A 46-year-old man presented to our institution, during the summer months, following referral by another hospital. The patient was in good health until 1 week before admission to our hospital, when he suddenly developed worsening headache, fever and depersonalization. Just before his illness, the patient, who had been residing in the UK for the previous 2 years, had just spent 2 weeks visiting friends and travelling extensively through Georgia, Alabama, Florida and Texas. There were no clues from his contact, sexual or past medical history. He had experienced no bites from animals. He had not spent anytime in the wild and had not driven through desert areas. He was heterosexual and monogamic.
His symptoms worsened during the next 72 hours, when he was admitted to an outside hospital. The patient started experiencing a subjective slowing of mentation, visual hallucinations as well as auditory hallucinations. On direct questioning, he also admitted to subjective perineal paraesthesias and dysaesthesias, without any rash present and the feeling of an erupting "cold sore" on his lip. He also described a vague episode of losing control of his bowel sphincter.
The patient was admitted to the outside hospital and empirical levofloxacin was started for a possible urinary tract infection, based on the presence of fever and perineal dysaesthesias. An HIV test was negative. Conventional blood cultures were negative. A urinary culture grew Escherichia coli but the results of the urinary analysis were unavailable. Because of worsening symptoms, on day 6 of the illness, the patient underwent an unenhanced brain CT that was suggestive of a small circumscribed brain haemorrhage. The patient was transferred to our hospital for further management.
On admission, the patient was complaining of subjective fever and headache. He was febrile with a tympanic membrane temperature of 38°C, normotensive and mildly tachycardic. His physical exam was significant for a slow mentation and generalized slowing of his verbal responses. However, he had an appropriate content, although he appeared tearful. Except for generalized mild weakness, his nervous system exam was otherwise normal, with the patient able to subtract serial numbers and perform tandem walking, albeit characteristically slowly. A chest X-ray was normal. Urine analysis and blood cultures were repeated.
The patient was started on ceftriaxone, doxycycline and acyclovir and a CT scan of the patient's brain was obtained after the infusion of iopamidol. The enhanced study revealed a 12 mm focus of increased attenuation consistent with a small haemorrhage adjacent to the posterior body of the left lateral ventricle. No abnormal enhancement was shown. There was no hydrocephalus and the brain parenchyma appeared otherwise normal (Figure ).
A lumbar puncture performed immediately thereafter revealed an opening CSF pressure of 19 cmH2O. The CSF analysis revealed a white blood cell (WBC) count of 0, a red blood cell (RBC) count of 0, a protein level of 0.3 g/L, and a glucose level of 4.3 mmol/L (the synchronous serum value was 5.3 mmol/L). A CSF PCR for viral isolates was ordered, the result of which became available 72 hours after the lumbar puncture had been performed. The CSF PCR was positive for HSV1 DNA and negative for Enterovirus as well as for Varicella Zoster Virus. A viral culture was not performed. Bacterial as well as fungal cultures of the CSF were negative.
The patient's symptoms worsened with increasing confusion before starting to improve on day 3 of the acyclovir (day 9 of the illness). A repeat HIV test was negative, both for antibodies for HIV 1/2 by ELISA and for antigens/antibodies by enzyme immunoassay. An MRI of the brain performed after injection of gadolinium on day 2 of acyclovir (day 8 of the illness) again revealed the small haemorrhage, unchanged in dimensions. No other lesions were identified and the remainder of the parenchyma appeared normal (Figures and ). The patient remained afebrile for the rest of his stay in hospital while his neurological symptomatology improved. An EEG was not performed. The patient was discharged to the outside hospital in very good health on day 7 of acyclovir, having returned to his premorbid mental condition (day 13 of the illness).


A 15 year old girl was brought to the emergency department with a history of sudden onset of paresthesia, involving initially the right leg, then, the right arm, the face and, subsequently the entire right side of the body, increasing during activity (walking) and ceasing during sleep, of two days duration. The patient described this as „the feeling of pins and needles“. There was no previous history of fever, headache, and neurological illnesses. She did not receive any medication. She was non-smoker. Clinical examination revealed a normal developed young girl, with normal memory, speech and orientation, with normal physical exam.
The preliminary impression of the emergency staff was of a functional disorder, and the patient was discharged home, with the recommendation to take calcium and magnesium supplements, being well known that the paresthesia of the mouth, hands, and feet is a common, transient symptom of the related conditions of hyperventilation syndrome and panic attacks. The patient was called back for a formal neurologic assessment scheduled for the next day. On the same day, the patient came back, with repeated involuntary movements involving her right side (foot, arm and face). She was admitted in the Intensive Care Unit and a diagnosis of Hemichorea-Hemiballismus (HC-HB) was made.
Hypotonia of muscles with normal power and normal deep tendon reflexes were present symmetrically. Her blood pressure was 110/55 mm Hg. Keyser Fleischer ring was absent at slit lamp examination.
This clinical symptom of spontaneous hemichorea was considered secondary to a poststreptococcal neurological disease, Sydenham's chorea, but was not associated with other clinical features of rheumatic fever (carditis, arthritis, erythema, rheumatic nodules) and neuropsychological features (dysarthria and emotional disorders). Also, the choreiform movements are rather more continuous in chorea Sydenham than paroxysmal as observed in the described case and the serum anti-streptolysin-O titre was < 200 IU.
Also, the possibility of continuous focal seizures (epilepsia partialis continua [EPC]) causing unilateral movements and CNS involvement (the contralateral basal ganglion, the thalamus and the subcortical areas) was considered. As a result, electroencephalography and brain CT and MRI scanning were scheduled.
Ischaemic and haemorrhagic strokes are the cause of chorea in most elderly patients, and these etiologies were excluded in our patient, based on the neuroimaging studies. Other differential diagnosis considered were: encephalitis, systemic lupus erythematosus, basal ganglia calcifications, Wilson's disease, thyroid disease and tuberous sclerosis. CSF was normal, anti-nuclear antibodies were negative, and serum ceruloplasmin and thyroxine levels were within the normal range. Also, the CT of the head did not reveal any lesion in the basal ganglia, as well as brain MRI exam. EEG was normal, even during the ictal recording, excluding the possibility of epilepsy [Fig. , Fig. ].
Multiple medications in different combinations were tried, including haloperidol, phenobarbital, clonazepam, diazepam, with minimal immediate benefit. Severe pain from the continuous right arm jerking was treated with perfalgan.
Other laboratory tests revealed: haemoglobin of 13 g%, total count of 8,800/mm3, differential count of N 60 E1 L29, and normal liver function tests. Her urea and serum creatinine were 20 mg% and 0.8 mg% respectively. Urine exam: glycosuria, without ketones. Blood glucose concentration was 367 mg% and glycosylated haemoglobin A1C was 13.9%. Estimated blood osmolality was 294 mosm/L and ketones were absent. Serum sodium: 132 mEq/L; potassium: 4.2 mEq/L; serum calcium and magnesium levels were normal. The diagnosis of diabetes was made and the patient was started on rapid analog insulin subcutaneous, until her blood sugar was brought below 250 mg%, following which long-acting insulin was started and continued for the first day. At the end of 24 hours, her blood sugar was 148 mg% and the involuntary movements had completely disappeared. She remained asymptomatic during her hospital stay and was discharged home on a combination of rapid-acting analog, before meals and long-acting analog insulin (subcutaneous) before dinner.
GAD antibodies were positive and C-peptide was low. Based on the presence of glutamic acid decarboxylase antibodies (9,000 U/ml; normal < 1. 4 U/ml), low C-peptide and high insulin requirements, we diagnosed type 1 diabetes mellitus.


A 72-year-old lady, normally fit and well, presented with a 5-day history of jaundice and abdominal pain. She was nauseated and had dark urine. On initial assessment, she was deeply icteric and her temperature was 38.2°C but she was haemodynamically stable. Systemic examination did not reveal any other abnormalities, specifically there were no stigmata of chronic liver disease. No organs or lymph nodes were palpable and the abdomen was soft and non-tender.
Biochemical analyses demonstrated a leukocytosis and neutrophilia; haemoglobin (Hb) 11.9 g/dL, white blood cell count (WCC) 13.9 × 109/L, neutrophils 11.4 × 109/L. An acute phase response was evident with C-reactive protein (CRP) 131 mg/L. A mixed cholestatic and hepatic picture of hepatic enzymes with alkaline phosphatase (ALP) 340 U/L, alanine aminotransferase (ALT) 240 U/L and gamma-glutamyl-transferase (γGT) 381 U/L was demonstrated; total bilirubin was 351 μmol/L. Hepatic synthetic function was preserved with albumin 30 g/L and prothrombin time (PT) of 13.8 seconds. A clinical diagnosis of cholangitis was made on the basis of Charcot's triad (abdominal pain, fever and jaundice), and empirical antibiotic therapy (oral ciprofloxacin 500 mg bd) was commenced.
An ultrasound of the biliary tree was performed demonstrating dilatation of the common bile duct to 1.5 cm with visualization of at least one stone in the lumen of the duct. Intrahepatic duct dilatation was also noted. Blood cultures confirmed a Lactococcus lactis cremoris septicaemia. The organism was sensitive to tazobactam/piperacillin and co-amoxiclav. In light of these results, antibiotic therapy was changed to intravenous tazobactam/piperacillin 4.5 g tds.
The patient proceeded to endoscopic retrograde cholangiopancreatogram (ERCP) where an impacted common bile duct stone was identified. Unfortunately, this was not amenable to endoscopic removal despite sphincterotomy; however two biliary stents were inserted with good drainage.
The patient recovered rapidly with resolution of her symptoms and signs and was discharged home 48 hours post-ERCP. Treatment was completed with 2 weeks of oral co-amoxiclav 625 mg tds.


A 91-year-old Caucasian male farmer presented at the Mayo Clinic, Rochester, Minnesota for evaluation of the acute complaint, "My feet aren't working." Specifically, he reported difficulty with balance leading to inability to walk, and extensive, painful bilateral ecchymoses of his heels (Figures and ). His distress and instability were alleviated only modestly by the use of a non-prescription cane. Barefoot ambulation was impossible. Barely functional ambulation was accomplished by wearing hard-soled shoes.
One month prior, the patient had been diagnosed with bronchitis at an outside clinic and was treated with a seven-day course of levofloxacin 500 mg by mouth, taken once a day (his estimated creatinine clearance was 32 mL/min using the Cockcroft-Gault equation). His bilateral heel pain developed insidiously over the first four days of fluoroquinolone treatment.
Even at 91, the patient had led an active lifestyle on his farm. He cooked all of his own meals, drove a tractor, and performed many other physical farm chores. On day seven of treatment, upon dismounting his tractor, he noticed sudden, severe pain in both of his heels and a compromised ability to ambulate independently.
The patient's medical history was otherwise notable for a mitral valve replacement with porcine xenograft 25 years prior, chronic hypertension, hyperlipidemia, degenerative spondylosis, depression and gastroesophageal reflux disease (GERD). He had no history of tendinopathy. The patient had never smoked, and had no exposure to second-hand smoke. He reported alcohol ingestion of two beers per month and caffeine consumption of three 8 oz cups of coffee per day.
In addition to the levofloxacin, the patient was on the following medications, with no recent changes: metoprolol ER 100 mg/d, isosorbide mononitrate ER 60 mg/d, hydrochlorothiazide/triamterene 25 mg/37.5 mg/d, spironolactone/hydrochlorothiazide 25 mg/25 mg/d, quinapril 20 mg/d, celecoxib 200 mg/d, glucosamine 1500 mg/d, sertraline 100 mg/d, omeprazole 20 mg/d, and acetaminophen 1000 mg every six hours as needed for arthritis-related pain. He had no known food or medication allergies.
On presentation to the hospital, the patient was afebrile and all vital signs were stable. Both heels were mildly edematous with overlying ecchymoses and were tender to palpation bilaterally. The patient had a palpable gap and mass-like defect distally with palpation along the left Achilles tendon. There was a similar gap, although no palpable mass defect, on the right. Dorsalis pedis and posterior tibial pulses were 2+ bilaterally, and capillary refill was less than two seconds in the great toes bilaterally. Thompson's test (also known as Simmond's sign) was abnormal bilaterally, with no movement of either foot. The patient could barely raise himself up on his tiptoes. In both lower extremities, ankle plantar flexion strength was 3/5, great toe flexion to test the flexor hallucis longus was 5/5, and ankle dorsiflexion to test the extensor hallucis longus was 5/5. The patient maintained full active and passive knee range of motion bilaterally. He demonstrated antalgic gait with significant difficulty in the toe-off (propulsion) phases bilaterally.
Radiographs of the lower extremities noted soft-tissue edema of the ankles. There were no noted bony abnormalities.
The patient was initially admitted to the hospital for in-patient care and placed on non-weightbearing status. Magnetic resonance imaging (MRI) of the ankles noted complete rupture of both Achilles tendons approximately 6 cm proximal from insertion upon the calcaneus, with the two ends approximately 3 cm apart on the left and 2 cm apart on the right. The patient was fitted with gravity equinus casts with heel extensions to keep the feet in plantar flexion. He was discharged from the hospital one day after admission.
Five weeks after hospital admission, the patient's casts were removed and he was fitted with controlled ankle motion (CAM) boots that were in plantar flexion at 15 degrees with resultant full equinus. Nine weeks after hospitalization, the patient was instructed to stop wearing the CAM boots and began wearing his own tennis shoes with three-quarter inch heel lifts to maintain relative plantar flexion.
At his initial presentation to the outpatient care center on the day of admission, the patient's primary care physician noted, "History of depression and anxiety: He is not anxious and depression is currently not a problem. He looks much brighter." However, at the meeting with his orthopedic surgeon nine weeks after hospital discharge, both the patient and family members noted decreased energy levels and general lack of enthusiasm. There was concern that these symptoms were fueled by his immobility.
Ten weeks after diagnosis, the patient presented to the Emergency Department with a 22-pound weight loss over the prior two months as well as generalized lethargy. He was hospitalized for evaluation where he was hydrated and his antihypertensive regimen was modified (quinapril, spironolactone, and hydrochlorothiazide were discontinued). He was discharged with blood pressures well within the normal range and with close follow-up with his primary care physician.
The patient was readmitted for inpatient care the following day with hospital-acquired pneumonia. He subsequently developed kidney failure, sepsis, heart failure, and a myocardial infarction. After consultation with the patient and his family, care was withdrawn and comfort care measures were initiated until the patient passed away 11 weeks after the initial diagnosis of bilateral complete Achilles tendon rupture.


The patient, a 33-year-old female Caucasian nurse, was referred to our Centre for Eating Disorders by her GP. She was affected by a severe untreated form of ANp with a duration of illness of 19 years. She smoked 15 cigarettes per day for over 15 years and drank 1 glass of wine at meals.
Four years previously, the patient had been kept under observation by the Psychiatry department for attempted suicide by medicinal overdose. The patient had also been treated with anti-depressives for about 15 years, although this therapy had been suspended about three months before her referral to our Centre.
No significant pathologies emerged in the review of the medical history of the patient's family. During the psychological assessment she reported the separation of her parents when she was a child and her difficulty in maintaining intimate relationships in adulthood. She embarked on her first diet following the death of her maternal grandmother; at this time she considered her weigh excessive (BMI 25). Three years prior to her arrival at the Centre, she had undergone a cone biopsy for adenocarcinoma in situ and had suffered a spontaneous abortion in the 3rd month of pregnancy.
She presented the main core eating disorder symptoms: she denied her underweight condition, she was obsessed with thoughts of food, weight and shape, she thought she couldn't stop bingeing and vomiting. She had decreased energy and difficulties in organizing her daily life. She worked compulsively and reported difficulties to relax. Affective disregulation and problems in her interpersonal relationships emerged in her clinical picture.
Upon her arrival at the Centre, she complained asthenia, lipothymia, ectopic heartbeat and abdominal pain; the intestine was not assessable due chronic laxative abuse. Binging (3–4 times/day) and the following severe purgative practices were disclosed: self-induced vomiting (28 episodes/week), laxative intake (1 cp day of senna) and diuretic use (occasional). Daily physical hyperactivity was also divulged: 2 hours of running or workout.
The diagnostic assessment revealed ANp and the concomitant Axis II Condition: Borderline Personality Disorder (according to the Diagnostic and Statistical Manual of Mental Disorders, Edition IV-TR) [].
The following data were revealed: weight 49 kg, height 1.67 m, BMI 17.5 kg/m2; blood pressure 125/85 mmHg; heart rate 72/min; respiratory rate 32/min; cutaneous temperature 36,2°C. Almost all of the teeth underwent odontoiatric cures or were substituted. Hair, nails and skin appeared normal.
Laboratory findings: serum total calcium 2.33 mmol/l, sodium 140 mEq/l, plasmatic proteins 7,6 g/dl with albumin 54,9% (4,17 g/dl). Hypokalaemia (3.1 mEq/l) was found and responded only to prolonged endovenous potassium (30 mEq/day of potassium chloride for 3 weeks), despite the patient's claimed cessation of the aforementioned purgative activity. Due to the persistent hypokalaemia, renin and aldosterone levels were evaluated, and the following data emerged: secondary hyperaldosteronism (Aldosterone > 100 ng/dl, active renin 408.9 μU/ml); creatinine in the normal range (0.8 mg/dl) and reduced creatinine clearance (70 ml/min); urinary electrolytes and ammonia were not available because the patient left the hospital against medical advice. Haemogas analysis in ambient air revealed pO2 127.80 mmHg, pCO2 38.8 mmHg, pH 7.39, HCO3- 22.80 mmol/l, and SO2 98.80%.
Oesophagogastroduodenoscopy (OGDS) showed grade "A" reflux oesophagitis (according to Los Angeles Classification []); abdominal ultrasound revealed bilateral reduction of the thickness of the renal cortex; renal scintigraphy exposed a bilateral delay in the arrival phase of the trace and no signs of obstructive uropathy were noted.


The 71-year-old Caucasian male subject without any comorbidity participated in the Dutch section of the European Randomized Study of Screening for Prostate Cancer (ERSPC). This study has been ongoing for almost 15 years in 8 European countries and aims to explore the feasibility of population-based screening for prostate cancer []. Almost 270.000 men have been randomized to the screening or control group. Prostate biopsy indications have changed during the course of the study, but include abnormal digital rectal examination (DRE) and/or transrectal ultrasound (TRUS) findings, and/or elevated levels of prostate specific antigen (PSA) in the blood serum and/or PCA3 (Prostate Cancer Gene 3) in the urine [].
In October 2007 our patient was screened using a measurement of the PSA serum level. His PSA was with 1.2 ng/ml below the biopsy-threshold of 3.0 ng/ml. However, as this man had also consented in participating in the PCA3 side study, his urinary sample (collected after DRE) was subjected to PCA3 analysis, which resulted in a score of 13. Since a threshold of PCA3 > 10 was used as a biopsy indication, this prompted DRE, TRUS, and lateralised sextant TRUS-guided prostate biopsies [].
No abnormalities were found during DRE and TRUS. Prostate volume measured by planimetric calculation was 30.9 cc. Histopathologic evaluation revealed no prostate cancer in the 6 biopsy-cores. However, in 2 of the 3 needle-biopsies that also contained rectal mucosa (number IV and V; taken from the left lateral side of the basis and middle of the prostate), a carcinoid was coincidentally found in the rectal mucosa. Small nests, glands and strands consisting of epithelial cells were present within the rectal muscularis mucosae (Figure ). These epithelial cells were characterised by an eosinophilic, finely granular cytoplasm, a round nucleus and inconspicuous nucleolus. No significant atypia, mitotic activity or necrosis was encountered. Additional immunohistochemical stainings showed strong expression of chromogranin and synaptophysin compatible with a carcinoid/low-grade neuroendocrine tumour. Molecular investigation eliminated the option of mixing of specimens.
Our patient was informed about the benign outcome of his prostate biopsies and the remarkable finding in the rectal mucosa by the principal investigator of the ERSPC and he was advised to make an appointment with the gastroenterologist. Besides constipation, no complaints of the gastroenterologic tract or lab changes were found. A colonoscopy was performed, during which two polyps were seen, the first at 2 cm from the anus and the second at 90 cm. The carcinoid was not detected during colonoscopy, probably because it was located in the submucosa. Both polyps were removed endoscopically and sent in for pathologic examination. The lesion in the rectum was a tubulovillous adenoma with low-grade dysplasia. The second was a hyperplastic polyp without any adenomatous changes. Because of the first finding, the patient was advised to undergo a control colonoscopy after 6 years. Until today the incidental finding of carcinoid did not have any clinical consequences for this patient.


A 49-year-old Male presented to our institution with 4-days history of productive cough with greenish phlegm, right-sided chest pain worse on inspiration, fever and sweats. On physical examination, he was febrile with a temperature of 102°F, heart rate of 92, Blood pressure of 143/88. He had rales in the lower lobe of the right lung; the rest of his physical examination was normal and did not reveal a friction rub. Chest radiograph showed right lower lobe consolidation, he was diagnosed with community-acquired pneumonia and started on antibiotic therapy. An ECG was done (Figure ); it revealed elevated ST segment "coved type" classical for Type 1 Brugada ECG. It did not show any changes suggestive of pericarditis namely, depression of the PR interval or diffuse saddle shaped ST elevation.
On further questioning the patient did not have any history of cardiac arrhythmias, syncope, past history of unexplained syncope, or family history of sudden death. Echocardiogram revealed a structurally normal heart with a normal ejection fraction, with no evidence of pericardial effusion. He had no rise in cardiac enzymes. He was discharged on oral antibiotic therapy. At one week follow up, the patient had recovered from pneumonia, and his ECG returned to normal.
Given his history the patient was considered low risk for an arrhythmic event and electrophysiological studies (EPS) were not pursued, he continues to follow up in the outpatient clinic.


A 54 year old female Caucasian patient presented to the orthopaedic outpatient clinic complaining of left arm and left knee pain. She had been diagnosed with malignant melanoma of the palpebral and forniceal conjunctiva 2.5 years before and had received treatment at the regional ocular oncology centre in the form of surgical excision, cryotherapy and adjuvant Mitomycin C.
During her oncological follow up 30 months following the original diagnosis, multiple bilateral pulmonary metastases all measuring <0.5 cms in diameter as well as a 4 × 2 cm right ischial lesion were identified. She was complaining of left arm and left knee pain and was therefore referred to the orthopaedic clinic.
The pattern of the pain was constant with occasional nocturnal exacerbations and was aggravated by weight bearing activities of both extremities. Clinical examination demonstrated localized areas of tenderness over the midshaft area of the left humerus as well as over the anteromedial aspect of the left proximal tibia. Furthermore a non-fluctuant swelling measuring 2 × 2 centimeters in diameter was palpable over the corresponding left proximal tibial metaphysis. All neighbouring joints examined normal. Her right ischial lesion was asymptomatic.
Radiographic evaluation demonstrated lytic lesions of the left humeral diaphysis and proximal tibial metaphysis with associated cortical involvement and ill defined zones of transition, however no evidence of fracture (Figure ). A bone scan confirmed the presence of three active areas corresponding to the lucent radiographic areas of the left humerus, left tibia and right ischium. It did not identify any further skeletal lesions
Regarding her osseous lesions she underwent intramedullary nailing procedures of both long bones on a semi-elective basis due to the danger of impending fracture. According to the Mirels classification for metastatic bone disease at risk of fracture, [] she scored 9 points for the humerus and 10 for the tibia.
A standard reamed and locked nailing technique was applied for stabilization of both bones with no associated intra-operative complications (Figure ). Venting of both bones was performed during the procedure in an attempt to reduce intra-osseous pressure and prevent the risk of fat and tumour embolisation. Intramedullary reamings, as well as specimens obtained via open curettage of the radiologically suspect lesions were sent to the histopathology department.
The patient had an uneventful recovery and was discharged home within 4 days. Histological examination confirmed the presence of devitalized bone and extensively necrotic, heavily pigmented epithelioid tumour, consistent with a diagnosis of metastatic malignant melanoma. There was a low mitotic count (1/mm2) and no significant lymphocytic infiltrate (Figure ).
At her latest follow up visit in the orthopaedic clinic 6 months post-operatively, she remains pain-free with no radiographic evidence of further metastatic spread of the involved bones. Further oncological input consisted of palliative radiotherapy to her right ischial and left humeral lesions, as well as bisphosphonate administration. No conjunctival recurrence has been identified 3 years following the original diagnosis.


A 33-year-old woman (G3, P3) presented referring intense dysmenorrhea and intermenstrual spotting since her third cesarean delivery, 1 year earlier. The patient's medical history and physical examination did not reveal any relevant finding. Two-dimensional-three-dimensional transvaginal ultrasound scans were performed with a Voluson 730 Expert system (GE Healthcare, Milwaukee, WI, USA) and IC5–9 (5–9 MHz) wide band Convex probe. Power Doppler settings were set to achieve maximum sensitivity to detect low velocity flow without noise (frequency, 5 MHz; power Doppler gain, -7.4; dynamic range, 20–40 dB; edge, 1; persistence, 2; color map, 5; gate, 2; filter, L1; and pulse repetition frequency, 0.6 kHz). The scan showed a hematoma (5.3 cm3) between the cesarean section scar and the bladder peritoneum. The bladder wall was not involved (Figure ). The lower uterine segment had a 9 × 12 mm wall defect and an anechoic track that seemed to communicate the blood collection with the endometrial cavity (Figure ). Afterwards, the power Doppler examination demonstrated the presence of active blood flow across the myometrium (Additional file ). Finally, the treatment performed was an abdominal hysterectomy and the pathologic study confirmed the process as being of ischemic origin (Figures and ).


Patient A is a 64 year old white female who presented with a large right breast mass. The mass had been present for at least 2 years, and the breast was swollen, streaked with grey and blue, and mildly tender. There was no personal or family history of breast cancer. Her past medical history was significant for a hysterectomy and oophorectomy at 46 years of age. Her first menstrual period was at age 13, and she had never been pregnant.
Physical exam revealed a well-nourished female with an obvious mass of the right breast. The mass measured 36 × 30 cm at the time of presentation. The skin of the breast was blue at the apex of the mass, and the nipple was massively enlarged and excoriated (Fig ). On initial presentation, there was no evidence of skin breakdown, but by the time of surgery, the patient had experienced loss of skin integrity. The contralateral breast was of normal size, with no significant masses on palpation. There was no palpable adenopathy in either of the axillary basins.
Fine needle aspiration was performed during the initial visit and revealed highly atypical cells suspicious of a malignant neoplasm. Core tissue biopsy showed mixed epithelial-stromal proliferation suggestive of a phyllodes tumor. CT scans of the chest, abdomen, and head showed no evidence of distant metastasis but did suggest invasion of the tumor into the chest wall. For this reason, initial surgical management only involved tumor resection, and breast reconstruction was deferred.
Right simple mastectomy was performed. Superior and inferior skin flaps were designed to allow skin approximation and closure after removal of the large tumor. These flaps included skin directly overlying the tumor that appeared normal (Fig ). The superior flap was raised to the level of the clavicle. Dissection revealed that the blood supply to the tumor was derived largely from collateral vessels arising from the skin. These vessels were large and friable, yet easily managed using standard techniques. The inferior flap was then raised, demonstrating tumor that was partly adherent to the inferior aspect of the pectoralis major muscle. No blood supply originated from the muscle. A portion of the pectoralis major muscle was excised with the tumor, and no invasion of deeper chest wall structures was noted. No lymphadenopathy was appreciated; therefore, an axillary lymph node dissection was not pursued. Two #19 Blake drains were placed beneath the superior and inferior flaps, followed by approximation of the flaps and skin closure (Fig ).
The pathologic findings of this procedure were consistent with benign phyllodes tumor. The tumor measured 30.0 × 25.0 × 20.0 cm ex vivo. Microscopic sections demonstrated large, simple ducts surrounded by a uniform, bland stroma (Fig ). The margin of resection was negative for the tumor with a tumor-free zone that ranged from 0.3 to 1.0 cm (Fig ). The Ki67 proliferation index of the tumor from patient A was 5 and 13 for the epithelial and stromal component, respectively (Fig ). The epithelial component Ki67 index from this specimen is typical of adenomas, whereas the index of 13 for the stromal component is consistent with benign yet brisk stromal proliferation. Mitoses were less than 3 per 10 high power field. Three axillary lymph nodes were present within the mastectomy specimen, and none of these showed evidence of malignancy. The patient is currently over 7 years post-surgery and has shown no evidence of local recurrence or distant metastasis.


Patient B is a 70 year old white female who presented with a large left breast mass. The patient was unsure how long the lesion had been present. Nonspecific findings consistent with a fibroadenoma were noted in the same region on a mammogram obtained 5 years previous to her presentation. Her past medical history was significant for hysterectomy at age 52. She had no personal history of cancer, although her family history was significant for lung and pancreatic cancers. She had used an estrogen and progesterone combination for hormone replacement in the past, the duration of which was unclear.
On physical examination, the patient's left breast had a multilobulated and relatively firm mass that measured approximately 12 cm in diameter and essentially replaced the entire breast. No cervical, supraclavicular, or axillary lymphadenopathy was noted. The contralateral breast showed no signs of a mass. Core tissue biopsy taken at the time of presentation suggested a diagnosis of cellular fibroadenoma or phyllodes tumor. Pre-operative CT scan revealed a 7.5 × 11 cm mass in the anterior portion of the breast, with no apparent mediastinal, lung, neck, or axillary lymphadenopathy.
Left modified radical mastectomy with dissection of level I and level II lymph nodes was performed. A right mastopexy was performed for purposes of symmetry. An elliptical incision encompassing the entire mass and the overlying skin was made. Collaterals in the skin supplied the tumor, and no deep invasion was identified. The superior and inferior skin flaps included skin that had been overlying the tumor. The tumor was excised along with the pectoralis muscle fascia. Axillary dissection was undertaken because of the presence of palpable level II nodes intra-operatively. A tissue expander was placed before final closure, as the patient desired reconstruction.
The pathologic findings of this procedure were consistent with a benign phyllodes tumor. The tumor measured 10.0 × 8.0 × 5.0 cm ex vivo. Microscopic sections showed large branching ducts surrounded by a uniform, bland stroma (Fig ); areas of hyalinization and myxoid change were rare. As with patient A, the margin of resection was negative for the tumor with a tumor-free zone that ranged from over 0.3 to 1.0 cm (Fig ). The Ki67 proliferation index of the tumor from patient B was 0.8 and 4 for the epithelial and stromal component, respectively (Fig ). No significant cytologic atypia or mitotic activity was noted. Sixteen lymph nodes were obtained, all of which were benign.
The patient had an unremarkable post-operative course and was able to start tissue expansion 19 days after her surgery. She had exchange of her tissue expander for a permanent implant 6 months after her mastectomy. She had an uneventful recovery from these surgical procedures and is currently 6 years post-surgery without complication.


A 60-year-old man was admitted for an examination to determine whether he had interstitial pneumonia. The patient had been previously hospitalised for two weeks at a different location with symptoms that included shortness of breath, a fever of 38.5°C, and a 7 kg loss of weight within the past month. At the aforementioned hospital, a chest radiograph indicated the presence of bilateral interstitial pneumonia. Subsequent microbiological investigations, including Ziehl-Neelsen staining and a PCR-based assay to test for the presence of M. tuberculosis on expectoration, indicated that there were no signs of such an infection. The patient was then transferred to our department for further evaluation. Clinical examination of the patient verified both a body temperature of 38 – 38.5°C and dyspnoea with 90% oxygen saturation under 6 L/min oxygen. The medical history of the patient was unremarkable, except for previous treatment for arterial hypertension. The total body tomodensitometry indicated the presence of nodules in both lungs, in the mediastinal lymph nodes, and in a right axilar lymph node. The pertinent laboratory assays were performed and indicated a value of 5.9 leucocytes/ml with 76% polymorphonuclear cells and 190 platelets/ml. The erythrocyte sedimentation rate was determined to be 28 mm for the first hour. The lactate dehydrogenase level was 612 IU/ml (normal levels are < 430 IU/ml), the gamma GT level was 699 IU/ml (normal levels are < 55 IU/ml), the bilirubin concentration was 13 μmol/l, the AST level was 96 IU/l (normal values are < 25 IU/ml), and the ALT level was shown to be 127 IU/l (normal values are < 45 IU/ml). It was suspected that the patient had already begun to develop pulmonary tuberculosis and thus was recommended to receive anti-tuberculosis therapy since it was reported that M. tuberculosis was isolated from an expectoration that was collected 14 days prior during the first hospital visit. Due to the observation that the patient's respiratory status had worsened, the patient was admitted into an intensive care unit for a period of four days. The results of direct microscopic examinations using Gram and Ziehl-Neelsen staining of a surgical lung biopsy were negative. This sample, cultured in BACTEC (Becton and Dickinson, Le Pont de La Claix, France) and in 5% blood agar in slant tubes (Labo Moderne, Dinan, France), remained sterile after a two-month incubation period. Subsequent histological examination discovered large B-cell lymphoma and further assessments confirmed that the patient had stage IV lymphoma that involved the lung, liver, and bone marrow. The patient then received the appropriate anti-lymphoma therapy.


A 69 year-old-man presented with abdominal distension and anal bleeding on defecation. For the last six months the patient was complaining of flatulence, periumbilical pain and sensation of incomplete evacuation. Apart from tenderness on deep palpation, blood on PR examination and increased bowel sounds, all other systems were found normal on clinical examination.
Colonoscopy revealed intraluminal stenosis of the colorectal junction and biopsy specimens were obtained. Biopsy confirmed a well differentiated mucinous adenocarcinoma of the rectosigmoid colon. There was no evidence of metastasis, based on abdominal computed tomography (CT), chest X-ray and endorectal ultrasound (US) 3D. Carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 19-9, and cancer antigen (CA) 50 were normal. Low anterior resection for colorectal carcinoma (CRC) with an end to end primary anastomosis was performed, while on exploration a mass in Meckel's diverticulum, 80 cm proximal to the ileocecal valve, was encountered (Figure ). The mass was 7.5 cm in maximal diameter (Figure ), while the size of the Meckel's diverticulum was 3 cm. Thus, this case is classified as an "intermediate risk" GIST according to the risk assessment of aggressive behavior in GISTs proposed by Fletcher et al. (size: 7.5 cm, mitotic count: 0-1/50 HPF) []. No evidence of liver metastasis or intra-abdominal metastatic spread was found. The patient underwent resection of the tumor together with partial resection of the small bowel in order to avoid rupture and intra-abdominal spillage. Tumor was excised, together with 3 cm of ileum on either side, and a lateral to lateral anastomosis was performed with the use of staplers.
The lesion in the colorectal junction was a stage C2 (Astler-Coller) tumour, 8 × 6 cm in size (Figure ), located in the rectosigmoid colon. Microscopic examination showed a well-differentiated adenocarcinoma, penetrating the bowel wall, without nerve and vascular invasion. However, one of the 23 resected lymph nodes was positive for metastasis. According to the TNM (tumor, lymph nodes, metastasis) classification, the disease was stage IIIb. Histopathological examination of the resected Meckel's diverticulum tumor revealed a stromal cell neoplasm with a few necrotic and hemorrhagic areas and a low index of mitotic count (0–1 mitoses/50 HPF) (Figure ). Immunohistochemical analysis revealed expression of C-kit (strongly positive), moderately positive stain for SMA, while markers for focal S-100 and CD 34 were negative (Figure ).
Patient's postoperative course was uneventful, and he was commenced on adjuvant chemotherapy with FOLFOX regimen (oxaliplatin i.v., 85 mg/m2(on day 1), leukovorin i.v., 200 mg/m2 (on days 1,2), 5 FU (fluorouracil) i.v., bolus 400 mg/m2 (on days 1,2), 5 FU i.v., 22 hours-infusion, 600 mg/m2 (on days 1,2), every 2 weeks for 12 cycles.
One year later he has no signs of local recurrence or metastasis.


A three-month-old female child was referred to our hospital for evaluation of apparent blindness. There was history of frequent episodes of flexor spasms with twitching of both eyes since one and a half months of age. Each episode recurred nearly five to six times per day associated with drooling of saliva. According to the parents, the child never turned towards light or sound. She was a second child born to a non-consanguineous marriage. It was a full-term normal delivery. There was no history of jaundice, fever or convulsion in the immediate neonatal period.
On examination, there was global developmental delay. The head circumference was in 10th percentile. On ophthalmic examination the child was neither responding to nor following bright light. Both the pupils were very sluggish in reaction. Anterior segments of both eyes were normal. The vitreous was clear and normal in both eyes. Fundus examination revealed bilateral optic nerve colobomas with variable-sized discrete dome-shaped loci of pale areas with sharp borders (chorioretinal lacunae) just nasal to the optic discs [Fig. , ]. The fovea was spared in both the eyes.
As the child had seizures, electroencephalography (EEG) was done by the neurologist. EEG showed burst of spike, polyspike, sharp and slow-wave complexes with suppression in between, predominantly over the right hemisphere. Bilateral synchronous and symmetrical discharges were also present along with slow waves of high amplitudes that were seen more on the right hemisphere. Thus, it showed burst suppression and hypsarrhythmia pattern. Computed tomography (CT) scan of the child revealed hypogenesis of the corpus callosum with small inter-hemispheric cyst [].
She was on anti-epileptic medications and subcutaneous injections of adrenocorticotropic hormone (ACTH) and was having good seizure control.


We report on a 75-year-old Caucasian woman, admitted in 1972 aged 39 for schizophrenia. She has been an informal inpatient since then. In her later years, her medical history includes atrial fibrillation, recurrent pneumonia, pulmonary fibrosis, small-vessel cerebrovascular disease, gallstones, and lupus anticoagulant without antinuclear antibody. Her regular drug treatment comprised clozapine, digoxin, furosemide, simvastatin, senna, lactulose, and zolpidem. She was on no calcium or vitamin D supplements. Aspirin had recently been replaced with warfarin, which was stopped shortly afterwards following the development of iron-deficiency anaemia. She was independently mobile and a smoker.
We investigated her for a mildly but persistently elevated alkaline phosphatase, with intermittently low phosphate and calcium (Figure ). Her albumin, bilirubin, alanine aminotransferase (ALT), and renal function were normal. Bone and liver isoforms of alkaline phosphatase were not measured. The diagnosis of osteomalacia was confirmed when in April 2008 her serum 25-hydroxyvitamin D level was found to be 10.5 nM, representing severe deficiency (Figure ). Coeliac serology was negative. She was commenced on calcium and vitamin D supplementation but fell and suffered a subcapital fracture of her femoral neck later that night, requiring hemiarthroplasty, subsequently complicated by pneumonia, wound infection, urinary tract infection, sepsis, recurrent hemiarthroplasty dislocation and prosthesis infection requiring excision arthroplasty.


A 28-year-old previously healthy man presented at the emergency department (ED) 48 hours after a hit in the left side of the abdomen by a fist, with gradual worsening of pain, nausea and bilious vomiting. Physical examination revealed a temperature of 37,6°C, a pulse rate of 80 beat per minute (bpm), a blood pressure of 110/70 mm Hg. The epigastrium, left upper and left lower abdominal quadrants were tender on palpation. On rectal examination the rectum contained no stool. Initial management of the patient involved intravenous fluid resuscitation, and nasogastric tube insertion, routine blood tests and supine abdominal x-rays. Initial laboratory values, including complete blood cell count, serum electrolytes, glucose, blood urea, creatinine, liver function tests, and lipase were all normal. Initially supine abdominal x-ray revealed dilated small-bowel loops with air-fluid levels, but no gas under diaphragm (Fig. ). Ultrasonography (US) of the abdomen showed free fluid in the peritoneal cavity with dilated small bowel loops without injuries of the parenchymatous abdominal organs. Diagnosis of hemoperitoneum was made, but with stability of vital signs, little abdominal tenderness, no signs of evident small bowel obstruction, and normal value of blood cell count, the patient was admitted in the surgery department for observation. During his hospital course his abdomen remained a little distended, with mild lower quadrant pain that was well controlled with analgesic pain medications. A repeat white and red blood cell count remained normal. Two days later, however, the abdominal pain was increasing, the vomits had turned fecaloid, and with absolute constipation. An abdominal computed tomography (CT) was performed which showed a targetlike lesion in the left upper quadrant with dilated small bowel loops proximally, suggestive of an ileo-ileal intussusception (Fig. ). Free fluid was seen in the paracolic gutters, pelvis and between bowel loops. There was no solid organ injury. Based to the clinical signs of small bowel obstruction and the result of CT, an emergent laparotomy was decided. At the exploration, the peritoneal cavity was filled with 500 cc of blood-stained serous fluid, while numerous dilated loops of small bowel were present. At approximately 90 cm from the ileo-ceacal junction, there was an ileo-ileal intussusception with a small mesenteric breach likely accountable of blood stained. There was no solid organ injury. The intussusceptum was gently milked out, revealing a 20-cm segment of ischemic ileum. The intussuscepted segment was edematous, but there was no bowel wall hematoma. Just proximal to this, at approximately 100 cm from the ileo-ceacal junction, a small dimple in the antimesenteric border was noted and proved to be a Meckel's diverticulum (Fig. ). Localized ileal resection with Meckel's diverticulum was undertaken. The postoperative recovery was uncomplicated, and the patient was discharged on the fifth day postoperatively. The pathological examination of the resected specimen showed a Meckel's diverticulum (3.5 cm in length) on the antimesenteric border with heterotrophic gastric mucosa.


A 40-year old Northern European male was first seen in the genetics clinic in 1994. He had a history of leiomyosarcoma of the thigh at age 36, treated with a compartmental resection and post-operative radiotherapy and male breast cancer (stage T2N0M0) for which he had a right mastectomy. The relevant family history at presentation was a paternal history of a father (an ex-smoker but non-drinker) with oesophageal cancer at 47, and a paternal grandfather and two paternal uncles who had been affected with colon cancer in their forties (Figure ).
Initial diagnoses considered included Li Fraumeni syndrome [], which is associated with germline mutations in the TP53 gene, due to the presence of a sarcoma and breast cancer in the proband. Mutations in the hMSH2 gene, which had been recently cloned at that time were also considered as the paternal branch of the family including the uncles and grandfather fitted the Amsterdam I criteria. Full sequencing of the TP53 gene from blood DNA was uninformative and mutation testing for mismatch repair mutations was not available at that time. Subsequently, BRCA2 was considered a candidate gene because of the presence of male breast cancer, but no mutations were found in either BRCA1 or BRCA2 by screening of the full coding sequences of these genes with dHPLC and large rearrangement testing by MLPA.
The patient went on to develop two further primaries – colon cancer at 48 years (a T1 tumour, treated with a sub-total colectomy) and prostate cancer at 50 years treated with brachytherapy. In addition, over the next decade the family history continued to evolve with the development of cervical adenosquamous carcinoma in his sister, an oligodendroglioma in his niece, a further case of colon cancer in a cousin and a prostate cancer in the proband's close relatives (Figure ). Immunohistochemical studies of his breast carcinoma and sarcoma showed loss of hMLH1 staining (Figure ) while hMSH2 and hMSH6 staining were normal. Staining was not available in the tumours from his immediate relatives, but an additional 8 cancers and one adenoma from other known mutation carriers in a different branch of the same family also showed loss of hMLH1 staining (data not shown) while hMSH2 and hMSH6 staining were normal. MSI testing was less extensively available in the family. While a high level of MSI was demonstrable in the proband's sarcoma (with three markers D5S346, D17S250, D2S123), it was not evident in his breast cancer, despite both tumours losing protein expression. This is likely to be a function of the known insensitivity of markers optimised for the detection of MSI in colorectal cancers, being used to try to detect MSI in other tumour types []. MSI was also demonstrated in 5 samples (4 cancers and one adenoma) from other known carriers in the second branch of the family.
Molecular analysis of the proband's germline DNA identified a missense variant in the hMLH1 gene (reference sequence NM_000249.2) in exon 2 at nucleotide position 200 (c.200G>A), which predicts substitution of glycine 67 with a glutamic acid residue (p.Gly67Glu). This putative p.Gly67Glu mutation segregates with cancer predisposition in nine family members (see Figure ). The proband is currently well and has surveillance with annual sigmoidoscopy and upper gastrointestinal endoscopy, annual chest wall examination, 6 monthly and PSA level measurements and sarcoma follow-up.


A 53-year-old female bidi smoker (pack year: 14) was admitted to our department with complaints of loss of appetite and left-sided chest pain for 5 months. On examination, the patient was alert and well oriented. She was not in obvious distress. Her vital signs were stable. The only significant finding on examination of the chest was reduced breath sound at the left lower axillary area with bi basilar crept in the infrascapular area.
Her chest radiograph revealed bilateral hilar prominence with left-sided pleural effusion []. A left thoracentesis revealed thin, grossly hemorrhagic pleural fluid that did not clot and did not clear on sequential samples and had no obvious odor. Thus, considering the age of the patient (53 years) and her smoking habits and hemorrhagic pleural fluid, a malignant process was considered in the differential diagnosis.
The pleural fluid was exudates with cytology showing 2,200 cells/cu mm with 88% lymphocytes and 12% neutrophils, red blood cell (RBC) count of 2,200,000/cu mm and pleural fluid hematocrit was 26%. Biochemical analysis revealed sugar 44 mg/dl, proteins 5.4 g/dl and adenosine deaminase 32 U/L (normal limit being less than 40 U/L). Pleural fluid cultures were negative for both pyogens and M. tuberculosis. Pleural fluid was negative for malignant cells on five consecutive occasions. Her pleural biopsy was performed by Abraham's needle, which was negative. Her PPD skin test was negative. A computerised tomographic scan of her chest revealed bilateral hilar lymphadenopathy with parenchymal opacity and left-sided pleural effusion [ and ].
Further, ultrasonography of the neck and abdomen, mammography and gynecological evaluation were performed to rule out any evidence of a malignant condition, but all were normal except for a deep cervical lymphadenopathy. An excisional biopsy of the upper deep cervical lymph node revealed a noncaseating granuloma. Serum ACE was 168 IU/L. Fiber optic bronchoscopy revealed no endobronchial abnormality. Bronchial brushing and bronchoalveolar lavage revealed predominance of lymphocytes and no malignant cells or AFB. A repeat thoracoscopic-guided pleural biopsy revealed a noncaseating granuloma.
Thus, a diagnosis of sarcoidosis presenting as hemorrhagic pleural effusion with bilateral hilar lymphadenopathy and deep cervical lymphadenopathy was made.
She was put on prednisolone 40 mg/day followed by in-tapered dosages. Her appetitite was improved and chest pain subsided gradually and without recurrence of symptoms of pleurisy [, ].


A 53-year-old well-built man slipped on the floor and landed on his back. He continued to suffer from sharp abdominal pains gradually increasing in severity for the following few days. The pain was localized in the epigastrium, left hypochondrium and the back. As he overlooked his fall, his local doctor attributed these pains to gastritis.
On the fourth day following his trauma, he presented to the Casualty Unit at Ain Shams University Specialized Hospital with shock and abdominal pain. He could not give relevant history as his level of consciousness continued to deteriorate. None of his family members who were accompanying him knew about his trauma.
His systolic blood pressure was 50–60 mmHg, and his heart rate was 130 bpm. Inspection showed an abdominal mass. The abdominal wall was tender and rigid on examination. The mass was fixed and not pulsating.
Intensive resuscitation measures started immediately. Blood was taken for cross match and investigations. The decision of exploration laparotomy was made. The patient was temporary resuscitated, and on the way to the operating room, he had a rapid CT examination (without contrast) to rule out a ruptured aneurysm due to the lack of proper history. It was difficult to maintain his vital signs that started to deteriorate again; so he was rushed to theatre.
The CT scan showed a huge multi-locular abdominal cyst with blood-dense fluid inside. The origin of the cyst was not clear due to its size. There was a tiny calcified structure floating in cyst cavity. Certainly, the possibility of a leaking aortic aneurysm was excluded. There was no other abnormal finding [Figures and ].
At the laparotomy, a huge dark blue cyst was filling most of the abdominal cavity and pushing the entire bowel to a small compartment. Opening the cyst revealed dark blood clots and de-fibrinated blood. The cyst was multi-locular as shown on the CT scan. The blood clots were removed and the loculi were traced down to the retroperitoneal space. The retroperitoneal space was full of blood clots of unidentified origin. There was no active bleeding. A small branched atheroma taking the shape of a blood vessel at its bifurcation was retrieved from the cavity of the blood cyst. Its diameter was about 4 mm. It denoted the previous rupture of a retroperitoneal blood vessel at its bifurcation (a lumbar artery). This represented the calcified structure identified at the CT scan.
The patient by this time received 15 units of blood and 12 units of fresh frozen plasma. As a consequence and due to the large size of retroperitoneal hematoma and the fact that there was no active bleeding or identifiable bleeder and the patient started to show signs of coagulopathy, the decision was not to interrupt the retroperitoneal hematoma. The cyst pseudo-wall, which actually was derived from the retroperitoneal wall, was closed by continuous vicryl suture to tamponade the remaining hematoma.
The patient was transferred to the ICU. He stayed there for 3 days and was transferred to the ward. He was discharged 10 days after his laparotomy.
One month later, a follow-up CT scan showed re-accumulation of some blood clots and mild left hydroureter and hydronephrosis. The patient was asymptomatic, but to avoid further pressure on his left kidney, he underwent an elective laparotomy. A smaller multi-locular blood cyst was identified, opened and evacuated. More blood clots were removed and the cyst wall was left open for drainage. The abdomen was closed with two drains inside.
The patient went home on the fifth postoperative day. Following his second laparotomy, he developed a wound infection. Some skin stitches were removed to help the pus draining. Six months follow up by abdominal ultrasound revealed no back pressure on the left kidney and absence of abdominal cysts or masses.


A 31 years old male presented with history of aches and pains in whole body especially marked in temporomandibular joints, lower legs and both hip joints lasting for 1 month. He was also suffering from fatigue and generalized weakness for the same duration. There was no history of fever, allergies, skin rash, cough, urinary and bowel complaints. He is employed in Navy as a marine, and is a non-smoker, non-diabetic and non-hypertensive. He had received anti-tuberculosis treatment 3 years ago for pulmonary Koch's. At the time of his present illness, he was not taking any medications. He was living in the sailors' accommodation with his colleagues, and there was no history of handling of any pets. Both his parents and his 5 siblings were healthy, and did not have history of major illness in the past.
On physical examination he was comfortable, afebrile, and did not have any bone tenderness. There was no pallor, jaundice or lymphadenopathy. Pulse was 78/minute and blood pressure was 110/75 mmHg. The heart and lungs were normal on auscultation, and there were no murmurs or added sounds. On abdominal examination liver was not palpable, while spleen was enlarged and palpable 3 cm below left costal margin. Neurological examination did not show any abnormality.
His complete blood counts showed Hb: 13.6 g/dl, total leucocyte count 48 × 109/l with 72% eosinophils, 21% neutrophils, 7% lymphocytes; and platelet count 167 × 109/l. The absolute eosinophil count was 34.5 × 109/l (34,560/cmm), and the eosinophils had heterogenous morphology in peripheral blood film (Fig ). His ultrasound abdomen revealed splenomegaly, while there was no enlargement of para-aortic lymph nodes, or presence of abdominal/pelvic mass and abscess. 2-D echocardiography showed normal sized cardiac chambers with good left ventricular contraction. There were no vegetations on the valves, no left ventricular hypertrophy and ejection fraction was >65%. Electrocardiography revealed sinus rhythm and no evidence of any abnormality including axis deviation, ischaemia, previous infarction or heart block. Chest X-Ray showed normal lung fields and cardiac shadow. Serum bilirubin, ALT, alkaline phosphatase, urea, creatinine, sodium, potassium, uric acid and blood glucose were within normal limits. Stool routine examination did not show any ova or cysts.
His bone marrow examination showed a hyperplastic marrow with depressed erythropoiesis and reduced megakaryocytes. Myelopoiesis showed increase in eosinophils and their precursors. There was infiltration by 40% blasts with high nucleo-cytoplasmic ratio, homogenous nuclear chromatin pattern and a thin rim of light basophilic cytoplasm (Fig ). The blasts were negative for Sudan Black B, acid phosphatase but displayed occasional block positivity with Periodic Acid Schiff stain. Flow cytometric analysis (FC500 Beckman Coulter) was done after incubation of bone marrow mononuclear cells with a panel of fluorescence labeled antibodies (obtained from Becton Dickinson, USA). The blast cell population showed strong reactivity (>95%) with B-cell markers including CD10, CD19, CD20, CD22 and cCD79a.
The blasts did not show expression of lymphoid T markers (CD3, 5 & 7) and myeloid markers (CD 13, 33 & cMPO). HLA-DR and cTdT also showed strong positivity. There were no detectable surface immunoglobulins or cytoplasmic light chains (IgM, IgG, kappa, lambda). The immunophenotype was consistent with common precursor B-lymphoblastic leukaemia. Cytogenetic analysis (Fig ) revealed karyotype 45 XY, t(7;12)(q22;p13),-9[15]/46,XY [05]. Routine examination of cerebrospinal fluid showed a protein level: 0.33 g/l, glucose: 4.4 mmol/l and occasional mature lymphocytes on Leishman's stain (There were no blasts seen in the cytospin smear).
The height and weight of the patient was 170 cm and 70 kg, respectively, and the body surface area was 1.7 m2. He was started on induction therapy based on UK ALL XII consisting of four drugs regimen, which included Inj vincristine 1.5 mg/m2 IV on day 1, 8, 16 and 24; Inj daunorubicin 60 mg/m2 IV on day 1, 8, 16 and 24; tab prednisolone 60 mg/m2/day × 28 days and Inj asparaginase 6000 units/m2 IM days 18, 19, 20, 21, 22, 23 and 24. He was also given intrathecal methotrexate 12.5 mg on days 1 and 8. The patient tolerated chemotherapy well, except that he developed an episode of gastroenteritis on 12th day of chemotherapy. He was rehydrated with IV fluids, and was administered Inj ciprofloxacin 400 mg b.d. and Inj Metronidazole 500 mg IV 8 hourly. For pneumocystis prophylaxis, he was given Co-trimoxazole 960 mg b.d 3 times a week. On the 20th day of the induction therapy, the complete blood counts showed correction of eosinophilia with a total leucocyte count of 8.1 × 109/l with 81% neutrophils, 12% lymphocytes, 05% eosinophils and 02% monocytes; Hb: 11.7 g/dl and platelet count: 170 × 109/l. His repeat bone marrow biopsy which was done on the 28th day of induction therapy showed active hematopoiesis with increase in eosinophil precursors and presence of 10% blasts in the marrow. Biochemical profile including serum urea, creatinine, electrolytes, bilirubin, ALT and uric acid were within normal limits. Serum LDH was 1254 U/ml (normal range: 250–500 u/ml). Due to his partial response to chemotherapy, re-induction therapy was given to him with the following drug combination: Inj vincristine 1.5 mg/m2 day 1, Inj daunorubicin 45 mg/m2 days 1 & 2; Inj etoposide 100 mg/m2 days 1–5; and Inj cytosine arabinoside 100 mg/m2 IV infusion 12 hourly days 1–5 and oral prednisolone 60 mg daily day 1–5 gradually to be tapered off in next two weeks. He was also given intrathecal Inj methotrexate 12.5 mg, on day 1 of second induction. The aforementioned chemotherapy regimen was repeated 4 weeks after the end of the cycle, when hematopoeitic recovery was adequate and the patient was stable. On 28th day of the intensification, the patient bone marrow was done which showed normal maturation of erythroid and myeloid series with less than 5% blasts, and normal number of megakaryocytes. The patient is scheduled for evaluation at Armed Forces Bone Marrow Transplant Centre, Rawalpindi, Pakistan for stem cell transplantation from matched sibling donor.


A 50-year-old man presented with a 4-week history of rectal bleeding with associated dyspnoea on exertion. His past medical history was unremarkable and there was no significant family history. He was a non-smoker and a social drinker. Physical examination including a digital rectal examination was unremarkable.
Initial investigations revealed a hypochromic, microcytic anaemia with a haemoglobin level of 8 g/dl and a ferritin level of 4 μg/L. Biochemical assessments of liver and renal functions were normal. Gastroduodenoscopy was normal and colonoscopy only revealed an incidental 2 mm benign tubular adenoma in the rectum.
Cross-sectional imaging was carried out. A MRI enteroclysis (Figure ) revealed a 22 mm peripherally enhancing soft tissue lesion in the right iliac fossa, and a CT enterography (Figure ) suggested that the mass lesion was arising either from the appendix or a Meckel's diverticulum.
A laparotomy was carried out via a grid iron incision. A Meckel's diverticulum was found to be adherent to the tip of the appendix in the right iliac fossa. There was a primary tumour arising from the Meckel's diverticulum and multiple sub-centimetre peritoneal deposits in the adjacent visceral peritoneum. These deposits were further distributed in the parietal peritoneum on the right side of the true pelvis and as tiny granular deposits in the greater omentum. A Meckel's diverticulectomy and en bloc appendicectomy was carried out and an omental deposit was sampled for histological assessment.
Gross examination of the specimen revealed a 40 mm diameter tumour arising from the mucosal aspect of the bowel wall of the Meckel's diverticulum. The tumour directly involved the peritoneal wall, and had invaded the serosal surface of the small bowel. The resection margins and the adhered appendix were tumour-free. A single omental deposit submitted separately was also involved by the tumour.
Histology of the tumour (Figure ) showed that it was composed of scattered small glandular structures and also scattered bizarre single tumour cells. The tumour cells expressed cytokeratin CK7, and CA 19.9. There was no expression of CK20, CDX2 or CEA. These findings support an upper gastrointestinal/pancreatico-biliary origin. Associated with the tumour were nests of cells with a pancreatic islet morphology, which expressed general neuroendocrine markers (CD56, synatophysin and chromogranin), and specific islet cell markers insulin and glucagon. Carcinoid markers serotonin and gastrin were negative. These appearances are consistent with the tumour being a pancreatic-type adenocarcinoma arising from ectopic pancreatic tissue in a Meckel's diverticulum.
The patient made good post-operative recovery. He was discharged following multi-disciplinary discussion among surgeons, radiologists and oncologists, with detailed out-patient follow-up arrangements in place, including an outpatient appointment with the pancreatic oncology specialist within a week of discharge.
Two weeks following discharge however, he developed food intolerance and small bowel obstruction was confirmed on CT scan. A second laparotomy was carried out and a dramatic increase in the volume of tumour was encountered (Figure ) with a significant increase in the size, number and extent of peritoneal deposits (Figure ). There was no single point of obstruction in the distal small bowel and in view of the encasement of distal ileum and proximal colon together with local mesenteric infiltration, an ileo-transverse colonic bypass was performed to relieve the obstruction.
Subsequent management was palliative and the rapid tumour progression continued until his death some 6 weeks after the initial operation.


A 30-year-old retrovirus positive male was referred for a bilateral slowly deteriorating vision over a six-month period. His CD4 and absolute lymphocyte counts at the time of referral were 120 cells × 106/L and 2300 cells/mm3, respectively. At the time of presentation, he was on a combination of trimethoprim and sulphamethoxazole. BCVA was counting fingers at 1 meter in both eyes. Old visual fields two months prior to his referral showed constriction in both eyes. The optic discs were pale in both eyes [Figs. and ]. There was no relative afferent pupillary defect. VEP showed decreased amplitude and increased latency in both eyes. At seven months follow-up, following HAART, his BCVA has improved to 20/60 and 20/40 in the right and left eyes respectively. The CD4 count at this follow-up was 210 cells × 106/L.


A 13-year-old retrovirus positive girl was referred to us for a routine ophthalmic evaluation. At the time of examination, she was unaware of the poor vision in the left eye. Her BCVA was 20/30 and counting fingers close to the face in the right eye and the left eye, respectively. Relative afferent pupillary defect was noted in the left eye. CD4 counts were 287 cells × 106/L. Mild optic disc pallor in the right eye and pale optic disc in the left eye was noted [Figs. and ]. Visual fields (HVF 30-2) in the right eye showed gross constriction [Figures and ]. After starting HAART, her BCVA at 20 months follow-up is 20/20 in the right eye and counting finger at 3 meters in the left eye. Serial visual fields also showed improvement in the right eye [Figures and ]. The CD4 count at this follow-up was 662 cells × 106/L.


A 31-year-old retrovirus positive male complained of decrease in vision in both eyes. His BCVA in both eyes was hand movements close to face. CD4 count was 189 cells × 106/L. Mild optic disc pallor was noted in both eyes. There was no relative afferent pupillary defect. Visual fields could not be done due to the poor vision. At six months follow-up after starting HAART, his BCVA is 20/200 in both eyes. The CD4 counts were not available at the last follow-up.


The patient is a 45-year-old man who was admitted for the first time in 1994 at the age of 31 for persistent headache. Work-up revealed a large left tentorial meningioma. He had no history of cranial radiation during childhood or clinical features of neurofibromatosis type I or II. He underwent gross total surgical resection. Pathologic evaluation, which was recently re-reviewed, showed an atypical meningioma with the following features: hypercellularity with sheets of monotonous meningothelial cells displaying a prominent mitotic activity with around 4 mitoses per 10 high power fields. In May of 1997, follow-up brain MRI revealed a recurrence in the vicinity of the original tumor bed. Surgery was performed with gross total tumor removal. Pathologic evaluation again showed meningioma with similar pathologic features. In September 1999, he developed multiple small tumor recurrences in the parietal, occipital and cerebellar lobes for which he underwent stereotactic radiosurgery (SRS) with excellent results on tumor control. In September 2001, the patient developed additional recurrent lesions in multiple sites in the infratentorial, retroclival, left optic nerve sheet, and foramen magnum regions.
He was again treated by stereotactic radiosurgery with good tumor control defined as a complete disappearance or progressive decrease in lesion size. In June 2003, he received further SRS treatment to new cerebellar, premedullary and craniocervical junction lesions. In February 2004, he developed numerous lesions outside previously treated sites and was given whole brain radiation therapy (WBRT) of 36 Gy as a palliative therapy because of the multiplicity and the progression of the brain lesions. Surprisingly many of the small lesions disappeared after WBRT and the patient remained asymptomatic until August 2005 when he developed left facial numbness. Brain MR imaging at that time showed a recurrent lesion in the left cerebellopontine (CP) angle, an area that was previously treated by SRS and WBRT. He was given 10 sessions of stereotactic radiotherapy (30 Gy in 10 fractions) and achieved a good partial response but this lesion grew back and caused progressive left facial numbness due to left Vth nerve compression. This was treated by another craniotomy and surgical resection. Histopathologic examination showed meningioma with the same pathologic features and additional elements like the presence of foci of geographic necrosis and a hemangiopericytomatous pattern of vasculature (Figure ). Mitotic count was now up to five per ten high power fields and Ki-67 labeling index was up to 15% (Figure ). The tumor was focally positive for epithelial membrane antigen (EMA) and negative for CD31 and CD34. The lack of CD34 immunostaining excluded the possibility of hemangiopericytoma or solitary fibrous tumor of the meninges. Occasional cells were weakly positive for S-100 protein. In July 2007, follow-up MRI showed tumor progression at the same CP angle site for which a redo SRS treatment was debated and finally delivered without significant acute toxicity. Of note, the question of chemotherapy was raised many times but the patient refused to receive any systemic therapy.
In November 2007 and because of persistent low back pain, the patient underwent MRI of the spine and pelvis. These showed two large masses in the left and right sacroiliac and gluteus muscle regions measuring 11 × 9 cm and 8 × 7 cm, respectively, causing bone destruction of the left sacral wing with extension in the left sacral neural foramina (Figure ). Surgical biopsy was performed and this revealed metastatic atypical meningioma, with similar characteristics to its intracranial counterparts. Further work-up included CT scan of the abdomen which revealed large bilateral renal metastases (Figure ). CT of the chest was negative. The patient was evaluated by medical oncology but declined systemic chemotherapy. Brain MRI showed no disease progression. He is now receiving palliative care for pain control.


A female patient 49-year-old, cook. First discreet skin changes, with increased compactness and hyperpigmentation of the right side of the face, were noticed about 4 years ago by the patient. Astringing skin sensation and periodic, weakly intensified pains in the right side of the face and head, treated as a migraine, accompanied the appearance of the changes. The patient did not go through any injuries and did not complain about other neurological aliments. The skin symptoms were disregarded by the patient and were treated as a variant of a regular condition (?!). Because of that the patient was not diagnosed or treated. Nobody from the patient's surroundings and the general practitioners noticed the progressing face asymmetry. The patient is not suffering from any other chronic diseases and does not take any medicine on a regular basis. The family history towards autoimmunological and neurological diseases was negative. In July 2008 the patient was admitted to our Clinic with suspected hemifacial atrophy ("en coup de sabre" scleroderma?).
Clinically, in admission to the hospital, strongly distinct face asymmetry could be observed. The right side of the face was clearly smaller. The mandible angle was lifted and smoothed. The lip redness on the affected side became thin and lifted. The cheek was sunken. The eyeball was situated deeper. The skin surrounding the changes was more coherent, thin and strongly seal-colored. There were linearly arranged, oval, sunken baldness focuses on the head's hairy skin, near the right temple. Skin surrounding these focuses was unchanged. The mucous and genitals membranes and nail plates were normal. The peripheral lymph glands – not enlarged (fig. ,).
In the performed laboratory tests (morphology with smear, fasting glucoses level, glycemia profile, AspAT, AlAT, bilirubin, GGTP, alkaline phosphatase, creatinine, urea, uric acid, protein with electrophoresis, ASO, Latex-R, Waaler-Rose test, VDRL, general urinalysis with culture) no aberrations were found.
Antigens against Borrelia burgdorferi in IgM class with a 1,26 titre (positive, norm up to 1,1) were found in blood serum. IgG antibodied – negative. Penicillin test – positive.
Histopathological examination of the right cheek change revealed traits of fibrosis, collagen fibers thickening, skin edema and skin adnexa and vessels atrophy, without an inflammatory infiltration. Image examination – x-ray of the chest, upper part of the digestive tract, abdominal cavity USG were all normal. Capillaroscopy – within the norm.
Head CT performed in a spiral technique, in transverse section, in forehead and fibular reconstructions, before and after the intravenous administration of contrast medium revealed only a bone septum on the right side of the sphenoidal sinus and the mucous membrane thickening within its area. The encephalon image – normal. NMR of the head – without pathology. Electromyography (the muscles end the nerves of the face: the right and left roundabout muscle of the mouth, the right and left facial nerve) – in the right roundabout muscle of the mouth the small impoverishment of the effort record. Conducition in both facial nerves without pathology. With an indirect, immunofluorescent method on Hep2 cells, no ANA antigen antibodies were found. Mycological examination on skin changes was also negative. Laryngological, dental consultation have not shown any abnormalities.
Neurological examination confirmed one-sided headaches in patient's anamnesis, without any focal symptoms of CNS damages. Suggested performing head CT and NMR and EMG (results a.b.).
During the patient's stay at the Clinic, cefuroxym (Plixym) in a dose of 2 × 1,5 g iv for 10 days was applied, continuing the treatment with oral cefuroxym (Zinnat) 2 × 250 mg for 4 weeks. Emollients and low-energy laser was applied locally (15 procedures). The patient was sent to the Infectious Diseases Outpatient Clinic in order to have a Borrelia burgdorferi infection confirmed with the use of Western-blot method (positive). Currently, the patient is under supervision of Dermatological Outpatient Clinic in order to continue the treatment and a possible committal to plastic surgery treatment after the pathological process is over.


Case 1: A 48-year-old Caucasian man presented to our institution in February 2004 with a short-segment bulbar urethral stricture. No previous history of trauma or sexually transmitted disease was reported at the time of presentation.
We initially performed urethrotomy using the Sachse technique without complications. Two years later, the patient complained again of decreasing urine stream and frequency.
As shown in Figure , maximal flow was 9.1 ml/sec (micturition volume 518 ml, micturition time 88 seconds).
Retrograde urethrography revealed a recurrent urethral stricture, as shown in Figure .


Case 2: Thirty-eight years before presentation, this 55-year-old Caucasian man had undergone an open urethral reconstruction after traumatic urethral damage. A recurrent stricture was treated with urethrotomy using a laser technique in 2006. A secondary recurrent urethral stricture developed during short-term follow up, as shown in Figure .
Uroflowmetry revealed a maximal flow of 5.9 ml/second (micturition volume 489 ml, micturition time 120.6 seconds).
In both patients, open surgery urethral reconstruction using Surgisis® as onlay patch was performed in the dorsosacral position. The urethra was exposed and incised. We identified a 3 cm long stricture in our first patient, and a 4 cm long stricture in our second patient.
End-to-end anastomisis of the urethra was not possible in either case. After incision of the urethra 0.5 cm distally and proximally of the respective stricture, a Surgisis® patch was cut and inserted, in the same way as a buccal mucosal free graft would be inserted, using a 5 × 0 monofile thread with longitudinal splines, over a 16-Foley catheter.
The procedure included insertion of a suprapubic cystostomy. The operation time was 144 minutes for the first patient. Because of the complicated preparation, operation time was 162 minutes for the second patien.. No perioperative complications were seen in either case. The transurethral catheter was removed in both patients on day seven postoperatively, and both patients were treated with ciprofloxacin 2 × 500 mg postoperatively for eight days.
On day 24 after the operation, retrograde urethrography revealed good healing in both patients (Figures and ). The percutanous cystostomy catheter was removed on day 25 in both patients.
Postoperative uroflowmetry performed on the first patient on day 25 revealed a maximal uroflow of 49.1 ml/sec (micturition volume 539 ml, micturition time 21.4 seconds), as shown in Figure . The same procedure performed on the second patient showed a maximal uroflow of 20.6 ml/second (micturition volume 563 ml, micturition time 64 seconds), as shown in Figure .


A self-sponsored (that is, uninsured) 36-year-old man diagnosed with chronic-phase (CP) CML (Sokal score 1.22 [low risk <0.8, high risk >1.2] and Hasford score 1158.6 [low risk <780, moderate 780 to 1480, high risk >1480]) had received imatinib 400 mg per day since the beginning of January 2004. After approximately 10 months of therapy, full hematologic and cytogenetic remission, then major molecular remission had been achieved with a %BCR-ABL/ABL International Scale (IS) score of about 0.01 compared to an initial value of 9. This status had been maintained for approximately three years. In January 2007, his BCR-ABL scored negative by nested RT-PCR.
Subsequently, the patient sought medical insurance and was switched by the insurer to the copy product imatib, at the same dose of 400 mg per day. In March 2007, after approximately three months of therapy with the 'copy' imatib, and despite a claimed compliance to the prescribed regimen, substantial hematologic changes were noted in the form of anemia (hemoglobin 9 g/dL), neutropenia (WBC 2300/mm3 with an absolute neutrophil count (ANC) of below 1000), thrombocytopenia (platelets 101,000/mm3) and loss of cytogenetic and molecular responses. Cytogenetic and molecular assessments demonstrated a 'positive' Philadelphia chromosome (22% Ph+ cells) and a %BCR-ABL/ABL ratio of 3, consistent with a disease relapse and a probable hematological toxicity to the agent. The spleen was still impalpable and the Sokal score was 1.16. Tests for tyrosine kinase mutations were not performed.
In May 2007, the patient resumed imatinib at a daily dose of 600 mg per day. In July 2007, after approximately two months of therapy with imatinib, laboratory values revealed a return to a full hematologic and cytogenetic response and in November 2007, after six months of therapy, the patient achieved a %BCR-ABL/ABL score of 0.01. Changes in hematologic laboratory parameters at baseline, following the change to the copy product with a loss of response and subsequent return to treatment with imatinib and reinstatement of response, are summarized in Table .


A 90-years-old Caucasian man presented for prostatectomy. His co-morbidities included atrial fibrillation, cardiac failure, ischaemic heart disease and hypertension, but he had no history of neuropathy. Medications included digoxin, lisinopril, bendrofluazide and nitrates. Laboratory parameters were normal. He made an informed choice of regional anaesthesia. Standard perioperative monitoring included electrocardiography, noninvasive blood pressure and pulse oximetry. Combined spinal/epidural anaesthesia was performed aseptically at the L3/4 space using a 16 G Tuohy needle and a 26 G Whitacre needle. Spinal anaesthesia was established with 2 ml of heavy 0.5% bupivacaine and an epidural catheter inserted for postoperative analgesia. The regional anaesthesia procedure was uneventful. Adequate motor and sensory block was achieved at 10 minutes. Sensory block to the T8 dermatome was confirmed by loss of cold sensation. An initial attempt at lithotomy positioning was associated with right leg myoclonus, which resolved on placing the patient supine. After 10 minutes, repeat lithotomy positioning produced similar myoclonus. Therefore, an epidural dose of 10 ml of 0.25% bupivacaine was administered, with complete resolution of myoclonus after another 10 minutes. Surgery and follow-up after 30 days were uneventful.


A 64-years-old Caucasian woman presented for ureterotomy. Her co-morbidities included bronchitis, coronary artery disease and diabetes mellitus, but she had no history of neuropathy. Medications included salbutamol, nitrates and metformin. The patient made an informed choice of spinal anaesthesia. Standard perioperative monitoring was used. Spinal anaesthesia was performed aseptically at the L3/4 space using a 26 G Whitacre needle and 2 ml of heavy 0.5% bupivacaine. The spinal anaesthesia procedure was uneventful. Adequate motor and sensory block was achieved at five minutes. Sensory block up to the T6 dermatome was confirmed by loss of cold sensation. The intraoperative course was uneventful. After arriving back on the ward 60 minutes after instituting spinal anaesthesia, the patient developed lower-limb myoclonus, lasting less than three minutes and resolving spontaneously. There was no recurrence of myoclonus and no sequelae. Subsequent spinal block with bupivacaine three months later was uneventful.


A 53-years-old Caucasian woman presented for pelvic surgery. Her co-morbidities included hypertension and rheumatoid arthritis but no neuropathy. Medications included oestradiol, bendrofluazide and dexamethasone. Previous regional block and general anaesthesia were uneventful. Serum vitamin B12 level was 191 ng/L (normal range 200-900 ng/L), but other laboratory parameters were normal. The patient made an informed choice of spinal anaesthesia. Standard perioperative monitoring was used. Spinal block was performed aseptically at the L3/4 spinal space with a 25 G Whitacre needle and 2.5 ml of heavy 0.5% bupivacaine plus diamorphine 300 mcg. The spinal block procedure was uneventful. Adequate motor and sensory block was achieved at 5 minutes. Sensory block up to the T6 dermatome was confirmed by loss of cold sensation. The intraoperative course was uneventful. However, after returning to the ward, about 90 minutes after instituting spinal block, she developed lower-limb myoclonus. The myoclonus lasted one hour and was treated with intravenous midazolam 4 mg. Subsequent follow-up for two weeks revealed no sequelae and no recurrence of myoclonus.


A 67-years-old Caucasian man presented for refashioning of a left below-knee amputation stump. His co-morbidities included diabetes, cardiovascular disease, peripheral neuropathy, obesity and asthma. Medications included insulin, amlodipine, lisinopril, gabapentin and salbutamol. Previous regional block and general anaesthesia were uneventful. The patient made an informed choice of spinal anaesthesia. Standard perioperative monitoring was used. Spinal block was performed aseptically at the L4/5 spinal space with a 25 G Whitacre needle and 2.5 ml of heavy 0.5% bupivacaine plus diamorphine 300 mcg. The spinal block procedure was uneventful. Adequate motor and sensory block was achieved at five minutes. Adequate sensory block up to the T8 dermatome was confirmed by loss of cold sensation. The intraoperative course was uneventful. However, at the end of surgery, about 60 minutes after the spinal blockade, the patient complained of repetitive muscle spasm in the absent amputated limb. The phantom spasm was distressful to the patient and was promptly treated with intravenous midazolam 5 mg. There was no recurrence of myoclonus and no sequelae.


A 34-year-old G4P3 Caucasian woman was followed up antenatally because of a stillbirth in her previous pregnancy. She had had mild pre-eclampsia in her first pregnancy and a Caesarean section was carried out after unsuccessful induction of labor. Her second pregnancy and delivery were uneventful. The reason for the stillbirth in her third pregnancy was found to be an umbilical cord knot.
In the pregnancy reported here, our patient had polymorphic eruption of pregnancy (PEP) from 26 weeks' gestation and had three separate courses of oral steroids. Anti-D-antibodies were also found to be increased but in quantitative analyses their concentration, however, remained low. She was hospitalized once for a short period in late pregnancy because of an abnormal fetal heart rate recording.
At 36 weeks' gestation, a hypoechoic, 3.6 × 4.2 cm rounded mass was noted within the placenta on ultrasound examination (Figure ). An ultrasound scan with umbilical artery Doppler measurement after 28 weeks' gestation was normal and it is likely that the leiomyoma had gone unnoticed probably because no special attention had been paid to the placenta on that occasion. Another explanation could be that the leiomyoma grew very rapidly in the third trimester of pregnancy and it was too small to draw appropriate attention in earlier scans.
She had induction of labor due to worsening of PEP at 38 weeks' gestation. A viable male infant weighing 3330 g was delivered with Apgar scores of 9 at one minute and 9 at five minutes. The placenta was removed without difficulty.
A round-shaped nodule was noted on the maternal surface of the otherwise normal placenta. The size of the nodule was 4 × 4 × 3 cm. It had a pale cut surface without hemorrhage, necrosis or calcification (Figure ).
Histologically, the nodule was composed of bundles of smooth muscle cells. Nuclei were round or oval shaped and there were no atypical features or mitotic activity (Figure ). No attached myometrium was identified.
Immunohistochemistry was positive for the smooth muscle actin antigen (Neomarkers, 1:500). Factor VIII related antigen (Dako, 1:750) and CD34 (Becton-Dickinson 1:20) marked only the endothelial cells, whereas cytokeratin of low molecular weight (Becton-Dickinson, 1:20), placental alkaline phosphatase (Dako 1:20) and desmin (Biogenex, 1:50) were negative. The method used for labeling was streptavidin-biotin. The tumor cells were positive for progesterone receptors but negative for estrogen receptors which is typical for leiomyomas during pregnancy [].
Chromosomes of the tumor were studied from paraffin sections by the fluorescence in situ hybridization technique with X- and Y-chromosome-specific probes and the tumor was found to carry XX chromosomes.


A 29-year-old Caucasian woman had a varus intertrochanteric osteotomy with trochanteric advancement for an old malunited femoral neck fracture. The femoral neck fracture was sustained in a childhood injury and was treated conservatively. The patient underwent reattachment of the greater trochanter for a failed trochanteric fixation approximately 4 weeks after her initial operation. She was discharged 2 days after the second procedure. Approximately 5 weeks later, the general practitioner referred her to the vascular surgeons with painless discolouration of the right leg. Clinical examination revealed a discoloured right foot associated with mild swelling and several small blisters on her toes. The most prominent feature was that the right foot exhibited bluish discolouration which evidently subsided to near-normal colour on elevation (Figure ). The femoral, popliteal, dorsalis pedis and posterior tibialis pulses were present and normal.
Handheld Doppler examination demonstrated a relative decrease in the audible quality of the biphasic pulse when compared to the normal side. Duplex scan of the right lower limb excluded the possibility of any superficial or deep venous thrombosis. The patient was commenced on 50% weight bearing status and was discharged home. A recent follow-up demonstrated significant improvement in symptoms since commencement of weight bearing status.


A 20-year-old Caucasian woman who presented with symptoms of right hip impingement underwent open debridement and repair of a torn acetabular labrum. The patient was discharged on the 5th postoperative day following an uneventful recovery period. She was to remain non-weight bearing for 6 weeks. Ten days following discharge, she presented to the clinic complaining of her right foot going blue and cold and with the complete absence of pain. The discolouration occurred when the limb was in a dependent position. Clinically, all peripheral pulses were present and normal. The patient was reviewed by a vascular surgeon who excluded the possibility of arterial insufficiency and deep venous thrombosis.
The patient was discharged with the advice to commence on weight bearing of the operated hip. In the follow-up clinic 5 months later, she was found to have complete resolution of her vascular symptoms.


A 60-year-old man with a history of hypertension, congestive heart failure, dyslipidemia and gastro-esophageal reflux disease was admitted for right shoulder rotator cuff tear. His medications included spironolactone 25 mg once daily, aspirin 325 mg once daily, pantoprazole 40 mg once daily, olmesartan 40 mg once daily, colesevelam 625 mg three times a day, furosemide 20 mg once daily and ezetimibe 10 mg once daily. The patient then underwent right shoulder arthroscopy and rotator cuff repair.
The postoperative course was uneventful until three weeks later, when he developed pain, swelling and a purulent drainage from his right shoulder. The patient returned to the emergency department and an arthroscopic irrigation and drainage was performed. Intraoperative fluid was sent for gram stain, culture and sensitivity, which later revealed the presence of Methicillin susceptible staphylococcus aureus, vancomycin-sensitive Enterococcus spp. and Serratia marcescens.
The patient had no known allergies. After reviewing antimicrobial susceptibility, he was started on vancomycin 1500 mgs intravenously (IV) every 12 hours (to treat both Staphylococcus aureus and Enterococcus spp) and ciprofloxacin 750 mgs by oral induction every 12 hours. The patient's vancomycin peak level was at 36.2 mcg/ml, and the trough level was at 14.7 mcg/ml after the third dose. The patient's shoulder pain and swelling improved after antibiotic treatment. He was discharged and allowed to go home on IV vancomycin and oral ciprofloxacin. His platelet count on the day he was started on vancomycin therapy was 253 × 103/mm3 (the normal range is 150 to 400 × 103/mm3). His complete blood count, vancomycin peak and trough levels were monitored in the infectious disease clinic. The platelet count was 231 × 103/mm3 in the first week and 272 × 103/mm3 in the second week. The platelet count was 6 × 103/mm3 in the third week after treatment.
The patient was admitted for further work-up of thrombocytopenia. In addition to vancomycin and ciprofloxacin, he received heparin flushes (50 units daily) for three weeks to maintain potency of the peripherally inserted central catheter (PICC). In the emergency department, his vital signs were reported as 37.4 degrees Celsius temperature, pulse of 88 per minute, respiratory rate of 18 per minute and blood pressure of 130/80 mmHg. Further examination revealed the presence of extensive petechial hemorrhages on both of his lower extremities. Peripheral pulses were present and equal in all extremities. A repeat platelet count in the emergency department yielded a result of 9 × 103/mm3.
On the first day after admission, administration of aspirin, vancomycin and heparin flushes of the PICC on the patient were discontinued. As part of his thrombocytopenia work-up, blood cultures, a disseminated intravascular coagulation panel and heparin-induced antiplatelet antibodies were obtained. Given the patient's presentation, vancomycin-induced anti-platelet antibodies were also ordered - this was done at the Blood Center of the Wisconsin Platelet and Neutrophil Immunology Laboratory, using immunofluorescence flow cytometry. These results were reviewed three days after the blood specimen was drawn. During this time, the patient received one unit of platelet transfusion, which raised his platelet count from 9 × 103/mm3 to 28 × 103/mm3. On the second day, the patient was given another unit of platelet transfusion, which further elevated his platelet count to 60 × 103/mm3. By the third day, his platelet count had increased to 271 × 103/mm3. He was discharged home on an initial dose of 100 mg intravenous tigecycline, followed by 50 mg IV every 12 hours. The patient continued with a follow-up at the infectious disease clinic and his platelet count was already at 344 × 103/mm3 after one week and 338 × 103 /mm3 after two weeks.
The differential diagnoses considered were: 1) disseminated intravascular coagulopathy; 2) heparin-induced thrombocytopenia (HIT); and 3) vancomycin-induced thrombocytopenia (VIT). Disseminated intravascular coagulopathy was ruled out because his prothombin time, fibrinogen level, D-dimer level and peripheral smear were all normal. Blood cultures also showed no growth. HIT was excluded by the absence of heparin-induced anti-platelet antibodies. A vancomycin-induced anti-platelet antibody test revealed IgG-positive antibodies detected in the presence of vancomycin. IgM antibodies were negative.