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A 59-year-old Chinese woman with a 10-year history of exertional dyspnea and palpitations was hospitalized for exacerbating symptoms of right heart failure from one month prior to admission. On physical examination, her pulse rate was 99 beats per minute, and blood pressure was 111/80 mmHg. She had moderate bilateral pitting leg edema, a distended jugular vein and mild dilatation of superficial neck and facial veins. An accentuated second heart sound without tumor plop was heard on auscultation. Electrocardiogram showed sinus rhythm with right bundle branch block. Chest X-ray and abdominal computed tomography were unremarkable. The results of lower extremity ultrasound were negative for deep venous thrombosis. A transesophageal echocardiogram (TEE) demonstrated a mobile and pedunculated giant mass (68 mm × 49 mm) in the enlarged right atrium (70 mm × 53 mm) arising from the anterior wall of the SVC (Figure ). The mass prolapsed into the right ventricle across the tricuspid valve during systole (Additional file : Video 1), resulting in tricuspid orifice obstruction and symptoms of right heart failure (Figure ).\nThe patient underwent surgical intervention through a median sternotomy and on normothermic cardiac arrest with the aid of cardiopulmonary bypass. To avoid mass fragmentation, care was particularly taken during venous cannulation after pericardiotomy. Briefly, an ultrasound probe was placed transversely on the patient’s right neck, and the short-axis of right internal jugular vein was clearly visualized. A venous cannula (15 Fr) was then inserted into the right internal jugular vein using the Seldinger technique. With the guidance of TEE, the tip of cannula was properly positioned in the distal segment of SVC. Similarly, TEE was performed to assess the location of the myxoma prior to the cannulation of inferior vena cava, keeping the cannulation site as far as possible to prevent a potential mass fragmentation. After opening the right atrium, a grey-green translucent mass in the atrial chamber with a pedicle attached to the anterior wall of the SVC was identified and was then completely excised, no endocardial adhesions in right atrium or ventricle was observed. A glutaraldehyde preserved autologous pericardium was used for patch reconstruction of the anterior wall of the SVC. The tricuspid valve appeared structurally normal, and tricuspid regurgitation was trivial. Histopathologic examination demonstrated a hypocellular benign tumor containing satellite polygonal cells with scant eosinophilic cytoplasm scattered throughout an acid-mucopolysaccharide-rich stroma (Figure ). Postoperatively, transthoracic echocardiography (TTE) showed normal biventricular function without any residual myxoma and significant tricuspid regurgitation, and the patient had an uneventful recovery and was discharged home at 7 days after surgery. |
A 64-year-old man was admitted to our clinic with similar complaints. He had undergone placement of the same type of penile prosthesis three years earlier. He reported the prosthesis had been functioning well, providing a high degree of satisfaction for him and his wife []. He had a 17-year history of DM (type II) with good control. He also described having trapped his penis against a toilet seat while sitting down to defecate four days earlier.\nAt presentation, both patients displayed fever (38.6°C and 39°C, respectively), and reported receiving broad spectrum antibiotics from general practitioners in their home towns. They denied any previous similar episodes since prostheses implantation. Physical examination in both cases revealed an erythematous, edematous and indurated penis with mildly macerated skin. The first patient also had ischemic spots over the penile shaft and localized soft swelling (3 × 2.5 cm) on the left side of the peno-scrotal junction (Fig. ). Penile and perineal palpation indicated intact devices in place, and this was further confirmed by radiography of the pelvis. However, the appearance of the patients' organs looked abnormal with poor concealment of the devices. The patients' white blood counts were elevated (13.200/mL and 14,100/mL, respectively). Urine analyses and cultures yielded negative results. Diabetes was well controlled in both patients as evidenced by normal levels of fasting and postprandial blood sugars and glycosylated hemoglobin levels. Ultrasound examination of the genitalia was performed to identify any possible hematoma but yielded no relevant results other than edema at the peno-scrotal junction of the first patient. Blood examination for bleeding, coagulation, prothrombin and partial thromboplastin times yielded normal results.\nAfter discussion in each case, we decided to perform an exploration and extrusion of each penile prosthesis. The operations were performed under spinal anesthesia. The tunica was opened and a significant volume of whitish-yellow purulent material was noted around both cylinders of the device in both patients. Cultures of this material in both patients yielded positive results for Staphylococcus epidermidis (S. epidermidis). The localized swelling seen at the peno-scrotal junction of the first patient was confirmed to represent soft tissue edema but not hematoma. Removal of the prostheses followed by continuous irrigation and suction drainage resulted in rapid and complete resolution of the local inflammatory process and infection-associated symptoms within three to four days and recovery was uneventful in both cases. |
A 47-yr-old woman presented to a local hospital with a painless lump in the right breast that had been present for 1 month. She had no history of other breast complaints or surgeries. Her menarche occurred at age 14 yr and she gave birth to 3 children. There was no family history of breast or ovarian cancer, but 2 of her family members died from late-onset cancers (). On physical examination, a poorly defined, firm mass was noted in the medial upper portion of her right breast, measuring approximately 3 cm, and no axillary or cervical lymphadenopathy was detected. Mammography demonstrated a lesion highly suspicious of cancer, and histological examination of the core needle biopsy of the lesion revealed invasive ductal carcinoma (IDC) of the breast. The patient was then transferred to our hospital for further evaluation and management of the cancer. Results for complete cell count, blood chemistry, and tumor markers (carcinoembryonic antigen; 0.8 ng/mL, cancer antigen 15-3; 5.3 U/mL) were all within reference intervals. Screening for metastatic disease by computed tomography and positron emission tomography showed no evidence of adjacent lymphatic, pulmonary, bone, or hepatic metastases.\nA pathologist reviewed slides from the other hospital and confirmed the diagnosis of IDC. The patient then underwent a partial mastectomy of the right breast with ipsilateral, axillary sentinel lymph node biopsies. The final pathology of the tumor was IDC, and the cancer was staged as pT2N0M0. The specimen showed comedo-type necrosis with calcification and had a maximum diameter of 2.2 cm. The Nottingham classification [] was II (moderately differentiated), and the total point score was 7 (2-3-2). The tumor cells stained positive for p53, and results for Ki67 were positive in 5% of the tumor cells. The carcinoma displayed no nuclear reactivity for estrogen receptors, progesterone receptors, or HER-2. Biopsy findings for 7 sentinel lymph nodes were all negative. Although frozen sections, removed during the surgery, were negative for malignancy, final pathology revealed malignant infiltrations in the deep layers of the inferior and medial margins.\nGiven the extensive family history of cancer, samples of peripheral blood (PB) lymphocytes and tumor tissue were assessed for TP53 mutation. Briefly, DNA was extracted from breast cancer tissue and mononuclear cells from PB, and 5 to 9 TP53 exons and intron-exon boundaries were studied. Analysis of PB revealed a germline heterozygotic A189V mutation that was homozygous in the IDC specimen (). Later, her 3 offsprings underwent genetic screening, and 2 daughters (aged 20 and 16 yr) were found to carry the mutation ( and ) despite absence of signs or symptoms of cancer. Patients (or their parents, if younger than 14 yr) gave informed consent for all molecular testing.\nAfter confirmation of the patient's TP53 mutation status, an interdisciplinary panel met to determine the utility of localized radiotherapy, based on the suspected radiosensitivity of individuals harboring a deleterious mutation in the TP53 gene [, ]. As partial mastectomy is generally followed by radiotherapy to increase the probability of tumor-free resection margins, risk of cancer relapse was determined to be greater than the risk of secondary carcinogenesis due to radiation. The patient has completed 4 cycles of adjuvant chemotherapy consisting of doxorubicin (60 mg, 32.8 mg/m2) and cyclophosphamide (500 mg, 273.2 mg/m2), and 6,400 cGy of adjuvant radiotherapy is planned. The patient is currently well, without any signs or symptoms of cancer recurrence. |
This was a 35-year-old married, multigravida female who was admitted to the Obstetrics and Gynaecology department of our institution for an elective exploration laparoscopy to retrieve a missed IUD. The patient was healthy otherwise. The patient’s obstetric history, an insertion of an IUD more than 9 years ago, was carried out at a private clinic. During a routine check-up 6 months after implantation, the IUD string had disappeared. A presumptive diagnosis of spontaneous expulsion was made. The patient underwent a new implantation of IUD, which was carried out at the same private clinic. The IUD was removed 2 years later. The patient has since had a successful pregnancy and the foetus was delivered by a Caesarean section (CS) 1 year after removal of the IUD. However, over the last 3 years, the patient has experienced difficulty conceiving. The patient has not experienced any complaints. During radiological tests, a foreign body in the right lower quadrant was detected by hysterosalpingogram. Based on these findings, laparoscopy exploration to retrieve the presumptive IUD was carried out.\nOn admission, the patient’s vital signs were normal. The patient was conscious and alert, with normal body-built habits. No anomalies were detected. No abdominal tenderness was observed. The results of her blood works were normal.\nThe patient underwent laparoscopic exploration. The obstetrics and gynaecology team were unable to locate the IUD in the free peritoneal cavity. However, the team identified adhesion at the level of the ileocecal junction and suspected a foreign body in the cecum with ileocecal fistula. The laparoscopic examination transitioned to an open laparotomy by route of the patient’s existing CS scar, and our team was called to carry out the procedure. A consent to carry out exploratory laparotomy was sought.\nThe laparotomy demonstrated that the IUD had penetrated the cecal wall through the base of the cecum. The IUD was palpated within the cecum (). The IUD was not fully mobile and was located approximately 8 cm from the appendix. In addition, ileocecal fistula was apparent between the terminal 7 cm of the ilium, and the entry point of the IUD at the base of the cecum (). A normal appendix was visualized at the base of the cecum (). Fibrosis in the uterine fundus was also observed. There were no other abnormalities to report.\nGiven the immobility of the foreign body and ileocecal fistula, a limited ileocecal resection was performed with a side-to-side anastomosis. We identified the missed IUD in the resected specimen (). The patient was discharged on post-operative day three with follow-up in the clinic. |
A 65-year-old woman complained of increasing pelvic pain and coccygodynia over the past 12 months. The patient described the pain as sharp, stabbing and localized to the lower pelvis with radiating to the anorectal area, and also complained of tenesmus. She had a traumatic injury on coccyx 50 years ago and retocele repaired with graft by surgery 15 years ago. At the beginning, she visited other clinics and had been diagnosed with levator ani syndrome. She took a daily dose of 225 mg pregabalin, 650 mg acetaminophen and 75 mg tramadol, and 25 mg sodium tianeptine. She also received superior hypogastric plexus block and caudal epidural blocks. But she was referred to our pain center because the previous therapies had been ineffective. Her pain score on the 10-grade visual analogue score system (VAS, ranging from 0 = no pain to 10 = absolutely intolerable pain) averaged 8/10. Pelvic MRI imaging showed 1.3 cm sized intramural leiomyoma. She was initially treated with caudal epidural block and ganglion impar block, but had the persistent presence of the pelvic pain and coccygodynia. We decided to perform a new technique for inferior hypogastric plexus block with a coccygeal transverse approach to reduce the pelvic pain and coccygodynia. A sufficient explanation was provided to the patient about the procedure and its complications and written consent was received from her. She was positioned prone on the table, with a pillow under the anterior superior iliac spine to flatten the normal lumbar lordosis. The midline of the sacrococcygeal area was cleaned with antiseptic, and sterile drapes were placed. The midline between S2 and S3 junction was the target anatomic landmark for the block (). An optimal sacral foramenal view was obtained as follows. The targeted sacral anatomic landmark was located approximately in the middle of C-arm fluoroscope screen in the anteroposterior view. A 22-gauge, 10-cm block needle was manually bent about 1 cm from its tip to form a 10 degrees angle (). This bend facilitated needle position toward the anterior aspect of the sacrococcygeal concavity. A skin entry point was just under the transverse process of the coccyx. After the local skin infiltration over the coccyx area, a 22-gause needle was slowly advanced to the inferior of the transverse process of the coccyx. The needle tip was then directed anterior to the coccyx but closed to the anterior surface of the bone until it reached the sacrococcygeal junction. A 22-gauge bent needle was directed superiorly and medially toward the sacrococcygeal junction with the guidance of the sacrum and coccyx. Lateral fluoroscopic imaging was used to identify the sacrococcygeal area, and midline position was confirmed with an AP view. We should pay close attention to needle depth to avoid rectal trauma because this structure lies close to the sacrum. Therefore, we frequently checked lateral and AP fluoroscopic imaging. The needle was advanced to the anterior surface of the sacrum until it reached midline between S2 and S3 junction level. With the needle in the proper position, after a negative aspiration of blood or stool, 1.5 ml of contrast medium was injected to confirm the retroperitoneal location (). Laterally, the contrast should appear smoothly contoured and hug the sacrococcygeal concavity like a teardrop. There should be a smooth contrast of the dye in the retroperitoneum between the sacrococcygeal region and the bowel gas. Next, for diagnostic and therapeutic purposes, a mixture of 2 ml of 2% lidocaine, 2 ml of 0.25% bupivicaine, and 10 mg of triamcinolone was injected after correct needle position was verified by fluoroscopy. She had significant pain relief with a drop of the VAS level from 8/10 to 2/10 immediately after block. She did not want neurolytic block. Further inferior hypogastric plexus blocks were performed twice in sequence at an interval of 3 months, which diminished VAS to 1/10. The nerve block reduced the amount of supplementary medication needed to control the pain. Pregabalin was reduced from 225 mg to 150 mg per day, and acetaminophen and tramadol was also reduced from 650 mg and 75 mg to 325 mg and 37.5 mg respectively. Her pain improved dramatically immediately after the nerve block (VAS score 2/10). There were no serious procedure-related complications. At present, 6 months following the first treatment, the patient has no problems in performing activities of daily living and works, including sitting and walking. The patient has maintained a VAS of 1-2/10. |
A 69-year-old man was admitted to a district general hospital with a flare of Crohn's colitis. His symptoms included bloody diarrhoea, with ten to fifteen episodes per day. He had a two-year history of ileocolonic Crohn's disease, and otherwise his past medical history was unremarkable. At ward level, he was alert, orientated, and independent with personal self-care.\nConventional treatment with 5-ASAs and azathioprine had failed to achieve remission, although he had been unable to tolerate doses greater than 100 mg of azathioprine due to nausea. As a result, he had become steroid dependent and had been taking continuous prednisolone for seven months prior to admission, with 20 mg being the lowest dose achieved during that time. Intravenous steroids (100 mg hydrocortisone qds) did not improve symptoms when he was admitted to hospital, and as per the initial outpatient plan discussed with the surgical team, biologic therapy was considered to be the next step for this gentleman. At the time of admission, he had suffered recurrent episodes of pyrexia. Three sets of peripheral blood cultures showed no growth and neither did serial stool cultures. Plain chest radiograph was unremarkable.\nHe was counselled and commenced on Infliximab treatment. Three days later, he suffered a clinical deterioration, with drowsiness and pyrexia. Glasgow Coma Scale revealed that eyes opened to voice, speech was limited to words only, not sentences, and he was able to obey commands (GCS 12/15). Full neurological examination was inhibited by patient drowsiness. All four limbs moved symmetrically against gravity, sensation appeared intact, and reflexes were equal and symmetrical. Limited cooperation inhibited assessment of limb coordination but horizontal nystagmus was noted in both right and left lateral gaze and speech was slurred. He had no rash or neck stiffness. A new cold sore was noted on his top lip.\nUrgent blood tests were sent alongside further blood, stool, and urine cultures. He underwent CT brain that day which showed no acute intracranial abnormality. He then underwent lumbar puncture. Results of these investigations are shown in . At the point of deterioration, he had been commenced empirically on acyclovir and high dose meropenem (2 g tds) to cross the blood-brain barrier.\nPrior to confirmation of the organism, lumbar puncture had revealed high protein and low glucose in cerebrospinal fluid (CSF), and he was commenced empirically on isoniazid, rifampicin, ethambutol, and pyrazinamide to cover for tuberculosis. These were stopped when Listeria was found in both peripheral blood cultures and CSF. It was shown to be sensitive to meropenem but antibiotics were changed to gentamicin and high dose amoxicillin (2 g qds) on the advice of Microbiology. They suggested a six-week course of amoxicillin and up to three weeks of gentamicin.\nMRI imaging revealed extensive T2 and FLAIR high signal centred on the cerebellar vermis with extension into the cerebellar hemispheres and brainstem, in keeping with rhombencephalitis.\nHe was transferred to the Intensive Care Unit (ICU) five days following Infliximab infusion due to fluctuating GCS in the range of 3–10/15 and was intubated in ICU because of concerns regarding airway protection. He transferred to ICU in the tertiary referral centre for neurology and neurosurgery for closer input, as he was deemed to be at high risk of developing obstructive hydrocephalus. In ICU, he underwent tracheostomy and was later weaned from mechanical ventilation. He also underwent gastrostomy insertion for long term nutrition maintenance.\nSubsequent neurological evaluation revealed prominent spastic quadriparesis with occasional spontaneous nonpurposeful movement in his upper limbs and a relatively fixed reduction of consciousness, with no evidence of awareness. He spent one month in ICU and was then discharged to ward level care. Active Crohn's disease was an ongoing problem, although medication was limited to steroids, and he was deemed to be too unwell to undergo defunctioning bowel surgery. No evidence of neurological recovery was demonstrated during the months that followed and he suffered from recurrent episodes of aspiration pneumonia. The latter was listed as primary cause of death ten months following Infliximab infusion, with Listeria rhombencephalitis and Crohn's disease listed as contributory factors.\nPrior to Infliximab treatment, this gentleman was already immunosuppressed. Long term steroid use alongside azathioprine already rendered him at risk of developing opportunistic infection. However, the serially negative blood cultures until the point of administration, followed by positive blood and CSF cultures 3 days following Infliximab, would suggest that this did play a role in his deterioration. This too is suggested by his dramatic neurological deterioration so soon after infusion. |
A 56 year old man, who complained of severe neck and back pain beginning as chest pain, visited the emergency room (ER). He had no medical history of pain, particularly originating from the spine. The chest pain occurred after an argument with another individual. He visited the ER immediately after the chest pain occurred. The laboratory findings showed elevated creatine kinase (CK), the muscle brain isoenzyme of CK, and troponin-I to 276 IU/L, 13.15 ng/mL, and 9.746 ng/mL, respectively. He was diagnosed with a non-ST-segment elevation myocardial infarction. He was treated with nitroglycerin, 250 mg aspirin following 200 mg per day, 60 mg enoxaparin every 12 hours, and 300 mg clopidogrel following 75 mg per day in the intensive care unit. Despite that the chest pain and laboratory findings improved, his back and neck pain progressed slowly with a visual analogue pain scale value of 8 or 9. He did not respond to pain killers, including opioids, and then abruptly developed paraplegia 3 days after the initial chest pain onset. He consulted the department of neurosurgery without a coronary angiographic evaluation.\nSpinal magnetic resonance images (MRI) obtained after the paraplegia showed a T1 low and T2 mixed heterogeneous signal intensity mass at the ventral epidural space from C2 to C4 and from T7 to L1, respectively. The mass compressed the cornus medullaris at the T10/L1 level and the spinal cord at the level of C2/3. Some high signals from the spinal cord were observed on T2 weighted images, indicating a spinal cord injury. Some of the T1 weighted images showed abnormally high signal intensity, indicating a multistage hemorrhage (). No abnormal coagulation findings were observed, including prothrombin time, activated partial thrombin time, bleeding time, and platelet count. He underwent an emergent operation to decompress the spinal cord.\nA right-side hemilaminectomy was performed from T7 to L1 under general anesthesia in the prone position. A hematoma was located at the ventral epidural space and had compressed the dura. The hematoma was hard, with no spinal cord pulsation. No active bleeding and no abnormal vascular structure were observed. Vital signs were stable during surgery.\nThe patient recovered from general anesthesia with no complications, but his neurological symptoms did not change. He started 75 mg clopidogrel per day and 12.5 mg carvedlol per day 14 days after surgery A coronary angiographic evaluation was not performed, as he declined the treatment.\nA follow-up MRI 2 months after surgery revealed several abnormal T2 weighted high-signal intensities and spinal cord atrophy, although no residual hematoma was found at the cervical and thoracolumbar areas (). No neurological recovery had occurred 7 months after the initial deficit. |
An 87-year-old woman presented with sudden headache, transcortical sensory aphasia and mild right sided weakness. Initial computed tomography (CT) and magnetic resonance imaging (MRI) of the brain showed an acute hemodynamic cerebral infarction of the left frontal and parietal lobes and a focal severe stenosis of the proximal left ICA. Echocardiography showed no evidence of abnormalities of the cardiac valves or of left ventricular dysfunction. Three days after admission, cerebral angiography showed a focal severe stenosis (75%) of the proximal left ICA without abnormal findings in either common carotid artery (). However, six days after admission, fever (40℃) suddenly developed with NIH Stroke Scale (NIHSS) score deteriorating from 4 to 10, due to additional aphasia and worsened weakness. Three days after the onset of fever, brain MRI showed no newly developed acute lesion, and echocardiography showed a newly visible 6×5 mm valvular vegetation of the non-coronary cusp of the aortic valve (). Blood cultures were positive for Staphylococcus aureus 4 days after the onset of fever as the offending microorganism. Intravenous antibiotic therapy was started immediately with a combination of cefazolin and gentamycin. Seven days after antibiotic therapy, the patient was diagnosed with bacterial meningitis, and cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 240/mm3 (leucocytes, 71%; lymphocytes, 29%), red blood cell count of 2900/mm3, glucose concentration: 50 mg/dL, protein concentration: 216 mg/dL, and pH 8.0. Twenty-six days after admission, chest CT, which was performed with the suspicion of the Lt. pleural effusion as the cause of the fever, showed an incidental 22×20 mm thin walled saccular vascular structure located 2 cm distal to the origin of the left CCA suggesting a mycotic aneurysm because of acute development, presence of ongoing fever and inflammatory infiltration around the saccular vascular structure (). Three days after the chest CT, the patient's fever and the results of repeated CSF analysis and blood culture were found to be normalized. Because of the latter evidence for complete eradication of septicemia and the patient's old age and cardio-neurologic risk factors for surgery, the patient was immediately subjected to an interventional procedure to treat the mycotic aneurysm. Thoracic aortography showed a saccular aneurysm in the proximal left CCA (). A 10 mm×5 cm polytetrafluoroethylene covered stent-graft (Hercules Vascular: S&G Biotech, Seongnam, Korea) was deployed within the proximal left CCA across the wide neck of the aneurysm (). The final thoracic aortography revealed a complete exclusion of the aneurysm and a widely patent implanted stent-graft (). During the 2 weeks after the procedure, intravenous antibiotic with cefazolin and anti-pletelet therapy with 325 mg aspirin and 75 mg of clopidogrel were continued, and patient's neurologic symptoms gradually improved. The final transesophageal echocardiography showed a subtly improved vegetation, compared with previous echocardiography.\nAfter 2 weeks of additional anti-pletelet treatment with the same medication regimen, the patient was discharged without neurological deficits.\nFollow-up chest CT 12 months after the procedure showed the aneurysm completely excluded and a widely patent stent-graft (). The patient remained asymptomatic during the 12-months follow-up period on continued anti-pletelet treatment with 100 mg aspirin and 75 mg of clopidogrel. |
A 39-year-old gentleman presented with persistent oral erosions and skin vesicles over the left forearm for 4 months in June 2007. There was associated voice change, foreign body sensation in eyes, and weight loss. Clinical examination revealed multiple erosions over lips, hard palate, and buccal mucosa with hemorrhagic crusts over the lips. There was a single resolving vesicle over left forearm. Nikolsky and bulla sign were negative. There was no palpable lymphadenopathy. The rest of the systemic examination was unremarkable.\nPerilesional lip biopsy under Direct Immunofluorescence (IF) showed fishnet pattern fluorescence for IgG in the lower third of epidermis and coarse granular contiguous positivity for C3 in the basal layer of keratinocytes. It was negative for IgA and IgM. He was started on Prednisolone and Azathioprine for one month, but his lesions did not improve.\nRoutine chest X-ray done showed right sided hilar mass (). Further evaluation with CT thorax revealed 6 × 3.8 cm, densely enhancing mass in the anterior and middle mediastinum ().\nHe had thoracotomy and debulking of the mass of 6 × 5 cm tumor in the right lobe of thymus, adherent to right phrenic nerve. There were no enlarged lymph nodes. Gross specimen showed an ill-defined tumor of size 2.5 × 3.5 × 3 cm with homogenous yellowish tan surface. Microscopy showed circumscribed spindle cell tumor composed of interlacing fascicles with storiform pattern in a background of lymphocytes (). Immunohistochemistry revealed cells positive for CD21 and CD35 leading to a pathological diagnosis of follicular dendritic cell tumor.\nPatient had 2 major criteria of PNP (a) polymorphic mucocutaneous eruption and (b) concurrent internal neoplasia and 2 minor criteria (a) Direct IF showing intercellular and basement membrane staining and (b) Indirect IF staining with rat bladder epithelium with intracellular IgG staining positive and diagnosed to have FDC tumor of the anterior mediastinum with Paraneoplastic Pemphigus.\nHe received postoperative radiation therapy to the residual mass in the anterior mediastinum (). He was treated with conventional anteroposterior-posteroanterior (AP-PA) technique, using 6 MV X-rays, 45 Gy in 25 fractions to midplane, and 5 fractions per week over 5 weeks. The skin and oral lesions subsided at the end of treatment. At 8-year follow-up, he is free of disease (). |
A previously healthy 21-year-old male presented to the emergency room with a 2 days history of increasing colicky abdominal pain mainly in the epigastric area. This pain was associated with nausea, vomiting and bloody diarrhea. He had no recent weight loss and no family history of bowel disease.\nUpon examination, the patient was afebrile, he had a tender abdomen with no peritoneal signs nor adenopathy. The patient’s skin, including the perioral area, appeared normal, as did the oral mucosa. Laboratory tests indicated low hemoglobin levels, high white blood count, with normal liver and renal function. A contrast enhanced computed tomography (CT) imaging of the abdomen revealed a long segment of jejunal intussusception and a filling defect in the second part of the duodenum, with right side hydroureter and hydronephrosis.\nPatient was consented for an exploratory laparotomy and taken to the operating room. During his surgery, a long segment of the proximal jejunum (67 cm) was found to be invaginated into a distal jejunal segment, which confirmed the diagnosis of intussusception (Fig. ). A mass of 6 cm could be felt at the lead point of the intussusception and the invaginated loop of bowel appeared to be compromised requiring resection of the diseased segment that contains the leading intramural polyp. Careful exploration of the rest of the abdominal cavity and intestine was done, and two additional masses were felt to be tethered inside the sigmoid colon. The sigmoid was redundant and easily resected with good oncological margins (Fig. ). Giving the patient’s young age, appendectomy was performed as well.\nPatient had an uneventful postoperative hospital stay and discharged on fourth day postoperative.\nHistopathology showed multiple polyps in the jejunal segment that exhibited features of PJS. These hamartomatous cauliflower-like pedunculated polyps ranged from 0.5 to 3.5 cm in size. The sigmoid mass showed a larger hamartomatous polyps 3.5 × 3.5 × 3 cm3 with low grade dysplasia while some of the jejunal polyps showed transmural infarction.\nHis postoperative upper and lower endoscopy showed numerous diminutive polyps in the gastric fundus and gastric body. It also showed multiple duodenal polyps (3–5 mm) with the largest found at the second part of duodenum involving the ampulla. These were excised and showed normal mucosa with no active or chronic inflammation, atypia or malignancy (Fig. ) and was booked for follow up endoscopy after 1 year. |
A 35-year old female patient visited our hospital with vision loss in the left eye, which had started 1 week before. She had previously been diagnosed with glaucoma in the left eye and was being treated with 1% brinzolamide/0.5% timolol maleate (Elazop; Alcon, Fort Worth, TX, USA). The BCVA was 20 / 50 in the left eye and 20 / 15 in the right eye. The IOP was 29 mmHg in the left eye and 18 mmHg in the right eye. There were 1+ inflammatory cells in the anterior chamber of both eyes. On the fundus examination, anterior vitreous cells were trace in the right eye and 2+ in the left eye. RCHs with engorged vessels were observed at the temporal area of the right eye and the inferotemporal periphery of the left eye (). Laser photocoagulation was performed (0.2 seconds) in the left and right eyes (300 and 190 mW, respectively). To control the inflammation, 1% prednisolone acetate (Pred Forte; Allergan, Irvine, CA, USA) was administered to the left eye, in addition to 30 mg of oral prednisolone for 1 week. The patient was referred to the hematology and oncology departments for a VHL evaluation, and no additional abnormality was found. After 1 month, the exudates increased, and fluorescein leakage was still observed around the RCH in the left eye during fluorescein angiography. The tumor was still in the active state, and laser treatment was considered insufficient because the tumor was located in the far periphery of the temporal retina. Triamcinolone (4 mg/0.1 mL) was injected into the subtenon, and cryotherapy was performed in the left eye. The patient underwent additional laser photocoagulation in both eyes when the fluorescein leakage increased during fluorescein angiography. After a total of two laser photocoagulations in the left eye and four in the right eye, the patient enjoyed a stable state for 6 months to the last follow-up (). |
A 51-year-old male patient had been diagnosed with squamous carcinoma, stage IIIa, two months prior, had twice been treated with cisplatin and gemcitabine combination chemotherapy, and was admitted for left upper lobe resection. Diabetes and hypertension were not detected in the medical history. At the time of admission, the blood pressure was 125/70 mmHg, heart rate was 64 beats/minute, respiration rate was 20 breaths/minute, and body temperature was 36℃. Plain chest radiography and chest computed tomography revealed a 2.9-cm tumor in the left upper lobe. An electrocardiogram was normal, and no abnormal findings were detected in blood tests. The thoracic cavity was approached via left posterolateral thoracotomy. Since adhesion of the pleura was severe, the adhesion was removed. Cardiac arrest occurred while dissecting the adhesion of the left lower lobe, immediately after the increase of the ST segment on electrocardiogram as well as the development of hypotension (60/40 mmHg) and bradycardia (40 beats/minute), after separating the vein and artery branching as well as the bronchus. Inotropics were used, and an intra-aortic balloon pump (Datascope®) was inserted via the left femoral artery while performing cardiac massage by pericardiotomy. After the insertion of an intra-aortic balloon pump, the heart rate recovered to a normal sinus rhythm, the blood pressure was 100/60 mmHg, and the arterial oxygen saturation level was 100%.\nAfter wound closure, surgery was completed, and the patient was transferred to the intensive care unit. After transferring to the intensive care unit, the patient remained stable for 10 minutes, cardiac arrest occurred simultaneously with a decrease in the ST segment on the electrocardiogram (). Thus, while performing cardiopulmonary resuscitation, an extracorporeal membrane oxygenator (Medtronic centrifugal Bio-pump®) was inserted into the right femoral artery and the vein by the Seldinger technique using a 17 Fr catheter and a 21 Fr catheter, and vital signs were stabilized. Afterward, echocardiography was performed, revealing apical ballooning and severe dysfunction of the left ventricle (). An emergency coronary artery angiogram was performed, and it was normal with the exception of 30% stenosis in the left anterior descending coronary artery (). The creatine kinase (CK) level was 2,976 U/L, creatine kinase MB (CK-MB) was 174 ng/mL, and troponin I was elevated to 26 ng/mL. Stress induced cardiomyopathy was diagnosed. Once vital signs were stabilized, catecholamine was terminated. 26 hours after surgery, the extracorporeal membrane oxygenator was removed. 48 hours after surgery, the intra-aortic balloon pump was removed. 3 days after surgery, blebs, edema, and discoloration were detected in the right extremities, and thus a peripheral angiogram was performed (). Compartment syndrome was diagnosed and a fasciotomy was performed. 4 days after the surgery, CK was 18,000 U/L, CK-MB was 73 ng/mL, and troponin I was reduced to 4.5 ng/mL. The artificial ventilator was removed 6 days after surgery. The patient was transferred to a general ward 11 days after surgery. The fasciotomy wound was sutured and the patient was discharged 20 days after surgery. At the time of discharge, echocardiography showed normal findings (). Currently, the patient has received follow-up care for one year and six months without significant complications. |
A 66-year-old woman with catatonic schizophrenia since 1972 was initially referred for blurred vision in 2012. She had been on chlorpromazine 100 mg daily for 13 years since 2000. On presentation, slit lamp and dilated fundal examination was unremarkable other than mild nuclear sclerosis cataract and the visual acuity was 0.3 (Snellen decimal) over both eyes. There were no abnormal corneal or lens capsular depositions and the cornea were clear bilaterally. The visual acuity remained the same for the following 2 years. In May 2013, chlorpromazine was switched to 5 mg daily olanzapine by her psychiatrist. She was not on any other systemic medications otherwise. In the latest follow-up in October 2015, there was a decrease in her visual acuity to 0.2 and 0.1 over her right and left eyes respectively. Slit lamp examination revealed bilateral diffuse pigmentary deposits over the full thickness of cornea (Figures and ), more significant at the interpalpebral region, as well as the anterior lens capsule (Figure ), which was not present in the previous follow-up 6 months ago. There was no significant progression of her cataract. The pupils could not be fully dilated. Gonioscopy was attempted to assess for presence of deposits at the angle but the patient could not cooperate. Fundal examination was normal and no pigmentary retinal deposits were present. General inspection showed no cutaneous pigmentation. Anterior segment optical coherence tomography (Visante, Carl Zeiss Meditec, Dublin, CA) showed the presence of depositions involving the full thickness of the cornea (Figure ). Specular microscopy revealed normal endothelial cell morphology, preserved hexagonal appearance, and the cell density was 3571 and 2958 over right and left eyes respectively. The clinical appearance of the corneal and lens deposition was classical of chlorpromazine-induced ocular toxicity, although the medication had been stopped for more than 2 years already when the ocular signs appeared. In view of the likely anti-psychotic agent related ocular toxicity, a letter explaining the ocular clinical findings was issued to her psychiatrist to reassess the need to continue the anti-psychotic agent. Olanzapine was subsequently stopped by her psychiatrist. |
A 42 year old Polish born male former semi-professional soccer player was seen on May 16th, 2003 in the emergency department, with the chief complaint of right leg pain. The patient had been playing soccer 10 days prior to this visit, and recalled a traumatic "tackle" injury to the posterior area of his right lower extremity. He denied experiencing any sensation of tearing or popping in the right knee during the index trauma, and was able to complete the game with only minor discomfort. On day 3 post-injury the patient noted severe pain in his knee and calf with ambulation. The patient visited his primary doctor on post-injury day 8 and was diagnosed with a right lower extremity soft tissue injury. A right lower extremity echo-doppler ultrasound (US), and a semi-quantitative D-dimer automated latex procedure were ordered to rule out a vascular disorder. The US investigation demonstrated a DVT in the distal femoral, popliteal, and distal calf veins, with a heterogenous mass (5 cm × 3 cm × 4 cm, resembling a hematoma) without a doppler signal in the right popliteal fossa. The D-dimer result was also positive for a suspected thrombosis (1.0–2.0 ug/ml; range = <0.25 ug/ml). The patient was instructed by his physician to proceed immediately to the emergency department for further evaluation and treatment.\nThe past medical and family history of the patient was non-contributory for a history of thrombophilia or other thrombotic major risk factors. The patient had a remote (11 years old) surgical history of a right-sided inguinal hernia that could have created scar tissue contributing to vascular obstruction and stasis. The initial emergency department examination demonstrated an exquisitely tender right calf with a 3 cm difference in mid-calf girth (10 cm. distal from each inferior patellar pole); a 1+ right knee supra patellar effusion; and a palpable popliteal mass with visible ecchymosis. Laboratory tests (CBC, Lytes, PT, PTT, ESR, CPK, Anti-throbomin, Factor V Leiden, Lupus Screen, ANA, Anti-Cardiolipin, Protein C, and Protein S) were negative for metabolic, hematological or familial abnormalities. A repeat US investigation confirmed the results of the previous outpatient results. The patient was anticoagulated simultaneously with unfractionated heparin and Warfarin sulfate. A multiview plain film x-ray examination of the right lower extremity demonstrated no fracture, dislocation, or bony mass.\nA magnetic resonance image (MRI) of the right knee was done several days after admission, to verify a torn right knee meniscal cartilage that had been previously diagnosed. The official MRI radiological report included a small free-edge tear of the posterior horn root junction of the lateral meniscus, chondromalasia (lateral patella and lateral femoral articular cartilage), and a moderate joint effusion with a bursal cyst or dilated semimembranous-gastronemius bursa.\nAnticoagulation was achieved on day 6 of the patient's hospitalization. He was discharged on 5 mg of warfarin per day, with instructions to continue the use of compression stockings. The patient was also advised to follow up with his primary physician for regular monitoring, and to avoid contact or collision activities during anticoagulation.\nThe patient was maintained on warfarin for six months, with weekly physician monitoring (symptoms, PT, INR) for the first three months post-injury. The monitoring interval was changed to once per month for the remainder of the treatment period. Hematologic investigations (APTT, PT, INR, Cardiolipin antibody, C-reactive protein, Lupant anticoagulant, Factor V Leiden, Antithrombin, ANA, Protein C, Protein S, and RPR) were obtained three months post injury. There were no contributory thrombophilic factors found in these investigations. Laboratory levels of Protein C activity 22% (range = 70–140%), Protein S activity 48% (range = 75–140%), INR 2.57 (range = 0.88–1.12), and PT 27.5 sec (range = 9.6–12.0 sec); APTT 38.5 sec (range = 23.4–35.4 sec) were found to be appropriately reactive to the anticoagulant therapy.\nThe patient underwent two arthrocentesis procedures to remove small amounts of serous fluid from the joint, and each time was injected with a lidocaine/corticosteroid combination. US examinations after the hospitalization period failed to demonstrate a recurrence or new onset of DVT, however residual echogenic material characteristic of a chronic thrombus was demonstrated in the popliteal vein. Compression stocking use was maintained after hospital discharge, and was discontinued after nine months. The patient returned to soccer after anticoagulation, with a full understanding of his increased risk of DVT recurrence.\nOne-year post injury the patient continued to suffer from intermittent right lower extremity discomfort and swelling often unrelated to activity. An elective arthroscopy was recently performed on the patient's right knee to investigate his long-standing meniscal disruption and effusion. The arthroscopy demonstrated several areas of arthrosis (patellar lateral and medial facets, lateral and medial femoral condyles), and a torn lateral meniscus. Appropriate partial lateral menisectomy and debridement, and chondroplasty of the areas of arthrosis were preformed. An arthroscopic examination of the posterior compartment demonstrated a small cleft-like area just medial to the semimembranosis where the Baker's cyst likely originated. The patient returned to the orthopedist one week post-op with a large (150 cc's) hemarthrosis that was aspirated from the knee. He was requested to follow-up in one month for re-evaluation. |
A 75-year-old Sri Lankan man with past history of hypertension and hyperlipidemia of 6-year duration and spontaneous right parietal intracranial hemorrhage 6 years ago with near normal recovery presented with painless swelling in his left supraclavicular area for the past 10 days. There had been no trauma or interventions done involving his neck and upper limb in the recent past. He did not have a history suggestive of ear, nose, throat, or oral infections and denied dyspnea, hemoptysis, back pain, lower urinary tract symptoms, or constitutional symptoms.\nAn examination revealed a nontender swelling in his left supraclavicular fossa due to a cord-like thickening of the left external jugular vein. There were no signs of infection either locally or involving his left upper limb. An examination of his oral cavity, ear, nose, and throat was unremarkable, and there was no lymphadenopathy. His upper limbs and face did not show evidence of venous congestion. Examinations of his cardiovascular, respiratory, central nervous, musculoskeletal and abdominal system were normal, but a digital examination of his rectum revealed a moderately enlarged, hard, irregular prostate gland.\nA venous duplex ultrasound scan of his neck confirmed thrombosis of his left internal jugular, extending into his external jugular and brachiocephalic veins (Fig. ). A contrast-enhanced computed tomography (CT) scan of his neck and upper chest demonstrated patent superior vena cava and right jugular veins, but his left internal jugular, external jugular, and left brachiocephalic veins were not visualized. However, it was unable to show thrombosis of these nonvisualized veins, as the study was done in the arterial phase. A chest radiograph did not show any masses or mediastinal widening.\nHis hematological investigations showed a hemoglobin of 11.4 g/dL, a white cell count of 8170/ mm3 (neutrophil 66 %, lymphocyte 21 %, middle fraction 13 %) and a platelet count of 530,000/mm3. The blood picture revealed evidence of inflammation. His erythrocyte sedimentation rate was 40 mm in the first hour (normal <20). His C-reactive protein level was 3 mg/l (normal <10 mg/L). A blood culture revealed no growth at 48 hours. Coagulation studies with activated partial thromboplastin time (APTT) and prothrombin time (PT) were normal. Thrombophilia screening was normal (antinuclear antibodies, anticardiolipin antibodies were not detected). His renal functions were normal, but liver tests revealed alkaline phosphatase (ALP) of 215 IU/L (53–128 IU/L) and gamma-glutamyltransferase (GGT) of 222 IU/L (normal <31 IU/L), while other enzymes were within normal range. His serum calcium was significantly elevated to 3.9 mmol/l. Human immunodeficiency virus (HIV) antibodies and venereal disease research laboratory (VDRL) test results were negative.\nHis prostate-specific antigen was greatly elevated to 257 ng/ml (normal <4 ng/ml). An ultrasound scan of his pelvis revealed a heterogeneously enlarged prostate with central calcification. A prostate biopsy revealed 30 % of tissue infiltrated by a conventional prostate adenocarcinoma of acinar type, which is predominantly composed of small glandular structures arranged in ill-defined nodules, giving the primary Gleason morphologic grade of 3, and less commonly of cribriform structures and large irregular glands, giving the secondary pattern as Gleason morphology grade 4. Perineural invasion, lymphovascular emboli or extraprostatic tissue infiltration was not demonstrated in the sections examined (Fig. ). There was a single lung metastasis in the lower lobe of his right lung, but no pleural effusion. There was no evidence of cervical or mediastinal metastasis.\nHe was immediately started on anticoagulation therapy with intravenous heparin followed by oral warfarin, to maintain his international normalized ratio (INR) 2–3. He showed a good response with treatment resulting in symptomatic relief and resolved neck swelling. He did not develop further thrombotic episodes while on anticoagulation therapy. He is currently being treated at the oncology unit with a chemotherapeutic regimen, which includes docetaxel and bicalutamide. |
The patient was an 18-year-old man who complained of right neck pain. Pain from the right neck to the back had been present for one year prior to his initial visit to our hospital. He had consulted another doctor approximately eleven months previously. No abnormalities were seen through plain radiography, and symptoms were alleviated by administration of a non-steroidal anti-inflammatory drug (NSAID). When the NSAID was discontinued six months later, symptoms recurred. Based on CT and magnetic resonance imaging (MRI), an osteoid osteoma in the superior articular process of C7 was suspected and the patient was referred to our hospital for surgery. There was tenderness at the paraspinal muscles of the right neck. Flexion and extension of the cervical spine exacerbated the right neck pain. No neurological abnormalities were noted, nor were there any abnormal blood test findings. Alignment also appeared normal on a plain cervical radiograph, and there were no obvious abnormalities. Upon closer inspection, however, indistinct lucency of the bone was observed in the right C6/7 facet joint (). On the plain CT scan, a nidus was seen in the right superior articular process of C7 (). On the contrast MRI, there were signal changes in the right superior articular process of C7, and a conspicuous contrast effect was seen in the surrounding tissue (). Osteoid osteoma of the right superior articular process of C7 was diagnosed based on these findings.\nMicroendoscopic surgery using a tubular retractor (METRx System Medtronic Sofamor Danek, Co., Ltd., Minneapolis, MN, USA) was selected because of its low invasiveness. A 2-cm incision was made 2 cm to the right of the midline, and an 18-mm in diameter tubular retractor was placed. After coagulation of the soft tissue, the right C6/7 facet joint was exposed. After excision of the C6 inferior articular process, the C7 superior articular process was removed using a chisel and rongeurs. Right C6/7 total facetectomy was performed. The right C7 nerve root could be confirmed when the C7 superior articular process was completely excised to the lateral side (). The operative time was 1 hour 29 minutes, and estimated blood loss was 5 mL. Pathologically, an osteoid formation covered with osteoblasts was seen. The pathological diagnosis was thus osteoid osteoma ().\nOn postoperative plain radiographs, the right C6/7 facet joint was completely resected (). No changes in alignment were detected. Postoperative CT confirmed complete resection of the tumor (). Postoperative MRI also showed that the tumor had been completely resected (). At 28 months after surgery, there had been no recurrence of symptoms. There was mild spondylolisthesis on C6/7. However, spinal instability such as increase of spondylolisthesis and/or posterior widening were not seen in the flexion-extension radiographs. |
A 30-year-old Thai female G2P0A1 at 37+1 weeks of gestation presented with a 1-week history of pruritic erythematous papules and plaques starting on the lower abdomen. The rash spread to all extremities and the trunk; however, mucosa, palms, and soles were spared. Neither abnormal symptoms nor signs of systemic involvement or fetal distress were detected.\nShe had been receiving regular antenatal care since she was 8 weeks pregnant. Her medications were 1 ferli-6 tab per day and 1 g calcium carbonate per day, which she had been taking since an antenatal care visit. She had undergone an abortion during the eighth week of pregnancy 5 years earlier. There was no history of a similar skin condition. She denied any previous herpes simplex infection. Physical examination revealed generalized discrete and confluent erythematous papules and plaques with central dusky red areas (targetoid lesions) on the trunk and extremities (fig. ). Some tiny pustules and vesicles were noted on both arms and the chest wall. Conjunctiva and oral and genital mucosa were unremarkable.\nA Tzanck smear from the vesicle showed the presence of polymorphonuclear cells but the absence of multinucleated giant cells. Gram staining of the pustules showed no organisms. Direct immunofluorescent study was negative for herpes simplex virus antigen. Additionally, a skin biopsy taken from the targetoid lesions on the left forearm illustrated focal parakeratosis with scale crust formation, irregular acanthosis and focal spongiosis of the epidermis, superficial perivascular infiltration of lymphocytes, and eosinophils with red blood cell extravasation. Direct and indirect immunofluorescent studies (HG factor) were all negative. Due to the diversity of skin manifestations, excluding the cause of the targetoid lesions and the negative result of laboratory investigations, PEP was diagnosed.\nSystemic corticosteroids were prescribed at the patient's first visit because pemphigoid gestationis could not be excluded. However, after the diagnosis of PEP was made, only topical corticosteroids and oral antihistamines were prescribed; the patient had a good clinical response. She delivered a healthy, term, male infant. |
A 46-year-old Chinese male with a history of hypertension presented with sudden syncope and came to his senses after ten minutes without headache. His respiratory rate was 21 breaths per min and the lungs were clear on auscultation. Cardiac examination revealed a grade II/6 diastolic murmur at the parasternal border. The pulse rate was 75 beats per min with normal sinus rhythm. The blood pressure was 109/76 mmHg in the left arm and 112/62 mmHg in the right arm. No remarkable abnormal was found in abdominal examination. Coagulation tests were normal. Arterial gas analysis on 3 L/min oxygen inspiration was pH 7.39, PaCO2 39.8 mmHg, PaO2 62.5 mmHg, SaO2 91.1%. A chest x-ray revealed widening of the mediastinum, a cardiothoracic ratio of 60%, and normal lung fields. Echocardiography revealed ascending aortic dissection and moderate aortic regurgitation with small to moderate pericardial effusion. Computed tomography scanning revealed ascending aortic to aortic arch dissecting aneurysm, in which the proximal part of right brachiocephalic trunk was also influenced. The left and right pulmonary arteries were normally enhanced with contrast medium. The patient underwent emergency operation for the thoracic aortic dissection, including Bentall procedure, interposition graft replacement of aortic arch, stented descending aorta with a shunt from a chamber around the aortic root to the right atrium. The patient was successfully weaned off bypass and transferred to the intensive care unit. The ratio of PaO2 to FiO2 after operation was 300. The haemodynamics was stable. However, the ratio of PaO2 to FiO2 fell to 150 gradually after operation. Two days after operation, the patient was conscious and cooperative, and his lung compliance and airway resistance were normal. But severe hypoxaemia ensued. In order to find out the cause of hypoxaemia, a chest computer temography was carried out but no evidence of atelectasis or pneumonia was shown. Pulmanary arteriography showed that an entire right lung field was defected without an extrinsic compression, which indicated embolism of the right pulmonary artery (Figure ). Considering the stable haemodynamics and the danger of haemorrhage, embolectomy and thrombolytic therapy were not applied in the patient. We took the anticoagulant therapy with low molecular weight heparin and warfarin, which sustained INR at 2-3. Pulmanary arteriography was reexamined every 3-4 day. The images indicated that thrombus gradually dissolved (Figure ). And the patient’s hypoxemia was improved. According to the effectiveness of treatment, we made sure that the entire right lung field defect in pulmanary arteriography was due to thromboembolism. Unfortunately, ventilator-associated pneumonia (VAP) occurred. Therefore, the tracheotomy tube was extubated until one month after operation. He survived for one year after discharging from the hospital without complications related to lung and heart. |
An 84-year-old-woman underwent a non-elective surgery because of an ankle fracture. Her weight and height were 62 kg and 150 cm, respectively, with body mass index of 27.6 kg/m2. She had left upper arm surgery eight days earlier in the same hospital. She fell in the bathroom while on the ward during the early morning two days previously. She hit her head and fractured her right ankle. She was unconscious when she was found by a nurse, but soon regained consciousness. She was not aware that she fainted. Her oxygen saturation (SpO2) was 88%, but increased to 94% with oxygen via a mask, with a blood pressure of 105/59 mmHg and heart rate 95 bpm. Although subsequent computed tomography (CT) of the head confirmed traumatic subarachnoid hemorrhage, with a small amount of blood in a region of the occipital sulci, no therapeutic intervention was deemed necessary for the head injury. However, she needed surgery for open reduction and internal fixation of the ankle fracture. She had atrial fibrillation, tachycardia of 120 bpm, diaphoresis and fever, and looked unstable at presentation before induction of anesthesia in the operating room (OR), although she responded appropriately to questions.\nThe surgery was performed under general anesthesia using desflurane and air combined with femoral triangle block and sciatic nerve block through a popliteal approach. Her airway was secured with a supraglottic device (#4 i-gel, Japan Medicalnext Co., Osaka). The surgery took one hour. Her anesthesia course of two hours and five minutes was unstable. Her heart rate varied between 95 and 140 bpm, systolic blood pressure varied between 70 and 110 mmHg, and frequent intermittent administration of phenylephrine was needed. Her SpO2 was 92-98%, though FO2 was maintained at 50%. Her body temperature was 38.5℃. After restoration of spontaneous respiration and confirming eye-opening to verbal stimuli, we removed the supraglottic device. She looked pale, although her SpO2 was 94% with an oxygen mask at 4 L/min. Because of her unstable hemodynamics and unexplained low SpO2 during and after surgery, we performed POC ultrasonography with a portable device (SonoSite M-Turbo, Fujifilm, Tokyo) using a sector probe (SonoSite, P21x) to rule out disorders in the heart and lung.\nLung sliding was identified on both lung surface, excluding possibility of pneumothorax. We found no fluid collection in the thorax. The apical four-chamber view revealed, however, a dilated right ventricle (RV), with reduced free wall motion of the RV with normokinesis of the apical RV wall (McConell’s sign) and a moderate tricuspid regurgitant (TR) jet. The peak TR pressure gradient was 41 mmHg. Further, we confirmed a D-shaped left ventricle (LV) during diastole in the parasternal short axis view along with a round-shaped dilated inferior vena cava in the subcostal short axis view. Ultrasonography did not detect any thrombus in the right heart or in the femoral veins. These images were not stored in the device, because the examination was not part of a routine work-up. Because there were no such abnormalities in the previous recordings of echocardiography before the first surgery, we diagnosed an acute RV overload, presumably resulting from a PE. We urgently ordered multidetector CT. CT angiography demonstrated filling defects in the right and left pulmonary arteries with an RV/LV diameter ratio of 1.5 (). CT venography showed only a small thrombus in the right popliteal vein and no residual thrombus in the greater veins such as the popliteal, femoro-iliac, or inferior vena cava. Her SpO2 was thereafter stable above 97% with oxygen supplementation via face mask for the following two days. She was carefully managed by cardiologists with oral anti-coagulant therapy (edoxaban). She was discharged from the hospital two weeks later. |
A 72-year-old woman with a medical history significant for sarcoidosis, paroxysmal atrial fibrillation, on apixaban, obstructive sleep apnea, hypertension, hyperlipidemia, and non-insulin–dependent type 2 diabetes mellitus, presented to the emergency department with sudden onset involuntary movements of her right arm and hand, which was followed by acute onset left-sided facial droop, dysarthria, and expressive aphasia.\nInitially, stroke was suspected; therefore, she underwent computed tomography (CT) imaging of the head without contrast. This showed a curvilinear hyperdensity in the left central sulcus region, left subinsular region, and inferior frontal operculum worrisome for an acute subarachnoid hemorrhage (SAH). CT angiography of the head and neck did not reveal overt vascular abnormalities. Further investigation with angiograms of the carotid and vertebral arteries successfully confirmed the absence of vascular lesions or aneurysms that may have accounted for hemorrhage. Noted in particular, there was no active extravasation of contrast evident during the study. Magnetic resonance imaging (MRI) of the brain showed curvilinear hyperintensity filling along the left central sulcus without evidence of acute blood within the sulcus (Figure ). The MRI also revealed a second area of focal parenchymal abnormality located anterior to the left frontal horn, with subtle mass effect and associated vasogenic edema. Cerebrospinal fluid (CSF) analysis from lumbar puncture did not reveal overt xanthochromia. Given these findings, intracerebral hemorrhage was felt less likely to be the cause of the patient's presentation, thus raising concern for an underlying inflammatory or neoplastic process.\nDue to concerns of an underlying malignancy, the decision was made to pursue a left frontal craniectomy with stereotactic biopsy of the abnormal leptomeningeal region within the left frontal lobe. Preliminary results from pathology revealed lymphocytic infiltration of the meninges, suggestive of either a lymphoma or inflammatory process. Final pathological results with molecular analysis supported a diagnosis of B-cell lymphoma. The lymphocyte population was comprised of mainly of CD20 + B cells (Figure ) and few scattered CD3 + T cells (Figure ). The B cells had no co-expression of CD5, CD10, nor BCL6. Studies also showed that they were negative for CD43 and TdT. The proliferation marker MIB1 was positive in <10% of lymphocytes, which was indicative of a low proliferation index. Cyclin D1 and in situ hybridization for EBER were negative, while PCR studies were positive for clonal rearrangement of IgH and Kappa light chain.\nAfter medical optimization, the patient was discharged home on dexamethasone and antiseizure prophylaxis, with instructions to continue care for her lymphoma with hematology/oncology as an outpatient. During follow-up, a whole-body fludeoxyglucose positron emission tomography (FDG PET) scan showed no evidence of FDG avidity nor pathologic lymphadenopathy outside of the CNS. The patient also underwent bone marrow aspirate and biopsy which effectively ruled out bone marrow involvement from her lymphoma. She then began treatment with whole brain radiation therapy (WBRT), completing a total dose of 2400 cGy over 12 fractions. Radiation therapy was well tolerated and was accompanied by several doses of memantine to mitigate possible neurocognitive effects. Following WBRT, the patient developed significant fatigue, ageusia, and episodic headaches without neurological deficits. Nevertheless, she subsequently began systemic treatment with single-agent rituximab, 375 mg/m2 once weekly, for a total duration of 4 weeks.\nSurveillance brain MRI demonstrated persistent enhancement of the central sulcus as well as FLAIR hyperintensity of the orbitofrontal region, despite unequivocal improvement. Findings suggested a low level of residual disease. White matter FLAIR hyperintensities that were new were thought to be radiation induced.\nA few months after completing treatment, the patient returned to the hospital with confusion, weakness, and malaise. She underwent initial evaluation with CT of the head which showed no acute intracranial abnormalities to explain her symptoms. An electroencephalogram showed absence of seizure-like activity. After an extensive workup, her symptoms were ultimately believed to be attributable to polypharmacy from her multitude of home medications.\nA repeat MRI of the brain performed 10 months after completion of systemic treatment remained unchanged as compared to prior MRI, and with no evidence of active intracranial disease.\nThe patient continues to be followed regularly in the outpatient setting with medical oncology and neurosurgery. She has shown no clinical evidence of disease recurrence to date, having completed therapy greater than 12 months ago. |
An-81- year old diabetic female presented with severe pain and swelling of left thigh in the emergency department in January, 2011. The previous night she woke up suddenly because of the severe pain in her left thigh. The pain was so severe that she couldn’t touch her thigh nor could she move it. She denied having any other symptoms. On examination, she was a febrile with pulse rate of 90 beats/min; respiratory rate of 16 breath/min and blood pressure was 160/100 mmHg. Systemic examination of chest, heart and abdomen was also normal. On local examination left thigh was swollen with difference of 12 cm between left and right, indurated and was excruciatingly tender to touch, maximum on anterolateral aspect without any erythema and cellulitis but was warmer than right thigh. Funds examination showed hypertensive along with background diabetic retinopathy changes. Peripheral pulses were symmetrical. There were no muscle fasciculations, muscle atrophy and tenderness of the spine. There was no evidence of neurovascular compromise. Neurological examination revealed absent ankle reflexes and absent vibration sensation at big toe and ankle bilaterally. Her urea was 86 mg % (10-35 mg%) and creatinine was 1.9 mg% (0.5-1.0 mg%) and rest of her routine blood tests were normal. Her random blood sugar was 320 mg% and blood ketones was negative. Twenty four hour urine revealed 800 mg of protein. D-dimer and antinuclear antigenwere negative. Creatine kinase was raised two time of the normal. Compressive Ultrasonography of left thigh was normal. MRI of pelvis and thighs showed high T2 signal and hypodense signal on T1 images of left thigh characteristic of fluid affecting subcutaneous and quadriceps with maximum involvement of vastes lateralis muscle of left thigh [Figures and ]. On i.v gadolinium there was uniform enhancement of the muscle with central non-enhanced area of necrotic muscle [ and ]. Fine needle aspiration was done which showed of muscle fibres in various stages of degeneration. Moreover, Sudden onset of excruciating pain and swelling without weakness in the thigh and with no signs of local and systemic inflammation, without any evidence of neurovascular compromise with small increase in creatine kinase, negative collagen network in a long standing diabetic woman having underlying micro vascular complications in the form of retinopathy, nephropathy and neuropathy is highly suggestive of diabetic muscle necrosis in our patient. The highly characteristic MRI findings further support the clinical diagnosis. The patient was treated conservatively with bed rest, analgesics and insulin. She starts showing improvement and was discharged after 24 days. |
The following is a description of the case of a 25-year-old woman with the initials S.K. in her second pregnancy who came to our antenatal consulting centre.\nThe first screening for blood count, blood group, biochemistry (ALAT, ASAT, creatine, urea, blood sugar) showed results within the reference range. Hbs Ag, HIV, Wasserman, IgG, IgM (toxoplasmosis), IgG, IgM (rubella), IgG, IgM (CMV) were negative.\nAt that time the woman was at 6 – 7 weeks gestation. Biochemical screening generally is done at 12 – 13 weeks gestation showed results within the reference range (low risk of development of a baby with an abnormality, low risk of developing preeclampsia in the second half of pregnancy and low risk of premature birth).\nThe patient came for a second comprehensive biochemical screening at 17 – 18 weeks gestation. The results showed the low genetic risk of congenital anomalies. Fetal morphology of the fetus was normal.\nS.K. came again for consultation at 22 weeks gestation in connection with the admittance of her first 3-year-old child to the hospital because of pneumonia. Serological tests of the child had shown elevated CMV titer - specific IgM.\nThen we made new serological tests of the patient and the results were as follows: CMV – specific IgG – 98; CMV – specific IgM – 2.1. It was then understood that the patient was most likely infected by CMV primarily in the first trimester of pregnancy. After consulting about the risk of transmission of CMV to the fetus the woman chose monthly ultrasound scans and refused amniocentesis.\nThe results of all ultrasound scans were normal until that time. At 24 weeks gestation fetal brain ultrasound scan showed thalamic calcifications bilaterally, hyperechogenic foci in the right side of the ventricular wall, asymmetric ventriculomegaly > 10 mm ().\nSimilar changes were imaged at 28 weeks gestation and also cerebellar developmental delay was noticed. Also, hepatomegaly was found at otherwise eutrpophically developing a fetus.\nAfter that patient, S.K. consented to do of amniocentesis as changes were already verified by ultrasound. Amniotic fluid analysis detected that the fetus was positive for CMV (CMV – specific IgM titer was 68), thrombocytopenia – 46 g/l. Levels of fetal liver enzymes were normal. Following consultation on the possible consequences of CMV infection of the fetus, the parents chose to continue with the pregnancy.\nIn the next ultrasound scanning to follow at 32 weeks gestation not only cerebellar developmental delay was noticed, but also of the head as a whole (microcephaly).\nAt 36 weeks gestation, in addition to the microcephaly already established, enlargement of the IV brain ventricle at the expense of underdevelopment of the cerebellum was noticed. Also, 2nd to 3rd stage of placenta maturity and low quantity of amniotic fluid was established ().\nThe patient was admitted to an obstetrics and gynaecology clinic for active monitoring. Cardiotocography was done on a daily basis. Upon the occurrence of two consecutive non-reactive NST and presence of late decelerations, a decision for delivery was taken. Because of the relatively immature fetus and low pelvic score a caesarian section delivery was done. A male fetus of weight 2,890 g and height 50 cm was delivered. The fetus was with skin petechiae and hepatosplenomegaly. Neurological examination showed no abnormalities. Thrombocytopenia was confirmed (Hg 66 g/l). The newborn baby was treated with Acyclovir i.v. – 5 mg / g / 12 h for 6 weeks ().\nPresently, the baby is six-month-old, of normal neurological status and preserved hearing. |
An otherwise healthy 18-month-old Caucasian female presented to the ophthalmology clinic at Boston Children's Hospital for the evaluation of esotropia of the left eye that was first noticed 8 months before presentation. She had a history of nasolacrimal duct obstruction that was treated conservatively and resolved spontaneously. There is no family history of strabismus or amblyopia. On her first ophthalmic examination, we were unable to measure the visual acuity using preferential looking test (PLT) due to poor cooperation; however, she had a clear fixation preference to the right eye. She had full ocular motility in both eyes and no nystagmus. In primary gaze, she had a left esotropia of 30 prism Diopters (PD) using Krimsky test; we were unable to measure her alignment in different directions of gaze or evaluate her stereopsis due to her level of cooperation on that first examination. Cycloplegic refraction was +1.25 in the right eye and +2.50 in the left eye. The remaining examinations including pupils and anterior and posterior segments were unremarkable. Patching of the right eye was prescribed for 2 h daily to treat the strabismic/anisometropic amblyopia of the left eye, along with full cycloplegic spectacle correction to correct any accommodative component of the esotropia. On further follow-up, she was noted to have decreased vision in the left eye seeing 20/130 compared to 20/63 in the right eye using PLT. She continued to have a left esotropia of 30 PD with correction and 40 PD without correction. The family was counseled about the likely need for strabismus surgery to treat this partially accommodative esotropia. She was later booked for a left medial rectus recession and a left lateral rectus resection to correct 30 PD of esotropia. During surgery, after isolating the medial rectus on a muscle hook, the muscle tendon width was noted to be shorter than expected and inferiorly displaced. Anterior pole test was performed and was negative confirming that the muscle was not transected, the muscle was secured on a 6-0 polyglactin 910 suture, and before detaching the muscle from the globe, further exploration was made which revealed another piece of muscle with similar short tendon width and more superiorly displaced medial rectus insertion. The position of the vertical rectus muscles was confirmed by hooking the two muscles to insure that the two medially inserted muscles are not the superior or inferior rectus muscle. It was concluded that these were two separate compartments of the medial rectus muscle, each tendon measured 5 mm in width, and the two heads were separated by 5 mm []. The two muscle compartments were separated at least all the way back to the sleeve where the muscle penetrates Tenon's capsule; further exploration beyond Tenon's was not performed to avoid complications and fat adhesion. Each insertion of the two heads of the medial rectus was imprecated with a 6-0 double-armed polyglactin suture as if it is a separate muscle the muscles were detached from the sclera. A decision was made to join the two compartments together as one muscle to allow for better control during adjustment and decrease the chance of inducing any vertical deviation. The inferior suture of the superior compartment of the medial rectus was tied to the superior suture of the inferior compartment [], it was noted that the muscle belly was significantly separated, and so, an augmentation suture was placed 4 mm from the distal ends of the two compartments []. The superior border of the now joint muscle compartments was attached to the sclera halfway along the original superior compartment insertion and the same for the lower suture, yielding a width of about 10 mm for the two joint compartments. Hang back technique was used and the muscle was recessed 4.5 mm; an adjustable suture using the short tag noose technique[] was used given the unpredictability of the response to the surgery in this scenario. The lateral rectus muscle of the same eye was then resected 6 mm, which was uneventful.\nAbout 1 h after the surgery, orthoptic examination showed orthotropia at distance and near using Krimsky test, no adjustment was needed, and the patient was discharged home. She maintained good alignment, and at the 1-month postoperative follow-up, her vision was 20/30 in the right eye and 20/40 in the left, she had 400 s arc of stereopsis, alternate prism cover test showed orthotropia at distance and near with correction and esotropia of 10 PD at near without correction. She continued to maintain good alignment over time (the latest follow-up was 10 months after surgery). |
An 11-year-old Sri Lankan girl presented with a 2-day history of fever, headache, vomiting, and altered level of consciousness. She had been experiencing polyuria and polydipsia during the past 2 weeks. There was no history of chronic headaches, visual disturbances, respiratory symptoms, or abdominal symptoms. She was not known to be diabetic. An examination revealed an unwell-looking febrile girl. Her height was 140 cm (25th centile) and her weight was 25 kg (3rd centile). There was no evidence of neck stiffness or positive Kernig’s sign. Following admission she developed generalized tonic–clonic seizures which required intubation and ventilation. Random blood glucose and electrolyte panel including sodium, potassium, calcium, and magnesium were normal. She was empirically started on antibiotics administered intravenously for possible meningitis. Magnetic resonance imaging revealed gross hydrocephalus with suprasellar mass most likely due to craniopharyngioma (Figs. , , and ). A ventriculoperitoneal shunt was inserted and she was started on 3 % hypertonic saline to reduce intracranial pressure. Her basal serum sodium levels were 140 mmol/l and she was commenced on a dose of 5 ml/kg 8 hourly, aiming to increase her sodium levels to 160 to 170 mmol/l. Her serum electrolytes were monitored 8 hourly. Her sodium levels rose to 163 mmol/l after the first 24 hours. It was decided to repeat another dose of 3 % hypertonic saline. However, during the latter part of the day she became polyuric and dehydrated. Her blood pressure was 80/60 and pulse rate was 130 beats per minute. She was hydrated with boluses of normal saline and commenced on hydrocortisone replacement administered intravenously. As her blood pressure failed to stabilize she was started on inotropic support with noradrenaline and dobutamine infusions. Her serum sodium levels were 226 mmol/l and further doses of 3 % hypertonic saline were stopped immediately. Other biochemical investigations were as follows: serum potassium 3.8 mmol/l (3.5 to 5.0 mmol/l), blood urea 8.1 mmol/l (2.5 to 8.0 mmol/l), serum creatinine 76 μmol/l (70 to 120 μmol/l), random blood glucose 8.5 mmol/l, serum ionized calcium 1.12 mmol/l (1.05 to 1.3 mmol/l), and serum magnesium 0.8 mmol/l (0.75 to 0.95 mmol/l). Her measured serum osmolality was 470 mOsm/kg with a urine osmolality of 280 mOsm/kg. There was no discrepancy between measured and calculated serum osmolalities. Her urine spot sodium was elevated at 116 mmol/l. A urine spot sodium of >100 mmol/l can be seen in hypernatremia following ingestion of salt or infusion of 3 % hypertonic saline. Considering the clinical and biochemical factors, hypernatremia in our patient can be attributed to infusion of 3 % hypertonic saline in the background of cranial diabetes insipidus.\nAs we considered a sodium level of 226 mmol/l not compatible with life it was decided to correct her sodium levels rapidly. She was treated with an immediate dose of desmopressin 400 micrograms administered orally and hydrated with 5 % dextrose administered intravenously and clear water via nasogastric feeding at a rate of 190 ml/hour to replace the fluid deficit of 7 liters over 36 hours. Her polyuria settled and her serum sodium levels dropped to 160 mmol/l on the following day. However, her cardiac status became unstable and a 12-lead ECG showed diffuse prolongation of QT intervals, ST depressions in leads V1 to V2, ST elevation in V3, and VT in V4 to V5 (Fig. ). An urgent echocardiogram was planned but she developed VT and went into cardiac arrest. In spite of defibrillation and subsequent resuscitation she died. |
The patient is a 67-year-old woman who presented with a near-obstructing adenocarcinoma of the right colon. She underwent an uneventful laparoscopic-assisted extended right hemicolectomy and was discharged in stable condition on post-operative day 5. She presented to our emergency department (ED) on post-operative day 10 complaining of diffuse abdominal pain, hematemesis and subjective fevers. Computerized tomography (CT) of the abdomen demonstrated a significant amount of free intraperitoneal fluid and associated pneumoperitoneum; she was started on broad spectrum antibiotics and taken to the operating room for an exploratory laparotomy. Upon entry into the abdomen, she was found to have a significant volume of succus and a small anastomotic leak. The anastomosis was resected and an end ileostomy was created. The patient's vital signs were stable and remarkable only for a low grade tachycardia throughout the procedure. She was extubated immediately after the operation. However, due to the patient's persistent obtundation following extubation, she was brought to the intensive care unit (ICU). While her oxygen saturation remained above 95% on supplemental oxygen with both oropharyngeal and nasopharyngeal airways in place, she failed to regain consciousness. When she was noted to be apneic, her respiration was supported with bag valve mask ventilation. The patient was given naloxone, glycopyrrolate and neostigmine to counteract the opioid and paralytic agents received during her procedure without any clinical improvement in her neurologic status. While bedside blood glucose testing was within normal limits, an arterial blood gas demonstrated a profound respiratory acidosis with a pH of 7.03, a PCO2 of 107 and a PaO2 of 375. She was re-intubated for hypercapnic respiratory failure and all sedating medications were held.\nShe continued to have no evidence of neurologic improvement, prompting cerebral imaging. CT of the head revealed acute cerebellar herniation with diffuse cerebral edema (Fig. ). Neurosurgery was emergently consulted and placed a decompressive external ventricular drain. Maximal medical therapy was initiated to further reduce the patient's intracranial hypertension. This included hypertonic saline, head of bed elevation to 30 degrees, maintenance of normotension and normoglycemia. She was also started on levetiracetam as seizure prophylaxis. A magnetic resonance imaging (MRI) was performed with findings consistent with the diagnosis of PRES (Fig. ).\nWith the initiation of treatment described above, the patient slowly began to recover neurologic function. By post-operative day 33, the patient was discharged to a rehabilitation facility. Five months later, she underwent a successful ileostomy reversal and was back to her pre-operative quality of life. She experienced complete resolution of her neurological symptoms and normalization of her neuroimaging (Fig. ). |
A 3-year-old boy came to our department with facial asymmetry. The history revealed that the child developed a swelling of 1.5 cm × 1 cm, oval in shape on left temporomandibular joint (TMJ) region noticed by mother just after few months after birth. The swelling gradually increased to the present size [], which made the mother curious to report to our department.\nThe swelling was non-tender, asymptomatic and firm in consistency. The swelling was slightly mobile, but mouth opening was normal.\nA computed tomographic scan was advised, which showed a large soft lobulated tissue mass over the left side of the TMJ, anterior to the coronoid process without a clear fat plane to the surrounding tissues [Figures and ]. Blood test results were within normal limits. Audiometry was carried out to assess the functioning of the ear.\nThe patient underwent wide excision of the mass under general anesthesia. Under standard skin preparation, local anesthesia with adrenaline infiltrated, preauricular incision [] was placed and the lesion was excised completely. Care was taken that the extent of incision does not cross the tragal notch, keeping the facial nerve in mind. Under hypotensive anesthesia, soft-tissue dissection was done to reach the tumor mass. Tumor mass appeared to be firm soft-tissue mass with a glistering shiny surface. Soft-tissue dissection was carried out around the tumor mass to reach the origin of tumor mass. It appeared to be attached to the anterior surface of TMJ, apparently to the periosteum. Tumor was excised in total [], rough bony surface was smoothened with a bone file. Betadine wash was given and the wound was closed in layers using 4-0 vicryl (polyglactin). Skin was sutured with 5-0 monofilament polyamide. Pressure dressing was placed. I.V antibiotics where continued for next 48 h. Patient was discharged after 48 h. Patient was given paracetamol orally. Pain was negligible post-operatively. Sutures were removed after 7 days [].\nIt looked like an encapsulated mass as we cut the mass in two halves. It was then sent for histopathological investigation.\nHistopathological examination revealed fibromatosis characterized by proliferating fibroblasts and was very aggressive in nature, but non-encapsulated.\nThe child's recovery was uneventful and there were no neurological deficits. Follow-up at 1 year showed no recurrence and the patient remains under careful follow-up. The mandible of the child was growing fine. |
A 41-year-old woman presented complaining of the sudden visual loss of the right eye while she was receiving the cosmetic forehead filler injection at a beauty salon 7 hours prior. She had no history of prior ocular or systemic disease, and no allergies to medications or known substances. During the procedure, the sudden visual loss was accompanied with severe ocular pain. According to the injector, hyaluronic acid (HA) filler mixed with lidocaine and epinephrine for local anesthesia was used; 2 cm3 of HA was injected into the right frontal area with a 23 gauge blunt cannula. During the process of external compression for hemostasis and shaping, the patient abruptly felt sharp pain in her right eye, followed by loss of vision.\nOn physical examination, the patient was alert, oriented, and coherent. On the right forehead, there were several areas of dark, the largest measuring about 8 by 5 cm. There were also several injection sites visible. The nasal dorsum skin showed black and purple discoloration with slight edema (Figure ). Visual acuity was no light perception OD and 20/20 OS. External ocular evaluation showed the right upper eyelid edema and ptosis. A dense right afferent pupillary defect was present. Examination of right fundus revealed a pink fundus with optic nerve edema (Figure ). A fluorescein angiogram showed normal retinal artery perfusion but several filling defects in the choroidal circulation (Figure A). Late hyperfluorescence in the choroid was observed. (T = 11 minutes after fluorescein injection) (Figure B). Visual evoked potential was prolonged by P100 (Figure A). Optical coherence tomography revealed thickening of the optic disc (Figure B).\nThe patient was diagnosed with right posterior ciliary artery occlusion. Packaging material confirmed that the material used was hyaluronic acid. Considering the patient was still in acute period and hyaluronidase was injected into the forehead, glabella, nose, and retrobulbar region (total 1500 U). The patient also received 2 hours of daily hyperbaric oxygen therapy, oral aspirin, oral acetazolamide, and intravenous of dexamethasone were also administered.\nAt 2-week follow-up of the patient's forehead and nasal skin improved significantly (Figure ) with improved visual acuity of the right eye to hand movements. Fundus examination revealed decreased edema of the optic disc. After a month of further recovery, the vision was unchanged. |
A 26-year-old young woman was admitted to the West China Hospital, Sichuan University, China, complaining of spontaneous nipple discharge in her left breast for one month. Her past history showed that she had accepted a lumpectomy on her left breast because of a palpable breast mass. The postoperative pathological report showed a complex fibroadenoma, with stromal cells proliferation, local lobulated structures were observed. She denied any family history of breast cancer or ovarian cancer.\nOn physical examination, a firm mass with a clear margin was palpated in lower inner quadrant near the nipple of the left breast, which measured approximately 2.5 cm in diameter. Single duct non-bloody discharge from the left nipple was evident after squeeze. There was no nipple retraction and skin dimpling evident.\nAn ultrasonography detected mammary duct ectasia and a solid-cystic mass measured 28 × 20 × 20 mm near nipple-areola complex (NAC) of the left breast (Fig. ). Left breast galactography showed mammary duct actasia and multiple irregular filling defects in the dilated duct (Fig. ).\nThe mass and the related mammary duct were excised through a circumareolar incision. Two intraductal neoplastic lesions measured 20 × 20 × 20 mm and 28 × 20 × 20 mm respectively were found in the dilated duct system. The cytology of the nipple discharge showed no tumor cells. The histological examination showed a biphasic tumor, with mesenchymal and epithelial components (Fig. A). The mesenchymal cells highlighted moderate stromal hypercellularity (Fig. B), marked nuclear atypia and occasional mitoses (Fig. C). Ki67 immunohistochemistry to assess the index of proliferation showed 20% to 30% positive (Fig. D). The histologic diagnosis was a borderline PT. The margin of resected tissue showed to be free of tumors.\nAfter operation, the patient is undergoing surveillance through ultrasonography and physical examination every 3 months. Till now, she has been followed up for 12 months, and no local or distant recurrence was observed. |
A 44-year-old female presented initially to an outside hospital with difficulty in speaking, right-sided facial droop and difficulty in walking. She also endorsed a 1-week history of intermittent headache. Magnetic resonance imaging (MRI) of brain demonstrated a ring-enhancing pontine lesion with surrounding vasogenic edema consistent with a brainstem abscess measuring 3.6 × 2.4 × 3.7 cm (). There were no areas of ischemia. Pertinent history revealed no dental, cardiac or pulmonary source of infection. She had no history of intravenous drug use.\nOn neurologic exam, she exhibited dysarthric speech with intact cognition and appropriate mental status. Pupils were 4 mm and were equal, round and reactive to light. She had nystagmus on right gaze and had a left gaze palsy. Face sensation was diminished to light touch on the right and she exhibited right facial weakness as well. Hearing was intact and palate elevated to the midline. Tongue had normal motion. She exhibited significantly increased tone with contracture in the right upper extremity. Strength was 4/5 in the right lower extremity, but sensation to light touch was intact throughout her extremities and trunk. Deep tendon reflexes were 3+ on bilateral upper extremities and 2+ on bilateral lower extremities.\nC-reactive protein (CRP) was 1.4 mg/dl and erythrocyte sedimentation rate (ESR) was 28 mm/h. Cerebrospinal fluid (CSF) studies were relatively benign. Cryptococcal antigen was negative and spinal fluid exhibited no xanthochromia. She was started on vancomycin, ceftriaxone and metronidazole for probable central nervous system abscess and was transferred to our facility for neurosurgical intervention.\nThree days after initial presentation, she underwent sub-occipital craniotomy for microsurgical abscess drainage. Initial consideration was given to a stereotactic procedure; however, an open approach was ultimately chosen due to surgeon preference. Intraoperative neuro navigation was used with subsequent creation of a posterior fossa craniotomy. This approach was chosen over a retrosigmoid approach, given the midline nature of the lesion. The dura was opened over the right cerebral hemisphere and tonsil at which time pus was expressed and was cultured immediately at the operative site. We were unable to dissect the roof of the fourth ventricle secondary to a large volume of pus and instead retracted the bilateral tonsils and resected a small amount of the inferior vermis. Facial colliculus was localized and an incision was made in the midline medial raphae. Incision into the brainstem did not express any purulence, so the wound was copiously irrigated and subsequently closed without advancing further into the brainstem. Cultures from the abscess grew step intermedius and antibiotics were narrowed accordingly. Over the next several weeks, the patient remained afebrile with no leukocytosis, but there was concern for persistent infection due to lack of clinical improvement. Repeat MRI demonstrated enlargement of the residual abscess (), and she was taken back to the operating room for repeat abscess drainage via the same sub-occipital craniotomy incision. During this procedure, the roof of the fourth ventricle was visualized and dissected through before localization of the vagal trigone. Midline raphae was once again opened and intraoperative MRI navigation confirmed the locations of the abscess. Microscopic dissection was performed in the midline between facial colliculi, and spinal needle was passed into the opening with subsequent aspiration of 9-ml purulent fluid, re-aspiration attempt and closure. Repeat gram stain and culture failed to reveal any organisms.\nShe presented to clinic for follow-up evaluation 11 weeks after discharge. Overall, she is doing very well and ambulating independently with a cane. On physical exam, CNII-XII are intact. She has no bulbar deficits. She has 4/5 strength in all major muscle groups on the right side. Repeat MRI has shown near resolution of the abscess (). |
A 55-year-old man presented a lush conjunctival hyperaemia and chemosis of the inferior bulbar conjunctiva in the left eye accompanied with dry eye symptoms, on March 2011. This lesion has been described for the first time three months earlier, and it had been the reason for five emergency hospital visits. In this period the patient has been treated with different drops and ointments, including topical steroids, anti-inflammatory, antibiotics, and eye lubricants, but none has proven any efficacy.\nOn March 2011, examination of the left eye disclosed an unilateral swollen and hyperemic inferior bulbar conjunctiva extending to both canthi; this was a light-pink-coloured lesion, painless, compressible and with an underlying transparent content (Figures and ); the inferior border of the mass was not identified.\nIn the patient's medical history is important to highlight a kidney transplant in 1999 by the Alport syndrome that is currently being treated with corticosteroids, cyclosporine, and azathioprine.\nOn ophthalmic examination, the best corrected visual acuity was 20/25 in both eyes. The biomicroscopy of the left eye revealed a punctate keratitis and the fundoscopy was normal. Intraocular pressure was 15 mmHg and pupils' reflexes were normal. The patient had no proptosis and no limitation on the eye movements. No signs of eye alterations associated with Alport's disease were found. No other systemic symptoms were pointed out by the patient.\nA computed tomography scan of the orbits and brain described a right and left maxillary and sphenoid sinuses, suggestive of sinus inflammation, with no involvement of the orbit (Figures and ).\nOn May 2011, an incisional biopsy was performed under local anaesthesia which proved to be diagnostic and therapeutic. Histology showed a lymphatic proliferation and ectasia with a network of empty bloodless channels lined by flattened endothelium with the presence of some blood vessels and inflammatory infiltrate (haematoxylin and eosin stain, ×100; ), which is consistent with the diagnosis of conjunctival lymphangioma.\nThe excision of the lesion led to the resolution of the case (Figures and ). Meanwhile the upper respiratory tract infection, which is likely to have exacerbated the size of the lymphangioma was resolved.\nTen months later the patient remains asymptomatic with no signs of recurrence of the lesion. |
A 24-year-old male visited our outpatient clinic for follow-up after totally corrected tetralogy of Fallot at the age of 1 year. At the age of 16 he had severe pulmonary regurgitation with volume overload of the right ventricle and ventricular arrhythmia, for which he underwent pulmonary valve replacement (PVR) with a homograft. He had remained under annual surveillance at the Department of Paediatric Cardiology until the age of 18, but upon transfer to the Department of Cardiology he withdrew from surveillance for several years. When he came back at the age of 24, he was asymptomatic and had a good exercise capacity. On auscultation he had a loud left parasternal systolic murmur at the second intercostal space. His saturation was 98 %. No other abnormalities were noticed. The electrocardiogram showed sinus rhythm with right axis deviation and a right bundle branch block.\nTransthoracic echocardiography showed a dilated and hypertrophied right ventricle with a moderately decreased systolic function and a moderate pulmonary valve stenosis (peak gradient 42 mmHg) with a mild pulmonary regurgitation. The pulmonary arterial pressure (PAP) could not be estimated. He underwent MRI to quantify the extent of right ventricular (RV) dilatation and dysfunction. The right ventricle was moderately dilated (RV end-diastolic volume 304 ml versus left ventricular end-diastolic volume 198 ml) and systolic function was mildly impaired (ejection fraction 45 %). Flow through the pulmonary artery was larger than through the aorta, and there was a consistently larger stroke volume of the right compared with the left ventricle, which could not be explained by valvular regurgitation. Magnetic resonance angiography revealed a partial aberrant pulmonary venous connection (PAPVC) of the right upper lobe to the superior caval vein (Fig. ). Subsequently, a cardiac CT was performed, which revealed an UCS type II (Fig. ). In addition, a pseudo-aneurysm was seen at the distal anastomosis of the homograft. |
A 47-year-old male, presenting a 32-year history of intermittent locking and loss of range of motion of the left elbow, with no recollection of associated trauma, was brought to our attention due to the considerable size of the elbow (Figure A), which had begun interfering with his job as a taxi driver and daily life. Clinical examination revealed a significant increase in size of the left elbow compared to the contralateral. The elbow lacked 40° of full extension and 85° of flexion and crepitation was noted when the elbow was brought from flexion to extension. Pronation and supination were substantially complete. Palpation of the elbow highlighted the presence of floaters in both the superficial and deep planes of the left elbow joint. No neurologic or vascular compression symptoms were observed. Routine laboratory data were normal. Other joints were normal.\nThe simple radiographs of the left elbow showed multiple rounded, calcified bodies widespread throughout the elbow joint (Figure A,B). Magnetic Resonance (MR) images showed the distribution of the calcified bodies spread throughout the elbow joint (Figure A,B,C). Diagnosis of synovial osteochondromatosis was made.\nOpen synovectomy was performed (by author A.S.) through anterior and posterior surgical access to the elbow. At surgery multiple calcific bodies were found adherent to the thickened synovium and within the joint space (Figures , and ). We removed and counted a total of 312 loose bodies, varying in size from a few millimeters to 3 cm (Figure ). Histopathology confirmed the diagnosis.\nPostoperatively, the elbow was supported in a sling for two weeks and then was mobilized progressively. The clinical and radiological evaluation at 6 months postoperatively showed marked reduction in the volume of the elbow, improvement of extension to 15° and flexion to 95°, no change in the preoperative prono-supination of the elbow, and no peripheral neurological deficits (Figures , and ).\nThe patient was assessed using the Mayo elbow performance score [] before surgery and at 6 months postoperative, with an increase from 50 to 80 points. |
A 72 year-old Indo-Caribbean man with three-vessel coronary artery disease underwent elective coronary artery bypass surgery on the beating heart with left internal mammary to the left anterior descending coronary artery and a saphenous vein graft to the posterior descending coronary artery.\nSurgery was uneventful and the patient returned to the intensive care unit in stable condition. Two hours later, however, due to sudden bleeding and cardiac arrest, he required resuscitation and re-exploration. In order to control massive bleeding from a tear of the aorta at the proximal venous anastomosis and the persistent depressed cardiac function, it became necessary to establish cardiopulmonary bypass. The hemoglobin (Hb) before re-exploration was 4.5 mg/dl. The tear in the aorta was repaired, and the venous graft re-implanted higher in the Ascending Aorta. Transfusion of 6 Units of packed red cells (PRC) and 3 Units of fresh frozen plasma (FFP) was required to achieve Hb of 8.8 mg/dl at the end of surgery. Weaning from cardiopulmonary bypass was achieved with no inotropic support; however, it was difficult to ventilate the patient. The lungs were very stiff and distended. Despite of high positive pressure and % FiO2 the blood saturation remained very low. This was soon followed by copious pulmonary secretion requiring bronchial suction (around 100 ml of fluid collected each time), every 5 to 10 minutes. The fluid was clear, yellowish, and not frothy. The total amount of collected bronchial fluid before transfer to ICU was over 1700 ml. An IABP was inserted, but any attempt to close the chest resulted in significant decrease in the systemic arterial pressure. The patient was therefore return to the intensive care unit with the chest open.\nRepeated bronchial suctions were required for about five hours before improvement in oxygen saturation. Bronchial secretion reduced and then suddenly stopped two hours after transfer to the ICU. Oxygenation improved and it was possible to close the chest the following day. Respiratory distress remained and the patient was extubated on day 5 postoperatively. He made a slow but uneventful recovery and was discharge home on day 20. |
An 89-year-old female with no relevant past medical history was referred to our centre on 9th January 2020 with reduced vision in her right eye and associated significant pain for 3 days. The best-corrected visual acuity (BCVA) was noted to be 0.36 logMAR in the right eye and 0.24 logMAR in the left eye. Slit-lamp biomicroscopic examination revealed right-sided periorbital erythema, conjunctival injection, a deep and quiet anterior chamber, and a clear cornea. She was also noted to have a vesicular lesion overlying her right eyebrow. Intraocular pressure was noted to be within normal limits in both eyes, and the right eye posterior segment examination was also normal. The left eye anterior and posterior segment examination was normal. In view of these examination findings, a working diagnosis of herpes zoster ophthalmicus was made, and the patient was prescribed high-dose acyclovir tablets (800 mg five times per day) and topical ganciclovir 0.15% gel three times per day.\nBy 4th March 2020, the BCVA in the affected eye had further deteriorated to 0.74 logMAR and anterior segment examination revealed persisting conjunctival injection and superficial punctate keratopathy, with the development of an inferior corneal epithelial defect measuring approximately 2 mm x 3 mm, confirmed with fluorescein staining. The patient was prescribed topical levofloxacin hourly. On clinic review two weeks later, the inferior epithelial defect had slightly increased in size, and 2+ inflammatory cells were observed in the anterior chamber. Due to this size progression, her treatment was switched from topical levofloxacin to chloramphenicol ointment three times daily, to provide further anti-microbial coverage. In view of the anterior chamber reaction, we also recommenced topical prednisolone sodium phosphate 0.5% three times daily, with the addition of a topical lubricating gel to be used up to 6 times daily.\nBy 28th April 2020, the anterior chamber reaction had largely resolved. However, the inferior corneal epithelial defect remained unchanged, prompting cessation of steroid medication, the commencement of preservative-free eye drop formulations, and continuing the generous use of topical lubricating agents, to promote healing. A bandage contact lens and a protective plastic shield were also utilised to encourage healing of the persistent inferior epithelial defect. However, despite these attempts, there was negligible healing of the epithelial defect. On the next clinic review, the epithelial defect now measured approximately 3 mm x 0.7 mm, and inferior stromal keratolysis with thinning was noted. Corneal sensation was also dramatically reduced in this eye.\nOn August 3rd, the BCVA had deteriorated to hand movements. On examination, a superior white dense corneal abscess was visualised. At this point, we sent a corneal scraping to the microbiology department for culture and arranged for urgent hospital admission. Corneal scrapings were inoculated on chocolate agar, Sabouraud dextrose agar, blood agar, starch ampicillin agar, and starch ampicillin agar with neomycin. Hourly topical ciprofloxacin 5% and hourly topical gentamicin 1.5% were prescribed. The patient was reviewed daily to closely monitor changes and to ensure treatment compliance. On successive review, the previously visualised epithelial defect had increased in size significantly, now encompassing almost the entire anterior surface of the cornea. In addition, a localised area of corneal perforation, which appeared to be self-sealed with prolapsed iris, was now visualised on the superior cornea for the first time. The anterior chamber was flat and a 2 mm hypopyon was visible.\nOn 8th August 2020, the microbiologist confirmed our corneal scraping had identified the rare bacterium Corynebacterium bovis using matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOF MS). Initial sensitivities to ciprofloxacin, vancomycin, clindamycin, rifampicin and resistance to penicillin were determined using European Committee on Antimicrobial Sensitivity Testing (EUCAST) clinical breakpoints []. The corneal scraping also isolated the organisms Staphylococcus epidermidis and Candida parapsilosis by way of direct culture. Due to the rarity of Corynebacterium bovis, and previous literature reporting pathogenicity predominantly in cattle, we proceeded to enquire about any recent animal contact. Our patient confirmed that she was recently feeding cattle near her residence. On the advice of our microbiology colleagues, we discontinued gentamicin 1.5% eye drops and added vancomycin 5% eye drops hourly with oral ciprofloxacin 750 mg twice daily. On this treatment regimen, the clinical presentation improved significantly, with a reduction in the size of the stromal infiltrate and improved visualisation of the underlying anterior chamber structures noted. Despite this, however, the previously visualised epithelial defect and stromal thinning had again progressed in size.\nBy 15th September 2020, the BCVA had deteriorated to perception of light. Due to the persisting localised perforation and very large central epithelial defect (Figure ), we decided to perform Gundersen conjunctival flap surgery with further intraoperative corneal scraping. Iridectomy of the prolapsed iris was performed and cyanoacrylate glue was subsequently utilised to seal the corneal perforation. We then proceeded to enclose the cornea with a conjunctival flap (Figure ). Postoperatively, the patient reported a substantial reduction in pain. Intraoperative corneal scraping did not isolate any organisms and in view of this, we decided to taper the antibiotic medications, commence topical nepafenac four times daily and continue the lubricating agents. During subsequent one-year follow-up of our patient, BCVA was noted to be perception of light; however, the patient reports no pain in this eye, and remains comfortable with the use of topical lubricating agents as and when required. |
A male patient aged 49 years reported to the Department of Periodontics, Sri Siddhartha Dental College and Hospital, Tumkur, with the chief complaint of deposits present on his teeth and he desired to get his teeth cleaned. Patient's medical history was not contributory. Patient had undergone extraction of upper right canine 2 years back, with uneventful healing.\nOn intraoral examination, stains and calculus were present along with generalized gingival inflammation and bleeding on probing []. Generalized periodontal pockets and attrition were present. Grade I mobility was present w.r.t. 12, 17, 25, 26, 35, and 36. Periodontal pocket measuring 7 mm was found w.r.t. 35 and 36, and no carious lesion was seen. The patient was advised orthopantomogram (OPG) which revealed presence of generalized bone loss along with a unilocular radiolucent area resembling a “tear drop shape” with a clear sclerotic lining, along with angular bone loss involving the mandibular left premolar and the mesial root of mandibular first molar [].\nThe vitality of the pulp was checked w.r.t. 35 and 36; it showed positive response as that of the contralateral side, and hence, endodontic involvement was ruled out. The patient was explained regarding the presence of lesion and a surgical excision of lesion was planned. The patient showed no symptoms, no history of swelling, discomfort, or pain, and was unaware of the presence of the lesion. Hematological investigation was done prior to surgery and was found to be normal. A comprehensive explanation was given to the patient regarding the intended surgical procedure to be done and an informed consent was taken before starting the procedure.\nFor surgical enucleation of the lesion, crevicular incision was given extending from canine till the first molar region [], with two vertical releasing incisions given, one on the mesial aspect of 33 and the other on the distal aspect of 36. A subperiosteal flap was raised [] and a surgical window was prepared [] between 35 and 36 using a straight fissure surgical bur under copious irrigation and the lesion was enucleated in the Department of Oral and Maxillofacial Surgery []. The biopsy specimen was sent to the Department of Oral Pathology for histopathologic investigation. Ten millilitres of blood was drawn from the median cubital vein using a 5-ml syringe with 25-gauge needle [] and it was centrifuged at 3000 rpm for 12 min for procuring platelet-rich fibrin [Figures –]. Platelet-rich fibrin obtained was mixed with osseo-graft (DMBM) [] which is a sterile bioresorbable demineralized bone matrix for bone void filling. The cavity was filled with the mixture of platelet-rich fibrin and DMBM, marketed by [Advanced Biotech Products (P) Ltd, Chennai, India]. The defect was closed using 3-O silk suture []. The patient was prescribed amoxicillin 500 mg, 3 times daily, for 5 days. The patient was advised to use chlorhexidine 0.12% (Periogard) as postoperative oral rinse for 30 days. Postoperative instructions were given to the patient to neither brush nor floss the surgical area for the first 4 weeks and to continue with the chlorhexidine (0.12%) oral rinse for 4 weeks. The patient was recalled after 7 days for suture removal at the surgical site and postoperative evaluation was done. The patient was recalled after 15 days and 3rd and 5th months for checkup and revaluation. After the 5th month, the surgical site showed good healing and an increase in bone height was seen [].\nHistological examination of the lesion was carried out as follows: The specimen was fixed in phosphate-buffered neutral formalin for 1 day. Later, 5-micron paraffin sections were obtained and stained with hematoxylin and eosin stain. Sections showed connective tissue stroma made up of bundles of thick, mature collagen fibers, resembling fibroma with plump fibroblast uniformly distributed. Also seen were many islands of odontogenic epithelium which appeared to be inactive []. The features were suggestive of COF (simple type). |
A 58-year-old Hispanic Caucasian man with diabetes mellitus presented to the Emergency Center with a 1-year history of progressive bilateral upper extremity weakness and episodes of orthostatic lightheadedness. He initially noticed weakness in his right-hand grip that gradually progressed over the next 6 to 8 months to involve the left hand and eventually both arms, to the extent that he was unable to hold objects or elevate his arms. He also complained of a tingling and burning sensation in both hands. His family had noticed mild bilateral facial weakness, described as reduced facial expression, without dysphagia or dysarthria. He did not complain of any lower extremity weakness or sensory symptoms. There was no bowel or bladder dysfunction, and he denied any erectile dysfunction. Prior to evaluation, he had been experiencing orthostatic intolerance that worsened to the point that he became non-ambulatory. His family had also noticed cognitive decline over the last year, with frequent forgetfulness and slow thought processing. On systems review, he reported mild xerostomia and xerophthalmia without dysphagia.\nA general physical examination, including cardiovascular, respiratory and abdominal systems, was normal. On initial neurological examination, he was awake, alert and oriented to person, place, time and situation. He had a Montreal Cognitive Assessment (MoCA) score of 16 out of 30, with deficits primarily in the visuospatial, executive and delayed recall domains. On cranial nerve examination, he had preserved pupillary responses, visual fields were full on confrontational testing, and he had normal fundoscopy bilaterally. His extraocular movements were preserved. He had bilateral facial weakness (facial diplegia) and decreased subjective sensation to light touch and pinprick in the left trigeminal nerve distribution. He did not have any hearing impairment and his uvula and palate elevated symmetrically. He did not have any weakness in his sternocleidomastoid, trapezius or tongue muscles. On motor testing, there was decreased tone in his upper extremities, with bilateral shoulder girdle and intrinsic hand muscle atrophy. On confrontational strength testing (based on the six-point Medical Research Council scale), he had normal neck flexion and extension strength. He had near symmetric proximal and distal weakness in the upper extremities, with strength of two to three out of five in all muscle groups tested, slightly worse on his right (Table ). His strength was normal in his lower extremities.\nOn multimodal sensory examination, he had subjectively decreased sensation to light touch and pinprick in his left radial nerve, left median nerve and right axillary nerve distributions. A sensory examination of his lower extremities was normal. His triceps and patellar reflexes were diminished bilaterally, with preservation of his other myotactic stretch reflexes. His plantar responses were flexor bilaterally, and he did not demonstrate any frontal cortical release signs. Automated blood pressure and heart rate measurements performed at the bedside with postural change demonstrated severe orthostatic hypotension with sympathetic α- and β-adrenergic compromise as follows: supine blood pressure, 142/90mmHg (mean arterial pressure, MAP, 107mmHg) with heart rate 68 beats/minute; sitting blood pressure, 97/64mmHg (MAP 75mmHg) and heart rate 77 beats/minute; standing blood pressure, 65/40mmHg (MAP 48mmHg) and heart rate: 81 beats/minute.\nHis elevated serum hemoglobin A1C of 7.9% (normal 4.3 to 6.1%) was consistent with suboptimal diabetes control. He had a normal thyroid function screen and serum vitamin B12 levels. The results of tests for serum rapid plasma reagin, human immunodeficiency virus antibodies and a hepatitis panel were all negative. A screen for systemic vasculitides revealed an elevated anti-SSA antibody titer of 28.4EU/mL (reference range: neg <16EU/mL, equivocal 16 to 20EU/mL, positive >20EU/mL), with a normal anti-SSB titer of 0.3EU/mL (reference range: neg <16EU/mL, equivocal 16 to 20EU/mL, positive >20EU/mL). The results of the following serum or blood tests were negative, non-reactive or normal: anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, complement 3 and 4 levels and rheumatoid factor titer.\nDue to his demonstrable cranial nerve deficits associated with his severe brachial diplegia and orthostatic hypotension, an infectious, infiltrative or inflammatory disorder affecting his cranial nerves and cervical nerve roots was considered. Cerebrospinal fluid analysis revealed a normal white cell count of 1/μL (normal 0 to 5), with an elevated protein level of 81mg/dL (normal 15 to 45mg/dL), and glucose of 90mg/dL (normal 50 to 80mg/dL) with serum glucose of 160mg/dL. A mildly elevated immunoglobulin (Ig) G synthesis rate of 3.8mg/day was detected (normal -9.9 to +3.3 mg/day), suggesting increased intrathecal antibody production. Magnetic resonance imaging (MRI) of his brain with and without gadolinium contrast was normal. MRI of his spine revealed mild spinal canal stenosis at C5–C6 due to a small central disc protrusion without cord compression. No changes suggestive of spinal cord or nerve root inflammation were observed.\nNerve conduction studies (NCS; Table ) suggested a primary axonal neuropathy. Mild conduction velocity slowing or prolonged distal latency, with reduced compound motor action potential amplitudes are consistent with this inference. There was no evidence of conduction block in any of the nerves studied. The normal tibial motor and sural sensory NCS provided evidence supporting the non-length-dependent nature of the patient’s axonal neuropathy. Monopolar needle electromyography revealed moderately severe chronic reinnervation changes in his radial, distal median, distal ulnar and axillary-innervated muscles bilaterally, with ongoing denervation changes in muscles innervated by his left distal median, right radial and bilateral axillary nerves only. Monopolar needle electromyography of cranial nerve VII innervated muscles revealed moderate chronic reinnervation changes bilaterally.\nThe electrodiagnostic data was consistent with chronic, moderately severe, axonal mononeuropathies affecting the patient’s radial, median, ulnar, axillary and facial nerves; slightly worse on the left, as seen in mononeuropathy multiplex. There was also evidence of moderately severe chronic reinnervation changes affecting the L2–L4 myotomes on the left, suggestive of subclinical lumbar radiculopathies (explaining his diminished knee reflexes on examination). Secondary chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is unlikely because the clinical presentation, physical signs with preserved reflexes, were not consistent with CIDP, despite the elevated protein on cerebrospinal fluid (CSF). Moreover, the electrodiagnostic data did not meet the European Federation of Neurological Societies/Peripheral Nerve Society criteria for CIDP.\nHe underwent a left superficial radial nerve biopsy that demonstrated a chronic vasculitic neuropathy with ongoing Wallerian degeneration, and severe end-stage axonal loss, as shown in Figure . This was consistent with a diagnosis of vasculitic mononeuropathy multiplex. A salivary gland biopsy (to evaluate for xerostomia) was normal. High-dose intravenous methylprednisolone was administered for 5 days followed by oral prednisone (1mg/kg/day) with strict glycemic control. A liberal salt diet, >2L fluid intake per day, JOBST® waist high compression stockings (to provide 30 to 40mmHg pressure), and fludrocortisone were used to treat the severe orthostatic hypotension. The patient was discharged to a rehabilitation facility for upper extremity physical and occupational therapy.\nAt 3-month follow up, the patient reported mild improvement in his upper extremity function, evidenced by interval objective improvement on confrontational strength testing (Table ) and improved facial expression. There was less orthostasis, with infrequent spells of postural lightheadedness despite non-compliance with compression stockings. The repeat MoCA score was unchanged, with stable deficits in visuospatial, executive function and delayed recall, although the patient and his family had noted a subjective improvement in his cognition. He was subsequently started on azathioprine, which was titrated upwards to a total daily dose of 2mg/kg/day alongside a gradual prednisone wean.\nAt 1-year follow up, he demonstrated further improvement in muscle strength (Table ) with stable cognitive deficits. He had further improvement in orthostatic hypotension, and was continued on fludrocortisone. His glycemic control had worsened with a hemoglobin A1C of 10%, and continued with a dose tapering prednisone regimen in addition to azathioprine. His hemoglobin A1C 1.5 years after hospital discharge was 9.2% on low-dose prednisone and therapeutic azathioprine. He continues to receive specialist endocrinological care for diabetes. His neurological examination at his most recent evaluation was stable, with no appreciable change on confrontational muscle strength testing. |
A sixty-four year old male presented to the emergency room after being struck by a motor vehicle. He was noted to have significant dyspnea with decreased breath sounds, midline vertebral tenderness, and a shortened, pulseless left lower extremity. The patient immediately received a chest tube for a pneumothorax, and was subsequently intubated. A popliteal artery and vein transection with ipsilateral subtrochanteric fracture (Fig. ) were also noted, and an emergent direct anastomosis and three compartment fasciotomy were performed. Further workup revealed compression fractures at L1 and L3 and transverse process fractures at L2/3, all minimally displaced, not requiring operative intervention.\nThe patient’s medical history was significant for peripheral vascular disease, prior myocardial infarction (with subsequent bypass graft x 4) and sick sinus syndrome (with pacemaker placement). One week after his initial injury, the patient was medically stable, and underwent an uncomplicated cephalomedullary nailing of his femur fracture (Fig. ).\nOn postoperative day five the patient suffered from both pneumonia and fasciotomy site infection. He returned to the operating room for multiple washouts, with deep cultures demonstrating methicillin-resistant Staphylococcus aureus (MRSA) treated with IV vancomycin. The patient’s femoral incisions healed uneventfully, and he was discharged home on hospital day 25.\nApproximately three months after discharge, the patient presented to his primary care provider with a new left leg discomfort and a warm mass on the anterior aspect of his thigh. The pain worsened, and the mass enlarged, becoming erythematous and indurated. Oral Amoxicillin-Clavulanate was started and the patient was sent for a CT scan, which revealed a fluid collection between the sartorius and vastus medialis muscles, in close proximity to the now-healed fracture site. The lesion extended to the distal medial thigh (Fig. ). The infection source was unknown, but all operative interventions used sterile technique. These authors believe the source was likely of earlier hematogenous origin from the pneumonia and/or fasciotomy site infections.\nThe patient was taken to the operating room where the abscess was drained. A sinus tract extended to the previous fracture site. Gaps of necrosis and soft tissue were isolated to approximately 4x5cm of bone. It was decided to remove the cephalomedullary nail. The necrotic bone and soft tissue were debrided back to healthy margins and appeared stable enough intraoperatively not to necessitate further fixation. The wounds were packed with betadine-soaked gauze sponges and allowed to heal by secondary intent while the patient received six weeks of IV vancomycin for cultures that grew MRSA.\nAfter a full course of antibiotics the patient experienced progressively worsening recurrent thigh pain and swelling. A bone scan demonstrated bony uptake, and a CT scan demonstrated a collection in the vastus lateralis (Fig. ). The patient was again brought to the operating room for aggressive debridement. Intraoperative cultures grew MRSA. After continued symptoms despite two additional debridements and intravenous antibiotics, the decision was made to utilize adjunctive hyperbaric oxygen therapy. Following partial closure of his wound he began a regimen of thirty HBO sessions at two atmospheres (atm) of pressure. After beginning therapy, a rapid improvement was noted in his condition, and his wound closed soon thereafter. The patient has remained asymptomatic for ten months following the final HBO treatment. |
A 30-year-old man presented with a 6-month history of horizontal diplopia without other symptoms. He was diagnosed with left-sided abducens nerve palsy by an ophthalmologist and referred to our hospital for further investigation. Other than bronchial asthma, his medical history was not significant. Neurological examination revealed left abducens nerve palsy without signs of impairment of any other cerebral nerves. His visual acuity was 1.2 on the right side and 1.0 on the left side. Laboratory test results, including HbA1c, C-reactive protein, and erythrocyte sedimentation rate, were normal. MRI with high-resolution T2-weighted imaging driven equilibrium radiofrequency reset pulse (T2WI-DRIVE) sequence showed pinching of the left abducens nerve between the elongated left VA and left AICA []. MRI showed no abnormal findings in the brainstem, cavernous sinus, or orbit. Based on these MRI findings, sandwich-type neurovascular compression was thought to be the cause of the abducens nerve palsy.\nBecause his symptoms did not improve spontaneously in 6 months, we decided to perform MVD for this patient. Surgery was performed using a standard lateral suboccipital approach. After the dural incision, the cerebellomedullary cistern was opened to release cerebrospinal fluid and allow sufficient cerebellar relaxation. The arachnoid membrane just above the lower cranial nerves was dissected. The lower cranial nerves were further dissected free from the choroid plexus to enable a clear view of the abducens nerve. The abducens nerve was found to be severely compressed from both sides by the VA and AICA []. Severe indentation of the abducens nerve was observed after moving the VA away from the abducens nerve []. The VA was first transposed and fixed to the dura mater of the petrous bone using a Teflon sling with the dripping of fibrin glue. Next, when we tried to mobilize the AICA toward the petrous bone, the AICA was found to penetrate the abducens nerve []. Because this penetration limited mobilization of the AICA toward the petrous bone, the AICA was attached to the pons with Teflon felt and fibrin glue to move it away from the main trunk of the abducens nerve. The neurovascular compression of the abducens nerve was resolved after these procedures [].\nPostoperatively, the patient presented transient dysphagia, presumably due to intraoperative retraction of the lower cranial nerves, which recovered after a few weeks. MRI demonstrated the disappearance of the neurovascular conflict of the abducens nerve with the VA and AICA []. The abducens nerve palsy gradually improved and eventually resolved 4 months after the operation. |
A 21-year-old woman presented with acute onset of abdominal pain with recent hematochezia and constipation. The pain was initially described as being most severe in the suprapubic area, followed by diffuse involvement of the entire abdomen, and ultimately localizing to the right lower quadrant. The clinical differential diagnosis at this point included acute appendicitis, ovarian cyst with possible rupture, urinary tract infection, internal hemorrhoids, inflammatory bowel disease, and pancreatitis. An abdominal computed tomography (CT) scan demonstrated an irregular, right adnexal mass measuring 8.8 × 7.8 cm (). A pelvic ultrasound also demonstrated a large right adnexal mass measuring 9.1 × 8.4 × 7.7 cm with internal vascularity. The mass was radiographically concerning for an adnexal tumor with possible ovarian torsion. The decision was made to perform a diagnostic laparoscopy and remove the adnexal mass. During the operation, the mass was noted to be an extrinsic sigmoid colon mass with active bleeding and hemoperitoneum (approximately 400 milliliters of blood) without involvement of the adnexa. The uterus, bilateral fallopian tubes, ovaries, and liver were grossly normal intraoperatively. The procedure was changed to an open laparotomy and the mass was resected along with the sigmoid colon and a low pelvic anastomosis was performed. The patient recuperated well after surgery. A CT scan was performed after six months to assess for residual or metastatic disease. The scan demonstrated multiple new ill-defined, low attenuating lesions in the liver, the largest measuring 6 cm in greatest dimension. A follow-up magnetic resonance imaging (MRI) scan showed several subtle, ill-defined areas of restricted diffusion that were not consistent with metastatic disease. Four years after surgery, the patient remains free of disease.\nGrossly, the mass was fragmented and 16 × 11 × 9 cm in size (aggregate measurement). The mass was well-circumscribed but unencapsulated and appeared to arise from the serosal surface of the sigmoid colon (). Cut surfaces were firm, tan-white to tan-yellow.\nHistologically, the tumor was composed of spindle cells with predominantly hypercellular and focal hypocellular areas and prominent hemangiopericytoma-like vasculature. Cytologically, the spindled cells had a scant amount of cytoplasm, mild to moderate cytologic atypia and pleomorphism, and 8 mitotic figures per ten high-power fields (Figures and ). The tumor had a focally infiltrative edge and hemorrhage but no necrosis. Immunohistochemical stains showed strong and diffuse positivity for CD34 and patchy Bcl-2 positivity. The neoplastic cells were strongly and diffusely positive for STAT6 by immunohistochemistry (). The tumor was negative for desmin, smooth muscle actin, inhibin, and CD117. |
A 42-year-old man who had undergone bilateral PRK two months prior was admitted to our ophthalmology clinic complaining of visual distortion in his left eye. The preoperative best-corrected visual acuity (BCVA) was 20 / 20, and the retinal examination was normal except for peripheral lattice degeneration in both eyes. The preoperative cycloplegic refractive error (spherical equivalent) was -4.5 and -5.0 diopters in the right eye and the left eye, respectively. Post-PRK uncorrected visual acuity was 20 / 20 in both eyes. Two months later, the visual acuity of the left eye had decreased to 20 / 70. Fundoscopy and macular optical coherence tomography (OCT) showed a stage II macular hole of the left eye (). Simultaneous OCT of the right eye showed vitreous traction on the fovea and mild elevation of the outer retinal layers ().\nOne month later, the patient underwent 23-gauge sutureless pars plana vitrectomy (PPV), localized posterior vitreous detachment (PVD) induction in the posterior pole, internal limiting membrane peeling and administration of sulphur hexafluoride gas as a tamponade in the left eye. During the operation, the patient was found to have inferotemporal peripheral lattice degeneration with multiple holes, around which a double line of barrier laser spots was introduced. PVD was not extended to the area of lattice degeneration. By the second postoperative day the macular hole had completely closed. Three weeks later, the SF6 was found to have been resorbed, and the patient's vision had improved to 20 / 40. Indirect ophthalmoscopy revealed an inferotemporal giant retinal tear (GRT) unrelated to the sclerotomies at the site of the previous lattice degeneration but that crossed the laser scars. The patient underwent PPV, endolaser photocoagulation and silicone oil injection. Postoperative examination showed successful retinal reattachment, and his BCVA reached 20 / 70 one month after the final surgery. Macular OCT revealed complete hole closure and restoration of the inner segment/outer segment junction (). Meanwhile, the patient complained of recent-onset progressive visual distortion in the right eye. At this time (4.5 month after PRK), OCT revealed increased vitreomacular traction and accentuated outer retinal layer distortion compared with the previous OCT, indicating a stage IB macular hole (). This traction accentuated one week later, and the vision of the right eye was reduced to 20 / 30 (). However, the degree of traction was decreased three weeks later, the vision in the right eye had improved to 20 / 25 and the posterior vitreous was attached (). Regular ophthalmic follow-up exams did not show any change over the next two months. |
The patient is an eight-year-old male with a history of chronic constipation since birth who presented to the emergency department after an episode of urinary incontinence that he did not feel. He was in his usual state of health until five days ago when he started to complain of pain in the posterior left thigh. The pain progressed over several days and became excruciating, radiating from the buttock to the back of his knee. The intensity of the pain awoke him from sleep. He also endorsed numbness of the left big toe. Trials of Motrin and naproxen at home did not improve his pain.\nUpon further questioning, pregnancy was uneventful, and the patient passed meconium soon after birth. His parents had been managing his constipation with over-the-counter suppositories at least once a month. A trial of polyethylene glycol did not help. At baseline, he has a bowel movement once or twice every two weeks. His last bowel movement was six days ago, and it was hard and small. His mother also reports that he has daily encopresis.\nOn physical exam, he was in excruciating pain. His abdomen was distended, with diffuse, mild tenderness to palpation. He walked with an antalgic gait. Tenderness to palpation over the left buttock was noted. Patellar reflex was 2+, and gastrocnemius reflex was 1+. Pulses were 2+ through the left lower extremity, and the sensation was notable for being slightly decreased in the left big toe.\nAt this time, the differential diagnosis was broad but suspected spinal cord compression and neuromuscular disorder were the most concerning, and thus pediatric neurology was consulted. They recommended an MRI of the spine to rule out spinal cord compression. Results showed marked distension of the rectosigmoid colon with intrinsic mass, likely fecal impaction, partially compressing the urinary bladder (Figure ). The mass measured approximately 7.9 x 6.5 x 10 cm in size. It was concerning for short segment megacolon, possibly due to Hirschsprung’s disease. The patient was transferred to another hospital for pediatric gastroenterology evaluation. There, he underwent fecal decompaction under anesthesia, followed by bowel cleanout. MRI of the left leg from hip to knee was within normal limits. The patient was also evaluated by neuromuscular medicine. EMG study revealed very mild, possible motor axon loss in the left fibular nerve, but it was not significant when compared to the asymptomatic right leg. His symptoms were most consistent with lumbosacral plexopathy, primarily affecting the L5 and fibular segments. It was thought that this could have been due to compression from his fecal impaction.\nFinally, the patient underwent rectal suction biopsy. Unfortunately, the biopsy was limited to the level of the muscularis mucosa, and no submucosal tissue was seen. Thus, the biopsy was unable to evaluate for aganglionosis. The patient's symptoms had improved after fecal decompaction, and his leg pain had resolved. As of now, there are no plans for repeat biopsy as the parents would like to pursue alternative therapies. |
A 39-year-old man was involved in a motor vehicle crash and sustained a pelvic fracture. The patient was initially treated conservatively at another hospital and 4 weeks of bed rest was advised. Six weeks after the injury, the patient started walking using double crutches. He was referred to our hospital 5 months after his initial injury with complaints of continued right posterior pelvic pain and the inability to sit comfortably. Plain pelvic radiography and CT scans revealed a fracture nonunion of the right sacrum bone and bilateral pubic rami (Figures and ). On the initial radiograph taken right after the injury, we found a fracture of the superior and inferior pubic rami, a longitudinal fracture of the sacrum (AO/OTA classification: 61-C1) in zone II (according to Denis), and avulsion of transverse process of the L5 vertebra.\nWe decided to attempt a 2-step procedure. This procedure consisted of CT-guided percutaneous placement of a guide pin for a cannulated screw across the sacroiliac joint under local anesthesia in the CT suite with subsequent iliosacral screw fixation, debridement of the nonunion tissue, and bone grafting through a posterior approach, and supplementary anterior external fixation under general anesthesia after moving to the operating theater.\nThe patient was brought to the CT suite and placed in a right lateral decubitus position on the scanning table. For intraoperative planning, a CT scan of the pelvis was obtained using a spiral CT scanner (Somatom Plus 4 Volume Zoom, Siemens AG, Forchheim, Germany; imaging parameters: 120 kV, 165 mA; slice thickness, 5 mm). Disinfection and draping were performed by an operator gowned with sterile surgical clothing. Local anesthesia consisting of 1% lidocaine was administered to the skin along the outer iliac periosteal surface. The operator made a small skin incision on the entry side and inserted a guide pin through the iliac wing across the sacroiliac joint to the mid-body of S1 using a Command 2 Console Power System (Stryker Instruments, Kalamazoo, MI). A repeated scan was taken at the level of the guide pin to check the depth, position, and angulation of the guide pin (). After final placement of the guide pin, the patient was transferred to the operating theater with the guide pin still in place.\nAfter induction of general anesthesia in the operating theater, the patient was positioned in the prone position. The screw tract was drilled over the previously placed guide pin. A 6.5 mm cannulated cancellous screw (the length was predetermined from the CT images) was then placed over the guide pin percutaneously. After the screw replacement, the right sacrum was exposed through a posterior approach. A partial hemilaminectomy of S1 and S2 was performed, the ligament flavum was excised, and the S1 nerve root was exposed (). The dural sac and S1 nerve root were retracted, and the nonunion site was exposed. We utilized the excised lamina as grafting bone. After debridement of nonunion tissue to refresh the nonunion site, the excised bone was morselized and grafted into the nonunion site. Once posterior fixation and bone grafting was accomplished, the patient was turned supine, and a supplementary anterior external fixator (Hoffmann II; Stryker, Mahwah, NJ) was applied (). The total blood loss was 60 mL. The external fixator was maintained for 4 weeks. Partial weight-bearing was permitted 4 weeks postoperatively, and full weight-bearing was permitted 3 months postoperatively. Nine months after the operation, radiographs and CT scans revealed that the fracture nonunions of the sacrum and pubic rami except the right inferior pubic rami had healed (Figures and ). At a 2-year followup, the patient was satisfied, because he was able to walk with pain-free without aid. He was able to sit without discomfort, and had no restriction in daily activities. |
A 34-year-old G5P1 woman whose last menstrual period was on 16 September, 2016, had received uremia maintenance hemodialysis for 4 years; she was diagnosed with pregnancy by pelvic ultrasound after approximately 16 weeks of amenorrhea. She had an underlying disease of chronic glomerulonephritis (CGN). The timeline of the patient care was shown in Figure .\nDuring the past years before pregnancy, the dialysis scheme of the uremic woman was 4-hour dialysis sessions 3 times weekly, and then the intensive dialysis and multidisciplinary cooperation according to the recommendations in the available literatures were performed on the pregnant woman. Firstly, the total weekly hemodialysis increased from 12 to 20 hours, the dialyzer with high efficiency biocompatible membrane was used, the average blood flow was from 180 to 240 mL/min and the dialysate flow was 500 mL/min. Low-molecular weight-heparin (bolus dose of 1000 IU followed by 250 IU every hour) was used to minimize the hemorrhagic risk and avoid coagulation of the dialyzer. Secondly, control of dry weight by slow continuous ultrafiltration in order to achieve the goal of 0.5 kg on weight gain per week. Thirdly, in order to target the postdialysis blood pressure below 140/90 mm Hg and to avoid intradialytic hypotension (<120/70 mm Hg), the dialyzed pregnant woman was treated by combination of ultrafiltration assessments and antihypertensive drugs, including long-acting calcium antagonist and alpha-methyldopa. Fourthly, management of anemia. The patient received subcutaneous recombinant human erythropoietin at a dose of 10,000 international units twice per week and intravenous iron administration of iron sucrose at a dose of 100 mg biweekly, as well as 10 mg of folic acid supplementation. In addition, nutritional supports were also performed on the pregnant women as follows: protein intake of 1 g/kg/d and 20 g/d more, calorie intake of 35 to 40 kcal/d. The dose of intake for calcitriol and calcium carbonate D3 was 0.25 μg/d and 0.6 g/d, respectively. With regard to the obstetric care, after the pregnancy was confirmed by pelvic ultrasound, the fetal biometries were assessed scheduled according to obstetric doctor's advice. The single umbilical artery, polyhydramnios and fetal growth restriction and no other abnormalities were found. After the management of the pregnant women on hemodialysis, her blood tests showed the hemoglobin (Hb) levels ranged from 9 to 11 g/dL, hematocrit (HCT) ranged from 25% to 30%, blood urea nitrogen (BUN) level was between 14.5 and 25 mmol/L and serum creatinine (Scr) was in the range of 804 to 1180 μmol/L, the calcium and phosphorus levels were kept in the normal range.\nIn April 25, 2017, at 31 weeks’ gestation and 4 days more, she was admitted to the obstetrics and gynecology department due to premature rupture of membranes and abdominal pain for 9 hours. Physical examination: T: 36.2°C, P: 106 beats/min, R: 18 beats/min, BP: 156/97 mm Hg. Abdominal ultrasound showed single live pregnancy, fetal heart rate was 144 beats/min, fetal growth restriction, and polyhydramnios (amniotic fluid index was 24). Her blood were examined: WBC: 10.1 × 109/L, N: 89.1%, L: 6.8%, RBC: 2.15 × 1012/L, Hb 73 g/L, HCT: 0.22 L/L, PLT: 237 × 109/L. ALT: 10 U/L, AST: 16 U/L, total protein: 57.2 g/L, albumin: 34.9 g/L. BUN: 19.2 mmol/L, Scr: 862 μmol/L, UA: 443 μmol/L. K+: 4.1 mmol/L, Na+: 140 mmol/L, Cl-: 100 mmol/L, Ca2+: 2.16 mmol/L, P3+: 2.18 mmol/L. Troponin I (cTnI) 0.729 μg/L. The left ventricular ejection fraction (LVEF) measured by color Doppler echocardiography was 0.59. Enlargements of left atrium and left ventricle, as well as slight of mitral regurgitation were detected. She was diagnosed with single pregnancy of 31+4 GWs (gestational weeks), fetal growth restriction, polyhydramnios and uremia. Then under general anesthesia, lower uterine cesarean section was performed and a female baby weighed 1700 g was delivered successfully. The baby, whose apgar scores were 8 at first minute and 10 at 5th minutes was sent to the neonatal intensive care unit because of her respiratory distress. And then she was discharged healthy after one week of intensive care. After the operation, the mother was sent to intensive care unit, hemodynamics monitor, ventilator-assisted breathing, continuous renal replacement therapy (CRRT) and other support therapy were performed. Four days later the mother's status was stable and she was discharged. Subsequently, she continued to receive regular dialysis. In the one year of postpartum follow-up, complications were not found in both the mother and the baby. |
A 41-year-old woman at 35 weeks' gestation was referred to Department of Anesthesia for analgesia during vaginal delivery. She was 160 cm tall and weighed 57 kg. She suffered from tuberculous pleurisy at 11 years old, diagnosed with tuberculosis-induced destroyed lung at 20 years old, and finally got left pneumonectomy at 25 years old. After the surgery, remnant right lung was bronchiectatic. She had frequent respiratory failure due to respiratory infections and was treated by intermittent admission with mechanical ventilation. At the early period of this admission, due to pneumonia on right lower lobe followed by respiratory failure, she was ventilated mechanically via endotracheal tube. Soon after, she got tracheostomy for prolonged mechanical ventilation. The lowest PaO2 checked during that period was 36.9 mmHg. It was difficult for her to be weaned from mechanical ventilation after recovery from acute pneumonia, so her ventilation was supported by synchronized intermittent mandatory ventilation (SIMV) or continuous positive airway pressure (CPAP). At 3 months after admission, she was diagnosed as 20 weeks' gestation. The patient elected to continue pregnancy, despite medical warning against influences of prior frequent maternal hypoxemia and heavy medications on fetus, increasingly difficult ventilatory management as she was approaching confinement. She stayed at ICU during rest period of pregnancy with ventilatory support by CPAP. At 35 weeks' gestation, the obstetrician decided to induce delivery, and injected misoprostol 50 µg subcutaneously at 4 hour intervals. Her chest x-ray showed tuberculous scar at right upper lung field, compensatory emphysematous change of whole right lung combined to left pneumonectomy state (). The last arterial blood gas analysis (ABGA) before onset of labor showed pH 7.362, PaCO2 49.3 mmHg, PaO2 241.4 mmHg, HCO3- 27.7 mmol/L, and 99.8% of oxygen saturation, while the patient was under assisted ventilation with CPAP at FiO2 0.6. Pulmonary function test was not available. Her hemoglobin value was 10.8 g/dl. The blood chemistry showed hypoalbuminemia (albumin 2.99 g/dl), but other laboratory findings were normal.\nWe conducted epidural anesthesia with 17-gauge Tuohy needle at L3-4 epidural space by midline approach at lateral position, and inserted a 20-gauge epidural catheter to cephalad. We injected 15 ml of 0.125% bupivacaine and fentanyl 20 µg via epidural catheter. A sensory level to T8 was achieved at 15 min after epidural block. Patient controlled epidural analgesia (PCEA) was applied with initial setting as continuous infusion of 0.125% bupivacaine 5 ml/hr. The bolus injection dose and lockout interval were set to 5 ml and 5 min each, under the control of an anesthesiologist responsible for extending the level of sensory block. Fetal heart rate and uterine contraction were monitored continuously. Because delivery could not be induced by regular injection of misoprostol for two days, elective cesarean section was decided to be performed on the third day from epidural anesthesia. We stopped PCEA and discussed the methods of anesthesia and possible complications with the patient and obstetrician. Both general and epidural anesthesia were easily performed because the patient already had a tracheostomy tube and an epidural catheter. But, the patient strongly refused to be ventilated with control mode ventilation (CMV) under general anesthesia. To be precise, she refused to be paralyzed by neuromuscular blocking agent due to fear of difficult weaning from CMV. The extension of epidural anesthesia up to T4 sensory level through epidural catheter and application of CPAP were planned. On the other hand, we also warned the patient that the level of anesthesia could be incomplete or excessive, and we would have to perform general anesthesia in that situation.\nThe patient was transported to operative suite with 5 L/min of supplementary oxygen through catheter into the tracheostomy tube. As soon as she arrived at operating room, we connected the anesthetic circuit to tracheostomy tube and applied 8 cmH2O of positive airway pressure with 40% of oxygen in air while the patient breathed spontaneously. The monitoring consisted of electrocardiography, noninvasive blood pressure, arterial oxygen saturation by pulse oximetry (SpO2). Her initial blood pressure was 130/80 mmHg, with heart rate of 75 beats/min and SpO2 97%. After checking patency of the epidural catheter and confirming no bloody aspirates with saline-filled syringe, we injected 15 ml of 2% lidocaine and 50 µg of fentanyl through the epidural catheter. Over the next 10 minutes, additional 10 ml of 1.5% lidocaine was injected epidurally to achieve a level of T4 sensory block to cold. As soon as such a level confirmed, cesarean section was started. A male infant weighing 2.53 kg was delivered within 5 minutes with Apgar scores of 7 and 8 at 1 and 5 min. We injected ephedrine 5 mg intravenously to compensate for hypotension post birth. Total operative duration was 35 minutes and total anesthetic duration was 55 minutes. The result of ABGA after baby birth showed pH of 7.425, PaCO2 40.0 mmHg, PaO2 169 mmHg, HCO3- 27.7 mmol/L, and 99.2% of oxygen saturation. A total 900 ml of Ringer's lactate solution was infused and the patient tolerated well the anesthesia and operation. Blood loss was approximately 500 ml. After completion of cesarean section, we removed the epidural catheter after injection of morphine 3 mg. She was transported to ICU while ventilated mechanically. While in the ICU, her ventilation was assisted with CPAP at the level of pressure support 8 cmH2O with FiO2 0.4. Her vital signs and ventilation parameters were stable. The ABGA showed pH of 7.446, PaCO2 39.7 mmHg, PaO2 32.3 mmHg, HCO3- 27.0 mmol/L, and 98.4% of oxygen saturation. After 2 days, weaning from ventilator was started, but it took 30 days. She was discharged at 77 days after cesarean section with home oxygen supplement. |
A 10-year-old boy presented to our unit with significant scars, keloids, and contractures in his anterior chest and neck that were formed secondary to burn injuries 4 years ago [Figure ]. With a past history of asthma, he was on inhalers on an occasional basis. Having been experiencing disfigurement-related emotional and psychosocial abuse after burn injuries, he expressed a strong desire to have his original appearance restored. Accordingly, a two-stage reconstructive procedure was performed.\nGiven severe hypertrophic scars in his pectoral and supraclavicular areas resulting from the original burn injury, the occipito-dorsal area was the only available and appropriate donor site of local autologous skin for neck reconstruction. Accordingly, bilateral pre-expansion of occipito-dorsal flaps was conducted. Under general anaesthesia in the prone position, the shape of the flap was designed in a way to match the recipient site and the occipital arteries were identified and marked on the skin using a portable Doppler ultrasound machine [Figure ]. Tissue expanders were positioned in a suprafascial plane inferior to the pedicle and deep to the center of the earlier defined occipito-dorsal flap, and the skin was closed directly. The expanders were inflated over a period of 3 months to a volume of 700 ml each. Prior to raising the flap, the occipital arteries were again dopplered and the flap was raised on a narrow isthmus, with precautions taken to ensure the flap remained above the fascial layer over the posterior trunk musculature. Once elevated, the flap was thinned to the layer in which the subdermal vascular network became visible through a layer of fat. Although designed as bilateral flaps, the two cavities converged as one. Upon rising, the expanders were removed. The donor site, measured 20 cm by 15 cm, was closed directly without drains. No significant donor site deformity was observed.\nTwo revision procedures were performed; the first one to address the dog ears in the posterior cervical region and the second one to remove excess adipose tissue by liposuction. As shown in Figure , these procedures achieved a satisfactory cosmetic result in terms of skin contouring, despite minimal scar hypertrophy. Moreover, these procedures resulted in a significant functional improvement; the patient was able to flex and extend the neck freely with no restrictions in lateral rotation. |
A 62-year-old white male with no significant medical history except for hypertension, presented to the emergency room of one of our community hospitals with a flu-like illness of 1 week duration and shortness of breath with hypoxia. His home medications were lisinopril 40 mg once daily and atenolol 50 mg daily. On initial presentation, his vitals were normal except for a pulse oximetry of 89% and a weight of 102 kg with body mass index (BMI) of 29.8 kg/m2. Even though he complained of low grade fever, his initial temperature was normal at 36.8°C. His cardiovascular system examination revealed a regular rhythm with normal venous pressure and heart sounds. The only positive finding in his physical examination was crackles in the back of the chest. His chest X-ray and CT scan showed multifocal bilateral infiltrates (). Initial ECG was within normal limits, with a normal PR interval of 160 ms. He was admitted to the hospital and started treatment with supplemental oxygen via a nasal canula and the antibiotics azithromycin and ceftriaxone. COVID-19 test by polymerase chain reaction (PCR) was returned positive later that day. Two days later, he developed crushing substernal chest pain with serial ECG changes suggestive of posterior myocardial infarction. Emergency coronary angiogram revealed occlusion of a large co-dominant proximal left circumflex artery (LCx), for which he promptly underwent primary percutaneous coronary intervention (PCI) with implantation of a drug-eluting stent, Xience Alpine, 3 × 15 mm (Abbott Vascular, Santa Clara, CA, USA), with excellent angiographic results (). Post-procedure, he was initiated on clopidrogel 75 mg/day in addition to aspirin 81 mg/day that was started previously. During the procedure, his respiratory distress worsened, requiring intubation and mechanical ventilation. He was transferred to our centre on the fifth day after the initial hospitalization because of worsening hypoxia and haemodynamic instability. Soon after arrival, he was placed on veno-venous extracorporeal membrane oxygenation (V-V ECMO). He was decannulated 3 days later while remaining on the ventilator. He was given a full 10-day course of hydroxychloroquine and also received the additional antibiotics piperacillin/tazobactam. Serum troponin I levels peaked at 40.47 ng/mL on day 5 of the hospitalization and then down-trended to <1 ng/mL (reference <0.03 ng/mL), though not completely reaching baseline. Other pertinent laboratory data included normal renal function, normal complete blood cell count with relative lymphopenia at 380 cells/mm3 and elevated lactate dehydrogensae (LDH) levels at 336 U/L (reference range 84–246 U/L) on admission. Interleukin-6 (IL-6) levels was at 14 pg/mL (reference range is <5 pg/mL) on day 3. C-reactive protein at 30.34 mg/dL (reference value <1), D-dimer levels of 33 976 ng/mL FEU (reference range <500) and ferritin levels at 1592 μg/L (reference range 20–300) were also elevated, on admission. On his 14th hospital day he had his first episode of asystole lasting 16 s. In the next 3 days, he had multiple sinus pauses without an escape rhythm, many lasting longer than 20 s (). These episodes occurred spontaneously without any negative chronotropic medications and without events causing an increase in intrathoracic pressure such as coughing, suctioning of the endotracheal tube, changing the patient’s position, etc. He had not been hypoxic or on any pressors or inotropes during this time. As expected, concomitant arterial pressure tracing also showed flatline, along with the episodes of asystole. At the end of each pause, the returning rhythm was atrial fibrillation that would spontaneously convert into normal sinus rhythm after several hours. His echocardiogram on the day when he had his first episode of asystole showed preserved left ventricular systolic function with an ejection fraction of 55–60% and posterior-lateral hypokinesia.\nInitially transcutaneous pacing was attempted but was not effective even at maximum outputs. The episodes continued for the next 2 days. As these episodes occurred some time after the index myocardial infarction and without provocation, the need for a permanent pacemaker was thought to be high. Because we wanted to minimize the number of procedures for the patient and reduce the risk of exposure for the healthcare staff during the implant and during the follow-up period, a decision to proceed with the implantation of a leadless pacemaker was made, without going through an interim temporary pacemaker.\nThe leadless pacemaker was inserted on the 17th hospital day after obtaining appropriate consent. Micra™ VR (Medtronic, Minneapolis MN, USA) was inserted in a standard fashion through the femoral vein (). Our pre-established COVID-19 protocol was followed, including adequate personal protective equipment and the procedure being performed in a designated, catheterization laboratory.\nOn completion of the procedure, the patient was transferred back to the COVID-19 unit, where he continued to remain on a ventilator for the next 10 days, followed by successful extubation.\nThe leadless pacemaker was interrogated wirelessly without added exposure risk to the staff on the day following the implantation and 5 days after the implant. Seven days post-implant the percentage of pacing was 3.4% and at 6 weeks post-implant it as 1.5%. A week after the implant, the patient underwent magnetic resonance imaging (MRI) of the brain due to mental status changes without any adverse effects on his pacemaker. He was successfully extubated 10 days after the leadless pacemaker implantation, and was eventually discharged on the 50th day of hospitalization to a rehabilitation facility, where he continues to recover gradually. His discharge medications included aspirin 81 mg/day, atorvastatin 80 mg/day, and metoprolol 12.5 mg twice per day. |
A 17-year-old female reported in an outdoor department of Oral Medicine at Government Dental College, Rohtak, with a 2-year history of persistent asymptomatic swelling of the upper lip and occasional gingival swelling (). Her medical history was noncontributory. There was no history suggestive of abdominal cramps, diarrhea, fatigue, weight loss, or any other gastrointestinal disorders. Systemic examination did not reveal any abnormalities. Examination revealed a nontender, diffuse, firm swelling of the upper lip. The surrounding facial skin showed diffuse erythematous swelling. The surface of the lip was smooth with no signs of scabs, bleeding, or exudation. No fissuring of the tongue, oral ulcers, or hypertrophy of the oral mucosa was noticed. There was no palsy of facial muscles. The patient had received intralesional triamcinolone injections in the past with temporary remissions and recurrences of the swelling. A chest radiograph, complete haemogram, erythrocyte sedimentation rate, serum folate, iron, and vitamin B12 levels, serum levels of angiotensin-converting enzyme, were ordered, which were in normal range. The tuberculin skin test for tuberculosis was negative. Ultrasonography of the upper lip revealed a mildly increased vascularity in the region. The diagnosis of cheilitis granulomatosa was confirmed on a histopathological examination, which revealed Langhans type giant cells, epithelioid cells, lymphocytes, and few neutrophils (). We decided to treat her with a combination of intralesional weekly injections of triamcinolone acetonide 10 mg/mL in the upper lip for 4 weeks, along with oral metronidazole 400 mg three times a day and oral minocycline 100 mg daily. There was a significant improvement in the labial swelling and erythema after 15 days of treatment. The gingival swelling also subsided after 20 days. After one month, metronidazole was withdrawn and minocycline was continued on alternate days for an additional one month. A recurrence of swelling of the upper lip was noticed after 4 months, which subsided with an injection of intralesional triamcinolone acetonide solution 10 mg/mL. In a 1-year follow-up, there was no further recurrence (). |
Written informed consent was obtained from the patient for her anonymized information to be published in this article.\nA 46-year-old female dental hygienist with no history of rheumatoid arthritis or trauma presented with metatarsalgia of the right foot. She was diagnosed with interdigital neuroma at a nearby hospital and received a local steroid injection on the plantar aspect of the second web space. The use of an insole was also prescribed. For 2 years thereafter, steroid injections were administered to treat any exacerbation of the metatarsalgia (10 injections of triamcinolone and one of betamethasone were administered). At 1 year after the primary injection, the second and third toes became bent and developed swelling, especially at the third MTP joint; she was subsequently referred to our department.\nPhysical findings indicated flexible hammertoe deformities of the second and third toes. The ranges of motion of the right second and third toe MTP joints at extension were 90° and 70°, respectively, whereas the corresponding ranges at flexion were both 0°. The ranges of motion in the proximal interphalangeal joints at extension were −30° and −60° in the second and third toes, respectively; the corresponding ranges at flexion were 70° and 90°, respectively.\nThe initial non-weight-bearing radiographs revealed no dislocation or arthritic changes in the second and third MTP joints (). After 2 years, dorsal dislocations of these joints were noted on a lateral radiograph (). Although no bone cyst or sclerosis was observed on the dorsoplantar radiograph, mild hallux valgus deformity was found. Magnetic resonance imaging revealed synovial fluid retention in the second and third MTP joints, and the plantar plates of both joints were ruptured from the proximal phalanx and retracted under the metatarsal head ().\nSurgery was performed for the second and third MTP joints and the hallux valgus deformity. The plantar plate disappeared, and the flexor digitorum tendon was exposed at the second and third MTP joints intraoperatively; the medial and lateral collateral ligaments (CLs) and the capsule were preserved and were sufficient for reconstruction. After cross-drilling the metatarsal head, the CLs were re-attached using non-absorbable sutures, and temporary fixation was achieved with a Kirschner wire. In addition, proximal oblique shortening osteotomies of the second and third metatarsal bases were performed. For the hallux valgus deformity, a distal soft tissue procedure and proximal osteotomy of the first metatarsal were performed, according to our operative indications.\nA short leg cast and non-weight-bearing walking were prescribed and continued for 3 weeks. At 4 weeks, partial weight-bearing in a short leg plaster shell, with active and passive range-of-motion exercises, was encouraged. At 7 weeks, the patient was instructed to wear shoes with arch supports, and full weight-bearing walking was allowed.\nCorrection of the deformity was achieved after the operation; however, pain in the third MTP joint recurred. A collapse of the third metatarsal head was observed at 5 months postoperatively (), and pain in the foot during walking gradually became worse. Therefore, resection arthroplasty because of necrosis of the third metatarsal head was performed at 15 months after the primary operation. At 1 year after reoperation, metatarsalgia improved, and visual analog pain score decreased from 8.6 points preoperatively to 1.8 points postoperatively.\nPostoperatively, the ranges of motion in the right second and third toes at the MTP joints for extension were 40° and 20°, respectively, while the corresponding ranges for flexion were 10° in both toes. Neither re-dislocation of the MTP joint nor recurrence of hallux valgus was observed (). |
The patient, a 51-year-old man, consulted a local hospital after noticing idiopathic pain in his lower right thigh. The patient had no medical history of note. A radiography revealed osteolysis with partial ossification (Figure a and b) in the region from the proximal tibial epiphysis to the metaphysis. The patient was referred to our department where a magnetic resonance imaging (MRI) scan revealed a bone tumor located in the proximal tibia. A tissue biopsy was performed, revealing atypical spindle-shaped tumor cells and multi-nucleated giant cells, as well as a neoplastic osteoid formation in the interstitial tissue, which led to the diagnosis of osteosarcoma (Figure c).\nAt this time no apparent metastatic lesions were observed. The administration of preoperative neoadjuvant chemotherapy with cisplatin (120 mg/m2 on day 1) and doxorubicin (30 mg/m2 on days 1 to 2) was not effective and the tumor continued to grow. On completion of two courses of chemotherapy a pathological fracture occurred and an amputation of the right femur was performed. The histological response rate of the resected specimen was less than 10% of the entire lesion. Following surgery, five courses of adjuvant chemotherapy with ifosfamide (3 g/m2 on days 1 to 4) and VP-16 (75 mg/m2 on days 1 to 4) were administered and the patient was discharged as disease free.During follow-up, a computed tomography (CT) scan at 9 months after discharge revealed multiple metastases in both lungs (Figure a), and chemotherapy was re-initiated. The chemotherapy did not result in any marked change in the pulmonary metastases. Although the patient’s general condition continued to be good, a tumor was palpated in the right shoulder approximately 1 year later. At approximately 3 years after recommencing chemotherapy, the tumor had grown to 7 cm in size and was causing intense pain. An MRI scan revealed a well-defined and markedly enhanced mass located in the trapezius muscle (Figure b, c, and d). Although positron emission tomography-CT (PET-CT) scan revealed an insignificant accumulation of the tracer in the pulmonary metastatic lesions (Figure ), the accumulation was comparatively high (standardized uptake value (SUV) of 4.6) in the tumor within the trapezius muscle (Figure ). With the exception of the trapezius muscle, any accumulation suggestive of metastasis was not found on the PET-CT scan. A thallium-201-scintigraphy revealed a high and even accumulation of the tracer within the tumor in the trapezius muscle. A thermography revealed a 1.5 degree increase in temperature inside the tumor compared with the contralateral side, which was suggestive of high activity.Based on these results, the tumor within the trapezius muscle was deemed to be malignant. As no growth of the pulmonary metastases or development of new lesions was observed, the tumor in the trapezius muscle was surgically removed. An intraoperative review of the tissue specimen by a pathologist showed atypical cell proliferation and osteoid formation, which led to a diagnosis of metastatic osteosarcoma. Consequently, wide and tumor-free resection was performed. Macroscopically, the resected tissue consisted of a solid tumor with bleeding and necrosis (Figure a). As with the biopsy specimen and the total cleavage hematoxylin and eosin stain (H & E) specimen, metastatic osteosarcoma was diagnosed (Figure b).The integrity of other tissues around the surgery area was damaged (Figure a) and the range of motion of the patient’s shoulder joint was limited after surgery (flexion: 120°, abduction: 105°) compared with the non-operated shoulder joint. However, the patient’s pain was eased after resection of the trapezius muscle metastatic lesion, and a good quality of life was maintained between chemotherapy treatments. Despite chemotherapy, at 14 months post-resection the pulmonary metastases began to grow rapidly (Figure b), and the patient died from respiratory failure. No local recurrence (Figure a) or new extrapulmonary metastases were observed after resection of the metastatic lesion in the trapezius muscle. |
The patient was a 52-year-old right-handed man in VS, according to the standardized VS diagnostic criteria developed by the American Medical Association. He had developed a trauma-induced brain injury (TBI) leading to a disturbance of consciousness, quadriplegia lasting 45 days, a GCS score of 6 (2 blinks, 1 verbal response, 3 motor response), and Rancho Los Amigos rating level I. Head computed tomography showed left temporal bone fracture with temporal, parietal, and occipital epidural hematoma, subarachnoid hemorrhage, and cerebral herniation. The right medial orbital wall was irregularly shaped, which was considered to be due to a prior fracture. His past illness history included craniotomy and tracheotomy 45 days before admission, and traumatic right eye injury 9 years earlier, without sequelae. The healthy subject was a 45-year-old right-handed man who drove for a living, and who had no previous history of head injury or cerebrovascular disease.\nBAEP was performed on the healthy subject and VS patient to rule out lesions to the auditory pathway.\nfMRI was performed in the healthy subject and VS patient during sound stimulation and movement-imagination tasks. Sound stimuli were divided into familiar–rest and familiar–unfamiliar sound stimuli. The movement-imagination tasks were designed to promote the imagining of playing tennis. The fMRI imaging data were analyzed using the FSL software package ().\nThe subjects were asked to alternate 30-s periods of task activity with 30 s of rest for a total of 3 minutes and 30 s. For sound stimulation, a familiar voice was provided by the closest family member to the individual prior to the onset of illness. The family member was instructed to speak the patient’s name and describe things that were of interest to the patient before the onset of their illness. The unfamiliar voice was provided by a person who had never been in contact with the patient. The instructions for the movement-imagination tasks were explained to the subject before scanning. The patient was instructed to imagine himself standing in the middle of a tennis court and playing tennis. The beginning of the movement-imagination period was cued with the word “tennis”, and the rest periods were cued with the word “relax”.\nfMRI was performed using an Ingenia 3.0T magnetic resonance system (Philips Healthcare, Best, the Netherlands), with conventional axial position T2 (TR = 2369 ms, TE = 107 ms), FLAIR (TR = 7000 ms, TE = 93 ms, TI = 2215 ms), T1 (TR = 2600 ms, TE = 20 ms, TI = 1040 ms), resting state brain scan (TR = 2500 ms, TE = 27 ms, NSA = 1, FOV = 230 mm), and task-oriented dynamic scan.\nWe obtained informed consent and support from the patient’s family to develop a rehabilitation and wake-up treatment plan. Rehabilitation treatment included rehabilitative nursing (e.g., optimal limb placement, nursing care for urine and intestinal function, air incision care), arousal therapy (e.g., environmental stimulation, sensory stimulation of sound, light, electricity, exercise therapy), joint mobility, standing bed, MOTOmed exercise trainer (RECK Technik GmbH, Betzenweiler, Germany), electrical stimulation of swallowing function, and acupuncture treatment. Amantadine was administered orally for 4 weeks according to the following schedule: 100 mg twice daily in week 1, 150 mg twice daily in week 2, and 200 mg twice daily in weeks 3 and 4. fMRI scans were repeated after treatment for 3 months.\nThis project was approved by the institutional review board of the First Hospital of Jilin University. This research did not increase the risk and economic burden of the patient; the patient’s rights were fully protected; and the project design was conducted in line with scientific and ethical principles. The patient’s relatives provided written informed consent to publish this case. |
A 53-year-old woman was taken to the emergency room after an accidental fall. At the moment of the fall, the patient was holding a glass bottle that shattered with the impact. A sharp piece of glass caused a deep wound with a length of about 3 centimetres on the right cheeks. The patient showed no signs of facial nerve injury. The wound was then toileted and sutured. After 10 days from trauma the patient began to complain of the appearance of a continuous colourless and odourless fluid from the wound, which increased after food intake. Therefore the patient came under our observation on 20th day from trauma. A clinical examination revealed on the wound scar a 3 mm orifice discharging a clear serous secretion, suggesting the diagnose of posttraumatic parotid fistula. The patients were invited to limit oral intake for a week in order to reduce salivary output; steristrips were placed to close the fistula and a compressive dressing was applied for 7 days, with no results. Due to severe discomfort caused by a large amount of secretion, a device for transdermal delivery of scopolamine (Transcop Recordati OTC S.p.A. Milan, Italy) was applied on the right preauricular region (). This device is a patch of circular form containing a reservoir of 1.5 mg of drug scopolamine, which is released into the bloodstream. The daily release of scopolamine is about 0.5 mg with a duration of a pharmacological three days for each patch. In the following 3 days, the patient reported significant reduction in salivary discharge from the fistula. The patches were replaced and the successive examination after 3 days revealed that the fistula was completely healed. The treatment was well tolerated and the patient referred only to a mild dryness of the mouth in the last 2 days of treatment. No recurrence was observed during a 3-month followup. |
Our inhouse specialist palliative care service (PCS) treated a 75-year-old man suffering from lung cancer. Originally, the patient was transferred from an orthopedic clinic where a pathological lumbar fracture was diagnosed. The patient was transferred to our internal medicine unit for further tumor examination. At the time of cancer diagnosis in November 2020, adenocarcinoma of the right upper lobe of the lung with osseous and lymphogenic metastases was far advanced, as well as metastases of the adrenal gland. Due to a rapidly worsening state of health and aggravating symptoms, such as dyspnoea and weakness, the planned radiotherapy and commencement of a tumor-specific therapy could not be carried out. Therefore, PCS management was initiated. During the patient’s hospital stay, his wife was his only visitor due to COVID-19 visitation restrictions. Before beginning PCS care, the patient had already been hospitalized for approximately 3 weeks in the internal medicine unit of the hospital, and an oropharyngeal swab for a SARS-CoV-2 PCR (polymerase chain reaction) test had last been performed on the day of admission to the hospital with a negative result.\nOn the day of transfer to the palliative care unit, the patient’s symptoms became significantly more severe. He suffered increasingly from shortness of breath and a cough, as well as developing a fever. Visitors were required to fill out a questionnaire before every visit asking about any potential contact with COVID-19 infected individuals and symptoms of infection, but a measurement of body temperature was not obtained. On admission to our palliative care unit, the patient’s wife denied that she or her husband had contact with anyone infected with COVID-19, and according to her questionnaire answers, she was free of symptoms. The patient’s symptoms were interpreted as being due to pneumonia from pre-existing lung cancer. Wearing a mask was impossible for the patient. The nurses along with other members of our multiprofessional palliative care team (social worker, psychologist, chaplains, physiotherapist, and doctors) used filtering face pieces class 2 (FFP2) tested according to the norm EN 149. The performance of FFP2 masks is mostly comparable with that of N95 respirators. However, the team members did not wear face shields or protective gowns at the bedside. Two days after transfer, the patient’s condition deteriorated, and his wife moved in to accompany her husband during the terminal phase. According to the hospital’s rules, relatives who are admitted must have an oropharyngeal swab for SARS-CoV-2 PCR. A few hours after the wife’s admission, the laboratory informed us that she was positive for SARS-CoV-2 with a cycle threshold value (ct value) of 15.5. Therefore, an oropharyngeal swab was also performed on the patient, which was positive test (ct value of 24). The patient’s wife was sent home for self-isolation in accordance with public health requirements.\nThe cancer patient died 4 hours after his wife went home. A report was made to the infection control team in cooperation with the hospital’s occupational health department to inform them of the patient’s and his wife’s infection with SARS-CoV-2. They ordered that all palliative care staff who worked during the couple’s stay on the ward be tested. To our knowledge, no other patients on the ward were positive for COVID-19, nor were other sources of infection identified.\nA COVID-19 PCR screening was performed on 18 staff members, irrespective of the type of contact protection measures they had been using. Most (n = 14) staff members were identified as having direct contact with the patient and/or wife. Testing was repeated every second day for 14 days so as to identify potentially infected staff during the COVID-19 incubation period. During this 14-day period, six staff members tested positive for SARS-CoV-2 (). In collaboration with the infection control team, the department decided to close the unit. This was necessary, first, to terminate the outbreak of SARS-CoV-2 and, second, because there was a shortage of staff.\nRespirator use was a key component of the infection prevention protocol. Donning and doffing respirators, as well as conducting appropriate seal checks, had been taught by infection control nurses in collaboration with occupational health in line with internal standards. All infected team members indicated they were confident that they had worn the mask properly. There is, however, no legal obligation in Germany to regularly conduct respirator fit tests. As a result, these tests were not conducted by occupational health prior to the outbreak. Re-using or re-processing respirators was not encouraged at the hospital. |
The first case is a 75 year old male previously known only for bilateral cataracts. He was diagnosed with stage III non-small cell lung carcinoma at the age of 74 years following investigations for a persistent cold. A routine X-ray revealed a right lower lobe lung mass which was diagnosed as non-small cell lung cancer (NSCLC) following a CT chest and bronchoscopy. He began gemcitabine but experienced an adverse reaction and it was changed to carboplatin and paclitaxel.\nPrevious to his cancer diagnosis and treatment, he lived in an autonomous seniors’ residence with his wife. He was retired but had previously worked as a laboratory technician and had a high school level education. He was independent in all his activities of daily living (ADLs) and most instrumental ADLs (IADLs) except for cooking and shopping which were always carried out by his wife. He ambulated independently. His wife noted that he was becoming more forgetful in the 4 years prior to his cancer diagnosis. However, once initiating carboplatin/paclitaxel the patient himself began complaining of forgetfulness and was referred to our clinic by his pulmonary oncologist. Cognitive testing showed a MMSE of 27/30 and a MoCA of 21/30 (normal score is ≥ 26). He denied any depressive symptoms and scored 2/15 on the geriatric depression scale (GDS) which is negative for depression. A CT head was significant only for an old lacunar infarct in the lentiform nucleus. A PET scan did not reveal any metastatic disease.\nA complete work-up was performed at the first visit and all blood tests were normal. A follow-up visit 5 months later while he was still receiving chemotherapy revealed cognitive testing scores of 30/30 on the MMSE and 23/30 on the MoCA test.\nTwo months after the cessation of the chemotherapy, the patient’s cognitive testing scores improved, with a MMSE of 30/30 and a MoCA of 27/30). The patient also reported that, subjectively, he found his memory to be improved.\nIt is important to note that the patient had a history of memory problems predating the cancer diagnosis and treatment by 4 years. In fact, it is possible that the patient may have been suffering from baseline mild cognitive impairment. This may have put him at higher risk of delirium secondary to chemotherapy. Furthermore, the improvement of his cognitive testing scores could be explained by a delirium which resolved given the relatively quick resolution of his cognitive deficits after cessation of chemotherapy. |
A 4-month-old male infant presented with a swelling arising from the upper jaw noted by his parents since 2 months, with difficulty in feeding and irritability []. History of pregnancy and delivery was normal and there was no history of medication during pregnancy. Growth and development of the infant were adequate for his age.\nOn intraoral examination, a swelling measuring about 3 × 3 cm in diameter was seen in the pre-maxillary region. It was located slightly toward right side and showed extension toward hard palate. Expansion of the anterior maxillary alveolar ridge with obliteration of labial vestibule was seen []. On inspection, swelling was smooth and the overlying mucosa was intact and stretched. On palpation, it was bony hard, fixed, non-fluctuant, and non-tender. No lymph nodes were palpable. An intraoral periapical radiograph revealed a multilocular osteolytic lesion. Patient was planned for surgical excision under general anesthesia. Incision was made through the labial mucosa. Lesion was exposed []. Its enucleation was done with curettage of septa present inside the lesion with normal surrounding bone.\nHistopathological examination of the excised tissue revealed sheets and chords of tumor cells in the background of dense fibrovascular stroma []. Another field showed areas of calcifications in a globular pattern with tall columnar cells showing reverse polarity, along with stellate reticulum [Figures and ].\nTumor cells were arranged in alveolus like spaces and in a pseudoglandular pattern. Individual tumor cells were recognized as two morphologically distinct types, namely large cells (densely pigmented cells, sparsely pigmented cells) and small undifferentiated cells (hyperchromatic cells) []. Irregular alveolar spaces are lined by larger cuboidal cells with moderate amount of cytoplasm and well-defined margins, some of which contained brownish pigment. Their nuclei were round to oval with finely dispersed chromatin and inconspicuous nucleoli. In addition, Small hyperchromatic cells with scanty cytoplasm were present within the spaces or seen as isolated nests within the fibrillar background [Figures and ]. Isolated clusters of the larger cells were also present. A characteristic biphasic pattern of cell distribution was seen. There was no evidence of atypical mitosis or necrosis in the tissue.\nBased on these findings a diagnosis of MNTI was made. For further confirmation of the diagnosis, 24 h urinary excretion of VMA was done and found to be increased, 2.9 mg/24 h, confirming the diagnosis. Post-operative course was uneventful. The 6 month follow-up of the patient showed no recurrence. |
A 77-year-old woman presented to our clinic with a mass on her left flank that had grown rapidly over 3 months. The patient had been diagnosed with NF-1 45 years ago. She also had asthma, hypertension, and atrial fibrillation, and had undergone percutaneous nephrostomy insertion in her left kidney to treat a urethral obstruction.\nClinical examination revealed a protruding firm nodule arising from a dermal neurofibroma in the patient’s left flank (). An ulcerated lesion with bloody discharge was present in the most prominent area, and the patient reported experiencing pain and tenderness. Magnetic resonance imaging revealed a well-enhancing mass (3.9×2.5×3.4 cm) with a broad base along the dermis, with a round bulging contour on the lateral side. The mass showed intermediate-to-high T1 signals with relatively homogeneous enhancement (). Histological examination showed infiltration of tumor tissue into the dermis, which was consistent with the appearance of interlacing bundles of neoplastic spindle cells with marked pleomorphism. The hypercellular areas consisted of clusters and sheets of epithelioid round cells admixed with fascicles of hyperchromatic spindled cells. No lymphatic or vascular invasion was identified (). Immunohistochemical staining was positive for S-100 protein in the tumor cell cytoplasm ().\nAfter diagnosis of the mass as a cutaneous epithelioid MPNST (CE-MPNST), complete surgical excision was planned. With the patient under general anesthesia, the grossly visible tumor was completely excised with lateral and deep resection margins of 30 mm and 15 mm, respectively (). After frozen biopsy to confirm the absence of malignancy, additional undermining was performed to elevate the surrounding subcutaneous tissue. A bilateral fasciocutaneous flap was elevated and advanced and was then closed layer by layer. The wound healed well after surgery, and no signs of local recurrence or metastasis were observed 15 months later ().\nThis study was approved by the Institutional Review Board of Kyung Hee University Medical Center on October 4, 2019 (IRB No. 2019-09-041) and was performed in accordance with the principles of the Declaration of Helsinki. Informed consent was obtained from the patient. |
A 27-year-old female presented in the surgical outpatient department with swelling in the left submandibular region and the floor of the mouth that had been present for six months. The swelling had increased gradually in size. The patient complained of difficulty in eating food. On physical examination, there was a non-tender mass, firm in consistency, not attached to the skin, measuring 5 × 4 cm in the submandibular region () and 2.5 × 1 cm in the floor of the mouth (). No nerve involvement was observed. On systemic examination, there was no swelling or café-au-lait spots all over the body. A family history of NF was absent. Laboratory investigations were within normal limits. An ultrasound of both masses revealed heterogenous echogenecity with ill-defined borders. The fine-needle aspiration cytology (FNAC) of the submandibular mass was inconclusive, but the FNAC of the swelling in the floor of the mouth revealed bland spindle cells in a haemorrhagic aspirate. A CT scan of the swelling in the submandibular region and the floor of the mouth revealed hypoattenuated masses. Excision of both the swellings was done simultaneously under general anaesthesia. The origin of the tumour was not obvious at surgery. The submandibular gland mass was an irregular, nodular, capsulated grey-white piece of tissue measuring 4.5 × 3 × 2 cm; it was firm in consistency (). The cut section was lobulated, with a white, hyalinised appearance. The mass from the floor of the mouth was an irregular white piece of tissue measuring 2 × 0.6 × 0.3 cm; it was firm in consistency and a small lymph node measuring 1 × 0.5 cm. The cut section was homogenous, grey-white, and glistening (). On examination under low-power magnification (10X), the submandibular gland mass was nodular and showed a tortuous mass of expanded nerve branches, which are seen cut in various planes of section. ( and ). The tumour was comprised of wavy serpentine nuclei with pink cytoplasm and a myxoid background, with areas of collagen bundles, and it was infiltrated by mild lymphocytic infiltrate. A diagnosis of plexiform neurofibroma was obvious on microscopic examination (). Histopathological examination of the mass in the floor of the mouth showed tissue lined by nonkeratinised stratified squamous epithelium. The subepithelial tissue revealed a tumour comprised of interlacing bundles of elongated cells with wavy nuclei, intimately associated with wire-like strands of collagen (). The background showed a myxoid appearance (). A diagnosis of diffuse neurofibroma was made. Although, immunohistochemically, the tumour was positive for S-100 protein, the diagnosis was obvious on light microscopy. |
A 44-year-old Peruvian woman, who had immigrated to Japan 20 years earlier, presented with postprandial upper abdominal pain of four months duration. She was found to have a gallbladder stone, which might have been the cause of her epigastralgia. Her past medical history was unremarkable except for a left renal stone. She had been pregnant three times and given birth to three children. On physical examination, there were no remarkable findings. As to laboratory tests, levels of aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), glutamyl transferase and total bilirubin were within normal ranges. Ultrasonography showed a few strongly echoic stones but there was no gallbladder wall thickening. Neither intra- nor extra-hepatic bile ducts were dilated. Routine preoperative computed tomography (CT) revealed a series of tortuous collateral veins at the liver hilum, irregularly surrounding the gallbladder from the neck to the fundus (Figure a, b). The extra-hepatic portal vein was occluded at the level of the spleno-portal junction (Figure c, d). There were no evidence of hypertrophy of the left liver, splenomegaly or ascites, suggesting that she was not cirrhotic. To check the anatomy of the biliary tract, we performed magnetic resonance imaging, which confirmed discontinuity of the common bile duct. This finding was assumed to have resulted from surrounding collateral vessels rather than a bile duct stone. Our diagnosis was symptomatic cholecystitis with CTPV. After being fully informed of her options, she provided consent to undergo surgery.\nWe considered SILS to be feasible because the cavernous vessels were not close to Calot’s triangle, and most ran from the middle to the left side of the hepatoduodenal ligament and liver hilum. Two distended collateral veins flowed extra-hepatically to the edge of the posterior segment of the liver. We were determined that these vessels could be sacrificed during the surgical procedure.\nThe operation was performed under general anesthesia, starting with a trans-umbilical incision. The peritoneal cavity was entered employing the open method, and a LAP PROTECTOR (HAKKO CO.,LTD. NAGANO,JAPAN, TM) was then inserted with EZ ACCESS (HAKKO). There were three holes, for two 5 mm ports and one 12 mm port. A flexible laparoscope (Olympus, Tokyo, Japan, TM) and two operating forceps were used. The pneumoperitoneum was set at 8 mmHg. Suture suspension of the gallbladder was not adopted. The courses of the cavernous vessels surrounded the neck of the gallbladder (Figure a). We first approached the cystic duct, with an assistant holding the neck of the gallbladder at the ventral position. Fragile cavernous vessels were encountered in this area, such that we kept the cystic duct together with these vessels. During the entire procedure, this process caused the most bleeding. Pulling the cystic duct out together with collateral vessels, employing a silk suture, we detached the cystic duct and the neck of the gallbladder from Calot’s triangle (Figure b). The cystic artery was ligated and transected near the neck of the gallbladder. After confirming the common bile duct, the cystic duct was ligated and clipped. There was bile oozing from the stump of the cystic duct, which was treated by ligation. The remaining surgical procedures were carried out with little difficulty. Hematoma was removed as extensively as possible, and no intra-peritoneal drainage was applied. Total operating time was 132 minutes and blood loss was 370 grams.\nThe patient was quite well postoperatively, with slightly increased AST (134 U/l), ALT (109 U/l) and ALP (188 U/l) on postoperative day 1, which decreased to 53, 78 and 181, respectively, the next day. Postoperative CT revealed that two extra-hepatic meandering vessels had been sacrificed but there were no hepatic perfusion abnormalities. She was uneventfully discharged on postoperative day 2. The liver enzymes dropped within normal ranges and she was asymptomatic on her last outpatient day of postoperative day 8. |
A 39-year-old Iranian male patient, a known case of AS since 15 years ago, referred to our clinic for his impacted mandibular wisdom tooth. He was operated for lumbar scoliosis and he had total hip replacement. He took 25 mg indomethacin daily, calcium 1000 mg daily, metothrexate 2.5 mg 4 days a week, prednisolone 5 mg daily, and folic acid 1 mg daily. There was no other systemic illness except mentioned including negative history of uveitis. Laboratory data revealed a positive HLA-B27, 1st hour ESR = 24 and 2nd hour ESR = 50, +++ CRP and mild hypochromic RBCs. Other data were within normal limits. Last bone densitometry was performed 10 years ago which was not significant regarding osteopenia or osteoporosis, though recent lateral neck radiography was suggestive of osteopenia of cervical vertebrae []. Oral panogram (OPG) revealed a left mandibular mesio-angular third molar []. Disk space was reduced and the borders of glenoid fossa and condylar head were sclerotic, yet no erosion and osteophyte was evident []. Mandibular border thickness was within normal limits (4-5 mm thick).\nIn oral examination, patient had class I angle occlusion. Mandible was limited in laterusive movement. No click or tenderness was noted examining temporomandibular joint. A 26-mm of maximum mouth opening was clarified. There were no other significant soft-and hard-tissue pathoses.\nA lateral neck X-ray was taken prior to the operation to detect any possible luxation of fracture of the cervical vertebrae which was normal. He got anesthetized using total 4 carpules each containing 1.8 cc of 2% lidocaine with 1:100,000 epinephrine solution. Patient had moderate limitation in cervical flexion and extension and a cushion was inserted behind his head to prevent subluxation or fracture of upper cervical vertebrae while the surgeon exerts unintentional heavy forces during the surgery. During a routine procedure, a flap was elevated and impacted right mesio-angular third molar was removed. A great care was made to avoid any heavy forces and rapid movement of the jaws and neck with regards to antiseptic and low traumatizing maneuver. Afterward, the surgical site was sutured and packed. Surgery was uneventful except for difficulty in accessing the site due to the limited range of mouth opening. The patient was discharged with prescriptions for oral analgesic and 400 mg cefixime for 7 days and 4 mg dexamethasone for injection. |
A 35-year-old male presented with the acute onset of neck pain and lower extremity weakness in the setting of hospitalization for sepsis with persistent leukocytosis and blood cultures positive for Streptococcus viridans and Candida glabrata. His past medical history included hypertension, type II diabetes mellitus, end-stage renal disease on dialysis, and non-ischemic cardiomyopathy. He had a history of a HeartMate 3 LVAD implantation four months prior complicated by redo-sternotomy for atrial valve replacement. He subsequently underwent tracheostomy and gastrostomy for airway and nutrition, respectively. At his baseline, he was able to ambulate independently, although he used a wheelchair in most instances. During his hospitalization, he also tested positive for COVID-19 (coronavirus disease 2019).\nOn physical exam, the patient had significant atrophy in his right lower extremity with flaccid paralysis and complete loss of tone. He had 2/5 strength in all muscle groups in the left lower extremity. He had a normal tone, was full strength, and normo-reflexive in the bilateral upper extremities. He was also found to be insensate in the right lower extremity and noted to have decreased sensation in the left lower extremity. His decline in the neurologic exam was partly attributed to critical illness polyneuropathy given his prolonged hospital and intensive care unit stay.\nDiagnostic evaluation\nA CT scan with contrast was initially performed that demonstrated mild erosion of the C6 and C7 vertebral bodies anteriorly with prevertebral phlegmon and a 7 mm prevertebral fluid collection concerning abscess, although there was no epidural collection or evidence of cord compression (Figure ). A CT scan of the thoracic spine was also performed, which was completely unremarkable (Figure ). Due to the patient’s LVAD, a CT myelogram was then performed instead of MRI. A cervical myelogram at C1-C2 was performed given the location of the suspected pathology, concern for dilution of the contrast media if conducted via lumbar puncture, and the need to visualize the superior border of the presumed pathology for pre-operative planning. This approach was chosen over lumbar injection due to concern that dye injected in the lumbar region would not travel to the region of interest. A 20-gauge, 10 cm needle was introduced into the cervical subarachnoid space at the level of C1-C2 under fluoroscopy, and 15 mL of clear CSF was obtained. 10 mL of iohexol-300 contrast was subsequently injected and the myelogram was performed. There were no complications, and the patient then underwent a CT scan of the cervical spine.\nThe CT myelogram imaging demonstrated a near-complete block of the ventral epidural space at the C2-C3 level with no to minimal contrast moving down the dorsal and lateral epidural spaces (Figure ). Changes of discitis and osteomyelitis were again seen at C6-C7 anteriorly and on the left side of the pre-vertebral space.\nSurgery\nAfter discussion with the infectious disease, neurology, neurosurgery, cardiac surgery, cardiac anesthesia, and cardiac ICU teams, a circumferential epidural compressive pathology was felt to be the reason for the patient’s symptomology. This was based on the symptomology and fluid collection and phlegmon seen on the CT of the cervical spine, as well as lack of contrast advancement on the CT myelogram. While other diagnoses were considered that would not improve with surgical intervention, based on the patient’s young age and potential to benefit based on a compressive etiology, surgery was recommended.\nAn emergent C3-C7 posterior cervical laminectomy at the level seen on the CT myelogram was planned with the use of intra-operative ultrasound. During the procedure, no dorsal or ventral epidural purulence or signs of infection was noted via gross visualization and ultrasonic probing. There were no other compressive lesions at this location.\nAfter decompression, the spinal cord appeared to be well decompressed circumferentially on ultrasound with surrounding CSF. The lamina and spinous processes were sent for permanent specimens, and a culture was performed of the epidural space. There were no intra-operative complications.\nPostoperative course\nPostoperatively and at three-month follow-up, the patient remained neurologically stable with bilateral lower extremity paraparesis and minimal sensation. The cultures taken during the operation were negative, and the permanent specimens were found to be unremarkable for signs of infection. This result could, however, be confounded as the patient had previously received empiric antibiotics. Additional CT imaging demonstrated post-operative changes without additional pathology (Figure ). Due to his lack of functional recovery and intra-operative findings and based on the clinical exam he was diagnosed with a suspected spinal cord infarct. |
An 80-year-old Japanese woman with no significant comorbidities noticed a bilateral tingling sensation on the anterior surface of her lower limbs.\nThe sensation was localized below her thighs; however, she felt neither numbness nor weakness, and could walk and ride a bicycle without any problems. Her symptoms persisted for about one month, which resulted in a visit to a local outpatient clinic. Laboratory studies performed in the clinic showed pancytopenia. Although the patient was examined at another general hospital, the cause of her condition was unknown. Subsequently, she experienced a high fever (a temperature of 38°C - 39°C) daily. However, she did not have any other accompanying symptoms, such as chills, pain, and appetite loss, and her general state was relatively normal. Despite a more detailed evaluation, the patient’s diagnosis was inconclusive, and she was observed as an outpatient. Five months after her first visit, she was taken to the emergency department of the hospital at which she was previously treated, because of sudden loss of consciousness. Laboratory studies showed that she had lost consciousness because of hypoglycemia, and further evaluation revealed that hypoglycemia was one of the signs of hypopituitarism. She received glucocorticoid and replacement therapy. Whereas treatment resulted in blood glucose level control, the tingling sensation gradually progressed. Although seven months had elapsed since her first visit, the causes of her symptoms remained unknown. Therefore, she was admitted to the Department of Hematology of our hospital for further assessment.\nHer past medical history was noncontributory.\nHer family history was noncontributory.\nOn physical examination, we observed the presence of a tingling sensation on the anterior regions of the lower limbs, under the thighs, and on both palms of the patient. Decreased vibratory sensation on both sides of the lower extremities was also noticed. Hepatosplenomegaly, lymph node enlargement, and skin eruption were not observed.\nBlood test results were as follows: White blood cell count, 300 cells/μL; Hemoglobin level, 9.0 g/dL; and Platelet count, 113000 platelets/μL, lactate dehydrogenase, 971 IU/L; Ferritin, 710 ng/mL; Soluble interleulin-2 receptor alpha, 3412 U/mL. No evidence of infection or solid tumor was observed on serum examination, culture, and imaging. Brain magnetic resonance imaging (MRI), however, showed enlargement of the pituitary gland (Figure and ). It did not appear to be a tumor as the entire pituitary gland was almost equally contrasted; no other abnormalities were present. We performed stimulating hormone tests, as the patient had been diagnosed with hypopituitarism in the previous hospital. The patient received an injection of four kinds of hormones [growth hormone (GH)-releasing hormone, corticotropin-releasing hormone, luteinizing hormone (LH)-releasing hormone, and thyrotropin-releasing hormone], and we monitored the levels of seven kinds of hormones [GH, LH, follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), cortisol, adrenocorticotropic hormone (ACTH), and prolactin] produced in response. Low levels of six of the seven hormones were observed, with the exception of prolactin, which confirmed the diagnosis of hypopituitarism.\nContrast-enhanced computed tomography scans of the abdomen and pelvis showed a hepatic cyst and mild splenomegaly. There was no evidence of tumor and lymphadenopathy could not be seen. Bone marrow aspiration and biopsy, performed to evaluate pancytopenia, revealed the presence of hemophagocytic lymphohistiocytosis (HLH) (Figure and ). There was no evidence of tumor involvement. She met five of eight criteria of HLH (fever ≥ 38.5°C, splenomegaly, peripheral blood cytopenia, hemophagocytosis in bone marrow, ferritin > 500 ng/mL, elevated soluble IL-2 receptor alpha two standard deviations above age-adjusted laboratory-specific norms)[]. We suspected lymphoma as a cause of HLH, as no evidence of infection or solid tumors were present. One of the most common causes of adult HLH is lymphoma. However, as the patient did not show lymphadenopathy, a random skin biopsy was performed, which showed that the tumor cells had proliferated predominantly within the small vessels of the dermis with no infiltration outside the vessels (Figure ). Immunohistochemical staining revealed positivity for the B-cell markers CD20 and CD79a in the absence of staining for T-cell markers. These characteristics were consistent with those of intravascular large B-cell lymphoma. |
A 44-yr-old female with tinnitus in the form of a high-pitched, 'whooshing' sound in the left ear visited our tinnitus clinic on April 11, 2012. The patient had a 6-month history of ear-ringing synchronous with the heart beat during physically stressful conditions such as fatigue, exhaustion, and emotional upset. It was heard about 50% of the time during the day and became louder when she experienced fatigue at her job in accounting. The patient described attenuation of tinnitus by manual compression of the left posterior auricular area. The patient did not complain of hearing impairment, fullness in the ear, hyperacusis, dizziness, or headache. She had no past head or neck trauma, no exposure to ototoxic drugs or extremely loud noise, chronic medical illness, or neuropsychiatric condition. The tinnitus was not audible even with a stethoscope around the left ear and mastoid area. The patient described that the Valsalva maneuver, or manual compression of the left internal jugular vein, reduced the loudness of the tinnitus, but it was unaffected by head position or compression of the right neck. The otoscopic examination and pure-tone audiogram were normal.\nAn axial temporal bone computed tomography with contrast enhancement revealed that the left MEV had a prominent opening to the sigmoid sinus and the large canal of the vein crossing the mastoid bone to the soft tissue, without other accessory MEVs (). The outer foramen of the MEV was located on the posterior-superior mastoid region. The diameter of the inner foramen (at the sinus side) of the left MEV was approximately 4.5 mm whereas that of the right MEV was 1.3 mm. The magnetic resonance image (MRI, Gyroscan, Philips, the Netherlands) of the posterior fossa with contrast enhancement showed an outstanding figure of the MEV enhanced together with the sigmoid sinus, also demonstrated on an MR-venogram where no other significant abnormality was found in the venous structures except a size discrepancy between the left internal jugular vein and the right, with the left being slightly larger ().\nDoppler of the left mastoid region detected the origin of the pulsatile tinnitus and displayed pulsating outward venous flow (from the sigmoid sinus to the scalp) with approximately 0.5 m/s of peak velocity at the orifice of the MEV (). However, no turbulence was detected by the Doppler waveform (confirmed by two professional sonographers) and the flow inside the mastoid bone was also not visible due to bony opacity. However, the Doppler recording seemed to be identical to the patient's tinnitus, which showed synchrony with her heartbeat and attenuation of the flow-signal by the Valsalva maneuver, which matched the timing of tinnitus-reduction described by the patient ().\nAlthough transfemoral venous embolization was recommended to obliterate the MEV, the patient preferred to adapt to the tinnitus and successfully modified her life style by avoiding stressful conditions and distracting attention from the tinnitus. |
A 58-year-old female presented with a chief complaint of left hip pain of 5 months’ duration. The patient had been seen approximately 10 months prior to presentation, shortly after experiencing a “clunk” in her right hip. She reported that her pain was stable and had not increased since that episode. Relevant history included a left primary THA approximately 25 years ago. The patient also reported a right primary THA at the age of 33 years, followed by a head and liner exchange 10 years later due to poly wear and broken tine. A right total knee arthroplasty procedure was performed approximately 1 year ago. Comorbid conditions reported included degenerative joint disease, thrombocytopenia, cirrhosis of the liver, lumbar spondylosis and anemia. The patient had been managing any ongoing hip pain with anti-inflammatories and routine monitoring of poly wear with annual radiographs.\nOn physical examination, a pain-free range of motion (ROM) of the affected hip was noted, although the patient demonstrated hesitation at the extremes of motion. Slightly reduced ROM was noted with internal and external rotation when compared with the right hip. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal. Radiographs were obtained and revealed severe polyethylene wear and asymmetry in the left hip (). Some acetabular and proximal femoral lysis was noted, although there was no change in the acetabulofemoral component interface.\nThe pre-operative plan for this patient was to exchange the polyethylene liner only; however, during surgery, it was observed that the locking mechanism on the poly component was incompetent. Furthermore, intraoperative measurement with the navigation system indicated anteversion of 5° (radiographic definition), revealing a cup component significantly more retroverted than the 18° indicated by the pre-operative radiograph (). A decision was made to exchange both the liner and the cup component ().\nSurgery was successful, and post-operatively, the patient was prescribed standard posterior hip precautions with toe-touch weight-bearing for 6 weeks. At 2 weeks post-op, the patient was progressing well. |
Our patient was a 40-year-old Black African woman with a medical history of HIV infection and mild depression. She was a non-smoker and had no known drug allergies. Her medication included venlafaxine, and reverse transcriptase inhibitors efavirenz (non-nucleoside) and lamivudine (nucleoside). She had originally attended 4 years previously with left nipple discharge associated with pain and discomfort of her left breast. Ultrasound imaging with core biopsies revealed multiple benign IDPs in her left breast and she underwent a Hadfield’s procedure (radical subareolar duct excision). Another Hadfield’s procedure was performed in the following year (2007) after recurrence of the benign IDPs. In 2010 she underwent a left subcutaneous mastectomy with implant reconstruction following development of a further IDP in her left breast. This form of surgical treatment was decided most appropriate due to the extent of the IDP, difficulty of radiological follow-up and to exclude atypia and risk of subsequent malignancy. In the mastectomy specimen a single IDP was present measuring approximately 38×22mm in maximum dimension. The IDP contained several suspicious foci of solid atypical proliferations, which after immunohistochemical staining were regarded as atypical ductal hyperplasia. The degree of atypia was not considered to amount to ductal carcinoma in situ (DCIS) and there was no evidence of invasive neoplasia. No axillary lymphadenopathy was noted at the time of the mastectomy. In situ hybridisation for the detection of human papillomavirus (HPV) was performed on two separate IDPs (in 2008 and the IDP in the mastectomy specimen in 2010). In both cases no HPV was detected with the probe set used (HPV 1, 2, 6, 11, 16, 18, 31 and 33). During follow up, 2 years after her left mastectomy (in 2012), she reported a small lump in her left breast. Ultrasound imaging revealed a new 9mm well-defined hypoechoic mass. This was shown on core biopsy to be a further IDP. Diagnostic excision of the lesion confirmed a benign IDP with hyperplasia, apocrine metaplasia and no evidence of atypia.\nIn 2013 she developed an enlarged palpable mass in her left axilla.\nOn ultrasound imaging the axillary mass corresponded to an abnormally enlarged lymph node with eccentric cortical thickening and loss of medullary fat (Figure A). No changes or abnormalities were detected in her left breast. Left axillary ultrasound-guided core biopsies of the lymph node revealed part of an IDP. As a result of this extremely unusual finding a diagnostic excision of the enlarged left axillary lymph node was performed. The lymph node measured 20mm in maximum dimension. The histology of the lymph node showed a reasonably well-circumscribed papillomatous proliferative epithelial lesion within an apparent encompassing duct. The lesion was confined to the node and comprised prominent tightly packed papillary fronds lined by a bilayer of luminal epithelial cells and an outer layer of basal cells supported by fibrovascular cores (Figures B and C); identical to an IDP of the breast. Cholesterol crystals, dense collections of macrophages and reactive stromatolites were also noted in part, signifying a long standing lesion and the latter indicative of previous core biopsy. No necrosis or significant atypia was evident and few mitoses were identified. At the periphery, benign lymphoid tissue was seen confirming the intranodal location of the lesion. In this surrounding lymphoid tissue small groups of duct-like structures were additionally noted (Figure D). In view of the curious finding of an IDP within an axillary lymph node immunohistochemical staining was performed for confirmatory characterisation of the lesion and exclusion of malignancy. The lesion and encompassing duct demonstrated mixed cytokeratin (CK) 5 and 14, p63 and smooth muscle myosin positivity (Figures E-G) with heterogeneous oestrogen receptor (ER) expression, indicating a benign lesion. A similar staining pattern was also displayed in the duct-like epithelial structures thereby determining their origin as breast. The histological appearances and immunohistochemical staining profile therefore substantiated a benign IDP within her left axillary lymph node, which was considered to have arisen from EBT.\nShe experienced an uneventful postoperative period and remains well at follow up appointments. Her recent annual contralateral mammogram (performed 1-month post-lymph node excision) revealed no significant interval change in her right breast when compared with previous mammograms, and no palpable axillary lymph nodes were identified. |
A 19-year-old male patient was incidentally found to have an abnormal shadow in the left thorax on chest radiography. He did not complain of any symptoms, such as coughing, dyspnea, chest discomfort, or neurologic symptoms. His previous medical and family history were unremarkable. No unusual findings were observed on a physical examination. His hematologic and serologic profiles, including inflammatory markers, were within the normal ranges. Plain chest radiography showed a well-defined mass in the paravertebral region (). Chest computed tomography (CT) revealed a 3.4-cm mass with a lobulated contour between the left ninth and tenth intercostal spaces. However, the CT images did not show foramen dilatation or central calcification. Furthermore, there was no radiologic evidence of invasion of the adjacent vasculature, soft tissue, or bony tissue; these findings were highly suggestive of a neurogenic tumor ().\nWe planned to excise the mass via video-assisted thoracoscopic surgery (VATS) in the left thorax. The lesion was a hypervascular mass located grossly in the paravertebral space and showed cystic changes or partial necrosis (). It was a tumor measuring 4.0×3.0×2.0 cm located laterally to the sympathetic trunk, but at some distance from the sympathetic nerve (). It abutted the intercostal nerve and surrounding tissue and seemed to originate from the intercostal nerve (). There were no definitive feeding vessels surrounding the mass. Thus, based on its macroscopic appearance, we assumed the mass to be a neurogenic tumor originating from the intercostal nerve. The tumor was completely removed, including excision of the affected intercostal nerve and periosteum adjacent to the rib because of severe adhesions to the mass. Frozen-section biopsy was performed intraoperatively, and the tumor was determined to be a lymphoproliferative lesion. Subsequently, the permanent histologic examination revealed atypical lymphoid hyperplasia, consistent with what is observed in hyaline-vascular–type Castleman disease (CD). Histologically, the tumor was composed of lymphoid follicles with hyalinized vessels surrounded by circumferentially arranged layers of lymphocytes in an onion-skin pattern (). The patient’s postoperative hospital course was uneventful, and he was discharged without complications on the second postoperative day.\nInformed consent of the patient was waived by Institutional Review Board. |
A 53-year-old woman with a medical history of the craniotomy for meningioma removal 10 years ago, was again scheduled the operation for her regrown tumor removal. She also had hypothyroidism for the past 10 years, which was treated with oral prednisolone at 20 mg/day and levothyroxine sodium at 50 μg/day.\nshows the results of blood chemistry tests performed at the time of admission to the hospital.\nThe patient was admitted to our ICU after the initial attempt of tumor removal, which resulted in failure because of severe hemorrhage prior to tumor handling. Surgery was then performed 3 months after ICU discharge, and the patient was once again admitted to the ICU after surgery. During both stays in the ICU the patient was administered 200 mL of Glyceol® over a period of 30 minutes, every 6 hours from 0:00 am. Despite her stable general condition, routine arterial blood gas analysis (Diagnostics 860, Chiron, CA, US) at around 6:30 every morning indicated reappeared hyperlactatemia. The fact that repeated measurements of her lactate levels were normal at other time points, made us to consider Glyceol® administration as the cause of her transient hyperlactatemia.\nTo exclude the possibility of impaired tissue perfusion caused by rapid infusion of hypertonic solutions as another cause of this transient hyperlactatemia, the patient was alternately administered Glyceol® and 20% mannitol solutions. The lactate levels increased gradually and peaked 45 minutes after Glyceol® administration, while no significant change was observed in case of mannitol. Blood glucose level increased slightly after Glyceol® administration but the increase was not significant []. This transient hyperlactatemia was reproducible by administration of Glyceol®.\nMetabolic abnormality was also considered another possible cause of her transient hyperlactatemia; however her amino acid analysis, urinary organic acid analysis and serum acyl carnitine analysis all showed normal results, and hyperammonemia, hypoglycemia, or ketonuria were not observed. In addition, impaired perfusion, infection and convulsive seizure were not observed during patient admission. Liver diseases including hepatitis, congenital metabolic diseases, glycerol metabolism abnormality, any diseases similar to Reye's syndrome, mitochondrial disorders and other conditions were all considered as differential diagnoses but were all unlikely because of her laboratory finfings. Moreover, Glyceol® administration produced hyperlactatemia even after correcting her hemoglobin concentrations in order to improve oxygen transport, while increased urinary excretion of lactic and pyruvic acids was found [].\nSince mannitol and Glyceol® administration resulted in different levels of lactate concentration, transient hyperlactatemia was unlikely to be triggered by impaired tissue perfusion caused by rapid infusion of hypertonic solutions.\nWe then performed a retrospective chart review and found other nine patients admitted to Jichi Medical University Hospital ICU after intracranial surgery and administered Glyceol® during the past year. All nine cases were confirmed to be without notable dehydration, infection or convulsive seizure before or after the administration of Glyceol®. We found that their lactate levels increased in general, peaked approximately 45 minutes after Glyceol® administration and returned to preadministration levels around 3 hours after []. No significant change in blood glucose was seen during Glyceol® administration. |
In October 2016, an 81-year-old man with chronic obstructive pulmonary disease (COPD) presented to his general practitioner with a 3-week history of increasing breathlessness but no cough. A chest radiograph identified a shadow in the lower zone in the left lung, and subsequent CT scan confirmed the presence of a 2.5 × 2.5 cm mass in the lower left lung and multiple mediastinal lymph nodes ( and ()). The patient underwent an endobronchial ultrasound guided biopsy of the paratracheal lymph nodes which revealed lung adenocarcinoma (T1c N3 M0). Tumour cells were strongly positive for CK7, thyroid transcription factor-1 (TTF-1) and with moderate focal expression of estrogen receptor (ER). They were negative for CK20, S100, PSA, CD56, synaptophysin and chromogranin. The tumour was negative for epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutations.\nHis previous medical history was COPD, diet controlled diabetes, and cancer of the prostate treated with radical prostatectomy in 2004 and in remission. He was not on regular medication and had no history of drug allergies. He was a retired salesman. There was no previous history of asbestos exposure. He was an ex-smoker (around 18 cigarettes daily for around 15 years) having stopped smoking 45 years ago. His ECOG performance status was 1. Physical examination was unremarkable.\nThe patient was offered chemotherapy and radiotherapy, but he declined as he was in his 80s and did not want any treatment that could adversely affect his quality of life. The decision was made to follow the patient up but without active treatment.\nA CT scan in December 2016 showed that the lung mass had increased in size to 2.7 × 2.8 cm though the mediastinal and left hilar lymph nodes had not changed in size. The patient was offered treatment but again declined. A chest X-ray in July 2017 showed progressive changes in the left lower zone but no significant collapse or effusion evident. The patient had a further CT scan in November 2017 which revealed near total resolution of the left lower lobe mass with only a small area of residual spiculated soft tissue remaining (1.3 × 0.6 cm) and a significant reduction in size and number of mediastinal lymph nodes ( and ()). The patient underwent another CT scan in January 2018 which showed stable appearances of the small residual opacity in the left lower lobe and mediastinal lymph nodes.\nOn further questioning, the patient stated that he had started taking CBD (“MyCBD”) oil 2% (200 mg CBD in 10 mL) from the beginning of September 2017. He took two drops (0.06 mL, 1.32 mg CBD) twice daily for a week and then nine drops (0.3 mL, 6 mg CBD) twice daily until the end of September. Following the November 2017 CT scan, the patient started taking nine drops twice daily but had to stop around a week later. The reason behind this was that the patient did not like the taste and caused him slight nausea. He was never physically sick. There were no other changes in the patient’s diet, medication or lifestyle from September 2017. Informed written consent was obtained from the patient. |
A 3-month-old female infant was admitted to our outpatient clinic on April 8, 2014 with parents’ complaints of bilateral white cloudiness at the pupillary zone perceivedd 1 month after birth. Preoperative ophthalmic examinations revealed complete bilateral lens opacification with clear corneas and anterior chambers. Since the infant did not cooperate with further examination of the posterior segment, we conducted B-scan ultrasonography of both eyes to screen abnormalities other than lens opacification, which showed negative results. Hence, she was diagnosed with bilateral congenital cataracts and underwent bilateral lensectomy, posterior capsulectomy and anterior vitrectomy under general anesthesia on April 9, 2014. Intraocular pressure (IOP) was OU 12 mmHg with bilateral corneal diameter of 10 mm measured before the corneal incision was made. Intraoperative examination and postoperative B-scan ultrasonography showed negative results of posterior segment stuctures. Therefore, the patient was discharged after an uneventful postoperative course.\nHowever, 6 months later, the infant was suspected to have bilateral developmental glaucoma with a mild enlargement of the corneal diameter, by a local hospital. She was then referred to our hospital again. The outpatient fundus examination revealed enlarged bilateral cupping with a cup-to-disc (C/D) ratio of 0.8 OU. IOP measured by schiotz tonometer was OD 19 mmHg and OS 26 mmHg on October 17, 2014, and OD 27 mmHg and OS 19 mmHg on October 21, 2014. The patient was then admitted to our inpatient department with the tentative diagnosis of bilateral developmental glaucoma. Ophthalmic examination showed IOP OD 52 mmHg and OS 20 mmHg (October 30, 2014; schiotz tonometer), mild opacification of the superior cornea in the right eye, clear cornea of the left eye, clear bilateral anterior chamber and visual axis zone. No retinal detachment was found with B-scan ultrasonography, and A scan showed axial lengths of OD 23.43 mm and OS 20.75 mm. The patient was scheduled to receive bilateral trabeculotomy on October 31, 2014. Her intraoperative examination under general anesthesia showed IOP OD 35.8 mmHg and OS 20.6 mmHg (schiotz tonometer), superior opacification of the cornea in the right eye with a diameter of 11 mm (Fig. ) and a clear cornea in the left eye with a diameter of 10.5 mm, clear bilateral anterior chambers, and increased C/D ratio of OD 0.9-1.0 and OS 0.8-0.9. Gonioscopy examination showed almost overall angle closure and no detection of trabecular meshwork in both eyes, except that the superior section in the right eye was vague due to the cornea opacification. Intraoperative ultrasound biomicroscopy detected bilateral shallow anterior chambers of OD 1.75 mm and OS 1.95 mm in depth with the pupil diameter of OD 2.15 mm and OS 2.07 mm, absence of the lens with a small amount of residual cortex out of the pupillary zone, and iris bombé with pupillary obstruction by vitreous herniation in both eyes (right eye in Fig. - and left eye in Fig. -). Middle-anterior positioned iris insertion, mildly extensive and anteriorly rotated ciliary process, and 360° of peripheral anterior synechiae (PAS) and iris-trabecular meshwork contact were also observed in both eyes with UBM. Therefore, we altered the surgical plan to anterior vitrectomy and goniosynechialysis. The postoperative IOP was OU 16 mmHg. The infant was administered TobraDex Eye Drops (Alcon Laboratories, Inc., Fort Worth, TX, USA) TID OU and 1 % pilocarpine (Bausch & Lomb Freda, Shandong, China) BID OU. One week after the surgery, her IOP was OD 15 mmHg and OS 16 mmHg. The whole changes of bilateral intraocular pressures in this case was shown Fig. .\nDuring the one-year follow-up in our medical centre after surgery, the infant showed no recurrent hypertension in the right eye. The intraocular pressure in the right eye maintained between 14 to 16 mmHg using TonoPen XL tonometer (Medtronic Ophthalmics, MN, USA) after oral administration of chloralhydrate. |
In August 2014, a 41-year-old male smoker was admitted to our hospital because of right pleural effusion. After obtaining the patient's informed consent, medical thoracoscopy examination was performed and many parietal pleural nodules were found in right lung. Histopathologic examination showed low differentiated adenocarcinomas in parietal pleural nodules which considered to be metastases rather than the primary tumor (Fig. ). Molecular testing using FISH was carried out on these parietal pleural nodules and found to be EGFR positive (exon 19 deletion). Considering the cancer was EGFR mutated, the patient began to receive treatment with 250 mg gefitinib daily since August 2014. The treatment was well tolerated and the chest computed tomography scan revealed a good response that the size of lesions in right upper lobe became smaller.\nUnfortunately, the chest computed tomography in November 2015 revealed the lesions in right lung became larger and new lesions were found in the left lung. Without the doctor's advice, the patient tried Tarceva, Sorafenib, BIBW2992, AZD9291, XL184, and Crizotinib successively. However, there was no obvious curative effect and the tumor gained progress. In February 2017, the patient was admitted to our hospital again. Positron emission tomography-computed tomography revealed that a mass in the right hilus pulmonis and multiple nodules in the bilateral lungs with high glycometabolism, which were considered to be primary cancer or metastases. After obtaining the patient's informed consent, a lung puncture biopsy under computed tomography guidance of the right lung mass was performed. Histopathologic examination showed small cell lung cancer (Fig. ) and the patient began to receive treatment with chemotherapy (etoposide 0.1 g day2–5 + cis-platinum 30 mg day2–4). Unfortunately, the chemotherapy treatment did not work and the right lung mass became larger. In order to get the latest pathology, a bronchoscopy was performed after obtaining the patient's informed consent. Interestingly, histopathologic examination showed squamous cell carcinoma (Fig. ). The patient died in April 2017 that survived for 32 months from lung cancer was found for the first time. |
This report concerns an 18-year-old female, known to have psoriasis vulgaris. The patient initially presented with the typical scaly inflammatory plaques, which were controlled with topical treatment in 2013. Despite her improvement at the time of diagnosis, the patient suffered from a severe relapse in 2018, in which the scaly plaques had involved 80% of her body. As an attempt to treat the flare-up, the patient was initiated on an anti-tumor necrosis factor, etanercept. The patient received the drug on a weekly basis, subcutaneously at a dose of 50 mg, for a period of seven months. Sequentially, the patient started to experience fever, night sweats, cough, dyspnea, and dysphagia. The symptoms were coincident with bilateral progressive supraclavicular swellings, which were increasing in size over a period of four months.\nClinical examination revealed the enlargement of cervical, supraclavicular, and submental nodes. The supraclavicular and cervical lymph nodes were tender upon palpation; however, the submental lymph node was non-tender and described as hard, immobile, with an estimated size of 1.3 cm. Skin examination findings were consistent with active psoriasis in which scaly patches on an erythematous base were reported. Other components of physical examination were insignificant.\nThe patient was suspected to have tuberculosis; however, the diagnosis was excluded due to the insignificance of the purified protein derivative and sputum culture results. Laboratory investigations revealed high C-reactive protein and high erythrocyte sedimentation rate, and other investigations were normal. The patient’s complaint was further investigated in October 2018 by a computed tomography (CT) scan of the neck and chest (Figure ). The radiological report was consistent with the patient’s presentation and clinical findings, in which the enlargement of different groups of lymph nodes, at multiple levels, above the diaphragm was recognized. The size of the greatest lymph node was measured to be 4.6 × 3 × 3 cm in the right supraclavicular group. Furthermore, the report stated that the findings of the CT scan are suggestive of lymphoma.\nIn November 2018, the patient was readmitted for biopsy; however, due to the heavy load on facilities, the biopsy was postponed to the following month. In December 2018, a right cervical lymph node was excised for biopsy under CT guidance. The pathological report denied the presence of malignant cells or granulomas from the provided sample. The report suggested reactive lymphoid hyperplasia and stated that the immunohistochemical markers CD15 and CD30 were absent.\nIn February 2019, the patient was readmitted to the medical ward to further investigate her lymphadenopathy. A CT scan showed further progression of the size of lymph nodes (Figure ). The report stated that the right submental lymph node was estimated to be 1.3 cm in size in the previous scan; however, it had grown to be 1.7 cm and was associated with a necrotic center. Although the lymph nodes in the left aortopulmonary window and right paratracheal region were also enlarged, the growth of the right axillary lymph nodes was of exceptional significance, in which the largest lymph node was estimated to be 2.6 cm in diameter. The scan also presented the mild compression that was applied on the trachea by the enlarged supraclavicular lymph nodes; however, it resumed its normal caliber in the mediastinum. The radiological report has also stated that there were no lung masses, nodules, or pleural effusion. It, however, suggested changes in the density of the liver, which may be indicating fatty liver changes. Thereby, it was recommended that the patient goes under further radiological studies, such as an abdominal and pelvic CT.\nIn October 2019, viral causes of lymphadenopathy such as Epstein-Barr virus, cytomegalovirus, and mumps were ruled out. CT scan was repeated and demonstrated further progression of the size of the lymph nodes, in addition to supraglottic narrowing as a result of mass effect (Figure ). Subsequently, the patient underwent a second excisional biopsy, as she started to experience significant unintentional weight loss, neck enlargement, dysphagia, altered voice, and further enlargement of the lymph nodes. The biopsy was taken from the right axillary lymph node. The pathological report confirmed the diagnosis of nodular sclerosis classical Hodgkin lymphoma stage IIIBSX. Contrary to the previous sample, the immunohistochemical markers CD15 and CD30 were positive. Fortunately, lymphoma was confined to the lymph nodes superior to the diaphragm.\nIn November 2019, the patient elected to be treated in a tertiary center given her logistics. We were allowed to access and trace her records. The other center ordered a positron emission tomography with 2-deoxy-2-[fluorine-18] fluoro-d-glucose integrated with computed tomography (18F-FDG PET/CT) (Figure ). The patient’s condition was managed with six cycles of Adriamycin, bleomycin, vinblastine, and dacarbazine (ABVD). Fortunately, the patient underwent complete remission. We had a telephone conversation with the patient, and she expressed the fact of having no active skin lesions as well. |
A 65-year-old man nondiabetic normotensive reformed smoker and ex-alcohol consumer with known case of ulcerative colitis and benign prostatic hyperplasia (under medications for 2 years) visited our center with complaints of decreased verbal output, decreased psychomotor activity and low mood for the last 1.5 months. The symptoms started in the form of memory loss (forgetting address, phone numbers, to turn on the lights in the evening, to locate headlight of the bike) with progression to the right-sided hand stiffness and ipsilateral leg weakness 3 months back. He then visited nearby medical center and was prescribed with medications (Escitalopram and Quetiapine), which did not improve his symptoms and his condition deteriorated further. Later on, he also developed a sudden difficulty of his speech with reduced speech output and inability to speak normally on the thirty-fifth day of the onset of his symptoms. Ten days prior to presentation to our hospital, he had no verbal output, no oral intake, inability to walk without support, and loss of control in urine and stool passage.\nHe had a history of disturbed sleep pattern for the last 1 month. There were features of low mood and non-compliant behavior at the time of presentation. He did not have a history of loss of consciousness or head trauma. There was no history of fever, swelling of limbs, headache, tremor, visual loss, seizures, weight loss, and exposure to toxic substances. There was no history of drug abuse. He was a non-vegetarian and had no history of psychiatric disorders. There was no similar history in the family.\nOn examination, the vital signs were stable. The Glasgow Coma Scale was E4V1M5, and pupils were bilaterally equal and reactive. The fundus examination was normal. He had patchy whitish lesion over dorsum of tongue and erythematous plaque over perineum. He had no signs of lymphadenopathy, meningism. Muscle tone was increased in all four extremities. Bilateral biceps, triceps, and knee reflexes were 3+. Planter reflexes were upgoing bilaterally. He also showed wide-based gait. Respiratory, cardiovascular, and abdominal examinations were normal.\nA complete blood count, hemoglobin, erythrocyte sedimentation rate, coagulation profile, liver, and renal function tests, C-reactive protein, serum electrolytes (Na+, K+, Ca+2, and Mg+2), serum glucose, and urinalysis were within normal range. Chest X-ray and Mantoux tests were also normal. Antinuclear antibody, complements C3, C4 were found to be negative. Cerebrospinal fluid (CSF) parameters showed no abnormality and adenosine deaminase in CSF was also within a normal range. CSF culture was sterile. Opening pressure during lumbar puncture was not elevated.\nT2-weighted magnetic resonance imaging (MRI) and FLAIR showed areas of high signal intensities in bilateral fronto-parietal lobe deep white matter (Figure ). The electroencephalogram showed bilaterally synchronous periodic pattern of bi- or triphasic sharp waves at 1 Hz (Figure ). Investigation of CSF 14–3–3 was not available in our center.\nThe diagnosis of probable CJD was made. Supportive care with anti-epileptics and antidepressants was provided. The patient was regularly followed up and his condition progressively worsened and died within 1.5 months of diagnosis. |
A 40 year-old Nigerian housewife was seen at the oncology clinic of the University College Hospital (UCH) Ibadan, Nigeria in June 2002 with a 1 year 8 months history of painful left breast lump which had been previously excised in another hospital but recurred 8 months before presentation at UCH. There was no information about histological diagnosis of the excised breast lesion from the first hospital. There were no systemic symptoms. She was Para 7+1 and had no family history of breast or ovarian cancer. Physical examination revealed globular enlargement of the left breast measuring 20 cm × 18 cm. The mass occupied the whole breast, was warm, multinodular and fixed to the pectoralis fascia. The ipsilateral axillary lymph nodes were enlarged, but examination of the other systems was normal. A clinical diagnosis of locally advanced cancer of the left breast was made.\nPlain radiograph of the chest and abdominal ultrasound scan were normal. A core-needle biopsy of the mass was done and histology showed a malignant neoplasm comprising islands of chondroblastic and osteoblastic stromal cells, with no normal breast tissue seen. A diagnosis of osteogenic sarcoma was made. The patient had a left modified radical mastectomy and latissimus dorsi musculocutaneous flap to cover an anterior chest wall defect. The mastectomy specimen weighed 350 g. Cut sections revealed areas of cystic degeneration and necrosis, with focal areas that were firm with a cartilaginous consistency. Conventional representative sections were obtained from each of the four breast quadrants, areola region, resection margins and axillary lymph nodes. Microscopic examination of the sections showed a malignant breast neoplasm displaying fibrosarcomatous, chondrosarcomatous (Figure ) as well as osteosarcomatous (Figure ) differentiation. There was metastasis to one of the lymph nodes. She was scheduled for radiotherapy to the chest wall but she defaulted. Contact tracing revealed that she died about 6 months after mastectomy. |
A previously healthy 6-year-old boy is transferred to the pediatric ward from an outside facility with findings of hypertension and bradycardia that were incidentally discovered during evaluation for abdominal pain associated with cough, congestion, frontal headache, and decreased appetite for 1 week. He had been started on prednisolone for a presumed diagnosis of wheezing-associated respiratory illness 4 days prior, but this was discontinued after 48 h when the patient was found to be hypertensive. His family denies the use of over-the-counter decongestant medications.\nThe patient was born full term with a cesarean section due to the previous two C-sections. His perinatal course was notable for transient tachypnea of newborn that was complicated with left small pneumothorax that spontaneously resolved. He had multiple surgeries for correction of bilateral club feet. His family feels that he sleeps more than usual for other kids in his age group. On reviewing his medical chart, his last normal heart rate (HR) and blood pressure (BP) were recorded when he was 3 years and 9 months old, and he has been mildly hypertensive with low HR since the age of 4.5 years. Family history was positive of the father with primary hypertension starting from the age of 29. His mother's uncle died at the age of 26 with heart attack, and his mother's great grandfather died suddenly at the age of 35 years. There is no known family history of renal disease or thyroid abnormalities. The patient does not have known allergies and is not currently on any daily medications.\nOn initial physical examination, the boy is alert, oriented, and not in pain or distress. His temperature is 97.5°F, HR is 54 beats/min, respiratory rate is 24 breaths/min, BP is 160/91 (99% – Stage 2 hypertension), and oxygen saturation is 99% on room air. Height is 1.13 m (8.7%), weight is 19.5 kg (14.5%), and body mass index is 15.3 kg/m2 (44.5%). He has Grade 2/6 ejection systolic murmur at the left lower sternal border with normal heart sounds. He has normal looking feet with a full range of movement but with bilateral scars. He does not have dysmorphic features, and his chest, abdominal, and neurological examination is completely normal.\nOn admission, the initial concern was that bradycardia and hypertension in the setting of headache might represent increased intracranial pressure. His headache resolved without intervention, and his neurological examination was reassuring. His HR and BP during his course did not vary significantly. HR stayed between 47–63/min, systolic BP 136–160 mmHg, and diastolic BP 75–97 mmHg. Initial workup showed normal complete blood count, electrolytes, kidney functions, and urinalysis.\nHis electrocardiogram (ECG) [] showed normal sinus rhythm with complete heart block as indicated by complete dissociation between P-waves and QRS complexes and junctional escape rhythm. Left axis deviation was also noticed. Echocardiography was negative for congenital heart disease and demonstrated normal ventricular function. There was, however, increased left ventricular (LV) mass with mild LV hypertrophy (LVH).\nLyme titers were within normal limits. The patient was also investigated for common causes of secondary hypertension. His thyroid-stimulating hormone was 3.44 uIU/mL and T4 was 11.3 ug/dL excluding hypothyroidism. Plasma renin activity was 5.18 ng/mL/h, which was within normal limits. His renal ultrasound was normal as well as his renal duplex that showed no evidence of hemodynamically significant stenosis bilaterally. Both renal veins were visualized and patent.\nGiven the fact that the patient had mild LVH suggesting secondary organ changes from hypertension, an angiotensin-converting enzyme (ACE) inhibitor was initiated. The patient was observed for 4 h after the first dose for any signs of hypotension or medication intolerance. He was then discharged home with diagnoses of likely congenital complete heart block and primary hypertension. He had scheduled follow-up with our pediatric cardiology facility.\nThe patient was followed as an outpatient with successful control of his hypertension. He demonstrated normal exercise tolerance and denied any cardiac complaints related to his bradycardia. A routine Holter monitor placed 15 months after his initial presentation showed several episodes of ventricular couplets, triplets, and a limited run of ventricular escape rhythm which was a new finding. He was referred to cardiac surgery for the placement of an epicardial pacemaker []. He tolerated the procedure well, and his baseline HRs reflected appropriate atrial sensing. Over the next several weeks, his hypertension resolved and his ACE inhibitor was discontinued. Over a 1-year follow-up, he has been asymptomatic with no recurrence of his hypertension. |
A 21-year-old woman visited our department complaining of a large painless swelling in the left submandibular region. The swelling had been recognized at its sudden onset two months earlier. Intraorally, her mouth floor was bluish and elevated. On palpation, the swelling revealed a soft, painless, and fluid-containing mass. The patient had no traumatic or surgical history, and the swelling did not cause difficulty in swallowing or speaking. Routine blood tests and the thyroid profile were within normal limits.\nPanoramic radiograph revealed no pathological changes. Contrast-enhanced computed tomography (CT) scan demonstrated a large rim-enhanced fluid attenuation mass occupying both sublingual spaces with an anterior connection (). The lesion extended into the left parapharyngeal space superiorly and compressed the left submandibular gland inferiorly (). Anteriorly, it extended to the right sublingual space in a horseshoe shape (). At the lower level of the lesion, several linear septa were noted (). A fluid-fluid level, which is the interaction between two fluids with different viscosities, was also noted (). Although the septation and fluid-fluid level within the lesion made the differential diagnosis from a cystic hygroma difficult, considering the location of the lesion in the sublingual space, it was diagnosed as a plunging ranula.\nUnder general anesthesia, an incision was made in the left lingual vestibule, and excision of the lesion along with extirpation of the left sublingual gland was performed. At surgery, the cystic lesion was found to be filled with a viscous and yellowish mucous fluid. After removal of the left sublingual gland, a cut-down tube was inserted into the middle portion of the left Wharton's duct.\nThe histopathologic examination of the specimen from the sublingual gland revealed ruptured acinar cells (). The patient made an uneventful recovery. The cut-down tube inserted into the left Wharton's duct was removed after 2 weeks. The patient has not experienced a recurrence 6 months postoperatively. |
In January 2007, a 38-year-old Chinese female diagnosed with right breast cancer underwent breast-conserving surgery and axillary dissection for an invasive ductal carcinoma that was estrogen receptor (ER) positive, progesterone receptor (PR) positive, HER-2 negative, and Ki-67 (25%–50%), with 4 metastatic lymph nodes in the 31 dissected lymph nodes. The pathological stage was IIIA (T2N2M0). After surgery, the patient received chemotherapy, radiotherapy, and hormonal therapy (tamoxifen) as adjuvant therapy. In December 2007, she developed three nodules in the right breast, and histology showed malignant cancer cells. She refused to undergo surgery due to personal reasons and chose to start capecitabine chemotherapy instead. Following five cycles of chemotherapy, the patient was revealed to have had a complete regression of the local tumor, and she then chose to perform a rigorous observation of the local tumor. By July 2009, she had again developed a new local lump in the right breast with progressive enlargement, but she did not undergo further inspections and treatment. Later, in September 2010, the patient was referred to our hospital with lung metastases, pleural effusion, multiple bone metastases, and asymptomatic BMs. Histopathologic examination of the lump in the right breast indicated that the tumor was ER positive, PR positive, and HER-2 negative. Magnetic resonance imaging (MRI) of the lump showed four hyperdense parenchymal metastatic lesions in the frontal, parietal, and cerebellum regions, with a diameter of 3–8 mm, along with a right frontal bone lesion and suspicious adjacent meningeal metastasis (). After a comprehensive consideration of treatment options and her poor performance status, we decided not to perform further cerebrospinal fluid (CSF) examination and chemoradiotherapy. She was treated daily with 1,000 mg of MPA from September 27, 2010 through November 23, 2010, the day she achieved a confirmed PR against the extracranial disease, to August 2011, when a follow-up of an MRI imaging of the brain showed a complete resolution of the brain parenchyma lesions (). The field of suspicious meningeal metastasis did not change significantly on the MRI scan, and the patient still did not have any meningeal metastasis-related symptoms. However, the lung metastases and local tumors of the right breast progressed, and then she stopped taking MPA. Subsequently, she was switched over to letrozole and goserelin acetate in August 2011, and this regimen showed a PR with a progression-free survival of 23 months. Regretfully, we could not evaluate the reaction of BMs to treatment further because the patient would not undergo a radiology examination of the brain during her follow-up. Nevertheless, that the patient did not exhibit any neurological symptoms during follow-up was an encouraging finding. |
In 2003, the Department of Oral Pathology and Surgery at the School of Dentistry, University of Athens referred a young 22-year-old female with Hajdu-Cheney Syndrome (HCS) to the Postgraduate Clinic of the Department of Periodontology, in order to receive periodontal treatment (Fig. ). The patient was diagnosed in 2001 with HCS after clinical, radiographic and histological examination (Fig. ). After gene examination of both parents, none of them was found bearing a mutation in the NOTCH2 gene []. Her physical examination showed that her height was 145cm and her weight was 45kg. The patient had thick coarse hair, low-set ears, small face and stature, thin lips, small mouth and short hands with clubbing of the fingertips (Fig. ). According to her medical history, the patient suffered from emphysema and allergic rhinitis, whereas oral intake of Vitamin D and calcium were prescribed daily for the treatment of osteoporosis [, ].\nDuring orthodontic treatment between the ages of 12 and 21 years, all of her first premolars were removed []. At the age of 20 years, the patient received non-surgical periodontal treatment (scaling and root surface debridement), as well as limited periodontal surgery in the lower anterior region [, ]. Detailed records regarding both orthodontic and periodontal treatment were not available. The patient was a non-smoker, visited her dentist every 6 months, brushed her teeth twice every day (Bass technique) and used dental floss and interdental brushes. At the time of the referral, the patient suffered from generalized advanced chronic periodontitis, increased tooth mobility and premature tooth loss []. Clinical and radiographic examination of both parents and her 4 years younger brother showed that the mother and the younger brother had normal dentition, whereas the father was diagnosed with chronic advanced periodontal disease with increased mobility of various teeth.\nThe patient was treated in collaboration with the Department of Prosthodontics. Clinical and radiographic examination of the patient revealed a number of significant findings. There was generalized horizontal bone loss of ~ 50%. However, alveolar bone loss around various teeth such as #4 (in place of #5), 14 and 24 was extensive (~ 100%). Tooth roots appeared short and cervical, whereas cervical resorption lesions were also evident (teeth #3, 10, 20 (in place of #19), 26) [, ]. The patient received non-surgical periodontal treatment in all four quadrants, which included scaling and root surface debridement. During this period, teeth #4, 14 and 24 were extracted due to extensive alveolar bone loss []. The maxilla was then rehabilitated with the placement of a provisional fixed partial denture of metal acrylic and the anterior region of the mandible with the placement of a Maryland bridge [] (Fig. ). Upon completion of the periodontal treatment, the patient was enrolled in a periodontal maintenance program.\nAfter careful consideration of the possible implications deriving from the patient’s condition (osteoporosis, generalized advanced periodontitis) and having taken her young age into account, we decided to proceed with the placement of dental implants, while implementing specific protocols such as longer healing periods. So, although in the current literature no other case of implant placement in a patient with HCS was described, in February 2005, a dental implant (Nobel Biocare, Replace Select Straight, TiUnite RP 4.3 x 13mm) was placed in the upper right first premolar region [] (Figs. , ).\nDuring the healing period, in March 2009, further teeth were extracted (#2,3,30). During the extraction of tooth #30, a bovine xenograft (Geistlich Bio-Oss Collagen 250 mg) was placed in the post-extraction site, in order to achieve ridge preservation [] and the region was rehabilitated with a resin-bonded bridge (Maryland bridge).\nFive years after placement and successful osseointegration of the dental implant in position #5, an additional implant (Nobel Biocare, Replace Select Tapered TiUnite Regular Platform (RP) 4.3 x 8mm) was placed in the upper right first molar region (Fig. ). Bone mineral density appeared physiological (Bone Type III) (Fig. ).\nSix months after implant placement, a porcelain fused to metal, three unit implant supported fixed partial denture 3 (4) 5 was placed in the upper right region (Fig. ). During this period of time, teeth # 18, 19 were extracted due to excessive bone loss.\nClinical and radiographic examination of the patient during the periodontal maintenance program in three months interval after implant placement revealed no abnormalities in the implant region. After successful oral rehabilitation of the posterior upper right region, 2 additional dental implants were placed in the posterior left region (during surgery tooth #20 - in place of #21- was extracted) and 1 in the posterior right region of the mandible (Straumann Standard Platform (SP) Tissue Level) (Figs. -).\nSix months after implant placement, a porcelain fused to metal, three unit implant supported fixed partial denture [] 19 18 was placed in the left region of the mandible, whereas a porcelain fused to metal implant supported crown was placed in the right region of the mandible (Fig. ).\nFive years after implant placement, clinical and radiographic examination of the patient during the periodontal maintenance program (in three months interval) revealed no abnormalities (Figs. -).\nFor the reader’s better understanding, Table presents the patient’s detailed dental treatment chronologically. |
A 40-year-old female, non smoker was referred by her family physician with migraine-type headache complaints and mild nasal congestion. The pain was located over the forehead and behind the left eye. Headaches occurred once every 3 weeks, triggered by weather and barometric changes with mild improvement during the menstruation. The duration of the headache was 3 days approximately and the pain was not associated with nausea, photophobia, vertigo or tinnitus. Its intensity was 9 on a 0–10 visual analogue scale.\nThe patient reported nephrotic syndrome at the age of 3, for which she had been on prednizolone for 10 years. A history of recurrent episodes of rhinosinusitis was also obtained.\nNasal endoscopy revealed a mild septal deviation, a right concha bullosa of the middle turbinate and a paradoxically curved middle turbinate on the left side. Coronal computed tomography (CT) scan confirmed the above findings and additionally revealed a superior concha bullosa and mild mucosal disease on the left side (Fig. ).\nThe patient underwent a detailed laboratory examination to exclude any other possible causes of headache. Whole blood cell count, urinalysis, thyroxin level, biochemical tests, tumor markers, as well as Mantoux test and monotest were normal. Chest radiography, electrocardiography, and ultrasonography of the thyroid gland were also normal. Biochemical and serologic tests of hepatic dysfunction were negative. Serologic tests of complement fixation titers of the plasma antibodies against various common viruses were performed and were found normal as well.\nThe patient underwent nasal rigid endoscopy after application of local anesthetic and decongestant, which revealed the presence of a large superior concha in close contact with the nasal septum (Fig. ). Direct application of local anesthetic (1% tetracaine hydrochloride solution) at the point of contact between the superior concha and the nasal septum improved headache by 4 points (score 5 at the scale of 0–10). Injection of local anesthetic (0.5 ml of 2% xylocaine with epinephrine 1:100.000) into the superior turbinate under endoscopic visualization eliminated the pain completely.\nThe patient was given endonasal steroids for 20 days without improvement. Then she was advised surgical intervention which she initially denied. The patient was followed for 3 months without any improvement and she, finally, decided to undergo surgery. Septoplasty and bilateral endoscopic sinus surgery was performed, including partial removal of both the pneumatized middle turbinates in conjunction with gentle lateralization and resection of the lower half of the left superior turbinate. The interior of the superior turbinate was found devoid of fluid or any other content. The patient reported prompt relief of her headache and at 13 months of follow-up postoperatively she remains free from headache or any other nasal symptoms. Although the patient did never report anosmia, she was examined by using the "Sniffin' sticks" test 1-year-postoperatively []. The examination showed that odor threshold, odor discrimination and odor identification were within normal limits. It appears, thus, that although part of the olfactory mucosa might had been removed by the partial resection of the superior turbinate, sufficient olfactory epithelium had remained intact, resulting in preservation of normal olfactory function.\nAlthough pneumatization of the middle nasal turbinate has been occasionally reported [], pneumatization of the superior and inferior turbinates are very rare findings [,]. The presence of a superior concha bullosa is not always recognizable with nasal endoscopy alone, due to the minimally accessible area of the upper nasal cavity. For this reason, the superior nasal turbinate has been called the forgotten turbinate []. Coronal CT-scan provides useful information for this inaccessible area.\nAssociation of a massive extensively pneumatized superior turbinate with headache is very rare. In these cases the superior turbinate is forced anteriorly and inferiorly at the area between the middle turbinate and the nasal septum, leading to intranasal mucosal contact []. Although the phenomenon of referred headache owed to intranasal mucosal contact was recognized as early as 1888 by Roe [] and has been since, occasionally, reported, with the advent of functional endoscopic sinus surgery and CT imaging, resurgence of interest in headache of nasal origin has been observed. Stammberger and Wolf [] reviewed the possible mechanisms involved in the genesis of referred headaches in the nasal area. According to them, afferent fibers from pain receptors in the nasal mucosa terminate in the same group of sensory neurons in the sensory nucleus of the trigeminal nerve, as fibers innervating cutaneous receptors, located at several peripheral segmental dermatomes of the ophthalmic and maxillary divisions of the trigeminal nerve. These two common pathways converge along the same final neurons to a common area of the cortex. Accordingly, the cortical center can not distinguish the original peripheral source of the pain impulses and they may be misinterpreted as coming from other skin areas, such as the temple, the zygoma or the forehead. The pain may be perceived also from other end-organs innervated by terminal branches within the trigeminal system, such as dura, intracranial and scalp vessels or the eye [].\nAn important issue in the generation of headaches of nasal origin is mediation of neuropeptides, such as substance P [,,]. These may be released by mechanical pressure induced in areas of contacting opposing mucosal surfaces, such as the superior turbinate and the nasal septum. Substance P can be liberated at both the central and the peripheral ends of a sensory neuron, mediating not only central pain reflexes, via afferent C fibers, but at the same time local reflexes at the nasal mucosa, resulting from reverse impulses and manifestating as vasodilation, extravasation of plasma, hypersecretion, and smooth muscle contraction. This axon reflex can explain why an initial small localized lesion, such as a limited mucosal lesion or area of nasal mucosal contact, may trigger severe long-standing headaches, frequently projecting to different areas of the head.\nMany areas of the nose and the paranasal sinuses have been implicated as causes of referred headaches, including superior concha bullosa as a rare occurrence. Clerico [] was the first who suggested the superior turbinate as a source of referred headache, with features consistent of common migraine. Two more reports on this issue followed [,]. Clerico [] proposed that before surgery, the application of local anesthetic and/or decongestant (diagnostic block) on the area of the superior turbinate, under endoscopic visualization, might confirm this anatomic variation as the source of headache. We performed this test, and although significant reduction of the pain was obtained, the pain was not completely eliminated. This was probably due to the fact that local decongestants and anesthetic sprays are deposited primarily in the anterior half of the nasal cavity and may not adequately reach the superior turbinate. Complete relief of headache was obtained only after injection of local anesthetic into the superior turbinate under endoscopic guidance. The positive finding of this diagnostic test and resolution of the symptoms after surgical intervention prove the association of our patient's headache with the presence of the massive superior concha bullosa.\nFinally, the presence of a nasal osteoma as a rare cause of headaches of nasal origin should be mentioned. Paranasal sinus and intranasal osteomas are histologically benign and slow-growing tumors, which are usuallly asymptomatic, but when they enlarge they may produce pressure symptoms such as headaches. They occasionally cause obstruction or infection and may grow into the orbit or intradurally causing neurological manifestations. Paranasal sinus osteomas usually occur in the frontal sinus and less frequently in the other sinuses []. A few cases of intranasal osteomas were also reported, mainly in the middle turbinate and once in the superior turbinate []. All cases of turbinal osteomas were characterized by accompanying headache, probably due to the same pathogenetic mechanisms implicated in headache caused by the presence of a pneumatized superior concha, as previously mentioned. CT scan may assist in differential diagnosis by depicting the lesion and providing detailed information concerning the bony structures of the region. |
In 2008, a 37-year-old male patient was examined at our institution for irregular postprandial dyspeptic complaints and pain in the epigastrium which had lasted for several months and receded spontaneously. Alternating stools occurred intermittently. Family medical history was insignificant and the patient had never suffered a serious illness. Neither physical nor laboratory examination revealed any pathological findings. Gastroscopic examination revealed multiple (several dozen) irregular flat polyps from 5 mm to approximately 15 mm in size, rather atypical in appearance with a central depression in the area of the descending duodenum, in locations except the ampulla of Vater (Figures and ). Histological examination of these lesions showed structures of the tubular or tubulovillous adenoma with mildly to moderately dysplastic epithelium and numerous Paneth cells (Figures and ).\nSince we assumed that the patient might suffer from FAP, he was first subjected to colonoscopy, the results of which were normal. This examination was followed by push enteroscopy, which confirmed the presence of polyps in the area of the duodenum only. Capsule enteroscopy ruled out the presence of polyps in the aboral part of the small bowel.\nSubsequently, a genetic examination for AFAP was initiated. A DNA analysis with direct detection of the most common mutations in the APC gene, using the PCR technique, did not confirm 5 bp deletion at codons 1309 and 1061 of the APC gene. Direct diagnosis of mutations in the APC gene using the DGGE method did not confirm a mutation in the screened part—exons 1–14 and exon 15 (approximately up to codon 1770)—of the APC gene. Afterwards we screened the patient for germline MYH mutations using the denaturing high-performance liquid chromatography (DHPLC) in combination with sequencing. No novel pathogenic mutation has been identified. Over several sessions, the polyps were removed endoscopically—large ones by means of mucosectomy and small ones by means of argon plasma coagulation. Following the endoscopic therapy, we checked the patient regularly each six months in the first year; at present, he comes for a checkup once a year. In each successive session, several (up to five) very small adenomas were found, which were removed using argon plasma coagulation. During the last checkup this year, two small polyps up to 4 mm in size were removed. The patient has no subjective complaints; the successive laboratory results are within the norm. |
A 60-year-old man with mental retardation of unclear origin who was otherwise healthy suffered a focal seizure with speech disturbance. Two intracerebral lesions were identified by magnetic resonance imaging (MRI) of the head (Figure ).\nThe patient's neurological status on admission was normal. There were no clues to phakomatosis in the patient's or in the family history. Neither did the clinical findings point in this direction. No further seizures occurred after initiation and starting phenytoin therapy.\nInitial MRI demonstrated a contrast-enhancing lesion in the left frontal lobe and a smaller lesion in the right frontal lobe (Figure ). No other focal lesions were identified. Laboratory tests were normal except for elevations of the following parameters: D-dimer level of 254, neuron-specific enolase level of 13.1, and lambda and kappa light chain levels of 1.63 and 4.64, respectively. The CSF cell count and protein content were normal.\nSince the lesions had no mass effect, initially a stereotactic biopsy was obtained from the left frontal lesion. Histologically, a semimalignant melanocytoma with the differential diagnosis of a MPNST was diagnosed. The lesion was then removed microneurosurgically. Postoperatively, the patient underwent whole-brain irradiation (30Gy). Due to the advanced stage of the malignancy and to gain control over further intracerebral metastasis, which were not visible on the MRI, no local radiotherapy such as radiosurgery was chosen. No postoperative or radiation-related complications were observed.\nFluorodeoxyglycose positron emission tomography (FDG PET) identified no body lesions except for an area of increased accumulation lateral to the right jugular vein, which corresponded to an enlarged lymph node, suggesting a nodal metastasis on MRI. PET even failed to demonstrate the right frontal lesion that was still present prior to cerebral irradiation. Only whole-body MRI (T2WI) identified several structures of increased signal intensity in the right thigh. One of the lesions was contiguous with the sciatic nerve (Figure and ). The radiologic criteria were indicative of a peripheral nerve tumor, suggesting that this was the primary tumor. Spinal MRI demonstrated further metastases at the level of S1 and S2 but no relationship to spinal nerves (Figure ).\nBased on the patient's poor prognosis due to extensive local tumor spread and the presence of distant cerebral and vertebral metastases and a high risk of neurological deficits associated with a resection of the thigh tumors, a removal was considered unjustified. Stigmata of neurofibromatosis were excluded, as were pulmonary and visceral metastases.\nThe first follow-up examination was performed after 3 months. MRI identified no tumor recurrence in the left frontal lobe and no progression of the lesion on the right (Figure ). The patient had no clinical or neurological symptoms and suffered no seizures on continuous phenytoin medication (300 mg/day). At the last follow-up 11 months later, MRI showed unchanged cerebral findings and no progression of the lumbar vertebral lesions. However, there was an increase in the size of the cervical lymph node metastasis, and MRI for the first time demonstrated metastases in the area of the right thigh. Nevertheless, the patient continued to be free of neurologic deficits or epileptic seizures and no further therapy was initiated.\nHematoxylin-eosin (H&E) staining demonstrated tumor tissue with spindled epithelioid cells, some of which contained melanin (Figure ). The cells were arranged in nestlike clusters with an altogether heterogeneous appearance. Immunohistochemically, strong expression of vimentin (dilution 1:600; Zymed, Wien/Austria) and S-100 (dilution 1:6000; DAKO, Glostrup/Denmark) was demonstrated (Figure ). The pigmented cells were positive for HMB45 (dilution 1:500; DAKO, Glostrup/Denmark) and there was isolated expression of EMA (dilution 1:100; DAKO, Glostrup/Denmark). The overall expression of Ki67 antigen (dilution 1:200; DAKO, Glostrup/Denmark) was low, but some foci with an index of 30% were identified. There was no immunoreaction to LU-5 (cytokeratin; dilution 1:500; Biomedicals, Augst/Switzerland), NF (neurofilament; dilution 1:200; Zymed, Wien/Austria), or SYN (synaptophysin; dilution 1:150; BioGenex; San Ramon/U.S.A.). Furthermore electron microscopy investigation showed a basal lamina, strongly indicating peripheral nerve origin. The histological diagnosis of MPNST was based on the demonstration of spindled cells and their arrangement, the pattern of immunoreactions as well as the electron microscopy investigation. Due to the overall low expression of the Ki67 antigen and the histological characterization, the tumor was graded WHO°I, according to the WHO classification for soft-tissue tumors[]. The histological diagnosis was verified by several reference pathologists. |
A female eight-year-old local Libyan cat was admitted to the Veterinary Teaching Hospital at the Faculty of Veterinary Medicine, University of Tripoli–Libya. The cat presented with a soft swelling in the rostral part of the skull and anorexia. A thorough clinical examination was carried out. The radiographical examination was performed to investigate bone involvement, and the right lateral view of the skull was acquired. In addition, a lateral chest radiograph was taken to investigate the presence of lung metastasis. Nasal swabs were collected from the nasal cavity and submitted for microbiological examination to investigate a fungal or bacterial infection. The decision for euthanasia was made, and the cadaver was submitted for postmortem and histopathological examinations.\nThe clinical examination revealed that there was a severe soft swelling involving the left craniorostral area of the skull causing pressure and deforming the left orbital area (see ). In addition, there was malodorous, mucohemorrhagic nasal discharge with severe dyspnea and stridor. The auscultation did not reveal any abnormal lung sounds. No signs of other body systems involvement were noticed.\nThe radiographic examination of the skull revealed that there was bone lysis involving the nasal bone with no evidence of bony proliferation (see ). In addition, the thorax radiograph showed no signs of tumor metastasis to the lung (see ).\nOn the microbiological examination, the culture plates showed no fungi or yeast growth on Sabouraud Dextrose Agar. However, there was bacterial growth on blood and MacConkey agar. The isolates were Gram-negative rods, lactose fermenting on MacConkey agar, and oxidase negative. Analytical Profile Index (API) 20E biochemical reactions showed the characteristics of Enterobacter species (data not shown).\nAt necropsy, the rostral part of the head was enlarged (see ). In the skull section, there were nasal deformity and partial bilateral obstruction of nostrils due to the presence of a tumoral mass with a mucohemorrhagic exudate as well as a proliferation of soft tissue, part of the tumor, involving the nasal structures. This caused bone deviation from right to left, affecting the eyeballs (see ). Blood-filled multilocular cavities of different sizes and shapes were present. No signs of metastasis were observed in the thoracic and abdominal cavities, cervical lymph nodes, lung, liver, or kidney (data not shown).\nThe histopathological examination has revealed the characteristics of poorly differentiated OSA. The tissue sections showed highly proliferating anaplastic mesenchymal cells in different shapes and types with pronounced osteogenic properties, where different stages of bony differentiation were seen. Blood cysts and spaces of variable shape and size were seen throughout the section. In addition, osteoclast-like tumor giant cells, angiogenesis, cartilaginous metamorphosis, and multiple necrotic areas were detected (see ). No relevant microscopic lesions were noticed in other major body organs. |
An 80-year-old man, who was followed up for peripheral arterial ischemic disease and iliac aneurysm for 2 years, presented with edema and ecchymoma on the left anterior surface of the thigh for 4 days. A history of distal gastrectomy for gastric cancer 2 years ago and low cardiac function without coronary disease was noted. The patient was previously a smoker, and had received cilostazol. An endovascular procedure was planned for the right ischemic limb after postoperative recovery from gastric surgery. The right common femoral artery (CFA) and superficial femoral artery (SFA) were occluded with an ankle-brachial index value of 0.3. The right common iliac artery had an aneurysmal change of 34 mm in diameter. The measurement of psoas muscle mass index at the third lumber vertebrae level was 4.62 cm2/m2.\nThe patient looked pale but was conscious. He was thin and weighed 40 kg (body mass index, 14.5) due to loss of appetite after gastric surgery; however, his left thigh was reddish, edematous and painful (). Hemodynamics, such as blood pressure and heart rate, were stable. Blood tests revealed a hemoglobin level of 3.41 mmol/l. Ultrasonography showed a 72 × 52 mm PFAA with a thick thrombus and hematoma extending into the adductors (). A venous thrombus was also observed in the left femoral vein. Enhanced computed tomography (CT) revealed a ruptured left PFAA 64 × 54 mm in diameter (). In addition, right iliac artery aneurysm and right CFA and SFA occlusion were also observed.\nEmergency surgery was performed due to an aneurysmal rupture associated with severe anemia. The junction of the profunda femoris artery (PFA) and the terminal portion of the aneurysm were marked using ultrasonography preoperatively. The left CFA, which was severely calcified, and SFA were exposed. PFA was also exposed at the junction and caudal end of the aneurysm. The femoral vein and its branches were engorged. Heparin administration followed by clamping of the PFA inflow and outflow of the aneurysm was performed. The aneurysm was filled with an atheroma and hematoma. A branch containing retrograde blood flow to the aneurysm was ligated. Aneurysmal PFA was interposed with PROPATEN 6 mm (W. L. Gore Associates, Inc., CA, USA). Transfusion was performed during surgery due to severe anemia.\nThe patient’s postoperative recovery was uneventful. On postoperative Day 5, enhanced CT showed an interposed PFA with no complications, perforating branches originating from the distal portion of the interposed vessel and a reduction in the hematoma (). The patient was discharged on postoperative Day 7. |
This is a 66-year-old patient, with four pregnancies, three normal deliveries and one abortion. She smoked from the ages of 10 to 51 years and had no family history of breast carcinoma. She reported the presence of progressively growing nodules in both breasts in 2005. In 2006, she underwent a mammography (Figure ) with suspicious findings and was referred to the hospital. She did not visit the hospital for fear of a positive diagnosis. In December 2006, she underwent another mammography, and was examined again in February 2007. Mammography showed a regular 9-cm nodule in the right breast, without skin retraction, with elastic firm consistency, diffuse bulging breast and negative axillary lymph nodes. Mammography also noted a 6-cm nodule in the left breast with bulging and skin retraction located in inter-medial quadrants and retro areolar region, hardened, partially mobile and negative axillary lymph nodes. She was referred to preoperative assessment and surgery. Incisional biopsies of both breasts were performed. Biopsy of the left breast revealed the presence of invasive ductal carcinoma (pT3pn0, pMx), Nottingham grade II, nuclear grade III. Biopsy of the right breast showed a probable benign phyllodes tumor. No core needle biopsy was performed because the technology was not available in our clinic.\nBased on the diagnosis and the size and location of the lesions, we decided to perform a simple mastectomy in the right breast and modified Madden mastectomy in the left breast.\nThe anatomopathological final result showed the presence of benign phyllodes tumor in the right breast (Figure ), which measured 9 cm in its longest axis, and invasive ductal carcinoma Nottingham grade II, nuclear grade III, which measured 7 × 6 cm in the left breast. Further evaluation indicated negative axillary lymph nodes and absence of metastasis (Figure ).\nFor histological assessment, fragments were dipped in Gender liquid at 4°C for 24 h and were cut into small pieces of 1 mm3 and post-fixed in a 1% OsO4 solution for 2 h, dehydrated and embedded in araldite. Silver or gray thin sections (60 to 90 nm) were selected on a Porter-Blum MT-B ultramicrotome. The ultra-slices were mounted on copper silver grids with 200 patches and stained with uranyl acetate and lead citrate. The fragments were fixed in formaldehyde 10% at 4°C. Approximately 24 h later the fragments were cut in cryostat. This protocol followed the routine procedures of our laboratory [-].\nFigure shows the histological evaluation of the of phyllodes tumor. Figure shows the histological results of the carcinoma in the left breast focusing on steroid Her-2/neu-receptor. Preoperatively, history and physical exam were normal; bilateral mammography, abdominal and pelvic computed tomography (CT), usg total abdominal and pelvic, chest imaging, and biochemical tests (complete blood count, platelets, liver function tests, and alkaline phosphatase) were all normal. However, bone scan indicated a low probability metastases.\nThe patient was given adjuvant therapy composed of radiotherapy and chemotherapy for phyllodes tumor and carcinoma, respectively. Chemotherapy included six cycles of the FAC regimen (5-fluorouacil, doxorubicin, dyclophosphamide). To date, the patient has not shown any clinical or laboratory alterations. |
The patient is a 51-year-old woman who underwent right hip arthroscopy with labral repair and femoroplasty with cam lesion debridement. After failing years of conservative management for unremitting right hip and groin pain, she elected to undergo right hip arthroscopy. Following surgery, she was made partially weight-bearing with an early range of motion to assist in recovery. She experienced an uneventful postoperative course until day five. While cleaning her kitchen, she extended and externally rotated her operative leg resulting in sudden and severe right hip pain accompanied by a fall to the ground and an inability to bear weight.\nUpon presentation, her right leg was shortened and externally rotated with intact neurovascular function. Radiographs revealed right anterior hip dislocation without evidence of acute fracture (Figure ).\nShe was consciously sedated, closed reduced, and placed in a knee immobilizer (Figure ).\nPostreduction computed tomography (CT) revealed an impaction-type fracture in the anterior aspect of the femoral head (Figure ).\nMagnetic resonance imaging (MRI) was also obtained, which revealed an impaction fracture involving the anterior margin of the right femoral head and neck junction (Figure ).\nSurgical pathology of the cam resection and femoroplasty ruled out the presence of bony pathology. By one week postoperatively, she was able to ambulate with a walker. Physical examination revealed painless hip flexion greater than 100 degrees, extension to neutral, internal rotation to 35 degrees, and abduction to 45 degrees. However, she still experienced a sensation of anterior hip popping and had crepitus anteriorly. Initial MRI and CT scan were re-reviewed, and the labral repair appeared to be intact. She was advised to limit external rotation and hyperextension of the hip with protected weight-bearing and crutch use.\nBy six weeks postoperatively, her preoperative anterior hip popping and crepitus had entirely resolved. She experienced no pain in the anterior hip capsule and no apprehension with hyperextension or external rotation. The patient had a stable gait without the use of assistive devices and was able to perform a full crouch without difficulty.\nThe patient did not remain symptom-free during her continued follow-up visit. By eight weeks postoperatively, she experienced a re-intensification of her right hip pain that she characterized as a deep ache in the joint. Her hip occasionally locked and was accompanied by a sense of instability. She denied a history of trauma - other than the recent hip dislocation - or inciting events. Physical examination revealed palpable crepitus in the anterior acetabular margin at 60 degrees to 90 degrees of flexion. Both internal and external rotation aggravated these symptoms. The patient could ambulate, although she preferred to take small steps with her right lower extremity to reduce pain. Radiographs of the right hip revealed a well-maintained joint surface and joint line architecture with no gross bony abnormalities.\nSubsequent MRI revealed right iliopsoas bursitis with filling defects in the joint recesses and the iliopsoas bursa suspicious for synovial proliferation and small intra-articular bodies (Figure ).\nAdditionally, new-onset small focal cartilage loss and osteochondral impaction injury in the femoral head secondary to microtrauma and instability were identified. Her symptoms were managed conservatively with activity modification and physical rehabilitation. Complete resolution of symptoms was reported by a six-month follow-up, and no further dislocations or instability had been reported at 12 months. |
A 42-year-old female patient, presented to our gynaecology outpatient department with complaints of lower abdominal pelvic pain and backache, dyspareunia, and difficulty in passing urine for the last 6 months. She had suprapubic pain with constant backache and heaviness in the perineum. Patient took medication from local practitioners for symptomatic relief. She presented to us when already catheterised with self-retaining Foley's catheter from outside for retention of urine for one day. There was history of similar episodes of retention of urine 4-5 times in the last 6 months for which she had to be catheterised once and again for about 5–7 days each time. The catheter was removed after toning of bladder.\nPatient was para one with one live issue 20 years old conceived spontaneously and delivered by normal vaginal delivery and had three spontaneous first trimester abortions, thereafter. Menarche was attained at the age of 13 years. Patient had irregular menstrual cycles occurring at every 15–20 days with bleeding lasting for 4-5 days; the amount of blood flow was normal. There was no previous illness or surgical intervention. Patient was a vegetarian, nonsmoker, nonalcoholic with normal bowel habits. She was moderately built and nourished. General condition of the patient was stable with mild pallor. Vitals were normal. Abdominal examination revealed a firm mass of 16-week size arising from the pelvis deviated more towards the left side. The mass had smooth surface with restricted mobility. On pelvic examination, cervix was hitched below the pubic symphysis, bleeding was present through the cervical os. Foleys catheter was in situ. Uterus was acutely retroverted; a mass of about 16-week size, irregular, firm in consistency was felt through posterior and the left lateral fornix. The uterus could not be differentiated from the mass. Base line investigations and renal function tests of the patient were normal. Ultrasonography revealed a large uterine fibroid of size 14 × 9 × 8 cm, which was subserous with normal bilateral adnexae. Right-sided hydroureteronephrosis was also reported for which IVP was done showing right-sided ureteric obliteration with bladder neck compression. Considering the above clinical findings and investigations, provisional diagnosis of subserous fibroid was made and abdominal hysterectomy was planned. A vertical midline infraumbilical incision was employed. Intraoperatively, uterus was found to be just bulky. A large retroperitoneal firm mass of size 10 cm × 8 cm was found arising from the posterior surface at the level of internal os (). Total abdominal hysterectomy was carried out along with removal of the large retroperitoneal mass (). Complete haemostasis was achieved and abdomen closure was done in layers. Cut section of the hysterectomy specimen showed a few small intramural fibroids on the anterior and the posterior wall of the uterus. The retroperitoneal mass depicted whorled appearance with no apparent degeneration or calcification. The hysterectomy specimen and the retroperitoneal mass were sent for histopathological examination.\nThe postoperative period of the patient was uneventful. The stitch removal was done on the seventh postoperative day. The stitch line was healthy with good healing. Histopathological examination confirmed the smooth muscle cell origin of the retroperitoneal mass consistent with diagnosis of retroperitoneal leiomyoma (). |
A 53-year-old Chinese female visited our hospital after noticing a mass in her left breast for one year and another mass in her right breast for five years. No family history of breast cancer was noted. Clinical examination showed a 4-cm left breast tumor, which was immobile, solid and irregular, without significantly enlarged accessible left axillary lymph nodes. A 4.5-cm immobile, solid, and cauliflower-like mass was found in the areola of the patient’s right breast. This mass exhibited skin ulceration and apparently had enlarged right axillary lymph nodes that formed an approximately 5-cm firm and immobile mass with irregular boundary. MMG and US results showed the bilateral breast masses and right axillary lesion suspicious for malignancy. Moreover, the left axillary lymph nodes were also reported to be suspiciously involved. Apocrine carcinoma was diagnosed in both breasts by core needle biopsy, and IDC-NOS was also found in the patient’s right axillary lesion. After 3 doses of cyclophosphamide epirubicin docetaxel (CET) neoadjuvant chemotherapy, the patient underwent bilateral modified radical mastectomy followed by adjuvant chemotherapy of the same regimen.\nMastectomy specimens with axillary contents were also placed en bloc in formalin for 48 h, and were then dissected. The right mastectomy specimen measured 20.5 cm × 19 cm × 4.5 cm (). A mass measuring 1.8 cm × 1.2 cm × 0.5 cm was identified in the areola of the breast. The cut surface of the tumor revealed firm and gray tissue with irregular boundary. Seventeen lymph nodes ranging from 0.3 cm to 2.5 cm in diameter were found in the right axilla. A 2.1-cm mass was also noted in the axilla. This mass was far from the breast parenchyma and its tissue texture was different from that of the other lymph nodes on the cut surface. The left mastectomy specimen measured 22 cm × 18 cm × 2 cm (). A mass measuring 1.5 cm × 1 cm × 0.7 cm was located on the side of the nipple. The mass was firm, with irregular boundary on the cut surface. Sixteen lymph nodes ranging from 0.3 cm to 1.8 cm in diameter were identified in the left axillary content.\nMicroscopic examination revealed that the tumors in the right () and left () breasts were apocrine carcinoma, with GCDFP-15 protein expression in each tumor (). These carcinomas exhibited grade II chemotherapy reaction in the Miller-Payne system[]. Ductal carcinoma in situ was also noted admixed with and adjacent to the invasive carcinoma in each breast (). The tumors spread to 1 of the 17 lymph nodes in the right axilla, and to 6 of the 16 lymph nodes in the left axilla. The right axillary mass consisted of IDC-NOS, with grade II chemotherapy reaction, adjacent to benign ectopic breast tissue (). No lymphoid tissue was identified in the mass lesion. The mass was far from the pectoral breast parenchyma.\nThe invasive components of carcinoma were also assessed for hormonal and proliferative marker expressions following the same immunohistochemistry procedures used in case one. The right breast tumor was negative for ER (<1%) and PR (<1%), and exhibited a HER2 reaction with an intensity of 2+. The tumor was positive for P53, with 90% of nuclei stained and the Ki67 labeling index was 15%. The right axillary accessory breast carcinoma was negative for ER (<1%) and PR (<1%), and showed stronger HER2 reaction (3+). This carcinoma had a lower P53 labeling (70%) and a higher Ki67 labeling (50%). The left breast tumor was negative for ER (<1%) and PR (<1%), and positive for HER2 (3+), with a Ki67 labeling index of 20% and a P53 labeling index of 70%. HER2 gene amplification was identified in all tumors via fluorescence in situ hybridization (FISH). All tumors were classified as HER2+ in molecular subtyping. |
A 68-year-old gentleman presented to the ED of a district general hospital in London with a history of worsening jaw pain following a fall at home 10 days prior, for which he had not sought any prior medical advice. History was difficult to obtain as the patient was a non-English speaker, however, reported an inability to eat and drink since the injury. Observations were within normal range and the patient was self-ventilating. On examination, he was found to have a bilaterally tender mandible to palpation with significant left-sided mandibular swelling. He was also found to be in diabetic ketoacidosis as a new presentation of diabetes mellitus (DM), which was stabilised with a sliding scale of insulin.\nA CT scan was performed which showed a displaced left mandibular condylar fracture, undisplaced mandibular symphysis and right mandibular condylar fracture. It also revealed a small collection within the floor of the mouth, and significant soft tissue swelling within the left masticator, parotid and parapharyngeal space displacing the airway to the right.\nAt this stage, a referral was made to our tertiary oral and maxillofacial surgery department due to suspected Ludwig’s angina, and the patient was transferred to our facility. On examination, the patient had notable swelling and tenderness across the left mandible and submandibular area, with some associated tenderness and swelling on the right side, a raised and tender floor of the mouth, with a maximum mouth opening of 4 cm.\nThe patient underwent incision and drainage of Ludwig’s angina in the operating theatre, via external bilateral submandibular incisions, revealing a large amount of pus in the submandibular, sublingual, submasseteric and left parapharyngeal spaces on the left side. The mandibular fractures were repaired with plating via an extra-oral symphyseal approach, and six Penrose drains were placed prior to closure. Due to ongoing airway swelling, the patient returned to the ICU intubated where he remained for four days and was extubated prior to step-down to the ward without further need for tracheostomy.\nRecovery was protracted, and the gentleman remained an inpatient for a further 48 days. There was a significant delay to the healing of the left neck wound, with multiple courses of antibiotics, including piperacillin/tazobactam (Figure ). CT neck with contrast 20 days post-operatively showed two complex intercommunicating abscesses in the left neck occupying the visceral space and the plane superficial to the sternocleidomastoid that were not amenable to drainage (Figure ), and the patient received twice-daily washout of the wound in addition to antibiotic therapy. The wound required debriding in the ward and was eventually closed 28 days post-operatively over a Redivac drain (Figure ). Healing was complicated by a new diagnosis of type one DM and subsequent poor glycaemic control, which rendered the patient immunosuppressed. |
A 66-year-old man had been diagnosed with Ta bladder cancer 6 years before he complained of dry cough in July 2009. He had a history of recurrent non-muscle-invasive bladder tumors and had therefore undergone 7 transurethral resections (TURs) and had received intravesicular chemotherapies (8 cycles of weekly mitomycin-C after the 4th TUR and 5 cycles of biweekly pirarubicin after the 5th TUR). All tumors were <1 cm, well pedunculated, and papillary. The number of tumors ranged from 1 to 6 in each respective TUR. The pathological findings of all TURs indicated the presence of urothelial carcinoma (stage Ta without carcinoma in situ, grade 1 or 2) without lymphatic or vascular invasion. The last TUR in January 2009 showed the same findings as the previous TURs, i.e., there were 3 tiny papillary tumors located at the right lateral wall, at the posterior wall, and adjacent to the left ureteral orifice, and pathological examination indicated results similar to those of the previous TURs. Chest radiography at 6 months after the last TUR detected a round nodule (diameter, 7.5 cm) in the right lower lung. We carefully rechecked the chest radiograph obtained in April 2008, which showed a small nodule (diameter, 1 cm) in the same area. These observations suggest that the lung metastasis had occurred more than 1 year previously. The initial diagnosis based on the computed tomography findings was primary lung cancer (). Therefore, initial treatment consisted of video-assisted thoracoscopic lobectomy. The histopathologic features of the pulmonary lesion and the TUR specimen of the bladder cancer were qualitatively similar. Immunohistochemistry showed that both the TUR specimen and the pulmonary lesion were positive for the urothelium-specific protein uroplakin Ia (UP-Ia) [] (). On the basis of these findings, the patient was diagnosed with pulmonary metastasis of recurrent Ta bladder cancer. Subsequently, he received 2 cycles of postoperative chemotherapy with the same gemcitabine and cisplatin regimen reported by von der Maase et al. []. Although we had planned 3 cycles of chemotherapy, the patient refused the third course. His bladder cancer recurred at 3 and 8 months after chemotherapy and hence he underwent TUR both times. The results of the pathological examination were the same results as for the previous TURs. Two and a half years after chemotherapy, chest and abdominal computed tomography once every 3 months detected no recurrence of the pulmonary lesions or other distant metastasis. |
A 57-year-old male patient presented with a left lumbal pain for 3 days. Physical examination with palpation revealed firm and mobile mass in upper left quadrant of the abdomen. No costovertebral tenderness was present. Urinalysis showed 3 erythrocytes. Laboratory data were as follows: blood urea nitrogen 16 mg/dL, creatinine 0.9 mg/dL, and hemoglobin 13.3 g/dL. Ultrasonography demonstrated a 14 cm vascularized, cystic, space-occupying formation with septations and solid components in middle and lower poles of the left kidney. Computed tomography identified a 14 × 11 cm cystic, space-occupying formation with many thick septae, which originated from anterior cortex of the left kidney and reached the level of pelvic inlet (). Doppler ultrasonography showed patent main renal vessels and vena cava, none with thrombus within. Thoracic tomography showed a millimetric nodule in the left lower lobe of the left lung. That finding was not considered metastatic, and a followup was deemed suitable for it. The patient was operated with left radical nephrectomy. Macroscopically, the nephrectomy material together with the surrounding fatty tissue weighed approximately 1500 grams. It was noted that the intact kidney tissue was restricted to a small area, and other areas were completely involved by the tumoral formation. The tumor was measuring 14 × 12 × 11 cm. It had a central necrotic zone on cross-section and was discharging a serohemorrhagic fluid. The tumor was observed to be well demarcated from the intact renal tissue by a smooth border and to have a pseudocapsule. Microscopically, tumoral cells had ovoid, round nuclei, coarse chromatin structure, and a narrow eosinophilic cytoplasm (). The tumor contained patchy areas of necrosis. Two to three mitoses were counted on 10 high power fields. In immunohistochemical studies, tumoral cells showed strong reaction with CD34 and CD99. Less than 1% of cells showed nuclear positivity with Ki-67 (). Despite repeated stainings with vimentin, no clear tumor evaluation could be made due to artifacts. The tumor was negative with Bcl-2, desmin, HMB-45, S100, FVIII, and CD31. Ewing sarcoma could not be ruled out. Molecular studies revealed no fusion related to the diagnosis of Ewing sarcoma. Histopathological, immunohistochemical findings, and molecular studies made the diagnosis of a solitary fibrous tumor. The patient is now currently free of disease at the 26th month of followup. |
A 68-year-old Caucasian male presented to our department with a two-month history of a small palpable nodule at the inferior angle of the right scapula. His medical history was remarkable for arterial hypertension.\nPhysical examination revealed a well-defined, non-tender and relatively mobile nodule at the inferior angle of the right scapula. There were no signs of infection and the overlying skin was normal. The remainder of the clinical examination was unremarkable. Ultrasonography demonstrated a well-circumscribed hypoechoic mass measuring 1.8 × 1.5 cm. Full blood count, biochemical tests and tumor markers were within the normal range.\nA surgical resection with wide margins of at least 2 cm was performed. Histological examination revealed a tumor measuring 1.8 × 1.5 × 0.7 cm consisting of elongated malignant cells characterized by nuclear polymorphic figures combined with mitoses. The surgical margins were free of disease. On detailed immunohistochemical analysis the tumor cells stained positive for smooth muscle actin (SMA), a1-antitrypsin, and vimentin [] and negative for desmin, S-100 protein, myocin and a1-antichymotrypsin. Based on immunohistochemical findings, the diagnosis of a subcutaneous leiomyosarcoma was established. Staging investigations including computed tomography scans of the chest and abdomen were all negative. Although a complete resection with wide surgical margins had been performed, adjuvant postoperative radiation therapy was administered due to the high mitotic rate of the tumor.\nTwo years after surgery, the patient was readmitted with a palpable small, non-tender nodule very close to the scar of the previous operation within the irradiated field. A tumor recurrence was suspected and a new surgical resection with wide margins was performed. Complete blood count and tumor markers were within the normal range.\nHistological examination and immunohistochemical analysis revealed a recurrent leiomyosarcoma measuring 1 cm in diameter. Staging investigations were negative. Adjuvant radiation therapy was not considered at this point by the multidisciplinary oncology team because the patient had received the maximum dose after the primary tumor resection. The patient is being followed up and is well without signs of disease six years after the resection of the recurrent tumor []. |
A 60-years-old female patient had a chief complaint of left intra-oral swelling since 2½months. The patient gave a history of exfoliation of maxillary left first molar before 2½ months. Patient She had a habit of snuff inhalation 3-4 times/a day since 13-14 years.\nIntra-orally, 3 × X 3 cm sized firm and tender swelling was present, which extended from maxillary left first premolar to maxillary left third molar region obliterating maxillary left buccal vestibule and palatally extending in the same region without crossing the midline, involving both soft and hard palate with normal overlying mucosa. Mobility of the involved teeth [maxillary left first and second premolar-Grade I, maxillary left second and third molar- Grade III] were present without any intra-oral sinus []. Left submandibular lymph nodes were enlarged, palpable, mobile and tender. OPG showed irregular radiolucency extending from maxillary left first premolar to maxillary left third molar with poorly defined border giving floating teeth appearance and angular (apical) root resorption of maxillary left first and second premolar, maxillary left second molar (mesial root). It also showed involvement of the left maxillary sinus []. PNS view showed homogenous haziness in left maxillary sinus without erosion/or destruction of lateral walls of maxillary sinus []. On the basis of clinical and radiographic findings, we thought of ameloblastoma converting into squamous cell carcinoma, squamous cell carcinoma of left maxillary sinus/or mixed tumor of minor salivary glands.\nFor further investigations, punch biopsy was taken from the palate. Histologic features were suggestive of pleomorphic adenoma of minor salivary gland. Patient was examined preoperatively. No evidence of spread or distant metastasis was found. After surgical removal of tumor with partial maxillectomy and resection of left side of hard palate, preoperatively prepared obturator was adjusted to cover the defect []. Histologically, excisional biopsy showed the features of adenoid cystic carcinoma of palate without lymphovascular invasion []. No metastasic nodes were seen. Patient was advised for post-surgical radiotherapy. Patient was given total radiotherapy dose of 60 Gy in 30 fractions (200 cGy/fraction for 6 weeks). Patient was advised for follow-up every 6 months. |
An 8-week pregnant 32-year-old primigravida patient without prior clinical symptoms of endometriosis applied to the polyclinic with complaints of hyperemesis. The subsequent pelvic ultrasonography showed a cystic mass of size 65 × 57 mm that was well circumscribed, heterogeneous, with internal echo, and containing a solid component of size 8 × 14 mm in the left ovary. CA 125 value was measured as 220. The patient was informed of the suspicion of malignancy and surgery was recommended; however, the patient chose to postpone the operation until the 2nd trimester because of the pregnancy. In the 12th week, the patient was admitted with complaints of left lower-quadrant pain, nausea, and vomiting; the ultrasonographic examination revealed an increase in the size of the mass, 77 × 65 mm, and increased arterial blood flow in the mass. The patient was operated based on her informed consent.\nIn the examination of the abdominal cavity, multiple endometriotic foci ‘‘gunpowder burns” on the pelvic side walls, in the pouch of Douglas, and on the intestinal surfaces as well as wide-spread intra-abdominal adhesions were seen. It was observed that both the ovaries were adherent in the Douglas pouch and that the left ovary contained an endometrioma of size 8 cm, whose content was drained during manipulation. While the capsule was being peeled, lesions of soft density, with irregular surfaces, and with adhesion in the Douglas pouch were observed at the base of the capsule that were spreading out of the ovarian capsule, also covering the surfaces of the right ovary and the uterosacral ligaments (Figures and ). The results of the frozen section showed decidualized endometrioma and decidual structures (Figures and ). The patient's postoperative care went without any problems; she was injected with 100 mg of micronized progesterone. After the fetal heart rate was checked, the patient was discharged on the 5th postoperative day. |
A 9-year-old girl was brought to the Child Guidance Clinic at the Department of Pediatrics at Medical College, Calicut, Kerala, with history of acute onset of change in behavior of 1 week duration. She became withdrawn and was not interested in play and other pleasurable activities. She was very irritable getting angry easily. Her speech was markedly reduced and she occasionally cried for no apparent reason. She also had severe loss of appetite and exhibited disturbed sleep. She had a non-specific febrile illness 3 weeks prior to the onset of the behavior change. The fever lasted for 1 week and there was no associated head ache, vomiting, skin rash, or diarrhea. The illness subsided with out-patient treatment. There was no history of any immunizations in the recent past. She was born of non-consanguineous marriage and her developmental mile stones were normal. She was going to school normally and had average academic performance.\nOn mental status examination, the child was cooperative for interview. Her psychomotor activity was reduced. Her speech was relevant and coherent with prolonged reaction time. Her mood was depressed. There were no delusions or hallucinations. Primary mental functions were intact. On nervous system examination, motor system, sensory system, and reflexes were within normal limits. There were no cerebellar or meningeal signs. A clinical diagnosis of moderate depressive episode (F-32-1) as per ICD 10 diagnostic criteria[] was made. The child was started on fluoxetine 10 mg per day.\nRoutine blood and urine examination was normal. CSF study was also normal. EEG showed frontal beta dominance and mild slowing of the background activity. MRI of brain showed hyperintense signals in T2 and FLAIR sequences involving bilateral corona radiata, gangliocapsular midbrain, middle cerebellar peduncle, and medial cerebellar hemispheres. The MR images were consistent with ADEM Figures and .\nAfter obtaining the MRI report, a diagnosis of moderate depressive episode secondary to acute disseminated encephalomyelitis (ADEM) was made and the child was treated with methyl prednisolone 30 mg/kg per day for 3 days. There was dramatic improvement in symptoms after the treatment with methylprednisolone. She was switched over to oral prednisolone 2 mg/kg/day which was given for 2 weeks and gradually tapered off. |
A 44-year-old woman was diagnosed with advanced gastric cancer (T4N3) for which total gastrectomy was performed. Twelve days after the operation, adjuvant chemotherapy was started with cisplatin and 5-fluorouracil. She received cisplatin (92 mg/day for 4 days) and 5-fluorouracil (1,530 mg/day for 1 day). Two days after the 1st chemotherapy, the patient presented with a sudden onset of right flank pain and dizziness. Emergency computed tomography (CT) imaging of her abdomen and pelvis was performed. A large thrombus was identified in the abdominal aorta at the origin of the renal arteries, and it involved the right renal artery causing renal infarction (). The CT scan prior to the chemotherapy showed a normal aorta at the origin of the renal arteries. Chest X-rays showed no abnormality. The electrocardiography and echocardiogram excluded arrhythmia or intracardiac thrombi. Initial laboratory findings were within normal limits; prothrombin time international normalized ratio 1.01, activated partial thromboplastin time 33.7 seconds, protein C activity 125%, antithrombin III 108%, blood urea nitrogen 13.8 mg/dL, creatinine 0.74 mg/dL, except for protein S activity 56%. Only protein S activity was lower than the normal limit (71 to 103%). A therapeutic intravenous infusion of unfractionated heparin was commenced. To minimize surgical burden to the patient who was on her 17th day after major surgery, hybrid surgery was chosen. Hybrid treatment was performed under general anesthesia. A transbrachial aortic angiogram was performed, which revealed a large filling defect in the aorta just at the origin of the renal arteries and there was no flow to the right renal artery. A cut-down of the right common femoral artery and a puncture of the left common femoral artery were performed. After gaining percutaneous access, a 10 × 40 mm balloon (ev3 Inc., Plymouth, MN, USA) was placed to occlude the left iliac artery to prevent contralateral embolization. And then, a 5 × 20 mm balloon (Cordis Co., Miami Lakes, FL, USA) was used to occlude the left renal artery (). Thereby, we could avoid renal artery embolization and contralateral groin cut down. Wire-directed balloon catheter thrombectomy was performed using a 5F over-the-wire Fogarty catheter (LeMaitre Vascular Inc., Burlington, MA, USA) via the right femoral access. An angiogram after thrombectomy revealed a residual filling defect in the aorta. The aortic thrombus was macerated using a Trerotola mechanical thrombectomy device (Arrow International Inc., Reading, PA, USA). A wire-directed balloon catheter thrombectomy was then performed using a 27 mm Equalizer balloon catheter (Boston Scientific, Cork, Ireland, USA). The completion angiogram demonstrated no residual thrombus with no embolus in the left renal artery or in the bilateral lower extremity arterial systems (). Left renal balloon occlusion was maintained for 41 seconds and the left kidney function was preserved after reperfusion. We used about 150 mL of contrast media (VISIPAQUE Injection, 270 mgI/mL; Amersham health, Cork, Ireland) and the postoperative creatinine level was 0.98 mg/dL. Chemotherapy was stopped after thrombectomy and the patient received systemic heparinization for 1 week and then received antiplatelets including aspirin, cilostazol, and atorvastatin calcium, indefinitely. Follow-up CT scan 7 days after the procedure showed complete resolution of the thrombus (). Eighteen days after the procedure, chemotherapy was restarted with only 5-fluorouracil, because cisplatin has renal toxicity and can cause another thrombus. After 5-months follow-up, she is doing well without another aortic thrombus. |
A 22-year-old, unmarried lady presented with recurrent seizures since her six years of age. The seizure started in her right hand and then became generalized. The seizure persisted for two to three minutes. There was no preceding prodrome, aura, or automatism. There was post ictal confusion but no post ictal paralysis. Her milestones of development were normal up to the age of six, except that she had mild mental retardation. She did not go to school. She could speak normally prior to her onset of the seizure. She had developed progressive speech regression since her 10 years of age and had become mute at her 12 years. She could follow the simple command. There was no family history of epilepsy. Her seizure was not controlled even after taking several anticonvulsants. Since her 10 years of age, she has experienced almost daily seizures. At the time of presentation, she experienced 5-10 seizures per day. She also had occasional rage attacks. She was on sodium valproate 1000 mg/day, carbamazepine 800 mg/day, and levetiracetam 1000 mg per day which were started at her 6, 9, and 16 years of age respectively. The patient was apathetic. She had expressive aphasia. There was no focal weakness. Superficial and deep tendon reflexes were normal. Her MRI of the brain (Figure ) revealed a complete band of gray matter located deep and parallel to pachygyric overlying cortex.\nThe thickness of the band was more in the posterior part of parietal and occipital cortex. An electroencephalogram (EEG) (Figure ) revealed bi-frontal slow waves which were marked during stage 1 sleep.\nWe gradually discontinued carbamazepine over 15 days, as we thought that it could exaggerate the seizure. We increased the doses of sodium valproate and added clobazam. We added clobazam 10 mg daily and increased the dose of sodium valproate to 1500 mg daily. At this, her seizure frequency was gradually decreased and her speech had gradually improved. After 15 days of discontinuing carbamazepine, her seizure was fully controlled. She began to speak and communicate during her 30 days of follow-up. Consequently, follow-up after six months revealed that she had experienced two transient brief attacks of seizure during the course of the period. Detailed history revealed that the seizures occurred during the missed dosage of the drugs. So, we did not make any dose adjustment and advised her strictly not to miss the dose of anticonvulsants further. Her final drugs were sodium valproate 1500 mg, levetiracetam 1000 mg, and clobazam 10 mg per day. |
The patient (JRS), a 58-year-old man was subjected to an excisional biopsy of a dark skin lesion in the left foot. On light microscopy, an acral melanoma was diagnosed, with a Breslow thickness of 1.5 mm. Clinical staging was T2 N0 M0, with a normal LDH (355 mg/dL) and normal chest and abdomen CT findings.\nBased on the clinical stage and Breslow thickness, a sentinel node biopsy and a wide-margin excision were carried out. On lymphoscintigraphic examination, a major uptake of radionuclide was localized in the popliteal and groin lymph nodes, which were excised and submitted to histopathological examination. These lymph nodes were deemed positive for metastatic melanoma and, consequently, a lymphadenectomy of the deep and superficial groin as well as popliteal regions was indicated. After this procedure, histopathological examination disclosed seven popliteal lymph nodes, all being disease-free.\nNormally, there are 2 to 9 lymph nodes localized within the fat tissue surrounding the nerves and major vessels of the popliteal fossa. Popliteal lymph nodes are deep structures encountered under the investing fascia of the leg, and they receive the lymphatic drainage of the deep structures of the distal leg and foot. Although infrequent, the lymphatic drainage from the skin is direct to these lymph nodes in some individuals. The surgical procedure of popliteal lymph node dissection involves en bloc removal of all fibrous, fatty, and lymphatic tissue in the popliteal fossa, with careful preservation of the nerves and vessels.\nThe patient is placed in the prone position with the knee slightly flexed. To gain access to the popliteal fossa, an S-shaped incision is performed (Figure \n). The lateral flap is raised first to the surface of the biceps femoris muscle proximally, and the lateral head of the gastrocnemius muscle distally and superficial to the level of Scarpa’s fascia. The medial flap is raised until the semitendinosus and semimembranosus muscle proximally and the medial head of the gastrocnemius muscle distally. Skin hooks or autostatic retractors are used to maintain raised flap traction.\nThe upper angle of the popliteal fossa is formed by the biceps and semimembranosus muscle. Medially to the edge of the biceps femoris muscle, the common peroneal nerve is identified through a layer of fat tissue. An ascending sharp dissection is made superficially to the nerve until the level of its origin from the sciatic nerve. This careful dissection continues distally until the surface of the peroneus longus muscle. At this point, the tibial nerve is also dissected in the popliteal space superficially to the popliteal vessels and both nerves are hooked with vessel loops to allow gentile lateral traction (Figure \n).\nEmerging from the lateral surface of the peroneal nerve, we can identify the lateral sural cutaneous nerve (Figure \n). This nerve is responsible for the sensory innervation to the posterolateral surface of the leg. The sural nerve is formed from the fusion between a communicating ramus of the lateral sural cutaneous nerve and the medial sural cutaneous nerve in the middle of the leg. If possible, this superficial communicating ramus should be preserved during the dissection over the lateral head of the gastrocnemius. In case of tumor involvement of the lateral cutaneous sural nerve or its communicating ramus, their sacrifice does not cause significant sensory deficit, if the medial cutaneous sural nerve is preserved. The medial cutaneous sural nerve has its origin from the tibial nerve and emerges from the popliteal space to run superficially in the groove between the two heads of the gastrocnemius muscle near to the small saphena vein in the middle of the back of the leg. Division of the medial cutaneous sural nerve results in cutaneous anesthesia.\nThe deep fascia is stripped off the surface of the gastrocnemius muscle, and the medial cutaneous sural nerve is hooked with vessel loops, like the lateral sural cutaneous nerve, both being held laterally. The popliteal vessels are now approached. The popliteal artery is medial to the popliteal vein and lies deeper. Both are located between the heads of the gastrocnemius muscle (Figure \n).\nThe descendent dissection continues and the small saphenous vein is ligated close to its insertion in the popliteal vein (Figure \n). All fibrous fatty tissue around the popliteal vessels is removed and some lymph nodes can be identified at this stage. A single lymph node can also be found between the back of the knee and the popliteal artery. Occasionally, there are two popliteal veins and the artery lies between them. The popliteal artery is divided into two major branches: the anterior and posterior tibial artery and a variable number of genicular branches. The surgical specimen is removed in continuity, with a proper identification of the nerves and vessels. As the final step, a closed suction drain is placed in the popliteal fossa.\nThe superficial lymphatics localized on the calf may accompany the short saphenous vein towards the popliteal fossa draining to popliteal lymph nodes. In a series from the Sidney Cancer Database\n[], there were 6.9% direct drainages to one or more popliteal lymph nodes among 236 lymphoscintigrams performed in patients with primary MM at or distal to the knee. Data from these lymphoscintigraphy studies revealed that lymphatic drainage to popliteal lymph nodes can take place anywhere on the leg and foot. However, metastatic disease in popliteal lymph nodes was clinically detectable in 0.31% of the cases only\n[]. In a series of Menes et al., popliteal lymph nodes were identified by lymphoscintigraphy in 9% of the 106 patients with MM below the knee or at more distal sites, and metastatic lymph nodes in the popliteal fossa were found in 2.8% of patients\n[].\nThere are two basic indications to perform popliteal lymph node dissection: i) grossly metastatic disease detected on clinical examination or ii) microscopic disease identified in sentinel node lymphadenectomy specimens\n[]. Popliteal node dissection is an uncommon procedure but adequately indicated according to data available in current literature\n[]. A thorough familiarity of the anatomical landmarks and technical details of the dissection procedure of the popliteal fossa is mandatory.\nIn 1980, Karakousis published an elegant description of this infrequent operative procedure with detailed information about the surgical anatomy and the technique\n[]. Since then, however, there is a paucity of published data on the technical aspects of popliteal lymphadenectomy. To choose the kind of incision, one must consider the optimal exposure necessary to reduce the risk of developing contracture scars. The most frequently used approach of the popliteal fossa by a medial route (described in vascular surgery textbooks to correct popliteal aneurysms or perform femoro-popliteal bypass), does not allow a proper exposure of the structures to accomplish radical lymphadenectomy\n[]. The long S-shaped incision used to access the popliteal fossa is designed to offer generous exposure and avoid deforming joint contracture. Other authors prefer a Z-plasty incision for the same purposes\n[,].\nTo guarantee sufficient exposure, a progressive dissection, initiated by the confection of the lateral flap, was continued throughout removal of all soft tissue. The subsequent surgical steps are followed according to the same principle of removing all fibrous and fatty tissue around, beneath, and alongside the popliteal vessels and nerves. After retraction of the flaps, an easy identification of the peroneal nerve and its ascending dissection until its origin in the sciatic nerve offers prompt identification of the tibial nerve. Subsequent recognition of the sural cutaneous nerves and their branches makes the dissection secure. The next crucial step involves the resection of all fat pad tissue close to the popliteal vessels. Meticulous inspection and palpation of the popliteal fossa must be performed not to leave any lymph node undetected. |
A 3-month-old girl delivered at term by normal vaginal delivery was referred to our institution with persistent cyanosis and respiratory distress since 2 weeks. She has a sister who had surgical repair of tetralogy of Fallot (TOF). When admitted, she was mechanically ventilated; her vital signs showed oxygen saturation of 50% on FiO2 of 100%; her blood pressure was 100/90 mmHg; and heart rate was 100-140 beats per min. Chest roentgenogram demonstrated cardiomegaly with central congestion and oligemic left lung with a band of atelectasis in the right upper lobe.\nAn echocardiographic study showed situs solitus, levocardia, d-looped ventricles, and normally related great arteries. It also showed TOF, pulmonary atresia (PA) with absent main pulmonary artery and hypoplastic (possibly confluent) pulmonary artery branches. There were major aortopulmonary collateral arteries (MAPCAs) supplying the hypo plastic pulmonary arteries. The inter-atrial septum was intact and the right superior vena cava (RSVC) was mildly dilated, draining into the left atrium (LA) [Figures and ]. The pulmonary veins were well seen and were normally draining to the LA, whereas the inferior vena cava and the hepatic veins drain into the right atrium. The LA, Left ventricle (LV), aortic root, and descending aorta were mildly dilated.\nThe LV systolic functions were good while right ventricle functions were fair to good.\nA cardiac computed tomography (CT) confirmed that superior vena cava (SVC) drains into the roof of the LA without communication with the right side system, whereas inferior vena cava does appear to drain into the right atrium with intact inter-atrial septum. The pulmonary veins were well visualized and draining to the LA. The right ventricle was small, with minimal contrast seen within. There were at least two collateral vessels arising from the aorta. The inferior collateral supplied the right lower lobe pulmonary artery and the more superior collateral vessel appeared to connect to the pulmonary artery confluence which then bifurcated into two hypoplastic pulmonary arteries. There was suspicion of presence of secondary supply to the left main pulmonary artery, as the peripheral left pulmonary artery appears of better caliber [; ].\nA diagnostic cardiac catheterization was performed. An injection in a peripheral vein in the left arm showed draining of the left innominate vein to the RSVC and consequently into the posterior LA []. It also delineated the presence of MAPCAs originating from the descending aorta and joining the hypoplastic pulmonary arterial tree. There were also two stenotic sites at the proximal parts of the pulmonary artery branches and normal pulmonary venous pattern |
A 41-year-old female with metastatic breast cancer presented to the emergency department with chest pain of 1 day duration. The chest pain started gradually, and was relieved by rest and exacerbated by exertion. She was started on capecitabine therapy 3 days before the onset of chest pain. She denied shortness of breath, nausea, vomiting, diaphoresis, fever, syncope, heartburn, and peripheral edema. The patient did not have a history of CAD or had known risk factors for CAD. She denied the use of cocaine. The patient did not describe symptoms suggestive of panic attack. On examination, her heart rate was 100 bpm and regular. Her physical examination was otherwise unremarkable.\nFive years before the current event, she underwent mastectomy and axillary lymph node dissection for a stage III (pT2N3) breast cancer. The tumor was ER+, PR+, HER2+, and she received adjuvant chemotherapy and trastuzumab, followed by tamoxifen. She was diagnosed with metastatic disease in the liver in 2014, and was started on trastuzumab, pertuzumab, and docetaxel. Fifteen months later, she had disease progression in the liver and was switched to trastuzumab-emtansine. Nine months later, she progressed again, and therapy was changed to lapatinib and capecitabine (1,500 mg b.i.d.). Three days after starting capecitabine, she experienced acute-onset chest pain.\nElectrocardiogram (ECG) testing showed normal sinus rhythm and no changes suggestive of coronary ischemia. Cardiac enzymes were negative. Complete blood count and chemistry panel were within normal range. CT angiography of the chest did not reveal any evidence of pulmonary embolism. A transthoracic echocardiogram documented normal cardiac function and a left ventricular ejection fraction of 60%. Her chest pain resolved after aspirin and analgesics were administered upon admission in the ER. A cardiology opinion was sought for possible angiography, but was not undertaken because of the patient's improving condition. She was discharged following complete resolution of chest pain. Oncology was consulted during the hospitalization, and capecitabine therapy was discontinued. Since then, she has had no complaints of chest pain. Repeat echocardiogram was normal as well. |
Previously well 60years old Sri Lankan Tamil male had dark urine for 3weeks which he ignored attributing it to change in the weather. He later developed purplish discoloration of fingers and toes associated with pain in extremities 10days prior to admission. He was admitted to the local hospital with progressively worsening shortness of breath even on mild exertion for seven days. On admission he had dry black discoloration of fingers and toes suggestive of dry gangrene. He did not recall any recent febrile illness or sore throat. There was no history of skin rashes, arthralgia or oral ulcers. There were no previous similar episodes.\nHe had never smoked and took alcohol only occasionally. Nor he did take any prescribed or recreational drugs. There was no history of viral hepatitis. He had not received any blood transfusions and nor there was any sexual promiscuity. He was a daily paid manual worker and had 3 children.\nOn further questioning he mentioned that they were displaced from their home due to floods and unusually cold weather and had to live in a temporary shelter one month prior to presentation. He was involved in carrying their belongings to dry land knee deep in cold rainwater. His urine colour turned dark about one week later.\nOn examination he was febrile and sweaty. He appeared ill but was not in pain. He had severe pallor and was mildly icteric. There was no finger clubbing. Fingers, toes and forefoot were discolored, shrunken and appeared lifeless (Figures and ). Pulse rate was 92bpm, regular with good volume. Jugular venous pressure was not elevated. Blood pressure was 110/70mmHg. On auscultation heart was in dual rhythm with an ejection systolic murmur in aortic area. All peripheral pulses were palpable. Respiratory system examination was normal. No palpable liver, spleen or other masses were detected on abdominal examination. Patient was conscious and rational. No neurological deficits were detected except absent sensation on peripheries which were discoloured.\nLaboratory investigations revealed, Hb-2.7g/dl, platelets-432000/l, WBC-15810/l (N 64, L- 19, E- 7, M 9) MCV-106.3fl, MCH-65pg, MCHC-61.1g/dl and reticulocyte count 14%. Total bilirubin 26.8mol/l, Indirect bilirubin 14.6mol/l, Direct bilirubin 12.2mol/l, AST-62u/l, ALT-16u/l, ALP-212u/l,Serum creatinine 89mol/l, Serum sodium 143mmol/l, Serum potassium 3.8mmol/l. Fasting blood sugar 4.7mmol/l erythrocyte sedimentation rate 30mm/Hr. Urine for haemoglobin was positive.\nHepatitis B surface antigen and Hepatitis C antibody were negative. Anti nuclear antibody and HIV serology were also negative. Mycoplasma IgM was negative. Epstein Barr virus IgM was positive with a titre of 1 in 1600. VDRL was non reactive. Blood picture revealed normochromic normocytic red cells, spherocytes, polychromatic cells, nucleated RBC and red cell clumps suggestive of acute haemolysis. White cells showed neutrophil leucocytosis with left shift. Platelets were normal in number with many platelet clumps. Direct antiglobulin test was positive with IgM and anti C3d specificity with strong auto-agglutination at 4C and room temperature and no auto-agglutination at 37C. Cold agglutinin titre was 1 in 2048.\nBlood film findings were compatible with severe cold auto-agglutinin mediated peripheral haemolysis with C3d specificity. Serum protein electrophoresis showed polyclonal increase in Gamma globulin region. Cryoglubulins were not detected.\nUpper gastrointestinal endoscopy showed multiple small antral ulcers and multiple small duodenal ulcers with no active bleeding.\nVascular surgeon decided no active intervention needed as patient had demarcated dry gangrene. Provisional diagnosis was cold autoimmune haemolysis associated with Epstein Barr virus IgM.\nPatient was transfused seven units of O positive red cells over a period of one week. He was started on folic acid 5mg daily. After the blood transfusions he improved symptomatically. Repeat blood film two weeks after admission showed resolution of haemolysis. Patient was advised to avoid cold and to wear gloves and stockings in cold weather. He was discharged home after arranging follow up for occupational therapy. Due to the loss of fingers and toes he was markedly disabled and had to stop working as a labourer. |
Case 1. The patient was a 55-year-old male who presented to the hospital with multiple episodes of vomiting, loss of consciousness, and repeated falls over the last day. He denied any chest pain, palpitations, or injury to his head. His medical history was significant for hypertension, diabetes mellitus, and end-stage renal disease. He received hemodialysis through his left forearm arteriovenous fistula one day prior to presentation. On presentation, the patient was hypotensive, with blood pressure of 90/50 mm Hg, was hypoxic, with an oxygen saturation of 88% of room air, had a heart rate of 79 beats per minute, and was afebrile. On physical exam, he was alert and oriented, with negative respiratory and cardiovascular exams. Neurological exam did not show any focal neurologic deficits. Laboratory data were significant for thrombocytopenia with a platelet count of 122 × 103/μL and a hemoglobin level of 17.3 g/dL. He underwent a CT scan of his head, which showed foci of gas in the cavernous sinus, anterior sagittal sinus, left side of the face, and left temporalis muscle (). He had not undergone any other procedures before presentation, and, by history, his hemodialysis had been uneventful. The patient's condition deteriorated rapidly; he became comatose and had a cardiac arrest. He was successfully resuscitated within five minutes. After resuscitation, the patient developed shock requiring vasopressor support. He was started on intravenous piperacillin-tazobactam and vancomycin for possible sepsis. In the presence of high pulmonary pressures and without any evidence of paradoxical air embolism, a bubble study to look for a patent foramen ovale was not performed. Adequate oxygenation was maintained throughout his hospital stay. He was not a candidate for transfer to another center for possible hyperbaric oxygen therapy due to his tenuous hemodynamic status. The patient's further course was complicated by hematemesis due to a Mallory-Weiss tear diagnosed by endoscopy. Sepsis work-up was negative. As his prognosis was poor, he was transferred to hospice care where he expired. |
A 42-year-old female, accountant by profession, recreational runner of approximately 30 kilometers per week, presented a 4-week history of deep, intense pain in the right groin, which appeared after usually 30 minutes of running. She denied any symptoms of the left hip. There was no history of trauma, alcohol abuse, steroid use, metabolic disorder or any relevant diseases. Her body height was 163 cm with body weight 51 kg, and her BMI was 19.2 Kg/m2. She had born two children and had a normal menstrual cycle. At the beginning of symptoms, she took analgesics with partial clinical improvement. However, due to persistence of pain, she was evaluated by her general practitioner (GP) who suggested x-rays and MRI of the pelvis and hip joints.\nAt the orthopaedic visit, physical examination revealed a slight ROM reduction of the right hip due to pain compared to the contralateral: flexion limited to 90°, extension 20°, external rotation 40°, internal rotation 10°, flexion-abduction 45° and adduction 30°. The neurovascular examination showed normal results of both lower extremities. The values of tumor markers, urine calcium level test and all blood tests prescribed in that occasion resulted normal except for vitamin D and PTH (). Radiographic examination including plain pelvis x-rays (antero-posterior and lateral views) did not revealed any bone alteration or sign of fractures (), while the MRI showed edema of the spongy bone in the femoral neck base and a suspicious fracture line in the inferior margin of the femoral neck (). The diagnosis was an FNSF at the right femoral neck base, which was classified according to Fuellerton and Snowdy as a Type II, compression-side, incomplete FNSF.\nDiscussing the MRI results with the patient, a conservative treatment was proposed, advising rest, using elbow crutches to avoid load on her right left limb for 30 days, then for further 20 days with assisted loading by crutches and finally, full weight-bearing at 2-month follow-up. Further, the patient was advised to take non-steroidal anti-inflammatory drugs (NSAIDs) for pain control and Cholecalcipherol 30.000 U.I./month to improve vitamin D levels.\nDuring the rehabilitation period, the patient underwent physiokinesis and magnetic therapy cycles. She was followed at 3, 6 and 12 months following the injury, being clinically, metabolically and radiographically assessed. At 3-month follow-up she was completely pain free with full right hip ROM on clinical examination. She was able to walk with complete load without pain, starting only stationary cycling and swimming, while a month later, she started normal physical activity, without complaint. The new x-ray imaging studies performed showed callus formation on the inferior aspect of the femoral neck. At 6-month follow-up, the blood level of vitamin D and PTH improved almost to normal values (). The 12-month follow-up MRI showed no signs of avascular necrosis (AVN), and there was radiographic evidence of a healed stress fracture (). |
A normally developed 5-year-old girl presented to the emergency department with a 1 month history of worsening abdominal pain that localized to the right upper quadrant with intermittent vomiting and fevers over the week prior to presentation. On physical examination, the child was febrile to 37.6°C with abdominal distension. A tender right-sided abdominal mass was found extending from the costal margin to the pelvis and beyond midline. Bowel sounds were heard only on the left. Abdominal CT imaging identified a large mass arising from the right kidney with at least one smaller lesion in the left kidney (Fig. A). Serum WBC and electrolytes were normal, with a serum creatinine of 0.40 mg/dl and a BUN of 7 mg/dl. Chest X-ray and pulmonary CT scans were negative for malignant disease.\nThe patient was given a presumptive diagnosis of bilateral (Stage V) Wilms tumor. The family consented for her to participate in the Children's Oncology Group trial AREN0534 which called for pre-operative chemotherapy in order to facilitate nephron-sparing surgery at the time of tumor resection. A central venous catheter was placed, and neoadjuvant chemotherapy with vincristine, dactinomycin and doxorubicin was initiated. Within hours of starting her therapy, we found that lactate dehydrogenase and uric acid were both elevated (1134 U/l and 6.3 mg/dl, respectively; Fig. ). Serum potassium and phosphate were both normal. The patient's hyperuricemia was felt to be consistent with tumor lysis syndrome, and allopurinol and alkalinized fluids were administered. The hyperuricemia soon resolved, and the patient maintained normal serum creatinine, potassium and phosphorus levels throughout her hospital stay. A follow-up CT scan after 6 weeks of therapy showed a marked response to chemotherapy of the right-sided lesion (Fig. B). The left-sided mass remained stable in size. We decided to administer another 6 weeks of chemotherapy to improve her candidacy for right partial nephrectomy instead of whole nephrectomy. However, despite further tumor shrinkage, total nephrectomy eventually had to be performed for the right kidney because no clear surgical plane could be identified at the time of resection (Fig. C). Pathologic interpretation of the right- and left-sided tumors confirmed Wilms tumor in each and a focus of anaplastic disease on the right (Fig. C). 10.8 Gy of radiation to the right flank was administered because of the pathologic finding of focal anaplasia, in accordance with the AREN0534 protocol. Presently the patient is well, with good renal function and in remission, now roughly 6 months after her end of therapy. |
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