A 53-year-old female with poorly controlled diabetes mellitus (DM) was brought to the emergency department with focal motor clonic seizures induced by forced voluntary eye closure due to rubbing her eyes. During hospitalization it was observed that seizures began when she closed her eyes strongly. Every time she repeated the eye closure the seizures recurred. The seizures started two days previously and occurred with each forced voluntary eye closure. She had no seizure with spontaneous eye blinking or sleeping, or with horizontal, vertical or rotatory eye movements. The seizures occured in the left orbicularis oculi, and then spread to the ipsilateral angularis oris and upper extremity, turning to the left side of the head. They lasted 2 to 3 minutes. The patient did not lose consciousness during seizures. She had had type 2 DM for eight years and her past medical history revealed no other significant disease. She had no history of seizures or other neurological disorder. She was using only insulin as her medication. The physical examination, including the neurological examination of the patient, revealed no abnormality. Her visual acuity, pupil reactions to light and eye movements were normal. The laboratory tests showed an elevated blood glucose level of 550 mg/dL but no evidence of ketosis. Serum osmolarity was 279.8 mOsm/L. Her ictal electroencephalogram (EEG) showed discharges of high amplitude spike-waves and multiple spikes-waves which localized to the right temporoparietal electrodes involving to the adjacent area. (). The photoparoxysmal response was not observed during the photic stimulation. Brain magnetic resonance imaging (MRI) was normal. Functional MR and single photon emission computed tomography (SPECT) were not performed. Seizure control was achieved immediately after the glucose level fell to normal levels. When the blood glucose levels decreased slowly to about 150 mg/dL in five days, the seizures ended completely. No anticonvulsants were used. During the next 3 months follow-up, no seizures occured. The patient had been free of seizures with effective control of blood glucose.


A 43-year-old Mexican Hispanic man arrived in our hospital with a chronic headache. His neurological examination was unremarkable. The imaging workup showed a giant basilar artery aneurysm, dimensions 32 mm × 20 mm (Figure ), and that the lesion was located at an angled portion of the vessel. For the management of this aneurysm, we decided to place a stent at the aneurysm neck in order to: 1) straighten the shape of the parent vessel; 2) promote a shift in the pattern of the inflow into the sac and the outflow from the lesion; and 3) foster the thrombosis of the aneurysm.
The lesion was reached through a left vertebral approach with a 6F guiding catheter (Envoy, Cordis, Miami Lakes, FL). The medical periprocedural management at that time (1997) was empirical, as no rules for anticoagulation or antiplatelet treatment had been defined for intracranial stents. The vascular neurologist advised that the patient be placed under full anticoagulation without any antiplatelet drug. A 3.5 mm × 12 mm balloon-expandable stent (BES) (AVE Medtronic; Advanced Vascular Engineering, Santa Rosa, CA) was advanced and deployed at the neck of the lesion (Figures ).
When trying to retrieve the balloon, the stent slipped backwards and its distal end tilted towards the sac. (Figures ). We therefore decided to carefully slip the stent forward into the aneurysm by inflating the balloon again and pushing the stent distally until the whole of it was floating within the aneurysm (Figures ). A 3.5 mm × 18 mm BES was advanced into the lesion and subsequently deployed within the parent artery to cover the full length of the diseased portion of the vessel, including the aneurysm neck (Figure ) In the immediate post-procedural angiographic runs, we observed a sluggish intra-aneurysmal vortex motion and a correction of the shape of the parent vessel to a 45-degree angle was conducted. The neurological status of the patient was unchanged and he was then discharged to the neurosurgical ward.
A control digital subtraction angiography (DSA) performed four hours later to counter clinical deterioration showed thrombosis of the aneurysm along the basilar artery (Figure ). Rapid recanalization of the vessel was obtained through a mechanical procedure (balloon angioplasty) with the use of antiplatelet treatment (ticlopidine 250 mg and aspirin 100 mg) (Figure ). The patient subsequently recovered and this episode left a pontine stroke as a sequela (Figure ).
At ten years after the operation, the patient has a minor paresis, with a modified Rankin Scale of 2. A new imaging follow-up with DSA and three-dimensional reconstruction has been performed, which showed that the aneurysm remains occluded (no recanalization), the parent vessel is still patent, and no in-stent stenosis is present (Figure to ). The clinical evolution of the patient is described in Table 1.


We report the case of a 70-year old Caucasian woman who was referred to the thoracic oncology unit of our hospital for the management of a retrosternal mediastinal mass. She had been well 8 weeks before admission when she experienced the sudden onset of sharp left anterior chest pain. The pain was worse in the area adjacent to the sternum and also worsens when she takes a deep breath. In 1999, she underwent radical left side mastectomy followed by CEF (cyclophosphamide, epirubin and fluorouracil) chemotherapy and radiotherapy. The clinical and histological characteristics of the primary breast cancer revealed a Stage IIIa adenocarcinoma with positive axillary lymph node metastasis. Her estrogen receptor assay, as well as the amplification of the human epidermal growth factor receptor type 2 (HER 2/neu) was negative. Expression of her progesterone receptors was defined as low (Reiner score for staining of tumour-cell nuclei). On admission our patient's vital signs were normal. She had neither jugular venous distension nor cervical or supraclavicular lymphadenopathy. Her chest was clear on auscultation. There was no tenderness on palpation of her ribs or sternum. The remainder of her examination results was normal.
Computed tomography (CT) scanning and magnetic resonance imaging (MRI) of our patient's chest revealed a 74.2 × 37.7 × 133.6-mm mass in her anterior mediastinum adjacent to the main pulmonary artery, the right ventricle, and ascendens aorta contiguous to the pericardium (Figures and ). There was no specific direct evidence of vascular invasion but we raised the question of pericardial invasion. Our patient was vigorously scrutinized for metastatic disease, which included routine blood chemistries and the determination of lipid associated sialic acid, carcinoembryonic antigen (CEA) and CA 15-3 serum markers. CT scan of her neck and abdomen for restaging revealed no other foci of metastatic disease. A bone scan showed uptake only in her sternum.
Our patient was anaesthetized and ventilated with a double-lumen endotracheal tube. An epidural catheter was also inserted for pain control during the peri-operative period. Our patient was placed at first in a right thoracotomy position with soft rotation of the coxa towards the surgeon. Standard thoracotomy incision was used to expose the serratus anterior muscle (SAM). The SAM was identified and mobilized by separating it from the chest wall and then carefully dividing its attachments to the first 4 to 5 ribs, with a periosteal elevator at first and then with a cautery. As dissection proceeded upward toward her axilla, the contribution of the lateral thoracic artery was seen entering the muscle on its anterior cephalic border. The blood supply to the serratus anterior may come from the thoracodorsal pedicle, from the subscapular pedicle, or directly from the axillary artery. In our case, our patient's blood supply came from the serratus anterior branch from the thoracodorsal artery, which originates as the largest branch from the subscapular artery. During the procedure these branches were identified and preserved. The harvested SAM was advanced and transposed within its arc of rotation towards the midsternal line to cover the defect.
The sternal incision started at the level of our patient's manubriosternal joint and extended inferiorly to her xiphisternum. The surgical resection was a vertical elliptical incision of the visible mass. Total sternectomy was performed at all layers encompassing our patient's skin, subcutaneous tissues, right pectoralis major muscle, all her costal cartilages of the first five ribs (Figure ), and the anterior part of her pericardium. Mobilization began first on one side of her sternum with exposure and section of the ribs. The ribs were divided laterally. Her right internal thoracic artery and the intercostals neurovascular bundle were ligated with absorbable suture. Lastly, the critical point of mass attachment to the heart was approached. Immediate closure of the defect was performed without cement but with a single 0.6-mm Gore-Tex cardiovascular mesh (W. L. Gore and Associates, Flagstaff, Arizona) which was cut to a size smaller than that of the defect. The mesh was thus effectively stretched when it was sutured to her chest wall so that any laxity in the reconstruction was alleviated (Figures and ). The serratus anterior myocutaneous flap was then secured with heavy non-absorbable suture over the Gore-Tex mesh.
Pathology revealed a poorly differentiated invasive carcinoma infiltrating our patient's sternum with the involvement of the pericardium (Figure ). The amplification of the human factor margins was clear, while immunohistochemistry was negative.
Epidural analgesia was employed in the immediate postoperative period. Postoperative respiratory function tests revealed satisfactory results and our patient could be relieved from endotracheal intubation a day after the operation. She did not have any problems in her daily activities or any occurrence of chest flailing or paradoxical movement of the chest. Scapular winging occurred although any effort was made to preserve the a third of the lower part of her serratus anterior muscle. No flap infection or wound dehiscence was noted, and she was discharged from the hospital nine days after the operation.
She received two additional cycles of CEF chemotherapy consisting of 2 cycles of oral cyclophosphamide at a dose of 75 mg/m2 on days 1 through 14, 60 mg/m2 of epirubicin on days 1 and 8, and 500 mg/m2 of fluorouracil intravenously on days 1 and 8. During her CEF therapy she also received antibiotic prophylaxis with ciprofloxacin at a dose of 500 mg orally twice daily. She is well 18 months after the diagnosis, and she exhibited no evidence of recurrent disease on serial CT and MRI scans of her chest, abdomen, and brain. She remains asymptomatic and the stability of her chest wall is well-preserved.


A 36-year-old-man without a medical history of pulmonary tuberculosis or BCG vaccination was admitted for dysphonia and dysphagia for 6 months. Laryngoscopic examination revealed thickening of the left vocal cord and the ventricular strip, with edema. Laryngeal CT scan [Figures and ] revealed a localized, regular thickening of the left vocal cord, associated with irregular thickening of the posterior laryngeal wall. The anterior commissure and sub-glottic region were normal. There were neither any cartilaginous abnormalities nor any cervical adenopathy. A biopsy was performed, which revealed caseo-follicular tuberculosis laryngitis. The chest radiograph and abdominal USG were normal. On further interrogation and investigations, it was found that the patient was negative for the human immunodeficiency virus and his sputum was negative for acid-fast bacilli.


A 7-year-old girl presented with a 2-week history of shoulder-tip pain, progressive fever and right upper quadrant pain. She had no history of vomiting, diarrhea or weight loss.
On examination, she was febrile and had a palpable, firm mass in the right upper quadrant. She had a temperature of 38°C, heart rate of 145/min and respiratory rate of 28/ min. Blood culture was negative and did not grow any organism. Serology for cytomegalovirus (CMV), Ebstein-Barr virus, hepatitis B surface antigen, hepatitis C and hydatid was negative. Serum α-fetoprotein levels of 0 and serum HCG <2 were recorded.
USG of the abdomen [] showed a large, mixed, complex solid-cystic lesion, which was predominantly a solid lesion with a heterogenous cystic component, within the right lobe of the liver with no flow or increased vascularity on color Doppler examination. CT scan revealed a well-defined, solitary, cyst-like hepatic mass []. No definite solid mass-like component, enhancing nodule or calcification/fat was appreciated. A few hyperdense areas were seen within this cystic-looking lesion. No vascular compromise or invasion was seen. No contrast enhancement was seen. Subsequently, an MRI of the abdomen was also performed [], which revealed the hepatic lesion to be predominantly hyperintense on the T2W images, but with central areas of low signal intensity. The T1W axial images [] revealed the lesion to be iso to heterogeneously hypointense and did not show any enhancement after intravenous contrast administration []. There was thus a discordance between the predominantly solid appearance on USG and the predominantly cystic appearance on CT scan and MRI.
She underwent surgical biopsy. Immunohistochemistry was performed, which revealed that tumor cells were positive for α-1-antitrypsin and α-1-antichymotrypsin and some cells were also positive for cytokeratosis. No positivity was seen for CD10 or desmin. Several CD68-positive macrophages were found. The myxoid morphology of the lesions, the presence of eosinophilic hyaline bodies and the immunohistochemical spectrum were typical for UES of the liver []. Rhabdomyosarcomatous differentiation was not seen. Based on these findings, we arrived at a final diagnosis of UES of the liver.
This patient is presently on chemotherapy (ifosfamide, doxorubicin and ondansetron) and follow-up imaging (CT scan) has revealed mild reduction in size. Future plans include surgery, if feasible, followed by radiation and postoperative chemotherapy. This is the currently accepted clinical practice.


A five-year-old boy presented with congenital anomaly of the left auricle. Antenatal history was uneventful and without any exposure to teratogenic agents. The child was full term normally delivered with no history of birth trauma. On examination, the left auricle was normal in size and shape but hanging from the temple by only the ear lobule [Figures , ]. The right side ear was normal. External auditory meatus and tragus were normal on both the sides.
No other congenital anomalies were found in both the cases. A special attempt was made to survey all the other structures that develop from the 1st. and 2nd. Branchial arches, - the mandible, maxilla, zygoma and squamous part of temporal bone, the muscles of mastication and facial expression, the tongue, the parotid and the cranial nerves and clinical examination revealed no abnormality besides the auricular malformation.
For surgical correction, the desired position of ear was marked with ink on the temple. After intubation, a paring incision was made on the tragal side ear and a vertical incision was given on the temple on the premarked side; the ear was reattached to the temple by fixing the ear cartilage to the fascia over temple region with non absorbable sutures and skin incision closed [].


A 66-year-old man underwent abdominoperineal resection of the rectum for advanced rectal cancer after preoperative chemoradiotherapy. During the operation, the root of the inferior mesenteric artery (IMA) was not ligated. The IMA was tagged and preserved, separating the nervous and lymphatic tissues from the root to a site just peripheral of the confluence of the left colic artery (LCA), then the superior.rectal artery (SRA) was ligated (). On day 3 post surgery, the patient experienced epigastric pain and vomited a large amount of bile-stained fluid. Plain abdominal roentgenograms showed marked gaseous distension of the upper small bowel. Under upper endoscopy, a decompression tube was placed at the upper jejunum 30 cm distal to the ligament of Treitz (). Because the third portion of the duodenum was bent caudally, the decompression tube could not be passed more distally. By day 5 post surgery, symptoms associated with ileus had disappeared. On the seventh postoperative day, the patient was awakened by epigastric pain, immediately followed by copious coffee-grounds diarrhea from the end colostomy. Although anemia and edema of the eyelids were present, the patient's general appearance was good. Upper endoscopy demonstrated a large amount of fresh blood in the stomach and a longuitudinal ulcerative lesion having a visible pulsative vessel in the base of the third portion of the duodenum (). Because of the severe pulsation and intermittent but spurting bleeding, hemostasis under endoscopy could not be performed. To identify the origin of bleeding, an emergency computed tomography (CT) was performed. Surprisingly, on arterial-phase CT revealed that the marking clip placed at the third portion of the duodenum was very close to the stump of the SRA (, arrow). This finding implied that the source of bleeding was the stump of the SRA. Thirty minutes after the emergency CT, the patient vomited a large amount of fresh blood and became hemodynamically unstable. Immediately after fluids resuscitation and transfusion with 4 packed RBC and FFP, the patient was transferred to the angiography room. Emergency angiography revealed active projectile bleeding from the stump of the SRA (). The stump of the SRA was in direct communication with the third portion of the duodenum (, arrow). Extraluminal hemorrhage was not identified. The length of the proximal portion of the IMA was considered to be sufficient for embolization. The stump of the SRA was obliterated using microcoils (TORNADO) between the root of the IMA and the tip of the ligation distal to the LCA (). Coil embolization was successful for achieving hemostasis. During the next 24 hours, the patient underwent fluid resuscitation and blood transfusion including 4 packs of RBC and FFP. Rebleeding did not develop after coil embolization. By the 10th day after coil embolization, symptomatic improvement and hemodynamically stable status without dopamine were achieved. On the 14th day after coil embolization, upper endoscopy revealed only the flexion of the third portion of the duodenum (). CT showed no sign of intraabdominal hemorrhage (). Edema and mild ischemic change of the end colostomy were identified as due to obstruction of the LCA arising from coil embolization. A diet was given from the 15th day after coil embolization. The clinical course was uneventful and the patient was discharged on the 40th postoperative day.
One of the rare points in the present case is the site of bleeding. Delayed postoperative hemorrhage in colorectal surgery has rarely been reported. All reports, including Japanese case reports, have demonstrated that the usual source of hemorrhage is a pelvirectal space associated with pseudoaneurysm of the ramification of the iliac artery and that the mechanism for formation of pseudoaneurysm was violation or exposure of the tunica adventitia of these vessels caused by lymph node dissection or postoperative anastomotic leakage [–]. In the present case, the source of hemorrhage was identified at the stump of the SRA. Although postpancreatectomy hemorrhage often occurs via active bleeding from the stump of the GDA, closely associated with anastomotic leakage at the pancreatojejunostomy [], our search of PUBMED showed no previous reports describing delayed hemorrhage from the stump of the SRA after colorectal surgery. In addition, a characteristic of this uncommon complication is that bleeding from the stump of the SRA was directly linked with the duodenum, leading to intraluminal hemorrhage without expansion into the abdominal cavity. Here we investigate the mechanism of this uncommon complication with a main focus on factors associated with surgical procedures in the present case. First, during lymph node dissection, the IMA was preserved and skeletonized from its base to its tributary (the peripheral side of the root of the LCA). The stump of the SRA was located approximately 4 cm distal to the base of the IMA (). Second, through the excision of the mesocolon, the peritoneum was resected from the infraduodenal portion to the bifurcation of the iliac artery, exposing the anterior aspect of the aorta, resulting in thebroad range of peritoneal defect. The peritoneal defect was repaired with an interrupted suture using 3-0 absorbable sutures. Because the transverse defect was quite broad, the suture line of peritoneal reconstruction yielded robust tension and contraction of the adjacent organs. Accordingly, the third portion of the duodenum was displaced downward (). Third, during the operation, an end colostomy was constructed with the sigmoid colon. During the maneuver of the left colon, the splenic flexure was not mobilized. Therefore, elevation of the end colostomy toward the abdominal wall yielded spasiticity of the mesenteric root of the left colon, including the stump of the SRA, leading to rotation of the stump of the SRA toward the cephalad portion very close to the anterior aspect of the duodenum (). Fourth, unfortunately, the patient developed palalytic ileus at the 3rd postoperative day. The flexion of the duodenum made it difficult to place the decompression tube distal to the ligament of Treitz. We infer that a strong force to the third portion of the duodenum during the insertion of the decompression tube violated the duodenal wall, and the stump of the SRA ().
In the present case, the patient developed delayed postoperative hemorrhage 4 days after placement of the decompression tube for postoperative ileus. Although we could not identify the formation of pseudoaneurysm on the emergency CT or angiography, it is assumed that exposure of the tunica adventitia of the IMA and contact between the decompression tube and the stump of the SRA caused a pseudoaneurysm of the stump.


A 20-year-old man underwent EPS for evaluation of recurrent palpitations. Baseline 12-lead electrocardiogram was normal. Catheter positioning induced a sustained narrow QRS complex tachycardia with 1:1 ventriculo-atrial (VA) relationship. Coronary sinus (CS) cannulation was extremely difficult due to anatomical reasons and could not be performed in the beginning of the study. During the tachycardia, there was a spontaneous change in CL from 346 to 265 ms. A significant QRS voltage alternans was also observed (). What are the possible mechanisms associated with this spontaneous change in CL? Is it possible to make a correct diagnosis of the tachycardia without the CS catheter appropriately positioned?


The patient was a 40-year-old man who met the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for schizophrenia. Onset of schizophrenia occurred in his early twenties. The typical antipsychotic drug haloperidol was administered for some time. After he stopped the medication (haloperidol 2 mg) because of tremor, he jumped from a second floor window due to delusions and hallucinations. He was then admitted to the hospital's emergency medical center with a right calcaneal fracture. His right leg joint was fixed in a plastic cast, and he was admitted. Treatment with blonanserin (8 mg) and flunitrazepam (2 mg, at night) was initiated for auditory hallucination. At 1 week later, the blonanserin was increased to 16 mg because his persecutory delusions and auditory hallucinations persisted. After the increase in dose (16 mg), the patient complained of leg restlessness. His global score on the Barnes Akathisia Scale [] was 3 ('moderate akathisia'). Substantial relief of akathisia was noted on the next day of fluvoxamine (50 mg) treatment, at which point his global score on the Barnes Akathisia Scale was 0. At 1 week later, the dose of blonanserin was increased to 24 mg since he still had psychotic symptoms. Fluvoxamine (50 mg) continued to be administered. He had no recurrence of the akathisia. After 1 month, he was discharged home because his psychotic symptoms were improved.


The patient was a 48-year-old woman who met the DSM-IV criteria for schizophrenia. The onset of schizophrenia occurred in her late twenties, and 10 years previously she had been admitted to a hospital emergency medical center with delusions and hallucinations. She was treated for this previous episode with haloperidol (6 mg), but she had stopped the medication due to EPS. She was admitted to the hospital emergency medical center with a recurrence of psychosis, including delusions and hallucinations. Treatment with blonanserin (8 mg), flunitrazepam (2 mg, at night), and levomepromazine (50 mg) was initiated. At 3 days later, the patient complained of leg restlessness. Her global score on the Barnes Akathisia Scale [] was 3. Substantial relief of akathisia was noted on the next day of fluvoxamine (50 mg) treatment, at which point her global score on the Barnes Akathisia Scale was 0. The dose of blonanserin was increased to 24 mg due to an abnormal experience. Fluvoxamine (50 mg) continued to be administered. After 3 weeks, she was discharged home because she had no recurrence of the akathisia.


The patient was a 63-year-old man who met the DSM-IV criteria for schizophrenia. The onset of schizophrenia occurred in his early twenties. He had been treated with olanzapine (10 mg) for the last 4 years, but he had a tendency to stop the medication due to appetite and body weight. He was admitted to the hospital due to delusions and hallucinations at his older brother's funeral. Treatment with blonanserin (8 mg) and etizolam (1 mg, at night) was initiated for auditory hallucinations and delusions. At 2 weeks later, the patient complained of leg restlessness. His global score on the Barnes Akathisia Scale [] was 2. Substantial relief of akathisia was noted after 14 days of fluvoxamine (50 mg) treatment. His global score on the Barnes Akathisia Scale was 0.


The patient was a 36-year-old man who met the DSM-IV criteria for schizophrenia. The onset of schizophrenia occurred in his early twenties. He was admitted to the hospital's emergency medical center with a cut to the right of the neck from an unsuccessful suicide attempt. Treatment with blonanserin (8 mg) and flunitrazepam (2 mg, at night) was initiated for auditory hallucinations. At 2 days later, the patient complained of leg restlessness. His global score on the Barnes Akathisia Scale [] was 3. Substantial relief of akathisia was noted on the next day of fluvoxamine (50 mg) treatment. His global score on the Barnes Akathisia Scale was 0. Blonanserin (8 mg), fluvoxamine (50 mg), and flunitrazapam (2 mg) continued to be administered. After 2 weeks, he was discharged home because he had recovered.


The patient was a 42-year-old man who met the DSM-IV criteria for schizophrenia. The onset of schizophrenia occurred in his early twenties. He had been treated with haloperidol (18 mg), chlorpromazine (150 mg), biperiden (6 mg), and haloperidol decanoate (100 mg) for some time. He tended to drink a lot of water due to mouth dryness. He was admitted to the hospital's emergency medical center because he had fallen at home. He was diagnosed with low sodium blood syndrome due to water intoxication, and he was treated with intravenous nutrition. After recovery, he was treated with blonanserin (16 mg) and flunitrazapam (2 mg, at night). At 2 days later, the patient complained of leg restlessness after the increase in blonanserin (24 mg). His global score on the Barnes Akathisia Scale [] was 3. Substantial relief of akathisia was noted on the next day of fluvoxamine (50 mg) treatment, at which point his global score on the Barnes Akathisia Scale was 0. After 1 week, he was discharged home because she had no psychotic symptoms.


55-year-old female presented with right flank pain and weight loss. CT scan demonstrated an 8.5-cm right lower pole enhancing renal mass suspicious for renal cell carcinoma (RCC) with renal vein thrombus. Metastatic workup was negative.


50-year-old female presented with right shoulder pain and left flank pain. CT demonstrated a left 8.0-cm renal mass with renal vein thrombus overlying the peri-aortic region. Metastatic workup revealed osseous metastases in the spine and left clavicle. (Figure ) Cytoreductive nephrectomy with thrombectomy was planned as part of a multi-disciplinary approach involving systemic targeted therapy with sunitinib (Sutent, Pfizer, NY) and radiation therapy.


Haiba, a woman aged 54, lived in a semi rural village on the very outskirts of Dar es Salaam in a household with her 12 family members. Five of these were her children. Her grown-up daughter was seriously ill from tuberculosis and required demanding daily care and medicine. Haiba was not alone in her care-giving role. Other females in the households assisted her, but being the mother of the ill daughter, Haiba had the primary care-giving responsibility for her daughter[] and since more than one person within the household was sick, it entailed choosing whom to help. Haiba chose her daughter's health to her own. This meant that she occasionally went without insulin in order to ensure that there was enough money within the household to buy her daughter's medicine.
Haiba's story illustrates how the needs of other relatives also had to be met which often compromised the needs of the person with diabetes. It further illustrates how the double burden of disease puts tremendous pressure on the remaining relatives[] and how prioritising was a continuous process that severely jeopardised the sustainability of the long-term treatment schemes necessary for survival.
In terms of financial support, our findings also show that there were limits to the obligations of kin. People were seeking out other ways of getting support as the mobilisation of resources had been extended to wider social networks. Many of the informants drew on support within their social network by approaching friends, colleagues or people within their local communities. A male informant explained to us in the following part of a home interview (Haamed, 35):
"Sometimes, when things get hard, I go to the business where I used to work and the colleagues they give me something. It is not fair every time to go to my brother."
Similar observations have been revealed in a recent study from western Kenya[]. This tells us of the need to revise the role of the family in general and include alternative support possibilities in our understanding of the conditions for illness actions in particular.
Furthermore, we argue that the diminished capacity due to hardship and deaths within the networks made the dynamics of illness action discontinuous as the intentions of the primary agent may be disrupted by other events. Such events may be the sudden death of the household provider or other relevant family members. The unpredictability and discontinuity of the life condition of the people with diabetes in the Tanzania study are illustrated through the story of one of the informants, Fatima, a woman of 32.


The first patient was a 41-year-old, 68 kilogram man with a past medical history of asthma, smoking, and hepatitis. The patient was found to have a right internal carotid artery terminus aneurysm by magnetic resonance imaging which was performed during an evaluation for recurrent headaches. The patient had no previous history of cerebral vascular accident (CVA) or subarachnoid hemorrhage (SAH). On the day of surgery, his preoperative vital signs included a BP of 111/64 mmHg and a heart rate (HR) of 59 beats/minute. The treatment plan was for coiling of the cerebral aneurysm in the interventional radiology suite under general anesthesia. Premedication included midazolam (2 mg) and fentanyl (50 μg) followed by placement of an arterial cannula in the right radial artery. The patient was transported to interventional radiology and positioned for comfort. Standard American Society of Anesthesiologists (ASA) monitors were placed. The initial BP was 100/62 mmHg with a HR of 94 beats/ minute. Following pre-oxygenation with 100% oxygen, anesthesia was induced with lidocaine (100 mg), fentanyl (200 μg), and propofol (total dose 150 mg). Endotracheal intubation was facilitated with vecuronium (10 mg). After endotracheal intubation, the BP was 105/52 mmHg with a HR of 71 beats/minute. The vital signs remained within 20% of baseline throughout the procedure with general anesthesia being maintained with desflurane (expired concentration 4-8%) and 250 μg of fentanyl. The procedure lasted approximately one hour and forty-five minutes. The aneurysm was only partially occluded thereby mandating the need to avoid hypertension during anesthetic emergence. Residual neuromuscular blockade was reversed with neostigmine and glycopyrrolate, lidocaine (100 mg) was administered, and the desflurane was discontinued. The systolic blood pressure (sBP) increased to 140-150 mmHg. A clevidipine infusion was started at 8 mg/hr with a decrease in the sBP to 120 mmHg within 2-3 minutes. The clevidipine infusion was decreased to 4 mg/hr and the sBP remained at 120 mmHg along. HR increased from 72 to 80 beats/minute following the start of the clevidipine during emergence. The patient's trachea was extubated and he was transported to the post-anesthesia care unit (PACU) with the clevidipine infusion at 4 mg/hr. His sBP remained at 110-120 mmHg. The clevidipine infusion was slowly weaned over the next 20 in the PACU in 2 mg/hr increments every 10 minutes. The patient was discharged home the next day without complications.


The second patient was an 83-year-old, 76 kg man with a past medical history of hypertension treated with lisinopril and hydrochlorothiazide and a distant history of tobacco use. During an evaluation for headaches, an MRI revealed an aneurysm of the left internal carotid artery (LICA) in the supraclinoid territory. There was no history of previous CVA or SAH. The morning of surgery, the patient's BP was 134/51 mmHg and the HR was 71 beats/minute. The patient had not taken his routine antihypertensive medications the morning of surgery. The treatment plan was for coiling of LICA aneurysm in the interventional radiology suite under general anesthesia. Preoperatively, an 18 gauge IV cannula and premedication provided by intravenous midazolam (2 mg). An arterial cannula was placed in the right radial arterial. The patient was transported to the interventional radiology suite and positioned to comfort. Standard ASA monitors were applied and the patient was pre-oxygenated with 100% oxygen. Anesthesia was induced with lidocaine (100 mg), fentanyl (100 μg), and propofol (total dose of 80 mg). Neuromuscular blockade was provided by vecuronium (10 mg). Immediately after endotracheal intubation, the BP was 105/70 mmHg with a HR of 60 beats/minute. Anesthesia was maintained with desflurane (expired concentration 4-6%) and 100 mg of fentanyl. The procedure lasted approximately one hour and twenty minutes. The vital signs remained within 20% of baseline throughout the procedure. Secondary to the anatomy of the aneurysm, coiling could not be accomplished. The patient's trachea was extubated during spontaneous ventilation with an expired concentration of 1 MAC of desflurane. Following tracheal extubation, the desflurane was discontinued. The SBP increased to 150-170 mmHg with a heart rate of 80-90 beats/minute. A clevidipine infusion was started at 2 mg/hour. Within 5-7 minutes, the sBP decreased to the 110-120 mmHg with an increase in the HR to 90-94 beats/minute. The patient was transferred to PACU with the clevidipine infusion at 2 mg/hr. The infusion was weaned over the next 30 minutes in 1 mg/hr increments in the PACU. He remained stable with the sBP ranging from 110-120 mmHg. The patient was discharged home the next day without complications.


The third patient was a 72-year-old, 85 kg man that found to have an ACOM aneurysm during a preoperative evaluation for an elective orthopedic operation. A CT scan of the head was obtained during the preoperative evaluation as the patient had neurologic symptoms similar to a transient ischemic attack. The patient's past medical history included a CVA in 2003 without residual neurologic deficit, osteoarthritis of the left shoulder and hypertension which was being treated with amlodipine and lisinopril. The treatment plan was to coil the aneurysm in the interventional radiology suite. On the morning of surgery, the patient did not take his usual anti-hypertensive medications. The preoperative vital signs on the morning of the procedure included a BP of blood 147/97 mmHg and a HR of 69 beats/minute. A 16 gauge intravenous cannula was started and following sedation with midazolam (2 mg) and fentanyl (100 μg), an arterial cannula was placed in the right radial artery. The patient was transported to the interventional radiology suite where standard ASA monitors were applied. Following preoxygenation, anesthesia was induced with lidocaine (100 mg), fentanyl (150 μg), and a total of 130 mg of propofol titrated to the BP. Neuromuscular blockaded was achieved with cisatricurium (20 mg). Following endotracheal intubation, anesthesia was maintained with maintained with isoflurane (end-tidal concentration of 0.5-1%) and fentanyl (total dose of 500 μg). Throughout the initial 2 hours of the procedure, the sBP varied from 100-120 mmHg with a diastolic BP of 70-85 mmHg. A clevidipine infusion was started at 2 mg/hour to control an increasing sBP up to 130-150 mmHg. The sBP returned to the range of 100-120 mmHg within 5 minutes of starting the infusion. The clevidipine infusion was continued for the next 90 minutes and the BP remained at 100-120 mmHg. A spike in the BP occurred with an increase of the sBP to 144 mmHg as the radiologist noted that there was bleeding from an intracranial vessel leading to the aneurysm (not the aneurysm itself) which occurred during the attempted coiling. Protamine was given to reverse heparin and the clevidipine infusion was increased 3 mg/hour. The sBP returned to its baseline value of 100-120 mmHg within 5 minutes. A CT scan of the head was obtained which demonstrated a subarachnoid hemorrhage with no change in the aneurysm. The patient was transported to the ICU with the clevidipine infusion at 3 mg/hr. This was continued for 4-6 hours in the ICU and then the patient was transitioned back to his routine oral anti-hypertensive medications and to oral nimodipine for preventing of cerebral vasospasm. His trachea was extubated the next day. The remainder of his post-procedure course was unremarkable without evidence of cerebral vasospasm or new neurologic deficit.


A 59-year-old woman was admitted to her reference hospital for dyspnea. Chest radiography showed a severe right pleural effusion. Her medical history included breast cancer (pT2pN1M0) diagnosed when she was 52, which was treated with surgery, adjuvant chemotherapy, adjuvant radiotherapy and hormonotherapy (3 years of tamoxifen and 2 years of letrozole). The patient did not have other diseases or congenital malformations and had not required previous abdominal or thoracic surgeries. The last normal follow-up was 2 months prior to her admission for the dyspnea. A thoracic tube was inserted, and 1,000 cc of pleural fluid was drained. After cytology revealed the presence of malignant breast cells, right-sided talc pleurodesis was performed. The patient had a good postoperative evolution, without fever or pain, and was discharged four days after the talc pleurodesis.
The patient came to our center for oncological treatment. A staging CT scan showed a heterogeneous hepatic lesion (9 × 6.5 cm) with air inside (Fig. ). In addition, bone and pleural affectation from the patient's metastatic breast cancer were observed. The patient was asymptomatic, without fever, abdominal pain or abnormal laboratory tests. A hepatic abscess was ruled out because of her clinical history, and a hepatic laceration made during the talc-injection procedure was suspected. Hormonal treatment (exemestane) was started. A new CT scan was performed one month later. A diffuse malignant hepatic infiltration was observed (Fig. ) without any tumor progression at distal sites. Laboratory analysis yielded the following values: bilirubin 1.66 mg/dL; GOT 146 UI/L; GPT 112 UI/L; LDH 2,934 UI/L; GGT 1,405 UI/L; and alkaline phosphatase 1,383 UI/L. An initial cycle of 50 mg/m2 doxorubicin hydrochloride and 500 mg/m2 cyclophosphamide was administered. The patient died four weeks later as a result of hepatic failure.


A 20-year-old woman presented with vesicovaginal (VVF) and rectovaginal fistula (RVF) due to obstructed labor. She underwent a temporary transverse colostomy followed by two failed attempts of VVF repair. One year later, the RVF was repaired successfully by the vaginal route and a simultaneous continent cutaneous urinary diversion procedure (right colon pouch with Mitrofanoff continence mechanism) was performed. She was then lost to follow-up and could not come even for colostomy closure due to poor socioeconomic condition. She presented after 10 years when she noticed a gritty sensation while passing catheter for pouch emptying. On evaluation, she had normal renal functions, with serum creatinine of 1.0 mg%, while an intravenous urogram revealed a large pouch full of stones []. In view of the large stone bulk, she was subjected to open surgical removal of stones with simultaneous colostomy closure. Stone analysis revealed that the stones were composed of calcium, magnesium and ammonium phosphate.


We report a case of stricture ureter following laparoscopic pyeloplasty, which was successfully repaired using an onlay buccal mucosa patch graft.
The patient, a 38-year-old married female attended our out patient department (OPD) with a history of left flank pain. She had a history of bilateral flank pain, for which she had undergone the following:
Multiple sessions of extra corporeal shockwave lithotripsy (ESWL) - for bilateral renal calculi (twice on the right side and five times on the left side from April 2004 to January 2006). Right laparoscopic pyeloplasty performed on 10, August 2006. Left laparoscopic pyeloplasty performed on September 2007; the stone could not be retrieved.
The left flank pain recurred after 2 months of the stent was removed. Her retrograde pyelography showed a renal calculus with a long upper ureteric stricture. In view of the concomitant renal calculus, a left percutaneous nephrolithotripsy (PCNL) with antegrade endopyelotomy was peformed in 2008 but the pain persisted upon stent removal. A repeat retrograde pyelography showed worsening of the stricture [].
Thus, an open repair of the strictured ureter using buccal mucosal onlay was performed on August 11, 2008. Per-op findings showed the stricturous segment to be 7 cm long. A graft was harvested from the right inner cheek and sutured to the stricturous segment with Vicryl 4/0 over a 7/14 Fr endopyelotomy stent. A omentum pedicle was wrapped around the graft []. A follow-up retrograde pyelography and intravenous urography showed excellent graft uptake, with no contrast leak, good patency of the repaired segment, and normal renal function [].


A 65-year-old man presented with a history of recurrent painless hematuria for several weeks. There was no history of other urological complaints. Cystoscopy showed a sessile ulcerated lesion measuring about 3 cm in diameter, in the right posterolateral wall of the bladder. A CT scan revealed a soft tissue tumor mass in the right posterolateral aspect of the urinary bladder wall involving the right ureteric orifice, with a consequent right-sided hydroureter (). There was no evidence of perivesical spread of the tumor or metastatic disease elsewhere. Transurethral resection of the tumor was attempted. The biopsy was reported as LELC with infiltration into the muscularis propria. Subsequently, a radical cystectomy obtained a specimen that measured 8.5×7×4 cm. A cut section revealed an ulcerated tumor mass measuring 3×3×1.5 cm at the right posterolateral wall of the bladder. On microscopy, the tumor was composed of diffuse sheets and cords of undifferentiated cells having large pleomorphic nuclei with coarse chromatin (Figures and ). Many of the nuclei had prominent nucleoli. The cytoplasm was moderate with poorly defined borders. The background showed dense lymphoplasmacytic infiltration with occasional eosinophils. The tumor showed transmural infiltration, but not invading the perivesical adipose tissue. There was no evidence of an in situ component in any of the examined sections. The entire tumor demonstrated similar morphology, without any associated component of conventional urothelial type carcinoma, or any other subtypes, such as squamous cell carcinoma or adenocarcinoma. The tumor cells were positive for pan cytokeratin (CK) (), CK7, CK 8 and Epithelial Membrane Antigen, but negative for chromogranin, vimentin and desmin. A diagnosis of pure LELC with evidence of muscular invasion was entertained. The patient had an uneventful post operative period. He is currently on follow-up and is free of symptoms, 12 months after the surgery.


A 3 -year-old boy was first seen in our department at the age of 20 days for a positive neonatal screening for PKU. He was born at 41 weeks of gestation to non-consanguineous parents, with a birth weight of 2810 g (10th centile). Family history was unremarkable for FD except for a maternal uncle deceased at the age of 53 years of cerebral stroke, and a grandmother suffers of systemic hypertension. A maternal niece has developed severe renal failure at birth and underwent to renal transplantation at the age of 19 years for polycystic kidneys (Fig. ). In our child an hyperphenylalaninemia due to BH4-deficiency was excluded by BH4 loading test (20 mg/Kg), analysis of urinary pterins, and determination of dihydropterine reductase activity on blood spot. Moreover, mutation analysis by restriction enzyme analysis was used to identify his genotype resulting homozygous for c.143 T>C mutation on exon 2 that changes in the protein Lys with Ser (p.L48S). The patient was subjected to a low-Phe diet and supplementation with Phe-free amino-acid mixtures. Treatment compliance was excellent with a mean of serum Phe value ~3 mg/dl during the day and good tolerance (440 mg Phe/day). Growth, neurological and psychological development were normal. At the age of 28 months, the boy began to show a slow growth, lack of appetite, severe abdominal pain and appearance often of episodes of gastroenteritis, resolving spontaneously and not related with the diet treatment. Laboratory routine investigations, sweat test, acid-base status, inflammatory parameters, stool culture, oven and parassite, faecal occult blood test, antigliadin antibodies (AGA), antiendomisium antibodies (EMA), tissue transglutaminase (tTG), were in the normal range. Symptoms of non specific enteropathy, such recurrent diffuse abdominal pain and diarrhea continued and at the age of 36 months he showed a deceleration of linear growth velocity (from 50th centile to 10-25th centile) although the BMI was in normal range. These symptoms combined with the familiar history, suggested us a possible FD. At clinical examination no angiokeratomas were found.
The diagnosis was confirmed by the reduced plasma a-galactosidase A (0,32 nmol/h/ml), decreased activity assayed in leucocytes [0,65 nmol/mg.prot/h (normal range: 26-80)] and the molecular analysis of GLA gene documented the hemizygous missense mutation g.5234G>A 2 in the exon 2 that changes in the protein Arg with Hys (p.R112H). In the mother, the mutation analysis showed that she carries the same heterozygous mutation. We performed a systematic pedigree analysis by the assay of GAL activity in the family and mutation analysis to brothers, sisters, nephews of the mother that resulted normal. The grandmother (II.2) and a brother (III.1) of the mother refused to undergo to molecular analysis (Fig. ).
Due to the lack of other clinical signs we decided not to start ERT but to perform a clinical follow-up every 6 months. Today the patient is 5-year-old, continues a diet therapy for PKU and severe abdominal pain is present periodically without triggering factors in absence of other symptoms.


An 84-year-old Caucasian man presented to the dermatology clinic with a new onset of red bristle-like lesions on the trunk. These lesions were without pain, tenderness, or pruritus. The patient is a diabetic and had a recent history of a painful drug rash secondary to hydrochlorothiazide, which was resolving at the time of examination. Medications used during treatment of his drug rash included predinisone, clobatesol and fluocinonide. In the setting of this resolving, painful drug rash, the new onset bristle-like spines were undetected by our patient, and were instead noted by his wife. Our patient is a retired veteran living with his wife in the rural countryside of the Colorado Front Range region. While he does not garden or directly handle plants, he enjoys the outdoors, and frequently takes walks along the country roads surrounding his home.
On examination, 5 to 6 3 mm erythematous papules were grouped along the right flank. Each papule possessed a central thin spine, extending up to 4 to 5 mm in length from the skin (Figure ). A punch biopsy was performed of a single papule and the differential diagnosis included foreign body, lichen spinulosus or one of the perforating disorders associated with diabetes (i.e. Kyrle disease, perforating folliculitis, reactive perforating collagenosis, and acquired perforating dermatosis). Microscopic analysis revealed the presence of a foreign body (Figure ) and a surrounding inflammatory infiltrate (Figure ). The foreign body consisted of a monomorphic and geometric pattern of cell walls, exhibiting the basic morphology of cactus spines [] (Figure ). A diagnosis of cactus spines with acute inflammation was thus established.


A 60-year-old non-diabetic, hypertensive man was seen one day after onset of decreased vision associated with severe watering, eyelid swelling and pain. Symptoms had started four days (February 2009) after uneventful phacoemulsification with intraocular lens implantation surgery for age-related cataract in the left eye.
On examination, the left eye visual acuity was light perception with accurate projection of rays. Slit-lamp biomicroscopy of the pseudophakic eye showed lid edema, congested conjunctiva, microcystic corneal edema, no corneal infiltrates, 1.0 mm hypopyon, 3+ cells and flare in anterior chamber and fixed dilated pupil.[] The intraocular pressure (IOP) was 31 mmHg done by applanation tonometry. Fundus examination showed vitreous exudates. On ocular ultrasonography, the retina appeared attached while low to medium reflective membranes with fine after-movements were noted in the vitreous cavity. Apparently the right eye examination was normal.
Acute pseudophakic postoperative endophthalmitis was diagnosed in the left eye. After informed consent, patient underwent a standard undiluted vitreous biopsy, pars plana vitrectomy and intraocular antibiotics were instilled; the antibiotics were vancomycin 1.0 mgm, ceftazidime 2.25 mg and dexamethasone 400 μgm. Postoperative topical medication included 3% ciprofloxacin and 1% prednisolone acetate eye drops every one hour, 1% homatropine eye drops four times a day and 0.5% timolol maleate eye drops and oral ciprofloxacin 750 mg twice a day.
The vitreous biopsy specimen was processed in the microbiology laboratory as per the institutional protocol.[] Direct microscopic examination of vitreous sample revealed gram-positive cocci in pairs, short chains and tetrads. A confluent growth of gram-positive cocci with alpha haemolysis on blood agar was observed after 24 h of incubation. The organism was further identified as Gemella haemolysans using Mini API Rapid ID 32 Strep. The organism was sensitive to cefazolin, gentamicin, gatifloxacin, chloramphenicol, and vancomycin and resistant to amikacin, ciprofloxacin, ofloxacin and moxifloxacin.
On the eighth day, the antibiotic regimen was changed to 5% fortified cefazolin (10 ml of distilled water added to 500 ml cefazolin injection vial) eye drops one-hourly for three weeks and oral chloramphenicol 250 mg three times a day for a week. Four weeks after surgery his best corrected visual acuity improved to 20/80 N 12 and IOP was 16 mmHg. All medication was discontinued and topical steroids were tapered over next four weeks.


A 53-year-old Guamanian-American man with seven pack-years of smoking, asbestos exposure as a child, and a family history of lung cancer suffered from a swollen, erythematous, painful tip of the left third finger. He first blamed the swelling on an embedded splinter, which he quickly dislodged with warm compresses and tweezers. However, the swelling persisted and the erythema deepened (see ). After two months of unremitting finger pain, he developed right hip pain subsequent to falling off a ladder. His primary care physician attributed the finger and hip pain to trauma, prescribed etodolac, and ordered a radiograph of the hip, which was unremarkable.
Two weeks later, the patient presented to the emergency department with sudden-onset chest pain, exacerbated by deep breathing. He was tachypneic, tachycardic, and slightly hypoxic. Computed tomography revealed a right upper lobe lung mass and right hilar adenopathy. Poorly differentiated adenosquamous carcinoma, characterized by positivity to mucin, CK7, TTF1, P63, and CK5/6, was seen on lung pathology.
The patient received high-dose intravenous narcotics but nonetheless reported persistent finger pain. Orthopedics was consulted. Two radiographic views of the left hand showed a highly aggressive lytic lesion involving the distal phalanx with permeative margins and slight immature periosteal reaction. There was significant associated soft tissue swelling or mass, as well as an associated minimally displaced pathologic fracture through the midportion of the phalanx. Additionally, there were adjacent tiny ossific or calcific fragments, possibly displaced bony fragments or dystrophic soft tissue calcification (see ). Taken together, the radiographic findings argued strongly against a traumatic injury, but instead supported a destructive and infiltrating process, such as lytic metastasis. The patient declined biopsy, elected comfort measures only, and died one month later.


A 28-year-old Japanese woman, gravida 1, para 1, was admitted with atypical genital bleeding and underwent polypectomy of the uterine cervix at 9 weeks' gestation. The 1-cm resected polyp was pathologically diagnosed as VPA (). The tumor is purely exophytic without invasion of the underlying stroma and lymphvascular involvement. Hence, she was referred to our hospital. As the polyp had no lymph capillary space invasion, we performed conization at 16 weeks' gestation when the patient decided to continue her pregnancy. The depth of surgical specimen was 1 cm and width of that was 3 cm diameter. No cancer cells were identified in the resected specimens. The final diagnosis was FIGO stage IB1. She delivered a healthy 2,946 g newborn vaginally at term 38 weeks, and she has been free of the disease for 44 months.


A 9-year-old native Hispanic girl with a history of plaque psoriasis was admitted to the emergency department of the Hospital Abina Patiño with a 4-week history of progressive skin desquamation. The condition started in her extremities and face, and then rapidly spread over her whole body.
A physical examination identified that the child was febrile, in moderate distress and had signs of moderate dehydration and severe malnutrition. Generalized skin redness and desquamation were seen over her entire body surface, accompanied by blepharitis, conjunctivitis and madarosis which were noted from an ocular exam (Figure ). Advanced onychodystrophy in her toenails and fingernails was noted bilaterally. Swelling, pain, and rigidity in her knees and elbows were also noted (Figure ).
Three months before she presented to our hospital, our patient was clinically diagnosed with plaque psoriasis and had been treated with topical corticosteroids and moisturizing creams. She had no pathological birth or related family history. Her parents also denied that she had experienced trauma, drugs, infections or any other similar triggers for her condition.
Based on the above observations, a clinical diagnosis of severe erythrodermic psoriasis with arthritis and secondary malnutrition was made. This diagnosis was supported by a histopathological study that showed parakeratosis and hyperkeratosis, elongation of rete ridges, and neutrophil infiltration (Figure ).
The initial management of our patient's condition included systemic treatment with methotrexate, fluid resuscitation, and well-controlled food intake. At the same time, her conjunctivitis and blepharitis were treated with artificial tears and antibiotics, respectively. Her skin was completely desquamated in the following two weeks and she achieved full skin recovery one month after she commenced treatment. Her arthritis also recovered in the first month of treatment and her malnutrition was progressively addressed with nutritional support. Her nail recovery, however, took a longer time and treatment to achieve any notable improvement.


A 70-year-old Arabic African man presented to the emergency department of the University Hospital Hassan II of Fez with a five-day intestinal obstruction with associated abdominal distension and vomiting. He denied intestinal bleeding or diarrhea. He gave a history of referred intermittent episodes of constipation for a period of 6 months.
When examined he was found to have general abdominal tenderness. His white blood cell count was 8000 elt/ml, his haemoglobin was 11 gr/dl, and his platelet count was 350 k/ml. His abdominal X-rays showed air-fluid levels. Abdominal scanner examination revealed a distension of his small and large bowels upstream a sigmoid colon process (Figure ). A sigmoidoscopy showed a stricture of his sigmoid colon. Our patient was taken immediately to laparotomy, which confirmed the presence of an occlusive sigmoid tumor. A defunctioning sigmoidostomy was later performed on our patient. A colonoscopy through the stomy revealed colitis and ileitis. A resection of his sigmoid colon was performed with continuity restored by end-to-end anastomosis (Figure ).
Meanwhile, pathological examination of our patient showed a well-differentiated adenocarcinoma of the colon (Figure ) arising from the areas of chronic transmural inflammation and ulcerations typical of Crohn's disease and extending through the bowel wall and invading the serosa (Figure ). The tumor was classified T3N+M0 according to the TNM classification. Post-operative chemotherapy with 5-fluorouracil and folinic acid (5-FU+Folinic acid) was recommended but this was refused by our patient. One year later he was still well except for some episodes of diarrhea.


A 25-year-old male patient was admitted to intensive care unit in unconscious state with an alleged history of suicidal hanging by neck. Patient was rescued by his relatives within few minutes and shifted to hospital within 30 minutes. On examination his pulse rate was 126/min and arterial blood pressure was 90/64 mmHg. His pupils were bilaterally dilated and nonreacting to light. On auscultation chest was bilaterally clear with adequate air entry, but patient was tachypnoeic with respiratory rate of 32/min. Upper airway reflexes were present. Patient had intermittent decerebrating movements. Pulse oximetry revealed SpO2 60% and arterial blood gas (ABG) analysis showed PaO2 54mmHg, PaCO2 28mmHg, pH 7.26, BE 9.2mEq/L and SaO2 64% on air.
Immediately, his trachea was intubated orally with 8.5 mm ID cuffed endotracheal tube after thiopentone sodium 200 mg and succinylcholine 75 mg I.V. Patient was put on ICU ventilator for controlled ventilation with respiratory rate of 12/min, tidal volume 500mL, PEEP 5cm of H2O and FiO2 1.0. Patient was given pancuronium and midazolam. After one and half hour of therapy, SpO2 further dropped to 52% and patient developed frank pulmonary oedema with extensive fine crepts all over the chest and pink frothy secretions appeared in the breathing system. Controlled ventilation was continued with PEEP. He was given furosemide 60 mg and morphine 6 mg IV and repeated 6 hourly. X-rays of cervical spine AP and lateral view revealed no bony injury. After 2hours patient's ABG was satisfactory and revealed PaO294mmHg, PaCO229mmHg, SaO294% on FiO21. His chest condition was markedly improved after 12 hours of ventilation. His ABG analysis depicted PaO2114mmHg, PaCO235mmHg, pH 7.41, SaO298.4% on FiO2 0.5. He regained his consciousness. He was put on weaning mode of ventilation Assisted Spontaneous Breath(ASB) and Continuous Positive Airway Pressure(CPAP) with FiO2 0.4 for next 12 hrs. After 24 hours (2nd day) he was fully conscious. His SpO2 was 99% on FiO2 0.4. Chest X-ray AP view detected no abnormality. ABG analysis revealed PaO2 116mmHg, PaCO2 45mmHg, pH 7.49 and SaO2 99% on FiO2 0.4. On 3rd day his trachea was extubated Post extubation his SpO2 was 97% on FiO2 0.4 by facemask.


A 12-year-old boy suffered severe polytrauma and sustained fractures, lacerated and avulsed wounds, primarily involving his limbs. His right leg, which had a threatening vascular injury, was debrided and kept under close observation. He underwent three procedures before a decision was taken to amputate his right lower limb, below knee. However an epidural was not performed, as sepsis was a consideration, and he was put on IV fentanyl infusion for postoperative pain relief.
Subsequently he was put on oral analgesics and rescue doses of IV morphine. On the fifth postoperative day, he complained of severe pain from the non-existing part of his leg with pins-and-needle sensations from the stump. The pain management team was then involved in managing his emerging phantom limb pain. We found an extremely anxious boy with a history suggestive of phantom limb pain and sensations. The pain was not continuous, varied from moderate to severe in intensity (average Visual Analogue Score 8/10), with a shooting character, which went to burning at times. On an average there were 15 – 20 episodes of severe pain (VAS of more than 6/10) per day. Hyperalgesia and cold allodynia were also noted. The boy also had generalised pain due to other injuries. A lumbar epidural catheter was inserted aseptically and he was put on continuous epidural analgesia with 0.1% bupivacaine, along with oral ibuprofen, gabapentin 100 mg BD, and amytryptline 10 mg HS. This made a drastic difference, with his pain score coming down to 3/10 from 8/10. However, he complained of increasing pain on the third day of epidural infusion. After checking for a functioning epidural, gabapentin was increased to 150 mg BD. On the next day, as the pain became more resistant, he was put on rescue doses of IV morphine. On the fifth day, the IV morphine used was 30 mg, a decision was taken to discontinue the epidural. As the pain showed increasing resistance to routine analgesics and opioids, we decided to initiate IV ketamine. After an ineffective trial of 150 mcg/kg, we decided to go with 300 mcg/kg with 2 mg midazolam, in a 60 ml solution, given over three hours, in a monitored setting. The VAS score decreased to 5/10 after two hours and to 3/10 that night, without any side effects. We pursued the same dose with alternate day infusions for 12 days. The use of morphine decreased substantially as the VAS scores decreased consistently. The number of severe pain episodes also reduced []. After six infusions the boy had no recurrence of limb pain for nearly 48 hours, after which he was discharged home. Further follow-up up to six months showed no recurrence, without any analgesic support.


A 16-year-old, unconscious female presented to Emergency with cyanosis and a greyish-brown hue, laboured respiration of 26/min, BP 150/100 mm of Hg, pulse rate 160/min, pupils with sluggish reaction, and SpO2 of 60% on air. Her chest was clear. Immediate intubation and ventilation with 100% oxygen and 6 cm PEEP improved the SpO2 to 84% only. There was a history of severe pain in the abdomen, nausea, vomiting, and dizziness, which was self-treated with tablet metoclopromide, about eight hours prior to unconsciousness. The patient was referred by a local practitioner who started an IV infusion and administered a shot of mephentermine and hydrocortisone after recording a BP of 40 mm Hg. History of ingestion of any drug was strongly denied by the companion. An urgent ultrasound abdomen ruled out any abdominal catastrophe and showed a generalized mild-to-moderate hepatic inflammation. Blood samples drawn for ABG had a chocolate brown colour, which did not improve on exposure to 100% oxygen and showed compensated metabolic acidosis []; X-ray of the chest and ECG were within normal limits, and WBC and liver enzymes were slightly raised. Serum creatinine and electrolytes were within normal range []. A clinical diagnosis of severe acute methaemoglobinaemia of unknown origin was made.
Five millilitres (50 mg) of methylene blue (prepared as 1% sterile solution) and ascorbic acid 500 mg were given IV. This improved her SpO2 to 92%, which dropped after about three hours, when 30 mg IV methylene blue was repeated. Intravenous Vitamin K, 10% dextrose, and an antibiotic were also added. Urine output was maintained above 100 ml/hour with proper hydration and frusemide, maintaining a normal central venous pressure (CVP).
She became conscious after six hours with a stable BP of 120/80 and HR of 120/minute. SpO2 was again 84% with ABG showing a saturation of 94%. IV methylene blue (30 mg) improved SpO2 to 97% over the next 15 minutes, only to return to 85% in the next three hours, with a similar response to another dose. Two units of fresh blood were transfused and this improved the SpO2 to 92 – 94%. She was extubated at 48 hours and maintained on a continuous positive airway pressure (CPAP) mask, with ABG showing a saturation of 93% and a PaO2 of 112, when she admitted to having consumed 250 ml of paint solvent (equivalent to 12.5 g of nitrobenzene). The SpO2 dropped back to 87% in next 12 hours.
With this waxing and waning picture of symptoms, six hourly gastric lavage with charcoal, purgation with polyethylene glycol (peg leg), intravenous methylene blue every six hours (three days) and then orally up to seven days, and IV ascorbic acid (500 mg) per day up to six days, was prescribed, till the smell of bitter almonds disappeared completely from the stools.
She improved rapidly after the seventh day with an SpO2of 90% on room air. International normalized ratio decreased to 1.08, although the liver enzymes were raised. She was discharged on the ninth day on oral iron, folate, ascorbic acid, and liver enzyme supplements and breathing exercises.


A 26-year-old white man diagnosed with acute pre-B lymphocytic leukemia (ALL) at age 10 refractory to chemotherapy for which he underwent a haplo-identical allogeneic stem cell transplantation (SCT) from his father who did not have any rheumatic and/or dermatologic inflammatory diseases including psoriasis. Except for a febrile and convulsive episode that lasted only a few days with a very good response to a short course of oral prednisone, he remained well until about 10 years later when he began to exhibit lower back pain and stiffness. On Christmas day 2003, he woke up with a painful, stiff and swollen right ankle which made walking very difficult. From December 2003 onwards the patient complained of right ankle pain, swelling and stiffness with difficulty in walking and only partial and transient clinical response to indomethacin, colchicine and allopurinol therapy. In January 2008, he presented to a local emergency room with a painful, stiff, and swollen right elbow for which he received a short course of oral prednisone. Over the subsequent 4 months, he continued to have right elbow and ankle pain and swelling accompanied by difficulty using his arm and walking. In May 2008, he was admitted to our University Hospital for left elbow and hand swelling and pain. On physical examination, blood pressure was 131/73, pulse 81, height 5'8", weight 215, BMI 31.6. He was in distress and pertinent findings revealed the presence of mild flaking and dryness of earlobes overlying skin, swelling, redness and tenderness of the second digit distal interphalangeal joint of left hand, swelling, tenderness, and decreased range of motion of right ankle, sausage digit deformity of the middle digit of the left foot, and enthesitis of the right Achilles tendon (Figures , , ). In addition, both sacroiliac joints were tender to palpation and a Schober test was positive. Past history: Hypertension, bilateral cataracts, and metabolic syndrome. Family history: Paternal grandfather had psoriasis and also suffered from stiff hands. Maternal grandmother had a history of rheumatoid arthritis for over 30 years. Laboratory findings: ESR: 56 mm/h (n < 20), CRP: 17.02 mg/dL (n < 0.80). Rheumatoid factor, CCP antibodies, ANA, and HLA-B27 were negative and/or normal. Hands and feet radiographs did not show erosions. Sacroiliac joints x-ray showed unilateral sacroiliitis (Figure ). Follow-up: patient is improved on symptomatic NSAID therapy.


A 59-year-old female with metastatic breast cancer (sites of metastases were bone and lung without liver involvement) was receiving chronic minidose of warfarin therapy (1 mg/day) for prophylaxis against catheter-associated thrombosis. Her prior chemotherapy included an adriamycin-based regimen given until disease progression. She had an hormone-receptor negative and high grade tumour, but she was in good general conditions, with an ECOG performance status of 0 and a life expectancy of more than 3 months. The laboratory tests were within the normal limits and her cardiac function was normal. The international normalized ratio (INR) level was monitored every week and was, prior to initiating capecitabine, always under the value of 2. In may 2005 she received the first course of chemotherapy using capecitabine 1000 mg/m2orally twice daily for a period of 14 days, followed by a rest period of 7 days and intravenous (iv) docetaxel 75 mg/m2 on day 1 and then every 3 weeks. Dexamethasone 20 mg was administered orally the night before and the day of chemotherapy and then at dose of 8 mg twice daily for a period of 2 days after docetaxel administration. Ondansetron, 8 mg twice daily, was given as an antiemetic on the day of docetaxel treatment. Prior to the docetaxel administration, ranitidine 50 mg was infused iv over 15 min, followed by 10 mg chlorpheniramine. Twenty-one days after initiating capecitabine, the patient's INR was markedly elevated (8, 87). Neither symptoms nor signs of bleeding were detected. The patient did not report any changes in dietary habits or physical activities, use of other drugs, alcohol or smoke, presence of fever or hyperthyroidism that could explain her condition. Twenty-four hours after the iv administration of Vitamin K 10 mg the INR value had dropped to 1.19. The warfarin was withheld and the patient did not develop any complications. The patient was treated with low molecular weight heparin subcutaneusly and the chemotherapy regimen was restarted without alterations of the coagulation parameters.


A 41 years old male patient previously healthy, presented with the history of laparoscopic repair of left inguinal hernia in a neighboring country 12 days ago. The patient noticed pain and redness around the port sites five days after the operation and reported to his doctor. He was given a course of antibiotics for one week but his redness, pain and swelling spread further on abdomen wall, thighs and scrotum. Two days prior to admission he was in severe pain, unable to move and had chills with rigor. He had nausea and loss of appetite. There was no known history suggestive of any pre-disposing- associated comorbid conditions.
He was toxic, tachycardic, emaciated, and febrile. The cellulitis and tense edema with tenderness was noticed involving the whole of the lower abdomen, scrotum, perineum, and the upper medial aspects of thighs. Skin blistering and ruptured bullae with foul smelling serous discharge were seen on the inner thighs []. No crepitus was felt in the affected area. His CT scan showed extensive inflammation of the subcutaneous tissues of anterior abdominal wall and thighs, fluid around the spermatic cords, collection medial to left obturator muscle, free gas in the subcutaneous planes. No extension of inflammation and fluid collection was seen in the retroperitoneum []. His laboratory parameters were as follow: White cell count: 19.7; Hemoglobin, 11.1 gm; Random blood sugar, 5.37 mmols; Urea, 7.19; Creatinine, 53.8; Na, 130. His liver and kidney functions were normal and was HIV negative. Blood cultures were taken. The clinical and radiological findings were diagnostic of NF.
He was resuscitated with IV fluids, oxygen, and parental broad-spectrum antibiotics, and was taken up for urgent surgical exploration. The diagnosis was established intra-operatively. Through a long left transverse inguinal incision the tissue planes were opened. The mesh was lying loose and infected and was removed. There was offensive smelling pus in all tissue planes sparing muscles. The incisions were extended further and all dead and necrotic tissues were excised []. He had several excisions of necrosed tissues over the course of one month. The blood and wound cultures grew Escherichia Coli, Coliform, Klebsiella, Proteus Mirabilis, and Staphylococcus Aureus. A split skin grafting was done to cover the exposed area and muscles []. No disability and recurrence of hernia was seen 6 months after the surgeries.


A 53-year-old Afro-Caribbean man was admitted to another institution with a two-day history of vomiting, hiccups and abdominal pain. He was felt to have gastroenteritis, given intravenous fluids, paracetamol and cyclizine and discharged from the accident and emergency department. Two days later he presented to his general practitioner (GP) with continuing epigastric and lower abdominal pain, vomiting, having not opened his bowels or passed urine for four days.
He had a history of hypercholesterolemia, but was on no regular medications aside from those prescribed two days earlier. He smoked ten cigarettes a day, denied alcohol intake and had no recent travel history. On examination he was apyrexial, clinically dehydrated, with vital signs of pulse rate of 108 per minute and blood pressure of 145/82. Physical examination revealed a generally tender but not peritonitic abdomen and an empty rectum, but was otherwise unremarkable. A urethral catheter was passed and a urine dipstick was strongly positive for blood, protein and less so for glucose and leukocytes.
Laboratory studies revealed a sodium level of 131 mmol/L, potassium level of 6.7 mmol/L, urea of 45.2 mmol/L, and creatinine of 1885 micromol/L (21.3 mg/dL). Of note were a raised C-reactive protein of 421, neutrophil count of 25.9 × 109/L and an erythrocyte sedimentation rate of 100. Blood gases revealed a pH of 7.19, a PO2 of 14.8 kPa, pCO2 of 5.18 kPa, HCO3 of 14.5 mmol/L with a base deficit of -12.9 on 28% inspired oxygen, and an anion gap of 28 mmol/l. An urgent renal ultrasound showed normal sized kidneys with no hydronephrosis and an empty bladder.
He was transferred urgently to the intensive care unit for continuous veno-venous hemodiafiltration and started on ciprofloxacin empirically in view of the history of abdominal pain and raised inflammatory markers.
He was transferred the next day to the renal unit at our centre. A computed tomography (CT) scan of his abdomen showed bilateral perinephric stranding suggestive of pyelonephritis but was otherwise unremarkable (Figure ). Investigations for underlying causes of the acute renal failure including auto-antibodies, complements and protein electrophoresis were normal.
The patient remained dependent on intermittent hemodialysis. He subsequently complained of back and loin pain, and blurred vision, and was intermittently confused and agitated. On day four of admission he reported having drunk 'battery acid' by mistake one week before his initial presentation, and his family reported a history of cocaine use. At this time there was no focal neurology elicited on examination, and no evidence of mucositis consistent with battery acid ingestion.
On day five of admission he developed respiratory distress due to acute pulmonary edema and possible aspiration pneumonia requiring emergency intubation, ventilation and transfer to the intensive care unit (Figure ).
Following a good response to antibiotics for aspiration pneumonia, he was extubated within 24 hours, and appeared alert and able to obey commands. Neurological assessment revealed bilateral dilated pupils with sluggish responses to light, and myoclonic jerks of his limbs. Subsequently he became more obtunded and was reintubated for a decreased level of consciousness and hypercapnia.
A CT scan of his brain showed no focal intra-cranial lesion, and a lumbar puncture was performed which showed an elevated opening pressure of 37 cmH20, markedly raised cerebrospinal fluid (CSF) protein at 2785 mg/L but normal CSF white cells 3 × 106/L and no organisms.
He had a tracheostomy inserted and was subsequently co-operative enough to comply with a neurological examination. This revealed bilateral palsies of cranial nerves III, VI and VII, and slow tongue movements but normal palatal movements. He also had distal lower limb weakness with diminished reflexes and down-going plantars and was beginning to complain of distal neuropathic pains. Electromyography and nerve conduction studies revealed a sensorimotor radiculoneuropathy with facial nerve involvement, similar to that seen in Guillain-Barre syndrome, with an atypical distribution.
Faced with a patient with acute renal failure and unexplained neurological disease, a review of the history of toxin ingestion and literature search was performed. The patient remained adamant that he had consumed battery acid, but by this stage he was lucid enough to use his mobile telephone to text his friend to bring in what was by this stage strongly suspected to be anti-freeze. An empty bottle of anti-freeze and coolant was brought in by his friend and the patient confirmed that this was what he had ingested. The product literature confirmed the presence of ethandiol or EG in concentrations of > 90%. As he was anuric for several weeks from admission, it was not possible to analyze a urine specimen for calcium oxalate crystals once this diagnosis became apparent.
Our patient continued to have a rocky course on intensive care complicated by acute respiratory distress syndrome (ARDS), presumed secondary to aspiration pneumonia complicating bulbar palsy, and a slow respiratory wean. He required continuous veno-venous hemofiltration for eight weeks, and is currently independent of dialysis but continues to have a severe degree of renal impairment with an estimated glomerular filtration rate (eGFR) of 13 mL/min. He is likely to require renal replacement therapy in the near future. Neurological recovery was also slow, but he was able to walk again about ten weeks after admission, although rehabilitation was also impaired by marked postural hypotension and persisting neuropathic pain.


A 24-year-old man was admitted to our hospital due to diarrhea, progressive jaundice, light stool, fatigue and excessive sweating for 18 days. He was diagnosed with TOF at age 3, and had undergone pulmonary valvotomy and closure of the foramen ovale at age 19. The former procedure failed, while the latter was successful. Since then hyperthyroidism was confirmed, and MMI (20 mg per day) was intermittently taken for 1 year because he refused to receive radioiodine therapy. Neither thyroid nor liver function had been regularly monitored during the treatment period or in the following 4 years. MMI (20 mg per day) was continuously taken by himself for 20 days prior to the onset of the symptoms, which, however, did not arouse his alertness, and MMI administration was continued until his admission. He denied use of any other concomitant prescriptions (including non-ADs), over-the-counter drugs or herbal remedies. The patient stated that there was no history of alcohol abuse, food allergies or liver disease.
Physical examination revealed a 112 heart beats per minute with evidences of tremor, generalized icterus, and pigmentation of the skin on the bilateral tibia. Marked carotid pulsation, jugular distension, and an enlarged thyroid gland with vascular murmur were observed. Thrill on palpation and mid-systolic murmur on auscultation were evident in the pulmonary area. A strong collapsing pulse and pistol shot sound was noted in the peripheral arteries. The liver edge and the spleen edge descended 1.5 cm and 3 cm below the costal margin, respectively, and peripheral edema was also noticed.
Laboratory tests revealed the following biochemical results (with the normal range in brackets): ALT 75 U/L (5 to 40), ALP 133 U/L (15 to 130), ALT/ALP ratio 0.56, TBIL 587.9 μmol/L (3.0 to 20.0), DBIL 288.2 μmol/L (2.0 to 6.0), FT4 154.8 pmol/L (7.90 to 14.10), FT3 30.8 pmol/L (3.86 to 6.00), thyroid-stimulating hormone less than 0.01 μIU/ml (0.340 to 5.600), PT 22.2 seconds (9.0 to 12.8), and international normalized ratio 2.3 (0.8 to 1.4). Viral serologies (hepatitis A, B, C, and E viruses; human immunodeficiency virus; Epstein-Barr virus and cytomegalovirus) and autoimmunity markers (antinuclear antibody, antimitochondrial antibody, antineutrophil cytoplasmic antibody, anti-smooth-muscle antibody, and anti-liver-kidney microsome antibody) were all negative. Screening studies were performed to detect genetic and metabolic liver diseases, which excluded hematochromatosis, Wilson's disease, and alpha 1-antitrypsin deficiency. The color Doppler echocardiography showed evidence of severe pulmonary stenosis, right ventricular hypertrophy, tricuspid incompetence with systolic regurgitation, and enlarged right atrium (Figure ). Moreover, ultrasonography of the abdomen revealed signs of hepatic parenchymal injury, inferior vena cava dilation and splenomegaly.
Drug induced lymphocyte stimulation test for MMI was performed, and the procedure was briefly described as follows: Lymphocytes isolated from the heparinized peripheral blood sample of patient were incubated with serial concentrations of the purified MMI (M8506, Sigma). After that, the proliferative response was assessed by measuring incorporated 3H-thymidine uptake. The patient showed a positive result, with the Stimulation Index of 2.19.
MMI was discontinued on admission. The patient was treated with PTU (50 mg 8 hourly) and propranolol (40 mg 3 times daily). Methylprednisolone (40 mg daily) and liver protecting preparation (e.g. diammonium glycyrrhizinate, ursodeoxycholic acid, and ademetionine) were also administrated. The patient underwent three sessions of plasma exchange, and an 8-hour continuous hemofiltration. His general condition, liver functions and other biochemical parameters gradually improved with ALT, ALP, TBIL and PT values, while FT3 and FT4 approximately restored to normal levels; however, two days later, his liver function worsened again (Figure ). A liver biopsy was performed on day 18 after admission. Pathological findings showed that the portal tracts were expanded by moderate inflammatory infiltration composed of lymphocytes, neutrophils and eosinophils. The portal tracts were surrounded by proliferative cholangioles, and some with bile plugs. Nodular regeneration of the hepatic parenchyma was delimited by loosened fibrous septa. Diffused swelling and enlargement of hepatocytes were detected within hepatic lobules, particularly around central veins. Feathery degeneration was also observed in some hepatocytes, indicative of intracellular cholestasis, but necrosis was absent within portal areas and lobules (Figure ). During the following 9 days, his liver function profiles progressively deteriorated, and grade II encephalopathy developed. The patient subsequently experienced hypoxemia, hypotension, decreased urinary outflow, and metabolic acidosis. Although mechanical ventilation and intensive therapies were applied, unfortunately, the progression of his medical conditions could not be suspended, and he eventually expired as a result of multiple organ failure on day 27 after admission.


A 55-year-old man, who was a former smoker and had chronic silicosis caused by 14 years of work in the granite industry, was admitted to the hospital after an episode of hemoptysis. The amount of blood expectorated was estimated at more than 200 mL. He also had a one-month history of productive cough with blood in the sputum. He had previous history of tuberculosis, with the last episode approximately two years prior, when he received isoniazid, rifampin, and pyrazinamide for two months, followed by four months of isoniazid and rifampin. He had been asymptomatic since then.
On physical examination, the patient was emaciated and pale. His blood pressure was 100/70 mmHg, his pulse was 104 beats/min, and his respiratory rate was 20 breaths/min. Lung auscultation revealed rhonchi and wheezing in both lungs. No other alterations were seen in the physical examination. A blood chemistry screening was normal, including negative finding by anti-HIV. Immunodiffusion tests were negative for Aspergillus.
A chest radiograph () and high-resolution computed tomography (HRCT) of the thorax () showed bilateral conglomerate masses, one with cavitation, associated with multiple small nodules, in addition to calcifications of the hilar and mediastinal lymph nodes, paracicatricial emphysema, architectural distortion, and enlargement of the central pulmonary arteries. No other parenchymal findings were suggestive of active tuberculosis.
The expectorated sputum was negative for acid-fast bacilli and the patient underwent a bronchoscopy that showed evidence of active bleeding. Direct examination of the bronchoalveolar lavage was negative for tuberculosis, fungi, or malignancy. Culturing was positive for Mycobacterium tuberculosis and negative for fungi.
Because of the enlarged pulmonary arteries, Doppler ecocardiography was performed, showing left ventricular diastolic function, mild tricuspid regurgitation, and pulmonary arterial hypertension with a systolic pulmonary artery pressure of 48 mmHg. The patient underwent an angiogram of the common bronchial trunk that showed marked hypervascularity and enlargement of left bronchial artery, which was selectively catheterized and subsequently embolized with polyvinyl alcohol particles (PVA). Bleeding stopped after embolization. The patient was treated for tuberculosis with isoniazid, rifampin, pyrazinamide, and ethambutol for two months, followed by seven months of isoniazid and rifampin. After the embolization and clinical treatment for tuberculosis, the patient progressed well, with improvement in his respiratory symptoms, and no rebleeding after a follow-up of two years.


A 31-year-old healthy woman with a history of primary infertility for 4 years was referred to our Center of Reproductive Medicine and Assisted Procreation in May 2008. The patient had the typical clinical and echographic criteria of polycystic ovarian syndrome (PCOS) []. Furthermore, in 2004, a diagnostic laparoscopy revealed patent tubes but with a tortuous course and a mildly dilated left fallopian tube. The male partner had normal semen parameters according to World Health Organization (WHO) standards []. In 2006, in another infertility center, the patient underwent two cycles of ovulation induction with intrauterine insemination without achieving pregnancy. In September 2008, at our center, the couple was included in an In Vitro Fertilization (IVF) program. Controlled ovarian hyperstimulation (COH) was performed using a flexible GnRH antagonist protocol with mild stimulation that involved the administration of recombinant FSH (rFSH) (Gonal-F; Serono, Geneva, Switzerland), 150 UI daily, from day five of spontaneous menstrual cycle. During ultrasound monitoring, when at least one follicle reached 14 mm in diameter, GnRH antagonist (Orgalutran 0.25 mg; Organon, Italia) 0.25 mg/day was added subcutaneously. After 9 days of administration of recombinant FSH, controlled ovarian stimulation was suspended for an increased risk of ovarian hyperstimulation syndrome (OHSS). After 2 months, the patient was enrolled in an oocyte vitro maturation (IVM) program. The patient received an oral contraceptive to induce menstruation, then an FSH “priming” was achieved with the administration of recombinant FSH (rFSH) (Gonal-F; Serono, Geneva, Switzerland), 150 UI daily for 3 days (from day three to day five). At day 8, transvaginal ultrasound monitoring showed right and left ovarian measurements of 4.3 × 3.1 cm and 3.9 × 2.7 cm, respectively, with several follicles in both ovaries, ranging from 7 to 11 mm in diameter. The day after recombinant chorionic gonadotropin 250 mcg (Ovidrel; Serono, Geneva, Switzerland) was administered. Thirty-six hours later, transvaginal oocyte retrieval was performed. After collection, the follicular fluid was filtered through a 70 μm cell strainer (Nunc) and was washed twice with flushing medium containing heparin (MediCult, Jyllinge, Denmark). At least 18 cumulus oocyte complex (COC) were collected. After washing all, COCs were placed in a single-well Petri dish (Becton-Dickinson), containing 0.5 ml of pre-equilibrated IVM medium (vial1- LAG 1 of IVM system medium; Medicult, Jyllinge, Denmark) for 3h and then placed in a new single-well Petri dish (Becton-Dickinson) containing 0.5 ml of pre-equilibrated IVM medium (vial 2-LAG 2 of IVM system medium; Medicult, Jyllinge, Denmark) supplemented with 0.075 IU/ml recombinant FSH (Gonal-F; Serono, Geneva, Switzerland), 0.1 IU/ml rHCG (Ovidrel; Serono, Geneva, Switzerland), and 10% maternal serum, inactivated at 56°C. The immature oocytes were stored in an incubator at 37°C and 5% CO2in a humidified atmosphere for 30 hours. After 30 hours of culture, all the oocytes were treated with 80 IU/ml hyaluronidase solution in order to remove the cumulus complex, then detected under a stereomicroscope. At least 14 oocytes to 18 reached the MII stage. According to cytoplasmic characteristics and presence of meiotic spindle signal, 12 oocytes were classified with good quality and those showing signs of mechanical damage or atresia were discarded. Unfortunately, as already worldwide known, the restriction of the Italian law, at the time of this report, allows to inseminate a maximum of three oocytes, while the resulting 9 good quality oocytes have been cryopreserved. The semen sample with normal sperm parameters was prepared as previously described []. Although normal results of the semen parameters we use ICSI for insemination and all 3 oocytes showed fertilization. Fertilization was assessed 16–18 hours after injection by the presence of two pronuclei. All the resulting zygotes were cultured in ISM1 medium as previously described []. The embryos were cultured for 2 days. Three good quality embryos, were transferred on day 3 after oocyte retrieval, as determined by Italian law. For luteal phase support, Progesterone 400 mg (Progeffik 200 mg; Effik, Italy) daily vaginal administration was commenced. Two days after embryo transfer, the patient presented to our clinic complaining of lower abdominal pain. She was afebrile and physical examination showed a point of maximal tenderness in the right lower abdominal quadrant. There was no vaginal bleeding nor any bowel symptoms, acute appendicitis and renal colic were excluded. The laboratory workup showed a white blood cell count of 22.000 migl./ml whereas hepatic enzymes, hematocrit and urine analysis were normal. Transvaginal ultrasound was carried out showing enlarged (10 × 7.5 cm) right ovary within coexistent mass, a small amount of fluid was revealed in the pouch of Douglas. The Colour Doppler examination was normal with presence of ovarian vascular flow bilaterally. Six hours after admission to the hospital, a worsening of clinical symptoms showed an acute abdominal pain. In view of these findings an explorative laparoscopy was carried out. The laparoscopic findings showed a twisted right adnexa whit an ischemic ovary. The enlarged cystic ovary had a bluish hue and measured about 10 cm in diameter. The surgeons proceeded to underwinding the twisted adnexa, pushing the ovary in the opposite direction of the torsion (). After a few minutes, there was recoloration and a decrease of the adnexal edema, signs of a successful recovery, and the ovary was preserved. The patient had an unremarkable postoperative course and was discharged to home the following day. Four weeks later transvaginal ultrasound showed a normal intrauterine 6-week pregnancy. The patient had a full-term pregnancy and delivered a healthy infant at 40 weeks of gestation.
To our knowledge, this is the first report of adnexal torsion after an IVM cycle.


A 56-year-old male presented to our clinic with bilateral giant inguinal hernias. His complaints were pain, bilateral inguinal mass and insufficient sexual activity. He was operated on four times before for right groin hernia. Concomitant diseases were arterial hypertension and diabetes mellitus. There were incision scars in the right groin region and bilateral giant inguinal hernias (). Laboratory findings were normal except for a slightly elevated blood glucose. Contrast-enhanced CT revealed that omentum, small bowel and colon were in the bilateral hernia sacs (). After evaluation of clinic signs and radiological findings, we decided to prepare the patient with PPP, after obtaining informed consent for the procedure. A peritoneal dialysis catheter was inserted into the abdominal cavity with a 3-cm lower midline incision under local anesthesia. Nitrous oxide was preferred for insufflation because of its inert structure. It was insufflated into the abdomen via a catheter. The first insufflation procedure was applied in the operating room and then at bed side (insufflator moved to the bed side). Daily insufflated gas volume, intraabdominal pressure and expansion of waist circumference at the level of umbilicus was recorded (). Insufflations went on for 18 days except day 11 because of a technical problem (). We determined that abdominal expansion did not increase any more after day 13 despite increased intraabdominal pressure. Waist circumference at the level of the umbilicus expanded and stayed at 11 cm at that time. During the procedures, we gave third-generation quinolones to the patient and an analgesic, when necessary.
The patient was operated on under general anesthesia on day 19. A Pfannensteil incision was preferred and there was sigmoid colon and 500 cc of fluid in the left hernia sac. Some small bowel segments, appendix vermiformis, cecum, and 200 cc of fluid was in the right hernia sac. We performed appendectomy for prophylaxis. The hernia contents were dissected easily from the hernia sac and the bilateral hernia contents were pushed into the abdomen easily. The peritoneum was closed with absorbable sutures. Stoppa technique was preferred and a 30×30 polypropylene mesh was placed and fixed to bilateral spina iliaca anterior superior, symphysis pubis, Cooper ligaments, and midline. Suction drains were placed on the mesh and in the scrotum bilaterally. An abdominal incision was closed layer by layer and a peritoneal dialysis catheter was taken out. The scrotum was elevated postoperatively. Mild shortness of respiration and abdominal distention was seen on postoperative day one. On postoperative day two, recovery was excellent and the postoperative course was uneventful (). Drains were removed on day 12 and the patient was discharged on postoperative day 14. A checkup after 11 months showed the hernia to be entirely cured.


A 63-year-old male presented with right giant inguinal hernia, pain and insufficient sexual activity. His concomitant diseases were coronary heart disease, arterial hypertension and diabetes. There was a giant right inguinal hernia and contrast-enhanced CT demonstrated omentum and a large mesenteric tissue with intestine segments in hernia sacs that displaced the penis laterally (Figure , ). His laboratory findings were normal.
We decided that reduction of hernia sac contents could cause an increase in intraabdominal pressure postoperatively, so the patient was prepared for hernia repair with PPP after providing informed consent. A silicone Foley catheter was inserted into the abdominal cavity and insufflated as described in the first patient. The first pneumoperitoneum was applied in the operating room and then at the bedside (the insufflator was moved to the clinic from the operating room). Daily insufflated gas volume, intraabdominal pressure and expansion of waist circumference at the level of umbilicus was recorded (). The waist circumference at the level of the umbilicus increased to 11 cm on the fourth day. With the experience of the first patient, we decided that expansion was enough for operation and the patient was operated on on the fifth day. A standard inguinal incision was preferred under general anesthesia. Small bowel segments, appendix vermiformis, cecum, and 300 cc of free fluid were in the hernia sac. The hernia contents were pushed into the abdominal cavity easily and a zig maneuver performed after prophylactic appendectomy. The peritoneum was closed and a 7×15 cm polypropylene mesh was inserted and fixed to the symphysis pubis, inguinal ligament and conjoint tendon. A suction drain was placed on the mesh and in the scrotum. An abdominal silicone Foley catheter was taken out. The scrotum was elevated postoperatively. Mild difficulty on respiration was seen on the first postoperative day. The drains were removed on day 12 and he was discharged on postoperative day 13 (). A checkup after 9 months was uneventful.