He had a history of renal cell carcinoma and had undergone left nephrectomy 1 year prior with no recurrence.

Prior to presentation, his evaluation included brain magnetic resonance imaging and neurologic evaluation with unremarkable results, and he was scheduled to undergo neuropsychological testing.Visual acuity was counting fingers OD, and 20/100 OS.

Motility and intraocular pressures were normal.

There was a right afferent pupillary defect.

Examination of the right eye revealed rubeosis iridis, a clear lens, neovascularization of the optic disc, retinal vasculitis, venous sheathing, and a dusky-appearing peripheral retina.

The left eye had a clear lens and a normal fundus on clinical examination.

Fluorescein angiography demonstrated a mixed retinal arteritis and phlebitis with extensive retinal and choroidal nonperfusion of the right eye with both retinal and optic nerve neovascularization.

The left eye demonstrated patches of active arteritis peripherally with a minimally affected posterior pole (Figure).Fluorescein angiogram at 1 minute demonstrating a mixed occlusive arteritis and phlebitis (yellow arrowhead) with extensive areas of retinal and choroidal nonperfusion (white arrowhead) in the right eye.


She had a history of “multiple lasers” of her right eye and blindness of her left eye from an unrepaired retinal detachment.

Her medical history included a pheochromocytoma, bilateral adrenal gland resection, and a pancreatic cyst.

Her father had a history of retinal detachment in his right eye; her 2 siblings did not have any medical or ocular issues.Visual acuity was 20/200 OD and no light perception OS.

She had daily frontal headaches without any associated visual aura, numbness, or weakness.

Anterior segment examination was unremarkable in the right eye and revealed phthisis bulbi of the left eye.

Dilated fundus examination of the right eye revealed prominent, engorged, and tortuous vessels with traction extending from the optic disc to the superior peripheral retina.

There was an associated thick fibrotic epiretinal membrane extending from the macula to the superior peripheral retina.

The retinal arterioles were attenuated and there was thickening of the macula with subretinal fluid found on optical coherence tomography.

In the superior retinal periphery, there was an orange, round, circumscribed mass with overlying tractional retinal detachment and numerous other smaller orange masses (Figure 1A).

Fluorescein angiography of her right eye showed early hyperfluorescence of the lesions with late leakage (Figure 1B).A, Wide-field scanning laser image of right fundus showing a round mass with an overlying tractional retinal detachment.

Associated engorged and tortuous vessels emanate from the optic disc.

B, Wide-field scanning laser fluorescein angiographic late-phase frame of right fundus demonstrating late leakage of engorged vessels.


Her disease recurred 1 year later, and she underwent haplotype-matched allogeneic SCT 8 months prior to admission.

The patient lived with her family, including her son who recently had a cough.

She was born in the Philippines and immigrated to the United States 3 decades prior.

She denied recent travel.On examination, her temperature was 38.3° C, pulse of 115 beats/min, blood pressure of 110/50 mm Hg, respiratory rate of 24 breaths/min, and an oxygen saturation of 90% on room air.

Cardiopulmonary examination revealed tachycardia, increased work of breathing and bibasilar crackles without wheezes.

Her laboratory studies revealed a white blood cell count of 4.2 × 106/mL (normal range, 3.4-10 × 106/mL), hemoglobin of 10.3 g/dL (normal range, 12-15.5 g/dL [to convert g/dL to g/L, multiply by 10]), platelets of 45 × 106/mL (normal range, 140-450 × 106/mL), and creatinine of 1.2 mg/dL (normal range, 0.5-1.0 mg/dL [to convert mg/dL to μmol/L, multiply by 88.4]).

A chest radiograph demonstrated bilateral opacities without pleural effusion or pneumothorax.

Two months prior to admission, she developed graft-vs-host disease requiring high-dose prednisone, rituximab, and intravenous immunoglobulin.

At the time of admission, she was receiving prednisone (40 mg/d) and tacrolimus for graft-vs-host disease and prophylaxis of infection with levofloxacin, valacyclovir, posaconazole, and thrice weekly dapsone.

On hospital day 2, she was intubated for hypoxemic respiratory failure.

Initial empirical treatment included vancomycin, cefepime, azithromycin, and oseltamivir.


His home medications included acyclovir, fluconazole, and cyclosporine.

Temperature on admission was 103.1° F, and other vital signs were unremarkable.

Thereafter, he had 2 more emergency department visits and was readmitted for recurrent fever.

A thorough physical examination revealed 2 nonpruritic skin bumps on the right forearm and left calf that both measured 1.0 cm × 1.5 cm.

Post-SCT bone marrow biopsy specimen analysis at day 30 showed no evidence of leukemic cells and 99.5% donor cells.

Complete blood cell counts with differential counts showed no evidence of peripheral blasts.

Laboratory and imaging work-up—including chest radiographs, blood culture, fungal culture, urinalysis, sputum culture, respiratory viral panel, fungitell and galactomannan assay, coccidioidomycosis serology, and cytomegalovirus and human herpesvirus 6 polymerase chain reaction assays—were all negative.

Both bumps were soft without pigmentation or ulceration.

Pathologic sampling of the respective lesions revealed a diffuse infiltration of large mononuclear cells with high nuclear-to-cytoplasmic ratio (Figure, A and B).

Immunohistochemistry staining was positive for CD4 cells and myeloperoxidase (Figure, C and D)A and B, Histologic evaluation of the skin biopsy specimens.

Vancomycin and cefepime were started for possible infection.

The patient was discharged with oral antibiotics after being afebrile for 72 hours.


She did not have any history of bleeding disorders, preceding trauma, or other precipitating factors such as recent heparin exposure, surgical procedures, underlying liver disease, or receipt of anticoagulation agents.

There was no family history of hematologic disorders.Her vital signs were normal.

Physical examination showed large ecchymoses on the left arm, right shoulder, left anterior chest wall, and flank.

Initial laboratory results showed isolated severe anemia.

Computed tomographic imaging showed a large soft-tissue hematoma in the left chest wall without evidence of internal hemorrhage.

Test results for other causes of anemia were unremarkable.

Laboratory values and mixing study results are shown in the Table.The patient has a common clotting factor inhibitor.The patient has an extrinsic clotting factor inhibitor.The patient has an intrinsic clotting factor inhibitor.The patient does not have a clotting factor inhibitor.


Her medical history was significant for asthma, but she had been symptom free for more than 7 years without medications.

The patient, a stay-at-home mother, denied prior toenail trauma, frequent sports activities, or hyperhidrosis of the feet.

She had undergone no previous diagnostic tests or treatment for her toenails.

She had used an over-the-counter antifungal cream intermittently to treat pruritus of her feet.

She reported no pain in the nails or difficulty ambulating.

Physical examination revealed thickening, yellow discoloration, and subungual hyperkeratosis of all 10 toenails (Figure, panel A).

Scale was present on the plantar surface skin and in the web spaces (Figure, panel B).

Examination of the fingernails, scalp, and skin was normal.A, Appearance of toenails on left and right feet.

Her father and sister had similar, but less severe, toenail problems.

She had no history of dandruff, skin problems, or joint pains.


He fractured the digit more than 30 years earlier.

He reported paroxysmal, intermittent pain that was exacerbated by cold weather.

Physical examination revealed distal nail plate splitting with accompanying longitudinal erythronychia (Figure, A) and tenderness on palpation of the nail unit.

Magnetic resonance imaging revealed a nail matrix lesion (Figure, B), which was excised using a transungual approach with partial nail avulsion.


She was taking no medications and these lesions were unchanged throughout an uncomplicated pregnancy.

There was no personal or family history of melanoma or eruptive nevi.

The patient noted that the lesions initially began on her thighs and rapidly multiplied throughout her skin.

Some of the lesions were pruritic and when scratched could be removed, leaving behind a hyperpigmented macule.

On physical examination, she had hundreds of 1- to 2-mm dark brown-black monomorphic papules throughout her trunk, extremities, palms, face, tongue, and sclera (Figure, A).

Findings from laboratory tests, including a complete blood cell count, comprehensive metabolic panel, and computed tomography of the chest, were unremarkable.

A punch biopsy was performed for histopathologic examination (Figure, B-D).A, Photograph of left thigh shows diffuse 1- to 2-mm dark brown-black macules and papules.

B and C, Punch biopsy of right arm shows a circumscribed proliferation of pigmented epithelioid melanocytic nests, located primarily at tips of rete ridges.

Superficial papillary dermis shows prominent pigment incontinence.

D, Melan-A immunostain shows low pagetoid migration of melanocytes with a lack of melanocytic confluence at the dermal-epidermal junction.

The patient described a sunburn several weeks prior to the initial eruption.


The lesion initially appeared as a small, bluish plaque at a young age and had gradually increased in size with subsequent development of wartlike features.

Aside from minor local pain and pruritus, the patient reported history of recurrent infections as well as oozing and bleeding after minimal trauma.

Physical examination revealed soft, compressible nodules overlying a friable verrucous plaque in a linear distribution involving the length of the right calf with minimal tenderness on palpation.

No other lesions were found on the body.

B, Biopsy specimen demonstrating epidermal verrucous hyperplasia, acanthosis, papillomatosis, and hyperkeratosis overlying dilated vessels in the dermis (hematoxylin-eosin, original magnification ×4).

C, Deeper section showing similarly dilated vessels in the deep dermis to the base of the specimen, indicating the probability of deeper extension (hematoxylin-eosin, original magnification ×4).

A deep punch biopsy specimen was obtained and sent for histopathological examination (Figure, B and C).A, Clinical photograph of extensive verrucous plaque on the right calf.


He had previously been referred to orthopedics by his pediatrician owing to multiple presentations for the same complaint.

He was born in the United States with no recent travel.

His pain was mild to moderate, woke him from sleep, and limited his physical activity.

According to outpatient records, his height had been unchanged for the last 2 years.A physical examination showed a well-appearing young boy with unremarkable heart, lung, and abdominal findings.

There was mild tenderness to palpation of the lumbar spine, and mild pain elicited with flexion and extension of his back.

His strength was 4/5 in bilateral lower extremities, with otherwise normal neurological examination findings.He had a white blood cell count of 6.2 × 103/µL (to convert to ×109 per liter, multiply by 0.001), a hemoglobin level of 10.9 g/dL (to convert to grams per liter, multiply by 10.0), and a platelet count of 611 × 103/µL (to convert to ×109 per liter, multiply by 1.0), with a normal peripheral smear result.

The results of a complete metabolic panel were unremarkable, and so were his lactate dehydrogenase and uric acid levels.

He had an erythrocyte sedimentation rate of 80 mm/h and a C-reactive protein level of 20 mg/L (to convert to nanomoles per liter, multiply by 9.524).In the emergency department, a radiograph of his chest (Figure, A) revealed a right paravertebral mass, destruction of left seventh rib, a compression fracture of T8, and bony erosion of L1 vertebra.

A computed tomographic (CT) scan (Figure, B) revealed paravertebral abscesses with T8 compression and destruction.

Mediastinal and hilar lymphadenopathy was noted on imaging but are not shown.A, Radiograph of the chest reveals a right paravertebral mass (left arrowhead), destruction of the left seventh rib (top right arrowhead), a compression fracture of T8 (middle right arrowhead), and bony erosion of L1 vertebra (bottom right arrowhead).

The patient denied recent trauma, fevers, weight loss, cough, rash, or sick contacts.


His medical and family history as well as review of other systems were unremarkable.

Physical examination revealed a positive Kussmaul sign and pulsus paradoxus but no cardiac murmurs.

An electrocardiogram demonstrated sinus tachycardia.

Results of a complete blood cell count and biochemical panel were within reference ranges.

A chest radiograph revealed convexity on the right heart border suggestive of cardiomegaly (Figure 1A).

Echocardiography demonstrated normal cardiac chambers and valves.

However, an echogenicity was noted compressing the superior vena cava and right ventricle.

The patient subsequently underwent computed tomographic imaging of the chest that revealed a large, 16.2 × 6.8 × 5.6-cm anterior mediastinal mass compressing the right cardiac structures, particularly the superior vena cava.

The mass consisted mostly of fat attenuation, but was interspersed with nodular densities (Figure 1B).

Tumor marker levels, including α-fetoprotein, lactate dehydrogenase, and β-human chorionic gonadotropin, were within reference ranges.

A, Radiograph showed a convexity on the right heart border and cardiomegaly.

B, Tomographic examination revealed a large, anterior mediastinal mass with fat attenuation interspersed with nodular soft tissue elements (asterisk).


He had been transferred from an outside institution with rectal bleeding requiring blood transfusion.

Twenty hours after the procedure, he reported abdominal pain.

The result of an upper gastrointestinal endoscopy performed at the referring institution was normal.

A colonoscopy had been performed at the referring institution, but visualization was poor, with fresh blood and clots noted in the ascending colon.

At angiography, no blush or bleeding vessel was evident.

Findings from computed tomographic scan of the abdomen and pelvis obtained at this time were unremarkable.

Endoscopic treatment of a right colon arteriovenous malformation with active bleeding was attempted.

The patient underwent urgent angiography and embolization of a right colic artery branch (Figure 1B).

The decision to embolize the right colic branch was based on the endoscopic findings and the presence of pooling contrast in the cecum noted on a computed tomographic angiogram (Figure 1A) performed at the referring institution.

He was treated with antibiotics and observed.

This was unsuccessful and bleeding persisted.


His medical history was significant for diabetes without retinopathy and radial keratotomy in both eyes for moderate myopia.

In the ensuing days to weeks after these urologic procedures, the patient reported fever, weakness, and decreased appetite, which resolved spontaneously after several days but resulted in persistent weight loss of approximately 15 lb.

Three months following this episode, visual symptoms developed.On examination, visual acuity was 20/400 OD and 20/20 OS.

Intraocular pressure, pupils, visual fields, and ocular motility were normal.

On slitlamp examination of the right eye, trace conjunctival hyperemia was present, the anterior chamber had occasional cells, the lens had mild nuclear/cortical cataract, and the anterior vitreous had 2+ cells.

Dilated fundus examination of the right eye showed grade 2 vitreous haze, mild optic disc edema, scattered elevated white chorioretinal lesions—some with mild surrounding intraretinal and subretinal hemorrhage—and a prominent macular lesion (Figure 1).

The patient had undergone 2 ureterorenoscopies over a 2-week period with laser fragmentation for nephrolithiasis.

A ureteral stent was placed followed by systemic ciprofloxacin.

The patient’s urinary symptoms subsequently improved.


His mother, also hyperopic, previously underwent prophylactic laser iridotomy for anatomically narrow, occludable angles.Best corrected visual acuity was 20/20 OU, with a manifest refraction of +7.75 −1.00 × 170 OD and +7.75 −1.25 × 010 OS.

He had a high hyperopic refractive error, and the magnification of his spectacle lenses highlighted the eccentric pupil.

He had no associated symptoms of decreased vision, ocular pain, diplopia, glare, or haloes and had no history of ocular infection, surgical procedure, or trauma.

Slitlamp examination confirmed mild corectopia in the right eye, along with 4 clock hours of iridocorneal touch nasally and a “hammered silver” appearance to the involved cornea (Figure 1).

On examination via gonioscopy, there were high peripheral anterior synechiae (PAS) above the Schwalbe line in this area, while the remaining angle was deep without PAS.

Intraocular pressures were 15 mm Hg OD and 14 mm Hg OS.

Pachymetry testing revealed symmetric central corneal thicknesses of 577 μm OD and 582 μm OS.

Both optic discs appeared healthy, with a cup-disc ratio of 0.2.


She also reported intermittent, binocular diplopia.

Results from a review of systems were otherwise negative, and she had not experienced recent trauma.

On examination, visual acuity was 20/20 in both eyes with subjective red desaturation OD.

Pupils were equal and without afferent pupillary defect.

Intraocular pressures were 24 mm Hg OD and 12 mm Hg OS.

Hertel exophthalmometry showed 4.5 mm of relative proptosis OD.

She had limitation of her extraocular muscles in nearly all fields of gaze OD, with the most obvious limitation occurring in abduction.

She had decreased sensation to light touch in the right cheek (cranial nerve V2).

Ocular examination revealed diffuse conjunctival injection OD with tortuous, dilated, corkscrew-shaped blood vessels (Figure, A).

Dilated fundus examination revealed mild optic nerve hyperemia and mild vascular tortuosity OD.

Vital signs and results from complete blood cell count and thyroid function tests were normal.

Computed tomography and magnetic resonance imaging, angiography, and venography of the brain and orbits revealed extraocular muscle enlargement and enhancement and a dilated superior ophthalmic vein OD.

She was started on topical antihypertensive drugs for elevated intraocular pressure (IOP) in the affected eye (30 mm Hg) and referred to our institution.


The patient reported the acute onset of foreign body sensation in his left eye while splitting wood 1 year prior.

He stated that his vision initially returned to normal after treatment, but had subsequently worsened.

He complained of tearing, photophobia, and burning in the left eye.The visual acuity was hand motions OS with a grossly constricted visual field by confrontation.

The anterior segment examination revealed mild edema of the cornea, a shallow anterior chamber, iris heterochromia (Figure 1A), and an intumescent white cataract with pigment deposition on the anterior lens capsule.

The cataract precluded visualization of the fundus.

B-scan ultrasonography did not reveal masses, retinal detachment, or foreign body (Figure 1B).Heterochromia iridis.

He attended a hospital emergency department at that time and was diagnosed with a corneal abrasion and treated with topical antibiotics.


On postoperative day 10, she developed seizures when walking and was immediately intubated.

Subsequently, she developed hypoxemia and hypotension associated with acute pulmonary edema and new cardiomegaly (Figure 1A).

Brain imaging revealed a new intracerebral hemorrhage in the right frontal and left occipital lobes, with narrowing of the internal carotid, basilar, posterior cerebral, and right posterior communicating arteries, suggestive of vasospasm or vasculopathy.

An electrocardiogram showed nonspecific ST changes with T-wave inversion (Figure 1B), and serum levels of troponin and creatine phosphokinase were negative.

Transesophageal echocardiography revealed new dilation of the left ventricle (LV), with an ejection fraction of 10%, functional mitral regurgitation, anterior and apical akinesis, and basal hypokinesis (Video 1, Video 2, and Video 3).

The right ventricle (RV) was distended, with moderate tricuspid regurgitation.

Recent pretransplantation coronary angiography did not reveal atherosclerosis.

Her cardiopulmonary status rapidly worsened, with cardiogenic shock and refractory hypoxemia (arterial blood pH, 7.12; arterial partial pressure of oxygen, 43 mm Hg; and partial pressure of carbon dioxide, 56 mm Hg), despite mechanical ventilation (rate, 24/min; tidal volume, 6 mL/kg; fraction of inspired oxygen, 100%; and positive end-expiratory pressure, 15 cm H2O), neuromuscular blockade, and administration of inotropes.Patient workup.

A, Chest radiographs were obtained on the morning of postoperative day 10 before (left) and after (right) the onset of pulmonary edema.

B, An electrocardiogram shows nonspecific ST changes and T-wave inversion.


Neurologic examination showed incomplete left eye closure with a grade 5 of 6 on the House-Brackmann scale.

Physical examination revealed no palpable parotid mass and no overlying skin changes.

Magnetic resonance imaging showed subcutaneous nodules focally infiltrating the superficial parotid gland with evidence of perineural spread along the labyrinthine segment of CN VII.

Fine-needle aspiration (FNA) with ultrasonographic guidance was nondiagnostic.

An open excisional biopsy demonstrated dense subcutaneous tissue overlying and invading the parotid gland.

Intraoperative frozen section revealed a spindle cell tumor.

Histopathologic examination revealed a subcutaneous mass with stellate extension into and around the parotid gland.

The tumor consisted of bland fusiform tumor cells in a storiform pattern near inconspicuous hyalinized vessels (Figure, A and B).

Immunohistochemical staining demonstrated diffuse positivity for CD34 (Figure, C), positivity for bcl-2, and negativity for CD99 and S-100.

Fluorescent in situ hybridization (FISH) further characterized the tumor with a translocation t(17;22)(q21;q13) and corresponding COL1A1/PDGFB fusion protein (Figure, D).A-C, Histopathologic images.

Treatment with steroids and antiviral agents marginally improved facial strength and allowed eye closure.

A superficial parotidectomy with facial nerve dissection and preservation was performed.

A, Tumor infiltrating around and within the parotid gland.

B, Fusiform tumor cells arranged in a storiform pattern.

C, Tumor cells strongly positive for CD34.


Examination revealed normal otoscopic findings, and an audiogram demonstrated moderate low-frequency CHL of 45 dB in the right ear and mild 30-dB CHL in the left ear with a normal tympanogram (Figure, A).

An axial computed tomographic (CT) scan performed at that time was interpreted as normal.

Owing to concerns of visual changes and possible associated genetic cause for hearing loss (HL), magnetic resonance imaging (MRI) was ordered 1 year after initial presentation and showed no central or peripheral otologic abnormalities.

Follow-up audiograms at 3 and 6 months showed similar persistent CHL despite normal otoscopy results.

After 30 months of persistent CHL with an unknown etiology, a repeated CT scan of the temporal bones was performed (Figure, B and C).

Two sets of tympanostomy tubes were placed the year before his initial visit for presumed otitis media–related CHL, but his hearing did not improve.

The patient and family decided to treat the CHL with bilateral hearing aid amplification and a frequency modulation (FM) system at school.

Operative intervention vs amplification was discussed, and the patient and family decided to continue with hearing aids because he had improved performance in school.

Surgical treatment will be considered in the future if there is a decline in hearing.A, Right-sided (45-db) and left-sided (30-db) conductive hearing loss in low frequencies (arrows).

O and X indicate right and left air conduction, respectively; opening and closing brackets, right and left bone conduction, respectively.

B and C, Axial computed tomographic (CT) scans of the temporal bones.


His medical history included hypertension and chronic rhinosinusitis.

On oral endoscopic examination, mild bilateral hyperemia of the tonsillar area and posterior pharyngeal wall were noted.

Fiber-optic laryngoscopy revealed a reddish, 2-cm supraglottic lesion involving medially the free margin of the suprahyoid epiglottis (Figure, A).

The neoplasm appeared highly vascularized on narrowband imaging (Figure, B).

For this reason, before attempting an incisional biopsy, contrast magnetic resonance imaging (MRI) was performed.

The MRI scan revealed an oval, 2.2-cm hypervascular mass arising from the free border of the suprahyoid epiglottis, which extended along the right aryepiglottic fold.

The mass appeared to be capsulated, with regular margins, and did not show laryngeal deep tissues invasion.

We proposed to the patient a surgical excision that could have been transoral or open according to the quality of exposure (which would be evaluated in general anesthesia).

After evaluating the optimal exposure using a Crowe-Davis retractor, a transoral excision using the da Vinci robotic system was performed.

The postoperative course was uneventful, and patient did not develop complications.

On the second postoperative day, pain was fully controlled with oral medications, and the patient tolerated oral intake.

He was discharged on the second postoperative day.A, Endoscopic examination of the supraglottic larynx revealing reddish supraglottic neoplasm arising from the free epiglottic border.

B, Narrowband imaging of highly vascularized supraglottic neoplasm.


He had a several-year history of joint, back, and abdominal pain; constipation; fatigue; and depression.

Laboratory workup revealed a normal intact parathyroid hormone (PTH) level (50 pg/mL; reference range, 13-88 pg/mL) and a slightly elevated 24-hour urinary calcium level (314 mg/d; reference range, 25-300 mg/d).

A technetium Tc-99m sestamibi scan showed no definitive lesion but demonstrated a small focus of possible increased tracer uptake near the mid-pole of the left thyroid lobe (Figure, A, arrowheads).

No abnormal masses were readily identifiable by ultrasonography or contrast-enhanced computed tomography (CT) of the neck.

Histological examination of permanent sections showed a thinly encapsulated parathyroid tissue (Figure, B) with approximately 30% displaying myxoid stromal change and focal presence of interspersed adipocytes (Figure, C, yellow arrowhead) bordered by a rim of compressed gland containing abundant stromal fat (Figure, C, blue arrowhead).

Examination at higher power showed chief cells in lobules, nests, and focal trabeculae with occasional clusters of clear and oxyphil cells (Figure, C and D).A, Technetium Tc-99m sestamibi scan with sodium iodide I-123 subtraction.

He underwent a parathyroid exploration and excision of a soft, ovoid tissue, believed to be a slightly enlarged left inferior parathyroid gland (120 mg; 1.0 × 0.6 × 0.3 cm).

Intracytoplasmic fat vacuoles were evident on intraoperative touch preparation.

Columns 2 to 4 show delayed images at 30 minutes, 1 hour, and 2 hours.

B-D, Histopathologic images (hematoxylin-eosin) of thinly encapsulated parathyroid tissue.


He was initially evaluated by an infectious disease physician and a local dermatologist, who had intermittently prescribed empirical antibiotics (clindamycin hydrochloride and doxycycline calcium) for a presumptive clinical diagnosis of methicillin-resistant Staphylococcus aureus (MRSA) infection for more than 1 year with minimal response.

Because no objective data including wound culture or biopsy were obtained during his prior evaluations, he sought an alternate clinical consultation given the appearance of new violaceous ulcerated lesions over his right lateral proximal calf (Figure, A) despite his actively taking doxycycline.

He endorsed spontaneous healing of previously involved sites despite the absence of antibiotic exposure but denied constitutional complaints, recent travel, or high-risk behavior.

His physical examination was unremarkable for hepatosplenomegaly or systemic adenopathy.

Laboratory evaluation including complete blood cell count, peripheral blood cultures, MRSA swab, human immunodeficiency virus/human T-cell lymphotropic virus testing, flow cytometry, and Lyme disease titers had unremarkable results.

Pathologic sampling of the lesions revealed V-shaped perifascicular infiltrative large lymphocytes with abundant amphophilic cytoplasm and prominent nucleoli (Figure, B and C).

Lesional cells exclusively involving the dermis stained positive for CD30, leukocyte common antigen, CD2, TIA-1, and CD4 and negative for CD7, CD8, CD43, CD56, and programmed cell death protein 1.

Scattered B lymphocytes were PAX5 positive and CD20 positive.

Scattered dermal dendritic and Langerhans cells were S100 positive.

T-cell receptor (TCR) gene rearrangement testing had negative results.

Systemic imaging did not reveal extracutaneous involvement, and screening endoscopy for upper and lower gastrointestinal involvement had unremarkable results.A, Photograph of right lateral proximal calf shows violaceous ulcerated nodule.


She had hyperlipidemia for which she took fish oil and red yeast rice extract.

She reported no fatigue, depression, memory problems, dry skin, or constipation.

Heart rate was 80/min and body mass index was 31 (calculated as weight in kilograms divided by height in meters squared).

Physical examination demonstrated a thyroid gland of normal size and consistency without palpable nodules.

Her laboratory values are reported in the Table.The patient has subclinical hyperthyroidism and does not need a repeat testing of a thyroid-stimulating hormone (TSH) level.The patient has subclinical hypothyroidism and does not need a repeat testing of a TSH level.The patient has subclinical hypothyroidism and should have the TSH level repeated in 1 to 3 months.


He experienced nausea and vomiting in the 2 weeks prior to surgery.

One week after the second operation, he reported an “inability to visually focus on objects” and excruciating, burning pain in the lower limbs, both proximally and distally.

On evaluation, the patient was alert and interactive, afebrile, and had no neck rigidity.

A primary gaze upbeat nystagmus was present, with superimposed gaze-evoked nystagmus in all directions (Video).

The remainder of the cranial nerve examination was normal.

He had neither motor deficits nor coordination problems.

Sensory examination revealed hyperalgesia and allodynia in the lower extremities.

Bilateral ankle reflexes were diminished.

He could not recall 3 items after a 5-minute delay.

The results of laboratory tests, including a complete blood cell count and comprehensive metabolic panel, were all within reference ranges.

Magnetic resonance imaging (MRI) of the brain showed abnormal signals of both medial thalami (Figure).Axial fluid-attenuated inversion recovery magnetic resonance imaging of the brain showing bilateral medial thalamic hyperintensity.

These areas demonstrated restricted diffusion on diffusion-weighted imaging (not shown).

Although the surgical procedure was uneventful, the postoperative period was complicated by an enterocutaneous fistula that required further surgical intervention.


The lesions were round, hypopigmented macules and were symmetrically distributed in the affected area.

The patient reported that the macules had appeared on his cheeks 2 years earlier and had gradually coalesced (Figure).

There was no hair growth at the site of the lesions, and the patient reported no symptoms.

The size of the lesions ranged from approximately 2 to 3 mm to 25 mm in diameter.

A skin biopsy was performed to rule out some kind of morphea.A, Hypopigmented macules on the face and neck.

B, Absence of hair growth in the affected area.

He was treated for tinea versicolor, without success.

C, Hematoxylin-eosin staining (original magnification ×10).

D, Hematoxylin-eosin staining (original magnification ×20).


He had been hospitalized 6 months prior for hypoxia.

The patient was referred for a second opinion.On presentation he had symmetric swelling of metacarpophalangeal joints (MCPs) and interphalangeal joints (IPs), preventing fist formation.

Dorsal MCPs had ulcers distal fingers were dyspigmented and atrophic, capillaroscopy was normal, and palmar IP creases had ulcerated lichenoid papules (Figure, A and B).

Chest computed tomography (CT) showed hilar lymphadenopathy, interstitial thickening, and perilymphatic ground glass opacities.

Bronchoscopy revealed plaquelike lesions, and transbronchial nodal aspiration of mediastinal nodes was negative for carcinomas and/or granulomas.

He had normal aldolase levels (4.5 U/L [to convert to μkat/L, multiply by 0.0167]), depressed creatine kinase (32 U/L), hyperferritinemia (1543 ng/mL), and T lymphocytopenia (absolute CD3, CD4, and CD8 counts, 328 μL, 233 μL, and 85 μL, respectively); the patient also had anti-SSA (Ro) antibodies, and immunoglobulin G anticardiolipin antibodies (19.5 units).

The patient tested negative for HIV, anti–Scl-70 antibodies, anti–β2-glycoprotein 1 antibodies, lupus anticoagulant, cryoglobulins, and anti–Mi-2 antibodies; prothrombin time, partial thromboplastin time, and tissue thromboplastin were normal.A, Edematous hands with crusted ulcers and surrounding hyperpigmentation overlying dorsal metacarpophalangeal joints and interphalangeal joints.

Prednisone was initiated for presumed sarcoidosis.

B, Ulcerating papules with crust located in the palmar creases of the priximal interphalangeal joints and distal interphalangeal joints.


In addition, the patient suffered from a splenic marginal zone lymphoma with bone marrow infiltration, had a history of splenectomy, and an IgM-κ paraproteinemia.

His hematologic condition was considered stable by his physician, who had also been treating the patient for hepatitis C with ledipasvir-sofosbuvir for 3 months.

On examination, there was a warm erythema on most of the abdomen, which appeared distended owing to hepatitis-induced ascites (Figure, A).

Laboratory results showed an elevated but stable white blood cell count of 19.04 × 103µL (reference range, 3.6-10.5 × 103µL), a recent rise of C-reactive protein levels to 179 mg/L (reference range, 0-5 mg/L), as well as a rise of IgM levels from 1060 mg/dL to 2220 mg/dL (reference range, 34-248 mg/dL) within the past year.

A biopsy procedure was performed on the abdomen (Figure, B-D).A, Light red erythema on most of the abdomen.

B, Interstitial infiltrate of deeply eosinophilic cells in the entire dermis and adjacent subcutis.

Hematoxylin-eosin staining (original magnification ×2).

C, Hematoxylin-eosin staining (original magnification ×40).


Two years prior, he was hospitalized with coma with no identifiable precipitant and an extensive workup done at that time only revealed an elevated ammonia level of 233 µg/dL (to convert to µmol/L, multiply by 0.714); etiology remained unclear but he improved with lactulose.

Prior to this admission, he was working in a restaurant, did not ingest any drugs or mushrooms, and had no operations and no family history of similar problems.

His mental status rapidly declined despite treatment with lactulose, necessitating intubation.

Within a few hours of transfer, his ammonia level peaked to 1960 µg/dL and he lost all brainstem activity due to diffuse cerebral edema (Figure 1B).A, Electroencephalography (EEG) showing diffuse polyspike complexes consistent with myoclonic seizures.

He was found to have hyperammonemia to 239.5 µg/dL and respiratory alkalosis (pH level, 7.482; partial pressure of carbon dioxide, 27.3 mm Hg, and partial pressure of oxygen, 109 mm Hg [to convert to kPa, multiply by 0.133]; and bicarbonate, 20.2 mEq/L [to convert to mmol/L, multiply by 1]).

Liver and kidney function were normal (protein, 6.4 g/dL, and albumin, 3.4 g/dL [to convert to g/L, multiply by 10]; direct bilirubin, 0.1 mg/dL, and indirect bilirubin, 0.8 mg/dL [to convert to µmol/L, multiply by 17.104]; alkaline phosphatase, 38 U/L, aspartate aminotransferase, 22 U/L, and alanine aminotransferase, 42 U/L [to convert to µkat/L, mutiply by 0.0167]).

Head computed tomography and cerebrospinal fluid analysis were unrevealing.

Ammonia levels progressively increased to 1120.5 µg/dL, requiring hemodialysis and sodium phenylbutyrate, which did not lead to significant clinical improvement.

On hospital day 6, he developed continuous myoclonus due to status epilepticus (Figure 1A), which was refractory to treatment with lorazepam and levetiracetam as well as continuous midazolam, lorazepam, and propofol infusions.

B, Head computed tomography showing diffuse cerebral edema, obliteration of basal cisterns, and transtentorial and tonsillar herniation.

Plasma amino acids and urine organic acids were requested.

Continuous venovenous filtration hemodialysis and carnitine treatment were started because of concern for inborn errors of metabolism.


A throat culture grew group A Streptococcus.

The illness began 1 week prior with low-grade fever and back pain.

The following day, she developed periorbital swelling and subjective high fever.

The back pain resolved, but she complained of fatigue, stiffness in her limbs, and sore throat.

She presented for reevaluation when she developed eyelid ecchymoses and conjunctival hemorrhage.

Four days prior to the onset of illness, she had completed a 10-day course of amoxicillin for acute otitis media.A 7-year-old girl with periorbital edema, ecchymosis, and bilateral conjunctival hemorrhage.A physical examination revealed a febrile patient with bilateral conjunctival hemorrhages, periorbital edema, and eyelid ecchymoses.

She had tonsillar hypertrophy with erythema and exudates.

Her liver and spleen were mildly enlarged.

Laboratory tests showed leukocytosis with a white blood cell count of 16.7 000/μL (to convert to ×109 per liter, multiply by 0.001) with a predominance of lymphocytes, mild thrombocytopenia (platelet count, 108 × 103/μL [to convert to ×109 per liter, multiply by 1.0]), elevated aminotransferases (alanine aminotransferase, 232 U/L [to convert to microkatals per liter, multiply by 0.0167]; aspartate aminotransferase, 261 U/L [to convert to microkatals per liter, multiply by 0.0167]), γ-glutamyltransferase (265 U/L), conjugated bilirubin (2.3 mg/dL [to convert to microkatals per liter, multiply by 0.0167]), and lactate dehydrogenase (2116 U/L [to convert to microkatals per liter, multiply by 0.0167]).

A rapid antigen detection test from a throat swab was positive for group A Streptococcus, so she was given an “antibiotic shot,” presumably penicillin.


The only medical history reported was a previous umbilical hernia repair.

On further discussion, it was discovered that he was involved in a motorcycle crash many years ago.

Other than a brief loss of consciousness, no significant injuries were sustained per the patient’s report.

He did undergo a formal trauma evaluation at that time; however, the radiographic images and medical records were no longer available.

In addition to complaints of dyspnea and chest discomfort, the patient reported 5 to 6 episodes of small-volume emesis over the last 6 months.

He denied any other gastrointestinal symptoms, such as heartburn, dyspnea, or constipation.

A large air-fluid level was seen on a recent chest roentgenogram, and subsequent computed tomographic scans of his chest were obtained (Figure 1).

The results of his examination were unremarkable, with the exception of bowel sounds being heard on auscultation of the left chest.


He was diagnosed with myocardial infarction 1 month earlier at another hospital and a coronary intervention was performed with 1 drug-eluted stent put in the left anterior descending artery.

Progressive dyspnea at rest was noted in recent days.

Physical examination revealed tachycardia and tachypnea.

His heart rate was 138 beats/min and respiratory rate, 25 breaths/min.

Chest auscultation revealed bilateral rales.

Heartbeat was regular, but with faint S1 and S2.

The extremities were cold, while no pitting edema was found.

Twelve-lead electrocardiography demonstrated persistent ST-T segment elevation in V2 to V6 leads.

Transthoracic echocardiography showed a hypoechoic mass around the apical region (Figure 1A).

Computed tomography of the chest revealed a large crescentic hypodense lesion surrounding the anterolateral wall of the left ventricle and apex (Figure 1B).A, Transthoracic echocardiography, apical 4-chamber view, showing a hypoechoic mass (arrowhead).

Review of systems and family history were unremarkable.

Laboratory findings were within normal limits.

LA indicates left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

B, Computed tomography of the chest, axial view, showing a hypodense lesion surrounding the anterolateral wall of the left ventricle and apex (arrowhead).


He was not taking any regular medication.

The rash caused a burning sensation; otherwise, he was feeling well.

He had a tender right submandibular lymphadenopathy but was apyrexial.A healthy teenaged boy presented with multiple target lesions and erythema on his right eyelids.

Examination revealed clusters of target lesions on the right upper and lower eyelids.

There were papillae in the upper palpebral conjunctiva and follicles and a few pustules in the lower palpebral conjunctiva.

The cornea was unremarkable with no staining, and results of a dilated ophthalmoscopy examination were normal.

Ocular movements were full, and there was no proptosis.

A few solitary lesions were found scattered on his nose and right cheek; however, his body was not affected.


During the office evaluation, the patient had an uncorrected visual acuity of 20/30 OD and 20/25 OS but was extremely photophobic and would not cooperate with any additional examination.

An examination under anesthesia was performed.

Intraocular pressures by Tono-Pen XL (Reichert) under light sedation were 13 mm Hg OD and 12 mm Hg OS.

Axial lengths by echography were 23.7 mm OD and 23.9 mm OS.

Retinoscopy showed bright reflexes in both eyes.

Anterior segment examination of each eye showed normal eyelids and lashes, conjunctiva, anterior chamber, iris, and lens.

The examination of the cornea of each eye was significant for punctate keratitis in the epithelial and subepithelial layers that stained lightly with fluorescein (Figure).

The corneal diameters were normal, and there was no evidence of Haab striae or stromal scarring.

The ophthalmoscopic examination was unremarkable.RetCam photograph demonstrating punctate keratitis in the epithelial and subepithelial layers of the cornea.


She also noticed subjective fevers, weakness, and spasticity in her left upper and lower limbs, along with right ear pain and decreased hearing.

Her postoperative course had initially been complicated by the development of a transverse sinus thrombosis on postoperative day 4, for which she was treated with anticoagulation.Over the next several days, she experienced marked worsening of her headaches, nausea, and blurred vision.

Repeated magnetic resonance imaging and venography of the head and neck demonstrated worsening of the cerebral venous sinus thrombosis, now extending into the right sigmoid sinus and jugular vein.

Additionally, opacification of the mastoid air cells on the right side was noted, consistent with mastoiditis.

Physical examination revealed otitis media on the right side.Ophthalmologic examination showed a visual acuity of 20/30 OD and 20/20 OS; color plates were 8 of 8 bilaterally, and there was no afferent pupillary defect.

Motility and confrontational visual fields were without abnormality.

Dilated fundus examination showed edema of the optic nerves bilaterally.

Spectralis MultiColor fundus images were obtained (Figure, A), as well as traditional spectral-domain optical coherence tomography images (Figure, B).Optical coherence tomography (OCT) of the patient’s optic nerves prior to lumbar puncture.


He also reported a single episode of binocular diplopia that lasted for 1 day and resolved spontaneously.

Otherwise, his medical history was unremarkable.On physical examination, there was mild right-sided ptosis and miosis.

After instilling 10% topical cocaine eyedrops, the right pupil did not change its size whereas the left pupil dilated by 2 mm, supporting a diagnosis of right-sided Horner syndrome.

Pain and temperature sensation were not evaluated.


No history of clinically significant fever was noted.

The electrocardiogram showed ST-segment elevation in leads I, aVL, II, III, aVF, and V3-6 (Figure 1A), which was accompanied by fluctuating elevation of troponin-T levels (1.2-12.0 ng/mL).

Angiography showed no evidence of coronary artery disease.

Transthoracic echocardiography demonstrated restricted diastolic filling with a low left ventricular ejection fraction (40%).

Late delayed enhancement images showed a striking sawtooth pattern of hyperenhancement in the left ventricular epicardium (Figure 1B) and right-sided enhancement of the anteroseptum.

Extensive myocardial edema was noted in the left ventricle via T2-weighted short tau inversion recovery imaging (Figure 1C).

Chest and abdominal computed tomography (CT) showed no inflammatory changes or lymphadenopathy.

Serum angiotensin-converting enzyme (ACE) levels were not elevated.

The brain natriuretic peptide level was elevated (1550 pg/mL).A, Electrocardiogram with ST-segment elevation in leads I, aVL, II, III, aVF, and V3-6.

Treatment for heart failure was initiated.

Cardiac magnetic resonance (CMR) imaging was then scheduled.


She did have a history of recent pericoronitis, but several courses of antibiotics were unhelpful.

The growth also caused malocclusion and ipsilateral upper lip numbness.

She reported no recent trauma; no difficulty speaking, breathing, or swallowing; no epistaxis, nasal congestion or nasal drainage; and no recent fevers.

Physical examination revealed a submucosal growth centered on the mesial aspect of the left maxillary alveolus.

Contrasted computed tomographic and magnetic resonance imaging showed a heterogeneously ossified lesion filling the left maxillary sinus, with local destruction of hard palate and alveolar bone (Figure, A and B).

Positron emission tomographic scans highlighted the fluorodeoxyglucose-avid nature of both the tumor and associated cervical lymphadenopathy.

A biopsy showed a tumor with lobular architecture, an incomplete peripheral ossified rim (Figure, C), and focal areas of osteoid matrix.

Higher power showed atypical cells with increased mitotic activity in a myxoid stroma (Figure, D).

Immunostains were negative for S100, pankeratin AE1/AE3, SMSA, and GFAP.A, Computed tomographic (CT) image of the head, coronal view.

B, Magnetic resonance image (MRI) of the face, coronal view with contrast.


He described the need to cough to clear the airway, but coughing provided no relief.

He noted some relief when bending at the waist or lying prone.

Flexible fiber-optic laryngoscopy revealed a large, irregular pedunculated mass on the left anterior false vocal fold (Figure, A and B).

The mass was seen to ball-valve in and out of the glottis with respiration.

Pathologic examination (Figure, C and D) revealed a 1.7 × 1.3 × 1.0-cm mass with a papillary-like architecture, expansion of the submucosa by benign mature adipose tissue, and variable amount of fibrous tissue.

Preparations for emergency tracheotomy were made.

In the operating room, with the patient, the anesthesia unit performed flexible fiber-optic laryngoscopy and advanced the endotracheal tube into the trachea over the flexible bronchoscope.

The patient was turned supine, and microdirect laryngoscopy was performed.

The mass originated from a stalk in the left anterior ventricle.

The position of the mass was discussed with the anesthesiology team, who felt comfortable performing prone intubation.

A video laryngoscope was used to ensure that advancing the tube would not shear the mass.

There was mild chronic submucosal inflammation without squamous epithelial proliferation.A, Direct laryngoscopic image of mass.

B, Direct laryngoscopy with retraction of mass to view stalk.

C, Hematoxylin-eosin, original magnification ×40.

D, Hematoxylin-eosin, original magnification ×200.


She referred only to minor head trauma 15 years earlier.

Findings from a physical examination were negative, while nasal endoscopy showed diffuse mucous rhinorrhea.

A CT scan of the paranasal sinuses showed complete opacification of the left sphenoid sinus, a double-lined appearance of the sinus walls (an inner bony sclerotic layer and a thin external one) (Figure, A), and 2 bony defects of the sphenoid sinus walls next to the cavernous sinus along the floor (Figure, B).

An MRI scan showed a concentric multistratified appearance of the sinus content.

On T2-weighted images (Figure, C), a hyperintense line peripheral layer consistent with fluid retention, an irregularly thick hypointense line, consistent with the sclerotic bone visible on CT, a crescent-shaped heterogeneous material in the lower part, and a black oval area in the upper part of the sinus were identified.

After gadolinium administration, volumetric interpolated breath-hold examination (VIBE) sequences revealed very intense enhancement of the oval black area in the upper part of the sinus, with no contrast enhancement of the remainder of the sinus (Figure, D).


His medical history was significant for atopic dermatitis.

He had no previous treatment with radiation or immunosuppressive medications.

On examination, he had a surgical scar, an indurated malformed auricle, a superficial right parotid mass infiltrating the overlying skin, and a 1.5-cm postauricular node.

Postgadolinium magnetic resonance imaging (MRI) showed infiltration into the cartilaginous tissue of the external auditory canal and ipsilateral cervical adenopathy (Figure, A).

Serum laboratory test results revealed an eosinophil count of 1109 cells/μL (reference range, 50-350 cells/μL), and an IgE level of 5.44 μg/mL (reference range, <0.27 μg/mL).

Flow cytometry was negative for signs of leukemia or lymphoma.

Fine-needle aspiration (FNA) revealed a mixed leukocyte population and was negative for malignant neoplasm, necrosis, and granulomatous disease.

Within the lymphoid tissue there was prominent follicular hyperplasia and a diffuse infiltrate of eosinophils (Figure, B).

There was an increase in small blood vessels within the germinal centers.

While some follicles had well-defined mantle zones, others demonstrated a spectrum of lytic changes accompanied by intrafollicular infiltrates of eosinophils (Figure, C).

The stroma was densely fibrotic with perivascular sclerosis (Figure, D).A, Magnetic resonance image (MRI) of a right parotid mass and pathologic preauricular and retroauricular lymph nodes.

An excisional biopsy of the postauricular node was performed.

B-D, Histopathologic images, hematoxylin-eosin.


He had no clinically significant medical, surgical, or social history.

His voice was breathy and raspy, and he projected his voice poorly.

Flexible Lindholm laryngoscopy revealed a large, right-sided, supraglottic, submucosal mass expanding the aryepiglottic fold and false vocal fold with hypomobility of the right vocal fold (Figure, A).

The lesion extended posterolaterally to the aryepiglottic fold and obscured visualization of the glottis.

The right laryngeal ventricle was effaced, but the mucosal surface of both true vocal cords appeared normal.

A computed tomographic (CT) scan to determine the extent of the lesion revealed a cystic mass with no protrusion out of the thyrohyoid space or into the subglottic airway (Figure, B and C).

The mass was completely removed using a pulsed potassium titanyl phosphate laser to make mucosal incisions just lateral to the aryepiglottic fold and cold instrumentation to manipulate and remove the mass.

Strategic needle decompression and angled endoscopes facilitated complete visualization and removal of the mass.

The paraglottic space was closed via endoscopic suturing.

He denied dyspnea, dysphagia, odynophagia, weight loss, and lymphadenopathy.

Intraoperatively, the lesion was fully visualized with a Lindholm laryngoscope (Figure, A).

The patient tolerated oral intake and was discharged home within 24 hours.

Considerable voice improvement and vocal fold mobility was noted at 6 weeks, with normal vocal fold movement, normal mucosal pliability, and complete glottic closure achieved at 1 year (Figure, D).


She reported no sick contacts, recent travel, recent antibiotic exposure, or nutritional supplement intake.

She denied use of tobacco, alcohol, or illicit drugs.

She initially had 10 to 12 watery bowel movements a day, which progressed to passage of bright red blood per rectum.

Vital signs were notable for elevated temperature (37.9°C), tachycardia (heart rate, 112/min), respiratory rate of 16/min, and blood pressure of 105/60 mm Hg.

Physical examination showed a soft nondistended abdomen without organomegaly and normal bowel sounds.

She had diffuse tenderness to deep palpation.

Laboratory evaluation revealed normal hematological indices, renal function, and hepatic function.

Computed tomography of the abdomen and pelvis demonstrated colonic wall thickening without perforation and stable prior pelvic lymphadenopathy.

No pathogenic organisms or parasitic ova were detected on stool culture.

Results of a stool Clostridium difficile toxin assay were negative.

Flexible sigmoidoscopy demonstrated grossly congested and erythematous mucosa in the rectosigmoid and descending colon.

Histopathology from the biopsies of one of the affected areas is shown in the Figure.


His medical history includes hypertension, benign prostatic hyperplasia, hypothyroidism, and chronic obstructive pulmonary disease, for which he takes finasteride, tamsulosin, levothyroxine, lisinopril, pantoprazole, and trospium.

He recently quit smoking and reduced his alcohol intake to 2 drinks daily but has an approximately 50 pack-year smoking history and a history of heavy alcohol consumption.

Family history and review of systems were unremarkable.

He denied pruritus, trauma, or contact with allergens or irritants.

Examination of the dorsal surfaces of the hands revealed five 0.2-cm to 0.6-cm tense, mildly hemorrhagic vesicles, a few 0.4-cm to 0.6-cm erosions with hemorrhagic crusting, scattered 0.5-cm pink scars, and milia (Figure).

Results of a basic metabolic panel, complete blood cell count, and urinalysis were normal.

Liver function tests revealed a total bilirubin level of 1.37 mg/dL (23.43 μmol/L), direct bilirubin level of 0.69 mg/dL (11.80 μmol/L), aspartate aminotransferase level of 100 U/L (1.67 μkat/L), and alanine aminotransferase level of 46 U/L (0.77 μkat/L).

Results of viral hepatitis and human immunodeficiency virus testing were negative.Dorsal surfaces of hands showing hemorrhagic vesicles, erosions with hemorrhagic crust, postinflammatory erythema and collarettes of scale, and milia.


She reported no occurrence of fever, rashes, oral ulcers, Raynaud phenomenon, chest pain, dyspnea on exertion, paresthesia, or joint concerns.

On examination, her temperature was 36.9° C, blood pressure was 134/81 mm Hg, pulse was 110/min, and oxygen saturation level was 91% breathing room air.

She appeared dyspneic, had no heart murmur, and had diffuse crackles especially at the lung bases and 2+ pitting edema of the legs without jugular venous distension.

No rashes, synovitis, or focal neurological deficits were found.

Laboratory evaluation showed a hemoglobin level of 7.5 g/dL from a baseline of 10.4 g/dL (reference range, 11.6-15.2 g/dL); a creatinine level of 6.5 mg/dL from a baseline of 1.2 mg/dL (reference range, 0.6-1.2; SI conversion to μmol/L, multiply by 88.4); and normal white blood cell count, platelets, and lactate.

Urinalysis showed the presence of red blood cells but no protein.

Chest x-ray showed new bilateral opacities.

Computed tomographic imaging of the chest showed moderate stable fibrosis with multiple ground-glass opacities in the left lung.

Based on these results, additional studies were performed (Table).The patient has antiglomerular basement membrane disease (Goodpasture syndrome).


She had a history of basal cell skin cancer but denied a history of internal cancer, as well as new medications.

Pertinent daily medications included metformin hydrochloride, sitagliptin phosphate, insulin glargine, somatostatin, and antihypertensives.

The lesions were mildly pruritic and would typically occur in crops of 3 to 4 on the arms, legs, trunk, and buttocks.

Individual lesions would last a few months before spontaneously resolving without scarring.

The patient denied new or progressively worsening systemic symptoms, including fevers, chills, night sweats, or rapid unexpected weight loss.

Physical examination revealed an obese but otherwise healthy-appearing white woman with multiple small 1.5-cm monomorphic and somewhat octagonal groupings of folliculocentric, erythematous, scaly, and hyperkeratotic papules at different stages of development distributed across arms, legs (Figure, A and B), trunk, and buttocks.

Skin examination otherwise had unremarkable results, including normal scalp, palms, soles, and nails, as well as no palpable cervical, axillary, or inguinal lymphadenopathy.

Two scoop shave biopsies of representative lesions were performed (Figure, C and D).Folliculocentric, octagonal, erythematous, and scaly papules on the left thigh.

C and D, Shave biopsy specimen (hematoxylin-eosin).


Her medical history included seasonal allergies, and she did not take any prescription medications.

She felt well and denied weight loss, night sweats, and any other systemic symptoms.Physical examination revealed scattered skin-colored papules on the right neck, a solitary 8-mm skin-colored nodule on the right jawline, and three 2- to 3-cm pink firm nodules on the right thigh (Figure, A and B).

A shave biopsy was obtained from the nodule on the right jawline (Figure, C), and the thigh nodules were excised.


She had consulted a dermatologist 18 months prior, who performed a biopsy of the lesion that was inconclusive.

Her medical history was relevant for multiple consultations with several neurologists in the past 2 years for intermittent moderate-to-severe unilateral headache with an unsatisfactory response to nonsteroidal antiinflammatory drugs and amitriptyline.

She was not taking any medication at the time of consultation.

Clinical examination revealed a 12-cm-wide, soft, nontender plaque with a raised, nodular, and slightly desquamative erythematoviolaceous border and a clear, atrophic center with an increase in wrinkle depth on her upper right arm (Figure, A).

Her neurological and mental state examination showed no abnormalities.

A biopsy specimen that included the border of the lesion was obtained (Figure, B and C).A, Annular plaque with raised borders and an atrophic and wrinkled center on the right arm.

No treatment was prescribed at the time.

There were no other mucosal or skin lesions.

No physical examination was performed specifically to the head and neck.

B, Hematoxylin-eosin stain (original magnification x20).

C, Orcein stain (original magnification x40).


The patient was born at full term via spontaneous vaginal delivery after an uncomplicated pregnancy with APGAR scores of 8 and 9 at 1 and 5 minutes, respectively.

His mother was varicella nonimmune and had no active rashes including in the perineal area.

Physical examination of the patient revealed widespread papulovesicular, crusted lesions on the arms, legs, face, scalp, and trunk (Figure 1).

The palms, soles, and oral mucosa were spared.

The patient was afebrile.Further workup included Tzanck smear, direct fluorescent antibody test for varicella, herpes virus culture, syphilis IgG antibody test, fungal culture, and bacterial culture.

While results were pending, the patient started empirical treatment with ampicillin, gentamicin, and acyclovir.


Two weeks after surgery, he was evaluated for persistent mild abdominal pain in clinic.

He returned to the emergency department 1 month later with a 2-day history of progressive abdominal pain, nausea, and vomiting.

Ultrasonography of the abdomen’s right upper quadrant showed gallbladder wall thickening with gallstones in the neck of the gallbladder consistent with acute calculous cholecystitis.

Computed tomography (CT) of the abdomen showed a 2.5-cm calcified mass with adjacent inflammatory changes in the left hemiabdomen that was most consistent with a lost gallstone (Figure 1A).

Results of a physical examination revealed mild abdominal tenderness in the left lower quadrant.

A second abdominal CT was performed (Figure 1B).A, Postoperative computed tomography (CT) of the abdomen demonstrating a lost gallstone in the left hemiabdomen (arrowhead).

He subsequently underwent a laparoscopic cholecystectomy.

The critical view of safety1 was obtained, and the gallbladder was removed from the fossa without difficulty.

On extraction of the gallbladder through the umbilical incision, a large stone in the gallbladder could be palpated.

After several attempts of extraction, the retrieval bag perforated and stones spilled into the abdomen.

Not all the spilled stones could be retrieved.

The patient had an uncomplicated postoperative course and was discharged to home on postoperative day 2.


He had a history of prolonged alcohol abuse.

A physical examination revealed stable vital signs and a normothermic, nontender, nonpulsatile, fixed lump in his upper abdomen (Figure, A).

A routine blood test revealed leukocytosis (white blood cell count of 12 000/μL[to convert to ×109 per liter, multiply by 0.001]), and his liver and kidney function test results were unremarkable.

His serum amylase level was 487 U/L (normal range, 28-100 U/L [to convert to microkatals per liter, multiply by 0.0167]).

A contrast-enhanced computed tomography (CT) scan of his abdomen was performed (Figure, B).Fixed and nonpulsatile abdominal lump (A) and contrast-enhanced computed tomography (CT) scan of the abdomen (B) (axial view).

The scan reveals a homogeneous collection of fluid (black arrowhead) encysted by a well-defined enhancing wall (yellow arrowhead).

Ten weeks previously, he was hospitalized and conservatively managed for acute pancreatitis.


Soon after the procedure, the patient began complaining of a large, linear “floater” in his central vision, which was very disturbing to him.

On examination, the implant was seen in the middle of the vitreous cavity in a vertical orientation and in the visual axis (Figure 1).

The patient was observed for 2 weeks with the hope the implant would settle down or move out of the visual axis, but this did not happen.Optos image of the patient’s right eye.

The fluocinolone acetonide intravitreal implant can be seen in the middle of the vitreous cavity, very close to the visual axis.

The left eye had undergone pars plana vitrectomy for the repair of a macula-involving tractional retinal detachment, but despite anatomical success, visual acuity remained count fingers, presumably due to a loss of retinal tissue from macular ischemia.

The right eye had undergone cataract extraction with intraocular lens implantation and a pars plana vitrectomy for nonclearing vitreous hemorrhage.

After this surgery, the patient was treated for persistent DME and received multiple intravitreous injections of bevacizumab, ranibizumab, triamcinolone acetonide, and a dexamethasone intravitreal implant, but the DME persisted, and visual acuity was 20/70 OU.

Therefore, a fluocinolone acetonide intravitreal implant (ILUVIEN; Alimera Sciences Inc) was injected.


She had a history of high myopia, astigmatism, and mild cataracts, as well as narrow angles, for which she had undergone laser peripheral iridotomy in both eyes a number of years earlier.

Her review of systems was normal, and she had no relevant family history of ocular disease.

The best-corrected visual acuity measured 20/100 OD and 20/200 OS, with manifest refractions of −9.00 −1.25 × 090 OD and −8.50 −0.75 × 086 OS.

Intraocular pressure measured 12 mm Hg OU.

The pupils were middilated and poorly reactive.

There were patent peripheral iridotomies bilaterally.

The lenses were displaced into the anterior chambers without any lenticular zonules visible.

There was central lenticulocorneal touch bilaterally with trace Descemet membrane folds at the points of contact (Figure).

The posterior segment examination results were unremarkable.


His vision was central, steady, and unmaintained in the left eye.

His visual acuity was 20/30 OD but the child was unable to read the distance chart with his left eye.

Worth 4-dot testing showed evidence of suppression in the left eye.

There was a relative afferent pupillary defect in the left eye.

Intraocular pressure was soft by palpation in both eyes.

The eyelids, conjunctiva, sclera, cornea, anterior chamber, iris, and lens were unremarkable in both eyes.

Fundus examination of the right eye was normal.

The fundus examination of the left eye revealed the findings shown in Figure 1.Fundus photograph of the left eye on initial presentation.


She did not report trauma, changes in vision, or foreign travel and did not take any topical ophthalmic medications.

Her best-corrected visual acuity was 20/25 OD and 20/20 OS.

Her pupils were round with no afferent pupillary defect, although the circular lesion did move in concert with the pupillary constriction and dilation.

The intraocular pressure was 14 mm Hg OU.

Slitlamp examination of the anterior segment showed a 2 mm × 2–mm circular iris lesion at the inferotemporal border of the iris.

The mass appeared to have a fluid-debris level (Figure 1A).

When the anterior segment was visualized with a goniolens (Figure 1B), we saw that the irideocorneal angle was open, that no neovascularization was present, and that a spherical mass about 2 mm in height arose from the pupillary margin.

Its nasal surface appeared white with speckled-brown pigmentation, while the remainder of the lesion had brown pigment (Figure 1B).

The anterior segment of the left eye and posterior segment of both eyes were unremarkable.A, Slitlamp photograph of anterior segment showed an iris lesion with a fluid-debris level (black arrowhead) inferotemporal to the pupillary border (white arrowhead).


After the PCI, the chest pain resolved, but the patient’s blood pressure was 90/60 mm Hg.

The electrocardiogram (ECG) at presentation revealed atrial fibrillation: concave upward ST-segment elevations of more than 1 mm in the inferior leads, more prominent in lead III than lead II, along with reciprocal ST-segment depressions in the anterior precordial leads.

The coronary angiogram (Figure 1A) confirmed this finding.

The left main, the left anterior descending, and the left circumflex coronary arteries were normal.

Another ECG (Figure 1B) demonstrated resolution of the ST-segment elevations in the inferior leads with a new rSR′ pattern with concave upward ST-segment elevations in leads V1 to V3.A, Coronary angiogram revealing complete occlusion of the mid-right coronary artery (black arrowhead) distal to a large right ventricular branch (white arrowhead).

B, Electrocardiogram (ECG) after a percutaneous coronary intervention reveals resolution of ST-segment elevations in inferior leads and a new rSR′ pattern with concave upward ST-segment elevations in leads V1 to V3.

A percutaneous coronary intervention (PCI) of the mid-RCA occlusion just distal to the right ventricular branch was performed.

This was suggestive of an acute inferoposterior myocardial infarction (MI), likely from complete occlusion of the right coronary artery (RCA).


Initial laryngoscopy with a Parsons laryngoscope identified airway deviation secondary to mass effect, with intubation ultimately achieved with assistance of a bronchoscope.

Examination revealed a large neck mass extending from the mandible to the clavicles, with mass effect causing neck extension and rotation.

The mass was multicystic, with prominent vasculature, and a small area of skin necrosis.

The patient underwent a magnetic resonance image (MRI) on day of life 3 which showed a 15.7 × 10.0 × 14.4-cm midline neck mass with solid and cystic components.

Flow voids were present throughout the mass.

The mass was isointense to hypointense on T1, and isointense to hyperintense on T2.

The patient also underwent a computed tomographic (CT) scan, which demonstrated calcifications present within the multicystic neck mass.

Owing to continued growth and risk of airway compromise, the patient was taken to the operating room on day 5 of life for resection of the mass and tracheostomy.

Following birth, the mass continued to grow, with inability to palpate the sternal notch by day of life 4 (Figure, A).

Pathologic results showed a multinodular 19-cm mass, 80% solid and 20% cystic, with multiple tissue types present (Figure, B-D).


Examination revealed a 5-cm, minimally tender mass deep to the left parotid gland.

Fine-needle aspiration was interpreted as a “well-differentiated squamous cyst.” Routine laboratory test results and hematologic markers were normal.

Cranial nerve examination findings were normal, and no overlying skin or mucosal changes were noted.

CT imaging (Figure, A and B) revealed a well-defined hypodense mass within the left masticator space measuring 5.0 × 3.5 cm, resulting in smooth remodeling of the left mandibular ramus.

The second left mandibular molar appeared to be missing.

On magnetic resonance imaging (MRI), the lesion was T2 hyperintense, mildly T1 hyperintense, without enhancement, with remodeling of left mandibular alveolar ridge.

No definite site of mandibular or maxillary attachment was noted (Figure, C and D).

He underwent resection via a combined transoral and transantral (Caldwell-Luc) approach.

Pathologic assessment demonstrated a squamous lined cyst with parakeratosis.Imaging of the face of a patient with a left jaw mass.

The mass was noted to be associated with an empty socket of the second mandibular molar, was not well circumscribed, and was notably adherent to some surrounding tissues, requiring meticulous dissection from the inferior alveolar nerve, temporomandibular joint capsule, and skull base.

A and B, Computed tomographic (CT) images.


Her medical history was significant for extensive craniofacial polyostotic fibrous dysplasia (FD), breast adenocarcinoma, and stage IV clear cell renal cell carcinoma with metastasis to the ipsilateral adrenal gland treated with radical nephrectomy.

Physical examination was remarkable for soft, tender nodules at the forehead and right orbit with right proptosis.

Neurologic examination results were normal, except for hypesthesia in a V1 distribution.

Sinus computed tomography showed a soft-tissue mass with involvement of multiple craniofacial bones with orbital, anterior, and posterior table defects.

Magnetic resonance imaging with contrast (Figure, B) showed interval growth at the frontal bones in the region of previously diagnosed FD.

Romanowsky-stained direct smears (Figure, C) showed loose billowing clusters of epithelial cells involved by strands of magenta extracellular tissue (black arrowhead).

Cytoplasm was abundant with coarse and fine textures.

Nuclei were large and round, occasionally with conspicuous nucleoli (blue arrowheads).

Hematoxylin-eosin staining (Figure, D) showed cells with abundant clear cytoplasm and nuclei with varying nucleolar prominence (blue arrowheads).

Immunohistochemical stains were positive for pancytokeratin, vimentin, CD10 and PAX-8.

A fine-needle aspiration (FNA) biopsy established the diagnosis.

A carbonic anhydrase IX (CA-IX) stain was noncontributory.A.

Multiple forehead nodules, oblique view.


His medical history was significant for emphysema but no previous skin cancers or surgery.

The lesion was growing in size and had begun to drain.

Prior to the visit, he had been evaluated in emergency care for the same complaint and was given a prescription of oral antibiotics; however, the lesion persisted.

On physical examination, the patient had a 2.5 × 2-cm, singular, umbilicated, ulcerated papular lesion of the left temple with overlying crusts and surrounding erythema and induration (Figure, A).

Computed tomography with contrast of the soft tissue revealed an abnormal mass in the site of the left temporal scalp lesion.

The mass appeared homogenous and was not particularly enhanced by contrast (Figure, B).

There was no accompanying surrounding lymphadenopathy.

A preoperative biopsy and low-power histological analysis revealed an epidermal proliferative process; vertically oriented anastomosing strands of basaloid epithelium were seen arising from multiple points along the epidermis (Figure, C).

In this case, there was concurrent well-differentiated carcinoma (Figure, C).

Afterward he was referred to a local dermatologist, who performed a biopsy of the lesion.

Ductal differentiation was observed on high power, and the mass had an intervening fibrovascular stroma (Figure, D).A, Left temple lesion.

B, Computed tomographic image with contrast, soft-tissue window.

C and D, Micrographs of tissue biopsy, hematoxylin-eosin.


He reported poor dental health and no exposure to tuberculosis.

He smoked cigarettes daily and consumed alcohol socially.

Significant medical history included excision of a mass at the ulcer site 8 years before that healed uneventfully.

Surgical pathologic examination revealed areas of histiocytes surrounded by lymphocytes and a focus of central necrosis.

The area bled, expressed serosanguineous drainage, and was prone to crust formation.

It was nontender, bled with manipulation, and appeared to be fixed to the underlying mandible.

Acid fast bacilli and fungal stains and cultures were negative.

There was a 1.5 × 1.5-cm ulcerated, submental lesion within the mid-portion of a scar.

Examination of the oral cavity revealed caries and periodontal disease.

There was no palpable cervical adenopathy.

Because the biopsy was concerning for malignancy, an excision with frozen section margins was then performed.

The lesion was present within old scar tissue and had an infiltrative growth pattern.

Microscopically there were epithelioid or spindle-shaped tumor cells with atypical vesicular nuclei and pale eosinophilic cytoplasm with areas of necrosis (Figure, A).

Tumor cells stained strongly positive for EMA, CD34, and pankeratin and demonstrated loss of INI-1 immunostaining (Figure, B and C).Histopathologic images.

B, Strong cytoplasmic staining with cytokeratin AE1/AE3 immunostain.

The patient received a course of antibiotic therapy.

When symptoms persisted, he underwent a biopsy.


She had no history of infections or recent travel.

Physical examination revealed a body mass index of 20 (calculated as weight in kilograms divided by height in meters squared), normal vital signs, and darkening of the palmar creases and buccal mucosa.

Morning laboratory tests were performed and are reported in the Table.Evaluate for congenital adrenal hyperplasia with serum 17-hydroxyprogesterone.Evaluate for primary adrenal insufficiency with a 250-μg corticotropin stimulation test.Evaluate for a pituitary adenoma with magnetic resonance imaging.Evaluate for a laboratory error by repeating tests for serum adrenocorticotropic hormone and cortisol.


She had a history of similar yet milder skin eruptions with sun exposure over the prior 2 years.

No other family members were similarly affected.

The physical examination findings were notable for acral edema and well-demarcated, tender petechial patches on the dorsal surface of the hands and feet (Figure, A and B).

A punch biopsy specimen from the affected area of her hand was obtained (Figure, C and D).In the clinical images, edema with petechial eruption is evident on the hands (A) and feet (B).

In the pathologic images, the hematoxylin-eosin–stained specimens from affected areas of the dorsal aspect of the hands show subtle thickening of vessel walls (C), in addition to extravasation of erythrocytes and fibrin thrombus formation (D).


The patient had a marfanoid habitus, disproportion of limbs, and an enlarged face.

Both lips were enlarged and felt nodular (Figure, A).

Multiple pink-whitish and translucent nodules were observed on the lateral and anterior surface of the tongue (Figure, B).

The rest of her physical examination did not reveal other cutaneous abnormalities, except for mild acne.

Biopsy results from tongue tissue are shown in the Figure, C and D.A, Both upper and lower lips were enlarged and felt nodular.

B, Oral examination revealed the presence of multiple small nodules located on the anterior and lateral surface of the tongue.


He reported that the lesions began on his face, then spread to his thighs and were mildly pruritic.

He did not have any other involvement and was in no pain.

On physical exam, multiple 1 to 3 cm purple papules with central black and hemorrhagic crusting were noted on his forehead, bilateral cheeks, and anterior thighs (Figure 1, A and B).

On his left flank, he had a large polycyclic, atrophic hyperpigmented plaque with a slightly erythematous and scaly border (Figure 1C).

The scalp, oral mucosa, back, chest, abdomen, arms, palms and soles were all spared.

Multiple toenails were noted to be dystrophic with hyperkeratotic subungual debris.

Over the next few days, the crusted papules and nodules eroded leaving smooth erythematous plaques with punched-out centers.

Testing for the human immunodeficiency virus (HIV) and hepatitis was negative.

Punch biopsy specimens from the left anterior thigh were taken for histopathologic analysis and fungal, bacterial, and atypical mycobacterial tissue cultures.

A skin culture was obtained of the polycyclic plaque on his left flank.A, Discrete and coalescing papules and nodules on the forehead and cheeks with central black and hemorrhagic crust.

B, Morphology on the thighs was similar to the face with friable, firm purple crusts overlying smoother dermal plaques.

C, Left flank with a large polycyclic, atrophic hyperpigmented plaque with a slightly erythematous and scaly border.


His medical history was significant for hypertension, hyperlipidemia, coronary artery disease after placement of a stent 7 years prior, right-lung empyema with decortication 8 years prior, and chronic obstructive pulmonary disease.

His family history was negative for neurological disease but positive for myocardial infarction and colon cancer.

He had a remote smoking history of 10 pack-years and no history of alcohol or illicit drug use.

Sixteen days later, the patient presented to the hospital again with a 2-day history of numbness and weakness in his left arm.

Significant neurological examination findings included fluent but dysarthric speech, dysphagia, marked left facial droop, and difficulty with multistep commands.

A motor examination revealed decreased left upper extremity strength (3/5 proximally and 4/5 distally), conspicuous loss of fine motor coordination, dysmetria, and dysdiadochokinesis.

Magnetic resonance imaging scans of the head were visually interpreted to show an acute infarct involving the posterior right frontal lobe (Figure 1).

An echocardiogram did not reveal evidence of an embolic source.

Hemogram and inflammatory markers were within normal limits (white blood cell count of 5600/μL [to convert to ×109 per liter, multiply by 0.001], erythrocyte sedimentation rate of 0 mm/h, and C-reactive protein level of 5 mg/L [to convert to nanomoles per liter, multiply by 9.524]).

Carotid arteries were unremarkable via ultrasonography.

Magnetic resonance imaging of the brain demonstrated an intra-axial necrotic lesion with adjacent vasculogenic edema primarily involving the right posterior frontal and anterior parietal lobes.Magnetic resonance imaging (MRI) of the brain at the time of initial presentation revealing hyperintensity in the right posterior frontal lobe (A) and hypointensity involving the right posterior frontal lobe (B).

The patient was discharged from the hospital 2 days later and was treated with aspirin and clopidogrel bisulfate.


Her medical history was unremarkable, except for hypertension, and she denied having any abdominal operations.Her laboratory results indicated the following: white blood cell count, 11670/μL (to convert to ×109/L, multiply by 0.001); sodium level, 132 mEq/L (to convert to mmol/L, multiply by 1); and creatinine, 0.6 mg/dL (to convert to µmol/L, multiply by 88.4).

She also had anorexia, and she had crampy abdominal pain during the past few days.

Similar symptoms occurred previously but were self-relieved.

She reported dull pain below the pelvic bone as we palpated gently over the abdomen.

In triage, her body temperature was 37.3°C, and she had a normal heart rate.

Physical examinations were notable for distended abdomen and hyperactive bowel sounds but negative for the peritoneal sign.

No gross abnormalities were present in the perineal area.

Abdominal radiography revealed segmental dilatation of the small bowel.

Further evaluation with computed tomography of the abdomen and pelvis was performed (Figure 1).A, Computed tomographic scan showing small-bowel ileus.

B, Computed tomographic scan showing a mass lesion in the right lower pelvic wall.

She was kept in the emergency department for observation.

However, she experienced little improvement in her primary symptoms.


Physical examination revealed at least 4 lower extremity edemas and an abdomen that was large, taut, and distended (Figure 1A).

A computed tomographic scan of the chest, abdomen, and pelvis was obtained (Figure 1B).A, In addition to lower extremity edemas, the abdomen of the patient was markedly taut and distended.

B, Representative computed tomography images with intravenous and oral contrast.

Note the patient’s descending colon was severely displaced by the retroperitoneal mass and was located on the patient’s right side.

The mass enveloped the left kidney without evidence of hydronephrosis.


Visual acuity was hand motion, and intraocular pressure was 17 mm Hg.

On examination, visual acuity  was counting fingers OD and 20/200 OS.

Anterior segment examination was unremarkable.

Dense vitreous hemorrhage precluded fundus examination of the right eye, and B-scan ultrasonography did not reveal any additional pathology.

The left fundus examination exhibited diabetic macular edema with central subfield thickness of 425 μm on optical coherence tomography and severe nonproliferative diabetic retinopathy, for which he had laser surgery for diabetic macular edema and panretinal photocoagulation.

On postoperative day 1, visual acuity was 20/200 and intraocular pressure was elevated to 35 mm Hg.

The conjunctiva had mild hyperemia with foci of subconjunctival hemorrhage, the anterior chamber was deep and quiet, the anterior vitreous contained no cells, and a few cobweblike, tan strands were present throughout the vitreous cavity.

The anterior chamber had minimal inflammation.

Extensive strands and veils were noted throughout the vitreous cavity (Figure 1).Anterior vitreous cavity (A) and wide-field fundus photograph (B) of the left eye demonstrating extensive transvitreal strands and sheets.

He subsequently underwent vitrectomy in the right eye for nonclearing vitreous hemorrhage with an uneventful postoperative course and improvement of his visual acuity to 20/100.

The patient was lost to follow-up and returned 4 months later with visual acuity 20/125 OD and counting fingers OS, with a vitreous hemorrhage in the left eye for which he underwent vitrectomy with thorough panretinal photocoagulation (1200 spots).

Topical timolol/acetazolamide and brimonidine were started twice daily, together with prednisolone acetate and moxifloxacin every 6 hours.

On postoperative day 3, the patient noted decreased visual acuity OS but he denied pain or discharge.


Three years prior to presentation, she reported difficulties with her vision.

She had difficulty comprehending some words while reading and also reported the feeling of a “blind spot” in her vision and a “part of her vision” that she could not see.

On further questioning, she had developed some recent difficulties with short-term memory and reported easily getting lost when driving.

She was found to have a left homonymous visual field defect.

She underwent repeated visual field examination every 6 months, showing progression of the visual field defect along with an increase in false-negative results.

She underwent 3 magnetic resonance imaging (MRI) scans of the brain, showing no neoplasm or stroke, and also underwent a stroke workup with negative results.

Review of the most recent MRI showed profound cortical atrophy of the parieto-occipital lobes with a slight predilection to the right side compared with the left.

Her best-corrected visual acuity was 20/20 OU, and color plate results were severely reduced in both eyes.

Dilated fundus examination findings were unremarkable.

Automated visual fields again showed a left homonymous visual field defect with high false-negative results (Figure, A).

She was unable to draw a clock and had simultanagnosia (Figure, B).A, Automated visual field testing (Swedish interactive thresholding algorithm [SITA]) showed a dense left homonymous visual field defect with high false-negative results.


His ocular history was significant for a motor vehicle crash resulting in likely left optic neuropathy (18 years ago), a procedure performed to change the color of his eyes from brown to blue (4 years ago), and bilateral laser in situ karatomileusis surgery (2 years ago).

His best-corrected visual acuity was 20/20 OD and 20/30 OS.

Anterior slitlamp examination of both eyes revealed the finding shown in Figure 1.

His anterior segment was deep and quiet, and his dilated fundus examination was unremarkable.

His intraocular pressure (IOP) was reproducibly higher in the right eye on 3 separate visits, averaging 20 mm Hg OD and 13 mm Hg OS.

His central corneal thickness was 496 μm OD and 480 μm OS.

He was being treated by outside ophthalmologists with loteprednol, nepafenac, timolol, and artificial tears.


Fourteen years earlier, the patient underwent a pituitary adenoma resection and external beam radiation.

Immediately after the resection, she developed slight ptosis and an adduction deficit of the right eye, presumed to be secondary to partial oculomotor nerve III (CNIII) damage.

Four years earlier, she developed intermittent esotropia of the right eye, presumed secondary to cranial nerve VI palsy.

At the present clinic visit, the patient reported the persistence of intermittent diplopia, which had remained unchanged for years, and denied other ocular or systemic complaints.

These episodes occurred more commonly following voluntary adduction.

On infraduction, the right upper eyelid simultaneously retracted, exposing 3 mm of superior sclera (Figure, B).

On adduction, the right pupil constricted slightly.

We noted 3 mm of relative right upper eyelid ptosis and anisocoria (3 mm OD and 4.5 mm OS in ambient lighting).

Pupils were round and reactive with no afferent pupillary defect.

The degree of anisocoria was the same in ambient and dim lighting.

Extraocular movements were initially intact; however, a few minutes later, the patient developed an intermittent esotropia of the right eye, with episodes of sustained adduction lasting up to 30 seconds followed by normalization of ductions and alignment (Video; Figure, A).

A magnetic resonance imaging (MRI) from 1 year prior showed a small amount of residual tumor within the right cavernous sinus, stable over years (Figure, C).A, Right eye esotropia after voluntary leftward gaze.

The remainder of the examination was within normal limits.

B, Right upper eyelid retraction after downward gaze.

C, Magnetic resonance imaging of the brain showing a very small amount of residual tumor (arrowhead) in the right cavernous sinus, creating a slight convexity of the lateral wall.


Although his right ankle pain and swelling initially improved, he presented 1 week later with left ankle and right knee pain and swelling.

He remained afebrile but continued to complain of persistent left ankle and right knee pain.On examination, he had a multitude of skin lesions, including a raised follicular rash on both shins; painful flesh-colored raised nodules on the right knee, left index finger, and elbows; and painful raised circular violaceous papulonecrotic lesions with surrounding erythema and induration on the bilateral shins, left knee, right upper arm (Figure, A), and bilateral buttocks.

He had a tender, nonerythematous, subcutaneous 1-cm nodule above the right olecranon.

Laboratory results were notable for an elevated erythrocyte sedimentation rate of 44 mm/h, a C-reactive protein level of 0.84 mg/L (to convert to nanomoles per liter, multiply by 9.524), an antistreptolysin O titer of 1150 IU/mL, and an anti-DNase B titer of 961 U/mL.

Admission laboratory results included a hemoglobin concentration of 9.3 g/dL (to convert to grams per liter, multiply by 10), indicating normocytic anemia; a white blood cell count of 11 500/μL (to convert to × 109/L, multiply by 0.001), with 64% neutrophils; an elevated erythrocyte sedimentation rate of 46 mm/h; and a C-reactive protein level of 0.57 mg/L.

Punch biopsy was obtained from a lesion (Figure, B), which showed a dermal neutrophilic infiltrate with normal Gram and Grocott methenamine silver stains.A, Painful raised circular violaceous papulonecrotic lesion with surrounding erythema on child’s right upper arm.

He was diagnosed with cellulitis and prescribed 10 days of sulfamethoxazole and trimethoprim.

Echocardiogram and electrocardiogram were normal, and he was treated with amoxicillin.

The results of the rapid strep test and throat culture were normal, but given his constellation of symptoms, he was diagnosed with acute rheumatic fever.

Four days after discharge, he developed new painful skin lesions on his elbows, forearms, and legs.

Hematoxylin-eosin stain reveals dense neutrophilic infiltrate in the dermis as well as papillary dermal edema (original magnification × 40).


She had reported intermittent chest pain without precipitating factors since the age of 8 years.

This had been evaluated by a pediatric cardiologist and was felt to be noncardiac in nature.

Persistence of pain and associated distress eventually prompted referral to adolescent psychiatry.

An electrophysiologist commenced treatment with flecainide and warfarin.

Warfarin was stopped after 6 months arrhythmia-free.

At our clinic, she reported intermittent, nonexertional, atypical chest pain and exertional dyspnea with a gradual decline in exercise capacity, confirmed by cardiopulmonary exercise test (oxygen consumption peak 65% predicted).

Electrocardiogram demonstrated sinus rhythm, a prominent biphasic p-wave, and occasionally prolonged interval between the beginning of the electrocardiographic wave representing ventricular depolarization and the end of the T-wave (QT, QTc up to 594 milliseconds) (Figure 1A).

Transthoracic echocardiogram revealed normal ventricular dimensions and systolic function with biatrial dilatation (left > right) (Figure 1B), dilated pulmonary veins, and abnormal diastolic filling.

Cardiac magnetic resonance imaging with gadolinium confirmed dilatation of the atria, pulmonary veins, and inferior vena cava with normal ventricular size, mass, and ejection fraction without enhancement suggestive of infarction, inflammation, or fibrosis.

Pericardium was of normal thickness.A, Electrocardiogram demonstrating prominent and biphasic P-wave and ST-T segment abnormalities.

At age 17 years she experienced 3 episodes of AF, each treated with direct-current cardioversion.

B, Four-chamber view of transthoracic echocardiogram.


Her family history was positive for breast cancer in her mother, and the patient was a lifelong nonsmoker.

She had a cough and fatigue at the time, but no other symptoms of upper respiratory tract infection at onset.

She attributed her fatigue to staying up late studying and had not tried any treatments, including antibiotics.

She denied any trauma, night sweats, fever, chills, weight loss, generalized pruritus or lymphadenopathy in other areas of her body, any voice change, dysphagia, odynophagia, hoarseness, hemoptysis, hematemesis, or weight loss.

Physical examination revealed palpable nontender, freely movable mass in the right supraclavicular region.

Palpation of the parotid, submandibular glands, and thyroid gland did not reveal any suspicious masses or tenderness.

No mucosal lesions, scars, or masses were found on intraoral examination, with clear oropharynx.

Computed tomography revealed a 2.0-cm, right-sided supraclavicular mass just anterior and superior to the right subclavian vein with central patches of hypoattenuation (Figure, A).

Results from initial ultrasonography-guided fine-needle aspiration were nondiagnostic.

Subsequent ultrasonography-guided core needle biopsy on supraclavicular aspirate showed a benign spindle cell proliferation arranged in a tissue-culture–like pattern with a myxoid to collagenous stroma (Figures, B and C).

Immunohistochemical stains demonstrated the cells to be positive for actin and negative for cytokeratin and S100 protein.


The swelling persisted despite a course of oral antibiotics prescribed by the primary care team.

His parents denied any recent fevers, night sweats, weight loss, pain, respiratory distress, nasal bleeding, or significant rhinorrhea.

The physical examination revealed a right infraorbital and maxillary swelling, with deformity of the right lateral nasal dorsum.

The remainder of the physical examination was unremarkable.

Flexible fiber-optic sinonasal endoscopy revealed a normal appearance of the nasal mucosa with no obvious obstruction, mass lesion, rhinorrhea, or bleeding.

Vision was grossly normal with no diplopia, and sensation of the right cheek was intact.

A contrasted maxillofacial computed tomographic (CT) scan and magnetic resonance imaging (MRI) were performed, revealing an expansile right maxillary mass, associated with roots of the upper molar and premolar teeth, with erosion through the anterior maxillary wall and some thinning and displacement of the inferior orbital wall (Figure, A).

The lesion was excised via a sublabial approach using both open and endoscopic techniques for better visualization.

Histopathologic analysis revealed a bland, monotonous proliferation of stellate spindled cells with a variable extracellular matrix ranging from loose myxoid (Figure, B) to fibromyxoid and collagenous (Figure, C).

There was also permeation of adjacent bone marrow spaces (Figure, D).A, Coronal view.

B-D, Histopathologic images (hematoxylin-eosin, original magnification ×4).


Results from a rapid strep test were negative, and observation was initiated for presumed viral pharyngitis.

Progression of neck swelling led to empirical treatment for bacterial pharyngitis.

Necrotic skin changes and persistent purulent neck drainage through the needle biopsy site required incision and drainage as well as incisional biopsy of the left side of her neck.

A neck computed tomographic scan with contrast revealed large bilateral asymmetric conglomerations of necrotic cervical lymph nodes measuring up to 9 cm in the greatest dimension (Figure, A).

Initial evaluation, including fiber-optic laryngoscopy, revealed the presence of significant bilateral tender lymphadenopathy in the absence of any lesions in the upper aerodigestive tract.

A core biopsy specimen yielded negative gram stain and aerobic and anaerobic bacterial, fungal, and acid-fast bacillus cultures.

Polymerase chain reaction (PCR) of nodal contents was negative for Bartonella henselae.

All the cultures once again returned with no growth.

Final pathologic examination showed necrotizing granulomatous inflammation (Figure, B) with no monoclonal lymphocyte population on flow cytometry.

Results from a test for human immunodeficiency virus and angiotensin-converting enzyme testing were negative.

Operative findings included abundant purulent debris and considerable necrosis of skin and neck musculature.

Four weeks after symptom onset, the patient was referred to the otolaryngology service.


His medical history was significant for chronic rhinosinusitis, allergic rhinitis, and asthma, for which he took fluticasone propionate and salmeterol (Advair) and albuterol.

A review of systems revealed epiphora and ocular crusting for 4 months.

The patient was lost to follow-up but returned several months later with 6 weeks of progressive bilateral parotid swelling (Figure, B).

A history of recent tuberculosis exposure was obtained.

Findings on nasal endoscopy included bilateral turbinate hypertrophy and significant nasal crusting.

A computed tomographic (CT) scan of the sinuses revealed diffuse mucosal thickening consistent with pansinusitis (Figure, A).

All laboratory results from an autoimmune workup were normal for angiotensin-converting enzyme (ACE) level, antineutrophil cytoplasmic antibodies, antinuclear antibody, and immunoglobulin levels.

His parotid glands were diffusely enlarged and tender, and his facial function was normal.

Radiologically, no masses or sialoliths were seen (Figure, C).

Test results for SSa/SSb levels, human immunodeficiency virus (HIV), polymerase chain reaction (PCR), mumps titers, rapid plasma reagin, amylase, cytomegalovirus PCR, and quantiferon testing were negative.

A superficial parotid biopsy revealed noncaseating granulomatous inflammation (Figure, D).

His only associated symptoms were fevers and fatigue.