A 37-year-old male presented at Accident and Emergency department with chief complaints of colicky abdominal pain, nausea and vomiting of twelve hours' duration. The pain was generalised in nature, moderate in severity, and not associated with any aggravating or relieving factor. There was no alteration of bowel habit. His past medical history included multiple blood transfusions for 'anaemia' since childhood, Hepatitis C and blue rubber bleb naevus syndrome (BRBNS). The latter was diagnosed following 'bowel surgery for internal bleeding' seven years ago at a different hospital. He had been treated with endoscopy-guided argon plasma coagulation and interferon α therapy to induce regression of gastrointestinal haemangiomas with limited success. No other family member had suffered from a similar condition.
On admission the vital observations were stable. General examination showed several subcutaneous compressible bluish skin lesions around neck, chest and abdomen (Figure ). Abdominal examination revealed soft and mildly distended abdomen with moderate epigastric tenderness. The bowel sounds and digital rectal examination were normal. Laboratory investigations showed haemoglobin 91 g/l, WBC 4.8 × 109/l, platelet 144 × 109/l. Urea, creatinine, electrolytes, liver function tests, amylase and coagulation screen were within normal limits. Plain X-ray of chest was normal. Abdominal radiograph showed distended loops of small bowel. Computed Tomography (CT) of abdomen revealed i)dilated loops of small bowel ii)'doughnut' signs, suggestive of intussusception, affecting small bowel at three different levels iii)subcapsular hepatic haemangiomas affecting segment six and iv)intramuscular haemangioma involving right quadratus lumborum muscle (Figure ).
He underwent laparotomy that revealed three irreducible small bowel intussusceptions at the levels of proximal jejunum, mid-ileum and distal ileum. Each of the intussusception was led by a large intraluminal haemangioma. There was also a localised perforation at mid-ileal level. Resections of the intussusceptions with primary anastomosis of small bowel segments and limited right hemicolectomy were performed (Figure ). The length of the remaining small bowel was 150 cm. Histology of the specimens confirmed intussusceptions of small bowel with gangrenous changes. Multiple haemangiomas involving serosa and submucosa were also noted. There was no feature of dysplasia or malignancy.
The postoperative course and follow-ups up to 6 months were uneventful. Further follow-ups were planned with gastroscopy, video capsule enteroscopy and colonoscopy.


A 17-year-old male with progressive visual loss and photopsia was admitted to our ophthalmology clinic. He had a history of blunt trauma with a basketball to his right eye 6 months ago and had begun to suffer from visual disturbances since then. His visual acuity (VA) was 20/400 in his right eye. Dilated fundus exam of his right eye revealed a giant tear in the superotemporal retina with a shallow retinal detachment involving the macula (Figure and ). His visual acuity was 20/20 and anterior and posterior segments were normal in the left eye. He underwent a three-port pars plana vitrectomy for the giant tear without crystalline lens extraction. Perfluorodecaline was used intraoperatively. Three weeks postoperatively, perfluorodecaline was observed in the anterior chamber in contact with the corneal endothelium (Figure ). No tilt or dislocation of the crystalline lens was detected on slit lamp biomicroscopy. We referred our patient to another eye clinic for ultrasound biomicroscopic (UBM) or endoscopic examination in order to determine zonular dialysis, but could not obtain these results as the patient refused (4)
After our attempt to remove the perfluorodecaline in the anterior chamber with a 27G needle failed, an anterior chamber wash was performed with balanced salt solution via two wide paracentesis. Two months after vitreoretinal surgery, his best-corrected visual acuity (BCVA) was 40/200 in the right eye. The vision and retina remained stable in his follow-up (Figure ).


A 62-year-old man with a history of gastroesophageal reflux disease presented with a one month history of epigastric pain, epigastric fullness, dysphagia, anorexia, and weight loss of 9 kgs. Clinical examination and blood tests were normal apart from elevated carcinoembryonic antigen (42.8 ng/ml; normal value < 5.0 ng/ml). Chest x-ray, electrocardiogram, echocardiography, and abdominal ultrasound (US) were normal. Esophagogastroscopy revealed an ulceroproliferative, intraluminar mass in the distal third of the esophagus obstructing the esophageal lumen. Biopsy showed small cell esophageal carcinoma. Due to esophageal lumen obstruction, endoscopic US was not feasible. Contrast-enhanced chest and abdominal computed tomography (CT) demonstrated a large tumor of the distal third of the esophagus without any lymphadenopathy or distant metastasis (Figure ).
The patient received preoperative chemotherapy with cisplatine and etoposide for 3 months with a significant reduction of the tumor size (Figure ). En block esophagectomy with two field lymph node dissection, proximal gastrectomy, and cervical esophagogastric anastomosis were performed. After an uneventful postoperative period, he was discharged on the 14th postoperative day.
Histopathology revealed a tumor (2.5 × 1.5 cm), 2 cm above the gastroesophageal junction, that was a small cell esophageal carcinoma infiltrating the submucosal and, focally, the muscular layer (Figure ). The margins of the specimen were free of tumor. Metastasis in two paraesophageal lymph nodes was found. Moreover, Barrett's esophagus, of intestinal type, with predominantly low grade and, focally, high grade dysplasia was identified in the lower esophagus. Immunohistochemical staining of the tumor cells was positive for chromogranin and neuron-specific enolase (NSE).
A diagnosis of primary small cell carcinoma of the distal third of the esophagus arising from dysplastic Barrett's esophagus was made. The patient received another 3 month course of postoperative chemotherapy with the same agents (cisplatine and etoposide) and was free of disease at review after 12 months.


A 63-year-old Caucasian man, previously fit and well, presented with a five-day history of shortness of breath associated with wheeze and dry cough. His symptoms had progressively become worse, limiting his exercise tolerance. He denied symptoms of hyperthyroidism such as heat intolerance or weight loss and reported no palpitations or chest pain. His past history was unremarkable with no history of ischaemic heart disease or diabetes and he was taking no regular medications. He lived independently at home with his wife, working six days a week and had stopped smoking 30 years ago. His systemic enquiry and family history were unremarkable.
The patient had tachycardia, irregularly irregular, at 122/min with a raised jugular venous pressure (JVP) and a respiratory rate of 24/minute. He had no peripheral oedema or cyanosis. Cardiovascular auscultation revealed a soft mitral murmur. Baseline full blood count, electrolytes and renal function were normal. Chest X-ray showed cardiomegaly, pulmonary congestion and a small right pleural effusion.
A diagnosis of Atrial Fibrillation (AF) with fast ventricular response was made and the patient was given intravenous diuretics and digoxin and anticoagulation was commenced with Low Molecular Weight Heparin. Despite 48 hours of treatment, the tachycardia persisted and the JVP remained elevated. Echocardiogram, though limited by tachycardia, showed no impairment of ventricular function.
Thyroid Function Tests showed TSH 6.2 (Normal Range = 0.40 – 4.00 mU/L), Free T3 of 12.5 (4.00 – 6.8 pmol/L) and Free T4 51(10–30 pmol/L). Repeat Thyroid Function Tests showed TSH 6.6, Free T4 57 and Free T3 19.4 confirming a pituitary cause for hyperthyroidism. Retesting at a second laboratory corroborated these values. Heterophilic antibodies, which can interact with immunoassays, were ruled out. Pituitary function tests showed testosterone levels were elevated at 43.10 (Normal range: 10.00 – 31.00 nmol/L) along with elevated FSH, 18.1 (Normal range: 18.1 U/L) and elevated LH at 12.4 (1.0–8.0 U/L). Growth Hormone (GH), IGF-1 and prolactin were normal.
An MRI of the brain showed a pituitary macroadenoma, 2.4 cm in diameter, abutting the optic chiasm, deviating the pituitary infundibulum and internal carotid artery. Visual field tests showed a defect in the right inferotemporal field with a normal field on the left. (Figure )
The patient was commenced on warfarin, but his International Normalised Ratio (INR) estimating his control on warfarin was markedly elevated with loading doses of warfarin and required reversal of anticoagulation with Vitamin K and introduction of low molecular weight heparin.
The patient was diagnosed as having a TSHoma and a decision was made to attempt neurosurgical removal. He was commenced on antithyroid medication (carbimazole) in the interim. Attempts to wean down his carbimazole resulted in an escalation of his symptoms and he was therefore maintained on this until successful trans-sphenoidal excision of his pituitary macroadenoma had been performed.
His AF persisted post-operatively, but was electrically cardioverted and he remains in sinus rhythm at twelve months follow-up off all treatment.
Post-operative MRI showed near total removal of the pituitary adenoma. (Figure ) Histology showed positive staining for GH, Prolactin and TSH. His TSH and T4 levels have remained normal post-operatively and glucagon stimulation test demonstrated adequate cortisol and GH response. His testosterone levels have also normalised after a transient fall post-operatively. GH, Prolactin and IGF-1 levels remained normal. FSH is persistently slightly raised at 9.1 U/L (1.0–7.0). The patient is asymptomatic, needing no treatment and back at full time employment. Arrangements are in place for a follow-up pituitary MRI.


A 16-year-old man with HIV infection was admitted to the inpatient department of the YRG Centre for AIDS Research and Education (YRG CARE) with severe crusted cutaneous lesions all over the body. He had a history of skin lesions that had developed initially over the scalp and forehead, later spreading all over the body over the course of one month with no signs of itching. By the time of admission, the skin condition had worsened rapidly and there was extensive, generalized, thick, hyperkeratotic, crusting, yellowish papule lesions that eventually disseminated across the body including the face, ear lobes, shoulder blades and entire trunk, with squamous lesions not sparing any region (Figure ). The patient presented with a temperature of 98.8°F and pulse rate of 80 beats a minute. The patient had a history of tuberculosis and had been on anti-tuberculosis therapy (ATT) for the past 3 years with poor adherence. Cardiovascular, respiratory and abdominal examinations were normal. Renal and liver function tests were also normal.
Laboratory investigations revealed a hemoglobin (Hb) level of 11.4 g/dl (normal values are in the range 12–17 g/dl), erythrocyte sedimentation rate (ESR) of 20 mm (normal range 0–14 mm), total thrombocyte count of 144 × 109/l (normal range 137–367 × 109/l), total leukocyte count of 18.2 × 109/l (normal range 3.9–9.4 × 109/l) and a total lymphocyte count (TLC) of 3.7 × 109/l (normal range 1.2–3.4 × 109/l). His absolute CD4 T-lymphocyte count (Beckman Coulter Inc., CA, USA) was 342 cells/μl (normal range 350–1411 cells/μl) and the CD4 T-lymphocyte percentage was 8%. His liver function test (LFT) revealed low alanine aminotransferase (ALT) at 28 IU/l (normal range 0–54 IU/l), normal total bilirubin of 0.4 mg/dl (normal range 0.4–2.3 mg/dl), direct bilirubin of 0.1 mg/dl (normal range 0.1–0.3 mg/dl) and a normal conjugate bilirubin of 0.3 mg/dl (normal range 0–1.5 mg/dl). His renal function tests revealed a low urine creatinine 0.5 mg/dl (normal range 0.9–1.3) and blood urea 11 mg/dl (normal range 9–33 mg/dl).
The differential diagnosis was initially either an adverse drug reaction, atopic dermatitis, dermatitis herpetiformis, psoriasis, ichthyosis, seborrheic dermatitis, erythroderma or Langerhans cell histiocytosis. However, following the suspicions of dermatologists of possible Acarus scabiei infestation, skin crusts were collected and mounted on 10% KOH preparation and observed under low- and high-power objectives. Numerous live and motile, adult A. scabiei mites that measured about 400 μm long and 300 μm wide were seen, which confirmed the diagnosis of Norwegian scabies. The patient was started with Ivermectin (6 mg) for 15 days and topical Permethrin cream with meticulous scrubbing and cleansing of the skin, which eventually resulted in complete resolution 4 weeks later. Intriguingly, in spite of quarantining efforts, one of the patient's acquaintances and a healthcare worker acquired the symptoms of itching, and had to be treated with topical Permethrin cream for a week. However, the diagnosis of scabies was not confirmed in either the acquaintance or the healthcare worker.


Our patient is a 31 year old male teacher, who was brought in by ambulance to the Emergency Department. Two weeks earlier he had sustained an injury to the right side of his neck due to a rugby tackle, with a fierce "hand off" to the jaw extending his neck and rotating it to the left. He continued to play the game without any ill effects. A week prior to admission he was seen by his family physician and given an antibiotic for "swollen gland" in the right side of his neck. On the day of presentation he had sudden onset of right sided neck swelling with pain in the neck and shortness of breath.
His vitals were stable (Pulse 54, Respiratory Rate 24 and O2 saturation of 100%). He was conscious with GCS of 15/15. There was an obvious right sided neck swelling with trachea deviated to the left without any stridor. There was no neurological deficit or any evidence of Horner's syndrome. Our initial clinical impression was that he had a ruptured aneurysm.
He was promptly intubated in resuscitation rooms and taken for CT scanning. CT angiogram of the neck vessels showed active extravasation of contrast from his right CCA (Fig. ) resulting in the formation of a large haematoma extending superiorly into the parapharyngeal space and inferiorly into the superior mediastinum. It resulted in compression and marked displacement of the airway to the left (Fig. ). The thyroid gland was also displaced and Internal Jugular Vein was effaced due to compression. Our impression was that he had ruptured pseudo aneurysm of the Right CCA and he was brought forward for emergency surgery.
His neck was opened on the right side using a lazy S incision. On opening his platysma, there was a bulging haematoma which was rapidly expanding. Control of the Right common carotid was obtained proximally at the level of sternal head of sternomastoid by deflecting it, and distally at the level of bifurcation of common carotid. Omohyoid muscle was also divided for access. He was heparinised and the right CCA was clamped above and below the site of injury. Haematoma site was exposed by reflecting the internal jugular vein laterally and taking its multiple branches medially between clips. Vagus nerve was identified and protected. The point of perforation was in the posteromedial aspect of the artery, with surrounding adventitia appearing somewhat ragged, suggesting a stretch injury (Fig. ). This appearance was consistent with rupture of a pseudo aneurysm. The arterial perforation site was extended in a cranio-caudal fashion to expose normal vessel wall. Examination of rest of the arterial wall appeared relatively normal with no evidence of true or mycotic aneurysm. Primary closure of the extended defect was carried out with polypropylene 6-0 suture in two layers (first layer – full thickness wall, second – periadventitia as reinforcement). The sternal head of sternocleidomastoid muscle was reattached.


A 36-year-old, postpartum, white female became increasingly symptomatic with sharp, low abdominal pain with the completion of each urination and gross hematuria. She denied night sweats or fever and any history of urinary tract infection, trauma, instrumentation or other urological problems. An ultrasound study of the kidneys and the urinary bladder revealed a broad-based polypoid mass (2.4 × 2.3 × 2.2 cm), located in the right posterolateral wall of the bladder. The patient subsequently underwent a transurethral resection of the aforementioned lesion.
Histologic examination of the excised mass displayed infiltration of the bladder wall (Fig. ) by an atypical spindle cell proliferation with histologic features of myofibroblasts (Fig. ) arranged in sheets with focal myxoid areas (Fig. ), whereas the overlying transitional epithelium was normal (Fig. ). In particular, the tumor cells demonstrated prominent nucleoli and nuclear pleomorphism; numerous normal mitotic figures (5/10hpf) and a few abnormal ones were seen. By immunohistochemical evaluation, the cells were: (a) positive for vimentin and ALK-1 (Fig ); (b) focally positive for cytokeratins 8/18/19, muscle specific and smooth muscle actins, and desmin; (c) negative for S-100, CD34, c-Kit (CD117), h-caldesmon and MyoD1.
These histologic findings posed a particular diagnostic problem and yielded a differential diagnosis of pseudosarcomatous myofibroblastic lesion versus low-grade leiomyosarcoma of focally myxoid type. Although the possibility of the former was taken into account, the diagnosis of malignancy could not be avoided, given the nuclear pleomorphism, abnormal mitoses and the infiltrative nature of the lesion. Based on the absence of an in situ urothelial neoplasm and the immunophenotype, this was considered to be more likely a smooth muscle tumor than a spindle cell carcinoma. Consequently, further adequate local excision was recommended. At that point, a staging work-up, including a bone scan, abdominal/pelvic MRIs and an intravaginal ultrasound, disclosed no definite evidence of radiographically residual intravesicular tumor and no evidence of extension or metastasis. Due to negative staging work-up and considering the rarity and complexity of the case, the patient was referred for close clinical follow-up and cystoscopic re-evaluation of the bladder excision site for potential residual lesion.
After five months' interval since the initial transurethral resection, a repeat cystoscopy was performed and disclosed scar tissue without any obvious tumor growth; additional biopsies were obtained from the surgical site. Microscopy revealed no sarcoma, but residual foci that simulated a reactive process.
Given that a sarcoma of the bladder would have already shown significant proliferative activity and comparing the initial slides with the re-biopsy slides, we issued a new diagnosis; in particular, we inclined more towards a diagnosis of pseudosarcomatous myofibroblastic lesion instead of a sarcoma. Due to the atypical features encountered and the fact that the biological potential of this entity cannot be accurately assessed, a close follow-up was warranted. The patient did not receive any adjuvant treatment. She is currently free of disease without evidence of tumor recurrence or metastasis by 3-year follow-up.


We dissected an upper limb of a 76-year-old male cadaver, for educational purposes. First, we exposed and then removed the fascia of the forearm and palm. The ulnar nerve and its dorsal ramus were exposed after reflecting the flexor carpi ulnaris tendon medially, by removing the flexor retinaculum and transecting the roof of Guyon's canal. The ulnar artery was removed in order to obtain a better view of the course of the ulnar nerve in this region. After careful dissection in the wrist area, we found a thin nerve branch, originating from the dorsal ulnar nerve branch approximately 3 cm proximal to the ulnar styloid process. This nerve branch, called Kaplan anastomosis, was parallel to the ulnar nerve. This nerve branch gave off many thin branches along its course for the synovial membrane of the joint, the abductor of the fifth finger and the skin of the area. The nerve branch then passed through Guyon's canal close to the pisiform bone and finally merged with the trunk of the ulnar nerve just before its division into the superficial and deep rami (Figures and ).
The normal course of the ulnar nerve in the forearm is between the flexor carpi ulnaris and the flexor digitorum profundus. The dorsal branch, which is responsible for the sensory innervation of the medial half of the hand and half of the digits, arises approximately 5 cm proximally to the wrist. In the hand, the ulnar nerve enters Guyon's canal underneath the superficial part of the flexor retinaculum and is divided into a superficial (sensory) and deep (motor) branch [].
Anomalies of the sensory innervation of the hand are uncommon []. In 1963, Kaplan described a nerve branch that arose from the dorsal cutaneous branch of the ulnar nerve and finally merged with the superficial ramus of the ulnar nerve []. Similarly, Wulle [] described a case of Kaplan anastomosis that merged with the superficial ramus of the ulnar nerve.
Hoogbergen and Kauer [] also found a Kaplan anastomosis. In particular, they found a significant case of a Kaplan anastomosis emerging from the dorsal cutaneous branch of the ulnar nerve approximately 2.5 cm proximally to the ulnar styloid process. It gave off three branches along its course. The first branch emerged just proximally to the ulnar styloid process and ran towards the radiocarpal joint. It was located between the abductor digiti minimi and the deep ramus of the ulnar nerve where the Kaplan anastomosis gave off two branches. One branch ran towards the abductor digiti minimi muscle, while the other ran towards the fifth carpometacarpal joint. It is of interest that eventually the Kaplan anastomosis merged with the deep ramus of the ulnar nerve [].
Our case differs from previous reported cases of Kaplan anastomoses in that the nerve is united with the trunk of the ulnar nerve just before its bifurcation into the superficial and deep ramus. Naturally we must distinguish between Kaplan anastomoses and dorsal cutaneous branch variations or ulnar-median nerve communicating branches. Paul et al [] reported a rare finding of the dorsal branch of the ulnar nerve which began in the upper quarter of the forearm and divided into medial and lateral branches. The medial branch merged from the hypothenar region with the deep branch from the ulnar nerve and the lateral branch became cutaneous. The communication branches between the ulnar and the median nerve are well recognized and the majority of cases are directed from the ulnar to the median nerve [,]. However, in most cases, these communication branches affect the sensory innervation of the digits.
Many authors have reported sensory communication branches between the ulnar and median nerves in the hand []. In 1991, Ferrari and Gilbert classified them []. Most authors found the incidence of communication branches between the ulnar and the median nerve to be over 90%, so this kind of anatomical variation should be considered as normal [].


A 75-year old gentleman was admitted to the Oncology/Haematology Ward in early September 2007 for severe shortness of breath. He had been fully investigated for a pleural effusion one month earlier in a neighbouring hospital. At that time drained pleural fluid revealed reactive lymphocytes with neither neutrophils nor eosinophils. However peripheral blood esosinophils were raised at 1.6 × 109/L, C-reactive protein (CRP) at 33 mg/dl and fibrinogen at 568 mg/dl. Cultures for bacteria and stains for acid-fast bacilli were negative. Several stool examinations and serologic tests were negative for parasites as well as an autoimmune screen (antinuclear antibodies, antineutrophil-cytoplasmic antibodies, anti myeloperoxidase antibodies). A right pleural biopsy done in mid August 2007 revealed sheets of pleura infiltrated by malignant epithelioid cells that on immune staining expressed CK7 (cytokeratin) with focal expression of CK5/6 whereas staining for carcino-embriogenic antigen, BerEP4, thyroid transcription factor-1 mesothelin, Wilms' tumour -1, CK20 or prostate specific antigen was negative, confirming a diagnosis of epithelioid mesothelioma. A drain was inserted through the right chest wall and opiates started (morphine sulphate 30 modified release bd, oxycodone). During the current admission the drain was re-sited and fluid examination revealed only reactive lymphocytes and few neutrophils. His peripheral blood eosinophils had risen to 21 × 109/L, CRP was up at 88 mg/dl and fibrinogen at 880 mg/dl. The patient was started on a prophylactic dose of tinzaparin (3500 IU/day). On the fourth day after admission the patient developed a swollen calf, his D-dimer was greater than 1000 mg/dl (cut-off normal >280 mg/dl) and an ultrasound scan confirmed a fresh popliteal vein thrombosis. Tinzaparin was increased to therapeutic levels for five days until warfarin brought the international normalised ratio within therapeutic range. A thrombophilia screen (including factor V Leiden, prothrombin 20210, protein C, protein S, antithrombin, lupus anticoagulant and anticardiolipin antibodies) arranged before commencing warfarin came back normal. Neither the FIP1L1-PDGFRA fusion transcript (deletion 4q12) nor other cytogenetic abnormalities were found on a cellular sample of peripheral blood. After 5 days later his general conditions deteriorated, he became progressively confused with increasing hypoxia and passed away for respiratory failure. Post mortem revealed a mesothelioma that had diffusely surrounded and invaded the left lung and pericardium without directly affecting vascular structures. No asbestos bodies were found and no pulmonary embolism was detected.


A 56 year old man presented with progressively worsening dyspnoea at rest. There was no history of chronic lung disease or cyanosis. On examination, he was found to have bilateral chest rhonchi and absent nasal cartilages. Investigation showed reduced FEV1 to 0.8 litres (23% predicted), and within normal basic blood tests. His medications included Prednisolone, Salbutamol and Seretide inhalers, and he was taking Mucolyn syrup regularly. Clinical diagnosis at time of referral was Relapsing Polychondritis, which was further supported by the bronchoscopy findings and a CT scan showing tracheobronchial thickening [,]. He underwent endobronchial stenting with a self-expanding metal stent (The Ultraflex™ Tracheobronchial Stent System, Boston Scientific, MA, US) in December 2005 to the trachea and separately to the left main bronchus; post operatively he was well and was discharged after 2 days.
On subsequent review his symptoms showed minimum improvement and his exercise tolerance was approximately 100 yards on the flat. Six months after his first bronchoscopy and stenting he had a silicon stent (The TRACHEOBRONXANE® Dumon® Silicone Stent, Novatech SA, France) inserted into the bronchus intermedius on the right side. During that procedure a subglottic stricture was noted and his airway was found to be very collapsible. Just prior to his planned discharge, he developed noticeable stridor and therefore the stent had to be removed urgently. He deteriorated to type 1 respiratory failure for which he was admitted to the Intensive Care Unit where he was intubated and ventilated. He was extubated and managed with CPAP in High Dependency Unit the following day. Unfortunately, his breathing became more laboured overnight, leading to readmission to Intensive Care Unit and intubation with an un-cuffed paediatric endotrachial tube. A second bronchoscopy was performed and showed significant oedema of the vocal cords, a subglottic stenosis, and the airway stents remained in good position. The distal trachea and right main bronchus were collapsing. There were relatively few secretions, and no evidence of infection. Following his second bronchoscopy and immediately after extubation, he again became hypoxic and witnessed a cardiorespiratory arrest from which he was successfully resuscitated.
He was taken to theatre, as an emergency, and CPB established through right femoral vessels cannulation. Transoesophageal echo was used for control of placement of the long venous cannula. Intra-operative bronchoscopy confirmed collapsing distal trachea. The right and left main bronchi were now seen with copious secretions which were aspirated. A 12 mm × 2 cm uncovered Ultraflex stent was inserted into the bronchus intermedius, and a percutaneous tracheostomy set was used to assist in performing an open tracheostomy. He was weaned from the CPB after 81 minutes, decannulated and the femoral vessels repaired.
He was weaned off the ventilator support over a two week period. Eventually, he required a transfer to a rehabilitation centre. His follow up at six months included a review by an ENT surgeon.


A 53 year old female with a longstanding high laryngo-tracheal post-intubation stenosis underwent elective follow-up bronchoscopy. She was fourteen years post-intubation for multitrauma. In February 2005 she underwent tracheostomy for worsening dyspnoea secondary to tracheo-bronchitis after Staphylococcal sepsis. Her past history was significant for right breast cancer, for which she had mastectomy and chemo-radiotherapy, and pneumothorax as a child.
Bronchoscopy showed severe narrowing of the left main bronchus (Figure ). Stenting was not attempted at that time, as inflamed mucosa was seen to predispose to bleeding which would have made airway management through the tracheostomy difficult.
Her preoperative electrocardiogram and her routine bloods including full blood count, urea and electrolytes, creatinin, cardiac enzymes, liver function tests and coagulation profile were within the normal range. She underwent elective bronchoscopy and stenting with Ultraflex, to the left main bronchus with CPB on standby. As a precautionary measure, just prior to airway intervention, the femoral vessels were exposed for potential cannulation. The bronchoscopic procedure was without complications and therefore CPB was not actually required (Figure ).


An 8-year-old boy presented to our clinic complaining of numbness of the little finger and the ulnar aspect of the ring finger. Ten days prior to presentation, the patient sustained a 1 cm laceration at the level of the distal wrist crease after falling on a piece of broken glass. On examination, he had weakness of abduction and adduction of the fingers. Movement of the thumb was unaffected.
The injury was managed at the emergency department by thorough wound irrigation. There was a partial irregular cut of about 30% of the radial aspect of the FCU with intact ulnar nerve and ulnar artery. The skin was sutured. After the primary management the patient was sent to our orthopaedic clinic for further follow up. The initial examination one week after the injury revealed a clean wound, no hematoma or swelling, normal sensation of the fifth and ulnar side of the fourth finger, and normal abduction and adduction of the digits. However a gradual numbness and weakness of intrinsic hand muscles was noted after 10 days that gradually worsened. On subsequent follow up a total ulnar nerve deficit was noted distal to the injury, at the wrist level involving motor and sensory branches.
Three weeks after the initial injury he developed marked weakness of all ulnar supplied intrinsic muscles with total sensory loss at the fifth and the ulnar side of the fourth fingers. Due to the progressive nature of his symptoms, exploration and decompression of the Guyon's canal was done under general anaesthesia. Exploration revealed normal healing of skin and subcutaneous tissue with excessive scar tissue at the radial edge of the FCU which spanned the ulnar nerve, narrowing the entrance of Guyon's canal and causing severe compression and cicriatrical constriction of the nerve.
The ulnar nerve was completely intact (Fig. ). No organized hematoma or lesion of ulnar artery was observed. Adhesions were released, excised and Guyon's canal was completely released. Physiotherapy was started immediately post-operatively, encouraging the patient to move the wrist and fingers. Sensation was markedly improved by the first post-operative day with nearly complete return of motor function at one week. At three months, the recovery was complete.


A 26 year old man presented to the urology service with a left testicular swelling. Clinical examination, followed by testicular ultrasound confirmed the presence of a testicular tumour. After a negative metastatic work – up, the patient proceeded to a left inguinal orchidectomy. This was followed by prophylactic para – aortic nodal irradiation to a total dose of 25 Gray (Gy) in 17 fractions. He then had a five year period of routine surveillance with clinical examination, tumour marker evaluation and annual computed tomographic (CT) scan. After five years a routine beta hCG was measured at 28.5 mIU/mL (normal 1.0 – 5.3 mIU/mL) and this raised concern regarding recurrence of his seminoma. This instigated a complete re – staging with CT Thorax/Abdomen/Pelvis and further metastatic work – up. These were all normal.
On further consultation, the patient admitted to self – administering intramuscular Nandrolone, an anabolic steroid for the previous one year. He had recently discontinued them and was taking hCG to minimise the side effects associated with their withdrawal. He discontinued hCG injections and his beta hCG normalised. He is well with no evidence of disease three years later.


A 58-year old woman presented to the gynaecology out-patient department with a 1-day history of increasing bilateral hip and suprapubic pain. She had a past history of carcinoma of the cervix 12-years prior to this admission, which was treated with a total abdominal hysterectomy, bilateral salpingo-oophorectomy with adjuvant radio- and chemotherapy. She developed a colo-vaginal fistula and bilateral ureteric obstruction 2-years ago due to complex pelvic sepsis, which was managed by fashioning a defunctioning loop colostomy and an ileal-conduit urostomy. However, the patient was otherwise well with no other significant medical problems.
On examination, the patient was dehydrated and pyrexic (38.6°C). Her blood pressure was 101/56 mmHg and pulse rate was 92/min. Abdominal examination revealed deep suprapubic tenderness with erythema of the perineum and inner thighs. Bowel sounds were normal. Initial haematological investigations demonstrated a haemoglobin level of 12.8 g/dl, white cell count of 19.1 × 109/litre, erythrocyte sedimentation rate of 109 mm/hour and a C-reactive protein of 357 mg/L. She was treated conservatively with analgesia, fluid resuscitation and intravenous antibiotics (benzyl-penicillin-2.4 g, clindamycin-900 mg, ciprofloxacin-400 mg) which were administered 3-times per day. On the second day post-admission, her condition deteriorated significantly and she was transferred to the high dependency unit (HDU) with septicaemic shock with a pulse rate of 110/min, blood pressure of 70/43 mmHg, and an oxygen saturation of 94% on 2 litres/min of oxygen therapy.
An urgent magnetic resonance imaging (MRI) scan of the pelvis revealed extensive oedema of the urethra, vagina and rectum with fluid collections within the proximal thigh adductors bilaterally which contained an air/fluid level within the pubic symphysis with extension into the retropubic space and superior to the urethra (Figure ). Subsequent surgical assessment identified extensive perineal and inner thigh cellulitis suspicious of necrotising fascititis. She underwent emergency debridement of the necrotic skin and subcutaneous tissues with drainage of pus. Post-operatively, she was transferred to the intensive care unit for inotropic support in the form of intravenous noradrenaline.
Histopathological assessment of a 20 cm × 7.5 cm ellipse of skin showed necrosis of the skin, dermis and subcutaneous fat with evidence of focal inflammation and pus within all tissue layers. Gram staining confirmed gram-positive cocci extending from the surface of the skin into the deep fatty tissue and arranged in chains, suggestive of streptococcal necrotising fasciitis. Cultures of swabs taken from the perineal wound isolated viridans group streptococci, coagulase negative staphylococci, enterococci and mixed anaerobes. The patient underwent repeated exploration and debridement of the wound in theatre under general anaesthesia on days five, seven, nine, twelve and fourteen post-admission.
The wound was suitable for VAC dressing (VAC Therapy™, KCI, Oxfordshire, United Kingdom) from day-9 after initial debridement (Figure ). Owing to the considerable pain and the position of the wounds, the VAC system had to be reapplied in theatre 3-times a week initially, and then reduced to twice weekly. Sequential wound assessment demonstrated marked improvements with visible granulation tissue following the application of the VAC system set at 125 mmHg continuous topical negative pressure (Figure ). Skin grafts obtained from the antero-lateral aspect of the left thigh were applied to the perineal and thigh wounds on day-20. The VAC system was then applied over the skin graft at a lower topical negative pressure of 50 mmHg.
On day-36, a repeat MRI was performed to investigate persistent bilateral groin sinuses. This demonstrated extensive oedema of all the muscle groups around the pelvis, most marked in the region of the obturators and the adductor muscles in the proximal thigh and bone marrow oedema in the symphysis pubis suggestive of osteomyelitis. Biopsy of the symphysis pubis corroborated the presence of osteomyelitis with collections of acute inflammatory cells and some reactive debris in the marrow space in combination with viable and necrotic bone. A gram stain showed some gram-positive organisms similar to those seen on the original biopsy, suggesting a residual nidus of infection in necrotic bone. The patient remained on long-term antibiotic therapy with continued application of the VAC dressing system as further surgical intervention was deemed inappropriate (Figure ). VAC therapy was discontinued on day-51. The patient was discharged 3-months post-admission with both groin wounds fully healed. She remains well 16-months later with no further signs of soft tissue sepsis or osteomyelitis.


A 55-year-old woman visited our clinic because of typical biliary colic. She had undergone cholecystectomy because of symptomatic gallstone disease 3 years earlier. For the last 6 months she had suffered from intermittently occurring colic. The pain was located in the right upper quadrant of the abdomen. The patient identified the complaint as being the same pain as she had experienced prior to the cholecystectomy. The colic was triggered by ingestion of fat. The patient also noted short periods of discoloured stools and dark urine without jaundice. In addition, the patient had classical reflux complaints with heartburn and acid regurgitation.
Laboratory investigations did not show any signs of cholestasis: aspartate aminotransferase (ASAT) 15 U/l (normal value 10 to 40 U/l), alanine aminotransferase (ALAT) 17 U/l (normal value 5 to 45 U/l), alkaline phosphatase 59 U/l (normal value 40 to 120 U/l) and bilirubin 9 μmol/l (normal value 1 to 15 μmol/l). However, an ultrasound investigation of the upper abdomen showed a slightly dilated common bile duct of 8 mm, with signs of small stones. Owing to the reflux complaints, an upper gastrointestinal endoscopy was performed. A hiatus hernia with reflux oesophagitis grade III according to Savary and Miller was diagnosed. It was decided that the patient should be treated with pantoprazol 40 mg daily. An ERCP was performed 4 weeks later. During this period there were no changes in the clinical condition with the exception of complete remission of the reflux complaints. A normal major papilla was seen. The pancreatic duct was normal. Despite several attempts it was not possible to gain access to the common bile duct. As the common bile duct was dilated it was decided to perform a precut papillotomy with the needle knife. Despite several attempts the common bile duct could not be cannulated and at that point the procedure was terminated.
Several hours later the patient complained of increasing pain in the upper part of her abdomen. The abdomen was tender with an absence of peristalsis. Examination of the blood revealed a serum amylase of 1142 U/l (normal value 60 to 220 U/l), ASAT of 1142 U/l (normal value 10 to 40 U/l), ALAT of 1220 U/l (normal value 5 to 45 U/l), alkaline phosphatase of 131 U/l (normal value 40 to 120 U/l) and γGT of 392 U/l (normal value 5 to 35 U/l). There was a leukocytosis of 15.6 × 109/litre. An X-ray of the abdomen showed air in the retroperitoneal space. The clinical diagnosis was post-ERCP pancreatitis with perforation due to the precut papillotomy.
Computed tomography (CT) scanning with contrast enhancement 2 days later showed a right-sided pleural effusion and a collection of air in the retroperitoneal space. The head and corpus of the pancreas were normal; some infiltration in the region of the tail of the pancreas was seen. There was no necrosis. The common bile duct was dilated with a diameter of 1 cm.
The liver enzymes and hyperamylasaemia returned to normal within 3 days. On account of persisting leukocytosis and a body temperature of 38.3°C antibiotic therapy was started (cefuroxim and metronidazole). Blood cultures were negative. Enteral feeding via a tube in the proximal jejunum was started. Eight days after the onset of the pancreatitis the patient again developed fever (39.5°C) without obvious explanation. Blood investigations still showed a leukocytosis (17.3 × 109/ml), with an acute phase reaction (elevation of the erythrocyte sedimentation rate and C-reactive protein). This time blood culture was positive for Pseudomonas aeruginosa. Antibiotic therapy was changed to ciprofloxacin. Her body temperature became subfebrile.
A CT scan taken 7 days later showed normalisation of the pancreas. The infiltration in the tail of the pancreas had almost subsided and the retroperitoneal air had disappeared. There was still pleural effusion and some ascites present. The clinical condition of the patient further improved, the fever disappeared and the abdomen was non-tender. The patient had normal stools. The treatment with opioids was tapered and normal oral feeding was started.
Sixteen days after the ERCP, when discharge of the patient was already being considered, her clinical condition deteriorated acutely. The patient became dyspnoeic, anxious and tachycardic, with a drop in blood pressure. Blood gas analysis showed respiratory alkalosis with hypoxaemia. Acute pulmonary embolism was suspected and treatment with anticoagulant therapy was started. Electrocardiography showed tachycardia with no signs of acute embolism or myocardial infarction. Cardiac ultrasound did not show signs of infarction or high pressures in the right side of the heart. The clinical situation worsened over the next 30 minutes. Ventricular tachycardia developed, respiratory arrest occurred and despite resuscitation the patient died within 1 hour.
Post-mortem examination showed no signs of acute myocardial infarction or pulmonary embolism. Both lungs showed signs of congestion compatible with the resuscitation. There was pleural fluid present. The culture was sterile. The pancreas showed signs of necrosis in the head and tail. There was fat necrosis in the retroperitoneum. No abscesses were seen. There were no signs of recent local bleeding. The common bile duct was dilated but there were no signs of stones in the common bile duct. A perforation opening at the level of the papilla was not detected. Two litres of ascites were present. There were no signs of systemic septicaemia, despite the fact that culture of the intra-abdominal fluid was positive for Enterococcus faecalis. Macroscopic examination was unable to identify any direct cause of death. Revision of the final CT scan did not reveal signs of necrosis.
Histological examination of the pancreas showed normal pancreatic tissue as well as areas with fatty necrosis. However, histological examination of sections of the lungs showed signs consistent with massive intrapulmonary fat embolism (Figures and ). The final diagnosis was death due to massive intrapulmonary fat embolism which occurred 16 days after the onset of a post-ERCP pancreatitis.


A 9-year-old boy presented with a 6.0-mm polypoid erythematous nodule with ulceration on his left chest. An excisional biopsy was done. Histologically, the tumor revealed several foci of superficial basal cell carcinoma along the epidermis. In the dermis, the tumor was composed of basaloid epithelial anastomosing cords that were separated by fibrovascular stroma connected to the overlying epidermis (Figure ). The histopathological features were that of a fibroepithelioma of Pinkus. The lesion was completely removed with clear biopsy margin. The patient is being followed for any possible local recurrence.


A 78-year-old man who was a chronic smoker presented to the maxillofacial department at a district general hospital with a 6-week history of difficulty in swallowing solids together with pain in his pharynx.
On examination, he was noted to have a 3 × 2 cm solitary pedunculated lesion on the right side of the anterior two-thirds of his tongue crossing the midline. His tongue mobility was normal and there was no palpable cervical lymphadenopathy.
Systematic examination of chest, abdomen and heart were normal. The lesion was biopsied and initially reported as a primary squamous cell carcinoma with some clear cell changes. His blood tests including renal functions were normal. His case was discussed in the head and neck cancer multidisciplinary team (MDT) meeting and subtotal glossectomy was planned after a staging MRI (magnetic resonant imaging) scan followed by adjuvant radiotherapy to the head and neck region. While awaiting an MRI, he presented to the hospital with severe pain in his oral cavity and difficulty in swallowing. His tongue lesion had doubled in size in a matter of two weeks and was now protruding outside the mouth (Figure ). It was considered unusual for primary squamous cell carcinoma of tongue to behave like that. The pathology was therefore reviewed at the same MDT meeting and this time the lesion was reported as partly squamous epithelium covered by fibromuscular tissue showing infiltration by a carcinoma, seen in the nests with extensive clear cell changes. The differential diagnosis was considered to be squamous cell carcinoma with clear cell changes, metastatic salivary gland neoplasm or metastases from RCC. It was decided to arrange an urgent CT scan and to debulk the tongue lesion surgically, to improve his symptoms. The patient had not described any suspicious urinary symptoms.
A CT scan of the neck, chest and abdomen revealed a 4.7-cm sized irregular mass in the left kidney suggestive of RCC (Figure ). There was no local extension and the left renal vein was clear. A solitary tongue lesion with no neck nodes was reported. No metastases were seen in the lungs, liver, adrenals, spleen and bones.
As per the MDT decision, he underwent a debulking surgery of the tongue metastasis, which was performed without complication. His swallowing improved significantly. Postoperatively, he received radiotherapy to his oral cavity delivering a dose of 60 Grays in 30 daily fractions over 6 weeks, which was well tolerated. Radiotherapy was given to treat the microscopic disease in his head and neck region.
A post-radiotherapy CT scan, 18 weeks after initial presentation, was arranged before radical nephrectomy, which unfortunately revealed early evidence of lung metastases. As the patient reported shoulder pain, a plain X-ray and bone scan were carried out and this revealed evidence of a solitary bone metastasis in the right scapula.
Following his debulking surgery and adjuvant radiotherapy, he underwent a radical left-sided nephrectomy. Histopathology confirmed a Fuhrman grade 3 clear cell carcinoma of the left kidney with extension into the superior perirenal fat but not into the renal sinus and with no microvascular infiltration. The maximal dimension of the tumour was 5 cm. The patient has subsequently been treated with interferon-alpha (dose: 3 MU, three times a week) as a systemic treatment for his metastatic disease. A repeat CT scan after six months of treatment showed a complete response with no evidence of any distant metastases.


A 62 year old man presented to our clinic with history of severe low backache over the last 3 months. He gives history of being treated for Early Carcinoma of Sigmoid colon immediately prior to the onset of backache. He had underwent laparoscopic resection of the tumour and subsequent anastomosis of the large intestine. The histopathology showed good tumour clearance. Initial workup for metastasis was negative. He developed anastomotic leak and an enterocutaneous fistula and was reoperated via a laparotomy. Defunctioning colostomy was done. When he presented to us, he had a colostomy bag and his sinus had healed. The backpain was intense when he attempted to move about. Resting in bed gave him some relief. His examination was negative except for paraspinal muscle spasm He had no neurological deficit.
His Erythrocyte Sedimentation rate was 116 mm/first hour. Radiographs of the Lumbosacral spine showed sclerosis of the L2,3 endplates. MRI showed spondylodiskitis of L2,3 vertebrae and L1,2 vertebrae(Figs. ,,,). The involvement of L2,3 was more with early changes in L1,2 disc space. The patient had been on long duration of antibiotics following the abdominal surgery.
Considering the MRI picture, an anterior debridement and biopsy via a retroperitoneal approach was thought of. But due to the colostomy wound and the laparotomy wound, the chance of contaminating the surgical wound was high. Also the possibility of peritoneal adhesions make anterior dissection difficult. Hence the lesion was approached via a posterior route. L2 laminectomy was performed, L2,3 disc space curetted out and sent for histopathology and culture. The spine was stabilized from L1 to L4 via pedicle screw instrumentation. Instrumentation in infected spine is now very well recognized as a therapeutic option to provide mechanical stability [,].
Cultures for bacteria including mycobacterium were negative. Myco 3 PCR for Tuberculosis was negative. Fungal Culture grown on Saborauds Tween 80 corn meal agar showed yeast cells of Candida tropicalis. The organism was sensitive to Fluconazole and resistant to Amphotericin B.
Patient was started on Fluconazole – 400 mg intravenously for two weeks and then orally for a period of 10 weeks. Patient was gradually mobilized. His ESR dropped 40 mm/first hour and he had good symptomatic relief. He later underwent colostomy closure uneventfully and is back to normal activities.


A 46 year old caucasian female presented with a one month history of a rash on the face and hands. She had also noticed generalised myalgia. There was no history of dysphagia, weight loss or night sweats. There had been no recent foreign travel. A past medical history of pernicious anaemia, treated with hydroxycobalamin injections, was noted. No other regular medications were being taken or had been started in the last month. Cardio-respiratory and abdominal examination was unremarkable. Power in all four limbs was graded MRC 5/5. A helitropic rash affecting both upper eyelids and a scaly violaceous eruption on the knuckles was noted. The full blood count, renal function and coagulation studies were normal. Serum B12 and folate levels were also normal. Serum creatine kinase (CK) was 9831 U/L (NR 20–180) and ESR was 54 mm/h (NR 0–20).
The history, clinical findings and blood tests all supported a diagnosis of dermatomyositis and therefore high dose prednisolone (60 mg OD) and methotrexate 10 mg per week with folic acid supplementation was commenced. The patient underwent a deltoid muscle biopsy which demonstrated patchy atrophy of fibres and inflammation around the fasicles compatible with dermatomyositis. Computed tomography of the abdomen, chest and pelvis was normal. Breast mammography revealed a normal parenchymal pattern with no features supportive of malignancy. Auto-antibodies including ANA and anti Jo 1 were negative. The patient was discharged 12 days later with significant improvement in symptoms. The CK continued to normalise 1888 U/L.
The patient was readmitted 21 days later with worsening dysphagia. Upper gastro-intestinal endoscopy demonstrated poor primary contractions with swallowing. Fibro-optic endoscopic evaluation of swallowing highlighted velo-pharyngeal dysfunction, inadequate clearance of bolus from the pharynx and evidence of residue in the valleculae and piriform fossa. Oesophageal and gastric transit studies confirmed oesophageal dysmotility affecting the medial and lower third of the oesophagus and mild gastric stasis. The prednisolone was increased to 60 mg. Given the findings of oesophageal and gastric delay, Intravenous immunoglobulin (IV IG) 40 g OD for three days was given, with a significant improvement in symptoms. Further IV IG was deemed unnecessary due to a paucity of symptoms. The patient was continued on prednisolone 60 mg for a further four weeks before being reduced and the methotrexate was increased to 15 mg per week. The patient continued to be followed up by both the gastroenterologists and rheumatologists. One year after her initial presentation, the patient described no dysphagia. Repeat fibro-optic endoscopy and oesophageal transit studies were not repeated given the resolution of symptoms.


A 56 year old female presented with headache, sinus pain, shortness of breath, cough productive of green sputum and haemoptysis. She had a history of bronchiectasis (diagnosed at age 20), hypertension, and a three month history of sinus problems with associated bilateral hearing loss. Chest radiograph revealed bilateral pleural effusions with apical opacities. Blood investigations revealed a C-reactive protein (CRP) of 454 mg/L and a creatinine of 76 umol/L. An initial diagnosis of lower respiratory tract infection was made and treatment with intravenous amoxicillin and erythromycin started. Pseudomonas was cultured from sputum after seven days, at which point intravenous gentamicin was started. She then developed pulmonary oedema and the haemoptysis worsened. Renal impairment also developed (urine protein/creatinine index 14395, urine protein 5.47 g/L, urine creatinine 3.8 mmol/L) and subsequently the gentamicin therapy was stopped. Her respiratory and renal function continued to deteriorate and she developed anterior t-wave inversion on ECG. Pulmonary haemorrhage secondary to systemic vasculitis was suspected. Blood investigations revealed haemoglobin (Hb) 9.0 g/dL, white cell count (WCC) 22.15 109/L, platelets (PLT) 522 109/L, CRP 227 mg/L, creatinine 159 umol/L, and positive cytoplasmic pattern anti-neutrophil cytoplasmic antibodies (cANCA) (ANCA protease-3 (PR3) 18 u/ml and ANCA myeloperoxidase (MPO) 1 u/ml). A diagnosis of Wegener's granulomatosis was considered most likely and intravenous methylprednisolone commenced. No upper airway lesions were identified on nasal endoscopy so no tissue biopsy could be taken. As a result of worsening respiratory and renal function she was intubated, ventilated and inotropic support with noradrenaline started. Nasogastric feeding was also commenced and plasmaphoresis undertaken. A renal biopsy was planned but she became progressively anaemic Hb 5.7 g/dL, thrombocytopenic PLT 35 109/L, and her liver function deteriorated with a prothombin time of 31 s, making renal biopsy unsafe in the presence of coagulopathy. Gastrointestinal haemorrhage was suspected as the cause of anaemia. Oesophago-gastro-duodenoscopy (OGD) was performed which revealed oesophagitis, gastritis and duodenitis consistent with vasculitis, see figure . These lesions were injected with epinephrine and intravenous omeprazole was commenced. At this point, 19 days after initial presentation, sloughing of her lingual mucosa was noted, see figure . The mucosal sloughing involved the entire anterior two thirds of her tongue bilaterally. After the addition of intravenous cyclophosphamide her respiratory and renal function stabilised. The lingual sloughing persisted, and over the next 14 days progressed to an area of well demarcated necrosis of the anterior two thirds of the tongue bilaterally, see figure . The necrotic area began to separate but unfortunately she developed further pulmonary haemorrhage and her renal and cardiac function continued to deteriorate despite plasmaphoresis and inotropic support. Her condition was deemed irretrievable and supportive care was withdrawn. She died 48 days after initial presentation with the cause of death reported as multi-organ dysfunction syndrome (MODS) secondary to Wegener's granulomatosis. No post mortem examination was performed.


A 29-year-old healthy gravida two, para one with previous caesarean section underwent a lower segment caesarean section at 36 weeks for premature labor under general anaesthesia.
Patient history details were as follows: Occupation: housewife; Ethnicity: Greek; Weight: 87 Kgr; Height: 167 cm; Medical history: one previous caesarean section, otherwise unremarkable; Family history: unremarkable; Patient habits and medication: non-smoker, no alcohol consuption, vitamin supplement during pregnancy.
Delivery of the fetus was uneventful. After the baby was born, an intravenous bolus of 10 i.u of oxytocin was administered. Uterine contraction was noted and gentle cord traction was applied in order to remove the placenta. With slight cord traction, complete inversion of the uterus, through the uterine incision occurred with the placenta remaining firmly attached to the uterine fundus (Fig. ). The inverted uterus was exteriorized at once and the placenta was manually removed. Several attempts for uterine reversion were done unsuccessfully for less than five minutes. Eventually, sevoflurane anesthesia was deepened from 1% to 5% and reversion of the uterus was finally achieved by gradually rolling the lowermost part of the posterior edge over the uterine fundus, thereby reverting that part that inverted last. The uterus was repositioned intraabdominally and an infusion of 20 i.u oxytocin plus 0.2 mg methylergometrine in 1000 ml Ringer's Lactated set maintained the uterine contractions. Sevoflurane progressively was reduced to the initial concentration. Uterine closure was followed by closure of the abdominal cavity. No significant changes in the haemodynamic status of the patient were noted during the operation. Blood loss was estimated at 1500 ml and two units of whole blood were transfused. After the end of cesarean section, 0.8 mg of misoprostol was given per rectum. The postoperative period was uneventful and the patient was discharged from the hospital on the 4th postoperative day.


A 41-year-old woman presented with a 2-month history of pruritus. Her medical history included morbid obesity (BMI, 56 kg/m2), hypertension, and type II diabetes. Her initial liver function tests showed moderately elevated total bilirubin and alkaline phosphatase levels and a normal alpha-fetoprotein (AFP) level (Table ). A computed tomography scan (CT-scan) revealed a large (14-cm), hypervascular mass that involved segment IV of the left lobe and segments V and VIII of the right lobe of the liver, partially occluding the proximal part of the common bile duct and causing moderate dilatation of the intrahepatic biliary system (Figure ). Percutaneous biopsy of the tumor confirmed well-differentiated HCC. In addition, biopsy of segment II of the left lobe revealed mild hepatitis with no evidence of steatosis. Volumetric measurement showed that segments I, II, and III accounted for less than 20% of the total liver volume and less than 0.45% of the patient's total body weight.
Surgical resection was initially ruled out because of a small-for-size remnant liver and abnormal pulmonary function tests that suggested a combination of restrictive and peripheral airway diseases (Table ). After discussing with the patient the risk of complications and potential liver failure associated with extensive liver resection, we elected to pursue locoregional therapy consisting of hepatic transarterial chemo/radioembolization with doxorubicin and yttrium-90 (Y-90) microspheres (Sirtex Medical Limited, Lake Forest, IL, USA). The patient was also placed on a weight-reduction program based on a hypocaloric Mediterranean diet, which has been proven effective for weight loss. Protein intake was calculated as 1 g/kg of body weight. The patient was also instructed to enroll in an aerobic and resistance exercise program in an attempt to improve her metabolic syndrome.
The treatment protocol consisted of 6 weekly injections of doxorubicin mixed with ethiodized oil, followed by 500- to 700-micron Embospheres (Biosphere Medical Inc, Rockland, MA, USA) alternated with Y-90 microspheres injected selectively into the right and middle hepatic arteries by interventional radiologists. The patient underwent 5 cycles of treatment; side effects were minimal and were related to postembolization effects. The total cumulative doses of doxorubicin and Y-90 were 200 mg and 40.4 mCi, respectively.
After 7 months of treatment, a follow-up CT scan of the abdomen showed no significant change in the size and enhancement pattern of the tumor. However, the patient's weight had decreased from 159 kg to 136 kg (so that BMI decreased from 56 to 48 kg/m2). This change was accompanied by improvements in most pulmonary function parameters (Table ) and reductions in the dosage of the patient's antihypertensive and antidiabetic medications. At that time, the decision was made to proceed with extended right hepatectomy to remove segments IV, V, VI, VII, and VIII after right portal vein embolization (PVE) to allow compensatory hypertrophy of segments II and III. A volumetric study performed 8 weeks after PVE showed that the caudate lobe and segments II and III accounted for 33% of the total liver volume.
The patient underwent an extended right hepatectomy. She was positioned on a bariatric operating table (Maquet surgical table; Getinge AB, Getinge, Sweden). Exploratory laparotomy was performed through bilateral subcostal incisions with upper midline extensions. A bariatric Thompson self-retaining retractor (Thompson Surgical Instruments, Inc., Traverse City, MI, USA) was used to elevate the costal margins and facilitate exposure. Despite extensive locoregional therapy, there was minimal inflammatory reaction and adhesions between the liver and adjacent organs. Intraoperative ultrasound was used to confirm the previously defined anatomic relation of the tumor with the intrahepatic vasculature. Hilar dissection and mobilization of the right lobe of the liver were carried out in standard fashion for extended right hepatectomy. Parenchymal transaction was performed with a dissecting sealer (TissueLink Medical, Inc., Dover, NH, USA). The total operative time was 630 min. Estimated blood loss was 720 mL. No transfusion of blood products was required.
The patient's postoperative course was uneventful, despite the long operative time and the technical difficulties encountered during mobilization of the liver because of the compensatory hypertrophy of the left lateral segment and the tumor's large size. The patient remained in the intensive care unit for 2 days and was discharged from the hospital on postoperative day 6. However, superficial wound dehiscence developed that involved the skin and the subcutaneous tissue. This was treated with vacuum-assisted closure (with the VAC Therapy system; KCI, Inc, San Antonio, TX, USA), which facilitated wound healing by secondary intention in 8 weeks.
Histopathologic examination of the excised tumor and portion of the normal liver revealed a well-differentiated 11-cm HCC. There were focal areas of necrosis and hemorrhage from previous chemoradiation therapy, but there was no evidence of microvascular invasion. In the normal liver parenchyma, there was evidence of postembolization effects, mainly focal areas of foreign body giant cell reaction, but minimal fibrosis and no steatosis. All lymph nodes were negative for malignancy. Currently, the patient is doing well, with no evidence of recurrence 17 months after tumor resection.


An 80-year-old male, a heavy smoker, was admitted to the hospital due to hematuria. Cystoscopy revealed multiple superficial small tumors ranged in size from 0.4–2 cm. Transurethral resection was performed and subsequent local chemotherapy by Mitomycin followed. The patient underwent cystoscopic resection of three recidiving superficial tumors 1 year later. The patient was alive and well without sign of disease 3 years after the second surgery.
The primary tumor was characterized by multicystic and papillary architecture and the presence of gland formation (Figure ). Cysts were lined with urothelial cells. Some areas had columns of cells arranged concentrically around eosinophilic PAS (periodic acid shiff)-positive material-filled gland spaces (Figure ). Additionally, numerous signet-ring cells were present in some parts (Figure ). Areas with gland-like lumina formation were also noted. Morphology of recidiving tumor was identical to that of the primary lesion.
Tissue for light microscopy was fixed in 4% formaldehyde and embedded in paraffin using routine procedure. Sections 5-μm thick were cut from the tissue blocks and stained with hematoxylin and eosin, and periodic acid Schiff (PAS). Immunohistochemical staining was performed using the following primary monoclonal antibodies: cytokeratins AE1–AE3 (NeoMarkers, Fremont, CA, USA), CAM 5.2 (Becton Dickinson, San Jose, CA, USA), CK 7 (DakoCytomation, Glostrup, Denmark), CK 20 (DakoCytomation), LeuM1 (Becton Dickinson), cyclin D1 (DakoCytomation), carcinoembryonal antigen (DakoCytomation), cerb2 (Novocastra, Newcastle, U.K.), p53 (DakoCytomation), EGFR (DakoCytomation), MUC1 (Novocastra), MUC2 (Novocastra), and polyclonal antibody Ki 67 (DakoCytomation). Primary antibodies were visualized using the supersensitive streptavidin-biotin-peroxidase complex (Biogenex, San Ramon, CA, USA). Appropriate positive control tissues used with the primary antibodies were employed.
Moderate to strong immunoreactivity was noted for cytokeratins (CK 7, CK 20, AE1–AE3, CAM 5.2) (Figure and ), LeuM1, and cyclin, while strong but focal reactivity was revealed for CEA, cerb2 and weak focal positivity for p53. Negative reaction for epidermal growth factor receptor (EGFR) was found. The expression of MUC1 and MUC2 was strongly positive. Positive staining was restricted to either small- or intermediate-size cysts or extended to signet-ring cells, in which reactivity was predominantly cytoplasmic.


A 56-year-old Caucasian man with type 2 diabetes mellitus, hypothyroidism, idiopathic thrombocytopenic purpura status post splenectomy in 1979, and remote testicular cancer status post orchiectomy and radiation therapy in the 1970s was admitted with 2 days of progressive fatigue, exertional dyspnea, low back pain and cranberry-colored urine. He had been started on metformin 500 mg twice a day 4 days previously for type 2 diabetes but called in to his physician the following day with complaints of "palpitation, heavy breathing, and tossing and turning last night" after taking the metformin, which he declined to continue. Two days before admission he was seen at an outside emergency room with hematuria and anemia; he was diagnosed with a urinary tract infection and started on oral ciprofloxacin. His other medications were pantoprazole, levothyroxine and glyburide. On the day of admission, vital signs were temperature 37.1°C, pulse rate of 133 per minute, respiration rate of 32 breaths per minute, blood pressure of 155/84 and pulse oxygen 94% on 6 liters O2. Physical examination was significant for respiratory distress, scleral icterus and generalized jaundice. There was no jugular venous distention and no enlarged thyroid gland or lymphadenopathy. His lungs were clear, heart sounds were distant, his abdomen was soft without masses or enlargement of organs, he had no rashes and no peripheral edema. Mild lumbar and thoracic spinous tenderness was noted; neurological examination revealed mild lethargy but otherwise normal mental status, with no focal findings. Laboratory studies (Table ) were significant for hemoglobin of 6.6 g/dl, which had dropped from 14.7 g/dl 4 days before, total bilirubin 6.6 mg/dl (direct 2.7 mg/dl), reticulocyte count 3.51%, lactate dehydrogenase 4829 U/l, and haptoglobin less than 6 mg/dl, all consistent with severe hemolysis. The direct antiglobulin (Coombs) test (DAT) was positive for anti-IgG and negative for anti-C3. The peripheral blood smear on admission significantly showed no schistocytes; 4% immature granulocytes and 4% nucleated red blood cells (RBCs) were noted. Other significant findings included marked leukocytosis to 46.1 K/cmm, acute renal failure, elevation of troponin-I and marked transaminase elevations (aspartate aminotransferase (AST) 1711, alanine aminotransferase (ALT) 806) with normal international normalized ratio and alkaline phosphatase. Blood and urine cultures showed no growth. Despite treatment with corticosteroids and transfusion of packed RBCs, the patient became increasingly dyspneic and agitated, complained of abdominal pain and developed hypotension followed by cardiorespiratory arrest approximately 8 hours after admission. Over the next 4 hours he was treated following the advanced cardiac life support protocol for recurrent bouts of pulseless electrical activity and asystole, with worsening hyperkalemia and metabolic acidosis. Despite transfusion, hemoglobin was noted to have declined to 3.3 g/dl. The patient died approximately 12 hours after admission.


A 38 year-old man diagnosed with HIV in 1987 (disseminated tuberculosis) and HCV, who was an ex-IDU, smoker (30 cigarettes per day), and alcohol consumer (30 g/day), with poor HAART adherence, and a CD4 nadir of 6 cells/mm3 in 2005, was seen on April 20th 2006 in a routine HIV control. He reported having an oppressive headache in the last week. The exploration only showed hypoesthesia in the right side of the face. A small ulcer in the cavum and an exophytic polypoid lesion in the back and upper area of the right nostril were observed by nasopharyngoscopy. Computed tomography visualized a mass in the cavum. A biopsy diagnosed a moderately differentiated squamous cell cancer. P.E.T. showed a hypermetabolic mass from the skull base to the right jawbone (Fig. ). In addition, P.E.T. also showed infiltration in the latero-cervical, supra clavicular and para-oesophagus nodes, in C3 and C6 (cervical vertebras), and in the liver (not shown). The patient restarted HAART on May 9th and was discharged. The patient was readmitted to the hospital on June 6th and he died one week later because of liver failure. The patient signed the informed consent to study HPV (June 6th) and his family authorized to publish this event.
Epstein-Barr Virus (EBV) and Human Papilloma Virus (HPV) were studied in biopsy and in blood serum sample (June 6th) by PCR real time and multiplex PCR kit, respectively. Furthermore, HPV was analyzed in samples from the oral cavity, anus, and penis. EBV was positive in the biopsy and in serum (63000 copies/mL) and HPV was positive in serum for two high risk oncogenic types: HPV-16 and HPV-33. HPV was also detected in the anus (HPV-16 and HPV-51) and in the penis (HPV-51).
We believe that our case illustrates the first report of an HIV-infected patient with a nasopharyngeal squamous cell carcinoma with a viremia by one EBV and two high risk oncogenic HPV-types, previous to his death. Although EBV appears to be the most important etiological factor for the
development of nasopharyngeal cancer and its presence in serum suggests metastasis [,], the HPV has been also implicated as an etiological factor in a subset of head and neck squamous cell carcinomas (HNSCC), and its presence in the sera has been related with an advanced HNSCC stage, or with a high risk for metastasis and with a poor prognosis [-]. Although we did not find HPV in the biopsy, we cannot dismiss its presence []. Moreover, he was HPV seropositive which could mean that the tumor was the source for it. The serum sample studied could only represent a single time point during the patient’s care, however HPV DNA in serum may represent occult haematogenous spread of cancer cells. So, it may be acceptable that the origin of the serum HPV could be the tumor.
Patients with HPV-positive tumors have a better overall survival than patients with HPV-negative tumors []. It has been observed that a normal host immunity may block metastatic disease []. So, the rapid evolution observed could be mainly related to the severe immunodeficiency HIV related. Indeed, the widespread metastatic lesions suggest the expression of chemokine receptor CXCR4 which has been associated with a high rate of metastatic potential of human nasopharyngeal carcinoma []. Likewise, other risk factors such as being smoker and an alcohol consumer could contribute to the aggressive clinical outcome as well.
In summary, this case suggests that in very advanced HIV patients with severe immunodeficiency, tumors may have a rapid evolution and different viruses etiologically related (HPV and EBV) can be detected in blood which could be associated with a worse and rapid outcome.


A 54-year-old Japanese man was admitted to our hospital complaining of a 3-month history of a sclerosing dermal lesion on the external genitalia (Fig. ). Computed tomography (CT) revealed numerous nodules invading various parenchymal organs and lymph nodes, suggesting an aggressive malignancy with systemic metastases. Histologic analysis of core needle biopsy samples from scrotal skin disclosed poorly-differentiated adenocarcinoma infiltrating the dermis with frequent lymph vessel invasion (Fig. ). Immunohistologically, the tumor cells were stained positive for cytokeratin 7 (CK7) in the cytoplasm and for thyroid transcription factor 1 (TTF-1) in the nucleus, but negative for cytokeratin 20 (CK20), suggesting that the tumor cells originated from either thyroid cancer or lung adenocarcinoma. The patient died of respiratory failure one month after admission, and an autopsy was conducted to disclose the origin of the cancer.
Grossly, massively spreading lesion (approximately 3 × 3 × 3 cm) with vague margin was noted in the right lung accompanying lymphangitic carcinomatosis, as well as a well-circumscribed nodule (8 mm in diameter) in the right lobe of the thyroid. We confirmed aggressive metastatsis at various loci including liver, bilateral adrenals, peritoneum, cardiac muscle of the right atrium, both thoracic (Th5) and lumbar (L5) vertebra, and lymph nodes within trunk except for head and neck. Microscopic examination revealed that the lung tumor was composed of adenocarcinoma presenting characteristic morphological structure of small tumor clusters with no fibrovascular cores surrounded by clear spaces (Fig. ), so-called 'carcinoma with micropapillary component (MPC)'. Moreover, these MPCs showed severe lymphovascular infiltration in parenchyma and in pleura. All these metastatic lesions were consisted of MPCs, whereas thyroid tumor was histopathologically composed of mainly follicles with atypical nuclear features such as ground-glass appearance and nuclear grooves characteristic of thyroid follicular variant of papillary carcinoma surrounded by MPCs (Fig. ). To further characterize this somewhat complex thyroid nodule with MPC-like clusters, we conducted immunohistochemical analysis.
Immunohistochemical analysis of tissue samples taken at autopsy confirmed that tumor cells in the lung MPCs, thyroid papillary carcinoma, and thyroid MPC-like clusters were all positive for CK7 but negative for CK20. TTF-1 staining demonstrated weakly positive in lung MPC and in thyroid papillary carcinoma follicular variant, whereas thyroid MPC-like clusters were negative. Furthermore, thyroglobulin was positive in thyroid papillary carcinoma with follicular variant, while negative in the MPC-like clusters in both thyroid and lung. On the other hand, lung adenocarcinoma and metastatic MPCs, including MPC in thyroid tumor (Fig. ), were exclusively positive for surfactant protein. These findings suggested that MPC-like clusters in the thyroid papillary carcinoma was metastatic tumor derived from lung cancer. Immunohistochemical analysis for D2-40 confirmed that the MPC was not located within a lymph vessel but in clear tissue space.


A 27-year-old male, non-resident Indian working in Qatar presented with right lower quadrant pain of one week duration. The pain was acute in onset, not very severe and was aggravated by movements. He was not having fever, nausea or vomiting. He had no urinary symptoms and the bowel movements were normal. He was on oral medications prescribed by the local physician and was having loss of appetite. On presentation his pulse rate was 86/mnt, BP was 130/80 mm of Hg. and temperature 98.6°F. Abdomen was soft and he had tenderness in the right lower quadrant, with rebound tenderness. Blood tests showed a total white blood cell count of 11200/mm3 (with 82% Neutrophils and 28% Lymphocytes) and the routine biochemical investigations were within normal limits. Ultra sonogram of the abdomen failed to visualize the appendix but the patient had probe tenderness in the right iliac fossa.
With a clinical diagnosis of appendicitis laparoscopy was done. One 10 mm port for camera at the umbilicus and two 5 mm working ports one in each iliac fossa were used. It showed a segment of ischemic omentum stuck to the parietal wall in the right lower quadrant (figure ). Appendix was normal. The segment of omentum was detached from the parietal wall (figure &) and excised. The excised segment was delivered in an endobag through the umbilical port (See additional file : Omental Infarction Video for an edited version of the laparoscopic findings and the procedure done). The post operative period was uneventful and he was discharged on the second post operative day. Histopathological evaluation showed focal ischemic necrosis and granulation tissue.


A 2 year and 11-month-old mestizo boy was admitted to the Hospital Infantil del Estado de Sonora (Children Hospital of Sonora State, Mexico) with muscle cramps, fine tremors on hands and feet for the last 2 days. His mother reported chronic diarrhea for the last year with 6 hospitalizations because of diarrhea and dehydration. During physical examination, upper abdominal distention was observed (Figure ), in addition to hypotrophic arms and legs and positive Chvostek's and Trousseau's signs. His weight and height were less than the fifth percentile for his age.
Blood count showed hemoglobin 101 g/L, white blood cells 8500/mmc, platelets 472,000/mmc, GVS 26 mm/h and reticulocytes 3%. Microcytic and hypochromic anemia was evident, with hematocrit 30%, mean globular volume 73 fL, serum iron 41 μg/dL and ferritin under 5 μg/L. Serum laboratory tests revealed hypocalcemia with total calcium of 5.7 mg/dL, sodium 133 mEq/L, potassium 3.2 mEq/L, chloride 103 mEq/L, glucose 82 mg/dL, AST 71 U/L, ALT 44 U/L, albumin 2.5 g/L, and C-reactive protein 0.5 mg/L. Billirubins, urine examination, and serial stool analyses for infectious etiologies, were negative.
The patient's tetany resolved after replacement of calcium and additional analyses were performed. IgA and IgG anti-gliadin antibodies as well as IgA anti-transglutaminase were positive, with index values of 3.5, 35.7 and 26.8, respectively. Index value was defined as the ratio of the absorbance of the test serum divided by the cut-off value []. Additionally, there was IgA reactivity to maize prolamins (zeins). The diagnosis of CD was confirmed by inflammatory cells infiltrate in the small intestinal mucosa and lymphocytes in the surface epithelium on duodenal biopsy, in a Marsh IIa/IIb classification (Figure ). After initiation of a gluten-free diet and lactose-free milk (at the beginning), mineral and vitamins supplements, the patient's symptoms completely resolved within 6 weeks. The clinical and nutritional response to the gluten-free diet was excellent. In a 2-month follow-up period, he presented normal blood counts and serum biochemical analyses. Additionally, his weight and height were in the 75 percentile for his age, antibodies titers were normal and there were no further episodes of tetany or diarrhea over 4 years follow up period.


A 38-year-old male motor-vehicle driver presented to the emergency department after falling on his right elbow and dislocating his elbow. On admission, there was a palpable radial pulse and full sensation in his forearm and hand. Radiography revealed this to be a posterior elbow dislocation, with fracture of the olecranon and radial head (Figure and ).
The elbow was reduced immediately and fixed with plaster. Computer tomography and 3D reconstruction suggested posterior fracture dislocation of the elbow, with olecranon oblique fracture and radial head comminuted fracture, without coronoid fracture (Figure and ). Surgery was carried out 6 days after injury. Posterior incision exposed the articular joint. Olecranon simple oblique fracture, radial head comminuted fracture and ulnar nerves were all visualized (Figure ).
We found that medial collateral ligaments were completely disrupted from the point of insertion to the distal humerus (Figure ). Medial collateral ligaments were attached to the distal humerus with a 5-mm Fastin suture anchor (Depuy Mitek) (Figure ). The comminuted radial head fracture was resected. The olecranon fracture was fixed with a lag screw, 12 cm in length and 7.5 mm in diameter, and a tension band wire (Figure ). The elbow was placed in a back slab. The postoperative period was uneventful. Gentle physiotherapy was started after the elbow was maintained in a splint for 2 weeks. Functional recovery was complete in about 3 months. Six months after surgery, the active range of motion was 0/10/130 degrees of extension and flexion. Pronation and supination were full. There were no signs of elbow instability.


A 63-year-old Caucasian man presented to his primary care physician with a 6-month history of intermittent right anterior neck and intraoral pain. The patient noted a tongue mass, which had grown substantially over the last several months. The mass made eating difficult at times and resulted in one episode of mild oral bleeding that resolved spontaneously. He was referred to our institution's department of otolaryngology/head and neck surgery for further evaluation.
The patient's past medical history is significant for RCC of the right kidney diagnosed 4 years prior and treated with right radical nephrectomy. An appropriate work-up at that time included a CT scan of the chest, abdomen, and pelvis and liver functions tests, all of which were negative for metastatic disease. He did not follow-up with his urologist as recommended after the surgery.
The physical exam revealed an erythematous, indurated 3 cm mass in the right anterior floor of mouth region that was tender to palpation. It was not fixed to the mandible and appeared vascular. The neck exam was positive for a 3 cm firm mass in the right thyroid lobe with no pathologic lymphadenopathy otherwise.
Biopsy of his anterior floor of mouth lesion was notable for persistent bleeding and revealed clear cell carcinoma, consistent with the patient's previous history of renal cell cancer (Figure ). Histologic evaluation revealed the presence of a solid nest of epithelial cells with clear cytoplasm and small, round hyperchromatic nuclei (Figure ). A rich vascular network was also noted. Immunoperoxidase testing was positive for CD10 and vimentin and negative for gross cystic disease fluid protein (GCDFP), S-100, HMB-45, muscle-specific antigen, and desmin, supporting the diagnosis of metastatic RCC (Figure ).
Original surgical, pathology and postoperative records were eventually obtained revealing the discovery of suspicious lymph nodes near the renal hilum during his original nephrectomy. The resected lymph nodes were found to harbor metastatic carcinoma and the patient was referred to a medical oncologist at that time to discuss additional therapeutic options. Unfortunately, he did not seek further care for his metastatic RCC. After receiving the news of his biopsy results in our clinic, the patient decided to return to his original institution for further care and died of metastatic disease within several months.


A 29-year-old man with no history of preexisting diseases presented with acute upper gastrointestinal bleeding in a local primary hospital. Endoscopy revealed a submucosal tumor located shortly distal of the papilla of Vater, bulging under the mucosa and forming a partly intraluminal mass. The mucosa showed a central ulceration, this being the origin of the massive bleeding. Because of persistent bleeding that could not be controlled by endoscopic interventional treatment, an emergency laparotomy was performed at the local primary hospital. At laparotomy, an encapsulated mass originating from the duodenal wall at the proximal third portion of the duodenum was identified, reaching to the pancreatic head. A ligation of tumor-feeding vessels was successfully performed to control the bleeding. After the emergency treatment, the patient was referred to our university hospital for further therapy.
Computed tomography visualized the tumor of the duodenum with a diameter of 1.8 × 2.3 × 2.5 cm (Figure ). The scan showed no metastases. 2 days after the initial emergency surgery, the patient underwent definitive surgery at our institution. No recurrent bleeding occurred since the emergency ligation of tumor-feeding vessels.
A relaparotomy was performed. The tumor was located in the proximal third portion of the duodenum, 3 cm distal of the ampulla of Vater (Figure ). It originated from the duodenal wall and protruded as a roundly shaped mass into the near of the pancreatic head. No infiltration of the pancreas or other adjacent organs was found, there were no suspicious lymph nodes. There were no signs of duodenal ischemia related to the haemostatic vessel ligation done at the first emergency operation. The tumor was treated by a limited resection of the distal second, third and fourth part of the duodenum, the proximal resection margin was located just distal of the ampulla of Vater. The bowel continuity was reconstructed by a latero-terminal duodenojejunostomy (Figure ) located opposite to the ampulla of Vater in order not to induce a stricture of the papilla.
The postoperative course was uneventful and the patient was discharged on postoperative day 13.
In the opened specimen, the tumor diameter was 2.5 cm (Figure ). The distance to the proximal resection margin was 0.5 cm; overall length of the duodenal segment was 9 cm. Histology revealed a GIST with a typical spindle cell pattern of the tumor cells (Figure ). There was focal necrosis. The main tumor mass was located subserosal. The tumor had a thin fibrous capsule, and it reached the muscularis mucosae, without penetrating it. There was a regular duodenal mucosa covering the tumor. Immunohistochemistry showed a strong positivity for KIT (CD117) and CD34, while desmin and smooth muscle actin were negative (Figure ). Mitotic activity was < 5/50 high power fields. No formal lymph node dissection had been performed, and as expected no lymph nodes were detected in the resected specimen.
As tumor diameter and low proliferative activity indicated a low risk of malignancy and recurrence, there was no indication for an adjuvant therapy with Imatinib, a tyrosine kinase inhibitor.


A 37-year-old white man, suffering from hepatitis B, presented to the emergency department with cough, low grade fever and night sweats. He was heterosexual with no history of intravenous drug use and worked as a bartender. Radiological examination of the abdomen and chest revealed no pathologies. Biochemical and hematological profiling showed: SGOT: 71 U/liter, SGPT: 61 U/liter, LDH: 931 U/liter, CRP: 28.33 mg/dl, leucocytosis (12,900/μL) associated with polymorphonucleosis (88.2%), Ht 35% and Hb 11.8 g/dl. The serologic examinations for HIV and hepatitis C were negative, as well as the Mantoux reaction.
The next day, the patient presented with dyspnea and auscultation revealed diminished breath sounds with diminished vocal resonance in the right hemithorax. A chest X-ray revealed a pleural effusion in the right hemithorax. Computed tomography (CT) scanning of the chest and abdomen revealed a pleural effusion and a liver abscess (Figure ). The abscess measured 14 × 9 × 7 cm, occupying a great percentage of the right lobe. An echogram of the liver showed septae within the abscess and for this reason echo- or CT-guided drainage was avoided. An operation was scheduled for the following day, but a rapid deterioration of the patient's clinical condition was observed that evening. The patient was febrile (oral temperature 39.2°C) with hypotension, tachypnea (32 breaths/minute) and tachycardia (110 beats/minute) and signs of an acute abdomen. Therefore, emergency surgery was deemed necessary. During exploratory laparotomy, a large volume of free fluid (~2200 ml) together with debris was found on entry into the peritoneal cavity. A rupture of the hepatic abscess at the position of segment VIII was found <Authors: and surgical drainage of the hepatic abscess (that contained many septae) was performed and two wide drains (32G) were placed in the remaining hepatic cavity. Finally, a thoracic drain tube (Büllau) was placed and gave only yellowish reactive fluid. The patient was hospitalized in the ICU for 14 days and for another 14 days in our department. The cultures of the pus were negative for any microorganisms. The diagnosis of an amebic abscess was made by the pathologists who identified E. histolytica in the debris (Figure ). The patient was discharged receiving metronidazole (Flagyl, Rhone Poulenc Rorer) 500 mg three times a day.


A 75 year old male was admitted as an emergency with a 12 day history of persisting vague lower abdominal discomfort and constipation. He also reported reduced urine output and lethargy. An ex-smoker, he was on treatment for high blood pressure and high cholesterol.
On examination he had a palpable abdominal aneurysm but was haemodynamically stable. Plain abdominal X-ray showed curvilinear wall calcification in a AAA (Fig. ). A CT scan was performed to exclude a leaking aneurysm and revealed a 7 cm infrarenal abdominal aortic aneurysm with fistulation into the inferior vena cava (Fig. and Fig. ).
The patient's constipation was treated with symptomatic improvement. During this period, preoperative assessments were performed and the patient scheduled for urgent planned repair of the AAA. However, before the theatre date he developed high output cardiac failure, manifesting as acute shortness of breath with acute pulmonary oedema and lower limb oedema. As a result he underwent emergency open repair of the aneurysm with a tube graft, together with closure of the fistula. He made an uneventful recovery and was discharged home 12 days post operatively.


A 4 and 1/2 year old Mexican girl with Down syndrome presented to the emergency department of a local tertiary care center with symptoms of fluctuating right arm weakness and difficulty smiling that started approximately 4 hours before admission. Her parents found her in bed that morning and noted that she had difficulty playing with one of her dolls because she kept dropping them with her right hand. Her smile also seemed a bit "twisted" according to her mother, and she walked with a limp on her right leg. There was no reported headache or vomiting nor did the child have any history of seizures.
On examination she was normotensive and afebrile. The child was sitting comfortably on the stretcher with her mother present beside her. The child had typical facial characteristics of trisomy 21. Her speech was delayed. Cranial nerve testing revealed a mild right-sided lower facial droop. Motor testing revealed a fluctuating 4+/5 MRC (Medical Research Council) Grade strength of her right upper extremity and right lower extremity. Long-tract signs included an equivocal right toe and a down-going left toe. She walked towards her mother with a slight limp favoring the right side.
Routine laboratory serum studies were unremarkable. Initial head computed tomography did not reveal any acute findings. Subsequent magnetic resonance angiography and imaging revealed acute ischemic changes in the left temporal-parietal area with left middle cerebral artery collateralization (see Figures and , respectively).
The differential diagnosis included transient ischemic attacks, ischemic stroke, dissection, hypoglycemia, cardiac source emboli, hypercoaguable states, seizures, and migraines [].
The patient was given aspirin 81 mg po qd and physical therapy. She was discharged home and eventually underwent an an encephalomyosynangiosis.
Her initial outcome post-operatively was satisfactory but unfortunately she was lost to follow-up.


A 56 year old Caucasian male presented to the ward via the podiatrist with a 5 day history of a hot, swollen and painful right foot leading to the inability to weight bear over the past 2 days. The patient had slipped down 2 steps while walking down a short staircase at home 6 days prior. The podiatrist had been seeing him regularly in the outpatient diabetic foot clinic for his left 1st metatarsal head plantar neuropathic ulcer. He had been put into a left total contact cast (TCC) for the past 1 month following debridement and dressing which resulted in good healing of the ulcer.
The patient is a known Type 1a diabetic since 1982 with established microvascular complications. He has end stage renal failure (ESRF) from diabetic nephropathy and has been on renal replacement therapy for the past 5 years. He has bilateral stable proliferative retinopathy with previous multiple laser photocoagulations and residual visual acuity of 6/36 right and 6/9 left. He also suffers from peripheral neuropathy with mild plantar neuropathic ulcers affecting the right and left feet in the past. He also has dyslipidaemia and hypertension.
There is a family history of Type 2 diabetes in the father and grandmother. He does not smoke or consume alcohol and works as a storeman. His list of current medications include; insulin Lispro (Humalog) 12 units three times a day (TDS) pre-meals subcutaneously (S/C), insulin Glargine 42 units once daily (OD) S/C, Metoprolol succinate 23.75 mg OD, Cilazapril monohydrate 2.5 mg OD, Erythropoietin beta 6000 units thrice weekly S/C, Simvastatin 40 mg OD, calcitriol 0.5 micrograms thrice weekly, calcium citrate 1200 mg once weekly, Aspirin 100 mg OD and Omeprazole 20 mg OD. He weighs 101.5 kilograms (kg) and stands 1.85 metres (m) tall, making the body mass index (BMI) 29.7 kg/m2.
Cardiovascular, respiratory and abdominal examination revealed no significant abnormalities. Neurological examination using Semmes-Weinstein 10 g (5.07) monofilament revealed loss of neuroprotective sensation bilaterally. There was also loss of proprioception and vibration sense bilaterally. Peripheral pulses were normal. The right foot was noted to be oedematous, erythematous and was tender to palpation around the dorsal midfoot. The cutaneous temperature of the right foot was 4°C higher than the left. The recently healed left plantar ulcer was also seen.
He had bilateral feet and ankle radiography, including weight-bearing films. The left foot and ankle films were unremarkable, showing no overt neuropathic arthropathy or Lisfranc joint problems. The right foot dorsoplantar weight-bearing film showed malalignment with lateral displacement of the 2nd metatarsal by 3 mm and a mild 2 mm lateral displacement of the first metatarsal consistent with a homolateral (Type B2) Lisfranc injury (Figure ). The lateral weight-bearing film showed the classical "step-off" point (Figure ).
Magnetic resonance imaging (MRI) was subsequently done. Axial and coronal T1 and Short T1 inversion recovery (STIR) sequences were undertaken. The left foot did not reveal any significant findings while the right foot scan showed high STIR signal within all the muscles of the flexor compartment, oedematous thickening of the interosseous muscles and low T1 with high STIR signal within the 2nd and 3rd metatarsal bases and tarsal bones consistent with acute (Stage 1) Charcot changes. A 6 mm lateral displacement of the 2nd and 3rd metatarsals was also detected. Oblique axial STIR views revealed a complete rupture of the Lisfranc ligament (Figure ).
He was treated initially with bedrest and analgesia followed by TCC for the right Lisfranc injury and acute Charcot. A prefabricated pneumatic walking brace (PPWB) was used for the left leg to prevent unequal distribution of pressure and thus possibility of further ulceration. We discharged the patient with the plan for the TCC to remain for the next 4 – 6 months (with 2 – 3 weekly re-casting) depending on resolution of the acute phase and achievement of anatomic alignment, followed by bracing.


A 47-year-old Caucasian man presented with a 1-year history of worsening right calf swelling, claudicant pain and foot numbness. Examination revealed an 8 cm aneurysmal swelling in the lower popliteal fossa: a posterior tibial artery aneurysm was confirmed on ultrasonography, angiography and magnetic resonance imagery (Figures , , ). The popliteal, anterior tibial and peroneal arteries were normal. There was no evidence of distal embolic pathology. The patient gave no relevant history of atherosclerosis, inflammatory arteritis or traumatic injury. He had however been treated 2 years before this presentation for subacute bacterial endocarditis following dental extractions. There had been confirmed radiographic evidence of mycotic embolisation to both kidneys and spleen; mitral valve vegetations were demonstrated on echocardiography. The patient was treated conservatively with an appropriate antibiotic regime, and his symptoms and elevated inflammatory indices eventually resolved.
The patient underwent elective surgical repair of the posterior tibial artery aneurysm with a reversed short saphenous vein jump graft. Postoperatively, he made an uneventful recovery. Histology showed pieces of aneurysm wall with attached skeletal muscle and thrombus. The aneurysm wall was fibrotic, with destruction of elastic tissue and an infiltrate of neutrophil polymorphs, consistent with an infective process (Figure ).
The posterior tibial artery aneurysm was considered to be mycotic and related to the previous history of endocarditis.