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The patient is a 29-year-old G2P1001 Hispanic woman with uncertain last menstrual period and no previous prenatal care who presented to Labor and Delivery for evaluation of preterm labor. She complained of nausea, vomiting, and acid reflux, which she had experienced throughout this pregnancy. Obstetric history included a prior full term Cesarean delivery without complications. Medical history revealed a history of kidney stones and pancreatitis. Surgical history was remarkable for cholecystectomy, appendectomy, and ureteral stone removal. All previous medical and surgical care took place in Honduras and no records were available.\nUltrasound established an estimated gestational age of 34 weeks with bilateral echogenic fetal kidneys. Amniotic fluid was normal with an amniotic fluid index (AFI) of 15.4. She was found to have contractions and her cervical exam changed from closed to 1 cm dilated. Given concern for preterm delivery, she was given a dose of betamethasone in accordance with recently published Antenatal Late Preterm Steroids trial demonstrating benefit between 34 and 36 weeks and 6 days' gestation []. Her contractions subsequently decreased and a repeat cervical exam was unchanged. She was discharged home with instructions to return in 24 hours for her second dose of betamethasone, but she did not return the following day.\nSeven days later, the patient returned to Labor and Delivery with contractions and diffuse abdominal pain. She reported vague and worsening discomfort across the entirety of her abdomen. She also complained of nausea, vomiting, and worsening acid reflux. She denied sharp or radiating epigastric pain, flank pain, or dysuria but noted polyuria, fatigue, and weakness. Her vital signs were within normal limits. Tocodynamometry demonstrated uterine irritability and contractions; however, her cervical exam remained unchanged from her evaluation one week before. Fetal heart tracing had moderate variability without acceleration. Ultrasound showed new polyhydramnios with an AFI of 41.3 with a biophysical profile of 8/10.\nDespite thorough and repeat history and physical exams, no focal signs or symptoms concerning for a specific etiology of her discomfort were elucidated. Her diffuse discomfort was attributed to significant uterine distension from polyhydramnios and GERD.\nHowever, labs demonstrated severe hypercalcemia, pancreatitis, and acute kidney injury: a corrected serum calcium of 16.9 mg/dL (ionized calcium 2.05), hyponatremia, hypochloremia, creatinine 1.4 mg/dL, BUN 41 mg/dL, amylase 334 U/L, lipase > 3000 U/L, WBC 15.8 K/mm3, and Hgb 9.7 g/dL. AST and ALT were within normal limits. An EKG was performed that showed ST elevations consistent with hypercalcemia. Troponins were negative. Focused physical exam was remarkable for a palpable thyroid gland (bilateral lobes) without rubor, calor, dolor, or bruits. Neurologic exam showed no focal deficits and full strength in bilateral upper and lower extremities. The patient remained alert and oriented × 3. Additional labs were drawn and were significant for low TSH (0.02 ng/dL), elevated free T4 (1.9 ng/dL), and significantly elevated PTH (937 pg/mL).\nThyroid ultrasound showed bilateral subcentimeter nodules and a 2.7 cm hypoechoic noncalcified solid lobulated nodule in the right thyroid lobe. A smaller, 0.7 cm nodule was also seen in the lower pole of the left thyroid lobe. A 0.6 cm predominantly cystic nodule was seen in the junction of the isthmus and right thyroid lobe. Abdominal ultrasound showed no dilatation of the intrahepatic biliary tree with a normal common bile duct. Florid bilateral nephrocalcinosis was present, consistent with longstanding hypercalcemia. Biliary etiology of her pancreatitis was deemed unlikely.\nFetal status remained reassuring with continuous monitoring. Aggressive IV fluid hydration was initiated with immediate improvement in pancreatitis but with minimal improvement in calcium levels. Given the patient's young age, severe hypercalcemia, very high PTH levels, and neck mass, there was concern for parathyroid cancer, not just parathyroid adenoma, for which the surgical treatment would be en bloc resection of the parathyroid gland as well as the thyroid gland, adjoining fatty tissue, lymph nodes, and surrounding muscles in order to achieve the best chance for surgical cure. A tissue biopsy of the thyroid nodule was obtained. Rushed pathology of a fine needle aspiration of the 2.7 cm thyroid nodule was concerning for parathyroid carcinoma.\nCalcitonin, cinacalcet, and zoledronic acid were added in succession, each with minimal improvement in hypercalcemia. For concurrent hyperthyroidism, she was also started on methimazole and propranolol in order to help prevent thyroid storm during possible surgical resection. Given incomplete administration of betamethasone one week before, the decision was made to administer a complete 2-dose course of betamethasone due to risk of premature delivery. Throughout the hospital course, continuous fetal monitoring showed reassuring fetal status. However, on the third day of medical management, the patient continued to have severe hypercalcemia refractory to medical management and fetal status began to deteriorate.\nFailing medical management, and in the setting of worsening fetal status, the endocrine surgery team provided emergent surgical management. Unexpectedly, intraoperative frozen section of one of two pretracheal lymph nodes was consistent with metastatic papillary thyroid cancer. She underwent bilateral exploration of parathyroid glands, total thyroidectomy, right central neck dissection, and right cervical thymectomy. After completion of the procedure, intraoperative PTH level decreased to 53, consistent with complete removal of the parathyroid lesion. Final pathology showed a parathyroid adenoma with atypia as well as occult papillary thyroid carcinoma with metastasis to a single lymph node.\nThe patient tolerated the procedure well and was transported to an ICU bed for close monitoring. She was closely monitored and started on calcium carbonate, calcitriol, and levothyroxine. Her calcium normalized within 12 hours and her pancreatitis resolved. Fetal status was reassuring following the procedure.\nOn postoperative day 2, at 36 weeks and 2 days' gestation, the patient began to contract painfully. She declined trial of labor and underwent an uncomplicated repeat C-section. She delivered a female infant weighing 3400 g with APGARS 7 and 8. The infant's calcium levels were elevated immediately following delivery with an ionized calcium of 1.66, but 24 hours later she was hypocalcemic and required calcium supplementation. The infant's hypocalcemia improved and stabilized with improved feeding and she was discharged home at 5 weeks of age with vitamin D3 supplementation. The infant also received an ultrasound that was consistent with neonatal nephrocalcinosis likely secondary to longstanding intrauterine hypercalcemia that may take months or years to resolve. A follow-up renal ultrasound is planned at 6 months of age.\nThe patient, now status postsurgical removal of thyroid and parathyroid glands, was discharged home on lifelong calcitriol, calcium supplementation, and levothyroxine with close outpatient follow-up with endocrinology. She will also follow up with endocrinology for further monitoring and evaluation of her thyroid function and for discussion of radioiodine therapy versus surveillance for thyroid cancer surveillance. |
A 35-year-old male reported to our department with a chief complaint of swelling over the left side of face and in front of ear since 3 weeks. Under the influence of alcohol, patient had a history of fall from slow-moving train 1 month back. Patient had a history of blunt chest trauma and was admitted under the department of general surgery for observation. The same patient presented to us 4 weeks later with a painless pulsatile mass in the left temporal region. Initially, patient noticed a very small pea-sized swelling in front of left ear, around 1 week after trauma. There was a history of the gradual increase in the size of swelling to present size since then, and patient was feeling pressure over the involved region. There were no changes over skin surface. Patient did not complain of headache, ear discomfort, visual disturbance, dizziness, hemorrhage, or any neurologic defect. He was concerned about the increasing size of the swelling.\nOn local physical examination, a well-defined roughly spherical-shaped globular, nontender, pulsatile mass of about 30 mm × 30 mm was seen over left preauricular region anterosuperior to the left tragus [], it was easily compressible on digital pressure. Swelling did not disappear on the compression of the ipsilateral STA, but aneurysmal pulsations were eliminated. Transmitted pulsations could be felt over posterosuperior region of the swelling. Computed tomography (CT) of brain was normal. On auscultation, bruit could be appreciated. Another pulsatile mass was present above the swelling mentioned, measuring approximately 10 mm × 10 mm in maximum dimensions.\nCT angiography revealed well defined, round to oval, hyperdense lesion measuring approximately 2.7 cm × 2 cm in left temporal space in the suprazygomatic region with nonenhancing hypodense area within the lesion suggesting partially thrombosed pseudoaneurysm from the superficial temporal branch []. Doppler ultrasound of left preauricular region revealed relatively well-defined lesion in the preauricular region on the left side measuring 3.0 cm × 2.6 cm × 3.0 cm in size. Lesion was seen in close relation to the STA. The artery showed normal triphasic waveform. Color Doppler showed “yin-yang” sign and “swirling pattern” waveform. These imaging features were suggestive of pseudoaneurysm. Part of the lumen of the pseudoaneurysm appeared heterogeneous, suggestive of partial thrombosis of the lumen. Another small pseudoaneurysm was seen adjacent to above-described pseudoaneurysm and appeared thrombosed [Figure and ].\nUnder general anesthesia, surgical exploration by Alkayat-Brahmley incision and temporal flap elevation was done []. The mass was excised and proximal and distal cut ends of the artery were ligated []. A 3.0 cm × 3.0 cm mass was resected []. A standard pressure dressing was applied for next 48 h. No bleeding or any other complication occurred. Biopsy specimen sent for histopathological examination confirmed pseudoaneurysm. The report stated hematoma in arterial wall beneath thinned out adventitia and fibrovascular stroma with extravasated red blood cells [Figure and ]. The patient recovered uneventfully after surgery and there is no recurrence after 1 year of surgery []. |
An 8-month-old female infant had coronary reimplantation at age 3 months for ALCAPA. Postsurgical ejection fraction showed early improvement with subsequent deterioration. A diagnostic left heart catheterization performed as part of a heart transplant evaluation revealed severe ostial stenosis of the LMCA. She was referred for PCI of the left main coronary artery to relieve her heart failure and preempt transplant. Her physical exam was significant for congestive heart failure and failure to thrive. The patient's echocardiogram showed markedly depressed left ventricular function. A cardiac computed tomography angiography (CTA) and initial diagnostic nonselective root aortogram demonstrated stenosis of the LMCA at the site of ALCAPA reimplantation. Selective left coronary angiogram revealed severe kinking of the reimplanted LMCA at the ostium ().\nThe procedure was performed in the Pediatric Cardiology interventional suite after extensive discussion and planning with Pediatric and Adult Interventional Cardiology, Pediatric Cardiac Anesthesia, Pediatric Cardiothoracic Surgery, and Pediatric Cardiac Radiology. General anesthesia and a femoral arterial approach were utilized. An ascending aortic root angiogram was obtained in 2 planes to assess the ostial left main stenosis. Due to the small size of the infant aorta, a 6 Fr JR-4 guide was reshaped to engage the left main coronary artery. A BMW wire was used to cross the lesion. Since the infant left main coronary artery was small but was expected to grow with age, a somewhat larger (3.0 × 8 mm Vision bare metal) stent was carefully implanted in the proximal LMCA at less than nominal pressure to avoid distal dissection. A poststent angiogram showed that the stent had moved during implantation and missed the ostium with residual stenosis of the LMCA origin. Hence, a 3.5 × 8 mm Vision bare metal stent was placed into the LMCA ostium overlapping with the previous stent distally and protruding 1-2 millimeters in the aorta proximally. The ostium and aortic overhanging portion of the stent were postdilated producing proximal flaring. The final angiogram confirmed excellent stent position and normal flow ().\nThe patient tolerated the procedure well and was discharged home on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel one day after PCI. She was followed in Cardiology clinic post-PCI and noted to have no change in her ventricular function. Nevertheless, she continued to do well clinically until six months post-PCI, at which time she demonstrated failure to thrive and required admission for initiation of continuous milrinone infusion. The left main stent was widely patent with normal Doppler flow signals as visualized by echocardiography (). She was listed as status 1A for orthotopic heart transplantation (OHT) and underwent transplantation one year post-PCI, at age 20 months. |
A 63-year-old female with a chief complaint of a progressive headache has been admitted to the Department of Neurosurgery. The headache first has been presented 4 months ago. Before that time, the patient had always been symptom-free, following a normal active life. The pain was pulsating, with a concentration in frontal and periorbital area with no particular radiation. When severe, it has been followed by eye irritation and involuntary tearing. Headache was progressive along the day, and most severe at night. The severity of the pain has also been intensified within the recent weeks comparing to time it started. The patient had no history of seizure or convulsion, aphasia, and diplopia. Otherwise, she gave a history of occasional vomiting, nausea, amnesia, and sphincter dysfunction in form of stress incontinency and equilibrium problems. Cerebellar tests were abnormal, and she could not walk on her own. She had a history of left kidney tumor, for which she had undergone partial nephrectomy for about three years ago. Furthermore, she gave a history of controlled diabetes, hypertension, and hyperlipidemia. No history of ischemic heart disease or cerebrovascular attack was mentioned. She had a drug regimen of insulin, losartan, memantine, atorvastatin, zinc plus, magnesium, propranolol, and venlafaxine. In her physical examination, cranial nerves were intact, with a Glasgow Coma Scale of 15/15. Cerebellar tests were abnormal with obvious equilibrium dysfunction and inability to self-manage walk. Both pupils were normal sized, symmetric and reactive to light. Visual acuity was at level of finger count out of three meters distance. Sensory and motor function of the four extremities were normal; and no sensory level was detected. The patient suffered from sphincter dysfunction in the form of stress incontinency.\nMagnetic resonance imaging (MRI) was performed for better evaluation. In T1 view a well-defined hypo-signal mass was detected in middle gyrus of each frontal lobe. The same hyper signal mass was detected in T2 view. Two totally discrete heterogeneous intraparenchymal lesions in frontal lobes lateral to falx cerebri was detected in flair view. Slight marginal edema was also seen []. As surgical removal is choice in approach to epidermoid tumors, the patient then underwent bifrontal craniotomy. Bicoronal skin incision was made, and dura was separately opened on the left and right. Since there was no inspection of tumor beyond the cortex, two separate cortical incisions were also made and the two separate tumors were totally resected from the middle gyrus of frontal lobe of both hemispheres. Right after the surgery up to her last visit, the patient has become symptom-free.\nFollowing the surgery, a cut of the tumor has been excised, and sent for pathology sampling. Microscopic review of the resected part reported normal brain tissue along with sections containing parts of cyst wall covered by squamous epithelium and huge amount of irregularly stratified keratin within its lumen which clearly emphasizes on diagnosis of a typical epidermoid tumor []. |
Our patient is a 13-year-old Risser 2 female with AIS consisting of a 53-degree right convex curvature curve from T4-T10 with a left convex thoracolumbar curve measuring 49 degrees from T11-L3 (Figure ).\nThe patient reported occasional back pain throughout her life, but this was never activity limiting. She denied any neurological symptoms, including numbness or tingling in her extremities. Menarche was at age 11. An MRI was obtained of the entire cord to rule out an intrathecal process, such as Chiari malformation, syrinx, or cord tethering, and was found to be normal without signal abnormality within the spinal cord at any level.\nAfter appropriate preoperative counseling, the patient and her family elected to undergo a posterior spinal fusion with instrumentation from T1-L1. The patient was positioned prone on a Jackson frame. Great care was used to place the head and neck in a neutral position, with the ears at the level of the shoulders. Arms were positioned in a manner that prevented traction on the brachial plexus. Elbows were bent to 90 degrees and the volar surface of the forearms was placed on foam pads after shoulders were abducted 90 degrees with 30 degrees of forward flexion. The patient underwent posterior instrumentation and fusion with hybrid fixation from T1 to L1. From incision to closure, the total operative time was four hours. Her estimated blood loss was 500 mls, and she received 53 ml of cell-saver blood autofusion prior to wound closure. Her mean arterial blood pressure (MAP) ranged from 95 mm Hg at incision to 75 mmHg at closure, with a high of 95 mmHg and a low of 59 mmHg. Neurologic status was monitored using SSEPs and transcranial MEPs without evidence of intraoperative abnormalities throughout the procedure. Prior to the procedure, her Hg was 11.2 and this was not rechecked immediately postoperatively. At the completion of the procedure, she was rolled supine on a hospital bed where she actively moved all major joints of upper and lower extremities on command prior to extubation. She was taken to the recovery room where she was noted to have full upper extremity and lower extremity function. Her arterial line was removed, and she was transferred to the floor after one hour.\nOn arrival to the floor, the patient did complain of slight numbness/tingling in her knees; however, her exam was normal and this was attributed to her prone positioning during surgery with pressure on the anterior surface of the knees.\nAt 11 pm (12 hours after the procedure), the patient began complaining of weakness in her upper and lower extremities as well as decreased sensation in all extremities. The patient was anxious and had periods of apnea, likely due to anxiety and narcotic usage. Her MAPs were between 62 and 65.\nExamination at this time revealed the patient was anxious and tachypneic. She was unable to move her lower extremities bilaterally (0/5 in all major muscle groups) with decreased sensation in the L3-S1 distribution. Left upper extremity exam at this time was completely normal while the right upper extremity demonstrated decreased sensation in C5 and T1 along with difficulty moving fingers and wrist on the right side (3/5 wrist flexion, wrist extension, and grip strength). The patient was given 1.5L normal saline at this time to help raise her blood pressure. Her hemoglobin at this time was 10.1.\nTwo hours after the onset of symptoms, the patient regained full strength and sensation in bilateral lower extremities and in her left upper extremity. Her right upper extremity regained full sensation, however, she continued to have weakness with elbow, finger, and thumb extension, as well as grip strength (all 3/5).\nAn MRI was subsequently obtained, which demonstrated a 4.2 cm longitudinal right-sided hemicord infarction from C5-C7 (Figures -).\nThe patient was immediately transferred to the pediatric intensive care unit (PICU) and started on methylprednisolone and a norepinephrine drip in order to maintain MAP >70.\nBefore discharge from the hospital, neurologic symptoms began to improve. She started having gradual improvement of right triceps function, however, she was still unable to fire finger or thumb extensors. She had full motor and sensory function in her left upper extremity and in her bilateral lower extremities.\nAt one month from the surgery, the patient had regained full sensation throughout her right arm from the C4-T1 distributions. Her strength on her right side was: biceps 5/5, triceps 4+/5, wrist extensors, grip strength, and extensor pollicis longus 4/5, and extensor digitorum communis and extensor indices 2+/5. Occupational therapy was started to work on strengthening and motion for her right arm. At four months from her surgery, she demonstrated improved coronal alignment but normal sagittal balance (Figure ).\nHer sensation remained intact in the right arm. Motor function demonstrated full grip strength and triceps function, mild weakness of her extensor digitorum communis (EDC) and extensor indicis proprius (EIP), and the inability to fully extend her fingers in her right hand. Occupational therapy was continued. |
An 83-year-old Caucasian female was scheduled for a colonoscopy under general anesthesia to investigate unexplained anemia (hemoglobin 115 g/L, mean cell volume 87.2 fL).\nShe had a background of hypertension, osteoarthritis, paroxysmal atrial fibrillation, and colonic diverticulosis. She had a past surgical history of total abdominal hysterectomy for uterine prolapse and right total hip replacement. She was independent in activities of daily living and had a performance status of 0.\nTo investigate the anemia, she was booked for oesophagogastroduodenoscopy (OGD), colonoscopy, and computed tomography (CT) scanning of the chest, abdomen, and pelvis to exclude malignancy.\nThe OGD was normal, and the CT scan revealed extensive diverticulosis in the sigmoid colon with associated narrowing and thickening of this segment of bowel. An outpatient colonoscopy was attempted under sedation but the patient was unable to tolerate the procedure. The procedure was abandoned and the patient was rescheduled for a colonoscopy under general anesthesia in the endoscopy suite.\nOn the day of colonoscopy, the patient was well. Induction of anesthesia performed by a consultant anesthetist was unremarkable. The colonoscopy was performed by a gastroenterology consultant and it was challenging because of poor bowel preparation and severe narrowing and tortuosity of a diverticular segment extending from the distal sigmoid to the mid descending colon. This segment was traversed, but at the level of the mid transverse colon, the patient's oxygen saturations dropped suddenly from 98% to 40% and there was an associated tachycardia of 160 beats per minute. Within 4 minutes of this sudden drop in oxygen saturation, the patient went into cardiac arrest, specifically pulseless electrical activity on the electrocardiogram monitor. The procedure was terminated and cardiopulmonary resuscitation (CPR) was commenced. The team that conducted the CPR noted that the patient had subcutaneous emphysema in the neck, chest and abdominal walls, and had a distended abdomen.\nDuring the second minute of cardiac compressions, the patient was found to have reduced air entry and hyper-resonance on percussion of the right hemithorax. This was attributed to a right tension pneumothorax and this was decompressed with a wide-bore cannula placed in the second intercostal space in the right midclavicular line.\nUpon decompression of the right tension pneumothorax, there was a return of spontaneous circulation and the oxygen saturation improved from 69% to 100%. An arterial blood gas revealed a pH of 7.36, partial pressure of oxygen of 15.2 on 15 L of oxygen, and a partial pressure of carbon dioxide of 6.08. A portable chest radiograph revealed bilateral pneumothoraces; the right-sided pneumothorax which was originally a tension pneumothorax had been converted to a simple pneumothorax, and on the left there was a simple pneumothorax. Two surgical chest drains were sited. The patient's temperature, pulse, and blood pressures were 36.0, 100 bpm, and 110/60 mm Hg, respectively. The abdomen once again was noted to be visibly distended and tympanic and there was a strong suspicion of colonic perforation.\nOnce stable, a CT scan of the chest, abdomen, and pelvis was obtained. This was reported by a radiology consultant as showing a large-volume pneumoperitoneum and free gas in the retroperitoneum with signs of perforation at the hepatic flexure of the colon. Note was made of bilateral pneumothoraces with extensive subcutaneous emphysema in the neck, chest, and abdominal wall and pneumomediastinum.\nShortly after this the patient was reviewed by the on-call surgical team and prompt arrangements were made for emergency laparotomy. At laparotomy, there was a perforation of the colon at the hepatic flexure with contained contamination around the proximal transverse colon and duodenum. A right hemicolectomy with exteriorisation of the ileal and colonic bowel ends as double-barrel stomas was carried out.\nPostoperatively, the patient was managed on the intensive care unit (ICU) and required cardiovascular (ionotropic) and respiratory support by way of mechanical ventilation for the first 4 days. She was treated for a lower respiratory tract infection and required reintubation for a short duration. She also received hemodialysis for 5 days. She was eventually discharged from ICU on nutritional support after a 28-day stay. At this stage, her stoma was healthy and functioning, and there were no ongoing surgical concerns. She was managed on a respiratory ward and started making progress. However, 6 days after being moved to the ward she deteriorated acutely and rapidly from a lower respiratory tract infection. She died 2 days later, 35 days after her original colonoscopy. |
A 69-year-old man was admitted to our hospital because of pain during urination and gross hematuria. There was no relevant medical history and no presenting complaints. Routine urine examination was positive for red blood cells and showed the absence of white blood cell, protein, and glucose. Blood urea, serum creatinine, and other biochemical blood tests showed no abnormal findings. There was no clinical sign of infection and no history of bladder catheterization. Ultrasound showed an irregular and isoechoic thickening of the left side of the bladder wall. Cystoscopic examination suggested a broad expanding mass on the left side of the bladder wall. Pre- and postcontrasted CT images revealed an irregular thickening of the left side of the bladder wall and an increased density of a surrounding fat tissue []. The irregular wall thickening showed isointensity relative to the bladder wall on T1-weighted images [], and inhomogeneous hypointensity on T2-weighted images [], and gradual and inhomogeneous enhancement were seen on dynamic contrast study []. In addition, there was obliteration of the normal hypointensity of the muscle layer of the bladder wall on T2-weighted images []. Furthermore, T1- and T2-weighted images including dynamic contrast study showed a stranding of perivesical fat [Figure and ], which suggested the perivesical fat invasion. The results of urine cytology showed no malignancy. However, imaging findings suggested an advanced bladder carcinoma invading muscle layer and perivesical fat.\nTransurethral partial resection of the bladder tumor was performed to obtain a histological diagnosis. Pathologic examination revealed a polypoid or papillary appearance of the mucosa, with submucosal edematous changes, neutrophil invasions, and granulomatous formations [Figure and ]. The patient was diagnosed as having a polypoid and papillary cystitis.\nHe was followed closely without any treatment, and both the irregular thickening of the bladder wall and the stranding of a surrounding adipose tissue nearly-disappeared on MR and cystoscopic findings after 3 months []. |
A 26-year-old gravida 2 para 1001 at 24 weeks of gestation, dated by last menstrual period consistent with 8 week ultrasound, presented to labour and delivery with 2 hours of severe, constant, right lower-quadrant pain as well as urinary retention, vomiting and syncope. She denied vaginal bleeding or amniorrhexis. She reported intermittent episodes of similar abdominal pain throughout the pregnancy, including an instance at 22 weeks where she presented to labour and delivery for sharp right lower-quadrant abdominal pain and vomiting that woke her from sleep. At that time, she had normal vital signs, fetal heart tones and bedside ultrasound. Labs were notable only for an elevated white cell count (WCC) and she was discharged with strict return precautions. Her obstetric history was significant for a bicornuate uterus diagnosed in her previous pregnancy for which she required a low transverse caesarean delivery secondary to malpresentation. Her first pregnancy was in her left uterine horn, this pregnancy was in the right.\nHer prenatal course was notable for markedly elevated alpha-fetoprotein (AFP) at 20.91 multiples of the median (MoM) at 17 weeks of gestational age. At 19 6/7 weeks of gestation, a fetal anatomic ultrasound demonstrated no structural abnormalities, specifically no neural tube or abdominal wall defects. But the fetus had asymmetric growth restriction. An amniocentesis for chromosome analysis was performed, which resulted in a 46 XY karyotype. The AFP in the amniotic fluid was within normal range at 1.78 MoM and no acetylcholinesterase was detected. At 23 5/7 weeks of gestation, just 2 days prior to admission, the estimated fetal weight was 397 g, below the 10th percentile for gestational age.\nAt the time of arrival to the hospital, the patient was ill, appearing with rigours but afebrile and haemodynamically stable. The patient’s respiratory and cardiac examinations were normal. She had right lower quadrant tenderness without guarding or rebound and her vaginal examination demonstrated a long closed cervix but marked tenderness in the posterior fornix.\nElectronic fetal monitoring demonstrated a baseline of 150 beats per minute with minimal variability, no accelerations and no decelerations. Her haemoglobin was 14.8 g/dL and WCC was 18x109/l. An abdominal ultrasound revealed an indeterminate tissue mass posterior to the uterus. Immediately following the ultrasound, an MRI of the abdomen/pelvis confirmed ill-defined soft tissue mass with free fluid. Over the next 5 hours, the patient’s vital signs did not change, but she declined clinically. She had worsening abdominal pain and distention. Then she developed abdominal guarding and rebound tenderness. At this point, variable decelerations were noted in the fetal heart tracings. Given her deterioration, the decision was made to perform an emergency exploratory laparotomy. General surgery was consulted in the event the source of her pain was not pregnancy related.\nIn the operating room, a vertical midline skin incision was made, and 1.5 L of blood was evacuated from the peritoneal cavity. The right horn of the uterus was torsed and necrotic. Bleeding was noted from an area of rupture on the lateral aspect of the uterine horn. The right fallopian tube and ovary were also necrotic. A hysterotomy was performed through a fundal incision to deliver the fetus followed by amputation of the right uterine horn and right salpingo-oophorectomy. An appendectomy was performed at the recommendation of general surgery. We speculate that the surgeon believed the appendix appeared inflamed with possible necrosis, and an appendectomy was performed to remove all doubt that appendicitis could be contributing to her symptoms. The baby was born alive with a heart rate in the 70 s, appeared grossly normal, but weighed 338 g. The patient declined aggressive interventions and elected to focus on the neonate’s comfort given fetal weight and gestational age. The infant expired after 45 min of life in the neonatal intensive care unit. |
A 32-year-old overweight male with recently diagnosed type 2 diabetes presented to an urban, university hospital ED with a chief complaint of palpitations, shortness of breath, light-headedness, and “feeling ill.” He had seen his primary care physician twice in the previous weeks for similar symptoms, and he had started an exercise program to address his new-onset diabetes. After an unsuccessful attempt to see his primary care physician again that day, the patient came to the ED for care. The triage nurse charted the patient’s chief complaint as “chest pain with shortness of breath for one week increased with exertion” and recorded a heart rate at 140. The remaining vital signs at triage were a blood pressure of 128/71 mm/Hg, respirations of 28, and a temperature of 35 degrees C. Room air pulse oximetry was recorded at 95%. At the time of his arrival, the ED was over 250% of capacity (patients/beds), and the institution was on ambulance diversion. Since all 40 licensed ED beds were occupied, the patient was placed on a gurney in one of several narrow hallways within the ED. Twenty patients were already receiving hallway care when the patient presented to the ED, and another 40 were in the waiting room. The triage nurse immediately performed an electrocardiogram (EKG) per ED policy, which was immediately reviewed by an attending physician on duty at that time. This physician noted there was no ST-elevation myocardial infarction (STEMI) on the EKG and, at the request of a nurse, wrote orders for a basic lab panel. As it was the end of shift, this physician had no further involvement with the patient and did not mention his/her involvement to the next attending. On average, attending physicians in this ED screen as many as 25 patient EKGs for STEMI while providing direct supervision to an additional 30 patients during a 10-hour shift.\nFour hours after triage, the patient was formally evaluated by an off-service PGY1 (post-graduate year one) resident. The resident was aware that an attending physician had already viewed the EKG and ordered labs. The resident charted the results, including the comments from the EKG, and performed a history and physical. The prior attending was off-shift, thus the resident presented the case to a new attending physician. At that time the ED remained crowded, with all its resources overwhelmed. The oncoming attending physician had immediately become overwhelmed with critically ill and injured patients and was repeatedly confined to the resuscitation room with medical or trauma codes. During the first 2 hours of the shift, this new attending physician performed over 10 initial EKG screenings. At 5 hours post-arrival, the resident was able to present the case to the new ED attending physician, who then examined the patient in the hallway. The history obtained by the resident noted the patient never actually had chest pain, and this was confirmed by the attending physician. The point-of-care glucose was 463 mg/dL, and the initial diagnostic impression was probable hyperglycemia with dehydration. Because the patient was in the hallway, there was no formal location to maintain his paper records, and the EKG was no longer available for review. This attending physician did know that, per ED policy, a patient with dyspnea and chest pain would have automatically received a triage EKG and assumed it had been reviewed by the prior attending physician. If the initial screening review of the EKG had been concerning, the patient would have been moved out of the hallway to a monitored licensed bed, or “doubled up” in the central treatment area of the ED. Six hours after presentation the patient’s laboratory studies returned with results consistent with the initial impression of possible mild diabetic ketoacidosis (DKA) and dehydration. The blood glucose was 417 mg/dL, bicarbonate 19 mmol/L, and an anion gap of 15. Venous blood gas pH was 7.34. PCO2 was mildly decreased. Other labs were within normal limits. The patient was treated with 3 liters of IV normal saline, as well as 5 units IV and 5 units subcutaneous regular insulin. A chest radiograph was performed and was normal. Oxygen saturation was checked multiple times and ranged from 95 to 98% saturation on room air.\nAfter therapy, the patient’s glucose decreased to the 200 mg/dL range, and a repeat chemistry panel showed normal bicarbonate with no anion gap. The patient’s heart rate ranged from 66 to 114 for much of the stay in the ED, and by time of discharge was normal. The dyspnea had improved. The patient passed an oral trial of fluids, felt improved, and wanted to return home. Because this was a new onset DKA, albeit mild, an informal discussion was held with the hospitalist about admission. The hospitalist, based on the quick resolution of symptoms and patient’s access to his primary care physician, recommended outpatient management. The patient was then discharged home with the final diagnosis of hyperglycemia, mild DKA, dyspnea secondary to metabolic acidosis, and dehydration. A more aggressive regimen for his diabetes was prescribed, and home equipment for self-monitoring ordered. Close follow-up with his primary care doctor was specified. The patient was discharged 8 hours after arrival in the ED. Discharge vital signs were 154/86 mm/Hg, heart rate 94, respiratory rate 20, temperature 37 degrees C, and 98% room air saturation. He never occupied a licensed ED bed and was never on a cardiac monitor, as these were all in use.\nTwo days later, the patient developed severe shortness of breath; therefore, 911 was called and EMS activated. The patient had a cardiac arrest en route to the same hospital from which he was discharged two days earlier. Resuscitative efforts were unsuccessful, and the patient expired. An autopsy was performed and showed multiple acute and chronic pulmonary emboli as the primary cause of death. The initial EKG was retrospectively interpreted by a cardiology attending physician as showing “right axis deviation, multiple ST and T-wave changes suspicious for anterior ischemia.” The autopsy did not show coronary artery disease or evidence of myocardial infarction. |
A 35-year-old male patient came with a history of right-sided inguinal hernia for the past 15 years, which became irreducible and painful since six days. He complained of severe back pain since three months. He was married for 15 years and had no sexual dysfunction. He had two children. There was no history of any drug intake by his mother during the first trimester of pregnancy. There was no family history of such disorder.\nOn physical examination, secondary male sexual characters were found to be well developed and had a normal penis. Right inguinal swelling was 8×6cm in size, tender and irreducible. The scrotum was well developed on the right side with soft testis in it and left side was poorly developed without a palpable testis. Rest of the physical examination was unremarkable. Clinical diagnosis of right-sided irreducible inguinal hernia with left cryptoirchidism was made.\nPatient was operated upon under spinal anesthesia. Peroperatively, the hernial sac contained a uterus-like mass with a tubular structure on each side []. One side of tube was attached to a 7 × 6 × 3.5 cm white, hard, irregular mass which was attached to the omentum. On pulling the cord structures, normal-appearing testis delivered from the right side of the scrotum. The cord was separated meticulously from the rest and the uterus along with the mass removed in toto. Right testis was replaced into the scrotum and hernia repaired by polypropylene. Postoperative course was uneventful.\nHistology revealed normal hypoplastic uterine tissue with attached fallopian tube. The mass was of malignant germ cell tumor with predominance of yolk sac elements. Additional components of embryonal carcinoma and teratoma were seen. Tumor was found to infiltrate spermatic cord. Few vascular emboli were also seen in the capsule. There was no ovarian tissue. Chromosomal analysis revealed 46 XY. Scan of the abdomen revealed multiple liver secondaries with multiple para-aortic and bilateral para-ileac lymph node involvement. There was thrombosis in the infrarenal aspect of the IVC and bilateral common ileac veins. Associated left side hydronephrosis was found. Right scrotal testis was normal. Chest X-ray was normal. In view of raised AFP, bHCG and LDH and nonpulmonary visceral metastasis, tumor was graded as poor risk Stage III. Even with anticoagulant therapy, DVT progressed relentlessly and he died of pulmonary embolism before the first cycle of BEP chemotherapy could be completed. |
An 85-year old Caucasian man was admitted to the hospital with a history of 2-3 weeks of anorexia, fatigue, headache and dyspnoea. The patient had prior to hospitalization taken penicillin per os (p.o.) for seven days for pneumonia without effect. His only medical history was a pacemaker implementation one year previously, due to III degree AV-block. After admission the patient was treated with intravenous (i.v.) G-penicillin and gentamicin on suspicion of pneumonia and endocarditis. Chest X-ray and echocardiography were normal. Unfortunately, blood and urine cultures were taken after institution of antibiotics and showed no growth. Due to poor clinical response antibiotics were changed first to i.v. mecillinam on day 7, and later to i.v. cefuroxime on day 9.\nDue to elevated alkaline phosphatase an abdominal ultrasound and CT were performed on day 14 showing an abscess measuring 10.5 x 7.2 x 8.7cm in the right liver lobe. By ultrasonic guided abscess drainage, 20 cubic cm of pus giving growth to K. pneumoniae was removed. Antibiotics were stopped after two days and the patient was discharged without any further treatment or follow up.\nThe patient was re-admitted to the hospital 109 days later due to collapse at home. On suspicion of urosepsis he was treated with i.v. cefuroxime and later supplemented with gentamicin. Liver ultrasound showed no abscess, but as blood culture showed growth of K. pneumoniae a new CT scanning was performed. The CT scan showed a new liver abscess about 2 cm in diameter, in close relation to the original liver abscess. The original liver abscess area was reduced to about 3 cm in diameter, and was hypodense with possible signs of infections/edema. Ten days after admission antibiotics was changed to ciprofloxacin p.o. for 41 days. After discontinuation of antibiotics, the patient was followed weekly with blood samples, and was after one month declared free from infection, as both CRP and leukocytes had remained normal.\nThe patient had no history of foreign travel and also no contact with people from Southeast Asia. Eighteen months after the last follow up the patient was doing well and had no sign of relapse.\nThe K. pneumoniae blood isolate was hypermucoviscous as shown by the formation of a mucoviscous strings when a loop was passed through a colony. Capsular serotype was K1 and it belonged to ST23 as determined by the K. pneumoniae MLST scheme described by Diancourt et al. []. The isolate was positive for the following virulence factors: aerobactin, allS, kfu and rmpA as revealed by polymerase chain reaction using specific primers []. |
A 15-year-old female patient (bodyweight 50 kg, height 160 cm) presented with syncope. Severe arterial hypertension was diagnosed (178/147 mmHg left arm, 102/83 mmHg left leg). She reported previous episodes of exercise independent headaches and nose bleeds. Auscultation revealed no cardiac murmurs, but an accentuated second heart sound and reduced pulses in the lower limbs. There were no clinical signs to suggest Alagille or William’s syndrome or clinical evidence of neurofibromatosis. Blood tests showed normal inflammatory markers and normal creatinine. The urine dip showed no markers for blood or protein. No regular medication was taken at the time she presented. The electrocardiogram showed normal sinus rhythm, no significant signs of left ventricular (LV) hypertrophy or abnormal repolarization. Echocardiography detected a severe concentric LV hypertrophy (14 mm diastolic septal diameter, 15 mm diastolic diameter of the LV posterior wall) and a long hypoplastic segment in the abdominal aorta with massive arterial collateralization. Cardiac catheterization confirmed the diagnosis of a midaortic syndrome with a minimum diameter of <1.5 mm and a gradient of 50 mmHg between the aortic arch and the femoral arteries (Figure ). The narrow part began directly under the diaphragm above the truncus coeliacus and continued down to the bifurcation of the arteriae iliacae including the renal arteries, with reversed flow in the caudal aorta up to the renal arteries. Because of the extraordinary length of the hypoplastic segment of 23 cm, we decided for a stepwise interventional therapy with a paclitaxel covered balloon. No additional computed tomography scan or magnetic resonance imaging (MRI) was performed. Consultation with our surgeon, supported the interventional approach. The proposed procedure was reviewed and approved by our institutional review board, extensively discussed with the patient’s family, and informed consent was obtained before proceeding.\nAfter balloon interrogation of the long stenotic abdominal aorta using a 6 × 20 mm Tyshak balloon (NuMED Inc., Hopkinton, NY, USA) to differentiate between rigid stenosis and hypoplastic parts, serial balloon dilation with a 7 × 40 mm paclitaxel covered In.Pact balloon (Medtronic, Minneapolis, MN, USA) (3 µg/mm2 Paclitaxel on the balloon) was performed (Figure ) from end to end of the stenosis. Planned redilations, to stepwise improve the aortic compliance and reduce the risk of dissection, were performed after 2, 4, and 8 months with Elutax balloons ranging from 8 mm to 12 mm diameter (Aachen Resonance, Düsseldorf, Germany) (2 µg/mm At the end of the last interventional procedure, a mild endothelial lesion at the former narrowest point of the aorta was noticed (Figure ). This lesion healed and after 2.7 years MRI showed a stable and adequate result (Figure ). Today the girl is in unrestricted physical condition. The blood pressure has markedly improved (139/64 mmHg right arm and 127/65 mmHg right leg) under therapy with atenolol and amlodipine.\nThe patient and patient’s family consented to the publication of this case’s history and the images presented. |
A 28-year-old man presented to our clinic three days after his first episode of vertigo. The patient was suffering from frequent episodes of severe spinning vertigo with mild nausea; each episode lasted for a few minutes. The patient complained of a severe whirling sensation with a clockwise direction during the ictus, and experienced a dull headache after the ictus. The patient reported that he did not suffer from agoraphobia, panic symptoms, or any recent stressful conditions. Nor was the ictus accompanied by ear symptoms, such as tinnitus, hearing loss, or aural fullness, and there were no other symptoms, such as paresthesia, motor deficit, or visual disturbances, including field defect, metamorphopsia, or color change. His symptom was not predictable and occurred without any position change. The patient did not lose consciousness during the onset of the symptom, and his family members had not witnessed any eyeball deviation or head turning during the episodes. The patient had no history of motion sickness or migraine. However, he had undergone an operation in the left cerebral hemisphere for the treatment of Moyamoya disease (encephaloduroarteriosynangiosis, EDAS) 3 years ago. Brain MRI revealed the presence of an osteoplastic craniotomy scar in the left lateral convexity (). No nystagmus was observed and his symptoms were not evoked by the hyperventilation maneuver. The patient showed bilaterally symmetrical saccade and smooth pursuit. A cerebellar function test was normal and a caloric test and audiometry showed normal responses. We assumed that the ictus was a manifestation of vestibular epilepsy. Therefore, the patient was admitted to the Epilepsy Monitoring Unit (EMU). He was monitored continuously for 24 hours a day with video and computerized EEG equipment. However, the episodes of vertigo were not accompanied by any significant EEG changes, such as sharp waves and spikes. Therefore, we suspected that the episodes might be psychogenic dizziness. The patient was responsive to benzodiazepine medication and psychological encouragement. |
An 82-year-old male patient was referred to our emergency department due to a neglected periprosthetic knee joint infection of his left knee. He had undergone a primary total knee arthroplasty 11 years ago in another institution because of painful osteoarthritis. Failure of the primary arthroplasty led to revision surgery two years later, at the same institution. The patient reported prolonged mild edema and moderate pain subsequent to the revision surgery and deterioration of symptoms during the past two months.\nOn admission, the patient reported severe pain in the left knee. This was the reason for the limitation of his daily activities. The patient was afebrile and no injury in the recent past was referred. Τhe knee joint was excessively swollen, with prominent erythema and warmth. Moreover, imaging by X-ray revealed a constrained revision prosthesis and no signs of fracture (Figure ). The range of motion was affected, with a major deficit in flexion and a 10 degrees deficit in extension.\nAn ultrasound of the knee joint was performed in the emergency department and revealed massive fluid accumulation in the joint. Blood samples revealed abnormal inflammatory markers. The C-reactive protein (CRP) was 20.3 mg/L and the erythrocyte sedimentation rate (ESR) was 67 mm/hr, but no leukocytosis was observed. Blood cultures were also obtained. The rest of the standard laboratory evaluation was normal.\nAs far as medical history is concerned, the patient reported myelodysplastic syndrome (MDS) and benign prostatic hyperplasia (BPH) under treatment. MDS could possibly be one of the reasons why leucocytosis was absent, even though, in many cases of chronic musculoskeletal infections, the white blood cell count is normal. The platelet count was normal (PLT: 262 X103/μL) and the red blood cell count (RBC) was 4.25 x106/μL with haemoglobin 11.1 g/dL. No known allergic reactions were reported.\nSurgical debridement of the joint was decided, and it took place in the operation room on the same day. During the procedure, pus was removed from the joint, several cultures were taken, and the joint was excessively debrided. After the operation, broad-spectrum empiric intravenous antibiotic therapy was initiated, consisting of piperacillin and tazobactam (4 g + 0.5 g) every six hours and vancomycin 1 g every 12 hours. Prophylactic dosage of low molecular weight heparin (LMWH) was also administered subcutaneously (enoxaparin sodium 4,000 IU once daily).\nThe cultures from the joint fluid and tissues revealed a multidrug-resistant extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli. ESBLs are enzymes that hydrolyze most beta-lactamase antibiotics, including penicillins, cephalosporins, and monobactams. On the other hand, blood cultures turned negative. Seven days after surgical debridement, the antibiotic regimen changed, based on the antibiogram. In collaboration with the department of infectious diseases of the hospital, therapy with intravenous meropenem and high dosage of tigecycline was initiated. The patient received a loading dose of 200 mg tigecycline followed by 100 mg every 12 hours in combination with 2 g meropenem every eight hours.\nSix days after the initiation of the therapy with tigecycline, the patient reported complaints of abdominal pain and nausea. No vomiting was referred. Liver function tests, as well as heart function tests and electrocardiogram (ECG), were normal. The abdominal ultrasonography did not reveal any abnormal findings besides the size of the spleen, which was at the upper normal limits. The symptoms subsided with the administration of proton-pump inhibitors (PPIs).\nFourteen days after initial tigecycline dosage administration, spontaneous swelling appeared on the left knee. Although systemic inflammatory markers and the patient's general condition were improving, the swelling of the joint progressively worsened within the next two days, despite ice therapy (Figure ). Simultaneously, a prolongation of the activated partial thromboplastin time (aPTT) and the international normalized ratio (INR) was noted, along with a vast decrease of fibrinogen (FIB) levels. On the other hand, the platelet count slightly decreased but remained in the normal range, over 150 X103/μL. Liver function blood tests were also normal.\nJoint aspiration was performed and 120 mL of blood was drained. The aspirate was sent for culture and sensitivity. Administration of low molecular weight heparin (LMWH) was interrupted. Fluid cultures were negative. Lack of platelet consumption, the good general condition of the patient, and an improvement in inflammation markers led us to rule out other causes of hypofibrinogenemia such as disseminated intravascular coagulation (DIC) and sepsis.\nHypofibrinogenemia worsened 18 days after the initiation of tigecycline treatment, with fibrinogen (FIB) reaching 158 mg/dL, aPTT 54.3 s, INR 1.78, CRP 11.8 mg/L, platelet count 181 X103/μL, white blood cell count (WBC) 4.3 x103/μL, haemoglobin 9.1 g/dL, and normal liver function tests. The hemarthrosis of the knee worsened, and the patient complained of severe pain of the joint. It was suspected that tigecycline was the causative factor of the hypofibrinogenemia that led to severe hemarthrosis. The antibiotic was discontinued, and the new antibiotic regimen consisted solely of intravenous administration of meropenem. During the next three days, eight fresh frozen plasma units were administered, along with vitamin K and 1 g of intravenous tranexamic acid. Following the discontinuation of tigecycline, the coagulation disorders became normal through the next six days. The fibrinogen levels reversed to the normal range (Table ).\nThis improvement was consistent with our initial hypothesis that tigecycline caused the coagulation disfunction. Despite the gradual improvement in hypofibrinogenemia, the severe hemarthrosis had to be surgically treated. The joint had to be debrided in the operation room 10 days after the discontinuation of tigecycline, as blood accumulation could not be aspirated because of blood clots. About 500 mL of clotted blood was obtained after the surgical debridement and no obvious site of hemorrhage was revealed (Figure ). No recurrence of hemarthrosis during hospitalization was observed. |
A 64-year-old-woman with no respiratory symptoms was referred to our hospital with a left lower lung mass detected in a chest X-ray during a routine health examination. She was a never-smoker and had no history of any medical conditions, except for pulmonary tuberculosis that had been cured by medication 15 years previously. The chest X-ray revealed a mass approximately 3 cm in size, which was located in the left lower lung field with a well-defined border (). The chest computed tomography (CT) revealed a 4×3-cm mass that was lobulated but not infiltrating the surrounding lung parenchyme in the left lower lobe mediobasal segment. The mass was homogenous with minimal necrotic findings in a small portion and was not enhanced upon contrast enhancement (). No abnormality was revealed by the bronchoscopic gross and cytological examination. The blood test and the tumor marker study were normal. The positron emission tomography (PET)/CT revealed that the maximal standardized uptake value (SUV) was 6.7 in the left lower lung mass without mediastinal lymph node uptake (). On the basis of the above examinations, we suspected lung malignancy that was in the operable stage; therefore, we planned surgical wedge resection biopsy and lobectomy if malignancy was confirmed. In the operation, the mass was resected by wedge resection with stapling and was diagnosed as adenocarcinoma upon a frozen section examination. Therefore, the patient underwent lobectomy, and the postoperative course was uneventful. Histopathologically, mixed squamous and mucin-secreting glandular epithelium covered the fibrovascular cores. In the focal area, mucin-secreting glandular epithelium showed a complex structure. Further, acantholytic squamous epithelial nests were mixed with mucin-filled epithelial cells with neutrophil and lymphoplasmacytic infiltrates (). Immunohistochemically, the tumor cells were positive for cytokeratin (CK5/6 and CK7) and p63 (). The Ki-67 proliferation index was less than 1%. These findings of the histopathological examination and immunohistochemical stain were compatible with mixed squamous and glandular papilloma. During the 18 months of follow-up, the patient has remained well and has not reported any medical problems. |
A 36-year-old Caucasian woman was evaluated with chief complaint of gluteal pain radiating to her leg. Her medical history was remarkable with gunshot injury to the affected leg with multiple pellets dispersed into her pelvis and proximal part of the thigh, as shown in Figs. and . She had gunshot injury 20 years ago. She was previously diagnosed as having lumbar disc herniation at L4–5 level. She underwent a previous discectomy outside our institution 2 years ago. A radiological examination revealed the presence of recurrent disc herniation, as well as multiple shotgun bullets in her pelvis and thigh. One of those bullets was deep into the sciatic nerve inside her quadratus femoris muscle.\nElectromyography (EMG) showed the presence of chronic sciatic nerve injury. Since it was clinically impossible to distinguish lumbar disc herniation from the sciatic injury, we decided to proceed with removal of the foreign object and neurolysis of the sciatic nerve followed by L4–5 discectomy and fusion. We decided to perform those procedures in two different settings. The first surgery included access to the sciatic nerve in the upper portion of her thigh and exposing the nerve fibrotic bands around the nerve. The dissection proceeded deep into the nerve within a muscle, where a bullet was found and removed. The distance from the bullets to the nerve was approximately 2 cm. Muscle tissue around the bullets was excised for analysis. For comparison, another specimen was obtained from the gluteal muscle, superficially away from the nerve and all the bullets. Two weeks later, she underwent scheduled L4–5 discectomy and fusion. Her postoperative course was uneventful. On follow-up examination at 6 months, she was essentially symptom free.\nA scanning acoustic microscope (AMS-50SI) developed by Honda Electronics (Toyohashi, Japan), whose schematic setup is shown in Fig. , was used in AI mode. It has a transducer with quartz lens, a pulser/receiver, an oscilloscope, a computer, and a display monitor. An 80 MHz transducer is installed within the microscope, which generates the signals and collects the reflected acoustic waves. Water is the coupling medium between the quartz lens and the substrate. For two-dimensional scans, an X-Y stage, controlled by a computer, is used. An oscilloscope analyzes the reflected signals from both the reference and target material after being collected by the transducer. As a result, acoustic intensity and impedance maps of the region of interest with 300 × 300 sampling points are obtained.\nThe principle of SAM in AI mode is demonstrated in Fig. . Distilled water is widely used as reference. The signal reflected from the target is\nwhere, S0 is the generated signal by the 80 MHz transducer, Ztarget is tissue’s AI and Zsub is the polystyrene substrate’s AI (2.37 MRayl). The tissue’s AI is calculated by combining the reflected signals from the tissue and the reference. The signal reflected from the reference iswhere Zref is the AI of water (1.50 MRayl). Then, the target’s AI is written aswith a constant signal S0 [] generated by the transducer.\nElectron microscopy-based imaging and chemical analysis studies were performed in a JEOL JIB-4601 focused ion beam scanning electron microscope (FIB-SEM) multi-beam platform coupled with an Oxford X-MaxN EDS system, as shown in Fig. .\nBlood samples were collected in test tubes containing ethylenediamine-tetraacetic acid (EDTA) and no anticoagulant on the day of the first surgery (foreign object removal) prior to the procedure. Then, 2 ml of 20% trichloroacetic acid (TCA) was supplemented into the blood samples to release the red blood cells (RBC) and other ingredients. The supernatant part was received from blood with TCA by centrifugation at 4000 revolutions per minute (rpm) for 20 minutes for the analysis of Pb and cadmium (Cd) within total blood. Coagulation of blood samples enabled serum trace element analysis: chromium (Cr), Fe, Cu, magnesium (Mg), manganese (Mn), selenium (Se), and Zn. The serum specimen was prepared using Hettich Universal centrifuge by centrifugation at 3000 rpm for 15 minutes, separating from cells immediately after and storing at − 20 °C until the analysis [].\nAfter weighing the left sciatic nerve tissue samples, they were digested with 2 ml of 65% nitric acid (HNO3) at 180 °C in the incubator for 1 hour. Then, 2 ml of 65% perchloric acid (HClO4) was added into the cooled mixture. Then, the mixture was digested at 200 °C in the incubator until the volume was halved. Digested materials were vortexed and diluted in water to a total volume of 10 ml. Concentrations were given in micrograms per gram (μg/g) wet tissue weight [].\nAll glassware were maintained at 10% (volume/volume; v/v) HNO3 before use, cleaned with deionized water, and dried in an incubator at 100 °C overnight. Pb, Cd, Cu, Cr, Fe, Mn, Se, and Zn elements were detected by inductively coupled plasma optical emission spectrophotometer (ICP-OES 6000, Thermo, Cambridge, United Kingdom). Measurements for each element were done three times and averaged. The ICP-OES was operated with argon carrier flow rate of 0.5 L/minute, plasma gas flow rate of 15 L/minute, sample flow and elusion rate of 1.51 L/minute, and peristaltic pump speed of 100 rpm, selecting the suitable wavelength for Pb, Cd, Cr, Cu, Fe, Mn, Se, and Zn, which were 220.353 nm, 228.802 nm, 267.716 nm, 324.75 nm, 285.213 nm, 357.610 nm, 196.090 nm, and 206.200 nm, respectively. Transport lines were obtained using 1.25 mm internal diameter polytetrafluoroethylene tubing. Element levels were indicated in micrograms per deciliter for serum (μg/dl) and μg/g for wet tissue. The standard concentrations for standard graph calibration were arranged from standard stock solutions of 1000 μg/ml for each analyzed element [].\nThe tissue samples were investigated by using AI mode of SAM. Figure shows the AI map of the tissue obtained away from the gunshot. The map was constructed by collecting the reflections of acoustic signals, generated by the transducer within SAM, from surfaces of the reference (water) and the tissue sample on the polystyrene substrate. At specific locations within the sample, the AI was calculated to be higher than 2 MRayl, indicating accumulation of elements with different elastic properties. Figure shows the AI map of the tissue obtained close to the gunshot. As can be seen in this image, almost everywhere had an AI of greater than 2 MRayl.\nSEM images of the tissue far away from the gunshot were obtained at magnifications of 5000 × and 500 ×, as shown in Figs. and , respectively. Similarly, SEM images for the tissue close to the gunshot were obtained at magnifications of 5000 × and 500 ×, as shown in Figs. and , respectively. The images were acquired at 5 keV energy for both tissue samples.\nThe SEM images show that the tissue far away from the gunshot keeps its original structure, whereas the tissue close to the gunshot seems to be deformed and torn up. These results demonstrate the degree of damage the impact of gunshot causes on soft biological tissues.\nTable represents the EDS measurements in SEM, carried out for determining the elemental distribution differences in the deformed tissues. The measurements show the percentages of the residue elements detected on tissues far away from the gunshot and close to the gunshot. According to the results, among all residue elements, Pb, Cr, Fe, and Mn are found to be higher in weight content in the region close to the gunshot, when compared to distant region. Cd and Cu levels do not differ much; however, Zn level is lower in the tissue close to the gunshot.\nWe determined Pb, Cr, Cd, Cu, Fe, Mn, Zn, and Se levels in both tissue samples. Pb, Cr, Fe, Se, and Mn levels were higher in the tissue close to the gunshot, conversely, Zn level was lower in this sample (Table ). Blood Pb and blood Cd, and serum Cr, Cu, Fe, Mn, Se, and Zn levels of our patient were also analyzed and the results are shown in Table , however, we did not observe significant differences when compared to reference values. |
A 48-year-old Polynesian, morbidly obese female with a BMI of 82, history of HTN, hyperlipidemia, obstructive sleep apnea and diabetes type II presented with 2 years of hoarseness. Her medications included Lipitor, Lasix, Indocin, Glucophage, Prilosec, Lantus, Humalog and Lisinopril. She had a 5-year pack per day smoking history as well as an 8-year use of crystal methamphetamine. Physical exam by the patient’s primary care physician revealed a small left upper neck mass. She underwent a thyroid ultrasound with FNA biopsy of the mass, which revealed papillary carcinoma of the thyroid. Flexible laryngoscopy revealed narrowing of the patients pharynx related to obesity and limited mobility of the left arytenoid. A preoperative CT scan of the neck revealed two large left peri-jugular lymph nodes with central necrosis. The patient underwent total thyroidectomy with left jugular lymph node dissection. A large tumor was noted at the superior pole of the left lobe of the thyroid, which extended into the tracheoesophageal groove causing damage to the left recurrent laryngeal nerve. Two large abnormal lymph nodes found just lateral to the jugular vein were positive for metastatic papillary carcinoma.\nAt the time of surgery, the patient weighed 510 pounds. Postoperative radioactive iodine therapy and whole body scan as well as external beam radiation therapy were recommended, however, was deemed unsafe for the patient due to the size limitations of the scanner. Eight months of strict diet regulations by endocrinology yielded a weight loss of 30 pounds and a patient who was still above the scanner capacity. She was ultimately referred to the bariatric surgery clinic and lost another 45 pounds during her 7-month preoperative phase. The patient’s weight on the day of her gastric bypass surgery was 421 pounds. Within 2 months, the patient lost 70 pounds and underwent bilateral jugular lymph node dissection for recurrent disease. Within 6 months, the patient weighed 314 pounds and was able to undergo radioactive whole body iodine scan, which revealed residual thyroid tissue in the left side of her neck. She underwent subsequent left radical neck lymph node dissection and debulking of a mass in her posterior triangle. |
A 74-year-old female presented to the emergency department (ED) with upper abdominal pain and melanotic stools. She had an elective open juxtarenal abdominal aortic aneurysm repair a month before her index presentation. She was hemodynamically stable. Her pertinent initial labs showed a hemoglobin of 6.7 g/dl (baseline 9.6 g/dl) with a hematocrit of 23%. Patient did not have any fever or leukocytosis. A CT abdomen with contrast done in the ED for abdominal pain showed nonspecific findings, i.e, irregularity of the “aneurysmal sac” with a small amount of fluid around the sac (see ) which was read by the radiologist as early postsurgical changes. She was admitted and was started on proton pump inhibitors. An esophagogastroduodenoscopy (EGD) was performed that revealed mild duodenitis. Her hemoglobin remained stable the next couple of days, and she was discharged home with a 6-8-week course of proton pump inhibitors. Two months later, she presented again with similar complaints with a drop of hemoglobin. A repeat EGD was performed that did not reveal any obvious source of bleeding, and she was discharged home after stabilization.\nA month later, she came for the third time into the ED with abdominal pain, hematochezia, and profound hypotension. Her pertinent laboratory findings include leukocytosis, low hemoglobin and hematocrit, thrombocytopenia, and transaminitis. She was resuscitated with IV fluids and blood transfusions. She was started on broad spectrum antibiotics after blood cultures were drawn. A CT abdomen and pelvis was performed which showed tiny foci of air at the anterior aspect of the native aneurysm wrap just inferior to the location where duodenum crosses (see ). At that time, a decision was made to perform push enteroscopy instead of simple EGD to evaluate second and third portion of duodenum which showed an aortoduodenal fistula with infected graft adherent to the bowel wall and extruding purulent exudate (see ). She underwent emergent surgical excision of the infected graft and bypass grafting to restore vasculature. Her blood cultures and cultures from the graft revealed methicillin-resistant Staphylococcus aureus (MRSA) and Streptococcus agalactiae. Aggressive management was continued with proper antibiotics in the intensive care unit, but her condition deteriorated, and she expired within several days. |
A 37 years-old unmarried premenopausal female presented in the emergency of our hospital with complaints of bleeding from ulcerative lesion in the left breast for a couple of hours. The patient had history of ulcer in the left breast for past 2–3 weeks which developed over the underlying huge breast lump. The lump was present for past 5 months but rapidly grew over the last 3 months to current size. There was no history of coagulopathy, trauma, chronic liver disease or history of similar illness in first degree relatives. The patient attained menarche at the age of 15 years. She is a non-smoker and denies history of contraceptive use or alcohol intake.\nOn examination in our emergency there was severe pallor with tachycardia. However the blood pressure was maintained. There was an oozing ulceration in upper outer quadrant of the left breast with underlying huge lump measuring 15 × 15 cm occupying the upper outer, lower outer and upper inner quadrants with deformed shape of the breast (a). The skin surrounding the ulcer was erythematous and edematous. Axilla did not show lymphadenopathy.\nBefore the development of breast lump, the patient had itchy lesion at the same site. The patient unfortunately attributed all these events to that itchy lesion and sought help late. There was no history of headache, shortness of breath, abdominal distension or bone pain.\nOn investigating the patient, she was severely anemic with hemoglobin of 5 gm% with normal total and differential counts. Coagulation parameters and liver function tests were normal. Chest X-ray showed no evidence of metastasis other than dense breast shadow on left side due to huge breast lump(a).\nMammogram revealed homogeneous radiodense lobulated mass occupying whole of left breast with subcutaneous thickening on the background of dense breast (b). Ultrasound (USG) of abdomen and pelvis did not reveal any abnormal findings. Trucut biopsy from the breast mass showed necrotic areas with fibrocollagenous tissue with proliferation of oval to elongated spindle cells showing mild degree of atypia.\nAfter discussion about the possibility of metaplastic versus malignant phyllodes tumor, the patient underwent modified radical mastectomy (MRM). Histopathological examination showed maximum tumor size of 14 cm with increased stromal cellularity, loss of stromal-epithelial balance and frequent mitoses more than 45 per 10 high power fields () typical of malignant phyllodes. All the resected margins, nipple and areola were free of tumor. Lymphovascular and perineural invasions were not identified. Seventeen axillary nodes retrieved were free of tumor.\nPostoperatively patient gained weight and was doing well. Three months after surgery, the patient started developing progressively increasing headache, nausea and vomiting for which she got admitted in our center. There was no local recurrence. However on further investigations, she had a huge cystic lesion with mural nodule in her brain (b,c,d). Contrast enhanced computed tomography (CECT) of chest, abdomen and pelvis showed lesions in lower lobe of left lung (a) of size 3.9 × 3.6 cm of +40 Hounsfield unit (HU) in posterobasal segment and right adrenal gland () of 5.8 × 5.1 cm of +30HU with significant enhancement in post-contrast images. Functional evaluation for the adrenal mass with urinary metanephrines and serum cortisol was negative. Patient refused biopsy from right adrenal gland and lung, but while preparing for burrhole biopsy from brain, patient succumbed to the disease. The patient underwent serial ultrasound of abdomen and pelvis during hospital stay which showed increase in size of 4 cm of adrenal mass in 15 days (tumor velocity). |
We present the case of a female born with birth weight 3.300 g by cesarean delivery in the 38th week due to labor dystocia after uneventful first pregnancy of a healthy 26-year-old (y-o) mother without addiction or continuous use of medication. Non consanguineous father; absence of neurological disease in the family. Left-hand was dominant. There was normal neuropsychomotor development until 5 years of age, when marked learning difficulties were observed at school. At 8 years, KS was diagnosed due to characteristic phenotypic traits such as eversion of the lower eyelid, elongated eyelid closure, arched eyebrows, long eyelashes, nasal tip facing down, high palate, and large and protruding pinna and fingertips with fetal aspect []. Furthermore, she had moderate conduction hearing loss and mild scoliosis, and scored 51 points on the intelligence quotient (IQ) test. Ophthalmologic evaluation was normal. At age 15, she had an unexplained episode of transient global aphasia with no trigger history of infection, cranial or cervical trauma, or pain. After referral to our service, the patient showed improvement of the transient deficit, presenting preservation of language (though with poor content, due to cognitive impairment). Physical examination did not detect motor deficit or other focal alterations. Magnetic resonance imaging (MRI) of the brain showed a hyperintense lesion in right posterior white matter, as shown in . A Doppler ultrasound of cervical vessels suggested severe right internal carotid artery (ICA) stenosis. A brain computer tomography demonstrated a bilateral patent carotid foramen, indicating a noncongenital ICA occlusion []. Digital subtraction angiography (DSA) showed right ICA occlusion at the bulbar portion, with compensatory perfusion of the ipsilateral hemisphere through anterior communicating artery, external carotid artery, and temporal branches anastomoses from the posterior circulation [], suggesting ICA dissection. Investigation of cardiologic and thrombophilic diseases were negative; her mother did not allow biopsy due to surgical risks (mainly visuals). Oral acetylsalicylic acid (ASA) was taken for 6 months, and no further treatment was recommended. Follow-up was done with MRI every 6 months to evaluate white matter, which did not show growth and pattern change, ruling out demyelinating, inflammatory, or neoplasic disease, and supporting primarily diagnostic hypothesis of gliosis. On 2-years follow-up, 3D-CTA identified complete spontaneous recanalization of ICA []. No other intercurrence was observed on the long-term follow up, but at age 16 a benign polyp of the gallbladder was removed.\nResearch was performed using PubMed database on articles published before 2016 September, using the following MESH terms: Kabuki syndrome, Kabuki makeup syndrome, Kabuki make-up syndrome, Kabuki make up syndrome or Niikawa-Kuroki syndrome combined with stroke, brain ischemia, brain hypoxia–ischemia, transient ischemic attack, cerebral infarction, carotid artery stenosis, carotid stenosis narrowing, vascular malformation, vascular anomaly, carotid arterial diseases, carotid arterial injury, or dissection. Only articles in English, Spanish, or Portuguese were included. A few articles met the review criteria.[] Other articles were included by decision of the authors aiming to improve discussion. |
A 19-year-old male presented in the emergency department with one episode of melena per day, for one week. It was associated with vomiting, shortness of breath and palpitations. His hemoglobin level on initial complete blood count was 5.80 g/dL, signifying severe anemia according to WHO guidelines []. His lab parameters on admission are presented in Table .\nImmediately packed red blood cells (RBCs) were requested from the blood bank. On forward typing his blood group was labeled as O positive and his serum showed strongly positive indirect Coomb’s test with a negative direct Coomb’s. On extended 11 cell panel antibody testing, his serum demonstrated pan-agglutination which matched with monoclonal panel cells having anti-Kell, anti-Lub, and anti-Kpb antibodies. On cross match with four O negative and four O positive packed RBCs, +4 incompatibility was seen with all. Meanwhile a detailed history of the patient revealed two distinct episodes of epistaxis in childhood and a family history of his paternal grandmother having an increased bleeding tendency. In view of his past history of fresh frozen plasma infusions, it was interpreted that the patient may have multiple alloantibodies in blood leading to gross incompatibility. Considering the urgency of the situation, one unit of the least incompatible (O negative) packed RBCs was issued after washing with normal saline thrice, to the emergency department. Transfusion was started under strict monitoring by the emergency department physicians. After slow transfusion of around 10 ml blood, the patient started shivering and his temperature spiked to 101°F with tachycardia and hypotension. The transfusion was stopped immediately and the patient was given intravenous antihistamine and hydrocortisone. Meanwhile, he was transferred to the intensive care unit (ICU) where he received intranasal desmopressin and intravenous factor VIII.\nTransfusion reaction workup revealed a grade 4+ pan agglutination in his serum. During repeat blood grouping, forward typing did not demonstrate any reaction to anti-A and anti-B antisera, like a normal O blood group. However, on reverse typing, his serum showed strong agglutination with group O pooled control cells. His post saline wash incompatibility with O negative red cell concentrate showed minor difference from grade +4 agglutination (pre-wash) to grade +3 clumping (post-wash). A fresh RBCs sample from the patient showed negative direct Coomb’s test, while fresh serum sample remained positive for indirect Coomb’s test. This workup strongly raised the suspicion of Bombay phenotype and his red cells were tested with anti-H lectin, which showed no agglutination. This confirmed his blood group as Bombay phenotype. The reactions observed with Bombay phenotype compared to other blood groups, on forward and reverse typing, are illustrated in Table .\nImmediately, voluntary donor pools were contacted in blood banks throughout the country. Overnight, a donor with Bombay negative blood group was arranged from Karachi. The packed RBCs were airlifted to Islamabad maintaining the cold chain. After crossmatching with recipient’s blood showed no reaction, the donor blood was transfused to the patient. Meanwhile, a distant relative of the patient from a nearby city, with Bombay positive blood group, consented to donate blood at our blood bank. Two days later, another unit of packed RBCs was transfused to the patient. His hemoglobin after two transfusions rose up to 7.40 g/dL. As his melena settled down on supportive therapy, an endoscopy was performed that suggested an underlying hiatal hernia. After surgical consultation, the patient was advised to reduce weight and discharged from the hospital, with a scheduled follow-up visit.\nIn view of the patient’s past medical history and family history, during the follow-up visit, a von Willebrand factor antigen, von Willebrand factor functional activity and factor VIII levels were ordered. His von Willebrand factor antigen level was <2.0%, von Willebrand factor functional activity was <4.0% and factor VIII level was 18.5%, consistent with type 3 von Willebrand disease. The patient and his family were counselled accordingly and referred to the hematology clinic. |
A 62-year-old woman presented acutely with severe sudden onset left-sided abdominal pain and several episodes of diarrhea with blood mixed in with stool. Her past medical history included coeliac disease and hypertension that was well controlled with ramipril 10 mg daily. On admission, observations were: temperature 36.4°C, blood pressure 115/50 mmHg, heart rate 75 bpm, respiratory rate 16, and oxygen saturations of 99% breathing on air. Examination revealed localized peritonitis of the left abdomen, and rectal examination showed altered blood with no stool. A computed tomography (CT) scan of her abdomen and pelvis showed an appearance consistent with colitis involving the transverse and sigmoid colon, the distribution suggesting ischemic colitis. She was initially managed conservatively with analgesia and intravenous antibiotics. Flexible sigmoidoscopy the following day showed an ischemic splenic flexure, and the decision was made for the patient to undergo a laparotomy. Preoperatively, the patient remained normotensive.\nOn the second day of her admission, the patient was taken to theater for a laparotomy. A low thoracic epidural was attempted for postoperative pain relief; however, the procedure was abandoned after one attempt due to a dural tap. Consequently, the patient had general anesthesia with systemic opioid analgesia and a rectus sheath block. Intraoperative findings revealed an ischemic left colon and proximal sigmoid colon; therefore, she underwent a Hartmann’s procedure. Intraoperatively, the patient remained hemodynamically stable, with an average blood pressure of 120/60 mmHg. Postoperatively, the patient was commenced on a morphine patient-controlled analgesia for pain relief and was anti-coagulated for the ischemic colitis. Investigations towards underlying conditions likely to have caused the ischemic colitis were also carried out. Screening for presence of the anti-phospholipid antibody, JAK2 mutation, and thrombophilia proved negative.\nPostoperatively, the patient developed an ileus. This was managed conservatively with nasogastric drainage and intravenous fluids. Her blood pressure rose from an average of 150/80 mmHg on postoperative day 1 to 190/80 mmHg on postoperative day 3, despite remaining on her usual dose of ramipril. On postoperative day 3, the patient complained of a frontal headache and “cloudy vision.” The headache and rising blood pressure was initially thought to be due to postoperative pain and dural tap; on postoperative day 3, she was commenced on a second antihypertensive, amlodipine. On postoperative day 4, headache, severe hypertension, and worsening vision continued. Neurological examination revealed no focal abnormality; however, fundoscopy showed blurred discs but no retinal hemorrhages or exudates. The patient was commenced on bisoprolol and underwent an urgent CT head scan ().\nThe CT head scan revealed bilateral areas of low attenuation in the left occipital lobe and to a lesser extent in the right occipital lobe. There were also some patchy areas of low attenuation in the right and left cerebellar hemispheres. There was neither mass effect nor enhancement.\nA subsequent magnetic resonance imaging scan of the head and magnetic resonance venography () showed patchy white matter edema most markedly in the occipital lobes but extending anteriorly to reach the frontal lobes, consistent with PRES.\nDespite these findings, blood pressure continued to be controlled with oral medication. However, on postoperative day 6, the patient developed status epilepticus. Repeat head CT excluded an intracerebral bleed. The patient was loaded with intravenous phenytoin, intubated, and blood pressure was tightly controlled with a mean arterial pressure of 85 mmHg. The patient was extubated the following day. Blood pressure continued to be tightly controlled with regular antihypertensives, and she remained on phenytoin to prevent further seizures.\nThe patient continued to improve and was discharged 21 days postoperatively with blood pressure controlled (systolic readings of 120–130 mmHg) on her usual dose of ramipril plus 10 mg amlodipine daily. The only residual neurological defects that she experienced on discharge were minor visual disturbances and memory problems. |
An 86-year-old man was admitted to our hospital with a 3-day history of acute abdominal pain. The patient had no previous medical history. A physical examination revealed marked right upper quadrant pain with normal bowel sounds. Murphy’s sign was positive. His vital signs were within the normal range. Abdominal ultrasonography revealed an enlarged gallbladder with surrounding fatty tissue inflammation. The blood biochemistry was essentially normal, including C-reactive protein (1.9 mg/dL) and total bilirubin (1.4 mg/dL) levels. An enhanced computed tomography examination revealed an enlarged gallbladder and incarcerated gallstone. Gallbladder wall enhancement was discontinued, and the fundus of the gallbladder was located centrally beyond the round ligament (Fig. ). The round ligament was attached to the right umbilical portion, which was associated with the anomaly of the intrahepatic portal vein system (Fig. ). Magnetic resonance cholangiopancreatography demonstrated the root of the cystic duct, while the middle portion of the cystic duct was unclear (Fig. ).\nWith the preoperative diagnosis of grade II acute gangrenous cholecystitis according to the 2018 Tokyo guidelines or gallbladder torsion, LC was planned. The first port was inserted into the umbilicus, and an enlarged and reddish gallbladder was observed. The gallbladder was swollen; however, torsion was not detected intraoperatively. The second port was placed in the epigastric area, while others were at the right hypochondriac and right lumbar regions. The gallbladder was attached to the left side of the hepatic round ligament (Fig. ). The cystic duct and the cystic artery were located in the normal positions. Severe inflammation and the narrow working space between the epigastric port and the gallbladder made it difficult to dissect Calot’s triangle; however, the cystic duct and the cystic artery were resected after the critical view of safety was confirmed. Due to the severe inflammation, a subtotal cholecystectomy was finally performed. The operative time was 178 min, and intraoperative blood loss was 50 mL. The pathological diagnosis was acute cholecystitis with a mucosal ulcer. The patient was discharged on the fifth day after surgery without postoperative complications. |
A 58-year-old male with a history of hypertension and diabetes mellitus presented to our emergency room. He complained of dysarthria and inability to sit, stand and walk since his awakening. On admission, he was alert and oriented. He was slightly dysarthric. His Mini-Mental State Examination score was 30. He showed neither hemispatial neglect nor disconnection syndrome. Muscle strength of all extremities and the trunk was not decreased. On sensory examination, vibratory sensation was slightly decreased on both feet, which was attributed to diabetes mellitus. Thermal, pinprick and positional sensation was perceived normally in all extremities and trunk. The finger-to-nose test revealed terminal dysmetria in the right arm. However, the heel-to-shin test showed no asymmetry. Rapid alternating hand movement was not disturbed on both sides. Deep tendon reflexes were normoactive without pathological reflexes. He did not show any resting or intentional tremor nor asterixis. When he attempted to sit, he grasped the bed rails only with both hands to pull himself up without using his axial and leg muscles, but retropulsion occurred soon after detaching his hands from the bed rails. When tested lying on the bed, he could maintain his legs elevated for more than 10 s. However, he could not stand by himself unless his caregiver supported him.\nCT of the brain did not show any intracranial hemorrhage. Then, an MRI of the brain was performed and diffusion-weighted imaging showed a high-intensity lesion at the medial frontal lobe on the left side (fig. ). A sagittal section of the double inversion recovery sequence revealed a high-intensity lesion at the cingulate gyrus between the VCA and VCP line and a corpus callosum body (fig. ).\nAfter 3 weeks of rehabilitation, he could keep standing and walk freely without assistance. His gait was not broad-based and the steps were regular in amplitude and direction. However, when standing on one foot and walking in tandem gait, lateropulsion to the right side persisted. With his eyes closed, lateropulsion to the right remained. After discharge, he could return to work, although the slight lateropulsion on tandem gait and standing on one foot persisted even at 1 year after onset. |
A 40-day-old female baby was referred to our division for an abdominal mass that had been diagnosed in another institution. Upon physical examination, she presented a pelvic mass extending to the gluteus and left thigh. Left lower-extremity paralysis was noted. Blood tests showed severe anemia and thrombocytopenia. In the following hours, her hematologic status worsened due to consumptive coagulopathy and the increasing volume of the mass. The CT scan done on admission showed an infiltrating pelvic mass (12 × 8 × 6 cm) extending through the sciatic foramen to the left gluteus and thigh (fig. ). The clinical aspect was pathognomonic of KMS.\nTransfusion, steroids and chemotherapy (vincristine, prednisone, rapamycin and cyclophosphamide) were started immediately. Coagulation parameters were normalized and the patient stabilized. Three months later, regression of the tumor volume (8 × 4 × 3 cm) was observed and interventional treatment became possible. Surgical dissection and ligature of the left internal iliac artery and sacral artery were performed. The main arterial supply of the pelvic mass was then embolized using a gelatin sponge (Spongostan Haemostatic®) under the fluoroscopy guidance of a portable C-arm tube in the operating room. At the control, complete regression of the pelvic mass and its vascularization were seen on the CT scan (fig. ). A clear sensitive-motor improvement was observed.\nThree months later, a second, similar, combined approach for the tumor occupying the left thigh was adopted. Surgical dissection of the left femoral artery and then partial embolization of the remaining tumor using a gelatin sponge (Spongostan Haemostatic) were successfully performed (fig. ). A third selective embolization of the arterial supply of the remaining tumor localized at the left gluteus region was planned for 2 months afterwards.\nA hybrid approach to the contralateral femoral artery was achieved in the angiographic room using Philips Allura flat-panel angiography. The right femoral artery was dissected and a 4-french, valved introducer was placed in the right common femoral artery. The contralateral, left lower-limb angiography done with a 4-french, shaped Cobra catheter (Glidecath, Terumo, Tokyo, Japan) showed the main supply of the hypervascular tumor in the gluteus (fig. ). Using a 2.7-french Echelon (EV3) microcatheter, selective catheterization of the profunda femoris artery feeders supplying the tumor was performed. Angiographic devascularization was achieved under fluoroscopy after injection of 0.8 ml of a nonadhesive, liquid glue, Onyx-18 (ethylene vinyl alcohol copolymer, Micro Therapeutics, Irvine, Calif., USA) (fig. ). Four months after treatment, the patient was stable. |
A.L., male, suffering from type 1 diabetes mellitus since he was 7 years old; the disease was metabolically compensated with stable insulin doses. At the age of 12 he was admitted for abdominal pain and a voluminous mass in right hypochondria was found; he was in good general conditions (32 kg of weight) and remaining physical examination was normal. His insulin requests were: regular insulin 5 IU before breakfast, 10 IU before lunch and 6 IU before dinner; NPH insulin 16 IU at bedtime. The liver ultrasound scan showed, at the VI liver segment, two hypo-isoechogenous oval lesions whose diameters were, respectively, 83 × 43 mm and 77 × 38 mm. CT scan (Fig. ) confirmed the presence of two masses, with an evidence of tumor capsule, that, after contrast injection, were hyperdense in early (arterial) phase and isodense, compared to the remaining liver parenchyma, in venous phase; it also highlighted a central hypodense "scar".\nRoutine blood tests were all normal and the detection of serological markers of HAV, HBV, HCV, HIV and CMV was negative: CEA and αFP were also negative. On the basis of the mild abdominal pain, and also for a formal request of parents, the child underwent surgical intervention: the two masses were completely removed. The gross appearance was that of lobulated, well circumscribed masses, lacking a fibrous pseudocapsule and showing a central scar with fibrous septa running to the periphery and partially demarcating nodular structures. At histologic analysis, both lesions were classic FNH showing a nodular hyperplastic parenchyma with a typical central fibrous scar, containing a proliferation of small bile ducts, irregular tortuous arteries with thickened walls, veins and capillaries. A discrete inflammatory infiltrate filled the fibrous septa surrounding the hepatocytic nodules (Fig. ). The child had a fully satisfactory post-surgery course in terms of metabolic compensation. The outbreak of fever justified a treatment with broad-spectrum antibiotic. After 7 years the child is in good health and no recurrence has been noted. |
A 54-year-old previously healthy male patient developed acute, left upper quadrant abdominal and left flank pain. This pain lasted several hours and then resolved spontaneously. When he was admitted to the hospital, on ultrasound and an abdominal and pelvic CT scan, he was found to have an 8-cm×7-cm×6-cm solid and cystic mass in the left (surrenal area) retroperitoneum containing bone and multiple soft tissue densities (). The tumor had calcification and was not well enhanced. There was no evidence of distant metastasis. The tumor was also examined by magnetic resonance imaging (MRI). We also diagnosed that the tumor originated in the left adrenal gland, because the normal adrenal gland could not be recognized by CT or MRI. The patient had hypertension for which he was taking amlodipine 5 mg daily. However, plasma levels of catecholamines, rennin, aldosterone, adrenocorticotropic hormone, and cortisol were within the normal range. Tumor markers, such as serum alpha-fetoprotein, lactate dehydrogenase, carcinoma antigen 125, neuron-specific enolase, and carbohydrate antigen 19-9, were examined because it was possible that the tumor did not originate from the adrenal gland.\nThe patient underwent resection of the lesion through a flank incision by 11th rib resection. The retroperitoneal dissection was tedious and difficult, but the mass was excised in its entirety (). The left adrenal gland was normal. The resected retroperitoneal cystic mass measured 8 cm×7 cm×6 cm and weighed 153 g (). The final pathological evaluation of the tumor was a mature teratoma without malignant components. Macroscopically, the specimen was a 6 cm ×5 cm ×4 cm fluctuating mass. On incision, cystic material came off and a thinly walled cyst was left. The cyst wall thickness was approximately 1 mm with only some minor excrescents. Histologically, the cystic cavity was lined by ciliated columnar cells () and the excrescents were hyalin cartilage islands under this epithelium with some lobules of seromucinous glands (). No immature elements were seen and the diagnosis was a mature cystic teratoma pathologically. Because these tumors usually represent metastasis from other primary sites, additional imaging with CT of the chest and scrotal ultrasonography was performed. No other primary tumor was identified. Therefore, we diagnosed the mass as a primary retroperitoneal teratoma. After 12 months of follow-up, the patient was free of recurrence. |
A 21 day-old girl was transferred to Samsung Medical Center due to extubation failure. The baby was born at the 35+1 weeks of gestation by emergency cesarean section due to spontaneous rupture of the membranes and premature labor. Apgar scores were 2 at 1 minute and 8 at 5 minutes. When the baby was born, she did not cry and became cyanotic and lethargic. Positive pressure ventilation was not effective, so endotracheal intubation was performed in the delivery room. At birth, weight, length, and head circumference were 2,030 g (25th percentile), 49 cm (75th-90th percentile), and 35 cm (>90th percentile), and she had low set ears. A large patent ductus arteriosus (PDA) was found and ligated 12 days after birth.\nWe conducted osteomeatal unit computed tomography (CT) to find the cause of extubation failure. CT scan showed bilateral choanal atresia, atresia of the left external auditory canal, and stenosis of the right auditory canal (). Thirty-five days after birth, she underwent a repair operation of the choanae, and we tried to extubate again. However, she was reintubated with an endotracheal tube because of sustained desaturation and tachypnea. We considered that the cause of extubation failure was an upper airway problem. She was identified to have postglottic stenosis through laryngomicrosurgery (). Forty-two days after birth, a tracheostomy was performed, and respiration stabilized without respiratory support.\nThe patient had a left aortic arch with aberrant origin of the right subclavian artery on chest CT and minimal left pulmonary artery hypoplasia without focal stenosis on echocardiography. Based on these results, we conducted the ophthalmic examination to identify other features of CHARGE syndrome, and found coloboma in her both eyes. Because she met two out of the three major criteria and two of the five minor diagnostic criteria, we concluded that she had typical CHARGE syndrome.\nWritten informed consent was obtained for a molecular genetic analysis of the CHD7 gene mutation from the parents. Direct sequencing analysis of the CHD7 gene was performed with genomic DNA isolated from peripheral blood leukocytes. As a result, a c.3896T>C (p. leu1299Pro) missense mutation in exon 16 of the CHD7 gene was detected, which has not been reported previously (). A familial study revealed that neither of the parents had the mutation. The polymorphism phenotyping program and the sorting intolerant from tolerant program predicted "possibly damaging" and "not tolerated." The amino acid residue L1299 is highly conserved across different species, and the L1299P variation does not occur in 200 control chromosomes from 100 healthy individuals.\nAfter discharge at 2 months of age, she has been followed up at the outpatient clinic regularly. At present, she is 11 months old and is using a hearing aid because of sensorineural hearing loss. Since she has had recurrent aspiration; thus G-tube feeding is required. Her height was 10th-25th percentile, body weight was 5th-10th percentile, and head circumference was 10th-25th percentile. The patient can sit alone but cannot stand with support. Hypoplasia of both kidneys was identified by abdominal ultrasonography, which was performed at 5 months of age. She has met two of the three major criteria and four of the five minor diagnostic criteria for CHARGE syndrome. |
A 55-year-old man was admitted to the Cardiovascular Surgery Department of our hospital for CAA detected by transthoracic echocardiography (TTE) during a routine physical examination. He had neither symptoms of cardiac diseases such as dyspnea, fatigue, chest distress, angina or arrhythmia nor family history of any cardiac diseases. Physical examination showed his heart rate was 78 beats per minute and the blood pressure was 138/80 mmHg. Grade III to-and-fro murmur was heard over the second intercostal space of his left sternal margin. Electrocardiogram (ECG) showed normal sinus rhythm and no significant ST segment or T wave anomaly was found. Chest radiography showed enlarged heart shadow. TTE demonstrated a giant right coronary artery (RCA) aneurysm with a fistula to the right atrium (RA), and the ejection fraction(EF) was 58% (Fig. a, b). The diameter of the RCA increased to 11 mm. Coronary artery computed tomography (CT) revealed a giant aneurysm (65*48 mm) originating from the distal RCA and draining into the RA (Fig. a, b, c). The results of coronary angiography (CAG) were consistent with the above results. Considering the giant size of the aneurysm, surgery was needed as early as possible. Median sternotomy revealed tortuous and dilated RCA, as well as aneurysmal dilation behind the right ventricle (Fig. a, b); a lateral branch originating from the acute marginal branch (AMB) of the RCA and being connected to the aneurysm. Since the surgery aimed to decompress the aneurysm and eliminate the shunt at the fistula site, identifying the entrance and exit vessels of the aneurysm was of vital necessity. To reduce the blood flow and pressure by closing the entrance vessel as much as possible without causing myocardial ischemia, the proximal RCA was ligated first. But intraoperative ECG monitoring showed elevated ST segment, ischemic myocardium and weakening contraction of the right ventricle (RV). Hence, the ligation was performed 3 cm from the distal end of the AMB. After ligation, no elevated ST segment was found. Transesophageal echocardiography (TEE) showed no ventricular wall motion abnormalities and the aneurysm was obviously downsized. The fistula was then occluded through the RA under TEE guidance in the absence of CPB. First, the guide wire and catheter sheath were inserted and passed through the fistula. Then a 30 mm atrial septal defect (ASD) occluder (BEIJING HUAYISHENGJIE) was applied to achieve maximal closure of the aneurysm (Fig. ). TEE showed the size of the aneurysm was obviously reduced, and no blood flow signals, ventricular wall motion abnormalities or shunt were observed (Fig. c, d). The patient was discharged 9 days after operation. Aspirin and clopidogrel were administered for 3 months. The follow-up revealed favorable outcomes and an improved quality of life for the patient. |
A 64-year-old Caucasian male with a medical history of hypertension and symptomatic bradycardia status-post pacemaker implantation presented to the emergency department with the chief complaint of swelling of the right upper extremity for three weeks. It progressed to a generalized swelling of the right shoulder and right side of the neck, restricting his arm movements. He also voiced the concern of worsening shortness of breath which started with the swelling. He did not report any personal or family history of thrombophilia. There was no previous history of any excessive upper extremity exertion or catheterization in the neck. Vital signs on presentation were a blood pressure of 127/61 mmHg, pulse rate of 79/minute, good volume, regular rhythm with no radio-radial or radio-femoral delay, respiratory rate of 19/min with a saturation of 93% on 3-liters nasal cannula, and temperature of 97.5oF. Physical examination revealed right upper extremity swelling without any sensory or motor deficits, right-sided neck swelling, and right-sided facial plethora. Examination of the contralateral arm, as well as the cardiovascular and respiratory systems, was normal. Biochemical investigations were within normal limits. The patient underwent a right upper extremity duplex ultrasonography which revealed an acute non-occlusive thrombus in the proximal right internal jugular vein (Figure ) and right subclavian vein (Figure ) at the cephalic vein confluence. At this point, Factor V Leiden, anti-thrombin III, protein C, and protein S levels were ordered which were normal. The patient was admitted to the medical ward and an intravenous heparin infusion was initiated. Chest radiography did not reveal any cervical rib, and computed tomography (CT) pulmonary angiography showed no evidence of pulmonary embolism. The swelling improved over the course of two days, and the patient was switched to oral apixaban for anticoagulation. He was discharged on apixaban for six months, and a complete resolution of his signs and symptoms was noted at his three-month follow-up examination. |
A 67-year-old male chronic smoker with medical history significant for chronic obstructive pulmonary disease was admitted for imaging guided biopsy of a 1.2 cm left lower lobe lung nodule found recently on a computed tomography (CT) scan of the chest. The nodule was highly suspicious for primary lung malignancy. The patient was placed in a prone position and lung parenchyma in the posterior lateral left chest was visualized. Under CT guidance, a 19-gauge guide was advanced into the left lower lobe and two separate 20-gauge core biopsy specimens were obtained from the mass. There was no hemorrhage or immediate post procedure complication. However, towards the end of the procedure, the patient started complaining of sudden onset of chest pain and became unconscious. No palpable pulses were identified. A code blue was called and cardiopulmonary resuscitation was begun according to Advanced Cardiovascular Life Support guidelines. The patient subsequently demonstrated ventricular fibrillation which responded to defibrillation shock and epinephrine. The patient had three cycles of chest compressions, one dose of epinephrine, and a shock of 200 J. He was successfully resuscitated and intubated for mechanical ventilation. A CT scan of the chest was obtained immediately after the resuscitation and it demonstrated development of a small anechoic area in the left cardiac ventricle consistent with air embolus (Figure ).\nThe vital signs recorded at the time were as follows: blood pressure of 130/80 mmHg, pulse rate of 90 beats per minute, respiratory rate of 18 breaths per minute, and normal oxygen saturation of 92% on room air. The patient was admitted to the intensive care unit. Bedside transthoracic echocardiogram (TTE) did not reveal evidence of an air embolus. Additionally, no cardiac wall motion abnormalities were noted. The patient remained hemodynamically stable for 24 hours, and he was successfully weaned off from the mechanical ventilator next day and discharged home in a stable condition. |
A 29-year-old woman known to have SLE for 6 years presented to the emergency department with a 5-day history of upper abdominal pain. She described the abdominal pain as dull and crampy, mild to moderate in intensity and localized to the epigastric and right upper quadrant regions. Two days before admission, the abdominal pain became constant and severe, and associated with nausea and vomiting but not associated with positional changes, eating, bowel movements or other factors. There had been no fever, chills, diarrhea, heartburn, hematemesis, melena or hematochezia. There was no history of herbal use, taking any new drugs or ingestion of unusual or undercooked foods and no recent travel or contact with ill persons. She was not known to have drug allergies and had no history of cigarette use, alcohol drinking or drug abuse.\nShe had been discharged from the hospital 2 weeks previously due the intrauterine death of her fetus at 30 weeks gestational age. She had been treated for SLE with low-dose prednisolone, with the addition of azathioprine and hydroxychloroquine and was maintained on pantaprazole as gastric prophylaxis. Her family history was notable for her mother who also had SLE.\nOn physical examination, the patient was afebrile. Her blood pressure was 158/90 mm Hg, pulse rate was 117 beats per minute, respiratory rate was 22 breaths per minute and oxygen saturation was 97% while breathing room air. The patient appeared to be in severe pain, with a pain score 8/10, and there were no jaundice, pallor, skin rash or mouth ulcers. The lungs and heart sounds were normal. Abdominal examination yielded right upper quadrant tenderness with no guarding or rebound tenderness, normal bowel sounds and no palpable organomegaly or masses. Results of the remainder of the complete multisystem examination were unremarkable.\nLaboratory studies revealed the following: serum sodium 132 mmol/L, potassium 4 mmol/L, and creatinine 54 μmol/L. A complete blood cell count revealed a hemoglobin level of 103 g/L, mean corpuscular volume 90 fL, mean corpuscular hemoglobin 30 pg, a white blood cell count of 10.8×109/L, an absolute neutrophil count of 9×109/L, lymphocyte count of 1×109/L, and an eosionophil count of 0.2×109/L, and a platelet count of 39×109/L. The hemolysis markers were normal. Serum iron saturation was 30%. Prothrombin time was 9.9 sec, partial thromboplastin time 34.2 sec, international normalized ratio of 1.1 and the fibrinogen level was normal. Serum liver biochemistry results showed a total bilirubin of 23.6 μmol/L and a direct bilirubin of 13.1μmol/L, alkaline phosphatase of 161 U/L, aspartate aminotransferase of 354 U/L, alanine aminotransferase of 429 U/L, albumin of 37 G/L. Serum amylase was normal. Stool examination for ova, parasites, and occult blood were negative. Urine analysis was normal. The erythrocyte sedimentation rate was elevated 125 mm/h. The complement levels were normal. Serologic studies revealed a positive antinuclear antibody test of 123.7 units and anti-ds-DNA test 200 units. Anti-SM, anticardiolipin antibody, antimitochondrial antibody, and anti-smooth muscle antibody were all negative. Immunoglobulin G was elevated at 26.5 g/L, and immunoglobulin M was normal. Viral hepatitis B and C screening tests were negative. The thyroid function test, vitamin B12 and folate levels were all normal. A chest radiograph, electrocardiogram and serum cardiac enzymes were all within normal limits. A computed tomography scan of the abdomen showed a normal liver size with multiple irregular hypodense lesions, mainly in the right hepatic lobe, which did not show arterial or venous enhancement ()\nThe patient was diagnosed initially with SLE flare up with liver involvement and autoimmune thrombocytopenia. She was started on high-dose methylprednisolone, 1 gram intravenously daily for 5 days, and intravenous immunoglobulin for 3 days. On the second day of management the pain dramaticaly disappeared and the liver enzymes started to improve as well as the platelet count. The patient initially was covered with broad spectrum intravenous antibiotics (pipracillin-tazobactam and metronidazole) due to the possibility of pyogenic or amoebic liver abscess, but since there was no evidence of infection, clinically or by laboratory investigation, and the her condition improved clinically and biochemically in the second day after receiving pulse steroids, the antibiotics were discontinued.\nAn ultrasound-guided biopsy from the liver lesions was non-conclusive, showing mild congestion and chronic mild inflammation with no granulomatous or atypical changes. Results of cultures from blood, urine and stool were negative. Amebiasis antibody was negative. She was discharged in good condition with no pain and normal liver enzymes and platelet count. Discharge medications included prednisolone tablet 40 mg daily and resumption of previous medications. A follow up CT-scan abdomen one month from discharge showed complete resolution of the previous lesions in the liver with normal liver parenchyma. |
Our patient is a 54-year-old Caucasian male with a history of cardiac and pulmonary sarcoidosis, hypertension, premature ventricular contractions (PVCs), and obesity who presented with acute onset right hemianopsia, memory recall difficulty, and alexia without agraphia. He was in his normal state of health and doing yard work when the symptoms began.\nIn the past year, incidental PVCs were found on 12-lead electrocardiogram (ECG) during a preoperative evaluation for dental work. Holter monitoring revealed a 12% PVC burden over 24 hours, indicating an indeterminate degree of ventricular dysfunction. Cardiac evaluation of the PVCs included transthoracic echocardiogram which revealed hypokinesis of the left inferior ventricular wall with an ejection fraction of 35%. Cardiac catheterization for investigation of structural blockages of coronary vessels yielded no significant CAD.\nThese findings were suspicious for an infiltrative process. This hypothesis was supported by cardiac MRI showing sarcoid infiltrates on T2-weighted images and by discovery of noncaseating granulomas on pulmonary node biopsy. He was diagnosed with cardiac sarcoidosis three months after initial presentation. During this time, he showed no clinical symptoms of systemic sarcoidosis or heart failure. An implantable cardioverter defibrillator was placed for primary prevention of arrhythmias secondary to cardiac sarcoid. He was doing well for one year until he presented with stroke symptoms.\nOur patient endorsed decreased vision on the right and described the words on his lawn mower being visible but not readable. He also acknowledged trouble with recalling names and specific events.\nUpon examination, our patient demonstrated normal speech and language. He was asked to write a simple sentence and performed the task without difficulty. When asked to read the sentence, he was unable to do so, representing alexia without agraphia. He showed right homonymous hemianopia. The remainder of the physical exam was normal.\nAt admission, initial computed tomography (CT) scan was negative. Subsequent brain magnetic resonance imaging (MRI) and magnetic resonance angiogram (MRA) confirmed a left posterior cerebral artery (PCA) infarction (). MRA of the neck was unremarkable. The stroke was suspected to be cardioembolic in origin due the PVC burden and reduced ejection fraction of 35% promoting possible thrombus formation. Transesophageal echocardiogram revealed no thrombus or patent foramen ovale (PFO) and supported the previous finding of hypokinesis of left inferolateral ventricular wall (). Hypercoagulable workup was nonrevealing. There was no family history of sarcoidosis or early age stroke.\nBy the time of discharge, our patient's visual symptoms returned to baseline and he was given high dose aspirin and atorvastatin for secondary stroke prophylaxis. Cellcept and prednisone were prescribed for management of sarcoidosis. A LINQ device was placed for continuous ECG monitoring. Lisinopril and metoprolol were maintained for pressure and rhythm control. |
A 46-year-old male deliveryman was admitted to the hospital in March 2018 with a 4-month history of progressive memory impairment. Four months before admission, he developed changes characterized by memory impairment; he could not remember where to deliver. He lost his quick intellect and responded slowly to certain situations. He did not talk much and was unable to say the right words at the right time. One month before admission, his symptoms became worse. He could not calculate correctly and complained of muscle trembling in the limbs. Then, a feeling of heaviness in his legs and double vision precipitated his admission. He had a history of type 2 diabetes mellitus. On admission, the patient was oriented, but his speech was slurred, with a Mini-Mental State Examination (MMSE) score of 14 of 30. He performed poorly on tests of cognitive function. Impairment was greatest for delayed and verbal recognition memory, and executive functions, language, and visuospatial functions were also impaired. Myoclonic jerks of the upper limbs were observed, with hypomimia and parkinsonian gait. During the next 1 month, he became increasingly confused, with difficulty to recognize family members. He acted like a child and needed to be taken care of. He could not wear socks independently and had difficulties putting on different pieces of clothing, but his motor function was normal. While hospitalized, routine hematological and biochemical examinations were normal. A vasculitis screen based on serological markers was negative. Diffusion-weighted imaging performed 5 months after onset did not show specific abnormality. An electroencephalogram (EEG) showed a mild slowing of the background activity, without periodic sharp wave complexes. CSF analysis demonstrated an elevated protein level (550 mg/dl) and increased cell count (17 × 106/L) with a lymphocytic predominance. The results of a thorough infectious workup conducted in CSF and serum were negative. The 14-3-3 protein was strongly positive in CSF. He was homozygous for methionine at prion protein gene codon 129, and prion protein gene sequencing revealed no mutations. A neurological autoantibody panel for serum and CSF revealed no evidence of antibodies to VGKC (LGI1/ Caspr2), GABAbR, GAD65, AMPA1R, AMPA2R, Hu, Ri, Yo, Ma2, CV2/CRMP5, and amphiphysin. However, CSF antibodies to the NMDAR were positive (1:100). In the presence of positive NMDAR antibodies, immunosuppressant treatment with intravenous immunoglobulin (IVIG) was commenced 18 days after admission. After 5 days of intravenous IVIG therapy, his cognitive performance improved, with an MMSE score of 19/30. Unfortunately, his family refused further treatment, and immunosuppressive treatment due to the economic problems, including high-dose intravenous corticosteroids, plasmapheresis, and cyclophosphamide, was discontinued. By 12 months from onset, there was a remarkable clinical improvement, and he only had slight acalculia. Eighteen months after the first neurological examination, he was alert, and the MMSE score was 24/30, during which he was unable to perform the serial-7 calculations. He was able to help his son to do the delivery work. During the follow-up (we followed him every 3 months, and the most recent follow-up was performed in April 2020), he remained in remission without any further treatment. |
A 54-year-old male patient presented with a two-day history of severe left-sided, lower back pain which disappeared with the appearance of left-sided lower limb pain felt deep inside the whole lower limb and described by the patient as intense internal pressure (VAS 8/10). On examination, power was 5/5 with no sensory deficit and normal reflexes. The patient received NSAID painkillers and active bed rest was advised. However, on the patient's insistence, a lumbar spine X-ray and MRI were done which showed mild IVD protrusion. The patient was reassured and sent home. A week later the patient presented to the ER with an 18-hour history of heaviness and difficulty in raising the left foot when walking, with numbness along the lateral part of the leg and dorsum of the foot. The pain was moderate (VAS 5/10). No sphincter-related symptoms were observed. According to the patient, the decreased pain caused the delay in presentation, against the instructions on first evaluation. On examination of the foot dorsiflexion was 2/5 (movement on gravity alleviation) with decreased sensation along the left L5 dermatome. There were normal reflexes and sphincters. The patient underwent immediate, new lumbar MRI which showed a large disc sequester with disc migration. His status was fully explained; he was admitted and underwent microdiscectomy L4/5.\nThe initial back pain lasted for 2 days, mostly caused by stretching and pressure on the weakened annulus fibrosis. This type of pain disappears or decreases once the annulus opens and nucleus pulposus leaks to the spinal or root canal. Initial left lower limb pain is a typical description of painful radiculopathy where mass pressure and inflammatory irritation of the nerve root and dorsal root ganglion cause neuropathic pain. This is different from nociceptive and referred pain types. Dorsal root ganglion hosts the cell bodies of sensory nerves with bidirectional connections (to the periphery and spinal cord). Injury to the nerve root motor fibers causes weakness.\nThe majority of patients with lumbar disc and radicular pain improve with conservative treatment. Surgical indications are acute or progressive motor weakness, sphincter dysfunction, intractable pain not responding to analgesia, and pain affecting patient daily life, not responding to 6 weeks of conservative treatment in the absence of acute surgical indications. In all cases, there should be a correlation between the clinical picture and MRI findings. In the current case, the patient has left L5 nerve root symptoms and signs (dorsiflexion weakness, normal reflexes, and dermatologic radiculopathy). The expected IVD prolapse occurred on either the left posterior-lateral L4/5 or left extreme lateral L5/S1 disc. Although there is a debate about dermatologic sensory distribution in root-originating symptoms and variations in clinical presentation (i.e., the L4/5 disc causing S1 root symptoms via compressing the root in higher position, groin pain with lower lumbar discs due to paravertebral sympathetic ganglion pathway entering at L1 or L2 nerve), we presented the commonly encountered scenarios. |
A 13-year-old girl diagnosed the previous year with CVID in the setting of pneumonia, low serum immunoglobulin levels, and absent antibody responses to immunizations, presented with worsening dyspnea. Whole exome sequencing did not reveal an underlying genetic explanation for the immune deficiency. A chest CT scan at the time of CVID diagnosis revealed only mediastinal lymphadenopathy. She was placed on monthly IgG replacement therapy and did well until she reported gradual worsening of dyspnea over 3 months. The dyspnea first manifested during competitive sports and progressed to an inability to walk up a single flight of stairs. Pulmonary function testing results () showed a restrictive pattern, and she was unable to complete the maneuvers for diffusing capacity of the lungs for carbon monoxide (DLCO). A follow-up chest CT scan revealed mediastinal and hilar lymphadenopathy, peripheral interlobular septal thickening, peripheral consolidation, and ground glass opacities (). Bronchoalveolar lavage obtained by bronchoscopy did not show any evidence of infection. Specific testing included bacterial, fungal, mycobacterial, and viral cultures along with PCR assays for influenza, respiratory syncytial virus, parainfluenza, human metapneumovirus, adenovirus, cytomegalovirus, Epstein-Barr virus, human herpes virus-8, and Pneumocystis jirovecii. She underwent a right lower lobe wedge resection biopsy via thoracoscopy. The biopsy () showed non-caseating granulomatous inflammation with aggregates of small lymphocytes, scattered multinucleated giant cells, scattered foci of organizing pneumonia, interstitial fibrosis focally in the subpleural space but not prominent or diffuse, and airway luminal compromise from adjacent lymphoid hyperplasia, confirming the diagnosis of GLILD.\nShe was treated with 4 doses of rituximab 375 mg/m2 given 4–6 months apart, based on clinical symptoms and pulmonary function testing, and azathioprine 50 mg daily for 18 months as IgG replacement therapy was continued. She responded well to the new therapy regimen with complete resolution of exercise intolerance and normalization of pulmonary function testing parameters (). She also had remarkable improvement of the CT scan abnormalities () with the follow up CT scan after completion of therapy demonstrating resolution of all abnormalities. |
A 25-year-old young woman was admitted to our hospital with intermittent periumbilical abdominal discomfort and pain. She had a history of depression and was otherwise a healthy individual. She complained that the discomfort was ongoing for six to eight months, and she usually rated it three to four out of 10 on the pain scale. There was no association with her menstrual cycle or food nor was there any associated nausea, vomiting, constipation, or diarrhea. There were no alleviating factors but she reported exacerbated discomfort with a strenuous workout at her school. The pain and discomfort were infrequent and usually occurred five to six times per month with a duration of one to two hours of constant brief episodes. It usually resolved spontaneously, and for this reason, she did not pay it much concern. There was no increase in frequency or intensity of the discomfort. She never noticed a fever nor any distention, bloating, or dyspepsia. There was no history of known abdominal trauma. She had no family record of any similar symptoms or history. Vital signs, including blood pressure, heart rate, respiratory rate, and body temperature, were all in normal ranges. However, while the physical examination was negative for tenderness, it revealed a non-specific mass of 5 cm x 3 cm that was palpable in the left upper quadrant. The mass seemed to arise from a deep origin below the abdominal wall; it had a smooth surface without any tenderness. It was freely mobile below the abdominal wall and appeared fluctuant. Blood test results found that the hemoglobin level was 11.6 g/dL (normal range 12 g/dl - 15.5 g/dl), the white blood cell was 10.5 K/µL (normal range 4 /lµ - 11 /µl), the platelet count was 149 K/µL (normal range: 150 K/lµ - 450 K/µl), the erythrocyte sedimentation rate was 5 mm/h (normal range: 0 mm/h - 29 mm/h), and the C-reactive protein level was 2 mg/L (normal range below 3.0 mg/L). Liver function tests, basic metabolic panel, amylase and lipase levels, and urinalysis were all within normal limits.\nContrast-enhanced computed tomography (CT) revealed a non-enhancing intra-abdominal mass (4.2 x 4.3 cm) with a heterogeneous pattern located on a proximal small bowel loop at the mesenteric border (Figures -). CT findings were not supportive to distinguish whether the mass was separated or attached to neighboring vessels or organs. Based on the history, physical examination, and imaging studies, a differential diagnosis of a gastrointestinal mesenteric tumor, stromal tumor, mesenteric hematoma, dermoid cyst, or desmoid tumor were made. Laparoscopy was performed to obtain an accurate visual diagnosis.\nExploration of the abdominal cavity identified a 4 cm mass (Figure ), which originated from the mesentery of the jejunum. The mesentery was shortened because of the location and size of the mass. Segmental resection of the jejunum and its mesentery, including the mass, was performed via a Da Vinci robotic system (Figure ). The procedure was completed with extracorporeal anastomosis of the jejunal segment. Macroscopically, the mass appeared to be a cystic mass of the jejunal mesentery and it measured 4.2 cm x 4.4 cm. The mass was cystic and the walls were pink-tan. The lumen of the cyst was dull trabeculae and demonstrated unremarkable rugal folds without mass lesions. It consisted of large amounts of grumous material and the overall change was degenerative in nature. Culture of the contents were sterile for bacteria, fungal, or tuberculous material. Histopathological examination of the resected tissues revealed a cystic wall that was made up of dense fibrotic tissue with scattered chronic inflammatory cells and lymphoid aggregates. The lesion did not show any significant epithelial lining with focal histiocytic or specific epithelium nor was there any proliferating/dysplastic lining. The final pathological diagnosis was (non-pancreatic) inflammatory pseudocyst. The patient had an uneventful postoperative course. We followed up with the patient in two weeks and again in three months. During the follow-up, the patient reported that removal of the cyst helped her abdominal pain and she improved clinically. |
A 62-year-old white female has a long history of schizoaffective disorder, bipolar type, since age 50, when she was first hospitalized on an involuntary civil commitment. Since then, the patient has had 10 psychiatric hospitalizations, including hospitalization at the state hospital for two years. She has had episodes of manic psychosis and depression. She also has borderline intellectual functioning. Fortunately, she has never had any suicide attempts. She was tried on numerous psychotropic medications including different adequately dosed antipsychotic medications as well as antidepressant medications for an adequate duration to ensure that they were on the therapeutic dose and ultimately, she was stabilized on a combination of clozapine and sertraline. There was no drug or alcohol involvement. Medical history is significant for hypothyroidism, history of basal cell carcinoma status post excision, osteopenia, vitamin-D deficiency, history of simple and complex endometrial hyperplasia without atypia, status post total abdominal hysterectomy and bilateral salpingo-oophorectomy. She is allergic to penicillin. Family history is significant for alcoholism in father and possibly post-traumatic stress disorder. Mother had a “nervous breakdown”. There was a significant family history of psychosis in maternal grandmother, and drug and alcohol abuse in brothers. The patient had a distant relationship with her parents. She was raped three times. In fact, her son is the product of one of the rapes. The patient is single. She has never been married. Due to the severity of her psychiatric illness, the patient has been on government disability benefit for the past nine years.\nThe patient is in treatment at a clozapine clinic at a not for profit outpatient clinic of a hospital system. During one of the visits, she appeared unwell, febrile with a temperature of 99.50 F and white blood cell count of 15.3 x 109/L (reference range: 4.8-10.8 x 109/L). She was a poor historian because of her limited intellectual capacity. She denied any physical symptoms except for leg and knee pain, but with her white blood cell count being elevated at 15.3 x 109/L, she was referred to the emergency room because of clinical suspicion of some severe underlying medical conditions like pneumonia, meningitis or cardiovascular disease. While in the emergency room, her leg was noted to be swollen. A left lower extremity ultrasound revealed extensive left lower extremity (external iliac, femoral, and popliteal) DVT (Figure ). Computed tomographic pulmonary angiography for pulmonary embolism (CTA PE) chest was negative for pulmonary embolism but did show ground-glass opacities compatible with left lower lobe pneumonia (Figure ). She did not have any evidence of phlegmasia cerulea dolens. Her inferior vena cava was patent, and the thrombus did not extend into the common iliac vein on the left. She was subsequently admitted to the medical floor. Diagnostic laboratory tests were taken on admission and on day three (Table ). She was started on a heparin drip. Vascular surgery was consulted, and no surgical intervention was necessary. She has eventually switched to rivaroxaban 15 mg two times a day for seven days and then 20 mg daily with dinner. Pneumonia was treated with a course of ceftriaxone and doxycycline combination which she completed. Due to the extensive DVT without any previous history nor family history of blood clots, COVID-19 was suspected. SARS-CoV-2 test was positive. |
A 65-year-old man presented with an intermittent right upper quadrant abdominal pain of 15 days duration. He was afebrile and had no history of abdominal surgery or trauma. On physical examination, the patient showed mild tenderness of the right upper abdominal quadrant. Leukocytosis was absent. Liver function tests showed transaminase and total bilirubin levels at normal levels, but an elevated γ-glutamyl transferase level (101 U/L). Levels of serum alpha-fetoprotein, carcinoembryogenic antigen, cancer antigen 19-9, and cancer antigen 72-4 were all within their normal ranges.\nAbdominal sonography showed a hypoechoic mass replacing gallbladder lumen and engulfing a gall stone with an indistinct margin between the mass and adjacent liver ().\nUnenhanced and contrast-enhanced arterial- and portal-phase multidetector-row helical CT of the gallbladder was performed under the impression of gallbladder carcinoma. Contrast-enhanced CT scans obtained during arterial- and portal-phases showed a heterogeneously enhanced and markedly thickened walls of the gallbladder body and fundus with an impacted gallstone and subtle, disrupted luminal surface enhancement, which formed a mass (). A second gallstone was also observed in the gallbladder, and intramural calcification was noted (). The mass of the gallbladder showed direct hepatic involvement and a perihepatic extension beyond the gallbladder (). The mass had infiltrated to the neighboring transversus abdominis muscle and gastric antrum with fatty infiltration around the gallbladder and in the greater omentum (). Pericholecystic lymph node enlargement was noted. In addition, hepatic parenchymal enhancement was observed adjacent to the gallbladder in arterial phase CT (), and this was followed by isoattenuation, relative to the normal liver, during the portal phase. As a result of the clinical and radiologic presentation, our impression was of gallbladder carcinoma with direct involvement of adjacent structures with omental seeding. We did not suspect actinomycosis of the gallbladder. Diagnostic laparotomy was then performed. Operatively, the diseased gallbladder was found to be perforated with severe adhesion to liver and greater omentum. Surgical findings initially appeared to be consistent with advanced carcinoma of the gallbladder. However, the intraoperative biopsy of a frozen section revealed inflammation with no evidence of carcinoma. Cholecystectomy was next performed.\nThe cut section of the resected gallbladder revealed that the gallbladder body wall and fundus were diffusely thickened with two gallstones, and had a fibrotic appearance (). Microscopic examination of the thickened wall showed inflammatory cell infiltration with fibrosis and intramural sulfur granules that contained tangled filamentous bacilli compatible with Actinomyces (). There was no evidence of gallbladder carcinoma.\nAfter surgery, the patient was treated with penicillin intravenously for 10 days, followed by oral therapy with amoxicillin for six months with no specific symptoms or abnormal laboratory findings. |
A 35-year-old male was admitted with progressive dysphagia of three weeks duration. He had dysphagia for both solids and liquids. There was no fever or odynophagia. Patient gave no history of ingestion of corrosives, pills or foreign bodies. He did not have cough, dyspnoea orthopnea or paroxysmal nocturnal dyspnoea. There was no history of vomiting, hemoptysis or hematemesis and weight loss. He gave a history of severe upper abdominal pain two months back. Pain occurred following a binge of alcohol and lasted for two days. Pain was relieved by symptomatic treatment from a local hospital. Patient did not have any further episodes of abdominal pain.\nOn clinical examination, the patient was found to be afebrile and the vital signs were stable. He was well built and nourished. There was no pallor, cyanosis, clubbing, jaundice and lymphadenopathy. There was no oral ulceration or candidiasis. There were no stigmata of internal malignancy. Chest examination was normal. Abdominal examination did not reveal any evidence of ascites or pancreatitis. There was no evidence of cranial nerve palsy, proximal muscle weakness or ocular defect. Investigations revealed a hemoglobin level of 13.5 gm%, total leukocyte count of 9800 cells/mm3 and an erythrocyte sedimentation rate of 15 mm/hr. Liver function and renal function tests were normal. Chest X-ray and electrocardiogram were normal. Esophagogastroscopy was performed, which showed stasis at the lower end of esophagus with an extrinsic compression of the lower esophagus. Ultrasound abdomen showed a large cystic lesion in the upper abdomen in close relation to the tail region of the pancreas. Rest of the abdomen was normal. The values for serum amylase and lipase were 734 U/L and 945 U/L, respectively. With these findings, a computed tomography (CT) scan of abdomen and chest was obtain after administering oral and IV contrast [Figures -]. Computed tomography scan revealed a pancreatic pseudocyst arising in the tail region of the pancreas and extending through the diaphragmatic hiatus into posterior mediastinum. The pseudocyst compressed the esophagus and produced dysphagia. |
In 2010, a 14-year-old girl presented with a chief complaint of HMB for 1 year. The medical history reveals umbilical cord bleeding and frequent mucocutaneous bleeding events such as cutaneous purpura and ecchymosis after birth. As she experienced recurrent episodes of severe epistaxis, the girl was admitted to the local hospital several times for medical treatment at the age of five. The patient was diagnosed with GT and occasionally received blood transfusions. One year before her hospitalization at our ward, she experienced menarche with excessive menstrual bleeding that required blood transfusion. Since, her menstrual period always lasted more than 9 days and did not cease spontaneously, a platelet or erythrocyte transfusion (usually more than one per period) was needed to stop the bleeding. The family history revealed that she was the only child from her parents’ non-consanguineous marriage. Physical examination showed no abnormalities, except for generalized pallor. A gynecological examination by speculum showed moderate bleeding and laboratory investigation yielded the following results: leukocytes, 5.0 × 109/L; hemoglobin (Hb), 4.5 g/dL; and platelets, 155 × 109/L. The prothrombin time (PT) and partial thromboplastin time (PTT) were normal. An abdominal ultrasound showed uneven endometrial thickness of 7 mm. The patient first received oral contraceptive therapy for two courses each for 21 day cycles. After a course of treatment, the menstrual bleeding stopped, her anemia symptoms were relieved, and the Hb level rose to 8.8 g/dL. However, the patient repeatedly forgot to take the medicine during the course of therapy and this poor compliance caused irregular vaginal bleeding, ultimately leading to worse academic and social performance with a Hb level of 9.5 g/dL. After communicating with her parents, we offered her an alternative treatment option and placed a LNG-IUS in her uterus under general anesthesia. One month after the operation, her Hb level rose to 10.2 g/dL, menstrual blood volume had significantly decreased with a shorter period and symptomatic relief compared to the preoperative condition when measured using Pictorial Bleeding Assessment Chart Score (PBAC). Five months later, the patient was amenorrheic and no HMB episode has been reported since. An ultrasound examination showed an endometrial thickness of 4 mm, and the LNG-IUS was in a good location. At 2-year follow up after insertion of LNG-IUS, the Hb level was found to be 13.8 g/dL. In 2015, the girl came to our ward to have the exhausted LNG-IUS replaced, and her growth and development were good. |
We report the case of a 32 year-old male patient who presented to our Emergency Department with acute onset of unbearable epigastric pain after severe emesis following food ingestion. The pain was radiating to his chest and back and increases by any movement. Due to severe pain and dyspnea, the patient was unable to lay supine insisted on remaining sitting up for the examination. He had an episode of hematemesis after the start of pain. His medical, family, and psychosocial history were irrelevant. He had no previous surgeries performed. Physical examination revealed an anxious patient who looked pale, and dehydrated. His vital signs were, a temperature of 37.5 C, heart rate of 103 beats/minute, and the rest were unremarkable. Examination of the cardiopulmonary system was unremarkable. Upon examining the abdomen, the epigastric area was tender with guarding in the upper abdomen but soft at the lower part. No rigidity was appreciated.\nHis laboratory investigations showed leukocytosis, WBC was 22 × 109/L. An electrocardiogram was done and showed sinus tachycardia. The chest (Fig. ) and abdominal x-rays (Fig. ) showed tiny air collection in the paraspinal space on the left side above the diaphragm, but no free air under the diaphragm and no evidence of pleural effusion.\nHe was admitted to the Intensive care Unit and underwent CT of the abdomen and pelvis, which revealed air around the distal esophagus with apparent thickening of the wall of the esophagus, the air was noted at the gastroesophageal junction with air bubbles in the gastro-hepatic ligament in the abdomen. A large intramural hematoma is noticed within the gastric fundus and basal infiltration of the left lung. Features were highly suggestive of rupture of the distal esophagus at the gastroesophageal junction with pneumo-mediastinum (Fig. ).\nThe diagnosis of Boerhaave’s Syndrome was made. Intravenous antibiotic and fluid hydration were initiated. With signs of peritonitis, hematemesis, and impending shock, he was intubated and taken for laparoscopic abdominal exploration with the possibility of thoracic exploration. As a result, Thoracic surgery team was consulted and involved in the course of management of the case.\nUpon entering the abdominal cavity, a generous hematoma was identified in the gastrosplenic ligament and filling the left upper quadrant area. No signs were indicating the presence of an abscess collection, nor a mass. Followed by dissecting through the pars flaccida on the right side of the stomach. The left side dissection initiated by cutting the greater omentum using a smart bipolar (Ligasure) device. The left crus of the diaphragm was identified, and the anatomy of the gastroesophageal.\n(GE) junction was elaborated. We identified a 2 cm longitudinal perforation within the lower third of the esophagus at the posterolateral wall (Fig. ). We continued the circumferential dissection of the esophagus, preserving the Posterior Vagus nerve. A 38-French gastric calibration tube was carefully advanced across the GE Junction into the stomach. The edges of the esophageal perforation were cleaned, and primary repair was performed with interrupted 2–0 polyglactin (Vicryl) stitches, (Fig. ). Then, an omental patch was sutured over the perforation area (Additional file 1: Video S1).\nA feeding jejunostomy was inserted to gain enteral access for postoperative nutritional support, and a nasogastric tube was advanced into the stomach under intraoperative guidance. Drains were placed intrabdominal and posterior mediastinal.\nThe patient was then shifted to the Intensive Care Unit. He was kept on the ventilator post-op and extubated the following day. He was kept on antibiotics and was started on jejunostomy feeding.\nOn postoperative day three, he was transferred to the regular surgical floor. Over a week duration, his leukocytosis resolved. On postoperative day 4, the patient was started on a clear fluid diet, which was well tolerated. One week postoperative, a CT scan of the abdomen-pelvis (Fig. ) was performed and confirmed the absence of fluid collections and contrast leak. He was discharged home on postoperative day eight but represented in the emergency room after 2 days with upper back and chest pain that aggravated with respiration. Examination of the chest revealed, left lower chest crepitations. He was afebrile and had a normal leukocyte count. A chest x-ray was done showing pleural effusion, for which he was re-admitted for further management. Upon admission, a repeat CT scan of the abdomen did not show any signs of contrast leakage and confirmed a left basal pulmonary consolidation and minimal left-sided pleural effusion. Pleural tapping with fluid analysis was performed, and he was managed with antibiotics and chest physiotherapy, which facilitated the resolution of the pleural effusion. He was discharged home in good condition after a week of hospitalization.\nHe was reassessed in the surgical clinics and was doing very well with no complains. An upper endoscopy was performed 2 months after the surgery and confirmed normal esophageal and stomach anatomy. |
A 28-year-old female with insignificant past medico surgical history presented with one day of acute onset pain in the periumbilical region that later migrated and confined to the RIF. She had associated intermittent fever, nausea, and loss of appetite. She did not have any urinary symptoms, bowel irregularities, or gynecological complaints. Abdominal examination was performed by two senior surgeons at two different occasions; the same day had findings of guarding and rebound tenderness at RIF. Hematological tests showed polymorphonuclear leukocytosis with left shift. Biochemical tests and urinalysis were normal. Urinary pregnancy test was negative. Abdominal radiographs were unremarkable. USG could not visualize appendix and was inconclusive except for probe tenderness in RIF. CT scan of the abdomen could not be done due to unavailability. A clinical diagnosis of acute appendicitis was made assigning an Alvarado score of 9/10. Laparotomy was performed using the Lanz incision in RIF. Intraoperatively appendix was found to be normal without evidence of inflammation or infection in RIF. In view of symptoms and signs, a possibility of other pathology was thought. Walking the bowel proximally up to 3 feet (1 m) did not show a Meckel's diverticulum or any other small bowel lesions. There were no obvious mesenteric lymph nodal enlargement and pelvic organs looked pristine. Approaching closure, just when the medial edge of the incision was retracted superomedially, a hemorrhagic lesion seemed to appear little deeper in the mid abdomen. Therefore, the incision was extended transversely from the medial edge to explore further. Entire bowel was explored and this revealed an ulcerated lesion measuring 7 × 5 cm arising from the antimesenteric border of the ileum 8 feet (2.5 m) from ICJ with localized interloop hemoperitoneum and inflammatory exudates as shown in . Resection of ileal segment containing the lesion was performed followed by restoration of bowel continuity and peritoneal toileting. The lesion was subsequently reported to be an ulcerated malignant ileal GIST.\nHistopathologically, gross examination confirmed the operative findings, and the cut section revealed a nodular lesion protruding out of the serosal surface measuring 7 × 5 cm along with 2 lymph nodes each measuring 2 × 1 cm.\nMicroscopically, the growth from the ileum had villous lining epithelium with focal ulceration. The submucosal region had a circumscribed nodule with proliferation of loosely cohesive spindle cells; some of which were arranged in vague storiform pattern and others in long fascicles. There were areas with epitheloid cells forming small anastomosing nests and cords. The areas in between these showed skenoid fibers along with focal areas of hemorrhage, infarction, and congestion as shown in . The mitotic figures were seen (8/50 high-power field). The lymph nodes were microscopically identified to be reactive, and the resected margins of the ileum were free of tumor.\nBased on tumor size and mitotic activity, possibility of a malignant GIST was suggested along with immunohistochemical analysis (CD117 and CD34) for further confirmation. The patient had an uneventful recovery and was discharged on the 8th postoperative day. She was advised to review a week later at the outpatients but failed to report. All possible contacts were used to trace her, but she remained inaccessible and lost to follow-up. |
A 45-year-old man presented with a one-month history of progressive back pain and hypesthesia in both L3 dermatomes. There were no motor weakness. He had undergone a right temporo-occipital craniotomy and partial removal of a huge HPC followed by whole brain radiotherapy at other university hospital in 2003 (). He underwent two more craniotomies with recurrent tumors removal at our institute in 2012 and 2013 (). Thereafter, he has been treated by gamma knife radiosurgery three times successfully for local recurrent and residual HPC. Since then, no local recurrence has been found. In March 2016, however, the first extracranial metastasis was found in the L2 vertebral body. Diagnostic workup including thoracolumbar magnetic resonance imaging (MRI), bone scintigraphy and thoracolumbar computed tomography (CT) revealed a solitary L2 body lesion. CT scans showed well demarcated osteolytic mass in the posterior aspect of L2 vertebral body with retropulsion to anterior epidural space (). T1- and T2-weighted MRIs showed an isointense tumor with strong contrast enhancement compressing the spinal cord (). Bone scintigraphy also showed hot uptake in L2 body. In consideration of the patient's relatively young age and a solitary lesion at the L2 body, we planned subtotal en bloc corpectomy and radical removal of the tumor via a transpedicular approach. Angiography performed prior to surgery revealed hypervascular tumor supplied by multiple arteries from the bilateral L2 and right L1 segmental arteries. Preoperative embolization of the feeders was done successfully through a super-selection of bilateral L2 segmental arteries using gelform particles one day prior to surgery. The patient underwent a L2 total laminectomy and radical total removal of the tumor with subtotal corpectomy. At surgery, a gray and reddish tumor filled the L2 vertebral body, which was curetted and drilled out easily under surgical microscope, and the tumor cavity filled with minced autologous bone. There was no invasion of spinal dura mater. Trans-pedicular screw fixation was performed from T12 to L4 to prevent postoperative instability. Postoperative MRI and X-ray showed the tumor was completely removed ().\nHistopathological finding revealed anaplastic HPC [World Health Organization (WHO) grade III] with numerous dilated, staghorn-type vessels with increased cellularity of the hyperchromatic tumor cells with oval nuclei which were surrounded by abundant blood vessels. Hematoxylin and eosin staining of metastatic spinal HPC () revealed more pronounced hypercellularity than intracranial HPC () and it showed increased cellular pleomorphism with mitotic count of ≥5 mitoses per 10 high-power fields in metastatic spinal HPC. Immunostaining of the tumor cells were negative for epithelial membrane antigen and CD34. The Ki-67 proliferation index of metastatic spinal HPC () was more increased by about 10% as compared with the cerebral lesion ().\nPostoperatively, his back pain and hypesthesia in the both L3 dermatomes improved. Adjuvant radiotherapy was not undergone as the postoperative MR images confirmed complete tumor resection. He was discharged without neurological symptoms and has been recurrence-free for the past six months. |
A 27-year-old woman (gravida 5, para 1) presenting with repeated fever and dyspnea was referred from a local hospital to our hospital for retained placenta. The patient had induced labor at 18 + 5 weeks gestation and subsequent curettage for adherent placenta 3 years ago. Ten days before the referral, she had a vaginal delivery at 40 weeks gestation and only partial placenta was manually removed due to placenta adhesion. Curettage was performed and postoperative ultrasound showed intrauterine scattered echogenic foci. In this situation, oxytocin was released continuously. Despite all this, the uterine contraction was good with little vaginal bleeding.\nThe patient developed a fever with a maximum temperature of 40.5°C 3 days later. Gram-negative bacilli were isolated from intrauterine secretion and ultrasound revealed placenta tissue measuring 7.3 × 3.6 × 6.0 cm3 without a clear boundary with myometrium. She was treated with meropenem 0.5 g, 8 hourly for 3 days, but the fever was still out of control. Thus, she was transferred to a superior hospital. Magnetic resonance imaging (MRI) revealed intrauterine placenta residue and partial penetration. Tienam 0.5 g, 6 hourly was used for 3 days and her body temperature raised to 42°C. Moreover, dyspnea was developed and Staphylococcus epidermidis was found in blood culture. Vancomycin 1 g, 12 hourly was added to the anti-infective therapy and continuous low flow oxygen was given. Laboratory result on serum procalcitonin was 1.49 ng/L and white blood cell count was 10.28 × 109/L and hemoglobin 84 g/L.\nIn consideration of deterioration of symptoms, the patient was referred to the emergency department in our hospital. Computed tomography (CT) of the chest revealed pneumonia and pleural effusion. After consultation of the infectious diseases department and the respiratory department, the patient continued with current treatment and was admitted to the intensive care unit (ICU) for further treatment. In the ICU, the patient had an intermittent fever with body temperature fluctuated from 36.5°C to 39.1°C accompanied with cough and dyspnea. Surplus pulse O2 (SpO2) maintained at 92% to 96% with oxygen-induced by nasal cannula at 4 L/min. The coagulation function test performed immediately after entering the ICU showed antithrombin III was 56%, fibrinogen degradation product was 8.6 μg/mL and D-dimer was 2.31 mg/L. Other coagulation parameters such as fibrinogen, prothrombin time and activated partial thromboplastin time were within normal ranges. The blood gas analysis revealed pH was 7.56, PCO2 was 33.75 mmHg, base excess was 7.6 mmol/L and HCO3 was 30.9 mmol/L and suggested a combination of metabolic acidosis and respiratory alkalosis. Hypodense filling defects in the bifurcation of pulmonary artery trunk and right main pulmonary artery, respectively (Fig. A) and pulmonary interstitial edema were found by contrast-enhanced CT. Additionally, pneumonia and pleural effusion were aggravated compared to the old CT image. According to the clinical manifestations, CT image and results of laboratory tests, a diagnosis of PE was established.\nGiven that the severe infection and PE, curettage for placenta residue should be delayed and treatment should be focused on controlling the infection and PE. Therefore, antibiotics continued on current protocol, diuretic and albumin were given and 0.4 mL Clexane was injected subcutaneously 12 hourly. Warfarin (2.5 mg per day) was added to anticoagulant therapy after consultation the next day. The level of the international normalized ratio (INR) was monitored daily. The patient's condition improved. On the fifth day of anticoagulant therapy, warfarin was adjusted to 3.75 mg per day due to INR was 1.13 and no hemorrhagic tendency.\nOn the seventh day in ICU, contrast-enhanced CT revealed disappearance of the hypodense filling defect in the pulmonary artery trunk and reduction in the right main pulmonary artery (Fig. B), alleviated edema and pneumonia and reduced pleural effusion. On the eighth day when the body temperature was within normal ranges for 3 consecutive days, antibiotic was changed to 4.5 g Tazocin, 8 hourly. The SpO2 remained good without oxygen intake. Clexane was stopped and warfarin was used alone. The patient was discharged from the ICU to general wards for continued therapy the next day.\nOn the twelveth day in our hospital, as the patient's condition stabilized, intravenous anti-infective therapy was stopped and oral administration of Cefdinir capsules was prescribed. Mifepristone 10 mg per day orally was started to promote necrosis of residual placenta. Warfarin was continued with 3.75 mg per day. The patient was discharged the next day.\nAfter 1 month of outpatient treatment, rivaroxaban tablets were prescribed instead of warfarin for continued anticoagulant therapy. Another month later, the patient underwent hysteroscopic resection of retained placenta. Postoperative ultrasound demonstrated no abnormalities and her menstruation returned to normal within several weeks. After 3 months of anticoagulant therapy, pulmonary perfusion scan showed normal findings which suggested completed recovery of PE. |
A 65-year-old woman with 4 days of neck and shoulder pain that affected her sleep in addition to left arm numbness was seen in our Pain Management Department. Prior to her arrival, the patient had taken some medications (specific details were not clear), but the pain did not improve and became intolerable. The patient had a history of hypertension that had not been treated regularly, and her highest blood pressure was 180/100 mm Hg. All of the patient's examinations and treatments were approved by the ethics committee of 903 Hospital.\nUpon arrival, the patient's vital signs showed hypertension with a blood pressure of 170/92 mm Hg; her other vital signs were normal. Physical examination showed a normal spine and extremities. There was slight tenderness over the cervical and the corresponding paravertebral area. The Spurling test, Jackson test, and left Eaton test were all positive. Sensation to pain and muscular tension of the extremities were normal bilaterally, and motor strength was grade 4/5 in the upper and lower extremities bilaterally. The biceps and triceps reflexes were normal bilaterally, and the Hoffmann sign was negative.\nWhen she arrived, the patient underwent an MRI scan that showed multiple disc herniation at cervical 3/4, 4/5, and 5/6, and the epidural sac was compressed by the disc herniation (Fig. ).\nThe initial diagnosis was cervical spondylosis and primary hypertension. It was decided to treat the patient conservatively with loxoprofen 60 mg twice a day, nifedipine sustained release tablets 10 mg daily, and an intravenous drip of 250 mL of 20% mannitol daily.\nTwo days later, the patient manifested clusters of tiny blisters along the C4 and C5 dermatome; the vesicular fluid was clear and there was no tenderness, suggesting the patient might have a concurrent acute herpes zoster infection. The antiviral drug famciclovir 0.25 g was started 3 times a day. The next day, the patient under went a nerve block procedure with an epidural puncture at the C7 to T1 space, and a catheter was inserted. The patient received an injection of 3 mL of the following mixture through the epidural catheter: 5 mL of 2% lidocaine, dexamethasone 10 mg, vitamin B1 100 mg, vitamin B6 100 mg, mecobalamine 1 mg, and 2 mL 0.9% saline, total volume 12 mL). The patient was observed for 10 minutes after the injection, and there were no signs of spinal anesthesia; the remaining volume of the mixture was subsequently injected and the catheter was removed.\nThe following day, the patient's pain had decreased and the clusters of blisters were somewhat reduced in size. A second epidural puncture and injection were performed, and the patient received the same nerve block mixture as before. The patient then showered and began to complain of body soreness, slight weakness, and a headache. Bilateral lung wheezing was heard on physical examination, and the patient was given 1 capsule of amoxicillin. However, the patient experienced severe pain of the shoulder, neck, and head accompanied by a low-grade fever (37.8°C), fatigue, and nighttime muscle aches. The patient also fell 1 time on the ward. Blood was tested due to these aggravated symptoms, and the white blood cell count was 24.27 × 109/L, neutrophil percentage was 92.41%, erythrocyte sedimentation rate (ESR) was 66 mm/h, hyperallergic C-reactive protein (CRP) was over 10 mg/L, and general CRP was 193.8 mg/L, suggesting an acute inflammation. The patient underwent a chest x-ray and cervical/thoracic MRI scan and was started on intravenous cefperazone/sulbactam 2 g twice a day and fosfomycin sodium. One day later the patient still complained of severe shoulder pain and headache; physical examination revealed C4 to T8 tenderness and neck stiffness; however, limb strength was normal. The MRI scan indicated epidural inflammation from C6 to T8 and an abscess formation (Fig. ).\nThe patient was moved to the intensive care unit to receive more intensive antibiotic treatment with vancomycin 1 g every 12 hours combined with imipenem/cilastatin sodium 1 g every 8 hours for anti-inflammation. Famciclovir was also changed to gentinovir 0.15 g twice a day for antiviral treatment. The patient's neck and back pain significantly improved after 4 days of anti-inflammation therapy, and the MRI scan showed significant absorption of the abscess (Fig. ). This therapeutic regimen was continued for 17 days, during which the white blood cell count decreased to 5.11 × 109/L, the neutrophil percentage decreased to 57.3%, the ESR decreased to 76 mm/h, the hyperallergic CRP decreased to 4.71 mg/L, and the general CRP was less than 10 mg/L. The patient's neck and back pain disappeared, and the clusters of blisters scabbed over. On physical examination, there was slight tenderness to percussion but no pressing pain or neck stiffness. After 3 weeks of anti-inflammation therapy, the antibiotics were gradually weaned. After over a month of anti-inflammation therapy, the epidural abscess was completely absorbed and the patient was discharged from the hospital (Fig. ). |
A 60-year-old African-American female (77 kg, 167 cm) with no known drug allergies presented to the operating room for emergent thrombectomy. Her symptoms included minimally responsive behavior and acute motor aphasia with right upper and lower extremity weakness. Her medical history was significant for depression, hyperlipidemia, scoliosis, end-stage lung disease secondary to fibrotic nonspecific interstitial pneumonia (NSIP), and World Health Organization Group 3 pulmonary hypertension []. Before her most recent admission for increasing dyspnea, she was a New York Heart Association classes III and IV on home oxygen (8–15 L/min oxygen requirement) and pirfenidone for her NSIP while awaiting lung transplant. In the months prior, she had multiple admissions and was treated with diuresis, steroids, and i.v. antibiotic therapy for similar complaints of worsening dyspnea thought to be a progression of her lung disease in the setting of a pulmonary hypertensive crisis and volume overload.\nThree months prior, the patient was again admitted for dyspnea at rest. Her initial blood, respiratory, and urine cultures were all negative with a decreasing white blood cell count. A transthoracic echocardiography showed borderline left ventricular hypertrophy (60% ejection fraction), stable right ventricular size increases with severely decreased right ventricular systolic function, mild tricuspid regurgitation, and pulmonary artery systolic pressures of 60 mmHg. Computed tomography (CT) angiogram of the chest failed to demonstrate pulmonary embolus or consolidation.\nThe patient was diuresed for 3 days, and her brain natriuretic peptide decreased; however, her oxygen requirement and dyspnea failed to improve. She was started on high dose i.v. steroids for presumed flare of her NSIP and prophylactic i.v. antibiotic coverage against healthcare-associated pneumonia. Eventually, she was transferred to the Medical Intensive Care Unit (MICU) where inhaled iloprost was started for symptomatic pulmonary hypertension, and venoarterial extracorporeal membrane oxygenation (VA-ECMO) diverted from the right internal jugular vein to the right brachiocephalic artery with a therapeutic heparin drip was initiated as a bridge to lung transplant.\nOne week following transfer, these measures were complicated by a decreasing hemoglobin and new onset hemothorax requiring partial thromboplastin time goal reduction. The patient subsequently became subtherapeutic on her heparin drip and developed new onset right upper and lower extremity weakness with a progressing motor aphasia. CT angiogram of the head and neck revealed distal left MCA-M1 occlusion. She was taken for emergent thrombectomy [].\nThe patient was brought to the neurological intervention suite, and standard American Society of Anesthesiologists monitors were attached, a left brachial arterial line was placed for invasive blood pressure monitoring, her high flow nasal cannula was replaced with bilevel positive airway pressure (BiPAP) with inspiratory positive airway pressure/expiratory positive airway pressure set at 20 cm H2O/5 cm H2O, respectively, on 100% FiO2, with proper end-tidal capnography monitoring, VA-ECMO, and the patient's heparin drip were continued throughout, and both of her peripheral i.v. catheters were maintained. Baseline vitals were sinus tachycardia at 102 b.p.m, blood pressure of 155/111 mmHg, respiratory rate of 24, and SpO2 of 91%. A baseline arterial blood gas was drawn demonstrating pH of 7.40, PaCO2 of 65 mmHg, PaO2 of 70 mmHg, and HCO3− of 40.8. Cefazolin 2 g was administered for antimicrobial prophylaxis, and 1 g of levetiracetam was administered for antiepileptic prophylaxis. A propofol drip was started at 30 ug.kg-1.min-1, and a phenylephrine infusion was used to maintain mean arterial pressures (MAPs) between 80 and 100 mmHg.\nBefore infiltration of the right groin by surgical team, a 10 mg bolus of propofol was administered. The patient remained sedated and hemodynamically stable with spontaneous respirations assisted with BiPAP throughout the entire case. During the case, propofol boluses of 10 mg were used to supplement the continuous i.v. infusion.\nOnce the surgical team had mechanically evacuated the patient's MCA clot, the phenylephrine infusion was halted, and a nicardipine drip was titrated to maintain MAPs between 65 and 85 mmHg. Propofol sedation was stopped upon closure and hemostasis of the right groin entry site. The patient was placed back on high flow nasal cannula and allowed to emerge from sedation, where an immediate neurological examination demonstrated improvement in speech as well as right upper and lower extremity strength. The patient was transferred back to the MICU on VA-ECMO, heparin drip, and a nicardipine drip. The patient subsequently was accepted for and underwent a double lung transplant 3 days after her MCA thrombectomy. |
A 73 years old male with a previous history of myocardial infarction, hypertension and hypercholesterolemia presented to our emergency department with generalized abdominal pain, distension and constipation for 1 week. He had multiple previous attendances with the same presentation (five admissions in 8 months), previously diagnosed as sigmoid volvulus and managed with either flatus tube insertion and/or flexible sigmoidoscopy. In all cases, decompression was initially successful with resolution of symptoms and signs of large bowel obstruction. He was discharged home with planned follow-up in the colorectal clinic including discussion for elective surgery to definitively manage the recurrent sigmoid volvulus. Unfortunately, he re-presented before outpatient work-up for surgery was possible. On re-admission, his examination revealed a distended, tender abdomen with stable observations and no evidence of peritonism.\nBlood tests on admission were unremarkable. Each admission, the patient’s plain abdominal films showed dilated large bowel loops consistent with sigmoid volvulus (). A subsequent computed tomography (CT) of the abdomen and pelvis with intravenous contrast revealed dilated large bowel and was reported as sigmoid volvulus with no evidence of perforation (). Caecal volvulus was not appreciated on this scan.\nOn the patient’s sixth admission, the decision was taken for definitive surgery in the form of a subtotal colectomy and ileostomy as he was not responding to conservative treatment despite endoscopic decompression. Intraoperative findings revealed a grossly distended sigmoid and right colon from a 360 degree twist. Mesentery at the recto-sigmoid junction was ischaemic with an ischaemic patch on rectum. Histological findings included congestion, oedema and haemorrhage consistent with the effects of volvulus.\nThe patient recovered well and was discharged on the sixth postoperative day. Unfortunately, he re-presented on day 11 post-operatively with vomiting. A plain abdominal film was consistent with ileus (), which was managed with wide bore nasogastric tube insertion, fluid and electrolyte balance. He was discharged and reviewed in clinic approximately 2 months later, with complete resolution of symptoms and a healthy stoma. He has since been discharged from regular follow-up. |
A 66-year-old obese female with essential hypertension, paroxysmal atrial fibrillation and atrial tachycardia was referred for a transesophageal echocardiogram prior to an elective electrophysiology study and ablation. On physical exam, she was morbidly obese with a body mass index of 37.7. Her cardiac exam was unremarkable with normal S1 and S2 heart sounds and absence of murmurs. The respiratory exam was unremarkable. Blood pressure and peripheral pulses were equal bilaterally. The chest X-ray was unremarkable. Mediastinum was within normal limits. Laboratory studies were unremarkable with the exception of mild normocytic anemia (hemoglobin of 10.2 g/dl).\nTransthoracic echocardiography revealed a normal sized left ventricle with an estimated ejection fraction of 60–65%. The left ventricular wall thickness and diastolic parameters were normal. The right ventricle was dilated but demonstrated normal systolic function. The aortic root, sinotubular junction and ascending aortic diameters were within normal limits. The aortic valve was trileaflet with no significant regurgitation. No other significant valvulopathy was noted.\nThe patient underwent a transesophageal echocardiogram in the EP lab under general anesthesia with endotracheal intubation due to high risk neck anatomy. The study confirmed normal left ventricular parameters and no significant valvulopathy. The left atrial appendage velocity was normal on pulse doppler imaging. There was no LAA thrombus. Evaluation of the descending thoracic aorta revealed an additional echolucent lumen located posteriorly (, ). Color Doppler imaging demonstrated flow directed away from the probe (). Pulse wave Doppler was suggestive of venous flow (). A possible Stanford type B dissection in the descending thoracic aorta could not be excluded. No dissecting flap was noted in the ascending aorta. Additionally, a small sized atheroma was visualized in the proximal descending thoracic aorta. The patient underwent CT angiography for evaluation of suspected aortic syndrome.\nCT angiography showed a normal descending aorta with no evidence of dissection, however it did reveal a dilated accessory hemiazygos vein (, , ). The left internal jugular and left subclavian were stenotic with a string-like appearance and there was an absent left brachiocephalic vein. |
A 27-year-old male underwent left parietal decompressive craniotomy and duraplasty for a vein of Galen aneurysmal malformation with left parietal intracranial bleeding with hemorrhage into the left lateral ventricle. After induction of anesthesia, a right subclavian CVC was placed under ultrasound guidance. Due to pre-operative low Glasgow coma scale (GCS), he was transferred to ICU for mechanical ventilation.\nChest X-ray (CXR) on arrival in ICU showed correctly placed CVC and bilateral clear lung fields. His feeding was started through a nasogastric tube. There was no change in CXR [] on 1st POD. In the evening during transfer for a computed tomography scan brain, he became agitated and started coughing. After that, he remained sedated comfortably. Overnight, his peak airway pressures increased that were unaffected by suctioning of tracheal tube or nebulization with salbutamol and ipratropium bromide. On examination, breath sounds were diminished and percussion note was dull over the right side of the chest. His CXR [] on 2nd POD showed massive pleural effusion on right side and mild on left side. Under ultrasound guidance, about 1400 ml of milky white fluid was aspirated []. Soon after drainage, airway pressures returned to baseline. The fluid was sent for analysis which revealed triglyceride levels of 285 mg/dl which correlates with lymphatic fluid (chyle). Microscopy and culture were negative for infection. Duplex ultrasound was negative for thrombosis in both subclavian veins and superior vena cava. There was normal venous pressure tracing from the catheter and free aspiration of blood from all three ports, but as we suspect chylothorax due to CVC, we removed the catheter. We did not came across such type of case, so we looked at the literature for further management. His enteral feeding was continued and he was observed clinically and radiologically (CXR and ultrasound daily). Due to persistent low GCS, he underwent tracheostomy on the 5th POD. He was discharged from ICU on the 7th POD and from hospital on the 11th POD. |
The second patient died was a 39-year-old female with univentricular heart (tricuspid atresia), who had had previously two cardiac surgeries (the last was atrio-pulmonary Fontan, 33 years earlier). The patient suffered from a serious right atriomegaly with frequent episodes of atrial tachycardia, so she was a candidate for Fontan conversion surgery. Pre-operative ventricular function was mildly reduced (50%). In the post-operative, the patient suffered from severe single ventricle dysfunction resulting in LCOS and the need for ECMO implantation. Both patients could not be weaned from ECMO due to multi-organ failure.\nSeven patients required pace-maker implantation due to post-operative sinus node dysfunction or atrioventricular conduction abnormalities. All patients were discharged on oral antiarrhythmic for 3–6 months and anticoagulants for 6 months. At discharge, 15 patients were in sinus rhythm, 5 had a stable pacemaker rhythm, 2 had atrial fibrillation, and 1 atrial flutter. One patient discharged in sinus rhythm had a pacemaker implant 5 months after the operation due to the presence of sinus node dysfunction.\nDuring a median follow-up of 14 months (IQR 7–27), there was no late mortality and 17/23 patients had an improvement of NYHA functional class. Five patients in NYHA III progressed to class II and 4 to class I; eight patients progressed from class II to class I.\nAt follow up electrocardiogram, 16 patients were in sinus rhythm, 6 with stable pacemaker rhythm, and 1 with permanent atrial fibrillation.\nRecurrence of arrhythmia occurred in 2/23 (8.6%) patients, more than 3 months after surgery. These patients presented at surgical ablation with history of atrial fibrillation lasting 4 and 19 years, respectively, and both had atrial fibrillation, which was treated with right-sided Maze rather than Cox maze III due to technical issues. Sixteen (69%) patients are in stable sinus rhythm, 12 without any anti-arrhythmic therapy. At median follow up of 14 months (IQR 7–27), freedom from recurrence of arrhythmia was 90.9% and cumulative risk of recurrence was 9.6% (). |
A 53-year-old man was referred to the pain management clinic for a 7 months history of intractable thoracic back pain and abdominal pain following surgical resection of a duodenal adenocarcinoma (stage IV). His pain was refractory to all treatments previously tried, with a reported maximal pain intensity of 10/10. His pain did not respond to methadone, hydromorphone, cyclobenzaprine, gabapentin, pregabalin nor lidocaine patches. Previous interventional therapies provided only temporary, if any, relief. These included neurolysis of the celiac plexus, neurolysis of the superior epigastric nerve, 12th intercostal nerve, and paraspinal trigger point injections. Given, his lack of response, the decision was made to move forward with a trial of intrathecal medication in preparation for a possible intrathecal drug delivery. At this time, he was receiving oral long acting morphine 100 mg three times daily, oral morphine 30 mg every 6 h as needed, tizanidine 4 mg three times daily as needed, and amitriptyline 25 mg every evening. The intrathecal drug trial was successful leading to the implantation of an intrathecal delivery system. During the implantation, the intrathecal catheter was successfully placed through a Tuohy needle at L3-4. In the course of the Tuohy removal, the epidural portion of the catheter was sheared. The fractured portion could not be removed. The decision was made to leave the sheared catheter in place. A second catheter was successfully placed at the same level and connected to the pump.\nIn the immediate postoperative period, the patient reported about 50% pain relief but 10 days after the procedure, he began to experience orthostatic headaches, nausea, vomiting, and the development of a painful lump in his right paraspinal lumbar area. The physical exam was unremarkable for any neurological deficits, but a tender mass was palpable in the left paraspinal area at L3-4. A pseudomeningocele in the subcutaneous lumbar tissue was demonstrated on computed tomographic (CT) imaging. Two intrathecal catheters were noted on CT imaging entering the spinal canal at the L3-4 level and a few millimeters of the proximal tip of the sheared catheter were visualized into the epidural space []. A CT with myelogram following injection of dye into the intrathecal pump showed CSF leakage and the pseudomeningocele at L3-4 [].\nThe patient was initially treated conservatively with bed rest for 48 h, but his symptoms did not improve over time. In addition, to the symptomatic pseudomeningocele and intracranial hypotension, the patient presented significant anxiety due to his concerns about the retained drain fragment. Surgical resection of the retained catheter with CSF leak repair was then recommended.\nThe patient underwent a minimally invasive repair of symptomatic CSF leak and removal of the sheared intrathecal catheter. Under general anesthesia with the patient prone on a Wilson frame, an 18 mm right-sided longitudinal incision 15 mm of the midline at L3-L4 was planned using fluoroscopy. Serial dilators were inserted and final 18 mm diameter retractor was docked at the junction of the inferior L3 lamina and facet complex.\nA L3 laminotomy and medial facetectomy were performed and upon removal of the ligamentum flavum, CSF became visible in the surgical field. The functional intact catheter was visible at the midline in the epidural space and some CSF was leaking around its insertion site in the dura. The second sheared catheter was identified following completion of a L4 laminotomy and CSF was freely leaking from its open end [].\nThe non-functional catheter tip was removed with micro bayonet curved tip forceps [], and the resulting dural defect was sutured primarily with a 5-0 TF-4 silk suture (Ethicon, Somerville, NJ) []. This particular suture is preferred by the senior author for dural closure through a tubular retractor because the needle has a semicircular shape which minimizes needle movements. A bayonet needle holder with a working distance of 6 cm is used to manipulate the needle and a knot pusher is employed to tie the knot. Additionally, a purse string suture was placed around the intact catheter to stop the CSF leak around it [Figure and ]. A Valsalva maneuver was performed up to 40 mmHg and held for 10 s to confirm the absence of residual CSF leak. A fine layer of absorbable polyethylene glycol hydrogel sealant (DuraSeal Spine Sealant System, Covidien, Waltham, MA) was applied over the sutures and hemostasis was achieved prior to closure.\nPostoperatively, the patient complained of nausea and abdominal pain that improved in the weeks following procedure. He further reported complete resolution of his postural headaches and was able to tolerate continued use of his functioning morphine pump. Complete resolution of his presenting symptoms with no evidence of CSF leak was confirmed at 8 weeks postoperatively. The patient continued to benefit from palliative care until his death 5 months after the procedure. |
A 12-year-old female of African ethnic origin was reported to the pediatric dental clinic of King Khalid University, College of Dentistry. She was the third child among her five siblings, with no history of hereditary diseases reported by the accompanying mother. The birth history of the patient was uneventful and was born as a full-term neonate of average birth weight by spontaneous normal delivery to healthy, nonconsanguineous parents. However, soon after birth, she suffered breathing difficulties and respiratory distress that necessitated her hospital admission for 37 days under observation. A diagnosis of mild nasal stenosis was made that did not require any intervention or treatment. The patient was then discharged, but there was no follow-up due to the patient's failure to appear for follow-up visits.\nOn extraoral examination, the patient had a noticeable convex facial profile, poorly distinctive philtrum of the upper lip, prominent nasal bone, narrow nose, and obviously incompetent lips (). Intraorally, the maxillary labial frenum was entirely absent, and the palate was narrow, high arched, and V-shaped with a prominent midpalatal suture (). The dentition was in the mixed dentition stage, with Angle's quarter cusp class II molar occlusal relation on the right side, while the left side indicated a full cusp class II relation. An extreme horizontal overbite (>7 mm) was noted. Rampant caries was evident with retained root stumps of primary molars. On the left side, the maxillary and mandibular teeth exhibited heavy plaque and calculus accumulation as compared to the right, indicating a right-side chewing dominance. No abnormality was detected with respect to the oral mucosa and gingival tissues, except for a small sinus tract related to the remaining root stumps of the maxillary right first primary molar (Figures –).\nAn SMMCI was present precisely at the midline, and the patient's mother reported its presence in the primary dentition as well. It exhibited mirror image symmetry between its right and left sides, which mimicked the anatomic contour of the distal surface of a normal maxillary central incisor (). The patient was referred for orthodontic evaluation and assessment. A true lateral view (lateral cephalogram) of the patient revealed a class II skeletal pattern with a downward and backward mandibular rotation. Both Anterior Nasal Spine (ANS) and Sella Nasion-Mandibular Plane (SNMP) angles showed a huge disparity from normal values, which reflected a highly prominent premaxilla (). The child was later referred to a pediatrician for the assessment of her overall physical status and for further investigation. The patient was categorized as underweight as her body mass index (BMI) at the time of consultation was 13.4, which put her below the fifth percentile in the growth chart. No abnormalities were detected in the child's intelligence quotient level, brain structure, or growth hormone levels. However, nasal stenosis was observed on frontal cone beam computed tomography ().\nThe treatment plan for the current case consisted of two main phases: a preparatory phase of comprehensive oral rehabilitation of dental diseases, including extraction of all residual roots of primary molars and restoration of carious permanent teeth, followed by a corrective phase that would involve complex orthodontic treatment. |
A 29-year-old male was referred to our neurovascular team after experiencing transient ischemic attacks, increasing in frequency and severity over the past 13 years, particularly worsening over the past three months. He was primarily experiencing staring spells accompanied by a right facial droop and slurred speech, but also noted that he was having episodes of right-hand weakness and decreased coordination. His was noted to have left lower extremity lymphedema with limb enlargement and varicosities that started as a child, which had progressed over the past 20 years. He had chronic headaches, but had never had seizure activity. Based on the clinical presentation, he was diagnosed with Klippel-Trenaunay Syndrome by his pediatrician. As part of the Klippel-Trenauna Syndrome with the lymphedema, he was frequently on antibiotics for cellulitis of his left leg, but denied any prior symptoms or issues with his right arm or leg. Additional significant medical history included hypertension, hyperlipidemia, and obesity.\nInitial imaging with a CT scan of his head showed multiple hypodense areas within the left frontal and parietal lobes. He was seen by his neurologist who obtained a brain MRI showing left frontal and parietal areas of T2 hyperintensity concerning for watershed infarcts. A magnetic resonance angiography (MRA) showed severe left and mild right distal internal carotid artery (ICA) and proximal middle cerebral artery (MCA) stenosis. He was started on daily Aspirin and came to our clinic for assessment where it was recommended he undergo digital subtraction angiography.\nThe angiogram confirmed the findings of the MRA, specifically identifying moderate narrowing of his left internal carotid artery at the carotid terminus, severe flow limiting stenosis at the proximal M1 segment of the left MCA with an abundance of Moyamoya vessels. The right internal carotid artery demonstrated mild, non-flow limiting arterial caliber narrowing at the carotid terminus with opacified Moyamoya vessels (Figure , ).\nBased on these findings and the recurrent watershed infarcts occurring with increasing frequency, an external carotid to internal carotid bypass surgery was discussed with the patient who elected to proceed.There were no complications with the surgery. The indocyanine green (ICG) run and intraoperative angiogram confirmed patency of the bypass (Figure ). At each of his three follow-up visits, he continued to experience improvement of his symptoms without any recurrent ischemic events.\nHe was seen in follow-up at one year after surgery where he had no neurological deficits and noted his transient ischemic attacks had resolved completely. Follow-up digital subtraction angiography was performed showing significant radiographic vascular proliferation from the bypass site with some regression of Moyamoya vasculature, Matsushima Grade B (Figure , ). |
The second case refers to a 48-year-old woman, a busy manager with a history of depression and sleep disturbance. She has had three terminations of pregnancy and one delivery by cesarean section. She smokes approximately ten cigarettes per day and has high cholesterol serum levels. She takes several medications: a selective serotonin reuptake inhibitor (escitalopram), two benzodiazepines (delorazepam and clonazepam), and a statin. She reports a four-year history of urinary symptoms: daily UUI episodes, mild stress urinary incontinence (SUI), and two episodes of nocturia per night. She wears pads every day. The urology consultation revealed some degree of pelvic pain, especially during vaginal examination. The urine dipstick was negative and there was no PVR. No specific causes of the symptoms such as urine tract infection were identified. The patient also complained of mild dyspareunia and occasional constipation. The urine culture turned out to be sterile, with no blood in urine, and the pelvic ultrasound scan and urine cytology were also negative. The cystoscopy, which was performed as a result of the presence of storage symptoms and to rule out a bladder tumor in this current smoker, was normal.\nIn OAB patients, it is of utmost importance to consider all comorbidities. Anxiety and depression may play a role, feeding a vicious circle. Moreover, medications to treat neurological or psychiatric disorders can influence OAB and be responsible for side effects [, ]. Gastrointestinal disorders are frequently associated with OAB, such as constipation in this case, but patients rarely raise the topic. An overlap exists between irritable bowel syndrome and OAB [].\nThe patient was prescribed a β3 agonist, pelvic floor muscle training (PFMT) and bladder retraining. Four months later, she noticed some degree of improvement, but had stopped the treatment as she felt that she had no time for PFMT. She was not compliant with the bladder drill either, and soon stopped the β3 agonist because she did not sense any real improvement. She also felt that she did not have the time to complete a bladder diary. She was prescribed fesoterodine 8 mg for three months. In parallel, her general practitioner asked for vaginal and urethral culture swabs, which were negative. After three months, her urinary urgency improved, but she said that the few remaining episodes of urgency were “killing her life” and that she did not want to be on pills for her whole life. Therefore, she refused to continue the treatment and requested an “easy fix”. Her reaction highlights the need for careful consideration of the consequences of incontinence in terms of QoL. A publication from Vaughan et al. [] reported that OAB and incontinence synergize to reduce QoL, especially in the domains of sleep, elimination, usual activities, discomfort, distress, vitality, and sexual activity.\nConsistent efficacy on urgency symptoms with a significant decrease in UUI and urgency episodes has been reported with fesoterodine at doses of 4 and 8 mg compared to placebo () [, , , ]; however, some patients may react differently. Patient satisfaction is an important driver of treatment success []. Patient expectations should be considered carefully in the context of OAB management. The achievement of patients' goals was measured in the Study Assessing FlexIble-dose fesoterodiNe in Adults (SAFINA study) [], a 12-week multicenter open label study with 331 OAB adults, using the Self-Assessment Goal Achievement (SAGA) questionnaire. Fesoterodine treatment resulted in 81.3% of patients declaring that their goals were “somewhat achieved/achieved” or that the result “exceeded/greatly exceeded their expectation”.\nOur case patient had very specific expectations; she refused to have an implant (neuromodulation), saying “I'm not going to be an android!” She accepted botox injections, and so a first set of injections was performed under local anesthesia. She found the injections “a little painful” and “a big annoyance”, but at the one-month follow-up visit after botox injection she reported no more UUI episodes and an improvement in frequency and the number of urgency episodes, as well as in QoL. Even though she stated that she did not like the idea of being a patient for the rest of her life, she accepted subsequent injections.\nThe clinical points that can be learned from this case are as follows:All OAB cases are different, and a thorough evaluation is mandatory to adequately address each case. It is important to assess other aspects, such as functional and psychological disorders that may influence symptoms, and to consider nonneurogenic OAB as a multifactorial disease. The major goal of initial therapy is to meet the patient's expectations regarding the reason for their visit, to improve their satisfaction, and their QoL. Due to fesoterodine's characteristics and flexible dosage, improvement of symptoms and achievement of the patients' goal are usually high with this medication. When patients have specific requirements, all options should be discussed and the patient's agreement obtained. A customized approach is a crucial factor for treatment success. OAB management should be personalized; beware of a simplistic application of a standardized treatment algorithm. |
A 33-year-old, male, right handed, realtor, of Malaysian descent, presented to hospital following a nocturnal seizure. His wife reported being awoken by a cry and found her husband convulsing. The patient's arms were flexed and his eyes open and rolled back. This lasted for approximately 1 minute and was followed by restless thrashing movements and awkward attempts to get up. There was some foaming at the mouth.\nOn admission there was some residual disorientation but no lateralizing symptoms or signs. The patient had been previously well, although one week prior he had had flu-like symptoms, including loss of appetite and general myalgia, as well as a swelling on the right side of his neck which had resolved on its own.\nThere was no history of previous seizures, meningitis, encephalitis, blackouts, loss of consciousness, head injuries, or febrile seizures. The patient reported no use of recreational drugs. Neither the patient nor his family members had a history of tuberculosis. The patient's most recent travel was an Alaskan cruise. There were mosquitoes but the patient had not been bitten. He had not been bitten by any ticks or animals. There were no exposures to sick people. The patient denied any history of sexually transmitted infections or other relevant past illnesses.\nIn hospital, the patient was started on phenytoin but continued to have further nocturnal seizures with post ictal periods of approximately 30 minutes. During the third seizure there was a twenty-one second period of asystole and a permanent pacemaker was placed the following day.\nPrior to the placement of the pacemaker, the patient was afebrile and had no headache, vision changes, or difficulty speaking or swallowing. There was no abnormality in bowel or bladder function. Gait was normal, and the patient's neurological exam was unremarkable except for gaze evoked nystagmus, thought to be a side effect of the phenytoin. Following the procedure, the patient reported feeling better and his wife reported that conversation with him was more normal, although he had forgotten details of events up to a week prior.\nThe same morning, however, the patient had a fourth seizure from sleep. The patient's phenytoin was optimized. Lumbar puncture (LP) showed WBC 7 cells/μL, RBC 1 cell/μL, protein 428 mg/L, and glucose 4.1 mmol/L. CT head with contrast was normal. The placement of the pacemaker precluded MRI.\nLevetriacetam was added, but the patient continued to have recurrent seizures. He developed additional symptoms. There was a right sided headache, right ear pain and tenderness, and an unusual sound in the right ear, which evolved into a hallucination of music. The patient also developed complex partial seizures; these involved speech arrest, leftward head and eye turning, as well as left arm posturing. The focal neurologic symptoms and focal seizures suggested a diagnosis HSV encephalitis, despite the normal LP results. A course of acyclovir was started and further investigations were carried out.\nResults of a second LP were also normal. PCR for Herpes simplex was negative. Cytology was negative, and repeat CT head with contrast was normal. SPECT showed a slight decrease in perfusion of the left side compared to the right. Repeat EEG showed nonspecific abnormality of the right temporal lobe. A biopsy was not done as there was a lack of a definable area to target.\nOver the first week of acyclovir therapy the patient showed significant improvement, and the headache and seizures resolved. The hallucination of music persisted for several days. The patient was discharged to complete a 3 week course of acyclovir. Tapering of the anticonvulsants resulted in breakthrough seizures, so the patient remains on levetriacetam and phenytoin. |
Case 2 involved a 45-year-old woman who reported continuous left hip pain since March 2015. She arrived at our hospital in November 2015. She also had a limited range of motion of her left hip. Her Merle d'Aubigné-Postel score was 10 points, with the following distribution: pain, 2 points; walking ability, 4 points; and mobility, 4 points.\nArthrography showed a honeycomb appearance around her left hip joint (). Upon MR imaging, axial images of the left hip joint revealed intra-articular and extra-articular mass lesions, one of which was located adjacent to the femoral vessels (). These examination findings suggested synovial osteochondromatosis forming a herniation sac. Based on the radiographic features, we considered that arthroscopic resection concomitant with an open anterior approach was suitable for complete resection.\nThe salient components of the surgical procedure were as follows. The patient was placed in the supine position on the fracture table and arthroscopic resection was performed. We could excise free bodies and osteochondromas existing in the acetabular fossa and the recess behind the labrum, but we could not excise those in the iliopsoas muscle and in the herniation sac near the obturator external muscle bursa. Then, we finished the arthroscopic resection and performed open surgery using an anterior approach. The anterior capsule was opened with a reverse T-shape incision. Osteochondromas remaining in the joint and those in the herniation sac near the obturator external muscle bursa were easily resected without surgical dislocation. Osteochondromas existing in the iliopsoas muscle were completely excised by bluntly splitting the muscle and herniation sac (). The capsule was repaired and fascia and skin closure was performed.\nThe patient began partial weight-bearing gait immediately after surgery and progressed to full weight-bearing at 4 weeks after surgery. Histopathological examination confirmed the diagnosis of a synovial osteochondromatosis. MR imaging performed 1 year after surgery showed that the herniation sac had diminished in size, with no apparent complications. At 1-year follow-up after surgery, the patient had slight pain in her left hip during activity and an improved range of motion. Her Merle d'Aubigné-Postel score improved to 17 points. |
An 8-month-old male infant developed a perianal mass during the first week of life which was treated as an abscess. The infant at that time had a full septic work-up that was negative and it was decided to treat him conservatively with antibiotic without incision and drainage. At the age of 2 months, he started having recurrent subcutaneous lumps on the lower extremities. At 5 months of age, he was provisionally diagnosed to have panniculitis and was hospitalized at that time for a muscle biopsy from the right thigh to confirm the diagnosis of panniculitis and evaluate other possible etiologies. After the muscle biopsy, he developed rapidly progressive bluish discolorations and indurations in the upper thighs which extended to the buttocks and scrotum over a period of 2 days (). The skin lesions progressed to hemorrhagic necrosis on the 8th day of hospitalization (). When the hemorrhagic necrosis developed, purpura fulminans was considered and protein C deficiency was suspected. He was started on regular fresh frozen plasma transfusion and later started on protein C concentrate and low-molecular-weight heparin. His course was complicated by compartment syndrome that required bilateral lower extremity fasciotomy followed by extensive debridement with artificial dermis (Integra®) application (Figures and ). Additionally, he developed anemia requiring multiple blood transfusions, thrombocytopenia, consumptive coagulopathy (prolonged prothrombin time (PT), activated partial thromboplastin time (aPTT), and low fibrinogen), and fibrinolysis (increased D-dimer) which were consistent with disseminated intravascular coagulation (DIC). His illness was further complicated by Gram-negative sepsis (Klebsiella oxytoca and Enterobacter cloacae), hypertension, and respiratory failure requiring ventilatory support. The infant was hospitalized for 3 months during which he gradually improved while receiving protein C concentrate. He was transferred to another facility for further care and skin grafting at the age of 8 months.\nHis growth parameters were appropriate for the age. His parents were cousins and they had 6 other older children who were reportedly healthy and there was no family history of any hematological diseases.\nProtein C level was found to be very low (less than 10%, normal: 68–143%) consistent with autosomal recessive PCD. The PROC gene was sequenced at PreventionGenetics LLC, Marshfield, Wisconsin, USA, and a novel homozygous missense mutation (c.1198G>A; p.Gly400Ser) was identified, confirming the diagnosis of autosomal recessive PCD. Protein C level was 56% in the mother and 73% in the father (normal: 68–143%), suggesting that both parents are carriers and have autosomal dominant PCD. Genetic testing showed that both parents are heterozygous for the p.Gly400Ser mutation in PROC, confirming the diagnosis of autosomal dominant PCD in both parents. Both parents were healthy with no history suggestive of thrombophilia. |
A 59-year-old man presented to the urgent care clinic at the School of Dentistry complaining of an upper lip mass for one-year duration. The mass started out as a small bump and had grown steadily since then. 3 months prior to his presentation, a draining parulis developed on the mass. The patient had no history of systemic symptoms such as fever, chills, weight loss, or fatigue. He was aware of a dark-colored “dead tooth” for several decades in the area of concern but denied any previous history of swelling in the area. The patient had recently moved to the United States from Nigeria and had previously been without access to adequate dental care. The patient said that a doctor in Nigeria told him that the lesion was likely cancerous.\nOn exam, there was a large, painless, fibrous, exophytic mass in the anterior maxillary labial vestibule (Figures and ). The base of the mass approximated the apex of tooth #8. A yellow purulent material was observed draining from the parulis (). Tooth #8 was discolored and was confirmed to be nonvital on pulp testing. There was a significant gap between teeth #7 and 8. Tooth #8 was displaced medially and was extruded relative to the adjacent dentition.\nA periapical radiograph revealed a large unilocular radiolucency associated with the apex of tooth #8 (). Cone-beam computed tomography again demonstrated a large cystic-appearing defect in the anterior maxilla with perforation of the buccal and palatal cortices . The lesion extended to the nasal floor on the ipsilateral side.\nThe patient was referred to the oral surgery department for excisional biopsy. After tooth #8 was removed, an incision was made around the base of the stalk that connected the mass to the labial and alveolar mucosa. Sharp dissection was used to free the mass, and the specimen was sent for histopathologic analysis. The mass communicated with a cystic lesion of the maxilla. The cyst was enucleated with a curette and also sent for pathology. Perforation of the cyst through the buccal and palatal cortices was noted during the procedure. Slight undermining of the wound margins allowed for closure with resorbable sutures.\nAt the patient's one-week follow-up (), he was doing very well. He reported minimal pain, no neurosensory disturbances, and no systemic or local symptoms of infection. He and his family were very relieved to learn that the lesion was benign. He was happy with his appearance after having the mass removed. |
A 73-year-old male (height, 158 cm; weight, 62 kg) was referred by the cardiology department to the rehabilitation department because of a 3-week history of left foot drop. He also complained of numbness and a tingling sensation on the left lateral side of the lower leg and dorsum of the foot. At the time of referral, the left leg and foot were soft and non-tender. Only the right dorsalis pedis was pulsatile, but not on the left side. Pain in the left lateral lower leg and dorsum of foot was scored 3/10 on the Numeric Pain Rating Scale. The Medical Research Council scale for weakness showed the following grades (right/left): hip extension 5/5, knee flexion 5/5, ankle dorsiflexion 5/1, and hallucis extension 5/1. He had no lower back pain and the straight leg raise reached 80° on both sides. A positive Tinel's sign behind the fibular neck on the left side was noted. In a nerve conduction study, there was no compound motor action potential in the left deep peroneal nerve on the left extensor digitorum brevis or tibialis anterior muscle recordings, and no evoked sensory nerve action potential in the left superficial peroneal nerve (). Needle electromyography showed abnormal spontaneous activity at rest and no motor unit action potential activity in the left tibialis anterior, peroneus longus, and peroneus brevis muscles (). Computed tomography (CT) angiogram showed proximal occlusion of the left anterior tibial artery (ATA) () without any abnormal findings of the soft tissue. This led to a diagnosis of left common peroneal neuropathy due to occlusion of the left ATA. The patient was treated with oral warfarin.\nThe patient's medical history was reviewed. He did not have diabetes mellitus. He received a mitral valve replacement 5 years ago due to mitral stenosis, and echocardiography showed a moderate degree of aortic stenosis and regurgitation. In addition, he had complete atrioventricular block and valvular atrial fibrillation; and had a pacemaker inserted three years prior to referral. However, he had been prescribed only an antiplatelet agent because of a history of cerebellar intracranial hemorrhage 2 years previously.\nApproximately 4 weeks prior to referral, he visited another hospital suffering from chest pain, and received percutaneous coronary angiography which took about 30 minutes. After percutaneous coronary angiography, he received conservative care in a general ward, without any physical restrain or requirement for absolute bed rest. He could ambulate the ward with only minimal assistance. Some days later, he complained of left leg weakness and a brain CT was performed to rule out an acute brain lesion. Magnetic resonance imaging (MRI) was contraindicated because of the cardiac pacemaker. The brain CT showed a subacute ischemic lesion in the right posterior temporal region but it did not clinically correlate with the weakness. Although he complained of foot drop and paresthesia, there were no symptoms of anterior compartment syndrome such as tenderness, redness or swelling of low leg. No deep vein thrombosis or abnormal findings of soft tissues were found upon ultrasonography of the left leg. After improvement of the chest pain, he was discharged home. Two weeks later he was admitted to the cardiology department in the present hospital due to chest pain, and was referred to the rehabilitation department. After diagnosis of the left common peroneal neuropathy and improvement of the chest discomfort with conservative therapy, he was transferred and received rehabilitation. |
An 80-year-old Caucasian female with history of hypertension and chronic back pain presented for emergent repair of a 7.2 cm aneurysm of the ascending aorta with Stanford classification type A dissection. Because the ascending aorta was unsuitable for arterial cannulation, the surgeon elected to perform axillary cannulation via the right subclavian artery with side graft anastomosis. The patient arrived to the operating room (OR) with nicardipine and esmolol infusions running through an 18-gauge peripheral intravenous (IV) line in the right antecubital (AC) fossa. Prior to induction of anesthesia, we disconnected the infusions from the right AC and administered medications though an 18-gauge IV in the left forearm. The patient also had a left radial arterial line (AL), and we placed the pulse oximeter and noninvasive blood pressure (NIBP) cuff on the RUE. After intubation, we placed a right radial AL, and the surgeons placed a left femoral AL. All arterial pressures correlated closely. Additionally, a 9-French central line was placed in the right internal jugular vein. The patient was cleansed and draped for surgery with her arms tucked to her sides.\nShortly after the procedure began, the right radial AL tracing went flat, and the pulse oximeter waveform was lost. We attributed this to the surgeon partially clamping the right subclavian artery in preparation for arterial cannulation. We switched the pulse oximeter to the left hand and relied on the left radial and femoral AL for pressure readings. Just prior to arterial cannulation, we noted that the right radial pressure returned, although about 20 points lower than the left radial/femoral. Immediately after initiating CPB, the right radial mean arterial pressure (MAP) increased to 200 mm Hg, and left radial/femoral MAP decreased from 60 to 30 mmHg. The perfusionist alerted the surgeon about the high line pressures and decreased CPB flows. After a brief attempt to troubleshoot and adjust the cannula with little improvement in pressure or flow, the surgeon proceeded with the operation. Over the next few minutes, the left radial/femoral MAP increased to 60 mmHg.\nAs deep hypothermic circulatory arrest (DHCA) was initiated, the right radial MAP decreased to 30 mmHg and left radial/femoral MAP decreased to 10. When CPB was reinstated, right radial MAP again increased to 200 mmHg. After 29 minutes of DHCA and 265 minutes of CPB, the patient was successfully weaned from CPB, and right radial MAP decreased to about 10 points lower than left radial MAP.\nDespite these issues, the surgery was otherwise uneventful. However, upon the surgical drapes being taken down, we noticed that the patient's RUE was swollen with blisters and bullae from the shoulder to the hand; yet, the skin of the upper arm where the NIBP cuff had been placed was normal as seen in figures. The IV in the right AC appeared to be infiltrated and weeping fluid even though we had not used it during the case and did not have any IV fluids attached to it (Figures and ). The IV and right radial AL were removed in the OR, and a Xeroform gauze dressing was applied to the RUE with the surgeons present. The intensive care unit nurses were instructed to elevate the arm and perform hourly neurovascular checks.\nOn postoperative day 1, the patient complained of tenderness and burning in the RUE, but she maintained adequate capillary refill, motor function, and sensation. Plastic Surgery was consulted to rule out compartment syndrome. They were unsure of the diagnosis but recommended nonoperative management and continued neurovascular checks. Eventually Dermatology was also involved, and they performed a punch biopsy of the patient's right dorsal hand. Their initial diagnosis was allergic contact dermatitis (ACD) due to the fact that the area of skin covered by the NIBP cuff was spared. However, the biopsy showed pauci-inflammatory dermal-epidermal blistering, which did not favor ACD. Direct immunofluorescence was also negative, ruling out localized pemphigus. Given the histologic findings, the final diagnosis was hydrostatic edema/bullae correlating with rapid edema during surgery. The patient continued to be managed nonoperatively with 1% triamcinolone ointment and gauze dressings, and within one month the blisters had completely resolved. |
A 34-year-old male patient presented with a 17-month history of intermittent left-sided upper abdominal and epigastric pain. The pain occurred one day following running, lasting three days. The pain was described as aching and stabbing in nature and radiated to the left flank, intermittently ranged in severity from 3/10 to 6/10 on the visual analog scale when present, and affected his ability to participate in recreational as well as physical activities.\nSymptom onset was correlated to ingesting a heavy meal consisting of biscuits and gravy with reported abdominal pain and sweats requiring urgent care. In the emergency department (ED), evaluation included a negative abdominal CT and he was discharged on antibiotics. The patient continued to have intermittent symptoms and self-managed by removing meats from his diet and intermittently taking dicyclomine and polyethylene glycol 3350.\nTen months later, the patient was seen for continued epigastric and left upper quadrant pain occurring randomly and not related to meals. The patient was subsequently referred to as gastroenterology. Upon examination, the pain was not provoked with abdominal auscultation. Murphy’s sign was negative. The workup included an assessment of H pylori to rule out peptic ulcer disease and an endoscope to assess for evidence of candidiasis or obstruction. Red flag symptoms to include anemia, blood in the stool, and weight loss were not present. Labs to include a complete blood count and comprehensive metabolic panel were negative. The working diagnosis was gastritis, and he was treated with pantoprazole 40 mg daily for two months. The patient followed up with gastroenterology as the pain worsened after running four miles and intense workouts. CT of the abdomen and pelvis with contrast, abdominal MRI, magnetic resonance cholangiopancreatography, MRI enterography, and nuclear medicine hepatobiliary studies were all normal. The patient was instructed to follow-up with his primary care provider as the examination did not indicate a gastrointestinal source of pain.\nThe patient did report a history of left-sided chest pain in 2017 that did precede his initial complaint of left side abdominal pain. During that period, the patient underwent a cardiology workup to include 12-lead EKG, laboratory studies, and a chest X-ray that were normal. The patient was seen by the Cardiology Clinic and wore an event monitor for two-weeks. No abnormal rhythms were noted, and the patient was discharged with a diagnosis of non-cardiac chest pain. An echocardiogram showed a mildly thickened left ventricle with a good ejection fraction of 60-65% and no dyskinesia or hyperkinesia. The patient was again seen in 2019 with a left-sided chest and tingling into the left arm and back similar to that in 2017. A 12-lead EKG was performed as well as a hemoglobin A1C panel and Lipid screen. Follow-on workup included an exercise treadmill test that was normal.\nAfter 17-months of recalcitrant left upper quadrant pain, the patient was referred to the Interdisciplinary Pain Management Clinic (IPMC). The patient’s primary goal was diagnostic clarity. His secondary goal was to run without pain.\nPhysical examination\nPhysical evaluation at the IPMC revealed that the patient’s pain was localized to the abdomen just below the costochondral cartilage and extending to a point midway between the umbilicus and axillary line the day following a run (Figure ). Deep palpation of the area did not reproduce pain. Palpation in conjunction with contraction of the abdominals (Carnett test) did not reproduce symptoms. Pressure applied to the area of the abdominal cutaneous nerve on the left side did not reproduce his pain. Thoracic ROM was assessed in standing. No pain was reproduced with motion along the cardinal planes but the combined thoracic extension and side bending to the right did reproduce his abdominal pain.\nMotion palpation testing\nWhile in prone, provocation testing includes several maneuvers with the goal of identifying biomechanical faults causing or contributing to the patient’s pain complaints. A rib spring maneuver is performed by pressing down on the left 11th rib angle in an anterior direction and then quickly releasing pressure so that the rib springs back up (Figures and 3). A positive test is indicated by a reproduction of the patient’s pain as in this case study patient.\nThe passive accessory intervertebral motion testing was performed in prone to the T1 through T12 spinous processes. The pressure is applied to each of the spinous processes assessing for any hypomobility or pain reproduction (Figures and 5). Commonly employed by physical therapists, this technique is considered to be valid in assessing spinal segmental hypomobility []. Intra-rater reliability is good and inter-rater reliability is moderate when assessing joint mobility and stiffness in the thoracic spine and ribs []. These maneuvers can be performed by primary care or emergency room providers. The restricted motion was assessed at T9 through T11 without pain reproduction.\nStrength and flexibility assessment\nFlexibility and strength assessments were made in supine. The treating physical therapist surmised that adaptive tissue tightening or muscular imbalance may have occurred due to the chronicity of the patient's complaint. The pectoralis minor and latissimus were tight on the left side compared to the right. The pectoralis major strength was assessed with manual resistance and no chest or abdominal pain was reproduced. Having the patient performing ten sit-ups assessed abdominal strength based on physical requirements in the U.S. Marine Corps. No pain was reproduced during the performance.\nIntervention\nThe patient was treated upon the initial evaluation with osteopathic manipulation techniques (OMT; Table ). OMT has been shown to be effective in the treatment of rib dysfunction []. A posterior rotation force was applied to the left 11th rib with audible cavitation (Figures -). Upon active thoracic ROM, the patient’s abdominal pain was not reproduced with combined extension and rotation to the right side.\nNo other treatment was performed at that time. The patient was asked to go jogging later in the day and assess for changes in pain along the abdomen the following day. The patient was asked to contact the clinic telephonically with the results.\nUpon telephonic follow-up, the patient reported that he did jog that day, and went snorkeling and bike riding the following day. The patient did not experience any left-sided upper quadrant pain, but he did note some flank pain as well as pain along the 11th rib and minor sternal pain. The patient wanted to go jogging again prior to his next clinic follow-up to determine if there was an actual treatment effect versus placebo effect from OMT.\nAt the second clinic visit two days later, the patient reported no abdominal or epigastric pain despite jogging the day previously. The patient did report pain at the left posterior superior iliac crest (PSIS; Figure ). A physical examination was performed. There was no abdominal pain reported with thoracic ROM or pain along the 11th rib with provocation testing. There was an asymmetry in the patient’s pelvic landmarks with his PSIS and iliac crest elevated on the left side as compared to the right suggesting sacroiliac joint (SIJ) dysfunction. This was confirmed by performing a thigh thrust. During the thigh thrust, the patient is supine with hip and knee flexed. The examiner cups the sacrum with one hand and applies force axially through the knee providing a shear force to the SIJ. A positive test is indicated by joint hypomobility, when compared to the opposite side, and reproduction in pain. There was also tightness noted along with the left piriformis and iliopsoas when assessed in prone.\nGiven signs and symptoms consistent with concomitant SIJ dysfunction, the patient was treated with a combination of SIJ OMT, deep tissue mobilization of the piriformis, and active release of the iliopsoas as described previously by Newman et al. []. The patient was instructed in a lumbopelvic strengthening program directed at the hamstrings, hip adductors, and abdominals to be done every other day, as well as stretching of the piriformis and iliopsoas muscles daily. The patient was asked to follow-up in one week.\nAt the third visit, the patient’s flank pain pattern returned. The patient ran three miles three times since the last visit. The patient did not report any abdominal or sacroiliac joint, SIJ pain either during or after jogging. He did report a constant pain along the 10th and 11th rib origin that radiated anteriorly to the 11th rib tip, which started the previous day (Figure ). Rotating the trunk fully to the left side reproduced this pain. Provocation testing revealed a reproduction of pain along the 11th rib and T10/11 segmental hypomobility. OMT to the 11th rib on the left side completely resolved his pain. As his abdominal pain goal had been met, his functional goal was revised to be able to jog seven miles without flank, back, or costochondral pain in four weeks.\nUpon follow-up at the fourth visit, the patient reported no abdominal or flank pain with jogging four miles. When he increased the distance to seven miles, the flank pain returned as well as pain along the costochondral cartilage extending to the distal sternum. This pain lasted two days and then subsequently resolved. Physical examination revealed pain along the 10th rib angle with thoracic rotation to the left side. Provocation testing to the 10th rib was positive for pain reproduction, but not at the 11th and 12th ribs. No pain was reproduced with deep palpation of the abdomen; however, there was pain along the costochondral cartilage extending from the 10th rib tip to the sternum. Following OMT to the 10th rib, instrument-assisted deep tissue mobilization was applied to the skin above the costochondral cartilage utilizing a directional (moving) cupping technique (Figure ) [].\nAt the fifth through seventh visits, the patient reported residual pain along the 10th rib and costochondral cartilage after activity lasting several hours. The patient had been increasing his activity level to include working out, running, and surfing. Treatment directed at the mobilization of the myofascial tissue along the costochondral cartilage was repeated. In addition, active release techniques were applied to the pectoralis minor and latissimus muscles to determine if tissue tightness contributed to rib mobility. After the performance of these techniques, the patient reported no pain with repeat provocation or ROM testing. The patient would continue to follow-up weekly for reassessment until his functional goals were met.\nUpon follow-up at the eighth visit, the patient reported a recurrence in pain along the abdomen, flank, and low back following surfing for two hours. The pain remained constant all day and night, thereby affecting his sleep. All of his symptoms resolved by the next day. The patient subsequently went jogging five miles the previous day and experienced tightness along the costochondral cartilage immediately afterward that has remained constant until this appointment. The patient rated his pain level as a 3/10 on a visual analog scale. The physical assessment did not demonstrate any segmental or rib hypomobility. The pain was reproduced with deep pressure applied to the attachment of the abdominals to the costochondral cartilage on the left side. The directional cupping treatment was repeated in the painful area. No pain was noted after treatment.\nApproximately five weeks after starting care, the patient came in for the eighth and ninth visits, the patient reported no flank, back, or costochondral pain with jogging seven miles. The patient continued to have mild tenderness along the costochondral cartilage with deep pressure; therefore, the directional cupping technique was employed to optimize tissue mobility in order to reduce the chance of recurrence. The following week, the patient returned for his tenth and final visit. The patient performed a series of intensive workouts to include jogging and surfing daily. There was no return of his pain. The patient was subsequently discharged from the IPMC. |
A 46-year old female patient, who had been suffering from autoimmune thyroid disease for eight years, presented at our clinic with an acute exacerbation of GO. Clinical examination revealed a convergent strabismus fixus with severe hypotropia of both eyes (Fig. ). The patient complained of increasing loss of eyesight and heavy retrobulbar pain. Visual acuity had deteriorated significantly from 0.6/0.5 to 0.1/0.1 within 3 months. A contrast enhanced orbital MRI scan showed distinct swelling of all extraocular muscles with bilateral compression of the optic nerve (Fig. ). There was no history of comorbidities except nicotine abuse. Laboratory tests showed a euthyroid biochemical status with TSH within the normal range, but elevated levels of Anti-Thyroid Peroxidase Antibody, Anti-Thyroglobulin Antibody and Thyroid Receptor Antibody. The patient’s daily medication comprised of 200 μg L-Thyroxin and 200 μg Selenium. Over many years, the patient had shown only mild to moderate symptoms of GO, but following a thyroidectomy, the symptoms had recently worsened dramatically. Since the disease could not be controlled by high-dose systemic glucocorticoid therapy, bilateral three wall orbital decompression had been performed twice previously. In the first step, the medial orbital wall had been resected via an endonasal approach. Due to ongoing findings as before, two months later partial resection of the orbital floor and fenestration of the lateral orbital wall via a combined transconjunctival/transcaruncular approach with piezosurgery had been performed. In addition, high-dose systemic glucocorticoid therapy was conducted prior to surgery and for the first two months after surgery. Glucocorticoid medication had to be gradually reduced until zero because the patient suffered from an upcoming depression and Cushing syndrome. Orbital radiotherapy for the treatment of thyroid eye disease had been considered as a therapeutic option, but the rapid progress of the disease with the growing risk of dysthyroid optic neuropathy forced us to act more quickly than orbital radiotherapy could perform []. Since the patient increasingly suffered from loss of vision and heavy pain attacks because of medial caudal squinting, we decided to correct the hypo- and esotropia surgically by releasing and repositioning the insertion points of the inferior and medial rectus muscle. Acute surgery was the last remaining treatment option.\nOperations on the left and right eye were performed consecutively with an interval of one week. The eye with the lower vision (left side) was chosen first. A forced duction test showed a complete fixation of the bulb. We opted for a transconjunctival approach (limbal incision) combined with lateral canthotomy to gain access to the dorsal part of the inferior part of the eye bulb. The insertion of the inferior rectus muscle was localized and then circuited with a squint hook (Fig. ). A non-absorbable polyethylene suture (Mersilene 4.0, Ethicon, U.S.) was placed at the anterior rim of the muscle before the muscle was detached from the outer bulb. This release in tension immediately resulted in the spontaneous elevation of the bulb. Lengthening of the muscle with an interposition graft (e.g. fascia lata) was not possible because of the deep retraction of the muscle. Instead, the polyethylene thread loop was directly fixed to the sclera at the former muscle insertion area, placing the muscle 12-15 mm dorsally with regard to its original fixation position. By marking of the original muscle insertion point with a non-absorbable polyethylene suture, an option could be preserved for a more precise muscle readaption at a later stage. Subsequently, the same procedure was carried out with the medial rectus muscle. Less tension allowed direct refixation of the muscle to the sclera without bridging by the polyethylene suture. The bulb was freely movable and remained vertically and horizontally in a primary position (Fig. ). Despite a significant exophthalmos, passive eyelid closure could easily be performed. The significant conjunctival contraction caused by the long-term hypotropia meant that only partial conjunctival wound closure with a polyglactin suture (Vicryl 7.0, Ethicon, U.S.) was possible. No postoperative complications occurred under the postoperative systemic antibiotic medication with Clindamycin of 3x600mg per day over three days supplemented by local application of Neomycin eye ointment for one week. Surgery of the right eye was conducted in the same manner (Fig. ) and under the same perioperative protocol one week later. Additionally, two mucosal grafts of 3.0 × 1.5 cm were harvested bilaterally from the inner cheek to be used for the bilateral reconstruction of the conjunctiva. The intraoral donor sites were closed primarily by using Vicryl 3.0 (Ethicon, U.S.). Starting from extreme eso- and hypotropia, the operation succeeded in repositioning the bulbs into the vertical and horizontal primary position with no restriction of passive movements. Three months postoperatively, the patient was free of pain and had a visual acuity of 0.3/0.6. Visual field testing (Goldmann perimetry) showed only slight concentric bilateral restrictions. Surprisingly, the patient did not suffer from diplopia despite the persistent restriction of active ocular mobility and a moderate bilateral exotropia (Fig. ).\nFollow-up examinations of the patient will be performed at close intervals, including ophthalmological check-ups and the testing of thyroid blood parameters. Contrast enhanced orbital MRI scans will allow the measurement of extraocular muscle volume, as described by Kolk et al. []. Orbital MRI scans were performed preoperatively and three months postoperatively (Fig. ) and the volumes of the extraocular muscles were calculated by using manual segmentation (Osirix Imaging software 5.9) (Table ). During this time interval, the total extraocular muscle volume increased from 24.91cm3 to 29.29cm3. Together with the ongoing high levels of thyroid-specific antibodies (Anti-Thyroid Peroxidase Antibody, Anti-Thyroglobulin Antibody and Thyroid Receptor Antibody), this indicated that the patient was still in an active stage of GO. Volumetric measurements of the extraocular muscles, based on follow-up MRI scans, will help to monitor the course of the disease. Further squint surgery, in terms of a precise readaption of the extraocular muscles, will be postponed to the future, when a more stable stage of the systemic autoimmune disease will be reached. |
The patient was a 34-year-old Turkish woman, gravida 2 para 1 with a normal vaginal delivery 15 years previously. Although she had not used any contraceptive method afterwards, she had not become pregnant. She was transferred to our hospital from her local clinic at the gestation stage of 13 weeks because of pain in the lower abdomen and slight vaginal bleeding. She did not know when her last menstrual period had been, due to irregular periods. At admission, she presented with a history of abdominal distention together with steadily increasing abdominal and back pain, weakness, lack of appetite, and restlessness with minimal vaginal bleeding. She denied a history of pelvic inflammatory disease, sexually transmitted disease, surgical operations, or allergies. Blood pressure and pulse rate were normal. Laboratory parameters were normal, with a hemoglobin concentration of 10.0 g/dl and hematocrit of 29.1%. Transvaginal ultrasonographic scanning revealed an empty uterus with an endometrium 15 mm thick. A transabdominal ultrasound () examination demonstrated an amount of free peritoneal fluid and the nonviable fetus at 13 weeks without a sac; the placenta measured 58 × 65 × 67 mm. Abdominal-Pelvic MRI (Philips Intera 1.5T, Philips Medical Systems, Andover, MA) in coronal, axial, and sagittal planes was performed especially for localization of the placenta before she underwent surgery. A non-contrast SPAIR sagittal T2-weighted MRI strongly suggested placental invasion of the sigmoid colon ().\nUnder general anesthesia, a median laparotomy was performed and a moderate amount of intra-abdominal serohemorrhagic fluid was evident. The placenta was attached tightly to the mesentery of sigmoid colon and was loosely adhered to the left abdominal sidewall (). The fetus was localized at the right of the abdomen and was related to the placenta by a chord. The placenta was dissected away completely and safely from the mesentery of sigmoid colon and the left abdominal sidewall. Left salpingectomy for unilateral hydrosalpinx was conducted. Both ovaries were conserved. After closure of the abdominal wall, dilatation and curettage were also performed but no trophoblastic tissue was found in the uterine cavity. As a management protocol in our department, we perform uterine curettage in all patients with ectopic pregnancy gently at the end of the operation, not only for the differential diagnosis of ectopic pregnancy, but also to help in reducing present or possible postoperative vaginal bleeding.\nThe patient was awakened, extubated, and sent to the room. The patient was discharged on post-operative day five with the standard of care at our hospital. |
A 39-year-old male with a history of schizoaffective disorder, bipolar disorder, and multiple prior suicide attempts presented with 10 hours of severe abdominal pain after ingesting over 100 gms of APAP two days earlier. On the morning of admission, the patient felt diffuse, severe abdominal pain, most prominent in the right upper quadrant, associated with nausea and vomiting. Upon evaluation in the emergency room, the patient was afebrile with a blood pressure of 110/66 mmHg, a heart rate of 100 beats per minute (BPM), and a respiratory rate of 16 with oxygen saturation of 99% on room air. His physical exam was significant for diffuse tenderness to palpation in right upper quadrant and epigastric area. The patient’s complete blood count was within normal limits. Other initial laboratory workup at the time of admission is shown in Table .\nThe patient was admitted due to transaminitis secondary to APAP toxicity and started on intravenous N-acetyl cysteine (NAC) protocol for 16 hours. The initial plan was to trend liver functions tests, international normalized ratio (INR), and APAP levels every six to eight hours and two hours prior to a 16-hour infusion being completed to determine if NAC was still needed. Table describes his trend of liver function tests and APAP levels.\nNAC was discontinued on Day 6 of hospitalization as the AST and ALT were less than < 3,500 units/L and APAP levels remained normal. However, despite normalization of liver function tests, his blood urea nitrogen (BUN) and creatinine trended up daily (data can be found in Table ).\nA nephrology consult was placed on Day 3 in the setting of the patient's rising creatinine. His urinalysis was negative for blood, protein, and white blood cells. Urine pH and specific gravity were also normal. Urine sodium was 34 mmol/L (normal: 30 - 90 mmol/L). Ultrasound of the retroperitoneum was negative for any evidence of obstruction. Initial differentials were initially acute tubular necrosis (ATN) from hypovolemia, acute tubular injury from APAP, or hepatorenal syndrome. We considered ATN, but there was no evidence of hypovolemia or poor perfusion as evidenced by a negative lactic acid and normal blood pressure, the absence of antihypertensives or diuretics, and normal urine sodium. Hepatorenal syndrome was also less likely, given the absence of hepatic encephalopathy and normalization of synthetic function. The etiology of acute renal failure was likely APAP toxicity, leading to tubular injury.\nWe planned to trend his creatinine and monitor for evidence of uremia or electrolyte imbalance, either of which would necessitate emergent hemodialysis. On Day 9, despite normalization of LFTs, the patient exhibited confusion and asterixis, consistent with uremia.\nHe underwent two hemodialysis sessions on Days 10 and 11. His creatinine improved afterward and continued to improve. His creatinine on discharge was 1.32 mg/dL (normal: 0.7 - 1.3 mg/dL). |
We present the case of a 42-year-old man who presented to the emergency department with a complaint of abdominal pain and diarrhea for 3 days. The abdominal pain started in the periumbilical region and was shifted to the right lower quadrant of the abdomen. The pain started gradually and had been progressing in severity. He described the pain as a stabbing in nature. It was exacerbated by movement and food intake. The pain was partially relieved by oral analgesic medications like paracetamol. The pain was associated with low-grade fever and decreased appetite. The patient also complained of diarrhea with five bowel motions/day. The stools were watery with no mucus or blood. He reported that diarrhea developed after he received an oral antibiotic therapy (cefuroxime) for a recent upper respiratory tract infection.\nThe past medical history of the patient was remarkable for diabetes mellitus that was well-controlled with oral antidiabetic agents. He did not undergo any previous abdominal surgeries. He had a smoking history of 15 pack-years. He had never drunk alcohol before. He worked as a taxi driver. The family history was unremarkable for any inherited gastrointestinal disorders.\nUpon examination, the patient appeared sick. He was not pale, jaundiced, or cyanosed. Vital signs revealed tachycardia (115 bpm), low-grade fever (37.5℃), normal respiratory rate (14 bpm), and maintained blood pressure (122/80 mmHg). The oxygen saturation was 99% on room air. Abdominal examination revealed a soft abdomen with diffuse tenderness. However, the tenderness was more pronounced in the right iliac fossa with a positive rebound sign. Further, the Rovsing sign was positive. Initial laboratory investigation revealed elevated leukocyte count and elevated inflammatory markers, including erythrocyte sedimentation rate and C-reactive protein. The renal and hepatic profiles were within the normal limits (Table ).\nIn light of the aforementioned clinical information, the patient was diagnosed as having acute appendicitis. A CT scan with intravenous contrast was performed to confirm the diagnosis. The scan demonstrated colonic wall thickening with edematous haustral folds suggestive of pseudomembranous colitis. Further, an endoluminal lesion was observed in the cecum with an average size of 6 cm. The lesion was well-defined and had a homogenous fat density with no solid component. The mass was causing a partial colonic obstruction. Such findings conferred the diagnosis of cecal lipoma (Figure ).\nThe patient was prepared for an emergency laparoscopy for further evaluation and management. The operation was done under general anesthesia and the patient was placed in the supine position. Limited segmental rection of the cecum with appendectomy was performed. The estimated blood loss was 10 mL and the total operative time was 100 minutes. The patient tolerated the operation with no complications. He had an uneventful recovery. Histopathological examination of the resected sample revealed the diagnosis of cecal lipoma and the associated acute appendicitis. The patient was discharged on the fifth postoperative day. After 3 months of follow-up, the patient remained asymptomatic with no active issues. |
A 27-year-old left-hand dominant male presented to our orthopedic elbow clinic complaining of bilateral elbow clicking and discomfort which had been present for several years. His painful symptoms were localized to the anterior aspect of both elbows and had slowly become more painful despite simple analgesia and physiotherapy treatments. He also described intermittent paraesthesia in the forearm, in particular after physical activity with the arm. The pain was exacerbated when working out in the gym, in particular with pull-ups, and while heavy lifting as a storeman. He was otherwise fit and well. Examination revealed the full range of movement of both elbows with no instability or weakness. Grip and grind tests were negative for pain bilaterally. There was no objective sensory disturbance, and Tinel’s sign was negative. Hook test for distal biceps rupture was negative and provocative testing of the biceps produced no pain. While moving the joint on the left side, a clicking sensation could be palpated over the lateral aspect of the biceps tendon that reduced digital pressure. Plain imaging and MRI scans of both elbows did not reveal any pathology, and the decision was made to explore the right elbow, as this was the most symptomatic. Under general anesthesia with tourniquet, an anterior curvilinear antecubital fossa incision was made. The lateral border of the distal biceps tendon showed evidence of compression of the LACN at the musculotendinous junction in forearm supination as illustrated in and . The tendon was partially resected, and the nerve confirmed to move freely without further entrapment (Fig. 3). An associated partial thickness tear of the long head of biceps distal hemitendon was debrided endoscopically. Postoperatively the patient was allowed an immediate gentle range of movement in a polysling. At 4 weeks after surgery, he was completely asymptomatic. The patient has given written consent for intraoperative images to be used for medical teaching. |
A 35-year-old woman with clinical features consistent with MS including tall stature (1.95 m), arachnodactyly and mild scoliosis presented to the emergency department with acute onset of chest pain in 2008. The year before she had experienced an episode of chest pain, but she did not seek medical attention at that time. Upon arrival a full work-up was initiated and a computed tomography angiography (CTA) revealed chronic DeBakey type I aortic dissection and aneurysmal degeneration of the aortic root measuring 7.74 cm and descending thoracic aorta (measurement 6.05 cm in maximum diameter) in axial view associated to a spiral dissection extending to both common iliac arteries (–). Interestingly the patient had a bovine aortic arch with left carotid artery emerging from the innominate artery; the dissection followed the inner curvature of the aortic arch and it did not extend to the supra-aortic vessels. Aneurysmal degeneration of the aortic arch was not present (). An echocardiogram confirmed aortic valve insufficiency. She was taken to the operating room for Bentall and De Bono procedure, replacing the aortic root and valve with a mechanical prosthesis, the patient was discharged home on postoperative day nine on systemic anticoagulation. Two months later, she underwent endovascular treatment of descending thoracic aorta using a 200×40 mm Zenith (Cook Inc., Bloomington, IN, USA) thoracic stent-graft that successfully isolated the aneurysm from the circulation. The distal thoracic aorta measured 3.3 cm and infrarenal portion 2.9, the decision was to maintain the patient under close surveillance. She was carefully followed in our institution by a multidisciplinary team, continuing her antihypertensive medical management with optimal blood pressure control. In 2012, a repeat CTA demonstrated aneurysm expansion of the thoracoadominal aorta measuring 6.4 cm and both common iliac arteries (measuring 2.3 cm in the right and 2.9 in the left) with imminent risk for rupture (). After discussions regarding the risks and benefits with the patient and her family, she was taken to the operating room for thoracoabdominal aortic and bilateral iliac arteries aneurysm repair.\nThe patient was placed in left lateral decubitus, a drain was placed for spinal cord protection, and subsequently a left thoracoabdominal incision was made via the 7th intercostal space crossing the costal margin and brought downward through the abdominal midline line ending just above the pubic symphysis. The left hemidiaphragm was circumferentially incised along its parietal insertion and the peritoneal sac was detached from the abdominal wall, the viscera were moved medially and the thoracoabominal aorta was totally exposed. The thoracic aorta endograft was clamped just above the diaphragm and reconstructions of the aorta and vessels were performed using a 22 mm five-branched Dacron graft, with the proximal end anastomosed to the stentgraft using pledgets and the graft branches to both renal arteries, celiac trunk, superior mesenteric artery and finally to the artery of Adamkiewicz (). Finally a bifurcated 20×10 mm graft was anastomosed to the distal tube graft and its limbs distally to the common iliac arteries bilaterally (). Total circulation was reestablished and hemostasis was ensured, and subsequently the thorax and abdomen were closed by layers. The surgery was completed successfully without complication and her hospitalization course was uncomplicated. The patient was discharged in stable condition in postoperative day 12 with preserved kidney function and without neurologic deficits in her lower extremities. The patient continued to be imaged in annual basis to rule out recurrent aneurysms or graft stenosis. demonstrate a CTA with three dimensional reconstruction of the aorta without new dissection or aneurysmal degenerations, and a schematic drawing of the complex hybrid repair with the prosthetic material utilized for the aorto-iliac reconstructions. |
A 44-year-old Nigerian female was admitted with a large, symptomatic abdominal mass. She was para 0, gravida 0 and in 2011 underwent open myomectomy through a lower midline abdominal incision for large, symptomatic fibroids. She also had a background of pulmonary tuberculosis (TB) which was treated in 1995, iron-deficiency anemia, and a benign goiter. We received the consent of all patients. Within the first few months following her open myomectomy she began to develop abdominal ascites, which was drained percutaneously on approximately three occasions in 2011-12. Owing to some personal circumstances, she did not attend her regular outpatient appointments and was eventually lost to follow-up. However, her abdomen continued to swell, with expansion of the skin and subcutaneous tissue that surrounded the scar.\nShe had no other relevant gynecological history and, aside from ferrous sulfate, she took no other regular medications. She was a non-smoker, denied alcohol use, and lived independently with her extended family. In 2016, five years following her original open myomectomy, she presented with a large abdominal mass that appeared to arise from the abdominal wall. This mass began to spontaneously discharge large volumes of brown fluid on the day of her admission. She was systemically well and gave no history of change in bowel habit or obstructive symptoms. She was not sexually active and had a normal menstrual history. She was not up-to-date with smear testing but denied intermenstrual bleeding. Her last menstrual period was one day previously.\nOn clinical examination she was thin, weighed 48 kg, with a body mass index (BMI) of 18. She was hemodynamically stable with a normal cardiorespiratory examination. She had a soft abdomen, with evidence of shifting dullness, and a large, irregular, firm mass that arose from the lower half of the abdomen overlain by her lower abdominal midline scar (). It measured approximately 30×20×10 cm. The overlying skin was of variable thickness with several small puncti on its inferior aspect, one of which discharged brown, odorless fluid. The mass itself was non-tender. Digital rectal examination was unremarkable. Bowel sounds were normal and could not be detected on auscultation of the mass. The clinical impression was that this was a large incisional hernia with evidence of ascites. Laboratory blood results revealed a microcytic anemia (hemoglobin count 10.1 g/dL, mean cell volume 63.6 fL), normal white cell count, renal and liver functions, and a mildly elevated C-reactive protein of 33 mg/L. Abdominal and chest radiographs were unremarkable. A computed tomography (CT) scan of her abdomen and pelvis confirmed the presence of a large, extraperitoneal lobulated space-occupying lesion with a mixed cystic and solid appearance that extended at least 20 cm caudally (). There was an 8×11×13 cm lesion in the uterus and a moderate amount of ascites, mainly in the lower abdomen and pelvis.\nA follow-up pelvic ultrasound scan (USS) demonstrated a bulky uterus that measured 15×11.5×9.7 cm with gross pelvic ascites. The differential diagnosis was a possible uterine malignancy with peritoneal and abdominal wall carcinomatosis or disseminated TB, particularly in light of her previous pulmonary TB. Assessment of her tumor markers showed that both the CEA and CA19-9 were within normal range; CA 125 was elevated at 89.8 U/mL (0-35 U/mL). Her hepatitis (A, B, C, E), human immunodeficiency virus (HIV), autoimmune serology and sickle cell tests were all negative. She underwent ultrasound guided peritoneal biopsy for TB screening, the histology of which showed chronic inflammation with no evidence of granulomatous inflammation or malignancy. Additionally, her ascitic fluid was negative for Mycobacterium tuberculosis. Two weeks following her original admission she underwent a laparotomy with excision of the large abdominal wall mass. This was carried out through an inverted T incision that encircled the lower midline laparotomy incision and the mass, but preserved the umbilicus. The extra-abdominal mass was of mixed cystic and solid components, and weighed 1.52 kg. It communicated with the abdominopelvic cavity through a 2 cm defect in the linea alba just below the umbilicus. The abdominopelvic cavity contained a large amount of odorless, brown fluid which flowed into the mass. There was an enlarged uterus bulky with fibroids. There were two large endometrioid cysts bilaterally in the region of the adnexae. The ovaries could not be clearly delineated and the fallopian tubes adhered to the pelvic walls. There was a large capsule that covered the small and large bowel, liver, gallbladder, and stomach. The mass was dissected free from the abdominal wall fascia and excised (). The endometrioid cysts that contained altered blood were drained. The large abdominopelvic capsule was stripped off of its adherent viscera, but it was not safe to strip it off in its entirety.\nThe fascial opening, which extended caudally by 5 cm, was closed with interrupted 1 Nylon sutures. The umbilicus was preserved. We left two large Robinson drains in the abdominopelvic cavity and two negative pressure (Redivac) drains remained in the subcutaneous space. The skin was closed with horizontal mattress sutures using 2-0 Vicryl Rapide. A negative pressure incision management system (PICO dressing) was applied to the wound. The final histology confirmed a 28×19×5 cm mass of endometrial tissue with no evidence of malignant transformation. The patient made a good post-operative recovery and was discharged one week following surgery with the abdominal drains and planned gynecological follow-up. She was assessed on a weekly basis in the General Surgery Outpatient Department in general surgery outpatients. All drains were removed 10 days following discharge (). The patient provided written informed consent for publication of this case report and accompanying images. She remains well. |
A 69-year-old female was referred to our clinic for an incidental finding of a large Morgagni hernia found on a recent CT chest scan for lung cancer screening. Patient reported occasional shortness of breath after prolonged ambulation but denied chest pain. She did have remote history of acid reflux symptoms but nothing recently. She denied issues with prematurity or issues with development as an infant, chest trauma, or MVA history. She did complain of occasional right shoulder pain but attributed this to arthritis. Denied history of heart attack, stroke, DVT, or PE. She had a 30-pack-year smoking history but quit a year prior. She was up-to-date on her colonoscopy, current within the past year. She denied hematochezia and melena, bowel habit changes or major body weight changes as well as any current abdominal pain. On examination her vitals were within normal parameters. Heart and lungs were unremarkable. Abdominal examination was soft with normal bowel sounds and nontender. Remainder of examination was unremarkable. Laboratory values included a normal CBC and BMP. A CT chest scan had demonstrated a large retroxyphoid hernia of Morgagni involving several loops of small bowel and transverse colon located in the right inferior hemithorax (Figs and ). No evidence of acute incarceration or strangulation were noted. A detailed discussion was undertaken with the patient regarding her hernia and she was consented for a laparoscopic repair with mesh.\nPatient underwent a laparoscopic approach in lithotomy positioning with the primary surgeon working between the legs. Three working ports were used, a 12 mm port at the umbilicus and two 5 mm ports; one in the LUQ and one in the RUQ. Upon initial laparoscopy multiple loops of small bowel were progressively reduced out of the hernia sac which also included the ascending colon and part of the transverse colon (Figs and ). All the small bowel and the colon appeared viable. The redundant parietal peritoneal hernia sac was excised out of the right inferior hemithorax utilizing a LigaSure (Covidien) (Fig. ). The falciform ligament was also taken down all the way to the diaphragm. The defect in the diaphragm measured to be approximately 9 cm by 4 cm. A section of Pariatex composite mesh was then trimmed to 2 cm in width by 9 cm in length. Three stay sutures of 0 Ethibond were placed laterally and in the middle of the mesh. This was placed into the peritoneal cavity after soaking it in vancomycin with local anesthetic. The sutures were then percutaneously brought through the diaphragm edge that was unattached to the anterior abdominal wall and then subsequently through the anterior abdominal wall. These were then tied thereby re-approximating the unattached edge of the diaphragm to the anterior abdominal wall near the xiphoid (Fig. ). Additional 0 Ethibond sutures were placed in between these initial ones percutaneously with a suture passer.\nAdditionally, another Pariatex composite mesh was then trimmed to 12 cm in width by 9 cm, soaked in vancomycin with local anesthetic and then placed into the abdominal cavity. It was positioned over the area of the repair and fixed into place with absorbable tacks around its caudad edge and centrally. Along the cephalad edge it was fixed with a running V-lock absorbable suture to the diaphragm. Fibrin glue was placed along this same edge (Fig. ). The ports were removed and incisions were closed.\nPatient’s postoperative course progressed well. She was monitored overnight and discharged the following day. She was seen for follow-up in 2 weeks out of surgery and did quite well. She was tolerating a regular diet and having bowel movements. A month after surgery another CT scan was obtained which demonstrated a postoperative seroma in the right inferior hemithorax (Fig. ). Currently, the patient is to be seen in a 6-month follow-up to have another CT scan at that time. |
A 15-year-old boy presented to the clinic with a right wrist pain, which is aggravated for 3 months ago. The patient hurt his right wrist after a fall while playing soccer a year prior to the presentation. The patient did not receive any treatment despite experiencing pain during laborious tasks, since he was able to perform daily activities. Upon physical examination, the radial side of the wrist had mild edema and evident anatomical snuff box tenderness. The patient displayed a limited ROM with flexion and extension angles of 70° and 60°, respectively, in the right wrist (80° and 90° in the left wrist, respectively). The radial and ulnar deviation angles in the right wrist were 15° and 50°, respectively (25° and 50° in the left wrist, respectively). When we examined the patient, the wrist showed mild swelling on the radial aspect as well as anatomical snuff box tenderness. He displayed limited ROM, flexion and extension angles of the right wrist were 70° and 60°, respectively (with 80° and 90° in the left). The radial and ulnar deviation angles in the right wrist were 15° and 50°, respectively (with 25° and 50° in the left).\nInitial plain wrist radiographs demonstrated nonunion of a fracture in the waist of the scaphoid (Fig. A). A computed tomography (CT) was obtained and indicated nonunion in the scaphoid waist and lateral intra-scaphoid angle of about 88°. The results induced the finding of humpback deformity (Fig. B).\nArthroscopic bone grafting and percutaneous K wires fixation was performed under general anesthesia. The mid-carpal joint arthroscopic findings revealed nonunion in the waist area, with punctate bleeding observed in proximal and distal fragments after arthroscopic debridement and removal of necrotic tissue, at the nonunion site. The associated injury was Geissler grade II instability at the volar side of the SL joint (Fig. C-G).[ We could get a complete bone union at 9 weeks after operation (Fig. H).\nAt 54 months’ follow-up, the preoperative pain of the patient improved on the VAS from 3 to 0, and the preoperative Quick DASH score also improved from 29.5 to 0. The ROM and grip strength improved from the preoperative normal range of 80% to 95% and 50% to 84%, respectively (Fig. I). |
A 53-year-old Caucasian woman was referred to our institution because of the suspicion of peritoneal carcinomatosis, raised by the findings of ascites at a transvaginal ultrasound performed as a yearly routine exam; a pre-surgical staging exam with computed tomography (CT) scan show thickening of the gastric walls, multiple omental nodules and ascites ().\nHer previous personal history was unremarkable and she denied any clinical symptom or cancer history.\nAt our hospital, she underwent an esophagogastroduodenoscopy and colonoscopy, with results negative for gastric/colon cancer.\nHer comprehensive metabolic profile revealed mild liver dysfunction with an alanine transaminase of 77 U/L and aspartate transaminase of 71 U/L. When tumour markers were assessed, CA125 demonstrated increased levels of 290 U/mL (normal values <35 U/mL), whereas carcinoembryonic antigen, CA 19.9 and other immunohistochemical markers were within the normal ranges. Serological assessment of HIV, hepatitis C virus and hepatitis B virus were negative.\nTen days later, the patient underwent an ultrasound-guided biopsy () with a diagnosis of suspicious carcinoma from the an unknown primary site.\nAfter 2 weeks, the patient received a CT scan of the thorax (to complete pre-operative staging), demonstrating a spontaneous (with no therapy) dimensional and numerical reduction of peritoneal lesions in the upper abdomen, partially included in the chest CT scan, as well as resolution of peri-hepatic and peri-splenic ascites ().\nSince there was no evidence of primary cancer at pre-operative examinations and the second CT scan revealed a partial resolution of peritoneal implants and ascites without therapy, the suspicion of an infectious disease was raised.\nThe pathological evaluation of the biopsies performed on the omentum and peritoneum revealed the presence of lymphoid aggregates with a central core of epithelioid cells with large eosinophilic cytoplasm, without atypia or mitosis () and with no immunohistochemical marker of oncologic malignancy. Due to the presence of necrotic nodules with histiocytes and giant cells, a Ziehl–Neelsen stain was performed to identify bacilli (), whose presence was then confirmed with molecular assays.\nBecause of the uncertain result of the biopsy and the conflicting results of the 2 CT scans, in order to rule out malignancy with certainty, the patient underwent a laparoscopic surgery in 2 weeks.\nDefinitive histological diagnosis excluded the presence of malignant cells and reported a necrotising inflammation caused by non-tuberculous mycobacteria. Hence, the patient was sent to a hospital with expertise in infectious diseases.\nA follow-up CT scan performed 1 year later confirmed a complete recovery of peritoneal findings. |
The patient is a 68-year-old male, immigrant to the US from Iraq, where he was a sheepherder. He has a long-standing medical history of echinococcal hydatidosis and known hepatic cystic disease for more than 30 years. He had been treated previously with cystectomies and hepatic lobectomy in his native country. Prior surgical treatment was complicated by intraoperative contamination and dissemination of the disease to the peritoneum and pelvis secondary (). Repeat exploratory laparotomy for palliative control of the extensive peritoneal and pelvic cystic disease was not curative and he was placed on lifetime maintenance therapy with albendazole. Serum titers against echinococcal antigen by an IgG-ELISA and cross-sectional imaging when necessary were employed to monitor disease status and response to therapy. Patient also has a 50-pack-year smoking history but otherwise has an unremarkable medical history. A routine abdominal CT scan obtained in late 2008 to monitor disease status revealed an incidental finding of a right lung base opacity. Dedicated chest CT confirmed a 2.5 × 1.6 cm right lower lobe nodule along the infrahilar region with possible post-obstructive atelectasis (). Whole body PET scan showed high FDG uptake in the perihilar soft tissue mass with SUV of 7, consistent with primary bronchogenic carcinoma. There were no foci of distant tumor metastasis but FDG-avid hydatid cysts were noted in the peritoneal and pelvic cavities. A biopsy of the lung lesion obtained via fiber optic bronchoscopy confirmed the presence of non-small cell lung cancer, favoring adenocarcinoma () with clinical staging of T4N0M0 (AJCC 6th edition). Thoracoscopic resection was attempted but aborted due to intraoperative finding of direct pericardial invasion by the tumor. The patient was treated with chemotherapy and radiation using a sequential approach due to significant postoperative debility that made concurrent therapy unsafe. Serial measurement of echinococcal serum antibodies with an IgG ELISA assay (ARUP Laboratories, Salt Lake City, UT) was performed to monitor disease activity. The patient received three cycles of systemic chemotherapy with cisplatin and docetaxel over a 3-month period followed by radiation therapy to the chest to a total dose of 66.6 Gy in 37 fractions and tolerated treatment with minimal toxicity. The most proximal echinococcal titer obtained prior to initiation of chemotherapy was 3.2. The repeat titer after completing two cycles of chemotherapy showed a drop in the titers to 2.2 down reaching a nadir of 1.8 (). A repeat measurement of echinococcal titer about 2 months into radiation treatment showed a nadir level of 1.0. Restaging scan including an abdominal CT scan after completion of chemoradiation was stable with a minimal decrease in the size of index intra-abdominal echinococcal cysts. Post-radiation, the patient received consolidation chemotherapy with three cycles of carboplatin and docetaxel and achieved complete response in the lung mass along with a further drop in the echinococcal titer to 0.5, the lowest value ever measured over the 10 years that the patient had been monitored for his chronic echinococcal infection at our center. Monitoring for disease recurrence with restaging scans continued while the patient was off chemotherapy. Although he continued to receive albendazole for his echinococcal disease during this time, there was a gradual increase in size of some of the areas of perihepatic echinococcal cystic lesion.\nFollowing recurrence of his cancer approximately 10 months later, patient was restarted on chemotherapy using a combination of carboplatin and pemetrexed. There was a similar reduction in the echinococcal titer with the resumption of chemotherapy. Due to treatment-related side effect, the patient elected to discontinue further chemotherapy following which the antibody titer gradually increased, reaching a peak of 6.32 within 4 months of the last dose of chemotherapy despite continued maintenance on albendazole. The patient is now approximately 6 years out from his original diagnosis of locally advanced lung cancer and remains alive and of chemotherapy. |
A 53-year-old man had injured his right hand in a motor vehicle crash, sustaining a composite wound exclusively to the dorsal aspect of the distal hand and the middle and ring fingers. More specifically, he suffered a comminuted intra-articular fracture of the proximal phalanx of the ring finger with a 6 × 8-cm overlying soft-tissue defect that also included the distal hand and middle finger to the proximal interphalangeal (PIP) joint level. The extensor tendon of the ring finger was disrupted, but not lost (). The volar surface of the right hand remained intact.\nThe wound was temporarily covered with artificial dermis and reconstruction was performed 14 days after injury. After surgical debridement, an 8 × 8-cm area of serratus fascia and a block of bone measuring 3 × 1×0.5 cm from the scapula on the angular branch of the thoracodorsal artery were harvested concomitantly (). The angular branch arose from the serratus anterior pedicle of the thoracodorsal artery and the length of the pedicle dissected to the bifurcation of the subscapular artery was 8 cm. After setting the harvested bone block in the defect and suturing the disrupted tendon, a fascial flap was placed over the wound. A split-thickness skin graft from the ipsilateral chest wall in the same operative field was grafted on the fascial flap. In the anatomical snuff box, the artery of the flap was anastomosed to the radial artery and the vein of the flap was anastomosed to the cephalic vein in end-to-end fashion.\nThe defect was reconstructed with good contours, whereas the joints of the ring finger were stiff. Six months postoperatively, the metacarpophalangeal (MP) joint had stiffened in 40° of flexion, and the PIP and distal interphalangeal (DIP) joints had stiffened straight. Grip strength was 11 kg for the right hand and 53 kg for the left, unaffected hand. However, since the stiffened fingers did not impede pinching or grasping, the patient required no additional surgery to improve range of motion of the ring finger (). |
A 67-year-old man with a history of chronic obstructive pulmonary disease, cerebral vascular accident, necrotizing pancreatitis complicated by pseudocyst requiring splenectomy and heart failure with preserved ejection fraction was transferred to our hospital following one month of treatment for pneumonia. He was a distant alcoholic but had since gone through rehabilitation and admitted to drinking one time per week and smoking four cigarettes a day. He had previously presented to his primary care physician with fever and malaise and was diagnosed with community-acquired pneumonia. He was treated with five days of azithromycin. He continued to worsen, and was admitted to an outside hospital with hypoxemia and right lower lobe pneumonia for which he was started empirically on vancomycin and piperacillin-tazobactam. His hospital course was complicated by respiratory failure requiring intubation for three days and a recurrent exudative right lung loculated effusion that required decortication and placement of a catheter that remained in place for two weeks. All blood and pleural fluid cultures were negative.\nOn transfer to our hospital for physical rehabilitation, the patient complained of mild shortness of breath. He denied hemoptysis, chest pain, orthopnea, nausea, chills or night sweats. Physical exam was significant for bilateral rhonchi with signs of consolidation in the right lower lobe. His labs were notable for a white blood cell count (WBC) of 17,000 cells/mcl with 87% neutrophils, and a chest radiograph revealed a right middle lobe infiltrate. He was continued on intravenous (IV) vancomycin and piperacillin-tazobactam at admission. Over the next two days his WBC climbed to 21,000 cells/mcl. Computed tomography scan of the chest revealed a right-sided empyema with extensive bilateral airspace disease consistent with severe pneumonia. A new chest tube was placed, which drained dark brown exudative fluid with gram-positive cocci on gram stain. The fluid was cultured and grew E. faecium resistant to ampicillin and vancomycin but sensitive to linezolid, gentamicin and streptomycin. The patient was started on linezolid and improved over the next two weeks, with resolution of the chest tube drainage. |
A 54-year-old Hispanic female initially presented to the hospital with a one-month history of dysphagia. Her past medical history is significant for stage IV adenocarcinoma of the right lung with metastases to the L2 spine in remission status post radiotherapy and chemotherapy, GERD, and intermittent asthma. Her medications included crizotinib. She was diagnosed with esophageal stricture and was admitted to the hospital for balloon dilatation. Shortly after the procedure though, she became hypotensive, tachycardic, and tachypneic, and she was admitted to the ICU.\nChest X-ray at this time demonstrated new right-sided infiltrates, thought to be secondary to aspiration pneumonia, and the patient was started on vancomycin and meropenem. There was also a concern for esophageal perforation, so a CT scan was performed, and it revealed a large right posterior thoracic mass with a mediastinal invasion that was obstructing the right pulmonary artery, in addition to an enlarged right heart. An echocardiogram that was also done showed right ventricular dilation, along with severe pulmonary hypertension, with a pulmonary artery systolic pressure of 75-80 mmHg.\nDespite optimal management, the patient continued to be tachypneic, hypoxemic, and dyspneic. As her respiratory status continued to decline, the patient was intubated, and the family decided to have a ‘do not resuscitate’ order for the patient. During her stay in the ICU, the patient became consistently tachycardic with a heart rate ranging from 100 to 120 beats per minute. Given her respiratory failure, active malignancy, and prolonged immobilization, the patient’s Geneva score was calculated to be 9, and a CT angiography (CTA) of the chest was ordered to rule out pulmonary embolism.\nCT angiography showed filling defect and concentric narrowing of the main right pulmonary artery, with pulmonary artery occlusion to the right lower lobe, likely due to arterial embolus or mass. The scan also showed invasion of the left atrium, as well as invasion of the left and right pulmonary veins (Figures -). The patient’s clinical status continued to worsen, and she was treated for distributive/cardiogenic shock with maximal blood pressure support, but she, unfortunately, succumbed to death. The time elapsed from admission to time of death was three weeks. |
A 45-year-old female presented to our clinic with abdominal pain for the last month. In addition the patient presented abdominal fullness, constipation, and loss of weight the last month. On physical examination abdominal discomfort was present. Medical history revealed a prior operation in the left arm for melanoma and axillary lymph node dissection 7 years ago with initial stage unknown and she received adjuvant high-dose interferon (Kirkwood regimen). In May 2014 she developed symptomatic iron-deficiency anemia and diffuse abdominal pain. Imaging exams revealed an obstructing abdominal mass originating from the small bowel and causing intussusception (). Laboratory examination revealed no remarkable findings. An exploratory laparotomy was decided and performed. During the operation indeed an intestinal intussusception was found () due to what appeared to be a distant melanoma metastasis (). Intestinal resection was performed with end-to-end hand sewn jejunojejunostomy. After careful checking no other distant metastasis was found in the abdomen. The patient had excellent postoperative course and was discharged at the 4th postoperative day.\nHistological examination of the tumor showed a malignant neoplasm consisting of large epithelioid atypical cells in solid arrangement which invades the mucosa, submucosa, and part of the muscularis propria. Immunohistochemistry revealed positivity of the tumor cells for HMB45 and Melan A (). One month after the operation the patient was subjected to 18FDG-PET/CT in order to rule out any other distant metastases. 18FDG-PET/CT result was normal except the thyroid gland that showed increased uptake (). Consequently it was decided to perform a total thyroidectomy. Two months after the first operation the patient was subjected to a total thyroidectomy. Pathology showed no signs of metastatic melanoma but revealed severe Hashimoto thyroiditis. The patient was referred for adjuvant immunotherapy. Molecular testing for the b-raf V600E mutation was positive. Between September and November 2014, she received first-line immunotherapy with ipilimumab at standard therapeutic regimen 3 mg/kg q3w for four cycles, which she tolerated without any remarkable toxicity. Subsequent radiologic and clinical controls showed no evidence of disease progression. The patient remains asymptomatic and free of disease 3 years after diagnosis and treatment of metastatic disease. The patient has given his consent for the case reports to be published. |
The patient was a 73-year-old man who was followed up for left shoulder pain for 1 year in another hospital. Magnetic resonance imaging (MRI) was performed because of progression of signs and symptoms, such as backache and lower limb weakness. Muscle weakness level was 4 in the manual muscle test, with slight difficulty of gait and muscle atrophy of the interossei dorsales muscle bilaterally. The patient complained of a moderate glove-and-stocking-type numbness on the four limbs. The MRI scan showed an area of increased signal intensity on T2-weighted images in the C5 region (). At discovery, the tumor was protruding into the spinal canal from the left side of the C5 vertebral body and pressed the dura mater from the front. The neurological symptoms were ascribed to the compression of the spinal cord and nerve roots by an expanding mass partly protruding into the vertebral canal (Figures and ). The metastatic lesion was found on neither the technetium bone scan () nor the positron emission tomography. The patient was treated with surgical resection of the tumor, followed by reconstruction in two stages. As the first stage, a posterior approach was selected for decompression. No heavy ion radiotherapy was performed because the tumor massively invaded into spinal canal and foramen, compressing the spinal cord and nerve root directly. Total laminectomy was performed for C4, C5, and C6. All the posterior elements, including the superior and inferior articular process and pedicles of C5, were resected by using piecemeal spondylectomy with air burr and Kerrison rongeurs. No bony element of C5 was restored without vertebral body, followed by fusion of C3 to T1 with pedicle screws. As the second stage, an anterior approach was performed to remove the total C5 vertebral body, lower bony endplate of the C4 vertebral body with the C4/5 disk, and upper bony endplate of the C6 vertebral body with the C5/6 disk. All these tissues were resected using an air burr and a Kerrison rongeurs. Complete intralesional resection of the tumor was performed by piecemeal, not en bloc resection, followed by spine column reconstruction by using a titanium mesh cage (). The patient did not undergo radiotherapy, because the tumor was located close to the cervical cord.\nThe pathological diagnosis was chordoma. On pathological examination, the cytoplasm of the tumor cells was acidophil with considerable nuclear pleomorphism (). It was lobulated and composed of an abundant myxoid stroma, with distributed nests, sheets, and cords of univacuolated, multivacuolated (physaliphorous), and glandular cells that showed almost some degree of nuclear atypia (). Immunohistochemical analysis revealed that the tumor cells were positive for cytokeratin AE1/AE3 (). Epithelial membrane antigen (EMA: ) and S-100 protein indicated a notochordal cell origin. The ratio of the MIB-1 index (Ki-67-positive cells) within the tumor was high (19.0%, ).\nRegarding the postoperative course, the patient underwent three additional spinal surgeries, because local recurrences of the initial lesion were found at 9 months, 4 years and 2 months, and 6 years after the first surgery (Figures and ). All three recurrences were located in front of the dura and were clearly encapsulated and isolated as a small oval lesion. These recurring tumors were treated with en bloc resection through the anterior approach, followed by replacement of the titanium mesh cage (). At 8 years and 4 months after the first surgery, the patient was ambulatory without lower and upper limb paralysis and demonstrated no neurological symptoms without recurrence (Figures and ). |
A 63-year-old lady was referred from ER to the ENT department, complaining of recurrent epistaxis episodes for the past 4 years. She also has history of left sided nasal obstruction, facial pressure, yellowish nasal discharge, protrusion of left eye and anosmia. She gave history of weight loss of around 7 kg in the past 3 months associated with decrease of appetite.\nBilateral nasal endoscopic examination showed a mass that easily bleeds on touch, filling the left nasal cavity and pushing the nasal septum to the other side.\nComputed tomography scan (CT) revealed a destructive mass in the left ethmoid/posterior maxillary and sphenoid sinus extending to the nasal cavity. It measured 4 × 4.5 × 6 cm, with extension posteriorly to involve the anterior superior border of the clivus, invading towards the pterygoid bone and reaching the carotid canal (Fig. ). MRI showed dural thickening lateral to the optic nerve on the left side but no clear intracranial neither periorbital extension. CT scan of chest, abdomen and pelvis were unremarkable for primary or metastatic tumour.\nThe tumour was treated with surgical excision; however, complete removal was not possible due to attachment to the optic nerve and carotid sheath. Post-operative radiotherapy was administrated.\nMultiple soft/tan and bone fragments were received for histological examination. Frozen section was performed for diagnosis and evaluation of margin status. The frozen section diagnosis was reported as “Malignant epithelial neoplasm with prominent clear cell change”. The tumour was extending to the resection margins.\nResected tissues were then fixed in 10% buffered formalin and embedded in paraffin. Permanent hematoxylin and eosin (H&E) sections revealed an infiltrative tumour with extensive bone destruction. The tumour consisted of polygonal to round cells arranged in nests and separated by fibrocellular and hyalinized fibrous septa. Most of the cells had a clear cytoplasm while few cells exhibited eosinophilic cytoplasm especially at the periphery of the tumour. The nuclei were round, uniform and centrally located with inconspicuous nucleoli. Mitotic figures and necrosis were not present. Perineural and lymph-vascular invasion were noted (Fig. ).\nThe differential diagnosis based on the H&E included squamous cell carcinoma with clear cell changes, mucoepidermoid carcinoma with prominent clear cell change, metastatic renal cell carcinoma and HCCC.\nImmunohistochemically, the tumour cells stained positive for EMA, CK5/6 (Fig. ), CEA and p63 and were negative for PAX-8, RCC, CK7, SMA and S-100 protein.\nFISH analysis of EWSR1 breakapart probe on paraffin-embedded tumour tissue showed evidence of a 22q12 rearrangement in 164 out of 200 (82%) of interphase nuclei scored (Fig. ).\nThe histological, immunohistochemical and molecular findings were consistent with primary hyalinizing clear cell carcinoma of the paranasal sinuses.\nOn follow-up, the patient showed no evidence of disease 4 months after the surgery. |
A 77-year-old lady presented to the emergency room with acute onset left hemiparesis.
The patient had a history of hypertension and Chronic Obstructive Pulmonary Disease (COPD) but was otherwise healthy and functionally independent. She was being treated with 2 antihypertensive medications: 5 mg amlodipine OD and 50 mg valsartan OD.
The patient had experienced a slight weakness in their left arm and left leg on the morning of admission but had not contacted the emergency services before a gradual worsening of the symptoms later that same day.
The paramedics found the patient to be awake with a left hemiparesis, left facial palsy and a mild dysarthria. The paramedics suspected an acute onset stroke, and the patient was admitted to our hospital as a stroke code.
Upon physical examination in the emergency room the patient had an National Institutes of Health Stroke Scale (NIHSS) of 11. The temperature was 36.7 °C, pulse of 90 beats per minute and blood pressure of 169/71 mm Hg. The initial prehospital oxygen saturation was 65% while on room air, subsequently increasing to 92% while breathing oxygen through a nasal cannula at a rate of 3 liters per minute. The respiratory rate was 22 breaths per minute.
An arterial blood gas obtained while the patient was receiving high-flow oxygen through a nasal cannula at a rate of 3 liters per minute showed a pH of 7.27, a partial pressure of carbon dioxide of 81 mm Hg (10.8 kPa), a partial pressure of oxygen of 60 mm Hg (8.0 kPa), a bicarbonate of 37.3 mEq per liter and a base excess of + 10.5 millimoles per liter.
A CT scan was performed including a pre- and intra- cerebral angiography. A subsequent perfusion scan was also performed. The CT examination was performed using the Siemens Somatom Definition Flash using GE Healthcare Omnipaque intravenous contrast and standardized protocols for |
A 24-year-old white man, a middle-distance runner (800 m) competing at national level (seasonal best/personal best of 1 minute 52 seconds), developed severe left heel pain in the pre-season in March 2013. His maximum perceived pain intensity was 10 cm on a visual analog scale (VAS) that ranged from 0 to 10 cm, with 10 cm expressing the worst perceivable pain; the athlete had to interrupt all running activity, and severe pain was perceived even when walking or standing. He continued training with aqua jogging and cycling. He got personalized hand-crafted orthopedic gel peads. Two months later he was attended by an orthopedic surgeon, who additionally prescribed oral intake of nonsteroidal anti-inflammatory drugs (NSAIDs) for 8 weeks. The athlete could continue his training but was not free from pain. When discontinuing medication in July 2013, pain returned immediately, and perceived pain intensity during walking was 10 cm on a VAS (range 0–10 cm). Eight sessions of ESWT were thus added to his treatment plan, and were conducted at a German Olympic center. He did not feel better after the treatment and reported a high level of frustration. An MRI was performed in January 2014 showing a calcaneal spur, signs of inflammation at the calcaneal tubercle, and structural changes of the plantar fascia, surrounded by a large edema (see Fig. ). In February 2014 he underwent an open plantar fasciotomy. Four weeks later he was allowed to perform the first units of regenerative running. Pain returned after approximately 1 week of training. An X-ray revealed no pathology and he was recommended to continue with soft training sessions. He received a peppering injection that reduced pain for 12 hours, and NSAIDs were re-prescribed. His running performance remained at a remarkably low level in comparison to his non-injured state, despite regular personalized training sessions. He presented himself at our out-patient clinic in July 2014 (for timeline see Fig. ).\nAn examination identified pain to palpation at the medial calcaneal tubercle and along the medial band of the plantar fascia. Thickening and enlargement of the proximal one-third plantar fascia was noted. Full and pain-free range of motion was noted to his ankle and foot. Standing caused moderate (VAS score, 5 cm) pain; walking caused severe (VAS score, 10 cm) pain. Latent myofascial trigger points could be found in the surrounding muscles: gastrocnemius medialis and lateralis, and tibialis posterior. Apart from these symptoms no abnormalities in his medical or family history which may have been relevant to the medical case were reported and he presented himself in a good mental condition. The diagnosis based on these findings was chronic plantar fasciitis (calcaneal spur syndrome).\nHe was treated with neural therapy (that is, injection of < 1 ml procaine 1%, which is a local anesthetic) of the surgical scar and along the surgical puncture channel. He lay in a supine position on a treatment table. Sessions took approximately 5 minutes. In total, three sessions (at baseline, at week 1, and after 4 weeks) were performed.\nAt the first treatment (March 2015), he described a slurping noise, like “if something filled up the pain origin.” Afterwards he could stand pain-free and walking (not running) was subjectively improved. After the third session the pain had been completely eliminated (VAS = 0 cm). He could return to sports at the former level. Since March 2015 no recurrence of the problem could be observed. No adverse events were observed. |
A 29-year-old male with a history of biliary atresia with failed Kasai procedure complicated with progressive cirrhosis and portal hypertension that received a left lateral segment living donor liver transplant (LDLT) from his biological father at 15 years of age. His immunosuppressive regimen included tacrolimus, and sirolimus. Eleven years after his LDLT, he developed advanced liver fibrosis and portal hypertension that manifested as refractory ascites. He received a splenectomy and a central spleno-renal shunt that eventually failed. He then underwent a side-to-side porto-caval shunt (PCS) at age 27 years. After 2 years with controlled disease, he presented with recurrent ascites and overt hepatic encephalopathy (HE) related to his progressive graft failure. His clinical course was also complicated by severe protein losing enteropathy due to his worsening portal hypertension (sprue was excluded by small bowel biopsy). Other causes of hypoalbuminemia were ruled out (e.g., kidney injury secondary sirolimus, as evidenced by 24-h urine collection with minimal protein and normal creatinine). Liver biopsy at this time showed stage 3-4 fibrosis. In addition, there was a paucity of interlobular bile ducts with degenerative changes in the remaining ducts, features compatible with chronic allograft rejection. A few months after, an abdominal ultrasound of the graft revealed a hepatic mass measuring 2.9 cm × 2.2 cm located in segment 2/3 and no evidence of intrahepatic duct dilation. Dynamic CT imaging showed a 3 cm lesion in the left lateral segment that was slightly hypodense and indeterminate in nature (Figure ). A dynamic magnetic resonance imaging (MRI) using liver mass protocol was performed due to the indeterminate nature of the lesion on CT and demonstrated increased vascularity of the lesion, raising suspicion for HCC. An ultrasound-guided percutaneous biopsy of the mass revealed a well-differentiated HCC (Figure ). Chest CT scan and bone scan demonstrated no evidence of extra hepatic disease. Alpha-fetoprotein (AFP) level was slightly elevated at 17 ng/mL (normal < 6 ng/mL). Anti-HBcAb (anti-hepatitis B core total antibodies) at this time and a year before showed negative results. The lesion was subsequently treated by percutaneous microwave ablation (PMWA).\nFollow up MRI was performed 1.5 mo after the ablation and showed no residual tumor (Figure ). The patient was subsequently listed for repeat liver transplantation. However, while on the wait-list he developed a second post-transplant malignancy, an EBV negative Burkitt’s type lymphoma. He received chemotherapy for the lymphoma but succumbed to complications due to the treatment that was in part limited by his advanced liver disease. |
A 53-year-old man presented with a gradually increasing mass located in the soft tissue of the oral cavity. The lesion was biopsied, and the pathology report showed increased infiltration of the buccal mucosa with monoclonal plasma cells. Immunochemistry demonstrated positivity for CD138, CIgA, and negativity for CD56, Cyclin D1 and CD20. Therefore, the diagnosis of soft tissue plasmacytoma was confirmed, for which he received localized radiotherapy with a total dose of 40 Gy, due to the absence of systemic disease as the bone marrow biopsy revealed the absence of neoplastic infiltration and serum and urine immunofixation were all negative.\nAfter five years, the patient noticed a painless swelling in his right testis. An ultrasound of the scrotum was performed that showed a hypoechoic mass in the right testicle with increased vascularization, and a normal-appearing left testis (Figure ). The patient subsequently underwent a right radical orchiectomy and the histopathology report showed testicular infiltration by a plasma cell neoplasm with identical immunophenotype (CD138+, CIgA+, CD56-, CD20-, Cyclin D1-) to the primary site in the oral cavity. Subsequently, the patient underwent a bone marrow biopsy that showed the absence of monoclonal plasma cell infiltration, and a PET/CT scan that was negative for reactive lesions suspicious of malignancy. In addition, serum and urine protein electrophoresis, as well as serum-free light chain assay were all within normal range, thus, excluding the presence of systemic disease, while complete blood count and full biochemical profile were normal.\nHowever, after one year, the patient presented again with painless swelling of his left testis that was attributed to disease relapse based on the imaging findings (Figure ). He refused to undergo left orchiectomy, thus he proceeded with systemic treatment based on lenalidomide, bortezomib and dexamethasone. Following 4 cycles of treatment, the patient underwent high dose melphalan with autologous stem cell transplantation. The blood tests of the patient revealed an increase in serum creatinine (1.3 mg/dl with 1mg/dl baseline level), normal calcium levels and normal complete blood count. Complete response was achieved with negative PET/CT scan and negative marrow minimal residual disease assessment. The patient continued on lenalidomide maintenance; however, six months later he was diagnosed with disease relapse in his left testicle (Figure ). A PET/CT scan was then performed, and showed a reactive lesion with an increased SUV max of 7 in the left testis, with no other loci suspicious of disease relapse. The blood analysis of the patient revealed no abnormal values. Since the patient refused surgery, he was initiated with next-line therapy, with bortezomib, cyclophosphamide and dexamethasone, he responded partially and still remains in remission (Figure ), while serum protein electrophoresis, immunofixation and serum-free light chain assay, all remain within normal levels. |
A 74-year-old male patient underwent left total knee arthroplasty (TKA) at our institution for degenerative knee osteoarthrosis. He had an uneventful postoperative course with no history of delayed wound healing or persistent drainage. Four years later, he presented with a 2-month history of a gradually developing painless swelling over the anterior aspect of the operated knee; the swelling was associated with a small sinus that was extruding a straw-coloured fluid. He had no history of fever, decreased appetite, or weight loss. He had no other musculoskeletal, respiratory, or systemic symptoms of note. He had no history of antecedent trauma, recent travel, or contact with infectious diseases. The patient is a known hypertensive, but the blood pressure was well controlled with treatment, and he is otherwise healthy. He is a retired teacher with no history of involvement in activities requiring excessive kneeling. He is ambulatory in his community and can walk comfortably with the assistance of a cane.\nThe patient's general physical examination results were within normal limits; positive physical findings were limited to the involved knee. There was an anterior knee swelling involving mainly the prepatellar area, approximately 7 cm in diameter, fluctuant, and not tender to palpation, with minimal surrounding erythema; the erythema was present mainly at the punctum. The punctum was draining a yellowish discharge on pressure (). There was no bony tenderness at the patella, distal femur, or proximal tibia. There was no detectable knee effusion, instability, or crepitus. The range of motion was well preserved (5–110°), as it was a prosthetic knee. It was only painful at the end of flexion as this movement compressed the prepatellar bursa.\nPlain radiographs of the knee showed a prepatellar soft tissue swelling (). There were no obvious bony changes, osteolysis, or loosening at the bone-prosthesis interface. Needle aspiration of the prepatellar bursa yielded 50 mL of slightly turbid straw-coloured yellowish fluid that was sent as per our protocol for cell count determination, microcrystal analysis, Gram staining, and Ziehl–Neelsen (ZN) staining for acid-fast bacilli (). Cultures for aerobic and anaerobic bacteria, Mycobacterium tuberculosis, Brucella, and fungi were requested.\nConsidering the patient's age, chronic presentation, and the presence of sinus, he was admitted with a diagnosis of infected prepatellar bursitis. The primary aims of admission were wound dressing, awaiting aspiration results, and further work-up. Aspiration results revealed normal cell counts, no crystals, and no organisms on Gram stain. To our surprise, ZN stain revealed acid-fast bacilli consistent with typical tuberculous infection; the bacterium was confirmed on culture 6 weeks later as Mycobacterium tuberculosis-sensitive to rifampicin, isoniazid, ethambutol, and streptomycin. Cultures for bacteria, Brucella, and fungi were negative. Aspiration was repeated and yielded similar results. The blood work-up showed normal total and differential white blood cell count and slight elevation of both erythrocyte sedimentation rate (ESR) (80 mm/hr; normal: 30–70 mm/hr) and C-reactive protein (CRP) (8 mg/L; normal: 0–4 mg/L). Tuberculin skin test revealed a negative result (<5 mm induration at 72 hrs), and further work-up including chest radiograph and echocardiogram revealed no evidence of systemic disease. A triple three-phase bone scan displayed normal uptake both at the bone-prosthesis interface and at the patella. An infectious disease consult was obtained. The patient was started on rifampicin (600 mg/day), isoniazid (300 mg/day), pyrazinamide (1500 mg/day), and ethambutol (800 mg/day) for 2 months and continued on the same dosage of rifampicin and isoniazid to complete a 6-month course.\nThree weeks later, the swelling significantly subsided in size and the sinus healed; therefore, the patient was discharged. He was reviewed at 6-week intervals at both the orthopaedic and infectious disease clinics for clinical progression and for any side effects of the medication. At the most recent 6-year follow-up, he was doing well with no evidence of local recurrence or prosthetic loosening (). |
Pleural effusion of usually greater than 500 ml that develops in a patient with cirrhosis and portal hypertension, in the absence of cardiopulmonary disease, is termed hepatic hydrothorax.\nWe report the case of a 56-year-old Caucasian male with hypertension and progressive painless jaundice who presented with shortness of breath of two weeks duration. The patient had a four year history of progressively increasing alkaline phosphatase of etiology for four years. There was no history of significant alcohol abuse or risk factors for viral hepatitis. On examination, his sclerae were icteric and there were spider naevi on the back. There was decreased air entry and dullness to percussion in the right lower lung field. Abdominal examination did not show organomegaly or free fluid. Labs showed direct bilirubinemia with a total bilirubin of 11.7, alkaline phosphatase 1261, AST 122, ALT 254, albumin 2.4 with normal platelet count and coagulation profile. Chest X-ray showed moderate pleural effusion (). ERCP revealed stricturing in the proximal and distal intrahepatic ducts with a beaded appearance. Common bile duct brushings were negative for malignancy. Liver biopsy showed findings suggestive of primary sclerosing cholangitis, prolonged obstructive biliary tract disease and moderate portal-periportal fibrosis. CT thorax and echocardiogram were negative for any mediastinal, pulmonary, pleural or cardiac pathologies that could cause pleural effusion. Thoracentesis revealed a transudative fluid with a serum-pleural fluid albumin gradient greater than 1.2, suggesting a diagnosis of hepatic hydrothorax. CT abdomen obtained at the time of admission did not show any ascites. The interesting aspect of this presentation was the absence of clinical or radiographic evidence of ascites.\nThe pathophysiology of hepatic hydrothorax involves the leakage of ascitic fluid from the peritoneal cavity into the pleural space through the embryologic defects, which are more prevalent in the right hemidiaphragm []. These defects arise from the rupture of pleuroperitoneal blebs as a result of raised intra-abdominal pressure from coughing, straining or ascites. The negative intrathoracic pressure aids the unidirectional flow of ascitic fluid to the pleural space through these defects. Diagnosis involves exclusion of cardiopulmonary disease, presence of transudative pleural fluid and demonstration of diaphragmatic defects when possible. The aim of treatment should be to relieve symptoms and prevent pulmonary complications by way of sodium restriction, diuretics, and therapeutic thoracentesis. Placement of a chest tube should be avoided as it leads to uncontrollable fluid loss and increased mortality. In resistant cases, pleurodesis with continuous positive airway pressure, videothoracoscopic repair of the defects [], and TIPS may be considered until a liver transplantation is performed, which is the definitive treatment. |
An 88-year-old man was referred to our hospital for emergent massive hemoptysis. His medical history was remarkable for chronic heart failure, moderate mitral regurgitation, atrial fibrillation, and chronic kidney disease. He was undergoing treatment with apixaban and pilsicainide for atrial fibrillation. He was severely hypoxic (SpO2: 80 under O2 15 L/min by oxygen mask) and hypotensive (systolic blood pressure: 80 mmHg) on admission. In the emergency department, we performed intubation into the right main bronchus through guided bronchoscopy; this was followed immediately by right side one-lung ventilation as portable chest radiography showed consolidation in the left upper lung. Bronchoscopy showed that the trachea was almost obstructed by haemorrhage and haematoma. He experienced cardiopulmonary arrest immediately after the airway was maintained. However, spontaneous circulation was restored by cardiopulmonary resuscitation. Contrast computed tomography (CT) demonstrated an aortic aneurysm at the aortic arch, which penetrated the upper lobe of the left lung (Fig. A,B). We suspected that it would be difficult to perform emergent surgery because of the patient’s poor general condition. Furthermore, we believed that there was no indication for endovascular stenting due to the following reasons: (1) the root of the left brachiocephalic artery was close to the penetrating portion of the aneurysm, at a distance of 12 mm. Thus, there might have been a high risk of obstructing blood flow to the brachiocephalic artery; (2) a risk of aortic injury might have been induced by stenting because the aortic arch was highly calcified. He was admitted to the intensive care unit, and we controlled blood pressure using nicardipine and discontinued anticoagulation therapy and performed platelet and fresh frozen plasma (FFP) transfusion for haemostasis. Bleeding from the APF decreased gradually due to astriction by haematoma. On the 17th hospital day, we performed bronchoscopy for the suction of haematoma, except in the bronchi of the left upper lobe, and adjusted the intubation tube for conversion to bilateral lung ventilation. On the 18th hospital day, we performed endobronchial occlusion with EWS to prevent fatal hemoptysis despite the risk of atelectasis. We inserted the EWS into each target bronchus with haematoma, with consideration of the risk of re-bleeding due to the removal of the haematoma. EWS sizes were as follows: (B1 + 2a: 7 mm; B1 + 2b: 7 mm; B3b + c: 7 mm; and B3: 7 mm) (Fig. A). B1 + 2c did not undergo EWS insertion because this bronchus was not responsible for bleeding on CT findings. There was no massive hemoptysis after bronchial occlusion with the EWS; subsequent mild hemosputum was controlled by a haemostatic drug. The patient was successfully extubated on the 22nd hospital day and was discharged on the 47th hospital day without complications and free from oxygen. Radiography showed that EWS had promptly fixed each bronchus (Fig. B). |
A 9-year-old female leucoderma patient presented to the stomatology department of a public hospital in Rio de Janeiro, Brazil. She complained of small nodules in the left parotid region that had developed over the course of 2 years. Her main complaint was of recurring periods of worsened symptoms characterized by the exacerbation and remission of gland volume that was possibly triggered by occasional otolaryngologic infections or unrelated to these infections. These symptoms suggest juvenile recurrent parotitis. Facial panoramic radiography revealed the presence of multiple circular radiopaque masses in the left parotid region (Fig. ). The ultrasound revealed increased volume of the left parotid, with imprecise borders, heterogeneous echotexture with hypoechoic and hyperechoic areas within it. These features were suggestive of an inflammatory process associated with calcifications in the parenchyma of the gland. CT scan revealed a dense mass in the left parotid; it was heterogeneous and included calcifications in its center (Fig. ). Because of the association between the patient’s clinical history, her clinical presentation, and the imaging findings, the possible origin of the calcified materials was questioned. There was evidence of sialoliths or dystrophic calcification associated with recurrent inflammation/infection. Sialoliths are typically symptomatic because of their association with secondary bacterial infections, which are generally treated with systemic antibiotic therapy. Spontaneous remission of bacterial sialadenitis associated with sialoliths is not expected. In addition, sialoliths generally observed as oval-shaped calcified masses or fusiforms on imaging. Because of the pediatric nature of this case, the clinical conduct selected to treat this patient was clinical follow-up and the use of imaging and functional assessments of the gland affected every 6 months or when any signs and/or symptoms appeared. After 48 months, the patient is asymptomatic, without periods of exacerbation of the condition. Recent ultrasound (Fig. ) demonstrates an improvement in the inflammatory aspect of the gland. Clinical and imaging follow-up will be maintained. |
A 37-year-old Caucasian male with a known history of aplastic anemia (AA), presented to a rural hospital after a ground level fall. AA was diagnosed 10 months earlier after he was investigated for pancytopenia. A bone marrow biopsy showed cellularity of only 10% and the presence of a small paroxysmal nocturnal hemoglobinuria clone (less than 0.2%). He received standard combination treatment for AA with cyclosporine 225 mg orally twice daily, horse anti-thymocyte globulin (ATG) 40 mg/kg daily for 4 consecutive days, and prednisone 1 mg/kg daily. His other medications included daily Pantoloc 40 mg orally, daily Valtrex 500 mg orally, and daily Dapsone 50 mg orally for Pneumocystis jirovecii prophylaxis due to a reported allergy to trimethoprim/sulfamethoxazole. He had recently quit smoking and denied alcohol use but actively used other recreational drugs, including marijuana, cocaine, and methamphetamine. He was unemployed. He had no known other medical co-morbidities and was taking no other medications prior to developing AA. The etiology of AA was felt to be idiopathic because he had no improvement after an initial trial of sobriety. AA improved following immunosuppressive therapy and, although human leukocyte antigen typing was performed, a subsequent bone marrow transplant was deferred not only because of the medical therapeutic response but also due to his ongoing recreational drug use. Although he was no longer transfusion dependent a month after starting immunosuppressive therapy, his treatment compliance waned overtime due to regular ongoing recreational drug use of cocaine and methamphetamines. He routinely used unsterilized tap water for illicit drug injections, but he denied other exposure to fresh or salt water sources at home or in the community.\nOn presentation to the emergency department he was not in distress, with a heart rate of 90 bpm and a blood pressure of 116/59. Severe pallor was noted upon examination, as well as a petechial rash and mild ecchymoses (Fig. ). The rest of his physical assessment was normal, including a neurological examination. Admission bloodwork revealed severe pancytopenia with hemoglobin of 22 g/L, a platelet count of 1 × 109/L, a white blood cell count of 3.7 × 109/L, and an absolute neutrophil count of 0.2 × 109/L (reticulocytes were not sent at admission, but 2 weeks into his hospitalization his absolute reticulocyte count was 12 × 109/L with a reticulocyte percentage of 0.5). All other admission blood work was normal, including liver function tests (total bilirubin 9 μmol/L (reference < 21 μmol/L), alanine aminotransferase 13 μmol/L (reference < 41 μmol/L), alkaline phosphatase 66 U/L (reference 30–130 U/L)) and renal function tests (creatinine 63 μmol/L (reference 59–104 μmol/L), glomerular filtration rate 120 mL/min (reference < 59 mL/min)). He was stabilized and transferred to a tertiary care center where he was restarted on treatment for relapsed AA with a regimen that included cyclosporine (5 mg/kg/day) and prednisone 30 mg daily in addition to five doses of ATG. He remained transfusion dependent throughout his hospitalization.\nOn day 10 after admission, he developed generalized, mild (3/10), colicky abdominal pain with an associated fever > 38.5 °C. He was started empirically on piperacillin-tazobactam (PTZ) 3.375 gm intravenously every 6 hours. Two sets of blood cultures, each consisting of an anaerobic and aerobic BacT/Alert bottle (bioMérieux, Laval, Quebec), were collected peripherally and from his central line. E. coli grew in each bottle set at 10 and 11 hours, respectively. He then developed watery, non-bloody bowel movements, 3–4 times a day, associated with rectal pain. Real-time PCR for Clostridium difficile A/B toxin on a stool sample was negative. Computerized tomography of the abdomen and pelvis was also unremarkable. Repeat blood cultures were negative at 24 and 48 hours after the initial positive set. He improved dramatically after 7 days of intravenous PTZ and was stepped down to oral ciprofloxacin 500 mg orally twice daily to complete a further 7 days of therapy.\nOn day 19 of admission he developed acute continuous severe (9/10), non-radiating dull rectal pain, associated with a high-grade fever (40.4 °C). Vancomycin 1.5 g intravenously every 12 hours and metronidazole 500 mg orally twice daily were empirically started and ciprofloxacin was continued in the same dosage. Blood cultures that were collected from peripheral venipuncture and a peripherally inserted central catheter line grew A. hydrophila at 11 hours. The peripherally inserted central catheter line was immediately removed the next day (day 20 after admission). The same day he also began to complain of vague, mild, bilateral leg pain. Delayed serum sickness due to recent ATG administration was considered a possible cause for his new symptoms because clinical examination did not show erythema, edema, or deformities on either of his legs. However, sustained bacteremia was diagnosed by recovery of A. hydrophila from repeat blood cultures (i.e., one anaerobic and aerobic bottle set from two peripheral venipunctures) positive after 11 and 16 hours of incubation. Bilateral leg pain steadily worsened in intensity (10/10) over the next 48 hours, and the area of distribution of pain extended to the lateral aspect of the right thigh although physical examination remained unremarkable. Creatinine kinase was increased at 470 U/L (normal range for males, 0–195 U/L). Ultrasound venous Doppler of both legs also showed no evidence of deep venous thrombosis. However, magnetic resonance images of both legs showed extensive bilateral patchy multi-compartment muscular and fascial inflammatory changes highly concerning for NF (Fig. , ).\nUrgent initial surgical debridement was performed that evening. An extensive four-compartment fasciotomy, debridement, and myomectomy were performed on both legs. Extensive ‘dishwater’ purulent material was found in multiple compartments of both legs, including (1) the superficial posterior compartment between the gastrocnemius and soleus muscles, and (2) the lateral deep compartment. There was also clinical evidence of severe muscle necrosis of the tibialis anterior muscles in the anterior compartment of both legs. He was admitted to the Intensive Care Unit post-operatively. After consultation with the Infectious Diseases service and review of the antibiotic susceptibility profile of the previously isolated A. hydrophila strain, antibiotics were changed to meropenem 1000 mg intravenously every 8 hours and clindamycin 600 mg intravenously every 8 hours. High dose intravenous immunoglobulin (2 g/kg) was also given. All prior antibiotics were discontinued.\nGram stain of tissue samples from the right tibialis anterior muscle showed no neutrophils but that gram-negative bacilli were present, and subsequently grew a heavy amount of A. hydrophila. Gram stain and anaerobic culture from the right vastis lateralis muscle also did not show the presence of neutrophils or organisms but grew scant amounts of A. hydrophila. A genus-level identification as Aeromonas was obtained for all isolates from blood and tissue samples by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry using a VITEK MS (bioMérieux, Laval, Quebec, Canada); since this technique has an accuracy of identification rate of 80–90% for species-level identification of Aeromonas [], all isolates were also analyzed using in-house bi-directional 16S rRNA gene cycle sequencing of the V1-V3 (approximately first 500 bp), as previously described []. Broth microdilution susceptibility panel testing was performed and interpreted using published guidelines []. All isolates were multidrug resistant to ampicillin, ceftriaxone, ciprofloxacin, and trimethoprim/sulfamethoxazole but susceptible to meropenem and tetracycline. The isolates were confirmed to produce an extended-spectrum β-lactamase (ESBL) using published guidelines and the Mast Disc Test (Mast Group Ltd., Merseyside, UK) []. Production of an AmpC β-lactamase was shown by resistance to cefoxitin disk (30 μg) testing and the Mast Disc test (Mast Group Ltd.).\nTwo additional extensive surgical procedures for removal of necrotic tissue from both legs were undertaken in the next 24 hours. Bilateral above-knee amputations were performed during the last debridement as a life-saving measure because of extensive rapid progression of bilateral leg necrosis, and the patient’s rapid clinical deterioration with severe unremittent hemodynamic instability during the operation. Post-operatively, he required aggressive resuscitation for septic shock in the Intensive Care Unit with intractable hyperkalemia and severe acidosis, and anuric acute kidney failure (creatinine 210 μmol/L; normal range for males, 50–120 μmol/L). Despite all therapeutic interventions, the patient went into cardiac arrest and passed away within 2 hours after the final surgery.\nPost-mortem examination at autopsy revealed findings related to the underlying AA, and evidence of septic shock secondary to extensive bilateral lower limb necrotizing myofasciitis. The bone marrow was markedly hypocellular and there was splenic enlargement at 331 g. The heart was enlarged (536 g). Cardiomegaly was likely a compensatory response to the AA due to the absence of atherosclerotic and hypertensive cardiovascular disease. In keeping with the patient’s severe septic shock, there was marked centrilobular necrosis of the liver, as well as petechial hemorrhages of the skin, heart, pleural surfaces, kidneys, and liver capsule. Histologic examination of skin and muscle from the left thigh showed necrosis of the muscle and deep subcutaneous adipose tissue, admixed with dense collections of gram-negative bacilli (Fig. , ). However, in keeping with the AA, there was notably an absence of an acute inflammatory response. |
A 12-year-old male obese child presented with a 1 day history of severe abdominal pain and fever. The pain was sudden in onset and severe in intensity. It started from the right iliac fossa and remained localized without any radiation. No relationship to intake of food or any posture was stated. It was continuous and pricking in nature. The patient also had a low-grade fever, which was continuous. This pain was associated with nausea but no vomiting. The patient had significant anorexia. There were no urinary or bowel complaints. There was no significant history of similar pain and the patient had enjoyed good general health before.\nUpon examination, he was an obese child in obvious distress lying in bed. His pulse was 130/min, his blood pressure was 110/65, and his temperature was 38°C. The rest of the general physical examination was normal. The abdominal examination showed tenderness in the right iliac fossa with rebound tenderness but no guarding or rigidity. There was no organomegaly and bowel sounds were present with an unremarkable rectal digital examination. The patient weighed 80kg.\nInvestigations revealed a white blood cell (WBC) count of 11.5 K/uL and hemoglobin was 14.4 g/dl. The rest of the serum chemistry values were normal. A plain abdominal radiograph was unremarkable and an ultrasound showed only minimal free fluid.\nWith a provisional diagnosis of acute appendicitis, the patient was taken to the operating room for an appendectomy. Upon opening of the peritoneal cavity, lightly hemorrhagic fluid was seen. On handling of the cecum, a torsed, gangrenous appendix epiploicae with 2 complete twists of the base was found []. It was transfixed and excised. The appendix was retrocecal in position and subhepatic in location with minimal inflammation and was kinked []. An appendectomy was also done.\nThe patient had an uneventful recovery and was discharged 2 days after the surgery. A peritoneal swab was negative for any growth. The histopathology was consistent with gangrenous appendix epiploicae. |
Patient is a 51-year-old woman with past medical history of hypothyroidism. She was complaining of dyspepsia so an upper endoscopy was done, revealing a mass in the greater curvature of the stomach, and a biopsy was taken. Pathology showed a poorly differentiated infiltrating adenocarcinoma with signet ring cells. A total radical gastrectomy reconstructed with esophagojejunal Roux-en-Y anastomosis was done. On the sixth postoperative day, purulent drainage was seen on the abdominal drain. And, an abscess was discovered at the level of the esophagojejunal anastomosis, surgery was required, the abscess was drained and a new esophagojejunal anastomosis was done high in the chest with autosutures. The patient persisted with poor medical condition; so an esophagogram identified a leak at the level of esophageal anastomosis, and after failed endoscopic placement of two metal stents to solve the leak, patient persisted with sepsis. Redo operation was performed and at thoracotomy an anastomotic leak, with free purulent fluid in the pleural cavity was found (Fig. A). An exhaustive washing of the pleural cavity was performed, stents were removed, thoracic esophagectomy was done, a feeding jejunostomy was made and a cervical esophagostomy was performed. Patient improved considerably after this, with adequate nutritional management through jejunostomy. She was discharged, and 6 months later she was hospitalized again for intestinal transit restitution with an esophagocoloplasty with interposition of the right colon via substernal route.\nEsophagocoloplasty was done, and hand-sewn anastomoses were made between the esophagus and the colon, drains were left in the abdomen and neck.\nOn the 10th postoperative day, an esophagogram was done to assess the neck anastomosis, which did not show any leakage or stenosis, which is why sips of liquids were initiated, attaining good oral tolerance, antibiotics were withdrawn, abdominal and cervical drains were removed and soft diet was initiated.\nOn the 13th postoperative day, serous fluid drained through the neck and became purulent a day after. A new esophagogram was done and an esophago-colonic anastomosis leak was discovered (Fig. B). An upper endoscopy was performed, localizing the fistula of 12 × 6 mm ( & Fig. C).\nPlastic surgery consultation was requested; management of the fistula with V.A.C. was decided.\nPartial opening of the cervical wound was done, and necrotic tissue debridement with extensive irrigation of the wound with saline and iodine over the cervical esophagus was performed. After this to protect the esophago-colonic anastomosis from direct contact with the V.A.C. a small paraffin gauze dressing (Lomatuell H, Paraffin Gauze Dressing) was placed over the cervical esophagus. The V.A.C. sponge was fashioned to fit the wound and placed over it. The adhesive drape was fixed to the neck skin and continuous suction between 100 and 125 mmHg was installed (Fig. A). In the first week, V.A.C. system drained about 50cc of saliva-like fluid daily and was changed every 2 days, once granulation tissue had begun to form over the wound, the system was changed every 5 days and no paraffin gauze was used (Fig. B). All V.A.C. changes were done in the operating room and during the first week of V.A.C. treatment, patient received total parental nutrition, on the 10th day patient was able to ingest liquids. Twelve days after initial use, the leak closed, since no fluid came out of the V.A.C. system, and after the patient resumed full normal diet, she was discharged home. On follow-up controls, the patient was in good condition (Fig. C). |
A 48-year-old Palestinian female patient with a history of trauma. The patient had slipped and fallen on her upper back, and she complained of progressively aggravating dyspnea at rest. Then, within the chest x-ray of trauma survey, found an incidentally huge mass occupying the left lung, irrelevant to the trauma. There was no past medical history, and the only surgical history consisted of one cesarean section 3 years prior to the visit. The patient was married and had four children. She was a non-smoker and had no recent history of traveling, weight loss or expectoration.\nExamination showed that the patient was stable with mild tenderness on palpation of the posterior upper back. Auscultation demonstrated absent breath sounds on the left. An abdomen examination concluded that there were splenomegaly.\nChest x-ray showed well-defined huge opacity of most left hemithorax with a shift of mediastinum to the right (Fig. ). CT chest/abdomen/pelvis with IV contrast revealed 20 × 15 × 18 cm3 well-defined mixed cystic lesion within the left lung containing multiple parts of the heterogeneous density with soft tissue elements and fat content. It also showed spots of wall calcification, where the lesion probably originated from the mediastinum, involving most of the left hemithorax. The mass compressed the mediastinal structures, great vessels, and airways (Fig. ). It is surrounded by a consolidation collapsed with a marked shift of mediastinum to the right side (Figs and ). No mediastinal lymphadenopathy and the right lung was clear. The spleen was enlarged with multiple cysts that varied in size with no significant enhancement post IV contrast in arterial and portal phases (Figs and ). The liver was unremarkable. Hematological tests were within normal limits. Mantoux test and Sputum culture were negative.\nThe decision was to perform a standard left anterolateral thoracotomy to remove the thoracic tumor after expiration because the cystic tumor was found to be very congested and vulnerable to rupture during the extraction (Fig. ). It emptied a large amount of thick, white/yellowish fluid and hair particles (Fig. ). The size of the tumor was extremely large, although no invasion to the mediastinum, vessels or to the airway had occurred. The tumor detached from the phrenic angle, diaphragm and all of the surrounding structures without any bleeding, air leak or complications. A laparoscopic splenectomy was done in the same session, and the spleen was extracted through the old cesarean incision scar for cosmetic purposes; the spleen shows multiple cysts on both visceral and diaphragmatic surfaces (Figs and ).\nThe patient was discharged on the 5th postoperative day. Histopathological examination revealed numerous fluid with soft tissue, squamous epithelium, adipose tissue, hair particles and calcification at the wall, which suggests benign mature intrapulmonary teratoma. The spleen contained multiple cysts that varied in size with mural calcification, which suggests cystic lymphangiomatosis of the spleen. The patient showed a good response in the follow-up with normal vital signs and labs. |
A 21-years-old Caucasian woman presented to a private dental clinic with a chief complaint of asymptomatic swelling in the gingiva observed four years prior. A gradual increase in size and no history of previous treatment were also reported during the anamnesis. The patient signed the informed consent, which represents the ethical approval of the faculty committee. Her medical and socio-economic histories were not contributory. The extra-oral evaluation did not reveal changes. The intraoral examination revealed a sessile nodule with a color similar to that of the mucosa and a focal erythematous area with a fibro-elastic consistency measuring 1.5 cm in the largest diameter extending from the inferior right lateral incisor to the inferior right first premolar. The lesion involved the vestibular and lingual gingiva, causing displacement of the inferior right canine (Fig. ).\nPanoramic reconstruction and parasagittal slices of the Cone Beam Computed Tomography (CBCT) showed a slightly superficial hypodense area between the inferior right lateral incisor and inferior right canine with reabsorption of the alveolar crest (Fig. ). Based on the clinical and immunological aspects, the main diagnosis hypotheses included peripheral ossifying fibroma, peripheral giant cell lesion, and ancient pyogenic granuloma. The peripheral odontogenic tumors were also included as a differential diagnosis. An excisional biopsy was performed and a clear separation was noted between the lesion and mandible bone during the trans-surgical approach. The histopathological analysis revealed a well-circumscribed proliferation comprising numerous islands and strands of epithelial polyhedral cells with well-defined borders and marked round nucleus in the connective tissue under the mucosal epithelium. Numerous nests, cords, and small islands of polyhedral cells with clear and vacuolated abundant cytoplasm were observed interspersed with the amorphous eosinophilic deposits (Fig. ). Immunohistochemistry was performed, which yielded positive results for CK-19 in the epithelial cells, except for the clear cells. Congo red staining showed the presence of amyloid-like deposits with apple-green birefringence under polarized light (Fig. ). A final diagnosis of a peripheral CEOT rich in clear cells was reached. No complications were observed in the postoperative appointment and a follow-up schedule was established. The patient has had no recurrence after 22 months (Fig. ). |
A 12-year-old male patient was reported to the Outdoor Patient Department of Pediatric and Preventive Dentistry, Pune, Maharashtra, with a chief complaint of pain and swelling in the lower left back region of the jaw since 15 days. Medical history was non-contributory. Extra-orally facial asymmetry was noted on the left side of the jaw with swelling extending anterio-posteriorly from the angle of the mouth to the lower border of the mandible (). The swelling had a smooth surface and the color of the swelling over the skin was normal. Palpatory findings revealed enlarged left submandibular lymph nodes tender on palpation. Intraoral examination revealed the expansion of the buccal cortical plate extending from the distal side of the left mandibular first premolar to the distal side of the first molar, measuring approximately 3 × 3 cm. The overlying mucosa was hard, red, and tender on palpation. It was smooth and no ulceration was observed. Also, the involved primary tooth was carious (). The panoramic view revealed unilocular radiolucency, which was well-defined and corticated extending from the distal surface of the mandibular left first premolar root to the distal surface of the mandibular first molar also involving the impacted second molar. Based on the above findings, a provisional diagnosis of radicular cyst was given.\nTo confirm the provisional diagnosis, fine needle aspiration cytology (FNAC) was planned. The procedure to be done was explained to the parents and the patient and their consent was obtained. The FNAC sample was sent to the Department of Oral Pathology and extraction of 75 was planned. Extraction of the involved primary tooth was carried out under local anesthesia (LIGNOX 2%), followed by aspiration of the cystic fluid and further irrigation with povidone iodine 5% (Indiamart). The socket was curated and the sample along with the extracted tooth was sent for confirmatory diagnosis. To prevent the loss of the impacted permanent premolar, the decompression technique was chosen as the treatment of choice. The cystic cavity was opened through the alveolar socket of 75, which helped to relieve the intra-cystic pressure of the cystic cavity further decreasing its size. A plastic stent made up of a needle cap was used to keep the cystic cavity in contact with the oral cavity and to open it for irrigation. The stent was stabilized using a ligature wire (26 gauge) and the patient was recalled after one week. A slight reduction in swelling and tenderness was noticed after 1 week. After 3 weeks recall, clinical and radiographic examination (orthopantomograph (OPG)), a gradual reduction in swelling and tenderness was observed (). At the third month recall, the swelling and pain had subsided completely (). The panoramic view also showed absence of radiolucency (). |
A 55-year-old Caucasian male, with a past medical history significant for tobacco abuse (41 pack-years), presented with shortness of breath accompanied by chest and back pain for two months. Blood workup showed a WBC count of 68,400 cells/µL, with an AEC of 27,360 cells/µL. A computed tomography (CT) pulmonary angiogram was performed, as he was hypoxic, and revealed a 3.6-cm speculated mass within the anterior right upper lobe, partially invading the anterior chest wall. It also revealed mediastinal and hilar adenopathy, an extensive osseous lesion (including compression fracture at T7), and a small pericardial effusion (Figure ). A CT of the abdomen and pelvis with contrast was performed and revealed a diffuse metastatic disease involving the liver, adrenal glands, spleen, and the bones. Magnetic resonance imaging (MRI) of the thoracic spine did not reveal spinal cord compression, but it did show the compression fracture at T7 and multilevel thoracic spondylosis. An MRI of the brain revealed a 5-mm lesion in the left occipital lobe, without edema or mass effect.\nThe hematology-oncology team was consulted for an evaluation of the metastatic disease and the eosinophilia. A core needle biopsy was obtained from a liver lesion and the result came back as poorly differentiated adenocarcinoma of the lung (cytokeratin 7, TTF1, and napsin-A were positive, while cytokeratin 2 and CDX2 were negative). Given his functional status, the decision was made to hold on systemic therapy and start on palliative radiation to the spine for pain control. The plan was to complete radiation sessions and then evaluate his functional status before starting systemic therapy.\nHe continued to have a high WBC count during the admission (Figure ). Therefore, a bone marrow biopsy was performed to rule out a hematologic malignancy and it revealed metastatic adenocarcinoma of the lung with no evidence of a myeloproliferative disorder. The flow cytometry from the bone marrow showed a CD5-positive clonal B-cell population, which was similar to the blood flow cytometry. Blood tests, including tests for Janus kinase 2 (JAK-2), calreticulin (CALR), MPL, BCR-ABL, and platelet-derived growth factor receptor (PDGFRA), were negative. The blood smear showed microcytic anemia with leukocytosis with absolute neutrophilia and eosinophilia. The serum immunoglobin E (IgE) was high at 377 IU/ml, and the tryptase level was low at 1.8 µg/L. Given these findings, his eosinophilia was related to a paraneoplastic process rather than a primary bone marrow disease.\nDuring the following days, the patient completed 13 sessions of radiation without improvement in his functional status, pain, or breathing. The case was discussed with the patient and his family; he decided that he would go with comfort measures, so he was discharged to the hospice facility. |
A 65-year-old man with severe chronic obstructive pulmonary disease (COPD) was admitted with a four-day history of chest pain and worsening shortness of breath. He explained the chest pain started suddenly when he tried to reach out for something on his computer table. It was located on the right anterior chest, sharp in nature, 7/10 in intensity, pleuritic, and worse with coughing and deep breathing. He had a past medical history of severe COPD with frequent exacerbations recently necessitating multiple antibiotics and steroid courses, coronary artery disease, gastroesophageal reflux disease (GERD), and hypertension. He had a 30-pack per year smoking history and quit about 10 years ago. He was a retired fireman living with his family.\nVitals signs in the emergency department (ED) were stable; he was breathing on ambient air. The physical examination demonstrated decreased breath sounds bilaterally without any wheezing or Ronchi. Moderate tenderness was present in the mid-axillary line in the fifth intercostal space, but no other abnormalities were noticed. Laboratory investigations were negative for any leukocytosis, troponin, or any other abnormalities. The electrocardiogram (EKG) showed a normal sinus rhythm. Computed tomography (CT) angiography was done to rule out pulmonary embolism (PE). The CT was negative for PE but showed mild peribronchial infiltrate in the right middle lobe and posterolateral lung herniation between the seventh and eighth ribs, with minimal subcutaneous emphysema along the right chest wall (Figure ).\nThe patient was admitted to the hospital and managed conservatively on broad-spectrum antibiotics, including vancomycin, levofloxacin, and 40 mg per day of prednisone. Two days later, his face swelled up suddenly with a change in the quality of his voice while he was eating dinner. An examination showed a swelling in the neck, diffuse crepitations on his body involving the face, all the way down to the buttocks. Repeat CT chest and neck showed extensive subcutaneous emphysema in the face, neck, chest, and mediastinum with a right-sided pneumothorax at the level of the previous lung herniation (Figures -).\nThe prevertebral and retropharyngeal air was demonstrated as compressing the oropharynx (Figure ). His oxygen requirement went up to 6 liters nasal cannula. A blowhole incision was made on the anterior chest wall, and he was observed in the medical intensive care unit (MICU). Surgery to close the defect was deferred due to his other comorbidities and the higher risk of post-operative complications. He improved gradually over the course of the next few days, completed the course of antibiotics with steroids, and was discharged to a rehabilitation center and did well post-discharge. |
A 56-year-old male without any previous medical history presented to our emergency room (ER) with multiple traumas from a 10 meter fall in a construction field. Physical examination revealed a male patient with a body mass index in the normal range and an acutely ill looking appearance. His right lower leg and ankle were swollen and bruised, and he had a 2 cm laceration wound on the plantar aspect of his right foot. The patient's right ankle had limited range of motion due to pain. The patient had tenderness at the right anterolateral aspect of the mid lower leg and anterior aspect of the ankle. There was grade 1 anterolateral instability of the left ankle. The neurologic examination was normal. Based on the patient's clinical history and physical examination, the orthopedic surgeon suspected a fracture of the right fibular diaphysis and ligament injury of the right anterolateral ankle.\nInitial radiographs of the ankle in the anteroposterior and lateral views showed fractures at the diaphysis at the fibula and anterior lip of the tibial plafond (Fig. ). The patient was not able to undergo ankle Mortise view because of his limited range of motion due to extreme pain. In a subsequent lower extremity computed tomography (CT), the orthopedic surgeon in the ER noticed a segmental fracture of the right fibular shaft and the anterior lip of the tibial plafond.\nTo evaluate the ankle ligaments, a turbo spin-echo (TSE) two-point mDixon technique applied to an ankle MRI (Table ) was performed after procuring written informed consent. In addition to the fractures of the right fibular shaft and tibial plafond, this MRI demonstrated a tiny chip fracture of the lateral talar dome. A tiny wafer-shaped talar dome chip fracture fragment about 7 (anterior–posterior diameter) × 3 (head to toe diameter) mm was clearly delineated only in the sagittal T2-weighted mDixon opposed-phase MRI (Fig. B). In T2-weighted mDixon in-phase imaging, which is considered a conventional T2-weighted image, there was a definite focal wedge-shaped cartilage defect at the corresponding area. However, there was only focal and subtle cortical irregularity and the cortical step-off was not definite (Fig. C). In a T2-weighted mDixon water-only image, which is considered a conventional fat-suppressed T2-weighted imaging, the cartilage lesion and focal cortical irregularity were once again noted, and the subcortical bone marrow edema was additionally confirmed. In these 2 sequences, a fracture was suspected, but the radiologists could not fully delineate the fracture line (Fig. D). In T2-weighted mDixon fat-only imaging, there were dark signal alterations at the subcortical region, but these were not considered fractures (Fig. E). T1-weighted imaging was obtained in the axial plane, and the fracture line was not depicted in this plane (Fig. F). In a CT image reviewed by an experienced musculoskeletal radiologist, there was a lateral talar shoulder cortical fracture at the identical area where the chip fracture was noted (Fig. A) from the T2-weighted mDixon opposed-phase image. In addition, there was a grade 2 injury to the anterior talofibular ligament with severe subcutaneous swelling of the ankle.\nDuring ankle arthroscopy, there was a free floating osteochondral fragment about 4 x 8 mm at the posterolateral talar shoulder, which was removed with basket forceps (Fig. ), and microfractures were performed at the posterolateral talar cortical fracture site.\nThe patient did well after the arthroscopy with recovery of full range of motion after 2 months. |
A 62-year-old female presented with a left RNP. At first presentation in our hospital, the patient reported progressive palsy starting with painless weakness only of her left wrist and long fingers extension 2 years ago. There was no history of any trauma or surgical procedure at her left upper extremity. Within these 2 years, the patient had a checkup by her family doctor and a neurologist. The diagnostic management included magnetic resonance imaging (MRI) of the cerebrum and cervical spine, electromyography, electroencephalography, and diagnostic analysis of blood and cerebrospinal fluid samples to exclude systemic specific or non-specific infectious or inflammatory or autoimmune diseases. No causes could be found that declared her RNP. So the diagnosis of a radial nerve mononeuropathy with unclear genesis was made, and the patient was treated by oral medication of glucocorticoids and vitamin B12. Additionally, the patient received a prefabricated wrist splint which immobilized only her left wrist in neutral position. Fortunately, stiffness or contractures in the wrist and all finger joints did not appear.\nOn the first clinical examination in our hospital, an incomplete but severe RNP was present. The strength of extension of the wrist and thumb's extension and abduction was completely lost according to grade 0 in Medical Research Council (MRC) scale (0-5), and the extension in the metacarpophalangeal (MP) joints II-V showed palsy grade 3 in MRC scale (Fig. ). The sensibility in the peripheral radial nerve area was completely lost. Electromyography revealed an advanced demyelinating radial nerve palsy, but not a complete neurotmesis. On physical examination, there was a painless and non-tender mass around the proximal radius. MRI revealed a submuscular, clearly demarcated and encapsulated tumor with a homogeneous and high-intensity signal similar to subcutaneous fat which surrounds the proximal radius shaft approximately a half part of its total circumference, and without visible septae inside the tumor after gadolinium injection (Fig. ). According to these findings, the diagnosis of a benign GL was made by the radiologist, and surgical removal of the tumor with exploration of the radial nerve was detected by us. The tumor was exposed typically through a volar approach. The radial nerve was carefully dissected, it was fixed to the capsule of the GL (Fig. ). The encapsulated GL with the size of 11x7x5 cm was completely removed in a monobloc manner. After that, an overstretching-related partial disruption of the nerve with a gap of 1 cm involving a half part of its overall circumference was visible (Fig. ). At this time (i.e. 2 years after first neurological symptoms) a sural nerve graft would be inappropriate, and a tendon transfer procedure was detected by us. This could not go beyond the scope of this first surgical procedure because the time of tourniquet already lasted 80 minutes. Additionally, a complete neurotmesis of the radial nerve was not found by electromyography, and so the patient was not cleared up by us on specificities of a tendon transfer procedure preoperatively. Furthermore, the potential risk of problems with wound healing would have been too high due to the necessity of another large surgical incision at this time. The diagnosis of a benign GL was confirmed by histological examination.\nSix weeks after removal of the GL, a triple tendon transfer procedure that included the transfer of the pronator teres (PT) to the extensor carpi radialis longus/brevis (ECRL/B), the transfer of the flexor carpi ulnaris (FCU) to the extensor digitorum communis (EDC), and the transfer of the rerouted extensor pollicis longus (EPL) to the palmaris longus (PL) was performed (Figs. , ). All tendon sutures were done in the Pulvertaft technique (end-to-side: PT to ECRL/B and FCU to EDC; end-to-end: EPL to PL). The wound healing was uneventful. The left upper extremity was immobilized in a plaster splint for 2 weeks. After that, the movement of elbow joint was freed, whereas the wrist was immobilized in the neutral position with a cast which additionally allowed the active flexion of all finger joints accompanied with its feather-related passive extension for another four weeks. Then, active strengthening of the wrist and all finger joints was started. Four months after surgery, the patient was completely able to perform her daily life activities again.\nAt the 10-months follow-up, strength of wrist extension, thumb's extension and abduction, and long fingers II-V extension had all improved to grade 4 in MRC scale that was accompanied with a sufficient circumduction of the thumb (Figs. -). The patient reported that she would undergo the same motion- restoring triple tendon transfer procedure again if it would be necessary. |
A 20-year-old girl wore orthokeratology lenses for years and used to clean the contact lenses with water from drinking fountain. The patient felt discomfort in the left eye off and on for 2 months and received topical levofloxacin eyedrops. The symptoms progressed to pain, photophobia, and tearing abruptly in 2 days, and the patient was referred to our clinic for severely stromal keratitis of the left eye. Visual acuity was 20/20 and counting finger in the right and the left eye, respectively. The left cornea demonstrated a large, irregular epithelial defect measuring 5 mm horizontally and 4.5 mm vertically accompanied with a deep stromal keratitis and radial neuritis [] on the 1st day of hospitalization. After taking samples from the scraped cornea and the lens cases, microbiological cultures for bacteria, fungus, and Acanthamoeba and polymerase chain reaction for Acanthamoeba were performed. The patient was started on topical chlorhexidine gluconate 0.02% and levofloxacin 0.5% ophthalmic solution hourly. On the 3rd day of hospitalization, the condition did not improve [] and topical voriconazole 1% was instituted hourly as an adjuvant for both fungal and Acanthamoeba infection. Surgical debridement and repeat cultures were performed on the third and 12th day of hospitalization due to no organism found in the prior samples and new stromal infiltration was noted [Figure and ]. The results finally confirmed the presence of Acanthamoeba on the 13th day of hospitalization. On the 15th day of hospitalization, after discussion with her family, oral voriconazole 200 mg twice daily was added to the concurrent therapies, which resulted in a rapid and almost complete resolution of the corneal inflammation [Figure -]. The triple combination therapy consisting of topical chlorhexidine gluconate 0.02% and voriconazole 1% and oral voriconazole was continued for a total of 1-month duration, followed by slowly tapering of the topical medications over the next 2 months. Liver function tests were normal throughout the course of treatment. Best-corrected visual acuity (BCVA) returned to 20/30 in the left eye 2 months from the initial treatment, and the cornea remained quiet. Final BCVA achieved 20/20 in the left eye 6 months later. |
A 39-year-old Nigerian woman presented to the rheumatology clinic with two-month history of cough, easy fatigability, and painful swelling of the ankles. The cough was dry, persistent, without any known aggravating or relieving factors. There was no history of orthopnoea or paroxysmal nocturnal dyspnoea. Fatigue had been persistent since onset of cough. It was worsened by moderate exertion but was not associated with respiratory distress. There was no fever or symptoms suggestive of any focus of sepsis. Both ankles were painful and swollen causing distress with mobility. She also had arthralgia in both knees and occasionally in the small joints of the hands. For several months prior to the onset of these symptoms, she noticed multiple recurrences of one or two painful spots on one or both legs or feet. These spots were not very distressing and there were several periods during which she forgot she had them. They seemed to disappear and re-appear at intervals and the patient never had to take any medication or see a doctor for that reason.\nThe described patient had sustained a slight injury to the dorsum of her right foot from a minimal domestic accident about a year earlier. This was treated with a few stitches with resulting good healing within a short period. However, a month prior to presentation, she started experiencing new onset of pain and palpable nodules within the inch-long scar () of the long-healed wound. On examination, two tender spots of EN () were identified on her feet. Faint but distinctive hyper-pigmented patches of early lupus pernio () were identified on her nasal alae. She was otherwise clinically stable.\nThe patient had presented at the pulmonology clinic where she was initially evaluated. Tuberculosis was ruled out by negative GeneXpert and sputum Acid and Alkaline Fast Bacilli tests. Chest radiograph showed bilateral hilar adenopathy and widespread reticulonodular infiltrates ().\nViral screening was negative for HIV, and hepatitis B and C. Serum electrolytes, urea, and creatinine were within normal ranges. Full blood count and urinalysis were also normal. The erythrocyte sedimentation rate was 32 mm/hr and reference range of C-reactive protein (CRP) – 0–16 mg/dl. Antinuclear antibody was positive at a low titre of 1 : 80 with a speckled immunofluorescent pattern. A diagnosis of LS was made and an assay of serum angiotensin converting enzyme (ACE) was ordered. Treatment with prednisolone, azathioprine, and naproxen was started. The ACE level came out to be 104 U/l (reference: 8–50 U/l). The cough subsided within a week on immunosuppressants but the arthritis persisted. The patient had intra-articular triamcinolone injection into both ankles and was also placed on hydroxychloroquine. This treatment led to resolution of the arthritis but only a slight reduction in fatigue was observed. After four months on treatment, the EN and lupus pernio healed; the serum ACE concentration reduced to 54 U/l, and ESR and CRP reduced to 15 mm/hr and 7 mg/dl, respectively. |
A 58-year-old male patient presented with a history of basal cell carcinoma on the left nasolabial sulcus for 17 years, having performed three previous excisions with local recurrence. He had a history of intense sun exposure in youth. He did not have primary or acquired immunodeficiency and denied prior radiation therapy or family history of oncology. The patient presented an ulceroinfiltrative lesion of 2.5 cm × 2.0 cm extending through the skin of the maxillary region and the left lateral portion of the nose. There were no palpable cervical masses. Anatomopathological study of the last approach, with deep margin compromised, and computed tomography evidenced infiltration up to periosteum. The patient opted for surgical treatment, so excision of the lesion was performed, with en bloc removal of the maxilla, lateral nasal wall, lateral portion of hard and soft palates on the left, and left neck dissection, levels I to IV. Anatomopathological study confirms the diagnosis of sclerosing basal cell carcinoma, with compromised margin in the region adjacent to the nasal root, perineural carcinomatous invasion, and vascular emboli, and the absence of lymph node metastasis. Posteriorly, he was subjected to adjuvant radiotherapy, presenting clinical remission after treatment.\nAt follow-up, 7 months after surgery, he presented with a painful mass with progressive growth in the left submandibular region, adhered to the mandible. PET-CT has showed hypercaptation of 1.9 cm in the left cervical level I and vertebral body of L5, with pathological fracture (Figures and ). Then, he was subjected to a new procedure, with modified radical neck dissection and marginal mandibulectomy, whose anatomopathological findings indicated sclerosing basal cell carcinoma compromising the submandibular gland and adjacent soft tissues, a very similar pattern to the primary tumor, with perineural and vascular invasion (Figures and ). Faced with this, metastatic disease was considered. Concomitant to this, a biopsy of the L5 lesion was performed, evidencing a histological appearance very similar to the primary tumor and submandibular lesion, compatible with bone metastasis (). Then, he was subjected to lumbar spine arthrodesis.\nIn postoperative follow-up, a new ulceroinfiltrative lesion was presented in the upper margin of the operative wound, nasal root region, and medial epicanto of the left eye, with induration up to the medial third of the lower eyelid, whose biopsy confirmed local recurrence without surgical proposal. He underwent chemotherapy with paclitaxel and carboplatin, interrupted by toxicity. The patient remains with clinically stable disease 21 months after diagnosis of the first metastasis. |
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