri, uncus, and cerebral peduncle and a second mass (measuring 2.1 × 2.1 × 1.7 cm) and was located along the right posterior frontal convexity, also causing mass effect. Two additional masses were detected immediately anterior to the second largest mass along the right posterior frontal lobe, measuring 1.3 cm each in the greatest dimension. There was no evidence of recurrent disease at the initial occipital site of presentation, nor evidence of drop metastasis or other enhancing lesions on spinal MRI [Figure , ].
The patient once again underwent respective surgery and all cranial tumors were removed successfully as seen on postoperative imaging [].
The patient is currently under close follow-up, with adjuvant radiotherapy and chemotherapy for her lung metastases without evidence of intracranial recurrence 12 months following her most recent resection seen on imaging.


A 33-year-old female with a 2-year history of dizziness was presented for review. The patient had no past medical history. The patient noted that her incidence of dizziness was getting worse, and a newly-onset bilateral nystagmus on the lateral gaze was presented on March 15, 2016. Therefore, it was recommended that the patient undergo a brain magnetic resonance imaging (MRI) on April 4, 2016. The brain MRI showed an approximate 3.4 cm×3.6 cm×5.7 cm sized high signal intensity (HSI), non-enhancing mass on the T2-weighted images at fourth ventricle (), and the formal reading of the MRI finding was a suspicious epidermoid cyst. The preoperative physical examinations showed dizziness and nystagmus on the bilateral lateral gaze. To rule out the LCN deficits, the neurosurgeons tested the loss of taste at the posterior one-third of the tongue (for CN XI), gag reflex (for CN XI, CN X), the presence of uvula deviation (for CN X), weakness of sternomastoid and/or trapezius muscle (for CN XI), and the presence of tongue deviation, dysarthria (for CN XII). The result of testing found that there was no abnormal finding on these tests. Then, on May 23, 2016, the patient was admitted at the Department of Neurosurgery and underwent a tumor removal surgery on May 24, 2016.


A 38-year-old female suffered from a 1-month history of diplopia and dizziness. The patient had no history of any other diseases. After visiting a local clinic, the patient was recommended to undergo a brain MRI. Next, she took a brain MRI on April 28, 2016. The brain MRI showed an approximately measured 5.2 cm×5.4 cm×4.8 cm HSI mass at the fourth ventricle on T2-weighted images, with strong diffusion restriction and scalloped expansion into bilateral cerebellum and brain stem (). As the previous case, the patient was diagnosed with a suspicious epidermoid cyst at the fourth ventricle. On the preoperative physical examinations, the incidence of nystagmus was seen in all directions and the left facial sense was decreased at the V2 area. Except for those noted and reviewed findings, there was no abnormality on the review of the lower cranial exams which were same tests in case 1. Therefore, the patient was admitted at the Department of Neurosurgery and went through tumor removal surgery on May 24, 2016.


A 63-year-old female presented to the emergency department with 2 days history of palpitations, shortness of breath and chest pain. She also reported chest heaviness with deep inspiration with both ambulation and at rest. Her past medical history was significant for hypertension controlled with medications. She denied any history of smoking. Electrocardiogram (EKG) performed in the emergency department showed patient to be in supraventricular tachycardia with a heart rate of about 170 beats per min () and blood pressure 123/83 mm Hg. Pulse oximetry showed 97% saturation on room air. On examination, she was in mild distress. Cardiac auscultation revealed normal S1, and S2 heart sounds without any gallops. No jugular venous distension was noted. Lungs were clear to auscultation.
The patient was given adenosine 6 mg followed by 12 mg dose two times without a change in rhythm. The patient was then given metoprolol 50 mg orally once and metoprolol 5 mg intravenously three times. Telemetry data showed that patient would go in and out of this rhythm even with the administration of the medications. Due to the arrhythmias refractoriness, the patient was started on amiodarone. On imaging, the initial chest X-ray was unremarkable for any acute changes and only showed pulmonary vascular congestion with cardiomegaly ().
After admission to the medical floor, patient blood pressure started to drop to 97/65 mm Hg, and her oxygen requirements went up. She required 2 L of oxygen via nasal cannula to keep oxygen saturation above 94%. Due to concern for pulmonary embolus (PE), a stat computed tomography (CT) angiogram chest was ordered, and it revealed multiple pulmonary emboli bilaterally, a large pericardial effusion, 7mm nodule in the right upper lobe and mediastinal adenopathy ().
The patient was started on low molecular weight heparin for acute PE. An echocardiogram was ordered which showed ejection fraction of 60-65%, apical diastolic collapse, and large pericardial effusion (). Cardiothoracic surgery was consulted, for urgent subxiphoid pericardial window and placement of a chest tube. About 800 mL of hemorrhagic fluid was removed. Analysis of the fluid revealed malignant cells positive for TTF1 and CK7 tumor markers indicative of primary lung adenocarcinoma. Immunohistochemical staining was performed on the sample, and it was positive for BRAF V600E mutation and PD-L1 expression.
The patient was started systemic therapy with dabrafenib and trametinib. The patient was discharged after clinical improvement and removal of a chest tube. She was given follow-up outpatient with oncologist and cardiologist.


A 66-year-old Caucasian woman with no significant past medical history presented to the emergency department with a 2-month history of progressively worsening dyspnea. The dyspnea was worse with exertion or laying down flat. She also complained of a productive cough, fatigue, and weight loss. She denied any sick contacts or recent travel. The patient has not been seen by a primary care physician for many years. She had 25 pack-years smoking history. She also endorsed occasional marijuana and cocaine use. Family history was notable for lung cancer in her mother.
Physical examination in the emergency room revealed a cachectic female in moderate respiratory distress who was alert and oriented. She was afebrile with a pulse of 106 beats per min, blood pressure of 119/76 mm Hg, respiratory rate of 24 breaths per min, and oxygen saturation of 99% on 2 L oxygen via nasal cannula. No jugular venous distension was noted. S1 and S2 heart sounds were distant with no audible murmurs, rubs, or gallops. Lung sounds were severely decreased in the right mid and lower fields but otherwise normal in the other fields. No edema, clubbing, or cyanosis was observed in the extremities.
Laboratory work up revealed leukocytosis (WBC 15.8 K/uL), hyponatremia 128 mmol/L, hypochloremia 92 mmol/L, and lactic acidosis 2.94 mEq/L. B-type natriuretic peptide and troponin were within normal limits. Arterial blood gas on 2 L oxygen revealed a pH of 7.45, a partial carbon dioxide pressure of 30 mm Hg, a partial oxygen pressure of 92 mm Hg, and bicarbonate of 23.1 mEq/L. A 12-lead electrocardiogram showed sinus tachycardia (). Chest radiograph revealed a cavitary lesion with an air-fluid level in the right upper lobe and an enlarged cardiac silhouette (). CT of chest, abdomen, and pelvis with contrast was performed, and it revealed a right upper lobe necrotic mass, pericardial effusion, and right pleural effusion along with right middle lobe medial segment collapse (). Extensive mediastinal adenopathy and bilateral adrenal masses were also noted. Echocardiogram revealed left ventricular ejection fraction of > 70% with right ventricular and right atrial diastolic collapse ( a-b).
The patient underwent emergent pericardiocentesis and placement of pigtail catheter to evacuate pericardial and pleural fluid, respectively, for therapeutic relief and fluid analysis. Approximately 850 mL of serosanguineous fluid was removed from the pericardial cavity. Later on, a pericardial window was placed by cardiothoracic surgery. Cytology studies indicated primary lung adenocarcinoma with positivity for Napsin-A and TTF-1. Further analysis revealed high expression of PD-L1 and positive BRAF c.1780G>A (p.D594N) mutation. Blood cultures and acid-fast bacilli smear performed on admission were negative for any acute infection. The patient’s shortness of breath improved during the hospital stay, and her electrolyte abnormalities were corrected. She was discharged to a skilled nursing facility once she was hemodynamically stable. She was given outpatient follow-up with an oncologist for treatment of stage IV non-small cell lung cancer.


A 57-year-old previously healthy female presented with worsening dyspnea of 2-week duration associated with an inability to lie down supine. She also had a fever, weight loss, and recurrent episodes of severe nocturnal cough. On physical examination, significant tachypnea and orthopnea were present with a temperature of 101°C on several occasions. Cardiovascular examination and other systemic examination were normal. Chest radiograph showed large mediastinal mass occupying the upper and mid-zone of the lung fields. Arterial blood gas analysis showed PaO2 of 42 and PaCO2 of 34 mmHg. Complete blood counts and biochemical reports including lactate dehydrogenase were within normal limits. After an initial stabilization with supplemental oxygen and noninvasive ventilatory support, multidetector contrast-enhanced computed tomography of the thorax revealed anterior mediastinal mass with critical airway narrowing (maximum luminal diameter of 3.9 mm at lower trachea) []. Due to significant airway narrowing and severe orthopnea, less invasive modalities such as bronchoscopic needle aspiration with or without images guidance were not feasible. Considering a possible lymphoma in the differential diagnosis, low-dose steroid for tumor debulking was started, but the patient showed no response and continued to worsen. Assuring patient safety along with the best clinical outcome, the patient was taken up for rigid bronchoscopy. A limited videobronchoscopy using ultra-slim pediatrics scope with a distal end outer diameter of 3.1 mm (BF-XP 190, EVIS Exera III, Olympus Medical Systems Corp., Japan) was performed to visualize the airway before the actual procedure [].
Under general anesthesia with airway block and spontaneous respiration, intubation was carried out using 12-mm rigid tracheobronchoscope with Hopkins telescope (Karl Storz, GMbH and Co., KG Germany). With the scope just above the carina, the predetermined area was punctured using the 18-gauge rigid needle with stylet (Karl Storz, GMbH and Co., KG Germany) [] and the needle was flushed with the stylet and few drops of saline to avoid bronchial contamination. The needle was jabbed to and fro in multiple directions while maintaining the continuous negative pressure by the retracted piston of the attached syringe. After terminating the suction, the needle was withdrawn from the lesion and the samples were divided for cytological, histopathological, and immunohistochemical evaluation []. Postsampling, temporary customized studded silicone “Y” stent was placed to stabilize the airway for interim symptomatic relief []. Appropriate positioning, adequacy of airway palliation with distal patency, and stability of the stent were ensured with check bronchoscopy after the procedure. Based on the cytological confirmation of lymphoma, debulking chemotherapy was initiated using low-dose cyclophosphamide plus vincristine in the hematology unit.
Histopathological section demonstrated diffuse infiltration by medium-to-large atypical lymphoid cells having round-to-irregular nuclei, coarse chromatin, and inconspicuous nucleoli [Figure and ]. On immunohistochemistry, tumor cells were positive for leukocyte-common antigen, PAX-5, and CD20 while negative for cytokeratin, CD3, and terminal deoxynucleotidyl transferase. Ki-67 labeling index was 95%–100% [Figure -]. These features were consistent with a diagnosis of Burkitt’s lymphoma and a dose-adjusted chemotherapy comprising of etoposide, prednisolone, vincristine, cyclophosphamide, doxorubicin, and rituximab was given. A significant clinical response was observed on review evaluation after the first cycle of chemotherapy prompting removal of the stent. The patient on last follow-up after six cycles of chemotherapy is free of symptoms with no evidence of disease.


A 54-year-old male patient presented a 14 cm × 10 cm large and 4.5 cm deep ulcerated wound with infiltrated nodular borders centered on the umbilicus (). The borders were sharply delineated. The patient had no particular medical or surgical history. He did not take any medication but was a heavy smoker (more than 30 cigarettes per day since the age of 18). The lesion appeared about 8 years ago as a small and easily bleeding fleshy tumor of the umbilicus. The patient did not seek medical attention as the lesion was not painful and because he thought that what had appeared spontaneously would also disappear spontaneously. There was no history of chronic umbilical inflammation, prior radiotherapy, or traumatism to the lesion site. On clinical examination, the lesion did not adhere to the underlying fascia or muscle plans. There were no loco-regional lymphadenopathies. There were no signs of a basal cell nevus syndrome or Gorlin syndrome. A clinical differential diagnosis of pyoderma gangrenosum, verrucous carcinoma, eroded spindle cell carcinoma (SCC), or eroded BCC was suggested. A 4-mm punch biopsy obtained under local anesthesia was suggestive for SCC (). Due to the clinical-pathological incoherence, a large excisional biopsy was performed revealing deep infiltrating morphea-form BCC ( and ). Immunohistochemical studies revealed strong positive stainings for BerEp4 and chromogranin A, but CD56 expression was only marginal (). Ki67 immunostaining revealed numerous positive cells. Keratin 20 immunostaining was negative. The final histological diagnosis was an infiltrating morphea-form BCC with neuroendocrine differentiation. Blood screening revealed no abnormalities. Magnetic resonance imaging (MRI) revealed a deep tumor infiltration until the muscular fascia ( and ). Ultrasound and computed tomography (CT) scan did not detect any further involvement of the loco-regional lymphatic ganglia.
The cutaneous tumor board decided, in accordance with the patient and his general practitioner (GP), for a two-stage sequential treatment plan, starting with a 3- to 4-month course of vismodegib 150 mg per day aiming at the reduction of the tumor mass followed by a new feasibility assessment for surgery. The common vismodegib-related adverse effects were observed in the form of alopecia, muscle cramps, and dysgeusia and later ageusia. The patient suffered most from the ageusia but accepted relatively well the other adverse events. Four months later, the lesion was significantly reduced in depth and extension and was not oozing or bleeding anymore (). The skin aspect was atrophic and cicatricial, not adhering to underlying structures. Ultrasound examination did not reveal any deep tumor infiltration. This significant shrinkage both in size and depth () finally allowed plastic surgery, respecting a 0.5 cm surgical margin. Histology only revealed cicatricial scar tissue without any sign of residual BCC, particularly at the borders of the lesion (). Until today, the follow-up is 6 months, and there are no clinical signs of BCC recurrence and ultrasound examination was unremarkable.


A 54-year-old male patient visited to emergency department for minor head injury after he slipped down on stairs. He underwent brain CT scan on approximately 2 hours after trauma (). He presented no clinical abnormality on initial neurologic examinations except mild headache; his vitals were stable, Glasgow Coma Scale (GCS) score was 15 (E4V5M6), pupils were normal bilaterally, and there was no history of loss of consciousness. Also, he had no recent history of any medical treatments or other hematologic disorders, hypertension, diabetes mellitus and alcoholism. No bony fracture, intracranial lesion, or mass effects were detected on CT scan. He was monitored and treated for symptomatic control in the emergency department. Then, the sudden onset of generalized tonic-clonic seizure was developed on 8 hours after trauma. Newly found acute subdural hematoma (ASDH) was detected in left cerebral convexity on subsequent brain CT and midline was shifted less than 2 mm (). There was no history of additional trauma while he was treated in the emergency department and no evidence of underlying medical dysfunction in laboratory findings. On further examination, hematologic test including coagulation profile and peripheral blood morphology was confirmed within normal range. The patient referred to neurosurgery department and admitted to intensive unit care. We followed-up repeated CT 24 hours after admission; there was no change of amount of hematoma. Though he sustained moderate headache, vitals were stable and GCS score was 15 without neurological deficit. The volume of ASDH did not change during serial CT on 3 and 5 days of admission. However, on 8 days of admission, upper and lower extremity motor grade of patient were deteriorated to grade 4 on right side. CT scan disclosed increasing amount of mixed-dense subdural hematoma (SDH) with mass effect (). There was no evidence of acute cerebral infarction or other intracranial lesions except SDH on diffusion weighted magnetic resonance image (). The patient became presenting intense headache and disorientation. Emergent surgical intervention of craniotomy with hematoma removal was performed and semisolid blood clot was evacuated. On the 1st post-operative day, CT showed no mass effect with midline recovery (). The patient's motor grade was nearly recovered to grade 5; however, recurrent ASDH was detected on follow-up CT scan on 3rd postoperative day (). Surgical intervention of craniotomy and hematoma evacuation was re-conducted in a same manner. The patient was discharged on the 10th postoperative day with GCS score of 15 and Glasgow Outcome Scale of 5 ().


A 2-year-old intact male Vizsla, with normal activity level, was evaluated for a 1-month history of right hind-limb lameness following trauma of the stifle caused by forceful direct impact against a solid surface, which occurred during physical activity. Prior to the injury there had been no history of medical problems. Clinical examination findings included a reluctance to walk, grade 3 lameness based on the Sumner-Smith scale (Sumner-Smith, 1993), decreased weight-bearing on the right hind limb, swelling of the cranial aspect of the stifle, as well as pain on deep palpation and passive manipulation of the joint. Complete blood count, serum chemistry and urinalysis results were within normal limits.
After 5 days of antiflammatory therapy with robenacoxib (2 mg/Kg), a slight improvement in lameness and a reduction in tissue swelling were observed.
Orthogonal radiographic views of the right stifle joint were obtained under general anaesthesia. Medio-lateral views demonstrated soft tissue radiodensity at the cranial aspect of the joint at the level of the distal half of the PL. On medio-lateral view, only the proximal part of the PL was clearly seen with distinct margins, while its distal part, along with the cranio-ventral margin of the infrapatellar fat pad, was ill-defined and indistinguishable from the background of periligamentous soft tissue opacity (). Abnormalities in intra-ligamentous radiodensity were not seen. Bony abnormalities were not visible at the level of the tibial tuberosity. The cranio-caudal view was not useful for radiographic evaluation due to superimpositions.
In order to characterise the soft tissue joint damage and to assess PL integrity, after the radiographic examination an MRI was performed under general anaesthesia using a 0.25 Tesla permanent magnet (ESAOTE VET-MR GRANDE: Esaote, Genoa, Italy). The MRI sequence protocol included sagittal, transverse and dorsal Gradient Echo-STIR, sagittal T2-weighted Fast Spin Echo, sagittal balanced steady-state free precession (bSSFP) sequence, and transverse and sagittal T1-weighted Spin echo, acquired before and after the intravenous administration of paramagnetic contrast medium (Magnegita® – gadopentate dimeglumine 500 mmol/ ml – insight agents®; 0.15 mmol/kg BW: Agfa Healthcare Imaging Agents GmbH, Köln, Germany).
Magnetic resonance imaging revealed swelling of the distal half of the PL, with increased intra-ligamentous signal intensity in fat-suppressed sequences. The damaged part of the PL was surrounded by irregularly marginated pathologic material, isointense on the T1- and T2-weighted sequences with inhomogeneous contrast-enhancement, resembling a clot (,). The abnormal material was seen more evidently adjacent to the inner surface of the PL, displacing the cranial aspect of the infrapatellar fat pad. Transverse spin-echo and bSSFP sequences oriented at the level of the distal PL insertion showed a focal linear defect in the medial area of the ligament section, originating from its caudal margin and extending toward the cranial margin. The cranial extension of the tear and involvement of the cranial ligament margin were not clearly assessable.
Multiplanar reformatting of the volumetric bSSFP sequence aligned according to the inner mid-dorsal axis of the PL showed complete disto-proximal extension of the lesion from the osteotendineous junction on the tibial tuberosity to the middle third of the PL (). At the level of the PL insertion, the tibial tuberosity showed a focal area of intraosseous pathological hyperintense signal in fat-suppressed sequences, compatible with a bone-marrow edema-like lesion (Starr et al., 2008) ().
In order to clarify any possible radiographically undetectable bone damage to the osteoligamentous junction at the level of the tibial tuberosity, an unenhanced CT scan of the right stifle was acquired immediately after the MRI examination, using a 16 slice-MDCT scanner (Somatom Emotion: Siemens, Forchheim, Germany) with the patient in sternal recumbency on the CT table under general anaesthesia. CT technical parameters were as follows: bone and standard acquisition algorithm, 110 kVp, 180 mAs, 0.6-mm slice thickness, pitch of 0.8 and 1 s/rotation. Three-dimensional (3D) multiplanar reformatted and volume-rendered images were obtained using dedicated 3D software (OsiriX DICOM-viewer: Pixmeo, Geneva, Switzerland). CT scans showed increased attenuation of the tibial tuberosity cancellous bone, with no sign of bone fracture or detached bone fragments at the osteoligamentous junction. The distal PL half was enlarged and surrounded by periligamentous accumulation of irregularly marginated material isoattenuating to the soft tissue. Such periligamentous swelling impeded identification of the boundaries of the distal PL half and exerted a compressive effect on the infrapatellar fat pad, which was caudally displaced. Discontinuities in PL structure were not evident (; ,; ,).
For a more detailed characterisation of the ligamentous injury the dog was subjected to ultrasonography of the stifle. B-mode ultrasound examination was performed with the dog maintained in lateral recumbency, using a portable ultrasound machine (MyLab TM Alpha, Esaote, Genoa, Italy) and a linear, 10–15 MHz high frequency transducer. Keeping the stifle normally flexed, the PL was examined from its cranial origin to its distal insertion in both the long and short axis planes. Transverse images were obtained with the ultrasound beam placed perpendicular to PL fibres, and longitudinal ultrasound images obtained by keeping the probe edge positioned over the patella. The scan technique was also extended over the lateral and medial sides of the PL. For dynamic ligament assessment, passive movements of flexion and extension were performed on the stifle joint while the ultrasound probe was held to the PL at different levels. Ultrasound videotapes and static images were collected and reviewed by both authors consensually.
The distal PL area appeared thickened with heterogeneous echotexture and a loss of fibrillary pattern (,). At this site a 10 mm (proximo-distal) anechoic defect, extending from the distal insertion to the midportion of the ligament, was detected within the PL fibres. The fibrillary defect appeared, on transverse images obtained at the level of the middle portion of the PL, as a 2 mm wide hypoechoic line in the medial half of the sections running from the caudal ligament margin to its centre.
At the distal insertion level the defect measured 3.8 mm and affected the entire PL section from caudal to cranial margin (,). The paratenon was not affected by the lesion.
Behind the patellar tendon the infrapatellar fat pad appeared inhomogeneously hyperechoic and caudally displaced by an accumulation of anechoic fluid interposed between the distal part of the PL and the tibial epiphysis (,).
The patient was discharged with an orthopaedic rigid knee brace. 30-day suspension of physical activity was recommended. One month later the dog appeared in good physical condition with significant clinical improvement of the hind limb lameness. Follow-up ultrasonography was recommended to monitor PL healing.


A 51-year-old woman with past medical history of hypertension was brought in by
emergency medical services after sustaining burns to the forearms. The patient
reported using aerosol cooking oil spray that ignited the flames. Examination
revealed second-degree burns to the bilateral volar aspect of forearms and the
dorsal aspect of bilateral hands with scattered regions of bullae, accounting
for a burn area of around 4%. The patient was discharged from emergency room
with topical silvadene for wound care. At the follow-up visit one week later the
burn wounds were noticed to have healed well.


A 31-year-old woman with no significant past medical history presented to the
emergency room with a complaint of burn wounds secondary to a flash fire. The
patient reported to have used an air freshener near a burning stove, which
flared up the fire causing burns to her right face, lips, neck, breast and
bilateral shoulders. Examination revealed superficial second-degree burns to the
right face and neck, first-degree burns to the right axilla, small second-degree
burns of the right breast and both anterior shoulders, accounting for an
approximate burn surface area of 5%. She was discharged with topical silvadene
and bacitracin prescriptions and was referred to follow-up as an outpatient. She
came back to clinic after three days; examination suggested similar findings,
blisters were debrided and she was recommended to continue topical silvadene
application. At the follow-up visit after ten days from the initial insult, the
burn wounds were noticed to have healed well with no prominent scarring.


A 66-year-old man with past medical history of diabetes mellitus, schizophrenia
and chronic alcoholism presented to the emergency room five days after using a
repellent aerosol spray next to the stove which was ignited. The patient
reported that initially he tried to treat the burns with local home wound care
and decided to come to the emergency room when he could no longer tolerate pain.
Examination revealed second-degree burns to the lower lip, nasal ala, forehead
and cheeks, first-degree burn to the right upper extremity on the anterior
forearm, and on the left upper extremity there were deeper second-degree burns
on the forearm, extending from the hand to the elbow with scattered bullae noted
on the dorsum of the hand and elbow region, accounting for a burn surface area
of approximately 7% (). The patient was subsequently admitted to Burn ICU, where bullae
were un-roofed, treated with local wound care using topical silvadene and
bacitracin, and supportive care (). The patient was discharged on
hospital day 12 with burns reported to be fully healed.


An otherwise healthy 55-year-old man complained of abdominal pain in January 2016. A pancreatic mass with multiple liver metastatic lesions was found through physical examination and abdominal sonography. In addition to a hypodense mass (36 × 32 mm), in the body of pancreas, the CT scan revealed a dilation of the distal part of the pancreatic duct and an involvement of splenic vein, superior mesenteric vein (SMV), and celiac trunk. Based on the poor general condition of the patient, he was not eligible for additional invasive investigational intervention or curative treatment.
The abdominal pain was not well controlled with methadone, 30 mg daily and paracetamol (acetaminophen), 500 mg QID.
The patient was a candidate for interventional pain management. Pre-procedural lab test assessments including coagulation tests, blood cell counts, and metabolic tests were in the normal range.
An experienced pain specialist performed a fluoroscopic-guided bilateral, retrocrural celiac plexus block, in the prone position, by using 20 gaged, 15 cm sharp, curved needles on February 9, 2016. Following negative aspiration and contrast approval, 7 mL of Marcaine 0.25% and 20mg Depo-Medrol were injected in each side. Subsequent to the procedure, the patient experienced dizziness and lack of energy. One week after the procedure, while the pain was well controlled and analgesics were tapered, a systolic blood pressure of 60 mmHg with positive orthostatic hypotension was recorded for the patient. The patient had no other sign and symptoms of cardiac or respiratory insufficiency in clinical assessment. Despite some general precautions such as hydration and routine workup to excluding other possible causes, the orthostatic hypotension had continued for the next 3 days. However, due to poor prognosis and patient conditions, willing advanced evaluation of hemodynamic and cardio-circulatory assessments was not considered. To restore the blood pressure, fludrocortisone 0.1 mg per day was prescribed and after a week, the blood pressure stabilized to 90/60 mmHg without orthostatic hypotension.
The patient was admitted to the palliative care unit on February 30 for severe constipation despite quite enough doses of laxatives. At the time of admission, he was receiving 10mg of methadone per day and physical examination revealed moderate ascites. Following palliative interventions, the patient was discharged a couple of days later with good control of his symptoms and passed away in May 2016 at home. An autopsy was not performed.


A 54-year-old woman was hospitalized because of lower back pain caused by trauma for 20 days. Lumbar magnetic resonance imaging (MRI) showed a fresh compression fracture at the L3 level (). Bone densitometry showed that the spine density was below average, with a mean spinal T-score of −2.98. A physical examination showed marked tenderness on palpation of the L3 region, with no other positive signs. Except for the incapacitating pain, the patient’s vital signs were stable and there was no evidence of infection. The white blood cell (WBC) count was 6900 cells/mm3 (normal range: 3000–10,500 cells/mm3. Haematological analysis demonstrated that the erythrocyte sedimentation rate (ESR) was 10 mm/h and the C-reactive protein (CRP) level was 0.6 mg/dL, both of which were well within the normal range. Considering that the patient’s low back pain persisted in the last 20 days, we chose to perform an L3 PKP (), and no complications occurred during operation. No antibiotic treatment was provided before, during, and after the operation. The patient’s low back pain was greatly improved after the operation, and she left the hospital 2 days later. Seven months postoperatively, she experienced recurrent back pain and underwent treatment at another hospital. The details of her treatment at this hospital were unclear. The patient was readmitted 10 months after the operation. Upon admission, she suffered from a low-grade fever, limited motion of the lumbar spine with paravertebral muscle spasm and extensive thoracolumbar vertebral tenderness. The resting results of a physical examination were normal. A chest X-ray showed a history of obsolete pulmonary tuberculosis. An imaging examination showed severe spondylitis at the L2–L3 level, with paravertebral abscess formation and bony destruction of L2 and L3 (). A haematological investigation showed that the WBC count was 11,060 cells/mm3, accompanied by 79.11% of neutrophil granulocytes, and the ESR and CRP level were increased (78 mm/h and 62 mg/dL, respectively). The serum T-SPOT.TB test showed that earlier secreted antigen target-6 in the Antigen A group was 10 (normal range: 0–6) spots, culture filter protein-10 in the Antigen B group was 17 (normal range: 0–6), and the result of the T-SPOT.TB test was positive. The results of the serum T-SPOT test suggested Mycobacterium tuberculosis infection. Medication for tuberculosis was started with the diagnosis of tuberculous spondylitis. After 4 weeks of tuberculosis drug therapy, the ESR and CRP levels were almost decreased to the normal ranges. The patient underwent posterior fusion and instrumentation from T12 to L5 without neural decompression (). Six months after surgery, the patient continued anti-tuberculous and anti-osteoporosis treatments, and low back pain appeared to be relieved after surgery. The patient can currently receive clinical reexaminations by herself, and there are no nerve lesions on both lower limbs.
The patient provided consent for this report.


A 45-year-old male patient, with known hyperthyroidism since 2012 (which was revealed later), noncompliant to antithyroid drug, presented in medicine emergency ward with complaints of acute onset weakness in all four limbs since early morning. He was having easy fatigability for past 3 days. He was unable to walk or stand unassisted. On physical examination, the patient was conscious oriented, afebrile but was having profound tremor, irritability, and breathlessness. His pulse rate was 96/min regular and blood pressure was 126/78 mmHg. There was no evidence of goiter or any eye and nail bed changes. Neurologic examination revealed power of 2/5 in the upper limbs and 1/5 in both lower limbs with diminished deep tendon reflexes and flexor plantars. Higher mental function including speech, cranial nerves, sensory system, and autonomic nervous system examination revealed no abnormality. Arterial blood gas (ABG) showed pH of 7.39, HCO3− – 18.1 mEq/L, pCO2 – 30.6 mmHg, pO2 – 63.1 mmHg, potassium (K+) – 1.58 mEq/L, chloride (Cl−) 95 mEq/L, and anion gap 8 mEq/L, suggestive of compensated respiratory alkalosis; however, electrocardiogram was normal. Laboratory investigation showed hemoglobin 14.9 g/L, total leukocyte count 9800 cells/cumm, polymorphs 76%, lymphocytes 23%, and platelet 1.76 lakhs cells/cumm. Random blood sugar was 109 mg/dl, sodium (Na+) 135 mmol/L, potassium (K+) 2.0 mmol/L, blood urea 40 mg/dl, and serum creatinine was 1.23 mg/dl. Liver function test showed total serum bilirubin 0.59 mg/dl and all liver enzymes were within normal limit. Serum protein was 6.7 mg/dL and serum albumin was 3.0 mg/dL. Serum ionic calcium 1.06 mmol/L (reference range: 1.1–1.35 mmol/L), total calcium 7.7 mg/dL, corrected calcium 8.5 mg/dL (reference range 8.5–10.2 mg/dL), serum magnesium 1.38 mg/dL (reference range 1.7–2.2 mg/dL), urinary Na = 48 mEq/L (normal value below 20 mEq/L), and urinary K = 26 mEq/L (normal value below 20 mEq/L). In the above patient due to traumatic catheterization, there was plenty of microscopic red blood cells (RBCs) in urine which could have lead to erroneously raised urinary Na+ and K+ due to hemolysis of RBCs. Patient may have also likely to have received diuretics by local practioners for breathlessness. He was supplemented with intravenous (IV) potassium chloride, magnesium sulphate with cautious monitoring, and supportive management. Patient's quadriparesis improved after K+ value returned to normal. Thyroid function test (enzyme-linked immunosorbent assay method) revealed free T3 (free tri-iodothyronine) 3.89 pg/ml (reference range: 1.71–3.71 pg/ml), free T4 (thyroxine) 10.0 ng/dl (reference range: 0.70–1.48 ng/dl), and thyroid-stimulating hormone (TSH) 0.0 μlU/ml (reference range: 0.35–4.94 μIU/ml). There was high free T3 and T4 with low TSH in serum, indicating hyperthyroidism. Antithyroid peroxidase (TPO) antibody was 749.53 IU/ml. 99m Technetium thyroid uptake and scan shows well-visualized thyroid gland with increased trapping function favoring hyperthyroid status-Graves' disease []. Finally, after thorough clinical examination and laboratory workup, a diagnosis of thyrotoxic hypokalemic periodic paralysis (THPP) due to Grave's disease was made.


A 58-year-old male presented to the emergency department in August 2015 with sudden-onset shortness of breath associated with sharp right-sided pleuritic chest pain. His only past medical history was of hypertension. Prior to this presentation he had been clinically well and was fully independent. He was a smoker with a 40 pack-year history. He did not drink alcohol and had no recent travel history.
On clinical examination the patient was unwell with a pain score of nine out of 10. His heart rate was 76 beats per min, his blood pressure was 210/100 mmHg, his respiratory rate was 20 breaths per min and his oxygen saturations were 98% on room air.
His chest examination showed reduced air entry on the right side with reduced percussion note. He had poor chest expansion on the right side. Heart sounds were normal, the apex beat was in the mid-clavicular line and jugular venous pressure was normal. He had no peripheral oedema.
These showed a C-reactive protein (CRP) of 48 mg⋅L−1 (normal range: <5 mg⋅L−1) and white cell count (WCC) of 6.05×109 L−1 (normal range: 4–11×109 L−1), with normal haemoglobin, platelets and renal function. A posterior to anterior chest radiograph was performed.
He was diagnosed with a large right-sided spontaneous pneumothorax with possible background emphysematous disease warranting further investigation given the patient’s smoking history.
A size 12 Seldinger chest drain was inserted in the emergency department. The chest drain was working well, with bubbling initially. A repeat chest radiograph showed improvement of the pneumothorax size; however, following a number of days there was persistent breathlessness and bubbling of the chest drain despite the use of suction.
He was assessed by the cardiothoracic surgeons, with radiographs which confirmed persistent pneumothorax, who performed a right-sided video-assisted thoroscopic surgery (VATS) with apical bullectomy and abrasion pleurodesis. Although a chest computed tomography (CT) scan can be useful for patients with persistent pneumothorax in order to identify loculated pneumothoraces and secondary causes, it was not performed and the patient was offered surgery to treat the persistent air leak and reduce the risk of recurrent episodes. Post-operative recovery was uneventful and the patient was discharged on the forth post-operative day. At a follow-up appointment the patient had recovered back to his baseline []. He was assessed in the community and diagnosed with emphysematous chronic obstructive pulmonary disease (COPD).


A 22-year-old male patient from Agarfa district, southeast Ethiopia, presented to Goba Referral Hospital with complaints of severe abdominal cramp, periumbilical pain which shifted to the right lower quadrant of the abdomen for 30-hours duration, and 2 episodes of nonbilious vomiting as well as high-grade fever. He had no past history or family history of TB. He had no cough, sweating, and weight loss, which suggested the evidence of pulmonary TB. Similarly, the patient had no history of subacute intestinal obstruction in the past, had no diarrhea and constipation, and had no urgency or pain during urination.
During admission, the patient was acutely sick looking and vital signs were as follows: blood pressure 90/60, pulse rate 104 beat/min, respiratory rate 26 breath/min, and body temperature 38.3°C. Examination of respiratory and cardiovascular systems was essentially normal. Local examination of the abdomen revealed that abdomen moved with respiration, there was direct tenderness below the umbilicus bilaterally, and rebound tenderness over the right lower quadrant of the abdomen. Laboratory studies on blood revealed hemoglobin to be 12 g/dL; white blood cell count 15,800/µL, neutrophil 88%, and HIV serology result negative.
With the clinical diagnosis of pelvic peritonitis secondary to perforated acute appendicitis, the patient was taken up for surgery. The peritoneal cavity was opened through the lower midline incision and 30 mL of thick offensive pus in the right lower abdomen and perforated appendix at the base was found. Then, the pus was drained, appendectomy and abdominal lavage were performed, and the abdominal wall was closed inlayer.
From the resected appendix, excisional biopsy was sent for histopathology, and the histological picture revealed granulomatous caseification lesion in the body of the appendix, which is diagnostic for extrapulmonary TB (). However, the intra-abdominal fluid, bowel, and omentum did not show any granulomatous lesions and no mesenteric lymphadenopathy. Based on these findings, the final diagnosis of perforated tuberculous appendicitis was made. After surgery, the patient took 1 g of ceftriaxone intravenously (IV) twice per day for 7 days and 500 mg of metronidazole IV 3 times per day for 7 days, and then started anti-TB treatment on the fourth postoperative day and continued it for 6 months. During the follow-up visits, the abdominal signs and symptoms were resolved and the patient had marked clinical recovery to date.


A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.


A 52-year-old man presented to us with complaints of painful defective vision of sudden onset associated with redness in both eyes for 3 days. He revealed treatment elsewhere with oral acetazolomide, topical timolol maleate, and intravenous methylprednisolone (IVMP) with no improvement. His best-corrected visual acuity (BCVA) was 1/60 right eye (OD) and 6/36 left eye (OS). Anterior segment examination in both eyes showed lid edema, circumcorneal congestion, corneal epithelial edema, Descemet's folds, multiple, fresh, pigmented keratic precipitates on the corneal endothelium, shallow anterior chamber (AC) (Van Herick Grade 1), fixed mid-dilated pupil, and glaucomflecken []. The intraocular pressure was 13 mmHg OD and 18 mmHg OS. The angle structures were not discernible on gonioscopy. The fundus view was restricted in both the eyes with faint disc edema in Grade 2 vitreous haze. Ultrasound B scan revealed 360° bilateral choroidal effusion []. A provisional diagnosis of bilateral uveal effusion syndrome with secondary angle closure was made. Thorough uveitis work up such as mantoux test, chest roentgenogram, Treponema Pallidum hemagglutination test, veneral disease research laboratory test, Hepatitis B surface antigen, HIV titers, serum antibody titers for herpes simplex, zoster, and cytomegalovirus were negative. However, he had neutrophilia, lymphocytopenia, and raised erythrocyte sedimentation rate. Peripheral smear showed iron deficiency anemia with no abnormal leukocytes. Systemic evaluation for other causes of immunosuppression beyond HIV included thyroid, renal profile, liver function test, hemoglobin electrophoresis, and bone marrow aspiration biopsy and cytology which were not contributory. We stopped acetazolamide and continued IVMP, topical prednisolone, and timolol maleate.
On day 3, BCVA remained 1/60 OD and 6/36 OS. With status quo anterior segment, the view of posterior segment cleared up in OS with Grade 1 vitreous haze. It had normal disc with multiple peripheral yellowish white retinitis patches []. Ultrasound B scan showed 360° choroidal detachment. Optical coherence tomography revealed fusion of inner retinal layers OD [] and thinning in OS [].
Promptly, IVMP was stopped, and parenteral acyclovir in the dosage of 500 mg three times a day was initiated. Oral steroid 60 mg/day was started after 48 h of antiviral therapy. The parenteral antivirals were reduced to twice a day due to intolerable side effects after discussion with our internist as unidentified immunosuppression was initially anticipated. However, detailed work up for it along with CD4 and 8 counts confirmed his immunocompetent status.
After 7 days of parenteral acyclovir, BCVA improved to 6/60 OD and 6/6 OS with complete resolution of retinal necrosis and choroidal detachment in the OS [Fig. and ]. It also showed regressing retinitis lesions and choroidal detachment in the OD [Fig. and ]. We shifted to oral valacyclovir 1 g/day along with tapering doses of oral steroids for 12 weeks. His BCVA improved to 6/24 OD and 6/6 OS, with corresponding cataract of Grade 2 and 1 posterior subcapsular cataracts (PSCC), respectively. The retinitis and choroidal detachment had fully resolved. He was normal till 3 years of follow-up with us. However, he consulted another ophthalmologist and underwent OD cataract extraction with intraocular lens implantation under periocular steroid cover devoid of oral antivirals. Postoperatively, intravitreal steroids were given at 3 periodic intervals. When reviewed again in our institute, he had no perception of light OD and BCVA of 6/12 OS. IOP was 4 mmHg OD and 12 mmHg OS. OD was pthisical with closed funnel retinal detachment (RD) on ultrasound B scan []. OS had normal fundus with a hazy media due to nuclear sclerosis and PSCC of Grade 2 [].


A 66-year-old male patient was referred to our department with a right intraventricular mass that had been diagnosed as anaplastic ependymoma on open biopsy at another hospital.
He had been followed because of diabetes mellitus, hyperlipidemia, and carotid artery stenosis but had been otherwise well. Two months before admission to our department, he had undergone magnetic resonance imaging (MRI) of the head, which incidentally revealed a mass lesion in the right lateral ventricle, for which he had been referred to the neurosurgery department at another hospital. He underwent a biopsy and the tumor was diagnosed as an anaplastic ependymoma. Although he had been initially referred to a Radiation Oncology Department for adjuvant radiation therapy, the provider referred him to our Department of Neurosurgery because of concerns that the residual tumor was not suitable for radiotherapy without prior cytoreduction.
Physical examination showed some short-term memory impairment, and ophthalmological examination revealed a visual field compromise (quadrantanopia) likely related to access corridor chosen for the biopsy. There was no focal motor weakness, major sensory deficit, dysmetria, or ataxia.
Computed tomography (CT) showed two hyperdense foci in the inferior horn and the atrium of the right lateral ventricle with peri-lesional edema of the ipsilateral temporo-occipital parenchyma [Figure and ]. The intraventricular lesions showed heterogeneous enhancement on postcontrast T1-weighted imaging (T1WI), on which the lesions appeared to arise from the choroid plexus [Figure –]. The postcontrast T1WI also showed additional tumor dissemination in the left lateral ventricle and around the brain stem []. Further whole-spine imaging showed leptomeningeal dissemination in the lumbar region (not shown).
The patient was taken to surgery and underwent subtotal removal of the tumor in the right lateral ventricle via an inferior temporal gyrus approach [Figure and ]. The tumor was solid, densely adherent to the choroid plexus but floating in the ventricle [].
Histopathologically, the tumor showed diffuse, tightly packed monotonous neoplastic cells with large, round, or slightly irregular nuclei and a scant to moderate amount of eosinophilic cytoplasm []. There were numerous mitotic figures and foci of focal necrosis. Perivascular pseudorosettes were not discernible. On immunohistochemical staining panels, the tumor cells were positive for leukocyte common antigen (LCA), CD20 [], CD30, CD79a, bcl-2, bcl-6 [], and MUM-1; and negative for cytokeratins, epithelial membrane antigen, S-100 protein, and glial fibrillary acidic protein.
Ophthalmological examination showed no intraocular lesions. CT of the chest, abdomen, and pelvis was interpreted as normal and bone marrow biopsy showed no atypical lymphocytic infiltrate. The patient was thus diagnosed with primary diffuse large B-cell CNS lymphoma likely originating in the choroid plexus.
The patient underwent chemotherapy with high-dose methotrexate (3500 mg/m2) every 14 days for three courses, followed by a course of chemotherapy with carboplatin (360 mg calculated by using the Calvert formula) and etoposide (80 mg/m2) 14 days after the third administration of high-dose methotrexate. After chemotherapy, cerebrospinal fluid (CSF) samples were obtained for cytology, which was negative for malignant cells. After the patient had undergone whole-brain irradiation (1.8 Gy × 22), postcontrast T1WI showed complete resolution of all previously visible CNS disease. Physical examination showed persistent quadrantanopia—unchanged from the patients status prior to subtotal removal of tumor—and amelioration of his short-term memory impairment. Because meningeal dissemination recurred during the follow-up period, the patient is currently again receiving chemotherapy with high-dose methotrexate in our department (8 months after surgery).


A 58-year-old male diagnosed with limited cutaneous scleroderma for 5 years (ANA positive, anti Scl-70 positive), presented with abnormal renal parameters (raised serum creatinine 2.7 mg/dl, hematoproteinuria) on routine investigations. He had a history of Raynaud's phenomenon for 20 years and digital ulcers for 7 years. He did not have any interstitial lung disease or pulmonary hypertension. On examination, there was depigmentation of the scalp, skin tightening of the face, telangiectasia, pitting scars, and sclerodactyly. His vital parameters were stable on admission with a pulse of 80/min, blood pressure (BP) 120/80 mmHg, and normal oxygen saturation. Urine analysis showed hematoproteinuria (urine protein/creatinine ratio = 0.6, red blood cells = 40–50/high power field) while the serum creatinine was 2.7 mg/dl. His complement levels were normal (C3 = 86.9, C4 = 13.10). ANA profile showed a positive result for Scl-70 with all the other antibodies being negative. P-ANCA was positive and the MPO-ANCA titers were significantly elevated at >200 IU/ml. Light microscopy of the renal biopsy revealed 10 out of 14 glomeruli showing complete and partial cellular/fibrocellular crescents. The underlying glomerular capillary loops were compressed and showed focal areas of fibrinoid necrosis. Interstitium showed mild chronic inflammation and focal areas of fibrosis. Vessels were unremarkable.[Figures and ]. Immunofluorescence did not reveal any positivity for immune deposits supporting the diagnosis of pauci immune (P-ANCA associated) necrotizing crescentic glomerulonephritis. He was given three doses of pulse methylprednisolone therapy (500 mg each) followed by injection cyclophosphamide 500 mg one dose during the same admission and advised to continue regular follow-up. He received 6 doses of cyclophosphamide followed by maintenance therapy with mycophenolate mofetil 1 g/day and oral prednisolone. His current serum creatinine is 1.34 mg/dl.


A 32-year-old Caucasian male presented in March 2009 with a 3-year history of multiple interconnecting comedones in the axilla and inguinal regions, as well as scarring from previous lesions. Embarrassment caused initial reluctance to seek medical assessment for his symptoms. He had a history of acne vulgaris, degenerative disk disease, congenital spinal stenosis, hypertension, obesity, and depression. His medications included oxycodone, irbesartan, labetalol, carbamazepine, folic acid, and sertraline. Initial treatment from 2009 to 2014 included antiseptic washes, topical clindamycin (with and without benzoyl peroxide), cloxacillin, tetracycline, cephalexin, doxycycline, amoxicillin/clavulin and desonide cream, all with limited benefit. Over the first 6 years of patient care, he had multiple visits to the clinic regarding HS lesion flares. The majority of the flares were treated effectively with low-dose intralesional corticosteroid (ILC) injections (ranged 2.5 to 5 mg/cc). Although ILC injections provided rapid relief for these individual lesions, they were insufficient for long-term disease stability. During his care period at the clinic, the patient was also diagnosed with diabetes, reduced smoking by switching to an e-cigarette, and lost 83 lbs.
Adalimumab, a tumor necrosis factor α (TNF α) inhibitor, was started in December 2014 as an 80 mg subcutaneous loading dose, followed by weekly 40 mg s/c injections with good response. His back pain improved significantly and his HS was relatively stable. He noted improved ambulation and no longer needed his assistive walking device. Adalimumab was well tolerated except for one episode of oral candidiasis.
He was maintained on adalimumab until February of 2015, when it was discontinued by a plastic surgeon while he underwent local excision of a persistent inguinal inflammatory nodule. While off adalimumab, his HS flared in the inguinal region, and required more ILC injections. His back pain worsened, and he required an assistive walking device once again. Adalimumab was re-started in March 2015 after a rheumatologist diagnosed him with SAPHO syndrome.
The adalimumab had reduced efficacy over time as new lesions began appearing and required increased potency and frequency of ILC injections. In December 2015, a weekly methotrexate dose of 10 mg (0.4 mL of 25 mg/mL) injection was added to the weekly adalimumab. Improvement was noted and flare-ups occurred less frequently. The patient began receiving intra-articular cortisone injections for inflammatory arthritis in his hands, wrists and arms with good response. He later complained of pain in the forearms and left clavicle, and as such, his methotrexate was increased to 20 mg weekly.
Currently, at 40 years of age, the patient maintains good control of his HS-SAPHO syndrome. His successful HS management plan included the following: HS flares relieved by ILC injections as needed, weekly 40 mg adalimumab, and weekly 20 mg methotrexate/folic acid. ILC requirements have decreased dramatically in recent years. Successful lifestyle changes over the duration of his case included weight loss, 2 years of smoking cessation, and increased control over his depression.


A man in his 70s was diagnosed with psoriasis vulgaris 20 years ago, which was well-controlled by the use of topical ointment (combination of vitamin D3 and steroid). The patient had become aware of a genital rash 10 years ago. Four years ago, he was referred to our department for a genital tumor. We made a diagnosis of EMPD with bilateral inguinal lymph node metastasis: T1N2M0, stage IV by skin biopsy and computed tomography scan. He was initiated on radiation therapy and monthly docetaxel chemotherapy for EMPD. For 3 years, he was stable with no distant metastasis through the penis, scrotum, both inguinal areas, or anus; however, the ulcers and nodules had not been cured. No significant adverse effects were observed during the course of treatment.
One day after completing the 37th course of monthly docetaxel, he experienced pain and warmth on both lower limbs. He was transferred to our department by ambulance the next morning. He had low blood pressure (80/48 mm Hg) and high temperature (39.4°C), and both lower limbs were erythematous and warm to touch (Fig. ). Group G thymosin-type lysin bacteria was detected in blood culture, and Group G Streptococcus was identified. He required emergency admission for septic shock from cellulitis of the lower limbs. Blood tests showed elevated inflammatory markers (C-reactive protein, 22.0 mg/dL; white blood cells, 22,000 cells/mm3) and disseminated intravascular coagulation (DIC) (Japanese Association for Acute Medicine acute-phase DIC diagnosis score, 4). Seven days after the infection, the psoriatic rash recurred, but the tumor nodule volume and the exudate from the tumor decreased (Fig. ). Ten days after the infection, the exudate from the tumor lesion decreased further, and the erosion area also shrank (Fig. ). Fourteen days after the infection, the tumor area further improved (Fig. ). Thirty days after the infection, the psoriatic rash in the lower abdomen had resolved, and the nodules with necrosis in the left inguinal region grew gradually (Fig. ). He recovered through therapy for DIC, although he had severe hemophagocytic syndrome due to Group G Streptococcus. We postponed the monthly docetaxel to 8 weeks after the last therapy for EMPD until his infectious condition improved (Fig. ). The tumor markers carcinoembryonic antigen and cancer antigen 19-9 showed low values during the infection (Fig. ).


A 32-yr-old man was referred to our hospital for further treatment after a transarterial chemoembolization (TACE) due to HCC. He had undergone a splenectomy after a motor vehicle accident at the age of 6. Furthermore, 16 yr previously, the patient was diagnosed as being a chronic hepatitis B-virus carrier, while 7 months prior he had been conservatively treated for jaundice. During a regular follow-up, a dynamic computer tomography (CT) was performed because serum alpha-fetoprotein (AFP) levels had increased to 128 ng/mL. The dynamic CT showed two hepatic nodules, which were primarily managed by TACE using adriamycin and lipiodol at other hospitals.
The patient had no significant family history of malignancy or B-viral hepatitis. Abdominal examination revealed a left paramedian scar with no palpable masses or hepatosplenomegaly. The findings from the remainder of the exam were within normal limits. The laboratory test results were within normal ranges except for aspartate aminotransferase levels, which were 45 IU/L (normal range, 13-34) and prothrombin time was 12.7 sec (normal range, 9.9-12.3). The patient's serology for hepatitis B was positive for HBsAg, anti-HBc Ab, HBeAg, and anti-HBe Ab and negative for anti-HBs Ab. Serum HBV-DNA quantitation levels were less than 0.5 pg/mL. Serum AFP was 17.29 ng/mL and serum protein induced by the absence of vitamin K (PIVKA II) was less than 10 mAU/mL.
The dynamic CT performed at other hospitals demonstrated a 2-cm and a 3-cm nodule in Segments IVa and VI, respectively. All lesions were located near the liver capsule. The lesion in Segment IVa was located in the subcapsular area of the liver parenchyma and the lesion in Segment VI appeared to grow exophatically. The lesion in Segment IVa showed a slight enhancement during both the arterial and portal phase and another lesion in Segment VI was slightly enhanced only in the portal phase (). Hepatic angiography showed a subtle vascular staining lesion only in Segment IVa and subsequent TACE was performed (). After three weeks of TACE, a follow-up CT scan showed a relatively homogenous lipiodol uptake in the Segment IVa nodule (), while the Segment IV nodule had no lipiodol uptake. The patient underwent magnetic resonance imaging (MRI) in our hospital to evaluate the lesion in Segment VI. The precontrast MRI showed that the lesions were low signal on T1-weighted images and high signal on T2-weighted images (). When analyzed using dynamic MRI, the lesion in Segment VI had enhanced arterial phases and was slightly hyperintensive to the liver parenchyma in the portal phases (). In addition, another lesion, which was not detected in previous imaging studies, was found in the inferior tip of Segment IVb ().
Though imaging studies showed atypical findings such as only slight arterial enhancement and no early venous washout, the patient's history of chronic hepatitis B and the elevated serum AFP levels during follow-up led to a diagnosis of HCC. The child classification was A, and his indocyanine green retention at 15 min was 28.4%. Even though his reserve liver function was decreased, surgical resection was thought to be possible when the anatomic locations of the hepatic lesions were considered. During the laparotomy, a 1-cm reddish brown nodule on the greater omentum was noticed, and small multiple nodules on the surface of the small bowel were further detected (). These observations, combined with a history of splenectomy, prompted us to strongly suspect splenosis. The 3 cm hepatic nodule in Segment VI was attached to the liver capsule and showed characteristics similar to other abdominal nodules (). The Segment VI and IVb lesions were excised and the frozen histological examination of these specimens was positive for splenic tissue (). Because the lesion in Segment IVa was covered with a fibrous capsule, the lesion was easily detached from the liver parenchyma and an enucleation could be performed. Pathological examination of the frozen and permanently fixed sections of this lesion found that this lesion also contained splenic tissue.


A 69-year-old male was diagnosed in February 2004 with stage IV extranodal marginal zone B cell lymphoma involving the mediastinal nodes, lung parenchyma and bone marrow.
Past medical history included one vessel disease, for which the patient underwent percutaneous coronary angioplasty; diabetes mellitus, and hypercholesterolemia. Medications included glimepiride, aspirin, isosorbide dinitrate, nicoradil, and atorvastatin. None of these drugs had been taken since the diagnosis of non-Hodgkin's lymphoma.
Following the 5th course of rituximab-CHOP chemotherapy the patient was admitted with neutropenic fever accompanied by generalized weakness and mucositis.
Empiric broad spectrum antibiotics were started along with granulocyte-colony stimulating factor. Despite recovery of the neutrophil count, the shortness of breath was aggravated and arterial blood gas analysis revealed hypoxemia (PaO2=55).
Gram stain and special stains of the sputum for acid-fast bacilli, pneumocystis carinii, and fungi were negative. Routine cultures for bacteria, fungi and mycobacteria yielded no growth. A chest X-ray showed progressive infiltrates in both lung fields. A computed tomography (CT) scan of the lung revealed bilateral patchy ground-glass opacities, suggestive of new onset interstitial pneumonitis. CT also showed a reduced primary mass in the right middle lobe, consistent with the initial primary lesion ().
Extrathoracic echocardiogram showed normal left ventricular contractility with unaltered ejection fraction. Cardiac enzymes were also normal. Ventilation perfusion scan showed no evidence of pulmonary artery embolism. Fiberoptic bronchoscopy revealed no evidence of endobronchial lesion. No malignant cells were found in the bronchoalveolar lavage fluid.
Gram stains, special analysis and cell cultures obtained from BAL and sputum following fiberoptic bronchoscopy were negative for bacteria, acid-fast bacilli, fungi and pneumocystis carinii. Bronchoscopy guided transbronchial lung biopsy was performed, showing interstitial thickening and type II pneumocyte activation compatible with interstitial pneumonitis ().
The patient was treated with prednisolone, 1 mg/kg a day, for 2 weeks. The dyspnea and tachypnea gradually improved, in addition to blood oxygenation and chest X-ray. A subsequent CT scan following prednisolone treatment showed marked improvement of the multifocal patchy interstitial infiltration and ground glass opacities; as well as a reduction in the primary lymphoma lesion.
After 42 days of hospitalization, the patient was discharged on a tapering prednisolone regimen. He experienced complete resolution of dyspnea and dyspnea on exertion. He was well on routine follow-up at the outpatient clinic, with no lymphoma progression or interstitial pneumonitis.


A 42-year-old female visited our emergency room (ER) with complaints of acute, diffuse abdominal pain. She had been treated for three days at a local clinic because of fever and right upper quadrant pain. She had no significant medical or medication history. The laboratory findings showed mild leukocytosis (11.2×103 cells/µL) and an elevated C-reactive protein level, and the hepatic parameters were markedly elevated. The serum hemoglobin level was 7.8 g/dL and she was transfused with whole blood.
The ultrasound examination performed on an ATL machine (HDI 5000, Bothell, WA) revealed a huge and heterogeneous lesion at the subcapsular area of the right hepatic lobe and also a perihepatic fluid collection (). The differential diagnosis was hepatic subcapsular abscess or a hepatic mass such as a cavernous hemangioma draping over the liver. MDCT was performed with a 4-channel scanner (Volume zoom; Siemens, Erlangen, Germany) with using following parameters; 120 kVp, 165 mAs, 3 mm collimation and a 1.5 mm reconstruction interval for the arterial and portal venous phases, and 7 mm collimation and a 5 mm reconstruction interval for the unenhanced and equilibrium phase images. After injection of 120 ml of non-ionic contrast material, the arterial phase images were obtained with a 40 sec delay, and 80 sec and 3 min delays were used for the portal venous and delayed phases, respectively. Coronal multiplanar reconstruction (MPR) was done at each phase.
On the unenhanced images, about a 9 cm-sized, low density, irregular-shaped lesion was seen at the right hepatic dome. Most of the lesion was not enhanced, but multiple, irregular and linear, septa-like densities were demonstrated which were of isoattenuation to the adjacent normal parenchyma on all phases (). The unenhanced images also revealed a huge, heterogeneous and mainly hyperdense lesion occupying the entire right subcapsular area, and this was suggestive of acute hematoma (). On the contrast-enhanced triphasic images, most of the lesion was not enhanced, except for multiple small enhancing foci that were gradually enlarged and isodense on all phases as compared with the liver parenchyma. The margin of the lesion at the junction with the normal parenchyma was shaggy and irregular. Another 1 cm-sized lesion was seen at the right hepatic lobe, and the lesion was of low density on the arterial phase; it showed peripheral isodense enhancement on the portal venous phase and it became totally isodense or slightly hyperdense on the delayed phase (). The MPR images helped us view all the above-mentioned findings at a glance ().
Angiography was performed for vascular embolization under the impression of rupture of hepatic tumor such as hepatic adenoma after the CT scan. The angiogram revealed a huge hypovascular area that conformed to the entire right subcapsular portion, which was compatible with hematoma, and an irregular parenchymal defect was seen in the hepatic dome without any feeding vessels, definite contrast accumulations or vascular malformations (). So, interventional procedures were not done and the diagnosis was not changed even after angiography.
The patient was given supportive care after angiography, but she suffered cardiac arrest that necessitated cardiopulmonary resuscitation. Finally, emergency right lobectomy was performed about 24 hours after her ER admission. At laparotomy, most of the portion of the right hepatic lobe was replaced by hematoma, and some inflammatory patches were present on the liver surface. A mass-like lesion was noted at segment 8, which had ruptured, and this resulted in a large amount of blood and necrotic material in the peritoneal cavity. On microscopic examination, the lesion was diagnosed as peliosis hepatis which was a blood filled cavity lined by fibrinous material and hepatocytes (). She was discharged about one month after surgery and has lived healthy without any symptoms or abnormal findings on follow-up CT examinations two years later.


A 55-year-old man, presented to our hospital, complained of a large pelvic mass, which was found incidentally during a routine ultrasonography. The patient had no history of abdominal or pelvic discomfort, nor any abdominal or pelvic surgery. In addition, the patient had no relevant medical or family history except for diabetes mellitus. Upon a digital rectal examination, a large mass with a stone-like hardness was palpated at 5-6 cm above the anal verge.
A single-phase helical CT (LightSpeed Ultra; GE Healthcare, Milwaukee, WI), spanning the whole abdominopelvic cavity, was performed. The CT scanning parameters included a beam collimation of 8 × 1.25 mm, a reconstruction interval of 1.25 mm, a pitch of 1.35, a rotation time of 0.8 seconds, a table speed of 13.5 mm/rotation, 120 kV and 160 mAs. Transverse CT images were obtained 70 seconds after the intravenous injection of non-ionic contrast material (120 mL) at a rate of 3 mL/sec (Ultravist 300; Bayer Schering Pharma, Berlin, Germany). Multi-planar reformatted coronal images were reconstructed with the transverse images. The CT images revealed a large, well-defined mass in the presacral space of the pelvic cavity, which seemed to have a long stalk arising from the left gluteus medius muscle (). The stalk traversed along the surface of the left iliac bone, and proceeded through the left sciatic foramen, and ended up connecting with the mass. The CT attenuation generated an easily recognizable mass, which was mainly composed of fatty tissue and calcification, with most of the stalk becoming calcified. The calcification in the mass was located peripherally in a linear and rosary pattern. Some focal areas of intermediate attenuation were identified as a mixture between fatty tissue and calcification, and occupied only a limited portion of the mass. These areas were revealed to correspond to chondroid tissue based on the histologic findings. MR imaging (Horizon 1.5T; GE Healthcare, Milwaukee, WI) was also performed with the use of a TORSO coil. On both the T1-weighted (366/8, echo train length of zero, 5-mm slice thickness, 2-mm gap, 256×192 matrix, 24-cm field of view, 2 signal acquired, and sequence duration of 3-4 minutes) and T2-weighted (4300/84, echo train length of ten, 5-mm slice thickness, 2-mm gap, 512×256 matrix, 24-cm field of view, 2 signal acquired, and sequence duration of 3-4 minutes) MR images, the mass was revealed to mainly consist of the hyperintense and signal void areas that represent fatty tissue and calcification, respectively (). Also seen are the focal areas of intermediate signal intensity, as shown on the CT images. The gadolinium-enhanced T1-weighted MR images obtained 30 seconds, 60 seconds, and 3 minutes after the intravenous injection of contrast material (Gadovist; Bayer Schering Pharma, Berlin, Germany), and the focal areas of the intermediate signal intensity around the calcifications observed at 30 and 60 seconds post-injection, became isointense as the surrounding fat tissue at 3 minutes post-injection. This finding represented a delayed enhancement (). No fat suppression technique was applied on our MR images.
The main mass was resected using a transabdominal approach, whereas the stalk was removed through the sciatic foramen. The surgical specimen consisted of a 13 cm, well-circumscribed, hard mass, with a severely calcified external surface. The cut surface of the resected specimen revealed a mass mixed with fatty tissue and calcification (). A histopathological examination revealed that the mass was composed of lipoma with chondroid metaplasia (), as well as extensive calcification within the chondroid tissue. In addition, fibrous tissue was also intermingled within the chondroid tissue. The final histological diagnosis was identified as a chondrolipoma.