# -*- coding: utf-8 -*-
NEW = {}

NEW[337] = [
    {"title": "Clinical paths", "content": "Every thyroid nodule identified in a child merits complete evaluation, given the higher relative malignancy risk compared with adults. The following are treated as pointers toward malignancy warranting expedited work-up: rapid nodule growth, a firm or hard nodule fixed to surrounding structures, satellite or enlarged cervical lymph nodes, a nodule 1 cm or larger with irregular or calcified borders, and new hoarseness or dysphagia."},
    {"title": "Diagnosis", "content": "Evaluation starts with a serum TSH and a neck ultrasound. If TSH is low, radionuclide scintigraphy is obtained to assess for an autonomous (hyperfunctioning) nodule; these are generally benign and usually do not need biopsy. If TSH is normal or elevated, ultrasound characterization of the nodule and gland follows; referral for ultrasound-guided fine-needle aspiration biopsy is made if the nodule is sonographically suspicious or 1 cm or larger. History is taken specifically asking about prior neck/head irradiation and family history of thyroid disease, medullary thyroid carcinoma, or MEN syndromes, since these change the pretest probability of malignancy substantially. A calcitonin level is checked and RET genetic testing is considered when there is a family history of medullary thyroid carcinoma, pheochromocytoma, hyperparathyroidism, or mucosal neuromas suggestive of MEN-2A or MEN-2B."},
    {"title": "Management", "content": "Urgent outpatient follow-up with a specialist experienced in pediatric thyroid nodules is arranged for any child in whom a nodule is found, since same-visit reassurance is not appropriate even for an asymptomatic, incidentally discovered nodule. Identifying a causative RET mutation can prompt prophylactic thyroidectomy on a defined timeline (by age 5 years for certain MEN-2A mutations, by 6 months of age for certain MEN-2B mutations), so early genetic counseling and testing in affected families is important."},
]

NEW[338] = [
    {"title": "Clinical paths", "content": "Any child with an unexplained symptom complex — altered mental status or behavior, seizure, cardiac dysrhythmia, hypotension or shock, respiratory distress or apnea, cyanosis, vomiting, or diarrhea — is approached with toxic ingestion on the differential, especially if the presentation does not fit a recognizable clinical syndrome. A slower-onset coma, or one preceded by delirium or abnormal behavior, favors a toxic cause over trauma. The classic accidentally-attractive agents — iron tablets resembling candy, and high-ethanol mouthwash without child-safety packaging — are kept in mind when taking an exposure history in a toddler."},
    {"title": "Diagnosis", "content": "Assessment starts with directed history (what agents were accessible, timing, quantity if known) and physical examination for symptom pairs that suggest a toxidrome: bradycardia or tachycardia, hypothermia or hyperthermia, respiratory depression or hyperpnea, hypotension or hypertension, mydriasis or miosis. Because ingestions are often unwitnessed, screening is also done for metabolic derangements — hypoglycemia, [[170|hyponatremia]], hyperammonemia — that can accompany or mimic ingestion. The type of exposure is weighed against known risk: caustic ingestion is the leading toxic exposure in children, with most cases from mild alkali agents (bleach, detergents) that can be relatively benign, but button battery ingestion is increasingly common and can be extremely dangerous, and liquid or strong alkali agents cause more severe injury than solids. The classically lethal-in-small-dose pharmaceutical categories are considered specifically — antimalarials, beta-blockers, calcium channel blockers, camphor, antidiarrheals, salicylates, opioids, and tricyclic antidepressants — since these carry disproportionate risk even in small quantities."},
    {"title": "Management", "content": "Initial emergency management in any responsive patient prioritizes airway, breathing, and circulation."},
]

NEW[339] = [
    {"title": "Clinical paths", "content": "Tinea capitis is suspected in a school-age child (peak 3-7 years) with patchy alopecia, broken or stubby hairs, scalp scaling, or a boggy inflammatory plaque (kerion), particularly when accompanied by posterior cervical or suboccipital lymphadenopathy - it is considered even when classic crusting or redness is absent."},
    {"title": "Diagnosis", "content": "A mycologic examination is performed looking for T. tonsurans, the cause of up to 95% of US cases; contact with kittens or puppies is asked about if M. canis (zoophilic) is suspected, and contact with other affected children, shared combs/hats/hairbrushes, or affected family members is asked about for T. tonsurans (anthropophilic) exposure. Because up to 60% of children with tinea capitis are asymptomatic carriers, and adult family members can also be asymptomatic carriers who perpetuate reinfection, screening of close contacts is considered when a child has recurrent infection."},
    {"title": "Management", "content": "Topical antifungals alone are not used - they cannot penetrate the hair shaft and will not clear the infection. Oral griseofulvin (first-line) is started for at least 8 weeks in children over 2 years of age, with administration advised alongside fatty food to improve absorption; oral terbinafine for 2-6 weeks is an alternative in children over 4 years. In children under 2 years, oral fluconazole is used; topical azole (e.g., clotrimazole) or allylamine (e.g., terbinafine) therapy is an option in this youngest age group only when the affected hairs are fine. A kerion is managed with the same systemic antifungal therapy - most patients, including those with a boggy, fluctuant-appearing kerion and tender regional adenopathy, respond well to griseofulvin without needing incision or drainage. Families are counseled about hygiene measures and shared-object precautions (combs, hats, brushes, bedding) to reduce spread to other household members and contacts."},
]

NEW[340] = [
    {"title": "Clinical paths", "content": "Varicella is suspected in a child with a brief prodrome of low-grade fever and malaise followed by a pruritic rash appearing in successive crops — typically about three — spreading centrifugally from the trunk and scalp outward, with lesions at multiple stages (papule, vesicle with a red halo, cloudy fluid, crust) present simultaneously. In a vaccinated child, breakthrough varicella is kept in mind if the rash looks milder or atypical. The timing of any maternal varicella exposure during pregnancy or around delivery is asked about: infection in the first half of pregnancy (especially 8-20 weeks) raises concern for fetal varicella syndrome (limb hypoplasia, dermatomal skin scarring, eye disease, CNS damage), while maternal varicella from 5 days before to 2 days after delivery risks severe, potentially fatal neonatal disease and needs urgent neonatal assessment."},
    {"title": "Diagnosis", "content": "Diagnosis is usually clinical with an exposure history; if confirmation is needed, PCR or direct fluorescent antibody of vesicular fluid or a scab scraping is used. An initial leukopenia followed by lymphocytosis and mildly elevated liver enzymes is expected if labs are drawn."},
    {"title": "Management", "content": "A child with varicella is kept in isolation until all lesions have crusted, or a minimum of 5 days if crusting is earlier; in a healthcare setting, an exposed, susceptible contact is placed under airborne and contact precautions in a negative-pressure room from days 8-21 after exposure (up to 28 days if they received varicella-zoster immune globulin). Supportive care is adequate for a healthy child; acyclovir/valacyclovir is reserved for adolescents, unvaccinated children 12 years or older, those with chronic skin or lung disease, and immunocompromised children, since these agents shorten disease duration. Urgent neonatal assessment is arranged when maternal varicella around delivery places the newborn at risk."},
]

NEW[341] = [
    {"title": "Clinical paths", "content": "Congenital toxoplasmosis is considered in any infant with hepatosplenomegaly, microcephaly or macrocephaly, abnormal tone, seizures, or intrauterine growth restriction, and specifically in any infant under 1 year with undiagnosed neurologic disease, especially when retinal lesions are present. A normal newborn exam does not exclude infection - most infected infants look normal at birth."},
    {"title": "Diagnosis", "content": "CSF analysis, a dilated eye exam, and CNS imaging are pursued when suspicion is raised by maternal history or other findings. On imaging, diffuse intracranial calcifications and hydrocephalus are sought; periventricular calcification on head CT should prompt toxoplasmosis serology alongside consideration of rubella, CMV, and herpes simplex. Hydrocephalus may be the only sign of congenital toxoplasmosis and typically requires shunt placement regardless of other findings. In an older child or adolescent presenting with visual symptoms, ocular toxoplasmosis is evaluated with T. gondii IgG/IgM serology plus dilated eye examination looking for focal necrotizing retinochoroiditis adjacent to a chorioretinal scar; PCR of aqueous humor can confirm the diagnosis but is rarely needed."},
    {"title": "Management", "content": "Confirmed [[155|congenital infection]] is treated with pyrimethamine, sulfadiazine, and folinic acid."},
    {"title": "Prognosis and outcome", "content": "Families are counseled that congenitally infected children who appear normal in infancy remain at risk for [[343|visual impairment]], [[114|learning disability]], or [[248|hearing loss]] emerging later, often in the second or third decade of life, so long-term ophthalmologic and developmental follow-up is warranted even after an initially reassuring newborn evaluation."},
]

NEW[342] = [
    {"title": "Clinical paths", "content": "Absence seizures are suspected in a child, typically 4-12 years old, with brief (a few seconds to about 20 seconds) episodes of staring or behavioral arrest, abrupt in onset and offset, without aura or postictal confusion, sometimes with subtle eye flutter, lip smacking, or other automatisms. Because episodes are often missed by the child and family, specific questioning about frequent daydreaming, inattention, or new school performance problems is warranted, since these can be the presenting complaint. If a child presents in a prolonged confused or dreamy state lasting hours, absence status epilepticus is considered and treated with a benzodiazepine."},
    {"title": "Diagnosis", "content": "Diagnosis is confirmed with EEG showing the classic 3-Hz generalized spike-and-slow-wave discharge; hyperventilation for 3-4 minutes is a simple office and EEG-lab maneuver that reliably provokes the seizure and supports the diagnosis. A normal neurologic exam and normal intelligence are expected in typical CAE — a finding of true falls, myoclonus, or developmental regression should instead raise concern for atypical absence or another [[206|epilepsy]] syndrome and prompt neurology referral."},
    {"title": "Management", "content": "Ethosuximide is started as first-line therapy for confirmed absence seizures; valproate or lamotrigine are reasonable alternatives. Carbamazepine is avoided, as it can worsen absence seizures."},
    {"title": "Prognosis and outcome", "content": "Families are counseled that the prognosis is excellent — over 90% of children become seizure-free with treatment, with remission typically by age 12 — but that seizures can occur many times a day until controlled, which can affect learning and carries some injury risk in the interim."},
]

NEW[343] = [
    {"title": "Clinical paths", "content": "By 3-6 months of age, persisting wandering nystagmus or poor visual regard/tracking should prompt urgent ophthalmology referral. In the first 1-2 years, persistent excessive tearing and eye redness, significant strabismus, and leukocoria (white pupillary reflex) are treated as red flags requiring prompt evaluation. Amblyopia - the most common cause of unilateral, preventable, permanent visual impairment in developed countries, affecting up to 5% of the population - is often insidious and will not be caught without systematic vision screening, so parental observation alone is not relied upon to exclude it. If an infant has poor eye contact, fails to fixate and follow, is unresponsive to visual threat, or shows wandering/roving eye movements with a normal eye exam (normal pupillary responses and eye movements on structural exam), cortical visual impairment from perinatal hypoxia, prematurity, hydrocephalus, congenital CNS anomaly, trauma, [[379|intracranial hemorrhage]], or periventricular leukomalacia is considered."},
    {"title": "Diagnosis", "content": "Visual behavior is screened at every well-child visit, since early detection of significant visual impairment - and of conditions that risk permanent vision loss if untreated - is one of the primary care clinician's most important responsibilities here. When abnormal eye movements are evaluated, they are characterized as rhythmic/swinging versus nonrhythmic, with waveform, direction, amplitude, frequency, velocity, and symmetry between the two eyes described, noting any associated nonocular muscle movement - vertical nystagmus in particular raises concern for a posterior fossa lesion. Referral to ophthalmology is made to determine etiology, and electroretinogram, visual evoked potential testing, brain imaging, and genetics/neurology consultation are pursued as indicated."},
    {"title": "Management", "content": "Once a vision-impairing condition without medical or surgical treatment is identified, early referral for tailored educational intervention, environmental modification, low-vision devices, and family support services is arranged rather than delaying care while awaiting a precise etiologic diagnosis."},
]

NEW[344] = [
    {"title": "Clinical paths", "content": "The distribution is examined first: acrocyanosis is confined to the hands, feet, and perioral/circumoral area, with the tongue, mucous membranes, and trunk remaining pink — this alone distinguishes it from central cyanosis, which involves the skin, lips, and tongue and needs prompt cardiorespiratory evaluation. Acrocyanosis in a newborn is expected in the first 6-24 hours of life (up to 1-2 days, or 24-48 hours with cold stress) and resolves with warming; in an older, normothermic infant, hypovolemia is considered. When a caregiver reports an alarming episode with crying, vomiting, coughing, or breath-holding, a careful history is taken and mental status change is observed for — true acrocyanosis occurs without major mental status change and the child otherwise looks well, whereas seizure, apnea, arrhythmia, or a congenital heart defect need to be excluded when the story or exam does not fit this pattern. If acrocyanosis appears in an adolescent, especially with other signs of autonomic dysfunction (orthostatic symptoms, cold limbs, excessive sweating), it is considered in that broader context rather than assuming a purely neonatal or cold-exposure cause."},
    {"title": "Diagnosis", "content": "Proper lighting is used, and diagnosis is confirmed with pulse oximetry rather than visual assessment alone, since visual assessment is not a reliable indicator of true oxygen saturation. If cyanosis extends beyond the classic distribution, persists beyond the first few minutes of life, or is accompanied by poor perfusion, mottling, or a change in mental status, oxygen desaturation is documented with pulse oximetry, and pre/postductal saturations, chest radiography, ECG, hyperoxia testing, and echocardiography are considered to distinguish a cardiac from a noncardiac or pulmonary cause."},
    {"title": "Management", "content": "No treatment is needed for benign acrocyanosis beyond warming the infant if it is cold-triggered. Supplemental oxygen is reserved for documented desaturation below target range on pulse oximetry, not for blue-looking extremities with normal saturation. If cyanosis extends beyond the classic distribution, persists beyond the first few minutes of life, or is accompanied by poor perfusion, mottling, or a change in mental status, prompt evaluation for cardiorespiratory disease is warranted."},
]

NEW[345] = [
    {"title": "Clinical paths", "content": "In a neonate with facial pustules in the first 2-4 weeks of life, neonatal cephalic pustulosis (comedones are absent) is favored when the picture is small, uniform dusky-pink papules/pustules on the face and scalp - but bacterial, viral, or fungal causes are still actively excluded, and other neonatal mimics such as milia, [[207|erythema toxicum neonatorum]], transient neonatal pustulosis, and sebaceous gland hyperplasia are considered. In an infant presenting between about 6 weeks and 1 year of age with open comedones and papules/pustules on the cheeks and chin, infantile acne is diagnosed - a true acne with a course that can last 1-2 years and a meaningful scarring risk (up to 25% of cases), so treatment is started rather than only observing. Hormonal/endocrine workup is reserved for infantile acne that is unusually severe or persistent, or accompanied by other signs of androgen or cortisol excess; routine hormonal testing is not needed otherwise."},
    {"title": "Diagnosis", "content": "Neonatal acne is managed with routine cleansing alone, and caregivers are reassured it resolves spontaneously within about 1-3 months without scarring."},
    {"title": "Management", "content": "Typical adolescent acne is started on topical therapy - a retinoid, benzoyl peroxide, and/or a topical antibiotic - as first line. For infantile acne, a topical retinoid (tretinoin cream or adapalene gel) combined with benzoyl peroxide is used as the initial regimen. Escalation to oral therapy occurs for severe or recalcitrant disease at either age: oral erythromycin (or azithromycin in infants) for more severe or refractory cases, with oral tetracyclines avoided in young children because of tooth discoloration. Oral isotretinoin is reserved for the most severe, scarring, or nodular disease at any age. Adolescents and families are counseled early about the risk of scarring and the emotional impact of acne, since both are recognized complications that argue for prompt, adequate treatment rather than a wait-and-see approach in more than mild disease."},
]

NEW[346] = [
    {"title": "Clinical paths", "content": "Any child with patchy [[370|hair loss]] is examined for the characteristic features of alopecia areata: sharply circumscribed, smooth, round or oval patches of complete hair loss with otherwise normal-looking underlying skin, and exclamation-point hairs (short, tapered, easily plucked) at the margin. Extent is assessed: single small patch versus multifocal or ophiasis-pattern loss versus progression toward alopecia totalis or universalis, since more extensive disease and childhood onset both predict a worse prognosis."},
    {"title": "Diagnosis", "content": "Nail pitting, striations, or leukonychia are checked for. Because inflammation is not a feature of alopecia areata, the presence of scaling, crusting, redness, pruritus, or regional lymphadenopathy should raise suspicion for [[339|tinea capitis]] instead, and warrants mycologic examination for Trichophyton tonsurans. Atopy is asked about and, since alopecia areata can rarely accompany other autoimmune conditions ([[290|Hashimoto thyroiditis]], [[270|type 1 diabetes]], Addison disease, vitiligo, ulcerative colitis), further evaluation is pursued only if the history or exam suggests one of these — most children with alopecia areata have no other autoimmune disease."},
    {"title": "Management", "content": "Topical corticosteroids are started as first-line therapy for localized alopecia areata, with referral to dermatology for consideration of other treatments if the response is inadequate, since no therapy has strong evidence of outperforming placebo."},
    {"title": "Prognosis and outcome", "content": "Families are counseled that about half of children regrow hair completely within about 12 months, though relapse is common, and that regrowing hairs are often initially grey before regaining color. Expectations are set based on prognostic features present: localized, later-onset disease in an older child, adolescent, or young adult carries the best prognosis, while childhood onset, an ophiasis pattern, coexisting atopy, or widespread hair loss predicts a more guarded course, including possible progression to alopecia totalis or universalis."},
]

NEW[347] = [
    {"title": "Clinical paths", "content": "In a child with sudden-onset epigastric pain radiating to the back, worsened by food and accompanied by vomiting, acute pancreatitis is considered. Most children are hemodynamically stable with nonspecific symptoms and can be managed conservatively, but the minority with necrotizing or hemorrhagic disease who present in shock or with jaundice and need immediate stabilization must be recognized."},
    {"title": "Diagnosis", "content": "Amylase and lipase are checked and abdominal imaging is obtained (ultrasound first-line, CT or MRI as needed). The diagnosis is confirmed when at least 2 of 3 criteria are met: consistent pain, amylase/lipase at least 3 times the upper limit of normal, and imaging consistent with pancreatitis - enzyme elevation alone is not relied upon, since nonpancreatic causes of hyperamylasemia exist. A history targeted at the common pediatric causes is taken: recent blunt abdominal trauma, biliary disease/gallstones (particularly relevant with rising adolescent obesity), multisystem illness such as HUS or [[254|inflammatory bowel disease]], and medication exposure - specifically valproic acid, L-asparaginase, 6-mercaptopurine, and azathioprine - as well as alcohol use in adolescents. If a child has a second episode, or any features suggesting genetic risk (family history, PRSS1/SPINK1/CFTR-associated conditions), a structured etiologic work-up is pursued rather than assuming idiopathic disease, since children with PRSS1 mutations in particular can progress to chronic pancreatitis more quickly. Chronic pancreatitis is considered - with evaluation for exocrine insufficiency (fat malabsorption, [[354|chronic diarrhea]]) and endocrine insufficiency (diabetes symptoms) - in a child with recurrent pancreatic-type pain and imaging showing pancreatic calcification or a dilated duct; pancreatic biopsy is not the standard diagnostic step in children as it can be in adults."},
    {"title": "Management", "content": "Conservative management is used for hemodynamically stable children with nonspecific symptoms."},
    {"title": "Prognosis and outcome", "content": "Families are counseled that pediatric outcomes with conservative management are favorable, with mortality under 0.4%, but that recurrent acute pancreatitis occurs in up to 10% of children after a first episode."},
]

NEW[348] = [
    {"title": "Clinical paths", "content": "On presentation with a possible exacerbation, the severity of obstruction and the risk of further deterioration are rapidly assessed, watching for wheezing, respiratory distress, tachypnea, and accessory muscle use, and asking about early warning signs the family may have already noticed (cough, chest tightness, retractions, audible wheeze). Exacerbations can follow two patterns — a days-long course from progressive inflammation and mucus plugging, versus an abrupt, asphyxial pattern from extreme airway hyperresponsiveness with a very high initial arterial CO2 — so a rapid or recent onset should not be falsely reassuring. High-risk features are identified on history — a prior severe exacerbation, prior ICU admission or intubation, poor controller adherence or inhaler technique, ongoing tobacco/air pollution or allergen exposure, and comorbidities such as obesity, rhinosinusitis, or food allergy — since a prior severe exacerbation is the strongest predictor of a future life-threatening episode."},
    {"title": "Diagnosis", "content": "Response is tracked with SpO2: a level below 92% after an hour of therapy is a good predictor that hospitalization will be needed."},
    {"title": "Management", "content": "Frequent bronchodilator treatments and a course of systemic (oral or intravenous) corticosteroid are started, which resolves most exacerbations. Any ongoing irritant or allergen exposure contributing to the episode is identified and removed. A written asthma action plan is provided or updated using PEFR zones relative to personal best (over 80% green, 50-80% yellow, under 50% red) with clear instructions for each zone and criteria for prompt clinician contact (severe symptoms, falling PEFR, or reduced SABA response). Follow-up is scheduled within 1-2 weeks of any hospital discharge to reassess control, reinforce the action plan, and review controller medication and inhaler technique."},
    {"title": "Prognosis and outcome", "content": "It is emphasized that most pediatric asthma deaths occur at home or in the community before medical care can be reached, making early home recognition and action plan adherence critical."},
]

NEW[349] = [
    {"title": "Clinical paths", "content": "Clinical presentation, not the hemoglobin number alone, guides urgency and the decision to transfuse - a child with chronic, compensated blood loss can tolerate a low hemoglobin relatively well and does not automatically need transfusion on lab value alone. It is recognized that severe or rapidly developing anemia can progress to hypoxia, [[285|congestive heart failure]], end-organ damage, and death, and requires prompt evaluation and treatment; when the cause is not immediately clear, diagnostic work-up and stabilization are pursued in parallel rather than sequentially. Children with cyanotic congenital heart disease or chronic respiratory insufficiency run a higher baseline hemoglobin, so a \"normal-range\" hemoglobin in these children can still represent a clinically significant, functional anemia relative to their own baseline."},
    {"title": "Diagnosis", "content": "The finding is confirmed against age- and sex-specific reference ranges before proceeding, since a hemoglobin that looks low by adult standards may be entirely normal for the child's age. A focused history is taken covering diet (milk intake, iron-fortified foods), growth and feeding history, symptoms of chronic disease, malabsorption, or blood loss, personal or family history of jaundice (including neonatal jaundice), gallbladder disease, splenomegaly, or splenectomy, and the child's ethnic background (relevant to hemoglobinopathies and G6PD deficiency). The reticulocyte count and MCV are used to classify the anemia by mechanism (decreased production vs. increased destruction vs. blood loss) and by red cell size (microcytic, normocytic, macrocytic) before a broader panel of specific tests is ordered."},
    {"title": "Management", "content": "Yearly screening is applied in high-risk children: prematurity or low birth weight, lead exposure, exclusive breastfeeding without supplemental iron past 4 months, a diet without iron-fortified foods, feeding difficulties, or poor growth."},
]

NEW[350] = [
    {"title": "Clinical paths", "content": "Occult or overt bacteremia is considered in a febrile child, particularly one under 2 years old with fever over 39°C and no clear source, with special attention paid to lethargy, irritability, altered mental status, tachycardia out of proportion to the fever, tachypnea or labored breathing, a bulging or depressed fontanel, nuchal rigidity, petechiae, or abdominal/flank tenderness — any of which raises concern for serious bacterial illness. Bacteremia in infants is often not accompanied by fever, and in newborns can instead present with apnea, bradycardia, respiratory dysfunction, temperature instability (fever or hypothermia), or abdominal distention. Vulnerable hosts are identified specifically — asplenic children, those with central venous catheters, neutropenic children, and those with short gut — since they carry substantially higher bacteremia risk and may have a confounding baseline tachycardia that complicates triage."},
    {"title": "Diagnosis", "content": "Blood cultures are obtained and vital signs are assessed carefully against age-appropriate normal ranges, since abnormal ranges vary substantially across childhood and subtle deviations can be missed without this context."},
    {"title": "Management", "content": "Empiric antibiotic choice is based on the most likely regional organisms for the child's age (S. pneumoniae, Staphylococcus, and H. influenzae predominate under age 2) and known local antibiotic resistance patterns, with quick adjustment if a specific risk factor points elsewhere — for example, a central venous catheter raising suspicion for coagulase-negative staphylococci, or travel/endemic exposure raising suspicion for typhoidal or nontyphoidal Salmonella or Brucella."},
    {"title": "Prognosis and outcome", "content": "Most children with pneumococcal bacteremia recover spontaneously, but the roughly 3-5% who develop meningitis or the additional 5% who develop another focal infection, most often pneumonia, are monitored for closely."},
]

NEW[351] = [
    {"title": "Clinical paths", "content": "When proteinuria is found incidentally in an otherwise well child, first classify by clinical context: if the child is acutely ill, recheck once recovered rather than pursuing work-up during the illness; if [[187|hematuria]] is also present, treat this combination as more concerning and evaluate completely. Conservative management is not appropriate when proteinuria is accompanied by edema, hypertension, hematuria, systemic complaints (rash, fever, arthralgia), or a significant family history of [[369|glomerulonephritis]] or renal failure."},
    {"title": "Diagnosis", "content": "In an otherwise healthy child with isolated proteinuria, the dipstick is rechecked; if repeatedly normal, no further work-up is needed. If dipstick remains positive, a urine protein-to-creatinine ratio is obtained on a first-morning sample. A ratio under 0.25 needs no further work-up. A ratio of 0.25 or higher should prompt specific evaluation for orthostatic proteinuria (paired supine and upright collections); if confirmed orthostatic, the family is reassured - this is a benign, common adolescent finding requiring no treatment or restriction. Persistent, nonorthostatic proteinuria, or any ratio of 1.0 or higher, requires a complete evaluation: urine culture, creatinine/BUN, total protein/albumin, cholesterol, C3, ANA, ASO titer, and renal ultrasound, with pediatric nephrology consultation. Total protein, albumin, cholesterol, and triglycerides are checked if [[310|nephrotic syndrome]] (proteinuria plus hypoalbuminemia, edema, and hyperlipidemia) is suspected. Complement (C3, C4) and streptococcal serology (Streptozyme, ASO, antihyaluronidase, anti-DNase B) are checked when post-streptococcal glomerulonephritis is possible (typically 4 days to 3 weeks after streptococcal pharyngitis or impetigo, with low C3/C4), and ANA testing (with low C3 and C4) is considered when SLE is a concern, particularly if hypertension or hematuria coexist."},
    {"title": "Management", "content": "Referral to nephrology is made and renal function is assessed (BUN, creatinine, electrolytes) when red-flag features are present. For a child followed with persistent asymptomatic isolated proteinuria who is otherwise stable, annual monitoring is arranged, with escalation to renal biopsy discussion if proteinuria exceeds 1 g/day or persists beyond 12 months."},
]