He was previously healthy and had no prior abdominal operations.

The rest of his history was noncontributory.

The patient noted pencil-thin stools that occurred during the past several months but had not had a colonoscopy in more than a decade.

He was mildly tachycardic but normotensive and afebrile.

Physical examination revealed a lethargic patient with a distended abdomen, diffuse rebound tenderness, and involuntary guarding.

No surgical scars or inguinal hernias were apparent on examination.

The only abnormal laboratory values were as follows: sodium concentration, 126 mEq/L (reference range, 135-145 mEq/L) (to convert to millimoles per liter, multiply by 1); lactate concentration, 58.6 mg/dL (reference range, 0-18.0 mg/dL) (to convert to millimoles per liter, multiply by 0.111); and white blood cell count, 18 500/μL (reference range, 3400-10 000/μL) (to convert to ×109/L, multiply by 0.001).

Computed tomography revealed diffuse free fluid but without free air and several loops of dilated small bowel with thickened, hypoenhancing bowel walls.

The mesentery was markedly edematous (Figure).

The rest of the small bowel were dilated and air and fluid filled but had normal bowel wall enhancement.

He was resuscitated with 2 L of lactated Ringer solution and underwent computed tomography of the abdomen and pelvis with intravenous contrast.

The colon was normal.Axial computed tomography image of the abdomen and pelvis.


The infant’s mother reported a small blue bump present at birth near the medial canthus.

Otherwise, the infant was stable, nontoxic appearing on examination, and feeding well.

The admitting team collected a complete blood cell count, basic metabolic panel, and blood cultures and performed a lumbar puncture for cerebrospinal fluid analysis, the results of which were within normal limits.

A maxillofacial computed tomographic scan was also obtained by the admitting service owing to concerns over displacement of the right globe (Figure 1).

By day 3 of admission, the edema and preseptal cellulitis had improved.External appearance of the right eye (A) with adjacent coronal maxillofacial computed tomographic scan on admission (B).

The white arrowhead indicates the lacrimal sac enlargement; black arrowhead, dilated nasolacrimal duct; and the yellow arrowhead, intranasal cystic mass.

The patient was admitted for broad-spectrum intravenous vancomycin and piperacillin/tazobactam for treatment of acute dacryocystitis with overlying preseptal cellulitis.

The patient continued treatment with intravenous antibiotics and on day 2 of admission, ophthalmology was consulted.

A bedside beveled percutaneous needle drainage was performed with a 25-gauge syringe.

The lacrimal sac was decompressed and 3 mL of purulent discharge was aspirated.


She had a history of chronic migraines and reported worsening headaches during the past 3 months.

The patient was not taking any medications and denied a history of illicit drug use.

The patient experienced intermittent episodes of numbness of her tongue, teeth, and upper extremities.

She reported intermittent tinnitus but denied transient visual obscurations or hearing changes.

Results of a review of systems were otherwise unremarkable.

Her best-corrected visual acuity was 20/100 OD and 20/70 OS.

Extraocular movements were intact, and pupils were round and reactive with no afferent pupillary defect.

Her intraocular pressure was 14 mm Hg OD and 10 mm Hg OS.

Results of the patient’s anterior segment examination were within normal limits.

Results of examination of her fundus are shown in the Figure, A.

Magnetic resonance imaging (MRI) of the brain revealed diffuse abnormalities on T2-weighted fluid-attenuated inversion recovery sequences (Figure, B).A, Color fundus photograph of the right eye demonstrates severe optic disc edema, retinal hemorrhages, cotton-wool spots, and macular exudates.

B, Magnetic resonance imaging scan of the brain in axial T2-weighted fluid-attenuated inversion recovery sequences reveals diffuse T2-weighted signal abnormality involving the cerebral hemispheres, brain stem, and cerebellum.


Her ocular history included optic neuropathy 5 years prior to presentation.

Her medical history included acute lymphocytic leukemia (currently in remission) after an allogenic hematopoetic stem cell transplant.

Two months before presentation, she developed Bell palsy on the right side of her face for which she was being treated with oral prednisone; her other medications were oral contraceptives and multivitamins.

As her Bell palsy was improving, she noted worsening of her visual acuity.

Her best-corrected visual acuity was hand motion OD and 20/400 OS.

A slitlamp examination revealed normal anterior segments in each eye.

The vitreous was free of cells in each eye.

A dilated ophthalmoscopic examination revealed mild optic nerve pallor (associated with her past episodes of optic neuritis) (Figure).


The patient returned 2 days later with persistent fever, worsening eyelid edema, and a new macular rash over her buttocks and shins.

Results of urinalysis revealed pyuria, and she was prescribed oral cephalexin, 250 mg every 12 hours, for a presumed urinary tract infection.

Motility and pupil reactions were normal.

There was moderate edema of the upper and lower eyelids bilaterally with erythema and several areas of shallow ulceration that were weeping a yellowish serous discharge (Figure, A).

This type of edema was associated with moderate hyperemia of the palpebral conjunctiva (Figure, B).

Results of the ocular surface examination revealed minimal bulbar conjunctival injection, the cornea was clear, and there was no discharge.

Cephalexin was discontinued, the patient was admitted, and a diagnostic workup was initiated, including swabs from the eyelid lesions and conjunctiva for bacterial cultures and viral polymerase chain reaction testing.

At this time, the ophthalmology service was consulted owing to concern for Stevens-Johnson syndrome precipitated by the treatment with cephalexin.On examination, her visual acuity was central, steady, and maintained in each eye.


There was no medical history of trauma, fever, or hematuria.

She was receiving therapy for mantle cell lymphoma and had previously undergone 1 cycle of the Nordic protocol (comprising cyclophosphamide, doxorubicin, vincristine, prednisolone, cytarabine, and rituximab).1 However, this resulted in tumor lysis syndrome and neutropenic sepsis.

The patient was reluctant to undergo further infusional therapy and was switched to ibrutinib, 560 mg, once daily.

During the 2-month period that she was receiving ibrutinib therapy, there were no concurrent administrations of anticoagulants.

At presentation, she was hypotensive (blood pressure, 79/45 mm Hg) with conjunctival pallor and left renal angle tenderness.

The patient’s hemoglobin count was low (7.6 g/dL; reference range, 12-16 g/dL; to convert to g/L, multiply by 10.0), which represented a significant decrease from the baseline (10.6 g/dL) measured 1 month before presentation.

She was also found to have acute-onset thrombocytopenia (40×109/L; reference range, 140-400×109/L) and leukocytosis (12.75×109/L, reference range, 4-10×109/L).

Her coagulation profile (prothrombin time) was normal.

A computed tomographic (CT) scan of the abdomen and pelvis was performed (Figure 1A) and compared with a similar scan performed 4 months prior (Figure 1B).

A, Findings from computed tomographic scan at presentation.

B, Previous findings from computed tomographic scan.


There was no history of illicit drug use, autoimmune disease, or cardiopulmonary disease.

Physical examination was remarkable only for asthenia.

Chest computed tomography (CT) demonstrated multiple pulmonary nodules, a spiculated mass in the right medial upper lobe, vertebral metastases, and small bilateral subsegmental pulmonary emboli.

Cranial CT showed scattered subacute embolic cortical infarcts and dural metastases.

Serum troponin was 2.6 ng/mL (type 2 myocardial infarction) with nonspecific electrocardiographic changes.

Transthoracic echocardiogram showed normal biventricular function with normal wall motion and shaggy, bulky masses on the tips of both mitral valve leaflets (Figure) (Video 1).

A saline contrast bubble study was negative for an intracardiac shunt, and commercial intravenous contrast showed no clot.

Transesophageal echocardiogram showed large, 1.4 × 0.5-cm, frondlike, mobile masses on the atrial surface of the mitral leaflets with mild mitral regurgitation.

In addition, a large 1.1  × 1.6-cm multilobulated, mobile mass was seen on the subvalvular chordae of the tricuspid valve, with trace tricuspid regurgitation.

Gated cardiac CT angiogram confirmed mobile hypoattenuating masses on the mitral valve leaflets that prolapsed to the left atrium during systole (Video 2).

No myocardial, pulmonary vein, or pericardial involvement was seen.Transthoracic echocardiogram.

A, Parasternal long axis showing masses on the tips of both mitral valve leaflets (arrowheads).

B, Parasternal long axis view showing mild mitral regurgitation.

C, Right ventricular inflow view demonstrating an echogenic mass on the tricuspid valve chordae (arrowhead).

D, Right ventricular inflow view showing mild tricuspid regurgitation.


She had no history of sinus infections or allergic rhinitis.

She had been treated with several courses of oral antibiotics and intranasal steroids without improvement of symptoms.

Nasal obstruction was constant and associated with right paranasal pressure.

Results from a head and neck examination, including cranial nerve, were normal, except for the results from nasal endoscopy, which showed a deviated septum and a soft-tissue mass emanating from the right middle meatus inferior to the middle turbinate that seemed to have a polypoid appearance superiorly and a papillomatous appearance inferiorly.

A computed tomographic (CT) scan of the sinuses without contrast showed complete opacification of the right paranasal sinuses with mass effect on the medial maxillary wall with mild hyperostosis posterolaterally.

A magnetic resonance image (MRI) of the face with contrast was obtained postoperatively to further delineate the mass and evaluate for intracranial extension.

Initial histologic stains showed the tumor to be positive for S-100 and actin (Figure, C and D) and negative for GFAP, CD34, and cytokeratin.

Additional immunostains showed the tumor to be negative for SOX-10 and B-catenin.Histopathologic images.

The patient underwent an endoscopic right sinonasal mass biopsy.

Intraoperatively, further excision of the mass was aborted owing to an unusual appearance of the mass as well as clear fluid exuding from the mass during microdebridement.

Pathologic analysis of the biopsied tissue revealed a uniform spindle cell tumor comprised of cellular fascicles and tumor cells with bland nuclei (Figure, A and B).

D, Smooth muscle actin immunohistochemical stain.


He had a history of asthma, chronic otitis media with effusion, and obstructive sleep apnea and had undergone 3 sets of tympanostomy tubes and an adenotonsillectomy.

Physical examination demonstrated a 3-cm firm and tender right parotid mass.

Clear saliva could be expressed from the Stensen duct.

A computed tomographic (CT) scan was performed, showing a discrete 2 × 2-cm necrotic mass in the right parotid gland (Figure, A).

A fine-needle aspirate (FNA) yielded a cellular sample with spindloid features, suggesting a neoplasm of uncertain subtype.

Additional studies, including flow cytometry and tissue cultures, were obtained.A, Coronal computed tomographic (CT) image demonstrating right parotid mass and level II adenopathy.

B, The normal parotid gland architecture is effaced by confluent granulomata with necrosis (hematoxylin-eosin, original magnification ×200).

Per recommendation of the head and neck multidisciplinary tumor board, the patient underwent total parotidectomy and neck dissection because the mass was grossly infiltrative of the parotid, and several enlarged level IB and II lymph nodes were observed at the time of surgery.

The mass was shaved off the marginal mandibular branch of the facial nerve because it was adherent to it.

He had no history of fevers or other constitutional symptoms.

A broad differential diagnosis was raised, including both benign and malignant salivary neoplasms.

Permanent histopathologic images showed normal parotid gland architecture effaced by confluent granulomata with Langhans-type giant cells and central necrosis (Figure, B).


His medical history was significant for prematurity, born at 26 weeks, and a 60-day intubation during a 99-day neonatal intensive care unit stay.

His noisy breathing had been present since birth, constant, exacerbated with feeding, sleeping, and supine positioning.

He fed poorly from the bottle with frequent choking, grunting, and irritability, and had minimal weight gain with 1 cyanotic event while feeding.

Nasopharyngolaryngoscopy showed no laryngomalacia, laryngeal lesions, or cord paralysis.Shortly after this visit, the patient presented to the emergency department with increased work of breathing, tachypnea, retractions, weak cry, and stridor.

Examination was significant for subcostal retractions, and biphasic stridor.

The physical examination was remarkable only for biphasic stridor and a weak cry.

A few days later he was taken to the operating room for direct laryngoscopy and bronchoscopy.During sedation, a prolonged expiratory phase with quick chest wall rise on inspiration and slow fall with expiration was observed.

Capnography showed a restrictive “shark fin” waveform (Figure, A).

The direct laryngoscopy and bronchoscopy were performed (Figure, C and D).Images show the (A) preintervention and (B) postintervention capnography wave form as seen on the anesthesia monitor.

Due to a lack of response to racemic epinephrine, albuterol, and steroids, he was admitted to the intensive care unit for heliox and intravenous steroids, resulting in mild improvements.

Endoscopy images on (C) expiration and (D) inspiration.

A viral panel was positive for rhinovirus.


His medical history included prostate cancer, hypertension, anxiety disorder, hyperlipidemia, gastroesophageal reflux disease, and diverticulosis.

His medications included omeprazole, alprazolam, amlodipine besylate, atenolol, simvastatin, and valsartan.

His intertrigo improved, but he then developed bright red, burning and painful nodules around his scrotum (Figure 1).

On physical examination, there were 2 symmetrical solitary erythematous nodules in the right and left inguinal folds adjacent to the scrotum.Clinical image of well-demarcated erythematous solitary papule in the right inguinal fold.


Physical examination revealed annular red plaques with scale and superficial erosions over the trunk and extremities.

Strikingly, plaques on both arms showed a corymbiform pattern, with a central and multiple satellite lesions (Figure, A).

On the lower limbs, infiltrated plaques with prominent crusts were seen (Figure, B).

Also, there were papulosquamous lesions on the left sole, but the palms were spared.

There was neither regional lymph node enlargement nor systemic involvement.

Two biopsy specimens from both types of lesions were obtained for histopathologic evaluation, showing an identical histologic pattern (Figure, C and D).

He had been treated with a course of high-potency topical corticosteroids without any improvement.


His medical history is significant for diabetes mellitus type 2 and hypothyroidism.

Medications included glipizide, metformin, and levothyroxine.A, Nodules are 4 to 6 cm in diameter on the right upper extremity.

He was renovating a commercial cannabis grow-house in California at time of onset.

He described the construction site as being filled with intoxicating mold.

He reported shortness of breath and a 20-pound weight loss.

Most concerning was the inability to use his right upper extremity.

Also, he developed a pathological fracture of his right foot (Figure, B).

Clinical examination of his forearms revealed several yam-size (4-6 cm), nontender, nonulcerated, boggy subcutaneous nodules in a sporotrichoid pattern and large nodules scattered on his trunk and abdomen.

There was no palpable lymphadenopathy or lower extremity lesions.

B, A pathological fracture on the fifth metatarsal on the right foot is indicated by the white arrowhead.

C, Histopathology shows pale, nodular aggregations of inflammatory cells in the deep dermis, extending into the fibrotic subcutis, as well as (D) aggregations composed of epitheliod histiocytes with few other inflammatory cells, so called “naked granulomas.”The patient’s laboratory tests showed fasting glucose of 122.0 mg/dL (reference range, 65.0-115.0 mg/dL); total calcium, 10.2 mg/dL (reference range, 8.5-10.5 mg/dL); blood urea nitrogen, 16.0 mg/dL (reference range, 10.0-24.0 mg/dL); creatinine, 1.30 mg/dL (reference range, 0.6-1.3 mg/dL); hemoglobin A1c, 6.7 (reference range, 4.0-6.0); 1,25-OH vitamin D 70, ng/mL (reference range, 15.9-55.6).Liver enzymes were within normal limits along with a negative purified protein derivative and quantiferon test results.

A culture from a cutaneous nodule with microbial stains for bacteria, fungal culture, and acid-fast bacilli was negative.

Computed tomography of the chest revealed hilar lymphadenopathy.

An incisional biopsy of a nodule on the right wrist was obtained, which showed nodular aggregations of epithelioid histiocytes with sparse peripheral lymphocytes, extending from the deep dermis into the subcutis (Figure C and D).


His medical history included diagnoses of eczema and multiple food allergies.

Owing to concerns about food triggers of his eczema, the child had a restrictive diet consisting solely of potato, pork, lamb, apples, cucumber, and Cheerios.

He also had a long-standing complaint of dry eyes.

The vision loss was not associated with pain, headache, fever, or photopsias (flashes of light).

On examination, the child’s visual acuity was limited to detecting hand motion at 30 cm.

His conjunctiva had dry, keratinized patches with foamy appearance (Figure 1A).

The cornea showed areas of marked epitheliopathy with opacity (Figure 1B).

His pupils were equal and reactive to light with no relative afferent pupillary defect.

His funduscopic examination showed mild optic nerve pallor.

He had normal extraocular movements.A, Photograph of the patient’s eye before treatment.

There was no history of redness, discharge, or trauma to the eyes.

Arrowheads indicate dry keratinized patches (Bitot spots).

B, Photograph of the patient’s eye before treatment demonstrating marked corneal epitheliopathy with opacity.


Other than a previous open hemorrhoidectomy, the patient had no significant medical history.

Of note, he had no family history of intestinal disease.On examination, he had a fever with a temperature of 39°C and tachycardia with a heart rate of 102 beats per minute.

This was associated with diarrhea, vomiting, fevers, and chills.

He denied any history of weight loss, melena, or hematochezia.

On abdominal examination, there was localized tenderness with guarding and fullness in the right lower quadrant.

Results from his blood laboratory investigations demonstrated leukocytosis, with white blood cell count of 17 000/µL (to convert to ×109/L, multiple by 0.001) and a C-reactive protein level of 205 mg/L (to convert to nmol/L, multiple by 9.524).

Transverse computed tomographic scan indicated a large right-sided inflammatory phlegmon measuring 7.5 cm in transverse diameter in a 48-year-old man.

He reported some relief of symptoms with loperamide.

He then underwent an exploratory laparotomy.

However, given the clinical history, the patient underwent a computed tomographic (CT) scan of the abdomen and pelvis with intravenous contrast (Figure 1).


The patient described a 4-day history of progressively worsening abdominal pain and diarrhea and denied fevers, chills, diaphoresis, or any previous similar episodes.

Her abdomen was distended and mildly tender, and her pain was disproportionate to the findings of her physical examination.

There were no abnormal laboratory test findings.

The abdominal computed tomography (CT) scan from her initial admission (Figure, A) and the abdominal CT angiogram on readmission (Figure, B) showed dramatic progression of her disease.A, Coronal view of computed tomography (CT) scan from 3 days prior to readmission demonstrating isolated duodenal thickening; B, coronal view of CT angiography scan on readmission demonstrating thickened small bowel and free fluid.


The patient was previously healthy and did not take any medications.Appearance of the optic nerves in fundus photographs taken 4 weeks after the patient’s injury at work.

On awakening, he reported that he was unable to see out of each eye.

He also had a left leg degloving injury, distal femur fracture, and posterior knee dislocation with bleeding through the open fractures and wounds.

He was profoundly hypotensive (blood pressure, 70/40 mm Hg) and anemic (hemoglobin level, 5.6 g/dL [to convert to grams per liter, multiply by 10]) from extensive blood loss.

Bedside examination revealed no light perception vision with 7-mm pupils that were nonreactive bilaterally.

Extraocular movements were full and there was no ptosis.

Slitlamp examination findings were normal, and fundus photographs of the posterior pole in each eye are presented in the Figure.

Magnetic resonance imaging of the brain performed earlier in the hospitalization was normal.

The optic discs are characterized by diffuse pallor, with no evidence of edema or hemorrhages.

He was urgently transfused and taken to the operating room for bilateral lower extremity irrigation and drainage and reconstruction of the left leg.

Unfortunately, postoperative infection necessitated a left leg above-knee amputation.The patient was admitted to the intensive care unit, intubated, and sedated for 1 month.


His medical history included ischemic heart disease and hypercholesterolemia, and he was an ex-smoker of 20 pack-years.Examination revealed unaided visual acuity of 20/20 OD and 20/20 OS.

He had been seen 2 weeks previously with similar symptoms and was diagnosed as having blepharitis and discharged with instructions for eyelid hygiene.

His symptoms failed to improve, and he visited his family physician the following week.

His physician prescribed a course of amoxicillin and clavulanate potassium, but the symptoms remained.The patient had no other ocular history or history of facial surgery.

He had no evidence of proptosis, no relative afferent pupillary defect, and a full range of extraocular eye movement.

Slitlamp examination demonstrated moderate bilateral blepharitis and extensive punctate keratopathy of the right eye.

Findings from posterior segment examination were unremarkable.

Examination of the cranial nerves demonstrated reduced sensation in the distribution of the ophthalmic and maxillary branches of the right trigeminal nerve, including complete corneal anesthesia.


The patient was born at term; had an unremarkable delivery; and had no history of developmental delay, trauma, or systemic illness.

There was no family history of strabismus, amblyopia, or congenital ptosis.

Her mother reported that, since infancy, the child’s left eye has twitched during feeding and mealtimes.

Her best-corrected visual acuity was 20/30 OD and 20/40 OS.

Pupils were reactive to light bilaterally, and there was neither an afferent pupillary defect nor anisocoria.

There was notable asymmetry in the following eyelid measurements: palpebral fissure height (10 mm OD; 5-6 mm OS) and margin reflex distance 1 (3.5 mm OD; 0.5-1.5 mm OS).

In addition, elevation of the left upper eyelid was observed with lateral jaw thrust but not with anterior-posterior jaw movements or with mouth opening and closing.

The levator function was 14 mm OU, and the margin crease distances were 5 mm OD and 6 mm OS.

Her ocular history was significant only for bilateral mixed astigmatism (−0.25 + 0.75 × 145 OD and −0.25 + 1.00 × 005 OS).


Her medical history includes breast cancer, diagnosed in 2000 and treated with lumpectomy and radiotherapy.

A mammogram, completed 4 months before her ophthalmology visit, was reported as stable.

More recently, she noted that her left eye “drifts out at times.” She also reported drooping of the left upper eyelid and binocular, variable horizontal or vertical diplopia at distance.

She also complained of itchy eyes but denied any pain or headaches.

On presentation, her visual acuity was 20/20 OD and 20/40 OS.

She had slightly decreased color vision (8/10 Ishihara plates) of the left eye and there was no relative afferent pupillary defect.

External examination revealed mild left proptosis and severely limited adduction of the left eye.

Both optic nerves appeared normal on retinal examination.

Magnetic resonance imaging of the brain (Figure 1) showed a 2.3-cm intraconal mass inseparable from the left lateral rectus muscle.

The mass medially deviated the left optic nerve and conformed to the shape of the orbital globe with mild bony remodeling of the lateral orbital wall.T1-weighted magnetic resonance imaging of the brain shows a 2.3-cm intraconal mass (black asterisk) molding to the left orbital globe with medial deviation of the optic nerve (blue asterisk).


A computed tomographic scan showed lytic lesions, and bone marrow biopsy findings revealed 30% κ-restricted plasma cells.

Three weeks after therapy initiation, follow-up SPEP-IF demonstrated an M-IgA κ at 0.1 g/dL.

Two months later, SPEP-IF demonstrated a new M-IgG κ band in the same electrophoretic position as the M-IgA κ, with the 2 distinguishable only by IF and measured at 0.1 g/dL.

Three months later, SPEP-IF demonstrated only the M-IgG κ, with the original M-IgA κ not detected.

Over the next 8 months, the patient received maintenance therapy with VRD-E, and monthly SPEP-IF consistently showed M-IgG κ at 0.1 g/dL, with the original M-IgA κ consistently not detected.

The serum free κ/λ ratio gradually decreased to 4.86 one year later.

He was assigned to the bortezimib-lenalidomide-dexamethasone–elotuzumab (VRD-E) arm of a phase 3 trial.

The Table summarizes assay data.Clonal evolution of myeloma cells to both IgG- and IgA-secreting cells.Immune dysregulation from multiagent therapy resulting in a new M-protein.New MGUS or B-cell lymphoproliferative disorder, such as monoclonal B lymphocytosis.Therapeutic monoclonal antibody at serum concentration detectable by SPEP-IF.


On arrival, he was afebrile, with a blood pressure of 120/80 mm Hg, heart rate of 35/min, respiratory rate of 16/min, and pulse oximetry of 98% on ambient air.

His examination revealed regular bradycardia without cannon A waves, clear lung fields to auscultation, and warm extremities.

Chest radiography revealed hilar adenopathy.

Electrocardiography showed sinus bradycardia, first-degree atrioventricular block, left posterior fascicle, and right bundle branch blocks (Figure 1A).

Transthoracic echocardiography revealed an ejection fraction of 50% without regional variation.

On exercise stress single-photon emission computed tomography, the patient completed 9 minutes of a standard Bruce protocol and developed transient high-grade atrioventricular block but had no ischemic ST-segment changes or defects on perfusion imaging.

Cardiac magnetic resonance imaging (cMRI) with gadolinium contrast-enhanced first-pass myocardial perfusion imaging at rest and contrast-enhanced late gadolinium enhancement imaging revealed low-normal left ventricular systolic function but no other abnormalities (Figure 1B).


On posttransplant day 10, he developed fever (38.4°C).

On posttransplant day 14 he developed new-onset pruritic, confluent, erythematous, blanching morbilliform macules and papules on his trunk and extremities (Figure, left).

Review of systems was notable for diarrhea and a 6-pound weight gain since transplantation and negative for headache, cough, shortness of breath, or abdominal pain.Left, Macules and papules on the trunk of the patient.

Right, Axial chest computed tomography of the patient.On examination, there was no lymphadenopathy or hepatosplenomegaly.

The patient’s heart rate was 100/min, blood pressure was 106/68 mm Hg, and he occasionally experienced mild hypoxia to 94% on ambient air.

Results of a basic metabolic panel were normal, with a blood urea nitrogen level of 10 mg/dL (3.57 mmol/L) and creatinine level of 0.7 mg/dL (61.88 μmol/L).

White blood cell (WBC) count was 7300/μL, and absolute neutrophil count (ANC) was 5480/μL.

Neutrophil recovery occurred beginning on posttransplant day 10, with WBC count of 700/μL and ANC of 532/μL on posttransplant day 10, correlating with the onset of the patient’s fevers.

Platelet count was 48 × 103/μL, and hemoglobin was 8.2 g/dL.

Results of liver function tests were normal.

Blood, urine, sputum, and respiratory viral cultures were negative.

Tests for cytomegalovirus, Epstein-Barr virus, human herpesvirus-6, adenovirus, parvovirus, cryptococcal antigen, aspergillus galactomannan antigen, β-glucan, and Clostridium difficile were negative.

Chest computed tomography demonstrated multifocal ground-glass and consolidative pulmonary opacities (Figure, right).

Computed tomography of the abdomen was unremarkable.

He was started on empirical treatment with cefepime; however, his fevers persisted despite antibiotic therapy.


Her pain was related to multiple vertebral fractures due to chronic steroid use for an inflammatory polyarthritis that was not responsive to hydroxychloriquine and methotrexate.

A comprehensive urine drug screen using immunoassay and mass spectrometry was ordered (Table 1).The patient is taking methadone, hydromorphone, and codeine.The patient is taking methadone, morphine, hydromorphone, and codeine.

Her pain medication regimen (methadone, 20 mg [3×/d]; immediate-release morphine, 30 mg [5×/d]; gabapentin, 1200 mg [2×/d]; duloxetine, 60 mg/d; and celecoxib, 200 mg [2×/d]) helped her independently complete instrumental activities of daily living.

She reported no adverse effects (eg, somnolence or constipation).


Dexamethasone was prescribed to reduce the risk of ATRA syndrome, a potentially life threatening complication seen in these patients and characterized by fever, pulmonary infiltrates, hypotension, and leucocytosis.After 12 days of treatment, the patient developed pyrexia and was started on empiric antibiotics.

Two days later he developed tender black spots on the scrotum that progressed to painful ulcers over 8 days (Figure, A).

As scrotal ulceration progressed, they enlarged and became necrotic with a black eschar.

Peripheral blood cultures and skin swabs from the lesions did not identify bacterial or viral infection.

Scrotal ultrasonography showed a subcutaneous hypervascular lesion with no abscess.

The development and progression of scrotal ulceration coincided with recovery in neutrophil count from 0.3 × 109/L to 1.2 × 109/L and persistent pyrexia.

A specimen was obtained for histopathology.A, Clinical photograph of scrotum and penis shows ulceration and necrosis of penile and scrotal skin with surrounding inflammation.

He was commenced on treatment with the PETHEMA LPA 20051 protocol consisting of all-trans retinoic acid (ATRA) and idarubicin, an anthracycline based chemotherapy.

Systemic antifungal and antiviral therapy were added with no improvement.

Acute promyelocytic leukemia (APML) was diagnosed by bone marrow aspirate morphology, immunophenotyping, and detection of the bcr1 variant of the PML-RARα fusion transcript in peripheral blood.


An abdominal computed tomographic scan showed findings consistent with bowel perforation, and she was admitted to the intensive care unit after emergent exploratory laparotomy.Her medical history was significant for 1 other episode of idiopathic bowel perforation 3 years prior.

Dermatology was consulted to evaluate an asymptomatic skin eruption that had been present for at least 8 months before her hospitalization.

Physical examination revealed numerous 5- to 10-mm nontender papules with a porcelain-white atrophic center and an erythematous halo, alongside scattered atrophic white scars (Figure, A and B).

The lesions were distributed across her trunk, neck, and upper and lower extremities.

Palms, soles, scalp, genitalia, and mucosal surfaces were spared.

Her neurological and mental state examination had unremarkable results.

A, Papules on the back with white atrophic center and an erythematous rim.

B, Lesions on the thigh similar to those of the back, alongside atrophic white scars.

C, Thigh biopsy shows hyperkeratosis and wedge-shaped avascular necrosis in dermis and subcutaneous tissue (hematoxylin-eosin stain, original magnification ×10).

D, Back biopsy shows occlusion of dermal blood vessels, perivascular lymphocytic infiltration, and mucin deposition (hematoxylin-eosin stain, original magnification ×40).

Biopsy specimens from her thigh and back were obtained (Figure, C and D).Clinical photographs and biopsy specimens.


The patient had a history of type 2 diabetes and hypertension and was treated with glimepiride, sitagliptin phosphate hydrate, and amlodipine besylate.

The patient also had polymyalgia, which was treated with a low dose of prednisolone.

The prednisolone therapy had been discontinued 2 months before her visit to the dermatology clinic when she had been hospitalized with pneumonia.

Multiple tense blisters had subsequently appeared on the palms.

The erythema did not respond to topical corticosteroid, oral roxithromycin (300 mg/d), or narrow-band UV-B phototherapy.

Physical examination at the first visit revealed scaly erythematous plaques on the whole body and tense blisters on the arms, hands, soles, and buttocks.

Neither scar formation or mucosal involvement was observed.

A skin biopsy specimen was obtained from a bulla on the forearm.

Histopathologic analysis revealed a subepidermal bulla with inflammatory infiltrates of neutrophils.

The results of an IgG chemiluminescence enzyme immunoassay for bullous pemphigoid (BP) 180 noncollagenous (NC) 16A were negative.

After treatment with oral prednisolone, 20 mg/d, the lesions healed without scar or milia formation (Figure 1).Clinical features before (A) and after (B) treatment with oral prednisolone, showing no scar formation.


Family history was noncontributory and her parents denied consanguinity.The child was hospitalized on multiple occasions during infancy for the fevers, and she had comprehensive sepsis evaluations, including lumbar punctures, with negative results.

The child had fevers (maximum temperature, 40°C) that lasted 3 to 5 days.

Her mother reported that the fevers resolved spontaneously but continued to recur almost every month.

The fever symptoms were associated with bilateral conjunctivitis, arthralgias, and irritability.

The hivelike, nonpruritic urticaria did not improve with antihistamine medication and there were no known precipitating or aggravating factors.

Despite extensive evaluation, a definitive source for the fevers was not identified, and the patient was referred to our institution.On physical examination, the patient was febrile (temperature, 39°C) and appeared fussy.

Findings from chest and abdominal imaging and bone marrow aspiration with biopsy were negative for a malignant process.

Skin examination confirmed nonpruritic, macular and urticarial lesions on the face, back, and lower extremities (Figure).

Bilateral conjunctival hyperemia without drainage was noted.

There was neither swelling nor redness of the joints.

Her right ankle and knee examination showed limited active and passive range of motion secondary to pain symptoms.

Findings from the remainder of physical examination were normal.Erythematous macular and urticarial lesions with areas of confluence on back and lower extremities.


The following day, the patient developed right upper extremity pain and swelling.

Physical examination revealed tense and tender swelling of the right upper extremity that was more marked in the upper arm and caused significant impairment in motor function, but sensation to touch and pin prick was intact (Figure 1A).

She was afebrile with a heart rate of 120 beats/min on admission and leukocytosis (white blood cell count, 23 000/μL [to convert to ×109/L, multiply by 0.001]).

Computed tomography of the abdomen and pelvis and transvaginal ultrasonography revealed a large intrauterine abscess.

The right radial pulse was absent, but biphasic Doppler arterial signals were present in the right radial and ulnar artery.

An attempt to insert a peripherally inserted central catheter (PICC) into the right basilic vein was unsuccessful.

An intravenous catheter in the left hand was established for the administration of antibiotics.


He had no history of previous surgery or trauma.

A physical examination revealed moderate epigastric tenderness with rebound and guarding.

His systolic blood pressure was 109 mm Hg, his diastolic blood pressure was 70 mm Hg, and his pulse rate was 100 beats/min.

Laboratory test results were remarkable for a white blood cell count of 13 970/μL, hemoglobin level of 8.4 g/dL, serum creatinine level of 1.67 mg/dL, serum amylase level of 57 U/L (reference range, 30-110 U/L), and serum triglyceride level of 282.42 mg/dL, with no evidence of coagulopathy.

Contrast-enhanced computed tomography (CECT) and mesenteric angiography were performed (Figure 1).A, Contrast-enhanced computed tomographic (CECT) image showing an intra-abdominal hyperdense mass (arrowhead) and free fluid in the upper abdomen.

B, Visceral artery angiogram revealing an aneurysm (arrowhead).

(To convert the white blood cell count to ×109 per liter, multiply by 0.001; hemoglobin level to grams per liter, by 10; serum creatinine level to micromoles per liter, by 88.4; serum amylase level to microkatals per liter, by 0.0167; and serum triglyceride level to millimoles per liter, by 0.0113.)


He denied notable ocular history aside from a recently documented elevated intraocular pressure (IOP) of 36 mm Hg OS and shallow anterior chamber (AC).

The AC was shallow, and episcleral vessels were congested.

Subsequently, a choroidal mass was discovered, and he was referred for our opinion.On examination, refractive error was +3.00 D OU, and best-corrected visual acuity was 20/25 OD and 20/40 OS.

Results of examination in the right eye were unremarkable, and IOP was 17 mm Hg.

Examination of the left eye revealed elevated IOP of 26 mm Hg while the patient was taking dorzolamide/timolol.

Ophthalmoscopic examination and wide-angle scanning laser ophthalmoscopy (Figure 1A) documented a ring-shaped peripheral ciliochoroidal mass accompanied by shallow serous retinal detachment inferiorly.

Globe transillumination revealed an undefined mottled choroidal shadow inferiorly.

B-scan ultrasonography (Figure 1B) and ultrasound biomicroscopy suggested an echolucent ciliochoroidal elevation without intrinsic vascular pulsations.

Magnetic resonance imaging of the orbits confirmed the ring-shaped ciliochoroidal elevation with nonenhancement of the mass.

Doppler ultrasonography showed normal flow parameters without evidence of a dural-cavernous fistula.A, Wide-angle fundus photograph demonstrating peripheral choroidal elevation, most prominent superotemporally, and numerous choroidal folds.

Laser peripheral iridotomy had been performed but failed to deepen the AC.


Serum GQ1b ganglioside IgG antibodies associated with internal ophthalmoplegia in Fisher syndrome were not detected.Within the following 2 weeks, progressive generalized autonomic dysfunction developed including reduced food intake and weight loss, constipation, urinary retention, anhidrosis, xerostomia, and xerophthalmia.

Ophthalmologic examination revealed bilateral mydriasis, with a reduced pupillary response to light and accommodation (Figure).

Uncorrected Snellen visual acuity was 20/32 OU for distance and 20/200 OU for near.

Results of slitlamp examination and ophthalmoscopy showed no abnormalities.Bilateral mydriasis with a reduced pupillary response to light and accommodation in an 11-year-old boy.Results of complete blood cell counts, serum chemistry examination, cerebrospinal fluid examination, and virologic studies of blood and stool performed for exclusion of infection were all negative.

Tumor, aneurysm, or traumatic lesion were excluded by cranial magnetic resonance imaging.

Ophthalmologic reexamination showed unaltered pupillary abnormality.

Results of Schirmer test without topical anesthesia showed 0 mm of tear production.

Lissamine green staining of the exposed interpalpebral areas showed moderate changes of the conjunctiva.

Mild corneal staining was evaluated with cobalt blue illumination after fluorescein instillation.

Diluted norepinephrine (0.1%) was instilled in both eyes, which elicited supersensitive dilatation of the pupils bilaterally owing to reinnervation and upregulation of the postsynaptic receptors, consistent with tonic pupils.


She also stated that she had pain to the eye.A, Slitlamp photography of the left eye demonstrating the pupil peaked toward the 9:30 area.

On slitlamp examination, a peaked pupil was noted (Figure 1).

No new pigment was noted on the ocular surface.

The patient subsequently underwent a complete excision of the tumor and supplemental cryotherapy to the resection bed.

Three months later, she had a new pigment deposition adjacent to the limbus in the area of the prior resection, for which she underwent additional excision and cryotherapy.

Pathology specimens from this excision were negative for atypia.

The patient was given mitomycin C as adjuvant therapy.Two months later, the patient presented for follow-up.

Pathological results confirmed the diagnosis of conjunctival melanoma.

She had an 11-mm pigmented conjunctival lesion that was suspicious for melanoma with significant involvement of the caruncle, bulbar conjunctiva, and palpebral conjunctiva.

The tumor had invaded the medial canthus and medial rectus insertion; however, no scleral invasion was observed during the intraoperative examination.

Her visual acuity and intraocular pressure were at baseline and within normal limits, respectively.


His ocular history was significant for mild nuclear sclerosis.

His current medications included multivitamins and fish oil.Automated Humphrey visual field (VF) shows a right, dense inferior arcuate scotoma (A).

His VF loss was recognized on automated Humphrey VF screening and had remained unchanged during the subsequent 5 years (Figure, A).

The VF loss is stable when compared with previous VF testing.

Color fundus photograph demonstrates small tilted right optic nerve with peripapillary atrophy (B).

GHT indicates Glaucoma Hemifield Test; MD, mean deviation; PSD, pattern standard deviation; and VFI, visual field index.Neuro-ophthalmic examination revealed visual acuities of 20/30 OD and 20/25 OS that matched with the density of his cataracts.

Color vision was within normal limits bilaterally.

Pupils were symmetric without afferent defects.

Applanation tonometry pressures were 18 mm Hg OD and 17 mm Hg OS.

Slitlamp examination revealed mild nuclear sclerosis in each eye.

Repeated automated Humphrey VF testing revealed bilateral inferior arcuate defects (mean deviation, −4.80 dB OD and −2.6 dB OS).


His posttransplant course was notable for moderate cellular rejection (International Society for Heart and Lung Transplantation grade 2R) within the first 6 weeks, which was treated with a pulse of corticosteroids.

Three days prior to this presentation, he experienced an episode of mild chest pain associated with radiation down his left arm and vomiting.

Over the preceding days, he developed progressive dyspnea on exertion, which prompted him to present to the emergency department.

His electrocardiogram (ECG) on presentation is shown in Figure, A.

His bedside echocardiogram showed anteroseptal akinesis with apical thrombus and reduced left ventricular function (Figure, B and Video).A, Patient’s admission electrocardiogram demonstrated new ST elevations of 1 to 2 mm in the anterolateral leads with Q waves in I, aVL, and across the precordial leads.

B, His bedside echocardiogram demonstrated anteroseptal akinesis with apical thrombus (arrowhead) and reduced left ventricular function.Order an emergent coronary angiogram and endomyocardial biopsy.

Subsequently, he had normal allograft function with no further rejection noted on routine surveillance biopsies.

He did not seek medical attention at that time as he felt the pain was unlikely to be coming from his heart.


She had a complex history of breast cancer on the left side that was first diagnosed in 1991 and was treated with lumpectomy, radiotherapy, cyclophosphamide, methotrexate, and fluorouracil.

In 2001, she experienced local disease recurrence and underwent complete mastectomy with axillary lymph node dissection on the left side and received adjuvant treatment with tamoxifen citrate and anastrozole.

In 2014, she developed axillary lymphadenopathy on the right side and was found to have metastatic disease.

She subsequently underwent axillary lymph node dissection on the right side, followed by treatment with doxorubicin hydrochloride and cyclophosphamide.

At the time of her evaluation, the patient’s physical examination was remarkable for discrete erysipeloid plaques on her chest, back, and right shoulder (Figure 1A).

The lesions were warm and indurated but nontender to palpation.

Her most recent mammogram and positron-emission tomography–computed tomography (PET/CT) showed no evidence of active disease.

Serum chemistry profile, complete blood cell counts, and hepatic and renal function testing had normal results.

Lesional skin biopsies were performed (Figure 1B).A, Clinical examination shows discrete erysipeloid plaques on the anterior chest.

B, Histopathologic analysis (hematoxylin-eosin stain, original magnification ×100).


Her birth history was unremarkable, and her growth and development were normal.

Her family history was unremarkable.Physical examination revealed 7 sharply marginated, irregularly shaped, polymorphic hyperpigmented macules of 10 to 15 mm in diameter, without scales, on the back and thighs.

There was no lymphadenopathy or hepatosplenomegaly.

The hyperpigmented macules were of orange hue, with unevenness of the pigmentation (Figure 1).


She had not visited a physician for several years but reported feeling well with no active symptoms.

She had no risk factors for hepatitis B, hepatitis C, or HIV and reported no use of nonsteroidal anti-inflammatory drugs or herbal medications.

One year ago, her urine was tea-colored during an upper respiratory tract infection.

Examination results were normal except for elevated blood pressure (154/90 mm Hg).

Although her hemoglobin concentration was low (10.5 g/dL; reference range, 11.6-15.2 g/dL), white blood cell count, platelet count, and electrolytes were normal.

Her kidneys appeared structurally normal on ultrasound.

Urine studies were performed (Table).Urinary tract infection is the most likely diagnosis.


She had a long-standing history of several outbreaks of skin lesions limited to both axillae and groin.

Previous episodes had been successfully treated with various topical drugs that were administered by her primary care physician.

No family history of similar lesions was recorded.

Physical examination revealed multiple annular erythematous plaques surrounded by a peripheral crusted and pustular collarette on her trunk (Figure, B).

No active lesions were present in her axillae, inframammary folds, or groin.

After obtaining informed consent, 2 biopsy specimens were taken from the periphery of the lesion for hematoxylin-eosin stain and direct immunofluorescence (Figure, C and D).

A skin swab specimen from a pustular lesion was taken for microbiological culture.A, Multiple erythematous and crusted plaques diffusely distributed on the dorsal trunk at presentation.

B, An erythematous annular plaque, surrounded by a crusted and focally pustular peripheral collarette.

C, Biopsy specimen revealing suprabasilar acantholysis (original magnification ×4).

D, Specimen from generalized lesions at clinical presentation (original magnification ×40).

C and D, Histopathologic images, hematoxylin-eosin.


The patient reported previous orolabial melanotic macules.

Her medical history was significant for hypertension, hypercholesterolemia, asthma, and breast cancer.

Medications included levalbuterol, nadolol, and cetirizine.

Family medical history was significant for breast cancer and social history was unremarkable.

Review of systems was positive for cutaneous ephelides.

Physical examination revealed a 7 mm × 6 mm asymmetric, heterogeneously pigmented lesion without indurated borders on the gingiva associated with the left maxillary central incisor tooth (number 9) (Figure, A).

A lesion similar in clinical appearance, although smaller, was observed on the gingiva associated with the right mandibular first premolar tooth (number 28) (Figure, B).

Biopsy specimens were obtained with a 3 mm punch instrument from both lesions for routine histology which demonstrated similar microscopic findings (Figure, C and D).A, Heterogeneously pigmented lesion of the gingiva associated with the left maxillary central incisor.

B, Heterogeneously pigmented lesion of the gingiva associated with the right mandibular first premolar.

C, Mucosal epithelium exhibiting spongiosis and a diffuse proliferation of heavily pigmented dendritic melanocytes that extend the full thickness of the epithelium (arrowheads).

Melanin incontinence is also noted (hematoxylin-eosin stain, original magnification ×100).

D, Squamous mucosa exhibiting spongiosis with diffuse pigmentation in the basal cell layer and dendritic melanocytes (arrowheads) in the stratum spinosum (hematoxylin-eosin stain, original magnification ×200).


Seventeen days after her last day of chemotherapy, while neutropenic, she became febrile and developed several vesicles with an erythematous base on the lower back (Figure, A) and left thigh.

Tissue and blood cultures and a punch biopsy specimen of a vesicle on the lower back were obtained.

Hematoxylin-eosin (Figures, B and C), gram (Figure, D), and periodic acid-Schiff stains were performed on the punch biopsy.

Testing for herpes simplex virus and varicella zoster virus were also ordered.A, Scattered vesicles with an erythematous base on the lower back.

B, Hematoxylin and eosin stain (original magnification ×200).

C, Hematoxylin and eosin stain (original magnification ×600).

D, Gram stain (original magnification ×600).


There was no history of tumors elsewhere.

She began to limp intermittently ten years earlier.

She refused further investigations until a year earlier, when she developed mild headache.

One month before hospital admission, her headache aggravated and became intolerable.

Her consciousness was intact, but her memory and concentration were poor.

A brain magnetic resonance imaging (MRI) showed multiple parenchymal lesions involving the pons, bilateral amygdala, and the left temporal pole (Figure 1A).

Magnetic resonance imaging showed minor focal enlargement of the lesions in the left temporal pole.

Enhanced MRI showed remarkable progression of the lesions in the left temporal lobe, involving the temporal pole and the parasylvian region, along with a newly developed mass in the third ventricle and obstructive hydrocephalus.

The lesions in the pons and the right amygdala remained stable (Figure 1B).

There were multiple congenital nevi distributed over the body, 2 of which on the legs were more than 5 cm in diameter, and another 3 on her back and face were more than 3 cm.

There were no focal motor or sensory deficits.

The rest of the neurologic and systemic examination was unremarkable.

Gene examinations showed a mutation in the N-ras-2 gene.A and B, T1-weighted axial brain magnetic resonance imaging at the levels of pons, midbrain, and thalamus, performed ten years earlier, shows multiple parenchymal lesions including the pons, bilateral amygdala, and the left temporal pole (arrowheads).

Sequence, spin echo; repetition time, 650.0 milliseconds; echo time, 14.0 milliseconds; field of view, 144 × 230; slice, 5.0 mm; window, 1054; contrast, 640.

C and D, Enhanced, T1-weighted axial brain magnetic resonance imaging at the levels of pons, midbrain, and thalamus, performed at the most recent hospital admission, shows remarkable progression of the lesions in the left temporal lobe, involving the temporal pole and the parasylvian region, along with a newly developed mass in the third ventricle (arrowhead) and obstructive hydrocephalus.


Ten days prior, he had presented to a referring hospital’s emergency department for nausea and vomiting and was given 20 mg of intramuscular dicyclomine.

He reported severe pain at the time and site of injection.

Within a few hours, he noticed swelling and purpura overlying the site of injection.Over the next 2 weeks, the swelling persisted and the purpura intensified, becoming black centrally (Figure A and B).

Pain worsened over this period, initially restricting use of the leg, then preventing any weight bearing, prompting his admission to our hospital 10 days after the injection.

He also reported numbness and occasional tingling of the skin involved.

The patient denied fever or chills, and his nausea and vomiting had resolved.A, Teenage boy with development of retiform purpura of the left thigh following intramuscular dicyclomine injection.

At 2 days after injection, red to purple retiform changes developed on the left thigh.

B, Worsening retiform purpura with central necrosis was noted 13 days after the injection.Findings of a physical examination were significant for retiform purpura of the left thigh, approximately 8 × 12 cm in size.

Palpation of the area elicited severe pain.

Popliteal, posterior tibial, dorsalis pedis, and femoral pulses were strong.

There was no swelling of the remainder of the leg, and findings of joint examinations were normal.

Sensation was intact throughout the leg with the exception of the skin involved, which had diminished light touch.Blood test results revealed a normal complete blood cell count, normal coagulation profile, and an elevated creatine phosphokinase level of 477 U/L (normal range, 22-198 U/L; to convert to microkatals per liter, multiply by 0.0167).

Magnetic resonance imaging of the thigh was completed, and a skin biopsy was performed for culture and histology.


She had presented to an outside emergency department 2 days prior with lower abdominal pain that subsequently localized to the right lower quadrant.

Her pain was accompanied by anorexia and nonbloody, nonbilious emesis.

She was noted to have voluntary guarding and focal right lower quadrant tenderness to palpation.

Laboratory analyses demonstrated a mild leukocytosis (white blood cell count = 14 × 103/μL [to convert to ×109/L, multiply by 0.001]) and normal urinalysis results.

Abdominal ultrasonography images were obtained that failed to show her appendix and demonstrated no secondary signs of inflammation.

Computed tomography images of the abdomen and pelvis were obtained, and the representative images are shown in Figure 1.

In our emergency department, pelvic ultrasonography images were obtained that failed to show both the appendix and right adnexal structures.Computed tomographic images.

Because of her notable tenderness, she was admitted for observation at the referring facility.

However, her right lower abdominal pain persisted, prompting further evaluation.

No antibiotics were initiated, and her activity improved with intravenous hydration.

She was transferred to our facility for surgical evaluation.


She had been recently treated at an outpatient facility for a viral illness with multiple episodes of forceful coughing.

There was no recent history of trauma to the neck or chest.Physical examination revealed normal vital signs and soft tissue swelling over the left supraclavicular area.

No overlying skin changes or crepitus were appreciated.

Laboratory data revealed leukocytosis (white blood cell count, 18 000/µL; to convert to ×109 per liter, multiply by 0.001).

A computed tomographic scan demonstrated extensive edema of the left neck, with fat stranding seen in the subcutaneous tissues extending into the left jugular, carotid, and esophageal spaces (Figure, A).

Mediastinal edema and bilateral pleural effusions were also seen on computed tomographic scan (Figure, B).

Owing to the concern for esophageal perforation, a barium swallow was performed, showing no extravasation of contrast.A, Computed tomographic scan shows extensive soft tissue inflammation in the left neck (arrowhead).


Her visual acuity was 20/20 OD and 20/70 OS.

Computed tomography scan results of her head did not reveal any acute intracranial pathology.

Her systemic inflammatory markers were elevated, including a left-shifted leukocytosis with a white blood cell count of 15 200 μL (normal values, 4100-8900 μL) (to convert to × 109/L, multiply by 0.001), a platelet count of 458 × 103 μL (150-450 × 103 μL) (to convert to × 109/L, multiply by 1.0), and a C-reactive protein level of 17.3 mg/L (<8.0 mg/L) (to convert to nanomoles per liter, multiply by 9.524).

Cerebrospinal fluid studies were suggestive of aseptic meningitis: elevated protein levels (0.139 g/dL, 0-0.035 g/dL) (to convert to grams per liter, multiply by 10.0), increased neutrophils (32%, 2% ± 4%), normal opening pressure, and normal glucose levels.On day 2 of her hospitalization, she complained of left-eye blurred vision.

Both eyes had normal pupillary responses, color vision, and intraocular pressures.

The results of an anterior chamber examination were unremarkable in each eye.

The results of a dilated fundus examination of both eyes revealed significant inflammation, including 1+ vitreous cell levels, marked disc edema, intraretinal hemorrhages, and extensive sheathing of the retinal venules (Figure).Bilateral fundus photographs of the right eye (A) and left eye (B) on presentation.


He was initially agitated and admitted to the intensive care unit with hemodynamic instability.

A significant amount of clear fluid was noted to be continually draining from the wound site.

The patient’s medical history at this point was unknown.From an ophthalmic standpoint, a single, deep laceration extended inferomedially from the right upper zygoma across the nasal dorsum and involving the eyelid-cheek junction (Figure 1).

The oral-maxillofacial surgery service was consulted for assessment of the facial lacerations, and the oculoplastic service was consulted for possible damage to the nasolacrimal system.


Her ocular history was notable for a previous uncomplicated cataract surgery in the left eye that had a good visual outcome.

On postoperative day 1, her visual acuity was 20/60 OD, attributed to mild corneal edema, with an intraocular pressure of 18 mm Hg.

At postoperative week 1, the best-corrected visual acuity was 20/50 OD, her intraocular pressure was 17 mm Hg, and there was no afferent pupillary defect.

The cornea was clear and there were trace anterior chamber cells.

A dilated examination revealed multiple spots of retinal whitening with tiny intraretinal hemorrhages concentrated in the posterior pole (Figure, A).

Optical coherence tomography revealed intraretinal cystoid abnormalities in the macula and hyperreflective patches in the nerve fiber layer and inner nuclear layer (Figure, B).A, Fundus photograph of the right eye demonstrating multifocal patches of inner retinal whitening in the posterior pole.

B, Optical coherence tomography through the macula demonstrating mild intraretinal cystoid abnormalities and hyperreflective thickened areas in the nerve fiber and inner nuclear layer, corresponding to the white retinal patches.

A dilated fundus examination was not performed.

The patient was referred urgently for consultation by a retina specialist.


His medical history was pertinent for a dual-chamber pacemaker implant 3 years earlier for intermittent symptomatic second-degree atrioventricular (AV) block.

Additional comorbidities included hypertension and well-controlled type 1 diabetes with no recent changes in his medications.

His pacemaker was programmed to a DDDR (dual-chamber, rate-adaptive) pacing mode with an AV delay of 300 milliseconds and tracking rates from 60 to 110 pulses per minute.

For the past several weeks he had noted generalized weakness and fatigue.

There was no associated loss of consciousness, chest pain, dyspnea, or palpitations.

Initial vital signs showed a systolic blood pressure of 110 mm Hg and results of physical examination demonstrated clear lungs.

Results of cardiovascular examination demonstrated no gallops, murmurs, or rubs.

Results of electrocardiography performed on admission are shown in Figure 1.


The patient had a history of IgGκ multiple myeloma, diagnosed approximately 6 months earlier.

At that time, flow cytometry showed a κ-restricted plasma cell population positive for CD38 and CD138 but negative for CD3, CD20, and CD45 expression.

Cytogenetic analysis with fluorescent in situ hybridization did not reveal high-risk genetic markers.

The patient demonstrated no evidence of end organ disease, and her myeloma was classified as stage II.

Physical examination revealed scattered red-violaceous nodules, with the largest measuring approximately 6.0 × 5.5 × 2.5 cm (Figure, A).

They were found in the mouth, the trunk, and on all 4 extremities.

The lesions were nonulcerated, round with a smooth surface, fixed, and firm and tender to touch.

An ultrasound-guided needle biopsy and immunohistochemical analysis of the largest lesion on the patient’s right shoulder were performed (Figure, B and C).

Since her initial diagnosis, she had completed 4 cycles of lenalidomide, bortezomib, and dexamethasone (RVD) therapy in addition to irradiation for lytic lesions of the thoracic and lumbar spine.


He was taking 20 mg prednisone and 150 mg azathioprine daily.On examination, he was afebrile and had diffuse rhonchi and expiratory wheezes.

A chest computed tomography (CT) scan revealed bilateral nodular infiltrates and a 1.3-cm cavitary nodule in the right upper lobe.

Blood and bronchoalveolar lavage fluid test results are presented in the Table.The patient does not meet criteria for invasive pulmonary aspergillosis.The patient is not at risk for invasive pulmonary aspergillosis and the results reflect colonization.


The boy was otherwise healthy, with an unremarkable medical history and with no history of trauma or exposure to radiation.

The lesion started as a hyperpigmented macule 3 years ago and since then had been gradually increasing in size and developing into a pink nodule.

The lesion was pruritic at times and sometimes bled with minor trauma.

On physical examination, there was a 1-cm well-circumscribed, symmetrical, pinkish, dome-shaped nodule with central erosions on the left cheek (Figure 1).

Hair, nails, and mucosae were of normal appearance, and the remainder of the examination was unremarkable.


Taking 2 to 3 tablets of hydrocodone/acetaminophen daily improved her back pain from 5 to 2 on a 10-point scale.

The patient had not achieved pain control with prior nonopioid pharmacologic pain management, including duloxetine and gabapentin.

Although past cocaine use was a risk factor for opioid misuse, a trial of hydrocodone was initiated, after discussion of risks and benefits, with a plan for careful monitoring.

A urine immunoassay drug screen was ordered to evaluate for medication misuse and illicit use (Table).The patient is not using hydrocodone but is using cocaine.The patient is not using hydrocodone but may be using cocaine.The patient may be using hydrocodone but is using cocaine.The patient may be using both hydrocodone and cocaine.

She reported no recent illicit substance or drug use and stated her last dose of hydrocodone was that day.

The state prescription drug monitoring program showed no other prescribers of controlled substances.


He reported no trauma, surgery, recent prolonged mobility limitation, or family history of thrombosis.

His only medication was aspirin, 81 mg daily.

On examination, his heart rate was 106/min, respiratory rate was 28/min, and swelling of the right calf was noted.

A heparin drip was initiated for suspected pulmonary embolism, which was confirmed with computed tomography pulmonary angiography.

Routine laboratory values were unremarkable.

Two days later, results revealed elevated titers of anticardiolipin and anti–β2 glycoprotein I antibodies and negative lupus anticoagulant screening assays (Table 1).Results should be repeated in 12 weeks to confirm diagnosis of antiphospholipid syndrome.

Warfarin was administered for long-term anticoagulation.

Given the unprovoked thrombotic events at a young age, a hypercoagulable state was suspected, and testing for the antiphospholipid syndrome was performed.


Detailed anamnesis revealed a history of intense diarrhea in prior months.

He complained of substantial, progressive seborrheic hyperplasia and flushing episodes over the past year, accompanied by ocular manifestations that included swelling of his eyelids.

Ophthalmological examination showed features of chronic blepharitis and lagophthalmos.

A biopsy specimen from the skin of the forehead was obtained and analyzed under hematoxylin-eosin staining (Figure, C).

A computed tomography (CT) scan completed the etiological investigation (Figure, D).A, Immunohistochemical analysis of the earlier lung tumor using chromogranin A; panoramic view shows that most of the cells diffusely express chromogranin (original magnification ×20).

C, Forehead skin shows scarce lymphocytic infiltrate close to follicular structure along with sebaceous hyperplasia (hematoxylin-eosin, original magnification ×40).

D, Liver computed tomographic (CT) image showing multiple metastatic hepatic masses.

B, Leonine facies presentation shows phymatous changes, diffuse erythema, pustular lesions, and seborrheic hyperplasia.


The lesions had been present for months and increased gradually.

Skin examination revealed multiple flaccid pustules on scaly, erythematous plaques on her trunk, with an annular and circinate pattern (Figure, A and B).A and B, Clinical presentation showed flaccid pustules on scaly, erythematous plaques on the trunk.

C, Subcorneal acantholysis of keratinocytes (yellow arrowheads) resulting in intraepidermal separation/blistering and an inflammatory infiltrate consisting of neutrophilic granulocytes (black arrowheads) (hematoxylin-eosin staining, original magnification × 100; inset original magnification × 400).

D, Discrete subcorneal intercellular IgA depositions (white arrowheads) (direct immunofluorescence with FITC-labeled antihuman IgA antibodies, original magnification × 400).

Treatment with topical steroids showed no lasting effect.


The tender area was beneath an adhesive bandage placed where she had received DTaP (diphtheria-tetanus-pertussis) and polio vaccinations 3 weeks earlier.

Removing the bandage revealed a tender indurated gray-violet plaque (Figure, A).

Otherwise, she appeared remarkably well, and her vital signs were normal.

White blood cell and neutrophil counts were low at 0.4 K/μL (normal range, 4.86-13.18 K/μL) and 0.18 K/μL (normal range, 1.60-8.29 K/μL), respectively.

Punch biopsy specimens were obtained for histopathologic analysis (Figure, B) and fungal culture (Figure, C).A, Gray-violet plaque on posterior upper arm at site of adhesive portion of bandage.

B, Broad nonseptate hyphae surrounding and infiltrating dermal blood vessels (hematoxylin-eosin; original magnification ×400).

Of note, occasional septae are seen in this specimen, consistent with the characteristic finding that mucormycetes are pauciseptate, rather than aseptate, molds.

C, Nonseptate hyphae with round terminal sporangia and free spores (lactophenol cotton blue mount; original magnification ×400).


History was notable for preterm premature rupture of membranes for 10 days.

The mother was otherwise in good health with normal prenatal care and had no history of sexually transmitted diseases.

During the first few days of life, the neonate had recurrent hypoxic episodes.

Per the primary team, the rash was first noted at 3 days of life.Physical examination demonstrated a small, ill-appearing neonate with multiple, grouped vesicles and punched-out ulcerations on his scalp, axilla, extremities, and scrotum (Figure, A-D).

He also had witnessed respiratory desaturations requiring urgent intubation.

Initial laboratory evaluation demonstrated a normal complete blood cell count and serum chemistry with the exception of a high lymphocyte count (34%, normal level <25% [to convert to proportion of 1.0, multiply by 0.01]) and high aspartate aminotransferase level (117 IU/L, normal level 8-39 IU/L  [to convert to microkatals per liter, multiply by 0.0167]).

A chest radiograph demonstrated increased pulmonary markings bilaterally.Neonate with grouped vesicles on an erythematous base on the scalp and bilateral lower extremities.

He was receiving intravenous antibiotics for suspected sepsis and bacitracin for the topical lesions.

The neonate was born via urgent cesarean delivery owing to breech positioning.


She had no family history of breast or ovarian cancer and no history of drug addiction or hyaluronic acid or free silicone injections in the breast.

She had neither fever nor skin redness but was experiencing fatigue.Initial presentation of the patient.

She denied any trauma to the breast.On physical examination, the patient had a 6-cm hard mass without nipple discharge or retraction and left axillary palpable lymph nodes.

A, Asymmetric mass in the upper quadrant of the left breast.

B, Breast ultrasonogram revealing hypoechogenicity of the breast tissue with periductal small cysts.The patient had stopped breastfeeding 10 months before the emergency department admission, and she had a recent history of pneumonia self-medicated with antibiotics.

Breast ultrasonography revealed diffuse nonspecific hypoechogenicity of the breast tissue with periductal small cysts (Figure 1B).

Mammography revealed asymmetric density and distortion in the left upper quadrants.Multiple 14-gauge ultrasound-guided biopsies in the upper quadrants of the left breast and fine-needle aspiration cytologic testing of an enlarged lymph node revealed granulomatous inflammation with epithelioid histiocytes, lymphocytes, plasma cells, and eosinophils.

Lymph nodes were normal.Blood test results were as follows: hepatitis B surface antigen, hepatitis C antibody, human immunodeficiency virus enzyme-linked immunosorbent assay, and whole-blood interferon γ release assay (QuantiFERON), negative; IgG cytomegalovirus, positive; fibrinogen level, 234 mg/dL (to convert to micromoles per liter, multiply by 0.0294); erythrocyte sedimentation rate, 4 mm/h; leukocyte count, 7660/µL (to convert to ×109/L, multiply by 0.001); no acquired immunosuppression; and no hematologic disorders.


He denied any history of systemic symptoms, pain, urinary symptoms, or abnormal bowel function but described 6 years of decreased appetite.

Contrast-enhanced computed tomography demonstrated an incidental right infrarenal, retroperitoneal mass measuring 9.7 × 7.7 × 9.1 cm (Figure 1A), with dilated tortuous supply from a lumbar artery branch and retroperitoneal lymphadenopathy.

Laboratory evaluation of plasma-free metanephrine levels showed a slight elevation in normetanephrine levels (1.21 nmol/L).

B, Flush aortogram outlining supply to the mass from a hypertrophied lumbar artery (blue arrowhead) and from a branch of the internal iliac artery (red arrowhead).At preoperative embolization, initial aortography identified the predominant lumbar artery branch and also demonstrated supply from a branch of the internal iliac artery (Figure 1B).

These branches were embolized and the mass was devascularized.

Twenty-four hours following embolization, surgical exploration was performed through a periumbilical midline incision.

With no evidence of distant metastasis (peritoneal or liver), the mass was resected with partial resection of the iliopsoas muscle to achieve negative margins in conjunction with aortocaval lymphadenectomy of the enlarged lymph nodes.

Given the dramatic arterial enhancement and hypertrophied perivascular plexus, biopsy was not performed, and preoperative arterial embolization was deemed appropriate to minimize intraoperative blood loss.A, Contrast-enhanced computed tomography scan demonstrating an incidental right infrarenal, retroperitoneal mass measuring 9.7 × 7.7 × 9.1 cm, with dilated tortuous supply from a lumbar artery branch.

The mass was running parallel to the right ureter, which was meticulously dissected, and the right kidney was successfully saved.

There were no complications, and the postoperative course was uneventful.


He denied risk factors for human immunodeficiency virus, and serologic testing results were negative.

He had completed treatment for keratouveitis and reported some residual blurring of his vision in the right eye.

His uncorrected visual acuity was 20/60 OD and 20/40 OS.

Pupillary responses, confrontation visual fields, motility, external examination, and intraocular pressure were normal.

Slitlamp examination revealed superficial keratitis and anterior stromal haze in the right eye but otherwise was normal.

Fundus examination (Figure, A) revealed a poor foveal light reflex with an irregular-shaped area of red discoloration in the fovea and surrounding subtle flecking of the retina in both eyes.

Spectral-domain optical coherence tomography (Figure, B) showed an irregular foveal contour with trace epiretinal membrane formation, with no evidence of foveoschisis or outer retinal changes.

Fundus autofluorescence was normal.A, Color fundus photograph demonstrating pseudohole formation with pigment mottling, right eye.

No other abnormalities were found on ophthalmoscopic examination.

B, Spectral-domain optical coherence tomography revealing distortion of foveal contour without epiretinal membrane formation, right eye.


She denied any history of hypertension, hyperlipidemia, type 2 diabetes, or human immunodeficiency virus exposure but had a 20 pack/year cigarette smoking history.Uncorrected visual acuity was 20/25 OU.

She denied eye pain, transient vision loss, photophobia, or photopsias but reported right-sided jaw pain migrating to include both temples, ears, neck, and left shoulder.

The jaw became more painful and fatigued with chewing, associated with an 3.6-kg weight loss over 3 months.

Automated perimetry revealed a small paracentral relative scotoma in the left eye.

Superficial temporal artery pulses were palpable without tenderness, and anterior segment examination was unremarkable in both eyes.

Fundus examination revealed healthy-appearing optic discs in both eyes and an arc-shaped area of retinal whitening in the nasal macula concentric to the optic disc in the left eye (Figure 1, A).

Optical coherence tomography through the lesion showed localized hyperreflectivity and thickening of the retinal nerve fiber and ganglion cell layers (Figure 1, B).

Fluorescein angiography revealed normal choroidal and retinal arterial perfusion.

Erythrocyte sedimentation rate was 2 mm/h, C-reactive peptide level was 0.49 mg/dL (to convert to nanomoles per liter, multiply by 9.524), and platelet count was 270 ×103/µL (to convert to ×109/L, multiply by 1).A, Fundus photograph shows a normal left optic disc with an adjacent arc-shaped patch of retinal whitening and no other macular pathology.

A mouth guard prescribed by her dentist for temporomandibular joint disease had provided substantial relief over the past 2 months.


She had been receiving care for dry eye syndrome, hyperopia, and presbyopia by another eye care clinician, and on routine examination a circumscribed elevation of her right iris was found.

She did not have any significant medical or family history, and review of symptoms was unremarkable.On examination, corrected distance Snellen acuity was 20/20 OU.

She noted intermittent shooting pain responsive to artificial tears in this eye; otherwise, she was without ophthalmic symptoms.

Intraocular pressures were 12 mm Hg OD and 10 mm Hg OS.

Slitlamp examination revealed a circumscribed elevation of the right iris inferotemporally (Figure, A).

Her iris was uniformly pigmented, and gonioscopy revealed an iridocorneal angle open to scleral spur with a circumscribed area of iris insertion anterior to the Schwalbe line inferotemporally, not deepening on compression.

Her lens was clear, and no iridociliary lesions were appreciated after pupillary dilation.

The optic nerve and fundus appeared normal.

The left eye appeared healthy with a uniformly deep anterior chamber.A, Low-powered slitlamp examination of the right eye showing irregularity of the posterior light reflection inferotemporally, indicating iris elevation.


When he descended to 35 ft during his dive, the patient experienced blurred vision in the right eye and sharp pain in the right temporal area.

At 50 ft of depth, vision in the right eye went completely black.

He ascended back to the surface at an appropriate speed and his vision recovered, but he was left with a mild residual blur.

This was associated with a pain and pressure sensation in the right eye lasting 30 minutes and noticeable bruising on the right upper eyelid.

After this episode, he noticed constant, binocular, diagonal diplopia in all gazes that was worse in upgaze.He was seen in our ophthalmology clinic the next day.

His visual blur had resolved, but double vision persisted.

On examination, visual acuity was 20/20 OU.

There was no relative afferent pupillary defect.

Color vision tested with Ishihara pseudoisochromatic plates was normal.

Confrontation visual fields were full in both eyes.

He had restricted supraduction and proptosis of 2.5 mm in the right eye.

There was ecchymosis of the right upper eyelid.

Results of dilated eye examination were unremarkable.

24-2 Humphrey visual fields were normal in both eyes.

Magnetic resonance angiography of the head showed no vascular abnormalities.

Magnetic resonance imaging of the orbits showed a fusiform heterogeneous peripherally enhancing extraconal mass within the superior orbit on the right, resulting in proptosis with downward displacement of the right globe (Figure).T1-weighted magnetic resonance imaging of orbit with contrast shows a fusiform heterogeneous peripherally enhancing extraconal mass within the superior orbit on the right (arrowhead), resulting in proptosis with downward displacement of the right globe.


At 48 hours after her skin lesions flared up, a change in her rhythm was noted on telemetry: her baseline sinus rhythm with heart rate of 90 beats per minute (bpm) was changed to bradycardia.

In the emergency department, chest radiography showed multifocal airspace consolidations involving both lungs.

Her baseline ECG obtained a day earlier showed normal sinus rhythm with first-degree atrioventricular (AV) block (PR interval of 240 milliseconds).

After 3 days in the intensive care unit, vasopressors were weaned off, and she was extubated.

Steroid and immunosuppressive medication doses were increased, and pulse methylprednisolone was started.

Her bone marrow transplant had been complicated with severe graft-versus-host disease (GVHD) of skin and liver, diagnosed by biopsies 1 month after her transplant.

She was subsequently diagnosed as having methicillin-resistant Staphylococcus aureus pneumonia.

Her hospital course was complicated with diffuse alveolar hemorrhage, possibly from pulmonary GVHD.

Because of respiratory distress, she was admitted to the intensive care unit.

Respiratory failure developed, and the patient was intubated and treated with vasopressors.

On hospital day 5, she was noted to have generalized erythematous skin with mild elevated liver enzyme, suggesting acute flare of chronic GVHD.

A 12-lead electrocardiogram (ECG) is shown in the Figure.

The patient denied symptoms associated with bradycardia.


He also had a medical history significant for obstructive sleep apnea, gastroesophageal reflux disease with Barrett esophagitis, diabetes, and degenerative joint disease.

In addition, he reported a 22.7-kg weight loss.

Findings from his head and neck physical examination were normal except for the laryngeal examination.

Laryngeal endoscopy revealed a large, well-mucosalized mass emanating from the left pyriform sinus, with mass effect on the larynx (Figure, A).

The bilateral true vocal folds (TVFs) were visualized and were normal, but the full range of mobility of the left TVF could not be assessed owing to mass effect.

A computed tomographic scan with contrast of the neck was obtained and revealed a 5 × 6-cm, nonenhancing, well-circumscribed laryngeal mass (Figure, B).

The tumor was originating from the left pyriform sinus and did not appear to be locally invasive.

Given these findings, the patient underwent direct laryngoscopy for transoral carbon dioxide laser–assisted excision without complications.

Microscopic examination of the mass demonstrated polygonal cells with peripherally placed nuclei and eosinophilic cytoplasm containing cross-striations (Figure, C).

Postoperatively, the patient reported improvement in dysphagia, voice quality, sleep, and breathing patterns.A, A large left pyriform sinus mass with mass effect on the larynx.

B, Preoperative computerized tomography scan showing a large laryngeal mass without local invasion.

C, Polygonal cells with peripherally placed nuclei and eosinophilic cytoplasm containing cross-striations (hematoxylin-eosin, original magnification ×40).


The patient had not received any chemotherapy or antimicrobial prophylaxis.

Cellular cytogenetics of his AML were notable for a 5q deletion and p53 mutation.

He had abruptly developed a painful eruption on his scalp, face, and left leg 24 hours prior to presentation after being scratched in these areas by his pet cat.

Physical examination revealed an ill-appearing, diaphoretic, thin man with multiple erythematous to violaceous, tender, edematous, targetoid nodules and plaques with central dusky appearance on the left forearm and right upper thigh (Figure, A).

Vital signs included temperature of 39.7° C, blood pressure of 141/69 mm Hg, and pulse of 122 bpm.

His white blood cell count was 1.8 × 103/µL (reference range, 4.5-11 × 103/µL; to convert to ×109/L, multiply by .001), and absolute neutrophil count was 246 cells/µL (reference range, 1520-6370 cells/µL).

Other laboratory values were remarkable for a red blood cell count of 2.13 × 106/µL (reference range, 3.9-5.5 × 106/µL; to convert to ×1012/L, multiply by 1), hemoglobin of 6.1 g/dL (reference range, 14-17.5 g/dL; to convert to g/L, multiply by 10), and platelet count of 14 × 103/µL (reference range 150-350 × 103/µL, to convert to ×109/L, multiply 1).

A brisk neutrophilic infiltrate was seen on histopathology (Figure, B).A, 1.5 cm-long, edematous plaque with dusky central erythema on upper thigh.

B, Punch biopsy specimen with hematoxylin-eosin staining (original magnification ×40); arrowhead indicates brisk dermal neutrophilic infiltrate.

Punch biopsy specimens from the right arm and left thigh were performed for histopathologic evaluation and tissue culture.


His mood had been controlled with bupropion, 300 mg/d, for the past several years; however, the recent death of his husband led to increased hopelessness, insomnia, and decreased energy.

His total score on the Patient Health Questionnaire 9 (PHQ-9) was 16 (Table 1).The patient has depressive symptoms of at least moderate severity.

Results of laboratory studies (thyroid-stimulating hormone, complete blood cell count, and metabolic profile) were unremarkable.


Her medical history was significant for chronic hepatitis B infection, for which tenofovir was initiated 4 months ago.

She was not taking any other medications.The patient was in no acute distress, and her vital signs were within normal limits.

The eruption had been present for approximately 8 months and consisted of asymptomatic, self-resolving, and continuously appearing macules and papules.

Review of systems was positive only for occasional arthralgias in her knees and ankles.

On physical examination, there were purpuric, erythematous macules coalescing into patches on the upper extremities, abdomen, and lower extremities (Figure).

A skin punch biopsy showed extravasated erythrocytes, a neutrophilic infiltrate, fibrinoid necrosis, and broken-down neutrophils releasing nuclear debris, consistent with leukocytoclastic vasculitis (Figure).

A second skin punch biopsy was performed for direct immunofluorescence, which was negative.

Results of a complete blood cell count and comprehensive metabolic panel were unremarkable.Physical examination of the lower extremities.

She had no oral or genital involvement and no joint effusions or deformities.

Dotted areas indicate areas of the skin that were biopsied.

Inset, Photomicrograph from first skin punch biopsy (hematoxylin-eosin, original magnification ×200).


Review of systems was remarkable for hypohidrosis, photophobia, and a history of recurrent sinopulmonary infections, including pneumonia, requiring hospitalization.

Physical examination revealed normal fingernails and toenails, dermatoglyphics, and dentition.

Additionally, there was no evidence of alopecia or keratoderma.

A punch biopsy specimen was obtained (Figure, C and D).A, Reticulate hyperpigmentation involving the lower and upper distal extremities, including the dorsal surface of the hand.

B, Diffuse reticulate hyperpigmentation of the trunk and flexures, including the posterior neck and axilla.

C, Hematoxlyn-eosin stain (original magnification ×200).

D, Congo red stain (original magnification ×200).

Family history was notable for similarly affected men on the patient’s mother’s side.


She had no significant past medical history and took no medications or supplements.

She denied any history of trauma or prior lesions at these sites and could not pinpoint any exacerbating or alleviating factors.

She denied fever, arthralgias, myalgias, or constitutional symptoms.

A physical examination revealed several 2-mm to 4-mm round, hyperpigmented macules symmetrically distributed over the lower extremities and dorsal feet (Figure, A).

A skin biopsy was performed (Figure, B-D).


She had no notable medical or family history.

The lesions first appeared in her right axilla 6 months prior and were asymptomatic.

The patient also noted a 3-month history of polyuria, polydipsia, and nocturia.

Review of symptoms was otherwise negative.

On physical examination there were no other sites of involvement including mucosal surfaces.

Shave biopsies were obtained from the right (Figure, C) and left axillae (Figure, D) and sent for histopathological examination.A, Clinical images show punctate yellow-brown papules on the upper eyelids and infraorbital rims; B, numerous red-brown papules in the right axilla.

C, Histopathology of a shave biopsy sample from the right axilla (original magnification ×200).

D, Histopathology of a shave biopsy sample taken from the left axilla (original magnification ×200).


Her medical history was significant for atopic dermatitis that was well controlled with topical triamcinolone, 0.1%, cream.

Three weeks prior, she had returned from school with 2 itchy papules on her right hand.

The papules continued to enlarge over the course of the day and progressed to form blisters.

The following day, she noticed similar lesions appearing on her left hand.

On further questioning, she recalled similar itchy papules appearing on her feet without progression to blisters.

Physical examination demonstrated numerous skin-colored tense bullae on her bilateral hands (Figure 1, A).

Xerosis was on the trunk and extremities.

On her dorsal and plantar feet, there were macerated, erosive plaques without vesicles or bullae (Figure 1, B).

Results of herpes simplex virus polymerase chain reaction, bacterial culture, potassium hydroxide preparation, mineral oil preparation, and direct immunofluorescence were negative.A, Bilateral palms with at least 20 tense, white-gold bullae, several with violaceous borders and overlying tapioca-like appearance, present diffusely but concentrated on the palmar surfaces.

B, Bilateral dorsal feet with macerated, erosive plaques.

She was evaluated by her pediatrician, who prescribed oral cefdinir and hydrocortisone, 2.5%, cream, but there was no substantive improvement.


Before this admission, she was healthy, with no previous medical problems.

She denied any change in her bowel habits or having experienced rectal bleeding.

She had a normal appetite and had no history of weight loss.

On examination, her vital signs were within normal limits.

She was mildly tender in the right iliac fossa and there was a large mobile mass, at least 10 cm in diameter, that was easily palpable in the right iliac fossa.

She was initially investigated with a computed tomography (CT) scan of the abdomen (Figure 1).

She underwent a colonoscopy that showed no intraluminal mucosal abnormalities or masses, but evidence of external compression at the cecum was noted.Coronal (A) and transverse (B) computed tomographic images show a large intra-abdominal cystic mass in the right iliac fossa.


Given a history of pancreaticoduodenectomy, the patient underwent computed tomography of the abdomen and pelvis with oral and intravenous contrast for further evaluation (Figure).A, Axial cross-section of patient's computed tomographic scan of his abdomen and pelvis after a Whipple procedure.

He admitted to nausea but no vomiting, fevers, or chills.

He reported having normal bowel movements and passing flatus without difficulty.

On examination, he was afebrile and not tachycardic.

He had a well-healed abdominal midline wound.

His abdomen was soft, not distended, and mildly tender diffusely, worse in the epigastrium, without rebound, guarding, or any palpable masses.

His bloodwork revealed an elevated lipase level of 2842 U/L (to convert to microkatals per liter, multiply by 0.0167) without leukocytosis or any electrolyte abnormalities.

Liver function test results were within normal limits.

The stomach is distended with oral contrast and an air fluid level.

A tubular solid structure can be seen within the body of the stomach.

B, Coronal view demonstrating the tubular solid mass within the distended stomach.


He had a history of chronic lymphocytic leukemia for which he had received allogeneic bone marrow transplantation; his course was complicated by extensive graft-vs-host disease including ocular manifestations.

His graft-vs-host disease was treated with systemic tacrolimus.

He also had a history of herpes simplex keratitis with fungal infection in the right eye that led to corneal perforation requiring penetrating keratoplasty.

His best-corrected visual acuities were 20/125 OD and 20/60 OS.

Slitlamp examination of the right eye revealed eyelid margin hyperemia, penetrating keratoplasty graft in place, a deep and quiet anterior chamber, a normal iris, and posterior chamber intraocular lens.

Examination of the left eye revealed eyelid margin hyperemia, an apparent soft tissue lesion on the palpebral conjunctiva of the left lower eyelid, inferior bulbar conjunctival injection, a small paracentral anterior stromal scar, a deep and quiet anterior chamber, a normal iris, and posterior chamber intraocular lens.

The conjunctival lesion had vascular and papilliform elements (Figure) and had not been noted on a routine examination 6 months prior.Clinical photograph showing a soft-tissue lesion on the palpebral conjunctiva of the left lower eyelid, accompanied by inferior bulbar conjunctival injection.


He denied experiencing decreased vision, pain, redness, photophobia, or recent trauma.

His best-corrected visual acuity was 20/25 OD and 20/30 OS, his intraocular pressures were 12 OD and 13 OS, and his pupils were reactive to light bilaterally without an afferent pupillary defect or anisocoria present.

His extraocular motility demonstrated a mild limitation on elevation and abduction.

His confrontational visual fields were intact.

His color vision was normal and his trigeminal and facial nerve function were intact.

His external examination revealed 4 mm of relative proptosis OS and 2 mm of hypoglobus OS.

His anterior slitlamp examination and dilated fundus examinations yielded unremarkable results.

The remainder of his review of systems was unremarkable.


His medical and surgical history included prostate cancer, status postcryotherapy, osteoarthritis, and migraines.

His social history was significant for active cigarette smoking and immigration from a Middle Eastern country.

His medications included naproxen at 500 mg as needed, tamsulosin at 0.4 mg daily, and aspirin at 81 mg daily.On examination, his best-corrected visual acuities were 20/40 OD and 20/25 OS.

His pupils were reactive, his extraocular motility was full, and the intraocular pressures were 16 mm Hg in both eyes.

He had no systemic symptoms and denied having eye redness, pain, and photophobia.

The results of the external examination and anterior slitlamp examinations were unremarkable, and there was no anterior chamber or anterior vitreous cell or flare.

The dilated fundus photography examination revealed yellow-gray, curvilinear, and puzzle piece–shaped subretinal macular lesions in both eyes (Figure).

The lesions were hyperfluorescent with hypofluorescent borders on fundus autofluorescence testing results (Figure).

Optical coherence tomography revealed that the involved areas exhibited a disruption of the outer retinal layers (including and deep to the outer nuclear layer) along with hyperreflectivity of the outer retina, retinal pigment epithelium, and choroid.

There was no involvement of the inner retina.

The patient underwent laboratory testing for syphilis and tuberculosis, which yielded negative results.Fundus photographs showing yellowish, puzzle piece–shaped, curvilinear lesions in the maculae of the right eye (A) and left eye (B).


His medical and ocular history included only pterygium surgery many years ago.

His social history was significant for multiple male and female sexual partners.On examination, his visual acuity was counting fingers OD and 20/70 OS.

His review of systems was otherwise negative for unusual findings, and he denied any pain, photophobia, or eye redness.

Pupils were reactive, extraocular motility was full, and intraocular pressure was 21 mm Hg OU.

The external and slitlamp examinations were unremarkable except for 1+ anterior vitreous cells in both eyes.

Dilated fundus examination revealed mild optic disc edema and hyperemia along with large, pale-yellowish, placoid lesions within the macula of both eyes (Figure 1).

Optical coherence tomography of both eyes (Figure 1, inset) revealed extensive disruption of the ellipsoid and interdigitation zones.

Contrast-enhanced magnetic resonance imaging and venography of the brain and orbits revealed an empty sella and hypoplasia of the left transverse sinus, without enhancement of the optic nerves.

A lumbar puncture revealed an opening pressure of 1.6 cm of water.Fundus photographs and optical coherence tomography of both eyes.

Examination of the posterior pole of both eyes revealed mild optic disc edema and hyperemia along with large, pale-yellowish, outer retinal lesions within or adjacent to the macula of both eyes.


Her heart rate was 135 beats/min, and her blood pressure was 160/100 mm Hg.

A 12-lead electrocardiogram documented wide complex tachycardia (WCT, Figure 1).


He passed his first kidney stone at age 27 and had 2 additional episodes of spontaneous stone passage.

He had no other significant medical history.

His typical daily consumption included 3 dairy servings, 2 to 3 L of water, 1 to 2 servings of animal protein (meat, poultry, fish, and eggs), and restricted dietary salt.

Family history was significant for nephrolithiasis in his mother.

Physical examination results were unremarkable (body weight, 77 kg).

Laboratory studies revealed normal serum levels of calcium, phosphorus, potassium, bicarbonate, creatinine, and parathyroid hormone.

His only medication was tamulosin (α1a-adrenergic receptor antagonist), which was prescribed as needed for stone passage.

His stone analysis showed 95% calcium oxalate (CaOx) and 5% calcium phosphate.

He reported no diarrhea or consumption of foods with high oxalate content (eg, spinach, beets, nuts, and chocolate).

Twenty-four-hour urine studies are shown in the Table.The patient has hypercalciuria due to distal renal tubular acidosis.The patient has hypercalciuria due to high animal protein intake.The patient has hypercalciuria due to high salt intake.The patient has hypercalciuria due to idiopathic hypercalciuria.


Her medical history included recurrent acute otitis media requiring tympanostomy tube placement.

At the 2-week follow-up, the swelling had largely resolved with a now-firm, slightly mobile, subcentimeter mass palpable in the anterior parotid gland.

Four days later the mass enlarged and became painful.

On physical examination, the left parotid gland was diffusely full and firm, which was consistent with viral parotitis.

A magnetic resonance imaging (MRI) study identified a 1.2 × 1.7 × 1.6-cm solid mass in the anterior parotid gland with well-defined borders and indention into the masseter muscle.

The mass was isointense to muscle on T1, hyperintense on T2, with strong contrast enhancement, heterogeneous internal enhancement and a central focal area of hypointensity (Figure, A).

Microscopically, the tumor was composed of spindle cells with elongated nuclei in a storiform pattern embedded in moderately dense admixed lymphohistiocytic infiltrate with no atypia (Figure, B).

Immunohistochemical analysis (IHC) was positive for activin-like kinase-1 (Alk-1) (Figure, C), vimentin, CD68, and factor XIIIa, and negative for smooth muscle actin (SMA), desmin, cytokeratin, and CD34.A, Postcontrast axial magnetic resonance image (MRI) demonstrating mass (arrowhead) with strong contrast enhancement, heterogeneous internal enhancement with a central focal area of hypointensity.

Gland massage, warm compress, sialagogues, and increased hydration were recommended.

The patient underwent a left superficial parotidectomy.

Grossly the lesion was nonencapsulated, firm, dark colored, and was located within the anterior superficial lobe of the parotid gland.

B and C, Histopathologic images, original magnification ×200.

B, Spindle cells with elongated nuclei in a storiform pattern embedded in moderately dense admixed lymphohistiocytic infiltrate with no atypia.