A 67-year-old Caucasian female with severe COPD who was receiving continuous oxygen treatment in addition to multiple bronchodilator and ant-inflammatory medications including fluticasone/salmeterol (Advair), tiotropium-bromide (Spiriva), ipratropium-bromide/albuterol-sulfate (DuoNeb) and budesonide (Pulmicort), presented to the hospital with sudden onset substernal chest pressure at rest which resolved spontaneously. She has no history of coronary artery disease, but limited cardiovascular risk factors including age and hypertension. Her physical examination was unremarkable with the exception of elevated blood pressure (158/92 mmHg). Serial electrocardiogram and cardiac enzymes during hospital course were within normal limits. For that reason, DST was scheduled. The patient received albuterol inhaler treatment 30 minutes prior to DST in addition to her scheduled bronchodilators as above. She underwent pharmacological stress test with dobutamine infusion at a maximum rate of 40 mcg/kg/min, a total dose of 28 mg, and atropine 0.2 mg. She reached to target heart rate with dobutamine/atropine combination. Blood pressure response was normal. During recovery the patient developed severe substernal chest pain that was similar to her prior pain and radiated to jaw. She appeared diaphoretic, pale and sick. Concurrent electrocardiogram showed 1.5 mm STSE in lead II, III, aVF, V3, V4 and V5 ( & ). There was only minimal improvement of chest pain with sublingual nitroglycerine. ST-segment remained elevated. Thus the patient underwent urgent cardiac catheterization. Coronary angiogram revealed no obstructive epicardial coronary artery disease ( & ). Chest pain resolved during catheterization while she was receiving nitroglycerine infusion and morphine. Thus our patient likely manifested coronary spasm with chest pain and STSE in the setting of albuterol and dobutamine combination. There was no evidence of myocardial necrosis based on biomarkers. The patient’s hospital course was uncomplicated. She remained chest pain free with medical management including long acting nitroglycerine.


An 11 year old right-handed girl with a history of a bilateral tumour in the neck was referred to our hospital for a second opinion. She had previously been examined at another hospital due to a tumour on the right side. Diagnosis was based on a conventional X-ray and a biopsy which showed bone tissue. No further treatment was done. We had no information available of the diagnostic and treatment considerations from that hospital. The girl also had symptoms such as paraesthesia and pain in the middle ring and little fingers, particularly on the right side, often during night time. The history of the patient included fatigue and pain while writing and working on a computer. She had problems carrying things in the hands, especially when the arm was pulled in the axial direction. Lifting the arms above the shoulder plane elicited similar symptoms in the fingers on the right side. She experienced intolerance to cold. Range of motion in the shoulder, elbow, wrist and fingers was normal, but she expressed pain in the three ulnar fingers during abduction above 90 degrees. She had impaired internal rotation/adduction/extension ("hand on the back") on the right side. Examination showed palpable cervical ribs bilaterally, where percussion in the area elicited symptoms in the three ulnar fingers. Subjectively, she expressed a somewhat impaired sensibility in the little fingers, particularly on the right side. The strength of the first dorsal interosseous muscle and the other ulnar nerve innervated muscles was equal (no atrophy in the extremity) to the contralateral side, but she had a positive Froment's sign. Two-point discrimination (2-PD) was 2-3 mm in all fingers. A normal pulse in the radial artery was noted even with the arm lifted. Assisted hand assessment (AHA) showed no abnormality. Isometric and dynamic tests of the right hand in a work stimulator (BTE Primus) showed 8-10% lower values than in the left hand. Electrophysiological investigation showed no abnormalities except a slightly increased F-wave (latency 18.9 ms; upper border 18.1). No EMG recordings were done from individual intrinsic muscles of the hand. Radiographs and CT of the cervical spine showed bilateral cervical ribs articulating against a bone prominence on the cranial surface of the first rib (Fig. ). The cervical rib with the "pseudoarthrotic" bony formation slightly dislocated the lower part of the brachial plexus ventrally. On MRI performed with the arms lifted, the space between the cervical rib, the bone formation and the clavicle decreased (Fig. ). MRI also showed fibrous tissue formation around the pseudoarthrotic bone formation. There were no similar findings of the brachial plexus on the left side despite the presence of a cervical rib.
When the patient was 12 years old, the cervical rib and the brachial plexus on the right side was explored supraclavicularly. The inferior trunk was riding over the cervical rib while the subclavian artery was located ventral to the cervical rib and the bone formation (Fig. ). The artery was not affected. The entire cervical rib including periosteum and fibrotic bands was resected. Thereafter, no anatomical structures disturbed the lower trunk. The postoperative events were uncomplicated, except initial pain during deep breath (conventional X-ray of the lungs showed no pathological findings). She was treated with the anti-inflammatory drug diclofenac to theoretically reduce new bone formation.
At regular follow-up at 1, 3, 6 and 12 months, she had no remaining symptoms from the lower trunk of the brachial plexus, except a slight allodynia around the scar during the first six months. She had no symptoms during full abduction. Cold intolerance was markedly reduced (none or insignificant) and a Froment's sign was not found. At one year follow-up, she had full range of motion and no impairment of strength compared to the contralateral side. Endurance, isometric and dynamic grip strength showed 9-18% higher values than on the left side. The girl was pleased with the surgical procedure. She continued her leisure activities in gymnastics.


A 16-year old right-handed girl with paraesthesia in the left arm, initially occurring periodically and later more frequent, since the age of 12 was referred to our hospital due to these symptoms. X-ray showed a cervical rib on the left side and a minor one on the right side (no symptoms on right side; Fig. ). She had similar symptoms as in Case One, such as paraesthesia and numbness in the three ulnar fingers of the left hand when carrying things in the hand, when a pressure was applied supraclavicularly (e.g. carrying a backpack) or when working with the hands above the plane of the shoulder. Percussion of the area of the palpable cervical rib on the left side elicited symptoms in the three ulnar fingers and "hands up tests" exaggerated the symptoms in the same fingers. The radial pulse was normal in all positions of the arm. She had good strength in all muscles of the upper extremity and a normal sensibility in the hand. Isometric test and endurance of grip showed 32% and 62%, respectively and weakness in the left hand compared to the right side (BTE Primus work simulator). Isometric test of the flexion in the left shoulder and endurance showed 16% and 54%, respectively lower values, compared to the right side. Electrophysiological examination showed no abnormalities. MRI showed a 6 cm long cervical rib from C7 on the left side, which articulated against a cranially oriented bony process from the first rib where the articulation was bulky (Fig. ). The left brachial plexus was slightly lifted up by the skeletal abnormality. On the asymptomatic right side a 2.5 cm long cervical rib was found, which had no contact with the brachial plexus.
The brachial plexus and the cervical rib of the patient were explored when the girl was 17 years. The brachial plexus was distorted at and adhered to the ventral edge of the cervical rib and the bony process from the first rib (Fig. ). The main part of the cervical rib including the bone process from the first rib was resected after the lower trunk was lifted up (Fig. ). The subclavian artery was not impinged by the bone formation. The direct postoperative events were without problems, but later she was investigated at the Department of Infectious Diseases due to fever of unknown origin. No cause of the fever was found and later she recovered completely. She was followed regularly as with Case One.
At one year follow-up she had no symptoms in the hand. The preoperative symptoms had disappeared although she still experienced a feeling of impaired strength in the left arm. She had full range of motion and it was not possible to provoke any paraesthesia. Tests of fine motor activity in the hand (Crawford pins and sleeve and Minnesota picking test) showed improved values. Tests in the work simulator showed improvement [isometric test 5% weakness (preoperatively 32%), endurance 54% weaker (preoperatively 62%), isometric test of extension with elevated arm 4% weaker than the right side (preoperatively 16%), endurance of flexion/extension with elevated arm similar value on the right side (preoperative 54% weaker)]. MRI follow-up 11 months after surgery revealed no occurrence of the resected cervical rib. There were no differences compared to the two CT-scans done at three and six months after surgery (done for other reasons; fever investigation and a fall from a horse). The patient was pleased with the surgery. She continued with her previous studies and leisure activities without restriction.


A 48-year-old male presented with progressively worsening pain in the thoracic spine radiating along the right eighth rib of four weeks duration and spastic paraplegia with bladder involvement of two weeks duration. He had undergone intralesional curettage for a progressively enlarging mass in the right eighth rib two years ago. The patient had received anti-echinococcus chemotherapy for six months. The radiographs revealed a residual cyst in the eighth rib with intrathoracic extension []. The vertebral column was not involved. The MRI revealed three separate well-circumscribed cysts. The residual extraspinal intrathoracic cyst had enlarged on the under-surface of the rib cage extending from the lower border of the seventh to the upper border of the tenth rib []. The cyst measured 5 cm in diameter. The cyst was multiloculated and hyperintense on T2 weighted images with a hypointense well-demarcated cyst wall. It had involved the rib head but the pedicle of the T8 vertebra was uninvolved. Two unilocular cysts measuring 2 cm in diameter were located at the level of the T8 and T9 vertebrae. One of these cysts was intraspinal and extradural and produced compression of the spinal cord while the other cyst was located outside the spinal canal in relation to the lamina of the T9 vertebra []. The eosinophil count, erythrocyte sedimentation rate and Casoni's test were within normal limits.
Using a right-sided posterior paramedian curvilinear incision [], a myocutaneous flap was raised towards the midline to expose the seventh to the tenth ribs from the posterior axillary line to their respective costo-vertebral junctions. The seventh, eighth, ninth and tenth ribs were extraperiosteally resected medially at the costotransverse junction and laterally beyond the lateral most extent of the cyst wall. The parietal pleura were incised at the periphery and chlorhexidine packs were placed inside the thoracic cavity to isolate the cyst. The cyst fluid was aspirated and 10 cc of hypertonic saline was injected into the cyst for its scolicidal effect. The cyst was gently separated from the lateral to the medial side by blunt dissection. The lateral part of the T8 pedicle was osteotomised along with the adjoining rib-head and the entire cyst excised. The T9 spinal cyst was excised en masse during T8 and T9 laminectomy. The T8 intraspinal cyst was gently lifted off the dura to achieve decompression of the thoracic cord. There was no communication between the intraspinal and extraspinal cysts. A single left ipsilateral rod and pedicle screw was used to stabilize the spine along with posterior bone grafting [].
The patient reached full functional status by six months and received albendazole for 12 months. Rod loosening was noticed after four years which was removed subsequently. Alignment of the thoracic spine was maintained and did not show any signs of collapse on follow-up radiographs. Magnetic resonance imaging (MRI) done at four years showed resolution of the cyst [].


A 53-year-old Caucasian woman presented with diffuse muscle weakness and pain. Past medical history was notable for gastroesophageal reflux disease, diverticulitis, intermittent lower back pain, and osteopenia. She took one dose of Risedronate, 35 mg for osteopenia. Within 15 hours, she developed severe aching muscle pain (10/10 on Visual Analog Scale) throughout the body with fevers, sweats, chills, tingling throughout the body, and loss of bladder control. In the Emergency Room, she was told she had a drug reaction from Risedronate and prescribed oxycontin for pain management. Evaluation included normal complete blood counts and electrolytes. Potassium and creatinine were mildly low at 3.4 mEq/L, and 0.5 mg/dL, respectively. The CO2 was elevated at 31.4 mEq/L (normal range 22.0–29.0 mEq/L), Calcium, creatine phosphokinase (CPK) and ESR were normal. Neurological examination in the emergency room was notable for decreased strength in proximal lower extremities graded at 4−/5 using the Medical Research Council (MRC) scale. Deep tendon reflexes were normal. The only medications patient was taking at the time of the event were Nexium 40 mg per day and Posture D vitamins.
Over the next three weeks, she developed severe muscle cramps, bilateral lower extremity edema, and progressive muscle weakness and could not raise her arms above her head. She had several falls and became wheelchair bound. Diffuse pain (8/10 on VAS) in the bones and muscles of her limbs and back was present.
She underwent electromyography (EMG) testing which demonstrated mild bilateral median neuropathies bilaterally and active denervation (fibrillations and positive sharp waves) only in the right deltoid muscle. MRI of cervical spine was normal. Methylpresnisolone, 24 mg with a six day taper was prescribed without clinical benefit.
One month post dose, she had proximal weakness in the upper and lower extremities with bilateral deltoid graded at MRC 3−/5, hip flexors at 3−/5, and hamstrings at 4/5. Proximal muscle weakness was evident on gait testing. She was admitted to an outside hospital. During her stay, the work up for following differential diagnosis was done: multiple myeloma, Gullian-Barré syndrome, chronic inflammatory demyelinating polyneuropathy. Systemic Lupus Erythematosus, Waldestrom's macroglobulinemia, Cushing disease, myasthenia gravis, hyperparathyroidism, and polymyalgia rheumatica. Work up included an MRI of brain with and without gadolinium, a lumbar puncture for cerebrospinal fluid analysis, and a whole body positron emission tomography scan, all which were normal. MRI of the muscle was not performed. Results of a second EMG study were similar to the previous test with the exception that the active denervation changes in right deltoid were absent. A muscle biopsy was considered at the beginning of the hospitalization, but was deferred because her aldolase and repeat CPK tests were normal. She started a program of physical and occupational therapy, and acupuncture.
The pain and weakness began to slowly subside approximately four months after the dose. By six months postdose, she improved to the point that she no longer needed a cane to ambulate. One year postdose, she reports easy fatigability, severe pain (7/10 on VAS) in the left biceps and back, and mild weakness in her legs. She has difficulty going up the stairs and standing from a lying position. Neurological examination was notable for mild proximal lower extremity and hand weakness with MRC grades of 4+ iliopsoas, 5− abductor pollicis brevis, 4+ abductor digiti minimi, and 4+ first dorsal interosseous bilaterally with some weakness on the finger extensions. No atrophy or fasciculations were seen.
Two and a half years after taking one pill of Risedronate, the patient continues to improve. She reports some weakness of her shoulders, difficulty carrying heavy things, and some shortness of breath with exertion. Recently, she underwent quantitative muscle testing (QMT) to asses her muscle weakness []. Isometric strength of ten muscle groups was measured bilaterally. Her percent of predicted strength values indicated extensive weakness throughout, with muscle strength of different muscle groups ranging from 31.5% to 76.4%, with the mean strength 50.5%.
A MedWatch form was filed with the FDA.


A 15 year old girl presented with a recurrence of ventricular tachycardia after having been externally cardioverted twice in a 24 hour period at a referring hospital. She had been diagnosed with a cardiac hemangioma when a murmur was noted at 5 years of age on a routine physical exam. Echocardiogram at that time showed a large mass in the RVOT with mild obstruction. Endomyocardial biopsy showed a non-specific vascular proliferation. A histopathologic diagnosis was confirmed when the tumor was resected shortly after the initial presentation. The tumor was infiltrative and encroached on the RVOT free wall and tricuspid valve, and hence was only incompletely resected. She continued to do well, and at 10 years of age, non-sustained polymorphic VT was noted on a routine screening Holter monitor. An EP study was performed and ventricular double extrastimuli (600:290:270) provoked sustained polymorphic VT. At that time, a transvenous single-chamber internal cardioverter defibrillator (ICD) was placed for primary prevention and the patient was started on Nadolol.
She remained asymptomatic for the next five years. Frequent episodes of non-sustained polymorphic VT were noted, but there were no ICD therapies or episodes of sustained VT. At 15 years of age, she presented to the emergency room with palpitations and 12-lead ECG demonstrated wide complex tachycardia at 180 bpm (shown in after amiodarone loading). The ICD was functioning appropriately, but the arrhythmia rate was slower than the defined VT/VF rate of 200 bpm, and hence no therapies were delivered. Tachycardia apparently terminated with amiodarone and she was discharged to home. She presented two days later with the same rhythm. On that occasion, both intravenous amiodarone and lidocaine had no effect on the rhythm, and external cardioversion with 50J restored sinus rhythm.
She was then transferred to our institution where Sotalol was initiated at 80 mg twice a day. Ventricular tachycardia recurred, and on both occasions was terminated with antitachycardia pacing using her ICD (). Sotalol was discontinued and therapy was transitioned to amiodarone and nadolol. The patient continued to have frequent episodes of VT despite several combinations of antiarrhythmic drugs including amiodarone, lidocaine and esmolol. Tachycardia could be reliably terminated with ventricular burst pacing from the ICD. The patient also reported that on several occasions she was able to successfully terminate tachycardia with vagal maneuvers. Adenosine was given during one episode and did not affect tachycardia.
When daily episodes of VT persisted despite maximal doses of amiodarone and nadolol, antiarrhythmic medications were discontinued for electrophysiology study and possible ablation. Left coronary angiography was performed at the beginning of the case, revealing a coronary fistula from the left coronary artery to the RV with a large contrast-filling vascular mass encircling the left coronary artery. Right coronary angiography demonstrated the same contrast-filling mass encircling the right coronary. The mass was presumed to be residual hemangioma with multiple blood supplies. A trans-esophageal echo with 2D and color doppler was also done, and showed the hemangioma to extend from the mid-portion of the RV septum to just under the pulmonary valve. At EP study, only several beats of nonsustained monomorphic VT were induced in the baseline state. Isoproterenol was infused, and longer runs of sustained monomorphic VT were reliably induced with ventricular burst pacing, ventricular triple extrastimuli, and with rapid atrial pacing. Attempts were made to perform entrainment mapping but were not successful because on some occasions tachycardia terminated with ventricular pacing, and on other attempts reliable capture could not be confirmed. Tachycardia terminated multiple times during the study. Termination was spontaneous and not associated with premature ectopic beats. Tachycardia could reliably be reinitiated on isoproterenol, both with ventricular burst pacing and with ventricular triple extrastimuli (500:320:320:280).
During sustained ventricular tachycardia, 3D mapping with CARTO was initially performed using a Biosense Webster EZ Steer catheter (4mm tip). Earliest areas of ventricular activation in tachycardia were noted along the border of the tumor, and earliest ventricular activation preceeded the QRS by 41 msec. Initial lesions placed along the tumor border were unsuccessful. Pace mapping from these sites showed paced QRS morphology similar to VT morphology in 11 of 12 surface leads. With similar findings at several points on the tumor border, the conclusion was made that tachycardia originated from within the tumor. Attempts to isolate the tumor with a series of lesions using an irrigated Navistar ThermoCool catheter were ultimately unsuccessful and tachycardia persisted. The case was ended and the patient was transferred back to the PICU in sinus rhythm. She underwent an upgrade to a dual chamber ICD with the intention of giving aggressive beta-blocker therapy.
Sustained tachycardia recurred and intravenous verapamil, which had previously not been tried, was given and tachycardia terminated. Oral verapamil was continued and there were no further tachycardia recurrences. She was started on oral Verapamil SR 240 mg daily and discharged from the hospital. She continued on Verapamil and did not have any recurrent episodes for one year. Subsequently, during a vigorous exercise the patient experienced two appropriate shocks. She had been noncompliant and was not taking verapamil at the time. Electrograms from the device demonstrated sinus tachycardia prior to an episode of VT ().


Ms. A, a 46-year-old woman, was admitted for global amnesia. She was awake and alert in the emergency room but was confused about her identity, past events in the last 2 days, and how she had arrived at the hospital. A head CT scan showed no acute disease. The psychiatry team was consulted, and it was discovered that Ms. A had a previous diagnosis of dissociative identity disorder (DID). Further investigation revealed that her family recently experienced enormous stress, which may have precipitated the current episode. During the psychiatric exam, she calmly sat with her eyes closed and insisted that they were already open when asked to open them. She also repeatedly fluctuated between referring to herself as “I” or “she.” When asked to write a complete sentence during the Folstein Mini-Mental State Exam, Ms. A took the pen with her right hand and effortlessly wrote, from the right margin to the left, the mirror image of “I’m tired of being here.” When asked to write the sentence again, she wrote the same sentence in the same direction as fluidly as she had done before (Figures and ). She later reported that she was normally right handed. Ms. A ultimately received a 24/30 on the Mini-Mental State Exam, with points deducted in orientation to place and time and in short-term memory. The amnesia began to clear toward the evening, and Ms. A agreed to continue her care at a local community hospital.
People with severe DID are known to fluctuate in various abilities, “such as fluency in a foreign language or athletic abilities [, ].” In some case studies, people with DID are able to switch handedness []. For example, one case study described a 27-year-old right handed woman who would regress into a left handed child []. One other case study described a left handed woman with a previous history of migraines and sensory and perceptive disturbances who mirror wrote with her right hand []. An exhaustive literature search was unable to yield reports of people with DID who spontaneously mirror wrote during their dissociative states, thereby making Ms. A's situation distinctive. It is not known why Ms. A began mirror writing as she did in her state. As is true for Leonardo da Vinci's mirror writing, one cannot help but wonder if there was a more profound level of meaning or purpose behind such reversed script.


A 45-year-old German Caucasian woman was transferred to our department of general surgery with a suspected esophageal perforation after endoscopic recovery of a pearl onion which was impacted in the middle third of the esophagus. After recovery of the pearl onion, upper gastrointestinal endoscopy revealed slightly bleeding mucosa at the site of impaction as well as an impassable stenosis. Her medical history, included relapsing periods of dysphagia since her childhood that were never examined by endoscopy or gastrografin swallow. At admission, she presented in a stable condition with normal laboratory findings. Clinical investigation revealed no abnormalities other than retrosternal pain as well as emphysema of the skin. Chest and abdominal radiography showed free intra-abdominal air as well as a pneumomediastinum. A gastrografin swallow was performed revealing leakage at the distal esophagus and pneumoperitoneum (Figure ). Explorative laparotomy and direct closure with hemifundoplication were performed and the mediastinum was drained.
Because of pathological drainage continuing on the tenth postoperative day as well as increasing white cell counts, we performed a gastrografin swallow that revealed mucosal irregularities and a double-barreled esophagus (Figure ). Upper gastrointestinal endoscopy identified an esophageal intramural dissection with complete obstruction of the true lumen at 35 cm, as well as mucosal bridges (Figure ).
These findings left us without any feasible conservative management options. The presence of mediastinitis due to a suspected transmural perforation prompted us to perform a transhiatal esophagectomy with cervical esophagostoma and blind closure of the stomach.
The pathology report showed the true esophageal lumen and a transmural perforation as well as a second lumen that was focally covered by a flat squamous epithelium with multiple ulcerations within the submucosal layer (Figure ). The postoperative course was uneventful and 3 months after esophagectomy, a reconstruction with a cervical esophagogastric anastomosis was performed and the patient was discharged on the 12th postoperative day after an uneventful course.


A 44-year-old Turkish woman admitted to the department of vascular surgery for her leg varices. She was on treatment with pentoxifylline and etodolac and her coagulation status was normal (prothrombin time=11 s, partial thromboplastin time = 25 s). The patient placed on the table in sitting position and her back was prepared and draped in the operating room. The patient instructed for full cervical and lumbar flexion, lumbar 4-5 intervertebral space was infiltrated with 1% lidocaine and a midline epidural catheter was easily placed into the L4-5 interspace using loss of resistance technique. No blood or cerebrospinal fluid was aspirated from the epidural space. An anesthetic test dose 5 ml of 2% lidocaine was injected and then continued 18 ml of lidocaine 2%. An anesthetic level to T11 was obtained. No adverse reaction was noted. During the operation, the patient felt motor loss in her legs. Epidural anesthesia was stopped and the procedure was continued and completed under general anesthesia. During the 4-h course in post-anesthesia care unit and 6-h course in the neurology intensive care unit, the patient’s sensory block decreased from T11 to L1 level, but motor block persisted. There was symmetrical loss of reflexes and flaccid paraplegia in the legs. Lower extremity sensation to light touch and pain returned, and the patient complained of pain at the dorsolumbar region. The patient urgently underwent magnetic resonance imaging (MRI), with suspicious epidural hematoma or spinal cord compression or ischemia. Thoracic and lumbar MRI images revealed intervertebral disc protrusion at T11-T12 level and an outstanding spinal cord compression ( and ). There was no evidence of hematoma and the spinal cord intensity was normal throughout the thoracic spine which ruled out spinal cord ischemia. There were osteophytes of the vertebral endplates in different levels of thoracic and lumbar spine. The patient was given methylprednisolone and transferred to the rehabilitation unit. Her sphincter control and anal reflex was intact, and tonus of the anal sphincter was normal. Over ten days of rehabilitation including range of motion and strengthening exercises, electrotherapy to the dorsal region and superficial heat, the patient’s dorsolumbar pain reduced, motor recovery was achieved with a weakness of 3/5 of the lower extremities. The patient was discharged after 20 days of rehabilitation with minimal weakness of the lower extremities and independent in daily living activities.


A 38-year-old, Turkish, Caucasian female patient presented with complain of intermittant cramping abdominal pain, nausea and vomiting which aggravated in the last 2 weeks. She had a history of cholecystectomy, performed 8 years ago. On physical examination, signs of anemia, jaundice and severe weight loss were inspected. The abdomen was distended and tender to palpation in the epigastrium and right upper quadrants with guarding, accompanied by reduced bowel sound. Laboratory examination revealed anemia (Hemoglobin: 8.1 g/dl), leukocytosis (13800/mm3), increase of erythrocyte sedimentation rate in first hour (105 mm/h), bilirubinemia (total bilirubin: 3 mg/dl and direct bilirubin: 1.82 mg/dl), increase of alchaline phosphatase (321 U/dl) and blood amilase (304 U/dl), prerenal azotemia (BUN: 50 mg/dl and creatinin: 1.24 mg/dl) and hypoalbuminemia (2.9 g/l). The levels of tumor markers were within the normal limits except CA-125, which was increased to 111 IU/dl. The abdominal ultrasound and computed tomography scan revealed a complex cystic retroperitoneal mass, 30 cm in diameter, extending from the subhepatic space down into the pelvis and was thought to be arised from the head of the pancreas. Dilatation of the intrahepatic and extrahepatic bile ducts and the Wirsung’s duct were accompanied by parenchymal calcifications and atrophy of the pancreas. The mass involved the porta hepatis and vascular structures, compressed the celiac trunk and superior mesenteric artery. The collecting system of the right kidney was dilated ( and ).
After one week of supportive treatment and transfusion of 2 units of blood, the patient underwent surgery. The exploration of the abdomen revealed a cystic mass, extending from the liver to the pelvis retroperitoneally, which elevated the cecum, ascending colon and partially transverse colon. The mass was perforated during the dissection and an abundant bile drainage was observed. The frozen section of the biopsy, taken from the capsule of this cystic mass showed no evidence of malignancy. Thereafter, the mass was thought to be a huge retroperitoneal biloma. The porta hepatis, the common bile duct and the duodenum were explored. In the retropancreatic portion of the common bile duct, a perforation site with a dimension of 3 × 3 cm was inspected and a Foley catheter was placed through this hole for a peroperative cholangiography which revealed dilatation of intrahepatic bile ducts was and normal level of biliary tract drainage into the duodenum. Thereafter, the retroperitoneum was cleansed with saline and drained and biloma was excised. The perforation site was repaired with 3/0 silk sutures with omentoplasty. T-tube placement was performed on the proximal choledochus and a peroperative cholangiography was repeated, which demonstrated a stricture in the common bile duct but free passage of contrast media into the duodenum ().
No complication was observed during early follow-up. On the postoperative 10th day, the T-tube was withdrawn following a cholangiography which revealed a sufficient passage of contrast medium into the duodenum and no leakage out of the biliary tract. There was no abdominal pathology, except findings of chronic pancreatitis and dilatation of the common bile duct, at ultrasonography imaging performed 3 months after the operation.


A 71-year old Greek female patient with a history of surgical resection of gastrointestinal stromal tumor (GIST) from the jejunum 21 months ago, presented with a CT follow-up diagnosis of a mass in the right inferior abdominal quadrant in contiguity with the abdominal wall and the uterus fundus. In order to exclude recurrence, a CT-guided biopsy was decided. The biopsy was performed under local anesthesia with an 18G semi-automatic biopsy gun (). Immediately after the second puncture the patient became hemodynamically unstable and control scan revealed active hemorrhage within the mass (). The patient was immediately transferred to the operating theatre where surgical tamponnage with retention sutures around the punctured region was performed. She turned hemodynamically stable 7 days later and remained in the Intensive Care Unit for 21 days. The patient spent another 20 days in the General Surgery department for complete recovery. Forty-one days after the biopsy the patient suddenly became hemodynamically unstable again. She was transferred to the Interventional Radiology suite, where an US Doppler examination revealed the presence of a 5.5 × 3.9 cm pseudoaneurysm in the punctured region with a neck width of 0.58 cm (). As this was considered as the cause of the hematocrit drop, treatment with percutaneous thrombin injection was decided. After local anesthesia a 21G needle was advanced under US-guidance and its tip was positioned in the middle of the pseudoaneurysm cavity away from the neck (). A solution of 1000 U/ml bovine-derived Thrombin Component (FloSeal, Baxter Healthcare, Fremont, CA, USA) was injected slowly at a rate of 0.1 ml/sec. The thrombotic process was controlled intermittently (in every 0.5 ml aliquots of the solution) with color Doppler. After a total amount of 1.5 ml of thrombin solution, almost complete pseudoaneurysm thrombosis was achieved (). No further thrombin injection was performed due to the patient’s hemodynamic instability. The patient’s hematocrit increased in the next six hours and she turned stable 12 hours later. The next day the patient complained of pain and hematocrit dropped again. An US examination revealed partial refilling of the pseudoaneurysm. Percutaneous embolization of the pseudoaneurysm was decided. Selective angiography of the internal iliac artery confirmed the presence of an IEA pseudoaneurysm (). Superselective catheterization of the IEA with a 3Fr microcatheter (SP, Terumo Europe) and subsequent embolization with 5 mm metallic coils (Cook, Denmark) was performed successfully. The coils were deployed proximal and distal to the pseudoaneurysm neck, in order to stop blood supply through the superior and the inferior epigastric branches (). The patient turned definitively stable and was released one week later. In the follow-up visit 6 months later no pseudoaneurysm recurrence was noted on US.


A 39-year-old African American man was referred to the outpatient neurology clinic with a two month history of distal upper extremities numbness and fine motor movement difficulties. He denied any neck pain, lower extremity symptoms, vision loss or any other neurological deficit. His physical exam was normal, including a detailed neurological exam. Laboratory evaluation six weeks prior had revealed normal basic chemistry profile, HGB 11.9 g/dl (MCV, and MCH values were not available at that time), and B12 203 pg/ml (normal; >180 pg/ml). He also underwent an EMG and nerve conduction study which revealed mild bilateral carpal tunnel syndrome. Other investigations conducted beforehand included MR imaging of the cervical spine three weeks prior, which revealed increased signal intensity within the core of the spinal cord at the level of C 3-4 on T2 weighted sagittal images. Axial images were not obtained at this level and contrast was not used in this study. A repeat of his cervical and thoracic MR imaging showed extensive posterior cervical cord flame-shaped lesions on T2 weighted images (,,,). Extensive laboratory evaluation was unremarkable including: basic chemistry profile, erythrocyte sedimentation rate, TSH, angiotensin converting enzyme, hemoglobin A1C, RPR, ANA, RF, serum protein electrophoresis, iron studies, Lyme IgG antibodies and heavy metals screen. His repeat Vitamin B12 level was 41 pg/ml, Methylmalonic acid 5.7 umol/l (normal; <0.4 umol/l), Homocysteine >50 nmol/l (normal; 5-18 nmol/l), folate 12.7 ng/ml. Pernicious anemia was suspected and investigation revealed positive intrinsic factor antibodies and negative anti-parietal antibodies. He received monthly injections of vitamin B12 replacement therapy. After six months his symptoms were resolved and his repeat spinal MRI showed resolution of the previous lesions.


A 57 year old Dutch Caucasian man was beaten by a group of youngsters. He had suffered brief loss of consciousness and was brought to the emergency room. He had a history of a mechanical aortic valve replacement and was therefore using acenocoumarol. He had no neurologic complaints and neurologic examination was unremarkable with a Glasgow Coma Scale score of 15. The laboratory workup revealed an INR of 5.1, much higher than the target of 2.5- 3.5. Initial head CT on the Emergency Room was read as normal (). He was admitted to the neurological medium care unit for clinical observation according to our current guidelines [,]. Neurologic examination was normal 10 hours after admission, but 12 hours after admission he suddenly complained of severe headache and subsequent developed a rapidly decreasing level of consciousness. On neurologic examination he now had a score of 9 on the Glasgow Coma Scale and a dilated right-sided pupil that was unresponsive to light. Emergent head CT scan showed subdural hematoma around the tentorium cerebelli compressing the brain stem and causing substantial midline shift (). Coagulation was normalized with 2500 IU of human protrombin complex and 10 mg vitamin K, and subsequently the patient underwent neurosurgery for evacuation of the hematoma. He made an excellent recovery.


A previously healthy, 4-year-old, Caucasian-Italian, uncircumcised boy came to our attention for the presence of a little, painless nodular lesion on the mucous face of the dorsal prepuce. The physical examination showed a sessile, bright red - blue, little nodule of around 3 mms in diameter, looking like a very small hemangioma. The history revealed it had appeared around six weeks earlier and it was now enlarging. No others symptoms, either local (bleeding and ulceration) or systemic, were reported and there were no other skin or mucosal abnormalities. Phimosis and Balano Preputial Adhesions (BPA) were absent. It was therefore decided to follow the boy. Twenty days after the first control, the lesion was not just one anymore, but other two satellite nodules occurred. The first lesion appeared bigger than before with a diameter of around 1.2 cm. The new two ones had a diameter of 3 and 5 mm respectively ( and ). After local excision of the lesions, the histopathological examination showed angiomatous tissue composed with congested capillaries and venules which were embedded in an edematous stroma containing a mild chronic inflammatory infiltrate (Pyogenic Granuloma). Even if the pathogenesis of such lesions is not always known, in this patient it is probably trauma related; parents reported traumatic BPA lysis with copious bleeding a few weeks before the appearance of the first lesion. After a follow up of six months no recurrences occurred.


A 46-year-old woman of Ethiopian descent presented to our emergency department with 3 weeks of worsening non-productive cough, dyspnea, fever, chills and night sweats. The patient’s medical history was significant for a three-year history of an uncharacterized rheumatologic illness marked by myalgias, arthralgias, two episodes of iridocyclitis, and a positive anti-nuclear antibody titer of 1:160, which had responded to treatment with systemic corticosteroids. Just three months prior to this presentation, she had developed thrombocytopenia with platelets to 37,000/mm3 which responded to prednisone (60 mg/day) which was slowly being tapered. Upon admission, her medications included prednisone (10 mg/day), calcium, and alendronate. Other past medical history included hypothyroidism and a completed treatment course for latent tuberculosis with isoniazid more than ten years prior. She worked as a cab driver and had a remote 20 pack-year history of smoking. She did not use alcohol or illicit drugs, and there was no family history of respiratory disease.
On examination, her temperature was 102.5 F with heart rate of 135 beats/minute, respirations of 33 breaths/min and oxygen saturation of 85% on 2 L/min supplemental oxygen. She was a moderately ill-appearing woman who had difficulty speaking in full sentences. Inspiratory crackles were present in bilateral lung fields and clubbing was absent. Her chest X-ray revealed diffusely increased interstitial prominence (). Laboratory evaluation indicated WBC of 6,700/mm3 with 16% neutrophils, 38% lymphocytes, and 38% atypical lymphocytes. All microbiologic studies were negative and bronchoalveolar lavage was non-diagnostic.
Chest CT showed diffuse patchy pulmonary interstitial opacities with peripheral predilection showing areas of septal thickening, ground glass, and subpleural honeycomb change () with para-aortic adenopathy. An open lung biopsy of the lingula revealed expansion of the interstitium by a diffuse lymphoplasmacytic infiltrate, intra-alveolar histiocytes and moderate interstitial fibrosis without fibroblastic foci or honeycomb lung (). Immunostains confirmed a polymorphic population of T and B-lymphocytes with variable degrees of alveolar filling by benign macrophages with no evidence of leukemic infiltrates. This suggested a histopathologic diagnosis of nonspecific interstitial pneumonia.
Because of the patient’s lymphoplasmacytic lung infiltrate, peripheral blood atypical lymphocytes, and cytopenias, a bone marrow aspiration and biopsy was conducted to assess for the possibility of a hematologic malignancy. Her aspirate revealed 55% blasts with the following immunophenotype by flow cytometry: cytoplasmic CD3+, surface CD3-, CD7+, CD5+, CD2-, CD1-, CD33+, CD13-, CD117-, MPO-, CD79a-, CD56-, CD34+, terminal deoxytransferase (TdT)+, CD10+, CD45 dimly +, consistent with biphenotypic acute leukemia.
Given our initial suspicion for respiratory infection in the setting of chronic immunosuppression, we began treatment with moxifloxacin to cover community acquired bacterial pneumonia and trimethoprim-sulfamethoxazole with high-dose prednisone for the possibility of PCP. By the third day of hospitalization, however, the patient showed marked improvement in her respiratory symptoms without any evidence of infectious etiology and all antibiotics were withdrawn.
The patient’s respiratory function continued to improve over a period of five days; supplemental oxygen was discontinued and steroids were tapered. Two weeks after her presentation she received standard induction chemotherapy for AML consisting of daunorubicin 60 mg/m2 by intravenous push for three days and cytarabine 200 mg/m2/day by continuous infusion for seven days. Her day 14 bone marrow biopsy revealed an ablated marrow and complete remission was achieved on day 28. She subsequently underwent matched related donor allogeneic peripheral blood stem cell transplantation using reduced-intensity conditioning. There were no respiratory difficulties during the induction period or at any time following the transplantation. However, her disease relapsed 157 days after transplant and she passed away on day 205.


A 52-year-old Malay male presented 32 years ago with a left inguino-scrotal hernia. A left inguinal herniorraphy was performed uneventfully and there were no other abnormalities. 10 years ago, his swelling recurred. He was operated for recurrent hernia. During surgery, he had a recurrent inguinal hernia and herniorraphy was performed. Post-operatively, he was asymptomatic until 5 years ago when started developing painless recurrent inguinal mass of a similar nature. It was initially reducible and was ignored by patient. However about 1 month prior to surgery, the mass became irreducible. There was no associated pain or obstructive bowel symptoms. Attempts to reduce the swelling were not successful. On table, an incision was made over the old scar and explored. There was no hernial sac or recurrences. The spermatic cord was isolated and traced distally into the scrotum. A large lipoma was seen arising from the inguinal cord (). It was dissected and excised. The cord was long and redundant (). The cord structures were preserved and no signs of invasion or malignancies were seen. Orchidopexy was performed and abdomen closed in the usual manner. He was well upon discharge. He was followed up in the clinic and post-operatively uneventful after discharge. He was discharged to be followed up at the primary care and has been problem free for almost 2 years since surgery. Histopathology reports confirmed the diagnosis of lipoma.


This is a case of a 65-year-old Jewish male who presented to our hospital complaining of a two-week history of sero-sanguineous oozing coming from a healing surgical wound overlying an ICD that had been implanted sixteen days prior to the day of admission at a different medical center. No purulent discharge was seen. The area became increasingly painful. The patient denied any fevers, chills, palpitations or other cardiovascular symptoms on admission. Vital signs were as follows: Temperature of 98.4°F, Blood pressure of 105/64 mmHg, Heart rate of 60 beats per minute, Respiratory rate of 14 breaths per minute and Oxygen saturation of 98% on room air. Physical examination revealed an eight-centimeter irregularly oval, warm, swollen, erythematous and tender area on the left anterior-superior chest wall. No local ulcers or new heart murmurs were noticed. Poor dentition, together with the presence of disheveling appearance was appreciated.
Past medical history was positive for non-ischemic dilated cardiomyopathy, congestive heart failure (NYHA class III), atrial fibrillation, essential hypertension and a recent syncopal episode. The patient had no history of alcohol, tobacco or illegal drug abuse. He was a retired messenger since 2004 and lived in a shelter. No family history of cardiomyopathy or oncologic diseases was noted.
Admission laboratory findings revealed mild leukocytosis together with mild normocytic normochromic anemia (). An electrocardiogram showed atrial paced rhythm at 60 beats per minute, a QRS complex of 102 msec and a QTc interval of 480 sec, no signs of ischemia were recorded. His home medications included Warfarin, Carvedilol, Lisinopril and Simvastatin.
Providencia rettgeri grew in two sets of deep wound cultures, one set of superficial wound cultures, one set of peripheral blood cultures obtained on the day of admission as well as from the culture of the removed device. The antibiotic resistance pattern was similar in all the cultures (). A trans-esophageal echocardiography did not reveal vegetations or signs of endocarditis.
The entire implanted system, including the cardiac leads of a dual chamber cardioverter-defibrillator, Medtronic®, model D224DRG, Secura DR was removed on day two of admission. The wound was left opened, and dry to wet dressings were applied locally. Resolution of the infection was seen after the patient received a four-week course of intravenous Cefepime two grams every twelve hours, subsequent surveillance blood cultures revealed no growth and second intention healing of the surgical wound ensued. An external defibrillator vest was initially placed and as soon as the antibiotic regimen was completed a new dual chamber cardioverter-defibrillator was placed on the right side of the thoracic wall. The patient was subsequently discharged with adequate follow-up.


A 13-year-old male presented with a fungating lesion on the scalp. He had sustained flame burns at the age of three. The lesion was never grafted and failed to heal completely. The primary care centre continued to manage the wound conservatively with frequent dressings. Eventually, a biopsy was performed and a well-differentiated squamous cell carcinoma was confirmed. He was referred to our tertiary centre for further management.
His main complaint was pain and a foul-smelling ulcer with a mucopurulent discharge. Specifically, the patient did not give any history suggestive of epilepsy or personality change. He was noted to be underweight for his age. On examination the lesion occupied the entire central vertex of the scalp []. The tumour measured 12 × 15cm. The central portion of the lesion was pulsatile. Bilateral cervical lymphadenopathy was present. On neurological examination no deficits were identified. No abnormalities were noted on the cardio-respiratory and abdominal examination. Blood investigations revealed microcytic anaemia and hypoalbuminaemia. The human immunodeficiency virus serology was negative.
Investigations included a skull radiograph, computed tomography (CT) and magnetic resonance imaging (MRI). These revealed extensive tumour infiltration of the soft tissue with underlying full thickness bilateral parietal bone erosion []. The depth of the infiltration included the dura and the cortex of the left cerebral hemisphere with underlying oedema of the brain []. A filling defect in the superior sagittal sinus indicated a thrombus. A chest roentegram and an abdominal ultrasound excluded metastatic disease in the lungs and liver respectively.
The cancer was staged clinically as T4N1M0. With Neurosurgical assistance the resection of the lesion was planned.
At surgery, the scalp, the involved cranial bones and dura were excised with 2cm tumour free peripheral margins. A suction-assisted resection of the involved cerebral cortex was done to the depth of normal brain tissue. The soft tissue defect measured 20 × 17 cm []. Our plan was to cover the defect with the anterolateral thigh flap. The tensor fascia lata was to serve as vascularised dural substitute. The flap harvest was abandoned after suitable calibre perforators could not be identified. A latissimus dorsi musculocutaneous flap was then used for cover. Lyoplant® (bovine pericardium) was used as a dural substitute. The flap was anastomosed to the superficial temporal vessels.
Histological diagnosis confirmed an invasive acantholytic squamous cell carcinoma, an aggressive pathological type which is poorly differentiated, extending into the deep dermis and subcutaneous tissue. The final histopathology result differed from the initial biopsy result due to a larger sample size of the former as well as poorly differentiated type cells were noted within the centre of the lesion. Abundant scar tissue and perineural invasion was noted with no vascular involvement. Brain and dura confirmed the presence of tumour in the deep resection margin. The interpretation of tumour clearance was inconclusive in view of the method of resection of the involved brain tissue.
The patient's postoperative recovery and wound healing was uneventful []. The patient had a near total right-sided hemiplegia of immediate onset following the surgery. Four weeks postoperatively, the bilateral cervical lymph nodes showed no signs of regression. Instead, the distribution and the size of the nodes had increased. A fine needle aspiration biopsy confirmed the presence of metastatic disease. Therapeutic bilateral selective cervical lymph node dissection, levels 1-5, was performed five weeks after the primary excision. Histology confirmed metastases to eight out of 90 lymph nodes. The patient was referred to the oncologists for further management. Three months later a large lymph node was detected in the left pre-auricular region which was excised and confirmed as metastatic disease. Chemotherapy was advised and six cycles of Taxotere and Cisplatin were administered. At nine months post surgical excision there was no evidence of local recurrence or metastatic disease. The patient defaulted on the subsequent planning of radiotherapy to the brain. At one year he presented to the oncologist with a history of seizures and weakness in the right upper and lower limb. A scalp recurrence was also noted. A CT scan of the brain showed left intraparenchymal parietal lobe mass lesion with solid and cystic components. The lesion was not amenable to neurosurgical intervention. The patient was offered palliative radiotherapy to the whole brain at a dosage of 3Gy each over nine cycles. The response was poor and the patient was discharged to the care of a hospice resulting in his demise three months later.


A 38-year-old female with hypertension, hypercholesterolemia, and positive family history presented to the ED one hour after the onset of a severe chest discomfort. Her ECG showed marked ST-segment elevations in leads I, aVL, V1–4. She was taken immediately to the catheterization laboratory after being given nitroglycerin, morphine, aspirin, and UFH. Angiography revealed a tight thrombotic lesion of the proximal LAD with a TIMI grade 2 blood flow (). After additional ACT-guided UFH and 600 mg of clopidogrel, a JL 3.5 F6 guiding catheter (Cordis, Miami, Fla, USA) was used to intubate the LCA, a 0.014-inch Asahi soft guide wire (Abbot, Redwood City, Calif, USA) was introduced into the distal LAD, a 2.0 × 20 mm Mercury balloon (Abbot, Redwood City, Calif, USA) was inflated once at 7 At to pre-dilate the lesion, and finally a 2.5 × 18 mm SES (Cypher, Cordis, Miami, FL, USA) was implanted at 16 At on the proximal LAD. The angiographic control showed a good result () and, as a result, no attempt was made to expand the stent with a noncompliant balloon.
Following the hospital discharge, the patient was instructed to take daily aspirin 100 mg for life, clopidogrel 75 mg for one year, bisoprolol 2.5 mg, ramipril 2.5 mg, and atorvastatin 10 mg. She was doing well until 280 days later when she was awakened early in the morning by the intensive chest pain accompanied by sweating and nausea. At the ED, her heart rate was 60/min, blood pressure 90/60 mm Hg, respiratory rate 18/min, and there were no pulmonary rales. The ECG demonstrated significant ST-segment re-elevations in leads V3–6. She received similar medication as previously, and was transferred to our catheterization laboratory again. The repeat angiography showed a thrombotic occlusion of the implanted stent (). An EBU 3.75 F6 Launcher guiding catheter (Medtronic, Minneapolis, Minn, USA) was used to engage the left main coronary artery, a 0.014” BMW guide wire (Abbot, Redwood City, Calif, USA) crossed the stent struts easily, and a 2.0 × 20 mm Mercury balloon (Abbot, Redwood City, Calif, USA) was gently inflated at 6 At to reopen the LAD. At this point, the IVUS using the Atlantis 40 MHz transducer (Boston Scientific, Maple Grove, Minn, USA) with a motorized pullback at 0.5 mm/s was performed to elucidate the mechanisms of the ST. The proximal LAD showed a positive vessel wall remodeling with maximum diameters within the external elastic membrane (EEM) at both stent borders of 4.5 mm and 3.5 mm, respectively (Figures , ). The vessel lumen, however, was encroached by a huge atherosclerotic plaque that comprised 59% to 74% of the measured area within the EEM and extended considerably beyond the outer stent margins. Near the distal part of the implanted stent, a severe stent fracture (SF) was found with complete strut separation over a wide distance (Figures –). The cross-sectional lumen area (CSA) at the site with missing struts was only 2.1 mm2. The decision was made to enlarge the stent with the balloon angioplasty. The noncompliant Mercury NC 3.0 × 20 mm balloon (Abbot, Redwood City, Calif, USA) was inflated successively across the stented segment up to 20 At with the resulting CSA of ≥ 6.5 mm2. The final angiographic result appeared excellent () and, therefore, the PCI was completed without additional stent placement.
The patient was then admitted to the CCU where tests addressing the antiaggregatory platelet function were carried out. The point-of-care testing using VerifyNow (Accumetrics, San Diego, Calif, USA) demonstrated a good antiaggregatory effect of aspirin with the ARU of 390 (normally, 620–672) and, on the contrary, a poor response to clopidogrel with the PRU of 245 (normally, 194–418) and only 10% inhibition, suggesting the clopidogrel resistance. The daily dose of clopidogrel was raised to 150 mg for the next year.
The further hospital course was uneventful. She experienced no additional adverse events until her outpatient visit 6 months later.


A 54-year-old man was admitted to the emergency department because of acute abdominal pain. He had a 3-month history of abdominal pain, bloating, anemia and three episodes of melena that resolved spontaneously. He was not using any specific medication and his medical history did not suggest any major disease. The physical examination showed a conscious patient hemodynamically stable whose temperature was 37°C, whose blood pressure was 130/80 mmHg and who had a good nutritional status and slightly discolored conjunctives. Abdominal examination showed a tenderness and a mobile hypogastric mass. The hemoglobin level was 8.2 g/dl and reduced hematocrit (24.9%) and iron level suggested chronic bleeding. The platelet count was 260,000/μL, white blood cell count was 10200/mm3 (79% neutrophils), blood urea was 0.25 g/L and the creatinine level was 10 mg/L. Liver enzymes and hemostasis laboratory data were normal. The patient was hospitalized in the gastroenterology department for etiological investigation. The upper digestive endoscopy and colonoscopy were normal. No gastric or colic lesions were found as an explanation of the melena. An ultrasound and abdominal computerized tomography (CT) were realized to explore the abdominal mass, which showed a large heterogeneous tumor of the small bowel (diameter of 12 × 11 × 8 cm) []; thus, the decision to refer the patient for surgery. But, during his hospitalization, before his transfer to the surgery department, the patient developed a fulminant gastrointestinal hemorrhage represented by a severe melena, with a hemorrhagic shock, sudden hypotension and shortness of breath, a profuse sweating and a tachycardia with a heart rate of 117 beats/min. He was admitted to the intensive care unit (ICU) with a swift assessment of his airway, breathing and circulation. Resuscitation was begun, after central intravenous access, with saline and conventional crystalloid solution and then transfusion of the red blood cells (6 units) was performed after blood grouping and cross-matching. An emergency exploratory laparotomy was performed under general anesthesia after hemodynamic stability and satisfactory control coagulogram (hemoglobin level 11.6 g/dl). Surgical exploration showed a pediculated tumor of the small bowel at 90 cm of the ileo-ceacal junction [], there was no hemoperitoneum and no other tumoral localizations were noted. A complete tumor resection with intact pseudocapsule and more than 1 cm of tumor-clear margins was performed. The patient recovered well without postoperative complications. Pathological examination revealed a malignant GIST. The tumor measured more than 12 cm in dimension and the mitotic rate was 20/50 high-power fields, with abundant tumor necroses. The tumor was focally positive for KIT (CD117) [Figure and ].


A 63-year-old man was admitted in the emergency room of the University Hospital of Hassan II with acute abdominal pain, hypotension, melena and severe anemia. His medical history revealed recurrent melena and upper abdominal discomfort over the last 4 months and did not suggest any major disease except hypertension treated for 3 years. He had no prior history of abdominal surgery or trauma. The physical examination revealed a conscious man with severe cutaneous paleness, a blood pressure of 90/60 mmHg, profuse sweating and a tachycardia with a weak and rapid pulse rate of 120 beats/min. There was no fever and there was minimal tenderness in the hypogastria at the abdominal examination. Laboratory data on admission showed a white blood cell count of 7,900/mm3, a hematocrit of 19% and a serum hemoglobin concentration of 6.4 g/dl, with a normal blood platelet level (390,000/mm3). Hemostasis laboratory data was normal. The patient was admitted to the ICU and was provided, by taking a central venous line (peripherally inserted central catheter) introduction of a nasogastric tube and urinary catheter, initial resuscitation by physiological serum and macromolecules and then transfusion with 8 units of red blood cells. After hemodynamic stability, a gastroscopy was performed, which did not demonstrate any gastric lesion responsible for this hemorrhage. No lesions or points of bleeding were found at the colonoscopy. But, the abdominal ultrasonography (US) realized after endoscopic explorations revealed the presence of a tissular mass in the left iliac fossa and the CT confirmed results of US and showed a solid tumor measuring (6 × 4.5 cm), probably a GIST of the small bowel [].
Even if hemodynamic parameters were normalized after resuscitation and transfusion, and the hemoglobin control level was 10.9 g/dl, and because of the persistence of the severe melena, it was indispensable to shift the patient to the operating room for an emergency surgery to control the source of bleeding. A laparotomy was performed. Exploration noted a tumor of the terminal ileum [] and no other tumoral localization was found. A small bowel resection removing the tumor was performed with terminoterminal anastomosis. Postoperatively, there were no complications and the patient made an excellent recovery. Histological examination described a stromal tumor with free margins. Immunohistochemical markers confirmed the diagnosis of GIST (CD 34 positive, CD 117 negative, AML negative) [Figure and ]. The re-evaluation, performed 6 months and 2 years later, showed complete recovery, without any sign of abdominal CT recurrence of the disease.


A 65-year-old Hispanic man from Bolivia with chronic lymphocytic leukemia (CLL) diagnosed 11 years before presentation and initially treated with alkylating agents, steroids and purine analogs, underwent an allogenic stem cell transplant from an HLA-compatible sibling a year before presentation. He developed cough and malaise eight months after the transplant for which he was admitted to another facility. Chest radiographs were reportedly negative and the patient was diagnosed with bronchitis and sent home on oral antibiotics. He continued to have intermittent cough productive of clear sputum associated with worsening malaise and weakness for about four months and was eventually evaluated at our hospital. Computed tomography (CT) of the chest revealed diffuse soft tissue thickening around the left main stem (LMS) bronchus (Figure ). This area was also intensely FDG-avid on PET scanning with a maximum standardized uptake value (SUV) of 7.4 (Figure ). The radiologic interpretation was consistent with leukemic infiltration of the bronchus or, less likely, localized graft-versus-host disease. Inflammation and mucosal thickening of the walls of the sphenoid sinuses were also noted incidentally on the same PET/CT scan and interpreted as sinusitis.
His medical history was remarkable for adult-onset asthma, two episodes of pneumonia several years ago, actinic keratosis and squamous cell carcinoma of the skin. He was a lifelong non-smoker and was on immunosuppression with prednisone and tacrolimus, and routine prophylaxis with atovaquone, valacyclovir and voriconazole. His vital signs were stable and his respiratory exam was unremarkable. He was thrombocytopenic (21,000/mm3), but not neutropenic (absolute neutrophil count 3,960/mm3).
An initial bronchoscopic exam revealed circumferential narrowing of the entire LMS bronchus (Figure ). The mucosa on the medial wall of the distal end of the LMS bronchus appeared to be necrotic and friable. This necrotic area measured about 1.5 cm in diameter. The necrotic area was washed with normal saline but biopsies were not taken because significant superficial bleeding was noted during minimal suctioning. Cytologic analysis of the bronchial wash revealed fragments of cartilage without diagnostic features. Stains and cultures for bacteria, AFB and fungus were negative. The patient's thrombocytopenia was known to be refractory to platelet transfusions. In an effort to safely expedite a diagnosis, a second bronchoscopy was performed utilizing convex-probe EBUS (Olympus UC-160F, Olympus America Inc., Center Valley, PA) with the goal of performing directed biopsies while avoiding vascular structures. Under ultrasound examination, a thickening of soft tissue was noted on the medial aspect of the LMS bronchus, underlying the area of necrosis visible endoluminally (Figure ). The thickening of the soft tissue on the anterior and lateral aspect of the distal LMS was also observed, with no evidence of a distinct lymph node in this location. With EBUS guidance, transbronchial needle aspiration (TBNA) biopsies were obtained from this abnormal region. On-site cytopathology evaluation revealed abundant necrotic material with multiple mycelia consisting of septate hyphae branching at around 45 degrees (Figure ), characteristic of aspergillus species. The patient tolerated the procedure, which was free of complications. Based on our findings, the patient was immediately started on high-dose intravenous liposomal amphotericin B and posaconazole. He was discharged after ten days of therapy, but re-admitted seven days later with worsening respiratory symptoms and partial left upper lobe collapse. He was discharged again after two more weeks of intravenous antifungals with clinical and radiographical improvement.


In the spring of 2001 a 51-year-old policeman consults his general practitioner (GP) with a painful, red spot on his upper limb. He is not ill, has no fever, has never smoked, uses a couple of beers each day and is known with hypertension, for which he is treated with atenolol ZOC 100 mg once daily. With a length of 1.86 meters and a bodyweight of 98 kilograms he is slightly over weighted.
The spot is there for a few days and looks like an oval shaped raised erythema. His GP diagnoses a superficial thrombophlebitis and prescribes conservative treatment: elevation of the leg and compresses. Within a few weeks the string disappears. Two years later the story repeats itself in exactly the same manner, but now the spot is located on the front of his left tibia. The GP again diagnoses superficial thrombophlebitis and prescribes a NSAID. The thromboflebitis again resolves itself in a few weeks.
A year later he consults again, this time with a swollen left calf, that started just above the ankle and a painful string at the inner side of the knee. Compression ultrasonography however shows no deep vein thrombosis, but again superficial thrombophlebitis. Treatment as before with NSAID. A year later he experiences a superficial thrombophlebitis for the fourth time (again diagnosed with compression ultrasonography) and a consulted specialist advocates screening on thrombophilia and possible malignancy. No thrombophilia is found, but PSA is slightly raised and because of a raised gamma-GT (123 U/l, which a month later spontaneously recovers to 63 U/l) a CT-scan of the abdomen is made. This reveals a solid mass in the left kidney and a solid mass in the suprarenal gland.
A partial nephrectomy and extirpation of the suprarenal gland is performed and biopsies of his prostate are taken. The pathologist diagnosis a renal cell carcinoma of the kidney, clear cell type with a diameter of 4.3 cm, Fuhrmann grade 111-IV, an adenoma of the adrenal cortex and adenocarcinoma of the prostate, Gleason score 6.
The patient recovers of the operation, distant metastases were not found. He is treated with prostatectomia for his prostate carcinoma. A year after the first operation a metastasis of the renal cell carcinoma is found in the right suprarenal gland, which is treated by extirpation. During the two years form his first to his third operation he suffered from deep venous thrombosis twice. Now, three years after the operation he has resumed working.
Retrospectively the renal mass was visible on a scan, made in 2001 because of his hypertension, that was difficult to treat at that time. This renal mass however was not noticed at that time.


A 50-year-old male presented with large multiple polypoidal growths on the penis and groin region for last 20 years. Twenty years back he had progressive itching on the tip of the penis and within few days he developed small skin-colored lesions with clear fluid oozing from them on scratching. He consulted a dermatologist, who prescribed topical ointment and oral medicines. The patient got relief with these medicines and remained asymptomatic for five years. Then again similar lesions erupted on the prepuce first and subsequently over the whole length of the penis. These lesions were progressively enlarging, became hard, not associated with pain but were very itchy. For the last five months, the scrotum and groin region had also been affected. Patient was able to have sexual intercourse during the initial four years. The wife didn't complain of any such lesion on her sexual organs and was found normal on examination.
On examination of the patient (), there were multiple polypoidal lesions on the skin of the penis, groin with average size of 2 cm. The intervening skin was normal and patient was able to urinate through slit-like opening. The scrotum skin was also involved but the lesions were not polypoidal.
The initial diagnosis of condyloma acuminata, acrochordons (Skin tags) and Bowen disease was kept and patient was investigated. The complete hemogram, liver, renal functions and immune status were found to be normal. The patient was taken for shave excision of the lesion under general anesthesia. The whole skin with lesion was excised up to the base of the penis. The thickness of the skin, excluding the lesion was about 2 cm. The mucosa of the penis was normal. The raw area was grafted with split-thickness skin graft. The histopathological examination of the tissue was found to be seborrheic keratosis (). On follow-up patient recovered well ().


A forty-year-old male welder with no past history of knee injury presented to another institution with left knee pain in September 2000. He underwent an arthroscopic partial menisectomy of the medial meniscus. In December 2004, 4 years after the primary surgery, he had a second arthroscopic partial menisectomy of the medial meniscus. However his left knee pain was not reduced. The radiographs of his left knee revealed a narrow medial joint space, femorotibial angle of 178 degrees, and posterior tibial slope [] of 9 degrees. In January 2005, when he was 44 years old, he received an opening-wedge HTO using a Puddu plate with a 15-mm opening block and osteochondral transplantation of the medial femoral condyle. The femorotibial angle was corrected to 170 degrees after the osteotomy, while the posterior tibial slope increased to 20 degrees. The Puddu plate was removed at 18 months after the osteotomy; however, he still had severe knee pain.
In January 2007, the patient first visited our institution for a second opinion, because he was recommended for another revision surgery to convert to total knee arthroplasty by the former hospital. He was unable to walk without a cane due to the left anteromedial knee pain. Physical examinations revealed quadriceps atrophy and no ligamentous laxity of the left knee. The range of motion was 140 degrees of flexion and -20 degrees of extension in the left knee, and 150 degrees of flexion and 0 degree of extension in the right knee. Severe left knee pain was observed with extension. The radiographs demonstrated complete bony union at the osteotomy site, a femorotibial angle of 169 degrees and posterior tibial slope of 20 degrees on the left side (Fig. ), and 178 degrees and 8 degrees on the right side. The mechanical axis of the left leg passed through the middle of the lateral femorotibial compartment. We concluded that the increased posterior tibial slope limited his knee extension, and that was the cause of the pain. We discussed with the patient the treatment options to reduce the knee pain that was his chief complaint. Since the patient was young and had a physically demanding job, we choose a medial closing wedge osteotomy to recorrect the posterior tibial slope rather than conversion surgery to total knee arthroplasty. Under arthroscopic examination, the transplanted cartilage on the medial femoral condyle was preserved; however, the medial meniscus was down-sized by the prior debridement. Degeneration of cartilage was evident due to impingement of the anteromedial edge of tibial plateau and medial condyle of femur with the extension of knee. The cartilage fibrillation observed on the medial femorotibial compartment was classified as grade III according to a modified Outerbridge classification []. The patellofemoral joint showed no arthrosis change, and lateral femorotibial joint surface had normal appearance, confirming a suitable indication for realignment osteotomy. A longitudinal skin incision was made on the previous operative scar over the anteromedial aspect of the tibia. The pes anserinus covered with scar tissues was dissected, and the superficial medial collateral ligament was exposed and detached from the tibia. The osteotomy guide wires were then inserted from the medial tibial cortex and were stopped at 1 cm short of the lateral cortex and 1 cm below the joint line. Two additional parallel guide wires were inserted to the proximal and distal of osteotomy line directed from anterior to posterior in the sagittal plane (Figs. ). These guide wires were used to estimate the correction angle of the posterior tibial slope. The osteotomy was performed, first from the medial cortex in the lateral direction according to the osteotomy guide wires, and second in the anteroposterior direction to remove the tibial bone in wedge shape and obtain full extension of the knee (Fig. ). The angular correction of the posterior tibial slope was achieved by closing the bony space that was created by osteotomy, applying a knee extension torque manually. At the end of the corrective procedure, the 2 guide wires made an angle of 15 degrees and full extension of the knee was obtained (Fig. ). Finally, a locking plate (LCP T-plate, Synthes®) was placed on the anteromedial tibia and fixed with 4 locking and 2 unlocking screws. Soft tissue releases were not performed due to the chronicity of the patient's flexion contracture. The postoperative radiographs showed 172 degrees of femorotibial angle and 8 degrees of posterior tibial slope (Fig. ). No immobilization was applied and range-of-motion exercise using a continuous passive motion machine was started from the day after the surgery. Partial weight bearing was permitted at 4 weeks and full weight bearing was achieved at 6 weeks. The patient returned to pain-free daily life including running and stair ascending and descending with -5 degrees of extension and 135 degrees of flexion. The bone union was completed and the postoperative alignment was maintained for 2 years after the revision osteotomy. The knee score of the American Knee Society [] was improved from 49 points of knee score and 35 points of functional score to 95 points and 90 points, respectively.


The patient, a 28-year-old woman with NF1 was regularly seen for follow-up of a cerebellar lesion, suspected to be a hamartoma. This lesion was accidentally discovered during a radiological exam performed for a facial neurofibroma, when she was 21 years old. Successive MRI-scans of the brain were performed.
At the age of 28, she was referred to our hospital because of complaints of progressive balance disturbance, ataxia of the right arm and leg, diplopia, and a sense of pulsation at the back of her head. She mentioned that a “bump” at the back of her head had increased in size over the preceding months.
Neurological examination revealed nystagmus of her right eye, diplopia, loss of sensibility of the face, and ataxia of the right arm and leg. Romberg's test was positive.An occipital/cerebellar solid mass of 4 by 5 cm was palpable.
An MRI-scan of the brain (Figures and ) showed a (sub)occipital right-sided bone defect, contiguous to a subcutaneous neurofibroma, and a lesion in the right cerebellar hemisphere that enhanced after Gadolinium administration (). In the left cerebellar hemisphere and the left superior colliculus other lesions were found, that both also enhanced upon Gadolinium administration.
Neurosurgical resection of the lesion was subsequently performed. Histological analysis revealed two distinct lesions: a mitotically active pleomorphic astrocytoma with pathologic vascular proliferation that was classified as glioblastoma multiforme (astrocytoma, grade 4) (Figures , , , and ) and a diffuse neurofibroma (Figures and ). The former showed leptomeningeal involvement, and the latter was restricted to the subcutis.
On immunohistochemistry, the first lesion was positive for GFAP (), the second negative (data not shown), but positive for S100 (). Approximately 10%–15% of the nuclei of the first lesion were positive for the proliferation marker Ki67 (MiB1) () and 1% of the nuclei of the neurofibroma (data not shown).
Approximately 30% of the cells in the first lesion showed immunopositivity for p53 ().
Upon recovery from surgery, the patient underwent both radiotherapy and chemotherapy. Six months later, MR-imaging showed progression of the tumor. After another six months metastases were present in the right frontal lobe and spine. The patient died shortly thereafter.


A 51-year-old Caucasian man who smoked and was afflicted with dyslipidemia presented at our emergency department complaining of typical angina and shortness of breath. He had a family history of coronary artery disease. He had been successfully treated with coronary angioplasty 12 years before presentation. A 4.0/16.0 mm AVE Micro stent (AVE Inc., Santa Rosa, CA, USA) was deployed in the proximal left anterior descending artery (LAD). The stent was postdilated with a 4.0-mm high dilatation force balloon (High Energy) at 14 atmospheres with good angiographic results. The patient was on therapy with aspirin, a statin, omega-3 fatty acids and a β-blocker and had remained asymptomatic up to his admission.
An electrocardiogram showed a marked ST-segment elevation in leads V2-V6, I and aVL, suggesting an extended anterior acute myocardial infarction (Figure ).
Emergency coronary angiography revealed total occlusion of the LAD with complete fracture of the mid portion of the stent (Figure and Additional file ). The circumflex artery had a non-critical plaque in the mid portion (50%) and the right coronary artery was normal.
A percutaneous coronary intervention (PIC) was performed. After predilation, two Cypher stents (Cordis, Miami Lakes, FL, USA) 3.0 × 33 mm in the middle part and 3.5 × 8 mm proximally, respectively, were superposed on the previous stent in the fractured occlusion area. Subsequently, a third Cypher stent 2.75 × 28 mm in the mid-LAD was deployed (Figure and Additional file , Additional file and Additional file ).
Overlapped segments with extensor balloon (3.5 × 20 mm) postdilation were performed. The affected coronary artery was successfully reperfused (final TIMI 3 flow) (Figure and Additional file ). The peak troponin T level was 82.89 ng/ml, myoglobin was greater than 1000 ng/ml, and creatine kinase-MB level was 217.30 ng/ml.
The patient was admitted to the coronary care unit and treated with double antiplatelet therapy (aspirin and clopidogrel) as well as a β-blocker, ACE-inhibitor, statin and diuretic. The patient's later course was uneventful, as cardiac biomarkers normalized.


A 33-year-old Caucasian male of Greek origin sustained a work accident. He fell from a height of 2 meters and landed on his right side. On admission he was conscious and well orientated with normal vital signs. His right shoulder and arm were painful, swollen and deformed. Clinical examination revealed a closed and neurovascular intact injury that had resulted to angulation of the arm with loss of the normal contour of the shoulder.
Radiographs showed an anterior dislocation of the shoulder with a transverse fracture of the middle third of the humeral shaft on the same side (Figure ). The arm was temporarily immobilized in a plaster slab. We have not performed a Magnetic Resonance scan (MRI) in order to investigate possible rotator cuff pathology, because of the lack of MRI equipment in our hospital. Thus, we decided that clinical examination at later would indicate the need or not of MRI. As soon as the secondary clinical survey was completed the patient was carried to the operating theatre. Under general anaesthesia, repeated attempts for closed reduction of the dislocated shoulder failed. Strong muscle contraction, despite the induction of muscle relaxation agents by the anesthetists, and extensive swelling of the soft tissues were obstructive of a successful reduction. Because of the unstable state of the fractured humerus and the risk for further soft tissue compromise and iatrogenic neurovascular damage, it was decided not to insist on reduction maneuvers. The surgeons preferred to attempt stabilization of the shaft fracture by intramedullary nailing prior to the reduction. Under fluoroscopy the entry point was targeted on the dislocated humeral head and an incision was made on the overlying skin. Although the anatomy of the region was altered, because of the dislocation, the anteriorly placed humeral head in the subcoracoid space facilitated, rather than obstructed, the guide wire and nail insertion. Intraoperative investigation revealed no rotator cuff or biceps pathology. Unfortunately a typical intramedullary nailing procedure could not be completed because after the proximal locking screw insertion, the image intensifier equipment suffered serious damage. The weakness for targeted distal locking which would subsequently result to rotational instability and the perspective of reduction manipulations, once the fixation was concluded, implemented the use of a rotational stability providing alternative. Thus a four holes small antirotational plate was placed on the anterior cortex over the fracture site. Four screws (2 at each side of the fracture) were inserted just medial to the nail. All screws were cortical and engaged both the anterior and posterior cortex of the bone enhancing the fixation and securing rotational stability. The shoulder was then reduced by gentle manipulation which sequentially included: external rotation, mild traction and inwards placement of the head into the glenohumeral joint (Figure ).
The limb was immobilized in a sling and only occasional flexion-extension of the elbow was allowed. Three weeks postoperatively the patient was encouraged to start Range of Motion (ROM) and muscle strengthening exercises of the shoulder. Bone union was demonstrated radiographically four months postoperatively (Figure ). Mild pain and restriction of shoulder abduction over 90 degrees were demonstrated, due to the impingement of the proud nail in the subacromial space. Therefore, 12 months after the operation and since bone union was secured, both nail and plate were removed. After the hardware removal, the pain symptoms drastically subsided. Full muscular strength and normal ROM were regained. The patient returned to his daily routine activities. At 3 years follow-up, the patient's shoulder is painless and retains a full range of motion (Figure ). No signs of shoulder osteoarthritic lesions or calcific tendonitis are evident in the latest radiographs.


A 62 year old man with nephrolithiasis history underwent an ultrasonography scan (US) with occasional report of cystic mass of 38 × 28 mm localized in the pancreatic body, close to the tail (April 2nd, 2008, as shown in figure ).
The radiologist recommended a Magnetic Resonance Imaging (MRI) and a fine needle agobiopsy to characterize the lesion interpreted as a pancreatic cystoadenoma or a dysontogenetic cyst. The MRI (performed on April 22nd - figure ) described a mass of 38 mm localized in front of the pancreas body and behind the lesser gastric curvature, maybe a supernumerary spleen, this hypothesis to be confirmed with a Computed tomography (CT) scan.
The CT scan was performed on May the 7th: it revealed a fluid, roundish mass less than 40 mm of maximum diameter between lesser curvature and pancreatic body with contrast enhancement as arterial blood, perhaps aneurysm of left gastric artery.
A Doppler Sonography (May 21st, see figure ) showed a thrombosis of a splenic artery aneurysm.
The patient underwent on June 18th to a transfemoral arteriography that demonstrated an aneurysm of the left gastric artery of 40 mm not confirmed in a selective arteriography performed on June 24th; showed in figure .
Another doppler sonography on the same day gave evidence of a peripancreatic iso-anechogenic mass.
A MRI (July 7th) displayed a sovramesocolic mass between lesser curvature and gastric body: gastrointestinal stromal tumor (GIST) or hemangiopericytoma.
On September 12th a contrast-enhanced sonography testified an ipo-anechogenic mass of 36 mm in the pancreatic body as a not active neuroendocrinal neoplasm; on the same date an endo-ultrasonography deposed for an extragastric mass, with no certain cleavage with pancreas (the brown words do not make sense to me) of 36 mm of maximum diameter and satellite lymphadenopathy.
The patient was admitted to our unit on October 13th after all the exams and procedures described above and with no certain diagnosis. His past medical history showed type II diabetes mellitus, hypertension, hyperuricemia and hypertriglyceridaemia. Laboratory tests were normal except for mild hyperglicemia (117 g/dL) and a slight γ-GT increase (104 IU/L). There was no serological indication of active HIV, B and C hepatitis, past Epstein Barr virus and Cytomegalovirus infections and tumor markers as CEA and CA19.9 were normal. A colonoscopy was performed that showed a diverticulosis. The patient underwent surgical operation for suspected pancreatic neoplasm. At laparotomy the pancreas appeared normal as well as the liver and other organs. (It was found) A voluminous well vascularized 4 cm mass was found along the lesser gastric curvature, not contacting the gastric body or the pancreas. The laparotomy was restricted to dissect the mass. The postoperative course was uneventful and the patient was discharged on 5th day. Frozen section of the mass showed an atypical lymphoproliferative process with no clonal rearrangement of IgH gene at molecular studies; the final pathological report described an angiofollicular lymphoid hyperplasia compatible with mixed variety, hyaline-vascular plasma cell type of CD made of preserved lymphoid tissue with follicles at various degree of maturation and diffuse hyaline involution and intervening sheets of plasma cells and capillary.
He is alive and free of recurrence at 4 months follow-up.


An 83-year-old Japanese man was admitted to the hospital complaining of general fatigue. Laboratory examination revealed marked increase of atypical lymphoblastic cells in peripheral blood. The diagnosis of acute lymphoblastic leukaemia was made, and combined chemotherapy (CHOP therapy) was started. During the initial course of chemotherapy, however, the patient suffered sudden cardiac arrest and, despite undergoing intensive efforts at resuscitation, died soon after the onset of symptoms; the cause of cardiac arrest could not be ascertained. At autopsy twelve hours after death, accumulation of 400 ml of fresh blood fluid was noted in the pericardiac space. The heart, weighing 460 g, showed markedly dilated and congested coronary veins (Figure arrows). A horizontal cross-section of the base of the heart revealed a fresh thrombus at the orifice of the coronary sinus (Figure , arrow). Histologic examination revealed extensive hemorrhagic change around the coronary vein (Figure , HE, ×40). Infiltration of leukemic cells was focally observed at the site of venous rupture; the cells, with small round nuclei, diffuse and dense chromatin content and scant cytoplasm, infiltrated almost all the organs, including the bone marrow cavity (Figure , HE, ×400). The final diagnosis of cardiac tamponade attributed to coronary sinus thrombosis was established histopathologically.


A 42-year-old Mediterranean male presented complaining of inability to sustain good oral care at the posterior aspect of the lower right jaw. The main problems were food impaction in the area and the subsequent malodor. The patient reported remarkable medical history, and he was a non-smoker. Clinical examination revealed local erytherma with noticeable bony defect distal to the second molar with obvious defect in the mesial wall of the third molar; the penetration depth was found to be up to 6 mm (Figure ).
Radiological evaluation confirmed the defect and it was attributed to the mesioangularly impacted lower third molar; there was marked dilation or thickening of the lamina dura secondary to the local inflammatory reaction. It was decided that the third molar should be extracted and concentrate of the patient's growth factors (PRGF) to be implanted into the bony defect to stimulate bone regeneration and promote healing(Figure ).
Preoperatively, 24 cc of the patient's blood (venous blood from a peripheral vessel) was obtained using a butterfly cannula. The blood was collected in five sterile glass tubes, pretreated with 3,8% trisodium citrate (anticoagulant factor) and then centrifuged at 460 g for 8 mins at room temperature (PRGF System, BTI Biotechnology Institute, Vitoria, Spain) []. After centrifugation, blood was separated into distinct layers, with the cellular fraction located at the bottom of the tubes and the plasmatic fraction located just above the red blood cell line. Plasma volume constituted 1 cc and was located just above the red blood cell line. This fraction appears to be very rich in growth factors []. A volume of approximately 5 cc of PRGF was collected in a tube and 50 μl of 10% calcium chloride (CaCl2) were added per 1 cc of PRGF []. CaCl2 activates PRGF and stimulates the formation of a semi-solid, scaffold-like mass which functions as a matrix for progenitor cells and maintains the regenerative area of the defect []. After activation, PRGF was mounted on a spatula and ready to be applied to the bony defect (Figure ).
The surgical part of this case study took place under local anesthesia. A transginigival incision was made after tissue infiltration with local anesthesia. A buccal mucoperiosteal flap was raised and bone was exposed. The third molar was elevated and removed, followed by debridement and curettage of all debris and granulation tissue in the area. Subsequently, the 'scaffold-like', CaCl2 activated PRGF was implanted in the bony defect. The volume of PRGF was adequate to provide full cover of the whole defect. The flap was carefully repositioned and sutured with horizontal mattress sutures. An immediate postoperative dental panoramic tomography was obtained and considered as the "baseline image" for this case study (Figure ). The patient was given full postoperative instructions, including contact details if postoperative complications to occur. Also, anti-inflammatory and antimicrobial cover was provided for 5 days.
At the first postoperative day, moderate pain was the main complaint and was controlled by NSAIDs. After two days, the pain subsided. No postoperative swelling was reported by the patient. There were neither symptoms nor clinical suspicion that would suggest alveolar osteitis (dry socket), indicating normal clotting and coagulation [,]. One week postoperatively, the sutures were removed and there was good tissue healing on examination.
On the fiftieth postoperative day, and according to the PRGF clinical protocol, radiographic evaluation took place and showed noticeable enhancement of density and radio-opacity in the third molar socket area, in comparison with the baseline image (Figure and Figure ). Further clinical examination showed significant reduction of periodontal pocketing by 3 mm and evidence of new bone formation.


A 31-year-old Turkish woman, weighing 78 kg, was scheduled for caesarean section under general anesthesia. She was not operated previously. Induction of anesthesia was achieved with 130 mg of propofol. Muscular relaxation was achieved before intubation with 12 mg of mivacurium. Isoflurane was used as the general anesthetic inhalation agent. The operation lasted for 30 minutes and the sectio-surgery was uneventful. After the surgery, the inhalation agent was discontinued and the patient received 100% oxygen. It was noted that emergence seemed to be prolonged after 10 minutes. All vital signs were stable, showing no signs of tachycardia or hypertension. Oxygen saturation remained 100%. After an additional 10 minutes, there was suspicion of a PChE deficiency. Peripheral nerve stimulator (PNS) produced zero twitches. Three milligrams of midazolam was administered intravenously for its sedation and amnestic effects. Later the patient was transferred to the post-anesthesia Care Unit (PACU) for observation and ventilator support. Sixty-two minutes later, spontaneous muscle twitching was noted. One hour and twenty-two minutes later from the initial use of mivacurium, the patient had regained sufficient motor function to meet extubation requirements. Blood samples were drawn and sent to confirm a PChE deficiency [Paitent's PChE value (normal range) 1017 IU/L (2000 to 11000 IU/L)]. The patient was transferred to a hospital ward for the evening and discharged two days later. The PChE values of the patient who was called for a control after two months was considered between the normal ranges (3124 IU/L).


A 47 year-old Turkish male, weighing 83 kg, was scheduled for laparoscopic cholecystectomy under general anesthesia. The patient had received two previous general anesthetics one for appendectomy 28 years ago and another for right inguinal hernia operation 19 years ago. It was learned that the case was applied succinylcholine during both of her previous operations and that he did not have a a history of a post-operative apnea etc. The patient had been using sertraline (100 mg/day) for 3 years due to major depressive disorder. Induction of anesthesia was achieved with 200 mg of propofol. Tracheal intubation was achieved with 17 mg of mivacurium. Isoflurane was used as the general anesthetic inhalation agent. The operation lasted for 25 minutes and further dose(s) of mivacurium were not required. After the surgery, the inhalation agent was discontinued, the patient received 100% oxygen but PNS produced zero twitches. All vital signs were stable, and oxygen saturation remained 100%. After an additional 20 minutes, there was suspicion of a PChE deficiency. Five milligrams of midazolam was administered intravenously for its sedative and amnestic effects. Later the patient was transferred to the PACU for observation and ventilator support. Two hours and twenty minutes later, spontaneous muscle twitching was noted. Three hours and fifteen minutes later from the initial use of mivacurium, the patient had regained sufficient motor function to meet extubation requirements. Plasma cholinesterase was found to have very low activity (788 IU/L). The patient was transferred to a hospital ward for the evening and discharged four days later.


A 73 year-old Turkish woman, weighing 43 kg, was scheduled for breast biopsy under general anesthesia. She had a cholecystectomy 32 years ago, a hysterectomy 23 years ago and an appendectomy operation 17 years ago. It was learned from the anamnesis of the patient that succinylcholine had been administered on three previous occasions during anesthesia without a prolonged effect. Following preoxygenation, induction of anesthesia was achieved using propofol 90 mg and later mivacurium 7 mg. Following tracheal intubation anesthesia was maintained with isoflurane. The procedure was completed within 20 minutes. But there was no clinical evidence of recovery of neuromuscular function and there was no response to train of four stimulation. Anesthesia was therefore maintained with isoflurane 0.5% in 50% nitrous oxide and oxygen. Because there was no evidence of improved neuromuscular function 60 minutes after administration of mivacurium. The patient was transferred to the PACU for continued mechanical ventilation and neuromuscular monitoring. Sedation was maintained with a continuous iv infusion of midazolam. Four hours and twenty minutes after the administration of mivacurium, train of four response ratio was 75%. Midazolam infusion was discontinued and clinical assessment confirmed recovery of neuromuscular function. Patient was extubated 340 minutes following the administration of mivacurium and further recovery was uneventful. Plasma cholinesterase was found to have very low activity (598 IU/L).