A 67-year-old female with a past medical history of chronic obstructive pulmonary disease and history of long-term tobacco abuse, who recently quit smoking, presented with shortness of breath, cough, myalgias, and malaise for one week. The patient had received two doses of Pfizer COVID vaccine, with the second dose in February 2021. In the ER, her vital signs were blood pressure (BP) 120/71, heart rate (HR) 78 bpm, respiratory rate (RR) 20 breaths/min, oxygen saturation 85% on room air, and afebrile. Laboratory assessment on admission is in Table . Nasopharyngeal swab for SARS-CoV-2 was positive. Chest X-ray on admission shows mildly patchy bibasilar pulmonary infiltrates and a calcified pulmonary nodule in the mid-right lung (2.0 cm) (Figure ). The patient was admitted to the general medical ward and started on 6 L per minute of supplemental oxygen via nasal cannula, remdesivir, dexamethasone, furosemide, azithromycin, and enoxaparin for venous thromboembolism prophylaxis. Despite multiple measures, the patient did not improve, requiring more aggressive management. Repeat chest X-ray showed slight interval improvement of bilateral pulmonary infiltrates and needed 4-5 L per minute via nasal cannula (Figure ).


A 58-year-old female with no significant past medical history presented with shortness of breath, fever, and cough for three days. The patient received two doses of the COVID vaccine, with the second dose in May 2021. In the ER, her vital signs were BP 105/96, HR 131 bpm, RR 20 breaths/min, oxygen saturation of 96% on room air, and febrile with a temperature of 102.0°F. Laboratory assessment is in Table . Nasopharyngeal swab for SARS-CoV-2 was positive. CT chest on admission shows no acute infiltrate and nonspecific nodules (Figure ). The patient was admitted to the general medical ward and started on antibiotics, dexamethasone, and remdesivir. The patient developed worsening hypoxia on Day 2, and CT chest showed widespread airspace disease throughout the lungs (Figure ). The patient required 4-5 L per minute via nasal cannula.


An 84-year-old female with a past medical history of hypertension presented with weakness, dry cough, and shortness of breath for four days. The patient had received two doses of the COVID vaccine, with the second dose in March 2021. In the ER, her vital signs were BP 133/93, HR 103 bpm, RR 22 breaths/min, oxygen saturation of 96% on 40 L per minute of supplemental oxygen via high-flow nasal cannula, and afebrile. Laboratory assessment is in Table . Nasopharyngeal swab for SARS-CoV-2 RNA was positive. Chest X-ray on admission shows worsening right pleural effusion with new opacity obscuring the lower two-third of the right lung and a new pleural-based opacity in the left upper lobe (Figure ). CT chest with contrast shows large right pleural effusion and associated right basilar consolidation and abdominal ascites. The patient was admitted to the telemetry unit and started on methylprednisolone, piperacillin-tazobactam, remdesivir, and baricitinib. The patient clinically deteriorated on Day 2 and was transferred to the intensive care unit for thoracentesis and possible intubation. Thoracentesis removed 1.95 L of bloody, serosanguineous fluid obtained, with partial resolution of the effusion (Figure ). On Day 3, the patient developed septic shock, florid renal failure, and lethargy and was started on intravenous fluids and norepinephrine drip. Chest X-ray showed near-complete opacification of bilateral lung fields and subsequently was intubated. On Day 4, tense ascites were noted and the patient underwent paracentesis, which removed 4.25 L of bloody, serosanguinous fluid. Renal replacement therapy started. The patient was deemed to have a guarded prognosis with multiorgan failure.


A 48-year-old male with a past medical history of type 2 diabetes mellitus and end-stage renal disease on hemodialysis presented with shortness of breath for three days. The patient was transferred from an outside facility where he was found to be hypoxic, saturating 79% on room air, chest X-ray showing infiltrates, and a positive nasopharyngeal swab for SARS-CoV-2 RNA. The patient had received two doses of the COVID vaccine, with the second dose in March 2021. Upon arrival to the general medical ward, the patient's vital signs were BP 132/79, HR 84 bpm, RR 18 breaths/min, oxygen saturation of 100% on 2-4 L per minute of supplemental oxygen via nasal cannula, and afebrile. Laboratory assessment is in Table . The patient was quickly weaned to room air, with SpO2 of 94-98%; hence, only supportive care was provided for COVID-19. On Day 1, the patient was found to have a right foot wound infection and was started on intravenous vancomycin and piperacillin-tazobactam. On Day 2, the patient was found to be hypoxic, put on 5 L per minute of supplemental oxygen via nasal cannula, and started on dexamethasone and remdesivir. Because of end-stage renal disease, the patient did not qualify for baricitinib. On Day 4, the patient required 10 L per minute of supplemental oxygen via high-flow nasal cannula, which he needed until Day 12, when we could start weaning down the supplemental oxygen over the next 3-4 days until Day 15 to room air. On Day 17, the patient was put back on 2 L per minute of supplemental oxygen via a nasal cannula which quickly escalated to 15 L on a nonrebreather mask within 2-3 hours, requiring the patient to get transferred to the intensive care unit on Day 18. At this time, he was put on bilevel positive airway pressure (BiPAP) with 40 L per minute of supplemental oxygen. Chest X-ray showed extensive diffuse airspace infiltrates, which significantly worsened from one week prior (Figure ). He was dialyzed without improvement from a respiratory standpoint and then intubated on Day 19. Subsequently, the patient was restarted on dexamethasone and broad-spectrum antibiotics despite completing 14 days' worth previously.


A six-year-old, 9.7 kg, male Cavalier King Charles spaniel was referred to the Cardiology Unit of the Veterinary Teaching Hospital of the University of Bologna with a two-month history of severe exercise intolerance associated with a syncopal episode. Clinical signs had developed during a local wave of COVID-19 approximately two weeks after the family of its owner had manifested symptoms of this viral disease and their positivity to SARS-CoV-2 had been confirmed by the local Health authority. Despite the dog’s clinical condition, evaluation at our institution was postponed and performed only after two months from the occurrence of the aforementioned signs due to the COVID-19 illness and related quarantine of the owners. The dog had been previously evaluated by the primary veterinarian several times since he was a puppy, as regular examinations were performed approximately every six months. Previous medical history was unremarkable and no cardiac problems had been identified at earlier examinations. The patient was an indoor dog that was being fed a high-quality balanced commercial diet. He had no known exposure to toxic agents or medications and was current on vaccinations and parasite prevention.
Upon presentation, cardiac auscultation revealed a grade II/VI left apical systolic murmur; the heart rate was 136 beats/min and the cardiac rhythm was regular. The femoral pulse was strong and synchronous with the heartbeat. Non-invasive systolic arterial blood pressure, assessed by a high-definition oscillometric device (petMAP graphic, Ramsey Medical, Inc., Tampa, USA), was 166 mmHg. Given the patient’s anxiety during physical examination, the pressure value was primarily interpreted as situational hypertension. Respiratory rate was mildly accelerated (44 breaths/min), likely due to the dog’s emotional stress, but lung auscultation was within normal limits. The remainder of the physical examination were unremarkable. Thoracic radiographs revealed mild generalised enlargement of the cardiac silhouette (vertebral heart scale 11.5, breed-specific reference interval 10.60 ± 0.50 []), with no obvious lung parenchymal abnormalities (). Sinus rhythm was observed on a six-lead surface electrocardiogram (Cube ECG, Cardioline S.p.A., Caverano, Italy) (). A transthoracic echocardiography was also performed by a board-certified cardiologist (GR) using an ultrasound unit (iE33 ultrasound system, Philips Healthcare, Monza, Italy) equipped with phased-array transducers (3–8 and 1–5 MHz) and continuous electrocardiographic tracing (, ). This showed LV volume overload and global systolic dysfunction without concomitant left atrial dilation (). Although the mitral valve leaflets were structurally and functionally normal, a mild mitral regurgitation with central jet was present. In light of the aforesaid findings, the valve insufficiency was hypothesized to be functional and due to the dilated cardiomyopathy (DCM) phenotype. No other echocardiographic abnormalities were identified.
Results of routine blood work, including complete blood count, serum chemistry and coagulation profile (prothrombin time, activated partial thromboplastin time, fibrinogen and antithrombin), were unremarkable. In light of the DCM phenotype, further laboratory tests included a thyroid profile and assessment of the serum concentration of cardiac troponin I (cTnI, IMMULITE 20000, Siemens, Erlangen, Germany). The former test ruled out hypothyroidism as a possible cause of LV systolic dysfunction (thyroxine 29.5 nmol/L, hospital reference interval [HRI] 13–51 nmol/L; thyroid stimulating hormone 0.12 ng/mL, HRI 0.03–0.38 ng/mL), while the latter unveiled MI (0.19 ng/mL, HRI < 0.15 ng/mL) [,]. The dog was started on pimobendan (Vetmedin, Boehringer Ingelheim, Ingelheim amRhein, Germany) at a dose of 0.25 mg/kg orally every 12 h, and several blood samples were collected with the aim of submitting them for investigation of infections responsible for MI. Initially, serological tests for Borrelia burgdorferi, Dirofilaria immitis, Anaplasma phagocytophilum, Ehrlichia canis, Leishmania infantum, Toxoplasma gondii and Bartonella henselae infection were performed (SNAP 4Dx, IDEXX Laboratories, Inc., Westbrook, U.S.A.; MegaFLUO LEISH, Vetefarma S.r.l., Cuneo, Italy; MegaFLUO TOXOPLASMA Gondii, Vetefarma S.r.l., Cuneo, Italy; Indirect immunofluorescence performed as described by Fabbi et al. []), yielding negative results. Given the family history as well as the ongoing and still unexplained MI, further serum samples were subsequently submitted for SARS-CoV-2 investigation [,]. Different serological assays were performed (using samples collected on the same day) to detect antibodies against the S and the N proteins of SARS-CoV-2. More in detail, specific neutralizing antibodies against the receptor binding domain of the spike protein were determined in serum samples using the SARS-CoV-2 surrogate virus neutralisation test (sVNT, GenScript cPass™ SARS-CoV-2 Neutralisation Antibody Detection Kit, GenScript Biotech Co., Ltd., Leiden, Netherlands) following the manufacturer’s instructions (positivity: ≥30% inhibition). Furthermore, SARS-CoV-2 neutralization assay (VNT) was performed as described by Rijkers et al. [] (positivity: titers ≥1/10). Lastly, a commercial multispecies enzyme-linked immunosorbent assay (ELISA; EradikitTM COVID19-Multispecies, In3Diagnostic, Turin, Italy; positivity: >20%) was performed. Pending serological results, no other therapies were prescribed in addition to pimobendan, but exercise restriction was recommended. Within two weeks, results from serological assays became available. All tests yielded a positive result ().
In light of such findings, approximately two weeks from presentation, another control was performed to recheck the clinical, cardiological and serological condition of the dog, and to obtain nasopharyngeal and rectal swabs for SARS-CoV-2 genome detection (using a real-time polymerase chain reaction (PCR) targeting E gene, as previously described by Corman et al. []). The owner reported an improvement in exercise tolerance and no further syncopal episodes. Physical evaluation was unremarkable, with the only exception being the heart murmur, which maintained unchanged characteristics. Echocardiography demonstrated a mild improvement of LV systolic function, although a DCM phenotype and a functional mitral regurgitation were still present, thus explaining the persistence of the heart murmur (). Blood samples were collected to monitor the antibodies against SARS-CoV-2 as well as the serum concentration of cTnI. All serologic assays were still positive () and cTnI was still over the HRI (0.17 ng/mL). SARS-CoV-2 molecular analysis yielded a negative result. Therapy as well as instruction at home were unchanged, and another recheck was planned within three weeks.
At that control, although the clinical and echocardiographic findings were stable compared to the previous examination, and two serological tests were still positive (i.e., sVNT and VNT), cTnI was normalised (0.09 ng/mL) and ELISA yielded a negative result for SARS-CoV-2 (). The dog continued to receive pimobendan and be revaluated regularly over the following weeks, showing a good clinical condition, stable echocardiographic parameters and a cTnI within the HRI. He is still alive and doing well at the time of manuscript writing (9 months from the occurrence of clinical signs and 7 months from the first evaluation at our institution).


We herein present a case that was recently managed at our institution, the Department of Surgery of the San Camillo Forlanini Hospital of Rome, Italy.
A 53-year-old man with previous history of alcohol-related liver cirrhosis presents to our department for routine follow-up. His comorbidities include hypertension managed with oral antihypertensive drugs and diabetes mellitus type 2. He has no significant allergies and never underwent any surgical procedure. He brings an ultrasound, which shows a 4 cm heterogenous mass in segment 8. His alfafetoprotein level is elevated to 76 ng/mL. He has no symptoms and looks in good performance status. We scheduled him for a triphasic CT scan, which shows a lesion of 4.3 cm with brisk arterial contrast and venous washout. According to the LIRADS classification, this lesion could be considered a class 5 with diagnostic features of hepatocellular carcinoma. The patient was discussed in our multidisciplinary tumor board including hepatobiliary and transplant surgeons, hepatologists, radiologists, pathologists, oncologists, and interventional radiologists. The plan was to submit the patient to curative intent treatments given his early presentation according to the Barcelona Clinic Liver Cancer Staging System (BCLC), namely surgical resection or liver transplantation; radiofrequency ablation was excluded given the tumor’s dimensions. Given the good performance status, the position of the lesion (which was right below the Glissonian capsule) and the liver function of the patients, the MDT decided to schedule the patient for surgery. We therefore saw the patient in clinic and discussed the procedure. Informed consent was signed, and liver function was tested using ICG retention rate. We used 0.5 mg/Kg corresponding to 40 mg in this 80 kg patient. The DICOM data of the CT scan of the patient were then submitted to our radiologist who performed a 3D reconstruction of the patient’s anatomy and the relationship of the lesion with the major vessels. Furthermore, the exact dimensions of the portal territories for segment 8 were reconstructed and showed on the model. We normally aim at the narrowest but still oncologically safe resection possible. The surgery is then planned on the model, identifying the borders of the resection and the exact location of the Glissonian pedicle to tackle and the hepatic veins to skeletonize and cut. Once the preoperative surgical plan is discussed between the surgeons and the radiologists, the patient can be scheduled for surgery. This generally happens 2 weeks from the administration of ICG to achieve a complete washout of the dye by the normal parenchyma and a retention by the tumor that will then be showed intraoperatively using the narrow band camera. The patient is scheduled for a laparoscopic anatomical segment 8 resection. In our experience, we use the so called “French position” to operate laparoscopic cases, with the patient standing in between the legs of the patient and two assistants on each side. Two screens in the operating room are dedicated to the endoscopic vision, one screen is dedicated to the intraoperative ultrasound, while one dedicated screen allows to show the preoperative surgical planning and therefore guide the resection throughout the case. We use a five-trocar technique with 1 umbilical port and 4 ports on the subcostal line. One port is epigastric and is very important for the dissection of the hepatocaval confluence. An extra 5 mm access is used to perform an extracorporeal Pringle manuever. Open laparoscopy access is gained at the level of the umbilicus. After inserting all the trocars, the narrow band camera is used to identify the HCC on the hepatic dome on segment 8, which is shining green because of the ICG administered 2 weeks before. Intraoperative ultrasound and doppler are then performed to confirm the border of the resection. Pringle manuever is prepared. Dissection is started from the hepatocaval confluence to immediately identify the middle and right hepatic veins. For segment 8 resections, no extensive right lobe mobilization is necessary unless exposure is limited. We then start our parenchymal transection using a combination of energy-based device clamp-crushing technique, CUSA dissection and bipolar coagulation. We identify the middle hepatic vein at its origin, and we carry our parenchymal transection in a cranio-caudal fashion, sweeping the liver parenchyma from the vein. This avoids any tearing on small peripheral branches of the middle hepatic vein. Slowly progressing caudally, we encroach the Glissonian pedicle for segment 8, going to the lesion and vascularizing the tumor bearing area. We test the pedicle using a bulldog clamp and checking with the doppler the absence of flow in segment 8 and the presence of flow in the remnant liver. We then ask the anesthesiologist to inject 1 mL of ICG intravenously. We will then see all the liver shining green but not segment 8, which is our resection area. Guided by the ICG we will then carry out the anatomical resection. The Glissonian pedicle is stapled, and the resection is carried out dissecting the whole resection area from the middle and right hepatic veins. Once the resection is finished, the vascularization of the remnant liver is checked both with the ICG and the doppler. A drain is generally not placed unless there are specific issues during the procedure. The patient was placed on a fast-track protocol with early feeding and mobilization and was discharged home on postoperative day 4. Follow up is now more than 1 year and the patient is currently in good health status with no signs of recurrence.


A 60-year-old Japanese male patient without any past medical history presented with dyspnea for 5 days in June 2019 (before the COVID-19 outbreak). He had no history of cigarette smoking, alcohol consumption, or sick contacts. He had a frequent cough, tachypnea (40 breaths per minute), low-grade fever (37.2°C), and hypoxemia (PaO2, 50.2 mm Hg on room air). He did not have wheezes or lung crackles and abnormal heart sounds on auscultation. Edema, skin rash, muscle weakness, myalgia, and arthralgia were absent. Blood tests revealed leukocytosis (10,300 cells/μl with 76% neutrophils, 2.0% eosinophils, and 14.0% lymphocytes) with high C-reactive protein levels (5.27 mg/dl). He had normal liver and renal function tests (aspartate aminotransferase 25 IU/L, normal <38 IU/L; alanine aminotransferase 30 IU/L, normal <40 IU/L; blood urea nitrogen 13.6 mg/dl, normal <20 mg/dl; and creatinine 1.04 mg/dl, normal <1.10 mg/dl) and no elevation of creatinine kinase (155 IU/L, normal <170 IU/L). Autoimmune screening did not identify any abnormalities, including anticyclic citrullinated peptide, anti-nuclear antibodies, anti-double-stranded DNA antibodies, anti-proteinase 3 (PR3) antibodies, anti-myeloperoxidase (MPO) antibodies, anti-Scl-70 antibodies, anti-Sjögren's syndrome-related antigen A (SSA/Ro52) antibodies, anti-aminoacyl-transfer RNA synthetase (ARS) antibodies, anti-Jo-1 antibodies, and anti-melanoma differentiation-associated gene 5 (MDA5) antibodies. Chest X-ray and computed tomography (CT) scan showed diffuse ground-glass opacification and consolidation in bilateral lung fields (Figure ). On the day of admission, the patient's condition deteriorated rapidly and he received noninvasive intermittent positive pressure ventilation (NPPV). The diagnosis of rapidly progressive interstitial lung disease with autoimmune disorders, such as severe inflammatory myopathy-related interstitial lung disease, could not be ruled out. Based on the diagnosis of ARDS of unknown etiology (PaO2/FiO2 235 with a positive end-expiratory pressure of 5 cmH2O), high-dose (1000 mg/day) intravenous (IV) methylprednisolone therapy was initiated. Empiric antibiotics (IV piperacillin-tazobactam and levofloxacin) were also given, although blood culture and urinary pneumococcal and Legionella antigen tests were negative. After 3 days of steroid pulse therapy, the patient improved dramatically and was weaned from NPPV and, thereafter, from oxygen support. The dose of IV methylprednisolone was reduced to half every 3 days and later it was switched to oral prednisolone (60 mg/day), which was also gradually reduced. Chest CT scan taken on the 13th day of admission revealed almost complete disappearance of abnormal shadows from the lung field (Figure ). He was discharged without dyspnea on the 26th day of admission. The steroid was tapered down gradually and discontinued 7 months after discharge. Although the patient had been asymptomatic for a while, he had a relapse of dyspnea in 10 months later after the first onset of ARDS. Upon the second admission, he had hypoxemia (PaO2 64 mm Hg) on O2 5L/min via face mask and started receiving NPPV therapy. Chest CT scan showed a mixture of diffuse ground-glass opacification and consolidation similar to roentgenological patterns observed previously (Figure ). The findings of physical examination and blood tests were not significantly different from the previous admission except that he had grasping pain in both thighs, proximal muscle weakness in extremities, and elevation of serum creatinine kinase (1741 IU/L). He had no skin eruptions, such as nail-bed telangiectasia, heliotrope rash, Gottron's papules, Raynaud's phenomenon, and hyperkeratotic lesions on his fingers (mechanic's hands). The short-tau inversion recovery sequence (STIR) of magnetic resonance imaging (MRI) showed inflammatory changes in both hamstring muscles (Figure ). However, the Euroline myositis line blot assay showed negative results for either myositis-specific antibodies (Jo-1, PL-7, PL-12, EJ, SRP, Mi-2, MDA5, and TIF1-γ) or myositis-associated antibodies (Ku, PM-Scl100, Scl-70, and SSA/Ro52). From these findings, the diagnosis of ARDS that relapsed along with an initial manifestation of seronegative PM was made. After 3 days of high-dose (1,000 mg daily) IV methylprednisolone therapy, the patient's dyspnea and muscle weakness improved dramatically and NPPV therapy was discontinued. Additionally, the diffuse abnormal shadows on the chest CT scan (Figure ) and the high signal on STIR MRI of the hamstring muscles (Figure ) disappeared. The dose of IV methylprednisolone was gradually reduced to 40 mg/day prednisolone, when the patient was discharged without respiratory and muscular symptoms on the 26th day of the second admission (Figure ). The steroid was tapered down gradually and discontinued 6 months after discharge.


A 75-year-old male presented to our hospital with worsening mental status. Gait instability and expressive aphasia were noted on the physical examination. He was otherwise hemodynamically stable, with unremarkable laboratory studies and a negative urine drug screen. Computed tomography (CT) of the head without contrast showed a large right frontoparietal lesion crossing midline with surrounding vasogenic edema (Figure ). Further characterization with magnetic resonance imaging (MRI) showed a 5.5-cm intra-axial mass within the deep white matter of the right frontal lobe, with gadolinium enhancement and prominent FLAIR (fluid-attenuated inversion recovery) signal concerning malignancy.
Later, the patient was started on dexamethasone, and a frontal stereotactic brain biopsy was performed. The initial pathology report showed a B-cell lymphoma with cells positive for CD20 immunostain (Figures -). However, due to its complexity, the sample was sent to an outside institution for a second opinion, which found the sample to be positive for the MYD88L265P mutation. Due to the strong association between this mutation and WM, quantitative serum immunoglobulins were measured, which showed an elevated IgM monoclonal paraprotein, confirming the diagnosis of WM.
The patient was started on treatment with rituximab, methylprednisolone, carfilzomib, and ibrutinib. The patient showed a good response by MRI at three months, and he was transitioned to oral ibrutinib only. Surveillance MRI at one year post-diagnosis showed patchy right frontal lobe enhancement indicating disease progression, although the patient had no clinical symptoms; he was then restarted on the initial chemo-immunotherapy protocol. However, ibrutinib was later held due to thrombocytopenia. Soon after, the patient presented to the hospital again with cognitive dysfunction, leg weakness, and falls, with MRI showing significant disease progression. At this point, his treatment was changed to palliative chemotherapy with high-dose methotrexate and rituximab. His disease responded avidly to this regimen, and he is currently completing a one-year course of treatment, with no radiologic or clinical evidence of recurrence (Figure ).


An 88-year-old woman (height, 150 cm; weight, 41 kg) with no history of drug allergy or general anesthesia was scheduled for transfemoral TAVI because of severe aortic stenosis (AS). The surgery was performed under general anesthesia to facilitate the use of transesophageal echocardiography and to manage any intraoperative complications. She was taking 0.625 mg/day bisoprolol, a selective β-1 blocker, for hypertension and chronic atrial fibrillation. Additionally, she was taking amlodipine for hypertension. Preoperative transthoracic echocardiography showed severe AS (aortic valve peak flow velocity: 4.73 m/s; mean aortic valve pressure gradient: 47 mmHg; aortic valve area: 0.41 cm2) and myocardial hypertrophy (left ventricular posterior wall thickness and interventricular septum thickness: 14 mm).
Pre-anesthetic medication for sedation was not administered. She received bisoprolol and amlodipine 3 h before entering the operating room. Figure shows the anesthesia record. General anesthesia was induced using midazolam and remifentanil; additionally, rocuronium was administered to facilitate tracheal intubation. She received total intravenous anesthesia: continuous infusions of propofol and remifentanil. Noradrenaline and dopamine were infused continuously through the central venous catheter to maintain blood pressure. AS disappeared after valve implantation. During the surgery, complete atrioventricular block occurred, and ventricular pacing (VVI mode: 60 ppm) was initiated. No other complications were associated with the surgical procedure. Postoperatively, she received 100 mg sugammadex through the central venous catheter, but 2 min later, her systolic arterial blood pressure (ABP) decreased unexpectedly to less than 40 mmHg. Simultaneously, ventilator monitoring revealed elevated peak and plateau airway pressures (60 and 40 cmH2O, respectively). No skin rash was observed on the body surface. Transthoracic echocardiography showed underfilling of the left ventricle without right ventricular dilatation or pericardial effusion. No abnormalities were observed in left ventricular wall motion.
The patient developed distributive shock, which was clinically diagnosed as anaphylactic shock caused by sugammadex because of the rapid onset of severe hypotension and bronchospasm. First, two boluses of 0.05 mg adrenaline were administered through the central venous catheter, followed by rapid volume resuscitation using crystalloid (1 L infusion within 30 min). The dose of noradrenaline was increased to 0.3 μg/kg/min. Consequently, the airway pressures returned to the original level, but the hypotension persisted. Thereafter, adrenaline was administered via bolus (0.1 mg twice) and continuous infusion (0.1 μg/kg/min); however, the increase in her ABP was minimal. Therefore, 1 mg glucagon was administered intravenously, and her systolic ABP immediately rose to 130 mmHg. An erythematous rash also appeared on her neck with the increase in ABP. Her general condition was stable after the therapeutic interventions. Ventricular pacing was continued because bradycardia with complete atrioventricular block was persistent during the interventions. She was admitted to the intensive care unit under tracheal intubation. Subsequently, the continuous infusion of adrenaline was discontinued, and the continuous infusion of noradrenaline was reduced. We also administered 125 mg methylprednisolone for 3 days. She was extubated 9 h after the onset of anaphylaxis, and circulatory agonists were discontinued the following day. She was discharged without complications on postoperative day 9. Blood tests revealed a total serum tryptase level of 7.3 ng/mL and 1.2 ng/mL at 1 h and 24 h after onset, respectively. We advised the patient to undergo allergy tests, such as skin prick tests or intradermal tests, to identify the cause of anaphylaxis. However, the patient refused these tests because she was elderly and unlikely to undergo surgery under general anesthesia in the future.
Written informed consent was obtained from the patient for the publication of this case report. This report was approved by the Institutional Review Board of Nagasaki University Hospital (Approval number: 21041932).


A 54-year-old man with a history of excessive intake of alcohol (100 g/day × 30 years) and locally grown tobacco use (500g/month × 30 years) was admitted to our hospital because of chronic persistent swallowing dysfunction for six months. White light endoscopy (WLE) revealed a 22 mm flat lesion in the middle esophagus.The lesion was covered with scattered leukoplakia, and normal vascular network could not be seen in the lesion (Fig. a). Narrow-band imaging (NBI) under endoscopy revealed the lesion with an indistinct brownish area, local white penniform area, and white tiny papillary surface structure (Fig. b). Further low and high magnifying endoscopy with NBI (ME-NBI) showed tiny irregular papillary microsurface structure with various shapes and sizes, and non-typical type B1 pattern of intraepithelial papillary capillary loops (IPCL) confined to the papillary microsurface structure (Fig. c, low magnification, and Fig. d, high magnification) according to the classification of Japan Esophagus Society (JES classification) []. Iodine staining endoscopy revealed a less-stained lesion (Fig. e) and showed more distinct white tiny papillary surface structure (Fig. f) than conventional WLE. Biopsy showed a low grade intraepithelial neoplasia. Chest and abdominal CT scan revealed no abnormal lesions.
According to the endoscopic manifestations under WLE, ME-NBI, and iodine staining endoscopy, combining with pathology, we considered the lesion to be early esophageal cancer. Therefore we chose endoscopic therapy. The lesion was completely resected with endoscopic submucosal dissection. Histopathology showed that the layer of neoplastic spinous cells was significantly thickened (Fig. a) with local keratosis presenting the appearance of the so-called church spire (Fig. b). The lamina propria papilla was elongated upward to the surface layer (Fig. c), and the nuclei in the basal region had double or more nucleoli. Tumor cell displayed expanding growth, and partial tumor cells broke through the basement barrier and invaded into superficial lamina propria (Fig. d). The IPCL were observed in lamina propria papilla with elongating upward to the surface layer growing underneath the layer of neoplastic spinous cells, which corresponds to the IPCL observed by ME-NBI (Fig. e). The lesion was histopathologically confirmed as early VCCE which was limited within the mucosal lamina propria (m2) and completely resected. There were no lymphovascular and neural invasions of cancer cells, and no cancer cells to be seen in the lateral and vertical margin of the resected specimen (the distance of the lesion to the closest margin of the resected specimen was 3.012mm) (Fig. ).


A 22-year-old healthy woman presented to the emergency department complaining of a five-day history of several red and painful areas that were associated with swelling of the lower extremities. Her complaint started one day after receiving the first dose of the Pfizer vaccine. She had received all vaccinations during childhood without any complications. There is no history of preceding infections including COVID-19 infection, sore throat, or diarrhea. In addition, she never complained of prior skin lesions or systemic diseases. She did not use any topical or systemic medication. All the laboratory investigations were normal. She stated that there is no history of contact with the sick patients and no family history of tuberculosis. Skin examination revealed multiple, tender, and erythematous nodules were present on her both legs. Based on the patient history, examination, and laboratory investigation all pointed to the vaccine-related erythema nodosum; however, we considered the Arthus-like phenomenon which can mimic the erythema nodosum lesions. She received oral ibuprofen 600 mg four times daily to relieve symptoms. Three days after receiving the treatment, she improved and the nodules started to flatten (Figure ). Two weeks later, on the follow-up examination, her symptoms had completely resolved.


A 77-year-old Japanese woman, para 7, who went through menopause at age 48, suffered sudden onset of left lower abdominal pain and visited a primary care doctor. Computed tomography (CT) revealed torsion of a left ovarian cyst, and she was transferred to our hospital for surgery. She had a history of left-side breast cancer and underwent total left mastectomy at the age of 67, with no recurrence thereafter. Although she was a carrier of hepatitis C, her liver function and coagulation remained normal, and she was being followed-up without medication. Furthermore, she was taking nifedipine and candesartan cilexetil for hypertension. Meanwhile, her family history and psychosocial history were unremarkable. She also had no history of trauma.
CT showed a 7.5-cm long elliptical mass in the left adnexal region that was continuous with the uterus (Fig. ). The ovary was atrophic because of the patient’s age, and difficult to identify; the appearance of blood and the continuity with the surrounding pelvic peritoneum were suggestive of retroperitoneal hematoma. Physical findings at admission were as follows: height, 144.5 cm; weight, 57.2 kg; body mass index (BMI), 27.4 kg/m2; blood pressure, 112/50 mm Hg; pulse, 72 bpm; and body temperature, 37.1 °C. Physical examination detected no significant findings. On external (body surface) and internal examinations, no palpable masses or tenderness were noted in the left pelvic area. Transvaginal ultrasound revealed an atrophied uterus; however, the bilateral adnexa could not be identified due to atrophy. The hematoma in the left pelvis could be identified. These findings were identical to those obtained by CT. Blood test results were a hemoglobin value of 9.5 g/dL, a hematocrit value of 28.4%, a white blood cell count of 7970/μL, and a C-reactive protein level of 0.05 mg/dL. Urinalysis revealed mild occult blood. After admission, the hematoma did not enlarge, and the hemoglobin and hematocrit levels did not decrease. After 11 days of bed rest, with no exacerbation of the inflammatory response, lower abdominal pain was relieved, and she was discharged. After discharge, we planned to investigate the cause of her bleeding on an outpatient basis, but 6 days after discharge, she was readmitted to our hospital after relapse of symptoms caused by retroperitoneal bleeding from the same site. The hematoma had grown to a size of 11.7 cm, and magnetic resonance imaging showed an abnormal vascular network extending from the left side of the uterus to the left adnexal area. Three-dimensional CT (3D-CT) similarly showed an abnormal vascular network on the left side of the uterus, and we suspected a possible arteriovenous malformation (AVM) or arteriovenous fistula (AVF) from the uterine artery to the left ovarian vein (LOV; Fig. ).
We decided that urgent treatment was needed for her repeated bleeding and performed vascular embolization therapy simultaneously with angiography. However, angiography of the internal iliac artery, including the left uterine artery, and the left external iliac artery, did not show AVM or AVF into the LOV. Angiography of the left renal artery confirmed that the contrast medium discharged from the left kidney did not flow into the inferior vena cava (IVC) but flowed back into the LOV (Fig. a). Subsequent venography also confirmed that the blood from the LRV did not flow into the IVC but regurgitated into the LOV and the lumbar vein (Fig. b). Left ovarian venography showed retrograde blood flow into a dilated and tortuous aneurysm in the pelvis and into the right internal iliac vein via a vein around the uterus (Fig. c). The cause of retroperitoneal bleeding was rupture of the LOV, the distension of which was caused by reflux. We performed embolization of LOV with N-butyl-2-cyanoacrylate and placed a coil centrally to prevent recanalization. Postembolization LRV imaging showed blood flow to the upper left lumbar vein and vertebral plexus (Fig. d). CT on the second day after the procedure confirmed good embolization of LOV and reduction of the retroperitoneal hematoma to a size of 6.4 cm (Fig. ). The patient then underwent regular outpatient follow-up, and the retroperitoneal hematoma gradually shrank and disappeared. At her final visit 2 years later, the hematoma had not recurred.
In this case, angiography confirmed the continuity of LRV and IVC but demonstrated no antegrade blood flow to the IVC. Therefore, we attributed LOV regurgitation to extravascular physical compression of LRV. After close examination of the CT images, we determined that LOV rupture was caused by NCS because the LRV was severely stenotic between the abdominal aorta and the SMA (Fig. ).


A 38-year-old woman presented with a 16-year history of ulcerative colitis being treated with mesalazine and infliximab. She had been undergoing routine colonoscopy examinations. Multiple random biopsies performed from the transverse colon to the rectum during colonoscopy suggested rectal cancer, for which she was referred to our hospital for surgery. A follow-up colonoscopy revealed the absence of the haustra between the transverse colon and rectum, without any obvious tumors. Histopathological examination of multiple random biopsy specimens obtained from the transverse colon to the rectum showed dysplasia with p53 overexpression in the rectum, which suggested cancer.
We performed laparoscopic proctocolectomy and D2 lymphadenectomy concomitantly with TaTME. The procedure involved two surgical teams. We inserted five abdominal ports, and the colon was mobilized from the ileocecal region to the rectum along with laparoscopy-guided dissection of blood vessels. The rectum was mobilized in the TME plane, and the left and right neurovascular bundles were incised. Transanal surgery was performed simultaneously using the laparoscopic procedure. We used the Lone Star Retractor System (Cooper Surgical, Trumbull, CT, USA), GelPOINT path transanal access platform (Applied Medical, Rancho Santa Margarita, CA, USA), and AirSeal system (ConMed, Utica, NY, USA) to ensure active smoke evacuation to aid in the visualization of the operative field. Circumferential mucosectomy was performed with preservation of the anal sphincter muscle. We used a purse-string suture and closed the rectal lumen to prevent mucus leakage and cancer cell dissemination. Mucosectomy was performed starting from the dentate line and extending into the anal canal. The circular and longitudinal muscles were incised, and the abdominal cavity was opened (Figure ). The specimen was extracted after a slight extension of the umbilical port site. We created an ileal pouch (J-pouch) and performed an ileal pouch-anal anastomosis. Finally, we performed a diverting-loop ileostomy. The operation time was 286 minutes, and the estimated blood loss was 52 mL.
Histopathological examination of the resected specimen revealed low-grade rectal dysplasia without any evidence of malignancy. It took some time to adjust to the ostomy pouch, and the patient was discharged 21 days postoperatively without any complications. The patient underwent loop ileostomy closure four months postoperatively and recovered without significant loss of the anal sphincter function. The anal sphincter function remained at four months after the second surgery. At four months after the second surgery, the patient is doing well.


A 25-year-old woman, without previous medical history, presented for infertility lasting for more than one year. Clinical examination was normal but abdominal and pelvic computed tomodensitometry (CT) revealed a cyst of the left ovary associated with abundant peritoneal ascites that could correspond to mucinous material. Pelvic magnetic resonance imaging (MRI) confirmed ascites and showed a heterogeneous mass of the left ovary measuring 8.4 × 6.8 cm with adipose, solid and cystic regions that were suggestive of a dermoid cyst. The right ovary and uterus seemed normal. No other lesion was seen in the rest of the body, notably in the digestive system. In this context, surgery by left oophorectomy with appendicectomy and omentectomy was performed 3 months after the first consultation, without resorting to additional hyperthermic intraperitoneal chemotherapy (HIPEC). Intra-operative examination revealed mucinous material inside the peritoneal cavity and a normal digestive tract with a normal appendix. There was no complication of the surgery. The 5-month follow-up based on clinical and imaging surveillance revealed no complaints. Without relapse, the patient was able to pursue her plan to have a child.
Macroscopically, the left ovary was cystic measuring 9.5 × 7 × 7 cm and weighing 305 g. It was ruptured on 4 cm. Its cut section revealed a heterogeneous and viscous mass with hair. The appendix, measuring 6 cm in length, and the omentum were macroscopically normal. Histologically, the ovarian cyst corresponded to a mature pluritissular teratoma with intermingled skin and pilosebaceous annexes, serous and mucinous glands, respiratory epithelium, adipose tissue and smooth muscle (Fig. ). The organoid areas with the aspect of a colon, representing about 20% of the ovarian cyst, were composed of colonic mucosa, muscularis mucosae, and submucosa from the surface to the depth. A thick muscularis propria was also observed. In the colonic mucosa, some glands were elongated and layered with moderate proliferating epithelial cells with minimal atypia, near to mucin pools stained with Alcian blue. The colonic epithelial cells were immunohistochemistry stained with CK20 and CDX2, and showed heterogeneous staining for CK7. These cells were negative for estrogen and progesterone receptors (Fig. ). The ovarian surface was covered with hyperplastic mesothelial cells and presented acellular mucinous pools, also found in the omentum. The left fallopian tube was normal. The appendix examined in totality was histologically normal besides mucin deposits on the surface of the serosa. It did not present any mucocele or LAMN/HAMN. All together, these data suggested a diagnosis of acellular PMP (according to Carr classification []) caused by a ruptured appendiceal-like mucocele associated with LAMN, in a left ovarian teratoma.
Next generation sequencing of the LAMN of the teratomatous mucocele revealed an activating mutation of KRAS gene c.35G > A corresponding to the p.(Gly12Asp) substitution (Fig. ). Complementary molecular analysis by SNaPshot showed an associated mutation of GNAS c.602G > A resulting in p.(Arg201His). No mutation was found by these two techniques on the other tissues of the ovarian teratoma (squamous, respiratory, adipose or smooth muscle elements) or in the normal appendix and ovarian parenchyma (Fig. ).


A privately owned two-year-old female guinea pig was referred for a repeated loss of material from the uterus and progressive weight loss. Anamnestically, the animal never conceived despite several attempts at mating. The day of the appointment, the pet expelled a large amount of hemorrhagic material. During the visit, the patient was quiet, depressed, and moderately responsive to stimulation. At physical exam, the patient showed tachypnea, vocalization upon manipulation of the abdomen that was tense, and dilated abdomen with a palpable mass. Ultrasonographic investigation evidenced a large well-defined 2 × 2 cm mass in the anatomic area of the uterus. The guinea pig underwent emergency surgery upon sedation with an association of butorphanol 0.7 mg/kg (Dolorex 10 mg/ml, MSD), medetomidine 0.07 mg/kg (Sedator 1,0 mg/ml, ATI), and ketamine 7 mg/kg (Imalgene 1000 100 mg/ml, MERIAL) administrated intramuscularly. Anesthesia was maintained with isoflurane 3% with a not cuffed endotracheal tube. The procedure was monitored with a multiparameter monitor, including ECG (II derivation) CO2, O2, and no invasive pressure and temperature. During the anesthesia, intravenous fluid (NaCl 0.9%) was administered at the rate of 5 ml/kg/h with infusion pump via intravenous catheter 24 G (Terumo). Surgical examination of the abdomen evidenced an enlarged and congested ovary and uterus and signs of peritonitis, including intra-abdominal fluid. The two organs were excised and submitted for histopathology. The patient was discharged on antibiotic (enrofloxacin 5 mg/kg bid/po Baytril flavour sosp os 25 mg/ml Bayer) and nonsteroidal anti-inflammatory drugs (meloxicam 0.3 mg/kg/sid/po Metacam sosp os 1,5 mg/ml flac 10 ml Boheringer) and ranitidine (3 mg/kg/bid/po Zantadine sol os 30 mg/ml Ceva) []. Histopathologic analysis revealed characteristic features of endometriosis both in the uterus and in the ovary. In detail, adenomyosis was described in the uterus because of the presence of ectopic glandular tissue in the muscular wall of the uterus (). On the other hand, at the level of the ovary, cystic enlargements filled with fluid were seen macroscopically; histologically, these cystic structures presented the classic glandular epithelium of the endometrium with one layer of cuboidal or tall cells, thus representing classic cystic endometriosis of the ovary (). Immunohistochemical staining was performed, by using the ABC method and diaminobenzidine, by means of specific antibodies for estrogen and CD10 in order to confirm the ability of the glandular epithelium to secrete estrogen and the presence of a stromal reaction surrounding the ectopic endometrial tissue (Figures and ) [, ]. The histopathological and immunohistochemical features described are strongly suggestive of endometriosis.
The guinea pig recovered from the surgery and was rechecked on a monthly basis. The patient died of unrelated causes three months later. A necropsy was performed at that time and did not show any sign of endometriosis.


A 49-year-old Japanese woman underwent an MRI examination in the referring hospital for an assessment of the orthopedic disease of her right hip joint, and the MRI revealed a tumor in her pelvis. She was referred to our hospital, where an MRI examination again showed tumor mobility (Fig. ), and a tumor derived from the intestinal tract was suspected.
In the contrast CT image (Fig. ), a mass approx. 45 mm in size was found on the right side of the pelvic floor, and in the blood vessel construction image, the tumor was nourished by vessels from the splenic artery to the greater omentum. In 18F-fluoro-2-deoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT), no abnormal accumulation was observed (Fig. ). The results of complete blood cell counts and biochemical tests were all normal. Cancer antigen 19-9 (CA19-9) showed a mild elevation at 37.8 U/mL (normal range < 37.0 U/mL), and carcinogenic embryonic antigen (CEA) was normal at 0.8 ng/mL (normal range < 5.0 ng/mL). Based on all of these results, the preoperative diagnosis was a suspected omental primary tumor or accessory spleen.
There was a danger of torsion irrespective of the presence or absence of malignancy, and the patient desires surgery to remove the tumor; the surgery was conducted concurrently with the diagnosis and treatment. The surgery was a single-incision laparoscopic-assisted greater omental tumor resection. A longitudinal incision was made approx. 4 cm around the umbilicus. A multichannel port (x-Gate®, Sumitomo Bakelite, Tokyo) was inserted in the wound. Observation of the abdominal cavity revealed a red and solid tumor mass of approx. 4 cm. Adhesion with the surrounding tissue was not observed. The greater omentum and the tumor were guided out of the body through the gate hole (Fig. ), and the tumor was excised together with the greater omentum. The tumor, a light brown tinged solid mass with a smooth border, was 5.2 × 3.8 × 3.5 cm in size with a well-defined border (Fig. ).
Histopathologically, the tumor involved large and small blood vessels (Fig. ), and tumor cells with eosinophilic cytoplasm were increased in number, in sheet form (Fig. ). In immunohistochemical staining, the tumor cells were found to be positive for HMB45 (Fig. ), Melan-A (Fig. ), and α-SMA (Fig. ), but negative for CD34, Desmin, c-kit, and s-100.
Based on the above results, the tumor was diagnosed as an omental PEComa. There has been no recurrence at 16 months after the surgery.


A 32-year-old Caucasian male with a known history of depression presented to the emergency department accompanied by police after a violent outburst following prolonged DFE abuse during a suicide attempt. On admission, he was emotionally labile and had contusions on his left shoulder and upper extremities due to a physical altercation with police. He was initially confused and verbally abusive, but within six hours he was oriented, cooperative, and able to provide a reliable history.
The patient stated that he had huffed keyboard cleaner several days per week for the past year; however, the frequency had increased over the last month to several times daily. Other than depression, the patient had no other known medical problems. He denied any personal or family history of kidney disease. The patient denied drinking alcohol, and he reported smoking one-half pack of cigarettes per day for the previous two years. He denied any other substance abuse except for DFE. He reported no use of nonsteroidal anti-inflammatory (NSAID) medications. During this episode of difluoroethane abuse, he had no loss of consciousness, but experienced frightening visual and auditory hallucinations as well as anxiety that persisted even after returning to his self-reported baseline mental status.
Initial labs revealed a WBC count of 21,000 with polymorphonuclear predominance of 81%, an elevated creatinine of 1.5mg/dL with no known baseline, BUN of 10mg/dL, GFR of 54 mL/min/1.73 m2, lactic acidosis, creatine kinase of 350 U/L, and a carboxyhemoglobin level of 3.1%. Urinalysis was significant for 3+ proteinuria, moderate blood, 14 RBCs, 3 WBCs, and 3 hyaline casts. He had a negative urine drug screen.
The patient received single renally adjusted doses of Vancomycin and Piperacillin-Tazobactam, intravenous 0.9% saline, and oxygen by nasal cannula while in the emergency department prior to admission. Over the next 24 hours, he received intravenous fluids and oxygen with subsequent normalization of lactic acid, creatine kinase, and leukocyte count. His creatinine down trended to 1.3mg/dL. However, 36 hours into admission, his serum creatinine inexplicably rose to 2.3 with a rise in carboxyhemoglobin to 3.6%, while his urine output remained stable (). Repeat urinalysis showed a small amount of blood with RBC of 2, negative proteinuria, and no evidence of infection.
His normal saline infusion was transitioned to bicarbonate with saline, but was discontinued after the patient developed pruritus. Ultimately, he was transitioned to normal saline at 75 ml/hour. A renal ultrasound showed increased echogenicity of both kidneys consistent with medical renal disease, without change in size, atrophy, or cystic lesions (). Thus, it is likely that the patient had some degree of chronic kidney disease (CKD) prior to admission. For the next three days, he continued to receive intravenous normal saline with subsequent improvement of creatinine and normalization of his urinalysis and was discharged with a creatinine of 1.6.


A 62-year-old Japanese female patient presented with a left abdominal mass. She was referred to our surgical outpatient clinic to undergo a detailed examination and treatment for the left abdominal mass. A clinical examination revealed an elastic soft, smooth-surfaced, painless, child-head-sized tumor with poor mobility, which was located in the left upper abdomen. Abdominal computed tomography (CT) demonstrated a child-head-sized mass with heterogeneous contrast at the left upper abdomen around the stomach, spleen, pancreas, and left kidney on a horizontal image () and coronal image ().
Magnetic resonance imaging (MRI) revealed a heterogeneously hyperintense mass on T1-weighted imaging (), a relatively uniform and hyperintense mass on T2-weighted imaging (), and a hypointense mass with an enhanced border on gadolinium- (Gd-) enhanced imaging (). A retroperitoneal tumor was diagnosed. Her laboratory data were white blood cell count, 4600/mm3; hemoglobin, 12.8 g/dl; hematocrit, 36.5%; and platelet count, 182,000/mm3, with normal electrolytes, as well as normal blood urea nitrogen levels, but slight liver dysfunction. Her serum levels of corticosteroid and/or androgen were 13.3 ng/ml (10.4–35.0 in female) and 173 pg/dl (35.7–240.0), respectively, which are within the normal ranges; however, her serum level of ACTH was elevated at 138.70 pg/ml (7.2–63.3).
The retroperitoneal tumor was resected (). The tumor was located at the left side of the stomach, posteriorly to the transverse mesocolon and pancreas, on the cranial side of the left kidney (Figures and ), but has not invaded the surrounding organs (Figures and ). The right adrenal gland was normal in size. The resected tumor was 20 × 18 × 10 cm in diameter and weighted 1500 g. An examination of the cut surface of the tumor revealed a multilobular yellow mass with bleeding in places ().
A histopathological examination with hematoxylin and eosin staining revealed that the tumor was composed of a proliferation of mature and variable-sized adipocytes admixed with aggregates of hematopoietic elements, associated with adrenal gland tissue in the peripheral region within the tumor (). These findings were compatible with AML.
The patient had an uneventful recovery and was discharged from the hospital on the 6th day after the operation. She has been followed up in our outpatient clinic without recurrence for approximately 12 years since undergoing the operation.


A 67-year-old Caucasian man came to our attention after a fixed oral prosthesis surgery. His past medical history was significant for a paroxysmal atrial fibrillation for which he was taking Amiodarone and Acenocumarol with stable International Normalized Ratio (INR) values. Following orthopantomography and CT scan, the procedure of implant insertion was performed with local anesthesia (Mepivacaine and vasoconstrictor) in area 36 [left lower jaw, designated according to the ISO system] [] without any complication. Acenocumarol had been discontinued 2 days before, switching to LMW heparin. The patient was discharged under antibiotic therapy (Amoxicillin and Clavulanic acid) and instructed to restart oral anticoagulant therapy after 2 days. About 48 h after the procedure, hiccup abruptly presented and failed to cease.
The patient did not report any further symptom, and no complications were found at the revision of the surgical area. Three days after the onset, the patient came to the emergency department due to this persisting symptom: Baclofen, Metoclopramide and Bromazepam were administered without significant clinical improvement. Both ENT, neurological examinations, blood tests and a brain CT scan failed to show any abnormality. Three days later, Chlorpromazine 25 mg b.i.d. was administered for 2 weeks. Furthermore, the patient was advised to program in the next few days a brain MR scan and chest imaging that were negative. Seven days following the surgical procedure, the stitches were removed and the wound did not show any problem. The hiccup continued resulting in significant distress and sleep deprivation. Providentially, it spontaneously ceased after 18 days. Neither relapses or neurological symptoms were reported in the later months.


The patient is a 55-year-old man with past medical history significant for two-year history of umbilical hernia, diabetes mellitus type 2, hypertension, gout, chronic kidney disease with proteinuria, diverticulosis, obesity, and osteoarthritis. The patient presented to the clinic because of umbilical hernia pain, which developed over the two months. The pain localized to the periumbilical region and left lower back, and it was exacerbated with food intake and sometimes relieved by 5 mg hydrocodone tablet. He also reported nausea and fifteen pounds weight loss over the two months, which he attributed to decreased food intake. The physical examination showed a 1 cm tender and irreducible mass superior to the umbilicus. The patient underwent herniorrhaphy and the gross examination of the surgical specimen did not reveal any masses or lesions.
The microscopic evaluation showed diffuse infiltration of the connective tissue by malignant cells with hyperchromatic nuclei, inconspicuous nucleoli, and abundant eosinophilic cytoplasm (). There were focal areas of gland formation with mucin production, consistent with adenocarcinoma. By immunohistochemistry, the neoplastic cells were strongly positive for pancytokeratin and CK7 () and negative for CK20, CDX2, TTF-1 and PSA.
The laboratory findings showed elevated levels of CA 19-9 (16,590 U/mL) and CEA (14.2 ng/mL). The patient underwent a subsequent computed tomography scan with intravenous contrast, which showed a 5.0 × 2.7 cm ill-defined and hypoattenuating mass located in the pancreatic tail and body (), with peripancreatic fat infiltration and vascular involvement of splenic artery and vein. In addition, the imaging showed peritoneal carcinomatosis, multiple ill-defined hypoattenuating lesions in the liver, and enlarged and hypoattenuating pericecal iliac lymph nodes. The patient had a prior noncontrast computed tomography scan four months earlier, which showed umbilical hernia with fat and no other lesions in the pancreas and abdomen ().
After the diagnosis, the patient refused chemotherapy and decided to undergo palliative care. The patient had rapid progression of the disease and died within two months of the initial histologic diagnosis of malignancy.


A 67-year-old Caucasian man with a significant history of recently diagnosed type 2 diabetes mellitus (T2DM) and essential hypertension presented to the hospital with chief concerns of diplopia with an extreme gaze, right eye pain, and sinus congestion for about two weeks.
At the time of admission, the patient was afebrile, had a blood pressure of 160/67 mmHg and pulse of 64/minute but had a white blood cell count of 14,540/µL. The patient’s blood glucose was 469 mg/dL, anion gap levels were within reference range, and his glycosylated hemoglobin (HbA1c) was 12.4%. Computed tomography (CT) and magnetic resonance imaging (MRI) of the orbit and face revealed severe sinusitis with possible orbital cellulitis and optic nerve compression (Figure ).
On the day of admission, the patient was started on an IV ampicillin and sulbactam combination (3000 mg/mL every six hours) and IV vancomycin (1500 mg/mL loading dose; 1250 mg/mL every 12 hours maintenance dose; target vancomycin trough of 10 to 20 mg/mL due to the severity of the infection). The patient was seen by the infectious disease (ID) team on day two of admission. The ID team recommended continuing vancomycin, switched the ampicillin/sulbactam combination medication to piperacillin/tazobactam (3375 mg/mL every six hours) and started the patient on empiric IV liposomal amphotericin B (400 mg/mL daily) given the concerns for invasive fungal infection. The patient was seen by ophthalmology team, and they recommended no acute surgical intervention. However, the otorhinolaryngology (ENT) team performed an endoscopy of the nasal sinuses on the second hospital day, and the patient required extensive debridement of the necrotic tissue of the right sinuses.
Biopsy results from the nasal sinuses showed broad hyphae with infrequent septations, haphazard branching, and numerous bizarre forms. These morphologic features were consistent with mucormycosis. Given this finding, the patient was continued on IV liposomal amphotericin B.
A second MRI of the orbit and face was repeated on the fourth hospital day and showed the progression of the disease including involvement of right retrobulbar fat and right optic nerve, persistent non-enhancing, and likely necrotic tissue extending from the right pterygopalatine fossa into the right masticator space (Figure ). Suspected osteomyelitis was noted at the base of the skull, and we noted asymmetric right frontotemporal pachymeningeal enhancement with wispy leptomeningeal enhancement along the middle cranial fossa, which was suggestive of meningitis.
The neurosurgery team was consulted as the patient had meningeal spread as well. The neurosurgery team deemed the patient inoperable.
Given the progression of the disease despite the standard-of-care treatment (i.e., surgical debridement, IV amphotericin B, and control of blood glucose), a literature search was done to find the next best step. Isavuconazole has been used, according to a few case reports [-], as salvage treatment in patients whose condition either failed the IV amphotericin B or were intolerant to it. Therefore, our patient was started on IV isavuconazole (372 mg/mL every eight hours) on the fifth hospital day, and IV amphotericin B (400 mg/mL daily) was continued. Since patient tissue aerobic and anaerobic cultures as well as blood cultures remained negative, piperacillin/tazobactam and vancomycin were discontinued on the fifth hospital day.
An MRI of the orbit and face was repeated 48 hours after the patient was started on isavuconazole and revealed a stable disease. The patient’s IV isavuconazole dose was reduced to 372 mg/mL daily (after receiving IV isavuconazole every eight hours for 48 hours). An MRI was obtained one week later, and it also showed stable disease with no further progression. The patient was switched to oral isavuconazole (372 mg daily), and IV amphotericin B (400 mg/mL daily) was continued. As the patient continued to improve, he was ultimately discharged after 19 hospital days on this regimen with a plan for outpatient follow-up evaluations with the ID, ENT, and ophthalmology teams. The patient was blind in his right eye with cranial nerves III, IV and VI palsies at the time of discharge. However, his left eye was completely intact with normal vision and movement.
During outpatient care, he continued to receive IV amphotericin B (400 mg/mL daily) and oral isavuconazole (372 mg daily). An MRI of the orbit and face after five weeks of this therapy showed some interval improvement of the infectious process (Figure ). After receiving IV amphotericin B (400 mg/mL daily) for 50 days, the medication was stopped, and the patient was continued on oral isavuconazole (372 mg daily). The patient's renal function was checked weekly as the patient was on IV amphotericin B. The patient had baseline creatinine of 1.0 mg/dL, it peaked at 1.8 mg/dL and returned to 1.4 mg/dL once the IV amphotericin B was stopped. Fungal cultures and blood samples were monitored for six weeks, and they remained negative.
An MRI of the orbit and face was obtained two months later while the patient was treated with oral isavuconazole (372 mg daily), and the imaging continued to show stable disease. Therefore, oral isavuconazole was stopped. By this time, the patient had isavuconazole for a total of four months (both via IV and oral doses). Besides headaches, the patient tolerated the isavuconazole well without any other significant side effects.
An MRI of the orbit and face was obtained again nine months after stopping oral isavuconazole, and his disease process has remained stable. Imaging at this time showed some improvement in the condition. The ID team stated the patient was cured. The ENT team still monitors the patient periodically, and, as of this writing, the patient has been over one year off of antifungal medications.
Regarding the patient’s diagnosis of uncontrolled T2DM, the patient was initially started on basal insulin while as an inpatient, but he was discharged on oral antihyperglycemic agents (metformin, 500 mg twice daily with meals and sitagliptin, 100 mg daily) given better control with oral agents at the time of discharge. His HbA1c improved to 5.0% from 12.4% in three months. The patient’s metformin has been stopped, and his sitagliptin dose has been reduced to 50 mg daily and is the only diabetic medication for the patient as of this writing.


A 20-year-old African American man was admitted to a psychiatric facility for psychosis. On initial presentation, the patient had an antalgic gait, which he attributed to his history of dopa-responsive dystonia. His mood was depressed and his affect was restricted. He had disorganized thought process and was slow to recall. He endorsed auditory hallucinations, paranoid delusions, depressive symptoms, frequent night awakenings, and persecutory nightmares. Per the ambulance report, the patient was wandering the streets in a confused state, so bystanders called 911. The patient stated that he had been homeless for the past 3 weeks. During this 3-week period, he admitted to not being complaint with his medications. Urine toxicology screen was negative.
Per medical records, he was diagnosed with dopa-responsive dystonia at age 11 after a 2.5-year history of progressive abnormal gait. He was initially misdiagnosed with tight heel cords at age 10 and treated with serial casting that resulted in good improvement on the right but marginal improvement on the left. His toe walking became more pronounced overtime accompanied by worsening left calf pain and stiffness, increasingly frequent falls, and new onset of intermittent torticollis. These symptoms worsened over the course of the day. He was eventually taken to an urban teaching hospital, where he was diagnosed with dopa-responsive dystonia based on clinical presentation and marked improvement on a levodopa trial. Magnetic resonance imaging of the brain and spine was unremarkable at the time.
At age 15, he was diagnosed with schizoaffective disorder bipolar type. His psychiatric history is also significant for multiple psychiatric hospitalizations, history of previous suicide attempts with medication overdose, and history of trauma. He also endorsed marijuana use since age 15 and daily tobacco use since age 18. He denies using any other illicit drugs. Per collateral information from his mother, his schizoaffective disorder has never been well controlled given the conflicting effects of his medications. She also mentioned that he was placed in individualized education programs as a child due to learning disabilities. His family history is significant for bipolar disorder on his maternal side. His family history on his paternal side is unknown. In addition to carbidopa-levodopa, his outpatient medications included sertraline, divalproex sodium, aripiprazole, and benztropine.
On hospital day 1, he was started on carbidopa-levodopa 25/100 mg tablet three times daily for dopa-responsive dystonia. On day 2 of his hospital course, sertraline 50 mg once daily, benztropine 2 mg twice daily, divalproex sodium 500 mg twice daily, and risperidone 0.5 mg twice daily were added to his medication regimen. We started him on a low-dose risperidone to avoid exacerbating his dopa-responsive dystonia symptoms. Physical exams were also performed daily to assess for dystonia and parkinsonian symptoms. His initial physical exam revealed an antalgic gait secondary to left lower extremity dystonia, which improved by hospital day 2 and resolved by hospital day 3. On hospital day 3, he became agitated and aggressive with staff members, which led to intramuscular administrations of haloperidol 10 mg, diphenhydramine 50 mg, and lorazepam 2 mg. He continued to endorse auditory hallucinations, so risperidone was increased to 0.5 mg in the morning and 1 mg at bedtime. His auditory hallucinations resolved and then returned on day 6. He reported hearing “good” voices and “bad” voices. He also continued to endorse depressive symptoms, multiple night awakenings, and persecutory nightmares. As a result, his risperidone dosage was increased to 1 mg twice daily. On hospital day 7, the patient reported hearing “mumbling” voices only and improvement in his sleep and depressive symptoms. On hospital day 8, his auditory hallucinations fully abated. By hospital day 10, he slept throughout the night, no longer had depressive symptoms, and had normal spontaneous speech. His thought process was linear, logical, and goal-oriented. His mood and affect was euthymic and full range. No psychotic symptoms were noted. The patient was compliant with his medications throughout the whole hospital course and his daily physical exams were negative for dystonia or parkinsonian symptoms since day 3 of his hospitalization. He was subsequently discharged on hospital day 14 with appropriate outpatient follow-up.


A thirty-three-year-old woman was admitted to our clinic at the 37th week of her gestation for delivery with a history of gravidity six, parity two, and abortion three. She had one previous cesarean section delivery. Her preoperative hemoglobin was 10.8 g/dL, prothrombin time (PT) 10.5 seconds, activated partial thromboplastin time (aPTT) 29 seconds, international normalized ratio 2.3, and platelet count 385x109/L. Transabdominal sonography and magnetic resonance imaging displayed total placenta previa, with myometrial invasion to the urinary bladder at the anterior wall of uterus (, ). The patient stated preoperatively that she preferred a conservative approach rather than hysterectomy in case of massive bleeding. After cesarean delivery of a transverse baby through a Pfannenstiel incision and removal of the placenta, a 5-6 cm area of tissue loss was detected at the anterior wall of the uterus and bleeding occurred from the cervix and posterior wall of the bladder. Pelvic packing was applied on the pelvic vessels for 20 minutes, the bleeding sites were sutured with 1.0 polyglactine sutures, and Sengstaken-Blakemore balloon catheter was placed in the uterus before suturing. A stomach balloon was filled with 250 mL saline and an esophageal balloon was filled with 400 mL saline to provide compression on the lower uterine isthmic and cervical bleeds, nevertheless, bleeding continued. Bilateral uterine and hypogastric artery ligations were planned due to hemorrhage. The left external iliac artery was accidentally held and bonded as the left hypogastric artery, which was released within a minute after distinguishing the vessels. Following this mistake, the uterine and hypogastric arteries were ligated on both sides. The patient lost about 2000 cc of blood due to the intraoperative hemorrhage as measured by adding 1650 cc blood in the aspirator and counted gauzes. She received erythrocyte suspension (3 units preoperatively and 4 unites postoperatively) and 3 packs of fresh frozen plasma. The patient had no findings of hypotension or shock at any time. The patient reported severe pain in both legs in the recovery room; it was observed that left dorsalis pedis and femoral artery pulses were absent. Doppler sonography showed a distinct stricture and triphasic flow loss on the left femoral artery. Diagnostic angiography was performed by a cardiologist. After a 6-F introducer sheath was inserted, it was confirmed that both external iliac arteries were occluded (). Intravenous heparin (100 IU/kg) was administered afterwards. A 6-F left internal mammary artery catheter was used with 0.035 hydrophilic guide wires to cross the occlusion. Angioplasty was performed first to the right and then contralaterally to the left external iliac artery with a standard balloon (8x80 mm). A completion angiogram concluded the procedure. The femoral access site managed manually with digital pressure. The balloon catheter was removed after 30 hours. The patient and her child were discharged on the 4th postoperative day with no further events. Informed consent was obtained from the patient.


A 76-year-old man was referred to our hospital for having lower back pain for 5 months, which was suspected to be L2/3 spondylitis on magnetic resonance imaging (MRI). He had previously undergone cervical laminoplasty for ossification of the posterior longitudinal ligament and diffuse idiopathic skeletal hyperostosis 19 years earlier. He had a history of hypertension and diabetes. Although a history of BCG vaccination was unknown, he had no previous history of tuberculosis infection. He had also undergone transurethral resection of a bladder tumor (TUR-Bt) and had been treated with intravesical mitomycin C (MMC) for the bladder cancer 1.5 years earlier. Four months later, he again underwent TUR-Bt, received intravesical MMC, and started BCG therapy for the recurrence of bladder cancer. After the sixth course of intravesical BCG therapy, he was aware of systemic weakness and loss of appetite, and was unable to walk. He appeared to have septic shock and therefore was treated in the intensive care unit. In spite of systemic analyses, the source of his infection and the causative bacteria could not be identified. He was subsequently diagnosed with hypercytokinemia caused by BCG therapy. He showed clinical improvement without the administration of antituberculosis drugs, and was discharged 9 months before he came to our hospital.
Except for a temperature of 37.2 °C, his vital signs were within normal limits. Although there were no motor and sensory disturbances in the legs, he was unable to walk owing to lower back pain. Physical examination demonstrated vertebral tenderness at the L2/3 level. Laboratory analysis demonstrated a normal white blood cell (WBC) count of 6300 /μL, a high erythrocyte sedimentation rate (ESR) of 53 mm/h, and a high C-reactive protein (CRP) level of 2.7 mg/dL. There were no other abnormal laboratory findings regarding anemic changes, kidney function, or liver function. The patient did not receive tuberculin skin testing.
There were no notable findings on electrocardiogram or chest X-ray. X-ray of the lumbar spine displayed collapsed endplates of L2/3. Sagittal T1-weighted MRI displayed a decreased signal in the L2/3 disc and the vertebral bodies (Fig. ). Sagittal T2-weighted MRI displayed an increased signal in the L2/3 disc and fluid collection in the anterior part of the vertebral bodies (Fig. ). Axial T2-weighted MRI displayed an increased signal around the posterior area of the vertebral bodies, which extended into the left epidural space and reached the peripheral muscle tissue and the area near the aorta (Fig. ).
On the second day of hospitalization, the patient underwent an L2/3 disc biopsy, but the general bacteria culture was negative, and the smear was negative for Ziehl-Neelsen staining. The patient’s blood culture was negative, and the result of T-SPOT.TB® (T-SPOT), which is a type of interferon-gamma release assay (IGRA), were also negative; the number of spots for both 6-kDa early secretory antigenic target (ESAT-6) and 10-kDa culture filtrate antigen (CFP-10) was 5 or less. The causative bacteria remained unidentified and therefore he was started on empirical therapy with intravenous ceftriaxone. On the fifth day of hospitalization, a plain computed tomography scan, which was performed for systemic examination, showed soft tissue development in the adjacent abdominal aorta at the L3 level (Fig. ), which was suspected to be an infectious aortic aneurysm. A 2-stage operation was planned for the spondylitis with adjacent infectious aortic aneurysm, to prevent rupture of the infectious aortic aneurysm, obtain spine stabilization, drain the abscess and make a diagnosis. On the tenth day in hospital, because the risk of rupture was considered to be low, the patient underwent an L2/3 laminectomy followed by posterior fixation using percutaneous pedicle screws at T12, L1, L4, and L5 as the first stage. Specimen cultures of the lumbar vertebrae, yellow ligament, necrotic tissue, etc., were negative for general bacteria, specimen smears were also negative for Ziehl-Neelsen staining, and there were no pathological findings of caseating granuloma or necrosis. On the fiftieth day of hospitalization, because the infection had been controlled but the inflammatory response was sustained, he underwent replacement of the aneurysm with a synthetic graft by vascular surgeons, and lesion curettage and L2/3 anterior interbody fusion by iliac bone transplantation as the second stage. Spinal surgery was performed in the transabdominal approach owing to the risk of rupture. On pathological analyses, the L2/3 intervertebral disc, vertebral bone, and tissue surrounding the vertebral bone and aorta showed caseating granuloma and necrosis with multinucleated giant cells and epithelioid cells upon hematoxylin-eosin staining, and positive bacilli upon Ziehl-Neelsen staining. The tuberculosis-polymerase chain reaction (Tb-PCR) result of the tissue was also positive, using COBAS® TaqMan® MTB Test, which is a real-time PCR system targeting the 16S rRNA gene region of Mycobacterium tuberculosis complex DNA. Owing to the patient’s history of BCG therapy, negative T-SPOT, pathological findings, and positive Tb-PCR, the pathogenic bacteria of the spondylitis was considered to be BCG. We then started multidrug therapy with antituberculosis drugs, including isoniazid (INH), rifampin (RFP), and ethambutol (EB), because BCG is typically resistant to pyrazinamide (PZA). PCR-based genomic deletion analysis was performed using the specimens to distinguish BCG from the other M. tuberculosis complexes. Specifically, multiplex PCR was performed utilizing region of difference 1 (RD1), which is present in the DNA of other M. tuberculosis complexes but is deleted in the DNA of BCG []. Primers ET1, ET2 and ET3 bind and amplify a 190-bp region in BCG, whereas a 160-bp region is amplified in the other M. tuberculosis complexes, as observed by electrophoresis on an agarose gel. A clinical isolate sample from our patient was identified as BCG with a deletion in RD1 (Fig. ). Specimen cultures from the first-stage and second-stage operation were later identified as members of the M. tuberculosis complex using a mycobacteria growth indicator tube. After therapeutic intervention, the patient’s WBC count, ESR level, and CRP level were improved and MRI displayed no signs of active infection in the spine, epidural space, peripheral muscle tissue, or aorta. On the ninetieth day after hospitalization, the patient was discharged from our hospital and transferred to a different hospital for physical rehabilitation.


A 42-year-old Cameroonian (black African) man with no relevant past medical history presented to our hospital with a 1-week history of fever and a 4-day history of no bowel movements. The fever was intermittent and worse in the evenings, and associated with headache, joint pains, and anorexia. He self-medicated an undocumented orally administered antimalarial medication but symptoms persisted. Three days later, he developed generalized abdominal pain, colicky in character, with a severity of 5/10 on a visual analogue scale. This was associated with progressive abdominal distension and an altered bowel pattern initially characterized by an inability to pass stool and flatus over 4 days but he denied any vomiting. A worsening of his symptoms prompted his visit to our hospital.
On examination, his mucous membranes were dry, his conjunctivae were pink, and his vital signs were normal. His abdomen was mildly distended with mild diffuse tenderness. There was neither guarding nor rebound tenderness. Percussion note was tympanic and bowel sounds were hyperactive. His rectum was empty per digital rectal examination and his prostate was not enlarged. The rest of the physical examination was unremarkable.
A rapid diagnostic (Alere™ Malaria Ag P.f, Abbott Rapid Diagnostics, USA) test for malaria was positive. Also, his complete blood count values were within normal ranges: white blood cell count of 6200 cells/uL, hemoglobin of 12.5 g/dL, and platelet count of 222,000 cells/uL. His metabolic panel was within normal range: serum sodium ion (Na+) of 140 mmol/L, serum potassium ion (K+) of 4.0 mmol/L, serum chloride ion (Cl−) of 98 mmol/L, serum creatinine of 0.9 mg/dL, alanine aminotransferase was 41.2 U/L, aspartate aminotransferase was 33.0 U/L, total bilirubin was 0.81 mg/dL, and alkaline phosphatase was 55.9 U/L. His human immunodeficiency virus serology was non-reactive. His rapid antibody test for typhoid fever was also non-reactive. There was no significant air fluid level or increased bowel gas on a plain abdominal radiograph and an abdominal ultrasound revealed mild free intra-abdominal fluid in all four quadrants.
We concluded on a working diagnosis of functional bowel obstruction secondary to malaria. He received three doses of intravenously administered quinine base infusion (600 mg in 500 ml of dextrose 5% to flow for 4 hours every 8 hours for 24 hours) and intravenously administered crystalloids (0.9% normal saline at rate of 1 liter 8 hourly for 48 hours) and was placed on “nothing by mouth.” He passed a small quantity of feces 48 hours after initiation of antimalarial medication, with complete resolution of the abdominal pain, distension, and bowel movements on the fourth day of hospital stay. A stool examination was done with no organisms identified. We then concluded on a final diagnosis of sub-acute intestinal obstruction secondary to malaria. He was then discharged on an orally administered artemisinin-based antimalarial combination (artemether/lumefantrine 20/120 mg, 4 tablets 12 hourly for 3 days). His 2-week follow up was unremarkable.


A 35-year-old para 0+6 Black African lady presented with a history of five first and one second trimester recurrent pregnancy losses. In addition, she had a nine-year history of irregular heavy bleeding associated with dysmenorrhea.
Her menarche was at 17 years of age with regular painful cycles that lasted 10 days. She was not on any contraceptive method and did not report any dyspareunia or urinary symptoms. Her first miscarriage occurred 11 years and was surgically managed by dilatation and curettage. Subsequently she noted changes in her menstrual cycle. Her menstrual cycle became irregular with a heavy flow for 10 days associated with severe dysmenorrhea and bowel symptoms of bloating and diarrhea. She used tranexamic acid one gram three times a day during her menses for the heavy prolonged periods and Mefenamic Acid 500 milligrams three times a day for the dysmenorrhea with reported relief of the symptoms.
The physical examination was unremarkable except for mild tenderness in the suprapubic region; she had grossly normal external genitalia and normal looking cervix.
Her initial hormonal profile was as follows:FSH: 4.5 IU/m (3.1-7.9 IU/L) LH: 10 IU/L (1-18 IU/L)
She had a recent pap smear one year ago that was normal.
Transabdominal and transvaginal (TVS) scans had shown separate right and left cornu with multiple cysts in the peripheral ovarian parenchyma features suggestive of bicornuate uterus and polycystic ovaries (). She also had a hysterosalpingogram (HSG) that was reported to have a uterus opacified with banana configuration oriented to the right with no delineation of fallopian tubes, findings suggestive of a unicornuate uterus.
Her past medical history was not significant. She was recently divorced, a condition she attributed to her history of several miscarriages in the context of an African cultural expectation of siring children.
She was subsequently scheduled her for hysteroscopy and diagnostic laparoscopy. She also gave consent for possible open Strassmans metroplasty.
On hysteroscopy, a normal looking endometrium was visualized with a right sided tubal ostia and a small tubal ostia on the left that did not appear patent (). Laparoscopically, a bicornuate uterus was found () with associated endometriosis at the vesicouterine fold. Open metroplasty was done (Figures and ). A fundal transverse incision was made and dissection done to the level of the endometrium after injection of subserosal vasopressin. Apposition of the two horns was done and the uterus sutured in layers (Figures and ). A copper intrauterine device was left in situ to separate the uterine walls and possibly reduce the chances of uterine synechiae though the evidence for this practice is still not conclusive. In addition, endometriotic deposits discovered at the vesico uterine fold were ablated.
She had an unremarkable follow-up after surgery with no complications reported.
A HSG 6 months after surgery revealed unification of the uterine horns but both tubes were not delineated.
Patient was lost to follow-up but two years later she presented having conceived spontaneously and a TVS revealed a single intrauterine pregnancy at 13 weeks. Her antenatal workup was as highlighted in .
She was subsequently followed up at the antenatal clinic and had no concerns till 33 weeks when she presented with a history of lower abdominal pain worsening over the past few weeks and right sided fundal tenderness pain score of seven out of ten on the pain assessment scale. The main concern at the time of assessment was possible uterine rupture. She did not have any features suggestive of bowel obstruction as she was passing stool and bowel sounds were present. She had a normal NST and an obstetric ultrasound that was done showed a single intrauterine pregnancy with normal biophysical profile and no features of placental abruption or slower uterine segment site dehiscence. She had no other investigations done at this time. The pain was significant enough to warrant an admission for which she subsequently received antenatal steroids for lung maturity and opioid analgesia for pain relief. However, the pain did not completely resolve and she underwent a caesarean delivery at 33 weeks and 5 days due to persistent lower abdominal pain. The outcome was a live male infant with a birth weight of 1950 grams and APGAR of 9, 10, 10. There was no evidence of uterine rupture although she had venous congestion and massive varicose veins bilaterally at the cornual areas. The previous metroplasty scar was intact.
She had a resolution of the abdominal pain postoperatively and had an unremarkable postoperative recovery. She was discharged on the fifth postoperative day.


A 58-year-old woman with a four-year history of hypertension-diabetes comorbidity presented to the outpatient department of the Nyakach County Hospital with edematous swelling of the face and upper and lower lips of 11-hour duration (Figure ).
There was associated dysphagia with stridor and hoarseness of voice. She did not have any pruritus, urticaria, or rashes. The tongue was swollen and was reported as hard in consistency. It was wedged between her teeth which prevented her from closing her mouth. Saliva was pooling and dribbling from her mouth. The patient had no history of smoking, angiotensin-converting enzyme (ACE) inhibitor-induced cough, atopy, or any recent use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Additionally, there was no prior history of a similar episode. The outpatient card indicated that the patient had tolerated a twice daily peroral dose of metformin 500 mg, a once daily peroral dose of glibenclamide 5 mg, a once daily peroral dose of hydrochlorothiazide 50 mg, and a once daily per oral dose of enalapril 5 mg for four years. Other aspects of her medical history were unremarkable. On examination, she had a pulse rate of 75 beats per minute, respiratory rate of 26 breaths per minute, and blood pressure of 140/72 mmHg. Pulse oximetry was not done. Her systemic examination was unremarkable. Review of her medication profile prompted us to suspect enalapril as the cause of the angioedema. Thus, we made use of the Naranjo probability scale to evaluate the likelihood that the observed effect was enalapril induced. Specific responses on this scale were one, two, one, zero, two, zero, zero, zero, zero, one for a cumulative score of seven, which ranks as probable. Therefore, a preliminary diagnosis of enalapril-induced angioedema was made and the enalapril was immediately discontinued. A 200 mg stat intravenous (IV) dose of hydrocortisone and a 20 mg stat dose of intravenous chlorpheniramine were administered and the patient was observed for one hour. The edema was noted to subside (Figure ) and a further three hour period of observation was allowed. The patient was then discharged on a once daily peroral dose of nifedipine 20 mg, a thrice daily peroral dose of chlorpheniramine 8 mg, and a tapered peroral dose of prednisolone as follows: 40 mg thrice daily for five days, 20 mg thrice daily for five days, 10 mg thrice daily for five days, and 5 mg thrice daily for five days. In addition, she was advised to continue with her usual doses of metformin, glibenclamide, and hydrochlorothiazide and to report to the hospital immediately if the swelling was to re-occur. On follow-up after one week, there was a marked change in facial appearance (Figure ), and at three weeks, the patient was symptom-free with a blood pressure (BP) of 142/78 mmHg (Figure ).


A 55-year-old male with a six-year history of hypertension presented to the Nyakach County Hospital with swelling of the upper lip of 10-hours duration (Figure ). The patient complained of restlessness and insomnia. There was no history of atopy or food or drug allergies. On examination, vitals were normal. Moreover, cardiovascular, respiratory, and abdominal examinations were unremarkable. The outpatient card indicated that he had tolerated nifedipine 20 mg, enalapril 5 mg, and hydrochlorothiazide 25 mg for six years. We suspected enalapril to be responsible for the edema and thus made use of the Naranjo probability scale to evaluate whether the observed edema was enalapril induced. The responses on this scale were one, two, one, zero, two, zero, zero, zero, zero, one for a total score of seven, which ranks as probable. Therefore, a preliminary diagnosis of enalapril-induced angioedema was made, enalapril withheld, and the patient immediately put on 4 mg intravenous dexamethasone injection and monitored for one hour. A gradual decrease in the swelling was observed about two hours after the intravenous dose of dexamethasone. The patient was discharged on a peroral dose of prednisolone tapered as follows: a thrice daily 20 mg dose for five days, a thrice daily 10 mg dose for five days, and a thrice daily 5 mg dose for five days. A twice daily peroral dose of cetirizine 10 mg was also given for 10 days, and the patient was advised to continue taking the nifedipine and hydrochlorothiazide, but to report immediately to the hospital if the swelling re-occured. After one week, the patient was reviewed and it was observed that there was a significant resolution of the swelling. On subsequent follow-up after three weeks, it was observed that the patient was symptom-free (Figure ).


A 41-year-old woman with no significant past medical history presented to the emergency department with a one-day history of nausea, vomiting, and diarrhea (six loose bowel movements within the previous 24 hours). Five days prior to her presentation, she presented to an urgent care clinic with body aches, chills, and fever. She tested positive for influenza type A and was prescribed Tamiflu. Her husband and several other family members also tested positive for influenza. On admission to the emergency department, she denied chills, fever, abdominal pain, numbness, or paresthesias. Nausea and vomiting were exacerbated by oral intake of food and fluid. She also complained of generalized weakness in her upper and lower extremities bilaterally, as well as shooting pain down the lateral side of her right lower extremity. On physical exam, she was noted to have dry mucous membranes. The rest of her exam was unremarkable. Vital signs on admission were a temperature of 95.5° F, pulse 94/min, respiratory rate 16/min, and blood pressure of 121/58 mmHg. She was started on 0.9% intravenous sodium chloride and Tamiflu. She was also started on ondansetron, prochlorperazine, and diphenhydramine for intractable nausea and vomiting. Her initial labs showed the following: white blood cell count (WBC) 13,200/mm3, hemoglobin (Hb) 21.5 g/dL, hematocrit 67.3%, platelet count 361,000/mm3, sodium 135 mEq/L, potassium 5.8 mEq/L, chloride 96 mEq/L, blood urea nitrogen 16 mg/dL, creatinine 1.1 mg/dL, glucose 169 mg/dL, calcium 8.4 mg/dL, and lactic acid 7.5 mg/dL.
After IV fluid administration, she stated she was starting to feel better, but this was short-lived. She continued to have generalized muscle pain, weakness, and feelings of heaviness in her lower extremities. At this time, there was no evidence of edema. Repeat labs showed continued elevated hemoglobin and hematocrit levels; therefore, phlebotomy was recommended. Hours later, the patient became lethargic and experienced numbness and tingling in her hands and feet. On generalized exam, her extremities appeared purple and cyanotic. She denied pain but once again described pressure in her lower extremities. Her pulses were unable to be obtained by Doppler ultrasound. She was transferred to the Intensive Care Unit where an arterial blood gas (ABG) depicted a pH of 7.148, pO2 146 mmHg, pCO2 25 mmHg, and a base excess of -18. Her albumin level was 2.4 g/dL, and she was started on replacement therapy. Her creatine phosphokinase (CPK) levels and liver function test were within normal limits. Neurology was consulted after episodes of sensory deficits to rule out Guillain-Barre syndrome.
On physical exam, she continued to have generalized weakness but presented with hyperreflexia of her deep tendon reflexes. It was recommended that a lumbar puncture be used to evaluate albuminocytologic dissociation and to possibly administer intravenous immunoglobulin (IVIG). After discussion, it was agreed that Guillain-Barre syndrome was unlikely and that further workup was not necessary. Labs showed no evidence of methemoglobinemia or carboxyhemoglobinemia. Heparin, insulin sliding scale, prochlorperazine, sodium bicarbonate, and IV fluids were administered. Her blood pressure began deteriorating rapidly, so Neo-Synephrine® was administered and the required doses of Neo-Synephrine escalated quickly. Repeat labs showed a continued elevation of the hemoglobin and hematocrit. Her WBC count increased significantly to 42,000/mm3. Labs confirmed that metabolic acidosis due to lactic acid continued to be present. She required intubation due to respiratory failure induced by her metabolic acidosis. She was coherent before intubation, and she only complained of generalized weakness and pressure on her lower extremities. Peripheral access was needed to run more lab work but was impossible due to the collapsibility of her veins. A central line was planned. However, the patient went into asystole and cardiopulmonary resuscitation (CPR) was attempted to resuscitate the patient to no avail.


An 80-year-old woman with a history of subarachnoid haemorrhage was brought to the emergency room because of speech problems. The patient was found in the morning by her relatives with severe speech comprehension and production difficulties. The exact time of symptom onset was unclear. Clinical examination at the ER revealed a sensory aphasia without other neurologic deficits. Stroke was suspected and the patient underwent a brain CT with an optimized stroke protocol consisting of an unenhanced CT, perfusion CT, and a CT angiography. Unenhanced CT showed no abnormalities, apart from already known and unchanged chronic hypodense gliotic changes in the left temporo-insular region (Figure ). Perfusion CT showed a normal to slightly diminished mean transit time (MTT), a diminished time to drain (TTD) and a clearly increased cerebral blood flow (CBF) and cerebral blood volume (CBV) in the entire left parietotemporal region (Figure ). No intra-arterial clots were seen on CT angiography. Urgent brain magnetic resonance imaging (MRI) was performed. Diffusion weighted images (DWI) showed subtle diffusion restriction in the left parietotemporal region, corresponding with the area of hyperperfusion on CT, without accompanying signal alterations on FLAIR (Figure ). Based on the clinical presentation and imaging findings, a nonconvulsive status epilepticus or postictal Todd’s paresis was suspected. An Electroencephalography (EEG) was performed within two hours of the MRI. Only interictal epileptiform changes were seen with sharp theta waves and spike waves in the left temporal region. These EEG findings were not compatible with an ictal state – seizure or status epilepticus – as the discharges were neither rhythmic nor continuous. Therefore, a diagnosis of postictal sensory aphasia was made, presumably after a focal seizure involving Wernicke’s area. An antiepileptic treatment with levetiracetam was started. There was gradual improvement of the patient’s speech difficulties over three days and she was discharged home after six days without residual symptoms.