He denied consuming tobacco or alcohol regularly.

He had type 2 diabetes mellitus for 2 years, which was well controlled with oral hypoglycemic agents.

There was no history of high-risk behavior for human immunodeficiency virus (HIV) acquisition.

The lesion had started as a small painless mass on the right lateral aspect of the tongue, which gradually grew and subsequently ulcerated.

It was asymptomatic except for causing mild difficulty in eating.

On physical examination, there was a single well-defined ulcer measuring 2 × 2 cm on the right lateral aspect of tongue with a clean base and irregular and elevated heaped-up margins (Figure 1A).

There was no underlying induration, friability, or bleeding on manipulation.

B, Biopsy from the ulcer showing a mixed cell infiltrate (hematoxylin-eosin, original magnification ×40).

C, Intracellular yeast forms within the histiocytes  (original magnification ×100).

The patient could not recall any history of trauma or tongue bite preceding the lesion.

A 3-mm punch biopsy from the edge of the ulcer was taken and sent for histopathological examination (Figure 1B and C).A, Tongue ulcer.


His visual acuity was hand motions, and intraocular pressure measurement was deferred in that eye.

Findings from examination of the left eye showed a penetrating injury with a 3-pronged barbed fishhook, with 1 prong lodged in the anterior chamber and another lodged in the lower eyelid (Figure 1).

The status of the crystalline lens was unclear owing to corneal edema.


She had undergone gastric bypass surgery 3 months before presentation, which was complicated by a gastric ulcer and stricture.

Other medical history included hypothyroidism and thyroidectomy for thyroid cancer diagnosed 10 years ago.

Her medication regimen included levothyroxine sodium and occasional bariatric chewable vitamins.

She denied alcohol or tobacco use or drug abuse.

There was a mild abduction deficit in both eyes as well as prominent upbeating nystagmus.

The amplitude of the nystagmus increased in upgaze and dampened with downgaze.

She was unable to read the control plate of the Ishihara test.

Her best-corrected visual acuity was 20/200 OD and 20/400 OS.

Her pupils were equally reactive, with no relative afferent pupillary defect.

Findings from an anterior segment examination were unremarkable.

Findings from a dilated fundus examination revealed disc edema in both eyes with peripapillary nerve fiber layer thickening and large intraretinal hemorrhages (Figure).A and B, Initial presentation of large intraretinal hemorrhages and disc edema in the left and right eye, respectively.

She had lost 34.5 kg since the procedure.


At the time of transfer, the patient was noted to have choking with feeds as well as a large volume of clear oral secretions that required frequent suctioning.

He was transported to a local emergency department.

Following a difficult orotracheal intubation with multiple attempts, the infant was transferred to a pediatric intensive care unit with a presumptive diagnosis of bronchiolitis.

During the next 2 days, he was weaned off mechanical ventilation and received oxygen via the nasal cannula.

He began feeding orally and was transferred to the general inpatient floor.

Based on these clinical findings, oral food and fluids were withheld from the patient and a fluoroscopic video swallowing study (FVSS) was performed (Figure 1 and Video).


She reported a weight loss of 40 kg during the previous 12 months concomitant with depression.

The patient had a history of cardiac arrhythmia, hypertension, and sigmoidectomy for diverticulitis.

Medications included lasilix, amlodipine, amiodarone, and atenolol.On examination, the patient appeared well.

The abdomen was soft without distension.

Her white blood cell count was 11400/μL (to convert to ×109/L, multiply by 0.001), her hemoglobin level was 11.5 g/dL (to convert to g/L, multiply by 10.0), and her platelet count was 233 ×103/μL (to convert to ×109/L, multiply by 1.0).

The C-reaction protein level was elevated to 41 mg/L (to convert to nmol/L, multiply by 9.524).

The results of renal and liver function, coagulation, blood level of electrolytes, total protein, albumin, antigen carcino embryonnaire, carbohydrate antigen 19-9, carbohydrate antigen 125, and β2 microglobulin tests were normal.

The patient had a normal esophagogastroduodenoscopy and colonoscopy.

Ultrasonography revealed a 10 × 8-m mass in the right hypochondrium.

Abdominal computed tomography scan revealed a thickened gallbladder wall infiltrating the liver parenchyma.

Magnetic resonance imaging showed a greatly enlarged gallbladder with a thickened wall without invading adjacent structures, a continuous mucosal line, and a hypoattenuated intramural nodule (Figure 1).


Findings from the prenatal ultrasound, most recently conducted at 33 weeks’ gestation, were normal.

The infant was active and well perfused, with a soft but distended abdomen and right-sided labial swelling.

Her Apgar scores at 1 and 5 minutes were 7 and 9, respectively.

Findings from the remainder of her examination were unremarkable.An abdominal radiograph revealed dilated small-bowel loops (Figure 1A).

Radiography of the upper gastrointestinal tract with water-soluble contrast showed a normal pattern of rotation.

Results of a suction rectal biopsy revealed ganglion cells to be present.

Serial abdominal radiographic images showed retained contrast in the terminal ileum 6 days following the gastrointestinal series (Figure 1B).A, Abdominal radiograph showing distended small-bowel loops with absent gas in the colon and rectum.

The infant’s postnatal course was remarkable for a febrile episode that was presumed to be due to chorioamnionitis in the mother and for which antibiotic treatment was initiated.


He reported no other illnesses and was taking only esomeprazole.

The patient noted chronic, left-sided abdominal pain related to his lymphoma and normal passage of stool and flatus.

He was afebrile and normotensive with a pulse rate of 104/minute.

A large, firm, tender mass located near the umbilicus was palpable in his abdomen, but there was no rigidity or rebound tenderness.

Laboratory studies (Table) showed an elevated lactate level of 6.3 mmol/L (reference range, 0.7-2.2 mmol/L) (56.8 mg/dL; reference range, 6.3-19.8 mg/dL).A computed tomographic scan of the abdomen showed diffuse lymphadenopathy and a large mesenteric mass abutting multiple segments of the small intestine and encasing the mesenteric vasculature.

His tachycardia improved, but blood lactate remained elevated between 4.7-7.2 mmol/L (42.3-64.9 mg/dL).

He received 3 L of intravenous normal saline in the first 24 hours because of concern about volume depletion and sepsis.

Serial abdominal examination results remained unchanged from the initial presentation.The patient has lactic acidosis from hypovolemic shock.The patient has lactic acidosis from mesenteric ischemia.


She has a history of hypertension and gastroesophageal reflux disease but no history of smoking.

Two hours prior to presentation, she choked on her food while at dinner and received repeated attempts at the Heimlich maneuver with successful dislodgement of a piece of ham.

The choking episode lasted for approximately 10 seconds, during which the patient was unable to speak.

On arrival, she was dyspneic and in respiratory distress.

Oxygen saturation was 80% with ambient air and improved to 99% with supplemental oxygen delivered via nasal cannula.

A 12-lead electrocardiogram showed normal sinus rhythm without acute ST or T-wave changes.

Brain natriuretic peptide level was 84 pg/mL.

The patient received a chest radiograph and a computed tomographic scan of the chest (Figure).

Transthoracic echocardiography demonstrated preserved systolic function, with no evidence of valve disease.Top left, Chest radiograph, posteroanterior view.

Top right, Chest radiograph, left lateral view.


During this period, he had been seen by his primary care physician as well as by hematology, dermatology, and cardiology specialists, who had told the patient his lesions were ecchymoses secondary to warfarin anticoagulation.The patient had no history of malignancy or exposure to communicable diseases.

He experienced a 15.8-kg weight loss during the past few months but denied any fevers or night sweats.

Physical examination revealed numerous slightly raised erythematous nodules throughout the neck, torso, and bilateral upper extremities (Figure, left).

Inspection of the oral cavity demonstrated 2 discrete erythematous patches with sharply demarcated borders on the soft palate (Figure, right).

The remainder of the physical examination was unremarkable.

Laboratory results revealed a prothrombin time of 11.6 seconds, an international normalized ratio of 1.0, a hemoglobin level of 12.1 g/dL, and a platelet count of 106 cells ×103/μL; results of a basic chemistry panel with liver function tests were within normal limits.

The skin lesion was biopsied, and results are pending.Left, Erythematous nodules on neck and torso (inset, close view).


Thirty years ago, he had abnormal liver function tests attributed to use of an unknown medication that resolved when the drug was discontinued.

He reports no jaundice, pruritus, or family history of liver disease and takes no medications.

He drinks 1 alcoholic beverage daily (≈100 g/week).

On physical examination, blood pressure was 108/63 mm Hg, pulse rate was 61 beats per minute, and body mass index (calculated as weight in kilograms divided by height in meters squared) was 23.4.

His liver was 7.0 cm by percussion and nontender, sclera were anicteric, there was no stigmata of chronic liver disease, and splenomegaly was absent.

The examination was otherwise unremarkable.

His laboratory values are reported in the Table.


Screening mammography (Figure, B) performed 4 weeks prior revealed a large grouping of left breast subareolar calcifications extending into the skin and nipple.

Follow-up ultrasonography demonstrated no discrete abnormal mass or shadowing but did show multiple echogenic foci consistent with findings on mammography.

An incisional biopsy specimen of the mass was obtained and sent for histopathologic evaluation (Figure, C).A, Firm, irregular, subareolar nodule of left nipple measuring 2 cm in diameter.

C, Biopsy specimen of the subareolar nodule (hematoxylin-eosin, original magnification ×20).


She had 2 older brothers, and the family had no medical history of note.

Physical and mental developments were normal.

Physical examination revealed mild xerosis with superficial skin erosions and erythematous residual macules from previous erosions.

Hair, nails, and mucous membranes were normal.

The mother explained that she often found the child peeling off skin with marked facility.

Symptoms improved in winter and worsened in summer.

Some of the lesions had an unusual linear geographic contour and were predominantly located at areas of friction (Figure, A and B).

Serological markers for celiac disease were negative.

A skin biopsy was performed (Figure, C).A, Clinical photograph of a disease outbreak.

Skin fragility can be seen as superficial erosions distributed predominantly around the trunk, some with geometric shape.

B, Photograph showing localized affectation of the disease.

Erythemato-desquamative well-demarcated plaque with peeling borders on right foot.

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

Remarkable detachment of the entire stratum corneum and mild psoriasiform epidermis hyperplasia with no other significant findings.


She was initially diagnosed with mastitis and received several courses of antibiotics for 2 months without improvement.

Subsequently she presented with back pain, paresthesias, shooting pain in the mandibular region, and diplopia.

A skin biopsy specimen from the breast was obtained (Figure, B).

Laboratory test results highlighted a hemoglobin level of 7.6 g/dL and a platelet count of 80 000/μL.

All of these conditions improved under treatment with oral corticosteroids, but the breast enlargement continued.

(To convert hemoglobin to grams per liter, multiply by 10; to convert platelets to number of cells × 109/L, multiply by 1.0.

)A, Enlargement and induration of both breasts.

B, Histopathologic specimen from the breast (hematoxylin-eosin, original magnification ×40).


At age 3 months, the patient was referred for ophthalmologic examination owing to a flat, hypopigmented lesion in the left temporal iris noted by the patient’s father.

The patient had multiple hypopigmented macules on his scalp, face, neck, back, limbs, and torso (arrowheads).

On examination, the patient fixed and followed with both eyes.

Pupils, motility, and binocular alignment were normal.

Dilated ophthalmoscopic examination revealed a well-demarcated hypopigmented lesion originating from the retinal nerve fiber layer and protruding into the vitreous cavity of the right eye (Figure 1B).

A similar lesion was seen along the left inferotemporal arcade (Figure 1C).

B-scan ultrasonography revealed a 4.0 × 2.9 × 2.2-mm lesion with no calcification, no retinal detachment, and no choroidal involvement (Figure 1D).

Given the suspected iris hamartoma and retinal astrocytic hamartoma, a systemic workup was commenced.A, Dermatologic manifestations.

B, A lesion was discovered in the right eye consistent with a retinal astrocytic hamartoma.

C, A similar smaller lesion was seen in the left eye.

D, B-scan ultrasonography revealed an elevated lesion emanating from the retina with no calcification or choroidal involvement.

Because of the constellation of findings, an initial diagnosis of linear epidermal nevus syndrome was made.

The family history was negative for any dermatologic or genetic diseases.


Best-corrected visual acuity was 20/20 OU.

Results of the pupillary examination, intraocular pressure measurements, motility, and confrontatiol visual field testing were normal in each eye.

Findings on the anterior slitlamp examination demonstrated rare anterior chamber cells and mild nuclear sclerotic cataracts in both eyes.

Results of the dilated fundus examination (Figure 1) demonstrated bilateral vitreous cells that were not dense enough to obscure retinal vessel details, as well as optic disc hyperemia, arterial attenuation, arterial and venous sheathing, hard exudates, and focal areas of retinal thinning.

There was no macular edema in either eye.

Results of a complete blood cell count were normal.Fundus photograph of the patient’s left eye at presentation.


One month prior to presentation, the patient’s mother noticed multiple annular, scaly patches on the patient’s scalp and upper back.

Both of the patient’s brothers developed similar patches.

Two weeks before presentation, the area on the scalp grew in size, becoming a tender nodule with yellow suppurative discharge.Results of the physical examination were notable for a somewhat tired-appearing boy with a 6-cm tender, red nodule on the right frontal scalp (Figure 1).

The nodule had a boggy consistency and thick yellow crust and was draining yellow material.

There was no hair within this area on the scalp.

On the patient’s right upper back was an annular scaly patch; significant posterior auricular and cervical lymphadenopathy was noted bilaterally.View on presentation of a boggy, erythematous nodule with suppurative discharge and loss of hair.


Physical examination findings were significant for mild left flank pain, but there was no costovertebral angle tenderness.

Laboratory results were within normal limits.

Axial imaging demonstrated an exophytic, retroperitoneal mass with solid and cystic components involving the left kidney, posterior abdominal wall, and mesocolon (Figure 1).

The mass measured 20 cm in its greatest dimension.

Findings on colonoscopy and mammography were negative.

Positron emission tomography–computed tomography did not reveal any other abnormality.Coronal computed tomographic image showing a retroperitoneal mass with a cystic component and involvement of adjacent kidney and mesocolon.

Red arrowhead indicates descending colon; blue arrowhead, left kidney invaded by mass; and yellow arrowhead, retroperitoneal mass with cystic component.


Physical examination revealed hepatomegaly and left lower abdominal tenderness.

The night after the procedure, the patient developed generalized peritonitis, and computed tomography revealed abundant free air (Figure 1B).A, Colonoscopic stent placement.

She had normal liver function test results and a carcinoembryonic antigen level of 23.8 ng/mL (to convert to micrograms per liter, multiply by 1).

Computed tomography of the abdomen and pelvis revealed a 9-cm, obstructed sigmoid colon mass with fistulous extensions to the bladder and small bowel and numerous metastases to the liver, peritoneum, and omentum.

The patient was referred to a gastroenterologist for stent placement (Figure 1A).

B, Computed tomogram depicting perforation.The patient went to the operating room for an emergency laparotomy.

Pathologic analysis of an endoscopic biopsy specimen revealed a moderately differentiated colon adenocarcinoma.


On day 3 of hospitalization, the dermatology service was consulted.The patient had a history of mild psoriasis, which significantly worsened 1 year prior to presentation, necessitating treatment with systemic agents and ultimately leading to a diagnosis of human immunodeficiency virus (HIV) infection.

Linear excoriations were noted diffusely.

Physical examination was remarkable for severe cachexia and diffuse plaques of thick, tan scale (Figure 1).

Hyperkeratotic areas were verrucous and fissured over bony prominences, including the elbows, knees, ribs, and clavicles.

Unroofed crust revealed a smooth, red, moist undersurface.Left, Diffuse plaques of thick, tan scale.

Dolutegravir and emtricitabine/tenofovir were continued, and diphenhydramine was prescribed for pruritus.


He was found to be tachycardic, hypotensive, in severe respiratory distress, and oliguric, and he had peripheral cyanosis and a lactate level of 3.1 mmol/L (reference range, 0.6-1.7 mmol/L) (27.9 mg/dL; reference range, 5.0-15 mg/dL).

The following morning, his central venous pressure was 13, stroke volume variation was 7%, and lactate was 3.0 mmol/L (27.0 mg/dL).

Mean arterial pressure of 60 to 65 mm Hg was achieved but lactate continued to increase to 4.2 mmol/L (37.8 mg/dL).The patient has epinephrine-induced β2-adrenergic stimulation driving his hyperlactatemia.The patient likely has sepsis, possibly with an uncontrolled infectious source, that requires further workup.The patient has decreased lactate clearance due to liver dysfunction and complicated by Ringer lactate solution.The patient is hypoperfused and requires further fluid and pressor resuscitation.

He was intubated, given empirical antibiotics for suspected community-acquired pneumonia, resuscitated with 3 L of Ringer lactate solution, and admitted to the intensive care unit.

However, blood pressure declined progressively through the night despite further fluid resuscitation and the addition of vasopressors (norepinephrine, vasopressin, and epinephrine) and hydrocortisone.


He has a history of pancreatitis several years prior, recent repair of a tibial fracture, ankle osteoarthritis, cholelithiasis, seizure disorder, and bipolar disorder.

He has a family history of type 2 diabetes in his father and brother.

His current medications include phenobarbital, levetiracetam, quetiapine, lorazepam, fluoxetine, tramadol, aspirin, celecoxib, and gabapentin, none of which were started in the past few months.

The rash is nonpruritic but is associated with burning pain.

Skin examination reveals hundreds of bright pink papules with central yellow hue distributed symmetrically over his dorsal hands, elbows, shoulders, and thighs (Figure 1).

The remainder of the examination is unremarkable.Left, Erythematous pink-and-yellow papules on the wrists.

The patient has had no fevers, shortness of breath, recent viral syndromes, or recent travel.


For the past 6 months, she noted when lying on her left side an inability to hear the television or her baby crying.

She also noted right-sided aural fullness and occasional right-sided headache.

Otoscopic examination results were normal.

A 512-Hz tuning fork examination showed a left-sided lateralization when the vibrating tuning fork was placed on the center of her forehead (Weber test) and bilateral air greater than bone conduction with the vibrating tuning fork placed in front of her ear canal vs her mastoid tip (Rinne test).

Facial motor and sensory function were intact and symmetric.

The rest of the head and neck examination was unremarkable.

An audiogram was ordered (Figure).This audiogram depicts sensorineural hearing loss (SNHL) consistent with early Meniere disease.This audiogram depicts a right-sided SNHL and impaired speech discrimination, which necessitate further investigation.This audiogram depicts a right-sided conductive hearing loss (CHL) with a notch at 2000 Hz, consistent with otosclerosis.


He also complained of multiple tender red lesions on his bilateral ankles and legs that appeared 2 days prior to admission.

Findings from a review of systems were negative for cough, sore throat, history of hepatitis, tuberculosis, sarcoidosis, inflammatory bowel disease, or sulfonamide use.Physical examination revealed several ill-defined, exquisitely tender erythematous subcutaneous nodules on his bilateral shins, medial feet, ankles, and right lower thigh without overlying ulceration, necrosis, or drainage (Figure, A and B).

A punch biopsy was performed, demonstrating pathognomonic histopathologic findings (Figure, C and D).


His medical history included severe peripheral arterial disease and a remote history of ruptured abdominal aortic aneurysm.

Physical examination of the left flank showed a well-defined 5 × 12-cm purpuric patch with a darker stellate patch within it (Figure, A).

Two punch biopsy specimens were obtained (Figure, B and C).A, Photograph of a purpuric patch on the left flank.

B, Biopsy specimen 1 (hematoxylin-eosin, original magnification ×40) showing needle-shaped clefts within the lumen of a blood vessel with minimal perivascular inflammation.

C, Biopsy specimen 2 (hematoxylin-eosin, original magnification ×40).

Eccrine ducts show cellular dyshesion and necrosis.

Three months before presentation, he underwent percutaneous endovascular stenting of a left popliteal artery aneurysm.


His medical history was notable for diabetes mellitus and hypertension, which was well controlled with a stable regimen of lisinopril and atenolol for several years.

He denied using any new medications or supplements or making recent dose adjustments in existing medications.

There was no history of a prior bullous eruption.

Physical examination revealed numerous small intact bullae and large erosions on the lateral feet, soles, and toes (Figure, A).

He denied having pruritus or spontaneous bleeding but reported discomfort from the pressure of intact bullae.

The extent of the bullae led to difficulty with ambulation.

There were also intact vesicles on the lateral palms along with erosions demonstrating evidence of previous bullae formation.

There were no vesicular or bullous lesions on the trunk, arms, legs, or mucosal surfaces.

Hematoxylin-eosin staining of a biopsy specimen obtained from a bulla on the foot was performed (Figure, B).A, Numerous small bullae in various stages of healing and large erosions on the feet with areas of denuded pink dermis on clinical presentation.

B, Biopsy specimen obtained from a bulla on the foot (hematoxylin-eosin, original magnification ×600).


He was previously diagnosed with conjunctivitis and treated empirically with artificial tears, ofloxacin drops (0.3%), and prednisolone acetate drops (1%) 4 times a day, without improvement.His visual acuity was 20/20 OD.

In addition, the patient had a right-sided intranasal mass.A, Slitlamp photograph of the patient’s right eye at presentation.

Examination findings of the anterior segment of the right eye revealed a raised, nonmobile, engorged perilimbal nodule in the inferotemporal sclera that was tender to palpation and did not blanch with phenylephrine drops (2.5%) (Figure, A).

The ultrasonogram demonstrated a noncystic, regular, dome-shaped lesion with medium to high reflectivity localized to the sclera without intraocular involvement (Figure, B).

The remaining results of the right-eye examination and the entire left-eye examination were within the reference range.

B, Anterior segment ultrasonography of the right eye at presentation.Laboratory test results demonstrated elevated inflammatory markers, with an erythrocyte sedimentation rate of 38 mm/h (reference range, 0-20 mm/h) and a C-reactive protein level of 190 mg/L (reference range, 0.08-3.1 mg/L) (to convert to nanomoles per liter, multiply by 9.524).

Results of serum antineutrophil cytoplasmic antibody (ANCA), rheumatoid factor, antinuclear antibody, angiotensin-converting enzyme, fluorescent treponemal antibody absorption, rapid plasma reagin, and tuberculosis skin testing were within their reference ranges.

Results of urine microscopy had 4+ red blood cells per high-power field.

His blood urea nitrogen and creatinine levels were within their reference ranges.


The patient’s history was negative for travel, recent vaccinations, or systemic illnesses.

The patient reported exposure to cats at home but had no recollection of direct trauma.

He denied having fever, nausea, headache, or other influenzalike symptoms.A, Unilateral isolated disc edema at initial presentation.

His best-corrected visual acuity was 20/20 OD and 20/200 OS.

Findings on pupillary, motility, and slitlamp examination of the anterior segment were unremarkable.

Findings on dilated fundus examination of the right eye were normal.

Figure 1A depicts the fundus findings in the left eye.

B, Development of macular edema with exudates 1 week after initial presentation.Findings on magnetic resonance imaging of the brain and orbits showed subtle enhancement of the left optic nerve.

No masses or demyelinating lesions were found.One week later, he presented to the ophthalmology office.

His best-corrected visual acuity had improved to 20/40 OS.

His examination was notable for the fundus finding shown in Figure 1B.


He had normal growth and development and no illnesses or fevers prior to presentation.

He had no contact with sick persons or with household members with similar skin lesions, and there was no history of recent sun exposure.

There was no family history of autoimmune disease, and the mother denied symptoms of dry eyes, dry mouth, cavities, or photosensitivity.A physical examination revealed a well-appearing afebrile male neonate with 5 annular plaques located on the frontal and posterior scalp.

The plaques emerged on day 17 of life and did not change in appearance or increase in number.

The thin red border had fine scaling and several pinpoint pustules.

In addition, there were faintly pink patches with scaling on the medial eyebrows and mesolabial folds.

There was no cervical or postauricular lymphadenopathy.


She was a current smoker and was taking aspirin and statin medication at the time of presentation.

Her most recent presentation was 1 week prior for a minor stroke with amaurosis fugax, slurred speech, right-sided weakness, and facial droop lasting longer than 24 hours.

Magnetic resonance imaging of the brain demonstrated subacute infarctions involving the left frontal and parietal hemispheres.

Workup at another facility prior to transfer included computed tomographic angiography of the neck, which showed chronic occlusion of the right ICA and 95% stenosis of the left ICA.On examination, the patient was afebrile with a heart rate of 69 beats/min and blood pressure of 134/69 mm Hg.

Pertinent findings included no carotid bruit, a regular cardiac rhythm, and equally palpable upper extremity pulses bilaterally.

The patient was neurologically intact, save for 4/5 motor strength in her right upper extremity.

Computed tomographic angiography of the head and neck was performed (Figure 1).Sagittal view demonstrates the left internal carotid stenosis (A indicates anterior; P, posterior) (A) and the distal extent of the findings (arrowhead) (B).


She underwent total thyroidectomy 15 years earlier for papillary thyroid cancer and is taking levothyroxine suppression therapy without evidence of recurrence.

She has well-controlled hypertension and hyperlipidemia.

Her other medications include losartan, atorvastatin, and ezetimibe.

She has no history of low trauma fractures (occurring from falls at standing height or less) or nephrolithiasis.

She has no family history of hypercalcemia.

Serum calcium levels before her thyroidectomy were normal.

Physical examination demonstrated no palpable thyroid tissue.

Her laboratory values are reported in the Table.The patient has hypercalcemia from thyroid suppression therapy.


He did report a history of injection drug use, opioid drug snorting, and tobacco abuse.

He also reported working as a gardener and having 2 dogs as pets.

He originally developed a pustule inside the nares, which gradually spread to involve the nose (Figure 1A).

The patient reported no fever, chills, headache, diplopia, cough, dyspnea, or hemoptysis.

Physical examination revealed an erythematous and deformed nose with small pustules and a perforated nasal septum.

A complete blood cell count showed a white blood cell count of 19 000 cells/µL; a chemistry panel showed a serum creatinine level of 1.7 mg/dL (150.3 μmol/L) and mildly elevated liver enzyme levels.

Results of a human immunodeficiency virus screening test were negative.

A computed tomography scan of the head, facial sinuses, and chest showed soft tissue swelling of the nose and several large cavitary lesions in the lungs (all lobes), with multiple bilateral nodular opacities (Figure 1B), but no intracranial lesions.A, Patient with pustulonodular lesion on nose and a Penrose drain.


His medical history was unremarkable and he was not taking regular medications.

The lesions appeared approximately 8 hours after taking two 25-mg doses of diclofenac, which was prescribed for low back pain.

He initially noticed itching over both hands and feet, followed by a burning sensation and the subsequent development of generalized purplish lesions.

He reported history of a similar though less severe eruption 4 months earlier at similar sites following diclofenac ingestion.

A clinical examination revealed multiple well-circumscribed, round to oval, purplish patches, erosions, and blisters on his trunk and feet (Figure).

Crusting over the lips and dusky red erosions and plaques on the penis, scrotum, and lower limbs were also noted (Figure).


The patient used standard finger sticks to test his blood glucose levels daily.

However, he had pricked his fingers for decades without incident.

The lesions were persistent, asymptomatic, and without aggravating or alleviating factors.

A review of symptoms was positive only for intermittent bloating and diarrhea.

Physical examination revealed multiple petechiae in a linear arrangement extending from the volar and lateral aspects of the fingers to the finger pads (Figure, A).

Results from initial laboratory tests, including a complete blood cell count, comprehensive metabolic panel, antinuclear antibody, erythrocyte sedimentation rate, rheumatoid factor, and cardiolipin antibody, were unremarkable.

Results from a urinalysis and transthoracic echocardiogram were also unremarkable.

Punch biopsies for histopathologic examination (Figure, B) and direct immunofluorescence (Figure, C) were performed.A, Petechial eruption on the fingers.

B, Histopathologic image showing subtle collections of neutrophils within the dermal papillae (hematoxylin-eosin, original magnification ×200).

C, Direct Immunofluorescence revealing granular IgA deposition within the dermal papillae and at the dermoepidermal junction (original magnification ×400).


He also reported easy bruising with minor trauma.

Physical examination showed trachyonychia (rough accentuated linear ridges) on 8 fingernails (Figure, A), thin and brittle toenails, diffuse nonscarring alopecia, and multiple purpuric patches on the forehead, scalp, chest, and arms.

He had substantial laxity of the skin on finger pads (Figure, A), and both sides of the gluteal cleft revealed soft, nontender, rugated, skin-colored linear kissing plaques with no vesicles, bullae, ulcers, or erosions present.A, Nail and cutaneous findings including trachyonychia of the fingernails and cutaneous laxity of the fingerpads.

B, Histopathologic specimen of the nail bed showing orange, amorphous and extracellular material deposited in the subungual dermis of the nail bed (Congo red special stain, original magnification ×10).

C, Same specimen under polarized light microscopy revealed intense apple-green birefringence of the amorphous material in the subungual dermis (lower half of the photomicrograph) (Congo red special stain, polarized light microscopy, original magnification ×10).


On arrival to the emergency department, the patient was intubated and resuscitated.

He underwent emergent chest, bilateral upper and lower extremity escharotomies, and a decompressive laparotomy for abdominal compartment syndrome.

Once the patient was hemodynamically stable he was taken to the operating room and underwent 4 operations for debridement and grafting, with the initial operation taking place 10 days after admission.

All were successfully treated with antibiotics.A, Newly excised burn wound with stitches at the amputation site and a large white nodule.

B, Close-up view of a burn wound newly excised to the subcutaneous tissue with black, plaque-shaped growth.

C and D, Histopathologic images, original magnification ×50.


On external examination, a pink, fleshy, pedunculated lesion with telangiectatic vessels on the surface was seen over the left caruncle (Figure 1).

Her best-corrected visual acuity was 20/20 OU.

Her ocular motility was intact in both eyes.


The patient wears spectacles for myopia but has no other ocular history and denies a history of trauma.

Her medical history is unremarkable, and her review of systems was negative, except for occasional back pain for which she takes tramadol hydrochloride orally.

The patient noticed the lesion when looking in a mirror 3 years prior to presentation.

The patient has had no visual changes or other symptoms but thinks the lesion may have grown slightly since first detected.

On examination, her corrected acuity was 20/20 OD and 20/25+ OS.

The results of pupil, motility, and confrontational visual field examinations were normal.

The intraocular pressure was 17 mm Hg OD and 18 mm Hg OS.

The patient’s manifest refraction was −14.50 + 2.50 × 089 diopters OD and −16.00 + 4.00 × 077 diopters OS.

The results of an anterior segment examination are that both the right eye and the left eye, except for the lesion identified (Figure 1), are normal.


She reported a pruritic, painful rash on her hands and feet and multiple painful joints.Animal exposures included 3 new puppies and rodent infestation in the home and neighborhood cats.

She did not report recent travel or arthropod bites.On examination, her right elbow and left knee were swollen and warm.

She reported pain with passive movement of the right shoulder and left wrist.

Petechial and pustular lesions were present on both hands and palms (Figure, A).

Her feet, including the soles, had many petechial lesions and a few purpuric lesions (Figure, B).A, Numerous scattered erythematous papules and petechiae with a few pustules on the palm and fingers of the left hand.

B, Many petechiae on the dorsum of the feet.Results of laboratory testing were significant for a white blood cell count of 5050/μL (to convert to ×109/L, multiply by 0.001) and a platelet count of 55×103 (to convert to ×109/L, multiply by 1).

Results of urinalysis and comprehensive metabolic panel were unremarkable .


She also lost more than 30 kg of weight during this period.

Physical examination revealed acute cachexia with conjunctival pallor and an immobile nontender mass in the left upper abdomen.

Her laboratory test results revealed a microcytic anemia and hypoalbuminemia.

The patient was scheduled for exploratory laparotomy and resection.A large central necrotic mass is shown in this computed tomography image of the abdomen.

Abdominal computed tomography was performed (Figure 1).


He had a long-standing history of gastroesophageal reflux disease that was only partially controlled with proton pump inhibitor therapy.

The symptoms were exacerbated by cessation of proton pump inhibitor medication, and he reported an associated 9-kg weight loss.

Results of laboratory testing were significant for iron deficiency anemia (hematocrit, 31% [to convert to proportion of 1.0, multiply by 0.01]) and hemeoccult-positive stool.

Upper and lower endoscopy, computed tomography enterography, PillCam capsule endoscopy, and a Meckel scan failed to identify a source of GI bleeding.

The patient received a retrograde double-balloon enteroscopy that showed an outpouching in the distal ileum (Figure, A) with an accompanying ulceration of the adjacent mucosa (Figure, B).

Exploratory laparotomy with small-bowel resection was performed, and the gross specimen is shown in Figure, C.A, Outpouching of the distal ileum.

B, Ulceration adjacent to the outpouching of the distal ileum.

C, Resected distal ileum revealing an ulceration of the mucosa.


She did not report any previous abdominal surgery.

The colicky pain did not migrate during that period and occurred in paroxysms at 9- to 10-minute intervals.

The patient was afebrile and had no nausea or vomiting.

Physical examination revealed mild tachycardia (96/min) and moderate abdominal distension without signs of peritonism; the bowel sounds were hyperactive.

Careful examination ruled out incarcerated hernias in the groin, femoral triangle, and obturator foramen.

Blood analysis results showed mild leukocytosis (total white blood cell count, 10.5 × 103/μL [to convert to ×109 per liter, multiply by 0.001]) without elevation of the C-reactive protein level (<3 mg/L [to convert to nanomoles per liter, multiply by 9.524]).

Serum electrolyte levels were within the normal range.

Computed tomography of the abdomen was conducted (Figure).Computed tomographic images of the abdomen.


She had evidence of bilateral carpal tunnel syndrome (positive Phalen test and Tinel sign bilaterally) and reduced deep tendon reflexes in the upper and lower extremities bilaterally.

On physical examination, she had no pallor, lymphadenopathy, or organomegaly.

Laboratory test results for complete blood cell count, serum calcium, serum creatinine, blood glucose, serum thyroid-stimulating hormone, and serum B12 were within normal limits.

Because of unexplained neuropathy, a workup to detect an underlying monoclonal gammopathy was done, including serum protein electrophoresis, immunofixation, and free light chain assay (see Table).The patient most likely has monoclonal gammopathy of undetermined significance (MGUS).This patient most likely has light chain monoclonal gammopathy.


During the prior 5 months, she experienced mild diarrhea, which was ultimately diagnosed as Crohn disease by colonoscopy with biopsy.Skin lesion progression and histopathological changes (hematoxylin-eosin, original magnification ×200).Physical examination reveals a pale, febrile patient with left leg edema and a rounded, swollen, and tender 10 × 10-cm ulceration on her left medial malleolus.

The lesion began as 2 sesame seed–sized violaceous, papulovesicular rashes with an erythematous halo on her left medial malleolus 12 days prior to presentation.

Within 1 week, more papulovesicles appeared, merged, and ulcerated spontaneously (Figure, A and B).

The ulceration expanded outwardly at a rapid pace, with increasing pain and a hemorrhagic exudative discharge (Figure, C [left panel]).

The ulceration has a raised rugged surface with thick hemorrhagic exudates and a surrounding violaceous-greyish necrotic border (Figure, C [left panel]).Laboratory tests show moderate anemia, hypoalbuminemia, and fecal occult blood.

Histopathology of skin lesions shows dermal edema with dense infiltration of neutrophils and vascular fibrinoid necrosis (Figure, C [right panel]).

Results of acid-fast staining, periodic acid–Schiff staining, bacterial and mycological cultures of skin biopsy specimens, and blood cultures are negative.

The lesion did not respond to treatment with systemic antibiotics, including vancomycin and meropenem.


She reported nonadherence to blood pressure medications.

She described the pain as “someone sitting on her chest” and reported associated diaphoresis and shortness of breath.

On physical examination, the heart rate was 99 beats per minute and blood pressure was 247/130 mm Hg.

An electrocardiogram showed sinus rhythm with left ventricular hypertrophy (LVH) and inferior T-wave inversion.

Laboratory values are shown in Table 1.An echocardiogram showed moderate LVH with preserved left ventricular systolic function and no segmental wall motion abnormalities.

The following day she underwent coronary angiography, which revealed only mild nonobstructive coronary artery disease with a 20% stenosis of the proximal left circumflex coronary artery.Chronic elevation in cardiac troponin T (cTnT) due to left ventricular hypertrophy.Type I non–ST-segment elevation myocardial infarction (MI) due to atherosclerotic plaque rupture.Type II non–ST-elevation MI related to acute increase in myocardial oxygen demand.


He was divorced 10 years previously and has since had multiple sexual partners.

His dysuria resolved and he now feels well.

His examination is normal, including the genitalia and skin.

Screening for other sexually transmitted infections reveals hepatitis B virus serologies consistent with previous immunization, a negative human immunodeficiency virus (HIV) enzyme immunoassay (EIA), and reactive syphilis test results (Table 1).The patient does not recall prior syphilis diagnosis or treatment.

He was diagnosed with gonococcal urethritis and treated with intramuscular ceftriaxone and oral azithromycin.

The local health department has no record of syphilis testing for him.The patient has latent syphilis and requires 2.4 million U intramuscularly of benzathine penicillin G weekly for 3 doses (total 7.2 million U penicillin).The patient has low titers representing the serofast state and does not require treatment.The patient has falsely elevated titers and should undergo repeat testing.The patient needs a lumbar puncture to assess for asymptomatic neurosyphilis.


She reports no new medications, foods, or oral hygiene products.

She has a history of hypertension, hypothyroidism, type 2 diabetes, gastroesophageal reflux disease, and seasonal allergies.

Her medications are valsartan-hydrochlorothiazide, levothyroxine sodium, metformin, insulin, and loratadine.

The lesions cause pain and difficulty brushing her teeth.

Intraoral examination shows generalized erythema and sloughing of the maxillary and mandibular gingiva, without evidence of dental plaque, calculus, or both, and white striae (Wickham striae) affecting the gingiva and mucosa (Figure 1).

She reports no involvement of other cutaneous or mucosal surfaces and no family history of oral lesions.


Her medical history was significant for hypothyroidism, seizures, and functional heart murmur.

Medications included levothyroxine sodium, mometasone furoate, levocetirizine, and benzonatate.

She reported that at the time of initial onset, multiple painful ulcers had appeared on the anterior maxillary gingiva.

She stated that the lesions had resolved spontaneously without treatment but recurred 8 years later as swelling and ulceration of the maxillary and mandibular gingiva.

She denied involvement of cutaneous surfaces and reported a history of ligneous conjunctivitis since childhood (Figure, A).

Review of systems was significant for easy bruising and prolonged bleeding.

Intraoral examination revealed generalized mild edema with rolled margins of the maxillary and mandibular gingiva accompanied by nodular ulceration of the left maxillary gingiva (Figure, B).

Biopsy specimens were obtained from the gingival ulcer (Figure, C and D) and buccal mucosa for routine histological and direct immunofluorescence analysis, respectively.

Also obtained were a complete blood cell count with differential and comprehensive metabolic panel; no abnormal findings were identified.A, Pseudomembranous masses affecting conjunctival mucosa of the left eye consistent with ligneous conjunctivitis.

B, Edema with rolled margins and nodular ulceration of the left maxillary gingiva.

C and D, Punch biopsy specimen from the maxillary gingiva showing aggregates of relatively amorphous, eosinophilic material beneath the epithelium and around blood vessels (C, hematoxylin-eosin, original magnification ×100; D, hematoxylin-eosin, original magnification ×200).


The mother, initially unavailable for examination because she remained at the facility where she had given birth, reported via telephone that she was healthy except for a urinary tract infection for which she had taken a 7-day course of nitrofurantoin monohydrate approximately 3 to 4 weeks before delivery.

She denied a history of herpesvirus infection, blistering disorder, or autoimmune disease.

On physical examination, the neonate exhibited extensive erosions rimmed by purulent vesicles involving the groin, neck, scalp, fingers, and left side of the upper chest (Figure, A and B).

Biopsy specimens were obtained, with results as shown in the Figure, C and D.A, Erosions rimmed with flaccid turbid vesicles involving the groin, thighs, and abdomen.

B, Large erosion with a rim of flaccid purulent vesicles and crusting on the left side of the chest.

C, Histopathologic analysis of truncal skin sample demonstrating suprabasilar acantholysis with an eosinophil-rich infiltrate (hematoxylin-eosin, original magnification ×40).

D, Direct immunofluorescence of perilesional skin from the right side of the chest demonstrates IgG in an intracellular “chicken wire” pattern involving the lower spinous layer (original magnification ×40).


The patient was not taking any medications at the time and denied any recent international travel.Physical examination revealed multiple annular plaques with raised erythematous-violaceous borders on the face, distributed mainly along the forehead and temporal region (Figure, A).

The eruption began on his upper back, at which time he felt well.

After returning from his trip, he noted that the eruption had become more prominent on his back and had spread to his face.

In addition, he began to have a febrile illness with joint pain and swollen nodes, which subsequently resolved without treatment.

The lesions continued to rapidly enlarge without scaling, and his plaques were not associated with itching or pain.

There were similar coalescing lesions found on back (Figure, B).

No other mucocutaneous findings were noted, and the rest of examination was unremarkable.

A punch biopsy specimen was obtained from a plaque on the right upper back and submitted for pathologic review (Figure, C and D).A, Multiple annular plaques with raised erythematous-violaceous borders are distributed mainly along the frontal and temporal region of the head.

B, Similar findings are seen on the patient’s face with more central clearing and attenuated coloring.

C, This pathologic specimen from a lesion on the upper back depicts distended sebaceous lobules with associated follicular dilatation and a mild chronic perivascular and perifollicular lymphomononuclear infiltrate.

D, This pathologic specimen from the upper back exhibits sebaceous lobules with sebocyte necrosis and an associated neutrophilic infiltrate that also includes scattered lymphomononuclear cells.

He then received significant sun exposure while on a 7-day trip to Miami, Florida.


He had undergone numerous chemotherapeutic regimens over the past 3 years, all of which had failed.

He acknowledged a mild, untreated seasonal rhinitis but otherwise had enjoyed good health prior to his cancer diagnosis.

He denied the use of heating pads but admitted to sitting on the hearth, directly in front of his fireplace, for long periods because of the cold weather and chills presumably from his underlying malignant neoplasm.

Physical examination revealed a large, reticulated, erythematous plaque with micaceous and silvery scale localized to the mid-back (Figure, A).

A punch biopsy was performed (Figure, B-D).A, Large, reticulated, erythematous plaque with silvery scale localized to the mid-back.

B, Mild hyperkeratosis overlying an epidermis with dysmaturation and apoptotic cells, increased small blood vessels, pigment incontinence, and perivascular inflammation with lymphocytes and eosinophils (hematoxylin-eosin, original magnification ×20).

C, Keratinocyte dysmaturation demonstrated by large keratinocytes with hyperchromatic nuclei and prominent nucleoli, and increased mitoses with starburst cells (arrowheads) (hematoxylin-eosin, original magnification ×60).

D, Squamous metaplasia and apoptosis of the eccrine ducts (hematoxylin-eosin, original magnification ×60).

For the past 4 months he had been receiving oral etoposide (daily for the first 3 weeks of each 4-week cycle), daily pancrelipase, and monthly octreotide acetate intramuscular injections.


Ocular history included penetrating keratoplasty with intraocular lens exchange and Descemet stripping automated endothelial keratoplasty in the right eye.

He described it as a central “band” of absent vision just below center.

On examination, visual acuity measured 20/40 OD and 20/60 OS, improving to 20/40 with pinhole.

A complete blood cell count, results of a comprehensive metabolic panel, erythrocyte sedimentation rate, C-reactive protein level, and computed tomography of the head without contrast were all normal.

Four days later in the Retina Clinic, visual acuity was unchanged.

Slitlamp examination of the anterior segment was normal.

Ophthalmoscopy revealed no vitreous cells, a posterior vitreous separation, cup-disc ratio of 0.3, normal retinal vessels, and a superior parafoveal crescent of translucent retina without associated edema or hemorrhage.

Fundus autofluorescence and fluorescein angiogram showed abnormalities in the superior macula (Figure 1).A, Fundus autofluorescence shows a superior parafoveal and perifoveal dark crescent at presentation, corresponding to the hypofluorescent region in part B.


Ophthalmology was consulted urgently in the recovery room because of complaints of vision loss and ophthalmoplegia in the right eye.

On examination, visual acuity was no light perception (NLP) OD and 20/20 OS.

Pupils were equal and round, with a 3+ relative afferent pupillary defect in the right eye.

Intraocular pressure was within normal limits in both eyes.

There was complete ophthalmoplegia in the right eye with no signs of restriction on forced ductions and normal motility in the left eye.

Visual field was full to confrontation in the left eye.

The right eye also demonstrated mild fullness of the orbit, right cheek skin erythema, trace proptosis, and trace conjunctival chemosis.

Posterior examination was significant for diffuse retinal whitening with a cherry-red spot in the macula in the right eye (Figure 1A).

There were no other neurologic deficits identified on examination.Case presentation.

B, Immediate postoperative magnetic resonance imaging showing enlarged extraocular muscles on the right side (arrowheads).A computed tomography scan without contrast did not show an acute intracranial hemorrhage and demonstrated diffuse enlargement of the right extraocular muscles.

Magnetic resonance imaging of the brain and orbits with contrast again showed enlargement and abnormal signal of the extraocular muscles on the right (Figure 1B); there was no evidence of cavernous sinus pathology.

A, Fundus photograph of right eye showing diffuse retinal whitening with a cherry-red spot.


She was born at 38.3 weeks via spontaneous vaginal delivery after an uncomplicated pregnancy to a 35-year-old, G3, now P2 mother with no significant medical history.

Results of maternal prenatal laboratory tests were all unremarkable.

She received regular prenatal care, and routine ultrasonography revealed no anomalies.

The Apgar scores were 9 at 1 minute and 9 at 5 minutes.

No resuscitation was required in the delivery room.

The newborn was already breastfeeding well, voiding, and stooling by the time of the initial examination.

Physical examination revealed a 3.5 × 4-cm mobile mass on the right lateral trunk at the midaxillary line at levels approximately T4 to T6.

The mass was firm and round, although when palpated it was not homogeneous or smooth.

There was no discoloration of the overlying skin.

Results of the remainder of the physical examination were normal.


The patient denied any history of abdominal surgery.

On examination, he was mildly distended and tender focally on the right side.

In the emergency department, a nasogastric tube was placed, yielding a moderate amount of dark, foul-smelling output.

Laboratory results were significant for a white blood cell count of 13 300/μL (to convert to ×109 per liter, multiply by 0.001) (bands 20%).

A contrast-enhanced computed tomographic scan of the abdomen and pelvis  demonstrated dilated small intestine (measuring up to 4.7 cm), with air-fluid levels extending to the terminal ileum (Figure 1A and B).

There were several loops of normal-caliber bowel proximal to the area of concern.

Dilated small intestine with air-fluid levels extending to the terminal ileum (A and B).

The decision was made to take him to the operating room for exploration given the lack of any previous abdominal surgical procedures and no other explanation for his symptoms.

Intraoperatively, a large portion of the small intestine was involved in dense adhesions.

After performing careful lysis on the distal involved bowel, a tightly coiled and twisted segment was encountered (Figure 1C).

At this point, further attempts to separate loops of small intestine would have been difficult, and the decision was made to resect this segment (approximately 110 cm) and perform a primary anastomosis.Cross-sectional computed tomographic scan of the abdomen.

C, Intraoperative image of involved small intestine.

Tightly coiled and twisted small bowel with adhesive bands.


His surgical history was notable for a coronary artery bypass graft 9 months earlier and γ-knife resection of an acoustic neuroma 10 years ago.Physical examination revealed a soft, nontender abdomen without obvious palpable masses.

He had been having recurrent gastrointestinal bleeding and melena during the past year.

He reported a 6.75-kg weight loss during the past few months but did not have abdominal pain, nausea, vomiting, fevers, or chills.

Inspection of the patient’s skin demonstrated multiple fleshy, soft cutaneous nodules (Figure 1A).

The patient’s laboratory testing was only notable for anemia with a hemoglobin level of 10.4 g/dL (reference range, 12-16 g/dL).

A prior extensive examination, including upper and lower endoscopy, upper gastrointestinal series with small-bowel follow-through, and capsule endoscopy did not reveal a diagnosis.

A computed tomography image of the abdomen and pelvis is shown in Figure 1B.A, Multiple cutaneous nodules and pigmented spots are evident on physical examination.

B, Cross-sectional imaging reveals a large, complex, septated, right-upper-quadrant abdominal mass.


In the past 2 years, she was thought to have a urinary tract infection (UTI) on 8 occasions and received antibiotic therapy 6 times.

Symptoms that triggered an evaluation for UTI included increased confusion, urinary frequency, cloudy urine, lethargy, hallucinations, and falls.

The patient reports no dysuria or abdominal pain but does chronically complain of voiding frequently.

She is afebrile with no abdominal, suprapubic, or flank tenderness, but her urine has a foul odor.

A catheterized urine specimen is obtained and results of urinalysis are reported (Table).

The urine culture reveals more than 100 000 colony-forming units (CFUs) per milliliter of Escherichia coli, which is sensitive to all antibiotics except ampicillin.The patient has a UTI because of chronic incontinence and a positive urine culture.A positive urinalysis and urine culture are always a UTI.Since the patient has a history of recurrent UTIs, these urine test results indicate that she has another UTI.

On this occasion, the family reports that she “doesn’t look right,” but the nursing staff states she is not confused.


He is a former smoker with a 12 pack-year history, having quit 40 years ago.He is afebrile, and other vital signs are normal.

The facial droop and leg weakness developed 3 weeks ago, while he was vacationing in upstate New York.

His symptoms have not progressed since initial onset.

He reports no rash, headache, joint pain, visual changes, fevers, night sweats, or weight loss.

On physical examination he has a left lower facial droop with sparing of the forehead muscles.

Lower extremity strength is preserved and reflexes are normal; however, he has a subtle gait abnormality characterized by slight dragging of his left leg with ambulation.

Tests for toxoplasma, Lyme disease, cryptococcal antigen, and human immunodeficiency virus are negative.

T1-weighted magnetic resonance imaging (MRI) of his brain demonstrates multiloculated ring-enhancing fluid collections involving the right basal ganglia, insula, and frontal lobe (Figure).

His cancer screening is up to date and unremarkable.


The patient recently returned from a trip to Puerto Rico.

He has no significant past medical history.

He noticed the lesions approximately 1 week after his return.

On physical examination, the patient is in overall good health.

Notable findings include 3 red, serpiginous lesions on the heel (Figure, A), lateral area of the midfoot (Figure, B), and ankle, some with vesicles.

Vesicles were also noted over the Achilles tendon.Serpiginous lesions on the heel (A) and lateral area of the midfoot (B) of the patient.


The patient is from India and arrived in the United States 1 month ago for graduate studies.

She reports no significant medical history and is unaware of any tuberculosis (TB) exposures.

She received the BCG vaccine as a child.

Laboratory testing showed normal chemistry and hematology values and a negative HIV test.

Because of the TST result, the patient has a chest radiograph performed, which was unremarkable.

The patient asks whether the positive TST result could be due to her BCG vaccination and wants further testing before beginning therapy.

Blood is drawn for an interferon-γ release assay (IGRA; see Figure for results).aExplanation of values: nil (the interferon-γ concentration in plasma from blood incubated without antigen [negative control]); TB antigen minus nil (the interferon-γ concentration in plasma from blood stimulated with 3 relatively specific TB peptides) minus nil; and mitogen minus nil (the interferon-γ concentration in plasma from blood stimulated with mitogen minus nil).

The TB response (TB antigen minus nil) is calculated as the difference in interferon-γ concentration in plasma from blood stimulated with TB antigens minus the interferon-γ concentration in plasma from blood incubated without antigen (nil).

Treatment for latent TB infection (LTBI) was recommended based on the positive TST, negative chest radiograph, and recent US arrival from a high-TB–incidence country.

Data are based on package insert available at http://www.quantiferon.com/irm/content/PI/QFT/2PK/US.pdf.cFor negative, positive, and indeterminate results, the probability of Mycobacterium tuberculosis infection is not likely, likely, and uncertain, respectively.The patient does not have LTBI.

The mitogen tube contains a mitogen (phytohaemogglutin-P) that is a nonspecific stimulator of T-cells.

It is used as a positive control to ensure the capacity to respond to antigens and also serves as a control for correct blood handling and incubation.bFor this IGRA, 1 mL of blood is drawn into each of 3 tubes (nil [negative control], mitogen [positive control], and TB antigens tube).

A positive IGRA test result occurs when all of the following criteria are met: (1) the nil value is less than 8 IU/mL; (2) the TB antigen minus nil response is greater than or equal to both 0.35 IU/mL and 25% of the nil value; and (3) there is a positive mitogen response.

No further evaluation is needed.The patient needs further evaluation for active TB disease.


His medical history included Parkinson disease, for which he took no medication.

Three months prior, he had noticed a small nodule on his calf, with no overlying skin changes or tenderness.

This progressed to a tender, nodular plaque while other lesions appeared.

The patient denied other signs or symptoms.

Laboratory findings showed an elevated lactate dehydrogenase (LDH) level at 439 U/L (reference range, 118-242 U/L) (to convert LDH to microkatals per liter, multiply by 0.0167).

Results from serum chemical analyses, complete blood cell count, and tests of liver functions were normal.

Physical examination revealed a healthy-appearing man with a 4.0 × 4.0-cm pink, firm, tender nodular plaque on his left calf (Figure, A), a 5.0-cm firm, subcutaneous mass on his right thigh, and a 0.5 × 0.5-cm subcutaneous nodule on his left cheek.

There was no cervical, axillary, or inguinal lymphadenopathy.

A punch biopsy specimen was obtained from each lesion (Figure, B and C).A, Clinical photograph of the nodular plaque on the left lateral calf.

B and C, Histopathologic images from the punch biopsy specimen demonstrating angiocentrism.

B, The large atypical lymphoid cells can be seen infiltrating a vessel (outlined by arrowheads) (hematoxylin-eosin, original magnification ×400).

C, Histopathologic image from the punch biopsy specimen showing positive EBER in situ hybridization.


She had a medical history of hypertension, hyperlipidemia, and tobacco abuse, requiring treatment with losartan and atorvastatin.Physical examination revealed punctate, blanchable telangiectasias coalescing to form large, retiform patches on her bilateral lower extremities, feet, and upper extremities (Figure, A).

They had first appeared on her lower legs 15 years ago and were slowly increasing in number and spreading to involve her feet and bilateral upper extremities.

The patient denied tenderness, pruritus, and edema.

There was no conjunctival or mucosal involvement.

Histologic findings from a biopsy specimen are shown in the Figure, B.A, Multiple telangiectasias coalescing to form large, retiform patches on the bilateral lower extremities.

B, Dilated, ectatic vessels in the superficial dermis with no associated inflammation or fibrinoid necrosis (hematoxylin-eosin, original magnification ×200).

She reported no family history of this problem and denied any personal history of anemia, epistaxis, hematemesis, melena, hematochezia, or hemoptysis.

The patient reported no dermatographism or purpura.


Her medical history was unremarkable, and she was not taking any medications at the time of presentation.

She reported pain, pruritus, and serous discharge associated with the plaques but denied any systemic symptoms.

Results of a physical examination revealed well-demarcated, moist, erythematous plaques and erosions in the bilateral inframammary regions (Figure 1A) and the intertriginous regions of the groin and scattered excoriated papules on the scalp.

A punch biopsy specimen of the plaque along the left inframammary region was sent for pathologic evaluation (Figure 1B-D).A, Well-demarcated erosive plaques on the bilateral inframammary region.

B, Abundant atypical cells within the epidermis and papillary dermis (hematoxylin-eosin, original magnification ×10).

C, Abundant atypical cells with reniform nuclei within the epidermis and papillary dermis (hematoxylin-eosin, original magnification ×40).

D, Immunohistochemical analysis (original magnification ×10).

Previous treatment with multiple courses of topical and systemic antifungals, topical and systemic corticosteroids, and oral antibiotics had failed.


The patient reported loss of consciousness and face trauma secondary to airbag deployment.

At the 10-week follow-up appointment, the patient reported that she was “miserable” because of vision loss; Snellen best-corrected visual acuity was 20/30 OD.

Visual acuity measured 20/200 OD and 20/40 OS.

In the right eye, external examination revealed ecchymosis and periorbital edema.

The anterior segment was within normal limits.

Examination of the posterior segment in the right eye demonstrated whitening of the macula with a central red spot consistent with posterior pole commotio retinae.

Flame-shaped hemorrhages and cotton-wool spots were noted (Figure 1A).

Optical coherence tomography (OCT) revealed subfoveal debris (Figure 1B).

Posterior segment examination was within normal limits.A, Fundus photograph of the right eye demonstrates whitening of the macula with a central red spot.

Flame-shaped hemorrhages and cotton-wool spots are present in the nasal macula and surrounding the superior arcade.

B, Optical coherence tomography of the right eye demonstrates subfoveal debris with distortion of the normal foveal architecture.

The patient was observed with serial examinations.


She denied any medication use and had no history of ocular surgery or known ophthalmic disorders.

Best-corrected visual acuity was counting fingers at 1 ft OD and 20/300 OS.

Slitlamp examination revealed fine keratic precipitates bilaterally, with 2+ anterior chamber cells in her right eye and 0.5+ cells in her left eye.

Dilated fundus examination of the right eye demonstrated a creamy white lesion emanating superiorly from the optic nerve associated with areas of intraretinal hemorrhage and extensive perivascular sheathing along the vascular arcades into the midperiphery (Figure 1A).

Ophthalmoscopic examination of the left eye showed a peripapillary preretinal gliotic lesion exerting mild traction on the macula with fine retinal striae and a macular star configuration of exudates (Figure 1B).

Spectral-domain optical coherence tomography revealed significant cystoid macular edema with associated subretinal fluid in the right eye and hard exudates without evidence of cystoid macular edema in the left eye.Baseline montage color fundus photographs.

A, Right eye demonstrates retinal whitening superior to the optic nerve adjacent to several pigmented chorioretinal scars.

B, Left eye demonstrates a preretinal gliotic lesion with a macular star.


Medical history revealed no other medical problems.

Her mother reported the lesion appeared at age 3 months, was previously diagnosed as a hemangioma, and was treated with observation.

She also reported the lesion originated as a “cystlike papule” that had continuously expanded.

In addition to causing cosmetic concerns, the lesion seemed to be irritated by clothing and would occasionally bleed and swell.

Since its appearance at 3 months of age, several abscesses formed underneath the region of concern requiring incision and drainage.

On physical examination, at the proximal posterior thigh, there was an 11 × 10-cm cobblestoned, gray plaque composed of numerous purplish, vesicular papules with surrounding satellite papules.

A 4-mm punch biopsy was performed (Figure, B and C).Translucent papules and histologic examination in a child.

A, Clinical examination shows numerous grouped translucent papules.

B and C, Dilated thin-walled vascular spaces containing valvelike papillary projections in the superficial dermis.


Her medical history was significant for hypertension and a previous laparoscopic cholecystectomy approximately 6 years ago.Coronal computed tomographic (CT) image of abdominal mass (arrowhead) (A) and axial CT image of peritoneal implant (arrowhead) (B).

High-resolution computed tomography revealed a 3 × 4-cm circumferential lesion in the second and third portions of the duodenum involving the pancreatic head (Figure 1).

Multiple nodules were noted along the peritoneal reflection of the right paracolic gutter.

The results of a biochemical analysis were remarkable with a total bilirubin level of 6.8 mg/dL (to convert to micromoles per liter, multiply by 17.104), an aspartate aminotransferase level of 394 U/L, an alanine transaminase level of 746 U/L, and an alkaline phosphatase level of 1146 U/L (to convert the last 3 analytes to microkatals per liter, multiply by 0.0167).


Medical history was significant for a total thyroidectomy for papillary thyroid cancer 7 years before as well as a strong family history of malignant breast cancer on the maternal side and colon and liver cancer on the paternal side.Physical examination revealed an 8 × 8-cm, tender, firm posterior right-flank mass that was mobile but fixed to the abdominal wall musculature.

Her case was presented at the soft tissue tumor board, and given that the patient was asymptomatic and pregnant, the decision was made to closely watch the progression of this lesion with serial imaging with a planned resection after delivery.Unfortunately, she developed premature rupture of membranes and lost the pregnancy.

Laboratory examination revealed no abnormalities.

Ultrasonography demonstrated a hypoechoic lesion measuring 3.3 × 3.6 cm with internal echoes and no significant flow (Figure 1A).

A noncontrast magnetic resonance image (MRI) revealed this to be a well-circumscribed T2 hyperintense lesion with diffuse surrounding soft tissue edema within the adjacent muscular and subcutaneous tissues abutting the posterior margin of the right chest wall and external oblique muscle at the level of the T11 to T12 intercostal space (Figure 1B and C).A, Ultrasonography demonstrating a hypoechoic mass in the musculature of the right flank.

B and C, T1- and T2-weighted images demonstrating an enhancing right-flank mass within the right-flank musculature.Because of the concern of malignancy, an ultrasonography-guided core biopsy was performed and demonstrated a myofibroblastic proliferation with immunostains positive for actin and negative for S100 and desmin.

Follow-up computed tomography was not able to identify the lesion but MRI showed that it was still present but decreased in size (2.4 × 1 cm) with interval resolution of surrounding inflammatory changes.

She subsequently underwent wide local resection of the lesion.


None of these therapies was of benefit.The patient reported no significant medical history and was not taking other medications.

He reported nasal congestion and pain, bleeding, and minor sloughing of nasal mucosal tissue.

On examination he had an erythematous plaque without ulceration on the right side of the neck (Figure, left).

Examination also revealed erythema and swelling of the left nasal ala extending to the infratip lobule (lowermost portion of the nasal tip directly above the nostril openings) and left alar rim as well as disruption of the nasal architecture with crusting of the left nare (Figure, right).

Cervical lymphadenopathy was present and most pronounced on the right side.

A biopsy of the nasal tissue revealed pseudoepitheliomatous hyperplasia, a lymphoplasmocytic inflammation, with no organisms found using special staining.Left, Erythematous plaque with crusting on the right side of the neck.

He was seen by 2 dermatologists, a family physician, and an otolaryngologist in Venezuela as well as 2 dermatologists, 2 family physicians, a nurse practitioner, and an infectious diseases specialist in the United States.

These 10 clinicians collectively prescribed oral amoxicillin, cefadroxil, cephalexin, azithromycin, clindamycin, and cefdinir as well as intramuscular ceftriaxone and topical bacitracin, mupirocin, and polymyxin B.

The remainder of the physical examination was unremarkable.


He had type 2 diabetes mellitus treated with insulin, metformin, glyburide, and pioglitazone.

He also had coronary artery disease complicated by a myocardial infarction and coronary artery bypass graft surgery 6 years ago.

He has had occasional night sweats but reported no fevers, weight loss, or change in appetite.

The general physical examination was unrevealing, as were oropharyngeal, cardiac, respiratory, abdominal, and lymph node examinations.

A complete blood cell count (CBC) showed a hemoglobin level of 14.6 g/dL and a white blood cell count of 24.1 × 103/μL with 25% neutrophils and 69% lymphocytes; platelet count was 189 × 103/μL.

A peripheral blood smear (Figure) showed red blood cells with mild anisocytosis (unequal size) and poikilocytosis (variation in shape).

The platelets were normal in number and appearance.

White blood cells were increased, with a lymphocytic predominance.

The lymphocytes were mature and appeared somewhat heterogeneous.

Smudge cells were noted (Figure, Left panel, lower right corner; Right panel, center).


She also had fine-textured hair, present since childhood with thinning noted in the past 7 years.

At the time, she denied a family history of similar skin findings but recently reported similar hand and foot findings in her mother.

Many of the papules were depressed centrally.

The lesions on her hands first developed in her 40s and were exacerbated by alcohol-based hand sanitizer at work.

They became more prominent with exposure to water but remained asymptomatic.

Two punch biopsies were performed from the left thenar eminence (Figure, C).A, Clinical photograph of the palm showing dozens of flesh-colored to translucent palmar papules.

There was no extension onto the dorsal aspect of the hands.

There were similar translucent papules over the margins of her feet, particularly her great toes, and hyperkeratotic yellow plaques with scattered pits over her bilateral soles, concentrated in areas of pressure.

B, Closer clinical view of the palmar papules over the thenar eminence, some with central depression.

C, Histologic image from a skin biopsy specimen from the thenar eminence (hematoxylin-eosin, original magnification ×40).

Occasional application of urea cream to her feet did not lead to significant improvement.


She had a history of type 2 diabetes mellitus, hypothyroidism, and hypercholesterolemia.

Her regular medications included metformin, insulin, rosuvastatin calcium, levothyroxine sodium, and aspirin.

She also had bilateral injected conjunctivae with periorbital swelling.

Examination revealed edematous labia and multiple perivulvar tender nodules on violaceous and indurated plaques sparing the vaginal mucosa and inguinal creases (Figure, A).

A punch biopsy of the perivulvar lesions was performed for histopathologic analysis (Figure, B and C) and tissue culture.A, Perivulvar plaques and nodules that developed after chemotherapy for acute myeloid leukemia.

Edematous labia with perivulvar violaceous plaques and nodules.

B and C, Skin histologic images from perivulvar plaques and nodules.

B, Spongiosis and hyperplasia of the epidermis with neutrophilic infiltrate within the dermis (hematoxylin-eosin, original magnification ×10).

C, Necrotic collagen and eccrine gland destruction (hematoxylin-eosin, original magnification ×10).


He reported no history of cutaneous diseases.

He had undergone heterologous bone marrow transplantation for chronic myeloid leukemia 18 years before and had hypertension controlled with lisinopril and hydrochlorothiazide and type 2 diabetes mellitus controlled by diet.

Physical examination revealed multiple hyperkeratotic purplish brown papules and plaques, more confluent in the perianal area, with well-demarcated keratotic prominent margins (Figure, A and B).

Dermoscopy showed structureless brownish pigmentation and erythema in the center, demarcated by a white-yellow hyperkeratotic scale at the periphery.

Therefore, 2 skin biopsies were performed (Figure, C).A, Multiple hyperkeratotic purplish brown papules and plaques on both buttocks, more confluent in the perianal area, with well-demarcated slightly elevated keratotic margins.

Because of suspicion of lichen planus annularis, the patient was treated intermittently with intramuscular triamcinolone acetonide depot and topical treatments such as corticosteroids, antifungal agents, pimecrolimus, and retinoic acid, resulting in subjective pruritus relief; however, the lesions did not show satisfactory improvement in 2 years’ follow-up.

C, Biopsy specimen (hematoxylin-eosin, original magnification ×400).


He denied any family history of similar eruptions and was not taking any medications aside from whey protein supplementation.

He felt well otherwise, denying fever, gastrointestinal upset, or any antecedent illness or exposure.

The cutaneous eruption had continued to spread despite topical and oral corticosteroid therapy, and diphenhydramine provided no relief from the pruritus.A, Initial clinical presentation of bullae on an erythematous base in a reticular pattern on the back.

B, Biopsy specimen from the mid-abdomen showing dense infiltration of the epidermis by numerous eosinophils (hematoxylin-eosin).

C, Biopsy specimen from the back showing abrupt necrosis of the epidermis and an intraepidermal blister filled with neutrophils and eosinophils.

The blister correlates with the bulla seen clinically.

The upper dermis showed a mixed infiltrate of lymphocytes, eosinophils, and neutrophils (hematoxylin-eosin).A complete blood cell count and comprehensive metabolic panel revealed only a minor lymphopenia (lymphocyte percentage, 16.8%; lymphocyte count, 1000/μL [normal, 1300-3600/μL]), a high monocyte percentage (13.6%; normal, 4.0%), but a normal absolute monocyte count.

(To convert lymphocyte count to ×109/L, multiply by 0.001.)

Results from assays for herpes simplex virus IgG, antinuclear antibodies, glucagon, and zinc were all within normal limits.On clinical examination, vesicles and bullae were found coalescing into large reticulated plaques with background erythema on the upper neck, inframammary areas, groin, mid back, and extending down onto the upper buttocks.

The bullae were eroded in some areas with hemorrhagic crust (Figure 1A).Punch biopsy specimens from characteristic lesions were obtained and sent for hematoxylin-eosin (H&E) examination (Figure 1B and C).


The patient’s medical history was notable for rheumatoid arthritis that had been well controlled with methotrexate for 15 years.

The lesion was first noted 6 months prior to presentation and was initially diagnosed as a chalazion.

The nodule increased in size during the next several months despite conservative measures including warm compresses.

Despite an initial decrease in lesion size, 6 weeks postinjection, new-onset ipsilateral extraocular motility deficits and palpable preauricular lymphadenopathy were noted.

A magnetic resonance image revealed an infiltrative process in the involved eyelid and lymphadenopathy (Figure, B and C).

Findings from systemic evaluation, including complete blood cell count, serum protein electrophoresis, serum lactate dehydrogenase, and whole-body positron emission tomography, were unremarkable.A, Swollen right upper eyelid.

Magnetic resonance images demonstrating diffuse eyelid infiltration (B, arrowhead) and lymphadenopathy (C, arrowhead).

Intralesional triamcinolone was then administered.

A biopsy revealed a mixed inflammatory infiltrate without evidence of neoplasia, supporting a diagnosis of chalazion.

A second biopsy of the eyelid lesion revealed large, atypical lymphocytes diffusely positive for CD20 and negative for CD5 and Bcl-1 (Figure, D-G), supporting a diagnosis of diffuse large B-cell lymphoma (DLBCL).


He had undergone trabeculectomy in the right eye with mitomycin C 4 years earlier.

On examination, his best-corrected visual acuity was 6/60 (−2.5 diopters sphere/0.5 diopters cylinder × 90) and 6/6 (0.5 diopters sphere) OD and OS, respectively.

His IOP was 36 mm Hg and 12 mm Hg OD and OS, respectively, while receiving the maximum-tolerated antiglaucoma medications.

Fundus examination was normal (Figure 1A and B), and B-scan ultrasonography revealed no mass lesion in the right eye.

The left eye was normal.A and B, Right eye at presentation showing marked red glow of the fundus (A) compared with the left eye (B).

On the first postoperative day, the anterior chamber was flat with corneolenticular touch (Figure 1C) and serous choroidal effusion.

The Ahmed glaucoma valve tube was ligated a week later, following which the IOP stabilized and choroidal effusion subsided.After 9 months, the IOP rose to 30 mm Hg, which could not be controlled medically.

Postoperatively, it again led to hypotony and a shallow anterior chamber.

The accompanying choroidal effusion was now associated with exudative retinal detachment, with retina-lenticular touch (Figure 1D) and the patient did not respond to conservative management.

C, First postoperative day following Ahmed glaucoma valve implantation in the right eye with a flat anterior chamber.

Note the iris plugging the opening of the Ahmed glaucoma valve tube.

D, Large serous retinal detachment and choroidal effusion following fibrous capsule excision.He underwent Ahmed glaucoma valve implantation in the right eye.

The anterior chamber repeatedly flattened despite viscoelastic injection, and the choroidal effusion persisted.

There was a tense fibrous capsule encapsulating the Ahmed glaucoma valve plate, which was excised.


The patient’s mother noted that both the pregnancy and the delivery were uncomplicated.

She denied ever having a miscarriage and had another healthy male child at home without any similar lesions.

The mother had a history of varicella as a child; she did not have a history of herpes simplex virus and had no oral or genital lesions at the time of delivery.

These papules had been present at birth and were persistent at the time of the patient’s initial hospital discharge.

Because no resolution had been noted over the next few days, the patient was taken to his primary care physician for evaluation and then sent to the emergency department for further workup.

On examination, the patient was noted to have 2- to 3-mm vesicles on the left upper extremity in a linear, bandlike distribution (Figure, A), and similar 2- to 3-mm deep-seated vesicles on his left medial thigh in a whorled configuration, approximately 4 × 3 cm in total size (Figure, B).

In addition, the patient had a 1-mm vesicle on his abdomen.A, Vesicles (2-3 mm in diameter) on the left forearm are in a linear, bandlike distribution.

B, Deep-seated vesicles on left medial thigh are in a whorled configuration.


Her medical history included a partial oophorectomy of a right ovarian cyst, hypertension, and vomiting and abdominal pain once a year that started 10 years earlier.

She had always been diagnosed as having adhesive ileus, and her symptoms always improved within a day after hospital admission.

A physical examination at admission revealed that her abdomen was slightly distended and tender to palpation on the right side of the paraumbilical point without muscle guarding.

The hematologic findings revealed slight anemia and amylasemia; her hemoglobin level was 9.3 g/dL (to convert to grams per liter, multiply by 10.0), and her amylase level was 168 U/L (to convert to microkatals per liter, multiply by 0.0167).

Abdominal computed tomography (CT) with intravenous contrast agent revealed a mass on the right side of the paraumbilical point (Figure 1).Contrast-enhanced computed tomographic scan through the abdomen showing a mass on the right side of the paraumbilical point.


Her medical history included gastroesophageal reflux disease, irritable bowel syndrome, hypothyroidism, hypertension, asthma, and obesity.

On palpation, the mass extended superiorly to the costal margins and inferiorly to the anterior-superior iliac spine; no fascial edge was palpable medially.

A computed tomographic (CT) scan demonstrated abdominal contents—including liver, ascending colon, and omental fat—protruding through a 12-cm defect.

Weight loss was counseled and 8 weeks allowed for optimization before exploration.


In addition to chronic hepatitis B, her medical history was notable for hypertension and her surgical history was significant for a recent liver biopsy.

The patient was symptomatic with intermittent left upper quadrant abdominal pain that was associated with nausea and constipation.

Physical examination revealed a soft, nontender, minimally distended abdomen with no palpable masses and no costovertebral angle tenderness.Laboratory test results at presentation revealed complete blood cell count, comprehensive metabolic panel, and amylase values within the reference ranges and a hepatitis B virus quantification level of 1590 IU/mL.

A computed tomographic scan of the abdomen and pelvis using intravenous contrast was obtained (Figure 1).Coronal computed tomographic imaging on initial presentation.

She reported no other gastrointestinal, genitourinary, or overall symptoms.


The patient did relate having many prior episodes of epistaxis since childhood.

Multiple red papules on the tongue (Figure 1), trunk, and limbs were noted during the physical examination.

The patient stated she had not noticed the red papules before.

Computed tomography (CT) of the brain showed a ring-enhanced lesion with surrounding edema on the left frontoparietal lobe.

There was no suggestion of otitis media or parasinusitis and no history of craniotomy, open head injury, or cyanotic heart disease.

Blood cultures were obtained when the patient was first seen, and the patient received ampicillin/sulbactam empirically.Multiple red papules on the tip and sides of the tongue.Consult a neurosurgeon to evaluate the brain CT finding; obtain a CT scan of the lung and abdomen and offer genetic counseling for the patient and her family.Consult a neurosurgeon to evaluate the brain CT finding; obtain a dermatology consultation and refer the patient to interventional radiology.


He was a graduate student who was doing well until he developed decompensated cirrhosis with variceal hemorrhage.

When he first presented, he had hypovolemic shock from acute blood loss related to variceal hemorrhage that was treated with many blood transfusions and variceal banding procedures.

He did not have any confusion, insomnia, or decreased mental alertness.

Jaundice was noted on the physical examination but he was alert and oriented with normal cognitive function.

He had a serum ammonia level measured as part of the routine liver transplant evaluation.

No tenderness was noted on his abdominal examination and he had mild ascites.

The Table lists results of laboratory analyses performed at admission and on hospital days 25 and 38.The patient has hepatic encephalopathy and should be treated.The patient has subclinical hepatic encephalopathy and should be treated.The patient is at high risk for developing hepatic encephalopathy and should be prophylactically treated.The patient does not have hepatic encephalopathy so no treatment is necessary.

When he was transferred to the liver unit on hospital day 25, his liver test abnormalities had mostly recovered and he had no further gastrointestinal bleeding.

During the inpatient liver transplant evaluation, his cognitive capacity and mental status remained stable and he had no symptoms of encephalopathy.

He received oral diuretics for the management of his ascites.


His myelofibrosis had been treated 2 years earlier with a splenectomy and allogeneic peripheral hematopoietic stem cell transplantation from a single-antigen mismatched unrelated donor.

A busulfan-based myeloablative regimen was used for preconditioning before the transplant.

He had received tacrolimus, but that was tapered off 4 months before his current problems began.

His only current medication is daily oral acyclovir.Vital signs were normal.

Subsequently, he noted development of a nonpruritic rash on his face, trunk, and extremities.

The rash was associated with intermittent fever, muscle pain, and weakness.

There were well-demarcated erythematous to violaceous scaly plaques on his forehead and cheeks, sparing the nasolabial folds and periocular regions (Figure, A).

Diffuse areas of reticulated hyperpigmentation were present across his chest and upper back (Figure, B).

There were violaceous, thin, flat-topped papules bilaterally on the dorsal surfaces of his hands (Figure, C) and the lateral soles of his feet.

Musculoskeletal examination revealed impaired ability to dorsiflex the wrists while bringing the palms together (“prayer sign”).A, Well-demarcated erythematous to violaceous scaly plaques on the forehead and cheeks with notable sparing of the nasolabial folds and periocular regions.

C, Violaceous, thin, flat-topped papules bilaterally on the dorsal surfaces of the hands.Results of liver function tests revealed an aspartate aminotransferase level of 41 U/L (0.68 μkat/L); alanine aminotransferase, 68 U/L (1.14 μkat/L); alkaline phosphatase, 147 U/L (2.45 μkat/L); and total bilirubin, 0.7 mg/dL (11.97 μmol/L).

After the transplant, he experienced acute graft-vs-host disease predominantly manifested by gastrointestinal symptoms.


His medical history was significant for hypertension, gastroesophageal reflux, and prostate cancer.

On examination, uncorrected visual acuity was 20/25 OU, pupils were equal and reactive to light without afferent defect, confrontational fields were normal, and ocular motility was full.

External examination was significant for decreased sensation in the distribution of the ophthalmic branch of the left trigeminal nerve.

A palpable mass was appreciated at the left supratrochlear notch.

There was 4 mm of proptosis and 2 mm of inferior globe dystopia, with increased resistance to retropulsion in the left eye.

Magnetic resonance imaging of the orbits demonstrated an infiltrating superomedial mass involving the extraconal and intraconal space on the left side (Figure 1).Magnetic resonance imaging of the orbits.

An 86-year-old man presents with an infiltrating mass of the left superomedial orbit demonstrated on T1-weighted axial (A) and coronal (B) images.


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

His pupil, intraocular pressure, motility, and confrontational visual field are normal in each eye.

The results of an external examination and a slitlamp examination of the anterior segment of both eyes are unremarkable.

A dilated fundus examination reveals clear vitreous in each eye and small yellow-white retinal lesions in the right eye.

The patient denies any history of recent illnesses (Figure 1).A, Color fundus photograph shows subtle yellow-white punctate lesions deep in the retina.

Fluorescein angiograms demonstrate hyperfluorescent lesions during the early and late phases and late optic nerve staining (arterial [B], venous laminar [C], and late [D] phase).


Three months prior to presentation, he had received a diagnosis of pneumonia; his condition improved after a course of azithromycin.

He denied ever having a fever, weight loss, contact with any sick persons, or sexual activity; using illicit drugs; or traveling outside of southern California.Examination revealed mildly tender, fluctuant masses at the base of his neck, each measuring 4 cm in diameter (Figure, A).

The left-sided mass had been spontaneously draining straw-colored fluid for 5 days.

Laboratory values included a white blood cell count of 13/μL (to convert to ×109 per liter, multiply by 0.001) (69% neutrophils, 21% lymphocytes, and 2.3% eosinophils [to convert to proportion of 1.0, multiply by 0.01]), a hemoglobin level of 12.3 g/dL (to convert to grams per liter, multiply by 10.0), and a platelet count of 337 × 103/μL (to convert to ×109 per liter, multiply by 1.0).

The results of a screening antibody test for human immunodeficiency virus and of a Mantoux tuberculin skin test were negative.

A chest radiograph revealed bilateral hilar adenopathy (Figure, B).

An excisional lymph node biopsy of the left-sided mass was performed (Figure, C).A, Bilateral level IV (low jugular) cervical adenopathy.

B, Chest radiograph showing bilateral hilar adenopathy.

C, Histological examination of the excised lymph node showing multiple spherules containing endospores (arrowheads) (hematoxylin-eosin, original magnification ×200).


Three months prior, he had an episode of native aortic valve endocarditis, necessitating aortic valve replacement with a pericardial bioprosthesis.

He developed postoperative acute renal failure, which progressed to chronic renal failure requiring dialysis via tunneled catheter.

Transesophageal echocardiography demonstrated a vegetation on his prosthetic aortic valve.

However, on postprocedure radiography, the tip of the triple-lumen catheter was not in the expected location (Figure 1).

Owing to his dialysis needs, a temporary dialysis catheter was placed in the right internal jugular vein.

As intravenous access was required for vasoactive medications and intravenous antibiotics, a triple-lumen central catheter was placed in the left internal jugular vein under ultrasonographic guidance.

The catheter was removed, and a new-stick insertion of a new catheter was attempted under ultrasonographic guidance.Chest radiograph showing left internal jugular catheter placement (arrowhead).

On this admission, he was found to have methicillin-resistant Staphylococcus aureus (MRSA) bacteremia.

He was diagnosed as having MRSA prosthetic valve endocarditis and admitted to the cardiovascular surgical intensive care unit prior to surgical intervention.In the setting of MRSA bacteremia, his tunneled dialysis catheter had been removed.

The catheter went in easily without resistance, was drop tested to confirm venous placement, and flushed and drew easily, and venous waveforms and pressures were transduced.


The patient had no history of oral or genital herpes lesions.

Her lesions improved with prednisone but recurred when treatment was discontinued.

No inciting factors were identified except a possible relation to her menstrual cycle.

She also reported concurrent painful oral lesions.

Erythematous, hyperpigmented, annular papules with dusky centers and bullae were observed on her arms and legs bilaterally (Figure, A, B, C).

Oral lesions were also observed and consisted of erythematous, crusted papules with superficial ulceration, gingival hyperplasia, and superimposed thrush (Figure, D).

Results of herpes simplex virus (HSV) 1 and 2 IgG serologic testing were positive.

Test results for pemphigus antibody panel, antinuclear antibodies, human immunodeficiency virus, and rapid plasma reagin were negative.


The patient reports experiencing no fevers or chills since the plaque developed.

On examination the bright reddish, irregularly shaped plaque measures 4.0 × 1.5 cm and has erosions on the surface (Figure 1).

The physical examination is otherwise unremarkable.


His blood pressure was 183/116 mm Hg despite taking lisinopril (40 mg/d) and verapamil (180 mg/d).

He had previously taken hydrochlorothiazide, which was discontinued due to hypokalemia approximately 1 month ago, as well as atenolol, which was stopped 2 months earlier.

As part of the workup for secondary hypertension, plasma aldosterone concentration and plasma renin activity were measured (Table 1).Primary aldosteronism is suggested; imaging is required for confirmation.Primary aldosteronism is suggested; confirmation requires an aldosterone suppression test.The results are unreliable; ARR should be measured 1 month after discontinuing lisinopril.


Soon thereafter, she was noted to be more forgetful and unsteady.

She was seen by an otolaryngologist for left-sided hearing loss and diagnosed as having Meniere disease.

She was treated for aseptic meningitis but continued to decline.

Head computed tomography findings were negative and the following day, the headache subsided.

Subsequently, brain magnetic resonance image findings showed numerous foci of enhancement throughout the brain (Figure 1).

Cerebrospinal fluid analysis results were normal except for mildly elevated protein (108 mg/dL).

Findings from cerebrospinal fluid Gram stain and cultures were negative.

Test results for human immunodeficiency virus, syphilis, enterovirus, West Nile virus, herpes simplex virus types 1 and 2, hepatitis, Cryptococcus, Lyme disease, Rickettsia, and Ehrlichia were negative.

Erythrocyte sedimentation rate and C-reactive protein findings were normal.

Results from antinuclear antibody, extractable nuclear antigen, rheumatoid factor, and antineutrophil cytoplasmic antibody tests were negative.

On examination, the patient had visual acuity of 20/20 OU.

Pupils, intraocular pressure, motility, and confrontational visual fields were normal.

External and anterior segment examinations were unremarkable.

Symptoms mildly abated with meclizine hydrochloride and a brief course of steroids.

Ophthalmology was consulted to evaluate the patient when she began to experience transiently blurred vision.

She was subsequently admitted to the hospital.

Dilated fundus examination findings were unremarkable.Axial brain magnetic resonance imaging.

B, Corresponding apparent diffusion coefficient image.


She was taking glatiramer acetate and tizanidine hydrochloride for MS.

The patient also noted decreased peripheral vision and pain on eye movements of the left eye.

She described a recent episode of gastroenteritis prior to the onset of visual complaints.

Her initial visual acuity was 20/50 in both eyes with a 1+ relative afferent pupillary defect in the right eye.

The patient had red desaturation in the left eye, and her color vision, which was determined by use of an Ishihara test, was decreased in both eyes.

Intraocular pressure and ocular motility were normal, and the results of an external examination, an anterior segment examination of both eyes, and a posterior segment examination of the right eye were unremarkable.