The case of a 25-year-old male patient who came into the emergency room after suffering trauma with left knee injury due to motorcycle accident is presented. Clinical examination revealed significant joint effusion and limited and painful mobility. Anterior and posterior drawer tests were difficult to evaluate because of pain. No laxity was observed. In the X-rays taken at the emergency room, concurrent avulsion fracture of anterior and posterior tibial spines was shown, Type IIIb (displacement and rotation offragment) and Type II, respectively, as classified by Meyers and McKeever [].A computed tomography scan was performed to confirm such lesions (); the size of the avulsed fragments was 11× 12 × 8 mm (ACL bony avulsion) and 19 × 12× 6 mm (PCL bony avulsion). Surgery was performed6days after trauma.
The operation was performed under general anesthesia. The patient was positioned supine with the limb placed in a standard leg holder with 90°flexion of the knee, and is chemia was applied to the root of the affected limb. The central transtendinous (usually employed by the authors for cruciate ligaments surgery) and the anteromedial and posteromedial portals were used. Arthroscopic diagnosis was made, confirming both lesions and ruling out other associated injuries. With the arthroscope placed in the central portal, and after removing synovial tissue and Hoffa’s fat pad to improve visualization, it was proved that bony avulsion of ACL could be reduced, with the help of a probe introduced by the anteromedial portal(). The posteromedial recess was addressed by introducing the arthroscope between the PCL and lateral wall of the medial condyle. The posteromedial portal was established so that the avulsion of the PCL could be observed (). For fixation of both avulsed fragments, the adjustable length suspension device ZipTight® (Zimmer Biomet, Warsaw, IN, USA) was used. This device has a pusher to facilitate the passage of the implant through a bony tunnel (). The PCL tibial avulsion fracture was treated first. An exhaustive debridement of the remnants of the synovial tissue was performed, and the bony fragment was reduced to its anatomical position. With the arthroscope placed in posteromedial portal, the PCL Guide (Biomet, Warsaw, IN, USA) was introduced through the anteromedial portal, positioning it on the avulsion of PCL insertion. With the guide set at 45°, a 2.4mm guide pin was introduced from the anteromedial aspect of tibial metaphysis (after performing a longitudinal 2-cm incision) through the avulsed fragment, displaying the output of the needle through the center of the bony fragment to avoid any possible damage to the popliteal neurovascular bundle. Over the guide pin, a tunnel was performed with a 4.5 mm cannulated drill bit(). Meanwhile, an assistant prepared the ZipTight implant, placing it in the end of its pusher. Once prepared, it was introduced in the tibial tunnel, carried by the pusher, to the intra-articular exit of the tunnel, through the avulsed fragment (). Once the implant appeared at the intra-articular exit of the tunnel, an obturator was introduced through the pusher until the implant came out entirely to the joint. By pulling the loops of the device, the implant was settled over the fractured fragment. Subsequently, the strands were fitted to the lateral grooves of the cortical button and side wires were pulled to adjust the knob to the tibial cortex. Continuing traction, fragment was reduced and fixed firmly in its bed (). Second, the fixation of the anterior cruciate avulsion fracture was carried out. With the arthroscope in the central portal, ACL bone avulsion was addressed. As in the posterior spine injury, exhaustive cleaning of synovial and small chondral remnants was performed. Using a probe, the bony fragment was reduced to its anatomical position. Through the anteromedial portal, an ACL Guide (Biomet, Warsaw, IN, USA) was introduced, open at 55°; a 2.4 mm guide pin was placed from the medial side of tibial metaphysis, using the same incision made for the posterior fragment, and crossing the avulsed bony fragment. Using such needle as a guide, a tunnel was performed with a 4.5 mm cannulated drill bit. Subsequently, another implant was placed, adjusted, tensioned, and fixed in identical manner to the posterior fragment ()
Passive mobilization of the knee started 24 h after surgery. Full weight-bearing of the limb was allowed with a knee brace in extension during the 1st 4 weeks. After the 4th week, the immobilizer was removed and progressive full knee flexion was allowed. The patient returned to his usual sports activity 6 months after the intervention. No post-operative complications appeared. At 18-month follow-up, the patient was conducting normal life and free of symptoms. At clinical examination, Lachman, anterior drawer, pivotshift, posterior drawer, and reverse pivot shift tests were negative. Range of motion was 130° flexion, with a 5°lack of extension. The International Knee Documentation Committee score was 83.80 points. Lysholm scale was 85 points. Patient resumed activities of daily living without any problem. Consolidation of both tibial spine avulsions was confirmed by anteroposterior and lateral X-ray () and by magnetic resonance imaging.


A 42-year-old male presented with multiple, discrete to confluent, and well-defined erythematous to dusky macules with superimposed bullae over the trunk and limbs for 3 days. He developed the lesions about 6 h after taking a combination pill of ibuprofen and paracetamol for joint pain. There were no associated constitutional symptoms, and general health of the patient was unaffected. Lips showed mild crusting. Genitalia had well-defined erosion over inner prepuce and glans penis. The patient also reported similar lesions of lesser severity at the same sites 2 years back, following intake of some over-the-counter analgesic for joint pain. Those lesions healed with hyperpigmentation. Based on history and clinical presentation, a diagnosis of GBFDE was made. Given the extensive involvement and risk of life-threatening consequences, rechallenge was not carried out. The patient was admitted and started on cyclosporine 5 mg/kg with excellent response and complete healing of lesions within 1 week [Figure –].


A 24-year-old male presented with widespread dull erythema over the body with superimposed vesiculobullous lesions over trunk and limbs that developed 2 h after taking medication for common cold. He had taken multiple medicines including cetirizine, paracetamol, and pseudoephedrine. On interrogation, he admitted to have 4–5 similar episodes in the past, each of increasing severity than the previous one. On those occasions, he had taken multiple medications before the episodes for complaints of fever and cold. The patient was in good general health except for the pain and discomfort in the lesions. Lips showed erythema. The patient was treated with cyclosporine 5mg/kg with excellent response within 5-7 days. The lesions healed with hypopigmentation [Figure and ]. Provocation was not carried out due to ethical reasons. The patient, however, reported after 6 months with severe burning and erythema in the healed lesions on self-administration of tablet paracetamol for fever, thereby confirming the cause of GBFDE.
GBFDE, a rare variant of FDE, has been defined as widespread blisters and erosions with typical well-demarcated FDE lesions involving at least 10% of the body surface area distributed on at least 3 of 6 different anatomic sites including the head and neck, front of the trunk, back, upper extremities, lower extremities, and genitalia.[] It has been associated with certain drugs, namely mefenamic acid, naproxen, cetirizine, ciprofloxacin, doxycycline, and nicotinic acid/laropiprant.[]
Clinically, GBFDE may either present as generalized oval shaped, brownish livid macules with superimposed blisters or as diffuse erythema with flaccid blisters. In both forms, there are areas of intact skin between the blisters. Mucous membranes are rarely involved, and usually, there is no fever and only mild malaise. A history of a similar previous localized event regarding an FDE can often be elicited. Recurrences can lead to more widespread skin detachment, and therefore, to a more severe disease course.[]
Histologically, GBFDE is characterized by necrotic keratinocytes that are either disseminated or present in the form of complete epidermal necrosis. The basement membrane zone shows vacuolization resulting in subepidermal blistering. The dermis usually exhibits a sparse superficial and often perivascular lymphohistiocytic infiltrate.
GBFDE can mimic SJS/TEN, staphylococcal scalded skin syndrome, and autoimmune bullous diseases such as pemphigus vulgaris and bullous pemphigoid, erythema multiforme major, and exfoliative dermatitis. In contrast to TEN, GBFDE consists of an absence or paucity of constitutional symptoms, well-demarcated blisters and erythematous patches, absence of small spots or target lesions, absence or paucity of mucosal erosions, absence or paucity of visceral complications, history of a similar eruption, and onset within hours of exposure to the associated drug. Most dermatopathologists also consider that the necrosis of the epidermis observed in GBFDE differs from that in TEN by more abundant infiltration by lymphocytes (including many regulatory T cells) and more pigment incontinence.[] However, in the acute stage, histological differentiation may be difficult or even impossible.
The distinction between GBFDE and SJS or TEN is important because of the presumed favorable prognosis of GBFDE. However, a case–control analysis of 58 patients with GBFDE matched by age and extent of skin detachment to 170 control patients with a validated diagnosis of SJS or SJS / TEN overlap, found GBFDE to have a nearly identical mortality rate to SJS/TEN, thereby questioning the benign nature of GBFDE.[] Therefore, the potential severity of GBFDE should not be underestimated, and it likely deserves the same symptomatic treatment and care as SJS or TEN. Severe cases of GBFDE should be regarded with the same level of urgency as cases of SJS/TEN, and the necessity of offering an effective treatment is of paramount importance.
Cyclosporine is a rapid and potent inhibitor of interleukin-2 (IL-2), and its suppressive action primarily is achieved by targeting T lymphocyte functions through IL-2, inhibition of macrophage activity, and inhibition of the activation of the Fas receptor–Fas ligand system. An additional mechanism of immunosuppression in cyclosporin A is the inhibition of CD8 T-cell activation, which in turn inhibits the apoptosis and destruction through either Fas ligand or perforin/granzyme pathway.[]
The mechanism of FDE involves intraepidermal CD8+ T cells that are present within the lesions and play a role in local tissue destruction. Clinically, resolved FDE lesions continue to harbor a substantial number of effector memory CD8+ T-cells at the dermal-epidermal junction, which allows for recurrence of the lesions in the same location. Based on the pathogenesis of FDE, Malviya et al. proposed that cyclosporine had a superior therapeutic effect over prednisone or IVIG by specifically targeting the activity of T cells.[] Considering the same, we also used cyclosporin in the above-mentioned cases with a favorable response in both our patients.


Our study presents an interesting case of a seventeen-year-old girl who was referred to the child psychiatry clinic with symptoms of depression and suicide attempt by taking medical pills. The patient was transferred to institutionalized care owing to intra-familial events. She had consistent problems of adaptation to the institutional surroundings and could not get along well with other children. As a result, she did not attend the school and displayed aggressive behaviours. At the initial psychiatric evaluation, she looked tired and sad with untidy hair and unkempt clothes. Her mood was clearly depressive and consistent with her affect. During the interview, she was reluctant, had minimal eye contact and answered with a subdued voice. She explained the reason for her suicidal behaviour that she blamed her loneliness and stated that she could not stand living anymore. During interview, no active suicidal ideations, delusions or hallucinations was observed. During the first interview, Beck Depression score was 44, State-Trait Anxiety Inventory (STAI)-1 score was 40 and STAI-2 score was 38. Based on Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV) criteria, she was diagnosed with Major Depressive Disorder and treatment with fluoxetine (20 mg/day), and aripiprazole (5 mg/day) was started. Two months after the initiation of the treatment, fluoxetine was doubled (40 mg/day) and this treatment regime was continued for subsequent four months, with aripiprazole (5 mg/day). This resulted in regression of depressive symptoms. During the next follow-up interview, she reported not having menstrual cycles for the past four months. Therefore, she was referred to an obstetrician immediately. She had no reports of menstrual irregularity, hirsutism, drug use or history of any related medical disorder prior to the treatment. There, she underwent pelvic ultrasonography examination which showed normal ovaries and endometrium. Analysis of blood test reports showed normal functions of thyroid, liver and kidney. Her pregnancy test was also negative. No pathology was detected in cranial magnetic resonance imaging. Finally, the pathology was reasoned to very high prolactin level in blood serum, which was shown to be 74 ng/ml, while the normal range being 4–20 ng/ml. After ruling out other possible causes of hyperprolactinemia, aripiprazole treatment was thought to be responsible for the observed symptoms. As an immediate change in therapy, aripiprazole was replaced with quetiapine (200 mg/day). Aripiprazole replacement successfully resulted in reduction of blood prolactin levels to 17 ng/ml and menstrual cycle returned to normal after two months of quetiapine treatment.


A 63-year-old male patient was referred to our hospital due to an alteration in his consciousness. Two weeks prior, he had suffered from a change in mentation and left hemiparesis, so the patient had been admitted to a provincial hospital. CT head scans demonstrated two sites with intracranial tumors: an irregular rim-enhancing mass at the right frontoparietal lobe and a sellar tumor. During hospitalization, the patient showed progressive neurological deterioration. Therefore, the patient underwent a decompressive craniectomy and was transferred to our hospital. At the tertiary hospital, he was fully oriented but had hemiplegia on the left side. Cranial T1W MRI with intravenous (I/V) gadolinium revealed an irregular, heterogeneously contrast-enhancing mass at the right frontoparietal lobe measuring 52 mm × 68 mm × 54 mm with central hypointensity indicative of necrosis [].
In addition, another tumor was noted in the sellar region with suprasellar extension, measuring 20 mm × 21 mm × 29 mm [Figure and ]. Pituitary hormones were found to be within normal values. An extended right frontoparietal craniotomy was performed to approach both tumors. However, the patients’ position was suboptimal to access the sellar region limiting the resection to a partial one at this site.
Histopathology of the right frontoparietal lesion revealed a glioblastoma multiforme [Figure and ] while the sellar tumor was identified as pituitary adenoma []. Since his hormonal profiles were normal, nonfunctioning pituitary adenoma was designated. The postoperative period was uneventful, and the patient was sent for adjuvant therapy. Unfortunately, the patient refused adjuvant therapy and was lost to for any further follow-up.


A 62-year-old female patient presented with progressively blurred vision in her right eye, which had occurred over the course of 1 year. On examination, she had normal visual acuity in her left eye but only 20/200 in her right eye. A cranial T1W MRI with I/V gadolinium revealed a homogeneously enhancing, board-based tumor at the planum sphenoidale with a dural tail sign, measuring 37 mm × 30 mm × 18 mm. Interestingly, a second enhancing sellar tumor with suprasellar extension was observed posterior to the former [Figure and ]. Therefore, the patient underwent a subfrontal approach for microsurgical resection. The anterior tumor showed a good arachnoidal plane for dissection but was attached to the dura of the planum sphenoidale. This tumor was subtotally removed due to high vascularity.
Histological characteristics were those of a meningothelial meningioma. Tumor cells formed lobules where they appeared to form a syncytium with oval nuclei, occasionally showing central clearing []. The tumor was immunostained and found to be positive for epithelial membrane antigen. After surgery, the patient developed Gram-negative septicemia and required antibiotic administration for 2 weeks. She recovered well and her vision, in the right eye, gradually improved too. At follow-up, she maintained independent daily activities. She does not wish to pursue a second surgery for the tumor residual.


A 61-year-old female patient presented with progressive headaches. Ten years prior, she had been diagnosed with an intraosseous meningioma at the right frontal base [Figure and ] for which she underwent a right-sided craniotomy for resection. Follow-ups with MRIs were obtained annually and showed stable residual disease. However, over the course of 3 months, before admission, she had begun to develop progressively worse headaches. After a repeat of an MRI, a newly infiltrative heterogeneously enhancing mass involving bilateral splenium of the corpus callosum was observed. To obtain a pathological diagnosis, an image-guided biopsy was carried out [Figure and ].
Microscopic examination revealed hyperchromatic nuclei and mitotic figures. However, no areas of necrosis, hemorrhage, or endothelial hyperplasia were observed. A diagnosis of anaplastic astrocytoma WHO Grade III was made []. Her hospital course was uneventful. Later, she was given a course of adjuvant external beam radiotherapy. She did not receive chemotherapy due to financial reasons. She has been followed up since, and she was still able to manage daily activities at the last follow-up.


A 50-year-old female patient presented with a chronic headache for 3 months and with progressively worsening visual field defects. On examination, a dense bilateral temporal hemianopia with normal visual acuity was detected. Her hormonal laboratory demonstrated mildly elevated prolactin (64.5 ng/ml) although all other hormones were within normal range. Cranial MRI revealed a heterogeneously enhancing sellar tumor with suprasellar extension and chiasma compression []. Two other hemispheric lesions were identified, which imposed as homogeneously enhancing solid nodules (1.1 cm on the right posterior parietal lobe and 1 cm on the left vertex with hyperostosis of adjusted skull). These were interpreted as likely meningiomas [Figure and ]. The patient underwent an endoscopic endonasal transsphenoidal approach for successful sellar tumor removal.
Microscopic examination of this surgical specimen showed epithelioid cells with a sheet-like growth pattern. A histological diagnosis of pituitary adenoma was made []. The postoperative period was without incident. The patient is being followed clinically and expectantly for her convexity lesions. Her visual field defects have improved since.


A 37-year-old female was referred from a provincial hospital due to a rapidly, worsening headache over a period of 2 weeks. According to her history, she had been suffering from progressive headaches for 5 years as well as from hearing disturbances on the right side for 1 year. Two weeks before admission, her headaches got rapidly more severe and she developed a bilateral papilledema. Cranial MRI revealed two tumors located in the pineal region and at the cerebellopontine angle (CPA), causing obstructive hydrocephalus.
A cranial T1W MRI revealed a nonenhancing large tumor at the pineal region with third ventricle extension. This tumor displayed restricted diffusion on diffusion-weighted MRI [Figure and ]. The second lesion imposed as a homogeneously enhancing cone-shaped tumor at CPA at the level of the right internal acoustic canal. The findings were compatible with vestibular schwannoma [].
The patient first underwent ventriculoperitoneal shunting for diversion of her cerebrospinal fluid. Later, an occipital transtentorial approach was chosen for pineal tumor removal. Near total tumor removal was achieved and the postoperative period was uneventful.
Histologically, the microscopic examination showed epithelium and lamellated keratin [], and the final diagnosis was epidermoid tumor. At last follow-up, she had recovered well and decided to postpone any CPA tumor surgery.


A 14-year-old female patient was hospitalized in our Cardiology Department for repeated episodes of PSVT which started at the age of 11. She was treated with Bisoprolol 2,5 mg but presented PSVT despite antiarrhythmic drugs. The 12-lead ECG showed minimal pre-excitation, with a small delta wave in leads V2–V3 but with a normal QRS complex of 100 ms and a normal PR interval in lead II of 160 ms. The three classical criteria for confirmation/exclusion of an accessory pathway were analyzed: there was a Q wave in lead V6, the precordial transition was after lead V1 and a R wave was present in lead avR. Therefore, the three criteria failed to confirm the presence of an accessory pathway. We measured the longest and the shortest PR interval and found a difference of 40 ms between leads II and V2. (Fig. ) Before the electrophysiological study, an echocardiogram showed normal ejection fraction and normal dimensions for the cardiac chambers, without any valvulopathy (Fig. ). During electrophysiological study 4 catheters were introduced through the right femoral vein: a quadripolar catheter at the level of the high right atrium, a quadripolar catheter at the level of the His bundle, a decapolar catheter at the level of the coronary sinus and the ablation catheter at the level of the right ventricle. During ventricular stimulation the retrograde conduction was through a left lateral accessory pathway, which was further confirmed by the activation through the coronary sinus catheter (Fig. ). As the accessory pathway was lateral, a trans-septal approach was performed using the Brockenborg needle for the septal puncture (Fig. ).
After the puncture a sheath was introduced inside the left atrium and a 4 mm tip catheter ablation at the level of the left lateral ring (Fig. ). Catheter ablation of the accessory pathway was performed using 35 W and 55 C. After ablation there was no anterograde or retrograde conduction through the accessory pathway. After 30 min the procedure was stopped and the patient returned to her room. The 12-lead ECG performed after catheter ablation was compared with the ECG before ablation and the three classical criteria were once again insufficient to establish the presence or absence of an accessory pathway.
Our criteria of PR variation of >30 ms confirmed the presence of the accessory pathway before ablation and the absence of the accessory pathway after ablation (Fig. ). Furthermore an adenosine test was performed to exclude the presence of the accessory pathway after ablation which produced a 2:1 AV block. After ablation the PR interval variation was 5 ms (Fig. ).


The patient is a 42-year-old Filipino woman with SLE. Chronic symptoms include discoid and malar rash, oral ulcers, photosensitivity, and polyarthritis. She has no history of renal or central nervous symptoms but has a history of pericarditis. She also has Raynaud disease, but no other notable medical problems. She denies an exposure to tuberculosis. Her medications include hydroxychloroquine, methotrexate, azathioprine, methylprednisolone, folate, pregabalin, and nifedipine.
At initial presentation to an outside provider, she noted new swelling and pain in her left fifth finger and the ulnar aspect of her left hand. She had a similar episode in the right hand 1 year prior, which was associated with a lupus flare and resolved with steroid treatment. Her left hand pain and swelling were also attributed to a lupus flare at the time of presentation, and methylprednisolone dosage was increased. When her symptoms did not improve 1 month later, she presented to our orthopaedic clinic. Her examination was notable for diffuse erythema and swelling in the fifth finger, extending into the palm, as well as a small cyst on the ulnar side of her dorsal hand (Figure ). She had a fusiform digit and pain over the flexor sheath but did not have pain with passive extension or a flexed digit at rest. A magnetic resonance image was obtained, and the results were consistent with tenosynovitis (Figure ). She received a cortisone injection in the fifth finger, which resulted in only a mild decrease in swelling. One month later, she elected to proceed with synovectomy.
In the operating room, a Brunner-type incision was made over the fifth finger, and purulence was immediately expressed. The incision was extended to the distal finger and palm to thoroughly evaluate the extent of infection, and synovectomy, irrigation, and débridement were performed after cultures were obtained. No “rice bodies” were noted, and no purulence was found distally in the carpal tunnel. After the volar procedure was completed, a small dorsal incision was made over the cyst, and purulence was also expressed. The area was not contiguous with volar infection. The skin was loosely closed with nylon sutures, and a soft dressing was placed.
The intraoperative acid-fast culture grew M tuberculosis, and all other cultures were negative. Subsequent evaluation of the patient found no evidence of previous or active pulmonary tuberculosis. Because of a recent history of headaches, she underwent neurologic evaluation and brain MRI, which revealed ring-enhancing lesions consistent with tuberculoma. She had no other neurologic signs or symptoms at the time of diagnosis and required no additional treatment for these lesions. She was treated with a standard four-drug regimen, and her azathioprine was discontinued during this course. Her hand infection healed uneventfully without any sign of persistent infection (Figure ).


A 62-year-old female was referred to the hospital for evaluation of hypokalemia. A few weeks prior to admission, she developed sore throat and difficulty swallowing. She also had noticeable change in her voice where it became more nasal. The patient had observed increase in weight and generalized swelling. She had a past medical history of alcohol abuse, hypertension and chronic obstructive lung disease (COPD), and was a smoker since childhood. Her family history was significant for a brother who was diagnosed with nasopharyngeal cancer. The patient was evaluated by an otorhinolaryngologist (ENT) and had a laryngoscopy showing a uvular lesion. A CT scan of the neck showed 2.9 cm left-sided mucosal/submucosal mass in the upper pharyngeal wall/left nasopharyngeal wall suspicious for nasopharyngeal carcinoma, with multiple enlarged regional lymph nodes. Biopsy of the lesion in the oropharynx revealed small cell cancer of the uvula (). The tumor tested positive for synaptophysin and TTF-1. Tests for p16 and HPV were not performed. The patient was referred to the oncology clinic and on follow-up visit, she had shortness of breath and excess wheezing. Her initial laboratory workup revealed hypokalemia, and accordingly she was sent to the emergency department (ED).
Upon arrival, her vitals were stable. On physical exam, she had moist oral mucosa without pharyngeal erythema. Her uvula was enlarged but not obstructing the pharynx. She had no palpable cervical lymph nodes. Chest examination revealed limited air entry with mild expiratory wheezes with coarse breathing sounds. Heart sounds were regular without murmur. She had 1+ lower extremity edema. Complete blood count (CBC) showed white blood cells of 11.7 × 103/µL, hemoglobin level 14.3 mg/dL, platelet count of 123 × 103/µL. INR was 1.2. Serum procalcitonin level was 171.37 ng/mL. Comprehensive metabolic panel (CMP) showed serum potassium 2.1 mmol/L, sodium level 145 mmol/L, normal blood urea nitrogen (BUN) and creatinine levels. Serum calcium level was 8 mg/dL, magnesium level 2.1. There was mild transaminitis with AST 147 U/L, ALT 119 U/L and alkaline phosphatase 123 U/L. Total bilirubin was 0.6 mg/dL and albumin level was 3 mg/dL. Chest X-ray showed hyper inflated lungs with coarse interstitial infiltrates along the right lung and left lower lung suggestive of atypical pneumonia. Computed tomography (CT) of the chest showed moderate emphysematous changes and infiltration suggestive of pneumonia without evidence of metastasis. Patient received azithromycin and ceftriaxone together with supplemental oxygen and bronchodilators. Magnetic resonance imaging (MRI) of the brain showed heterogeneous, mildly enhancing, T2 bright mass along the left fossa of Rosenmuller, compatible with her malignancy (). Enlarged bilateral retropharyngeal and cervical lymph nodes were noted. Non-specific dural thickening and enhancement were concerning for malignant spread. Further diagnostic workup for tumor staging included CT scan of the abdomen which showed nodular cirrhotic liver with innumerable metastatic deposits within the liver measuring up to 3.2 cm (). A nuclear medicine bone scan showed no evidence of osseous metastasis. Though patient was not known to be diabetic, her admission hemoglobin A1c (HbA1c) was 6.4, and throughout her hospital stay, she was noted to be hyperglycemic with blood glucose ranging from 159 - 336 mg/dL. She was also found persistently hypokalemic requiring frequent potassium supplementation. Accordingly, adrenocorticotropic hormone (ACTH) was requested and showed a level of 479 pg/mL. Serum aldosterone level was 4.8 ng/dl, and renin activity was 1.1 ng/ml/hr.
Patient was diagnosed with late metastatic small cell carcinoma of the uvula and she was determined to be a poor candidate for chemotherapy given worsening thrombocytopenia and generally poor condition. Palliative radiation was offered in view of dural metastases but the patient was not amenable to further treatment at this point. The patient decided in favor of comfort measures and was accordingly set up for home hospice care upon discharge.


This is a 49-year-old male with hypertension and chronic kidney disease. He presented to the Emergency Department on the 28th of March 2017 with right-sided weakness and inability to speak. He was found to have recent acute/early subacute infarct along left middle cerebral artery territory.
On 6th of April 2017, the patient was transferred to Qatar Rehabilitation Institute to be enrolled in an active rehabilitation program. Upon assessment, he was found to have global aphasia, dense right-sided weakness, maximally assisted in bed mobility and transfer, and totally assisted in activities of daily life.
During his hospital stay, he had episodes of elevated liver enzymes and the suspected medications (atorvastatin 40 mg orally daily and escitalopram 20 mg orally daily) were suspended with continuous monitoring of the liver enzymes. Liver enzymes started to decrease within few days after the suspension but did not reach the baseline. A week after suspending escitalopram, he was started on (oxybutynin 5 mg orally twice daily) for overactive bladder. Within a week of starting oxybutynin, liver enzymes increased again ( and ). A thorough medication review was done by the assigned clinical pharmacist and none of his medications was known to result in high liver enzymes. After discussing this with the physician, oxybutynin was the only suspected medication to be responsible of this elevation in liver enzymes as it was the newest medication added to his therapy, and hence, it was suspended.
To rule out inflammatory, autoimmune, or any other underlying causes, the gastroenterology team was consulted to evaluate the case. Their primary assessment was “drug-induced hepatitis.” Their recommendations were to stop any suspected hepatotoxic medication and to do further investigations. These included full workup of hepatitis, hepatitis A virus immunoglobulin M, hepatitis C virus antibody, hepatitis E virus immunoglobulin M, antinuclear antibody, anti-smooth muscle antibody, antimitochondrial antibody, anti-liver kidney antibodies, and celiac profile – immunoglobulin A, anti-tissue transglutaminase antibodies, ceruloplasmin, and α-1 antitrypsin. All the required tests were negative and the ultrasound of the abdomen showed normal findings. Within a week of discontinuing oxybutynin, both ALT and AST were decreased to values lower than 3 times the baseline.
As the patient was lost to follow-up, consent for publication of this case was not possible. However, the case details have been sufficiently anonymized and approval for publication has been obtained from the organization’s medical research center.


A 22-year-old man was presented to the hospital with symptoms of progressive dyspnea, paroxysmal nocturnal dyspnea, intermittent cough, and bloody sputum. No previous history of any systemic diseases was reported by the patient. There was no personal history of tobacco use and recreational drug abuse. The patient admitted to have self-administered stanozolol, clenbuterol, and triiodothyronine (T3) to increase his muscle mass and his strength for 10 days, and discontinued after symptoms of chest discomfort and exertional dyspnea 12 days before his admission to the hospital. During the first 7 days, he consumed stanozolol 10 mg/day and clenbuterol 40 μg/day, and then doubled the dose during the next 3 days. The dose of T3 was 25 μg/day for the reported 10 days of administration. On admission, vital signs showed body temperature 36.5 °C, heart rate 102 bpm, blood pressure 118/78 mmHg, and respiratory rate 20 breaths/min. Physical examination revealed icteric sclera and mild pitting edema of the bilateral lower limbs. Cardiovascular examination showed muffled heart sounds, gallop rhythm, and grade 2/6 systolic ejection murmur at mitral auscultatory area. The relevant lab reports are listed in .
The electrocardiogram showed sinus tachycardia and left ventricular hypertrophy (). The transthoracic echocardiography () revealed ejection fraction 20%; left atrium (36 mm); right ventricle (30 mm); left ventricle (62 mm); diffused hypokinetic ventricular wall motion, severe tricuspid regurgitation, moderate mitral regurgitation, pulmonary artery systolic pressure (45 mmHg), and mild pericardial effusion. The pulmonary CT () showed bilateral pneumonia, pleural effusion, and pericardial effusion. The abdominal ultrasonography () showed cholestasis and intestinal fluid. During admission period, patient was managed with symptomatic and supportive medical therapy. His blood biochemistry reports including cardiac markers and the liver function test showed gradual improvement and he was discharged after 12 days of hospitalization.


A 6-year-old boy reported to our outpatient department (OPD) as a follow-up case of hydrocephalus with dorsal meningocele with complaints of mild, intermittent chest pain for 1 month. He did not have any fever or dyspnea. He underwent VP shunt procedure with a medium-pressure flexible shunt and repair of dorsal meningocele at 1 month of age and was doing well till date. He was followed up at our OPD every 6 months and was asymptomatic. Clinically, the VP shunt chamber could be palpated in the neck as it was shifted down. His vitals were stable, chest was clear, abdomen was soft, and there was no neurological deficit. His weight gain and height was appropriate for age.
Routine blood investigations and chest X-ray were carried out. Blood reports of complete blood count and electrolytes were normal. The anteroposterior (AP) and lateral view of chest X-ray revealed supradiaphragmatic coiling of VP shunt in the right side of chest wall. There was no pleural effusion or hydrothorax []. Non contrast CT scan (NCCT) thorax was carried out to confirm migration of the VP shunt in the thoracic cavity []. NCCT of brain revealed downward migration of VP shunt outside lateral ventricle.
Initially, a neck incision was made to retrieve the shunt; however, because of failed attempt, video-assisted thoracoscopic removal of shunt was carried out and it was retrieved totally.


An 18-month-old male infant, diagnosed as a case of steroid-resistant nephrotic syndrome, born of nonconsanguineous marriage, was admitted with complaints of not able to sit and head drop for 1 day.
The patient was diagnosed to be a case of infantile nephrotic syndrome at the age of 1 year with puffiness of face, edema feet, and oliguria. There was no renal dysfunction, hematuria, or hypertension. Family history of kidney disease was absent. He was treated with full dose steroid (2 mg/kg/day) for 4 weeks and additional 2 weeks with no remission. Renal biopsy showed minimal change disease with no deposits on immunofluorescence. He was started with cyclosporine A (6 mg/kg/day), alternate day steroids (1.5 mg/kg/day), oral enalapril and furosemide. Trough cyclosporine (C0) blood level after 4 weeks of initiation was 95 (target: 80–120 ng/ml). In the subsequent months, the patient was admitted twice, 5–7 days each with an interval of 2 weeks for infective diarrhea and treated with antibiotics, zinc, and fluid management. Diuretics were intentionally withheld and not restarted. Serum electrolytes at the time of last discharge were normal. The infant intake reduced to predominantly milk, due to cough, cold, and wheezing, few days before the weakness developed. There was no history of fever, dysuria, or vomiting. There was no history of weakness in the past. There was weight loss of 800 g (10% body weight) from previous hospital visit.
On admission, the infant was limp but conscious. General examination showed mild pallor and minimal pedal edema. Weight of the child was 7.4 kg (expected 10.5 kg, <3rd percentile WHO standards, Grade II malnutrition of Indian Academy of Pediatrics classification). Urine output was normal with approximately 1 ml/kg/h. Vital parameters were normal. Neurologically, the infant was conscious, but irritable. There was no cranial nerve palsy. There was head drop with weakness of extensors of neck. Tone was decreased in all the four limbs. He was able to sit only with support in tripod position []. Deep tendon reflexes were depressed and planters were absent. Other systemic examinations were normal.
Suspecting hypokalemic paralysis, electrocardiogram (ECG) was done which showed flat T- and U-waves []. Investigations revealed hypokalemia (serum K+ = 2.1 mEq/L), hypocalcemia (corrected serum Ca = 6.9 mg/dl), hypomagnesemia (serum Mg = 1.6 mg/dl), hypoalbuminemia (serum albumin = 2.0 g/dl), and hypercholesteremia (serum cholesterol = 216 mg/dl) with blood urea of 3 mg/dl and serum creatinine of 0.12 mg/dl. Random blood sugar was 106 mg/dl and complete blood count was normal. Thyroid profile was normal.
Arterial blood gas analysis was normal (pH = 7.40, HCO3− = 22.3 mmol/L, PCO2 = 36 mmHg, PO2 = 83.3 mmHg, and SaO2 = 95%) and urinary electrolytes (mEq/L) were Na: 9, K: 2.2, Cl: 12, creatinine: 5. Urinary K was <20 mEq/L with FeK of 2.5% (average 10%). Transtubular potassium gradient (TTKG) calculated was 0.5 (<4) ([urinary K × serum osmolality/serum K × urinary osmolarity] ×100), suggesting extrarenal losses. Spot urine protein creatinine ratio was 0.34 (normal <0.2). Spot calcium creatinine ratio was 0.34 (normal <0.8 for infants) and FeNa was 0.34 (normal <2). Urine routine and microscopy showed trace proteins and no white blood cells or red blood cells. Serum 25-hydroxyvitamin D3 level was 3 (normal = 9–37.6 ng/ml).
The patient was started on KCl infusion (4 mEq KCl in 100 ml fluid) along with injection MgSO4 50% 0.2 ml/kg intramuscular for 2 days; head drop improved rapidly and the patient completely recovered within 48 h. Repeat serum K+ level was normal (3.7 mEq/L). The patient was discharged on oral potassium supplement (syrup Potclor 20 mEq/15 ml) of 1 mEq/kg.


This is the case of a 29-year old male from the Peruvian jungle who was HIV positive for about 6 years, has not been receiving highly active antiretroviral (HAART) therapy, and with a CD4 count of less than 50 cells/mm3. The patient complained of diffuse abdominal pain lasting for 1 month, subsequently localized to the right lower quadrant, with an intensity of 9/10, associated with fever, chronic diarrhea, and a 6-kg weight loss. On physical examination, he looked chronically ill with pallor, and his abdomen had rebound tenderness on the right lower quadrant. Laboratory examinations showed severe hypochromic microcytic anemia, leukocytosis, hypoalbuminemia, and azotemia.
A flat abdominal X-ray showed pnemoperitoneum and air fluid levels (Fig. a). He was taken to the operating room, where 1 L of pus and a 1 cm perforation, approximately 40 cm proximal to the ileo-cecal valve, with ileal wall thickening were found. A segmental ileal resection and ileostomy were performed. The gross specimen in (Fig. b) shows the ulcer in the terminal ileum, and histopathological examination revealed the presence of caseating granuloma with yeast, compatible with histoplasmosis (Fig. c).
Therapy with amphotericin and itraconazole was started with a favorable response. The patient required hemodialysis for chronic kidney disease, probably due to HIV-associated nephropathy (renal biopsy was not performed). It is important to remark that there was not any sign to suspect CMV infection.


A 45-year-old male patient visited (September 2015) the outpatient department (OPD) of Dr. Sarvepalli Radhakrishnan Rajasthan Ayurved University Hospital, Jodhpur, Rajasthan, for the complaints of passage of hard stool for 3 months and profuse bleeding P/R, pain per anum (near 3 O’clock pile mass may be due to erosions near pile mass) and feeling of something coming out per anum since 1 month.
History of present illness revealed that the patient was apparently normal before 3 months. Gradually, he experienced the passage of hard stool. The problem increased day by day. The patient experienced something is coming out per anum for 2 months. Later, he developed pain per anum during defecation which lasted for the whole day and profuse bleeding P/R for 1 month. Past history revealed sclerotherapy (conservational treatment) in 2014. The patient was under allopathic medicines for the above complaints and did not tried any other system of medications. The disease re-occurred after 1 year in 2015.
Personal history revealed that the patient is a vegetarian, with reduced appetite, irregular food habits, more intake of spicy sweet and chilled foods, disturbed sleep, frequency of micturition 3–4 times per day, straining to pass stool and had no addiction to opium. The patient has a daily routine of two-wheeler riding. There was no genetic linkage of the disease noticed in the family.
General examination of the patient showed pallor vitals were pulse rate 74/min, respiratory rate of 18/min, blood pressure 120/84 mmHg and body weight of 60 kg. Per abdominal examination showed shrunken abdomen and no tenderness.
On local examination, skin of anal verge was found indurated. On digital rectal examination, tender but sphincter tone was normal. Proctoscopic examination confirmed two 2nd-degree (late stage) internal hemorrhoids at 3 O’clock position and 11 O’clock position. Lesions near the 3 O’clock position revealed pile mass. Blood discharge per anum was seen [].
Based on the clinical presentation, the patient was diagnosed as a case of later 2nd degree internal bleeding piles at 3 O’clock and 11 O’clock positions. According to Ayurveda, the patient was diagnosed as a case of Raktarsha (bleeding piles).
The patient was advised for ligation and plication procedure followed by Matra
Basti with Jatyadi oil. Before planning treatment, complete blood count and other tests were done to rule out conditions such as anemia, clotting disorder, diabetes mellitus, other infective disorders, human immunodeficiency virus, Venereal Disease Research Laboratory, and hepatitis. Ligation with surgical linen Barbour thread number 20 on 11 O’clock (to slough off the pile mass) and plication with absorbable chromic Catgut on 3 O’clock internal hemorrhoid (as mucosa is eroded near the 3 O’clock pile mass, it may bleed on transfixation) were done under local anesthesia followed by Matra
Basti with Jatyadi oil.[]
Patient's consent was taken prior to operative procedure. Bowel preparation was done with soap water enema and the patient was kept fasting for 12 h before the surgery. Injection TT was administered I/M for prophylaxis. Lignocaine sensitivity test was done before surgery.
Ligation of 11 O’clock position pile mass by surgical linen Barbour thread number 20
The patient was placed in a lithotomy position. Painting and draping was done. A hemorrhoidal plexus block with liberal local infiltration of 2% lignocaine was given thereafter. The hemorrhoidal masses at 11 and 3 O’clock positions were identified. Gentle digital anal stretching of no more than 6 (3 + 3) fingers (Recamier/Maisonneuve procedure) was done. Intracanal packing was given to avoid soiling during operation Revelation of the “Triangle of Exposure:” The skin-covered component of each of the main piles was seized with Allis tissue holding forceps usually in the 3, 7 and 11 O’clock positions and retracted outward, keeping the Allis tissue forceps in anatomical positions. This revealed the “Triangle of Exposure,” i.e., the mucosal component or internal hemorrhoids at the upper pole and dermal component in the grip of Allis forceps at the lower pole. The internal pile at 11 O’clock position was grasped with a pile mass-holding forceps. The forceps attached to the right anterior pile were taken in the palm of left hand drawn outward and the left index finger was used to stabilize the inner aspect of the pile mass The base of the pedicle of internal hemorrhoidal mass at 11 O’clock was transfixed and ligated by passing a round-body curved needle loaded with the surgical linen Barbour thread number 20.
Plication of 3 O’clock position pile mass by absorbable chromic Catgut
The hemorrhoid at 3 O’clock position was held by pile-holding forceps and round-body curved needle with absorbable chromic catgut passed through the hemorrhoid mucosa. It was done repeatedly till the tightening of stretched pile mass mucosa by folding the mucosal surface in tucks. The pile mass got reduced in size. Gauze soaked in Jatyadi oil was placed inside the canal. One end of the anal packing given initially was withdrawn out for facilitating easy removal and a T-bandage was tied [].
After operation, common analgesics and anti-inflammatory drugs were given to the patient. Isabgol husk was prescribed 1 tsf at bedtime for 4 weeks and a light fibrous diet till healing of the wound. The dressing was removed the next morning after a lukewarm sitz bath. From the 2nd day, Matra
Basti with 50 ml of Jatyadi oil was administered P/R once daily. The treatment was continued for 4 weeks.
Sloughing off of hemorrhoidal masses with automatic removal of linen thread at 11 o’clock position occurred in 10 days and absorption of chromic Catgut at 3 o’clock position occurred in 20 days. Wound healing was monitored daily till discharge of patient from the hospital.
The patient was advised to attend the OPD for examination once a week for 4 weeks. For this 4-week period, the following medicines were prescribed to reduce pain and inflammation and promote healing: orally: Triphala powder (5 g at sleep time with lukewarm water), tablet Gandhaka
Rasayana (250 mg twice a day after food), tablet Maha
Shankha
Vati[] (250 mg twice a day before food) and tablet Triphala
Guggulu[] (2 tablets of 500 mg each thrice daily before food); P/R: Matra Basti with Jatyadi oil. Plain lukewarm water sitz bath was advised after each defecation.
During each follow-up visit, signs and symptoms were assessed. There was moderate-to-mild pain, burning sensation, tenderness, inflammation and brownish black discharge on the first and second visits. During the third and fourth visits, there was no pain, tenderness, discharge or anal stricture and the internal hemorrhoids had completely resolved [].
After this 1-month treatment, the following medications were prescribed for 3 months orally to cure digestive impairment. Drakshasava (10 ml twice daily with equal amount of water after meals), Abhayarishta[] (10 ml twice daily with equal amount of water after meals) and capsule Cytozen twice daily. Relief from signs and symptoms was seen after follow-up of 3 months. No recurrence of the signs and symptoms occurred in the follow-up period. The patient got cured with no complications of the therapy [].
Diet and lifestyle guidelines (high-fiber diet, adequate water intake, no straining or suppression of natural urges, avoiding over exertion and avoiding staying up late) were suggested to the patient and the patient was expected to follow these guidelines for at least 1 year.


A 72-year-old woman was admitted to our hospital for a hepatic mass, which was incidentally identified during a routine health checkup. The patient denied a history of jaundice, vomiting, flushing, or diarrhea before admission. Physical examination revealed a palpable mass in the right upper quadrant of her abdomen. The mass showed a hard texture with an unclear boundary. Laboratory tests showed her blood chemistry was normal. The serum alpha fetoprotein (AFP) level was normal (5.37 ng/mL, reference range 0–7.2 ng/mL), and the hepatitis B virus surface antigen and the hepatitis C virus antibody were negative. Abdominal ultrasonography revealed a huge intrahepatic lesion, which was considered to be hepatic cancer. Dynamic contrast-enhanced abdominal computed tomography (CT) showed a low-density mass measuring 13 × 7 × 6 cm in both, the right and left hepatic lobes (Fig. ). The mass showed heterogeneous enhancement in the arterial phase; however, a decrease in enhancement was observed in the venous phase with no enhancement in the central cystic portion on a triple-phase scan. 18F-fluorodesoxyglucose positron emission tomography (18F-FDG PET) and fused PET/CT showed increased uptake by the mass, which was indicative of a hepatic tumor. Whole-body 18F-FDG PET showed no abnormal activity except for the hepatic lesion. We performed a biopsy for a conclusive diagnosis. Histopathological examination showed a poorly differentiated malignant tumor. Immunohistochemical examination showed that the tumor was positive for cytokeratin (CK), synaptophysin (Syn), chromogranin A (CgA), cluster of differentiation (CD) 56, and thyroid transcription factor (TTF)-1 and negative for cytokeratin (CK) 7. The positive nuclei demonstrated the Ki-67 proliferation rate was 15%. Based on the World Health Organization 2010 classification, this patient was diagnosed with a NET (grade G2).
Based on CT findings, we originally planned to perform a right hepatic trilobectomy. The indocyanine green test performed for preoperative evaluation of hepatic function indicated acceptable hepatic function, although the postoperative residual hepatic volume systematically evaluated using the Hisense Group CAS surgical plan was only 17.87% of the original hepatic volume. The postoperative residual hepatic tissue was insufficient to maintain normal physiological function. Therefore, we selected the surgically safe ALPPS procedure. The first stage of the operation performed laparoscopically included cholecystectomy, ligation of the right portal vein, and partial splitting of the hepatic tissue between segment IV and the left lateral hepatic lobe. No postoperative bleeding and/or bile leakage were reported, and the patient recovered uneventfully.
Contrast-enhanced CT showed the volume of the left hepatic lobe increased significantly a week postoperatively (Fig. ). Remnant hepatic volume was 31% of the standard hepatic volume after evaluation by the Hisense Group CAS surgical plan. Right hepatic trisegmentectomy was performed (Fig. ), and the patient recovered uneventfully with regular follow-up as an outpatient for a year. Postoperative follow-up data are shown in Table . No tumors were identified in any other location during follow-up. The patient received Tegafur at a dose of 80 mg/day for 6 months postoperatively. Histopathological examination showed small cell carcinoma (13 × 7 × 6 cm) in the right hepatic lobe, and immunohistochemical examination showed the tumor was positive for CK, Syn, CgA, CD56, and TTF-1, and negative for hepatocyte, AFP, CK19, CD34, blood vessels, and p53. The positive of Ki-67 was 40%. Interstitial vascular tumor thrombus was not identified using CD31 and D2-40 stains (Fig. ).


An 18-month-old male child with right microphthalmia and complete corneal opacity, midline cleft palate and a repaired cleft lip presented to us with a cystic swelling protruding into his oral cavity. The child had undergone repair of his cleft lip at 10 months of age. Examination of the oral cavity demonstrated a wide complete cleft palate that allowed direct visualization of a completely compressible cystic swelling showing cough impulse.
Computed tomography (CT) head showed a defect in the floor of sella and sphenoid sinus through which the floor of third ventricle was herniating like a cerebrospinal fluid (CSF)-filled sac [Figure and ]. Magnetic resonance imaging (MRI) of the head demonstrated the CSF-containing sac extending through a bony defect at the base of skull passing through the sella and sphenoid sinus into the oral cavity. This CSF-filled sac was actually the floor of the third ventricle which was herniating through the defect, probably containing the structures of the lateral wall of third ventricle, i.e., thalamus or hypothalamus proximally. In addition, both medial orbital walls were seen to be widely separated. There was agenesis of the corpus callosum [Figure and ]. As the sella was affected, we carried out a complete battery of endocrine evaluation that revealed hypothyroidism and necessitated initiating oral thyroxine replacement.
After ensuring that thyroid functions were optimized, the child was taken up for transcranial repair of the encephalocele. Bi-frontal craniotomy with an extradural approach was used to access the third ventricle herniating into the sphenoid and posterior ethmoidal sinuses. The sac was opened to inspect its contents. The cavity was empty and seemed to be lined by ependyma indicating herniation of the infundibular recess and third ventricular floor through the bony defect; proximal part of the sac also contained part of the hypothalamus and thalamus. Excision of the distal part of the sac with re-positioning of normal brain tissue was done and the remaining part of the sac was plicated. The cavity was obliterated with fat and the dural defect was sealed with fascia lata overlay graft, reinforced with small bone piece and fibrin glue. Postoperative CT scan showed complete obliteration of the sac. The patient was discharged on the 7th postoperative day and referred to plastic surgery for repair of the cleft palate. At 6 months follow-up, the child was doing well without any CSF leak.


A 62-year-old woman presented with an 18-month history of progressive headache, generalized weakness, and bilateral exophthalmus more relevant on the right. Neurological examination demonstrated diplopia on the right lateral gaze and bilateral decrease of visual acuity, especially in the right eye, without visual field deficit. Endocrine workup revealed hypocortisolism (cortisol: 49.3 μg/l, normal: 70–250 μg/l; ACTH: 8.3 ng/l, normal: 9–60 ng/l) and hypothyroidism (TSH: 0.84 mUI/l, normal: 0.270–4.20 mUI/l; T4: 5.1 ng/l, normal: 9.5–18 ng/l). Computer tomography (CT) and magnetic resonance imaging (MRI) scans showed a large (62 mm) extradural lesion invading sphenoid, right maxillary sinus, both cavernous sinuses (CSs), anterior and posterior ethmoid bone, orbits, and anterior and middle skull base with bone invasion extending to the clivus []. The patient was initially managed with a 15-day course of steroids (prednisolone 80 mg twice a day): bilateral exophthalmus remarkably improved, and a MRI (1 week after steroid interruption) showed a significant volume reduction (44 mm) []. At our skull base meeting, it was decided to proceed with Stage I EEA for tissue biopsy that suggested the diagnosis of a pituitary adenoma and therefore induced to offer a Stage II EEA surgical resection to the patient. Surprisingly, the MRI realized for navigation protocols the day before surgery (6 weeks after discontinuing steroids) showed a dramatic volumetric increase of the lesion. Surgery was undertaken using image-guided surgery with MRI and CT imaging fusion. The first step consisted in making a nasoseptal flap.[] The lesion consistency was quite soft in its upper and superficial-anterior part, whereas the lower and deeper posterior portion involving the clivus, the internal carotid artery (ICA), and the CS was firmer, oozy, and fairly adherent. The tumor invaded and eroded the petrous bone; the ICAs were uncovered and identified with the help of a micro-Doppler probe. At the end, the resection was subtotal and the nasoseptal flap was lined over tuberculum sellae, sellar floor, clival recess, and ICAs and sealed with fibrin glue. The postoperative course was uneventful, and the patient was discharged after 3 days. The histopathology of the lesion confirmed a GPA with a Ki-67 of 1%. Immunohistochemistry analysis showed that cells had an epithelial phenotype with positivity of anti-pan-keratin staining and neuroendocrine differentiation with positive anti-chromogranin A, synaptophysin, CD56, and NSE antibodies. PS100, vimentin, GFAP, and TTF1 were absent. Furthermore, there was a positivity of 5%–10% of the cells to anti-ACTH antibodies (polyclonal) and negativity for all other hormones.
Early postoperative MRI confirmed residues in the right orbit, the right frontobasal region as well as the lower clivus, and both CSs []. At 6-week follow-up, the clinical examination showed the resolution of diplopia and exophthalmus, with improvement of the visual acuity; hydrocortisone and thyroid replacement therapy were weaned off after 6 months due to normal hormonal assessment. At 6 months, MRI showed once again a limited progression of the residue. The case was discussed at our neuro-oncology meeting and given the lesion's aggressive behavior despite a Ki-67 of 1%, and it was decided to start a radiotherapy treatment. No further progression of the residue was seen at the 12-, 24-, 36-, and 48-month follow-up, and the patient remained asymptomatic with a normal pituitary function.


A 56-year-old man fell from a height of 2 m and was brought to our hospital. His consciousness level on arrival was depressed (Glasgow Coma Scale score of 10), and he exhibited left hemiparesis. Cranial CT revealed a right epidural hematoma and linear skull fracture [Figure and ]. Scalp swelling was prominent in the right temporooccipital region, and the patient was believed to have hit his head in this region [, arrow]. No spinal fracture was identified on cervical–spinal CT [Figure and ]. The patient was admitted for emergency craniotomy, and removal of hematoma was performed. The postoperative course was favorable, his consciousness level returned to alert, and his left hemiparesis was alleviated. Two days postoperatively, however, he began to complain of neck pain that was exacerbated in weight-bearing postures such as sitting or standing. The neck pain gradually worsened, and cervical MRI was performed 5 days postoperatively. No abnormal finding was detected on T1- or T2-weighted imaging [Figure and ]; however, high-signal intensity at the C4–C5 posterior ligament complex, including the inter- and supra-spinous ligaments, was demonstrated on T2 fat-suppression sagittal MRI [].
The patient was conservatively treated with immobilization in a rigid cervical collar and closely monitored neurologically and radiographically. Although neurological examination exhibited no muscle weakness and his sensory examination remained intact, cervical CT 10 days after surgery revealed C5 vertebra anterior subluxation [Figure and ]. Posterior fixation surgery was performed 21 days after admission [Figure and ]. The postoperative course was uneventful, and the patient's neck pain was alleviated. The patient was discharged 4 weeks after surgery with no neurological deficit.


A 40-year-old female presented with hard swelling over the left side of her forehead and vertex since birth. She had progressively increasing headache for the past 12 years, dimished vision of the left eye, and tingling of the left arm for the past 1½ months. Clinical examination revealed diffuse bony swelling over the left side of the forehead right up to the midline and extending up to coronal suture posteriorly and up to superior temporal line laterally [Figure and ]. Her visual acuity on the left side was 6/36 with normal acuity (6/6) on the right side with optic atrophy on the left side. There were no other motor or sensory deficits. Other systemic examinations, birth and family histories were noncontributory.
Computed tomography (CT) of the head revealed irregular partially calcified hyperdense extra-axial lesion measuring 26 mm × 18 mm × 18 mm along the left sphenoid wing [Figure –]. Multiple calcified hyperdense extra-axial dural-based masses were also seen along the left frontoparietal convexity, interhemispheric fissure, and over the superior surface of the left tentorial leaflet. In addition, there was hyperostosis of the overlying left frontal and parietal bones [Figure –]. Contrast-enhanced magnetic resonance imaging (CEMRI) of the brain revealed a heterogeneously enhancing lesion with moderate perilesional edema of the left medial sphenoid wing and adjacent basi-frontal region, encroaching upon the left optic canal [Figure –] with another rounded homogeneously enhancing lesion along the superior surface of the left tentorial leaflet, causing buckling of the underlying gray–white matter [Figure and ]. There were no abnormalities of calcium metabolism or any other hormonal function. A provisional diagnosis of the left medial sphenoid wing and left tentorial meningioma in a case of congenital skull anomaly was considered. Diffuse meningiomatosis was considered as differential diagnosis.
She was subjected to skull base approach (left pterional craniotomy with orbito-zygomatic osteotomy) with the aim of removal of soft tissue component of the lesion, decompression of bony lesion around optic foramen, and decompression of the left optic nerve.
Intraoperatively, craniotomy was difficult due to uneven inner surface of the cranium, and a high-speed drill was used to perform the craniotomy. Dura was found adherent to uneven inner surface of the bone along with multiple intradural [Figure –] calcifications adherent to the underlying surface of dura along with irregular knobby calcifications projecting from the underlying surface of the pterional osteoplastic bone flap [], making way through the dura, covered with thin flimsy innermost layer of dura with no attachment to the underlying pia mater of the brain. Removal of soft tissue component and decompression of the bony components of the medial sphenoid wing lesion were achieved along with cauterizing its dural attachments (Simpson's Grade II excision). The patient showed significant improvement in her headache and vision postoperatively. She is under regular follow-up, and close monitoring by serial CEMRI brain has been planned so that further surgery or radiosurgery may be considered if recurrence in the operated lesion or growth in the residual lesion is seen.
Histopathological examination of the soft tissue lesion was consistent with transitional meningioma (WHO Grade I), and bony lesion revealed lamellar bone architecture with marrow elements without tumor cells [].


A 67-year-old male smoker with a 35 pack year smoking history was reviewed in the rapid access lung clinic following an episode of hemoptysis. Pulmonary function tests showed an obstructive pattern with a forced expiratory volume in one (FEV1) postbronchodilator of 1.55 (58%) and a forced vital capacity (FVC) of 3.87 (113%). The FEV1/FVC ratio was 40%. A chest radiograph demonstrated lung hyperinflation. The patient underwent further assessment with volumetric computed tomography (CT) scan with contrast of the thorax. This revealed a 1.1 cm × 1.2 cm lesion posterior to the bronchus intermedius in the apical subsegment of the right lower lobe, on a background of paraseptal emphysema []. No CT enlarged mediastinal lymph nodes were identified. A careful comparison to a previous scan performed 2 years previous identified a lesion at the same location that measured 0.6 cm × 1.0 cm at that time.
The patient underwent flexible bronchoscopy without identification of an endobronchial lesion. Washings and brushings from the right lower lobe were negative for malignant cells, and no organisms grew in culture. Following a multidisciplinary team discussion, a positron emission tomography (PET) scan was performed which identified the lesion adjacent to the bronchus intermedius. There was minimal (18) F-fluorodeoxyglucose uptake with a maximum standardized uptake value (SUVmax) of 2.6 []. Despite the negative PET scan, the lesion remained suspicious for malignancy as there was documented persistence and slow growth. A CT-guided biopsy was considered high risk as the lesion was centrally located.
The patient underwent an EBUS under conscious sedation in an ambulatory setting. This revealed a 0.9 cm rounded homogeneous lesion posterior to the bronchus intermedius []. No mediastinal lymphadenopathy was identified. An EBUS-guided transbronchial needle aspiration (TBNA) was performed [] which revealed atypical cells suspicious for malignancy. A repeat EBUS-TBNA confirmed a well-differentiated adenocarcinoma which was negative for EGFR mutations. A diagnosis of Stage IA – cT1aN0 M0 lung adenocarcinoma was made, and the patient successfully underwent a curative right lower lobectomy. Final pathology was consistent with a pT1aN0 M0.


A 45-year-old male presented with a 3-month history of cough. Chest X-ray and computed tomography (CT) showed a 3.8-cm-sized mass in the right lower lobe and multiple enlarged mediastinal lymph nodes (–) in which 18F-fluorodeoxyglucose uptake was detected (). For diagnosis and nodal staging, endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) and biopsy were performed. Aspirates from both lymph nodes and lung mass were highly cellular. Some tumor cells were cohesive enough to form 3-dimensional clusters, but others were dispersed in single cells (). Frequent crush artifacts and naked nuclei were easily identified. Tumor cells were poorly to undifferentiated with scanty cytoplasm and irregular nuclear contour. Nuclear chromatin was fine to granular and nucleoli were small but occasionally identified (). Unexpectedly, a few scattered dyskeratotic cells were noticed (, ). Many neutrophils and necrosis were present in the background (). Biopsy of mediastinal lymph nodes showed sheets of metastatic undifferentiated tumor cells with large area of necrosis and peritumoral neutrophilic infiltration (). Tumor cells had scant and delicate amphophilic cytoplasm. Nuclear chromatin and contour were similar to the findings of aspirate smears. Foci of abrupt squamous differentiation were identified more often than in cytology (). Under additional immunohistochemistry (IHC) staining, these tumor cells showed a very high proliferation index of up to 70% in Ki-67 (1:200, Dako, Glostrup, Denmark) and were positive for pan-cytokeratin (1:500, Dako), p53 (1:4,000, Thermo Fisher, Rockford, IL, USA), p63 (1:200, Biocare, Concord, CA, USA), and NUT (1:100, C52B1, Cell Signaling Technology, Danvers, MA, USA), and up to 70% of tumor cells expressed programmed death-ligand 1 (PD-L1; RTU, 22C3, Dako) (, ). Tumor cells were negative for Oct3/4 (1:50, Santa Cruz Biotechnology, Dallas, TX, USA), chromogranin (1:400, Dako), CD99 (1:50, Dako), CD45 (1:1000, Dako), CD56 (1:200, Leica Biosystems, Novocastra, Newcastle upon Tyne, UK), and thyroid transcription factor 1 (TTF-1; 1:50, Dako), which can help rule out the possibilities of other malignancies.


A previously healthy 32-year-old male presented with a persistent cough for 3 months, blood-tinged sputum and chest pain. On chest CT, a 5.5-cm-sized consolidative lung mass accompanied by enlarged mediastinal lymph nodes was identified at the left lower lobe (, ). Abdomen-pelvis CT showed multiple necrotic masses scattered throughout both lobes of the liver and bilateral adrenal glands (), and positron emission tomography highlighted multiple hypermetabolic bony lesions in the whole spine, bilateral ribs, pelvic bones, sternum and both scapulae (). Cytology of lymph node aspirates from EBUS-TBNA showed dispersed and clustered tumor cells in the background of necrosis (). Some tumor cells had large vesicular nuclei with open chromatin, prominent nucleoli, scanty cytoplasm and a high nuclear to cytoplasmic (N/C) ratio. Naked nuclei were frequently identified in scattered individual cells. However, others exhibited more abundant amphophilic to eosinophilic cytoplasm and granular nuclear chromatin with a lower N/C ratio, which could be considered squamous differentiation (–). Biopsy of the mediastinal lymph nodes and liver showed metastatic carcinoma in a necrotic background composed of two morphologically different tumor cell components: poorly differentiated cells with hyperchromatic nuclei and scanty cytoplasm, and squamoid cells with less hyperchromatic nuclei, prominent nucleoli and ample cytoplasm (, ). By IHC, tumor cells were positive for p63, p53, and NUT, negative for TTF-1 and CD56, and had a relatively low Ki-67 proliferation index of approximately 25% (, ). PD-L1 IHC test revealed low expression of about 1% of the tumor.


A 65-year-old never-smoking woman presented to a local hospital, because an abnormal shadow was detected at the right lower lung field by annual chest X-ray. She had no subjective symptoms. Computed tomography (CT) revealed a 5-cm well-circumscribed tumor in segment 6 of her right lung, which was in wide contact with the parietal pleura (Fig a,b). An enlarged subcarinal lymph node was suspected of being metastasis (Fig c). A CT-guided percutaneous needle biopsy of the lung tumor was performed, and a diagnosis of adenocarcinoma was made. She was referred to our hospital for treatment. Since there was no evidence of distant metastases, we performed right lower lobectomy with lymph node dissection (ND2a-2), and combined resection of the parietal pleura with video-assisted thoracoscopic surgery.
Macroscopically, the lesion was a well-circumscribed tumor of 7.0 × 4.5 × 4.2 cm in size with a soft, fleshy, and pale tan-white cut surface. A histopathological examination showed biphasic proliferation with carcinomatous and sarcomatous components with a sharp border between both components (Fig ). The carcinomatous component consisted of glandular structures of atypical cells that possessed chromatin-rich nuclear and clear cytoplasm, confirming high-grade fetal adenocarcinoma (H-FLAC) (Fig a,b). Morule formation was not seen in the carcinomatous components. In contrast, the sarcomatous component consisted of immature spindle cells that differentiated into chondrosarcoma (Fig c–e). Immunohistochemically, the glandular structures expressed membranous beta-catenin and focal α-fetoprotein (Fig ). The expression of p53, murine double minute 2 (MDM2), cyclin-dependent kinase 4 (CDK4), and thyroid transcription factor 1 (TTF-1) were not confirmed. A diagnosis of the blastomatoid variant of pulmonary carcinosarcoma was thus established.
The tumor infiltrated the parietal pleura, but there was no invasion of tumor cells on the detached surface of the parietal pleura. As expected before surgery, the involvement of the subcarinal lymph node was confirmed, although no other lymph node metastases were confirmed. The tumor was ultimately staged at pT3, pN2, M0, G3, R0, UICC stage 3A by the UICC 7th classification. The mutations in epidermal growth factor receptor (EGFR) gene and v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) gene, and the anaplastic lymphoma kinase (ALK) translocations were not detected. She received cisplatin (80 mg/m2, Day 1) plus vinorelbine (25 mg/m2, Day 1 and 8) every three weeks for four cycles as adjuvant chemotherapy six weeks after the operation and remained alive two and a half years after surgery with no evidence of local recurrence or distant metastasis.


The patient was a 70-year-old man with a 9-year history of Parkinson’s disease, started with diffuse bradykinesia and postural instability. In his past medical history, he suffered from impaired glucose tolerance, hypertension, dyslipidemia and Obstructive Sleep Apnea Syndrome. Moreover, he was treated with prophylactic antiepileptic therapy (Phenobarbital 50 mg/day) for a meningioma of left temporal lobe.
About 5 years after onset of PD, he started to present motor fluctuations with wearing-off symptoms, progressively worsened by the appearance of unpredictable and sudden off periods. The clinical worsening also included camptocormia and paroxysmal freezing of gait with frequent fallings. Moreover, he complained about insomnia secondary to nocturnal hypokinesia with difficulty in turning in bed, night-time leg cramps and morning akinesia. With the passing of time, all these symptoms became poorly controlled on oral dopaminergic therapy.
For this reason, he was admitted to our Neurological Department as a suitable candidate for Levodopa-carbidopa intestinal gel (LCIG) treatment. He underwent naso-intestinal evaluation with LCIG (Duodopa®-gel) followed by permanent treatment with LCIG via percutaneous endoscopic gastrostomy and jejunal tube (PEG/J).
The assessments, performed at baseline and at follow-up visits, included: Unified Parkinson’s Disease Rating Scale, motor fluctuation data obtained from patients diaries (“on” without dyskinesia, “on” with dyskinesia, and “off”), PDQ-39 Questionnaire, PD Sleep Scale-2 (PDSS-2) and Epworth Sleepiness Scale (ESS).
Prior to LCIG treatment, daily oral dopaminergic medication consisted of Rotigotine transdermal patch (4 mg/day, administered from 8:00 a.m. to 8:00 p.m.), Rasagiline (1 mg/day), melevodopa/carbidopa (Sirio®, 500 mg/day, administered five times daily) and two tablets of slow-release levodopa/benserazide (Madopar HBS®, 100/25 mg, administered at 10:00 p.m).
After PEG/J placement, all oral levodopa therapy was interrupted, including evening therapy with levodopa/benserazide.
LCIG monotherapy (total daily dose: 1080 mg, administered from 7:00 a.m. to 10:00 p.m.) significantly reduced motor fluctuations and akinesia (by approximately 60%), allowing him to walk longer distances, and with partial effectiveness on paroxysmal freezing and camptocormia (, ). During follow-up visits, the parameters of LCIG continuous infusion were gradually reduced to 870 mg daily because of the appearance of axial dyskinesias.
For the treatment of nocturnal disturbances, the administration of Rotigotine was shifted from daytime to overnight (from 10:00 p.m. to 7:00 a.m.), when the patient was not receiving LCIG treatment. After that, he reported an improvement of night’s sleep, with better movement fluency and disappearance of morning akinesia. The assessments showed a reduced diurnal hypersomnolence and, consequently, an improved global quality of life ().


A 47-year-old woman was brought to our ED with a 1-month history of progressive
dyspnea associated with general weakness. The patient presented with chills, body
weight gain, and hair loss, but had no signs of fever, cough, chest pain,
neurological defects, bleeding focus, trauma history, or cold. She had a history of
thalassemia but was not receiving any medication for this condition.
On arrival in the ED, the patient showed lethargy and poor response. Her vital signs
were as follows: respiration rate 26 bpm, pulse rate 62 bpm, temperature 31.6°C, and
blood pressure 111/66 mmHg. Her pulse rate subsequently decreased to 58 bpm and her
blood pressure decreased to 82/44 mmHg. Physical examination showed pale conjunctiva
and general edema ()
with no other findings such as bloody or tarry stools on digital examination.
However, the patient had a surgical scar in the thyroid region of her neck. An
initial finger-stick test indicated a blood glucose level of 158 mg/dL. Laboratory
tests detected leukopenia (white blood cell count, 3100/µL), severe anemia
(hemoglobin level, 3.6 g/dL), mildly elevated C-reactive protein (6.59 mg/L) and
aspartate transaminase levels (38 U/L), hyponatremia (sodium level, 129 mEq/L), and
hypokalemia (potassium level, 3.3 mEq/L). Examination of renal and liver functions,
as well as troponin-I, albumin/calcium, and cortisol levels showed no specific
results. Electrocardiography indicated sinus bradycardia, and chest radiography
indicated cardiomegaly (). Echocardiography showed increased pericardial effusion without
tamponade.
Assessment of the history of the surgical scar indicated that the patient had
developed hypothyroidism 5 years after undergoing thyroidectomy, but was receiving
no regular medication for this condition. The results of the above analyses and the
presence of hypothermia, decreased mental status, and general edema suggested that
the patient had myxedema coma. She was administered oral thyroxine sodium
immediately (two tablets, 0.1 mg thyroxine sodium/tablet) once daily for 10 days,
followed by a maintenance dose of one tablet once daily; intravenous hydrocortisone
(100 mg hydrocortisone/vial) once daily; and methylprednisolone (one vial, 40 mg
methylprednisolone/vial) every 8 hours for 1 day. Hypothyroidism was confirmed by
assessment of her thyroid hormone levels (thyroid-stimulating hormone, 90.540 µIU/mL
[reference range, 0.35–5.50 µIU/mL] and free thyroxine, 0.22 ng/dL [reference range,
0.93–1.56 ng/dL]).
The patient also received supportive care, including intubation for progressive
respiratory failure and hypercapnia, inotropic agents including intravenous dopamine
followed by norepinephrine for hypotension, blood transfusion for severe anemia,
rewarming with a heat lamp, and general intensive care unit arrangements. Her
hypothermia resolved within 1 day and her condition then improved gradually after
extubation for 11 days, and she was subsequently discharged. The patient provided
written informed consent for publication of this report.


An 81-year-old man was referred to our department for treatment of stenosis in the descending colon secondary to ischemic colitis. A colonoscopy and barium enema examination revealed that a long segment of the descending colon had a narrowed lumen (Fig. ). Blood tests revealed a slightly elevated serum creatinine level (1.3 mg/dL [normal range, 0.6–1.1 mg/dL]). The plain abdominal computed tomography revealed multiple large bilateral renal cysts. The largest cyst was 12 cm in diameter, and there were more than 20 cysts in total (Fig. , c). Although the patient's family history was unremarkable, further testing was recommended to determine whether the patient had polycystic kidney disease. However, the patient and his family declined further testing after they were provided with information on polycystic kidney disease.
To treat the stenosis, laparoscopy-assisted colectomy was planned. Under general anesthesia, the first trocar for pneumatoperitoneum and the laparoscope was introduced through an incision at the umbilicus. Intra-abdominal pressure of 8 mm Hg was created to enable observation of the peritoneal cavity. We observed no pathological ascites and no strong adhesion between the inner surface of the abdominal wall and the internal organs. To insert the surgical instruments, a 5-mm port was placed at the right upper abdomen and a 12-mm port was placed at the right lateral abdomen. The small intestine was relocated to the right side, with the left side of the body slightly elevated. The cysts of the left kidney were visible through the thin mesentery of the transverse and descending colon (Fig. , b). Four large renal cysts of the left kidney were fenestrated with a monopolar scalpel, and the serous fluid of the cysts was aspirated. This created a larger working area for the surgery (Fig. ) and enabled observation of the splenic flexure.
The descending colon and distal part of the transverse colon were mobilized from the lateral side to the midline, and further fenestration and aspiration of renal cysts was performed as necessary. After mobilization of the descending colon and distal transverse colon was completed, a 3-cm incision was made at the umbilicus and the colon was extracted through it. The region of interest was then resected and an anastomosis was completed using functional end-to-end anastomotic technique. The surgery took a total of 140 min, and there was minimal estimated blood loss. The postoperative course was uneventful, and the patient was discharged 9 days after surgery. Inflammatory cell infiltration and fibrosis were present in the resected specimen, consistent with postischemic colitis.


A 62-year-old male progressing from headache and altered behavior to altered consciousness and stupor over several hours was admitted to our hospital. His medical history included excessive alcohol intake of approximately 800 g per week for a minimum of 20 years, and he indicated that he often cooked fish himself using an electric heater while consuming alcohol. He also had a pet turtle in his bedroom. He also had a history of pneumonia which was successfully treated 10 years ago and macrocytic anemia which was noted during a routine medical health screening.
On admission, his vital signs were as follows: body temperature, 39°C; pulse rate, 120 beats per minute; and blood pressure, 142/65 mm Hg. He was confused, could not follow verbal commands, and exhibited neck stiffness. His pupils were round, 3 mm in diameter, and his light reflex was sluggish. Roving eye movements were observed. There was no obvious weakness in his extremities, and he did not have a positive Babinski sign.
Cranial computed tomography images showed a small hematoma with perifocal edema at the trigone of the left lateral ventricle (Fig. ). Laboratory test results were as follows: white blood cells, 12,200/mL; platelets, 6.9 × 104/mL; red blood cells, 313 × 104/mL; mean red blood cell volume, 109.9 fL; hemoglobin, 12.4 mg/dL; C-reactive protein, 15.0 mg/dL; aspartate aminotransferase, 1,047 IU/L; alanine aminotransferase, 203 IU/L; γ-glutamyl transpeptidase, 547 IU/L; blood urea nitrogen, 29.4 mg/dL; and creatinine, 2.25 mg/dL. Examination of the cerebrospinal fluid (CSF) revealed a bloody appearance, with an opening pressure of 100 mm H2O, a cell count of 2,683/µL with only polymorphonuclear cells, a protein concentration of 1,165 mg/dL, and a glucose concentration of 0 mg/dL. CSF Gram stain revealed many gram-negative bacilli which were phagocytosed by the polymorphonuclear leukocytes (Fig. ). Blood and CSF cultures were positive for E. tarda, which was susceptible to several antibiotics including meropenem. The definitive diagnosis was meningoencephalitis due to E. tarda infection. The patient was initiated on intravenous dexamethasone at 0.15 mg/kg, followed by 2 g meropenem every 12 h. Eight hours after admission, his blood pressure declined, and intravenous continuous infusion of dopamine was started; however, the blood pressure did not increase sufficiently. Nine hours after admission, the patient developed general tonic seizures, bilateral mydriasis with no light reflex, and an abnormal eye position without oculocephalic reflex. His consciousness deteriorated to deep coma, and 375 mg fosphenytoin sodium hydrate was initiated. The CSF examination on the second hospitalization day revealed a cell count of 864/µL which included only polymorphonuclear leukocytes. Despite the reduction in the CSF cell count, the patient never regained consciousness and died from cardiopulmonary arrest despite resuscitation on the third hospitalization day.


A 40-year-old female patient was referred with a complaint of soft-tissue mass in her dorsal side of the tongue. According to the history, this lesion occurred 2 months ago; however, she neglected it until the patient recognized the expansion of the lesion size. Clinical examination showed that there was a pink-colored lesion located on the dorsal side of the tongue and was approximately 0.5 cm in length []. There was nothing abnormal in her systemic review. The lesion was completely excised, from its connection to the tongue under local anesthesia [Figures –], with diode laser. Immediately after laser therapy, the patient described a remarkable pain comfort []. One week later, the patient had no more pain, early healing, and reduction in the lesion size []. Two weeks later, the lesion was approximatively healed with no pain or discomfort []. One month later, we noted a complete tissue healing with no sign of recurrence [].


The patient was born by Cesarean section at 39 wk of gestation to a 34-yr-old G3P2001 mother following a pregnancy notable for maternal genitourinary Group B streptococcal infection and the presence of IgM and IgG antibodies to cytomegalovirus (CMV) in maternal serum. The mother had previously lost a 3-yr-old female child diagnosed with twice relapsing acute megakaryoblastic leukemia and concentric left ventricular hypertrophy in the absence of a discernible cardiac defect on transthoracic echocardiogram. Ultrasound of the patient obtained at 21 wk of gestation showed dilated lateral ventricles (11 mm in diameter), indicating mild fetal ventriculomegaly on this otherwise normal evaluation. Subsequent ultrasound evaluations at 27 wk and 34 wk of gestation demonstrated affirmed ventriculomegaly. Head ultrasound obtained shortly after birth revealed continued dilatation of the cerebral ventricles and prominent choroid plexi in the lateral and third ventricles.
At 5 mo, the patient came to the attention of our pediatric neurosurgical service after a surveillance magnetic resonance imaging (MRI) of the head showed markedly dilated lateral and third ventricles with prominence of the extra-axial spaces in the frontal and temporal regions, abnormal prominence of the choroid plexus, and two choroid plexus cysts with no evidence of aqueductal stenosis or other intraventricular obstructions (). Initial examination by our team did not reveal clinical signs of hydrocephalus (i.e., full and bulging fontanel, progressive macrocephaly) but was notable for positional plagiocephaly and dysmorphic facial features (flattened left facial structures and asymmetrically set ears). The patient also had sensorineural hearing loss of the left ear and global developmental delay. A diagnosis of hydrocephalus associated with diffuse villous hyperplasia of the choroid plexus (DVHCP) was made. In the setting of no clinical signs of hydrocephalus and subsequent MRI evaluations showing no significant increase in ventriculomegaly, the patient was managed conservatively with surveillance MRIs with a plan to pursue CSF diversion surgery if indicated. The patient experienced delays in attaining developmental milestones: he sat independently at 12 mo, pulled to his knees at 16 mo, and possessed a vocabulary of fewer than 10 words at 21 mo.


A 36-year-old woman underwent laparoscopic myomectomy for multiple uterine fibroids. A primary 10-mm supra-umbilical port along with three 5-mm lateral ports was used to perform the surgery. The left lateral 5-mm port was later converted to a 15-mm port for specimen retrieval. The surgery lasted for 302 min and sixty fibroids were removed. A full-thickness closure of the left lateral 15mm port was done using polyglactin suture.
On day 2 of surgery, the patient developed nausea and vomiting not relieved with antiemetics and prokinetics. Computed tomography scan revealed a right para-umbilical full-thickness abdominal defect measuring 1.7 cm × 1.0 cm containing a short segment of the small bowel []. Laparoscopic evaluation showed a 4–5-cm ileal loop herniating through the right lateral 5-mm port []. The bowel loop was freed from the peritoneal defect and the hernia site was repaired.
As the primary surgery was prolonged and the uterus was being manipulated from the lateral ports, fascial necrosis could have occurred and led to widening of the incision and subsequent herniation of the small bowel.


While performing a total laparoscopic hysterectomy for a 42-year-old woman, it was noticed that a small part of the plastic cannula in the left lateral port had broken and was lodged in the subfascial tissue. The fascial incision was extended to remove the broken piece and not sutured subsequently. Three weeks later, the patient presented with complaints of pain on the left lower port site. Ultrasound was suggestive of a left lateral abdominal wall hernia of small bowel loops and mesentery in between the subcutaneous fat and muscle layers. Laparoscopic evaluation showed a 5-cm peritoneal defect with ileal loops surrounded by inflammation and dense adhesions [].
Any extension of the incision during the primary surgery should have warranted a port closure and hence we acknowledge the role of an iatrogenic PSH in this case.


A 17-day-old boy presented with 24-hour history of repetitive vomiting, minimal urine output, and low body temperature (lowest rectal temperature, 34°C; normal range, 36.6°C-38.0°C). He was pale, lethargic, and dehydrated. His vital signs were as follows: heart rate of 160 bpm (normal range, 110-160 bpm), blood pressure of 82/55 mm Hg (normal systolic range, 65-85 mm Hg; diastolic range, 45-55 mm Hg), and respiratory rate of 48/min (normal range, 35-55/min) with normal oxygen saturation. His heart and lung auscultation was unremarkable. He had a soft and nontender abdomen, with palpable hepatosplenomegaly. Mild peripheral edema and petechial lesions over his face, palate, feet, and buttock were observed. He had normal external male genitalia. On presentation, biochemical testing was compatible with severe AKI, hyponatremia, hyperkalemia, and metabolic acidosis (). Moderate leukocytosis and severe thrombocytopenia were noted. Blood cultures were drawn before antibiotics were started. Urine culture was not performed as the patient was anuric. Intravenous (IV) fluid resuscitation (0.9% sodium chloride 20 mL/kg) was initiated along with broad-spectrum antibiotics (ampicillin and cefotaxime). Hyperkalemia was promptly treated with IV 10% calcium chloride (0.2 mL/kg) to stabilize the cell membrane and sodium bicarbonate (2 mmol/kg) before being transferred to the pediatric intensive care unit.
The patient was born at term from an unremarkable pregnancy, except for maternal systemic hypertension in the third trimester. He was breastfed for 10 days and then switched to infant formula because of feeding difficulties. He was reported to be sleepy and not peeing often since birth. A skin rash over his extremities was observed on days 8 and 15 of life. The patient had not received any medications before presenting to emergency department.
In the first 24 hours, the patient required invasive mechanical ventilation for respiratory failure. He developed a diffuse maculopapular rash. His hyponatremia, hyperkalemia, and metabolic acidosis were corrected as per standard guidelines. He remained anuric and developed generalized edema despite high dose of diuretics (IV furosemide 2.5 mg/kg every 4 hours). His thrombocytopenia (as low as 16 × 109/L) was refractory to platelet transfusions. Few urine drops were sent for culture and urinalysis () 8 hours after admission. Urine microscopy did not reveal any casts. His abdominal ultrasound showed bilateral nephromegaly (right and left kidney long-axis measurement of 7.7 and 8.2 cm, respectively, without dilatation of the collective system) with a mild heterogeneous renal parenchyma and hepatosplenomegaly. To exclude a malignant process, a bone marrow biopsy was performed and revealed normal features. Further investigations showed low complement, high C-reactive protein, and high ferritin levels (). No schistocyte was seen on the blood smear. Plasma lactate dehydrogenase, haptoglobin, pyruvate, ammonia, creatinine kinase, triglycerides, and cortisol levels were normal. Urinary biomarkers of tubular dysfunction were not tested.
In the following 48 hours, the patient developed a disseminated intravascular coagulation, requiring fresh frozen plasma and cryoprecipitate transfusions. Blood and urine cultures as well as viral studies (including parainfluenza, influenza, pneumoviruses, adenoviruses, bocaviruses, rhinovirus, herpex, human herpesvirus-7 [HHV-7], cytomegalovirus [CMV], and varicella-zoster) were negative. Because of severe fluid overload, continuous venovenous hemofiltration was initiated and then discontinued due to hemodynamic instability. The patient’s clinical condition was rapidly and progressively deteriorating despite optimal antibiotic treatment and supportive care. As the clinical presentation was atypical and the etiology of AKI unclear, the decision to perform a kidney biopsy was made.
Following optimization of the coagulation profile with blood products, a kidney biopsy was performed under ultrasound guidance and general anesthesia. Light microscopy showed a massive dense multifocal cellular infiltration of neutrophils, eosinophils, and lymphocytes with few plasma cells (). Tubular injuries including tubulitis, breaks of tubular basement membrane, and necrosis of tubular cells () were seen. Neither fibrosis nor tubular atrophy was observed. Glomeruli showed ischemic collapse () or mesangiolysis and double contours of the glomerular basement membrane (). There was no evidence of endo- or extracapillary proliferation, or cast identified in the glomeruli. Immunofluorescence studies were negative (including albumin, fibrin, IgG, IgA, IgM, C3, and C1q). No microorganism was demonstrated with Gram and Grocott stain. Poor quality of tissue was studied under electronic microscopy, which did not show any glomeruli.
A skin biopsy was performed on areas affected by the maculopapulous rash. It revealed edema of the papillary dermis with mild superficial perivascular infiltrate of lymphocytes, histiocytes, and neutrophils. Few foci of extravasated red cells were observed. The epidermis was normal. These findings were suggestive of an urticarial lesion.
Histopathological findings were consistent with a severe ATIN as well as some features of thrombotic microangiopathy (TMA), including mesangiolysis and double contouring of the glomerular basement membrane. Neutrophil infiltration originating from renal tubule pointed toward an infectious process originating from the renal tubules. The severity of the inflammatory process was reflected by the significant renal parenchyma destruction. Histopathological findings were consistent with an acute pathological process. The patient’s clinical presentation combined with biochemistry abnormalities (including hypocomplementemia), imaging, and histopathological findings was suggestive of acute bacterial pyelonephritis. Skin biopsy findings showed an inflammatory process suggesting urticarial-like lesion, which can be seen with ATIN.
The histopathological findings prompted the initiation of IV methylprednisolone pulses (10 mg/kg/day on days 5, 6, and 7), followed by oral prednisolone (2 mg/kg/day). Antibiotics were given for 10 days. Peritoneal dialysis was initiated to help fluid management. His condition stabilized following the steroid pulses and then progressively improved with normalization of his renal function over several days. Extended investigations (including antinuclear, anti–double stranded DNA [dsDNA], anti-histone, anti-sjögren’s-syndrome-related antigen A (SSA), anti-sjögren’s syndrome type B (SSB), antiparietal cell, and anti–smooth muscle antibodies and lymphocyte immunophenotyping) were normal. Cytogenetic analyses were unremarkable (normal Comparative Genomic Hybridization (CGH), karyotype 46XY). The patient was extubated and peritoneal dialysis discontinued after 12 days. His hematology and biochemistry profile (including his complement) normalized. Oral prednisolone was slowly weaned and then discontinued after 12 weeks.
At 1-month follow-up, the patient had a normal renal function. His follow-up renal ultrasound showed a left pelviectasis (described by the radiologist but no measurement given) with a left thin and slightly heterogeneous renal parenchyma. Left grade III vesicoureteral reflux was diagnosed on voiding cystourethrogram (VCUG). At 10-month follow-up, renal scintigraphy with dimercaptosuccinic acid revealed normal kidney function, without scarring. His renal ultrasound and VCUG normalized at the 18-month follow-up. He has maintained a normal blood pressure, urinalysis, and renal function over the past 5 years.