{"articles": {"452": {"sections": [{"id": "4451122ad1a443b5bbb72a9142f24e7e", "slug": "how-to-read-a-rash", "title": "How to read a rash", "content": "Every rash yields to the same five questions, asked in order. First, the primary lesion: is it a macule or patch (flat), a papule or plaque (raised, solid), a vesicle, pustule, or bulla (fluid-filled), a wheal (transient, edematous), or purpura (does not blanch with pressure, meaning blood outside the vessel rather than dilated vessels within it)? Second, distribution: truncal versus acral, flexural versus extensor, dermatomal, photo-exposed, or following the lines of an external contact. Third, the child's age, since the newborn's transient pustuloses, the toddler's viral exanthems, and the adolescent's autoimmune eruptions rarely overlap. Fourth, timing: did the rash precede the fever, follow it, or appear on a fixed day of a predictable illness, and how did it evolve, spread, or change color over hours to days. Fifth, itch and systemic signs: a pruritic eruption points toward an allergic or eczematous process, while fever, mucosal involvement, lymphadenopathy, joint pain, or a toxic appearance point toward an infectious or inflammatory one and change the urgency of the workup. Applied consistently, these five questions turn a confusing blur of red spots into a short differential, and they are the frame every section below is written around.", "parent_id": null, "variant": "long"}, {"id": "3cc5baf41dbc4c079a162a29e6dc37c4", "slug": "measles-the-morbilliform-rash-and-koplik-spots", "title": "Measles: the morbilliform rash and Koplik spots", "content": "The photograph shows the classic morbilliform (measles-like) eruption: blanching erythematous macules and papules that begin on the face and hairline and spread downward over the trunk and limbs over about three days, often becoming confluent, together with the pathognomonic Koplik spots, tiny white-gray specks on a red background on the buccal mucosa that appear just before the skin rash. The rash follows a cephalocaudal spread and coincides with the peak of the child's fever and the classic triad of cough, coryza, and conjunctivitis. The photograph and full account are in [[158|Measles]].", "parent_id": null, "variant": "long"}, {"id": "cd916ee9ad0d4bafbceb94f169bd01c8", "slug": "rubella", "title": "Rubella", "content": "The rubella rash consists of pink-red macules and fine papules that begin on the face and spread inferiorly to the trunk and extremities, typically within the first 24 hours; it is classically brief, fading in 2 to 3 days, which has earned it the name \"three-day [[measles|measles]].\" After respiratory exposure the virus replicates in the respiratory epithelium, spreads to regional lymph nodes, and produces a viremia before the rash appears; postauricular and suboccipital lymphadenopathy often precede the eruption and are a useful clue, since the rash itself is milder and less confluent than measles and Koplik spots are absent. The incubation period averages 14 days (range 12 to 23). Treatment is supportive; the real stakes are in pregnancy, where maternal infection in the first trimester causes congenital rubella syndrome, which is why the disease matters far more as a target of MMR immunization than as an illness in the child sitting in front of you. A postnatally infected child needs only reassurance and exclusion from contact with pregnant contacts until the rash has resolved and the child is no longer considered infectious.\n\n![Rubella: Rubella rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/af7aab94db654766ab43d8b5486bc160.jpg)", "parent_id": null, "variant": "long"}, {"id": "cb82aacfe34647ce88c6530032984c20", "slug": "roseola-rash-as-the-fever-breaks", "title": "Roseola: rash as the fever breaks", "content": "Roseola infantum (exanthem subitum, \"sixth disease\"), caused chiefly by human herpesvirus 6, presents with 3 to 5 days of abrupt, high fever in an infant or toddler who otherwise looks reasonably well; the fever resolves by crisis or lysis, and only then does the rash appear, a discriminating sequence that separates roseola from exanthems that erupt while the fever is still climbing. The rash itself is a faint pink or rose-colored, nonpruritic, 2- to 3-mm macular or maculopapular eruption that begins on the trunk and spreads peripherally, with discrete lesions that rarely coalesce; scalp involvement can occur. Mechanistically the pattern reflects the timing of viremia, which is controlled by the immune response that also breaks the fever, so the rash marks the tail end of viral replication rather than its peak. The child's fever height relative to how well they look, and the risk of a [[febrile seizure|febrile-seizure]] during the febrile phase, are the usual reasons for evaluation; once the rash appears the illness is essentially over, and management is reassurance and supportive care.\n\n![Roseola: rash as the fever breaks: roseola 001. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/f42e6032602546a080873653ee0852cc.jpg)", "parent_id": null, "variant": "long"}, {"id": "572fedd22a014fbba734827c218eb120", "slug": "erythema-infectiosum-slapped-cheeks-and-lacy-reticular-rash", "title": "Erythema infectiosum: slapped cheeks and lacy reticular rash", "content": "Parvovirus B19 has a particular tropism for erythroid progenitor cells at the pronormoblast stage, which is why erythema infectiosum (fifth disease) begins with mild fever and upper respiratory symptoms before an intensely erythematous \"slapped cheek\" rash appears, often with striking circumoral pallor. Days later a symmetric, lacy, reticular (net-like) pink rash spreads over the extremities and trunk; this second-stage rash characteristically flares with heat, sun exposure, or exercise for one to several weeks afterward, a distinctive recurring pattern unlike any other childhood exanthem. Peak incidence is between 5 and 15 years of age; transmission is respiratory with an incubation of 4 to 28 days (mean 16 to 17). By the time the rash appears the child is past the infectious viremic phase and can return to school. The same erythroid tropism explains the disease's two serious complications: transient aplastic crisis in children with a chronic [[hemolytic anemia|hemolytic-anemia]] such as [[sickle cell disease|sickle-cell-disease]], and fetal hydrops if a nonimmune pregnant contact is infected, both reasons to ask about exposures even though the rash itself needs no treatment beyond reassurance.\n\n![Erythema infectiosum: slapped cheeks and lacy reticular rash: Erythema infectiosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/fdfc6a73ae1b4aa19edaf3cb0e8caf5b.jpg)", "parent_id": null, "variant": "long"}, {"id": "b39626d8b70740d8b5fa03ae4b5cf0f2", "slug": "scarlet-fever-sandpaper-rash-strawberry-tongue-desquamation", "title": "Scarlet fever: sandpaper rash, strawberry tongue, desquamation", "content": "Scarlet fever is a reaction to pyrogenic exotoxins from group A streptococcus, usually accompanying streptococcal pharyngitis. Its fine, papular, sandpaper-textured rash begins on the neck and upper chest and concentrates in skin creases as linear petechial streaks (Pastia lines), while the face shows flushed cheeks with circumoral pallor. After several days the rash is followed by desquamation of the hands and feet, alongside a strawberry tongue. The photograph and full account are in [[430|Rashes & Exanthems]].", "parent_id": null, "variant": "long"}, {"id": "6578250ff3084124b75c4808cc63923b", "slug": "varicella-lesions-in-all-stages", "title": "Varicella: lesions in all stages", "content": "Varicella's hallmark is the simultaneous presence of lesions in every stage of evolution on the same patient, from erythematous macules to papules, vesicles (a \"dewdrop on a rose petal\"), pustules, and crusts, distributed centripetally with heavier involvement of the trunk and scalp than the limbs, and often with a handful of lesions on mucosal surfaces as well. New crops continue to appear for several days, which is why lesions of every stage are visible together rather than a rash of uniform lesions. The photograph and full account are in [[340|Varicella Zoster]].", "parent_id": null, "variant": "long"}, {"id": "fc138a2fad334e049c6100cf6aaf40ea", "slug": "hand-foot-and-mouth-disease", "title": "Hand, foot and mouth disease", "content": "Hand, foot and mouth disease is caused by coxsackievirus, commonly A16, or, in more severe outbreaks, enterovirus A71. It produces gray-white oval vesicles on an erythematous base concentrated on the palms, soles, and buttocks, together with painful erosions on the tongue, buccal mucosa, and palate, in a young child who is often otherwise only mildly unwell with low-grade fever. The mouth pain, more than the skin lesions, is usually what drives a family to seek care. The photograph and full account are in [[141|Pediatric Dermatology]].", "parent_id": null, "variant": "long"}, {"id": "221080c27bec4cf2af4a4ac7703b0b0b", "slug": "gianotti-crosti-syndrome", "title": "Gianotti-Crosti syndrome", "content": "Gianotti-Crosti syndrome (papular acrodermatitis of childhood) is a reactive eruption seen most often between 1 and 6 years of age, historically linked to [[hepatitis B|hepatitis-b]] but now attributed more often to Epstein-Barr virus, cytomegalovirus, parvovirus B19, human herpesvirus 6, coxsackievirus, and other common childhood [[viral infections|viral-infection]]. The lesions are monomorphic, flat-topped, lichenoid papules that appear in crops and are notably acral: they favor the face, buttocks, and extremities and characteristically spare the trunk, sometimes becoming confluent over pressure points such as the knees and elbows. Skin biopsy, when performed, is nonspecific, showing a perivascular mononuclear infiltrate with epidermal spongiosis, so the diagnosis rests on the distinctive clinical pattern rather than histology. The acral distribution with trunk sparing is the key discriminator from other viral exanthems and from Gianotti-Crosti's more common look-alikes, which tend to be truncal. The eruption is self-limited, typically resolving over several weeks without scarring, and treatment is symptomatic only, directed at itch if present; the workup, if any, is aimed at identifying an associated infection such as hepatitis rather than at the rash itself.\n\n![Gianotti-Crosti syndrome: Gianotti-Crosti syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/d6c800ce92c940a0a6fb0cfc79e962af.jpg)", "parent_id": null, "variant": "long"}, {"id": "5e4cedf639de4b2cb7d83138a21bc01d", "slug": "erythema-toxicum-neonatorum", "title": "Erythema toxicum neonatorum", "content": "[[Erythema toxicum neonatorum|erythema-toxicum-neonatorum]] is a benign eruption of unknown cause that affects roughly half of full-term infants and appears somewhat less often in preterm infants. Lesions are firm, yellow-white, 1- to 2-mm papules or pustules surrounded by a blotchy erythematous flare, which has earned the eruption the nickname \"flea-bite\" dermatosis; the palms and soles are always spared. Lesions typically begin 24 to 48 hours after birth (occasionally as late as the tenth day), unlike transient neonatal pustular melanosis, which is already present at delivery, and a Wright-stained smear of the pustule contents shows an infiltrate rich in eosinophils with no organisms, again distinguishing it from an infectious pustulosis. The course is brief, three to seven days, and the lesions resolve completely without residual pigmentation. No treatment or workup is needed beyond recognizing the pattern and reassuring the family that the eruption is entirely benign; the two facts worth carrying forward are the timing (after birth, not at birth) and the eosinophilic, sterile nature of the pustule contents.\n\n![Erythema toxicum neonatorum: Toxic erythema of the newborn. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/4d4730dacc894f158f9f6a426b351a92.jpg)", "parent_id": null, "variant": "long"}, {"id": "ce5761f7330b445797442ef6e9e219f5", "slug": "milia", "title": "Milia", "content": "Milia are tiny, 1- to 2-mm, firm, whitish-yellow papules that arise on the face, most often the nose, forehead, and cheeks, in as many as 40% of newborns. They are keratin retention cysts, formed when keratinous and sebaceous debris becomes trapped within the follicular opening rather than shedding normally, which explains both their firmness (unlike a pustule, they are not denuded by gentle pressure) and their eventual resolution once the follicle matures and clears. Their intraoral counterpart, small keratin-filled cysts on the palate, is called an Epstein pearl and is found in up to 60% to 85% of newborns. Most facial milia clear spontaneously within the first month of life without any treatment. Milia acquired later in childhood usually follow local skin trauma such as a burn or blister, and widespread or persistent milia occasionally point toward a genodermatosis such as oral-facial-digital syndrome or epidermolysis bullosa, which is the one situation in which the family should be asked about associated findings rather than simply reassured.\n\n![Milia: Neonatal centrofacial milia. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/1d5b2aac7d07456e94e9e80db2236c7b.jpg)", "parent_id": null, "variant": "long"}, {"id": "0ace8aa054104fceace34be89b037420", "slug": "neonatal-cephalic-pustulosis-neonatal-acne", "title": "Neonatal cephalic pustulosis (neonatal acne)", "content": "Neonatal cephalic pustulosis, commonly called neonatal acne, becomes apparent within the first two to four weeks of life and affects roughly one in five newborns. It presents as multiple 1- to 2-mm dusky pink papules and pustules concentrated on the face, especially the nasal bridge and cheeks, and sometimes the scalp. Comedones are absent, which is the key point separating this condition from true infantile acne, a distinct and later-onset disorder (usually presenting around three to six months) that does show comedones, can scar, and often needs active treatment. The mechanism here is thought to be a hypersensitivity-type inflammatory reaction to Malassezia yeast species (M. furfur, M. sympodialis) colonizing the sebaceous follicles, on a background of transient stimulation of the newborn's sebaceous glands by residual maternal and fetal androgens, rather than a true acneiform process. The eruption is self-limited and clears within weeks without scarring. No treatment is required; the family needs reassurance and a clear explanation of why this is not \"baby acne\" in the sense the term is usually used, since that distinction determines whether any treatment is warranted at all.\n\n![Neonatal cephalic pustulosis (neonatal acne): Neonatal cephalic pustulosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/88e71fb680804d44b998af1bac6c188d.jpg)", "parent_id": null, "variant": "long"}, {"id": "e7888d8c6d5e451bacfcc6bb0affb948", "slug": "transient-neonatal-pustular-melanosis", "title": "Transient neonatal pustular melanosis", "content": "Transient neonatal pustular melanosis is present at birth, which is the single most useful fact separating it from [[erythema toxicum neonatorum|erythema-toxicum-neonatorum]], its main mimic, which instead appears after a day or two. Three lesion types can be seen together in the same infant: fragile, evanescent superficial vesiculopustules that rupture within 24 to 48 hours, a ring or collarette of fine scale left where a pustule has ruptured (sometimes surrounding a small hyperpigmented macule), and hyperpigmented macules alone, which can persist for weeks to months after the pustular phase has resolved. Lesions favor the forehead, neck, chin, and lower back, and occasionally involve the palms and soles. A Wright-stained smear of pustule contents shows neutrophils rather than the eosinophils of erythema toxicum, and no organisms are seen on stain or culture, confirming the sterile, self-limited nature of the process. No treatment is required, and the family can be reassured that even the residual pigmented macules will fade over time without scarring; the diagnosis is made on the combination of timing (present at birth) and the coexistence of pustules, collarettes, and pigmented macules on the same infant.\n\n![Transient neonatal pustular melanosis: Transient neonatal pustular melanosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/e35145c6a288485282a18f8f30965235.jpg)", "parent_id": null, "variant": "long"}, {"id": "d84ed2b65f0b47e7aca35939e1f638a4", "slug": "infantile-seborrheic-dermatitis-cradle-cap", "title": "Infantile seborrheic dermatitis (cradle cap)", "content": "Cradle cap is a physiological finding in infants under three months of age, reflecting an overactive infantile sebaceous gland driven by residual maternal hormones together with local Malassezia yeast colonization. The photograph shows the typical greasy, yellow, adherent scale over the scalp, though the same process can extend to the eyebrows, nasolabial folds, retroauricular skin, and diaper area; the eruption is not itchy, which distinguishes it from [[atopic dermatitis|atopic-dermatitis]], and its course is self-limited over the first several months of life. First-line care is simple: regular emollients and a mild, non-medicated baby shampoo, with gentle removal of loosened scale rather than aggressive scrubbing. For more widespread, symptomatic, or persistent disease, a 2% ketoconazole cream or a mild topical corticosteroid such as 1% hydrocortisone (sometimes combined) is effective, and topical calcineurin inhibitors are a further option for refractory or facial disease that a family wants to avoid treating with repeated steroid courses. Resolution without treatment is the rule, and the family's main need is reassurance that the greasy scale, however alarming it looks, reflects a benign and temporary imbalance rather than poor hygiene or an infection.\n\n![Infantile seborrheic dermatitis (cradle cap): Cradle cap. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/ee838d963605462692ed010daf00f05f.jpg)", "parent_id": null, "variant": "long"}, {"id": "2cfc44723b1b4e098c1bc6e9cffd6c55", "slug": "diaper-dermatitis-irritant-versus-candidal", "title": "Diaper dermatitis: irritant versus candidal", "content": "Irritant diaper dermatitis is the most common dermatologic problem of infancy, affecting roughly half of all diaper-wearing infants at some point. It results from prolonged skin contact with urine and feces, overhydration of the stratum corneum, and friction, and it characteristically involves the convex surfaces most exposed to the wet diaper (the buttocks, lower abdomen, and upper thighs) while sparing the deep skin folds, since urine and feces pool less there. Recognizing that fold-sparing pattern is the first step in distinguishing simple irritant dermatitis from a superimposed candidal infection, discussed separately. Management is straightforward and highly effective: frequent diaper changes, scheduled diaper-free intervals to let the skin dry, gentle cleansing with a soft cloth and lukewarm water rather than repeated wiping or vigorous washing (which itself worsens the irritation), and a barrier ointment such as zinc oxide or petrolatum applied at each change. Allergic contact dermatitis from dyes or fragrances in diapers or wipes is a less common variant, distributed at the waistband or diaper edges rather than in the perianal area, and responds to switching to dye-free, fragrance-free products.\n\n![Diaper dermatitis: irritant versus candidal: Napkin dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/a4742b1ce1c24c369c715d3d22a52fa5.jpg)", "parent_id": null, "variant": "long"}, {"id": "a4cae3e11a30468d8e49c86764473e0d", "slug": "candidal-napkin-dermatitis-thrush-satellite", "title": "Candidal napkin dermatitis thrush satellite", "content": "Candidal diaper dermatitis is the most common infectious complication of the diaper area and often follows a course of oral antibiotics, which suppresses competing bacterial flora and allows Candida overgrowth. Unlike simple irritant dermatitis, it produces confluent, beefy-red, weeping plaques with a scalloped, overhanging edge of scale that characteristically involves the deep skin folds (the groin and gluteal creases), and it is studded at its margins with the discrete satellite papules and pustules that give the condition its name. Diagnosis is usually clinical, but a potassium hydroxide preparation of a satellite lesion shows budding yeast and pseudohyphae if confirmation is needed, and culture can be reserved for cases that fail to respond as expected. A practical rule used in practice is to treat any diaper rash that has persisted beyond three days presumptively with a topical antifungal, since candidal superinfection is common by that point even when the eruption began as simple irritation. First-line treatment is topical nystatin, clotrimazole, or miconazole applied with each diaper change alongside the usual barrier measures, continued until the rash has fully cleared rather than only improved.\n\n![Candidal napkin dermatitis thrush satellite: Napkin dermatitis thrush. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/86660d1ddb8a4782ab73efc43dabb387.jpg)", "parent_id": null, "variant": "long"}, {"id": "beb9c3734b654508a4ee1f273c89560b", "slug": "mongolian-spot-dermal-melanocytosis", "title": "Mongolian spot dermal melanocytosis", "content": "Mongolian spots (congenital dermal melanocytosis) are flat, poorly circumscribed, slate-gray to bluish-black macules or patches, most often over the lumbosacral area and buttocks though they can occur anywhere, ranging from 1 to 10 cm and sometimes appearing in clusters. They are extremely common in darkly pigmented infants (seen in roughly 85% to 100% of Asian and over 60% of Black newborns, but under 10% of White newborns) and are present at birth. The color reflects melanocytes that became arrested in the dermis during their embryonic migration from the neural crest toward the epidermis, rather than a true nevus or an area of bruising, which is the discrimination that matters most clinically: because the lesions can resemble bruises, documenting their presence, distribution, and size at birth in the medical record protects the family from a later, mistaken concern for inflicted injury. Most Mongolian spots fade gradually over the first several years of life and need no treatment. Extensive or unusually persistent dermal melanocytosis is occasionally a clue to an underlying lysosomal storage disease, such as Hurler, Hunter, or GM1 gangliosidosis, and warrants a closer look at the infant's overall growth and development.", "parent_id": null, "variant": "long"}, {"id": "f9a48bf843414e2583fb0c4e560bfad2", "slug": "infantile-hemangioma", "title": "Infantile hemangioma", "content": "[[Infantile hemangioma|infantile-hemangioma]] is a vascular tumor, not a malformation: it is usually absent or barely visible at birth, proliferates rapidly over the first few months as endothelial cells multiply, and then involutes slowly over years, a growth pattern that itself distinguishes it from the vascular malformations discussed elsewhere in this section. The photograph and full account are in [[156|Infantile Hemangioma]].", "parent_id": null, "variant": "long"}, {"id": "c2e1abb5c26d4547ae157b5a9e847d40", "slug": "port-wine-stain", "title": "Port-wine stain", "content": "A port-wine stain is a capillary vascular malformation, not a tumor: it is present at birth, grows only in proportion to the child, and does not regress the way an [[infantile hemangioma|infantile-hemangioma]] does, instead becoming darker, thicker, and more nodular over years. Clinically it appears as a sharply demarcated, deep pink-to-purple patch, most often on the face, affecting some 0.3% to 0.5% of children equally in both sexes. Its clinical significance turns almost entirely on location: a facial port-wine stain that involves the ophthalmic (V1) division of the trigeminal nerve, covering the forehead and upper eyelid, carries roughly a 26% risk of Sturge-Weber syndrome, compared with about 6% for any facial port-wine stain regardless of distribution. Sturge-Weber syndrome, caused by a somatic mosaic mutation in GNAQ, combines the cutaneous capillary malformation with an ipsilateral leptomeningeal vascular malformation and often glaucoma, and can present with [[seizures|seizures]], [[intellectual disability|intellectual-disability]], or hemiparesis depending on severity. Any infant with a V1-distribution port-wine stain therefore needs ophthalmologic evaluation for glaucoma and a low threshold for neuroimaging if there are neurologic signs. Pulsed dye laser, started early, is the standard treatment for the skin lesion itself.\n\n![Port-wine stain: Port-wine stain. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/c22df116adda4117a244fe001c6d84f2.jpg)", "parent_id": null, "variant": "long"}, {"id": "23fb57df099c41f7999ca7ea35a10eb6", "slug": "caf-au-lait-macules", "title": "Caf\u00e9-au-lait macules", "content": "Caf\u00e9-au-lait macules are light to medium brown, round or oval patches with smooth, well-demarcated borders, ranging from under a centimeter to many centimeters across and often most numerous on the trunk. A single small caf\u00e9-au-lait macule is common in the general population and is not itself a concern, but the number and size of the lesions matter: six or more caf\u00e9-au-lait macules greater than 5 mm in a prepubertal child (or greater than 15 mm after puberty) is one of the diagnostic criteria for [[neurofibromatosis type 1|neurofibromatosis-type-1]], which requires two of seven total criteria (the others being two or more neurofibromas or one plexiform neurofibroma, axillary or inguinal freckling, an optic pathway glioma, two or more Lisch nodules on the iris, a distinctive bony lesion such as sphenoid dysplasia or tibial pseudarthrosis, or a first-degree relative who meets the criteria). The macules' smooth border is itself a discriminating feature, in contrast to the irregular, \"coast of Maine\" border of the pigmented macules of McCune-Albright syndrome. The practical next step in a child with multiple caf\u00e9-au-lait macules is to count and measure them, examine the axillae and groin for freckling, and refer for genetics and ophthalmology evaluation if criteria are met.\n\n![Caf\u00e9-au-lait macules: Caf\u00e9-au-lait macule. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/8417c4b8f6de4b28a53a84d3c2b2e5a5.jpg)", "parent_id": null, "variant": "long"}, {"id": "0b4178d60bdb46bfa555dd11e06e5785", "slug": "nevus-sebaceus", "title": "Nevus sebaceus", "content": "Nevus sebaceus is a congenital, hairless, orange-yellow, slightly raised plaque most often found on the scalp or face, present at birth and often becoming more waxy, verrucous, and nodular around puberty under the influence of rising androgens. It arises from a somatic mosaic mutation in HRAS or KRAS, disrupting the same growth-signaling pathways implicated in a range of benign and, less often, malignant skin tumors that can develop within the lesion over a lifetime, most commonly trichoblastoma, syringocystadenoma papilliferum, or trichilemmoma, with basal cell carcinoma occurring only rarely. Older teaching held that 10% to 15% of these lesions undergo malignant transformation, but more recent series put secondary tumor development, most of it benign, at around 14% over a lifetime and true malignant transformation far lower than once believed. Because of the small but real chance of secondary tumor formation and the cosmetic change expected at puberty, management options include either periodic monitoring through adolescence or elective surgical excision, often timed before puberty both for cosmesis and to preempt the tissue changes that follow hormonal activation of the lesion.\n\n![Nevus sebaceus: Naevus sebaceous. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/d9fcd8efe6a94ed09ab52928f7b89797.jpg)", "parent_id": null, "variant": "long"}, {"id": "08e6ba1606954312bf65630fb126ffcb", "slug": "impetigo-honey-crusted-and-bullous", "title": "Impetigo: honey-crusted and bullous", "content": "Impetigo is a superficial epidermal infection with two patterns: the common, nonbullous form shows thin vesicles that rupture quickly to leave the classic honey-colored crust, most often around the nose and mouth, while bullous impetigo shows flaccid bullae over an inch across that rupture to leave a thin, varnish-like crust. The photograph and full account are in [[430|Rashes & Exanthems]].", "parent_id": null, "variant": "long"}, {"id": "22bc70ffe71144b1b8c2ddbbe53b97f4", "slug": "cellulitis", "title": "Cellulitis", "content": "[[Cellulitis|cellulitis]] is a [[bacterial infection|bacterial-infections]] of the dermis and subcutaneous tissue, one layer deeper than the superficial infection of erysipelas, and that depth is exactly what produces its defining physical sign: erythema, warmth, tenderness, and swelling with borders that fade gradually into normal skin rather than the sharply raised, well-demarcated edge of erysipelas. Group A streptococcus and Staphylococcus aureus are the leading causes overall, with the lower extremities and feet the most frequently affected sites; in infants under three months, group B streptococcus is an important additional cause and can be associated with [[bacteremia|bacteremia]]. A break in the skin barrier, whether from trauma, an insect bite, tinea pedis, or an underlying condition such as [[atopic dermatitis|atopic-dermatitis]], is the usual portal of entry, and because the causative organism sits within intact skin rather than at an open wound, cultures from the leading edge have a low yield, so most cases are treated empirically. Signs that should prompt urgent reassessment rather than routine outpatient antibiotics include rapid progression, lymphangitic streaking, abscess formation, pain out of proportion to examination findings, or systemic illness, all of which raise concern for a deeper or necrotizing process.\n\n![Cellulitis: Cellulitis of the left leg. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/6c8b5ceb542f448dbf014a109efd83e2.jpg)", "parent_id": null, "variant": "long"}, {"id": "d0cea4514be24428abc54177739be36e", "slug": "staphylococcal-scalded-skin-syndrome", "title": "Staphylococcal scalded skin syndrome", "content": "Staphylococcal scalded skin syndrome is caused not by direct [[skin infection|skin-infections]] but by hematogenous spread of an exfoliative (epidermolytic) toxin from a distant staphylococcal focus, most often the nasopharynx, conjunctivae, or umbilicus, produced predominantly by phage group 2 strains. The toxin cleaves desmoglein-1, a protein that holds keratinocytes together within the granular layer of the epidermis, causing the superficial epidermis to separate from itself while sparing the deeper dermis, which is why gentle lateral pressure on seemingly normal skin causes it to shear away (a positive Nikolsky sign) and why the disease, despite its dramatic and generalized appearance, spares the mucous membranes, in contrast to toxic epidermal necrolysis, where necrosis extends through the full thickness of the epidermis and mucosal surfaces are severely involved. It occurs mainly in infants and young children, who develop fever, malaise, and marked skin tenderness, often preceded by a localized crusting infection around the eyes, nose, and mouth, followed by widespread erythema and superficial peeling. Because the process is toxin-mediated rather than a true skin infection, treatment centers on systemic antistaphylococcal antibiotics together with supportive skin and fluid care similar to that used for a burn, rather than topical therapy alone.\n\n![Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/79792c718a2a4fc3943173c1e5247abc.jpg)", "parent_id": null, "variant": "long"}, {"id": "cfb8af41e0dd4e52bc4a887082cde190", "slug": "erythema-migrans", "title": "Erythema migrans", "content": "Erythema migrans, the rash of early [[Lyme disease|lyme-disease]], begins as a red macule or papule at the site of an Ixodes tick bite that expands over days to a large annular patch, often with central clearing that gives it the classic \"bull's-eye\" appearance, though uniform erythema without clearing is at least as common in practice. The photograph and full account are in [[191|Lyme Disease]].", "parent_id": null, "variant": "long"}, {"id": "0be2341bbceb4bd19fa90f0c8ed2b951", "slug": "tinea-corporis", "title": "Tinea corporis", "content": "Tinea corporis produces an annular, scaly plaque with a raised, active, often vesicular or pustular border and a clearer center, growing outward as the dermatophyte advances through the stratum corneum while the older, central skin resolves behind it. One or several plaques can appear anywhere on the trunk or limbs, and the annular, expanding shape with the more active edge is what separates it from other scaly plaques such as nummular [[eczema|eczema]]. The photograph and full account are in [[141|Pediatric Dermatology]].", "parent_id": null, "variant": "long"}, {"id": "80ec8597a717491aa2cfd2958f7867e6", "slug": "tinea-capitis-and-kerion", "title": "Tinea capitis and kerion", "content": "[[Tinea capitis|tinea-capitis]] presents with patchy scale and broken hairs on the scalp, often with cervical or occipital lymphadenopathy that helps distinguish it from simple dandruff or seborrheic dermatitis. If the host mounts an exuberant inflammatory response to the dermatophyte, a kerion can develop: a boggy, tender, pus-filled, sometimes scarring plaque that is often mistaken for a bacterial abscess but is a reaction to the fungus rather than a true infection needing incision and drainage. The photograph and full account are in [[339|Tinea Capitis]].", "parent_id": null, "variant": "long"}, {"id": "92db13b6a54f49ffa8a534d9d1e9b5f9", "slug": "tinea-pityriasis-versicolor", "title": "Tinea (pityriasis) versicolor", "content": "[[Tinea versicolor|tinea-versicolor]] produces multiple fine, finely scaling, round-to-oval patches on the trunk and upper arms that appear lighter than surrounding skin in tanned or dark complexions and pink-to-tan in pale skin, which is where the name \"versicolor\" comes from. It is caused by overgrowth of the skin's own commensal Malassezia yeast, favored by heat and humidity, rather than a true dermatophyte, and the pigment change can persist for weeks even after treatment clears the yeast. The photograph and full account are in [[401|Tinea Versicolor]].", "parent_id": null, "variant": "long"}, {"id": "c55c51a78279447f8d758c819545b486", "slug": "tinea-pedis", "title": "Tinea pedis", "content": "Tinea pedis in children takes several forms. The interdigital type is the most common, producing pruritic maceration, fissuring, and scaling most often in the third and fourth web spaces; the \"moccasin\" pattern instead produces confluent, dry, hyperkeratotic scaling across the entire sole and sides of the foot without much inflammation, and a vesiculopustular form can also occur, especially on the instep. All patterns are caused by dermatophyte invasion of the keratinized stratum corneum, most commonly Trichophyton rubrum, and a potassium hydroxide preparation showing septate hyphae confirms the diagnosis when needed. The moccasin pattern in particular must be distinguished from simple interdigital maceration, contact or [[atopic dermatitis|atopic-dermatitis]] of the foot, and juvenile plantar dermatosis, a shiny, glazed, fissured eruption of the weight-bearing sole related to friction and occlusive footwear rather than infection; a KOH preparation settles the question when the clinical picture is ambiguous. Recurrence is common because the fungus persists in shoes and socks even after the skin clears, so footwear hygiene is part of treatment. A topical imidazole applied twice daily for two to four weeks clears most cases; the more hyperkeratotic moccasin pattern and refractory or extensive disease often need a course of oral antifungal therapy instead.\n\n![Tinea pedis: Moccasin tinea pedis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/ecd3011f82fb4f57ae775ffcd9b6573d.jpg)", "parent_id": null, "variant": "long"}, {"id": "598df19aae6b44a69665515b8699c610", "slug": "molluscum-contagiosum", "title": "Molluscum contagiosum", "content": "Molluscum contagiosum presents as skin-colored, dome-shaped, waxy papules with a characteristic central dell (umbilication), most often clustered on the trunk, face, and extremities, and affects an estimated 5% to 11% of children between infancy and age 16. Individual lesions are usually painless, though itching, surrounding redness, or a low-grade eczematous reaction around a lesion can occur as the immune system begins to clear it, and this inflammation often precedes spontaneous resolution rather than signaling worsening infection. The photograph and full account are in [[141|Pediatric Dermatology]].", "parent_id": null, "variant": "long"}, {"id": "b5e9db8ee5c545eeb8eab3cfc747539a", "slug": "common-and-plantar-warts", "title": "Common and plantar warts", "content": "Common and plantar warts are caused by cutaneous human papillomavirus types, most often HPV-1, -2, -4, and -7, which infect the squamous epithelium and drive a localized, benign overgrowth of the epidermis. Common warts are skin-colored, rough, minimally scaly papules and nodules found most often on the hands, ranging from a few millimeters to several centimeters and sometimes coalescing into plaques through autoinoculation, while plantar warts occur on weight-bearing soles and are often flattened by pressure into the skin. The clinical trick that separates a wart from a callus is that a wart obliterates the normal parallel skin lines (dermatoglyphics) running across the site, while a callus preserves them, since a callus is simple pressure-induced thickening of otherwise normal skin rather than a growth of infected epithelium. Diagnosis is almost always made by inspection alone; biopsy is reserved for atypical, treatment-resistant, or worsening lesions. The great majority of HPV infections in children are subclinical, and roughly 90% resolve spontaneously within two years as cell-mediated immunity clears the virus, which is why observation alone is a reasonable choice; when treatment is wanted, options include salicylic acid, cryotherapy, and cantharidin.\n\n![Common and plantar warts: Common warts. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/bac8d53ab1fc4b2eb2add1b6ce28230c.jpg)", "parent_id": null, "variant": "long"}, {"id": "30ba414b87de477cbc950f0a07f9bba8", "slug": "herpetic-gingivostomatitis-mouth-gums-primary-herpes-simplex", "title": "Herpetic gingivostomatitis mouth gums primary herpes simplex", "content": "Primary herpetic gingivostomatitis, caused by herpes simplex virus type 1, peaks in children between about six months and three years of age and begins with fever, irritability, and painful, swollen, easily bleeding gums (gingival hyperemia and edema) together with regional lymphadenopathy. Painful vesicles then erupt across the gingiva, tongue, buccal mucosa, lips, and hard and soft palate, rupturing quickly into shallow ulcers covered by a gray-white membrane and surrounded by a red halo, often coalescing into larger painful erosions that make oral intake difficult. This anterior, gum-involving, whole-mouth distribution distinguishes it from herpangina, a coxsackievirus infection confined to the posterior pharynx and soft palate that spares the gingiva, and from simple aphthous ulcers, which lack fever, vesicles, or gingival swelling. Management is chiefly supportive: pain control, and attention to hydration, since oral pain can lead to refusal of fluids severe enough to require intravenous support in a young child. Oral acyclovir, started early in the course, can shorten the duration of lesions, fever, and viral shedding, and is generally reserved for more severe presentations or immunocompromised children rather than given routinely for mild disease.\n\n![Herpetic gingivostomatitis mouth gums primary herpes simplex: Herpes simplex on the cheek. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/e8da12bbb9f9470dbffa427fe61fa586.jpg)", "parent_id": null, "variant": "long"}, {"id": "afbc6bc21d8745b481c5d63c92fed5c4", "slug": "eczema-herpeticum", "title": "Eczema herpeticum", "content": "[[Eczema|eczema]] herpeticum is a herpes simplex virus superinfection of skin whose barrier is already broken, almost always by underlying [[atopic dermatitis|atopic-dermatitis]], and is one form of the broader group of conditions called Kaposi varicelliform eruption, in which a second infection (herpes simplex, coxsackievirus, or vaccinia) spreads widely across preexisting dermatitis rather than staying localized the way it would on normal skin. It presents as widespread, monomorphic vesicles and pustules that quickly break down into characteristic punched-out erosions scattered over areas of active or recently active dermatitis, usually with fever and malaise, and it can look at first glance like simple bacterial impetiginization of eczema; the clustering of uniform, punched-out lesions rather than the honey-colored crust of impetigo is the clue that should raise suspicion. Because the underlying process is viral and can disseminate, especially in a child with a large area of disrupted skin barrier, eczema herpeticum is treated as a dermatologic emergency rather than managed with topical care or antibiotics alone: it requires systemic acyclovir or valacyclovir, and any periocular involvement needs urgent ophthalmology evaluation because of the risk of herpetic keratitis and vision loss.\n\n![Eczema herpeticum: Eczema herpeticum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/febda93809e94f67acb5069cbde57aa9.jpg)", "parent_id": null, "variant": "long"}, {"id": "1ce68fd9c73342f593fe19c328fab9ba", "slug": "herpes-zoster-in-a-child", "title": "Herpes zoster in a child", "content": "[[Herpes zoster|herpes-zoster]] results from reactivation of latent varicella-zoster virus that has persisted in a dorsal root ganglion since the child's primary varicella infection, traveling back down the sensory nerve to erupt as grouped vesicles on an erythematous base confined to a single dermatome, usually in a unilateral band. It is uncommon in otherwise healthy children and shows no seasonal pattern; contrary to intuition, exposure to a case of varicella actually boosts cell-mediated immunity to the virus and lowers the chance of reactivation, so zoster is not \"caught\" from a case of chickenpox. The lifetime risk of zoster after a childhood varicella infection is at least 30%. Unlike in adults, postherpetic neuralgia is uncommon in healthy children, so treatment of an otherwise uncomplicated case is optional; when treatment is chosen, oral acyclovir at 20 mg/kg per dose (maximum 800 mg) shortens the illness if started promptly. In an immunocompromised child, however, zoster can disseminate and become life-threatening, and these children should receive intravenous acyclovir at 10 mg/kg (or 500 mg/m2) every eight hours rather than oral therapy.\n\n![Herpes zoster in a child: Herpes zoster. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/b5670e962deb4e0580baa5e4a9c5bfdc.jpg)", "parent_id": null, "variant": "long"}, {"id": "41062eb0533348199046423d276d0754", "slug": "scabies-burrows-and-the-infant-pattern", "title": "Scabies: burrows and the infant pattern", "content": "Scabies produces intensely pruritic, excoriated papules with threadlike burrows classically found in the finger webs and flexor wrists, worse at night, and reflecting a delayed hypersensitivity reaction to the mite, its eggs, and its feces rather than to the burrowing itself. Infants show a different, more diffuse pattern involving the scalp, face, palms, and soles, sites otherwise spared in older children and adults, with bullae and pustules more prominent than obvious burrows, which can make the infant presentation easy to miss. The photograph and full account are in [[430|Rashes & Exanthems]].", "parent_id": null, "variant": "long"}, {"id": "0fa31a7b601d493886ac05e4ff516c89", "slug": "head-lice", "title": "Head lice", "content": "Head lice (Pediculosis capitis) infestation is confirmed by finding live lice or, more often, nits, the eggs cemented firmly to the hair shaft close to the scalp; the firm attachment is the key discriminator from dandruff or hair-care debris, which slides freely along the hair rather than staying fixed at one point. Adult and nymphal lice feed on scalp blood and deposit saliva and fecal matter on the skin, and it is sensitization to these deposits, not the bite itself, that produces the hallmark symptom of pruritus, which is why pruritus typically does not appear until some weeks into an infestation rather than immediately at exposure, a delay that often surprises families who expect itching to start right away. Transmission is by direct head-to-head contact and, less often, by shared fomites such as combs or hats. First-line treatment is a topical pediculicide such as permethrin 1%, applied to dry hair and rinsed after the recommended contact time; because most agents are less reliably ovicidal than they are lousicidal, a second application seven to nine days later is usually advised to kill lice that hatch after the first treatment, together with wet combing to remove residual nits.\n\n![Head lice: Head lice eggs. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/73a42a35423741faa38cfed3af15a2c3.jpg)", "parent_id": null, "variant": "long"}, {"id": "6163c00ea7174aa9921e798f549918e2", "slug": "pityriasis-rosea-herald-patch-and-christmas-tree-pattern", "title": "Pityriasis rosea: herald patch and Christmas-tree pattern", "content": "Pityriasis rosea is a common, benign, self-limited papulosquamous eruption most often affecting adolescents and young adults, more frequent in winter, with a suspected but unconfirmed viral trigger, current evidence pointing toward human herpesviruses 6 and 7. It begins with a single, larger \"herald patch,\" an oval plaque with a fine collarette of scale at its edge, easily mistaken at this stage for tinea corporis; days to weeks later, numerous smaller oval, scaly papules and plaques erupt over the trunk, their long axes running along the skin's natural cleavage lines so that on the back they fan out in a pattern that has been likened to the branches of a Christmas tree. This orientation along cleavage lines, together with the preceding herald patch, is what separates pityriasis rosea from guttate psoriasis and from a viral exanthem, neither of which shows the same patterned alignment. The disease resolves on its own over roughly six to eight weeks without scarring, so the main task is recognition and reassurance; antihistamines or emollients can be offered for associated itch, but no antiviral or antifungal treatment changes the natural course.\n\n![Pityriasis rosea: herald patch and Christmas-tree pattern: Pityriasis rosea. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/4127f84870ea470687f9fd73192c2968.jpg)", "parent_id": null, "variant": "long"}, {"id": "fe0d639924a0485ea8ac79333a54b1ff", "slug": "atopic-dermatitis-by-age", "title": "Atopic dermatitis by age", "content": "[[Atopic dermatitis|atopic-dermatitis]]'s morphology and distribution shift with age: infants show weeping, crusted patches on the cheeks and extensor surfaces, while older children and adolescents develop lichenified, dry, scaly plaques concentrated in the flexural creases, both driven by chronic pruritus (itching in the past 12 months) plus features such as early onset, personal or family history of atopy, and generalized xerosis. The photograph and full account are in [[195|Atopic Dermatitis]].", "parent_id": null, "variant": "long"}, {"id": "a0230f40abd143d1b0df212c6a638fbf", "slug": "allergic-contact-dermatitis", "title": "Allergic contact dermatitis", "content": "Allergic contact dermatitis is a type IV, T-cell-mediated delayed hypersensitivity reaction to a specific sensitizing allergen, which requires prior exposure and sensitization, unlike irritant contact dermatitis, a direct toxic effect on the skin that can occur on first exposure to a strong enough irritant in anyone. The clinical signature of an allergic reaction is a sharply demarcated patch of erythema, edema, vesicles, or bullae whose shape mirrors the pattern of contact rather than any natural anatomic distribution, so a geometric or linear configuration, the outline of a watch strap, an adhesive bandage, or a henna tattoo, is itself strong diagnostic evidence of an external cause. Poison ivy and related plants illustrate the mechanism well: their oil (urushiol) becomes fixed to epithelial cells within about 20 minutes of contact and cannot spread further after that point, so lesions that appear to \"spread\" over subsequent days actually reflect staggered contact with different amounts of oil rather than true migration of the reaction; thorough washing within minutes of exposure can prevent the eruption entirely. Management is identification and avoidance of the allergen plus topical corticosteroids for established lesions.\n\n![Allergic contact dermatitis: Adhesive plaster reaction. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/b7f60ab8f40d43d68b3cd71b166ccc53.jpg)", "parent_id": null, "variant": "long"}, {"id": "1ec6e02e59d94a3ba0cd120ce734467a", "slug": "guttate-psoriasis", "title": "Guttate psoriasis", "content": "Guttate psoriasis presents with a sudden shower of small, drop-shaped (guttate, from the Latin for \"drop\"), scaly papules scattered over the trunk and proximal limbs, often erupting one to three weeks after a streptococcal pharyngitis in a child with no prior psoriasis history. Removing the fine scale can produce pinpoint bleeding, a finding also seen in plaque psoriasis, and the eruption can either resolve completely or mark the first presentation of chronic plaque psoriasis later in life. The photograph and full account are in [[141|Pediatric Dermatology]].", "parent_id": null, "variant": "long"}, {"id": "c0a33e9e243f43b8b52fb5378b56151e", "slug": "urticaria", "title": "Urticaria", "content": "Urticaria consists of pruritic, erythematous, edematous wheals or plaques that characteristically wax and wane, with any individual lesion resolving within 24 hours even as new ones appear elsewhere, a fixed-versus-fleeting distinction that is the single most useful discriminator in the differential. The wheal forms when mast cells degranulate and release histamine, causing plasma to leak from small dermal blood vessels into the surrounding connective tissue, which produces the superficial swelling; deeper, similar leakage into subcutaneous tissue produces the accompanying [[angioedema|angioedema]] seen in some patients. Triggers include infection (streptococcal and viral), medications, and foods, though many cases remain idiopathic. Two mimics are worth distinguishing by name: urticaria pigmentosa, a form of cutaneous mastocytosis with fixed reddish-brown macules that develop a hive-like wheal only when stroked (a positive Darier sign) rather than waxing and waning spontaneously, and urticarial vasculitis, in which individual lesions are fixed for longer than 24 hours, are often painful rather than itchy, may bruise as they resolve, and are accompanied by fever or joint pain. Ordinary urticaria is treated with non-sedating H1-antihistamines, dosed up to fourfold higher than usual in resistant cases, reserving epinephrine for accompanying angioedema or [[anaphylaxis|anaphylaxis]].\n\n![Urticaria: Urticaria. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/c5fc1820968843a1ab6436512e837deb.jpg)", "parent_id": null, "variant": "long"}, {"id": "8affcdaa790b4140bbd189416fa7e9aa", "slug": "erythema-multiforme-target-lesions", "title": "Erythema multiforme: target lesions", "content": "Erythema multiforme is a hypersensitivity reaction confined to the skin and, often, the oral mucosa, without the systemic toxicity of its more severe look-alikes; herpes simplex virus is by far its most common trigger, and the eruption may appear even after the preceding cold sore has already healed, with Mycoplasma pneumoniae a distant second cause, especially in children. The defining lesion is the target (iris) lesion: three concentric zones, a dusky or blistered center, a paler ring of edema, and an outer rim of erythema, distributed classically on the extensor surfaces of the hands, feet, and limbs, and appearing in crops over several days rather than all at once. What separates erythema multiforme from urticaria is that its lesions are fixed in place for days rather than migrating or resolving within hours, and what separates it from Stevens-Johnson syndrome is the near-absence of significant mucosal involvement and of the widespread epidermal detachment and systemic illness that define the more severe reaction. Management is symptomatic for an isolated episode; when episodes recur in step with herpes simplex outbreaks, suppressive antiviral therapy is used to prevent further flares rather than treating each episode as it occurs.\n\n![Erythema multiforme: target lesions: Cutaneous adverse reaction to anticonvulsant, erythema multiforme target lesions. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/dd7fc3aca3f941bd977cd6540ab767b9.jpg)", "parent_id": null, "variant": "long"}, {"id": "218ca2ef307b476eb939f9031acb7aa4", "slug": "erythema-nodosum", "title": "Erythema nodosum", "content": "Erythema nodosum is a septal panniculitis, inflammation confined to the fibrous septa of the subcutaneous fat rather than the fat lobules themselves, that produces tender, erythematous, poorly demarcated nodules, most typically over the shins, bilaterally. It reflects a delayed (type IV) hypersensitivity response to a circulating antigen rather than direct infection of the skin, which is why it is best understood as a reactive marker of an underlying process elsewhere: streptococcal pharyngitis is the most common identifiable trigger in children, alongside [[tuberculosis|tuberculosis]], coccidioidomycosis, histoplasmosis, [[inflammatory bowel disease|inflammatory-bowel-disease]], sarcoidosis, and certain drugs, notably oral contraceptives and sulfonamides. The condition is more common in adolescents than younger children and, throughout life, considerably more common in females. Because the nodules themselves are a reaction rather than the primary disease, evaluation is directed at finding the trigger, for instance a throat culture and streptococcal serology, a chest radiograph if sarcoidosis or tuberculosis is suspected, and a review for inflammatory bowel symptoms, rather than at the skin alone. Treatment is symptomatic (nonsteroidal anti-inflammatory drugs, rest, and leg elevation) together with treatment of the identified underlying cause; the nodules typically resolve over several weeks without scarring, sometimes passing through the color changes of a resolving bruise as they fade.\n\n![Erythema nodosum: Erythema nodosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/7f29e6763eb54f2aa45ddf3e91e5564d.jpg)", "parent_id": null, "variant": "long"}, {"id": "6abff670892a497d9ea29306f32c37ea", "slug": "morbilliform-drug-eruption", "title": "Morbilliform drug eruption", "content": "Morbilliform (measles-like) drug eruptions account for the large majority, roughly 75% to 80%, of all cutaneous [[drug reactions|drug-reaction]] in children, making this the pattern to know first when a rash appears in a child on a new medication. Lesions are erythematous macules and papules that begin on the trunk seven to ten days after a first exposure to the culprit drug (or within a day or two on re-exposure in an already-sensitized patient), then spread peripherally to the extremities and face while sparing the mucous membranes, often with pruritus but with mild or no systemic symptoms. That mucosal sparing, together with the absence of skin pain, blistering, or a positive Nikolsky sign, is exactly what needs to be checked and documented, since it is what separates an ordinary morbilliform drug eruption from the early stage of Stevens-Johnson syndrome, which the eruption can otherwise resemble. If those severe features are absent, and if the medication is important enough to warrant continuing, it can sometimes be continued with close monitoring; if not needed, stopping it allows the rash to resolve over roughly seven to fourteen days without further treatment beyond antihistamines for itch.\n\n![Morbilliform drug eruption: Morbilliform drug eruption. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/8eca460943a34fb5bcc2c6ec8236a3f8.jpg)", "parent_id": null, "variant": "long"}, {"id": "9f511596c8254eea8de2748192610e3f", "slug": "keratosis-pilaris", "title": "Keratosis pilaris", "content": "Keratosis pilaris is a common, autosomal dominant disorder of follicular keratin plugging that produces small, rough, skin-colored to reddish papules, often described as looking like permanent goosebumps, concentrated on the extensor surfaces of the upper arms, thighs, cheeks, and buttocks; the individual lesions are discrete and do not coalesce into plaques, which distinguishes the texture from a true inflammatory dermatitis. It is more common in children who also have [[atopic dermatitis|atopic-dermatitis]] and tends to worsen in the dry winter months, then gradually subside through adolescence and into the third decade of life, an expected natural course worth mentioning to families concerned about a persistent rough texture. No treatment is required, since the condition is entirely benign and self-limited over years, but for cosmetic bother, regular use of a bland emollient to reduce dryness, or a keratolytic preparation such as a 10% to 40% urea cream or a 12% lactic acid lotion, can smooth the texture of the skin, though these can themselves cause mild irritation and should be introduced gradually. Reassurance about the benign nature and typical improvement with age is usually all that is needed.\n\n![Keratosis pilaris: Keratosis pilaris. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/388cda26223842dab6b1778b442507ba.jpg)", "parent_id": null, "variant": "long"}, {"id": "8d66f2ab080a4c089ee26eb8320cbb6c", "slug": "periorificial-dermatitis", "title": "Periorificial dermatitis", "content": "Periorificial (perioral) dermatitis is a papulopustular eruption of small, uniform, erythematous papules and pustules clustered around the mouth, with a narrow, characteristically spared rim of normal skin immediately adjacent to the vermilion border, and it can extend to involve the perinasal and periocular skin as well; it is considered a variant of rosacea rather than a form of true dermatitis or acne. The condition is strongly linked to, and typically worsened by, exposure to topical or inhaled corticosteroids, and a common iatrogenic cycle in practice begins with an initial irritant dermatitis that is treated with a topical steroid, which suppresses the eruption temporarily but drives a rebound flare of periorificial dermatitis when the steroid is withdrawn, prompting further steroid use and perpetuating the cycle. A severe, papulonodular, granulomatous variant exists that can be mistaken for sarcoidosis on skin biopsy. The essential first step in treatment, and the one most likely to be resisted by a frustrated family, is complete withdrawal of all topical steroids and other facial irritants, accepting an expected initial flare; topical metronidazole or erythromycin is then used for milder disease, and an oral tetracycline-class antibiotic, in a child old enough to receive one, for more resistant cases.\n\n![Periorificial dermatitis: Perioral dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/400920a84cbf47ea9bd4747f8e9bfb36.jpg)", "parent_id": null, "variant": "long"}, {"id": "1e31c41b711543a88a8631873e8b30f4", "slug": "pityriasis-alba", "title": "Pityriasis alba", "content": "Pityriasis alba presents as ill-defined, hypopigmented (not fully depigmented) patches with a fine surface scale, most often on the face, in children between about 2 and 6 years of age, and represents a mild, often subclinical form of [[eczema|eczema]] rather than a distinct disease process; low-grade inflammation disrupts melanocyte function locally, leaving behind lighter, though never fully white, skin once the visible inflammation has faded. The lesions are self-limited, typically clearing over several months to a couple of years without scarring or permanent pigment change. The most important discrimination to make, and the one families most often ask about, is from vitiligo: vitiligo produces sharply demarcated patches of complete depigmentation without surface scale, while pityriasis alba shows fuzzy, ill-defined borders, incomplete lightening, and a fine scale, and it is entirely reversible over time. Management is reassurance that the condition is not vitiligo, together with regular emollients to reduce the associated dryness and scale, and a mild topical corticosteroid can be used briefly during any acutely inflamed phase; the pigment evens out on its own as the underlying low-grade eczema resolves.\n\n![Pityriasis alba: Pityriasis alba. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/8b090c14fec24ae58107e7e2087f0704.jpg)", "parent_id": null, "variant": "long"}, {"id": "fac4392d2d64445598691173b53f17fc", "slug": "acne-vulgaris", "title": "Acne vulgaris", "content": "[[Acne vulgaris|acne-vulgaris]] in adolescents shows the full range of the pilosebaceous unit's response to androgen-driven sebum overproduction and follicular plugging: open and closed comedones, inflammatory papules and pustules, and, in more severe disease, nodules and scarring cysts, concentrated on the face, chest, and back. Comedones, absent in the neonatal and infantile acneiform eruptions discussed elsewhere in this atlas, are what confirm this is true acne rather than one of its early-life mimics. The photograph and full account are in [[345|Acne Vulgaris]].", "parent_id": null, "variant": "long"}, {"id": "57919b893e324cadb52ff606c846bf12", "slug": "iga-vasculitis-henoch-sch-nlein-purpura-palpable-purpura", "title": "IgA vasculitis (Henoch-Sch\u00f6nlein purpura): palpable purpura", "content": "IgA vasculitis produces palpable, nonblanching purpura concentrated on the buttocks and extensor surfaces of the lower legs, reflecting IgA immune-complex deposition in small dermal vessels, typically in a child between about 3 and 10 years old who otherwise looks well, unlike the toxic-appearing child with [[meningococcemia|meningococcemia]] discussed elsewhere in this atlas. Accompanying joint pain, abdominal pain, and renal involvement complete the classic picture and guide how closely the child needs to be followed. The photograph and full account are in [[436|Henoch-Sch\u00f6nlein Purpura]].", "parent_id": null, "variant": "long"}, {"id": "f5c0702d04f440e0968ee1b4706d079f", "slug": "meningococcemia-petechiae-and-purpura-fulminans", "title": "Meningococcemia: petechiae and purpura fulminans", "content": "[[Meningococcemia|meningococcemia]]'s rash begins as scattered, nonblanching petechiae, seen in more than 80% of cases as the disease progresses, and in fulminant disease can evolve within hours into purpura fulminans, confluent, retiform purpuric plaques caused by disseminated intravascular coagulation and thrombosis of dermal vessels triggered by endotoxin-driven activation of the coagulation cascade and diffuse endothelial injury. The clinical picture before the rash is fully established is what should raise suspicion: leg pain, cold hands and feet, mottled or abnormal skin color, and a prolonged capillary refill time can precede the petechiae and reflect early shock. Complications of severe purpura fulminans include focal skin infarction and necrosis, most often of the lower limbs, occasionally severe enough to require amputation (in roughly 2% of survivors, with amputation delayed until the tissue has clearly demarcated), and, in survivors, growth disturbance from epiphyseal injury caused by the underlying disseminated coagulation. Because the disease can progress from fever to [[septic shock|septic-shock]] over a matter of hours, this is a true emergency: empiric antibiotics should not be delayed for confirmatory testing, with ceftriaxone 50 mg/kg per dose every 12 hours (or cefotaxime) started immediately alongside aggressive treatment of shock. The combination of fever, toxic appearance, and rapidly evolving petechiae or purpura is what separates this from IgA vasculitis, in which the child looks well, and from immune [[thrombocytopenia|thrombocytopenia]], in which there is no fever or toxicity.\n\n![Meningococcemia: petechiae and purpura fulminans: Petechiae due to meningococcal disease. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/9fdfbc0c86d34beb885cc4a928099c81.jpg)", "parent_id": null, "variant": "long"}, {"id": "beab6662072d4bdd969a5bc3a2343c9d", "slug": "kawasaki-disease-the-mucocutaneous-findings", "title": "Kawasaki disease: the mucocutaneous findings", "content": "[[Kawasaki disease|kawasaki-disease]]'s mucocutaneous findings include a polymorphous truncal rash, bilateral non-exudative conjunctival injection, red and cracked lips with a strawberry tongue, and erythema and edema of the hands and feet followed by periungual desquamation in the second to third week of illness. These findings, together with fever lasting five days or more and cervical lymphadenopathy, make up the diagnostic criteria, and their combination in a young child with a high, poorly explained fever should prompt urgent evaluation for coronary artery involvement. The photograph and full account are in [[5|Kawasaki disease]].", "parent_id": null, "variant": "long"}, {"id": "bafc3600e9d8454eb8a402e093681ffa", "slug": "stevens-johnson-syndrome", "title": "Stevens-Johnson syndrome", "content": "Stevens-Johnson syndrome is a severe mucocutaneous reaction in which keratinocyte necrosis leads to partial-to-full-thickness epidermal detachment; by definition, Stevens-Johnson syndrome involves less than 10% of body surface area, toxic epidermal necrolysis more than 30%, with an overlap zone in between. About 15% of pediatric cases follow an infection, chiefly Mycoplasma pneumoniae or herpes simplex virus, while roughly a third to half are triggered by a medication, most often sulfonamides, anticonvulsants, beta-lactam antibiotics, or nonsteroidal anti-inflammatory drugs. The rash begins as erythematous, target-like macules and papules that evolve into vesicles, bullae, and sheet-like erosions, but the feature that sets Stevens-Johnson syndrome apart from erythema multiforme and from staphylococcal scalded skin syndrome is severe involvement of two or more mucosal surfaces, ocular, oral, or genital, together with skin that is painful to touch and a positive Nikolsky sign extending down to a raw, bleeding dermis rather than the superficial split of scalded skin syndrome. Overall pediatric mortality is under 8%. Management begins with immediate withdrawal of the suspected causative drug and supportive care equivalent to a burn unit: fluid and electrolyte management, wound care, nutrition support, and pain control, with ophthalmology and urology involved early for mucosal complications; the role of systemic corticosteroids remains controversial and unresolved.\n\n![Stevens-Johnson syndrome: Stevens Johnson Syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/88002536c1bf41f48c8b66bcc87d1a4e.jpg)", "parent_id": null, "variant": "long"}, {"id": "e2ccc9b83daa4e5db2e0bac02290b38b", "slug": "malar-butterfly-rash-of-lupus", "title": "Malar butterfly rash of lupus", "content": "The malar rash of [[systemic lupus erythematosus|systemic-lupus-erythematosus]] is an erythematous or violaceous, sometimes maculopapular, eruption across the cheeks and the bridge of the nose that characteristically spares the nasolabial folds, a distribution that is the single most useful feature separating it from seborrheic dermatitis and rosacea, both of which involve the folds. The rash is photosensitive in roughly 30% of patients, and sun exposure can both trigger the cutaneous eruption and flare systemic disease activity, reflecting a shared underlying photosensitivity in the disease's immune dysregulation. The malar rash is one of the classification criteria for systemic lupus erythematosus, alongside discoid lupus lesions, oral or nasal mucosal ulcers, more general photosensitivity, nonerosive arthritis, renal disease (proteinuria or cellular casts), neurologic disease, cytopenias, and specific autoantibodies including anti-double-stranded DNA and anti-Smith antibodies, so its presence should prompt a broader systemic evaluation rather than treatment of the skin in isolation. Initial management of the skin lesion itself is strict sun protection with a broad-spectrum sunscreen and topical corticosteroids for localized disease, while the systemic workup, antinuclear antibody, anti-dsDNA, complement levels, and urinalysis, proceeds in parallel given the implications for kidney and other organ involvement.\n\n![Malar butterfly rash of lupus: Malar 'butterfly' rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/1cab7607bb7146aaa0d15642b7542c69.jpg)", "parent_id": null, "variant": "long"}, {"id": "b6e48326137d4abeb95fb9f90880cdbc", "slug": "juvenile-dermatomyositis-heliotrope-rash-and-gottron-papules", "title": "Juvenile dermatomyositis: heliotrope rash and Gottron papules", "content": "[[Juvenile dermatomyositis|juvenile-dermatomyositis]] most often announces itself with its rash before muscle weakness follows, and its two cutaneous findings are considered pathognomonic, present in more than three-quarters of affected children. The heliotrope rash is a violaceous to lilac discoloration of the upper eyelids, often with periorbital edema, named for its resemblance to the color of the heliotrope flower, while Gottron papules are flat-topped, erythematous-to-violaceous papules distributed symmetrically over the extensor surfaces of the finger joints (the metacarpophalangeal and interphalangeal joints), and also frequently seen over the elbows and knees. Both findings reflect an underlying immune-mediated vasculopathy that targets the small blood vessels of both skin and muscle, which is also why dilated, dropped-out, and tortuous nailfold capillaries are a supportive examination finding, visible with simple magnification at the base of the fingernails. Once these skin findings raise suspicion, evaluation includes muscle enzymes (creatine kinase and others), MRI or biopsy of an affected muscle, and nailfold capillaroscopy, along with screening over time for calcinosis cutis and for lipodystrophy with [[insulin resistance|insulin-resistance]], recognized later complications of the disease. Treatment is systemic immunosuppression, typically corticosteroids together with methotrexate.\n\n![Juvenile dermatomyositis: heliotrope rash and Gottron papules: Gottron papules over joints. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/4a4a00ee0b1b4bc2ad21982a4be8343b.jpg)", "parent_id": null, "variant": "long"}, {"id": "bf506482add542a38dc59b38f535054e", "slug": "lichen-sclerosus", "title": "Lichen sclerosus", "content": "Lichen sclerosus in children affects the anogenital area in as many as 75% of cases and occurs predominantly in prepubertal girls, presenting as white, atrophic, porcelain-like patches and plaques that often form a figure-of-eight or hourglass pattern encircling the vulva and perianal skin. Minor friction from ordinary childhood activities such as bicycle riding can produce visible purpura, fissures, or bleeding within these fragile plaques, and this trauma-induced bruising and tearing is important to recognize because it is easily, and sometimes wrongly, mistaken for a sign of sexual abuse; recognizing the classic white, atrophic morphology surrounding the finding prevents that error. Left untreated over time, the disease can progressively distort normal genital architecture, including resorption of the labia, narrowing of the vaginal introitus, and painful fissuring that predisposes to secondary infection, and contrary to older teaching that the disease resolves at puberty, many postmenarchal adolescents continue to have active disease. First-line treatment is a high-potency topical corticosteroid such as clobetasol 0.05% ointment applied twice daily for two to four weeks, followed by a maintenance regimen, sometimes with a topical calcineurin inhibitor, and ongoing follow-up with gynecology or dermatology given the chronic, relapsing course.\n\n![Lichen sclerosus: Axillary lichen sclerosus. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/8d2b0f1b58574babbcd5b7a1355e448b.jpg)", "parent_id": null, "variant": "long"}, {"id": "f596ea24bbc64abf8e9611248d99178a", "slug": "vitiligo", "title": "Vitiligo", "content": "Vitiligo produces sharply demarcated, completely depigmented macules and patches, distinct from the incomplete lightening and blurred borders of pityriasis alba, resulting from autoimmune destruction of melanocytes: roughly 80% of patients with active disease carry anti-melanocyte antibodies, and melanocyte-specific CD8-positive T lymphocytes are directly implicated in attacking pigment-producing cells, with disease activity tracking antibody titers. New patches can appear at sites of skin trauma, a Koebner-type phenomenon, and the disease occurs in two broad patterns: segmental vitiligo, limited to one dermatomal-type distribution with rapid onset and progression that then tends to stabilize, and generalized vitiligo, often familial and associated with other autoimmune conditions, particularly autoimmune thyroid disease, and occasionally with [[alopecia areata|alopecia-areata]]. A rare but important association is Vogt-Koyanagi-Harada syndrome, in which autoimmunity against melanocytes in the eye, inner ear, and meninges accompanies the skin disease, producing uveitis, [[hearing loss|hearing-loss]], and aseptic [[meningitis|meningitis]]. Because of the thyroid association, a reasonable evaluation in a child with new vitiligo includes screening for autoimmune thyroid disease. Treatment options include topical corticosteroids or calcineurin inhibitors for localized disease and phototherapy for more extensive involvement, with counseling about sun protection for the depigmented, unprotected skin.\n\n![Vitiligo: Ankle vitiligo suitable for ruxolitinib cream. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/fec211ef079d4bef973feceb01e25a3d.jpg)", "parent_id": null, "variant": "long"}, {"id": "d253f8e25fce49c18cd7ac4964c0a363", "slug": "alopecia-areata", "title": "Alopecia areata", "content": "[[Alopecia areata|alopecia-areata]] causes rapid, complete hair loss in sharply defined round or oval patches on the scalp, and sometimes the eyebrows, eyelashes, or other body sites, with the skin within the bald patch appearing entirely normal, without scale, scarring, erythema, or broken hair stubble of varying length. That normal-appearing skin is the key discriminator from [[tinea capitis|tinea-capitis]], which typically shows scale, broken hairs, and sometimes an inflammatory kerion, and from trichotillomania, in which hairs are pulled out at irregular lengths over an irregularly shaped patch rather than a clean, round area of total loss. In severe disease all scalp hair can be lost (alopecia totalis) or all scalp and body hair (alopecia universalis). The disease is T-cell-mediated, with lymphocytes attacking the hair follicle while sparing the surrounding skin, which explains the sharp, \"punched-out\" quality of the patches; lifetime incidence is 0.1% to 0.2%, and more than half of affected people are under 20 years old at onset. On close examination, short, tapered \"exclamation-point\" hairs are often visible at the margin of an active patch, and nail pitting can accompany more extensive disease. Topical or intralesional corticosteroids are the mainstay of treatment, and many patches regrow spontaneously without any treatment at all.\n\n![Alopecia areata: Eyebrow loss in alopecia areata. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.](/uploads/media/e867caa9f7154a12bf68454ec7f57852.jpg)", "parent_id": null, "variant": "long"}, {"id": "2f5ebf884bf34777b547b54244408697", "slug": "rashes-compared", "title": "Rashes compared", "content": "| Rash | Primary lesion | Distribution | Age | The giveaway |\n|---|---|---|---|---|\n| Measles | Morbilliform macules and papules | Face and hairline spreading to trunk and limbs | Any age, unvaccinated | Koplik spots before the rash |\n| Rubella | Fine pink macules and papules | Face spreading inferiorly within 24 hours | Any age, unvaccinated | Brief course, postauricular nodes |\n| Roseola | Faint pink macules | Trunk spreading peripherally | Infants, toddlers | Rash appears as fever breaks |\n| Erythema infectiosum | Slapped-cheek erythema, then lacy rash | Cheeks, then extremities and trunk | 5-15 years | Rash flares with heat or sun |\n| Scarlet fever | Fine sandpaper papules | Neck and trunk, Pastia lines in creases | School age | Strawberry tongue, later desquamation |\n| Varicella | Vesicles on red base | Centripetal, trunk and scalp heavy | Any age, unvaccinated | All lesion stages at once |\n| Hand, foot and mouth disease | Oval vesicles, oral erosions | Palms, soles, buttocks, mouth | Under 5 years | Painful mouth plus acral vesicles |\n| Gianotti-Crosti syndrome | Monomorphic lichenoid papules | Face, buttocks, extremities, trunk spared | 1-6 years | Acral distribution with trunk sparing |\n| Erythema toxicum neonatorum | Papules or pustules with erythematous flare | Widespread, palms and soles spared | Newborn, 24h-10 days | Eosinophils, sterile smear |\n| Milia | Tiny white-yellow papules | Nose, forehead, cheeks | Newborn | Firm, keratin-filled cysts |\n| Neonatal cephalic pustulosis | Pink papules and pustules, no comedones | Face and scalp | 2-4 weeks | No comedones (unlike true infant acne) |\n| Transient neonatal pustular melanosis | Pustules, collarettes, pigmented macules | Forehead, neck, lower back | Present at birth | Present at birth, neutrophils on smear |\n| Cradle cap | Greasy yellow scale | Scalp, eyebrows, folds | Under 3 months | Non-itchy, physiological |\n| Diaper dermatitis, irritant | Erythema on convex surfaces | Buttocks, thighs, sparing folds | Diaper-wearing infants | Spares the skin folds |\n| Candidal diaper dermatitis | Beefy red plaques, satellite pustules | Skin folds, perianal spreading out | Diaper-wearing infants | Satellite pustules, fold involvement |\n| Mongolian spot | Slate-gray macule or patch | Lumbosacral area, buttocks | Present at birth | Fades over years, not a bruise |\n| Infantile hemangioma | Red vascular papule or plaque | Anywhere, often head and neck | Weeks to months | Proliferates then involutes |\n| Port-wine stain | Flat deep pink-purple patch | Face, unilateral | Present at birth | Grows with the child, does not regress |\n| Caf\u00e9-au-lait macule | Smooth-bordered brown macule | Trunk, anywhere | Any age | Six or more suggests NF1 |\n| Nevus sebaceus | Orange-yellow hairless plaque | Scalp, face | Present at birth | Becomes verrucous at puberty |\n| Impetigo | Honey-crusted erosions or flaccid bullae | Face, around nose and mouth | Preschool age | Honey-colored crust |\n| Cellulitis | Erythema, warmth, poorly demarcated | Lower extremities most often | Any age | Border fades into normal skin |\n| Staphylococcal scalded skin syndrome | Diffuse erythema with superficial peeling | Generalized, flexures accentuated | Infants, young children | Nikolsky sign, mucosa spared |\n| Erythema migrans | Expanding annular red patch | Site of tick bite | Any age | Expands over days, may clear centrally |\n| Tinea corporis | Annular plaque with active border | Trunk, limbs | Any age | Central clearing |\n| Tinea capitis | Scaly patches, broken hairs | Scalp | School age | Occipital lymphadenopathy |\n| Tinea versicolor | Fine scaling hypo- or hyperpigmented patches | Trunk, upper arms | Adolescents | Fine scale, pigment change |\n| Tinea pedis | Interdigital maceration or moccasin scaling | Feet | Older children, adolescents | Web-space fissuring, KOH-positive |\n| Molluscum contagiosum | Umbilicated dome papules | Trunk, face, extremities | Young children | Central dell |\n| Common and plantar warts | Rough papules | Hands, soles | Any age | Obliterates skin lines |\n| Herpetic gingivostomatitis | Oral vesicles and ulcers | Gingiva, tongue, lips, mucosa | 6 months-3 years | Gingival swelling and bleeding |\n| Eczema herpeticum | Punched-out erosions on dermatitis | Areas of active eczema | Children with atopic dermatitis | Monomorphic punched-out lesions |\n| Herpes zoster | Grouped vesicles on red base | Single dermatome, unilateral | Any age, prior varicella | Dermatomal band |\n| Scabies | Excoriated papules, burrows | Finger webs, wrists; infants: face, palms, soles | Any age | Nocturnal pruritus, burrows |\n| Head lice | Nits fixed to hair shaft | Scalp | School age | Nits do not slide off hair |\n| Pityriasis rosea | Oval scaly plaques | Trunk, along cleavage lines | Adolescents | Herald patch, Christmas-tree pattern |\n| Atopic dermatitis | Erythematous, later lichenified plaques | Cheeks in infants, flexures later | Any age | Chronic pruritus, flexural in older children |\n| Allergic contact dermatitis | Sharply demarcated erythema, vesicles | Site of contact | Any age | Geometric or linear shape |\n| Guttate psoriasis | Small drop-shaped scaly papules | Trunk, proximal limbs | Children, adolescents | Follows streptococcal pharyngitis |\n| Urticaria | Edematous wheals | Anywhere, migratory | Any age | Individual lesions resolve under 24 hours |\n| Erythema multiforme | Target (iris) lesions | Extensor hands, feet, limbs | Any age | Three-zone target lesion |\n| Erythema nodosum | Tender erythematous nodules | Shins, bilateral | Adolescents | Panniculitis, marker of another disease |\n| Morbilliform drug eruption | Erythematous macules and papules | Trunk spreading out, mucosa spared | Any age | Onset 7-10 days after a new drug |\n| Keratosis pilaris | Small rough follicular papules | Upper arms, thighs, cheeks | Children, adolescents | Gooseflesh texture, no coalescence |\n| Periorificial dermatitis | Papulopustules around mouth | Perioral, sparing vermilion rim | Young children, women | Worsened by topical steroids |\n| Pityriasis alba | Ill-defined hypopigmented patches, fine scale | Face | 2-6 years | Incomplete lightening, not vitiligo |\n| Acne vulgaris | Comedones, papules, pustules | Face, chest, back | Adolescents | Comedones present |\n| IgA vasculitis (Henoch-Sch\u00f6nlein purpura) | Palpable purpura | Buttocks, extensor lower legs | 3-10 years | Well child, purpura plus joint or belly pain |\n| Meningococcemia | Petechiae, purpura fulminans | Widespread, evolves rapidly | Any age | Fever plus toxic appearance |\n| Kawasaki disease | Polymorphous rash, mucosal changes | Trunk, hands and feet, mucosa | Under 5 years | Conjunctival injection, strawberry tongue |\n| Stevens-Johnson syndrome | Target lesions, bullae, erosions | Skin plus 2 or more mucosal sites | Any age | Severe mucosal involvement, skin pain |\n| Malar rash of lupus | Erythematous or violaceous malar patch | Cheeks and nasal bridge | Adolescents, more girls | Spares the nasolabial folds |\n| Juvenile dermatomyositis | Heliotrope rash, Gottron papules | Eyelids, extensor finger joints | Children | Precedes muscle weakness |\n| Lichen sclerosus | White atrophic plaques | Vulva, perianal skin | Prepubertal girls | Figure-of-eight pattern |\n| Vitiligo | Completely depigmented macules | Anywhere, often symmetric | Any age | Sharp borders, no scale |\n| Alopecia areata | Complete hair loss in round patches | Scalp | Under 20 years | Normal-appearing skin in the patch |", "parent_id": null, "variant": "long"}, {"id": "bff6d6694d514f599ed59936616f7190", "slug": "in-short", "title": "In short", "content": "- Roseola's rash appears only after the fever breaks; most other viral exanthems erupt while the fever is still present.\n- Erythema infectiosum's parvovirus B19 targets erythroid progenitor cells, which is why it can trigger aplastic crisis in [[sickle cell disease|sickle-cell-disease]].\n- Gianotti-Crosti syndrome is acral (face, buttocks, limbs) with trunk sparing, unlike most other viral exanthems.\n- [[Erythema toxicum neonatorum|erythema-toxicum-neonatorum]] appears 24 hours to 10 days after birth with an eosinophilic, sterile smear; transient neonatal pustular melanosis is present at birth with a neutrophilic smear.\n- Neonatal cephalic pustulosis has no comedones; true infantile acne, which appears later, does.\n- Candidal diaper dermatitis involves the skin folds and has satellite pustules; irritant diaper dermatitis spares the folds.\n- A facial port-wine stain in the V1 trigeminal distribution carries about a 26% risk of Sturge-Weber syndrome.\n- Six or more caf\u00e9-au-lait macules over 5 mm (prepubertal) is a diagnostic criterion for [[neurofibromatosis type 1|neurofibromatosis-type-1]].\n- Staphylococcal scalded skin syndrome splits the superficial epidermis and spares mucosa; toxic epidermal necrolysis splits full-thickness and involves mucosa.\n- A wart obliterates normal skin lines; a callus preserves them.\n- Eczema herpeticum on top of [[atopic dermatitis|atopic-dermatitis]] needs systemic acyclovir, not topical antibiotics.\n- [[Herpes zoster|herpes-zoster]] in a healthy child rarely causes postherpetic neuralgia, unlike in adults.\n- An ordinary hive resolves within 24 hours; urticarial vasculitis lesions persist longer and can bruise.\n- Morbilliform drug eruptions spare mucosa and skin pain; their presence signals possible early Stevens-Johnson syndrome instead.\n- [[Meningococcemia|meningococcemia]] needs empiric ceftriaxone the moment it is suspected, without waiting for confirmatory tests.\n- Pityriasis alba has ill-defined, incompletely lightened, scaly patches; vitiligo has sharp, complete depigmentation without scale.\n- Lichen sclerosus purpura from minor trauma is easily, and wrongly, mistaken for abuse.", "parent_id": null, "variant": "short"}, {"id": "540f5f17dd5741de9092351e0d3b3b43", "slug": "the-rashes-that-cannot-wait", "title": "The rashes that cannot wait", "content": "[[Meningococcemia|meningococcemia]] can progress from fever to [[septic shock|septic-shock]] within hours. Do not wait for a lumbar puncture or blood culture result: draw cultures if they can be obtained without delay, then give empiric ceftriaxone 50 mg/kg per dose (or cefotaxime) immediately, and treat shock aggressively with fluid resuscitation and, if needed, vasopressor support and airway management. A nonblanching petechial or purpuric rash with a toxic-appearing, febrile child is the trigger to act, not a reason to wait for it to evolve further.\n\nStaphylococcal scalded skin syndrome needs systemic antistaphylococcal antibiotics started promptly, since the disease is toxin-mediated and will keep spreading until the source is treated, plus burn-unit-style supportive care: careful fluid balance (large areas of denuded skin lose fluid and heat like a burn), gentle handling to avoid further shearing of skin, and pain control. Topical therapy alone is not sufficient.\n\nStevens-Johnson syndrome requires immediate identification and withdrawal of the causative drug, since continued exposure worsens the reaction. Move quickly to supportive, burn-unit-level care: fluid and electrolyte management, wound care to the denuded skin, nutrition support, and pain control, with early ophthalmology and urology consultation for ocular and genital mucosal involvement to prevent long-term scarring.\n\n[[Eczema|eczema]] herpeticum needs systemic acyclovir or valacyclovir started as soon as the widespread, monomorphic, punched-out vesicular eruption on dermatitic skin is recognized; antibiotics for presumed bacterial impetiginization will not control it. Any periocular involvement is an ophthalmologic emergency and needs same-day evaluation for herpetic keratitis.\n\n[[Kawasaki disease|kawasaki-disease]] is a clinical diagnosis in the first hour: fever for 5 days or more plus at least four of conjunctival injection, oral or lip changes, polymorphous rash, extremity changes, and cervical lymphadenopathy should prompt echocardiography and treatment with intravenous immunoglobulin plus high-dose aspirin without waiting for all features to appear, since the goal of treatment is preventing coronary artery aneurysm and the benefit is greatest early in the illness.", "parent_id": null, "variant": "clinical"}], "content": null}, "453": {"sections": [{"id": "b6d98904d8c24551875fac3a0a357882", "slug": "how-to-read-a-pediatric-film", "title": "How to read a pediatric film", "content": "A pediatric film is read against a moving target: the same shadow is pathology at one age and pure anatomy at another, so technique and age are checked before the pattern is. The standard chest study is a posteroanterior and lateral view, upright, in full inspiration; a well-inflated lung places the diaphragm at roughly the eighth to tenth posterior rib. Anything less is a portable AP film, what most sick infants get: taken supine, magnifying the heart and mediastinum, and prone to rotation, checked against the medial ends of the clavicles relative to the spinous processes, which can itself mimic cardiomegaly or unilateral hyperinflation.\n\nThe single largest trap in a young child's chest film is the thymus. In the first years of life it fills much of the anterior mediastinum, has a smooth wavy or straight border on the right (the \"sail sign\"), and can be mistaken for cardiomegaly, a mediastinal mass, or lobar collapse; it shrinks with age and physiologic stress and is absent in DiGeorge syndrome. A pneumomediastinum can lift that same thymus off the heart into its own, unrelated \"spinnaker\" sign.\n\nOn the skeleton, an open growth plate is a lucent band at the metaphysis, not a fracture, and its width and regularity change with age and site; nearly every fracture pattern in this article is a variation on how a still-growing bone bends, buckles, or separates at this weak point rather than breaking cleanly the way mature bone does. A systematic read of every film - airway, bones, cavity contents, soft tissues - catches the incidental finding at the edge of the image as reliably as the one the film was ordered for.", "parent_id": null, "variant": "long"}, {"id": "3ffd0cbc830f423b89e74ce9424ee529", "slug": "neonatal-respiratory-distress-syndrome-ground-glass-lungs-and-air-bronchograms", "title": "Neonatal respiratory distress syndrome: ground-glass lungs and air bronchograms", "content": "The film behind this entry is a premature neonate on day zero, already intubated for hyaline membrane disease, the historical name for surfactant-deficient respiratory distress syndrome (RDS); ventilation has re-expanded the lungs, and here the pressure needed to do it has caused a pneumothorax. Untreated, the disease looks different: low lung volumes, a diffuse, uniform reticulogranular or \"ground-glass\" haze, and air bronchograms, air-filled bronchi standing out against airless, collapsed alveoli around them. The heart is usually a normal size, though a prominent thymic shadow and the low lung volume make it look large.\n\nThe mechanism is a lack of surfactant, produced by type II pneumocytes from roughly 24 to 28 weeks of gestation and not fully functional until about 35 weeks; without it, surface tension collapses the alveoli into miliary atelectasis and interstitial edema, and the more preterm the infant, the more severe the picture. The main mimic is transient tachypnea of the newborn, which is hyperinflated rather than under-aerated and shows fluid in the fissures rather than a uniform haze; congenital pneumonia can look identical on imaging, which is why cultures are sent alongside the film rather than relying on the radiograph to separate the two.\n\nAt the bedside, RDS is treated with exogenous surfactant and continuous positive airway pressure or mechanical ventilation as needed, and both its incidence and severity are reduced by antenatal corticosteroids given to the mother ahead of a preterm delivery.\n\n![Neonatal respiratory distress syndrome: ground-glass lungs and air bronchograms. Findings are consistent with hyaline membrane disease in a premature neonate complicated by pneumothorax from barotrauma. The lungs are well expanded as the patient is intubated. In a non-intubated patient with HMD the lungs would demonstrate redu... Case courtesy of Andrew Dixon, Radiopaedia.org, rID: 10264 (CC BY-NC-SA 3.0).](/uploads/media/7ab0388d195d48e89234af93e2685cf0.png)", "parent_id": null, "variant": "long"}, {"id": "adb012663207489b8b0237d54eb5bd93", "slug": "transient-tachypnea-of-the-newborn-fluid-in-the-fissures", "title": "Transient tachypnea of the newborn: fluid in the fissures", "content": "This term newborn's film was taken to sort out increased work of breathing, and transient tachypnea of the newborn (TTN) is one of the three diagnoses that dominate that list in a term baby, alongside neonatal infection and meconium aspiration. The classic appearance is hyperinflated lungs with prominent perihilar, bronchovascular streaking radiating from the hila, and fluid layering in the horizontal, or interlobar, fissure; mild cardiomegaly is common.\n\nThe mechanism is simple retention: fetal lung fluid that is normally squeezed out during vaginal delivery and cleared by the lymphatics in the first hours of life instead clears more slowly, particularly after cesarean delivery or a very fast labor, leaving the interstitium and fissures wet rather than the alveoli filled. This is the opposite physiology from respiratory distress syndrome, and the film reflects it: TTN is hyperinflated and RDS is under-aerated, with a uniform ground-glass haze rather than streaky perihilar markings.\n\nThe baby is tachypneic, sometimes strikingly so, but is not in significant distress - no grunting, minimal or no retractions - and the diagnosis is really one of exclusion once RDS and pneumonia have been considered. Management is supportive: supplemental oxygen if needed, monitoring, and time. Symptoms resolve within about a day, occasionally two, and the film clears alongside them; a baby who is not improving on this timeline should be re-evaluated for one of its two mimics rather than assumed to have unusually slow TTN.\n\n![Transient tachypnea of the newborn: fluid in the fissures. In a term baby, the most common causes of increased work of breathing that can be seen on a chest x-ray are: Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 94073 (CC BY-NC-SA 3.0).](/uploads/media/00e5ab398d894aed96a8e0fd148d1357.png)", "parent_id": null, "variant": "long"}, {"id": "b8ca99fa1e2b43218b45e8cec945e122", "slug": "meconium-aspiration-coarse-patchy-opacities-with-hyperinflation", "title": "Meconium aspiration: coarse patchy opacities with hyperinflation", "content": "This full-term boy's first-day film shows the classic combination for meconium aspiration syndrome: asymmetric, patchy lung opacities together with increased lung volumes. Other examples in the same family add coarse, rope-like interstitial densities radiating from the hila and a flattened diaphragm from air trapping.\n\nThe mechanism is aspiration of meconium-stained amniotic fluid, usually in the setting of perinatal stress or post-maturity; meconium is both an airway irritant and a surfactant inactivator, so small airways obstruct unevenly - some completely, producing atelectasis, others only partially, producing a ball-valve effect that traps air distally - while the alveoli that do fill develop a chemical pneumonitis. The patchiness and the hyperinflation together are the fingerprint: RDS is diffusely under-aerated and uniform, and TTN is hyperinflated but without the coarse patchy opacities.\n\nAir leak is the complication to watch for, since 10 to 15 percent of infants develop a pneumothorax or pneumomediastinum from air trapped behind obstructed airways at high pressure. At the bedside, the film's role is confirmatory rather than the trigger for treatment - clinical distress with meconium-stained fluid is enough to start respiratory support - but it flags the infant who needs closer surveillance for air leak. The radiographic findings correlate poorly with clinical severity, so a relatively clean film does not rule out a sick baby, and a striking one does not always predict the worst course.\n\n![Meconium aspiration: coarse patchy opacities with hyperinflation. This a full-term baby boy during his first day of life presenting with signs and symptoms of respiratory distress. The asymmetric patchy lung opacities with increased lung volumes are classic findings of meconium aspiration, on chest radiograph, w... Case courtesy of Naim Qaqish, Radiopaedia.org, rID: 74578 (CC BY-NC-SA 3.0).](/uploads/media/6ffc0ea5fa3646d5a217f29b89b84468.png)", "parent_id": null, "variant": "long"}, {"id": "da3ff6aab10842ccb9b920a17bcb468b", "slug": "congenital-diaphragmatic-hernia-bowel-in-the-chest", "title": "Congenital diaphragmatic hernia: bowel in the chest", "content": "The frontal film of this newborn shows what a Bochdalek-type congenital diaphragmatic hernia looks like once repaired and healed: well-expanded, well-grown lungs, after early surgery and a course complicated by bilateral chylothoraces. Before repair, the same chest instead shows multiple air-filled bowel loops occupying part or most of one hemithorax - almost always the left, since 80 to 90 percent of these hernias come through the posterolateral Bochdalek defect on that side - with an indistinct or absent hemidiaphragm and the mediastinum pushed toward the opposite side.\n\nThe mechanism is a failure of the diaphragm to close during fetal development, allowing abdominal viscera (stomach, spleen, and bowel, occasionally liver or kidney) to herniate into the chest early enough to compress the developing lung; the result is pulmonary hypoplasia, most severe on the side of the hernia but often bilateral, together with abnormally muscularized pulmonary vessels that predispose to pulmonary hypertension after birth. This combination, not the hernia itself, is what makes the disease dangerous.\n\nOn the film, gas-filled loops in the thorax separate CDH from other causes of neonatal respiratory distress at a glance, though a nasogastric tube coiling up into the chest is a useful confirmatory clue. At the bedside, the priority before any thought of surgical repair is stabilizing the pulmonary hypertension and hypoplasia - gentle ventilation, inhaled nitric oxide, sometimes extracorporeal life support - since these, not the anatomic repair, determine survival.\n\n![Congenital diaphragmatic hernia: bowel in the chest. This is a congenital diaphragmatic hernia (Bochdalek type). They underwent timely neonatal repair with complication of bilateral chylothoraxes. At follow-up, the lungs have expanded and grown well. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 203697 (CC BY-NC-SA 3.0).](/uploads/media/5134bb4630e940edbef91359593e0fb2.png)", "parent_id": null, "variant": "long"}, {"id": "2128952dd93440788c537eb7c0496c39", "slug": "pneumothorax-in-the-neonate", "title": "Pneumothorax in the neonate", "content": "In the newborn, a large pneumothorax on a supine film rarely shows the sharp visceral pleural line an upright adult film would. Instead it declares itself as a hyperlucent hemithorax with unusually sharp costophrenic and cardiac borders, a deep, well-defined costophrenic sulcus (the deep sulcus sign), and sometimes a thin lucent stripe tracking along the mediastinum. It complicates surfactant deficiency, meconium aspiration, and positive-pressure ventilation, and a sudden clinical deterioration on the ventilator should prompt a look for it before a film is even taken.\n\nThe film and full account are in [[396|Pneumothorax]].", "parent_id": null, "variant": "long"}, {"id": "d15710b8a2e14c69bd616c4ff3350e0e", "slug": "croup-the-steeple-sign", "title": "Croup: the steeple sign", "content": "Croup narrows the subglottic airway symmetrically, and on a frontal neck film that narrowing tapers the airway into an inverted V, the \"steeple sign,\" in place of the normal shouldered contour below the vocal cords. The finding is neither sensitive nor specific: it can be absent in a child with croup and present as a normal variant, or rarely in epiglottitis, and does not track with how sick the child looks. Croup remains a clinical diagnosis, and a neck film is reserved for an atypical course, obtained only once the airway is secure.\n\nThe film and full account are in [[131|Pediatric Otolaryngology]].", "parent_id": null, "variant": "long"}, {"id": "d9fa8671861b4f72be2d2550e300d53b", "slug": "epiglottitis-the-thumb-sign", "title": "Epiglottitis: the thumb sign", "content": "On a properly positioned lateral neck film, taken with the neck extended and the airway distended by inspiration, an inflamed epiglottis loses its thin curl and swells into a round, thickened shadow resembling an adult's thumb pressed into the airway - the thumb sign. The finding is suggestive but never worth chasing in a child who looks unwell: when epiglottitis is strongly suspected, imaging is skipped in favor of airway visualization and stabilization in a controlled setting such as an operating room, since laying the child flat for a film can precipitate complete obstruction.\n\nThe film and full account are in [[331|Epiglottitis]].", "parent_id": null, "variant": "long"}, {"id": "9e78f05b92c54acb8d3c5b77ffc0c362", "slug": "retropharyngeal-abscess-prevertebral-soft-tissue-widening", "title": "Retropharyngeal abscess: prevertebral soft tissue widening", "content": "A lateral neck film in retropharyngeal abscess shows the prevertebral soft tissue thickened well beyond the width of the adjacent vertebral bodies, often with an anterior, convex bulge pushing the airway forward; on CT the same space contains a low-attenuation collection with an enhancing rim if the process has organized into a drainable abscess rather than cellulitis.\n\nThe mechanism is infection, usually extending from pharyngitis, tonsillitis, or a penetrating injury to the posterior pharyngeal wall, tracking into the retropharyngeal space - a potential space running from the level of the adenoids down to the esophagus at C4-C5 and generously supplied with lymph nodes in young children, which is why the disease is mostly one of early childhood.\n\nThe finding is deceptively easy to overcall: retropharyngeal soft tissue looks thickened on almost any film not taken in full inspiration with the neck extended, because expiration buckles the trachea forward and mimics the same convexity (a \"pseudo-abscess\"). A useful check is the ratio of retropharyngeal soft tissue width to the adjacent vertebral body, which is close to 1:1 in infancy and falls to about 1:2 by school age; soft tissue wider than half the vertebral body width is the threshold worth acting on.\n\nAt the bedside, a confidently abnormal film or ongoing suspicion prompts contrast-enhanced CT to distinguish cellulitis from a collection large enough to need surgical drainage, alongside high-dose intravenous antibiotics regardless of which is found, and otolaryngology involvement to decide between the two.\n\n![Retropharyngeal abscess: prevertebral soft tissue widening. Signs of prevertebral infection, such as edema, cellulitis, or abscess formation, should be suspected in children presenting with neck pain or headache, especially on plain radiographs, which are the first-line imaging in these patients, and on no... Case courtesy of Mostafa Elfeky, Radiopaedia.org, rID: 240692 (CC BY-NC-SA 3.0).](/uploads/media/61343ea842184ee0aed723eb13d3cf14.png)", "parent_id": null, "variant": "long"}, {"id": "8eba1f8c994840a78657d07510d181af", "slug": "bronchiolitis-hyperinflation-and-peribronchial-thickening", "title": "Bronchiolitis: hyperinflation and peribronchial thickening", "content": "This 1-year-old's film shows the peribronchial cuffing typical of bronchiolitis without a focal consolidation to suggest bacterial pneumonia instead - thickened walls around the small airways seen end-on as ring shadows, together with the hyperinflation, flattened diaphragms, and increased anteroposterior chest diameter that come from small-airway narrowing and air trapping. Patchy subsegmental atelectasis, where mucus plugs a bronchiole completely, can also appear and should not be mistaken for pneumonia.\n\nThe mechanism is diffuse inflammation and edema of the small airways, almost always viral - respiratory syncytial virus is the dominant cause - causing partial obstruction that traps air distally on exhalation more than it blocks it on inhalation, which is why hyperinflation rather than collapse dominates the picture. What separates bronchiolitis from bacterial pneumonia on imaging is largely what is absent: no lobar consolidation, no significant pleural effusion, no cavitation.\n\nAt the bedside, this distinction rarely needs a film at all; bronchiolitis is a clinical diagnosis in a wheezing infant with a viral prodrome, and a chest radiograph is reserved for a child who looks sicker than the typical course, has focal findings on examination, or is not improving as expected, because an unnecessary film in a wheezy infant more often triggers antibiotics for a viral illness than it changes management.\n\n![Bronchiolitis: hyperinflation and peribronchial thickening. Bronchiolitis refers to small airway inflammation. In young children, the most common cause is viral infection with respiratory syncytial virus (RSV) the most common agent. Case courtesy of Sally Ayesa, Radiopaedia.org, rID: 172882 (CC BY-NC-SA 3.0).](/uploads/media/b9e018791ca541ea941dddb06d90d1f5.png)", "parent_id": null, "variant": "long"}, {"id": "86df6088345c4c4182aef1e42c842e21", "slug": "round-pneumonia", "title": "Round pneumonia", "content": "This 7-year-old girl's round opacity over the right upper lobe was mistaken clinically for shoulder pain before the film showed its source: a right upper lobe pneumonia abutting the pleura, round enough to be read as a mass at first glance. Round pneumonia is a shape, not a different disease from ordinary bacterial pneumonia, most often caused by Streptococcus pneumoniae; the round appearance comes from an age-related quirk of lung anatomy.\n\nThe collateral air channels that let infection spread sideways across a mature lung - the pores of Kohn and canals of Lambert - are not yet fully developed before about age 8, so infection in a younger child expands outward as a sphere from its point of origin rather than following the fissures and airways into the wedge-shaped lobar pattern seen in older children and adults. On the film, an acute rather than obtuse angle where the opacity meets the chest wall favors a lung origin over a pleural-based mass.\n\nIn a child under 8 with the classic symptoms of pneumonia - fever, cough - that acute angle and the age alone are usually enough, and no further imaging is needed to exclude a true mass. The action that follows is a short course of antibiotics and, if there is any lingering doubt, a follow-up film after treatment: resolution of the \"mass\" confirms it was pneumonia and closes the question without biopsy or CT.\n\n![Round pneumonia. A good example of round pneumonia, which typically occur in the pediatric population. Case courtesy of Ian Bickle, Radiopaedia.org, rID: 190005 (CC BY-NC-SA 3.0).](/uploads/media/296a13db931249b191e4a48d211d202a.png)", "parent_id": null, "variant": "long"}, {"id": "97341465c9b644c5b343a713ffa9240e", "slug": "lobar-pneumonia-with-effusion", "title": "Lobar pneumonia with effusion", "content": "A lobar pneumonia that has gone on to seed the pleural space shows a recognizable pattern on frontal and lateral films: a dense lobar opacity with a fluid meniscus tracking up the chest wall alongside it, best confirmed on a lateral decubitus view that lets free-flowing fluid layer out along the dependent side. Loculated fluid may not shift on that view and instead points toward an organizing empyema rather than a simple parapneumonic effusion.\n\nThe film and full account are in [[150|Pneumonia]].", "parent_id": null, "variant": "long"}, {"id": "e33cdc714bd54d65a9f82d6059ab65fb", "slug": "inhaled-foreign-body-unilateral-air-trapping", "title": "Inhaled foreign body: unilateral air trapping", "content": "This patient's presentation - sudden dyspnea, wheeze, cough, and a witnessed choking or \"screeching\" episode - captures why an inhaled foreign body is often diagnosed clinically before any film is taken, and why the film can be unremarkable if the object still allows some air past it in both directions. When it produces a one-way, ball-valve obstruction, lodged classically in a mainstem bronchus (the right more often than the left, given its straighter takeoff), the affected lung inflates on inspiration and cannot fully empty on expiration, so it stays hyperinflated and hyperlucent while the unobstructed lung deflates normally.\n\nThe mechanism is purely mechanical: the object's edge and the airway wall act as a one-way valve rather than a fixed obstruction. Because this is a dynamic finding, a single inspiratory film can look deceptively normal; the sign is unmasked by comparing an inspiratory film with an expiratory one, or, in a younger child who cannot cooperate with breath-holding, left and right lateral decubitus views, and watching for the mediastinum to shift away from the trapped, still-inflated side on the view meant to deflate it. A radiolucent object leaves no shadow of its own, so this indirect sign, not a visible foreign body, is usually what the film actually shows.\n\nOnce suspected, the definitive next step is not more imaging but rigid bronchoscopy, which is diagnostic and therapeutic in the same procedure.", "parent_id": null, "variant": "long"}, {"id": "65edce0cc2034f58b09d6ab3ccd05b3e", "slug": "swallowed-coin-in-the-esophagus-en-face-on-the-frontal-film", "title": "Swallowed coin in the esophagus: en face on the frontal film", "content": "In this 3-year-old, the swallowed coin lies lodged high in the esophagus, seen en face - flat and round - on the frontal film, which is the tell for its location. The distinction is orientation, not appearance: an object caught in the coronal, disc-like esophagus lies broadside to a frontal x-ray beam and appears as a full circle, while the same object in the sagittal, slit-like trachea or larynx turns edge-on and appears as a thin line on the frontal view (and broadside on the lateral) - the reverse of the esophageal pattern.\n\nThis follows directly from the two structures' different cross-sectional shape, and it lets a plain film separate an airway foreign body, which usually causes immediate respiratory symptoms, from an esophageal one, which more often causes drooling, refusal to eat, or throat pain with a quieter airway. Esophageal coins commonly lodge at one of three physiologic narrowings, most often the upper esophageal sphincter just below the cricopharyngeus. A coin that has moved on a repeat film, as happened here after overnight observation, is drifting toward the stomach rather than fixed in place.\n\nAt the bedside, a coin at or above the level of the clavicles, one causing symptoms, or one that has not moved on a repeat film after a period of observation is an indication for endoscopic removal rather than continued watching.\n\n![Swallowed coin in the esophagus: en face on the frontal film. Swallowed coin in the esophagus in a 3-year-old child. Note the transverse orientation, a foreign body in the trachea is more likely to have an AP orientation and will probably also result in symptoms +/- pulmonary changes (e.g. atelectasis) Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 8286 (CC BY-NC-SA 3.0).](/uploads/media/8dc290c4a4324329b482e211e7db3422.png)", "parent_id": null, "variant": "long"}, {"id": "2688754145674c229ca6146fecfccf01", "slug": "button-battery-in-the-esophagus-the-halo-sign", "title": "Button battery in the esophagus: the halo sign", "content": "An hour after this 20-month-old swallowed it, her chest film showed a round, radiopaque, 22-millimeter object lodged in the proximal esophagus with a halo, or double-rim, sign: two concentric circles produced by the battery's beveled edge, distinguishing it at a glance from the single uniform density of a coin. A lateral view sharpens the distinction further, showing a step-off at the rim rather than a coin's flat profile, and the lucent trachea running anterior to the object confirms it is esophageal rather than tracheal.\n\nThe urgency here has nothing to do with size and everything to do with electrochemistry: a lodged battery completes a circuit through moist tissue, generating hydroxide at its negative pole and causing liquefactive necrosis that can perforate the esophagus within two hours, quite apart from any pressure or chemical leak from the cell itself. This is why an esophageal button battery is removed emergently regardless of the child's symptoms, in contrast to a coin, which can often be observed.\n\nWhile removal is arranged, giving honey or sucralfate by mouth, if the child can swallow safely, has been shown to slow the injury. Once out, the mucosa is inspected endoscopically, because the same mechanism that caused the injury can go on to cause a tracheoesophageal fistula, perforation, mediastinitis, or delayed vessel injury even after the battery itself is gone.\n\n![Button battery in the esophagus: the halo sign. A radiograph of her chest was done approximately one hour after ingestion showing a round radiopaque 22 mm foreign body in the proximal esophagus. The object had a halo sign /double rim sign which indicated the manifestation of two circular pieces... Case courtesy of Ashmitha Kumar, Radiopaedia.org, rID: 164310 (CC BY-NC-SA 3.0).](/uploads/media/284386d7eace4bdabc119bde4278dd5e.png)", "parent_id": null, "variant": "long"}, {"id": "cced1d94c6d848edb52fbd9936283b39", "slug": "cystic-fibrosis-upper-lobe-bronchiectasis", "title": "Cystic fibrosis: upper-lobe bronchiectasis", "content": "By adolescence, cystic fibrosis has usually left its mark on the upper lobes first: bronchiectasis seen as ring shadows (a dilated, thick-walled airway in cross-section) and tram-track opacities (the same airway in longitudinal section), against a background of hyperinflation, peribronchial cuffing, and mucoid impaction. On CT the same disease shows the signet-ring sign, a dilated bronchus paired with its smaller adjacent pulmonary artery, and low-attenuation regions of air trapping on expiratory images that can be invisible on a plain film.\n\nThe upper-lobe predominance and the age of onset are the pattern to recognize: cystic fibrosis damages airways from repeated infection and impaired mucociliary clearance working from the top down over years, in contrast to the acute, usually lower-lobe-predominant, and rapidly reversible changes of viral bronchiolitis, with which early cystic fibrosis can otherwise be confused on a single film. The underlying mechanism is a defective CFTR chloride channel that thickens airway secretions, so mucus plugs small airways, traps bacteria behind the plug, and each infection leaves the airway wall a little more dilated and scarred than before.\n\nAt the bedside, the plain film is a surveillance tool rather than the test that changes management on the day: it is obtained annually or with an exacerbation, but a CT scan, scored for the extent of bronchiectasis and air trapping, tracks disease progression and predicts future exacerbations better than either the film or pulmonary function testing alone.\n\n![Cystic fibrosis: upper-lobe bronchiectasis. The classic chest radiographic findings of cystic fibrosis include: Case courtesy of Hazem M. Almasarei, Radiopaedia.org, rID: 161586 (CC BY-NC-SA 3.0).](/uploads/media/29222ebb939e4c96aaa6ab5341011ade.png)", "parent_id": null, "variant": "long"}, {"id": "6f6c7e8f85de45e1b50f4853aff12bf2", "slug": "tetralogy-of-fallot-the-boot-shaped-heart", "title": "Tetralogy of Fallot: the boot-shaped heart", "content": "The classic tetralogy of Fallot chest film shows a boot-shaped heart, or coeur en sabot: a normal-sized left atrium and ventricle beside a hypertrophied right ventricle that lifts the cardiac apex upward, with a small or absent main pulmonary artery producing a concave waist where its shadow should bulge. Pulmonary vascularity is reduced rather than increased, and a right-sided aortic arch is present in about a quarter of cases.\n\nThe film and full account are in [[268|Tetralogy Of Fallot]].", "parent_id": null, "variant": "long"}, {"id": "4a00561f37754aea9b30008b5db792c2", "slug": "transposition-of-the-great-arteries-egg-on-a-string", "title": "Transposition of the great arteries: egg on a string", "content": "Transposition of the great arteries produces the \"egg on a string\" sign only in a minority of cases, but when present it is distinctive: a globular, egg-shaped cardiac silhouette, from an enlarged right atrium and right ventricle, the chambers now doing double duty, sitting atop a narrow superior mediastinum, the \"string.\" Most films instead look ordinary, or show only mild cardiomegaly with increased pulmonary vascular markings, which is one reason the diagnosis in a cyanotic newborn cannot be excluded by a normal-looking film.\n\nThe mechanism behind the sign is the abnormal side-by-side, rather than the normal spiral, relationship between the aorta and pulmonary artery in transposition; this narrows the great-vessel silhouette at the mediastinal waist while the systemic ventricle (anatomically the right ventricle) hypertrophies below it to push blood through the aorta. The heart looks different from the boot of tetralogy of Fallot mainly in vascularity: transposition usually has normal to increased pulmonary blood flow rather than the reduced flow of tetralogy, because the two circulations run in parallel rather than one being obstructed.\n\nAt the bedside, the film is never the deciding test; profound cyanosis unresponsive to oxygen in the first hours of life is a duct-dependent emergency, and the next steps are an echocardiogram to confirm the anatomy and a prostaglandin E1 infusion to keep the ductus arteriosus open until balloon atrial septostomy or surgical repair can be arranged.\n\n![Transposition of the great arteries: egg on a string. This case was donated to Radiopaedia.org by Radswiki.net Case courtesy of The Radswiki, Radiopaedia.org, rID: 12036 (CC BY-NC-SA 3.0).](/uploads/media/4ee3d21c224c489f809f2bf441e0783b.png)", "parent_id": null, "variant": "long"}, {"id": "627641be97b24a519b087fddd26fdb61", "slug": "total-anomalous-pulmonary-venous-return-the-snowman", "title": "Total anomalous pulmonary venous return: the snowman", "content": "The snowman sign belongs specifically to the supracardiac form of total anomalous pulmonary venous return, in which all four pulmonary veins drain not into the left atrium but into a confluence that empties upward into a vertical vein and then the left superior vena cava, before returning to the right atrium. That extra vessel running alongside the superior mediastinum widens it into a second, upper \"head\" sitting atop the cardiac silhouette's \"body,\" giving the two-lobed snowman, or figure-8, outline together with cardiomegaly and increased pulmonary vascularity. The sign takes months to appear, since the collateral pathway needs time to dilate, so it is essentially never seen in the newborn period even when supracardiac TAPVR is already causing cyanosis.\n\nThe other anatomic types look entirely different: when the anomalous vein instead drains below the diaphragm (infracardiac, or \"type 3,\" TAPVR), the connection is typically obstructed, and the film shows a normal-sized heart with severe pulmonary venous congestion and edema rather than any snowman contour, because the physiology is one of obstructed outflow rather than a volume-loaded chamber. This makes heart size and pulmonary vascular pattern, not the presence or absence of a snowman, the more reliable bedside clue to obstruction.\n\nAny cyanotic, tachypneic newborn with this picture needs an urgent echocardiogram to define the drainage pattern and look specifically for obstruction, since obstructed TAPVR is a surgical emergency rather than a stabilize-and-wait ductal-dependent lesion.", "parent_id": null, "variant": "long"}, {"id": "7b6dd407510245ccb203a8d1b6f21c0b", "slug": "coarctation-of-the-aorta-rib-notching-and-the-figure-3-sign", "title": "Coarctation of the aorta: rib notching and the figure 3 sign", "content": "In an older child or teenager with coarctation of the aorta, the frontal chest film shows the figure 3 sign: a double bulge along the left upper mediastinal border, the aortic knob above and the poststenotic dilation of the descending aorta below, with the coarctation itself as the notch between them. Lower down, the ribs - typically the third through eighth, posteriorly - show scalloped undersurfaces from chronic pressure erosion by dilated, tortuous intercostal collateral vessels, a finding called rib notching.\n\nBoth signs are consequences of the same obstruction: coarctation narrows the aorta, usually just distal to the left subclavian artery near the ligamentum arteriosum, so blood reaches the descending aorta and lower body partly by an alternate route, retrograde through the internal thoracic and intercostal arteries, which enlarge under the extra flow and, over years, erode the bone they run along. This is why rib notching takes years to develop and is essentially never seen in an infant with coarctation, however severe; a newborn instead presents with a duct-dependent circulation and cardiogenic shock as the ductus closes, with no time for collaterals to form.\n\nIn the child old enough to have developed both signs, they confirm a diagnosis usually already suspected from upper-body hypertension with diminished or delayed femoral pulses, and the next step is an echocardiogram to define the anatomy before referral for surgical or catheter-based repair.\n\n![Coarctation of the aorta: rib notching and the figure 3 sign. Aortic coarctation can be difficult to identify on chest x-ray and routine review of aortic outline, as well the inferior rib notching, which is known as Roesler sign when coarctation is the cause, which is necessary if one is to make the diagnosis. Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 6279 (CC BY-NC-SA 3.0).](/uploads/media/879e39526b69402c8d967f3cffd8482c.png)", "parent_id": null, "variant": "long"}, {"id": "d5264e8aa6fc442c8855240d3afea580", "slug": "left-to-right-shunt-cardiomegaly-and-pulmonary-plethora", "title": "Left-to-right shunt: cardiomegaly and pulmonary plethora", "content": "A large ventricular septal defect enlarges the heart on the side that handles the extra volume: the left ventricle and left atrium receive the shunted blood after it recirculates through the lungs, so the cardiac silhouette grows along its left border while the aorta, carrying a normal or reduced forward stroke volume, stays unremarkable in size. An atrial septal defect shifts that pattern one chamber earlier - a dilated right atrium and right ventricle, a prominent main pulmonary artery segment, and again a small aortic shadow. In both, the lungs show pulmonary plethora: engorged vessels visible further into the periphery than normal, and end-on vessels, small round densities where a vessel is caught in cross-section, more numerous than expected for the field.\n\nThe mechanism is the same regardless of which septum is defective - blood takes the path of least resistance from the higher-pressure left side to the lower-pressure right side, recirculates through the lungs, and returns to overload whichever chamber sits downstream of the defect, enlarging it by volume rather than by pressure. This pattern distinguishes a left-to-right shunt from cyanotic lesions with reduced flow, like tetralogy of Fallot, at a glance: more vessels rather than fewer.\n\nAt the bedside, cardiomegaly and plethora in an infant with a murmur and feeding difficulty around six to eight weeks of age - when pulmonary vascular resistance has fallen enough to unmask the shunt - prompts an echocardiogram rather than further films, to size the defect and plan medical or surgical management.", "parent_id": null, "variant": "long"}, {"id": "4d89a99d7fb04d5087afd67c39dca718", "slug": "necrotizing-enterocolitis-pneumatosis-intestinalis-and-portal-venous-gas", "title": "Necrotizing enterocolitis: pneumatosis intestinalis and portal venous gas", "content": "This preterm infant's film, taken at 8 days of life, actually shows NEC's worst-case complication: perforation, seen as the football sign, a large oval lucency outlining the whole peritoneal cavity with the falciform ligament visible as a line down the middle, confirmed on the lateral view. That free air is downstream of the two signs that define NEC itself: pneumatosis intestinalis, a bubbly or curvilinear lucency within the bowel wall, most often the right lower quadrant, and portal venous gas, branching lucent streaks over the liver where gas has tracked from the bowel wall into the mesenteric and portal venous system. Both are considered pathognomonic for NEC in a premature infant, a step beyond the nonspecific findings - diffuse gaseous distention, loss of the normal symmetric gas pattern, or a single dilated loop that stays fixed on serial films - that raise suspicion but do not confirm it.\n\nThe mechanism is ischemic and infectious injury to an immature bowel wall, most often in a preterm infant recovering from another stressor; gas produced by bacteria invading the damaged wall dissects into the submucosa (pneumatosis) and, once it enters disrupted mucosal vessels, travels to the portal system. Once the wall is compromised enough to perforate, gas escapes freely into the peritoneum.\n\nAt the bedside, pneumatosis or portal venous gas without perforation is managed medically - bowel rest, decompression, antibiotics - with serial abdominal films or cross-table lateral views to watch for free air; a football sign or free air on any view is a surgical emergency.\n\n![Necrotizing enterocolitis: pneumatosis intestinalis and portal venous gas. X-rays demonstrate necrotizing enterocolitis with perforation, and resulting pneumoperitoneum (seen as the football sign on AP view with visible falciform ligament, and confirmed on lateral film). This child was transferred to a tertiary neonatal ... Case courtesy of Alice Spencer, Radiopaedia.org, rID: 67382 (CC BY-NC-SA 3.0).](/uploads/media/43eecfd6a09143a7b9b2d6647a77b38c.png)", "parent_id": null, "variant": "long"}, {"id": "59fcb61e98a04239b264bf2ad5624395", "slug": "duodenal-atresia-the-double-bubble", "title": "Duodenal atresia: the double bubble", "content": "A neonate with duodenal atresia shows two air-filled, dilated structures on a plain abdominal film - the stomach and the obstructed duodenal bulb proximal to the atresia - separated by the pylorus and giving the double-bubble sign; critically, there is no gas at all distal to the two bubbles, because the obstruction is complete.\n\nThe mechanism is a failure of the duodenal lumen to recanalize during early fetal development, and it is strongly associated with trisomy 21 (present in roughly a quarter to a third of cases) and with other atresias, so the film of one prompts a careful look for the others. The double bubble is not unique to atresia: a duodenal web or annular pancreas can produce the same two-bubble appearance if the obstruction they cause is complete, and only surgery distinguishes among them. The sign that does separate true atresia from a partial obstruction such as malrotation is the complete absence of distal gas, since any air seen beyond the duodenum means the lumen is at least partly patent and points instead toward malrotation with a partially obstructing band or a less severe web.\n\nClinically, duodenal atresia announces itself antenatally with polyhydramnios or postnatally with bilious or nonbilious vomiting, depending on whether the atresia is above or below the ampulla, in the first day of life, and the double bubble on a plain film is usually enough to proceed straight to surgical repair without further contrast imaging.\n\n![Duodenal atresia: the double bubble. Duodenal atresia in a neonate. Confirmed at surgery. Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 6352 (CC BY-NC-SA 3.0).](/uploads/media/d6c4a95362ab4d8d833775ecc2226743.png)", "parent_id": null, "variant": "long"}, {"id": "b400b3bee4524c329fc0117be266bb1f", "slug": "pyloric-stenosis-on-ultrasound-the-thickened-elongated-pylorus", "title": "Pyloric stenosis on ultrasound: the thickened, elongated pylorus", "content": "On ultrasound, hypertrophic pyloric stenosis looks exactly like its name: an elongated, thick-walled pyloric channel that will not open, most often measured at a muscle wall thickness of 4 millimeters or more and a channel length of 16 millimeters or more in a vomiting infant between 2 and 8 weeks of age. Real-time scanning confirms the diagnosis by watching fluid fail to pass through the closed channel over several minutes, the functional counterpart to the fixed measurements.\n\nThe film and full account are in [[262|Pyloric Stenosis]].", "parent_id": null, "variant": "long"}, {"id": "e323e2c12619473aa4f8fafb43ca63ab", "slug": "intussusception-the-target-sign", "title": "Intussusception: the target sign", "content": "On ultrasound, intussusception forms a target, or doughnut, sign in cross-section: concentric rings of bowel wall and mesenteric fat where one segment of bowel has telescoped into the segment just downstream of it, and a pseudo-kidney sign in the longitudinal plane along the same axis. The finding is now sensitive and specific enough that ultrasound has replaced contrast enema as the first study in a child with the classic history of intermittent colicky pain, vomiting, and later currant-jelly stool.\n\nThe film and full account are in [[441|Surgical Abdomen]].", "parent_id": null, "variant": "long"}, {"id": "42e62faa3ad44f1db080f950d3972060", "slug": "malrotation-with-midgut-volvulus-the-corkscrew-duodenum", "title": "Malrotation with midgut volvulus: the corkscrew duodenum", "content": "An upper GI contrast study is the gold standard for malrotation, correct more than 93 percent of the time, and in an unrotated bowel the key finding is simply a duodenum in the wrong place: the duodenojejunal junction, which should lie to the left of the spine and level with or above the duodenal bulb, is instead displaced inferiorly and to the right. When the abnormally mobile, narrow-based mesentery this creates has twisted on itself - midgut volvulus - the same study instead shows the corkscrew sign, a spiraling column of contrast winding through the twisted duodenum and proximal jejunum, sometimes narrowing to a beak-like point where the lumen is compressed. On ultrasound, the same twist can be inferred indirectly by finding the superior mesenteric vein lying to the left of the artery instead of its normal position to the right.\n\nThe mechanism is a failure of the normal fetal rotation and fixation of the midgut, leaving the small bowel mesentery attached to the posterior abdominal wall across an abnormally short base instead of the usual broad diagonal one, which lets the entire midgut twist around the superior mesenteric vessels and cut off its own blood supply.\n\nThis is why bilious vomiting in an infant is a surgical emergency until proven otherwise: the corkscrew sign, or even a convincingly abnormal duodenojejunal junction without frank volvulus, is reason enough to proceed directly to the operating room rather than wait for further deterioration, since delay costs bowel.\n\n![Malrotation with midgut volvulus: the corkscrew duodenum. CT features of intestinal malrotation complicated by midgut volvulus. Case courtesy of Ammar Haouimi, Radiopaedia.org, rID: 211348 (CC BY-NC-SA 3.0).](/uploads/media/aaf02da1e6a0414ca4be5ad2243b4dc0.png)", "parent_id": null, "variant": "long"}, {"id": "025bc64b90944f5586d49e07180aef19", "slug": "hirschsprung-disease-the-transition-zone-on-contrast-enema", "title": "Hirschsprung disease: the transition zone on contrast enema", "content": "In this 5-month-old, an unprepped contrast enema shows the classic sign of Hirschsprung disease: an abrupt transition zone where a normal-caliber or dilated proximal colon narrows sharply into the smaller-caliber, aganglionic distal segment that cannot relax to let stool pass.\n\nThe mechanism is a failure of neural crest cells to migrate all the way to the end of the hindgut during development, leaving the distal bowel, almost always beginning at the rectum and extending a variable distance proximally, without the Auerbach and Meissner plexuses that normally coordinate peristalsis and relaxation; that segment stays tonically contracted, and the bowel just above it dilates against the obstruction over time. The study works best after the first month of life, because the proximal bowel may not have had time to dilate enough to show a clear transition in a newborn just days old; in that setting, or in the roughly 1 in 10 cases where the study is falsely normal at any age, the more subtle clue is a rectum no wider than the sigmoid colon above it, the reverse of the normal relationship. No prior cleansing enema is given, since that can transiently distend the aganglionic segment and hide the transition zone.\n\nAt the bedside, a positive or even a merely suspicious study is followed by a suction rectal biopsy, which is the test that actually confirms the diagnosis by showing absent ganglion cells and hypertrophied nerve trunks.\n\n![Hirschsprung disease: the transition zone on contrast enema. Features of Hirschsprung disease with a transition zone in the distal colon. Case courtesy of Tee Yu Jin, Radiopaedia.org, rID: 71552 (CC BY-NC-SA 3.0).](/uploads/media/25e77c1e976a497a9f73b782e3ee2665.png)", "parent_id": null, "variant": "long"}, {"id": "96e42888aec0443ead8b7caf2124efbf", "slug": "meconium-ileus-soap-bubble-right-lower-quadrant", "title": "Meconium ileus: soap-bubble right lower quadrant", "content": "This 2-day-old's plain film shows the soap-bubble sign of meconium ileus: a mottled, granular lucency in the right lower quadrant produced by gas bubbles trapped within abnormally thick, inspissated meconium in the terminal ileum, alongside dilated proximal small bowel loops of differing caliber and a notable absence of air-fluid levels, because the meconium is too viscid to layer the way liquid stool would. A contrast enema, if performed, adds a microcolon - a colon that looks abnormally small and unused because it has never had a normal volume of stool pass through it - and small filling defects in the distal ileum sometimes called rabbit pellets.\n\nThe mechanism runs back to cystic fibrosis in more than 80 percent of cases: defective CFTR chloride transport leaves meconium abnormally dehydrated and protein-rich, and it impacts in the terminal ileum, the narrowest point in the fetal small bowel, causing a lower small bowel obstruction before birth. The disease can be simple, an obstruction alone, or complicated by volvulus, atresia, or perforation with meconium peritonitis, which is what separates the two most consequential next steps.\n\nAt the bedside, simple meconium ileus is treated with a hyperosmolar water-soluble contrast enema, which is diagnostic and often therapeutic at once, drawing fluid into the bowel to loosen the impacted meconium and relieve the obstruction without surgery; evidence of perforation, volvulus, or peritonitis on the initial film instead means proceeding directly to laparotomy.\n\n![Meconium ileus: soap-bubble right lower quadrant. Typical imaging findings in meconium ileus. Associated with cystic fibrosis. Case courtesy of Juan Carlos Santizo Castillo, Radiopaedia.org, rID: 97076 (CC BY-NC-SA 3.0).](/uploads/media/eafadc2705c44e49a0a0020888c853b5.png)", "parent_id": null, "variant": "long"}, {"id": "248152d5bfb4457aaf8332ab7f4af020", "slug": "posterior-urethral-valves-the-keyhole-sign-on-vcug", "title": "Posterior urethral valves: the keyhole sign on VCUG", "content": "The keyhole sign for posterior urethral valves actually appears on two different studies at two different times, and it is worth being precise about which is which. Prenatally, on fetal ultrasound, it is the combination of a dilated posterior urethra continuous with a distended bladder, shaped together like a keyhole, alongside bilateral hydroureteronephrosis; this constellation is essentially pathognomonic and is how about half of cases are found before birth. After birth, the diagnostic study becomes a voiding cystourethrogram, and the sign there is really an abrupt caliber change rather than a literal keyhole: a markedly dilated posterior urethra that narrows suddenly at the level of the valve leaflets into a normal or small-caliber bulbar and penile urethra, often with a thick-walled, trabeculated bladder and diverticula from years of voiding against an obstruction present since early fetal life. The valve tissue itself is thin and frequently not directly visible; the diagnosis rests on the abrupt caliber change, not on seeing the leaflets.\n\nThe mechanism is a congenital membrane or ridge of tissue in the posterior urethra that obstructs urine flow in a male fetus, and the severity of the resulting oligohydramnios, from reduced fetal urine output, predicts the degree of pulmonary hypoplasia the infant will have at birth, often the more immediately life-threatening problem.\n\nAt the bedside, a male infant with a palpable bladder, a poor stream, or antenatal hydronephrosis goes to VCUG to confirm the valves, with early urologic referral for endoscopic valve ablation.\n\n![Posterior urethral valves: the keyhole sign on VCUG. Posterior urethral valve is a common cause of obstructive uropathy in infants. Severe cases are usually diagnosed with antenatal ultrasonography. Voiding cystourethrogram (VCUG) is the modality of choice for the diagnosis of posterior urethral val... Case courtesy of Hidayatullah Hamidi, Radiopaedia.org, rID: 52571 (CC BY-NC-SA 3.0).](/uploads/media/1fb1abc195954eddbec6f30433dcc915.png)", "parent_id": null, "variant": "long"}, {"id": "c1d0e936cb1b43ffab68a75d2ce58c3d", "slug": "vesicoureteral-reflux-on-vcug", "title": "Vesicoureteral reflux on VCUG", "content": "This 9-year-old's voiding cystourethrogram shows bilateral reflux of different severity in each kidney - grade III on the right, grade II on the left - illustrating that VUR is graded per renal unit rather than as a single diagnosis for the child. The five-point fluoroscopic grading scale runs from reflux confined to a non-dilated ureter (grade I) up to gross ureteral, pelvic, and calyceal dilation with tortuosity and loss of the normal papillary impressions (grade V); a nuclear cystogram, which uses far less radiation but has much lower spatial resolution, can only sort reflux into three bands - mild, moderate, or severe - and so is better suited to following a reflux already characterized on fluoroscopy than to grading it the first time.\n\nThe mechanism is a ureterovesical junction that fails to act as a one-way valve, usually because the intramural, submucosal tunnel the ureter travels through the bladder wall is too short; contrast, or infected urine, that should stay in the bladder instead washes back up the ureter toward the kidney. Bladder trabeculation, as seen here, points to an element of voiding dysfunction or outlet obstruction working alongside the reflux rather than a purely anatomic ureteral problem.\n\nAt the bedside, the grade drives management: low-grade reflux is often watched for spontaneous resolution with or without prophylactic antibiotics, while higher grades or breakthrough febrile UTIs on prophylaxis move the conversation toward longer prophylaxis or surgical correction.\n\n![Vesicoureteral reflux on VCUG. This case demonstrates bilateral vesicoureteric reflux - right grade III and left grade II, with bladder trabeculation. Case courtesy of Varun Babu, Radiopaedia.org, rID: 19476 (CC BY-NC-SA 3.0).](/uploads/media/2a21a57d71d84af295f340a748baa3d8.png)", "parent_id": null, "variant": "long"}, {"id": "d26ba85f2d644af182e01b7d2233754a", "slug": "medullary-nephrocalcinosis", "title": "Medullary nephrocalcinosis", "content": "Medullary nephrocalcinosis on renal ultrasound is calcium deposited within the renal pyramids rather than the cortex, seen as increased echogenicity that starts at the tips of the pyramids and, as it worsens, can involve the whole pyramid and eventually cast a posterior acoustic shadow the way a kidney stone does; the cortex itself stays normal, which is the detail that keeps this from being confused with more diffuse renal disease.\n\nThe finding needs to be separated from a normal newborn mimic, transient renal medullary hyperechogenicity: a harmless, self-resolving brightening of the pyramids in the first weeks of life caused by Tamm-Horsfall protein rather than calcium, which clears on a repeat scan within a month without any of the metabolic workup nephrocalcinosis demands. True nephrocalcinosis reflects a sustained excess of calcium or phosphate delivered to the distal tubule and collecting duct, where urine is most concentrated and least buffered against precipitation; the two settings that produce it most often in children are distal renal tubular acidosis, which cannot acidify urine enough to keep calcium in solution, and prolonged furosemide use in a premature infant, which causes hypercalciuria as a direct drug effect. Hyperparathyroidism and other causes of hypercalciuria or hyperoxaluria follow the same final pathway.\n\nAt the bedside, an echogenic-pyramid finding on ultrasound prompts a metabolic screen - serum electrolytes and a urine calcium-to-creatinine ratio at minimum - rather than a repeat scan alone, since the underlying cause, not the calcium itself, is what needs treating to prevent progressive renal damage.\n\n![Medullary nephrocalcinosis. An infant suspected to have Liddle's syndrome, screened for nephrocalcinosis. Case courtesy of Hani M. Al Salam, Radiopaedia.org, rID: 9899 (CC BY-NC-SA 3.0).](/uploads/media/1db64e2194ca47f4b993722146182ee2.png)", "parent_id": null, "variant": "long"}, {"id": "5a108b81016e42fc9be834bb33a22129", "slug": "wilms-tumor-a-renal-mass-displacing-the-kidney", "title": "Wilms tumor: a renal mass displacing the kidney", "content": "This 3-year-old's abdominal imaging shows a large right-sided renal mass, bulky enough to distort the kidney's normal shape and, on cross-section, to displace the inferior vena cava rather than invade it outright in most cases - though Wilms tumor's well-known tendency to grow into the renal vein and extend along the IVC, occasionally as far as the right atrium as a tumor thrombus, means these vascular structures are specifically evaluated with Doppler ultrasound whenever a solid renal mass is found.\n\nCT with contrast follows to confirm that the mass is truly intrarenal, the detail that most reliably separates it from neuroblastoma, which arises outside the kidney and displaces rather than replaces renal tissue, to map its extent, look for nodal spread or liver metastases, and assess the contralateral kidney, since 5 to 10 percent of cases are bilateral. The mechanism is a nephroblastoma arising from persistent, undifferentiated metanephric blastema that should have completed its differentiation into mature nephrons before birth; Wilms tumor is the most common malignant kidney tumor of childhood, typically presenting as a painless abdominal mass found incidentally by a parent or on a routine exam, occasionally with microscopic or gross hematuria.\n\nAt the bedside, a solid renal mass on ultrasound in a preschool-age child goes to contrast CT of the abdomen, with chest imaging to look for pulmonary metastases, before any biopsy, since most centers proceed to surgical resection first and confirm the histology on the specimen rather than risking tumor spillage with a preoperative biopsy.\n\n![Wilms tumor: a renal mass displacing the kidney. This case demonstrates the typical appearance of a large right-sided Wilms tumor. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 8084 (CC BY-NC-SA 3.0).](/uploads/media/22f9ebc6bb4a410ca1c83e6cc7fc1da3.png)", "parent_id": null, "variant": "long"}, {"id": "43c0094eec5d4ba98ee2fb2308856bbf", "slug": "neuroblastoma-a-calcified-suprarenal-mass", "title": "Neuroblastoma: a calcified suprarenal mass", "content": "Neuroblastoma and Wilms tumor sit side by side as the two most common solid abdominal masses of early childhood, but they look different enough on cross-sectional imaging to usually be told apart before any tissue is taken. Neuroblastoma typically appears as a lobulated suprarenal or paraspinal mass, heavily and irregularly calcified in a majority of cases, that encases and lifts blood vessels - the aorta and its branches - off the spine rather than merely pushing them aside, and that not infrequently crosses the midline, a detail with staging significance defined relative to the vertebral column.\n\nThis behavior reflects where the tumor comes from: neural crest cells of the developing sympathetic nervous system, most often in the adrenal medulla but anywhere along the sympathetic chain from the neck to the pelvis, growing as an infiltrative mass that surrounds normal structures in its path rather than one that displaces them cleanly the way an encapsulated renal tumor does. Calcification and vascular encasement, together with an extrarenal origin confirmed on CT, are what separate it from Wilms tumor, which is intrarenal, less often calcified, and displaces rather than encases the great vessels.\n\nAt the bedside, a suprarenal mass with these features prompts urine catecholamine metabolites (vanillylmandelic and homovanillic acid) and a metaiodobenzylguanidine (MIBG) scan, which is both diagnostic - most neuroblastomas take up the tracer - and a staging tool, since it screens the rest of the skeleton and marrow for metastatic disease in one study.\n\n![Neuroblastoma: a calcified suprarenal mass. Neuroblastomas (NBL) and nephroblastomas/Wilm's tumors (WT) represent two of the most commonly detected solid tumors in childhood 1. These are the two crucial differential diagnoses to be considered with any renal mass identified in a child of thi... Case courtesy of Candice Norris, Radiopaedia.org, rID: 50955 (CC BY-NC-SA 3.0).](/uploads/media/72524c1ab75044cf8399d315d12e484f.png)", "parent_id": null, "variant": "long"}, {"id": "79430f44cb8a473ca38bcd4fceac62cf", "slug": "osteosarcoma-the-sunburst-and-codman-triangle", "title": "Osteosarcoma: the sunburst and Codman triangle", "content": "The classic osteosarcoma radiograph combines a destructive, mixed lytic and blastic lesion at the metaphysis of a long bone, the distal femur being the single most common site, with two periosteal reactions that, together, announce an aggressive process before biopsy confirms it. The sunburst pattern is spiculated new bone laid down perpendicular to the shaft, following tiny blood vessels the tumor has recruited as it breaks through the cortex; a Codman triangle is the wedge of periosteum lifted and partly ossified at the tumor's margin, where growth has outpaced the periosteum's ability to keep laying down bone smoothly along the shaft.\n\nBoth signs exist because osteosarcoma outgrows the bone's normal remodeling, in contrast to a slow-growing or benign lesion, which gives the periosteum time to thicken solidly around it instead. Tumor osteoid extending into the adjacent soft tissue is a further marker of cortical breach that a benign lesion would not produce. The tumor typically arises in the second decade, coinciding with peak growth velocity at the metaphysis, most often near the knee - distal femur or proximal tibia - or the proximal humerus, the sites of the fastest-growing physes in the body.\n\nAt the bedside, this appearance in an adolescent with weeks of activity-related bone pain and swelling prompts MRI of the entire bone and adjacent joint to define disease extent, staging with chest CT (the most common site of metastasis), and biopsy at a center equipped to plan the eventual limb-sparing resection, since a poorly placed biopsy tract can compromise that surgery later.", "parent_id": null, "variant": "long"}, {"id": "ccd3f2ff7b1e46d5bab89cf0c4d46b0b", "slug": "ewing-sarcoma-onion-skin-periosteal-reaction", "title": "Ewing sarcoma: onion-skin periosteal reaction", "content": "Ewing sarcoma's signature is a multilayered, lamellated periosteal reaction, the \"onion-skin\" sign, laid down in successive shells as the tumor repeatedly outgrows and lifts the periosteum, sometimes with Codman triangles at both ends of a permeative, moth-eaten lytic lesion within the bone. The distinguishing detail from osteosarcoma is location as much as pattern: Ewing sarcoma favors the diaphysis of long bones and flat bones such as the ribs and pelvis, reflecting its origin from primitive neuroectodermal cells within the bone marrow cavity rather than from bone-forming cells at the growth plate, whereas osteosarcoma is a metaphyseal, growth-plate-adjacent disease.\n\nBecause Ewing sarcoma is a marrow tumor first, it frequently causes fever, weight loss, and an elevated white count alongside local pain and swelling, a systemic picture that leads it to be misdiagnosed as osteomyelitis more often than osteosarcoma is. It belongs to the family of \"small, round, blue cell\" tumors of childhood, distinguished from its look-alikes - neuroblastoma, lymphoma, rhabdomyosarcoma - by strong CD99 surface expression and, in most cases, a specific t(11;22) chromosomal translocation.\n\nAt the bedside, an onion-skin lesion in a child or adolescent triggers the same broad staging survey as osteosarcoma - MRI of the entire bone to define extent, CT of the chest, a bone scan, and bone marrow aspirate and biopsy from at least two sites, since marrow involvement changes both prognosis and treatment intensity - before multiagent chemotherapy, surgery, and often radiotherapy are sequenced together.\n\n![Ewing sarcoma: onion-skin periosteal reaction. Ewing sarcoma is one of the most common primary malignant bone tumors in children. Case courtesy of Leonardo Lustosa, Radiopaedia.org, rID: 231652 (CC BY-NC-SA 3.0).](/uploads/media/9dfaab6df91443a494c8d5f787a7f58c.png)", "parent_id": null, "variant": "long"}, {"id": "28e1fe5cd2504a758d4e215951af8deb", "slug": "slipped-capital-femoral-epiphysis-on-the-frog-leg-view", "title": "Slipped capital femoral epiphysis on the frog-leg view", "content": "The frog-leg lateral view is what makes a subtle slipped capital femoral epiphysis visible: with the hips abducted and externally rotated, a line drawn along the superior femoral neck (Klein's line) that would normally clip the lateral edge of the femoral epiphysis instead passes above it, because the epiphysis has slipped posteriorly and medially off the neck like a scoop of ice cream sliding backward off its cone. An anteroposterior view alone can miss exactly this degree of slip.\n\nThe film and full account are in [[87|Pediatric Orthopedics]].", "parent_id": null, "variant": "long"}, {"id": "e0d1021e84ee4bf79da0934b1c7c937a", "slug": "legg-calv-perthes-disease-the-fragmented-flattened-femoral-head", "title": "Legg-Calv\u00e9-Perthes disease: the fragmented, flattened femoral head", "content": "Legg-Calv\u00e9-Perthes disease moves through a radiographic sequence rather than one static appearance: early sclerosis and slight flattening of the femoral epiphysis, then fragmentation into irregular densities as dead bone is resorbed, and finally reossification that can leave the head permanently flattened and enlarged if it heals out of a spherical shape. The femoral head looks small, dense, and fragmented compared with its normal, round counterpart on the other side, which is the detail that usually prompts the film in the first place.\n\nThe film and full account are in [[87|Pediatric Orthopedics]].", "parent_id": null, "variant": "long"}, {"id": "a1f9ae78a84f4f6e9bb268e7f6b6303a", "slug": "developmental-dysplasia-of-the-hip-on-ultrasound", "title": "Developmental dysplasia of the hip on ultrasound", "content": "This 2-day-old girl's hips were scanned because breech presentation is a major risk factor for developmental dysplasia of the hip, and the study shown here is actually a normal one, Graf type Ia, used to illustrate the measurement the whole technique depends on: an alpha angle greater than 60 degrees and a beta angle less than 55 degrees, indicating a well-formed bony acetabular roof and a well-covered femoral head. The alpha angle measures the slope of the bony acetabular roof relative to the ilium and reflects how much of the roof has ossified; the beta angle measures the cartilaginous roof and reflects how well the femoral head is still covered by cartilage that has not yet ossified.\n\nAs dysplasia worsens, both angles fall: the bony roof is shallow and poorly formed, the cartilaginous labrum is pushed upward and everted rather than cupping the head, and in a frankly dislocated hip the femoral head sits lateral and superior to the acetabulum altogether, sometimes with a delayed or absent ossific nucleus. Ultrasound works because it directly images the mostly cartilaginous infant hip that plain radiographs cannot assess before the femoral head ossifies around 4 to 6 months of age; it is the screening test of choice for infants younger than about 4 months.\n\nAt the bedside, a normal Graf type Ia study like this one needs no further workup even in a breech infant, while a lower alpha angle or any instability on the dynamic Harcke maneuver moves the infant into bracing with a Pavlik harness rather than watchful waiting.\n\n![Developmental dysplasia of the hip on ultrasound. Developmental dysplasia of the hip is a complex disorder encompassing various hip problems, including neonatal instability, acetabular or femoral dysplasia, hip subluxation, and hip dislocation 1. Case courtesy of Cesar Matias Parra, Radiopaedia.org, rID: 240724 (CC BY-NC-SA 3.0).](/uploads/media/ab744b83120d484aacd0f6139927b1ef.png)", "parent_id": null, "variant": "long"}, {"id": "ed0f6f41049c445d8edd193ffeb62fad", "slug": "salter-harris-fractures-of-the-physis", "title": "Salter-Harris fractures of the physis", "content": "A Salter-Harris fracture crosses the growth plate itself, and the five-part classification (Salter-Harris I through V) exists because the exact path the fracture line takes through the physis, metaphysis, and epiphysis predicts both how it is treated and how likely it is to arrest growth: a straight separation along the plate carries the best prognosis, while any pattern that crushes the germinal layer of cartilage, as in a type V injury, carries the worst, often invisible on the initial film.\n\nThe film and full account are in [[406|Pediatric Fracture Eponyms]].", "parent_id": null, "variant": "long"}, {"id": "18fd0e40d08644c7bea0ed1e8948bed4", "slug": "toddler-s-fracture-the-spiral-tibial-line", "title": "Toddler's fracture: the spiral tibial line", "content": "A toddler's fracture is a low-energy, nondisplaced spiral or oblique fracture through the distal or mid tibial shaft, typically from nothing more dramatic than a fall while running or a leg twisted awkwardly underneath a jumping or tumbling toddler - exactly the mechanism here. On the initial film the fracture line can be subtle to the point of being nearly invisible: a faint, obliquely oriented lucent line through otherwise normal-looking cortex, easy to miss if the differential for a limping toddler does not include it.\n\nThe mechanism is torsional: a rotational force applied to a young child's tibia, whose cortex is more porous and pliable than an adult's, produces a spiral fracture line rather than the transverse break the same force might cause in stiffer, more mineralized bone. Because the initial film is so often equivocal, the fracture frequently declares itself only in retrospect, on a follow-up film obtained about ten days later that shows periosteal new bone forming along the fracture line as it heals - confirmation that a real injury was there all along.\n\nAt the bedside, a toddler who refuses to bear weight with a normal or equivocal tibial film, and no other findings to suggest a different diagnosis, is often simply immobilized in a walking cast or splint on clinical suspicion alone, with the follow-up film serving to confirm rather than to make the diagnosis before treatment starts.\n\n![Toddler's fracture: the spiral tibial line. This child (our son) jumped off his bed and landed awkwardly, twisting his leg and sustaining a spiral fracture of the tibia: a toddler fracture. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 9317 (CC BY-NC-SA 3.0).](/uploads/media/0896a1e3ca0345c29ad5123e7ff40e21.png)", "parent_id": null, "variant": "long"}, {"id": "9010ea147ea5405b9c05d2de43d0a6ba", "slug": "buckle-torus-fracture-of-the-distal-radius", "title": "Buckle (torus) fracture of the distal radius", "content": "A buckle, or torus, fracture of the distal radius shows no true fracture line at all: instead, the cortex bulges outward in a smooth, localized hump at the junction of the metaphysis and diaphysis, where the bone has failed under compression by buckling rather than breaking. No visible cortical break does not mean no fracture, and the diagnosis rests on recognizing that subtle bulge rather than looking for a lucent line.\n\nThe mechanism is a fall onto an outstretched hand, transmitting a compressive, axial load through bone that, in a young child, is still porous and springy enough to crumple locally rather than snap. This is what makes a buckle fracture inherently stable: because the cortex has folded rather than separated, there is no fracture surface free to displace further, and the injury heals predictably in three to four weeks with simple immobilization alone.\n\nThe distinction that matters at the bedside is from a greenstick fracture, which fails in tension on one cortex while the opposite cortex stays intact and can still angulate further if not immobilized correctly; a buckle fracture will not. Recognizing a buckle fracture for what it is prevents the overtreatment - unnecessarily rigid casting, orthopedic referral, repeated films - that a benign, self-limited injury does not need, and a removable splint plus a normal return to activity in a few weeks is generally all that is required.\n\n![Buckle (torus) fracture of the distal radius. This case Case courtesy of Aayush Agrawal, Radiopaedia.org, rID: 223829 (CC BY-NC-SA 3.0).](/uploads/media/3ebdf63e87d3402bbb2c507417c3a923.png)", "parent_id": null, "variant": "long"}, {"id": "7c337d2c47894f968c41f619411bd544", "slug": "greenstick-fracture", "title": "Greenstick fracture", "content": "A greenstick fracture, like a young, green branch that bends and splits along one side without snapping cleanly in two, fails on the tensile, convex side of the bone while the compressive, concave side stays in continuity, showing plastic deformation, a bend without a true fracture line, rather than a break. The fracture line seen on the film therefore only crosses part of the bone's diameter, stopping at the midline rather than running all the way across as a complete fracture would.\n\nThe mechanism is the same immature cortex responsible for buckle and toddler's fractures: pliable, porous pediatric bone bends substantially before it fails, and a bending force great enough to break an adult bone outright instead partially fails a child's bone on one side only. The clinical complication follows directly from the physics: the intact concave cortex, still under some residual bend, tends to spring the bone back toward its deformed position even after reduction, so an angulated greenstick fracture sometimes has to be deliberately completed - broken the rest of the way through - to let it be straightened and stay straight in a cast. Left unaddressed, this recoil can lock in an abnormal angulation as the fracture heals.\n\nAt the bedside, an acceptable degree of angulation for age and site can be treated with immobilization alone, but the threshold that would be tolerated in an adult complete fracture may not apply here.\n\n![Greenstick fracture. This fracture pattern is consistent with a &quot;greenstick fracture&quot;, as there is disruption of the cortex on the outer (convex) side with only bowing of the inner (concave) side of the fracture. It is typically seen in children, whose bones... Case courtesy of Sharifah Intan, Radiopaedia.org, rID: 31084 (CC BY-NC-SA 3.0).](/uploads/media/5df01e3b55f54157b73fb3a0d858ba96.png)", "parent_id": null, "variant": "long"}, {"id": "702653f07bb84577887ac77b784e39c2", "slug": "supracondylar-fracture-the-posterior-fat-pad", "title": "Supracondylar fracture: the posterior fat pad", "content": "On a lateral elbow film, a posterior fat pad is never visible in a normal joint - it sits tucked invisibly within the olecranon fossa - so whenever it becomes visible, lifted up and out as a triangular lucency behind the distal humerus, it means the joint is distended with fluid, and after trauma that fluid is blood. This is the finding in this 3-year-old, together with the sail sign: forward displacement of the anterior fat pad into a triangular shape resembling a ship's sail from the same joint effusion.\n\nNeither sign is the fracture itself; it is indirect evidence of one, and in about 70 percent of children with a positive fat pad sign but no fracture line visible on the film, a supracondylar fracture is present anyway, simply too subtle or nondisplaced to see directly. A second, complementary check is the anterior humeral line, drawn along the front of the humeral shaft on the lateral view: it should pass through the middle third of the capitellum, and if it instead clips the anterior third or misses the capitellum altogether, the distal fragment has been displaced posteriorly, as commonly happens with a supracondylar fracture from a fall onto an outstretched, hyperextended elbow.\n\nAt the bedside, a positive fat pad sign in a child with a history and examination consistent with elbow trauma is treated as an occult supracondylar fracture, immobilized and referred to orthopedics, even when no fracture line can be found, because waiting for one to become visible risks a displaced fracture healing in a worse position.\n\n![Supracondylar fracture: the posterior fat pad. On annotated image lateral view: Positive posterior fat pad sign as indicated by yellow line in the olecranon fossa. This is not seen on normal elbow radiographs. Case courtesy of Afra Alfalahi, Radiopaedia.org, rID: 54689 (CC BY-NC-SA 3.0).](/uploads/media/e7c26a52a4ab425f9efd6994621c7b43.png)", "parent_id": null, "variant": "long"}, {"id": "a4bf9719f7cb425aab608a133c460c75", "slug": "osteomyelitis-periosteal-reaction-and-lucency", "title": "Osteomyelitis: periosteal reaction and lucency", "content": "This 5-year-old's story captures why osteomyelitis is diagnosed by more than the plain film: despite fever, leg pain, and swelling with confirmed infection, his radiograph showed no periosteal reaction at all, and it was ultrasound that found subperiosteal fluid tracking along the proximal tibial diaphysis. Radiographic change genuinely lags behind the clinical picture in acute osteomyelitis; the earliest sign, deep soft-tissue swelling adjacent to the metaphysis, does not appear until about three days after symptoms begin, and the more familiar findings - a lytic, permeative area of bone destruction, often eventually rimmed by reactive sclerosis, with periosteal new bone laid down alongside it - can take a week or more to develop, by which point the child has often already been treated.\n\nThe mechanism is hematogenous seeding of the richly vascular, sluggish-flow metaphysis just beneath the growth plate, where bacteria, Staphylococcus aureus most often, lodge and multiply before the periosteum has had time to react; pus that forms under the periosteum, as on this child's ultrasound, lifts it away from the bone and is what eventually calcifies into the visible periosteal reaction. Laboratory markers, an elevated ESR and CRP, are more reliably abnormal early than either the white count, normal in up to half of children with osteomyelitis, or the film.\n\nAt the bedside, a normal or equivocal plain film in a child with a clinical picture concerning for osteomyelitis does not exclude the diagnosis, and MRI or ultrasound, as here, should follow rather than a repeat plain film taken a few days later.\n\n![Osteomyelitis: periosteal reaction and lucency. A child presented with fever along with right leg pain and edema. Laboratory study revealed infection. The radiograph was negative for a periosteal reaction. However, the ultrasound showed subperiosteal fluid involving the proximal tibial diaphyse... Case courtesy of Maulik S Patel, Radiopaedia.org, rID: 85571 (CC BY-NC-SA 3.0).](/uploads/media/04f343a0e517452b9afa18936bf51124.png)", "parent_id": null, "variant": "long"}, {"id": "7cac5678f9094aabbbf3e84552441254", "slug": "rickets-cupped-frayed-metaphyses", "title": "Rickets: cupped, frayed metaphyses", "content": "On a wrist film, rickets loosens the sharp, flat-to-convex border of the growth plate into a frayed, indistinct edge and reshapes it from convex to concave - cupping - most easily seen at the distal radius and ulna, alongside widening of the growth plate itself from an accumulation of unmineralized osteoid. The same changes appear wherever growth is fastest, including the knees and the costochondral junctions, where they produce the rachitic rosary felt along the chest wall.\n\nThe film and full account are in [[325|Rickets]].", "parent_id": null, "variant": "long"}, {"id": "d305efce1f7a4aa68afcbd46a831041c", "slug": "scoliosis-and-the-cobb-angle", "title": "Scoliosis and the Cobb angle", "content": "The Cobb angle is measured on a standing, full-spine radiograph by drawing lines along the endplates of the most tilted vertebra above and below the curve's apex, then measuring the angle between perpendiculars dropped from each; the number that results is what separates a curve worth watching from one that needs bracing or surgical referral, far more reliably than the same curve judged by eye.\n\nThe film and full account are in [[224|Scoliosis]].", "parent_id": null, "variant": "long"}, {"id": "8e0fc195d1d0487ab9c1d28ee0fe5174", "slug": "abuse-the-classic-metaphyseal-corner-lesion", "title": "Abuse: the classic metaphyseal (corner) lesion", "content": "The classic metaphyseal lesion is a fracture through the very edge of the growth plate's primary spongiosa, and depending on the angle it is photographed at, it can look like two different injuries that are actually the same one: seen face-on, only the corners of the metaphysis fracture visibly, leaving a small triangular chip of bone at the medial or lateral edge (the \"corner\" or \"chip\" fracture); seen obliquely, the whole disk-shaped fragment separates and resembles the curved handle of a bucket (the \"bucket-handle\" fracture).\n\nThe mechanism is shearing and torsional stress applied across the metaphysis - violent shaking, or forceful pulling and twisting of a limb - strong enough to fracture the weakest, most recently formed bone in the body without the bending or direct-impact forces that cause an ordinary long-bone fracture. This is exactly why the finding is so specific: a mobile, weight-bearing child generates bending forces from falls and stumbles, not the shearing forces needed to produce this pattern, so a metaphyseal corner fracture in a non-ambulant infant, as in this 1- to 2-year-old, is not explainable by routine handling or a minor accidental fall. Unlike a shaft fracture, healing here usually proceeds without the prominent callus or periosteal new bone that would otherwise date the injury on a follow-up film.\n\nAt the bedside, this single finding is sufficient grounds for a full skeletal survey and a child protection evaluation, regardless of what history is offered, because its specificity for abuse is higher than almost any other radiographic sign in pediatrics.\n\n![Abuse: the classic metaphyseal (corner) lesion. Appearances are consistent with a metaphyseal corner fracture. Case courtesy of Jan Frank Gerstenmaier, Radiopaedia.org, rID: 22589 (CC BY-NC-SA 3.0).](/uploads/media/b6c07c4551e04cd9995c2001a14dd3d1.png)", "parent_id": null, "variant": "long"}, {"id": "4194e8c8a3d347c7bffb4ca69aa7be0b", "slug": "abuse-posterior-rib-fractures", "title": "Abuse: posterior rib fractures", "content": "This 6-week-old's evaluation shows how posterior rib fractures are often actually found: not on the initial plain film, which can be unrevealing in the first week after injury, but on a bone scan or a skeletal survey repeated after ten to fourteen days, once healing callus has calcified enough to be visible as a bulbous or ring-shaped density at the rib head or the costovertebral junction. Posterior rib fractures carry among the highest specificity of any finding for abuse: in a child under three with no rib fracture explained by a clear accidental mechanism, the positive predictive value for non-accidental trauma approaches 95 to 100 percent.\n\nThe mechanism is anteroposterior compression of the chest severe enough to lever the rib head against the transverse process of the vertebra - characteristically, an infant gripped around the thorax with the thumbs pressed into the back during violent shaking - a fundamentally different stress than the two-finger or two-thumb technique used for infant cardiopulmonary resuscitation, shown not to cause rib fractures even when done forcefully.\n\nAt the bedside, any rib fracture in a nonambulatory infant without a clearly adequate accidental explanation warrants a full skeletal survey, or a bone scan when an early survey is falsely reassuring, as here, and involvement of a child protection team; a fracture found at a different stage of healing than the reported timeline of injury is itself an additional red flag.", "parent_id": null, "variant": "long"}, {"id": "f23171ce4cee47c1a5f9a8aa1d730780", "slug": "linear-skull-fracture", "title": "Linear skull fracture", "content": "A linear skull fracture is a simple, sharply marginated lucent line crossing the calvarium without displacement or branching, and it accounts for roughly three-quarters of all pediatric skull fractures, whether from an accidental fall or an abusive injury - its shape alone does not distinguish between the two. What does raise concern, in either setting, is a fracture that is complicated: one that crosses suture lines, that is bilateral or multiple, or that is diastatic (widened) or depressed, since these patterns carry a materially higher chance of an associated intracranial injury underneath, and multiple or bilateral fractures in particular are more often seen in abuse than in an accidental fall from a single point of impact.\n\nThe mechanism of the simple fracture is straightforward: a blunt impact exceeding the skull's elastic limit, propagating a crack along the path of least resistance through the bone, which in an infant's thinner, less mineralized calvarium takes comparatively less force than it would in an older child. Most linear fractures need nothing beyond observation, since there is no bone to reduce and no fragment to elevate.\n\nAt the bedside, the main action a linear fracture prompts is a follow-up film at two to three months to confirm normal healing and to exclude a growing skull fracture - a rare complication where a dural tear beneath the fracture line lets the leptomeninges herniate into the gap and pulse it progressively wider rather than let it heal.\n\n![Linear skull fracture. Fell out of a carry-cot it from a low height, bumped her head, and sustained a nondisplaced left parietal fracture. Case courtesy of Ya\u00efr Glick, Radiopaedia.org, rID: 94296 (CC BY-NC-SA 3.0).](/uploads/media/b38b815133484f14b4fc86f1f86ccc01.png)", "parent_id": null, "variant": "long"}, {"id": "55ff582f04ab4bb29d43d9841e90489e", "slug": "abusive-head-trauma-subdural-hematoma", "title": "Abusive head trauma: subdural hematoma", "content": "On CT, a subdural hematoma is a crescent-shaped collection that follows the curve of the brain's surface, distinct from the lens-shaped, biconvex epidural hematoma that bulges inward against the brain; a subdural can also cross suture lines freely, since it lies beneath the dura rather than being contained by the periosteal attachments that limit an epidural. In abusive head trauma specifically, a few features raise the suspicion of a shaking or shaking-with-impact mechanism well above that of an accidental fall: bilateral collections, blood of clearly different ages, an interhemispheric location along the falx, and involvement of the posterior fossa or parieto-occipital region.\n\nThe mechanism is rotational, angular acceleration-deceleration of an unsupported infant head - repeated forward and backward motion during shaking - that shears the bridging veins crossing the subdural space between the brain's surface and the dural sinuses, producing multiple small hemorrhages rather than the single large bleed typical of a focal impact. This same rotational injury tears retinal vessels, which is why subdural hemorrhage, retinal hemorrhage, and encephalopathy travel together often enough to be called a triad, though not every case shows all three.\n\nAt the bedside, any infant with an unexplained or inadequately explained subdural hemorrhage, particularly one that is bilateral, of mixed ages, or interhemispheric, needs a dilated fundoscopic examination for retinal hemorrhages, a skeletal survey to look for fractures at other stages of healing, and involvement of a child protection team before the family's explanation is accepted at face value.\n\n![Abusive head trauma: subdural hematoma. Gradually increasing head circumference in the first several months of life. There was no record of head trauma at birth or in infancy. Infant referred to a neurosurgeon for macrocephaly. Imaging revealed large subdural collections. Subdural tap ... Case courtesy of Joseph Scheller, Radiopaedia.org, rID: 83160 (CC BY-NC-SA 3.0).](/uploads/media/04f7a01c9d124838acf186e82d0b3e1a.png)", "parent_id": null, "variant": "long"}, {"id": "c8d3c2b0c11146338787a00beaa1ff2a", "slug": "hydrocephalus", "title": "Hydrocephalus", "content": "Hydrocephalus is read on imaging as ventricular enlargement out of proportion to the surrounding brain, and the pattern of which ventricles are enlarged points directly at the cause: dilation of both lateral ventricles and the third ventricle together (triventricular hydrocephalus) suggests an obstruction at or below the level of the aqueduct of Sylvius, while enlargement of all four ventricles points to a problem with CSF resorption further downstream, such as after a hemorrhage has scarred the arachnoid granulations.\n\nIn a premature infant, this is tracked with serial cranial ultrasound through the still-open anterior fontanelle rather than with CT or MRI, because posthemorrhagic ventricular dilation develops in 30 to 50 percent of infants with severe intraventricular hemorrhage, is initially asymptomatic, and needs to be caught by a screening study before it becomes clinically obvious. The mechanism is an imbalance between CSF production, which continues steadily from the choroid plexus, and its flow or resorption, which is obstructed either by a structural blockage in the ventricular system or by blood products and inflammation clogging the arachnoid villi where CSF is normally reabsorbed; the ventricles reshape from their normal slit-like contour into a distended balloon shape as pressure inside them rises.\n\nClinically, this shows up first as a head circumference crossing percentiles, split sutures, and a tense, full fontanelle in an infant whose sutures have not yet fused, and any of these findings on a growth chart is the trigger for the imaging that confirms the diagnosis, not the other way around.\n\n![Hydrocephalus. Hydrocephalus is a rare manifestation of Joubert syndrome (JBTS). Its recurrence among multiple affected family members in published reports suggests that this association is unlikely to be coincidental. Rather, it may represent a distinct phenoty... Case courtesy of Magdi Mahsoub, Radiopaedia.org, rID: 218284 (CC BY-NC-SA 3.0).](/uploads/media/b4df6cc4cd2e47b5b0c4133c966e06d2.png)", "parent_id": null, "variant": "long"}, {"id": "fa0c1c73b0d54c0b8273a5184aaac90c", "slug": "atlantoaxial-instability-in-down-syndrome", "title": "Atlantoaxial instability in Down syndrome", "content": "Atlantoaxial instability is assessed on a lateral cervical spine radiograph by measuring the atlantodens interval, the gap between the back of the anterior arch of C1 and the front of the odontoid process of C2; a value up to about 4.5 millimeters is accepted as normal in a child with Down syndrome, compared with 2.5 millimeters in the general population, reflecting the generalized ligamentous laxity, and specifically laxity of the transverse ligament that normally holds the odontoid snugly against the atlas, characteristic of the condition.\n\nThe mechanism is this laxity itself: without the transverse ligament holding it firmly in place, the atlas can shift forward relative to the axis with neck flexion, and severe or symptomatic instability can compress the spinal cord between the posterior arch of C1 and the odontoid, or stretch the vertebral arteries running through the same region, producing both upper and lower motor neuron findings or vertebrobasilar symptoms respectively. Most children with a widened atlantodens interval are entirely asymptomatic, and progression from hypermobility to true instability over time is uncommon, seen in only a small minority followed over several years.\n\nAt the bedside, a widened interval on a standard lateral view without neurologic signs or symptoms restricts the child from contact and collision sports and activities requiring extreme neck flexion or extension, while any neurologic finding, or a clearly abnormal interval, prompts flexion-extension MRI to look directly at spinal cord impingement and signal change, rather than relying on the plain film measurement alone.", "parent_id": null, "variant": "long"}, {"id": "40950bec808a4fe4bcdf468c5e408182", "slug": "signs-compared", "title": "Signs compared", "content": "| Sign | Modality | What it shows | The diagnosis | First action |\n|---|---|---|---|---|\n| Ground-glass haze with air bronchograms | Chest radiograph | Diffuse, low-volume, uniformly hazy lungs | Respiratory distress syndrome | Surfactant, CPAP or ventilation |\n| Fluid in the fissures | Chest radiograph | Hyperinflation with perihilar streaking and fissural fluid | Transient tachypnea of the newborn | Supportive oxygen, observe |\n| Coarse patchy opacities with hyperinflation | Chest radiograph | Asymmetric patchy opacities, hyperinflated lungs | Meconium aspiration syndrome | Respiratory support, watch for air leak |\n| Bowel loops in the chest | Chest radiograph | Air-filled bowel in a hemithorax, mediastinal shift | Congenital diaphragmatic hernia | Stabilize pulmonary hypertension before repair |\n| Deep sulcus / medial stripe | Chest radiograph, supine | Hyperlucent hemithorax, sharp sulcus | Neonatal pneumothorax | Needle or tube decompression |\n| Steeple sign | Neck radiograph, frontal | Symmetric subglottic narrowing | Croup | Clinical diagnosis; dexamethasone, nebulized epinephrine |\n| Thumb sign | Neck radiograph, lateral | Swollen, rounded epiglottis | Epiglottitis | Secure the airway in the operating room; do not lay the child flat |\n| Prevertebral soft tissue widening | Neck radiograph, lateral; CT | Soft tissue wider than half the vertebral body | Retropharyngeal abscess | Contrast CT, IV antibiotics, ENT |\n| Peribronchial cuffing with hyperinflation | Chest radiograph | Ring shadows around thickened airways, no focal consolidation | Bronchiolitis | Supportive care |\n| Round opacity, acute pleural angle | Chest radiograph | Spherical parenchymal opacity | Round pneumonia | Antibiotics; follow-up film for resolution |\n| Lobar opacity with meniscus | Chest radiograph, decubitus | Consolidation plus a fluid meniscus | Parapneumonic effusion / empyema | Antibiotics; drain if loculated |\n| Unilateral hyperinflation on expiration | Inspiratory/expiratory or decubitus films | Air trapped on the obstructed side | Inhaled foreign body | Rigid bronchoscopy |\n| En face round density in the esophagus | Chest radiograph, frontal | Coin lying broadside, coronal plane | Esophageal coin | Endoscopy if proximal, symptomatic, or not moved on repeat film |\n| Halo (double-rim) sign | Chest radiograph | Concentric rings from a beveled disc battery | Esophageal button battery | Emergent endoscopic removal |\n| Upper-lobe ring shadows and tram tracks | Chest radiograph; CT | Bronchiectasis worst in the upper lobes | Cystic fibrosis | Annual imaging; CT scores exacerbation risk |\n| Boot-shaped heart | Chest radiograph | Uptilted apex, concave pulmonary segment, reduced flow | Tetralogy of Fallot | Echocardiogram; manage hypercyanotic spells |\n| Egg on a string | Chest radiograph | Globular heart on a narrow mediastinum | Transposition of the great arteries | Prostaglandin E1; echocardiogram |\n| Snowman (figure-8) | Chest radiograph | Two-lobed superior mediastinal contour | Supracardiac TAPVR | Urgent echocardiogram for obstruction |\n| Figure 3 sign, rib notching | Chest radiograph | Double aortic contour; scalloped ribs | Coarctation of the aorta | Echocardiogram; surgical or catheter repair |\n| Cardiomegaly with pulmonary plethora | Chest radiograph | Enlarged chamber downstream of the defect, engorged vessels | Left-to-right shunt (VSD/ASD) | Echocardiogram to size the defect |\n| Pneumatosis intestinalis, portal venous gas | Abdominal radiograph | Bubbly bowel wall gas; branching hepatic lucencies | Necrotizing enterocolitis | Bowel rest, antibiotics; surgery if perforated |\n| Double bubble, no distal gas | Abdominal radiograph | Two dilated gas bubbles, nothing beyond | Duodenal atresia | Surgical repair |\n| Thickened, elongated pylorus | Ultrasound | Muscle wall \u22654 mm, channel \u226516 mm | Hypertrophic pyloric stenosis | Pyloromyotomy |\n| Target / doughnut sign | Ultrasound | Concentric bowel-within-bowel rings | Intussusception | Air or contrast enema reduction |\n| Corkscrew duodenum | Upper GI contrast | Spiraling, beaked contrast column | Malrotation with midgut volvulus | Emergent surgery |\n| Transition zone | Contrast enema | Abrupt caliber change, dilated to narrow | Hirschsprung disease | Suction rectal biopsy |\n| Soap-bubble right lower quadrant | Abdominal radiograph | Mottled lucency, no air-fluid levels | Meconium ileus | Hyperosmolar contrast enema |\n| Keyhole sign | Prenatal ultrasound; VCUG | Dilated posterior urethra and bladder | Posterior urethral valves | VCUG; endoscopic valve ablation |\n| Graded reflux of contrast | VCUG | Contrast washing up the ureter, grades I-V | Vesicoureteral reflux | Grade-based prophylaxis or surgery |\n| Echogenic pyramids | Renal ultrasound | Increased echogenicity sparing the cortex | Medullary nephrocalcinosis | Metabolic workup (electrolytes, urine calcium) |\n| Intrarenal mass displacing vessels | Ultrasound, CT | Bulky mass distorting the kidney | Wilms tumor | Contrast CT staging; surgery |\n| Calcified suprarenal mass encasing vessels | CT | Calcified mass lifting vessels off the spine | Neuroblastoma | Urine catecholamines, MIBG scan |\n| Sunburst, Codman triangle | Radiograph, MRI | Spiculated periosteal reaction, lifted periosteal wedge | Osteosarcoma | MRI, chest CT staging, biopsy at a treating center |\n| Onion-skin periosteal reaction | Radiograph, MRI | Multilayered periosteal shells | Ewing sarcoma | MRI, chest CT, bone scan, marrow biopsy |\n| Klein's line miss | Frog-leg lateral radiograph | Line along the femoral neck passes above the epiphysis | Slipped capital femoral epiphysis | Non-weight-bearing; surgical pinning |\n| Fragmented, flattened femoral head | Radiograph | Sclerotic, fragmented, then reossifying epiphysis | Legg-Calve-Perthes disease | Containment management |\n| Low alpha angle, shallow roof | Hip ultrasound | Alpha angle <60\u00b0, poor femoral head coverage | Developmental dysplasia of the hip | Pavlik harness |\n| Fracture through the physis | Radiograph | Salter-Harris I-V pattern | Physeal fracture | Classification-guided reduction |\n| Subtle spiral lucent line | Tibial radiograph | Faint oblique fracture line, or none until healing | Toddler's fracture | Immobilize on clinical suspicion |\n| Cortical bulge, no fracture line | Radiograph | Smooth compressive bulge at the metaphysis | Buckle (torus) fracture | Removable splint |\n| Unicortical break | Radiograph | Fracture on the convex side, intact concave side | Greenstick fracture | Reduce, sometimes complete the fracture |\n| Posterior fat pad, sail sign | Elbow radiograph, lateral | Lifted posterior fat pad, displaced anterior fat pad | Supracondylar fracture (occult) | Immobilize and refer even without a fracture line |\n| Soft tissue swelling, later lucency | Radiograph; ultrasound, MRI | Radiographic change lagging the clinical picture | Osteomyelitis | MRI or ultrasound; do not wait on a repeat film |\n| Cupped, frayed metaphyses | Wrist radiograph | Widened, frayed, concave metaphyseal border | Rickets | Vitamin D/calcium/phosphate workup |\n| Cobb angle | Standing spine radiograph | Angle between the most tilted endplates | Scoliosis | Angle-based observation, bracing, or surgery |\n| Metaphyseal corner (bucket-handle) lesion | Radiograph | Chip or bucket-handle fragment at the metaphysis | Abusive fracture | Skeletal survey, child protection team |\n| Posterior rib fractures | Radiograph; bone scan | Callus at the rib head or costovertebral junction | Abusive injury | Skeletal survey, child protection team |\n| Linear lucent line | Skull radiograph, CT | Sharp, undisplaced fracture line | Linear skull fracture | Observation; follow-up film if diastatic |\n| Crescent-shaped collection | Head CT | Concave collection crossing suture lines | Subdural hematoma (consider abuse) | Fundoscopy, skeletal survey, child protection team |\n| Ventricular enlargement | Cranial ultrasound, CT, MRI | Dilated ventricles, pattern depends on cause | Hydrocephalus | Serial imaging; neurosurgical referral |\n| Widened atlantodens interval | Lateral cervical spine radiograph | Gap between C1 arch and odontoid >4.5 mm | Atlantoaxial instability | Restrict contact sports; flexion-extension MRI if symptomatic |", "parent_id": null, "variant": "long"}, {"id": "8f5eff4e7b7243399a3e3ad3c5259f11", "slug": "in-short", "title": "In short", "content": "- Check technique first: a rotated or supine AP film can mimic cardiomegaly or unilateral hyperinflation on its own.\n- The infant thymus has a smooth \"sail sign\" border and can be mistaken for cardiomegaly or a mediastinal mass; it shrinks with age and is absent in DiGeorge syndrome.\n- Ground-glass haze with low lung volumes and air bronchograms is respiratory distress syndrome; hyperinflation with fluid in the fissures is transient tachypnea of the newborn.\n- Meconium aspiration shows asymmetric patchy opacities with hyperinflation and a 10 to 15 percent risk of pneumothorax or pneumomediastinum.\n- The steeple sign of croup and the thumb sign of epiglottitis are both overrated at the bedside: croup and epiglottitis are diagnosed and managed clinically, not by film.\n- An inhaled foreign body causing a ball-valve obstruction shows unilateral air trapping on expiratory or decubitus films, not a visible object; rigid bronchoscopy is diagnostic and therapeutic.\n- A coin lies broadside (en face) in the coronal esophagus and edge-on in the sagittal airway; a button battery shows a halo/double-rim sign and is removed emergently regardless of symptoms.\n- Boot-shaped heart (tetralogy of Fallot) has reduced pulmonary vascularity, unlike egg on a string (transposition) or the snowman sign (supracardiac TAPVR), which usually have normal or increased flow; rib notching and the figure 3 sign of coarctation instead take years of collateral flow to develop.\n- Pneumatosis intestinalis and portal venous gas are pathognomonic for necrotizing enterocolitis; free air (the football sign) is a surgical emergency.\n- Double bubble with no distal gas is duodenal atresia; the corkscrew sign on upper GI contrast is midgut volvulus and is a surgical emergency regardless of how well the child looks.\n- Target sign on ultrasound (intussusception) and thickened, elongated pylorus on ultrasound (pyloric stenosis, wall \u22654 mm, channel \u226516 mm) have both replaced contrast studies as first-line imaging.\n- The keyhole sign of posterior urethral valves is prenatal (dilated posterior urethra and bladder); after birth, VCUG shows an abrupt caliber change at the valve.\n- A solid renal mass that is intrarenal and displaces vessels is Wilms tumor; a calcified suprarenal mass that encases and lifts vessels off the spine is neuroblastoma.\n- Sunburst periosteal reaction with a Codman triangle is osteosarcoma (metaphyseal); onion-skin periosteal reaction is Ewing sarcoma (diaphyseal, marrow-based, and can mimic osteomyelitis).\n- A posterior fat pad on a lateral elbow film is never normal and implies an occult supracondylar fracture in about 70 percent of cases even without a visible fracture line.\n- Radiographic change in osteomyelitis lags the clinical picture by days; a normal plain film does not exclude it, and MRI or ultrasound should follow.\n- A metaphyseal corner (bucket-handle) fracture or a posterior rib fracture in a non-ambulant infant is abuse until proven otherwise and warrants a skeletal survey and child protection evaluation.\n- A subdural hematoma that is bilateral, of mixed ages, or interhemispheric, especially with retinal hemorrhage, points to abusive head trauma from rotational shear on the bridging veins.", "parent_id": null, "variant": "short"}, {"id": "67e03e851e1b4107b2a6cf5e63e8626c", "slug": "films-that-change-the-next-hour", "title": "Films that change the next hour", "content": "**Epiglottitis.** A thumb sign, or even a strong clinical suspicion alone, means the film is finished mattering: the child goes straight to a controlled airway - laryngoscopy in the operating room - without being laid flat, agitated, or sent through radiology unaccompanied.\n\n**Tension pneumothorax.** A hyperlucent hemithorax with a deep sulcus or mediastinal shift on a deteriorating, ventilated newborn or trauma patient is not a film to wait on; needle decompression or chest tube placement happens on the clinical picture, and confirmation follows rather than precedes it.\n\n**Necrotizing enterocolitis with free air.** Pneumatosis and portal venous gas buy time for medical management - bowel rest, decompression, antibiotics - but a football sign or free air on a cross-table lateral changes the plan instantly to the operating room.\n\n**Malrotation with midgut volvulus.** A corkscrew duodenum, or even just an abnormally positioned duodenojejunal junction in a bilious-vomiting infant, is treated as a twisted, ischemic bowel until surgery proves otherwise; every hour of delay is bowel that may not survive.\n\n**Button battery.** A halo sign in the esophagus is removed emergently regardless of the child's symptoms, on the clock of a two-hour window before liquefactive necrosis can perforate the esophageal wall; honey or sucralfate may be given while removal is arranged, never in place of it.\n\n**Abusive fractures.** A metaphyseal corner lesion or a posterior rib fracture in a non-ambulant infant, found on any film for any reason, triggers a full skeletal survey and a child protection evaluation the same day, independent of the history offered for the injury that prompted the original film.", "parent_id": null, "variant": "clinical"}], "content": null}}, "assets": {"4305": {"caption": "Neonatal respiratory distress syndrome: ground-glass lungs and air bronchograms. Findings are consistent with hyaline membrane disease in a premature neonate complicated by pneumothorax from barotrauma. The lungs are well expanded as the patient is intubated. In a non-intubated patient with HMD the ", "alt_text": "Neonatal respiratory distress syndrome: ground-glass lungs and air bronchograms. Findings are consistent with hyaline membrane disease in a premature neonate complicated by pneumothorax from barotrauma. The lungs are well expanded as the patient is intubated. In a non-intubated patient with HMD the ", "title": "Hyaline membrane disease", "path": "media/7ab0388d195d48e89234af93e2685cf0.png"}, "4306": {"caption": "Transient tachypnea of the newborn: fluid in the fissures. In a term baby, the most common causes of increased work of breathing that can be seen on a chest x-ray are: Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 94073 (CC BY-NC-SA 3.0).", "alt_text": "Transient tachypnea of the newborn: fluid in the fissures. In a term baby, the most common causes of increased work of breathing that can be seen on a chest x-ray are: Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 94073 (CC BY-NC-SA 3.0).", "title": "Transient tachypnea of the newborn", "path": "media/00e5ab398d894aed96a8e0fd148d1357.png"}, "4307": {"caption": "Meconium aspiration: coarse patchy opacities with hyperinflation. This a full-term baby boy during his first day of life presenting with signs and symptoms of respiratory distress. The asymmetric patchy lung opacities with increased lung volumes are classic findings of meconium aspiration, on chest ", "alt_text": "Meconium aspiration: coarse patchy opacities with hyperinflation. This a full-term baby boy during his first day of life presenting with signs and symptoms of respiratory distress. The asymmetric patchy lung opacities with increased lung volumes are classic findings of meconium aspiration, on chest ", "title": "Meconium aspiration", "path": "media/6ffc0ea5fa3646d5a217f29b89b84468.png"}, "4308": {"caption": "Congenital diaphragmatic hernia: bowel in the chest. This is a congenital diaphragmatic hernia (Bochdalek type). They underwent timely neonatal repair with complication of bilateral chylothoraxes. At follow-up, the lungs have expanded and grown well. Case courtesy of Jeremy Jones, Radiopaedia.org, r", "alt_text": "Congenital diaphragmatic hernia: bowel in the chest. This is a congenital diaphragmatic hernia (Bochdalek type). They underwent timely neonatal repair with complication of bilateral chylothoraxes. At follow-up, the lungs have expanded and grown well. Case courtesy of Jeremy Jones, Radiopaedia.org, r", "title": "Congenital diaphragmatic hernia (with follow up)", "path": "media/5134bb4630e940edbef91359593e0fb2.png"}, "4309": {"caption": "Bronchiolitis: hyperinflation and peribronchial thickening. Bronchiolitis refers to small airway inflammation. In young children, the most common cause is viral infection with respiratory syncytial virus (RSV) the most common agent. Case courtesy of Sally Ayesa, Radiopaedia.org, rID: 172882 (CC BY-N", "alt_text": "Bronchiolitis: hyperinflation and peribronchial thickening. Bronchiolitis refers to small airway inflammation. In young children, the most common cause is viral infection with respiratory syncytial virus (RSV) the most common agent. Case courtesy of Sally Ayesa, Radiopaedia.org, rID: 172882 (CC BY-N", "title": "Bronchiolitis", "path": "media/b9e018791ca541ea941dddb06d90d1f5.png"}, "4310": {"caption": "Round pneumonia. A good example of round pneumonia, which typically occur in the pediatric population. Case courtesy of Ian Bickle, Radiopaedia.org, rID: 190005 (CC BY-NC-SA 3.0).", "alt_text": "Round pneumonia. A good example of round pneumonia, which typically occur in the pediatric population. Case courtesy of Ian Bickle, Radiopaedia.org, rID: 190005 (CC BY-NC-SA 3.0).", "title": "Pediatric round pneumonia (mimicking shoulder pain)", "path": "media/296a13db931249b191e4a48d211d202a.png"}, "4311": {"caption": "Swallowed coin in the esophagus: en face on the frontal film. Swallowed coin in the esophagus in a 3-year-old child. Note the transverse orientation, a foreign body in the trachea is more likely to have an AP orientation and will probably also result in symptoms +/- pulmonary changes (e.g. atelectas", "alt_text": "Swallowed coin in the esophagus: en face on the frontal film. Swallowed coin in the esophagus in a 3-year-old child. Note the transverse orientation, a foreign body in the trachea is more likely to have an AP orientation and will probably also result in symptoms +/- pulmonary changes (e.g. atelectas", "title": "Ingested foreign body - coin in esophagus", "path": "media/8dc290c4a4324329b482e211e7db3422.png"}, "4312": {"caption": "Button battery in the esophagus: the halo sign. A radiograph of her chest was done approximately one hour after ingestion showing a round radiopaque 22 mm foreign body in the proximal esophagus. The object had a halo sign /double rim sign which indicated the manifestation of two circular pieces... C", "alt_text": "Button battery in the esophagus: the halo sign. A radiograph of her chest was done approximately one hour after ingestion showing a round radiopaque 22 mm foreign body in the proximal esophagus. The object had a halo sign /double rim sign which indicated the manifestation of two circular pieces... C", "title": "Button battery ingestion", "path": "media/284386d7eace4bdabc119bde4278dd5e.png"}, "4313": {"caption": "Cystic fibrosis: upper-lobe bronchiectasis. The classic chest radiographic findings of cystic fibrosis include: Case courtesy of Hazem M. Almasarei, Radiopaedia.org, rID: 161586 (CC BY-NC-SA 3.0).", "alt_text": "Cystic fibrosis: upper-lobe bronchiectasis. The classic chest radiographic findings of cystic fibrosis include: Case courtesy of Hazem M. Almasarei, Radiopaedia.org, rID: 161586 (CC BY-NC-SA 3.0).", "title": "Cystic fibrosis", "path": "media/29222ebb939e4c96aaa6ab5341011ade.png"}, "4314": {"caption": "Transposition of the great arteries: egg on a string. This case was donated to Radiopaedia.org by Radswiki.net Case courtesy of The Radswiki, Radiopaedia.org, rID: 12036 (CC BY-NC-SA 3.0).", "alt_text": "Transposition of the great arteries: egg on a string. This case was donated to Radiopaedia.org by Radswiki.net Case courtesy of The Radswiki, Radiopaedia.org, rID: 12036 (CC BY-NC-SA 3.0).", "title": "Transposition of great arteries - egg on a string", "path": "media/4ee3d21c224c489f809f2bf441e0783b.png"}, "4315": {"caption": "Coarctation of the aorta: rib notching and the figure 3 sign. Aortic coarctation can be difficult to identify on chest x-ray and routine review of aortic outline, as well the inferior rib notching, which is known as Roesler sign when coarctation is the cause, which is necessary if one is to make the", "alt_text": "Coarctation of the aorta: rib notching and the figure 3 sign. Aortic coarctation can be difficult to identify on chest x-ray and routine review of aortic outline, as well the inferior rib notching, which is known as Roesler sign when coarctation is the cause, which is necessary if one is to make the", "title": "Coarctation of the aorta", "path": "media/879e39526b69402c8d967f3cffd8482c.png"}, "4316": {"caption": "Necrotizing enterocolitis: pneumatosis intestinalis and portal venous gas. X-rays demonstrate necrotizing enterocolitis with perforation, and resulting pneumoperitoneum (seen as the football sign on AP view with visible falciform ligament, and confirmed on lateral film). This child was transferred t", "alt_text": "Necrotizing enterocolitis: pneumatosis intestinalis and portal venous gas. X-rays demonstrate necrotizing enterocolitis with perforation, and resulting pneumoperitoneum (seen as the football sign on AP view with visible falciform ligament, and confirmed on lateral film). This child was transferred t", "title": "Neonatal pneumoperitoneum secondary to perforated necrotizing enterocolitis", "path": "media/43eecfd6a09143a7b9b2d6647a77b38c.png"}, "4317": {"caption": "Duodenal atresia: the double bubble. Duodenal atresia in a neonate. Confirmed at surgery. Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 6352 (CC BY-NC-SA 3.0).", "alt_text": "Duodenal atresia: the double bubble. Duodenal atresia in a neonate. Confirmed at surgery. Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 6352 (CC BY-NC-SA 3.0).", "title": "Duodenal atresia (congenital)", "path": "media/d6c4a95362ab4d8d833775ecc2226743.png"}, "4318": {"caption": "Malrotation with midgut volvulus: the corkscrew duodenum. CT features of intestinal malrotation complicated by midgut volvulus. Case courtesy of Ammar Haouimi, Radiopaedia.org, rID: 211348 (CC BY-NC-SA 3.0).", "alt_text": "Malrotation with midgut volvulus: the corkscrew duodenum. CT features of intestinal malrotation complicated by midgut volvulus. Case courtesy of Ammar Haouimi, Radiopaedia.org, rID: 211348 (CC BY-NC-SA 3.0).", "title": "Midgut volvulus", "path": "media/aaf02da1e6a0414ca4be5ad2243b4dc0.png"}, "4319": {"caption": "Hirschsprung disease: the transition zone on contrast enema. Features of Hirschsprung disease with a transition zone in the distal colon. Case courtesy of Tee Yu Jin, Radiopaedia.org, rID: 71552 (CC BY-NC-SA 3.0).", "alt_text": "Hirschsprung disease: the transition zone on contrast enema. Features of Hirschsprung disease with a transition zone in the distal colon. Case courtesy of Tee Yu Jin, Radiopaedia.org, rID: 71552 (CC BY-NC-SA 3.0).", "title": "Hirschsprung disease", "path": "media/25e77c1e976a497a9f73b782e3ee2665.png"}, "4320": {"caption": "Meconium ileus: soap-bubble right lower quadrant. Typical imaging findings in meconium ileus. Associated with cystic fibrosis. Case courtesy of Juan Carlos Santizo Castillo, Radiopaedia.org, rID: 97076 (CC BY-NC-SA 3.0).", "alt_text": "Meconium ileus: soap-bubble right lower quadrant. Typical imaging findings in meconium ileus. Associated with cystic fibrosis. Case courtesy of Juan Carlos Santizo Castillo, Radiopaedia.org, rID: 97076 (CC BY-NC-SA 3.0).", "title": "Meconium ileus", "path": "media/eafadc2705c44e49a0a0020888c853b5.png"}, "4321": {"caption": "Posterior urethral valves: the keyhole sign on VCUG. Posterior urethral valve is a common cause of obstructive uropathy in infants. Severe cases are usually diagnosed with antenatal ultrasonography. Voiding cystourethrogram (VCUG) is the modality of choice for the diagnosis of posterior urethral val", "alt_text": "Posterior urethral valves: the keyhole sign on VCUG. Posterior urethral valve is a common cause of obstructive uropathy in infants. Severe cases are usually diagnosed with antenatal ultrasonography. Voiding cystourethrogram (VCUG) is the modality of choice for the diagnosis of posterior urethral val", "title": "Posterior urethral valve with grade V vesico-ureteric reflux", "path": "media/1fb1abc195954eddbec6f30433dcc915.png"}, "4322": {"caption": "Vesicoureteral reflux on VCUG. This case demonstrates bilateral vesicoureteric reflux - right grade III and left grade II, with bladder trabeculation. Case courtesy of Varun Babu, Radiopaedia.org, rID: 19476 (CC BY-NC-SA 3.0).", "alt_text": "Vesicoureteral reflux on VCUG. This case demonstrates bilateral vesicoureteric reflux - right grade III and left grade II, with bladder trabeculation. Case courtesy of Varun Babu, Radiopaedia.org, rID: 19476 (CC BY-NC-SA 3.0).", "title": "Vesicoureteric reflux", "path": "media/2a21a57d71d84af295f340a748baa3d8.png"}, "4323": {"caption": "Wilms tumor: a renal mass displacing the kidney. This case demonstrates the typical appearance of a large right-sided Wilms tumor. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 8084 (CC BY-NC-SA 3.0).", "alt_text": "Wilms tumor: a renal mass displacing the kidney. This case demonstrates the typical appearance of a large right-sided Wilms tumor. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 8084 (CC BY-NC-SA 3.0).", "title": "Wilms tumor", "path": "media/22f9ebc6bb4a410ca1c83e6cc7fc1da3.png"}, "4324": {"caption": "Neuroblastoma: a calcified suprarenal mass. Neuroblastomas (NBL) and nephroblastomas/Wilm's tumors (WT) represent two of the most commonly detected solid tumors in childhood 1. These are the two crucial differential diagnoses to be considered with any renal mass identified in a child of thi... Case ", "alt_text": "Neuroblastoma: a calcified suprarenal mass. Neuroblastomas (NBL) and nephroblastomas/Wilm's tumors (WT) represent two of the most commonly detected solid tumors in childhood 1. These are the two crucial differential diagnoses to be considered with any renal mass identified in a child of thi... Case ", "title": "Neuroblastoma", "path": "media/72524c1ab75044cf8399d315d12e484f.png"}, "4325": {"caption": "Toddler's fracture: the spiral tibial line. This child (our son) jumped off his bed and landed awkwardly, twisting his leg and sustaining a spiral fracture of the tibia: a toddler fracture. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 9317 (CC BY-NC-SA 3.0).", "alt_text": "Toddler's fracture: the spiral tibial line. This child (our son) jumped off his bed and landed awkwardly, twisting his leg and sustaining a spiral fracture of the tibia: a toddler fracture. Case courtesy of Jeremy Jones, Radiopaedia.org, rID: 9317 (CC BY-NC-SA 3.0).", "title": "Toddler fracture", "path": "media/0896a1e3ca0345c29ad5123e7ff40e21.png"}, "4326": {"caption": "Buckle (torus) fracture of the distal radius. This case Case courtesy of Aayush Agrawal, Radiopaedia.org, rID: 223829 (CC BY-NC-SA 3.0).", "alt_text": "Buckle (torus) fracture of the distal radius. This case Case courtesy of Aayush Agrawal, Radiopaedia.org, rID: 223829 (CC BY-NC-SA 3.0).", "title": "Torus fracture - distal radius", "path": "media/3ebdf63e87d3402bbb2c507417c3a923.png"}, "4327": {"caption": "Greenstick fracture. This fracture pattern is consistent with a &quot;greenstick fracture&quot;, as there is disruption of the cortex on the outer (convex) side with only bowing of the inner (concave) side of the fracture. It is typically seen in children, whose bones... Case courtesy of Sharifah In", "alt_text": "Greenstick fracture. This fracture pattern is consistent with a &quot;greenstick fracture&quot;, as there is disruption of the cortex on the outer (convex) side with only bowing of the inner (concave) side of the fracture. It is typically seen in children, whose bones... Case courtesy of Sharifah In", "title": "Greenstick fracture", "path": "media/5df01e3b55f54157b73fb3a0d858ba96.png"}, "4328": {"caption": "Supracondylar fracture: the posterior fat pad. On annotated image lateral view: Positive posterior fat pad sign as indicated by yellow line in the olecranon fossa. This is not seen on normal elbow radiographs. Case courtesy of Afra Alfalahi, Radiopaedia.org, rID: 54689 (CC BY-NC-SA 3.0).", "alt_text": "Supracondylar fracture: the posterior fat pad. On annotated image lateral view: Positive posterior fat pad sign as indicated by yellow line in the olecranon fossa. This is not seen on normal elbow radiographs. Case courtesy of Afra Alfalahi, Radiopaedia.org, rID: 54689 (CC BY-NC-SA 3.0).", "title": "Supracondylar fracture with posterior fat pad and sail signs", "path": "media/e7c26a52a4ab425f9efd6994621c7b43.png"}, "4329": {"caption": "Osteomyelitis: periosteal reaction and lucency. A child presented with fever along with right leg pain and edema. Laboratory study revealed infection. The radiograph was negative for a periosteal reaction. However, the ultrasound showed subperiosteal fluid involving the proximal tibial diaphyse... C", "alt_text": "Osteomyelitis: periosteal reaction and lucency. A child presented with fever along with right leg pain and edema. Laboratory study revealed infection. The radiograph was negative for a periosteal reaction. However, the ultrasound showed subperiosteal fluid involving the proximal tibial diaphyse... C", "title": "Acute osteomyelitis of tibia", "path": "media/04f343a0e517452b9afa18936bf51124.png"}, "4330": {"caption": "Ewing sarcoma: onion-skin periosteal reaction. Ewing sarcoma is one of the most common primary malignant bone tumors in children. Case courtesy of Leonardo Lustosa, Radiopaedia.org, rID: 231652 (CC BY-NC-SA 3.0).", "alt_text": "Ewing sarcoma: onion-skin periosteal reaction. Ewing sarcoma is one of the most common primary malignant bone tumors in children. Case courtesy of Leonardo Lustosa, Radiopaedia.org, rID: 231652 (CC BY-NC-SA 3.0).", "title": "Ewing sarcoma", "path": "media/9dfaab6df91443a494c8d5f787a7f58c.png"}, "4331": {"caption": "Abuse: the classic metaphyseal (corner) lesion. Appearances are consistent with a metaphyseal corner fracture. Case courtesy of Jan Frank Gerstenmaier, Radiopaedia.org, rID: 22589 (CC BY-NC-SA 3.0).", "alt_text": "Abuse: the classic metaphyseal (corner) lesion. Appearances are consistent with a metaphyseal corner fracture. Case courtesy of Jan Frank Gerstenmaier, Radiopaedia.org, rID: 22589 (CC BY-NC-SA 3.0).", "title": "Metaphyseal corner fracture (child abuse)", "path": "media/b6c07c4551e04cd9995c2001a14dd3d1.png"}, "4332": {"caption": "Linear skull fracture. Fell out of a carry-cot it from a low height, bumped her head, and sustained a nondisplaced left parietal fracture. Case courtesy of Ya\u00efr Glick, Radiopaedia.org, rID: 94296 (CC BY-NC-SA 3.0).", "alt_text": "Linear skull fracture. Fell out of a carry-cot it from a low height, bumped her head, and sustained a nondisplaced left parietal fracture. Case courtesy of Ya\u00efr Glick, Radiopaedia.org, rID: 94296 (CC BY-NC-SA 3.0).", "title": "Skull fracture - infant", "path": "media/b38b815133484f14b4fc86f1f86ccc01.png"}, "4333": {"caption": "Abusive head trauma: subdural hematoma. Gradually increasing head circumference in the first several months of life. There was no record of head trauma at birth or in infancy. Infant referred to a neurosurgeon for macrocephaly. Imaging revealed large subdural collections. Subdural tap ... Case court", "alt_text": "Abusive head trauma: subdural hematoma. Gradually increasing head circumference in the first several months of life. There was no record of head trauma at birth or in infancy. Infant referred to a neurosurgeon for macrocephaly. Imaging revealed large subdural collections. Subdural tap ... Case court", "title": "Subdural hygroma with membranes", "path": "media/04f7a01c9d124838acf186e82d0b3e1a.png"}, "4334": {"caption": "Retropharyngeal abscess: prevertebral soft tissue widening. Signs of prevertebral infection, such as edema, cellulitis, or abscess formation, should be suspected in children presenting with neck pain or headache, especially on plain radiographs, which are the first-line imaging in these patients, an", "alt_text": "Retropharyngeal abscess: prevertebral soft tissue widening. Signs of prevertebral infection, such as edema, cellulitis, or abscess formation, should be suspected in children presenting with neck pain or headache, especially on plain radiographs, which are the first-line imaging in these patients, an", "title": "Retropharyngeal abscess", "path": "media/61343ea842184ee0aed723eb13d3cf14.png"}, "4335": {"caption": "Developmental dysplasia of the hip on ultrasound. Developmental dysplasia of the hip is a complex disorder encompassing various hip problems, including neonatal instability, acetabular or femoral dysplasia, hip subluxation, and hip dislocation 1. Case courtesy of Cesar Matias Parra, Radiopaedia.org,", "alt_text": "Developmental dysplasia of the hip on ultrasound. Developmental dysplasia of the hip is a complex disorder encompassing various hip problems, including neonatal instability, acetabular or femoral dysplasia, hip subluxation, and hip dislocation 1. Case courtesy of Cesar Matias Parra, Radiopaedia.org,", "title": "Developmental dysplasia of the hip", "path": "media/ab744b83120d484aacd0f6139927b1ef.png"}, "4336": {"caption": "Hydrocephalus. Hydrocephalus is a rare manifestation of Joubert syndrome (JBTS). Its recurrence among multiple affected family members in published reports suggests that this association is unlikely to be coincidental. Rather, it may represent a distinct phenoty... Case courtesy of Magdi Mahsoub, Ra", "alt_text": "Hydrocephalus. Hydrocephalus is a rare manifestation of Joubert syndrome (JBTS). Its recurrence among multiple affected family members in published reports suggests that this association is unlikely to be coincidental. Rather, it may represent a distinct phenoty... Case courtesy of Magdi Mahsoub, Ra", "title": "Hydrocephalus associated with a molar tooth sign", "path": "media/b4df6cc4cd2e47b5b0c4133c966e06d2.png"}, "4337": {"caption": "Medullary nephrocalcinosis. An infant suspected to have Liddle's syndrome, screened for nephrocalcinosis. Case courtesy of Hani M. Al Salam, Radiopaedia.org, rID: 9899 (CC BY-NC-SA 3.0).", "alt_text": "Medullary nephrocalcinosis. An infant suspected to have Liddle's syndrome, screened for nephrocalcinosis. Case courtesy of Hani M. Al Salam, Radiopaedia.org, rID: 9899 (CC BY-NC-SA 3.0).", "title": "Medullary nephrocalcinosis", "path": "media/1db64e2194ca47f4b993722146182ee2.png"}, "4282": {"caption": "Tinea pedis: Moccasin tinea pedis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Tinea pedis: Moccasin tinea pedis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Moccasin tinea pedis", "path": "media/ecd3011f82fb4f57ae775ffcd9b6573d.jpg"}, "4283": {"caption": "Periorificial dermatitis: Perioral dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Periorificial dermatitis: Perioral dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Perioral dermatitis", "path": "media/400920a84cbf47ea9bd4747f8e9bfb36.jpg"}, "4284": {"caption": "Gianotti-Crosti syndrome: Gianotti-Crosti syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Gianotti-Crosti syndrome: Gianotti-Crosti syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Gianotti-Crosti syndrome", "path": "media/d6c800ce92c940a0a6fb0cfc79e962af.jpg"}, "4285": {"caption": "Pityriasis alba: Pityriasis alba. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Pityriasis alba: Pityriasis alba. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Pityriasis alba", "path": "media/8b090c14fec24ae58107e7e2087f0704.jpg"}, "4297": {"caption": "Caf\u00e9-au-lait macules: Caf\u00e9-au-lait macule. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Caf\u00e9-au-lait macules: Caf\u00e9-au-lait macule. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Caf\u00e9-au-lait macule", "path": "media/8417c4b8f6de4b28a53a84d3c2b2e5a5.jpg"}, "4298": {"caption": "Nevus sebaceus: Naevus sebaceous. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Nevus sebaceus: Naevus sebaceous. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Naevus sebaceous", "path": "media/d9fcd8efe6a94ed09ab52928f7b89797.jpg"}, "4299": {"caption": "Cellulitis: Cellulitis of the left leg. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Cellulitis: Cellulitis of the left leg. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Cellulitis of the left leg", "path": "media/6c8b5ceb542f448dbf014a109efd83e2.jpg"}, "4300": {"caption": "Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Staphylococcal scalded skin syndrome", "path": "media/79792c718a2a4fc3943173c1e5247abc.jpg"}, "4248": {"caption": "Rubella: Rubella rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Rubella: Rubella rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Rubella rash", "path": "media/2f7313e5f18d437b8e3afc7a95357621.jpg"}, "4249": {"caption": "Roseola: rash as the fever breaks: roseola 001. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Roseola: rash as the fever breaks: roseola 001. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "roseola 001", "path": "media/df7f45225e8340388c06a1bbd18cf3f8.jpg"}, "4250": {"caption": "Erythema infectiosum: slapped cheeks and lacy reticular rash: Erythema infectiosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema infectiosum: slapped cheeks and lacy reticular rash: Erythema infectiosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Erythema infectiosum", "path": "media/79644463c9e94bcfa452682aa65917e4.jpg"}, "4251": {"caption": "Erythema toxicum neonatorum: Toxic erythema of the newborn. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema toxicum neonatorum: Toxic erythema of the newborn. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Toxic erythema of the newborn", "path": "media/5757dec7281b4dfb9b518b57244bbd35.jpg"}, "4252": {"caption": "Milia: Neonatal centrofacial milia. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Milia: Neonatal centrofacial milia. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Neonatal centrofacial milia", "path": "media/8c9b42b10e03472aaafbc7a2ed564458.jpg"}, "4253": {"caption": "Neonatal cephalic pustulosis (neonatal acne): Neonatal cephalic pustulosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Neonatal cephalic pustulosis (neonatal acne): Neonatal cephalic pustulosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Neonatal cephalic pustulosis", "path": "media/0b899521355a4850b6e7330fdd83e6ed.jpg"}, "4254": {"caption": "Transient neonatal pustular melanosis: Transient neonatal pustular melanosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Transient neonatal pustular melanosis: Transient neonatal pustular melanosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Transient neonatal pustular melanosis", "path": "media/9c769d4a60db4692b3ca423611b87d73.jpg"}, "4255": {"caption": "Infantile seborrheic dermatitis (cradle cap): Cradle cap. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Infantile seborrheic dermatitis (cradle cap): Cradle cap. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Cradle cap", "path": "media/46b39106122e4c6b833c2181e0010d2a.jpg"}, "4256": {"caption": "Diaper dermatitis: irritant versus candidal: Napkin dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Diaper dermatitis: irritant versus candidal: Napkin dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Napkin dermatitis", "path": "media/55625280da8c425282ebc83cfb71a71f.jpg"}, "4257": {"caption": "Candidal napkin dermatitis thrush satellite: Napkin dermatitis thrush. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Candidal napkin dermatitis thrush satellite: Napkin dermatitis thrush. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Napkin dermatitis thrush", "path": "media/2ba59d61a45c48c3b12eed73b9a15b95.jpg"}, "4258": {"caption": "Port-wine stain: Port-wine stain. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Port-wine stain: Port-wine stain. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Port-wine stain", "path": "media/1a98f62b74924cabb428bba352ae2e40.jpg"}, "4259": {"caption": "Caf\u00e9-au-lait macules: Caf\u00e9-au-lait macule. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Caf\u00e9-au-lait macules: Caf\u00e9-au-lait macule. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Caf\u00e9-au-lait macule", "path": "media/d3be86ec44a0425584796e75369113d3.jpg"}, "4260": {"caption": "Nevus sebaceus: Naevus sebaceous. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Nevus sebaceus: Naevus sebaceous. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Naevus sebaceous", "path": "media/f56d0da8cce6433b8f0d6e519ca19131.jpg"}, "4261": {"caption": "Cellulitis: Cellulitis of the left leg. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Cellulitis: Cellulitis of the left leg. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Cellulitis of the left leg", "path": "media/56e02af8cc0e493786aaf8460ffa2bd9.jpg"}, "4262": {"caption": "Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Staphylococcal scalded skin syndrome", "path": "media/a305e5606e3b45e29792d0708d2e9942.jpg"}, "4263": {"caption": "Common and plantar warts: Common warts. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Common and plantar warts: Common warts. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Common warts", "path": "media/3e5ac415335d47e7a2642b8430f0bc3c.jpg"}, "4264": {"caption": "Head lice: Head lice eggs. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Head lice: Head lice eggs. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Head lice eggs", "path": "media/f7f1d7176c6e47ae8bcb30559aa7b69f.jpg"}, "4265": {"caption": "Herpetic gingivostomatitis mouth gums primary herpes simplex: Herpes simplex on the cheek. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Herpetic gingivostomatitis mouth gums primary herpes simplex: Herpes simplex on the cheek. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Herpes simplex on the cheek", "path": "media/4f06f4fe04c447b480b16a6ee1e067b5.jpg"}, "4266": {"caption": "Eczema herpeticum: Eczema herpeticum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Eczema herpeticum: Eczema herpeticum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Eczema herpeticum", "path": "media/47562658b5684cb9aad46e2a03cba85e.jpg"}, "4267": {"caption": "Herpes zoster in a child: Herpes zoster. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Herpes zoster in a child: Herpes zoster. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Herpes zoster", "path": "media/b5670e962deb4e0580baa5e4a9c5bfdc.jpg"}, "4268": {"caption": "Pityriasis rosea: herald patch and Christmas-tree pattern: Pityriasis rosea. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Pityriasis rosea: herald patch and Christmas-tree pattern: Pityriasis rosea. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Pityriasis rosea", "path": "media/4127f84870ea470687f9fd73192c2968.jpg"}, "4269": {"caption": "Allergic contact dermatitis: Adhesive plaster reaction. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Allergic contact dermatitis: Adhesive plaster reaction. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Adhesive plaster reaction", "path": "media/b7f60ab8f40d43d68b3cd71b166ccc53.jpg"}, "4270": {"caption": "Urticaria: Urticaria. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Urticaria: Urticaria. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Urticaria", "path": "media/c5fc1820968843a1ab6436512e837deb.jpg"}, "4271": {"caption": "Erythema multiforme: target lesions: Cutaneous adverse reaction to anticonvulsant, erythema multiforme target lesions. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema multiforme: target lesions: Cutaneous adverse reaction to anticonvulsant, erythema multiforme target lesions. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Cutaneous adverse reaction to anticonvulsant, erythema multiforme target lesions", "path": "media/dd7fc3aca3f941bd977cd6540ab767b9.jpg"}, "4272": {"caption": "Stevens-Johnson syndrome: Stevens Johnson Syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Stevens-Johnson syndrome: Stevens Johnson Syndrome. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Stevens Johnson Syndrome", "path": "media/88002536c1bf41f48c8b66bcc87d1a4e.jpg"}, "4273": {"caption": "Erythema nodosum: Erythema nodosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema nodosum: Erythema nodosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Erythema nodosum", "path": "media/7f29e6763eb54f2aa45ddf3e91e5564d.jpg"}, "4274": {"caption": "Meningococcemia: petechiae and purpura fulminans: Petechiae due to meningococcal disease. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Meningococcemia: petechiae and purpura fulminans: Petechiae due to meningococcal disease. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Petechiae due to meningococcal disease", "path": "media/9fdfbc0c86d34beb885cc4a928099c81.jpg"}, "4275": {"caption": "Morbilliform drug eruption: Morbilliform drug eruption. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Morbilliform drug eruption: Morbilliform drug eruption. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Morbilliform drug eruption", "path": "media/8eca460943a34fb5bcc2c6ec8236a3f8.jpg"}, "4276": {"caption": "Keratosis pilaris: Keratosis pilaris. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Keratosis pilaris: Keratosis pilaris. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Keratosis pilaris", "path": "media/388cda26223842dab6b1778b442507ba.jpg"}, "4277": {"caption": "Alopecia areata: Eyebrow loss in alopecia areata. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Alopecia areata: Eyebrow loss in alopecia areata. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Eyebrow loss in alopecia areata", "path": "media/e867caa9f7154a12bf68454ec7f57852.jpg"}, "4278": {"caption": "Vitiligo: Ankle vitiligo suitable for ruxolitinib cream. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Vitiligo: Ankle vitiligo suitable for ruxolitinib cream. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Ankle vitiligo suitable for ruxolitinib cream", "path": "media/fec211ef079d4bef973feceb01e25a3d.jpg"}, "4279": {"caption": "Malar butterfly rash of lupus: Malar 'butterfly' rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Malar butterfly rash of lupus: Malar 'butterfly' rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Malar 'butterfly' rash", "path": "media/1cab7607bb7146aaa0d15642b7542c69.jpg"}, "4280": {"caption": "Juvenile dermatomyositis: heliotrope rash and Gottron papules: Gottron papules over joints. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Juvenile dermatomyositis: heliotrope rash and Gottron papules: Gottron papules over joints. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Gottron papules over joints", "path": "media/4a4a00ee0b1b4bc2ad21982a4be8343b.jpg"}, "4281": {"caption": "Lichen sclerosus: Axillary lichen sclerosus. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Lichen sclerosus: Axillary lichen sclerosus. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Axillary lichen sclerosus", "path": "media/8d2b0f1b58574babbcd5b7a1355e448b.jpg"}, "4286": {"caption": "Rubella: Rubella rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Rubella: Rubella rash. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Rubella rash", "path": "media/af7aab94db654766ab43d8b5486bc160.jpg"}, "4287": {"caption": "Roseola: rash as the fever breaks: roseola 001. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Roseola: rash as the fever breaks: roseola 001. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "roseola 001", "path": "media/f42e6032602546a080873653ee0852cc.jpg"}, "4288": {"caption": "Erythema infectiosum: slapped cheeks and lacy reticular rash: Erythema infectiosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema infectiosum: slapped cheeks and lacy reticular rash: Erythema infectiosum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Erythema infectiosum", "path": "media/fdfc6a73ae1b4aa19edaf3cb0e8caf5b.jpg"}, "4289": {"caption": "Erythema toxicum neonatorum: Toxic erythema of the newborn. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Erythema toxicum neonatorum: Toxic erythema of the newborn. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Toxic erythema of the newborn", "path": "media/4d4730dacc894f158f9f6a426b351a92.jpg"}, "4290": {"caption": "Milia: Neonatal centrofacial milia. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Milia: Neonatal centrofacial milia. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Neonatal centrofacial milia", "path": "media/1d5b2aac7d07456e94e9e80db2236c7b.jpg"}, "4291": {"caption": "Neonatal cephalic pustulosis (neonatal acne): Neonatal cephalic pustulosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Neonatal cephalic pustulosis (neonatal acne): Neonatal cephalic pustulosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Neonatal cephalic pustulosis", "path": "media/88e71fb680804d44b998af1bac6c188d.jpg"}, "4292": {"caption": "Transient neonatal pustular melanosis: Transient neonatal pustular melanosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Transient neonatal pustular melanosis: Transient neonatal pustular melanosis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Transient neonatal pustular melanosis", "path": "media/e35145c6a288485282a18f8f30965235.jpg"}, "4293": {"caption": "Infantile seborrheic dermatitis (cradle cap): Cradle cap. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Infantile seborrheic dermatitis (cradle cap): Cradle cap. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Cradle cap", "path": "media/ee838d963605462692ed010daf00f05f.jpg"}, "4294": {"caption": "Diaper dermatitis: irritant versus candidal: Napkin dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Diaper dermatitis: irritant versus candidal: Napkin dermatitis. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Napkin dermatitis", "path": "media/a4742b1ce1c24c369c715d3d22a52fa5.jpg"}, "4295": {"caption": "Candidal napkin dermatitis thrush satellite: Napkin dermatitis thrush. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Candidal napkin dermatitis thrush satellite: Napkin dermatitis thrush. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Napkin dermatitis thrush", "path": "media/86660d1ddb8a4782ab73efc43dabb387.jpg"}, "4296": {"caption": "Port-wine stain: Port-wine stain. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Port-wine stain: Port-wine stain. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Port-wine stain", "path": "media/c22df116adda4117a244fe001c6d84f2.jpg"}, "4301": {"caption": "Common and plantar warts: Common warts. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Common and plantar warts: Common warts. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Common warts", "path": "media/bac8d53ab1fc4b2eb2add1b6ce28230c.jpg"}, "4302": {"caption": "Head lice: Head lice eggs. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Head lice: Head lice eggs. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Head lice eggs", "path": "media/73a42a35423741faa38cfed3af15a2c3.jpg"}, "4303": {"caption": "Herpetic gingivostomatitis mouth gums primary herpes simplex: Herpes simplex on the cheek. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Herpetic gingivostomatitis mouth gums primary herpes simplex: Herpes simplex on the cheek. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Herpes simplex on the cheek", "path": "media/e8da12bbb9f9470dbffa427fe61fa586.jpg"}, "4304": {"caption": "Eczema herpeticum: Eczema herpeticum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "alt_text": "Eczema herpeticum: Eczema herpeticum. Image sourced from DermNet (dermnetnz.org), CC BY-NC-ND 4.0.", "title": "Eczema herpeticum", "path": "media/febda93809e94f67acb5069cbde57aa9.jpg"}}, "links": [{"article_id": 452, "media_id": 4248}, {"article_id": 452, "media_id": 4249}, {"article_id": 452, "media_id": 4250}, {"article_id": 452, "media_id": 4251}, {"article_id": 452, "media_id": 4252}, {"article_id": 452, "media_id": 4253}, {"article_id": 452, "media_id": 4254}, {"article_id": 452, "media_id": 4255}, {"article_id": 452, "media_id": 4256}, {"article_id": 452, "media_id": 4257}, {"article_id": 452, "media_id": 4258}, {"article_id": 452, "media_id": 4259}, {"article_id": 452, "media_id": 4260}, {"article_id": 452, "media_id": 4261}, {"article_id": 452, "media_id": 4262}, {"article_id": 452, "media_id": 4263}, {"article_id": 452, "media_id": 4264}, {"article_id": 452, "media_id": 4265}, {"article_id": 452, "media_id": 4266}, {"article_id": 452, "media_id": 4267}, {"article_id": 452, "media_id": 4268}, {"article_id": 452, "media_id": 4269}, {"article_id": 452, "media_id": 4270}, {"article_id": 452, "media_id": 4271}, {"article_id": 452, "media_id": 4272}, {"article_id": 452, "media_id": 4273}, {"article_id": 452, "media_id": 4274}, {"article_id": 452, "media_id": 4275}, {"article_id": 452, "media_id": 4276}, {"article_id": 452, "media_id": 4277}, {"article_id": 452, "media_id": 4278}, {"article_id": 452, "media_id": 4279}, {"article_id": 452, "media_id": 4280}, {"article_id": 452, "media_id": 4281}, {"article_id": 452, "media_id": 4282}, {"article_id": 452, "media_id": 4283}, {"article_id": 452, "media_id": 4284}, {"article_id": 452, "media_id": 4285}, {"article_id": 452, "media_id": 4286}, {"article_id": 452, "media_id": 4287}, {"article_id": 452, "media_id": 4288}, {"article_id": 452, "media_id": 4289}, {"article_id": 452, "media_id": 4290}, {"article_id": 452, "media_id": 4291}, {"article_id": 452, "media_id": 4292}, {"article_id": 452, "media_id": 4293}, {"article_id": 452, "media_id": 4294}, {"article_id": 452, "media_id": 4295}, {"article_id": 452, "media_id": 4296}, {"article_id": 452, "media_id": 4297}, {"article_id": 452, "media_id": 4298}, {"article_id": 452, "media_id": 4299}, {"article_id": 452, "media_id": 4300}, {"article_id": 452, "media_id": 4301}, {"article_id": 452, "media_id": 4302}, {"article_id": 452, "media_id": 4303}, {"article_id": 452, "media_id": 4304}, {"article_id": 453, "media_id": 4305}, {"article_id": 453, "media_id": 4306}, {"article_id": 453, "media_id": 4307}, {"article_id": 453, "media_id": 4308}, {"article_id": 453, "media_id": 4309}, {"article_id": 453, "media_id": 4310}, {"article_id": 453, "media_id": 4311}, {"article_id": 453, "media_id": 4312}, {"article_id": 453, "media_id": 4313}, {"article_id": 453, "media_id": 4314}, {"article_id": 453, "media_id": 4315}, {"article_id": 453, "media_id": 4316}, {"article_id": 453, "media_id": 4317}, {"article_id": 453, "media_id": 4318}, {"article_id": 453, "media_id": 4319}, {"article_id": 453, "media_id": 4320}, {"article_id": 453, "media_id": 4321}, {"article_id": 453, "media_id": 4322}, {"article_id": 453, "media_id": 4323}, {"article_id": 453, "media_id": 4324}, {"article_id": 453, "media_id": 4325}, {"article_id": 453, "media_id": 4326}, {"article_id": 453, "media_id": 4327}, {"article_id": 453, "media_id": 4328}, {"article_id": 453, "media_id": 4329}, {"article_id": 453, "media_id": 4330}, {"article_id": 453, "media_id": 4331}, {"article_id": 453, "media_id": 4332}, {"article_id": 453, "media_id": 4333}, {"article_id": 453, "media_id": 4334}, {"article_id": 453, "media_id": 4335}, {"article_id": 453, "media_id": 4336}, {"article_id": 453, "media_id": 4337}]}