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A 47-year-old female patient was admitted to our hospital with a few hours history of personality change, cognitive dysfunction, and headache. She also had a 12-year history of abortion and thrombocytopenia. She was drowsy, with a Glasgow coma scale of 14. The platelet count was markedly decreased to 58,000/µL, and physical examination showed splenomegaly. Computed tomography (CT) of the abdomen showed a cirrhotic liver with splenomegaly. However, she had no history of hepatitis. Lumbar puncture was performed after platelet transfusion, and no red blood cells were found in the cerebrospinal fluid.\nMagnetic resonance (MR) imaging and CT of the brain were performed for evaluation of suspected intracranial lesions. A T1-weighted axial image showed a target-like thrombosed aneurysm located in the right anterior sylvian fissure (). Ovoid high signal intensity was suggestive of a hematoma surrounding the posterior aspect of the aneurysm. A T2-weighted axial image also showed a thrombosed aneurysm and a posteriorly located hematoma with a surrounding dark line (). Difference in signal intensity was observed between the posteriorly located hematoma and the thrombosed aneurysm on T1- and T2-weighted images, i.e. on T1- and T2-weighted images, the posterior hematoma showed homogeneous high signal intensity, whereas the thrombosed portion of the aneurysm showed intermediate and inhomogeneous high signal intensity (). A gadolinium-enhanced axial image showed no definite enhancement of the lesions (). On precontrast CT scan (), the thrombosed aneurysm showed a highly attenuating wall. This high attenuation on CT images presented as high signal intensity on T1- and T2-weighted images. The posteriorly located hematoma abutted the aneurysmal sac. The hematoma also differed in density from the highly attenuating aneurysm wall. No evidence of subarachnoid hemorrhage was observed on MR or CT images. Digital subtraction angiography was performed, and 2 unruptured aneurysms were detected in the right middle cerebral artery ().\nSurgical intervention was not performed because of continued thrombocytopenia. Instead, coil embolization was performed immediately. After embolization, follow-up angiography showed faint staining of the contrast media on the capsule of the hematoma posterior to the thrombosed aneurysm (). Immediately after coil embolization, follow-up CT of the brain showed capsular enhancement in the aneurysmal sac and the posterior hematoma (). The aneurysmal sac and hematoma were decreased in size 4 days after coil embolization (), and they had almost completely disappeared 4 months later (). After 1 year, MR imaging of the brain showed that the hematoma in the right temporal lobe had completely disappeared (). Ovoid high signal intensity suggestive of a hematoma abutted the posterior aspect of the aneurysm. A T2-weighted axial image also showed the thrombosed aneurysm and the posteriorly located hematoma with the surrounding dark line (). Difference in signal intensity was observed between the posteriorly located hematoma and the thrombosed aneurysm on T1- and T2-weighted images, i.e. on T1- and T2-weighted images, the posterior hematoma showed homogeneous high signal intensity, whereas the thrombosed portion of the aneurysm showed intermediate and inhomogeneous high signal intensity (). A gadolinium-enhanced axial image showed no definite enhancement of the lesions (). |
A 10-year-old girl was referred to the Department of Otorhinolaryngology and Oral and Maxillofacial Surgery, Eskilstuna Hospital, Sweden, for evaluation of facial chronic swelling at the left side. According to the parents, the whole family was on holiday at the Mediterranean coast 8 months before they visited our department. A few weeks after patient's return to Sweden, the patient experienced swelling of regional lymph nodes at the left side of the neck. No further investigation was done. Two months later, the patient had noticed a slight swelling at the left side of cheek () and showed restricted mouth opening. The general practitioner suspected TMJ-like symptoms and referred the patient to Dental Oral Rehabilitation Center. Dental examination did not give any hint of inflammatory dental foci. There was no previous history of viral or bacterial infection. Periapical radiographs showed no significant pathology that could explain the patient's symptoms. Magnetic resonance imaging (MRI) showed inflammation adjacent to the left side of ramus mandible.\nOn the basis of these findings the patient was then referred to the Department of Otorhinolaryngology and Oral and Maxillofacial Surgery for further investigation. Panoramic CBCT demonstrated loss of the normal trabecular pattern with radiopacity within ramus/angulus mandibulae and incomplete development of germs of the third molar at the left side (). Moreover, sectional images of CBCT showed typical periosteal reaction, lytic lesions, and new-bone formation at the left side, from ramus mandibulae to incisura/collum mandible (Figures –). Bone scintigraphy showed increased tracer uptake only at the left side of the mandible ().\nAlthough the diagnosis of osteomyelitis was considered probable, the possibility of a tumorous lesion could not be excluded. The patient was submitted to diagnostic bone biopsy. Under general anesthesia, several bone biopsies were then taken for histological and microbiological examination. The histological findings were consistent with chronic inflammation. No signs of malignancy were seen. Bacterial cultures showed no growth of organism, such as mycobacterium tuberculosis. The blood samples did not show any significant abnormalities. The patient was given per oral clindamycin 150 mg every 8 hours and prednisolone 5 mg every 24 hours. After 8 weeks of drug treatment, decortication of mandible and additional curettage of the medullary bone were performed. The third-molar germ was also removed. Six months later, CBCT showed continued radiopacity of the mandible at the left side without any signs of active inflammation (radiolucency) (Figures and ). Extraoral photo of patient showed a slight diffuse swelling at the left side ().\nThe CBCT 3D image showed continued thickness of collum mandibulae and processus coronoideus (Figures and ). After surgery, she has received NSAID to reduce her intermittent extraoral swelling. Further investigation, treatment, and follow-up are necessary to control the patient's disease at her temporomandibular joint site. |
A 44-year-old female office worker sustained a right anterior glenohumeral dislocation with an associated avulsion of the greater tuberosity, as described by Mutch et al. []. Open reduction and internal fixation of the fracture were performed with a tension band technique, using an anchor screw and nonabsorbable sutures []. The functional outcome was poor. The patient was painful and had marked weakness in external rotation and abduction. Active forward flexion and abduction were 40° with full passive motion, and active external rotation was 30°. Her single assessment numeric evaluation score [] was of 40 %. Past medical history was significant for noninsulin-dependent diabetes mellitus and obesity (BMI 42). Radiographic evaluation demonstrated a complete osteonecrosis and resorption of the greater tuberosity (Fig. ) with a suspicion of massive rotator cuff tear involving both supraspinatus and infraspinatus tendons, without retraction. There was a state 1 Goutalier fatty infiltration of the supraspinatus and infraspinatus muscles. The electromyographic evaluation of the axillary nerve was normal. It was decided to reconstruct the defects with a fresh-frozen Achilles allograft tendon with attached calcaneal bone. Written informed consent was obtained from the patient for publication of this case report and accompanying images.\nUnder general anaesthesia and interscalene nerve block, the patient was placed in the beach chair position, with the operative arm draped free. An open anterosuperior incision with a deltoid split was performed in order to expose the greater tuberosity defect. The long head of the biceps was already resected. The remaining posterosuperior rotator cuff was carefully dissected, and the proximal humeral head was debrided. The quality of the cuff tissue was poor. The Achilles tendon allograft with attached calcaneus was then prepared (Fig. a). The calcaneus was shaped to fill proximal humeral head defect. The Achilles tendon was then split longitudinally, with the deep layer used to reinforce the rotator cuff repair and the superficial layer used to stabilise the allograft to proximal humeral diaphysis. Then, the bony portion of the allograft was secured to the humeral head with a 4-mm malleolar screw under fluoroscopic control. The native rotator cuff was then repaired onto the bony graft with a combination of an anchor (Haelix®, DePuy Mitek, Inc., Raynham, MA) and bone tunnels in the graft. The deep split of Achilles tendon was then sewn into the native posterosuperior rotator cuff to reinforce the repair (Fig. b). Finally, the superficial Achilles split was return on itself and attached laterally with another anchor (Haelix®, DePuy Mitek, Inc., Raynham, MA) in order to stabilise and cover the allograft.\nPostoperatively, the patient wore an abduction sling for 6 weeks and was allowed to perform pendulum exercises only. Passive mobilisation was performed from weeks 6 to 12. Then, strengthening with progressive loads was initiated, and the patient returned to full activities level. At 6- to –12-month follow-up, she was pain free and recovered a full active range of motion compared to the opposite side, with an active antepulsion of 150° and an active external rotation of 50°. The SANE score was of 95 %. On plain radiographs, the bony portion of the allograft was integrated with the proximal humerus. The arthroscanner showed a good integrity of the tendinous graft (Fig. ). |
A 66-year-old male was referred to Niigata University Hospital after being found to have tracheal deviation on an X-ray obtained to diagnose the cause of dysphagia. He had a history of smoking and drinking for 46 years. A physical examination showed no significant findings, and laboratory tests, including serum tumor markers such as CEA and CA19-9, were normal. Endoscopy revealed an approximately 50 mm esophageal submucosal tumor, which was located 25 cm from the incisors (Fig. ). A chest CT scan showed a well-demarcated, enhancing homogeneous tumor measuring 51 × 41 mm in the upper third of the esophagus (Fig. ). No regional lymph node enlargement was observed. Endoscopic ultrasonography (EUS) showed a large tumor of low echogenicity in the esophageal wall, originating in the submucosa layer (Fig. ). EUS-FNA-mediated histopathological examination revealed a proliferation of spindle-shaped cells in a fasciculated, disarrayed architecture, with nuclei in a palisading pattern, followed by a preoperative diagnosis of esophageal schwannoma was made in this current case.\nGiven that the 50-mm tumor was located at the anterior wall in the upper third of the esophagus, we performed tumor enucleation using a cervical approach. We placed the skin incision in a longitudinal fashion along the anterior border of the sternocleidomastoid muscle extending to the sternal notch, which facilitates use of a combined transthoracic approach if needed (Fig. ). After transection of the left sternocleidomastoid muscle, the tumor was easily identified (Fig. ). After mobilization of the esophagus, the tumor was excised to include all esophageal layers (Fig. ). Although preservation of the mucosal layer with tumor enucleation is a less invasive technique, in our case, full-thickness excision was indicated because of dense adhesions between the tumor and the surrounding esophagus as well as thinning of the mucosal and muscular layers. We inserted an endoscope to act as a stent during transverse closure of the esophagus and performed a leak test that was negative (Fig. ). The anastomosis appeared healthy and well perfused, and we were careful not to injure the blood supply to the surrounding esophagus. Post-procedure, neither dehiscence nor stricture was found by fluoroscopy. Following this normal post-operative test result, we removed the nasogastric tube and permitted the patient to start eating.\nThe resected tumor measured 52 × 40 × 31 mm in size (Fig. ), and the cut surface on gross examination was yellowish and elastic (Fig. ). Consistent with the EUS which showed that the tumor was originating in the submucosa layer, pathological analysis confirmed that the submucosa was the originating layer (Fig. ). High-power photomicrographs of the tumor showed spindle-shaped cells in a fasciculated and disarrayed architecture (Fig. ). Immunohistochemically, the cells stained positive for S-100 protein (Fig. ), but were negative for KIT (Fig. ), CD34 (Fig. ), desmin (Fig. ), and α-smooth muscle actin (SMA) (Fig. ). This was consistent with the tumor being a benign esophageal schwannoma. The patient recovered without any post-operative complications and was discharged on the 12th post-operative day, which is standard for an open esophageal enucleation. There has been no evidence of recurrence over a current follow-up period of 3 years.\nEsophageal schwannoma is one of the most common types of neurogenic tumor. Benign disease is uncommon, but malignant schwannoma is even more rare []. Although esophageal schwannoma is often difficult to diagnose preoperatively [], an accurate preoperative diagnosis could lead to less invasive surgical treatment. Therefore, although this is a rare entity, it is important to suspect esophageal schwannoma by clinical examination and subsequent pathologic biopsy to establish an accurate preoperative diagnosis.\nRegarding the presentation of esophageal schwannoma, while some patients are asymptomatic, symptoms generally correlate with tumor size due to the mass impinging upon surrounding structures, which can result in dysphagia, dyspnea, chest pain, pneumonia, or hemoptysis []. On review of our own retrospective series of four patients with esophageal schwannoma, including this current case, three patients presented with progressive dysphagia. Table summarizes the characteristics of our patient series. Obtaining an accurate preoperative diagnosis of esophageal schwannoma is very challenging. EUS-FNA may be useful for both the diagnosis and management of this disease []. Although EUS-FNA may have several procedural risks, such as bleeding and infection, these risks are minimal []. In general, it is considered to be a safe, reliable, and accurate method for obtaining a tissue diagnosis in the evaluation of submucosal lesions of the gastrointestinal tract. In this case, we could make a preoperative diagnosis by EUS-FNA. Even if preoperative diagnosis was difficult to make, using operative rapid pathologic diagnosis method may also be useful.\nWhile surgical resection offers radical treatment for esophageal schwannoma, the approach should be determined based on tumor size, location, and patient condition. Esophagectomy or local resection consisting of full-thickness excision and tumor enucleation are mainly performed. As a more radical approach, esophagectomy may lead to a high incidence of post-operative complications, such as recurrent laryngeal nerve paralysis, pulmonary compromise, or chylothorax [, ]. In contrast, local resection is a sufficient approach for the curative treatment of benign schwannomas and is less likely to result in serious morbidity []. Furthermore, tumor enucleation is quite technically feasible because the esophageal schwannoma does not usually involve all layers of the esophageal wall and is typically limited to the submucosa []. However, enucleation may not be a preferred approach for very large tumors because this has been associated with higher rates of esophageal stenosis [].\nWhen the tumor is located in the upper third of the esophagus as in this case, a cervical approach for enucleation has been reported [, ]. Conversely, a transthoracic approach presents more difficultly for resection of a tumor located in the cervical esophagus because of its deeper operative field and narrower working space. In this case, the tumor was located at the anterior wall in the upper third of the esophagus that we could address using the cervical approach. In our series of four patients with esophageal schwannoma, three patients underwent tumor enucleation and one patient underwent esophagectomy due to the excessive size of the tumor (90 × 67 mm).\nOur case represents the first case report of tumor enucleation through a cervical approach. Recently, however, video-assisted thoracic surgery (VATS) has been used more, as this minimally invasive approach has been shown to result in less post-operative pain and shorter hospital length of stay than the open thoracotomy approach. However, in certain cases, such as in one of our patients, VATS may not provide exposure that is adequate for tumor access. In very large submucosal tumors, VATS may lead to an increased risk of mucosal injury during extensive submucosal dissection [].\nThere are a few reported cases of malignant esophageal schwannoma [, ]. In these cases, regional lymph node dissection was performed, and the patients did not experience any recurrences. In contrast with radical lymph node dissection in esophageal cancer (adenocarcinoma or squamous cell carcinoma), lymph node dissection for esophageal submucosal tumors is controversial. When an esophageal submucosal tumor is suspected to be malignant based on concerning preclinical or radiographic findings (such as local invasion or enlarged suspicious lymph nodes), lymph node dissection should be considered. Radical esophagectomy with regional lymph node dissection may also be needed in certain cases to minimize potential recurrence. In this case, we achieved successful tumor enucleation for a large benign submucosal tumor; however, we emphasize that surgery to treat benign esophageal tumors, including schwannomas, should be performed on a case-by-case basis. |
A 78-year-old man has affected by abdominal pain, vomiting and weakness and has evaluated at June 2013. Studying his medical history, he had hip joint replacement surgery, then in initial physical examination has shown no significant finding, except a few tenderness on the middle abdominal quadrant. In laboratory assessment, complete blood count, renal function tests-alkaline phosphatase and lactate dehydrogenase were normal, but hemoglobin and transaminases were abnormal as follows: Hb = 9.1 mg/dl, AST = 71 u/lit, ALT = 656 u/lit.\nIn abdominal CT scan, there was a 71 × 61 mm mass at the aortic bifurcation in favor of tumoral lesion or adenopathy.\nSurgery has recommended and in pre-operative evaluation he has referred to cardiologist. ECG had no significant and specific changes and in echocardiography, a large mass with diameter of 74 × 60 mm has seen in right atrium () and LV ejection fraction was 65%. Also, in thoracic sections of CT scan, an intra-cardiac mass has seen ().\nBases on these new findings management of the patient has changed to cardiac surgery and open heart surgery has recommended and performed at August 2013. Pathologic examination of removed cardiac mass has reported as below after immunohistochemistry study: HMB 45 and CK: negative; CD20: positive. Compatible with non-Hodgkin lymphoma in favor of B-cell origin ( and ). He has referred to oncologist after recovery of heart surgery (September 2013).\nIn evaluation of medical history and further physical examination, he had no history of fever and sweating, but weight loss of 2 - 3 kg during recent weeks. Karnowsky performance status was 80%. At physical examination, he had an adenopathy of 2 × 1 cm at left jugulodigastric chain, and the another of 3 × 1 cm at left supraclavicular area and physical exam was normal otherwise.\nIn bone marrow biopsy, BM was hyper cellular, and involved with lymphoma infiltration. The patient has planned to treat by R-CHOP chemotherapy regimen (Rituximab-cyclophosphamide-Doxorubicin-vincristine-prednisolone).\nHe could not provide Rituximab due to economic problems, therefor he has received only CHOP regimen. After first cycle of treatment, cervical adenopathies have disappeared and at the end of seventh cycle, imaging of the neck , chest and abdominopelvic cavity by CT scan had no positive finding of disease but the patient has not satisfied to undergo BM biopsy for second time.\nPatient treatment has completed after eight cycles of CHOP chemotherapy regimen at February 2014, but he was in good condition, without any evidences of disease after six months of follow up. |
A 42-year-old female presented for neurosurgical evaluation with persistent neck pain and numbness in her left fingers 2 years after a traumatic fall on stairs with head strike without loss of consciousness. She initially presented to an outside hospital and on examination had left-sided neck and upper extremity (UE) pain, with paresthesias and reduced UE strength bilaterally and pain-limited lower extremity strength bilaterally. Her presentation was most concerning for a central cord syndrome spinal cord injury (SCI). Facial lacerations and bruising, headache and dizziness were concerning for a concussion. Brain and cervical computed tomography (CT) scans were negative for acute intracranial processes or cervical fractures, dislocations or spondylotic changes and she refused an MRI due to claustrophobia. Without MRI or flexion/extension radiographs, the outside hospital physician was not comfortable clearing her cervical spine. She was discharged maintaining a rigid cervical collar and recommended to follow up outpatient with neurosurgery.\nBy approximately 6 months post-injury she had regained most motor function and, without consulting a physician, self-discontinued the rigid cervical collar without any acute deterioration in neurological status. Her chronic neck and left shoulder pain and weakness did not improve with acetaminophen or occupational therapy. She did not disclose her fall history to her primary care provider (PCP) and was referred for neurosurgical evaluation. This occurred during a declared state of emergency in the northeastern USA due to COVID-19. The patient lived in rural New England, over 1 hour away from our hospital, and did not have the means to get to appointments, especially with public health measures in response to COVID-19.\nDuring telemedicine evaluation, she discussed her fall. She had not understood the significance of her trauma and experienced symptoms consistent with postconcussive syndrome (PCS), including persistent problems with memory, concentration and decision making. Without telemedicine, she would have been advised to see a neurologist for brain and optic nerve MRI, visual evoked potentials, and lumbar puncture with cerebrospinal fluid analysis (CSF) to work up multiple sclerosis. A non-contrast T2-weighted cervical MRI from 1 month before neurosurgical evaluation revealed a 4 mm area of hyperintensity within the spinal cord at the C4–C5 level consistent with previous spinal cord injury (). Anteroposterior (AP), lateral and flexion/extension radiographs were recommended to assess for cervical instability, though these were not possible with COVID-19 restrictions. She was counseled regarding risks and benefits of future surgical decompression and fusion to prevent progression and stabilize the cervical spine, though surgery is unlikely to return function. After 1 year of relative clinical stability without her cervical collar, it was not deemed necessary to restart its application. Six weeks after evaluation she continued to experience neck pain with arm weakness and numbness without symptom progression. |
A 70-year-old male was admitted to our hospital because of a severe headache, fever, and confusion. The patient had been well until 5 hours before admission, when fever up to 39.6°C and mental status change developed. He had a history of Waldenstrom macroglobulinemia last treated 10 months ago, chronic HBV infection, chronic obstructive pulmonary disease, hypertension, and benign prostate hyperplasia.\nOn examination, he was confused, with a Glasgow Coma Scale of 11/15 (eye opening response 2/4, best verbal response 4/5, and best motor response 5/6), and febrile and had nuchal rigidity. Due to presumed bacterial meningitis, he was immediately treated with ceftriaxone, vancomycin, ampicillin, and dexamethasone, according to European guidelines on empiric treatment of bacterial meningitis, while a computed tomography (CT) of the head was performed due to decreased level of consciousness and did not reveal any abnormality. A lumbar puncture was performed and revealed 6960 white blood cells (WBCs) per field at the cerebrospinal fluid (CSF), while 98% were neutrophils. Latex and gram stain of the CSF were negative, while a culture of the CSF and blood cultures were sent. The patient was admitted to the Internal Medicine Department. Ceftriaxone, vancomycin, ampicillin, and dexamethasone were continued. On the fourth day of hospitalization, both CSF and blood cultures grew S. pneumoniae that was sensitive to penicillin and then antimicrobial treatment was deescalated to ceftriaxone only. On the third day of hospitalization, his fever and symptoms resolved completely, while the inflammatory markers decreased.\nHowever, on the fourth day of his hospitalization, the patient developed bradycardia down to 40 beats per minute, which was associated with mild dizziness while standing without improvement of the heart rate, with the electrocardiogram showing a sinus bradycardia (). Because of the CNS infection, the possibility of intracranial hypertension was suspected, and a fundoscopy was performed, which did not show signs of increased intracranial pressure. Since no other cause of bradycardia was noted, even after all medications were recalled, a 24-hour rhythm recording (Holter) was performed, which revealed sinus bradycardia as a basal rhythm during the 24 hours, with a lowest heart rate of 30 beats per minute, as well as three episodes of nonsustained ventricular tachycardia. A transthoracic heart ultrasound was performed and revealed an ejection fraction of 55%, mild left ventricular hypertrophy, left atrial dilation, and a small amount of pericardial fluid. Due to the absence of an obvious reversible factor that could be associated with the bradycardia and the presence of symptoms, the placement of a permanent pacemaker was considered. Surprisingly, some days before the placement of the pacemaker, a medical doctor that was on a night shift discovered that the patient's wife was administering to him eye drops containing timolol, a b-blocker used for glaucoma, which she started doing the night before the bradycardia had developed, without letting any member of the staff know. The eye drops were stopped and the bradycardia resolved along with the patient's symptoms. A repeat 24-hour rhythm recording (Holter) was performed the following days and was normal. The patient was discharged and during follow-up there was no recurrence of the bradycardia. |
A 67-year-old male patient was admitted to our Physical Medicine and Rehabilitation outpatient clinic with complaints of difficulty in opening his mouth, oral leakage during liquid food consumption, and speech difficulties. His medical history revealed that he was admitted to the neurology outpatient clinic with complaints of vertigo, the difficulty of speaking, and understanding 12 months prior. The complaints of the patient were found to be compatible with a transient ischemic attack. Doppler ultrasonography revealed 95% stenosis in the internal carotid artery. Carotid endarterectomy and consequent patch angioplasty were performed by the cardiovascular surgery team and no postoperative complications were seen. After one month of the operation, his present complaints were started; however, these were not considered to be associated with operative complications.\nOn physical examination, he had an incision scar on his right sternocleidomastoid muscle. He could fully close his eyes, raise the eyebrows symmetrically. Nasolabial folds were symmetrical in the smiling position. However, the elevation of the right lower lip was evident, when the patient opened his mouth (Figure 1). Other neuromuscular examination findings were normal. An electrophysiological study of the facial nerve was conducted. Although the compound muscle action potential (CMAP) in the right orbicularis oculi by stimulating the zygomatic branch of the facial nerve was normal, CMAP of the right mentalis muscle by stimulating the MMBFN was absent (Figure 2a). Needle electromyography of the mentalis muscle revealed a single fiber activity at maximal voluntary activation. Sonographic evaluation of the mentalis muscle showed a decreased muscle thickness in the right side, compared to the left side (2.3 mm vs. 3.1 mm, respectively) (Figure 2b). The patient was diagnosed with marginal mandibular nerve paralysis. A total of 15 sessions (five days a week for a total of three weeks), stretching and proprioceptive neuromuscular facilitation exercises, and massage were applied. Electrical stimulation was also administered to the lip depressor muscles for strengthening. After this program the fluid leak from his mouth and speech difficulty were fully recovered. A written informed consent was obtained from the patient. |
A 49-year-old male with no prior medical history presented to the ED approximately 4 hours after being stung on the right forearm by a lionfish while cleaning his home salt-water aquarium. The patient reported that he felt a sting followed by immediate pain and bleeding from the puncture site. He became diaphoretic with continued pain and experienced minimal relief after removing the barbs from the puncture site, taking aspirin and ibuprofen, and soaking his arm for 2 hours in a warm water bath. The patient presented to the ED for further pain management.\nOn initial exam the patient was noted to have erythema, edema, and urticaria extending up the right arm from his fingertips to the lower portion of the humerus, with a visible puncture wound at the volar aspect of the forearm (). He reported continued burning pain, described as 10/10 pain, although he did feel that it had plateaued since exposure. He denied chest pain, palpitations, shortness of breath, lightheadedness, or nausea/vomiting/diarrhea. His initial blood pressure was 139/95 mmHg, heart rate 105 beats/minute, respiratory rate 24 respirations/minute, and temporal temperature 37.2°C.\nThe medical toxicology service was consulted and the patient was treated per their recommendations. The extremity was submerged in a hot water bath for 30 minutes with subjective, immediate improvement in symptoms (). After 10 minutes of the water bath, the patient also received parenteral hydromorphone 1 mg every hour for 4 hours for continued pain. An X-ray performed to evaluate for residual foreign body was negative, and tetanus vaccination was administered. The patient had improvement in pain and was admitted to the observation unit for overnight monitoring and continued pain management with parenteral analgesics.\nThe following morning, 6 hours after the last dose of analgesic medication, the patient's pain score was reported as 0/10 and the swelling and erythema were improved. He received a total of 4 mg hydromorphone and 10 mg oxycodone during his hospitalization. All laboratory values, including creatine kinase, remained within normal limits and the patient was discharged home approximately 20 hours after envenomation. |
An 8-year-old Chinese boy with no specific family or psychosocial history was admitted to our hospital with an emergency occurrence of purpura, severe hematemesis, large bloody stools, and sharp abdominal pain. His symptoms had begun 2 weeks prior to admission, with abdominal pain and an erythematous pinpoint rash on his arms. The rash developed from his upper limbs (opisthenar and arms) to his lower limbs. Laboratory examination in the outpatient clinic revealed no abnormalities in indicators such as white blood cell count, platelet count, and hemoglobin. After oral medication (specific unknown), his abdominal symptoms began to reduce, as did the purpura. Ten days prior, the rash progressed mostly on the legs, and he experienced deeper abdominal pain in the form of persistent pain with abdominal gassiness and emesis. He was admitted to another hospital with a diagnosis of HSP. Seven days prior, he had melena. After fasting and fluid replacement, there was no obvious improvement in the symptoms. Half a day prior, his face and lips appeared pale, and he had increased abdominal pain, accompanied by numerous bloody stools and hematemesis. He was immediately treated with methylprednisolone, posterior pituitary injection, somatostatin, and hemocoagulase, together with the infusion of large blood products (Table ). At this stage, the patient still produced large amounts of blood in the vomit and stool. His vital signs were extremely unstable, and he was transferred to the pediatric intensive care unit of our hospital. The patient had purpura with lower limb predominance and abdominal pain (consistent with one of the following 4 criteria: abdominal pain, histopathology, arthritis or arthralgia, and renal involvement), and was diagnosed with HSP.[\nOn admission, he had severe anemia, with a blood pressure of 76/44 mm Hg, pulse of 135 beats/min, and respiratory rate of 25 breaths/min. There was also a palpable purpura rash on both legs, tenderness in the abdomen, and absence of bowel sounds. Routine blood examination revealed a hemoglobin level of 70 g/L, white blood cell count of 11.48 × 109/L, and platelet count of 13 × 109/L. The liver function test showed albumin 10 g/L. The serum electrolytes showed sodium 140 mmol/L, potassium 2.92 mmol/L, chloride 112.1 mmol/L, and bicarbonate 15.9 mmol/L (Table ) with coagulopathy. Therefore, HSP complicated with an alimentary tract hemorrhage was diagnosed. He was immediately treated with intravenous methylprednisolone (2 mg/kg per day), infusion of blood products, and somatostatin but after 2 days after treatment (day 3), he still had massive gastrointestinal hemorrhage, poor circulation, a reduced level of consciousness, and unstable vital signs. Abdominal ultrasonography and plain abdominal radiography revealed no enterobrosis. The patient was also evaluated by pediatric surgeons, and the continuation of medical treatment was suggested. However, his condition deteriorated, and he needed to rely on a life-supporting blood transfusion. He developed signs of peritonitis with abdominal distension. Gastrointestinal tract perforation was suspected. A contrast-enhanced computed tomography (CT) scan of the whole abdomen revealed curved liquid samples and gas shadows on the left and front of the stomach, supporting the possibility of gastrointestinal tract perforation (Fig. ). On day 4, an emergency laparotomy was performed. The surgery revealed that the anterior wall of the descending duodenum was thinner with a 1 cm × 1 cm diameter perforation, and the posterior wall had a 3 cm × 1 cm ulcer, which had penetrated into the peritoneum of the pancreas and experienced active bleeding from the broken end of the vessel. The intraoperative hemorrhage volume was approximately 3000 mL, including intragastric bleeding and intestinal blood clots. Pathological examination indicated chronic inflammation of the intestinal wall mucosa in the descending part of the stomach and duodenum, with hemorrhage, ulceration, interstitial congestion, and edema. Immunofluorescence microscopy of paraffin sections showed granular and lumpy IgA focal deposition in the blood vessel walls (Fig. ). Postoperatively, he was administered nasal continuous positive airway pressure-assisted ventilation, anti-infection treatment, albumin transfusion, platelet transfusion, abdominal drainage, methylprednisolone, fluconazole antifungal treatment, and wound dressing. The general symptoms gradually improved, vital signs were stable, and abdominal pain was relieved. The drainage tube was assessed after discharge, the abdominal CT was repeated after 1 month and the duodenostomy tube was removed 50 days after surgery. There was no evidence of rebleeding during the 2-month follow-up assessment. |
In June 2016, a 19-year-old male developed acute abdominal pain after consumption of alcohol. The patient did not complain about fever, nausea, vomiting, diarrhea, or jaundice. He had a history of alcohol drinking and no history of smoking. After admission to our facility, he signed an informed consent form and received examination and treatment. The results of the laboratory examination showed that the levels of blood amylase, lipase, carcinoembryonic antigen, CA125, and CA199 were normal. Abdominal CT scan revealed a cystic structure located in the pancreatic tail with a size of 6.5 cm × 4.6 cm and regular margin of margin enhancement in both arterial and portal venous phases []. Magnetic resonance cholangiopancreatography showed that this location was not communicating with the pancreatic duct [Figure and ]. In addition, EUS examination provided the following information: (1) uniform ultrasound echo in the pancreatic parenchyma and no expansion of the pancreatic duct; (2) cyst-solid space-occupying lesion with a size of 4.2 cm × 4.1 cm, smooth inner wall of 0.28 cm thick, four-layered echo of the partial pancreatic wall similar to that of the stomach, and no separation or nodule; (3) CDFI showed rich blood flows around the lesion and no blood vessels inside. The contrast-enhanced EUS showed pronounced enhancement of the pancreatic cyst-wall and no enhancement inside the pancreas [Figure , and ]. Then, a 19G fine needle was punctured inside and 40 mL of brown fluid was extracted []. Next, elective laparoscopy was performed to resect this pancreatic space-occupying lesion, resulting in a mass with the size of 4 cm × 4 cm × 5 cm, soft texture, clear border, and no adherence to the surrounding tissues. No other anomalies were observed during this surgery. Subsequently, pancreatic mucinous cystoadenoma was considered by the surgeon. Finally, postoperative pathology examination showed that this sample was gastric tissue that had mucosa, submucosa and muscularis propria but lacked serosa. Fewer glands were found in this mucosa than in normal stomach, indicating gastric hypoplasia []. The resected segment of the pancreatic space-occupying lesion was approximately 11 cm long []. The inner wall was white, the outer wall was dark red, the thickness was 0.3 cm, and a nipple-shaped protuberance was found on the inner wall (tip) []. Accordingly, the diagnosis was malformation of heterotopic gastric mucosa in the pancreas. |
A 59-year-old caucasian female was diagnosed with thyroid papillary carcinoma after total thyroidectomy in 2001. Diagnosed with postsurgical hypothyroidism under treatment with levothyroxine, 100 micrograms per day. There was no other previous medical history of interest. The patient did not consume tobacco or alcohol.\nIn 2008, a computerized tomography scan (CT) showed locoregional relapse and surgery was performed with resection of locoregional recurrence and left cervical lymphadenectomy. In November 2011, pulmonary relapse was treated with I-131 since November 2011 until March 2012 (total accumulated dose: 850 mCi). In October 2016, a CT scan showed a progression of the disease with cervical and pulmonary progression. The patient started sorafenib, 400 mg twice a day. Stable disease was maintained during 20 months. In June 2018, patient presented an episode of abrupt instability and cervical pain. The magnetic resonance imaging (MRI) (Fig. ) showed a new metastatic lesion in the skull base with destruction of bony structures of the left occipital-petrous region. At this point, a molecular study of the cervical node was performed and a mutation in BRAF was found.\nDue to the lack of alternative therapeutic options, treatment with vemurafenib–trametinib was requested as a compassionate use. In August 2018, patient was started on the combination of dabrafenib 150 mg twice a day and trametinib 2 mg once a day. MRI in October 2018 showed a slight decrease of the metastatic lesion in the skull base (Fig. ). In addition, the patient showed evident clinical improvement with decreased initial headache and cervicalgia.\nA follow-up PET–CT scan was performed in January 2019. Tumor was on radiological partial response. In addition, there was intestinal pneumatosis with mild sign of pneumoperitoneum (Fig. ). Patient had no digestive symptoms and the abdominal medical examination was completely normal. Also normal neurological examination was verified. Routine physical examination showed blood pressure 110/60 mmHg, heart rate 80 bpm and 36.5 degree centigrade temperature. Blood test showed normal liver function: AST 21 U/L, ALT 16 U/L, bilirubin 0.19 mg/dL and normal renal function: creatinine 0.7 and glomerular filtrate > 90 mL/min. Blood count values were normal: leukocytes 7.6 × 1000/µL, hemoglobin 12 g/dL and platelets 417 × 1000/µL.\nThe surgery department recommended conservative treatment unless new abdominal signs or symptoms were seen. Intravenous metoclopramide 10 mg/8 h and paracetamol 1000 mg/8 h were administrated. Both drugs, dabrafenib and trametinib, were discontinued after the PI diagnosis.\nOnly 10 days after the discontinuation of targeted therapy, tumor progression was shown with clinical deterioration due to intracranial hypertension and the patient died 4 weeks later because of intracranial disease progression. Because the cause of death was related with tumor progression, autopsy was not performed. |
A previously medically free 48-year-old female was referred from the dermatology clinic with a complaint of generalized pruritic urticaria refractory to conventional treatment of non-sedating antihistamines (allerfin 4 mg + XYZAL 5 mg) and topical corticosteroids (mometasone 0.1% QD). The pruritic urticaria started three days prior to presentation; however, she has been having similar episodes over the past few months but never as severe as her current presentation. General laboratory investigations were performed and the results were significant for undetectable TSH levels. Given these results, the patient was referred to Internal Medicine where further history and examinations were performed. The patient revealed to have been suffering from moderate cardiac palpitations, weight loss, heat intolerance, polyphagia, oligomenorrhea and diarrhea over the past four months. The patient had originally dismissed these symptoms as perimenopausal symptoms. On physical examination, the patient was found to have urticarial rash, staring look, fine tremors and a stage 3 goiter. However, all these thyrotoxic signs and symptoms were mild in this patient and she was notably negative for eye symptoms, lid lag and lid retraction.\nThe patient was started on propranolol 20 mg BID and complete thyroid function tests with thyroid antibodies were performed alongside an ultrasound of her thyroid and cervical lymph nodes. The ultrasound showed a mildly enlarged thyroid, measuring about 12 cc in size, with heterogeneous hypoechoic pattern and decreased vascularity that is suggestive of post-inflammatory thyroiditis. There were no suspicious focal thyroid lesions and cervical lymph nodes looked benign bilaterally (Figure ).\nLab results came back typical for primary hyperthyroidism with high free T3 and T4 but low TSH. Also, TSH receptor antibodies and anti-thyroglobulin antibodies came back positive which confirmed the diagnosis of GD. Notably, the patient IgE titer was also elevated.\nAfter confirming the diagnosis, the patient was started on carbimazole 10 mg BID and was booked for follow-up in six weeks. During the first week of treatment, the patient developed a shortness of breath and a severe pruritic rash. She discontinued the medication by herself and her symptoms improved over the following week. Once the patient returned to baseline, she restarted carbimazole 10 mg QD, yet again she developed a shortness of breath and a severe pruritic rash. She discontinued the medication and presented to the clinic the following day. In the clinic, her hyperthyroidism was found to have gotten worse. The patient has also developed lid lag and lid retraction which were absent on the original presentation. Blood was sent for thyroid function tests (TFTs) which came back even higher than her original lab results. Her gamma-glutamyl transferase (GGT) was also elevated suggesting some hepatotoxicity from carbimazole. The patient was switched to propylthiouracil (PTU) 50 mg TID and was evaluated for possible radioactive iodine therapy.\nAfter six weeks on PTU, the patient was reevaluated and she showed a marked improvement in her symptoms. Even her initial complaint of pruritic urticaria is now completely controlled on a low dose of antihistamines; however, she still had some lid lag and fine tremors. Laboratory studies also showed a marked improvement in TFT and GGT which normalised after discontinuing Carbimazole. The patient was followed up every six weeks and showed continuous improvements; by her sixth month of treatment, she was found to be clinically euthyroid with normal free T3 and T4 levels. |
A 40-year-old male patient presented to a hospital in December 2011 with a right-sided thyroid mass and hoarseness. An ultrasound scan (USS) and fine needle aspiration cytology was consistent with MTC. The blood laboratory analysis of the patient revealed high serum levels of calcitonin and CEA, 222 pg/mL and 18 ng/mL, respectively. In December 2011, the patient underwent a total thyroidectomy and bilateral neck lymphatic dissection with a good recovery. Histological analysis of this specimen revealed a 17 mm MTC. In total 49 lymph nodes were removed from the right central, paratracheal, right lateral neck, and 13 lymph nodes contained malignant deposits. These were positive for MTC (12 lymph nodes from the right and one lymph node from the left cervical). Tumor tissue examination for the RET oncogene mutations was negative and no familial or personal history was positive for a genetic syndrome. The postoperative serum calcitonin and CEA levels were 1.99 pg/mL (normal range: 0–18 pg/mL) and 0.9 ng/mL (normal range: 0–3 ng/mL non-smoker), respectively. A USS of the neck did not reveal lymphadenopathy. Following normal urinary catecholamine, metanephrine determination the patient proceeded to a surveillance program. The patient made a good recovery with a normal serum calcium on no supplements at 2 weeks follow-up. However, in the subsequent months the calcitonin levels began to rise to pre-reoperative surgery levels suggesting low grade persistent disease. A computed tomography (CT) scan and USS of the neck were performed in July 2012 revealing only cytologically proven small metastatic lymph nodes. The patient underwent a repeat uncomplicated selective neck lymph dissection. Histological analysis confirmed that lesions showed features consistent with metastatic MTC. Immunocytochemistry revealed calcitonin expression and nuclear TTF-1 expression supporting MTC. In the subsequent months serum calcitonin and CEA levels began to rise. Skin nodules began to grow and by August 2014, serum calcitonin and CEA levels reached 411 pg/mL and 31.51 ng/mL. A fluorodeoxy-d-glucose–positron emission tomography (FDG-PET) scan of the whole body, performed in August 2014, revealed widespread evidence of metabolically active disease involving the right retropharyngeal space, upper right side of larynx, right superficial, depth axillar conglomerated lymph nodes, paraesophageal lymph nodes, IVa and VIII liver segments, aortocaval, peripancreatic, para-aortic, and pericaval areas consistent with widespread disease. Since surgery was not possible we considered the use of tyrosine kinase inhibitors (TKIs) (vandetanib, cabozantinib, etc) as first line therapy but these drugs are only available after systemic cytotoxic treatment in Turkey with special permission. Therefore, we treated our patient with capecitabine (1,700 mg/m2) from day 1 to 14 and temozolomide (200 mg/m2) from day 10 to 14 every 4 weeks. Assessments of tumor measurements, serum calcitonin, and CEA were made before treatment and followed-up. After two courses of treatment, the patient was referred to the clinic in December 2014 with improved performance and was asymptomatic with normal hemoglobin, calcium, urea, and creatinine levels. The calcitonin and CEA levels decreased to normal range ( and ). The radiologic imagines (thorax and abdominal CT) revealed significant shrinkage of axillary, para-aortic, and paracaval lymph nodes and shrinkage rate including liver lesions was more than 50%. The chemotherapy was well tolerated, with no diarrhea or hematologic toxicities. |
A 3-year-old female child was brought to the hospital with complaints of cough, difficulty in breathing, fever and swelling over the right side of chest, neck and face for last 2 days. She had no history of any similar episode in the past. Physical examination revealed that child was conscious but tachypneic and febrile. SCE was present all over the right side of face, neck and chest. Auscultation revealed diminished air entry with fine crepitations on the right side of the chest without any rhonchi. Her X-ray of the chest depicted SCE and pneumomediastinum with infiltrates in the middle zone of the right lung without any evidence of collapse of the lung and the presence of fluid or air in the pleural cavity. There was no evidence suggestive of foreign body (FB) [].\nShe was initially diagnosed as a case of pneumonitis with barotrauma and put on antibiotic therapy. As there was no clinical improvement and cause of SCE without pneumothorax was also not clear, therefore, diagnostic bronchoscopy under general anesthesia was planned.\nStandard monitors were applied for monitoring heart rate, noninvasive blood pressure and pulse oximetry. Injection glycopyrrolate-0.05 mg was given intravenously. Anesthesia was induced with an inhalational technique using oxygen, nitrous oxide (50:50) and halothane 1-2% delivered through Ayre's T piece face mask with spontaneous ventilation. Anesthesia was maintained with oxygen, nitrous oxide and halothane. Succinylcholine 20 mg was administered intravenously (IV) and direct laryngoscopy was attempted but it revealed no abnormality. It was followed by tracheobronchoscopy with Richard Wolf rigid ventilating bronchoscope size 5 mm OD. Left side bronchoscopy revealed normal study, but on the right side a granulation tissue was detected. On careful examination and removal of granulation tissue, a FB was detected just near the origin of apical branch of right main bronchus, embedded in the mucosa. It was retrieved safely but with great difficulty. It was a plastic piece in tortoise shape with multiple sharp pointed projections measuring 5 mm × 9 mm []. During the procedure, the child was ventilated gently through bronchoscope with oxygen, nitrous oxide (1:1) and halothane 1-2%. Besides the initial dose, only two intermittent doses of succinylcholine (5 mg IV each) were required. She maintained her all vitals and oxygenation throughout the procedure.\nShe was given steroids (dexamethasone-2 mg and hydrocortisone-50 mg) intravenously. Her trachea was intubated with a tracheal tube (4 mm ID) to provide chest physiotherapy and endotracheal suction was done to remove secretions. Lignocaine 1% 1 mL was instilled intratracheal through endotracheal tube to reduce the irritation of the tracheobronchial tree and hence, to control cough reflex. The trachea was extubated when the child was awake. During postoperative care, she was given humidified oxygen by face mask (FiO2: 0.35) for 6 h. She maintained her SpO2 above 96% in postoperative period. SCE reduced gradually within next 48 h without any subsequent intervention. On 3rd day, X-ray of the chest revealed no abnormality [], and the child was discharged to the care of her parents. |
A 64-year-old woman sustained total scalp avulsion when her long hair was pulled into a spinning machine. She was not wearing a helmet (). The avulsion started from the top of the nose, crossed the upper one-third of both ears and extended down to the lower occipital area. Neurological examination revealed intact bilateral extraocular muscle and normal facial sensory responses.\nEmergent replantation of the avulsed scalp was performed under general anaesthesia, with an interval between the injury and revascularisation of 4 hours (). The right superficial temporal artery (STA) and superficial temporal vein (STV) had sufficient length, with STA diameter of 1.0 mm and STV diameter of 1.1 mm, enabling direct anastomosis. Immediately after anastomosis of the right STA and STV, abundant blood supply was noted throughout the entire scalp, including the left temporal area, with perfusion from the circumferential edge. The left STA and STV were narrow and short, and additional anastomosis resulted in much less blood flow without use of a vein graft. Four drains were inserted in the occipital space between the scalp and skull. We did not use thrombolytic drugs during and after surgery. Postoperative congestion occurred with concomitant effusion between the epicranial aponeurosis and skull; however, the symptom improved gradually with the aid of drains.\nThe scalp mostly survived; however, partial skin necrosis (3.0×4.0 cm2) developed in the lower left occipital region. Therefore, the lesion was debrided and reconstructed with a split skin graft 2 weeks after the operation. The wound healed well, and thick hair growth was clearly observed. As of 2 months after the first operation, exuberant hair was evident (). Another finding was that the patient’s hair growth pattern was different between the sides, that is, the right temporal area had greater hair growth compared with the left. At 1 year postoperatively, her hair had grown sufficiently, and right eyebrow movement was observed (). Although sensory paralysis and dysfunction of the left frontal muscle remained, the patient was very satisfied with the aesthetic result. |
A 10-year-old girl presented with a painful, palpable left temporal mass. She exhibited no neurological deficits nor signs or symptoms of systemic illness. Head CT demonstrated a spiculated tumor arising from the left temporal bone, resulting in substantial mass effect on the temporal lobe (Fig. ). There was no evidence of an extracranial primary lesion. She underwent craniotomy for gross total resection of the lesion. Intraoperatively, the tumor was markedly adherent to dura but without intradural extension. Histological analysis demonstrated a small round blue cell tumor, with prominent CD99 staining of tumor cells. Fluorescence in situ hybridization (FISH) was positive for the EWSR1 rearrangement diagnostic of EWS (Fig. c). The family initially pursued homeopathic treatments including nutritional support and tumor monitoring using serum anti-malignin antibody, a non-specific and non-sensitive marker of malignancy.\n,\n The patient experienced a local recurrence at 3 months after presentation. Repeat complete resection of the tumor demonstrated intradural tumor extension although systemic work-up including chest CT and bone marrow biopsy remained negative for extracranial disease. She was treated according to the Children’s Oncology Group (COG) interval compression arm of AEWS0031 with a regimen of vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide/etoposide. She underwent focal radiation with a delay to concurrent chemotherapy due to an interval infection, and then completed continuation compressed therapy. Two years after her initial presentation, she was found to have local recurrence as well as bony metastases to the spine. She was subsequently treated with local irradiation, followed by complementary therapies which included high-dose IV vitamin C and a special diet high in whole fruits, vegetables, whole grains, and no processed sugar. Her disease progressed further with widespread bony dissemination, also treated with focal palliative radiation to the spinal metastases. Bone marrow biopsies at the time of each recurrence showed no evidence of malignancy. She died nearly 3 years after presentation. |
A 42-year-old male patient presented to our emergency room of Istanbul Medipol University Hospital with a low-velocity gunshot injury. We detected one entry point on the posterior aspect of the thigh, just superior to the popliteal groove. No exit wound was detected on physical examination. There was swelling around the knee and range of motion was limited due to pain and swelling. Neurological and vascular examinations revealed intact. Following the initial assessment, the vascular examination was confirmed by Doppler ultrasonography of the related extremity. There were no signs of compartment syndrome in the preoperative physical examination. A bullet was detected in the knee joint on the initial X-rays (). Intravenous antibiotics including cefazolin and ornidazole were started following the initial assessment.\nPreoperative computed tomography (CT) scans revealed an undeformed bullet just superior to the intercondylar eminence of the tibia in coronal plane and inferior to the patella in sagittal plane (). A knee arthroscopy was planned and performed under general anesthesia, 4 hours after the patient's admittance. Using standard anteromedial and anterolateral arthroscopic portals, the anterior cruciate ligament, and medial and lateral menisci were found to be intact. A non-displaced flap-like osteochondral defect, approximately 1 cm × 1 cm in size, was detected on the medial femoral condyle. A midline, 1 cm long mini-incision was performed through the patellar tendon as the Swedish portal is called. This extra portal allows direct access to the intercondylar notch and insertion of a large-sized grasper (). The bullet was removed using this portal. The knee joint was debrided and irrigated with 3,000 mL of saline solution. Immediately after releasing the tourniquet, swelling of the anterolateral compartment of the leg and pulse deficiency was detected in the dorsalis pedis artery on the foot. Thus, we performed an anterior and lateral compartment release through a single lateral incision fasciotomy.\nActive knee flexion exercises up to 90° were started on the first postoperative day. However, weight bearing was not allowed on the surgical side due to the chondral lesion. On the third day after surgery, the incision of fasciotomy was primarily closed. No signs of infection were detected at follow-up visits. CT and magnetic resonance ımaging was performed in the 6th postoperative week in order to evaluate the bone and chondral healing (). Complete union was detected at the fracture line, and the chondral lesion seemed to be healed without an additional intervention. |
A 31-year-old woman visited our emergency room after a minor hit to her occipital region. At the first examination, her consciousness was clear without neurological deficits. Computed tomography (CT) scans showed only a subcutaneous hematoma in her occipital region []. However 2 h later, her consciousness got worse drastically and second CT scan revealed remarkable enlargement of her subcutaneous hematoma [Figure and ]. Her scalp ruptured leading to massive external bleeding, and she went into hemorrhagic shock, so an emergent surgery was performed to stop the bleeding.\nAfter the evacuation of the hematoma, the sources of the bleeding were identified as the occipital artery and the entire surface of the subcutaneous connective tissue. They were cauterized, and the bleeding was controlled. We resected her extended skin for effective astriction. The next day, soon after the removal of her bandage, her head bulged again, and a second emergent surgery was performed.\nDiffuse bleeding from subcutaneous connective tissues continued. They were cauterized entirely, and a collagen sheet coated with bovine thrombin, and bovine aprotinin (TachoComb®) was used []. Her extended skin was cut off adequately by plastic surgeons and wrapped in bandages again [].\nAfter the second surgery, her subcutaneous hematoma did not expand. She received blood transfusions in the intensive care unit but bled from her back to the thoracic cavity. She died of cardiac tamponade 48 days after onset.\nOur patient was suspected of having a connective tissue disease because her clinical findings suggested multiple system fragilities. She had hypertelorism, short and downslanting palpebral fissures, a long philtrum, and thin upper lip. Her fingers were slender, and her vertebral column showed the scoliosis. In addition, she repeated dislocations of the shoulder joint and diverticulitis. Autopsy findings showed hyperextension of the skin, a massive subcutaneous hemorrhage and repeated dislocations of the shoulder joint. Autopsy diagnosis was compatible with EDS. |
A 45-year-old female presented with arthritis of bilateral hips secondary to developmental dysplasia of the hip (DDH) with chief complaints of pain, difficulty in ambulation and significant restriction of the activities of daily living. On clinical examination, the patient had an antalgic gait with relative shortening of 2 cm of the left lower limb. Flexion deformity of 20° was noted bilaterally with further flexion up to 90° with additional fixed adduction deformity of 15° on the left side and a fixed abduction deformity of 20° on the right hip. Radiographic evaluation revealed Crowe Grade 1 dysplasia on the right and Grade II dysplasia on the left side (). Bilateral uncemented “ceramic on poly” THR (Pinnacle, Corail, Depuy Synthes) was done in the same setting in the lateral decubitus position utilizing the posterolateral approach to the hip joint. Size 44 mm Pinnacle cup with two acetabular screws with a polyethylene liner with an uncemented size six Corail femoral stem with a 28 mm ceramic femoral head was used on both sides. On the left side, additional bone grafting of superior acetabular defect was done with bone graft obtained from the osteotomized femoral head. The surgical wounds were closed in layers with no surgical drains in situ. Immediate post-operative radiographs showed optimal alignment. The patient was mobilized with a walker and weight bearing as tolerated. The patient was discharged on the fourth post-operative day. The surgical wounds were examined on the 14th post-operative day, and suture removal was done. The surgical scar was healthy. However, on clinical examination, the hips were lax with exaggerated range of motion. Repeat radiographs revealed bilateral dislocation of the hip with a periprosthetic fracture in the left femur. There was no history of trauma on enquiry. Closed reduction under anesthesia was attempted unsuccessfully on the right side.\nBilateral open reduction was planned. Both acetabular components were stable. On the left side, femoral fracture extended up to the 8 cm distal to the lesser trochanter. The component was unstable, and there was a change in the femoral stem version. The prosthesis was extracted, and the femoral stem was revised using a long distal fitting revision stem (20 cms × 12 mm Biorad, Medisys). The proximal periprosthetic fracture was treated by reduction and was stabilized by encerclage wiring. Although pre-operative radiographs showed only a dislocation an undisplaced proximal femur fracture similar to the left side was found intraoperatively. The prosthesis was unstable with a change of version. Stem was revised with a distal fitting long revision stem (12 mm × 20 cms, Biorad Medisys). The fracture was reduced and was stabilized by encerclage wiring. Post-operative radiographs revealed optimal alignment. Bed side physiotherapy was instituted, and Medical therapy for osteopenia was instituted. Post-operative recovery was uneventful with drain removal done on the second post-operative day and suture removal done on the 14th post-operative day. The fractures united uneventfully, and the patient is ambulatory at the latest follow-up at 6 months (). |
A 32-year-old male presented at our institution with a history of pain over the lateral aspect of the left foot for 2 years of insidious onset. He complained of pins and needle sensation over plantar aspect of the left foot. There was no significant history of trauma. He noticed swelling behind the left knee in the past 6 months which was initially peanut shaped and gradually progressed to the present size.\nOn examination, there was an oval mass of 2 × 3 × 1 cm, firm, non-pulsatile, non- fluctuant, non-transilluminating in the left popliteal fossa () which was mobile in both directions. Skin over the swelling was pinchable. The patient was neurologically stable except with decreased sensation over lateral aspect (plantar region) of the left foot. Notably, the left popliteal and dorsalis pedis pulses were felt.\nMagnetic resonance imaging (MRI) of the left popliteal fossa revealed encapsulated round to oval shaped, eccentrically placed lesion seen within the intermuscular space in the posterior aspect of knee joint. Lesion shows homogenous isointense on T1 and heterogeneous hyperintense signal on T2. There are hypointense foci seen within the hyperintense area on T2 which is suggestive of fascicular sign. The sagittal image showed continuity of mass lesion with the tibia nerve displaying fat split sign, lesion measuring 2 × 3 × 1 cm (, , ).\nUnder spinal anesthesia, the patient underwent neurolysis of tibial nerve and excision biopsy of tumorous lesion (, ) by incising the epineurium of tibial nerve since the tumorous lesion was eccentrically placed. As there was no disruption of tibial nerve continuity, no nerve repair was done. Gross resected specimen of tumorous mass of 2 × 3 × 1 cm and the cut specimen showing areas of hemorrhage, necrosis, and cystic spaces interspersed along the tumorous lesion (, ). Histopathological examination (×40) of the lesion showed biphasic tumor consisting of compact hypercellular Antoni A areas and myxoid hypocellular Antoni B areas and nuclear palisading around fibrillary process of Verocay bodies without any neural elements seen (). Immunohistochemistry (IHC) staining of the resected lesion revealed strong positivity for S-100 staining ().\nThe patient was regularly followed up at timely intervals for 9 months since the excision of the lesion. The follow-up period was uneventful. The patient had improved sensation over lateral aspect (plantar region) of the left foot and without any recurrence of tumorous lesion during the follow-up period. |
A 67-year-old woman who complained of gross hematuria for 3 days was admitted to our department on November 21, 2012. The patient reported hematuria without fever, and denied having low back pain or edema of lower limbs. She had been diagnosed with diabetes, but was not undergoing regular treatment. Her main laboratory examination and ancillary investigation results were as follows. Routine urine test showed occult blood in the urine, with ++ cells/μL. Biochemical examination showed a blood sugar level of 8.36 mmol/L. The serum creatinine (SCr) level and estimated glomerular filtration rate (eGFR) were 93.5 μmol/L and 60.78 ml/min/1.73 m2, respectively. Urine cytology test showed the presence of tumor cells twice. Enhanced abdominal computed tomography (CT) revealed a soft tissue density in the upper calyx of the left kidney, suggesting pyelo-carcinoma (Fig. ). Computed tomography angiography (CTA) identified the blood vessels that supply the tumor region (Fig. ).\nAfter admission, the patient received aggressive perioperative treatment in order to improve her cardiac and renal function, and to control her blood sugar levels, so as to improve her tolerance to surgery. Ureteroscopy detected a papillary neoplasm with a pedicle in the upper calyx of the left kidney. Subsequently, the patient underwent LPN with segmental renal artery clamping. After entering the retroperitoneal space and dissociating the renal artery and renal vein, the target artery was clamped beyond the final bifurcation before entering the parenchyma. Access and clamping strategies for target arteries were preoperatively determined on the basis of the 3D models by the radiologist and surgeon. After incision of the left renal parenchyma and exposure of the upper calyceal neck, the tumor was found confined to the upper calyx. Later, the renal calyx and parenchyma were sutured successively after complete resection of the neoplasm. During the operation, a double J tube was placed for drainage of urine and for postoperative infusion therapy. The tumor was found to be confined to the upper calyx of the left kidney. Histopathological examination of the surgical specimens confirmed a diagnosis of papillary Grade I carcinoma of the renal pelvis, with massive hemorrhage, with the tumor measuring 18 mm × 10 mm × 7 mm and confined to the mucosal layer (Fig. ). All surgical margins were negative.\nThe patient received postoperative intravesical instillation of pharmorubicin fortnightly for 3 months. Subsequently, the double J tube was removed. A cystoscopy was performed every 3 months for the first 3 years. CT was performed to check for the recurrence or metastasis of the tumor every 6 months for the first 3 years, and annually thereafter. There was no evidence of recurrence during the follow-up period for more than 43 months after surgery till the time of writing this report. The most recent SCr level and eGFR of the patient were 82.9 μmol/L and 69.78 mL/min/1.73 m2, respectively. |
A 46-year-old nulliparous woman presented after having experienced pain in the right side of her groin and labia majora for four months, as well as a lump that was increasing in size. She had previously undergone three laparotomies for ovarian cystectomy at 20, 10, and 8 years prior to this visit due to her severe progressive pelvic pain. The pathological examinations of surgical specimens obtained from all three operations indicated ovarian endometriosis.\nThree years prior to this visit, she experienced progressive pelvic pain and she also noticed a growing mass at the right labia majora. She underwent total abdominal hysterectomy (TAH) with bilateral salpingooophorectomy (BSO) and excision of a 3.7 × 2.5 cm labial mass. Pathological examination revealed adenomyosis and multiple leiomyomas in the uterus as well as endometriotic cysts in both ovaries. The labial mass contained focal atypical endometriosis on a background of benign endometriosis (Figures and ). The patient had an uneventful recovery. However, she did not return to follow-up after this operation. She had no history of hormonal replacement therapy (HRT).\nOne month before this visit, she had undergone an incision biopsy of her labial mass at the provincial hospital, and the pathological report indicted only apocrine hidrocystoma. Nevertheless, the mass had increased in the size with accompanying progressive pain.\nUpon presentation at our hospital, there was a 7x4-cm hard mass at the right labia majora extending to the right groin area. The mass seemed to be in continuity with the pubic symphysis that would require pubic bone excision and reconstruction with flap surgery to achieve complete resection. However, the patient refused such extensive surgery. Based on the previous pathological diagnosis of endometriosis of the vulva in this patient, she was then initially treated with two doses of GnRH agonist followed by one 150 mg dose of depot medroxyprogesterone acetate. These medications were administered with the aim of shrinking the bulk of the mass. However, the mass developed into an ulcer and rapidly increased in size (). A second biopsy of the mass was then performed. The pathologic examination showed a papillary growth structure lined by round tumor cells with clear cytoplasm and pleomorphic nucleoli (). shows residual atypical endometriosis that had merged with the tumor. The patient's tumor exhibited focal cytoplasmic staining for napsin A. A diagnosis of clear cell adenocarcinoma of the vulva with coexisting atypical endometriosis was made based on these pathological findings.\nComputed tomography of the abdominopelvic region showed an ulcerative mass at the right labia majora and nodal metastasis at the bilateral external iliac and superficial inguinal regions that varied in size from 2.0 to 3.5 cm. Other CT findings were unremarkable.\nAs this case was considered inoperable, systemic chemotherapy consisting of paclitaxel and carboplatin was administered. The growth of the tumors stabilized during the first two cycles of chemotherapy but rapidly progressed thereafter. Palliative treatment under multidisciplinary care was subsequently initiated. Pelvic radiation was administered to slow down the progression of disease and to alleviate pelvic pain. At 17 months after her initial presentation, the patient passed away due to the progression of the disease and severe sepsis. |
A 23-year-old Caucasian woman was presented at the ED of our hospital after having lost her consciousness in a bus. Bystanders reported convulsions during this event. At our ED, the woman was too weak and too confused to answer questions, therefore taking a correct history was not possible. Her medical records showed substance abuse: cocaine, cannabis, amphetamines, crack and GHB. At time of presentation at the ED, she was awake, but with diminished consciousness and incoherent thoughts, which was scored as a Glasgow Coma Score (GCS) of 14. Except for tachycardia, vital signs and electrocardiography were normal.\nShe was diagnosed with GHB intoxication and admitted to the medical ward for observation because her consciousness was still slightly lowered. The evening of the day of admittance, she became very agitated, had hallucinations and recognized no persons other but her boyfriend. Vital signs remained stable. Lorazepam was started at 1 mg 4 times per day and raised to 1 mg 6 times per day. As the agitation increased, she had to be physically restrained. Being still uncooperative, she received 5 mg haloperidol and 50 mg clorazepate.\nThe next day she remained disoriented and still had hallucinations. Because of her uncooperative behaviour, she was transferred to the psychiatry ward, next to, but separated from the hospital, where she was treated with clorazepate 50 mg daily, oxazepam 25 mg 3 times per day, biperiden 2 mg 2 times per day and haloperidol in a rising dose up to 5 mg 3 times per day.\nSix days later, her psychiatrist sent her back to the ED because of deterioration with loss of motor control and fever. The patient was again very agitated. Physical examination showed no abnormalities and neither did a computer tomography (CT) of the brain. At that time she had a fever of 39.3 °C, a blood pressure 109/76 mmHg, and a pulse rate of 132/min. Pulse oximetry showed an oxygen saturation of 97%, while her respiratory rate was 33/min and she now scored a GCS of 10 out of 15 (E2 M5 V3). Laboratory investigation showed WBC 20.000/μl, C-reactive protein (CRP) 50 mg/dl and a highly increased creatinekinase (CK) of 6000 U/l. Again she was admitted to the medical ward for observation and treatment with lorazepam. The next day, the situation worsened with hypoxia (pO2=8.2 kPa), a rising CK (9800 U/l) and extreme motion restlessness of extremities with choreatic movements and peri-oral hyperkinesias. The choreatic movements, resembling Huntington's disease, prompted us to consider a cause related to the GABA system, leading eventually to the diagnosis of GHB withdrawal syndrome. Bruises were visible on knees and elbows. With the diagnosis of severe GHB withdrawal syndrome and rhabdomyolysis she was admitted to the Intensive Care Unit (ICU). The midazolam (50 mg/h) and clonidine (120 mcg/h) needed to manage the unrest, inhibited patient's coughing reflexes and lead to diminished clearance of secretions of her upper airway, resulting in hypoxia, which necessitated intubation and mechanical ventilation. Even despite these high doses of sedatives, she still sometimes had phases of being awake and sitting upright in bed. Because of rhabdomyolysis, she received 6 L infusion fluid intravenously per 24 hours. There were no signs of renal failure at any time. After three days the neurological situation had improved significantly. The patient was extubated despite having need of high doses of midazolam and clonidine, which could be decreased over days. Temperature, CK, WBC and CRP returned to normal values. Eight days after admission to the ICU, the patient was discharged to the medical ward with oxazepam 80 mg 3 times per day. Soon thereafter she could be discharged from the hospital, without any obvious neurological sequelae.\nHer parents later reported that over the last three months for admittance, their daughter was using GHB every two to three hours. Based on information given by her parents and other relatives, our patient daily GHB intake was estimated between 60 and 90 g. Patient later confirmed this. |
A 41-year-old man started with migraine-like attacks and behavioral changes that evolved in a few weeks to confusion and gait instability. After 30 days of the initial symptoms, he was brought to the emergency room when he presented a reduced level of consciousness and global aphasia. At admission, physical examination revealed an aphasic and stuporous patient in postictal state; there were no motor deficits or meningism. Vital signs were within the normal range. The patient had a history of desmoplastic medulloblastoma in his right cerebellar hemisphere at age of 20. The lesion was treated with right occipital craniotomy resection followed by a 56 Gy two-dimensional cranial radiation therapy (36 Gy/18 fractions in the whole brain and 20 Gy/10 fractions in the posterior cranial fossa). The spinal cord was also irradiated with 30 Gy in 20 fractions. He had no other chronic diseases, no history of seizures, or ischemic cerebrovascular events.\nAt the neurology ward, the patient underwent a brain MRI that revealed new and prominent left hemisphere gyriform contrast enhancement associated with increased T2 and FLAIR signal involving predominantly the left occipital and temporal lobes (Fig. ). MRI also showed small areas of restricted diffusion within the left occipital lobe, compatible with subacute infarction. Cerebrospinal fluid analysis showed only a slight increase in proteins (71 mg/dL). Electroencephalogram showed disorganized rhythms, without epileptiform discharges or periodic activity. Four-vessel angiography showed no vascular lesions.\nThe patient initially received carbamazepine (800 mg/day) for seizures, remaining free from new spells after recurrent seizures in the first few days of hospitalization. Intravenous methylprednisolone (1,000 mg/day for 5 days, with tapering schedule with prednisone) and verapamil (160 mg/day) were administered with fast recovery of consciousness and gait abnormalities. After corticosteroid therapy, aphasia had almost completely remitted, and he reported no headache crises. At follow-up, the patient remained with mild language impairment, his new MRI after 7 months showed resolution of previous abnormalities (Fig. ), and the new electroencephalogram normalized. |
A 32-year-old man was admitted to our hospital because of a bulge in the left inguinal region. He had no pain and no urinary symptoms. Physical examination revealed a non-tender, reducible bulge in the left inguinal region. His body mass index (BMI) was 19.0 kg/m2. Laboratory data were all within the normal range. Computed tomography (CT) performed 5 years before admission for other disease showed a left indirect inguinal hernia. In addition, a small protrusion of the adipose tissue into the left femoral canal and a portion of the bladder pulled to the left femoral ring were observed retrospectively (Fig. ). Preoperative imaging studies were not performed. Based on a diagnosis of left indirect inguinal hernia, we planned for TAPP.\nThe patient was placed in the supine position under general anesthesia. A urinary catheter was inserted before the operation. A 10-mm port was placed for the laparoscope at the umbilicus and two 5-mm ports were placed at each flank. Laparoscopy and intraperitoneal observation revealed a left indirect inguinal hernia with sliding of the surrounding tissue. There were no other peritoneal indentations (Fig. a). We incised the peritoneum and dissected the preperitoneal space toward the Retzius space along the vesicohypogastric fascia. We found a mass covered with the vesicohypogastric fascia that was pulled into the femoral ring (Fig. b). The mass was confirmed to be a portion of the bladder; the mass expanded when we injected saline through the urinary catheter (Fig. c). We first dissected the protruding bladder all around from the preperitoneal tissue sliding with the bladder because the protruding bladder had developed severe adhesion to the hernial orifice. Then we reduced the protruding bladder carefully without causing injury. The length of the herniated bladder in the femoral canal was about 1 cm. The diameter of the femoral ring was 1 cm. An aberrant obturator artery was observed (Fig. d). After additional dissection, we repaired the left myopectineal orifice with ULTRAPRO Partially Absorbable Lightweight Mesh (15 × 10 cm, Johnson & Johnson, Cincinnati, OH) (Fig. e). Operative time was 101 min. The patient was discharged on postoperative day 1 without complications. No recurrences or symptoms were noted at the 12-month follow-up. |
We present a the case of a 50 year old woman (history of malnutrition, chronic obstructive pulmonary disease) accepted in the Digestive and Surgery Division due to an intestinal obstruction of 3 days. The patient underwent emergency surgery for intestinal obstruction, with removal of impacted bezoar in the ileocecal valve. After 48 h, the patient started in sepsis by intestinal suture dehiscence. Right hemicolectomy was performed urgently with cleaning of the peritoneal cavity. After 72 h of operation, in the ICU, the patient situation turn to worse by a suture dehiscence of the anastomosis, requiring a new emergency surgery. Due to septic state by a colonic dehiscence and disseminated peritonitis, and the inability to perform anastomosis, colectomy and terminal ileostomy. A Bogotá bag laparostomy was precised due to the abdominal Compartimental syndrome (intra-abdominal pressure index of 25, intraabdominal pressure measurements was done intravesically).\nIn the ICU the APACHE II score was in the first week 15 (first week range 8–17) and the Mannheim peritonitis index was 34 (first week range 28–36). OA scoring by Bjórcket al was 2B (Fig. ). After stabilization in the ICU the Bogotá bag was removed 6 days later, and we placed dynamic closure system (ABRA®) (Fig. ). IAP measurements were performed in the patient during ABRA treatment in the ICU, but no pathologic values were recorded. The measurement of the abdominal wound was: 15 cm wide and 27 cm length. The ileostomy in the lower right quadrant functioned normally. The fascia was approximated one cm per day. Sixteen days later we proceeded to the primary closure of abdomen (Fig. ).\nThe patient was discharged from the ICU after 2 days since the primary closure. Finally the patient was discharged a week from the Hospital. There was no dehiscence of skin and wound had healed properly in the follow up after 3 years (Fig. ). |
A 26-year-old Asian female presented to the emergency room for increased urinary frequency, severe pain, and burning overnight. She was unable to hold urine; however, she had no abdominal pain, blood in the urine, abnormal or cloudy urine color, strong or foul urine odor, or fever. Her menstrual periods had always been regular. She had a 5-year-old healthy child and no history of any obstetric or gynecological problems. She had a pulse rate of 90 beats/minute and blood pressure of 100/60 mmHg. Her body mass index was 22 kg/m2. Investigations showed hemoglobin of 13.5 g/dL (normal range: 12–16) and a total white blood cell count of 6,800/mm3 (normal range: 4,000–11,000); urine microscopy test did not reveal any red blood cells or white blood cells. Her kidney function tests were within normal limits. The woman had presented to an outpatient clinic the day before for neck pain and headache; with a diagnosis of torticollis, she was prescribed tizanidine 2 mg three times a day and acetaminophen 500 mg four times a day. She developed symptoms an hour after the second dose of tizanidine, ie, within 10 hours of initiation of the drug. She had been on famotidine 40 mg once a day for 4 weeks for dyspepsia. She never had an episode of cystitis or urinary infections before. There was no history of any allergies or predisposing conditions that could have been responsible for the acute onset of this adverse event. Tizanidine treatment was subsequently discontinued and the patient was treated with hydration; her symptoms gradually improved within 24 hours. After stabilization, the patient was referred for urological consultation and ultrasonography of the urinary tract that failed to show any evidence of the current urinary problems. Urine culture did not yield any microorganism growth. The Naranjo probability scale was used to evaluate the possible causal relationship between tizanidine and the acute urinary symptoms. The scoring obtained by this algorithm was 4, which indicates a possible causal association between the drug and the adverse reaction. The Naranjo probability scale categorizes adverse drug reaction (ADR) probability based on predefined weighted questions evaluating factors like temporal association of drug use and ADR occurrence, previous reports of ADR, alternative explanation of the event, drug level, dose–response relationship, etc. Scoring for Naranjo algorithm follows: >9= definite ADR; 5–8= probable ADR; 1–4= possible ADR; 0= doubtful ADR. |
An 11-year-old girl was reported to ambulatory care with fever and headache for 2 weeks. Prior to these symptoms, the patient was in normal health. She had febrile episodes (100–102 °F) without chills or rigors. The fever was associated with severe headache on the right side and was not associated with any vomiting, nausea or aura. The patient did not have any other significant complaints, clinical signs or symptoms pertaining to the ear, nose, throat or chest, or bleeding diathesis except for a history of falling 2 years previously when she was 9 years of age.\nWe admitted the patient for further evaluation. On clinical examination, the patient had tenderness over the right mastoid bone with an intact tympanic membrane. With the above history, a provisional diagnosis of acute mastoiditis of the right side was made. Pediatric neurology, endocrinology, and ophthalmology consultations were obtained. On fundoscopy, the patient had bilateral papilledema with normal vision on both sides and was referred for further imaging with magnetic resonance imaging (MRI) of the brain which revealed no space-occupying lesions in the brain.\nRoutine investigations were all within normal limits except for erythrocyte sedimentation rate which showed a three-fold increase in the first hour. Subsequently the Mantoux test was performed which was positive (22-mm induration) and there was increased serum homocysteine.\nSubsequently the patient was worked up for tuberculous OM, and a bone scan was performed for OM of the temporal bone. The patient had a positive Mantoux test (22-mm) and 99Tc- MDP triple phase bone scan with single-photon emission computed tomography (SPECT-CT) of the temporal bone which suggested asymmetric uptake with increased radiotracer accumulation in the right temporal bone posteriorly. The patient was kept on AKT but did not respond.\nHigh-resolution computed tomography (HRCT) scan of the temporal bone showed mild sclerosis and cortical destruction involving the right temporal bone (). With these findings, the patient was taken up for debridement to obtain tissue for histopathological diagnosis.\nThe patient underwent right cortical mastoidectomy under general anesthesia. There was a mass with soft cheese-like material on the sigmoid sinus bony plate. The sigmoid sinus plate was eroded, and the mass was tracked medially and found to be compressing the lumen of the sigmoid sinus. The mass occupied the space between the sigmoid sinus bony plate and the membranous lumen, misleading the diagnosis as lateral sinus thrombosis (). The disease was cleared overall and the sigmoid sinus was found to be normal with good flow as confirmed by needle aspiration.\nTissue was sent for histopathological examination which revealed Mucor mycosis-induced OM of the right temporal bone (). Postoperatively, the patient received 2g cumulative dose of Amphotericin-B (liposomal) along with voriconazole 50mg per day for 3 weeks.\nThe patient was strictly monitored for liver and renal function tests. The patient was free from symptoms after 3 weeks, with regular follow-ups to date. Post-operative magnetic resonance imaging (MRI) of the brain () and magnetic resonance venography (MRV) () after 6 months revealed post-canalised sigmoid sinus of the right side with good flow contour. |
An 18-year-old Burmese man, with no significant medical history at the time, visited the Emergency Department for intermittent abdominal pain that had acutely worsened. He reported no fevers, shortness of breath, lightheadedness, fatigue, blood in the stool, tarry stools, changes in bowel habits, weight loss, nor any other symptoms other than severe abdominal pain. His vital signs were normal. Physical examination was remarkable for left upper quadrant abdominal tenderness and mild abdominal distention. Also, small, dark blue-colored spots on the lips () as well as the fingers were noted (). Laboratory testing was notable for hemoglobin of 8.3 g/dL with an unknown baseline. He had a mean corpuscular volume of 74 fL, a red blood cell distribution width of 17.2%, as well as an iron panel with iron level of 18 µg/dL, iron-binding capacity of 362 µg/dL, and ferritin of 35 µg/dL findings consistent with iron-deficiency anemia.\nAbdominal computerized tomography (CT) scan was performed and showed findings of a segment of large intestine invaginating into the adjoining intestinal lumen at the level of the splenic flexure (). The patient was taken to the operating room where he underwent exploratory laparoscopic bowel resection in order to surgically treat an intussusception that had caused large bowel obstruction. He was found to have multiple large polyps of varying sizes which were sent for histopathological evaluation. The pathology report showed hamartomatous polyps consistent with Peutz-Jeghers polyposis. There was no malignancy and the margins were negative. The patient was started on oral iron supplementation and referred to a gastroenterologist for further evaluation. He underwent colonoscopy where he was found to have many polyps throughout the colon and rectum (), the largest of which were removed and sent for histopathological evaluation. The histology revealed a polyp with proliferation of the smooth muscle bundle () on hematoxylin and eosin stain (× 400). Immunohistochemistry (IHC) stained positive for smooth muscle actin (SMA) (× 100) indicating smooth muscle origin with central core branching of the smooth muscle () consistent with hamartomatous polyps. Also, the patient underwent genetic testing, which was positive for a germline mutation in the STK11 (LKB1) gene, confirming the diagnosis of Peutz-Jeghers syndrome. His family members have since been referred for genetic testing and colonoscopy as they none of the family members had a colonoscopy done. |
We present a case of a 52-year-old married man, who has the sixth grade, and works as a mechanic. He has no previous history of medical conditions. As a psychiatric background, he reported depressive symptoms following the death of his only son 22 years ago.\nThe patient was referred to treatment at the psychiatry department of Hospital de Braga for the first time by his family doctor for collecting various objects, predominantly stones, papers, and damaged pieces of cars that were deposited unorganized in the patient’s house. The patient collected these items because he thought they were valuable and/or usable in the future, but recognized that the collection was exaggerated. He could not discard any of these items, even if he never used them when needed. He reported to get anxious when someone else discarded some of these items. This behavior had started about 20 years earlier and it worsened with time. Despite, the thoughts of the possible use of these items were the reason why he could not throw out the possessions, these thoughts were not considered intrusive, repetitive, or egodystonic. The garage, attic, and surroundings of his house were cluttered with these objects (Figure ). The clutter in his house is classified in to seven categories according to the clutter image rating (, ).\nOn admission, in the mental status examination, it was observed that the patient was vigil, calm, and oriented; his mood was depressed; his speech was organized, logic, and coherent; and there were no psychotic symptoms.\nA psychotherapeutic plan for the patient was designed. The goals were to understand and educate the patient on his symptoms and beliefs, so he could understand the need of treatment. Cognitive restructuring of the beliefs and exposure to non-acquire and discard the objects saved were also explored. Along with the psychotherapeutic plan, a pharmacological treatment with fluvoxamine 100 mg id and trazodone 150 mg id was made, to treat the coexistent depressive symptoms and insomnia. During the first 6 months of treatment, the patient continued to buy and collect objects. Then, fluvoxamine was gradually augmented to 100 mg tid and quetiapine 200 mg was added to the treatment plan, with progressive improvement in the symptoms and the patient being able to sell/recycle most of the items after 9 months of this treatment (Figure ). The patient is currently medicated with quetiapine 100 mg id for insomnia and organized the spaces cluttered (Figure ). The patient and his wife were very gratified with the results.\nThis study was performed in accordance with the provisions of the Declaration of Helsinki 2008 and was approved by the ethics eommittee of Hospital of Braga. We obtained informed written consent from the patient authorizing publication of clinical case and his photographs. His anonymity has been preserved. |
A 59-year-old female patient visited our oral and maxillofacial department clinic complaining of a sense of discomfort in the right posterior palatal area. The patient did not remember exactly when the symptom began. The patient had no other concerned medical history. On clinical examination, a dome-shaped mass of 2.0 × 2.5 × 1.0 cm with clear border and no ulceration was observed in the right posterior palatal area. On the next days of admission, incisional biopsy was performed under local anesthesia. Pleomorphic adenoma (with central coagulative necrosis, most likely traumatized pleomorphic adenoma) was reported histopathologically. Hence, the patient underwent simple mass excision with safety margin under general anesthesia without any additional examination (Fig. ). Postoperative histopathologic report was epithelial myoepithelial carcinoma with positive basal resection margin. Magnetic resonance imaging of the head and neck and whole-body positron emission tomography were performed for further examination, but there was no evidence of distant metastasis (pT2N0M0, stage II) that was shown (Fig. ). Postoperative radiation therapy was administered to the primary site at the Department of Radiation Oncology, and the total radiation dose was 6148, 5400, and 4500 cGy at the operation site, border area, and lateral cervical lymph node level IB and II, respectively, for 39 days. There were no significant complications other than oral mucositis.\nAfter radiation therapy, a 1.5 × 1.0 cm fistula occurred in the right site, which was the operated site, and a fistula closure was done using two-flap palatoplasty under general anesthesia at 8 months after radiation therapy. However, the operated right side flap, which had poor blood circulation after radiation therapy, was necrotized (Fig. ). We removed the necrotized flap under general anesthesia and designed a facial artery myomucosal island flap containing the right mucosal membrane and buccinators, using the facial artery as a trophic blood supply to the flap. The flap was transposed by tunneling to restore the defect through the lingual side of the mandible. The donor was restored using the ipsilateral buccal fat pad flap. After the operation, the nasal and oral opening was closed and properly healed up (Fig. ). |
A 20-day-old male baby was admitted to the Department of Pediatric Surgery with a 24-hour history of abdominal pain and distension accompanied by bilious vomiting. His body temperature was 39.8°C, pulse 150 beats/min and blood pressure 90/45 mmHg. The physical examination revealed an extremely tender and massively distended abdomen with no peristalsis. A nasogastric tube that was inserted, produced a large amount of bilious fluid. Laboratory investigation revealed blood cell count 17,800/mm3, erythrocyte sedimentation rate 35 mm/h, whereas all other findings were normal. An upright plain abdominal radiograph revealed intestinal obstruction with air-fluid levels and massively distended and oedematous intestinal loops in the upper abdomen (Figure ). Ultrasonography examination did not disclose the cause of the ileus. As the patient's clinical status was rapidly aggravated an immediate surgical exploration was necessitated.\nAt operation an inflamed mass was found in upper left quadrant, in which the splenic flexure, the spleen, the greater omentum and loops of the small intestine participated. Careful dissection of the adhesions, between the greater omentum and the intestinal loops, revealed a small amount of pus and an inflamed spherical mass (4 × 4 cm in size). This mass was full of pus and adherent to the antimesenteric border of the splenic flexure of the colon and shared a common muscle wall with it (2 × 2 cm in dimension). The spherical mass was isolated from the colon and removed easily. Examination of the colon and the mass did not reveal any communication between them. The muscle coat of the colon was simply sutured. The histopathological examination of the excised specimen showed histological patterns resembling the colon, resulting in the final diagnosis of colonic obstruction due to an inflamed and purulent non-communicating spherical duplication in the splenic flexure of the colon.\nThe postoperative course was uneventful and the baby was discharged on the 6th postoperative day. |
A 52-year-old woman presented to the emergency room with intense pain and swelling of the left leg and lumbar area, accompanied by high fever. According to the patient, the pain occurred 6 days ago without traumatic events. After assessing the patient’s medical history it was known that 23 years ago she delivered a baby via Caesarean section. Unfortunately, an early postoperative period was complicated: laparotomy, hysterectomy and cholecystectomy were performed due to pelvic abscess formation and peritonitis. At a subsequent time the patient remained healthy until her current hospitalization.\nClinical evaluation revealed swelling of the previously mentioned areas and painful palpation. There was significant redness in the lateral middle part of the left thigh. Initial blood workup showed elevated levels of serum C-reactive protein (518 mg/L) and procalcitonin (4.4 ng/mL). Due to a septic condition, the patient was admitted to the intensive care unit.\nFor further evaluation, a computed tomography (CT) scan was performed. It revealed free air in the left leg () and presacral abscess draining to the left gluteal area and thigh through the greater sciatic notch (). Moreover, it showed fixated ileum to the abscess. To treat thigh phlegmon, multiple incisions and fasciotomies were performed in the left gluteus and thigh, releasing a large amount of purulent discharge. Thigh phlegmon gradually resolved, however, the origin of the presacral abscess was still unknown. CT data () and postsurgical colonoscopy with terminal ileoscopy raised suspicion of an ileal fistula causing bowel content evacuation to the presacral space. The second surgery was performed. Ileal diverticulum was found approximately 10 cm from ileocecal valve. A fistula was connecting the lumen of diverticulum with presacral abscess. Ileal fistulectomy and presacral abscessotomy were performed. Postoperative course was uneventful and the patient was discharged from the hospital. Histological examination of the surgical specimen identified the perforated ileal diverticulum, forming fistula to the presacral abscess. According to the pathology report, the ileal diverticulum was more likely congenital. |
A 31-year-old female patient presented to our clinic with pink-red pimples that she had had since birth, and that were dispersed throughout the right gluteal region, down to the right femoral area, and had grown over time in both number and size. The patient reported that her lesions became infected twice per year. Nothing in particular was noted in her family history or her laboratory tests.\nThe dermatological examination showed vesicle-like lesions that began in the right gluteal region and extended to the inner side of the right femoral area. These were 1–5 mm in diameter, had colors varying between yellowish pink and red, and while some had a tendency to form groups, other were dispersed throughout the area [Figure and ]. A punch biopsy was taken from the patient, and histopathology revealed that there were many dilated lymphatic ducts and lymphocyte groups around these ducts in the superficial dermis []. Because some lesions were hemorrhagic and others had a translucent yellowish color, a PDL was applied for the hemorrhagic lesions and cryotherapy for the translucent yellowish ones. PDL with a cap that is 5 mm in diameter, a 350 ms pulse time, and 585 nm wave length was used on the patient's lesions. The laser treatment consisted of 5 sessions at 4-week intervals, beginning with a dose of 7 J/cm2, and in every session the dose was increased by 0.5 J/cm2, so that the final dose was 9 J/cm2. Meanwhile, cryotherapy was applied to the translucent yellowish vesicles in 5 sessions of double freeze–thaw cycles at 3-week intervals. With the combination of PDL and cryotherapy, the patient's lesions regressed [Figures , and ]. We followed up this patient for nearly two years. Small sized new lesions measuring a few millimetres appeared during this time and we performed cryotherapy (five sessions at three month intervals). After treatment, significant improvement was observed in the patient's lesions. |
A 20-year-old female patient with hemoglobin-SS sickle cell disease, osteonecrosis of the right hip with chronic right hip pain, and asthma presented complaining of pain in both thighs for 5 days. The pain began after ice-skating but she denied any direct trauma to her limbs. On presentation, she was febrile and tachycardic, with leukocyte count of 25.3 × 109/L and hemoglobin of 7.0 g/dL. There was no tenderness to palpation of the hips bilaterally and no tenderness to palpation of the joints, but an ill-defined swelling to the right anterior thigh was noted which the patient reported was chronic.\nAn initial diagnosis of sickle cell vasoocclusive painful crisis with systemic inflammatory response syndrome was made, and sepsis work-up was done. She was started on analgesics and intravenous fluids and also received a simple blood transfusion. On hospital day (HD) 2, she was noted to have persistent fever and leukocytosis and so was started on intravenous Levofloxacin empirically. At that time, her left thigh pain appeared to be worsening, with a new area of swelling and warmth but no tenderness. X-rays of the left hip and left thigh were done, which showed heterogeneous appearance of the proximal left femoral shaft, which was thought to be likely secondary to sickle cell osteodystrophy, infarct, or infection.\nThe patient's blood cultures obtained on admission had shown no growth and her urine culture was negative. Her chest X-ray showed no evidence of pneumonia. However, clinically, she did not appear to be improving, with persistent pyrexia and leukocytosis. Her C-reactive protein levels were elevated at 7.8 mg/dL, for which her dose of Levofloxacin was increased and Vancomycin was added. Due to increasing suspicion for osteomyelitis, an MRI of the left lower extremity was done. It demonstrated 2 areas of loculated fluid collection: the first was in the proximal left thigh anteriorly, in the quadriceps muscle, measuring approximately 1.8 × 2.0 × 4.0 cm. The second was in the proximal left thigh laterally, between the quadriceps muscle and subcutaneous tissue, and measured approximately 2.8 × 3.0 × 10.0 cm. These areas had low signal intensity on T1 weighted imaging and high signal intensity on fluid sensitive sequences. An abscess was noted within the left proximal femur, with a communicating tract extending from the abscess within the bone to the overlying muscle and subcutaneous tissue (). The radiological findings were consistent with a Brodie's abscess.\nOrthopedics consultation was sought and the patient subsequently underwent incision and drainage of the left thigh abscesses in the operating room. A large amount of pus was found within the thigh muscles, which extended down into the bone. Two defects were also identified in the bone where the pus appeared to be extruding from. The area was debrided and irrigated, a Jackson Pratt drain was left in situ, and the wound was closed. Clindamycin was added to her antibiotic regimen. Postoperatively, leukocytosis began trending down slowly and the patient became afebrile. She was started on physical therapy for early mobilization, which she tolerated well. Wound cultures obtained during the incision and drainage surgery showed no growth of organisms. On post-op day (POD) 3, the drain was removed.\nHer postoperative course was subsequently complicated by persistent fevers that started on POD 4. High sensitivity C-reactive protein (hs-CRP) was obtained and noted to be significantly elevated at 101.54 mg/L (normal < 0.5 mg/L). CT scan of bilateral lower extremities showed anterior thigh abscesses, involving multiple muscle groups of both lower extremities. Her antibiotics were switched to Imipenem. She was taken back to the operating room where she underwent incision and drainage of the left and right thigh abscesses. A copious amount of purulent material was found within the anterior soft tissue of the right thigh, which communicated with a hole in the proximal femur. Exploration of the left thigh revealed small amounts of pus and a hematoma around the femur, as well as the previously identified defects in the bone. Jackson Pratt drains were left in the right and left thighs. Wound cultures obtained were negative again, with no organisms seen on gram stain.\nUnfortunately, she continued to spike fevers and leukocytosis persisted. Repeat blood cultures, urine culture, and chest X-ray were negative. A repeat CT scan of the lower extremities was done, showing residual abscess in the iliopsoas muscle and vastus lateralis muscle of the left thigh and in the right thigh. Antibiotics were switched to Vancomycin and Levofloxacin but then subsequently changed to Linezolid and Piperacillin-Tazobactam. Percutaneous ultrasound-guided drainage of the residual bilateral thigh abscesses was undertaken: 3 right thigh abscesses were identified and approximately 4.5 mL of purulent fluid was drained; approximately 4.0 mL of fluid was aspirated from the left thigh fluid collection. Postprocedure CT scan showed minimal residual abscess fluid. Jackson Pratt drains were kept in situ and continued to drain moderate amounts of serosanguineous fluid.\nThree days after percutaneous drainage, the patient remained afebrile and her leukocyte count was consistently trending downwards. She had a repeat CT scan of the lower extremities, which showed decreased fluid collection and soft tissue swelling of the thighs compared with prior studies, bony changes consistent with sickle cell osteodystrophy, and chronic osteomyelitis. She was discharged to a long-term acute care hospital to facilitate continued intravenous antibiotic therapy with Vancomycin and Piperacillin-Tazobactam for at least 6 weeks. She presented for follow-up in infectious disease clinic 3 weeks later and was noted to be doing well with no fever episodes and significantly decreased pain. Repeat hs-CRP was significantly lower at 33.75 mg/L. She was continued on antibiotics for the proposed course. |
A 76-year-old woman diagnosed with an aortic arch aneurysm was admitted to our hospital for worsening dyspnea on exertion. The patient presented without hoarseness or symptoms of airway obstruction. The dyspnea had started 2 weeks before admission and gradually worsened until provoked by light exercise. The patient was referred to our department for treatment. Upon admission, the physical examination showed a blood pressure of 95/70 mmHg, heart rate of 100 beats/min, and oxygen saturation of 95% as measured by pulse oximetry. After light exercise, her oxygen saturation decreased to 90%. Laboratory tests showed increased liver transaminase (64 U/L and 100 U/L of aspartate aminotransferase and alanine aminotransferase, respectively) and brain natriuretic peptide concentrations (1967 pg/mL). A computed tomography (CT) scan showed that a large 70-mm diameter saccular aortic arch aneurysm had substantially compressed the periphery of the pulmonary artery and that a large thrombus had protruded into the main trunk of the pulmonary artery. No other CT findings of chronic pulmonary thromboembolism, including abrupt narrowing, obstruction, or calcified thrombi, were found in the pulmonary artery branches (). Echocardiography showed preserved left ventricular ejection fraction of 61.5%; decreased left ventricular dimension of 26.6 and 18.2 mm in diastole and systole, respectively; profound pulmonary hypertension characterized by a right ventricular systolic pressure of 95.9 mmHg; moderate to severe tricuspid regurgitation; and pulmonary stenosis indicated by a peak velocity of 3.84 m/s and a peak pressure gradient of 59.2 mmHg. Echocardiography did not show intracardiac or extracardiac left-to-right shunt flow. The patient was preoperatively diagnosed with a large saccular aortic arch aneurysm that caused the pulmonary stenosis. An urgent aortic repair was scheduled on day 6 of hospitalization.\nDuring anesthetic induction, the patient’s systolic blood pressure was temporally decreased to 40 mmHg. During the surgery, transesophageal echocardiography showed no intracardiac or extracardiac left-to-right shunt flow. A median sternotomy was performed, and a serous pericardial effusion was found in the pericardial space. The ascending aorta was intact on inspection. A cardiopulmonary bypass was established with an ascending aorta cannulation, bicaval venous cannulations, and placement of a left ventricular vent via the right superior pulmonary vein. The patient’s body temperature was cooled down to a tympanic temperature of 26°C, and the cardiopulmonary bypass was arrested. The ascending aorta was incised, and a selective cerebral perfusion via the three supra-arch branches was initiated; the cerebral circulatory arrest time was 5 min. Aortic arch opening revealed a thrombus filling the entrance of the saccular aneurysm at the lesser curvature of the aortic arch. First, the aortic wall was trimmed at the distal portion of the thoracic aorta over the entrance of the saccular aneurysm, and a four-branched 26-mm vascular prosthesis (Japan Lifeline Co., Ltd., Tokyo, Japan) was then anastomosed to the distal thoracic aorta. After the distal anastomosis, the lower body perfusion was resumed via a side branch of the prosthesis; lower body ischemia time was 59 min. After removing the thrombus from the aneurysm, a 3-cm diameter foramen was detected at the bottom of the aneurysmal sac in contact with the lumen in the main trunk of the pulmonary artery (). No obvious pus or tumor was present inside or surrounding the aneurysmal cavity. She was diagnosed with ductus arteriosus aneurysm. The pulmonary stenosis was considered to have been caused by not only the external compression but also the thrombus protrusion into the pulmonary artery. The foramen in the anterior wall of the pulmonary artery was closed using a vascular patch () and proximal anastomosis was performed. Following tricuspid annuloplasty, the vascular prosthesis was declamped; the myocardial ischemia time was 170 min. The three supra-arch vessels were reconstructed. The duration for cardiopulmonary bypass, selective cerebral perfusion, and surgery were 274, 199, and 440 min, respectively.\nThe postoperative CT scan showed disappearance of the pulmonary artery stenosis and successful placement of the three-branched vascular prosthesis (). Echocardiography confirmed a 33-mmHg decrease in right ventricular systolic pressure and reduction in trivial tricuspid regurgitation. The preoperative dyspnea experienced by the patient on exertion was relieved. The pathological examination showed that the thrombus protruding into the pulmonary artery was composed of thrombotic materials alone without any vascular wall components. Postoperatively, the patient experienced a parietal lobe stroke. However, she gradually recovered after rehabilitation and was discharged on postoperative day 61. |
A totally health 13-years old boy, without a family history of congenital heart disease was referred to our institution for cardiac evaluation due to a systolic non-common murmur detected from a primary care physician during the systematic school examination. He denied before any exertion intolerance, chest pain, palpitations, dyspnea, syncope or prae syncope. His review of systems and medical history were negative. He had no history of myocardial infarction (MI), arrhythmias, or stroke. His family history was positive for hypertension in his maternal grandparents. However, he and his family denied any cardiac disease, including congenital cardiac disease and sudden death in young adults.\nCardiac examination revealed a regular rhythm with normal S1 and S2. He had a grade 2 out of 6 continuous murmur noted at the apex. There were no S3, S4 or click. He had 2 plus pulses bilaterally in both upper and lower extremities. An electrocardiogram showed normal sinus rhythm with poor precordial R-wave and with no conduction or repolarization abnormalities.\nChest radiography revealed normal heart silhouette with a prominent localized bulge at the apex of left ventricle (). An echocardiogram showed normal cardiac connections, normal left ventricular size and function, dimensions, and wall thickness. The window to evaluate left ventricular apex was poor and careful examination confirmed a diverticulum diameter 4.5 x 4.3 cm, in the inferoapical/apical–lateral walls of the left ventricle (LV) (). By color-Doppler systolic inflow and diastolic outflow was noted, being continuously with other part of the left ventricle. Myocardium with prominent trabeculation was seen along the lateral wall of the chamber. Wall-motion analysis showed that the muscle of the chamber thickened during systole. No thrombus was seen. In addition, the aortic valve was bicuspid without any hemodynamic disturbances. The right ventricle looks smaller with normal contractility (). There are no any other morphologic or hemodynamic disturbances and, all time during examination normal rhythm was noted. Holter monitoring demonstrated scant supraventricular extrasystoles with repeat phenomena, and rare ventricular extrasystoles in pairs. |
The patient was a 31-year-old healthy male who is self-employed in the shipping industry as a repairman of fiberglass boats. After consuming half a bottle of locally produced arrack (alcohol 38 % W/w) he ingested an estimated volume of 150 ml of MEKP containing solvent (60 % MEKP in phthalate solution) as an act of deliberate self-harm. He was unaware of the level of toxicity of the substance.\nThe patient developed severe throat and epigastric discomfort soon after ingestion. He was admitted to a regional hospital where he was given activated charcoal. A nasogastric tube was inserted in anticipation of erosive complications. Over the next 24 hours, his symptoms progressed with worsening irritation of the throat, development of abdominal pain, difficulty in breathing and noticeably reduced urine output. He was transferred to our tertiary care unit for further management of progressive multi organ involvement.\nOn general examination he was alert and coherent with Glasgow coma scale score of 15. There were multiple ulcerations in his mouth and oropharyngeal region. Nasogastric tube contents revealed coffee ground aspirate. Respiratory examination revealed rapid shallow breathing with a respiratory rate of 40 per minute. Auscultation of the lungs was unremarkable and oxygen saturation was 99 % on room air on pulse oxymetry. He was tachycardic (heart rate:104 beats per minute) with normal blood pressure and adequate peripheral perfusion. Severe guarding and tenderness over the epigastrium was present in examination of the abdomen. Bowel sounds were sluggish.\nPreliminary investigations revealed progressively rising serum creatinine and blood urea. He had a neutrophil leukocytosis (Table ). Arterial blood gas analysis showed a high anion gap metabolic acidosis with a pH of 7.21. Serum potassium was elevated at 6.4 mmol/L, which persisted through the first week of hospital stay. Ultrasound scan of the abdomen showed normal sized kidneys with evidence of acute renal failure. Subsequent complete blood counts showed a reducing trend in hemoglobin and platelets. Bite cells, Heinz bodies and fragmented red cells were also seen. Serum lactate dehydrogenase level was elevated. Direct Coombs test was negative. The reticulocyte count was 1.5 % showing an inadequate bone marrow response. Hemolysis settled by the second week of the illness.\nThe patient was managed in the ward. Acute management included intravenous sodium bicarbonate to correct acidosis and medical management of hyperkalemia. Urgent hemodialysis was followed by regular renal replacement therapy for the next four weeks. Repeated blood transfusions (8 units during the first week) were required to maintain hemoglobin levels.\nGastric protection was instituted with intravenous proton pump inhibitors. Parenteral feeding was initiated due to intolerance of oral feeds. On third day the patient developed large volume coffee ground aspirate through the NG tube, which later became bilious. This heralded distal duodenal obstruction, which was confirmed by a gastrografin study. This resolved after 2 weeks and liquid feeds were gradually started as tolerated. However, he had persistent odynophagia. Upper gastrointestinal endoscopy performed on day 28 revealed inflammatory lesions extending from upper esophagus to duodenum. There were slough, exudate and fibrotic bands but significant stricture formation was not seen (Fig. ).\nThe patient was discharged on the 29th day. He was tolerating semisolid diet despite having persisting odynophagia. He had lost 4.7 kg during his hospital stay. His follow up plan included a repeat endoscopic assessment in 3 months time, psychiatric assessment and follow up with the medical unit. He was also referred to the dietitian for nutritional support and supervision.\nBy his first review in 2 weeks the renal functions had returned to baseline. First follow up endoscopy at 3 months revealed slough, which was cleared by the passage of the endoscope. This resulted in temporary relief of odynophagia. However it recurred and the odynophagia persisted for six months. At 6-month review he was tolerating normal feeds with only slight discomfort. He has lost further 7 kg (weight on admission 68 kg) but features of other nutritional deficiencies were not present. One year after ingestion, he was asymptomatic and was gaining weight. |
A 78-year-old man presented with macroscopic hematuria, urinary frequency, and accidental leakage of urine. His past medical history only included benign prostatic hyperplasia. Initial assessment by fibroscopy showed a unique tumor developed on the anterior wall of the bladder. The patient underwent transurethral resection of the bladder tumor. Pathological analysis reported high-grade muscle-invasive urothelial carcinoma of the bladder (pT2 stage). The uro-computed tomography (CT) scan did not show any abnormality regarding the upper urinary tract. Metastatic workup with thoracic and abdomino-pelvic CT scan showed clinically localized bladder cancer. The patient was then referred to our department to undergo a curative intent surgery according to the multidisciplinary committee recommendations. Bilateral extended pelvic lymphadenectomy with radical cystoprostatectomy and ileal neobladder reconstruction were performed. Definitive pathological analysis rendered pT2N0M0 high-grade urothelial carcinoma (TNM 2009) with free surgical borders, associated with prostatic adenocarcinoma Gleason score 7 (3 + 4), grade 4 involving 20 % of both prostatic lobes. A total of 15 days after surgery, the patient developed penile pain. Physical examination showed painful induration located on the right corpus cavernosum of the penis. PET/CT imaging showed a high focal intense uptake of 18F-FDG in the right corpus cavernosum of the penis (Fig. ). The report concluded that there was a high suspicion of metastatic spread to the penis. Complementary penile magnetic resonance imaging (MRI) associated with simultaneous fine needle biopsy were realized. Penile MRI showed low to intermediate signal intensity as compared with the surrounding corpus cavernosum on an axial T2-weighted image (Fig. ). Histopathological examination from the right corpus cavernosum biopsy revealed carcinomatous tumor emboli from the urothelial carcinoma of the bladder (Fig. ). The patient was referred to the medical oncologist for appropriate treatment of the metastatic disease. Concomitant radio-chemotherapy was decided according to the genitourinary tumor board recommendations. This treatment included local radiation associated with cisplatin-based regimen chemotherapy. The patient received chemotherapy with a combination of gemcitabine and carboplatin followed by radiotherapy. Despite such intensive combined treatment, metastatic cancer progression occurred and the patient died.\nPenile metastases are extremely rare events. The most common primary tumors concern the urogenital system (i.e., bladder, prostate, and kidney) or the rectum-sigmoid colon [–]. Indeed, physiopathology of metastases to the penis is still unclear. Several mechanisms of dissemination have been described. A usual way of spread seems to be the retrograde venous dissemination from the pudendal venous system into the dorsal venous system of the penis. However, alternative ways have been evocated such as retrograde lymphatic spread into penile lymphatic channels, iatrogenic implantation secondary to instrumentation, or direct extension from the primary tumor [–]. Interestingly, most cases of penile metastasis are metachronous. The time interval between primary tumor and penile metastasis ranges from 3 to 60 months. Indeed, about two thirds of all penile metastases are diagnosed at a meantime of 18 months after the detection of the primary tumor []. Moreover, penile metastases are usually symptomatic. Most frequent are malignant priapism due to the tumor infiltration of the corpus cavernosum (>40 %), intense penile or perineal pain (≈10 %), penile nodules or ulceration, generalized swelling of the penis, and various urinary symptoms [–]. As previously reported, penile metastases from urothelial carcinoma of the bladder may be detected by either pelvic CT scan or MRI [–]. Classically, the corpus cavernosum is the site of involvement of metastatic penile carcinoma whereas the glans penis and corpus spongiosum are rarely involved []. Even though MRI may able to distinguish metastatic lesion from primary tumor of the penis, the presence of penile lesion must be pathologically confirmed. Percutaneous biopsies are also possible using penile block as anesthesia []. However, as presented in our case report, penile metastasis may be asymptomatic without any clinical sign of the lesion at the time of staging. Indeed, abdomino-pelvic MRI and/or CT scan do not systematically include the penis in routine clinical practice. In this context, diagnosis may be more tricky and challenging. FDG/PET-CT analysis may represent a valuable non-invasive technique which correctly identifies such lesions providing an extensive staging in a single session. Although 18F-FDG/PET-CT has been shown to improve baseline staging in the nodal staging of bladder cancer [], controversy stills exists in relation to the widespread use of PET/CT in clinical practice []. One of the main reasons is its additional cost for a test with low sensitivity [].\nDefinitely, accurate staging of bladder cancer is crucial to guide physicians in establishing the best therapeutic strategy and to avoid useless curative intent treatment option. Once penile metastasis has been diagnosed, the prognosis is poor and death occurs rapidly []. The average survival in patients presenting with penile metastasis is very short (i.e., 4 months from diagnosis), as it is highly associated with advanced disease []. Conversely, only a few cases of synchronous metastasis have been described. Overall, penile metastases must be considered as a non-curable advanced multi-systemic disease requiring palliative therapy such as local radiotherapy and systemic chemotherapy. Partial or total penectomy may be discussed in order to palliate painful symptoms. However, curative intent surgery should be avoided. In our case report, metastasis became evident 15 days after surgery, which is very prompt. Indeed, the patient was asymptomatic and the abdomino-pelvic CT scan did not show any abnormality at baseline staging. Hence, we hypothesize that penile metastasis was already present at time of surgery. Arguably, this case report strengthens the impact of 18F-FDG/PET-CT for detecting asymptomatic penile metastasis originating from muscle-invasive urothelial carcinoma of the bladder. |
The case involves an 18-year-old male with known rheumatic heart disease (RHD) since 11 years of age who was on irregular treatment. The patient presented with shortness of breath (SOB) for two weeks. The patient was diagnosed, admitted, and treated as decompensated heart failure and improved. After one month, the patient returned with fever and SOB. On examination, he was conscious, oriented, and cooperative, but he was ill, pale, and toxic with third degree finger clubbing. Auscultation revealed decreased air entry in the chest bilateral basally, palpable hyperdynamic apex beat of the heart shifted to the sixth intercostal with palpable systolic thrill with diastolic murmur. Chest radiograph (CXR) revealed an enlarged left atrium of the heart. Transthoracic and transesophageal echocardiography (TTE and TEE) showed a dilated left atrium () and destroyed and perforated leaflets of the tricuspid valve with severe (grade IV/IV) aortic regurgitation (AR) and stenosis (). There were also multiple masses on the aortic valve, the longest at 20 mm implanted like a membrane on the left ventricular outflow tract with vegetation or a subarctic membrane about 14 mm away from the aortic valve (). There was also thickening of the mitral valve associated with severe mitral regurgitation (MR) on color flow mapping (CFM) () with fenestrated anterior leaflets of the mitral valve.\n(TEE) confirmed the above, showing detracted aortic valve leaflets () and detecting the presence of a subaortic membrane () and minimal pericardial effusion (). The presence of severe mitral regurgitation (MR) was confirmed with perforation of the anterior mitral valve leaflet (). There was also significant vegetation between the chordae tendinae.\nThe left ventricle was normal in dimension with good contractility and 63% ejection fraction (EF) apart from mild concentric hypertrophy. The right heart appeared normal in dimension apart from severe pulmonary hypertension causing moderate secondary TR (III/IV). Abdominal ultrasound imaging (US) revealed a congested and enlarged liver, inferior vena cava (IVC), and spleen. Blood culture revealed staphylococcus aureus. This was a case of aggressive IE severely destructing the aortic and mitral valves with vegetation-like masses and an incidentally discovered sub aortic valve membrane.\nThe patient was admitted to the cardiology department and treated with excessive antibiotics according to the guidelines of European society of cardiology for one month. The patient referred for open heart surgery. Surgical resection of the sub aortic membrane was done and both aortic and mitral valves were replaced with prosthetic valves. The patient was discharged after surgery in good health.\nPost-operative TTE images show the prosthetic aortic and mitral valves () with good functioning on CFM () and good positioning of both () however, CFM revealed the remnants of mild TR (). In this evaluation, the patient was a symptomatic and regular on daily warfarin. |
A 36-year-old man presented with left-sided headaches associated with vertiginous giddiness for 3 months. A magnetic resonance imaging (MRI) scan of the brain revealed a 5.7 cm left temporal mass with significant left cerebral edema and midline shift []. The patient underwent preoperative angioembolization of the tumor followed by a left pterional craniotomy and excision of the tumor. Histopathological examination of the resected specimen revealed a meningothelial tumor predominantly consisting of cells with eccentrically placed nuclei, occasional prominent nucleoli, and abundant eosinophilic cytoplasm, consistent with a diagnosis of a meningioma with predominant rhabdoid features []. Extensive tumor necrosis was also noted []. Immunohistochemically, the tumor cells showed diffuse strong positivity to vimentin with focal expression of epithelial membrane antigen (EMA) and cytokeratins AE1/3 []. Placental alkaline phosphatase, activin receptor-like kinase 1 and desmin were not expressed by the tumor cells. The patient recovered well postoperatively and received gamma knife radiosurgery 2 months later for treatment of residual tumors.\nFive months following the initial surgery, a routine follow-up MRI scan of the brain showed tumor recurrence in the left middle cranial fossa measuring 7.9 cm with a midline shift, marked sulcal effacement, basal cistern distortion and left uncal herniation []. An emergency left decompressive craniectomy and excision of the recurrent tumor was performed. On postoperative day 3, the patient developed wound dehiscence over the lateral aspect of the craniectomy incision with the significant cerebrospinal fluid (CSF) leak. Computed tomography (CT) scan of the brain revealed increasing ventricular dilatation with intracranial herniation, and a VPS was implanted. The patient subsequently recovered well.\nThe patient re-presented 1 month later with abdominal pain and distension associated with anorexia, lethargy and confusion. He was disoriented, and his abdomen was distended with generalized tenderness. A CT scan of the brain revealed recurrence of a 7.9 cm left frontotemporal tumor with associated perilesional edema [] while a CT scan of the abdomen revealed moderate amounts of ascites with diffuse peritoneal enhancement suggestive of ongoing peritonitis []. The VPS was explanted with the placement of separate extra-ventricular and peritoneal drains in view of a possible VPS infection. The patient remained septic and critically ill even after removal of the VPS and administration of broad-spectrum antibiotics, requiring increasing inotropic and ventilatory support. CSF and peritoneal fluid cultures were negative. There were 2–3 L of serous fluid drainage from the peritoneal drain daily and multiple samples of peritoneal fluid sent for cytology and culture did not show any malignant cells or infective organisms.\nDiagnostic laparoscopy was attempted to elucidate the cause of persistent sepsis, but conversion to a laparotomy was necessary due to dense intra-abdominal adhesions. Intra-operatively, the peritoneal surfaces, greater omentum, serosal surfaces, and mesentery of the small and large bowel were studded with multiple flesh-colored tumor nodules. Histopathological examination of a segment of greater omentum revealed adipose tissue coated and infiltrated by an extensively necrotic tumor which was composed of predominantly epithelioid cells with moderate amount of clear or eosinophilic cytoplasm and marked pleomorphic, irregular, and hyperchromatic with prominent nucleoli []. Some tumor cells had a rhabdoid appearance [], with eccentric nuclei displaced by rounded intracytoplasmic eosinophilic inclusions, and some had a spindled appearance. The tumor cells stained strongly with vimentin and EMA []. Morphologically and immunohistochemically, the omental biopsy was similar to that of the primary brain tumor which supports the diagnosis of IAM from the primary brain tumor via the VPS. The patient continued to deteriorate and subsequently died 4 days after laparotomy, secondary to massive bilateral pulmonary embolism. |
A 38-year-old japanese man with no previous cardiovascular disease was admitted to our hospital because of paroxysmal nocturnal dyspnea and low grade fever of four weeks duration. He had the history of the resection of subcutaneous abscess in the neck, several days before the onset of symptom. On admission, blood pressure was 104/40mmHg with a regular pulse of 102/min. His body temperature was 37.4C. An early systolic murmur and a diastolic blowing murmur with thrill were detected at the left parasternal border. Increased pulmonary vascular marking was observed in his chest X-ray and the cardio-thoracic ratio was 50%. Electrocardiogram revealed a prolonged P-Q interval of 0.28 second, left ventricular hypertrophy and ST depression in the left precordial leads. After admission, first-degree of atrioventricular block normalized in 0.18 second of P-Q interval. Echocardiography was performed with a Tohshiba 65A after normalization of P-Q interval, which revealed the dilated and hyperkinetic left ventricle and the slightly dilated left atrium. M-mode echocardiography showed premeature mitral valve closure (), and the left ventricular end diastolic dimension was 6.4 cm and the end systolic dimension was 4.4 cm. The right coronary cusp and left coronary cusp of the aortic valve were extremely elongated and the left Valsalva sinus was dilated. Both aortic cusps were prolapsing and no coaptation was seen. Severe aortic regurgitation was observed on color Doppler flow imaging. In late diastole, mitral regurgitation which ran just behind the posterior mitral leaflet and extended to the posterior wall of the left atrium was detected (). The diastolic mitral regurgitation began with the atrial systole and disappeared with the ventricular systole ().\nAlthough several blood cultures were all negative, the diagnosis of acute aortic regurgitation due to infective endocarditis was made from the clinical history and destructive changes of the aortic valve. After intensive antibiotic therapy for three weeks, aortic valve replacement was performed. At surgery, commissural rupture between the right coronary cusp and the left coronary cusp was detected and an abscess was present in the root of the left coronary cusp. No abnormalities were detected in the mitral apparatus. After aortic valve replacement, the diastolic mitral regurgitation disappeared completely. |
A 63-year-old man reported pain in the lateral aspect of his right hindfoot during ambulation for 6 years. During the initial examination, a bony protrusion was palpated on the lateral aspect of his right hindfoot (). The patient complained of pain at the same site during walking.\nPlain radiographs and computed tomography (CT) images of his right foot showed HPT, bony overgrowth surrounding the peroneal tendon, and OP, an ossicle on the outer anterior side of the calcaneus (). Magnetic resonance imaging (MRI) showed a low-intensity lesion on T1-weighted image and a high-intensity lesion on a short T1 inversion recovery (STIR) image around HPT (). Bone marrow lesions of HPT were suggested, while OP did not show any signs of inflammation. Dynamic ultrasonographic images confirmed HPT and OP causing impacts accompanied with active eversion of the foot, and the pain was released by lidocaine injection between the HPT and OP (). On the basis of these findings, we assumed that the lateral foot pain stemmed from inflammation around the HPT caused by the impacts between the HPT and OP and not from POPS. Therefore, we decided to perform only HPT resection, without OP removal.\nA lateral incision was made parallel to the peroneus longus tendon. During operation, we observed that traction of the peroneus longus tendon caused the HPT and OP to collide with each other (). There was no apparent fracture or diastases of OP during inspection. The protuberance of the HPT was resected with a chisel. The resection of HPT released OP to glide smoothly along the peroneal tendon track. A 3 cm longitudinal tear of the peroneus longus tendon between the HPT and OP was confirmed and sutured with 3-0 PDS by using tubularization. The wound was irrigated and closed, and a sterile dressing was applied. Full weight-bearing was allowed postoperatively, as tolerated. The postoperative course was uneventful, and the patient returned to normal activities without any kind of functional disability. We compared the outcomes of the surgery, using the Japanese Society for Surgery of the Foot (JSSF) scale, an objective standard rating system [, ], and the Self-Administered Foot Evaluation Questionnaire (SAFE-Q) []. The SAFE-Q is an ankle-specific subjective evaluation method consisting of six subcategories (i.e., pain and pain-related, physical functioning and daily living, social functioning, shoe–related, general health and well-being, and sports activity [optional]). The preoperative JSSF score of 71 points (maximum score of 100 points) significantly improved to 100 points after one year. Compared to the preoperative condition, all subscale scores in the SAFE-Q improved after 1 year: pain and pain-related, 48 to 72 points; physical functioning and daily living, 41 to 82 points; social functioning, 62 to 88 points; shoe-related, 50 to 74 points; and general health and well–being, 58 to 76 points. Plain radiographs taken one year after the surgery showed no signs of HPT recurrence (). |
The patient was a 74-year-old female; 152.9 cm in height and 56.0 kg in weight at the time of her initial examination; a housewife; and described as gentle in her personality. Her chief complaints were lack of motivation, irritability, loss of appetite, and weight loss. Her medical history included hypertension and dyslipidemia at the age of 68, and she had undergone a colectomy at the age of 73 in January X−1. She had no remarkable family medical history, but her husband had Lewy body dementia and was in need of long-term care. Regarding the history of here present illness, she came to our clinic in December X−1 for abnormal behavior based on amnesia and paranoia, such as buying too many vegetables that she could not use, rotting them in the refrigerator, being unable to clean her room, and repeatedly washing her clothes while saying “my husband is dirty.” She had high neuropsychological test scores of 28 on the MMSE and 16 on the FAB; and her ADLs were not abnormally rated low, as indicated by scores of 33 on the DASC-21, 7 on the Lawton IADL scale, and 2 on the level of support required. Neurological examination showed no tendon reflex, left-right hyperactivity, or pathological reflex; and no atrophy was observed in the medial temporal lobe on magnetic resonance imaging (MRI) with coronal transection imaging. However, cerebral blood flow SPECT showed significant blood flow reduction in the anterior part of the bilateral precuneus, which led to the diagnosis of Alzheimer's disease.\nShe was attending local clinics for internal medicine and orthopedic surgery, but her conditions were poorly controlled, with polypharmacy and a diastolic blood pressure of over 100 mmHg. In our hospital, the patient was not treated with anti-dementia medication and adjustments to her medication regimen were initiated. She was also diagnosed with colorectal cancer and underwent a colectomy in January X. After discharge from the hospital, she weighed 50.6 kg, but her weight increased to 54.4 kg in July X with repeated dietary and nutritional guidance aimed at improving the breakfast menu with a focus on increasing energy levels. However, in September X, depressive symptoms such as “feeling lightheaded and agitated” became noticeable, with frequent missed meals and a decrease in the amount of food intake, which decreased her weight by 1.1 to 53.3 kg in 2 months. Muscle mass measured by a body composition analyzer (InBody 270) using bioelectrical impedance analysis was 32.6 kg. The weight after removing the body fluid weight (24.5 kg) from the total body weight (53.3 kg) was 28.8 kg. Since September X, she started taking 3.75 g of Ninjin'yoeito once before bedtime for her loss of appetite and weight loss.\nIn November X+1, her appetite improved and she weighed 56.7 kg, with an increase of 3.4 kg. Her muscle mass was 33.0 kg with an increase of 0.4 kg. The weight after removing the body fluid weight was increased by 3.9 kg (56.7–24.0 kg = 32.7 kg). |
We report the case of a 54-year-old woman who was diagnosed with tumor in the body of the pancreas, using computed tomography (CT). Magnetic resonance imaging (MRI) of the abdomen also revealed a tumor mass located at the pancreatic body; hence, pancreatic cancer was suspected. Artery invasion was seen near the celiac axis (Figure ).\nThe patient underwent abdominal vascular ultrasonographic scanning of the hepatic vein, inferior vena cava, superior mesenteric vein, splenic vein, and portal vein, which showed that the blood flow was unobstructed prior to the surgery. The blood flow volume of the splenic vein was 14.5 cm/s and that of the superior mesenteric vein was 18.8 cm/s. The diameter of the portal vein was 1.1 cm and its blood flow volume was 28.8 cm/s. The patient underwent IRE ablation under balanced general anesthesia for pancreatic cancer because the tumor mass was considered unresectable because of tumor infiltration of the celiac axis root and major abdominal blood vessels. Furthermore, multiple metastases were established in the lymph nodes of different regions. Before the IRE ablation, we performed tumor mass biopsies. The patient was admitted to the hospital after routine blood tests, which showed normal levels of leukocytes, neutrophils, erythrocytes, leukocytes, platelets, and amylase. These levels increased on postoperative day (POD) 2. The levels of C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor (TNF) were also increased on POD 2. The amylase level of the drain from the IRE was 922.8 U/L on POD 3, which was 6 times higher than the upper limit of the normal serum amylase level, indicating the presence of postoperative pancreatic fistula according to the International Study Group on Pancreatic Fistula classification[]. The drain amylase level reached the normal serum range on POD 5 and after the drain removal. The levels of cancer antigen 199 in the serum were decreased after the surgery. The re-evaluation MRI scan following the IRE ablation demonstrated thrombosis of the portal vein trunk on POD 7 and revealed that the tumor size had decreased (Figure ).\nNon-occlusive PVT did not affect the patient’s general condition, and the patient was discharged from the hospital on POD 8 because she showed no other complications. The patient currently has good quality of life. |
A 53-year-old male presented to our institution with a 70-pound weight loss for evaluation of an ampullary lesion. His clinical history included Type 2 diabetes, diabetic gastroparesis, and a family history of lung, colon, and prostate cancer. Magnetic resonance cholangiopancreatography at that time showed a dilated extrahepatic biliary system with a filling defect within the distal common bile duct (CBD). The pancreatic duct was normal. No intrahepatic abnormality, vessel involvement, or pancreatic mass was seen. The considerations included a stone or a mass lesion. He had undergone esophagogastroduodenoscopy and colonoscopy at an outside facility about 2 months previously, where an ampullary polyp and an ileocecal tubulovillous adenoma were identified. Further workup at that time was precluded due to complications from a fall. He was referred to our facility for endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasound (EUS).\nERCP performed at the Cleveland Clinic showed a large polyp at the ampulla along with bulging of the ampulla and extension into periampullary area as a flat, sessile component of about 2 cm in size []. The polyp was friable and bled on touch. There were a distal CBD stricture and intrahepatic ductal dilation seen on retrograde cholangiogram. On EUS, the lesion appeared confined to the mucosa, without extension into deeper wall layers. The polyp extended into the distal CBD causing a stricture, whereas the proximal CBD was mildly dilated at 9 mm. There was no vessel invasion or abutment, and no suspicious lymph nodes were found. During the ERCP, biopsies of the ampullary polyp were obtained together with brushings of the distal CBD stricture, and a biliary plastic stent was placed.\nSubsequent computed tomography scan of the abdomen did not show any contiguous organ involvement, liver lesions, or enlarged lymph nodes and no ascites was noted. The patient was anicteric and liver function tests were normal. Serum tumor marker levels were within normal range (cancer antigen: 19.9–84 U/ml and carcinoembryonic antigen: 2.3 ng/ml).\nThe CBD brushing sample was received in 30 ml of CytoLyt solution which was clear and colorless but containing multiple particles. A ThinPrep Papanicolaou-stained slide showed a cellular preparation containing cohesive clusters, strips, and single columnar cells dispersed in a clean background. Two distinct cell populations were present; the first showing bland flat honeycomb sheets of typical benign ductal epithelium [] and the second showing mild architectural atypia/disorganization and discernible nuclear pseudostratification/palisading, the latter seen best at the periphery of the larger two-dimensional groups []. In this second population, the columnar cells were slender and taller than usual biliary epithelial cells, had basal, elongated, and slender nuclei occupying at least a third to half of the cell length, with smooth nuclear contours, and hyperchromatic evenly dispersed chromatin []. Single dispersed cells were observed but did not display overt nuclear atypia []. Mild inflammation was present, but necrosis not identified. A cytologic diagnosis of “Mildly atypical epithelial cells” was rendered with an accompanying comment that the cytological findings were similar to that seen in the surgical biopsy from the patient's ampullary polyp, which showed features of a tubular adenoma (TA). In this case, the use of “mildly atypical epithelial cells” was preferred over “low-grade dysplasia” or “adenomatous epithelium” at our institution as there are no defined criteria for “low-grade dysplasia” in cytology brushings, and the use was avoided to prevent misunderstanding and confusion with a clinically significant high-grade dysplasia by the clinical team.\nAmpullary polyp biopsies were received in formalin as multiple pieces aggregating to 2.6 cm and hematoxylin- and eosin-stained sections showed features of a TA with low-grade dysplasia. No high-grade dysplasia or invasive carcinoma was identified.\nThe lesion was not amenable to local endoscopic resection based on its location, size, and involvement of distal 1 cm of the CBD. Based on the patient's significant weight loss, family history of cancer, and the large size of the lesion, a pancreatoduodenectomy (Whipple procedure) was performed to exclude an underlying malignancy.\nFinal histology confirmed an ampullary TA with low-grade dysplasia, 3 cm in largest dimension, extending into the distal CBD []. No high-grade dysplasia or mucosal invasion was seen. Thirty-four peripancreatic and periduodenal lymph nodes were examined and were negative for malignancy. The patient's postoperative course was uneventful, and he was discharged to home on day 8. At 1 month, he continues to feel well, with improved appetite and tolerating a regular diet. |
A 22-year-old female with no prior medical history developed fever and productive cough for 5 days which was treated with azithromycin. Her symptoms progressed to high-grade fever, hemoptysis, and left sided pleuritic chest pain. Her white blood cell count was 24,000/μL with 90% neutrophils and a computed tomography (CT) scan of chest revealed opacification of the left lung with air bronchograms, multiple varying sized cavities with abscess formation with a left pleural effusion []. PVL producing CA-MRSA was isolated from sputum and blood. Broad spectrum antimicrobial treatment for cavitary pneumonia which included vancomycin was initiated. Blood and sputum cultures grew MRSA positive for PVL. Left pleural ultrasound identified a complicated pleural effusion with septations. Pleural fluid from a diagnostic left sided thoracentesis grew MRSA as well and left sided tube thoracostomy was performed.\nIntensive Care Unit transfer was necessitated by massive hemoptysis requiring endotracheal intubation and mechanical ventilation. Her right main stem bronchus was selectively intubated followed by embolization of the left upper and lower bronchial arteries. Heavy sedation was maintained to decrease cough with continued selective right lung ventilation. Additional antibiotics including linezolid, clindamycin, and rifampin were begun to optimize antimicrobial coverage for MRSA. Thoracic surgery consultation was obtained and left pneumonectomy was recommended given a degree of lung necrosis. A repeat CT chest on day 6 showed the progression of the pneumonic process with complete opacification of the left lung with multiple air bronchograms. Also noted was the involvement of the right lower lobe with a cavitary lesion with surrounding centrilobular nodules []. Bilateral and progressive lung involvement impeded planned surgical resection.\nThe patient subsequently developed severe hypoxemia with PaO2/FiO2 ratio <100 on FiO2 0.8 and positive end-expiratory pressure (PEEP) of 12 cm H2 O on volume-control ventilation on day 7 of hospital course. Deep sedation and neuromuscular blockade were begun. In an attempt to salvage the right lung from spillage and contamination from the necrotic left lung, vigorous pulmonary toilet, and frequent bronchoscopies to remove copious purulent material [] were performed twice daily. The procedure was frequently limited by worsening hypoxemia. On hospital days 8-9, patient had PaO2 64 on volume-cycled ventilation, FiO2 1, PEEP 14 cm H2 O despite sedation, and neuromuscular blockade. Serial PaO2/FiO2 ratios <100 along with oxygenation index >40 (highest oxygenation index = 46) prompted consideration for ECMO to provide oxygenation support and to prevent acute lung injury in the lesser involved lung, while the fulminant CA-MRSA infection was being treated. On day 9, VV ECMO was initiated via left subclavian and left femoral veins for severe hypoxemia, and the patient was positioned with her right lung up at all times []. An aggressive toilet bronchoscopy strategy was utilized twice daily to remove as much necrotic and infected endobronchial material as possible to prevent spoilage of the right lung. An adult bronchoscope was used for toilet bronchoscopy. Examination of the right lung was carried out before removing purulent discharge from the left to avoid cross-contamination.\nThrombocytopenia due to linezolid necessitated substitution with ceftaroline therapy while continuing clindamycin and rifampin. On day 18, she was decannulated from VV ECMO. There was a concern for seeding of the right lung with a single cavity as seen on imaging on day 22 []. Nevertheless, clinical parameters remained stable without fever, worsening leukocytosis or hypoxemia. Aggressive weaning was continued while optimizing the patient for tracheostomy and percutaneous gastrostomy tube on day 25. As her nutritional status improved, and there was no further evidence to support infection of the right lung and she underwent a left extrapleural pneumonectomy with intercostal muscle flap buttressing of bronchial (day 31). The surgical pathology revealed extensive necrosis predominantly around the airways, widespread pulmonary intra-arterial thrombosis with extensive organizing acute lung injury [Figure and ]. Rapid clinical improvement ensued thereafter with decannulation from tracheotomy on day 43 and discharge to a skilled nursing facility (SNF) on day 47. She has survived her stay at the SNF and has been discharged home without the need for supplemental oxygen. |
The patient, a 40-year-old male, presented to our clinic with a history of right knee pain predominately along the medial aspect. His medical history includes prior examinations and treatments by another physician for right knee pain which provided minimal relief. The patient’s pain originated 2 months prior, wherein he experienced moderate pain that became sharp when squatting and bending, as well as stiffness while sleeping. The pain subsided with extension of the extremity, but loading of the joint re-aggravated the pain. Physical examination showed good range of motion (ROM), slight patellofemoral crepitus, and no meniscal signs along the medial joint line.\nMRI with no contrast was obtained, which demonstrated full-thickness chondral fissuring of the lateral patellar facet, mild abnormal signals of the proximal patellar tendon and Hoffa’s fat pad, and intact ACL and posterior cruciate ligament (PCL). The patient was treated with an ultrasound-guided injection of 2 cm3 of 1% lidocaine without epinephrine and 1 cm3 of Kenalog-40. He experienced immediate pain relief in his knee and was scheduled for clinical follow-up in 6 weeks.\nThe patient first presented to our office approximately 6 weeks following last examination and treatment from previous physician. He presented with medial pain of the right knee that was sharp but minor in nature. The pain was predominately activity-related and the patient was able to ambulate on his own. The patient stated that he was active as a bodybuilder and was a professional fighter for the prior 12 years. Our physical examination showed an antalgic gait with the patient favoring the affected extremity. The patient also exhibited minimal focal tenderness below the medial joint line and a negative McMurray test. Patient’s ROM was 0–120°+ and the knee was stable in reverse pivot and varus and valgus stress. When positioned in deep flexion, the patient experienced pain along the medial side of the knee. I personally reviewed the previous MRI the patient received while under previous physician’s care. Upon examination and imaging review, the patient was prescribed a lidocaine cream for pain management, and Pilates for stretching exercises were recommended. The patient was subsequently scheduled for follow-up in 6 weeks.\nThe patient returned to our office for 6-week follow-up visit. Approximately 2 weeks prior, he had experienced an injury to his right knee while teaching a kickboxing class, which had caused severe pain. The pain was severe enough in nature to cause difficulty and discomfort while sleeping. He had applied the previously prescribed lidocaine for the pain, but it offered only little relief to the knee. A physical examination was performed, which resulted in similar results as the previous examination—antalgic gait, minimal tenderness along medial joint line, medial pain in deep flexion, and no pain when in varus or valgus. We discussed the patient’s injury history and it was our recommendation to perform an in-office diagnostic arthroscopy (mi-eye 2™) due to the continued pain and discomfort with a negative MRI. The patient agreed with this recommendation and was scheduled to return for mi-eye 2 procedure in approximately 2 weeks with the goal to visualize pathology and develop a treatment plan.\nUpon return for the in-office arthroscopy, the patient was positioned lying down with a “bump” placed under the right knee for flexion (). The procedure was performed in a sterile environment, and the knee portals were aseptically prepared. The patient was given an analgesic injection of 1% lidocaine (5 cm3). The mi-eye 2 was inserted into the right knee and immediately—within approximately 20 s—the intact ACL was visualized () and a tear of the mid-body of the medial meniscus was identified ( and ). Through the duration of the procedure, minimal saline was needed—approximately 4 cm3. Following visualization, we discussed the treatment options with the patient, who ultimately opted for surgical intervention.\nThe patient was scheduled for surgery 2 days later to address the meniscus tear visualized with mi-eye 2. In addition to the mid-body tear of the medial meniscus, surgical findings included grade II changes to the medial and lateral edges of the patella and radial tear of the posteromedial aspect of the medial meniscus. The mid-body meniscal tear previously visualized using mi-eye 2 was confirmed ( and ) and the meniscus was debrided to a stable rim (). The patient was discharged following recovery from anesthesia and allowed for weight-bearing on his right knee as tolerated. He was scheduled for follow-up 3 weeks post-operatively.\nFollowing 2 weeks of surgery, the patient reported good functional motility and resolution of medial-sided joint pain. |
A 61-year-old female was found to have a palpable thyroid nodule on routine physical examination by her primary care physician. The patient was then referred for a thyroid ultrasound which showed a 2.1 cm, left-sided thyroid nodule. The patient underwent an ultrasound guided fine needle aspiration (FNA) biopsy which revealed a papillary thyroid carcinoma. The patient was referred to ENT and subsequently had a total thyroidectomy. She was referred to our endocrine clinic for postsurgical management of her T1b N1a MX stage 3 papillary thyroid carcinoma 4 weeks after total thyroidectomy. The tumor size was 1.7 cm in maximum diameter and was unifocal. At the time of surgery, the surgical margins were positive and focal lymphovascular invasion was observed with 1 out of 6 dissected lymph nodes positive for metastatic disease. The patient was prepared for radioactive iodine remnant ablation with a low iodine diet and thyrotropin alfa injections. An initial diagnostic SPECT/CT (Philips Precedence 16P) scan was performed 24 hours after administration of 5.3 mCi of Iodine-123 (I-123). The scan showed uptake in the left posterior thyroid bed and anteriorly at the level of the hyoid bone, both likely representing residual thyroid tissue. Physiologic uptake was also noted in the salivary glands, nasopharyngeal mucosa, and gastrointestinal tract. Additionally, a large (8 cm × 9 cm × 8 cm) heterogeneous left anterior mediastinal mass with mixed solid and cystic architecture was noted. This mass did not demonstrate uptake of the I-123 tracer (Figures and ). A CT-guided biopsy of the mass returned only hemorrhagic material. Serum thyroglobulin tumor marker was found to be low at 0.3 ng/dL and TSH was >125 uIU/mL, which suggested the mass was not metastatic thyroid cancer. Based on these laboratory findings, it was decided to continue with ablation therapy and 157 mCi of Sodium Iodide-131 (I-131) was administered to the patient. Posttreatment SPECT/CT one week later showed uptake of radioactive iodine by the mediastinal mass (Figures and ). After a repeat CT-guided biopsy was nondiagnostic, the mass was removed via sternotomy.\nSurgical pathology sections demonstrated a multiloculated mass composed of cystic spaces lined by a variety of epithelial types, including areas of low-cuboidal (), mucinous columnar with goblet cells (), ciliated columnar, and keratinizing stratified squamous epithelium. There was no significant cytological atypia or increased mitotic activity. The intervening stroma was densely fibrotic with patchy chronic inflammation, glandular elements, and numerous hemosiderin-laden macrophages—providing evidence of previous hemorrhage (). Grossly, the cystic contents ranged from dark brown, likely due to previous hemorrhage, to clear fluid. Adjacent to the cystic spaces, there was a peripheral remnant of normal involuting thymic tissue showing Hassall corpuscles and associated lymphoid tissue (). These findings are consistent with a benign multilocular thymic cyst. |
A 27-year-old woman, gravida 1 para 0, underwent the routine prenatal examinations in our hospital from 6 gestational weeks. Till 30 gestational weeks, the prenatal course was unremarkable, including systemic prenatal ultrasound diagnosis and the routine fetal cardiac screening (at 24 gestational weeks). Fetal growth was within the normal process and the alpha fetal protein was 23.91 U/ml (the normal reference value:0–25 U/ml).\nAt 30 gestational weeks, the B-mode ultrasound revealed that the liver of the fetus was enlarged with a heterogeneous solid mass located in the right quadrant of the fetal abdominal cavity, with a close relationship to the liver. The mass measured 5.8cmx4.7cmx5.2 cm and pushed the portal vein and gall bladder. The lesion seemed to have an ill-defined margin, irregular shape, partial capsule with multiple cystic cavities inside, and maximal diameter of 2.1 cm. The portal and hepatic veins were not dilated. In the color Doppler ultrasound, the mass appeared to be highly vascularized (Fig. ) and RI was 0.67. The three-dimensional power Doppler ultrasound showed the feeding vessels were mainly around the lesion but there were less vessels inside it (Fig. ). Due to the rapid enlargement of this mass and the imaging features of ultrasound, the diagnosis of HBL was highly considered. But IHH, mesenchymal hamartoma or other rare liver tumors such as hepatic cysts or adenomas could not be ruled out.\nAccording to the pediatrician, the final diagnosis depended on the postnatal biopsy of the hepatic lesion and the prognosis of HBL was uncertain. Finally, the parents chose to give up this fetus because of the uncertain outcomes involving tremendous emotional and economic impacts on the family. Furthermore, they refused to take any further prenatal examination, like fetal MRI. A male fetus was aborted, weighing 1409 g and measuring 36 cm long.\nMedical ethics committee of West China Second Hospital of Sichuan University have approved this case report and the autopsy was performed. The liver of the fetus was enlarged, about 8 cm long and the mass was located in the right lobe, pushing the portal vein (Fig. ). The histological diagnosis was IHH (Fig. ).\nThe written consent was obtained from the patient for publication of case details and images. |
A 19-year-old man was admitted to our department with repeated haemoptysis. He had been followed up for neutrophil migration failure and bronchiectasis at the paediatrics department in our hospital since birth. Five months before the admission, the patient was referred to our department with haemoptysis for 2 weeks. Although airway bleeding associated with bronchiectasis was suspected, his symptom was improved with carbazochrome sodium sulfonate hydrate and tranexamic acid. Three months before the admission, he visited again because of recurrence of haemoptysis. Plain CT showed lobular central granular shadows in the right middle lobe, left lingular segment and bilateral lower lobes. He was admitted for evaluation of the source of bleeding. On admission, his height was 168.5 cm, and his weight was 53.5 kg. His vital signs were blood pressure, 103/49 mm Hg; pulse rate, 81 beats/min; pulse oximetry, 99% in room air; and body temperature, 36.7℃. Physical examination showed coarse crackles in both lung fields. Laboratory examinations showed no abnormality. Chest X-ray showed bronchial wall thickening in the right middle and left lower lung field and the surrounding ground-glass opacity and consolidation (). Plain chest CT also showed bronchial wall thickening and dilation in bilateral lung fields, partial mucoid impaction and multiple centrilobular granular shadows in the right middle lobe, lingular segment and bilateral lower lobe (). Contrast-enhanced CT showed hyperplasia and tortuosity of the bilateral bronchial artery; however, it was difficult to obtain a detailed evaluation of the origin and running by the axial views (). The three-dimensional (3D) image showed that the right bronchial artery branched from the left subclavian artery and was running on the dorsal side of the aortic arch ( and ). On the other hand, the left bronchial artery branched from the aortic arch and perfused to the left lingular segment. In 4D CT, the pulmonary artery was imaged again after the bronchial artery was imaged, indicating a bronchial artery–pulmonary artery shunt on both sides ( and ). Bronchial angiography confirmed the branching of the right bronchial artery from the left subclavian artery and shunting to the pulmonary artery ( and ). Additionally, the left bronchial artery branched from the aortic arch and perfused to the left lingular segment consistent with the CT findings. |
A 28-year-old man referred to our department with a 7-week history of left hip limping, difficulty walking, and inability to bend forward. He had aided waddling gait and poor tolerance of weight bearing. There was no history of any major trauma. His vital signs were normal. The examination of the hip elicited an impaired restriction of flexion and both internal and external rotation, with a 2-cm shortening of the left leg. A Harris hip score of 65.5 was achieved by the patient. His distal neurovascular status was intact ().\nOther examinations showed poor secondary sexual characteristics with a Tanner’s pubertal and axillary stage of 2. He worked in an automobile repair shop and had normal social activities. A survey of his past medical history showed that at age of 17 years, blurred vision, meningeal signs, and abnormal secondary sexual development were noted; and after investigations, brain magnetic resonance imaging showed a lobulated intra- and suprasellar mass, 38 × 32 × 24 mm in diameter, with extension posteriorly into the interpeduncular cistern and extension superiorly and insinuation into the third ventricle. Consequently, in December 2001, he underwent brain surgery for craniopharyngioma. Ten years later, his previous symptoms recurred, and in April 2011, he underwent a second brain surgery for tumor recurrence. At the meantime, he had been followed up by an endocrine clinic.\nAccording to the patient’s past history, he was born full term with a birth weight of 3.5 kg and his early development was described as normal (menarche was at age of 14 years). Since that age, he had always weighed between 49 and 57 kg. During these years, he was under medical therapy for hormonal disorders. There was no history of delayed dental maturation, hyposmia, or a family history of delayed puberty. He had no midline defects. Complete pituitary evaluation is depicted in .\nIn 17 July 2013, the patient was admitted to our hospital, and we performed the standard treatment for SCFE: fixation with a single screw and a prophylactic fixation in the contralateral hip ().\nPostoperatively, the patient had an uneventful recovery and was discharged 2 days after surgery with instructions for weight-bearing status and followed up through both orthopedic and endocrine clinics. He came on regular follow-up visits, and based on clinico-radiological evidence of union, full weight-bearing walk was advised in the fourth month. |
A 42-year-old male presented to us with complaints of diffuse abdominal pain and abdomen distension for 2 days. He had a history of constipation for 2 days, but no vomiting. The patient was brought after an episode of seizure for 3 min, followed by a brief period of altered sensorium. He was diagnosed with a seizure disorder 9 years ago for which he was on irregular medications. He is a chronic alcoholic for the past 25 years and had an episode of alcohol binge drink 2 days ago. On examination (height – 168 cm; weight – 45 kg), the patient was drowsy with a Glasgow Coma Score (GCS) of E3V4M6-13/15. His blood pressure was 80/48 mm of Hg. His heart rate was 102/min; the respiratory rate was 22 per minute and the temperature was 99°F. Abdomen examination revealed mild abdomen distension, diffuse tenderness with neither guarding nor rigidity, and absent bowel sounds. Digital rectal examination showed altered dark-colored stools. Respiratory system examination showed the presence of equal air entry bilaterally with basal crepitations.\nThe capillary blood glucose (CBG) at admission was 32 mg/dl. After initial stabilization with intravenous fluids, 25% dextrose, and supportive measures, further investigations were done. A complete blood count showed an elevated total count of 15.4 × 109/L with a neutrophil predominance. X-ray abdomen showed multiple air–fluid levels. CT of the abdomen showed diffuse dilatation of the jejunal and ileal loops and the collapse of the large bowel with a transition point probably at the terminal ileum or ileocecal junction. All these features suggested a small bowel obstruction and the patient was planned for an emergency laparotomy as per the hospital protocol in emergencies. The patient responded well to the initial resuscitation with intravenous fluids, 25% dextrose, and inotropes, and his GCS improved to 15/15 and CBG increased to 180 mg/dl. The patient did not develop any further seizures.\nDuring the emergency laparotomy, the following were found: (1) dilated jejunal and ileal loops, (2) collapsed large bowel, and (3) at 20 cm from the ileocecal junction, there was an ileoileal intussusception []. The involved ileal segment was resected and stomas were fashioned. On examining the specimen, it was found that 7 cm of proximal ileum had telescoped into the distal part and that the telescoped part was gangrenous.\nPostoperatively, the patient had a cough with expectoration and he revealed that he had similar episodes for the past 1 month. A chest X-ray which was done preoperatively showed opacity in the left middle zone. Subsequently, the CT chest which was performed showed evidence of consolidation with air bronchogram in the left lower lobe and evidence of cavity with surrounding consolidation in the anterior aspect of the left upper lobe, suggesting an active infection in the lung []. Sputum smears examined with Ziehl–Neelsen stain did not reveal any acid-fast bacilli, but molecular testing by nucleic acid amplification (GeneXpert) was positive for Mycobacterium tuberculosis with moderate sensitivity to rifampicin. The histopathological examination of the resected bowel segment confirmed the presence of numerous epithelial granulomas with aggregations of epithelioid histiocytes and scattered Langhans type of giant cells, suggesting a tuberculous origin of the lesions [Figures and ]. Subsequently, the patient was started on antitubercular treatment with isoniazid, rifampin, pyrazinamide, and ethambutol according to the local national guidelines. This leads to the conclusion that the small bowel obstruction was due to intussusception and the lead point for the intussusception would have been the tuberculous lesion. The patient recovered well postoperatively and is awaiting reversal of his stoma. |
A 23-year-old Indian female patient reported to the Department of Conservative Dentistry and Endodontics with a chief complaint of yellowish discoloration and poor appearance of her teeth with the rehabilitation of the same. Family history and medical history was non-contributory. Patient was unmarried, well qualified medical student and there was no history of similar condition in the family. Her parents and siblings were fine and no other family member presented with similar dental findings. Her past dental history disclosed that she underwent root canal treatment of 36 due to caries involvement. Extra-oral examination disclosed normal mouth opening and no temporomandibular joint problems. The patient was healthy with no co-morbidities.\nOn intraoral examination, the enamel thickness was highly thinned down and partially flaked off from few surfaces of teeth. Teeth revealed well defined pitted surfaces along with yellowish brown discoloration. Surfaces of teeth were rough with minimal enamel present. The teeth also revealed short clinical crowns with multiple spacing between teeth. The occlusal plane was uneven worn-down posterior teeth. On frontal view, the patient presented with deep bite with less horizontal overlap. Dentin which was exposed were brown in color. The periodontal examination revealed normal healthy gingiva with no abnormalities (Fig ).\nRadiographic examination included full mouth Orthopantomogram (OPG) and Intraoral periapical radiograph (IOPA) showed features of AI. (Fig ) Occlusion was assessed after obtaining the diagnostic casts. Based on clinical and radiological examination, it was diagnosed as hypoplastic type of amelogenesis imperfecta. Based on the arrived diagnosis, a full mouth rehabilitation was planned. A well formulated treatment plan involving endodontic, and prosthetic department was charted out to furnish a functional occlusion with good esthetics and further prevent the tooth loss. The entire treatment plan was explained to the patient and informed consent was obtained. The initial phase of the treatment consisted of endodontic therapy. Based on OPG reports, it was decided that pulp space therapies should be performed on 37, 46, 47, 16, 17, 26 followed with retreatment with respect to 36 and fixed prosthesis was planned for the entire dentition.\nTreatment protocol: Patient was asked to check her on diet to maintain oral hygiene. The mock presentation of full coverage prosthesis were executed on upper and lower casts and presented to the patient. She was contented with the anticipated outcome and prognosis of the overall treatment plan was satisfactory. The subsequent rehabilitation plan was formulated.\nDefinitive treatment plan:Patient motivation for the treatment and maintenance of oral hygiene, Endodontic treatments of #37, 47, 47, 16, 26, Providing temporary bridges on all posterior teeth for reconstruction of the lost occlusal vertical dimension, Trial of fixed partial dentures and, Periodic follow-ups at 1 year and 2 year intervals followed by augmentation of oral hygiene measures.\nEndodontic treatment was performed with respect to #37, 47, 47, 16, 26 under rubber dam and local anesthesia. 3% sodium hypochlorite (Vishal Dentocare Pvt Ltd, India) was used as irrigant in all the treated teeth. The working lengths for all teeth was obtained using hand K file (Dentsply Inc, Maillefer, Dentsply India), Root ZX II Apex locator (Morita, Irvine, CA), and finally confirmed using intraoral periapical radiograph. #16, 26 showed the presence of MB2. Cleaning and shaping of all the canals were performed with hand K files and Protaper rotary files (Dentsply Inc, Maillefer, Dentsply India) under copious irrigation with 3% sodium hypochlorite and enlarged upto F2 file size. Retreatment was performed with respect to #36. Three rounds of calcium hydroxide as intracanal medicament (CALCICURE, Voco) were placed for #36. All the access cavities were given temporary seal dressing (cotton pellet and intermediary restorative material, Cavit G, 3M ESPE GmbH, Neuss, Germany). All the obturation was completed using F2 protaper gutta percha cone (Dentsply, Maillefer, Dentsply India) with AH Plus sealer (Dentsply, Sirona, Dentsply India). The next stage of treatment was the restorative and prosthetic phase. Fixed partial dentures were planned.\nRestorative treatment included the Post endodontic restoration of # 37, 46, 47, 16, 17, 26 and 36 with composite restoration (Filtek Z 350 XT, 3M ESPE, St, Paul, MN, USA). As per radiographic findings, the impacted teeth was retained as the patient was not willing for any surgical extrusion procedure. The deciduous 63 was included in the tooth preparation. All third molars (#18, 28, 38, 48) were not extracted as they had not erupted.\nProsthetic treatment included the tooth preparation on #17, 16, 15, 14, 24, 25, 26, 27, 34, 35, 36, 37, and 44, 45, 46, 47 to receive metal ceramic crowns. Diagnostic impressions were made using alginate (3M ESPE Alginate Impression Material). The diagnostic casts were then mounted on semi adjustable articulator (Hanau Articulator, Teledyne Hanau Buffalo, NY, USA) using Hanau facebow. The tooth preparations were performed quadrant wise so that the patient was adjusted with the new occlusion. First the posterior teeth were prepared and the temporary acrylic bridges (Integrity™ Temporary Crown & Bridge Material, DENTSPLY, USA) were fixed to increase the occlusal height. Temporary acrylic crowns were placed for 1 month to assess the patient’s forbearance to the new occlusion. Once the patient was habituated to the new occlusal height, then final maxillary and mandibular impressions were prepared with poly vinyl polysiloxane impression material (Aquasil Ultra Putty Soft Regular and Aquasil Ultra LV, Dentsply USA). Interocclusal records in centric occlusion were taken and the working casts were mounted on semi-adjustable articulator (Hanau Articulator, Teledyne Hanau Buffalo, NY, USA). Trial with metal ceramic restorations was done and finally cemented with self-adhesive resin (RelyX Unicem 2 Clicker A2 Universal Self-Adhesive Universal Resin, 3M-ESPE, USA). Then the anterior teeth were prepared for metal ceramic restorations. The patient was regularly monitored at 1 week, 1 month, 3 months, 6 months and at 1 year and 2 years intervals using clinical and radiographic examinations (Figs. , and ). Patient was highly satisfied with the treatment outcome and the gingival condition was maintained, esthetic impairment and the dentinal sensitivity was resolved. |
A 62-year-old white female with a history of hypertension, which is well controlled, was found to have a new irregular density with microcalcifications on screening mammogram. Biopsy showed invasive mammary carcinoma of the ductal type. Tumor was grade 3, ER negative, PR negative, and HER2-neu negative by immunohistochemistry staining. She was diagnosed with stage IIA (T2, N0, M0) breast cancer. She has never smoked and has no history of drinking.\nShe underwent lumpectomy with sentinel lymph node biopsy. Her tumor measured 3.2 cm with negative margins. Lymph node biopsy was negative. She met the criteria for adjuvant chemotherapy treatment. She was enrolled in clinical trial BR003. The trial investigates the benefits of adding carboplatin to the standard chemotherapy in patients with triple-negative breast cancer in the adjuvant setting. She was planned to receive dose-dense adriamycin/cyclophosphamide for 4 cycles followed by weekly Taxol for 12 weeks plus carboplatin every 3 weeks for 4 cycles. She received 4 cycles of adriamycin 60 mg/m2 and cyclophosphamide 600 mg/m2 every 2 weeks for 4 cycles with pegfilgrastim support. She was then started on paclitaxel 80 mg/m2 with carboplatin adjusted for an area under the curve of 6 mg/mL/min.\nShe tolerated 6 cycles of weekly Taxol as well as 2 doses of carboplatin with the exception of mild neuropathy and mild cytopenia. Three days after her cycle 6 of Taxol, the patient presented to the emergency room with abdominal cramping and diarrhea for 1 day prior to admission. She also reported multiple episodes of large amounts of bright red blood with bowel movements. Her symptoms were associated with generalized weakness and fatigue. She denied any fever, chills, nausea, or vomiting. Evaluation upon hospitalization revealed stable vital signs with no fever. Abdominal examination revealed mild diffuse tenderness with no guarding or rebound tenderness.\nLaboratory examination revealed normal white blood cells with absolute neutrophilic count of 6.9 ×109/L, hemoglobin of 9.4 g/dL, and platelet count of 83 × 109/L. Chemistry profile was remarkable for potassium of 3.3 mEq/L. Stool for occult blood was positive. Stool PCR testing was negative for multiple organisms including Campylobacter, Clostridium difficile (toxin A/B), Salmonella, Yersinia enterocolitica, enteroaggregative E. coli, enteropathogenic E. coli, enterotoxigenic E. coli, Cyclospora cayetanensis, Entamoeba histolytica, Giardia lamblia, adenovirus, rotavirus A, and Cryptosporidium. Abdominal X-ray showed no evidence of bowel obstruction or ileus. The patient underwent colonoscopic evaluation, which revealed moderately severe ischemic colitis in the splenic flexure, descending colon, and sigmoid colon (Fig. ). The cecum, ascending colon, transverse colon, and rectum appeared normal. These findings, along with the lack of significant cardiovascular risk factors and previous events, suggested that her condition is likely related to chemotherapy. Pathology showed acute colitis, favoring ischemic colitis (Fig. , Fig. ).\nThe patient was treated with intravenous fluid hydration and bowel rest. Her diarrhea as well as her abdominal cramps resolved within 3 days. She was discharged home and her chemotherapy was held for 2 weeks. After carefully reviewing the literature, the patient was offered to continue on single-agent paclitaxel, with close monitoring after explaining the possibility of relapse. Single-agent weekly paclitaxel was resumed and carboplatin was discontinued. She was able to tolerate the remaining 6 cycles of weekly paclitaxel well. |
A 52-year-old man was diagnosed to have WM 2 years ago. At that time, the complaints of diminution of vision led to the discovery of serous retinal detachments in macular area of both the eyes and retinal hemorrhages suggestive of a hyperviscosity state. The diagnosis of WM was confirmed with bone marrow biopsy. The patient was treated with multiple cycles of chemotherapy for over a year. Thereafter, the blood counts were stable. However, the vision did not improve. He was reexamined at this stage, 2 years from the diagnosis and 1 year after the chemotherapy was over.\nHis best-corrected vision was 20/60 in both the eyes. The anterior segments were normal. Retinal examination revealed a circular punctate yellowish lesion at macula, with atrophic pigmentary changes in both the eyes. The temporal rim of these lesions appeared to reveal a slightly elevated serous detachment. This was more clearly evident in autofluorescence images that showed a complete absence of autofluorescence at the fovea covering about 1 disc area. The outer area showed spotted appearance similar to a leopard's skin with hypoautofluorescence in the center surrounded by hyperautofluorescence. The outermost rim showed tiny hyperfluorescent specks. The same pattern was seen in fluorescein angiography. There was neither leakage nor pooling of the dye. The spectral-domain optical coherence tomography (OCT) images showed the elevation of retina, with retinal thickening and small cystoid spaces. There was disorganization of the outer retinal layers. The inner segment–outer segment junctional photoreceptor layer and external limiting membrane layers were absent. The RPE layer was thinned out and atrophic. The area between the outer retinal layers and the RPE showed moderately reflective, nearly homogeneous material. Along the RPE, a few clumps of highly reflectile material were seen [].\nElectroretinographic studies showed normal rod and cone responses, but multifocal electroretinography revealed reduced foveal and parafoveal responses and minimally reduced perifoveal responses. Blood tests revealed normal blood counts and no abnormal cells. In view of the degenerative and atrophic changes at macula, no intervention was advised, and the patient was offered visual rehabilitation with spectacles. |
A 17-year-old African American female with a negative past medical history except intermittent asthma presented to the emergency room complaining of cough and chest pain for the past two weeks in addition to rib pain, back pain, and weakness for about one month. The chest pain had been worsening upon deep inspiration over the past few days. The pain was unlike what the patient had experienced previously associated with acute asthma exacerbations and was refractory to beta-agonist treatment.\nOne month prior, she had given birth to a 32-week gestation infant after an unremarkable pregnancy and delivery. Two weeks prior to this presentation, the patient had been seen in another emergency room for similar symptoms. A chest X-ray and computed tomography (CT) of the chest was performed then which were read as normal.\nUpon examination in the emergency room, the patient was noted to be afebrile and on pulse oximetry was saturating at 98% on room air. An electrocardiogram showed sinus tachycardia at 110 beats per minute with possible left atrial enlargement and no S-T segment or T-wave abnormalities. A chest X-ray revealed a right basilar opacity and bilateral pleural effusion consistent with a diagnosis of pneumonia (). Treatment with intravenous antibiotics was initiated, and the patient was transferred to the pediatric floor.\nOn the floor, additional history of having experienced swelling of her lower limbs and joint pain in her hands was obtained. Physical examination revealed the following findings: right-sided metacarpophalangeal, wrist, elbow, and knee swelling and erythema, decreased range of motion of both knees, bilateral conjunctival erythema, bilateral nonpitting pedal edema, mild diffuse abdominal tenderness, a confluent erythematous maculopapular rash involving both upper and lower extremities, and a malar rash.\nLaboratory investigations were notable for a white blood cell count of 2.4 thousand per cubic millimeter (nl 4.8–10.8 thousand per cubic millimeter) with 84% neutrophils (nl 40–80%), 9% bands (nl 0–6%), and 6% lymphocytes (nl 15–50%), a creatinine level of 1.24 milligrams per deciliter (nl 0.3–0.8 milligrams per deciliter), hemoglobin level of 9.6 grams per deciliter (nl 10.7–17.3 grams per deciliter), an albumin level of 2.9 grams per deciliter (nl 2.7–4.8 grams per deciliter), an erythrocyte sedimentation rate of 72 millimeters per hour (nl 0–20 millimeters per hour), antinuclear antibody titer of 1:2560 with a homogeneous pattern (nl < 1 :80), and an anti-double-stranded DNA antibody level of >1000 iU/ml (nl ≤ 30). Urinalysis was positive for protein of 100 milligrams per deciliter (nl negative) and white blood cells of 12–20 per high power field (nl negative). This was followed by a spot urine protein-to-creatinine ratio which revealed significant proteinuria (871 millligrams per gram creatinine (nl 80–200 milligrams per gram creatinine)) consistent with SLE related kidney disease. All other laboratory values including rheumatoid factor, complement studies, and coagulation studies were normal. Additionally, bilateral lower extremity venous duplex studies showed no evidence of deep vein thromboses.\nAfter approximately forty-eight hours on the pediatric floor, the diagnosis of SLE was confirmed—the antibiotics were discontinued and the patient was started on high-dose intravenous methylprednisolone. Soon after the steroids were started, the patient became hypertensive (180/114 mmHg) and bradycardic with unbearable headaches prompting transfer to the pediatric intensive care unit. Upon transfer, the patient's physical and neurologic examinations were normal except for mildly decreased air entry at the lung bases. An echocardiogram was performed which showed an ejection fraction of 55–60%, mild to moderate mitral regurgitation, peak systolic pulmonary artery pressure of 45 mmHg (moderately increased), normal-sized pulmonary arteries, moderate to severe tricuspid regurgitation, a mildly dilated right atrium, and a less than 50% variation in respirophasic changes in the inferior vena cava and hepatic veins. The patient was started on intravenous hydralazine and oral nifedipine. A second chest X-ray was unchanged. A repeat electrocardiogram showed marked sinus bradycardia at 42 beats per minute with a prolonged QTc interval of 462 milliseconds and flipped T waves in the anterior leads. The patient was then transferred to a tertiary facility for management of her pulmonary hypertension, dysrhythmia, and further investigation and management of her nephrologic and rheumatologic disease. |
Our proband is a 39-year-old male who was first seen in our clinic at age 35. In his early medical history, he reports that he was hypermobile (Beighton score of 7/9), small in stature, and had a high-arched palate. He has had several joint dislocations involving the digits and patellae, the first of which occurred around 12–14 years old. Due to family history including cardiomyopathy in three paternal uncles, father, and sister, the proband was investigated by a cardiologist at 16 years old. No heart problems were found, though his other symptoms were suggestive of an underlying connective tissue disorder and he was labeled as having “either Ehlers–Danlos or Loeys–Dietz syndrome.” Years later, the proband was found with a pulmonary artery aneurysm after he was hospitalized for a spontaneous pneumothorax in 2008. The proband was closely followed after this incident due to a worsening of the aneurysm and severe pulmonic regurgitation (PR).\nAt age 35, the proband's pulmonary artery aneurysm had grown to 5.7 cm. Aside from his severe PR, he was experiencing moderate mitral regurgitation, mild tricuspid regurgitation, severe left atrial enlargement, and biventricular failure with an ejection fraction of 22%. Surgery was now necessary. A pulmonary artery resection with pulmonary homograft valve 27 mm implantation was performed with resultant symptomatic improvement and an improved ejection fraction to 45%. The surgeons had noted myxoid degeneration in the pulmonary valve, supporting the presence of a connective tissue disorder. At age 37 he was found to have gallbladder stones and underwent a laparoscopic cholecystectomy. Days after the surgery, he returned to the hospital with acute respiratory distress, shortness of breath, and fever. Investigations revealed he had contracted Klebsiella pneumonia. He was hospitalized once again, and developed acute liver failure, acute renal failure, and respiratory failure requiring ventilator support, acute-on-chronic systolic heart failure, and pulmonary artery hypertension. The proband returned home after his multiorgan system failure had subsided, though he later experienced dyspnea and exercise intolerance. Pulmonary function tests were performed and found he had reduced left lung volume with restrictive disease of unknown etiology. This finding, along with his existing connective tissue disorder and pulmonary artery aneurysm, led to the proband being referred to medical genetics with suspicion of Loeys–Dietz syndrome.\nDuring a genetics consultation, the proband agreed to multigene panels for thoracic aortic aneurysm and dissection and cardiomyopathy. The tests were negative, finding no pathogenic variants related to Loeys–Dietz, Ehlers–Danlos, or Marfan syndrome. As a next step, whole-exome sequencing (WES) and mtDNA analysis were performed. WES uncovered the likely pathogenic variant c.1039 C>T (p.R347X) in TAB2 in a heterozygous state, which we propose is responsible for the symptoms seen in the patient. This variant inserts a stop codon near the middle of the protein, resulting in TAB2 truncation and dysfunction.\nKnowing of the likely pathogenic variant afflicting our proband, his sister was evaluated as well. She is a 36-year-old female who had a ventricular septal defect that was repaired in her infancy, right bundle branch and atrioventricular block, right ventricular dilation and diminished RV function, mild dilation of the aortic root, hypermobility (Beighton 5/9), unilateral sensorineural hearing loss, myopia, and mildly sloped shoulders. The similarity of her phenotype to the proband's was not a coincidence, as she was found to have the same TAB2 variant. Probands mother was negative for the familial variant, suggesting likely paternal inheritance.\nIn the time since the proband's genetic testing, he has continued to follow with the cardiology clinic. EKG shows severe biventricular enlargement, an LV ejection fraction of 33%, a right bundle block, enlarged atria (the right more severely so), and mild aortic and mitral valve regurgitation. He developed brief episodes of chest pain, neck swelling with underlying lymphadenopathies, and volume overload. His pulmonary valve regurgitation and pulmonary artery aneurysm have worsened since his surgery at age 35, with the aneurysm reaching 5.2 cm. These symptoms prompted his placement on the cardiac transplantation list at age 39. The proband has been considered for a percutaneous pulmonary valve replacement or some form of mechanical circulatory support including a left ventricular assist device (LVAD), biventricular assist device (BIVAD), or total artificial heart while he waits for a transplant. |
A 50-year-old woman was referred by her dentist for the evaluation of mandibular swelling. The patient had osteoporosis treated with risedronate. Physical examination revealed swelling of the mandibular symphysis with chin deformation. The tumor did not seem to adhere to the skin but extended from the mandibular left first premolar to the mandibular right canine. The anterior buccal floor was deformed, and the inferior alveolar nerve was preserved. An excisional biopsy of the buccal mass was performed, confirming an initial diagnosis of chondrosarcoma. The histological plates were reinterpreted, leading to a final diagnosis of chondroblastic osteosarcoma. Cartilaginous tissue with chondroid matrix was observed in which chondrocytes with cytonuclear abnormalities were found (Figure ). Immunohistochemistry was not contributory, because it did not detect any IDH1 and IDH2 variants. Craniofacial computed tomography scan (Figure ) revealed a 32-mm-long axis lesion in the symphyseal region responsible for an osteolysis on both sides of the mandible. This scan did not reveal any suspicious lesions elsewhere. No suspected hypermetabolic focus or submandibular and cervical lymph node involvement was found in positron emission tomography imaging.\nIt was decided to implement neoadjuvant chemotherapy with doxorubicin 80 mg and cisplatin 140 mg over three cycles. Due to the lack of significant evolution in the tumor mass, an interrupted pelvi-mandibulectomy with bilateral lymph node dissection was performed along with reconstruction with a fibula free flap. The histological analysis after the tumor resection showed a lobulated architecture of the tumor, with pleomorphic cells associated with a predominantly cartilaginous matrix and a matrix in the form of thick immature bone areas (Figure ). The lymph nodes were free of malignant cells. The final diagnosis was conventional osteosarcoma with a chondroblastic predominance. The patient underwent 60-Gy adjuvant radiotherapy in 33 fractions. At the time of writing, the patient was still undergoing treatment and will be followed in the long term. |
A 55-year-old male with history of atrial fibrillation, HHT, hyperlipidemia, hypertension, prostate cancer status post prostatectomy, remote smoking, and obesity was scheduled for a Maze procedure for treatment of atrial fibrillation. Medications for this patient included estradiol TD nasal spray, cromolyn sodium nasal spray, mupirocin 2% nasal ointment, aspirin, digoxin, metoprolol, and pravastatin.\nPreoperatively he was seen by Hematology for assessment of the use of anticoagulation therapy for atrial fibrillation in the setting of HHT. As mentioned, this patient was currently on only aspirin for anticoagulation given the risk of bleeding with HHT. After consultation, recommendations were to avoid further anticoagulation unless proved to be medically necessary in the setting of his cardiac pathology. Further recommendations revealed close follow-up with his physician as well as ongoing laboratory markers to evaluate for anemia.\nThe patient was also seen preoperatively in the Outpatient Preoperative Assessment Center in preparation for his surgery. Pertinent physical exam findings at that time revealed several telangiectasias on the tongue, lips, and right cheek. Exam of the airway revealed a mallampati class II, full cervical range of motion in all planes, and aforementioned small focal telangiectasias of the tongue but none noted in the posterior oropharynx. The patient was determined to be an ASA physical status 3 with good cardiac functional capacity. He also was determined to be high risk for obstructive sleep apnea as determined by the STOP BANG questionnaire.\nLaboratory data included a hemoglobin of 15.1 g/dL, hematocrit of 43.6%, and electrocardiogram showing atrial fibrillation with a rate of 68. A chest x-ray reviled no cardiopulmonary pathology. There was a recent transthoracic echocardiogram completed revealing an ejection fraction of 59% with left ventricular hypertrophy and a mildly dilated left atrium. There were no signs of diastolic dysfunction, and the heart was otherwise structurally normal. Furthermore, there was also documented evidence of a negative lexiscan cardiolyte stress test preformed 3 months prior.\nThe patient was originally diagnosed with atrial fibrillation 8 years ago and had undergone successful cardioversion to normal sinus rhythm after his initial presentation. He had spontaneously converted back to atrial fibrillation approximately 5 months prior to his planned surgery and had since been experiencing ongoing dyspnea on exertion and palpitations.\nSignificant to his history of HHT, he previously had experienced frequent episodes of epistaxis and does follow with an otolaryngologist. His epistaxis was complicated by a deviated septum in the setting of HHT, and he subsequently underwent septoplasty for surgical repair. After this nasal surgery he was started on a nasal estrogen for treatment of his epistaxis. Estrogens have been shown to be beneficial in the treatment of epistaxis secondary to HHT. It is postulated that estrogens may improve the integrity of the vascular endothelium or cause microhemostasis in the microcirculation. Since initiation of treatment and nasal surgery the patient’s episodes of epistaxis have been rare.\nOn arrival in the preoperative holding area, an 18 gauge IV was started and a right radial arterial line was inserted for hemodynamic monitoring. The patient was transferred to the operating room where standard ASA monitors were applied and pre-oxygenation commenced. General anesthesia was induced with fentanyl, midazolam, lidocaine, propofol, and rocuronium. The patient was intubated with a left double lumen endotracheal tube (ETT) using a MAC 3 blade revealing a Cormack-Lehane grade I view. Careful attention with gentle manipulation was used during direct laryngoscopy and no telangiectasias were appreciated in the posterior oropharynx. The ETT was pretreated by soaking in warm sterile normal saline to allow pliability and lubricated to facilitate smooth intubation and avoid airway trauma and rupture of any possible oropharyngeal telangiectasias. After successful intubation, correct positioning of the ETT was confirmed by bronchoscopy. After induction of general anesthesia, a cordis centeral venous catheter was inserted in the right internal jugular vein for central venous pressure monitoring and access for fluid and blood resuscitation if needed. A transesophageal echocardiogram (TEE) was performed ruling out an intracardiac thrombus or any significant structural heart disease. General anesthesia was maintained with isoflurane, oxygen, fentanyl, and vecuronium. Single lung ventilation ensued on the left for access to the heart via thoracotomy on the right chest wall. Prior to induction, the patient was in atrial fibrillation with a rate of 111. Intraoperatively successful cardioversion was performed 3 times for rates in the 160s. The surgery was successful without complication, and the patient remained in normal sinus rhythm with a rate of 70 at the conclusion of the procedure. Near the end of the procedure 2 lung ventilation resumed and the patient was treated with ondansetron for prevention of postoperative nausea and vomiting. The patient’s neuromuscular blockade was reversed with neostigmine and glycopyrolate. The double lumen ETT was exchanged for an 8.0 single lumen ETT under direct visualization with a size 4 McGrath video laryngoscope. Due to the high risk for obstructive sleep apnea (OSA) the decision was made to transfer the patient to the intensive care unit intubated where he was able to recover from anesthesia and was successfully extubated later in the day. Estimated blood loss from the case was 50 cc, urine output was determined to be 200 cc, and the patient received a total of 2700 cc of crystalloid throughout the procedure. |
The patient is a 69-year-old man with hypertension on amlodipine, hypogonadism on testosterone therapy, and chronic polyuria thought to be due to central diabetes insipidus on intranasal desmopressin at 10 µg twice daily who presented to the emergency department from his primary care physician’s office 6 months after initiation of desmopressin with 1 month of progressive fatigue, anorexia, dizziness, weakness, and gait instability that worsened in the week prior to presentation. He denied any fevers, headaches, neck pain, chest pain, nausea, vomiting, diarrhea, dark stools, or leg swelling, but did note increased thirst with up to 1 gallon of water intake daily for several weeks. His past medical history also included hyperlipidemia, obesity with mild obstructive sleep apnea, gastroesophageal reflux disease with esophagogastric fundoplication, and benign prostatic hyperplasia with green light photovaporization.\nOn examination in the emergency department, the patient had normal vital signs and was alert but was very lethargic and had an unstable gait. A non-contrast computed tomography scan of the head on the day of admission demonstrated no acute intracranial processes. However, a basic metabolic panel revealed a sodium level of 96 mmol/L, which was down from 125 mmol/L 2.5 months prior to presentation, and down from a value of 134 mmol/L at the initiation of desmopressin 6 months prior. Additionally, the patient’s urine sodium level was 37 mmol/L and he had normal thyroid-stimulating hormone and cortisol levels. Given the patient’s profound hyponatremia with changes in mental status, hypertonic saline was administered and admission to the medical intensive care unit was initiated.\nIn the medical intensive care unit, the patient was placed on an 800-mL/day fluid restriction, taken off the hypertonic saline, and placed on a dextrose infusion to match urine output. The patient required infusion of over 11 L of 5% dextrose (Fig. ) to match a high urine output, which peaked at 7.4 L on the second day of admission and then tapered down to 1.5 L by hospital day 5 (Fig. ). Over the course of 4 days in the medical intensive care unit, the patient’s sodium levels steadily increased to 125 mmol/L (never rising above 8 mmol/L in a day) with improvement in his mental status and symptoms (Fig. ). The patient was then transferred to the medicine unit with stabilization of his serum sodium levels between 130 and 132 mmol/L on repeated checks prior to discharge home.\nAt discharge, the patient was instructed to discontinue his desmopressin. Repeat sodium levels on outpatient follow-up remained stable between 136 and 139 mmol/L. However, as seen in Fig. , comparing a magnetic resonance imaging study of the brain obtained on day 3 of admission to one obtained on day 25 after admission revealed a slight irregular T2 hyperintensity in the central part of the pons, likely consistent with central pontine osmotic myelinolysis. Despite this finding, the patient eventually returned to his baseline mental status with no permanent neurologic deficits observed at the 2-year follow-up. The central diabetes insipidus continued for several months and then went into remission. |
A 35-year-old pregnant woman was admitted to our emergency room 4 weeks prior to her due date because of a sudden headache and unconsciousness. Computed tomography (CT) showed a massive cerebral haemorrhage in the right hemisphere, and she was immediately taken to the operation room for an emergency caesarean section. After the foetus was delivered, she underwent a craniotomy to remove the cerebral haematoma. After 8 h of surgery, the patient was taken to the ICU for further treatment.\nThe patient developed dilated pupils without a pupillary response. The CT scan showed mild pneumonia (Fig. a and b) on day 1. Moxifloxacin was started to treat her pneumonia and to prevent surgical site infections. Laboratory examinations on admission revealed a leukocyte count of 10*10^9/ml and a C-reactive protein level of 21.9 mg/L. As the pneumonia progressed, the patient developed febrile fever with a temperature between 38.5–39.5 °C and developed more grossly purulent tracheobronchial secretions, and laboratory studies showed an increased leukocyte count. Meanwhile, no pathogen was found as multiple sputum cultures, blood cultures and IgM for Chlamydia and Mycoplasma all came back negative, which ruled out common hospital acquired pneumonia caused by Streptococcus pneumoniae, Klebsiella pneumoniae or Staphylococcus aureus. Despite starting moxifloxacin at admission and meropenem and vancomycin on day 3 after admission, her pneumonia worsened, and she soon developed hypoxemia (oxygenation index 55–85 mmHg). The CT performed on day 12 showed more exudation and atelectasis than previously (Fig. c and d).\nSince the bacteriological culturing protocol failed to demonstrate a responsible pathogen and our current antibiotic therapy failed to control the pneumonia, we came to realize that the pathogen could be an uncommon pathogen for severe pneumonia. We sent a sample of bronchoalveolar lavage fluid for pathogen detection by next-generation sequencing (NGS) at BGI-Shenzhen on day 13 after admission. The NGS test was performed on the BGISEQ-500 platform []. Within 24 h, the NGS results identified 252 DNA sequence reads (out of 18,188,496) and 621 RNA sequence reads (out of 38,214,718) corresponding to P. micra. After we eliminated all the sequence reads of the human host and the unclassified reads, P. micra reads accounted for 83.17% (DNA) and 60.53% (RNA) of the total microbial reads (Fig. ). The second pathogen identified by NGS was Stenotrophomonas maltophilia, which could be a co-pathogen. Thus, the NGS results suggested that P. micra was the main pathogen causing pneumonia. On day 14, we adjusted the antibiotic therapy from meropenem and vancomycin to ornidazole for P. micra and sulfamethoxazole for Stenotrophomonas maltophilia according to our local antibiotic sensitivity pattern.\nAfter starting ornidazole, a prone position was given and daily bronchoscopic sputum suction, the hypoxemia improved. A CT scan performed on day 24 found less infiltration (Fig. e and f) and fewer lesions of atelectasis. Bronchoscopy showed less sputum and less bronchial oedema.\nUnfortunately, due to the patient’s massive cerebral haemorrhage, she was diagnosed with brain death based on electroencephalogram (EEG) and her clinical status. |
A 28-year-old female was referred to our hospital with sudden severe headache and vomiting. She fell into a coma during transportation, and was initially treated in the intensive care unit. Prior to this event, she had been in good health except that she often experienced migraine-like headaches. On admission, she was assessed as Glasgow Coma Scale 4 (E1V1M2), and her blood pressure was 125/84 mmHg, heart rate was 67/min (regular in rhythm), respiratory rate was 16/min, body temperature was 36.2oC, and routine laboratory blood tests showed no remarkable abnormalities. Her pupils were 2.5-mm prompt when reacting to direct light on the right side and 3.0-mm sluggish when reacting to direct light on the left side. Non-contrast computed tomography (CT) of her head revealed a large heterogeneous-dense space-occupying lesion in the trigone of the left lateral ventricle with midline shift to the right. The oval-shaped lesion was approximately 6.5 × 5.0 × 5.0 cm in size with intraventricular hemorrhage (IVH), which extended forwards into the third and fourth ventricles (Fig. ). CT angiography showed no vascular abnormality such as aneurysm, vascular malformation, or tumor stain. The patient was thus a relatively young female with no symptoms until onset who had developed a massive intracranial hemorrhage, which made it difficult initially to consider hemorrhage due to meningioma.\nOur first impression derived from these findings was acute intracranial hemorrhage in the left ventricular trigone, although the cause of the hemorrhage was unclear. Her clinical status was so bad that urgent extraction of the hematoma was performed in order to save her life. A massive hematoma was removed and the enlarged left lateral ventricle was opened through the occipital pole cortex via a left occipitoparietal craniotomy. The hematoma consisted of one part that could be easily evacuated and another part, located mainly on the deep side, that was solid and bled easily. The surgery was terminated after confirming that a large amount of the hematoma had been debulked, leaving a portion in which hemostasis was difficult. Histological examinations of the solid part revealed a meningioma with massive hemorrhage within the tumor and many irregular vessels, including softened thin-walled vessels, closed vessels, etc., at the peripheral area of the tumor (Fig. ). Closed arteries with organized reaction suggested a possibility of old hemorrhage. Spindle-shaped tumor cells were arranged in fascicular or storiform structures, and a few psammoma bodies were observed. Nuclear atypia or mitosis was rarely seen, and the Ki-67 proliferative index was less than 3 %. The tumor also extended to the choroid plexus, suggesting its derivation. The diagnosis of the 1st surgical specimen was fibrous meningioma, WHO grade 1. The intracranial hematoma was therefore thought to be due to intratumoral hemorrhage in a left lateral ventricular trigone meningioma. Postoperatively, the patient recovered well, but was diagnosed with right homonymous hemianopsia, right hemiparesis, and right abducens nerve palsy. Cerebral angiography was performed 5 days after the first operation and did not show any abnormality such as aneurysm, vascular malformation, or tumor satin. However, follow-up head CT demonstrated a residual tumor in the trigone of the left lateral ventricle (Fig. ).\nAt 42 days after admission to our institution, 2nd surgery was performed to remove the residual tumor using the same approach as in the 1st surgery. The tumor was found to be relatively soft and well-demarcated. It arose from the choroid plexus, with arterial blood supplied from the medial and posterior lateral choroidal arteries, and was removed completely. Microscopic examinations of the 2nd surgical specimen yielded a diagnosis of fibroblastic meningioma with a Ki-67 proliferative index of l − 2 %. Abundant hemosiderin deposits, indicating prior hemorrhage, were visible within the tumor. The patient’s 2nd postoperative course was uneventful, and no residual intraventricular tumor was found on her follow-up imaging (Fig. ). She was discharged from our hospital after the 30th post-2nd-surgery day. She was seen to be in a good state at the 15-month follow-up, demonstrating recovery from her right hemiparesis and right abducens nerve palsy, although her hemianopsia was not resolved. |
A 66-year-old female with a past medical history of hypertension, hypothyroidism, and gastroesophageal reflux disease presented to an outside hospital with abdominal bloating and discomfort. An ultrasound performed at her initial presentation noted a large left upper abdominal mass. She was referred for a whole body positron emission tomography-computed tomography (PET-CT) scan that demonstrated a large 24 × 12 cm left upper abdominal tumor coming off the tail of the pancreas and abutting the greater curvature of the stomach. The patient also had hypermetabolic metastases within the liver.\nThe patient underwent an image-guided biopsy of the large lesion. Pathology demonstrated a bland spindle cell neoplasm consistent with GIST. Immunohistochemistry was positive for CD117 and CD34. One-two mitoses were identified on the entire core tissue, and Ki-67 showed 1-2% proliferative index. The patient was started on imatinib (Gleevec) and demonstrated a metabolic response to therapy with a slight decrease in the size of the tumor.\nFour months after the initiation of imatinib therapy, a follow-up CT demonstrated the prior GIST, which had decreased in size to 13.2 × 8.9 × 12.9 cm (). Multiple hepatic lesions were once again identified, although most of them had decreased attenuation and showed a decrease in size. However, a 2.8 × 2.6 × 1.9 cm ovoid, mixed density, and partially calcified left kidney mass in the mid to lower pole was also identified, radiographically consistent with a primary RCC.\nGiven that the patient had an excellent radiographic and clinical response to imatinib and an enlarging left renal tumor that was radiographically concerning a primary RCC, resection of both the gastric and renal masses was recommended. The patient underwent a simultaneous radical resection of the large upper abdominal mass, consisting of en bloc subtotal gastrectomy, distal pancreatectomy, and partial omentectomy, as well as left radical nephrectomy, 10 months after initial presentation.\nGrossly, a 14.7 × 8.7 × 7.3 cm large mass stemming from the wall of the stomach was identified. The mass appeared tan-gray and lobulated on cut resection surfaces, with scattered edematous areas. Microscopically, the tumor demonstrated greater than 95% necrosis, consistent with the radiographic findings of response to imatinib. Scant areas demonstrated viable spindle-shaped tumor cells with vesicular chromatin and abundant cytoplasm arranged in fascicles and sheets, consistent with a GIST. The mitotic rate was low, with 0 mitoses identified per 5 mm2 (0-1 mitoses per 10 high power fields) (Figures and ). Gene mutation testing showed a KIT exon 11 deletion/substitution KPMYEV 550–555 L. PDGFRA mutation testing was not performed.\nThe nephrectomy specimen demonstrated a 3.6 × 3.2 × 1.8 cm hemorrhagic mass in the lower renal pole that abutted the renal sinus fat and came within 0.2 cm of the perinephric fat (). On hematoxylin and eosin- (H&E-) stained sections, the renal mass was focally well-circumscribed, though in a few areas it exhibited tumor extensions into adjacent parenchyma. It consisted of variably sized nests of cells separated by thin, fibrovascular septa (). The neoplastic cells were round to polygonal and demonstrated mainly voluminous clear to focally eosinophilic granular cytoplasm, distinct cell membranes, and mildly to moderately atypical vesicular nuclei with occasional nucleoli (). Some of the cells were binucleated to trinucleated. In several areas, the tumor nests demonstrated one to multiple rounded hyalinized structures. These hyalinized foci were usually lined by cells with higher nuclear-to-cytoplasmic ratio than, but similar nuclei to, the large cells comprising the majority of the tumor nests. Within scattered tumor nests, there was cellular dyscohesion away from the hyalinized foci with only the layer of small cells remaining, imparting a focal papillary or pseudopapillary appearance. Abundant psammomatous calcifications were seen throughout, often within the hyalinized areas. The tumor cells were positive by immunohistochemistry for vimentin, MART-1/Melan A, and the renal tubular marker CD10 (scattered focal membranous positive). They showed strong and diffuse nuclear positivity with transcription factor E3 (TFE3) (), and they were negative for cytokeratin AE1/AE3, epithelial membrane antigen (EMA), cytokeratin 7, carbonic anhydrase 9 (CA9), and HMB-45. Cytogenetic studies performed on fresh tissue from the tumor demonstrated an unbalanced rearrangement characterized by an (X;22) translocation at Xp11.2 and 22p11.1, consistent with an Xp11.2 (TFE3 gene) translocation-associated renal carcinoma (). As the tumor invaded the renal sinus fat, it was classified as pathologic TNM stage pT3a pNX MX, or Stage III.\nOn six-month follow-up, the patient was doing well. She was continuing on imatinib therapy due to the metastatic disease involving her liver, which also demonstrated the same KIT exon 11 mutation as her primary GIST. |
A 29-year-old male patient reported to the Department of Prosthodontics and Crown and Bridge, with a chief complaint of unesthetic appearance and difficulty in chewing food. History revealed that patient had undergone surgery for oral tumor present on the lower right posterior region of the jaw 1 year back, which resulted in a large hard and soft tissue deformity []. On examination of the maxillary arch, all the teeth were intact with good periodontal conditions. Mandibular arch examination revealed missing lower right canine, premolars, and first molar. Mild recession on the distal side of the lower right lateral incisor was seen. The restorative space of this Kennedy Class 3 defect was >15 mm []. Radiographic examination revealed 20% bone loss with lower right lateral incisor but no clinical mobility. Considering the extent of the defect, the required prosthesis was planned not only to restore the missing teeth but also to restore the deficient part of the ridge as well.\nTreatment options suggested were removable cast partial denture, and an implant supported FDP. The patient was not willing for a removable prosthesis and also could not afford the cost and elective surgery associated with an implant-supported prosthesis. Entirely tooth-supported conventional FDP could not be used in this situation because of the unfavorable long-term prognosis.\nConsidering the clinical findings, a fixed-removable dental prosthesis using cement retention for the fixed metal fused to ceramic bar framework and ball retention for the RPD was planned for the rehabilitation of the long span Kennedy Class 3 partially edentulous space in the lower right posterior region of the jaw. The patient was explained about the treatment procedures, and informed consent was obtained.\nDiagnostic impressions of the maxillary and mandibular arches were made using irreversible hydrocolloid (Tropicalgin, Zhermack, Italy). The casts were poured with model plaster (Kalabhai, Kaldent, India) and were articulated using facebow and centric bite record. On these casts, a diagnostic wax pattern was fabricated of the missing teeth. A putty index of this pattern was made using addition silicone putty material (Aquasil, Dentsply, Germany) to fabricate temporary restoration at a later stage.\nThe abutment teeth were prepared to receive porcelain fused to metal restoration with lower right central incisor, lateral incisor, and second molar and all metal restoration with the third molar. A two-stage putty-light body impression of the lower arch was made and poured in die stone (Pearlstone, Asian Chemicals, India). Temporary FDP was fabricated using the putty index and cemented using temporary cement (Temp-Bond, Kerr Corporation, Romulus).\nWax patterns were fabricated for all the prepared teeth and a wax custom bar running over edentulous deficit ridge was connected to these prepared wax patterns. Ball attachment patterns (Rhein 83, USA) were attached to the custom bar in the region of second premolar and first molar. Selection criteria for precision attachment were based on location and length of the edentulous span; function, retention required, and economical constraints of the patient.\nSpruing, investing, casting, and finishing and polishing of this nickel–chromium (Ni-Cr) alloy framework were done. Framework try-in was done in patient's mouth to assess the fit and availability of interarch space. After satisfactory try-in, the ceramic (VITA Zahnfabrik, Germany) layering was done for all the retainers, except for lower right third molar. The bisque trial was done to evaluate the shade and fit of the fixed prosthesis [].\nThe single-stage putty-light body addition silicone pick-up impression of the lower arch was made with retention caps secured over the ball attachment. The cast was poured using die stone. Temporary denture base and the wax occlusal rim were fabricated covering the edentulous area. The jaw relation was recorded followed by articulation and teeth arrangement was done to achieve unilateral balanced occlusion with disclusion of all nonworking side teeth on lateral excursion. Waxed denture try-in was done followed by acrylization with heat-polymerized acrylic resin (Trevalon HI, Dentsply, India). Laboratory remounting and finishing and polishing of the prosthesis were done []. Standard retention caps were inserted in the slot present on the intaglio surface of the RPD.\nCementation of a metal framework with auxiliary attachment was done using Type 1 Glass ionomer cement (GC Gold Label 1, Japan) and the removable denture was attached to this framework using the ball attachment []. Postinsertion, hygiene, and home care instructions were explained to the patient. Recall visits of 1- and 3-month follow-up of the prosthesis were found to be satisfactory in terms of function and esthetics. |
A 62-year-old woman was admitted in the hospital in June 2011, with a diagnosis of cervical spondylotic myelopathy. The patient began to experience neck and back pain with stiffness 7 years ago. The symptoms developed slowly, until the gait disturbance and hand clumsiness began to appear in 2010. Initially she received conservative treatment and it was less effective. However, her symptoms progressed and at the time of presentation she was wheel chair bound. She didn't have any history of trauma with no relevant past medical or similar family history.\nPhysical examination showed cyan pigmentation on the nose, sclera, and the ear auricle and also in other parts of the body (). There was kyphosis at the thoracolumbar segment, resulting in a restricted movement at neck and back. Positive Romberg and Tandem gait sign and the finger-escape sign were observed. The grip-and-release test was 8 movements at both hands in 10 seconds, which was obviously inferior to the normal criterion of above 20 movements. Paresthesia on both hands and radial side of the left forearm and no motor weakness was observed. No pathological reflexes were observed on either side. The preoperative Japanese Orthopedic Association myelopathy (JOA) score for her was 7.\nCT scans indicated multilevel degenerative disc disease from cervical to lumbar spine, including narrowing, calcification, osteophytosis and vacuum phenomenon (, ). MRI showed the cervical spinal compression in multi-segment by disc extrusion and ligamentum flavum redundancy simultaneously ().\nAs the color of the patient's urine turn to dark after exposure to air after two hours, the patient's urine sample was screened for metabolic disorder. The measured value for HGA was 1220.03 while the normal value should be 0. So, we confirmed the presence of alkaptonuria.\nAs the patients' cervical spine had normal lordosis and multi-level stenosis, we performed the modified laminoplasty. This involves C3 laminectomy, C7 upper semi-laminotomy, and C4–6 open-door laminoplasty with implantation of man-made coral bone interposition. This was in contrast to the conventional cervical laminoplasty technique that involves a laminoplasty from C3–7 completely. During the operation, the ossificated nuchal ligament and the ligamentum flavum between C2–3 were stained black in color due to the deposition of the oxidized HGA pigmentation (). After surgery, the patient recovered uneventfully (). The cervical JOA score improved from 7 preoperatively to 9 at discharge and reached 11 at one year postoperatively. She was satisfied with the treatment although she had difficulty in climbing stair case without crutches. |
A 26-year-old Hindu male educated up to class 8th without any past and family history of psychiatric disorders, well-adjusted pre-morbidly, presented to the hospital with the history of being treated by cardiothoracic surgeon for multiple self-inserted nails in pericardium. History revealed that the patient had continuous illness of 4 years characterized by symptoms of muttering and smiling to self, being suspicious towards family members, decreased sleep, aimless wandering behavior, aggressive and assaultive behavior against family members, which was mostly unprovoked, poor self-care, and impaired biological functions. Mental status examination revealed blunted effect and prominent auditory hallucination in the form of people discussing among themselves about him and his actions. For the above symptoms, he was seen by a psychiatrist two years back, but the patient did not show much improvement as he remained poorly compliant to prescribed medications. In the mean time, the patient started having self-injurious behavior in the form of piercing nails and safety pins in his chest wall just adjacent to his left nipple. This behavior was not evident to his parents as he would do this mostly when he would be alone. His injury was noted by his uncle when he had fever and was taken to a doctor who noticed an infective swelling over left chest wall on the side of nipple. When inquired about any chest injury, the patient admitted about his self-mutilating behavior of piercing his chest wall with nails and safety pins. Radiological examination of the chest showed multiple foreign body in the chest wall and pericardial cavity. He was referred to a cardiothoracic surgeon for treatment. After being treated for foreign body in chest and pericardial cavity, patient's guardian came to the hospital for treatment of psychiatric symptoms. On asking the reason for the self-mutilating behavior, patient told that he did it to relieve his feeling of burning sensation in left side of chest and palpitation. The patient did not attribute his self-injury behavior as a response to auditory hallucination. He also said that he did not have much perception of pain during this behavior. Physical examination revealed multiple scar mark over left chest wall and postoperative scar marks over sternum []. Patient was prescribed with tablet trifluperazine 10 mg and trihexyphenidyl 2 mg, and was asked to follow up after 1 month. After 1 month of treatment, patient showed good improvement in psychopathology, and there were no reports of self-injurious behavior during this period. |
A 74-year-old man with a past medical history significant for coronary artery disease complicated by dilated congestive cardiomyopathy and chronic atrial fibrillation, status post implantable cardioverter defibrillator placement and aortic bioprosthetic valve replacement presented to the hospital after an episode of hematochezia accompanied by nausea and pallor. On arrival, he was noted to have melenic stools, hypotension, and an acute drop in hemoglobin from a baseline of 8–9 to 5.6 g/dL. He was resuscitated with intravenous fluids and packed red blood cells and was intubated. A bedside esophagogastroduodenoscopy revealed irregular-appearing mucosa in the second part of the duodenum, concerning for malignancy (Fig. , ), as well as several duodenal ulcers (Fig. ). A computed tomography scan of the abdomen and pelvis demonstrated arterial phase extravasation of blood into the duodenum (data not shown). Interventional radiology embolization was performed to control active bleeding of anterior pancreaticoduodenal arcade. The patient continued to have melenic stools, and his hemoglobin continued to fall, necessitating vasopressor support despite volume and blood product resuscitation. The patient was deemed a poor surgical candidate given his cardiac comorbidities, and the patient's family decided to initiate hospice care. The patient expired a short time thereafter, and an autopsy was performed.\nAt autopsy, gross examination revealed evidence of massive upper gastrointestinal bleeding including bloody gastric and intestinal contents. In the duodenum, near the ampulla, there was a circumferential area of mucosal irregularity measuring 4 cm in length, corresponding to the area seen on endoscopy (Fig. ). A 1-cm mucosal ulceration was also identified within the area of mucosal irregularity. Histologic examination of the area of mucosal irregularity revealed extensive benign BGH with no evidence of dysplasia or malignancy (Fig. ). A duodenal ulcer was also noted with extension of acute and chronic inflammation and fibrin through the muscularis propria and into the adjacent adipose tissue (Fig. , ). |
A 43-year-old man was admitted to the Endocinology Section of this hospital because of palpitations, weight loss of two years’ duration and recent onset of exertional dyspnea. The physical examination, laboratory and histological findings, including serum thyroxine, TSH level and needle biopsy of the thyroid, were compatible with hyperthyroidism and congestive heart failure. He was initially treated with propylthiouracil (300 mg daily), and the heart failure symptoms improved with appropriate care. On admission, serum HBsAg was tested as a part of routine clinical tests and was found to be positive. The patient denied any history of hepatitis exposure or any family history of hepatitis B or exposure to blood products. Serum aminotransferase activities were within normal limits. HBeAg and HBV–DNA were not detected in the serum. The patient was discharged on the 21st hospital day with markedly improved general condition. Two months later, propylthiouracil was substituted with methimazole (30 mg daily) for better compliance. Seven months later, the patient was readmitted to the hospital because of nausea, general malaise and jaundice of two weeks’ duration and transferred to the Hepatology Section. He denied any use of illicit drugs, herb medication or alcohol during the period. On examination the patient appeared acutely ill and icteric, although he was clinically euthyroid. No Spider angiomata, skin rash or palmar erythema was noted. The pulse was irregular with a rate of about 80 due to atrial fibrillation. The edge of the liver was palpable 5 cm below the right costal margin with a vertical span of 13 cm. The liver was diffusely tender.\nNo evidence of ascites was found. The hematocrit was 42 percent; the white cell count was 6400; with a normal differential count, the platelet count was 81,900/mm3. Agranulocytosis or eosinophilia had not developed during the illness. The serum protein was 7.1 g/dl (albumin 4.6 g and the globulin 2.5 g) and the bilirubin was 5.0 mg/dl (direct 3.5 mg and indirect 1.5 mg). The serum alanine aminotransferase (ALT) was 180 U/L (normal <40), the serum aspartate aminotransferase (AST), 848 U/L (normal <40), and the alkaline phosphatase, 848 IU/L (normal: 64–238). The prothrombin time was 13.7 seconds with a control 11.3 seconds. The T3 RIA was 109.85 ng per 100 ml (normal: 90–210), the thyroxine 3.01 ug per 100 ml (normal: 5–13) and the TSH 19.85 uU per ml (normal: 0.3–5). Serum HBsAg and antibody to hepatitis B core antigen (anti-HBc) were positive, but HBeAg, IgM anti-HBc, and HBV-DNA by dot and slot blot hybridization were negative. Antibody to hepatitis C virus (Anti-HCV) by Elisa method was negative. An ultrasonographic examination of the abdomen revealed a diffusely enlarged liver, although the spleen was not enlarged.\nThe methimazole was discontinued and symptomatic care was given. During the next four weeks the patient’s condition deteriorated rapidly (). From the 21st hospital day, dexamethasone was administered at a dose of 10 mg daily. On the 27th hospital day, hepatic encephalopathy developed and the patient died four days later. A postmortem needle autopsy of the liver was performed (, ). The histologic findings revealed a micronodular cirrhosis secondary to a hepatitis B virus infection with moderate septal/portal inflammation, marked cholestasis and scattered acidophilic bodies. No HBsAg or HBcAg was detected in the liver by peroxidase-antiperoxidase method. |
An 89-year-old man was admitted to the hospital with left hip pain after a fall from a window. The left leg was amputated above the knee 50 years ago due to a trauma, and the patient had chronic stump pain and right knee osteoarthritis that resulted in limited walking ability (community ambulation with cane)[ and inability to perform basic activities of daily living[ with his limb prosthesis. There were no other underlying diseases.\nThe type of fracture was A1.2, according to the AO/OTA classification, and the displaced fracture fragment formed an anterior angle (Fig. ). The preoperative ASA classification was stage II, and the mean dual-energy X-ray absorptiometry T-score of the femoral trochanteric area was –3.7, indicating severe osteoporosis.\nSurgery was planned using a PFNA II, and fracture reduction was performed in the supine position on the fracture table under general anesthesia. The stump of the affected side was fixed to the boot piece using a skin-pulling band. Unlike the usual procedure for skin traction, the band was not only fixed to the stump but also wrapped around the anterior and posterior thigh due to the aseptic drape and skin incision. The band was fixed using skin tape and surgical Ioban (3 M, Maplewood, MN); it was then fixed to the ankle part of the boot piece so that the lower side of the boot piece (ankle side) could support the stump along with the skin traction band (Fig. ). Subsequently, sufficient traction and rotation could be applied. The state of reduction was evaluated by C-arm fluoroscopy, and it was confirmed that proper traction and internal rotation were obtained; however, anterior angulation of the fracture site remained. Anatomical reduction was performed using a kidney clamp through an incision, and internal fixation was performed using a standard 130° nail with a 200-mm length and 9-mm diameter (Fig. ).\nFracture union was achieved at 6 months postoperatively, and there were no fracture-related or general complications during the 2-year follow-up. Walking ability[ (community ambulation with cane) and activities of daily living were restored.[ |
A 46 year old male was an alcohol-intoxicated restrained passenger in a head-on motor vehicle collision, suffering blunt force abdominal trauma. At the collision site EMS recorded a Glasgow Coma Score of 15 with stable vital signs. He was transferred to Cabell Huntington Hospital where he was intubated and found to be tachycardic and profoundly academic to an arterial pH of 7.19 with accompanying base deficit of -11. Hemoglobin was 12.9, hematocrit 37.1, PT 11.5 sec, and APTT 23.5 sec. CT showed acute thoracic aortic rupture with a large volume of blood inferiorly along the aorta, right middle and lower lobe lung contusions, and a 4 cm laceration along the inferior lobe of the liver with blood in the renal hilum suggesting right renovascular injury and free fluid within the pelvis (a). He was transferred to Saint Mary’s Medical Center for emergent management of aortic rupture.\nEmergent surgical management of the ruptured thoracic aorta was completed by the cardiothoracic team. Upon completion, initiation of exploratory laparotomy was begun, noting blood in the peritoneum and bile staining in the right upper quadrant associated with the transverse and hepatic flexures of the colon. The gallbladder was visibly distended, firm to palpation, and discolored but showed no signs of rupture. Subcapsular hematoma was appreciated along the right posterior lobe of the liver but showed no signs of actively expanding or gross laceration. Open cholescystectomy with intraoperative cholangiogram was performed on a thick, distended and grossly-discolored gallbladder consistent with hemorrhage into the gallbladder lumen (b). Conray contrast was used to demonstrate a completely intact biliary tree with extravasation noted from the common bile duct. Duodenal injury was ruled out by passing methylene blue through the orogastric tube with no extravasation appreciated and colon was assessed via direct visualization by Kocher maneuver and mobilization of the hepatic flexure. Due to the duration of the thoracic aorta repair and the exploratory laparotomy, the decision was made to place a 16-French T-tube in the common bile duct in addition to two large #24 Jackson-Pratt tubes in the vicinity of the bile duct (). The patient was maintained on ventilator in the neurotrauma intensive care unit. In the postoperative period the T-tube drained golden brown bile and was well-tolerated.\nUrine collection via Foley catheter showed blood-tinged urine that persisted until POD 10 but then spontaneously resolved. During this time on POD 6 the patient underwent gastrostomy with placement of percutaneous gastrostomy and tracheostomy tubes. Due to the PEG becoming disloged on POD 8 the patient underwent exploratory laparotomy and gastrostomy with jejunostomy tube placement and removal of foreign body. Evaluation on postoperative day 10 showed successful drainage of the operative site via T-tube (c). The patient continued to improve and was discharged on POD 28 with T-tube and J tubes in place.\nRecovery was complicated during the outpatient course as frank blood began appearing in the patient’s urine on POD 39 and the patient began complaining of pain around tube sites. CT urogram showed no residual renal injury and was presumed to be due to residual posttraumatic blood accumulation. Of note, a small amount of fluid was appreciated in the anterior right middle and upper abdomen along the inferior right lobe of the liver not seen previously but consistent with postoperative seroma. A urinary tract infection was diagnosed and managed medically. T tube cholangiogram revealed no abnormalities and the the T-tube was removed along with J-tube on POD 54. The remainder of the patient’s recovery period was uneventful with regards to hepatobiliary procedures, however frank blood in the urine persisted for an additional 6 months due complications of subclinical traumatic kidney injury sustained during the motor vehicle collision. |
A 41-year-old right-handed woman who had complained of a 3-year history of progressive ataxia and dizziness was visited by a neurologist. Throughout these years, she was visited several times by general physicians. She had a history of falling along with ataxia, and no blurring of vision was noted. Neurological examination revealed no cranial nerve deficit. MRI demonstrated high-signal lesions in the left frontal lobe involving corpus callosum on fluid-attenuated inversion recovery imaging [].\nAfter that, with a diagnosis of MS, according to McDonald criteria (2005) the patient was treated by β-interferon 1a for about 1 year. She had been complained of nausea, vomiting, fatigue, and drowsiness as side effects of β-interferon 1a during therapy. The ataxia, as chief compliant was also continued. After 1 year and with the stress of her husband death, she presented with slowing and clumsiness in a way that she could not walk without help more than 50 m. Neurological examination revealed impaired tandem gate, positive Romberg sign, and positive bilateral Babinsky. New MRI showed that the lesion is extended to left frontoparietal lobe [].\nAlthough brain tumor was suspected, the patient treated with β-interferon 1a for more six months until a magnetic resonance spectroscopy (MRS) was done and a commission of neurologists and neurosurgeons suggested astrocytoma and suspected MS for the patient.\nFinally, a neurosurgeon did stereotaxis, and pathology revealed Grade II astrocytoma. With this diagnosis the tumor excited by craniotomy and followed by 1 month of radiotherapy. After that, ataxia and clumsiness reduced but she was not visited by neurologist and received no therapy for MS for 6 months. After that following a severe cold, she presented with difficulty in walking and slowing in a way that could not walk without help more than 10 m. Hence with a diagnosis of relapse of MS she received pulse therapy of corticosteroid for 5 days, twice in 2 weeks and followed by Extavia (β-interferon) for 2 months. With therapy walking ability improved and she could walk about 100 m without help.\nDuring follow-up, neurological examination revealed impaired tandem gate, positive Romberg sign, and positive bilateral Babinsky. Cranial nerves were intact, but quadriparesis (more severe in right side), and clumsiness was present. Last MRI showed multiple high-signal plaques around the corpus callosum and high-signal lesion in left parasagital area due to excision of the tumor []. |
A 69-year-old man was referred to our institution for the treatment of persistent AT. He had a history of mitral valve plasty for mitral regurgitation due to mitral valve prolapse and coronary artery bypass grafting for angina pectoris 19 years before the ablation and paroxysmal AF was first diagnosed in the following year. The frequency of AT has increased starting at 14 years before the ablation, and cardioversion was performed each time. He was admitted for radiofrequency catheter ablation of AT because of palpitations during exercise and increased brain natriuretic peptide levels. A 12-lead electrocardiogram showed an AT with a tachycardia cycle length (TCL) of 304 ms and positive P-waves in leads I, II, III, aVF, V4, V5, and V6 (Figure ). With informed consent, the patient underwent an electrophysiological study and ablation.\nEndocardial mapping of the atrium was performed using a PentaRay catheter (Biosense Webster, Diamond Bar, CA, USA) with the CARTO mapping system (Biosense Webster). Checking the activation map of the left atrium (LA) during AT with a TCL of 304 ms and activation on the CS propagating from distal to proximal, we suspected that the AT was localized re-entrant tachycardia in the LA anterior wall (Figure ). However, because a small part of the TCL was still not covered by the LA mapping, a second map was acquired in the right atrium (RA). The activation map of the RA showed a focal activation pattern starting from the RA septum. When the maps of both atriums were combined, the propagation of the tachycardia on the activation map exhibited the centrifugal activation from the LA anterior wall, and the conduction from the RA to LA was not well understood (Video 1). While, a coherent map demonstrated that the propagation ran from the RA high septum to the LA anteroseptum via an interatrial connection, and turned to the RA septum from the LA septum via the Bachmann bundle with clockwise rotation. Furthermore, the high-septum interatrial connection appeared to have a conduction delay because conduction velocity vectors near the connection were thicker relative to the surrounding areas (Figure and Video 2). On a voltage map, a wide low-voltage zone (LVZ) extending from the LA anterior wall to the LA and RA septums was documented (Figure ). Entrainment mapping revealed a short post-pacing interval (PPI) [PPI-TCL <20 ms] in the RA and LA septums, and finally, the AT was diagnosed as BiAT with a re-entrant circuit involving both atrial septums (Figure ). On the ripple map of both atriums, a propagation reciprocating near the assumed high-septum interatrial connection was visualized (Video 3), and clear double potentials were recorded near the site (Figure ). The preceding potentials were considered to be far field potentials due to amplitude lower than the following potentials, and the TCL (304 ms) was completely covered by adding the activation time of the preceding potentials (36 ms) to the activation time of the endocardial potentials of both atriums (268 ms). Given these, the preceding potentials were considered to be potentials of an epicardial interatrial connection. Ablation began with 35 W of radiofrequency using an irrigated catheter (ThermoCool SmartTouch™ Surround Flow, Biosense Webster) on the epicardial interatrial connection with a conduction delay from the endocardial side (Figure ). After 17 s of ablation, BiAT was terminated and sinus rhythm (SR) was restored without pause (Figure ). Additional burns at the area near the successful site of ablation were applied; subsequently, pulmonary vein isolation and LA roof ablation were also performed using a 28-mm cryoballoon (Arctic Front Advance, Medtronic, Minneapolis, MN, USA). All procedures were completed without any complications. No AT was induced by atrial burst pacing under isoproterenol infusion. After the ablation, the patient was followed up without any antiarrhythmic drugs, and SR was maintained during 3 months of follow-up. |
A 68-year-old postmenopausal woman presented with symptoms of urinary incontinence. She attained menopause at the age of 50 and is not sexually active for the past 15 years. She had four uneventful vaginal deliveries. Her first visit to a gynecologist was in 2012 for itching, burning of the vulvovaginal area, and repeated urinary tract infections. Local examination of the genitalia showed a fissure at the fourchette, decreased vaginal rugae, and increased friability with petechiae. The vaginal pH was 7, and the pap test reported an atrophic smear. Transvaginal ultrasound was consistent with postmenopausal status. She was started on daily conjugated equine estrogen 0.625 mg cream for 15 days, followed by twice weekly for 6 months. The fissure was not healing at day 15, and biopsy from the fissure site showed nonspecific inflammation. She was to continue local estrogen therapy. Two years later, she returned with complete fusion of labia minora from clitoris to the posterior fourchette with a tiny opening at the anterior one-third of the introitus through which she was voiding and had stopped estrogen therapy. This time, the labia were manually separated under local lignocaine cream. She was lost for follow-up and returned 3 years later with dribbling of urine. She was not on any medication. A routine urogynecological evaluation was performed with history and detailed examination. Local examination of the genitalia had signs of atrophy with a CLF of the genitalia []. Introitus was not identified due to labial fusion. The cough test was negative, and postvoid residual volume was 40 ml on abdominal ultrasound.\nUnder short general anesthesia, patient is positioned in lithotomy. Surgical separation and restoration of labial anatomy were done. A midline vertical incision is given along the midline raphe, which opened up a normal urethra, vaginal introitus, vagina, cervix, and uterus. The vaginal pH was 7. Labial skin edges were freshened and sutured to the vaginal epithelium using 2-0 vicryl []. Vulvar biopsy reported as patchy inflammation. Surgical correction of CLF was uneventful.\nImmediate postoperative care was with a third-generation cephalosporin antibiotic and analgesics. Vaginal pack and the indwelling catheter were removed after 24 h. She was started on daily vaginal conjugated equine estrogen of 0.625 mg cream for 15 days and then twice weekly for 6 months. The pseudo-incontinence has resolved entirely. She has been local estrogen therapy 0.5 mg estriol once weekly for 1 year. There was no agglutination of labia with complete resolution of urinary symptoms after a follow-up of 3 years. Vaginal pH is 5 at 3-year follow-up []. |
A 50-year-old woman was admitted to our Breast Unit because of a typical appearance of inflammatory cancer in the left breast with small, well-circumscribed, solitary nodules in the trunk and in the base of the neck. Her left breast appeared swollen, red and oedematous. Bilateral mammography showed a 3 cm mass in the left breast with increased skin thickness. Mammogram was normal in the right breast. Biopsy confirmed the presence of lymphangitis carcinomatosis sustained by HER2-overexpressing, HR-negative IDC. Staging CT scan showed no sign of systemic disease and she started neoadjuvant therapy with Epirubicin plus Cyclophosphamide according to a dose-dense schedule (every 2 weeks).\nAfter four cycles she complained of pain in her right hip. Bone scan revealed the presence of multiple metastases in the spine and pelvis. MRI confirmed neoplastic lesions in all vertebra and pelvic bones (). She underwent radiotherapy to the proximal part of her right femur and subsequently initiates first line therapy with Trastuzumab, Pertuzumab and Docetaxel. She rapidly reached clinical benefit: the inflammatory signs of the left breast gradually faded and the skin nodules decreased. Consistently, the MRI performed after 6 cycles demonstrated a dramatic reduction in number and size of bone metastases ().\nAfter 9 months of treatment (12 cycles) she noticed reddening of her trunk and a swollen, oedematous right breast, the contralateral one, resembling a cutaneous infection. Topical steroids, oral nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics were prescribed without any benefit. A biopsy of the para-areolar skin was performed and histological examination disclosed a HER2-overexpressing IDC. New small nodules appeared in the skin of the trunk and the pre-existing ones increased in size (). Nevertheless, disease remained in partial response in the bone and with no other site of metastatic spread as revealed by MRI () and CT scan, respectively. She discontinued treatment and started a second line therapy with TDM-1. |
A 47-year-old lady with underlying diabetes mellitus and hypertension, presented with lethargy and progressive body weakness for 2 weeks, shortness of breath, and orthopnoea for 3 days. She was admitted in the Intensive Care Unit (ICU) and treated as Gullien-Barriere Syndrome with AMAN variant and Streptococcus Hemolyticus bacteraemia after a couple of investigations. Intravenous immunoglobulin, as well as 2 courses of antibiotics (ceftazidime and amoxicillin clavulanate, followed by meropenem), was administered through a central venous catheter. In the second week of ICU admission, she developed an upper gastrointestinal bleeding and required inotropic support and endoscopy. She developed a rash over the upper trunk after intravenous sedations (benzodiazepine, propofol and fentanyl), so blood transfusion was given. Subsequently, the allergic reaction resolved after chlorpheniramine was given.\nTwo days later, we noticed a 6 × 5 cm non-tender bluish blister over the right cubital fossa at the previously placed intravenous cannula. The wound was dressed using purilon gel and foam every alternate day. After 3 weeks, the wound became sloughy and bedside wound debridement was done (). The wound measured about 8 × 5 cm with exposed subcutaneous fat. It did not heal despite regular dressing; thus, the patient was referred to the plastic team for further wound management. Wound debridement, basilic vein ligation, and vacuum dressing were done by the plastic team in the operation theatre (). After 1 cycle of vacuum dressing and no organism growth from the tissue culture, another wound debridement was performed with a delayed wound closure (). Postoperative recovery was complicated with congested and swollen tissue, which was treated conservatively by upper limb elevation. The oedema subsided eventually and sutures were removed at day-14 post operation. The patient was able to move her right upper limb in full range of movement and later transferred out of the ICU to the neuromedical ward. Later she was discharge and followed up in plastic clinic in 2 weeks, then 1 month and 3 months. Her wound was healed well and there is no functional disability. |
A 10-year-old boy visited the Department of Pedodontics with the complaint of being unable to chew on his right side. Upon examination, the lower arch contained the following teeth: 36, 35, 34, 73, 32, 31, 41, 42, 83, and 46 (). The upper arch contained teeth consistent with the intertransitional period, except that 14 had erupted (). Upon history taking, it was gathered that 84 and 85 had been extracted a year ago due to extensive caries and severe pain. An orthopantomograph (OPG) revealed half root completion of the unerupted 44 and 45 (). It was decided to construct a LHLD (functional lingual arch with hinge-type lockable dentulous component) in order to maintain the edentulous span until the eruption of 44 and 45, and to relieve the child of his chewing disability. After band adaptation on 36 and 46, alginate impressions were made of both the arches, into which the prepared bands were placed ( and ). Casts were poured with dental stone. A lingual arch incorporated with two molar tubes (on the edentulous side) was fabricated using 0.9 mm wire on the lower cast (). Wax up was done on the edentulous span containing artificial molar teeth (to replace 84 and 85), such that the molar tubes were incorporated into the wax up in order to later serve as hinges for the dentulous component. On the buccal side of the dentulous component, another molar tube was placed, such that it was parallel and in alignment with another buccal tube welded on the buccal surface of the molar band ( to ). The lingual arch was then soldered to the bands ().\nPlaster blockout of the undercuts and buccal tubes was done (). Acrylization was carried out using self-cure acrylic by the putty method. An index was made of the wax up () using addition silicone (Elite HD, Zhermack, Germany), following which the cast was dewaxed (). Artificial teeth were incorporated into the index () and self-cure acrylic was mixed with monomer and placed into the index. The index was reseated on the edentulous ridge on the cast until the acrylic mixture had completely polymerized (). An "Angry Birds" sticker was laminated and placed on the buccal surface of the dentulous component and covered with a thin layer of clear acrylic. The appliance was then gently removed from the cast ( and ).\nThe tubes on the buccal surface were incorporated in order to pass the locking wire (0.64 mm) that formed the locking component of the appliance ( and ). The efficacy of the hinge (molar tubes attached to the lingual arch) was verified by rotating the dentulous component around its hinge axis ( and ). Finishing and polishing was carried out for the acrylic and metal components. The appliance was evaluated for any mucosal interferences or occlusal disharmonies, following which the appliance was inserted intraorally by cementing the bands onto 36 and 46 using luting glass-ionomer cement ( and ). The patient was recalled the next day for a check-up, following which another general evaluation was done after a week. |
A 56-year-old African American female with a past medical history of colon cancer of 3 years of status post-low-anterior-resection and chemotherapy presented to the emergency room with 3 months of progressive, debilitating left hip pain, 40-pound weight loss, and weakness. She denied flank pain, hematuria, or bright red blood per rectum. On exam, the patient was afebrile, with a heart rate in the 110s and systolic blood pressure in the 90–100s. She appeared cachectic. On abdominal exam there was a well-healed low midline incision. There was no flank pain but there was left lower quadrant discomfort and limited range of motion of the left leg with associated hip pain. WBC count was 14,900, hemoglobin was 6.5 g/dL, hematocrit was 20.1%, and the platelet count was 462,000. BUN was 19 and creatinine was 1.4. The urinalysis was significant for a pH of 7.0, moderate hemoglobin, and large leukocyte esterase with negative nitrites. There were >50 WBCs and 10–25 RBCs and many bacteria. Urine culture was 20,000 CFU with more than 3 organisms present. Blood culture was positive for vancomycin sensitive Enterococcus faecalis.\nCT scan of the abdomen and pelvis with intravenous contrast revealed a 22 cm × 11 cm enhancing left retroperitoneal fluid collection extending along the length of the psoas muscle and tracking into the left hip. The left kidney had a duplicated collecting system with moderate hydronephrosis of the upper pole moiety. The renal pelvis of the lower pole moiety was obstructed with a 3 cm stone with apparent loss of integrity of the renal pelvis with urine extravasation. The lower pole parenchyma had calyceal ballooning and significant cortical thinning. The right kidney also had a duplicated collecting system with a preserved upper pole parenchyma and no hydronephrosis. The lower pole renal pelvis was obstructed with UPJ calculi and a focus of air consistent with emphysematous pyelitis. There was dilation of the proximal renal pelvis without parenchymal atrophy (). These abnormal CT findings were highly of chronic pyelonephritis/XGP secondary to chronic obstruction versus less probable malignant transformation.\nThe patient was admitted to the hospital, resuscitated, and covered with broad-spectrum antibiotics. Two large bore retroperitoneal drains were placed percutaneously with drainage of purulent fluid. Abscess culture was significant for Proteus spp. and E. faecalis. Percutaneous nephrostomy tubes were placed in both the upper and lower pole moieties. Following defervescence, the patient was taken to the fluoroscopy suite for further evaluation. Retrograde pyelography confirmed complete bilateral ureteral duplication with no vesicoureteral reflux. There was contrast extravasation from the left lower pole moiety confirming urine leak from the renal pelvis. The lower pole of the right renal pelvis had significant stone burden but preserved integrity (). On Mag-3 renal scan with furosemide washout, the left kidney contributed with 28% of overall renal function, with approximately 90% of that from the upper pole moiety. There was minimal contrast uptake in the lower pole ().\nThe patient was taken to the operating room for an open left retroperitoneal washout and open lower pole heminephrectomy. A stent was placed in the left upper pole ureter to assist with intraoperative identification and preservation. Via a left flank incision, the left retroperitoneum was explored and significant fibrosis and inflammatory rind was encountered around the lower pole of the kidney. The lower pole was completely mobilized and a common sheath with both ureters was identified. The sheath was opened and the stented upper pole ureter was identified and excluded. The lower pole ureter was traced cranially to the renal pelvis and a 2 cm necrotic defect was noted in the collecting system. The pelvis was opened and several large stones were removed. The lower pole parenchyma was markedly thinned and amputated. The exposed cortex was fulgurated with cautery and the defect was reapproximated with liver sutures and hemostatic agents. Significant necrotic rind was washed out of the retroperitoneal space along the psoas muscle and a large bore drain was left in place. The patient tolerated the procedure without complication.\nThe gross pathologic specimen consisted of several fragments of irregular, pink-brown kidney with orange-white discoloration with white fibrous surfaces and multiple pale yellow lesions with scalloped borders. The uninvolved parenchyma was pink-tan and smooth. Additional fragments of dusky green-yellow necrotic tissue and calculi were also submitted. Microscopic examination of the kidney fragments revealed focal xanthomatous changes and obstructive uropathy. The necrotic fragments showed acute inflammatory exudate with fibrin residues.\nThe patient was discharged from the hospital several days after surgery with significant improvement in left hip pain. Interval CT scan 2 months after surgery revealed almost complete resolution of the retroperitoneal abscess and preservation of the left upper pole moiety (). |
A 36-year-old female patient reported to Department of Periodontology, Dr. D.Y Patil Dental College and Hospital, Pimpri, Pune with the chief complaint of a swelling in maxillary left front tooth region of the jaw since 1-year. The patient had noticed a small growth in the anterior region 1-year back, which had gradually increased to the present size, and it was associated with pain due to food lodgement. Past dental history revealed incomplete root canal treatment initiated 6 months earlier in the maxillary left lateral incisor. There was no contributory medical or drug history and no associated deleterious habits.\nThe intraoral examination revealed a swelling that measured 2.4 cm × 1 cm in size, extending from vestibule to gingival margin apico-coronally and from distal aspect of maxillary right central incisor to mesial aspect of maxillary left canine mesiodistally []. It was a firm, nontender growth, pale pink in color with a reddish component on attached gingiva of the maxillary left lateral incisor. The surface of the lesion appeared to be nodular, and the swelling was sessile. There was minimal bleeding on probing, and there was no purulent discharge from the gingival sulcus. Periodontal probing was performed and a pocket depth of 5 mm mesially, and 8 mm distally of the maxillary left lateral incisor was recorded.\nAn intraoral periapical radiograph [] revealed periapical radiolucency at the apex of the tooth and an intrabony defect distal to the maxillary left lateral incisor. Laboratory investigations (complete blood profile) revealed no abnormalities in the blood counts.\nA provisional diagnosis of pyogenic granuloma secondary to chronic irritation was given based on the clinical and radiographic investigations.\nThe initial phase of treatment consisted of nonsurgical periodontal therapy-scaling, root planing, and oral hygiene instructions. An endodontic consultation was taken and on pulp vitality testing tooth was found to be nonvital. The provisional diagnosis given was primary endodontic lesion with secondary periodontal involvement. The root canal treatment of the involved maxillary left lateral incisor was planned and completed. At 3 months recall, clinical examination showed neither a significant change in the size of the gingival growth nor a significant reduction in probing depth. However, no periapical radiolucency was detected at this time.\nAs the swelling involved the attached gingiva and was located in the esthetic zone, an excisional biopsy would have lead to considerable loss of keratinized tissue. Since, there was combined pocket due to swelling, therefore we did not raise conventional flap. Keeping in mind that there was also an intrabony defect associated with maxillary left lateral incisor, an internal bevel gingivectomy was planned in order to conserve keratinized tissue and facilitate access to the underlying bone defect. Under local anesthesia (2% LOX, Neon Labs lignocaine with 1:80,000 adrenaline), a mucoperiosteal flap was raised by giving internal bevel, sulcular, and interdental incisions. The intrabony defect adjacent to the maxillary left lateral incisor was debrided, and the root surfaces of the teeth were planned []. The tissue on the undersurface of the gingival swelling was curetted and sent for histopathological examination. Management of the intrabony defect comprised of placement of platelet rich fibrin (PRF) into the defect []. For preparation of PRF, 20 ml of blood was drawn from the antecubital vein and centrifuged in two glass tubes (10 ml each) at 3000 rpm for 12 min. Two plugs of PRF were obtained in separate test tubes. One plug was used as a graft material, and the other was compressed and used as a membrane.[] The flap was then sutured back to its original position, and a periodontal dressing was given. The patient was prescribed amoxicillin (500 mg thrice a day for 5 days), diclofenac (50 mg twice a day for 5 days) and was instructed to follow standard postoperative instructions. Ten days later the periodontal pack and sutures were removed, and the healing was found to be satisfactory. At 3 and 6 months follow-up [Figures and ], there was complete soft tissue healing with no recurrence of the lesion. At 6-month recall, the pocket depth was 1 mm mesially and 3 mm distally of the maxillary left lateral incisor. Radiographic evaluation at 6 months also showed good bone fill [].\nHematoxylin and eosin, stained section stratified squamous epithelium of the tissue specimen showed a hyperplastic parakeratinized. A highly cellular connective tissue with the plump proliferation of the endothelial cells and fibroblasts, with evidence of multiple budding capillaries was seen. Chronic inflammatory cells in a collagenous matrix, predominantly lymphocytes, and plasma cells were also noted. These findings were consistent with the histopathological diagnosis of a telangiectatic granuloma []. |
In January 2017, a 19-year-old boy came to our attention with macroscopic hematuria and progressive anemia. The patient reported mild asthenia, with no other systemic symptoms. Blood investigation including inflammatory test (CRP and procalcitonin) were normal. Sonography identified a mass that, on abdominal magnetic resonance imaging (MRI), appeared as a locally thickened and edematous mucosa of the anterior wall of the bladder. A transurethral resection was performed at the local hospital. The patient arrived to our center 7 weeks later and an endoscopic evaluation was performed with no evidence of a residual mass. The histology of the tumor initially resected was reviewed revealing an ALK-positive IMT. The tumor was characterized by spindle cells with ovoid nuclei containing prominent nucleoli and eosinophilic cytoplasm. The tumor cells were interspersed in a myxoid stroma with a heterogeneous inflammatory infiltrate (, left). Immunohistochemistry was positive in more than 50% of cells for classical IMT markers, such as ALK, alpha smooth muscle actin and desmin, and there was focal expression of cytokeratins (CK) 8/18/19. Positivity for ALK varied, with cells showing more or less diffuse cytoplasm staining (, right). On staging, CT scanning revealed multiple small nodules in both lungs, mainly in the upper left lobe (, top), and 18 fluorodeoxyglucose-PET showed a 29 × 18 × 29 mm osteolytic lesion in the left iliac bone, subsequently confirmed by bone CT scan. A diagnosis of metastatic ALK-positive IMT was made and an anti-ALK therapy (entrectinib 600 mg/day) was adopted (). Treatment response was assessed after 3 months, indicating stable disease. As CT images confirmed a stable condition in terms of the number and size of lung and bone metastases, entrectinib administration was continued. Three months later, CT scanning revealed excavated pulmonary micronodules suggestive of initial drug response, whereas after 9 months a substantial reduction of the nodules, in particular the excavated pulmonary micronodules in the right lung, and a persistent bone metastasis was observed. One year after starting the therapy all lung metastases disappeared (, bottom) and the bone lesion was much reduced in size (23 vs. 29 mm), showing sclerotic margins around the central lytic area. During the treatment the patient was followed monthly for the 1st year with progressively longer intervals in the 2nd year. No side effects were reported apart a mild episode of diarrhea in the 2nd month of treatment. Blood investigations including blood count, renal and liver function and CRP were always normal. Due to the favorable safety profile of entrectinib, the therapy continued and 33 months after starting the treatment the patient remains in complete remission.\nAs a part of an ongoing study on sarcomas, we tested for the presence of CTCs in patient's whole blood samples, prior to and throughout the treatment, using the CellSearchTM system (CS): the only EpCAM-based CTC enrichment system approved by the FDA (Food and Drug Administration) for the In vitro Diagnostic (IVD) detection and collection of circulating tumor cells in cancer patients (). According to the system, an event is classified as CTC when its morphological features are consistent with that of a cell expressing the epithelial cell adhesion molecule (EpCAMhigh/+) and exhibiting a CK+, DAPI+ and CD45− phenotype (). However, since EpCAM expression may change during tumor evolution and CTC expressing low levels of EpCAM are discarded by the CellSearch system, cells expressing no or low EpCAM (EpCAMlow/−) were also collected through an antibody-independent Automatic Sample Collection Device (ASCD) coupled to our CellSearch system and subsequently stained for CK, CD45, and DAPI (). Finally, to capture circulating ALK-positive IMT cells, a customized assay with a FITC-conjugated anti-ALK antibody was designed () and results were expressed as the total number of ALK+CTCs per 7.5 ml of peripheral blood (). As summarized in , which reports findings obtained through liquid biopsy, EpCAMhigh/+ cells were found in the blood before starting entrectinib administration (, T0), with one in two of them being ALK−, whereas no cells were detected at the end of the first treatment cycle when the disease was reportedly stable (, T1). The 6-month assessment revealed 2 ALK+/CK+/CD45− and 2 ALK−/CK+/CD45− circulating tumor cells (, T2). EpCAM was variably expressed in the 2 ALK+ cells (1 EpCAMhigh/+ and 1 EpCAMlow/−), whereas both of them were positive to CK, negative to CD45 and had intact nuclei stained by DAPI. At this time, concomitant CT images revealed persistent focal pulmonary ground-glass opacities with excavated micronodules of branching “tree-in-bud” morphology, suggesting a partial response to entrectinib. After 9 months of targeted therapy, no more circulating IMT cells were detected and this situation remained the same up to the last follow-up (, T3). This last CTCs assessment was performed prior to CT images of complete pulmonary metastasis reduction, hence earlier than clinical response. Since then, our patient exhibited a continuous improvement in symptoms over the time and no additional adverse events were reported. |
An 18-year-old boy underwent ACL reconstruction with an autograft of quadruple hamstring and anterior half of the peroneus longus tendon of his left knee after a twisting sports injury six months prior to surgery. The diameter of the autograft was 7 mm, which was suspended with an Endobutton (Smith & Nephew, Memphis, TN, USA) at the femoral tunnel. An 8 mm × 25 mm PEEK interference screw (Smith & Nephew, Memphis, TN, USA) was used to fix the graft in the 7-mm tibial tunnel. The patient recovered well and was discharged two days post-operation. His wound healed well after two weeks, so the sutures were removed in an outpatient department, and knee flexion was encouraged. Forty days after the operation, the patient came back and complained of tibial wound rupture for one day after a 1-week history of swelling and pain over the anterior aspect of the proximal tibia. Knee examination showed a 1-cm rupture in the tibial wound without obvious redness and effusion, but with focal soft-tissue swelling and moderate tenderness around the wound. The knee joint also had no obvious swelling. Laboratory evaluation revealed no systemic signs of infection, with an ESR of 35 mm/h, CRP of 2.9 mg/L, and WBC of 6.9 × 109/L. The knee joint fluid evaluation revealed no signs of infection, with a nucleated cell count of 900 × 106/L. The joint fluid smear of bacterium and fungus was negative. The MRI scan revealed the intact screw extrusion from the tibial tunnel to subcutaneous tissue (Fig. ).\nSurgery was performed to remove the screw. When the wound rupture was incised and enlarged, the screw was found in the subcutaneous tissue surrounded by a small amount of clear fluid. The whole screw was removed, and its surrounding soft tissue was fetched for germiculture. After the debridement of the adjacent soft-tissue and tibial tunnel, sufficient irrigation was performed, and a vacuum sealing drainage dressing (VSD) covered the wound with a continuous negative pressure suction to promote healing.\nVSD was removed after three days, and wound dressing was performed every three days. The cultures of preoperative joint fluid and intraoperative soft tissue were both negative. Therefore, he was discharged from the hospital with a smoothly healed wound two weeks post-reoperation. After two years, he recovered uneventfully, with a knee joint range of motion of 120° of flexion to 0° of extension. The Lachman test was positive, but the pivot-shift test negative. He was able to return to simple sport activities, such as jogging, without continued symptoms. The MRI scan showed a continuously regenerating ACL (Fig. ). |
A 30-year-old male presented with symptoms of hypoesthesia and dysesthesia of the L5 nerve root distribution, with right positive Lasègue, and normal strength and reflexes for 60 days. The patient presented no comorbidities, except the previous treatment of a testicular seminoma with orchiectomy and adjuvant RT 20 years ago. The radiation dose utilized for the treatment of the seminoma was 30.6 Gy, irradiating the cervical and para-aortic regions. There was no personal or family history of neurofibromatosis. He had undergone coronal, sagittal, and axial T2-weighted contrast-enhanced magnetic resonance imaging (MRI) of the lumbar spine that revealed a contrast enhancement of two nodular formations placed in the L4 nerve root, the first located proximally, measuring 1.1 cm × 0.6 cm, and the second distally in the right lateral recess of the spinal canal, measuring 2.1 cm × 0.9 cm []. Investigation with a neurophysiologic study of lower limbs, genetic analysis, and brain, cervical, and thoracic MRI was indicated.\nThe results of the electroneuromyography of lower limbs revealed subacute and chronic right L5 neuropathy without muscle denervation. The genetic analysis was normal. The brain and cervical spine MRI were normal [].\nA surgical indication for diagnosis and treatment as well its complications were discussed with the patient and his family. The patient was afraid of motor deficit complications and decided to control the pain with physiotherapy and oral analgesic medication. The patient was closely observed. The pain was well-controlled with physiotherapy and oral analgesia when necessary during 6 months. After this period, the patient complained of a progressive increase of sciatica, the paresthesia became worse, and the motor strength was quickly and severely reduced with Grade 2 dorsiflexion of the right foot strength. The lumbar MRI showed that a tumor of the nerve root had grown [].\nSurgery was indicated and accepted by the patient and his family. The surgical planning was total tumor removal with free margins. A right hemilaminectomy from L3 to S1 was performed. After the incision of the dura mater, a fusiform tumor was visualized adjacent to the L5 foramen and adjacent of the cauda equina nerve roots. The L4 nerve root was individualized and sectioned proximal to the upper margin of the tumor. The distal tumor was dissected, and the nerve root distally to the tumor was individualized and sectioned. The entire segment of L4 nerve root was resected with clear margins []. The dura mater was sutured with 4.0 mononylon. The paravertebral muscle was tightly sutured to avoid cerebrospinal fluid (CSF) leak. The subcutaneous tissue and skin layer were closed in the standard fashion.\nThe patient was discharged from hospital 3 days after surgery with better resolution of pain, hypoesthesia in the L5 dermatomes, and motor strength Grade 3 of the L5 nerve root. The anatomopathological and immunohistochemical studies showed a hypercellular malignant spindle cell tumor with a high mitotic index and moderate pleomorphism in a nerve root, compatible with a malignant peripheral nerve sheath tumor (MPNST) [].\nThirty days later the patient reported somnolence, anisocoria, diplopia, severe Grade 2 paraparesis, neurogenic bowel with flaccid anal sphincter tone, and neurogenic bladder. Sagittal T1-weighted contrast-enhanced MRI of brain and spine demonstrated a hypertensive hydrocephalus, leptomeningeal enhancement, and contrast-enhanced masses throughout the cervicothoracic spinal cord surfaces []. The patient underwent urgent cervical decompression via C7-T2 laminectomy with partial resection of the fibrous tumor and a ventricular catheter to monitor intracranial pressure and CSF drainage. Biopsy staining with hematoxylin and eosin revealed features characteristic of the malignant peripheral nerve sheath.\nThe patient died from acute respiratory failure 48 h after the second surgery. The patient's total time of survival from the time of MPNST diagnosis was 9 months. |
A 74-year-old male, history of a left A2 aneurysm, presented after a motor vehicle accident at low speeds. At the scene, the patient exhibited confusion. He sustained abrasions above his left eye, around his nose, and above his lip. Upon further investigation, patient had also had a syncopal episode on the prior day, where he fell and hit his head as well. Besides the confusion, he exhibited no focal neurological deficits. A computed tomography (CT) head demonstrated a 4 cm × 6 cm hyperdensity and edema with mass effect on left frontal area (). The concerns included possible traumatic brain contusion, aneurysmal hemorrhage (given history of left A2 aneurysm), or hemorrhage from an underlying tumor given profound edema. The patient was started on fosphenytoin. A CT angiography of the head demonstrated a pericallosal cerebral aneurysm (). A magnetic resonance imaging of the brain demonstrated a bifrontal, enhancing brain lesion with surrounding edema, concerning for a high-grade glioma (). Subsequently, he was started on intravenous decadron.\nThe patient was discussed at the brain tumor board, where the plan was to address the aneurysm followed by resection of the mass versus close monitoring with subsequent imaging. The high risk of rehemorrhage, given the possibility of an aneurysmal hemorrhage, motivated prompt treatment of the aneurysm. The patient was taken to the angiography suite. An anterosuperiorly projecting azygous A2 aneurysm, measuring 4.5 mm × 5.5 mm with a neck width at 3.5 mm and a small daughter sac, was completely obliterated with primary coiling (). Visualization of the external carotid arteries and internal carotid arteries bilaterally did not show any tumor blush. The following day, he underwent a left craniotomy along a forehead skin crease for mass excision. Final pathology revealed glioblastoma. The patient recovered well from both procedures, with a baseline neurological exam. The patient subsequently underwent hypofractionated radiation and temodar. The Medical College of Wisconsin does not require Institutional Review Board approval or patient consent for this case study. |
A 56-year-old man presented with a history of 6 months hypogastric pain. In order to investigate the cause, colonoscopy was performed using conscious sedation with intravenous midazolam (2.5 mg) and meperidine (25 mg). The rectal mucosa was normal, but there were multiple diverticula in sigmoid colon and also some small sessile polyps (<1 cm) near the junction between sigmoid and descending colon. Biopsy samples were taken and the scope was gently advanced toward cecum. There were multiple scattered diverticula up to ascending colon and another small sessile polyp was also found in cecum, from which other biopsy sample was taken ().\nThe procedure was completed without any complication during colonoscopy. About 5 minutes later, the patient complained of severe colicky abdominal pain, which recurred every 5 minutes and was accompanied by diaphoresis.\nOn physical examination, blood pressure was 110/80 mmHg, heart rate was 80/min and the patient had no fever. The abdomen seemed distended and bowel sounds were high-pitched. Also, the abdomen was tympanic on percussion, but there was no tenderness or guarding.\nPlain abdominal radiography showed multiple colonic air-fluid levels and distention of the colon, especially in the right side ().\nSince there was no subdiaphragmatic free air and no free air between intestinal loops, the probability of perforation was ruled out. Immediately, the patient underwent second colonoscopy, but the scope could hardly pass through sigmoid colon because of spasm and edema at the site of previous polyp biopsies. The scope was gently advanced toward cecum and simultaneously decompressed the entire colon by suctioning the entrapped air. After performing the second colonoscopy, the colicky abdominal pain was relieved and abdominal distention was significantly decreased. The patient remained in hospital for close observation. Fluid and electrolytes were supplemented intravenously. Oral feeding was not permitted. Complete blood cell counts showed leukocytosis. White blood cell count was 19×109/L and hemoglobin was 15 mg/dL. Serum amylase and lipase levels and electrolytes were within normal ranges. After 2 hours, the patient passed flatus and after 12 hours, he passed liquid stool. The next day, white blood cell count was reduced to 1010/L and the patient had no pain or diaphoresis. He tolerated liquids and then full meals, and therefore, he was discharged during the second day. |
A 36-year old woman was referred to a tertiary unit at 29+5 weeks of gestation due to fetal cardiomegaly and mild ascites (Fig. a, b), which was detected on a scan undertaken for suspected small for gestational age. The woman was nulliparous with a low-risk first trimester combined screening test and unremarkable anomaly scan. She was rhesus B negative and underwent non-invasive prenatal testing that determined the rhesus genotype of the fetus to be rhesus B negative. Otherwise, no red blood cell antibodies were reported. Of note, the maternal grandmother was known to have sideroblastic anaemia that was diagnosed at 17 years of age. The mother of the unborn fetus and her brother had undergone testing as children but were told that no further follow-up was needed. Unfortunately, additional information regarding and genetic testing for this family history was not available. The woman had mild macrocytic anaemia with haemoglobin of 10.4 g/dl and a mean corpuscular volume of 104 fl. The woman had not received any preconceptional or genetic counselling.\nUpon arrival, the first scan in our department demonstrated a middle cerebral arterial (MCA) peak systolic velocity (PSV) value above 1.5 Multiples of the Median (MoM). Fetal biometry was normal, as was the amniotic fluid index and umbilical artery doppler. Dexamethasone for fetal lung maturation was administered, and an uncomplicated in utero fetal blood transfusion (IUT) was performed at 30+3 weeks of gestation. The pre-transfusion fetal haemoglobin was 4.4 g/dl, which was increased to 14.1 g/dl following 120 mL of blood transfusion through the intrahepatic portion of the umbilical vein (Fig. ). Investigations to determine the underlying cause of fetal anaemia included microarray comparative genomic hybridization, serology to exclude congenital infection, a peripheral blood film and fetal bilirubin to detect haemolysis. These preliminary investigations were normal. A fetal MRI brain was performed, which showed no abnormalities. In the subsequent weeks, the MCA-PSV improved, as did the cardiomegaly.\nAt 35+3 weeks of gestation, the MCA-PSV increased to above 1.5 MoM. The options of delivery and ex-utero transfusion versus IUT were discussed with the multidisciplinary team and with parents. As it was considered that an IUT would allow pregnancy to proceed to term, it was decided to proceed with IUT. A second IUT took place with a pre-and post-transfusion fetal haemoglobin of 9.7 and 15 g/dl, respectively. The MCA-PSV remained stable until 37 weeks and three days when a caesarean section for breech presentation was planned. Fetal biometry was consistent with previous measurements, and the amniotic fluid index and umbilical artery doppler were normal. The woman was counselled regarding the need for delivery and likely need for exchange transfusion in the neonatal period. Delivery of a female infant via caesarean section due to breech presentation was performed at 37 + 4 weeks. The birth weight was 3150 g, and apgar scores were 8 and 10 at 1 and 5 minutes, respectively.\nSubsequently, the infant again became anaemic, requiring regular 3–4 monthly blood transfusions but she is making good developmental progress. Her anaemia was unresponsive to pyridoxine. Iron levels should be closely monitored to detect the need for chelation therapy in future care plans, since iron toxicity is a major cause of morbidity and mortality in XLSA [].\nFetal and maternal blood was collected for DNA extraction, at the time of the first IUT. DNA was sequenced by next-generation sequencing for 11 genes associated with sideroblastic anaemia. Analysis was performed using Agilent SureSelect XT custom enrichment technology and Illumina DNA sequencing. Significant maternal cell contamination of the fetal blood sample was excluded using the ABI AMPFLSTR Identifiler PCR Amplification Kit. A heterozygous variant in the ALAS2 (NM_000032.4) gene was identified in both the mother and the fetus. The c.488G > A; p.(Arg163His) variant identified affects a conserved amino acid and is absent from the gnomAD controls database []. The variant was therefore classified as pathogenic according to the American College of Medical Genetics (ACMG) variant interpretation guidelines []. The findings for both the mother and the fetus were confirmed by Sanger sequencing. These results were available two days following delivery and verified a heterozygous ALAS2 c.488G > A; p.(Arg163His) and SLC4A1 c.876 + 5G > A mutations in both the baby (Fig. a) and the mother (Fig. b). X-inactivation studies [, ] were undertaken. There was no significantly skewed X-inactivation in the sample provided from the baby. The level of X-inactivation in the mother could not be determined, as she was uninformative for the AR locus []. |
A twenty-year-old male patient reported to the department with the chief complaint of tooth discoloration and constant pus discharge in relation to upper right central incisor (). Past dental history revealed trauma of twelve years' duration and had not undergone any treatment for the affected tooth. Intraoral examination showed a pus discharging sinus in relation to upper right central incisor and radiographic examination revealed open apex. It was a case of chronic periapical abscess of right upper central incisor with an open apex. It was decided to do a nonsurgical approach to close the apex as the root tip appeared thin and fragile. The root canal was accessed and thoroughly irrigated with 3% sodium hypochlorite solution and saline as final rinse. Biomechanical preparation of the root canal was done using standard hand instruments (K-files) up to size #90. One-visit MTA apexification procedure was chosen as it was more predictable and less time consuming. Mineral trioxide aggregate (Angelus, Brazil) was mixed and slowly packed into the canal till the apical area was densely filled. A moist cotton pellet was placed over the MTA and the patient was recalled after one week and rest of the canal was obturated with gutta-percha. Radiograph was taken and evaluated every 3 months. Tooth was asymptomatic and one-year follow-up showed radiological signs of healing (). But the periapical sinus did not heal even after a year.\nSurgical option was chosen to treat the nonhealing sinus. The lining epithelium of the sinus was excised and removed using tissue forceps and scissors. The frenal attachment adjacent to the sinus opening was also removed to avoid the tissue tension. Periapical curettage was done through the surgical opening (). A combination of beta-tricalcium phosphate and hydroxyapatite (Sybograf-T) was placed at the surgical site. Platelet rich fibrin was prepared in accordance with the protocol developed by Freymiller and Aghaloo. Intravenous blood (by venipuncturing of the antecubital vein) was collected in a 10 mL sterile tube without anticoagulant and immediately centrifuged at 3,000 rpm for 10 minutes. PRF was separated from red corpuscles base using sterile tweezers just after removal of PPP (platelet-poor plasma) and then transferred into a sterile dappen dish and was placed over the site. The tissues were approximated and sutured using resorbable Vicryl 3-0 black suture. The patient was back after one week for suture removal and the wound healing was found to be satisfactory. The complete healing was achieved at 4-week time. Discoloration of the tooth was managed by all ceramic crown and patient was recalled for further review (). |
A 32-year-old Caucasian female presented to the emergency department with an acute onset of shortness of breath (SOB). Her past medical history was significant for recurrent VTE of unknown etiology with removal of an inferior vena cava filter due to misplacement. She had no family history of thromboembolic disorder and no past medical history of smoking or oral contraceptive usage. Her first episode of PE was spontaneous about six years ago followed by multiple episodes of VTE that required thrombolysis on three separate occasions. Her comprehensive hypercoagulable workup in the past included factor V Leiden mutation, JAK2 V617 mutation, Lupus anticoagulant, antithrombin III activity, PNH flow cytometry, factor II gene mutation, protein C, protein S, anti-cardiolipin antibody, anti-beta-2 glycoprotein-1 antibody, and homocysteine levels, which were all unremarkable. She had recurrent PE on many therapies including warfarin (with therapeutic international normalized ratio of 2.5-3.5), rivaroxaban, apixaban, dabigatran, heparin, and fondaparinux. She also had a history of rash secondary to enoxaparin making management more complicated. Her pertinent physical exam findings on presentation included hypoxia on 2 liters of nasal cannula with oxygen saturation at 96%, respiratory rate of 22 and decreased breath sounds bilaterally in the lung bases with no signs of deep vein thrombosis (DVT). A computed tomography (CT) scan of the chest with contrast on admission showed new pulmonary emboli on the right side.\nAt this point it was challenging to decide the next step in management since she had failed most known anticoagulants in the past. This also caused much physical, psychological, and financial burden on the patient due to recurrent hospitalizations over a short period of time.\nThe hematology service was consulted, and after a thorough discussion with the patient, rivaroxaban 15 mg twice daily was initiated since she had failed the 20 mg once daily dose in the past. Unfortunately, after about three weeks of rivaroxaban treatment she presented with another episode of PE. She was started on therapeutic heparin at this time with activated partial thromboplastin time (aPTT) range between 90-140 seconds. A higher aPTT range was selected given her recurrence. She required large doses of heparin to maintain her aPTT, but after it was maintained at the new therapeutic goal, her breathing eventually improved and she did not require further oxygen supplementation. At this time, the hematology service decided to combine two oral anticoagulants to prevent further episodes of PE since she has had recurrence on heparin. They initially recommended combining a second oral anticoagulant with rivaroxaban such as apixaban or dabigatran, but due to the patient’s health insurance coverage issues and the higher price of novel oral anticoagulants, two drugs from this class did not seem feasible. Instead, she was started on warfarin with a therapeutic goal INR range of 2-3 along with rivaroxaban 15 mg bis in die (BID). At the time of writing this manuscript, six months since the patient was seen, she has had no recurrence of PE or signs of bleeding. |
A 55-year-old female came with complaints of on and off right lower quadrant abdominal pain for 1-year. The patient also had urinary complaints such as intermittency, burning, and frequency. She denied any episodes of fever, chills, gross hematuria, or dysuria. Her past medical and surgical history were insignificant. The per abdominal examination was normal, but on bimanual pelvic examination a mass on the right side near the bladder neck area was palpable.\nUltrasonography (USG) suggested a well-circumscribed polypoidal soft tissue lesion projecting in urinary bladder lumen and attached to the posterior wall and base of the bladder with no internal vascularity []. Intravenous pyelography demonstrated a large filling defect in the bladder and normal functioning kidneys []. To know the detailed anatomy, magnetic resonance imaging (MRI) was done, which showed a large, well-defined rounded, soft tissue lesion of size 67.6 mm ×51 mm at posteroinferior aspect of urinary bladder, close to anterior surface of the cervix and vagina. The mass was isointense to the skeletal muscles on T1 and T2 images. It also showed small focal irregular cystic areas of necrosis []. The finding was suggestive of a benign lesion, probably leiomyoma. The urine cytology smear showed large numbers of squamous cells; few degenerated cells and bacteria, but atypical cells were not seen.\nOn cystoscopy, a large smooth sessile growth arising from the right posterolateral wall was noted []. The right ureteric orifice was not visualized. Transurethral resection (TUR) of the lesion was performed, and resected specimens were sent for histopathological examination. At the completion of the resection, the previously palpable pelvic mass could no longer be appreciated by bimanual examination.\nOn postoperative day 1, the patient's urine was clear, the Foley catheter was removed, and the patient was discharged on oral antibiotics. The histopathological examination showed spindle cells in sheets and fascicles oriented in different planes. There was no epithelial lining seen. There was no atypia, mitotic activity or other indices of malignancy. The impression of leiomyoma was made []. On follow-up at 3 months, the patient was asymptomatic, and USG was normal. |
A previously healthy 25-year-old White man presented with a 1-year history of blurred vision in the right eye, headache, and weight loss of about 30 kg. On physical examination, he had a body mass index of 28 kg/m2 and visual field defects in the right eye. Initial MRI showed a lightly spotted heterogeneous 19 × 16 × 19 mm tumor located suprasellarly, close to the pituitary gland with no ingrowth or association with the pituitary gland (Fig. A). Endocrine evaluation revealed secondary hypogonadism with low follicle-stimulating hormone, luteinizing hormone, and testosterone but intact thyrotroph and lactotroph axes. An ACTH test was performed with a subnormal cortisol response (30-minute cortisol 248 nmol/L, reference > 420 nmol/L) and low plasma ACTH concentration, indicating secondary adrenal insufficiency, and the patient started treatment with hydrocortisone. The somatotroph axis was not evaluated. Visual field measured by perimetry revealed visual field defects in the right eye.\nThe tumor was initially diagnosed based on MRI as a craniopharyngioma for which reason the patient was referred to craniotomy as standard treatment. At surgery, the tumor appeared gray and reddish, and was capsulated and fragile with easy bleeding, unlike craniopharyngiomas with sharp, irregular borders, which have a tendency to adhere to vital neurovascular structures and often consist of cystic and/or solid parts []. The pituitary tumor was partially resected, and a small amount of capsule remnant underneath the optic chiasm could not be surgically removed. Perioperative frozen section histological examination described the tumor as a possible malignant lymphoma due to lymphocytic infiltration.\nThe patient was transferred to the Department of Endocrinology at Odense University Hospital for further diagnostic workup and management of pituitary hormone deficiencies. Postoperatively, the patient was still affected by headache and visual deficits on ophthalmologic assessment. MRI showed regression of the pituitary mass (9 × 6 × 8 mm), but remnant pituitary tissue was located just below the optic chiasm (Fig. B). Pituitary hormone insufficiency of all anterior axes and diabetes insipidus was diagnosed, and treatment with hydrocortisone, levothyroxine, testosterone, growth hormone, and desmopressin was implemented.\nEndocrine evaluation did not support a hormone-producing adenoma. Sellar lymphoma is a very rare disease often related to immunodeficiency, for example HIV-related, or seen in immunocompetent patients who are over 60 years old []. Metastasis was not suspected; the patient did not suffer from cancer in another location. Workup for infectious and rheumatologic etiologies was not indicative of secondary hypophysitis, nor was drug-related infiltration of the pituitary gland a possible differential diagnosis. Final histological diagnosis showed lymphoid reaction with predominant CD20 positive B-cell infiltration and no sign of significant IgG4 involvement. The patient was diagnosed with autoimmune hypophysitis.\nTen months postoperatively, the patient reported impaired vision. MRI showed that the remnant tissue lifted and exerted pressure at the optic chiasm. Perimetry confirmed progression of visual field defects in the right eye and now involvement of the left eye. Because of progression of visual field defects, treatment with glucocorticoid pulse therapy was initiated: methylprednisolone 500 mg infusion for 3 days, followed by reduced prednisolone doses, that is, 37.5 mg per day. Follow-up MRI after 1 month of glucocorticoid treatment (11 months postoperatively) demonstrated significant reduction of the pituitary mass and decreased pressure at the optic chiasm. Perimetry was unchanged. Treatment with prednisolone continued for 3 months.\nThe patient had intolerable adverse effects to glucocorticoid treatment with excessive weight gain of about 50 kg and cushingoid features. The need for long-term treatment led to initiation of steroid-sparing treatment with 150 mg azathioprine per day under gradual tapering of prednisolone (13 months postoperatively). Visual field defects improved, and repeated MRI showed additional regression of the remnant pituitary mass. Perimetry revealed stable conditions. Due to stable condition over 26.5 months, treatment with azathioprine was reduced. Control MRI after one and a half month showed recurrence with increasing mass in sella turcica causing mass effect on the optic chiasm. Treatment was resumed: azathioprine 100 mg per day in combination with prednisolone 37.5 mg per day.\nDespite additional 11 months treatment with azathioprine and prednisolone treatment (52 months postoperatively), control MRI showed further progression with increasing pituitary mass size (11 × 6 × 7 mm) reaching the optic chiasm (Fig. C). Treatment with rituximab was initiated: 1000 mg infusions 14 days apart, repeated every 12 months. This resulted in almost complete regression of pituitary mass (3 × 2 × 7 mm) evaluated by MRI (Fig. D). Rituximab treatment was discontinued after 25 months (77 months postoperatively) because of stable disease. To date, the patient has been followed up for ten and a half years postoperatively. According to control MRI 4 years after end of treatment with rituximab, he is in sustained remission with unchanged pituitary mass size and no affection of the optic chiasm. |
A 72-year-old male with past medical history significant for CLL presented with four days of progressively worsening fever, cough productive of blood streaked sputum, and back pain. Almost two months prior to presentation, he had traveled to Southeast Asia with his family, during which he had a brief diarrheal illness that resolved within 24 hours without intervention. Four days prior to hospital admission, he noticed decreased exercise tolerance, followed by right-sided back pain, and progressively worsening cough and fever.\nThe patient's past medical history included a remote history of renal cell carcinoma with partial nephrectomy and CLL diagnosed two years prior to presentation with lymphocytosis and lymphadenopathy (Rai stage I)—baseline white blood cell count (WBC) of 12 K/uL. He had never required treatment for CLL prior to presentation and had immunoglobulin levels within normal limits several months prior to infection (IgA 119 mg/dL, IgG 730 mg/dL, IgM 51 mg/dL). He was otherwise well, not on any prescription medications, and very physically active.\nOn presentation to the hospital, he was febrile to 38.9°C and short of breath, with a WBC count of 30.2 K/uL (95% lymphocytes, 2% bands). Chest X-ray revealed an area of consolidation in the right upper lobe with associated area of cavitation. The patient was admitted and started on vancomycin, piperacillin-tazobactam, and azithromycin. Sputum culture collected at the time of admission returned positive for innumerable Salmonella species within 24 hours of collection; further, it was identified as Salmonella enteritidis when sent to the New York City Department of Health for serotyping. One set of blood cultures drawn on admission resulted positive in one out of two bottles four days after they were drawn, identified as Salmonella enteritidis and also serotyped by the New York City Department of Health. There was no growth from repeat blood cultures drawn one day following positive result while on empiric antibiotics. Susceptibilities performed by E-test showed Salmonella enteritidis susceptible to ceftriaxone, after which antibiotic regimen was changed to ceftriaxone 2 grams intravenous (IV) daily.\nComputed tomography of the chest performed in the first 24 hours of admission revealed multiple bilateral pulmonary emboli and a large right upper lobe cavitary mass with adjacent ground glass opacities and septal thickening, as well as moderate bilateral axillary, mediastinal, and upper abdominal adenopathy (). Further microbiologic studies revealed positive BioFire FilmArray® Gastrointestinal Panel (BioFire Diagnostics, Salt Lake City, Utah, USA) for Salmonella sent five days after admission when the patient developed diarrhea, and stool culture sent at the same time with rare Salmonella enteritidis, also typed by the New York City Department of Health with the same susceptibilities.\nHe defervesced within hours of administration of antibiotics and was treated with four weeks of ceftriaxone 2 grams IV daily. Follow-up imaging showed complete resolution of cavitary pneumonia. PET scan was performed for CLL monitoring one month after admission, showing cervical, axillary, hilar, mediastinal, upper abdominal, and iliac chain lymphadenopathy with low-grade metabolic activity, as well as uptake in the right upper lobe of the lungs indicating residual inflammation. During the following two weeks, the patient developed recurrent fevers for which he received GAMUNEX®-C (immune globulin injection [human], 10% caprylate/chromatography purified), but fevers persisted. Gallium scan was performed to evaluate for residual infection, which revealed strong radiotracer uptake in the right hilum with corresponding 6.3 × 4.2 cm lymphadenopathy seen on CT chest obtained at the same time (), as well as mild uptake in the right upper lobe of the lung. He was started on cefpodoxime 200 milligrams orally twice daily, with resolution of fevers after one week of therapy, on which he continued for 4 months. Surgical excision for source control was not attempted due to difficult to access location of infected lymph node and patient's response to antibiotic therapy with no recurrent infection. He continues to be followed closely, with no evidence of recurrent or persistent salmonellosis on evaluation with clinical exam and laboratory testing. |
A 69 years-old fit male with an active life was admitted to our institution. He suffered from cervico-brachialgia, arisen 3 weeks before, and fever. He affirmed lack of appetite and weight losses during the last month, together with mild–moderate dyspnea on the previous 4 days.\nHis clinical history briefed hepatic steatosis and surgery 30 years before due to left colon cancer.\nThe transthoracic echocardiogram (TTE) diagnosed a severe mitral regurgitation (MR) due to IE; it was confirmed by transesophageal echocardiogram (TEE), which showed two vegetations on the atrial face of mitral valve, sized 11 × 10 mm on the posterior leaflet and 7 × 5 mm on the anterior leaflet (). The blood culture was positive for Streptococcus alactolyticus, and consequently, the following intravenous antibiotic therapy was prescribed: Gentamicin (80 mg × 3 every day for 2 weeks) and Ceftriaxone (2 g × 2 every day for 4 weeks).\nThe cervical magnetic resonance imaging (MRI) confirmed the presence of non-specific inflammation of vertebral soma C5 and C6, endorsing spondylodiscitis.\nThe total body computed tomography (CT) was remarkable for a hypodense area of 13 mm in the spleen and a lumbar lymph node of extended size. This was probably related to infarction derived from a septic embolism.\nTo assess the possible sites of infection, the patient underwent odontoiatric evaluation. The result was negative for dental foci, but the musculoskeletal and joint ultrasound of his right ankle and foot showed a synovitis of phalangeal metatarsal joint.\nA colonoscopy did not show any pathological lesions beside the left hemicolectomy. The second TTE showed a size reduction of the valve vegetations. Nevertheless, owing to the presence of severe MR and the high risk of embolism, cardiac surgery was scheduled.\nThe patient underwent surgery 16 days after the beginning of the antibiotic therapy, started and later confirmed with blood cultures results, the day after the admission at the Hospital. Intra-operatively, the diagnosis of IE was confirmed, identifying huge vegetations on the atrial face of mitral valve leaflets ().\nThe mitral valve was replaced for a tissue valve (Perimount Magna 31, Edwards Life Sciences Irvine CA). Histology did not reveal any polymorphs, no organisms were identified on Gram stain, and routine cultures failed to grow any organism because of the antibiotic therapy. Streptococcus alactolyticus was identified on mitral valve tissue using polymerase chain reaction (PCR).\nThe post-operative course was complicated by a Third-Degree Atrioventricular Block requiring a DDD pacemaker (PMK) implant, after a watchful and wait period in which temporary epicardial pacing was used. Standard antibiotic prophylaxis with cefazolin was used before PMK implantation in addition to tailored therapy for IE. A pericardial effusion required sub-xiphoid surgical drainage.\nThe intravenous antibiotic therapy was continued after the operation for 12 days and stopped 5 days before discharge.\nThe patient was discharged with a good clinical condition on his 17th post-operative day. |
A 41-year-old male with a past medical history of HyperPP, asthma, and hypertension, underwent laparoscopic sigmoid resection after failing conservative management. Neurology was consulted for preoperative evaluation, and the patient was prescribed a high carbohydrate diet as tolerated with a carbohydrate load the day prior to the surgery. The patient was also prescribed acetazolamide 500 mg oral two times daily up to the day of the procedure.\nThe day prior to the procedure, the patient tolerated bowel prep well and fasted eight hours. Preoperative electrocardiogram (ECG) and laboratory values were normal, including serum potassium of 4.3 mEq/l and serum glucose of 82 mg/dl. The operating room temperature was increased to 72°F, to avoid hypothermia. The patient was transported to the operating room, where standard American Society of Anesthesiologists (ASA) monitors were applied. An intravenous infusion of 5% dextrose in normal saline was initiated in order to maintain adequate glucose levels throughout the operation, which was eventually changed to normal saline to avoid hyperglycemia. All fluids were infused through a warming device, and a forced-air warming blanket was placed on the patient. The patient was pre-medicated with midazolam 2 mg IV, pre-oxygenated and induced with propofol and fentanyl. The patient was intubated and paralyzed using rocuronium, titrated to effect using a twitch monitor. An arterial line was placed in the left radial artery and was used for blood pressure monitoring and frequent arterial blood gas sampling. Serial potassium levels were monitored hourly and ranged from 3.1 to 3.9 mEq/l. Rescue medications such as insulin, glucose, 8.4% sodium bicarbonate, calcium chloride, furosemide, and albuterol were immediately available to treat a potential hyperkalemic crisis.\nThe duration of the procedure was four hours. The patient was extubated successfully with no complications and transferred to the post-anesthesia care unit. The patient did not exhibit signs of muscle weakness and was discharged home on a post-operative day five in stable condition. |
A 23 years old male patient admitted with h/o dysuria, pyuria and loss of appetite since 3months. He was a known case of chronic renal failure and reflux nephropathy. On investigating, patient’s renal parameters were found to be very high. His serum creatinine was 8.9 and blood urea was 175. So, he was started on haemodialysis. The next day, patient complained of inability to move bilateral lower limbs following an episode of seizure. Neurological opinion was opted to rule out the cause of seizure. Orthopedic opinion was not considered as the patient did not sustain any trauma. All possible investigations were performed to know the cause of seizure. His calcium was 4mg/dl. Hypocalcaemia was the cause for his seizure. Patient was treated for hypocalcaemia. Next day, patient continuously complained of bilateral hip discomfort, therefore orthopedic evaluation was carried out and a radiograph of pelvis was taken which showed vertical subcapital displaced fractures of bilateral neck of femur (). Working on this patient, he had hypocalcaemia, hyperphosphatemia (6.2 mg/dl), increase ALP (alkaline phosphate) and hyperparathyroidism (488 pg/ml). From these parameters diagnosis of, pathological bilateral neck of femur fracture with hyperparathyroidism due to renal osteodystrophy was made.\nIn this patient, considering age, general condition & prognosis an elective surgery bilateral uncemented modular bipolar hemiarthroplasty was performed (-intra operative and - post operative X-ray). Reasons for choosing this surgery were (1) 3 days old fracture due to delay in diagnosis (2) bilateral subcapital vertical displaced fracture with high chance of vascular compromise causing avascular necrosis (3) poor prognosis for internal fixation as patient had osteoporosis secondary to renal osteodystrophy (4) patient was planned for elective renal transplantation within next 3 months and after that patient might require higher dose of steroids and other immunosuppressant which further increases the chance of avascular necrosis and failure of internal fixation. Post-operative period was uneventful. Patient was mobilized on 5th day post op () and was discharge on 11thday after suture removal with vit-D3 & calcium supplements and weekly twice dialysis. |
This 33-year-old man was admitted via the emergency room due to recurrent fever and right upper quadrant abdominal pain. Since his childhood he suffered from easy fatigue and was informed that he had had a palpable enlarged spleen from birth. His younger brother had been previously diagnosed at private clinic 3 years ago with congenital spherocytosis due to splenomegaly, pancytopenia, and increased peripheral ovalocytes. Therefore, this 33-year-old patient was also evaluated and received splenectomy several months later under the impression of congenital spherocytosis (At that time, his RBC fragility test was negative, but peripheral ovalocytes was 26%). According to operative findings at the clinic, his liver was grossly nodular and enlarged, so a liver biopsy was done. Following the biopsy, he was diagnosed at the private clinic as having liver cirrhosis.\nSeven months before entering our hospital, diarrhea with fever and chills developed. At that time, he was diagnosed with amebic colitis and treated with antibiotics. Four months before admission to our hospital, right upper quadrant abdominal pain with fever developed, so he was checked and managed as a cholecystitis patient. However, the fever and abdominal pain continued to fluctuate in severity thereafter. Two days prior to his admission to our hospital, severe abdominal pain and fever were aggravated.\nOn admission to our hospital, the patient’s temperature was 39.3°C, the pulse 92, and the respiration 24. The blood pressure was 110/70 mmHg. On examination, the patient was relatively well-nourished but appeared acutely ill. No rash, lymphadenopathy, or jaundice was evident. The liver was 3 finger-breadth’s palpable on the epigastrium, which was hard and tender. The kidney was not palpable. We reviewed the microscopic findings of the obtained previous liver biopsy specimen, which had been done 3 years ago. Microscopic finding showed preserved normal hepatic cell cords with diffuse portal and periportal fibrosis surrounded by proliferated bile ductules and bizarre-shaped ectatic bile ducts (). Abdominal computed tomography findings revealed Caroli’s disease and hepatomegaly accompanied by multiple renal cysts (). We diagnosed him with congenital hepatic fibrosis and Caroli’s disease, complicated by cholangitis. As a result, due to suspicion of hereditary causes, we reevaluated and tested his family members, including the Case 2 and Case 3 patients. The laboratory and imaging findings are summarized in . |
Here, we present a 48-year-old female without any significant past risk factors or medical history, coming with a 4 × 3 cm well-defined, irregular, non-ulcerated, non-erythematous, non-tender and firm swelling over the left shoulder arising from the superficial plane. Initially, the swelling was smaller in size and was diagnosed as sebaceous cyst by a fine needle aspiration cytology (FNAC) done 3 years back. The patient did not follow up and now reported with complaints of rapid increase in size in the past 6 months. The patient did not have any symptoms and routine physical examination was normal ().\nThe patient was evaluated and magnetic resonance imaging of the left shoulder was done, which showed a solid cystic mass lesion with haemorrhagic areas involving superficial and deep subcutaneous plane with no intramuscular/bony involvement, with the possibility of a soft tissue sarcoma. There was no nodal involvement on radiological imaging ().\nWide local excision with intraoperative frozen section was carried out. Margins of 1 cm on all side were given clearance and deep margins till pectoralis and deltoid muscle was dissected. Frozen section came out as skin adnexal tumour with tumour-free margins ().\nThe soft tissue specimen with skin had a cut surface of tumour grey brown in colour with friable necrotic areas. On microscopic examination, the section showed stratified squamous epithelium with an underlying neoplasm composed of lobules of epithelium in a diffuse growth pattern. The epithelial cells show nuclear pleomorphism and are basaloid cells. The tumour also showed closely packed well-developed ducts with extensive areas of necrosis. Few mitotic figures were present in between. Focal areas of necrosis with comedo carcinoma-like appearance were seen. The tumour stained positive for pancytokeratin, cytokeratin 5/6, Ki-67 and S-100. These histological features and stains supported the diagnosis of hidradenocarcinoma.\nThe patient was sent for adjuvant radiotherapy after healing of the surgical site and is currently undergoing radiotherapy (). |
A 19 year old male patient weighing 61 kg who had been admitted with 50 cc of paraquat ingestion in an attempt to suicide, was brought to the poisoning emergency department of the Khorshid Hospital in Isfahan on September 16, 2018, about 2 hours after repeated nausea and vomiting. Glasgow Coma scale, and vital signs were normal, blood pressure was 120/80 mmHg, pulse rate was 90/min, respiratory rate was 18/min, and the temperature was 37°C, and O2 saturation was 95'. Cardiac and pulmonary examinations were normal at the time of admission.\nThe patient had a history of hypothyroidism that was controlled by levothyroxine tablets. Treatment began with a nasogastric tube and gastrointestinal (GI) washing at the time of admission. GI washing continued until the GI secretions were clear and then 60 grams of activated charcoal was gavaged to the patient and subsequently maintained for the nasogastric tube. Dithionite test was performed and the result was positive (dark blue). A catheter was immediately implanted for hemodialysis through the right femoral vein, and the patient underwent hemodialysis three times and every time for 8 h. 2 h after each hemodialysis, a dithionate test was performed to evaluate the toxicity reduction.\nOther treatments for the patient include antioxidant administration of N-acetylcysteine 300 mg/kg/day, infusion of Vitamin C 150 mg/h, Vitamin E, 300 units every 8 hours in the form of intramuscular injection, and methylprednisolone 10 mg/kg IV. Pantoprazole ampule 40 mg was administered twice a day to protect GI tract, and a full dose of silymarin, 6000 mg/day. Every other day chest X ray was taken and the patient was in a respiratory recovery condition, which suddenly worsened after 21 days of hospitalization and the patient said he had cervical pain and his breathing had gotten very difficult. After physical examination, the right cervical emphysema was detected.\nImmediately chest X-ray and lateral neck graphy performed and surgical and lung service consultation were requested. In graphies, the air was seen in the soft tissue of the neck and the frontal area of the trachea as well as in the mediastinum. Bilateral pneumothorax without mediastinal shift was observed. The diagnosis of severe emphysema of superfcial and deep spaces of the neck, followed by bilateral pneumothorax and severe pneumomediastinum was established [Figures -]. The bilateral chest tube was fixed and the patient was transferred to the pulmonary intensive care unit (ICU). During hospitalization, broad-spectrum antibiotic was administered to the patient due to fever and symptoms of pulmonary infection as well as sepsis. In addition to continued treatment of paraquat poisoning, supportive ICU care and treatment by lung and surgical services were also performed.\nDuring hospitalization, level of alanine aminotransferase (ALT) got abnormal from day 12 of hospitalization, then it decreased to the normal range from day 23, but at day 27 it increased remarkably and reached 691 U/L. The level of Aspartate transaminase (AST) was in normal range during hospitalization but increased to 1372 U/L on day 27. Since the forth day of hospitalization, the level of Blood urea nitrogen (BUN) ascended and got out of normal range. During hospitalization, the level of BUN had fluctuation with the maximum level of 54.6 mg/dL recorded on the 21st day. Creatinine level got abnormal since day 3 of hospitalization and increased since day 11 of hospitalization and remained abnormal. Hb level was less than normal and the patient was anemic during hospitalization. Since day 21, Platelet level got out of the normal range and got into a downtrend. The international normalized ratio (INR) level was in the range of 1.27–1.52 and on the 27th day reached 2.29. The patient was died on the 27th day due to severe pneumomediastinum and despite treatment with experimental. |
A 46-year-old gentleman presented with increasing back pain and pain in the left hip for six months. This pain was associated with numbness in the left leg. Over the previous two weeks, his symptoms had become intrusive, resulting in an ability to walk only with the aid of crutches. The patient reported of no weight loss and no bowel or bladder dysfunction.\nOn examination, there was tenderness in the lower thoracic spine, lumbar spine, and over the iliac crest on the left side. Neurological examination revealed reduced sensation over the left leg from the groin to the foot. Power was reduced in left toe extension and left ankle dorsiflexion to Medical Research Council (MRC) grading of 3/5. On the right side, sensation was reduced over the little toe. Reflexes were bilaterally brisk in the lower limbs, but plantar reflex was normal.\nFull blood count, erythrocyte sedimentation rate (ESR) and calcium levels were normal. Computed tomography (CT) scanning revealed multiple areas of bony destruction in the vertebrae and left iliac bone. () Magnetic resonance imaging (MRI) revealed destruction of T5, T10, L3, and L5 vertebrae with abnormal tissue causing severe compression of the spinal cord and nerves in these areas ().\nPlasma electrophoresis was performed to check for multiple myeloma. This revealed that IgA and IgM levels were normal. However an abnormal band was detected on plasma electrophoresis. Further analysis revealed an excess of kappa light chains with a value of 200.5 mg/L (normal value 3.3–19.4). Free lambda chain values were normal. These tests suggested a diagnosis of BJP-kappa myeloma.\nTuberculosis can present similarly to MSCC, in that spinal canal involvement can cause radiating pain and limb weakness []. It was, however, an unlikely differential diagnosis. The typical manifestations of spinal tuberculosis involve vertebral bone destruction, narrowing of intervertebral disc space and paraspinal abscess []. Despite MRI revealing vertebral bone destruction, there was no evidence of paraspinal abscess.\nThe possibility of osteomyelitis was also ruled out upon haematological testing. ESR in osteomyelitis tends to be raised to a level greater than 100 mm/h []. The patient, however, had a normal ESR and did not present with features of systemic infection.\nPrimary bone tumours may affect the spine and manifest with cord compression. The incidence of primary bone tumours affecting the spine is reported to be between 4 and 13% []. Boussios et al., after review of literature, reported on 69 cases of Ewing’s sarcoma affecting the spine and presenting with cord compression []. In their report, the average age of the patient was younger with a median age of 17.95 years. Multiple myeloma is the most common primary bone tumour of the spine. The multiple vertebral involvement in this case would be in favour of either metastatic disease or myeloma.\nLastly, the probability of MSCC was increased by the presence of both motor and sensory symptoms. Radicular pain and sensory complaints tend to be initial symptoms in patients with lumbar metastases, whereas weakness in the limbs is more pronounced in patients with thoracic metastases []. As T5, T10, L3, and L5 were all affected, it was concluded that the patient would be treated for spinal cord compression.\nThe aim of treatment would not be curative, but rather aimed at improving quality of life []. In view of the cord compression, neurological deficit and the mechanical instability caused by vertebral collapse, surgery was proposed as the initial treatment option in this patient. Biopsy was performed from the iliac bone lesion. Biopsy confirmed the diagnosis of myeloma. Histology revealed a highly cellular tumour composed of solid sheets of cells with plasmacytoid morphology. There was a high mitotic rate. Immunohistochemistry revealed a strong expression of CD138 but not for CD56, CD20 or CD3. The proliferation index Ki-67 was approximately 20%.\nSubsequently, the patient underwent spinal decompression and spinal stabilisation at the lumbar and thoracic areas. () Histological analysis of surgical specimens was similar to that of the biopsy of the iliac bone confirming a diagnosis of multiple myeloma. Post-operatively radiotherapy was initiated in line with National Institute for Health and Care Excellence (NICE) guidelines []. The patient was also referred to the local haematology unit for oncological treatment of the myeloma with the surgical procedure resulting in restoration of mechanical stability to the spine and the surgical decompression offering relief from cord compression and recovery of the neurological deficit.\nThe operation was successful, with numbness in the left leg improving within 3–4 days. The pain subsided within one month and the patient could walk short distances without the use of crutches.\nAt one-year follow-up, the patient regained full function of the spine and hip. Ambulation status was restored, and lower limb power returned to normal (MRC score of 5/5). |
A 24-year-old man was admitted to our hospital with the signs of advanced chronic renal failure (CRF) in 2006. In his past history, he had developed kidney and bladder stones since he was 5-year-old. In his family history, his sister exhibited an elevated urine Ox concentration and his brother presented with kidney stones and renal failure. Unfortunately, they refused to cooperate with physicians to perform required tests until transplantation. Immediately in 1st day of admission, blood urea nitrogen (BUN) and serum creatinine (Cr) were determined 165 and 16.5 mg/dl, respectively, and also protein and glucose were detected in urine. The diagnostic findings indicate shrunken hyper-echogenic kidneys with hydronephrosis. Multiple stones with different sizes were observed in calyces of both kidneys. The bladder wall was thickened (4.7 mm), and urinalysis did not reveal any crystals. The patient underwent hemodialysis (HD) three times per week for 4 months. Four months after admission, the patient underwent bilateral nephrectomy. Based on the findings obtained in bilateral radical nephrectomy, chronic pyelonephritis with nephrolithiasis was confirmed. Microscopic examination revealed glomerulosclerosis and tubulointerstitial fibrosis. About 2 years later (September 2008), the patient underwent living kidney transplantation with a diagnosis of ESRD. The primary graft function was acceptable? but 3 days after transplantation, the urine output suddenly dropped to 30-50 cc a day. Therefore, a renal biopsy was taken. Tissue sections containing glomeruli and tubules were obtained. The following histopathological data were gathered: The glomeruli showed no conspicuous changes, mild to moderate atrophy with mononuclear inflammatory cells and occasional eosinophilic infiltration of interstitium, some tubules contained marked Ox crystals, and some contained granular and white blood cells casts. Following the acute rejection, anti-thymocyte globulin (ATG) was administered for the patient. After few days of ATG administration, the drug was discontinued because of fever. The possibility of PH1 was considered when a lot of Ox crystals were observed in the renal allograft biopsy and also by ruling out the other causes of hyperoxaluria. Therefore, pyridoxine therapy was commenced (dose, interval, and route of admin).\nIn January 2009, the patient's serum Cr and BUN levels were 4.8 and 38 mg/dl, respectively. The patient's computed tomography (CT) scan and radiography demonstrated cardiomegaly, bilateral pleural effusion with congestion, and calcification at the right pulmonary hilum and parenchyma. The molecular diagnostic polymerase chain reaction test revealed the persistence of cytomegalovirus. After few months, the patient refused to continue the treatment and finally he died 1-year later. |
The patient is a 67-year-old woman who complained of loss of strength, affecting predominantly the proximal muscles, in both the upper and lower limbs, over the last three years. The patient reported recently marked difficulties in climbing stairs and walking. Symptoms presented fluctuated initially, becoming continuous at the time of assessment. Bulbar or respiratory symptoms did not accompany them.\nHer past medical history was remarkable for the presence of small cell carcinoma of the lung in treatment with carboplatin and etoposide; the patient has been a smoker from age 16 and is a moderate alcohol drinker. On neurological examination, manual muscle strength testing was 5-/5 in the proximal upper limbs and 4+/5 in the proximal lower limbs. The sensation was preserved to all modalities. The bicipital, patellar and Achilles deep tendon reflexes were absent bilaterally.\nNeurophysiologists performed electroneurography, EMG, RNS, and single-fibre EMG. Electroneurography for nerve conduction studies (NCS) revealed normal motor and sensory conduction velocities and expected characteristics of the evoked potentials, helping us rule out polyneuropathy secondary to chemotherapy treatment. During the needle EMG, they studied the right vastus lateralis muscle, which showed no evidence of abnormalities, ruling out a myopathy possibility.\nFor the RNS test, they studied the right median nerve. The responses were recorded using electrodes applied over the abductor pollicis brevis muscle. It demonstrated a significant drop (>10%) in the amplitude of the fourth potential to the first one. Moving next to the single-fibre EMG, the right vastus lateralis muscle was studied, which showed the presence of an increased jitter in four of the six pairs, with an increase of the average jitter value. In one of the pairs analyzed, there was a block (Figure ).\nThese findings were consistent with an alteration of the neuromuscular transmission at the postsynaptic motor end-plate level, which is compatible with MG.\nHer laboratory studies showed that anti-acetylcholine receptor (anti-AchR) antibodies (Ab) testing was negative (0.38 IU/mL). In the presence of clinical and neurophysiological data suggestive of MG, physicians repeated the laboratory workup (which includes anti-AchR Ab, anti-striated muscle Ab and anti-MuSK Ab), highlighting an anti-AchR Ab value of 0.75 IU/mL (a grey area of positivity). After one year, a control analysis showed an anti-AchR Ab value of 1.15 IU/mL (positive). Also, a chest radiograph and computerised tomography (CT) were performed, not observing the presence of an associated thymoma. |
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