[
  {
    "article_id": 313,
    "article_title": "Preterm Birth",
    "section_id": "5fc25f1b18e84102b9bf07fa582c8056",
    "section_title": "Ongoing care of the former preterm infant",
    "variant": "clinical",
    "imperatives": 2,
    "content": "For any preterm infant, gestational age at birth (and, closely related, birthweight) is the single most useful piece of information for anticipating risk - the earlier the birth, the higher the risk of respiratory disease, IVH, NEC, retinopathy of prematurity, and long-term neurodevelopmental impairment, with the highest risk concentrated in infants born at or before 25 weeks. Start enteral feeding as early as feasible even in very preterm infants, since nutrition is closely tied to long-term head growth and neurodevelopmental outcome, and [[214|malnutrition]] (particularly in VLBW infants) is specifically linked to smaller head size, poorer psychomotor/mental outcomes, and higher rates of [[164|cerebral palsy]] and autism.\n\nIn primary care follow-up, always correct chronologic age for degree of prematurity when assessing growth and [[10|developmental milestones]], and plan for longer well-child visits to properly evaluate nutritional status, developmental trajectory, and family coping. Screen proactively - not just reactively - for the recognized long-term risks of prematurity: [[378|language delay]], visual-perceptual problems, minor neuromotor dysfunction, attention and executive function difficulties, learning disabilities, and social/emotional problems, since these can be subtle and are common even in children who look well at early exams, including those born late preterm (33-36 weeks) who are often mistakenly treated as low-risk. Track growth parameters, especially head circumference, as an early marker of nutritional adequacy and neurodevelopmental risk. Given the described association between preterm/low birth weight and later hypertension, consider incorporating blood pressure monitoring into longer-term follow-up for children with a preterm birth history, while recognizing the evidence here is still preliminary."
  },
  {
    "article_id": 314,
    "article_title": "Refractive Error",
    "section_id": "e4b29dbcc0b341fa8e5d3c8df0426567",
    "section_title": "Approach at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "When a child fails vision screening, or a parent/teacher reports squinting, eye rubbing, sitting too close to the television, headaches, or fatigue with visual tasks, refer for a comprehensive ophthalmic evaluation including cycloplegic retinoscopy rather than relying on instrument-based (autorefractor) screening alone, since autorefraction can overestimate myopia in children. Prioritize referral in children with recognized risk factors for refractive error - prematurity, Down syndrome, a parent with refractive error, or connective tissue disorders such as Stickler, Marfan, or Ehlers-Danlos syndrome - even in the absence of specific complaints, since young children may not reliably report visual symptoms themselves.\n\nOnce a significant refractive error or anisometropia is identified, arrange prompt correction with glasses as first-line treatment to prevent amblyopia and strabismus - the risk that drives the urgency of treating refractive error in children rather than in adults. Reserve contact lenses for very high or markedly asymmetric refractive errors or for adolescents who decline glasses. Only consider referral for off-label laser refractive surgery in the specific circumstance of a child who cannot tolerate glasses or contact lenses (due to neurobehavioral impairment or severe compliance issues) and has an amblyopiogenic refractive error, recognizing this is not a routine or approved pediatric treatment. Ensure any child treated for amblyopia or anisometropia has consistent follow-up to confirm the corrective strategy (glasses, contacts) is being used as intended, since compliance failures in this population directly translate into missed windows for preventing permanent [[343|visual impairment]]."
  },
  {
    "article_id": 316,
    "article_title": "Otitis Externa",
    "section_id": "48d711ed90204ec4acea3cfb8338199f",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Confirm the diagnosis using the 48-hour onset criterion plus tragal/auricular traction tenderness, and gently debride the canal both to confirm the diagnosis directly and to allow topical medication to reach the inflamed skin. Start first-line topical combination antibiotic-corticosteroid drops (polymyxin/neomycin or a fluoroquinolone) for uncomplicated cases, and add oral analgesia given how painful this condition typically is. If canal swelling is too severe for drops to penetrate proximally, place a wick — and refer to ENT if the swelling is severe enough that you cannot visualize the tympanic membrane, since these patients need specialist canal management and a temporary wick.\n\nEscalate to oral ciprofloxacin for cases not responding to topical therapy or when [[353|cellulitis]] has spread beyond the external canal, and evaluate for malignant otitis externa with imaging in any diabetic or immunosuppressed patient who has disproportionate pain, otorrhea, or new cranial nerve findings — do not manage this population with topical therapy alone. If drainage persists beyond 2 weeks despite appropriate treatment, refer to otolaryngology; if it persists beyond 6 weeks, evaluate for cholesteatoma; and if it persists beyond 3 months despite multiple antibiotic courses, consider MRSA as the likely organism and adjust antimicrobial coverage accordingly.\n\nFor prevention, counsel families to dry the ear canal after swimming, avoid cotton swabs and other objects that disrupt the protective cerumen layer or cause canal trauma, and consider drying drops (e.g., dilute acetic acid or alcohol-based solutions) for children with recurrent episodes, particularly frequent swimmers, since disruption of the natural cerumen barrier is the central mechanism driving this condition."
  },
  {
    "article_id": 318,
    "article_title": "Phenylketonuria",
    "section_id": "73209fb7e5fb4e309306b89e661c11b3",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 3,
    "content": "Ensure every newborn receives screening in the first few days of life, and specifically repeat testing by the second week of life for any infant screened before 24 hours of age, since delayed detection risks irreversible neurologic damage that begins to occur by about 8 weeks of age. If an infant presents with vomiting, irritability, an eczematous rash, and a musty/mousy odor — particularly if fairer in complexion than unaffected relatives — consider PKU even if newborn screening was reportedly normal or is pending, and pursue plasma phenylalanine and phenylalanine:tyrosine ratio testing; a urine ferric chloride test can be a rapid adjunct in the emergency setting when the characteristic odor prompts suspicion.\n\nOnce PKU is confirmed, initiate a phenylalanine-restricted diet with a phenylalanine-free medical formula as soon as possible, and refer to a metabolic disease clinic and a nutritionist experienced in PKU for ongoing, careful dietary monitoring — the treatment is lifelong, not just an infant/childhood intervention. Support continued breastfeeding if the family wishes, but only with close specialty clinic oversight to balance breast milk's phenylalanine content against formula and dietary needs. Counsel families explicitly that aspartame-containing products must be avoided completely, since this common sweetener is a hidden phenylalanine source.\n\nDifferentiate classic PKU from the rarer biopterin-related variants by checking urinary pterins and blood dihydropteridine reductase activity, since these variants need additional treatment with neurotransmitter precursors beyond diet alone — missing this distinction means diet alone will not prevent neurologic damage in these patients. For any young woman with PKU approaching or during childbearing age, emphasize strict return to (or maintenance of) phenylalanine restriction before and throughout pregnancy, since maternal PKU can cause fetal harm irrespective of the fetus's own genetic status. Monitor treated children with phenylalanine level testing coordinated by the metabolic clinic to confirm control is achieved early (ideally by 3–4 weeks of age) and sustained over time, since both the timing and the consistency of control drive long-term cognitive outcome."
  },
  {
    "article_id": 319,
    "article_title": "Puncture Wound Infection",
    "section_id": "9d309f1a32434eb191ba1a55c37e1859",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "For a straightforward foot puncture wound, perform thorough irrigation, update [[266|tetanus]] prophylaxis as indicated by the child's immunization history, and consider a course of antibiotics per local practice; counsel families that the majority of these wounds heal without complication using this approach. Ask specifically whether the puncture occurred through a shoe, particularly a sneaker, since this raises specific concern for Pseudomonas infection and should influence empiric antibiotic selection if infection develops. Obtain a plain radiograph for puncture wounds, especially those over the metatarsophalangeal joints or other weight-bearing areas, to look for a radiopaque foreign body (glass, metal) or bony penetration; if suspicion for a retained foreign body remains despite a negative plain film, pursue ultrasound, CT, or MRI, since organic material is often radiolucent.\n\nReassess promptly if [[353|cellulitis]] develops after a puncture wound — treat with IV antibiotics and add surgical drainage if an abscess forms — and escalate the workup if signs of infection persist beyond the expected course, since this may indicate a retained foreign body or deep infection ([[227|septic arthritis]], chondritis, [[175|osteomyelitis]]) requiring surgical debridement and a 10–14 day systemic antibiotic course covering S. aureus and Pseudomonas. For purulent cellulitis/abscess, use ultrasound to confirm a drainable collection when exam is unclear, perform I&D for mild-to-moderate disease, and add TMP-SMX or escalate to IV vancomycin with I&D based on abscess size, extent of cellulitis, and systemic signs (fever, hypotension) or immunocompromise.\n\nFor animal or human bite puncture wounds, assess wound severity and location (hand/face carry higher risk), and give amoxicillin-clavulanate prophylaxis for 5 days when the wound is moderate/severe, the patient is immunocompromised, or there is possible penetration of the periosteum or joint capsule or significant edema — do not withhold prophylaxis on these higher-risk bite wounds while waiting to see if infection develops."
  },
  {
    "article_id": 320,
    "article_title": "School Refusal",
    "section_id": "7ffb6a3944ba4720b88f415d5864312b",
    "section_title": "Evaluation and management",
    "variant": "clinical",
    "imperatives": 2,
    "content": "When a child is missing school 2–3 days per week for 2 or more weeks, first distinguish school refusal from truancy and from ordinary illness-related absenteeism: confirm the parent is aware the child is at home (ruling out truancy), and look for the characteristic pattern of somatic symptoms confined to weekday, term-time mornings that resolve by midday, without underlying organic explanation. Use a sensitive, holistic history-taking approach — the first conversation itself begins building the therapeutic alliance needed to shift the family away from avoidant behavior — and systematically explore child-related factors (age-appropriate fears, temperament, academic performance), family factors (parental illness, family stress, overdependency dynamics), and school factors (bullying, violence, academic pressure) rather than assuming a single cause.\n\nAlways ask directly about bullying (traditional and cyber) and about violence or fear of violence at school, given how commonly these contribute to school-associated refusal and how serious the downstream emotional consequences can be. Screen for anxiety disorders (especially separation anxiety in younger children), depression, oppositional defiant disorder, panic disorder, and agoraphobia, recognizing that 20–30% of affected children will not meet criteria for any specific psychiatric diagnosis — a normal screen does not exclude school refusal as the correct diagnosis. Directly ask about suicidal ideation given documented cases among school refusers, and treat any positive response as requiring immediate, serious follow-up rather than downplaying it as anxiety.\n\nTailor management to age and underlying dynamic: for a younger child with separation-anxiety-driven refusal, work toward gently increasing tolerance of separation from parents (for example, practicing overnight stays with relatives or friends) while arranging a prompt, early return to school rather than prolonged time at home, since delay tends to entrench the avoidance pattern. Engage the family and the school collaboratively in a shared plan, and involve cognitive-behavioral therapy, relaxation techniques, and, when an anxiety or depressive disorder is present, consider SSRIs as part of a comprehensive treatment plan. Frame physician involvement itself as marking a turning point that signals to the child and family the seriousness of the symptoms and the need to change the avoidant pattern, and counsel families explicitly about the meaningful long-term risks (school non-completion, later psychiatric care, disrupted independence) of unaddressed school refusal to support engagement with treatment rather than continued accommodation of avoidance."
  },
  {
    "article_id": 321,
    "article_title": "Hypoglycemia",
    "section_id": "ad610ccd0f1749d293d816d54e5be9c8",
    "section_title": "Immediate management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Treat hypoglycemia immediately once recognized or confirmed, with the goal of restoring and keeping glucose above 70 mg/dL — a target that matters most in hyperinsulinism, where the child cannot fall back on ketones as brain fuel while glucose is low. In a child with diabetes, this means prompt carbohydrate treatment, and patients and families should be taught to always carry a source of carbohydrate along with a glucose meter when away from home, aiming to normalize glucose quickly without giving so much carbohydrate that it rebounds into hyperglycemia. Diazoxide can be used for hyperinsulinism, including the syndromic hyperinsulinism of [[323|Beckwith-Wiedemann syndrome]]. Beyond the initial glucose correction, long-term management turns on identifying the underlying cause, since that determines the definitive treatment and the risk of recurrence."
  },
  {
    "article_id": 321,
    "article_title": "Hypoglycemia",
    "section_id": "375111a834674bc3a2162cf4c7064921",
    "section_title": "Recognizing and confirming hypoglycemia at the bedside",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Suspect hypoglycemia in any infant or child with autonomic signs (shakiness, sweating, pallor, dizziness) or neuroglycopenic signs (irritability, lethargy, confusion, seizures), remembering that neonates and infants are frequently asymptomatic or show only subtle findings such as cyanosis, apnea, hypothermia, hypotonia, jitteriness, or poor feeding. A blood glucose below 60 mg/dL (3.3 mmol/L) confirms hypoglycemia in infants and children outside the first 72 hours of life. Whenever the glucose is below 50 mg/dL (2.8 mmol/L), obtain a critical sample before treating, since this is the point at which a diagnostic fasting or provocative test would also be stopped. A simultaneous insulin level above 2 µU/mL at a glucose below 60 mg/dL, together with low ketones and low lactate, points to hyperinsulinism; absent ketonemia and ketonuria with an appropriately suppressed insulin instead points to a fatty acid oxidation defect. In a patient with known diabetes, hypoglycemia is defined at a higher threshold, below 70 mg/dL, and does not need this same critical-sample workup."
  },
  {
    "article_id": 322,
    "article_title": "Undescended Testis",
    "section_id": "7f87cce6a9a145c5a775520bec73124e",
    "section_title": "Bedside Approach to the Boy with an Empty Scrotum",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Examine in a warm room with warm hands. Inspect for scrotal asymmetry - a hypoplastic hemiscrotum suggests the testis has never descended. With the child supine or sitting, attempt to guide the testis down the inguinal canal into the scrotum. If successful, hold it in the scrotum for 30 seconds to fatigue the cremaster: a retractile testis remains down, a true undescended testis springs back up. Do not order a scrotal ultrasound to try to find a non-palpable testis - it does not change management and should be reserved for a painful or mass-like scrotum. If the testis has not descended by 6 months of age (corrected for gestational age), refer for surgery rather than waiting further, since spontaneous descent essentially does not occur after this point. A UDT found together with an inguinal hernia should go to surgery at the time of diagnosis, not be deferred to 6 months."
  },
  {
    "article_id": 324,
    "article_title": "Nasal Fracture",
    "section_id": "c62c548d6aaa40ce8de8550711559519",
    "section_title": "Septal Hematoma and Timing of Reduction",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Perform an intranasal speculum exam on every child with nasal trauma specifically to look for a septal hematoma - this requires urgent incision and drainage, since an untreated hematoma causes pressure necrosis of the avascular septal cartilage and a saddle-nose deformity. If swelling limits assessment of deformity, plan re-examination in 2-7 days once it resolves. A fracture with visible deformity or functional (airway) compromise should be reduced, typically by closed reduction under general anesthesia, with the goal of reduction within about 7 days of injury; a child with persistent nasal deformity at 4-5 days post-injury needs urgent referral to a subspecialist to restore anatomic alignment."
  },
  {
    "article_id": 325,
    "article_title": "Rickets",
    "section_id": "99351d70bcae433e99d9fd5a656eb509",
    "section_title": "Bedside evaluation",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In a child with bony deformity, fracture out of proportion to trauma, failure to thrive, or nonspecific bone pain, start with a dietary and social history, since most rickets is nutritional; a family history can suggest 1-alpha-hydroxylase deficiency or renal phosphate wasting, and prior response to vitamin D treatment can help localize the defect. Examine for craniotabes, frontal bossing, delayed fontanel closure, rachitic rosary, Harrison groove, and widened wrists and ankles, and check for hypocalcemic signs — tetany, seizures, or stridor from laryngeal spasm. Confirm with radiographs showing metaphyseal cupping, splaying, and fraying, bowing, cortical narrowing, or stress fracture lines, alongside laboratory testing of calcium, phosphorus, and vitamin D levels, since all patients with rickets have an abnormality in calcium and/or phosphorus."
  },
  {
    "article_id": 325,
    "article_title": "Rickets",
    "section_id": "968fa8fe65f24cc39103acd54153f474",
    "section_title": "Monitoring high-risk infants",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In preterm or low-birth-weight infants, particularly those under 27 weeks gestation or under 1500 g, monitor calcium, phosphorus, and alkaline phosphatase weekly and check serum bicarbonate periodically, since [[387|metabolic acidosis]] promotes bone dissolution. Obtain at least one screening radiograph for rickets at 6-8 weeks of age in high-risk infants, with additional films as clinically indicated. For prevention, ensure breastfed infants receive vitamin D supplementation of at least 400 IU/day, per the American Academy of Pediatrics recommendation."
  },
  {
    "article_id": 326,
    "article_title": "Vitamin D Deficiency",
    "section_id": "c524129f98f74c87b47308e9a7cc9f7a",
    "section_title": "Recognition and workup at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Consider vitamin D deficiency in an infant or child with hypocalcemic symptoms (tetany, seizures), [[246|growth failure]], lethargy, irritability, hypotonia, craniotabes, or recurrent respiratory infection, particularly in an exclusively breastfed infant without supplementation, a child with dark skin pigmentation, prematurity, fat malabsorption (cholestatic liver disease, cystic fibrosis, IBD), anticonvulsant use, or a vegan diet using unfortified soy or rice milk. Screen with serum 25-hydroxyvitamin D: a level under 15 ng/mL defines deficiency and 15-20 ng/mL defines insufficiency. Expect the classic pattern of low-normal or low calcium, low phosphate, high alkaline phosphatase, and high PTH in vitamin D-deficient [[325|rickets]]; in very young infants, [[368|hypocalcemia]] (including seizures) may be the presenting feature rather than overt rickets."
  },
  {
    "article_id": 327,
    "article_title": "Splenic Injury",
    "section_id": "f1a0dca075894503a588d838076f1ff9",
    "section_title": "Initial Management of Blunt Splenic Injury",
    "variant": "clinical",
    "imperatives": 2,
    "content": "In a hemodynamically stable child with blunt splenic injury on CT, manage nonoperatively with observation; interventional radiology is only rarely needed, and this approach now succeeds in more than 95% of pediatric cases while avoiding the complications, transfusion needs, and longer hospital stay associated with surgery. Use CT findings to guide the timing of safe return to usual activity, and do not routinely order follow-up imaging once the child is stable. Reserve laparotomy for the rare child who is not hemodynamically stable, and prefer splenic repair over splenectomy whenever the spleen can be preserved, given the long-term infectious risk of asplenia."
  },
  {
    "article_id": 327,
    "article_title": "Splenic Injury",
    "section_id": "b6fc7ce97db24e10a0926c0d19f24705",
    "section_title": "Preventing Postsplenectomy Sepsis",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Any child left asplenic - after trauma splenectomy or from functional asplenia such as [[162|sickle cell disease]] - needs lifelong precautions against overwhelming infection with encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae type b, Salmonella). Start prophylactic penicillin or amoxicillin, especially in children under 5 years of age, and ensure pneumococcal conjugate, Hib, and meningococcal vaccines are up to date. Counsel families that risk of fulminant septicemia is highest in young children and can be increased up to 350-fold compared with an immunocompetent child, so any fever in an asplenic child warrants urgent medical evaluation."
  },
  {
    "article_id": 328,
    "article_title": "Compartment Syndrome",
    "section_id": "cbf55ebf1fae4aff940b616da52a849e",
    "section_title": "Immediate management",
    "variant": "clinical",
    "imperatives": 2,
    "content": "As soon as compartment syndrome is suspected, remove or split any cast or splint immediately, and elevate the affected extremity only to the level of the heart — not above it, since elevation above heart level reduces tissue perfusion and worsens ischemia. Obtain urgent orthopedic consultation without delay; definitive treatment is prompt, wide fasciotomy of the affected compartments. Admit all children with an open fracture, or with a diagnosis of or concern for compartment syndrome, for ongoing orthopedic care given the high risk of infection and neuromuscular injury. In the rare neonatal presentation of a swollen, paralyzed, dysvascular limb with a sentinel forearm lesion, emergency surgical fasciotomy is the only treatment that may salvage limb function."
  },
  {
    "article_id": 328,
    "article_title": "Compartment Syndrome",
    "section_id": "a83fbb6646b94c65b2ca89180b5c6753",
    "section_title": "Recognition in the child with a limb injury",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Suspect compartment syndrome in any child with an extremity fracture or blunt/crush injury — especially a tibial shaft, proximal tibial metaphyseal, supracondylar humerus, or displaced forearm fracture — who has pain out of proportion to the injury, or pain that is increasing despite analgesic administration. In children, rely on the \"3 As\" — anxiety, agitation, and an escalating analgesia requirement — rather than the classic \"5 Ps\", since paresthesia, pallor, pulselessness, and paralysis are late findings and a child may show only a single sign. Examine for pain with passive stretch of the toes or fingers, and for a tense, non-compressible, swollen compartment. Consult orthopedics urgently for any such concern, and obtain compartment pressure measurement when feasible: an absolute pressure of 30 mmHg or more, or a value within 30 mmHg of the diastolic blood pressure or mean arterial pressure, supports the diagnosis."
  },
  {
    "article_id": 330,
    "article_title": "Herpes Zoster",
    "section_id": "09495af432e745fb998512e0ab9ff2cc",
    "section_title": "Bedside recognition",
    "variant": "clinical",
    "imperatives": 3,
    "content": "Suspect herpes zoster in a child with grouped vesicles on an erythematous base confined to one to three dermatomes and not crossing the midline, especially over the thorax or a cranial nerve distribution, sometimes preceded by burning pain, itching, or paresthesia in that area. Ask about risk factors that raise suspicion and prognosis: varicella acquired in the first 1-2 years of life, intrauterine VZV exposure, maternal varicella during pregnancy, or immunosuppression (including [[372|HIV infection]], where zoster is about 10 times more frequent than in healthy age-matched children). Perform an ophthalmologic examination whenever the ophthalmic (V1) branch of the trigeminal nerve is involved, because of the risk of corneal involvement. Recurrent or multidermatomal shingles should prompt evaluation for an underlying T-cell immune defect."
  },
  {
    "article_id": 331,
    "article_title": "Epiglottitis",
    "section_id": "7e0157d21a1544bca950264a1e6aebcf",
    "section_title": "Airway Management and Antibiotics",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Involve otolaryngology (and, where available, a pediatric anesthesiologist and pediatric surgeon or otolaryngologist) immediately for controlled evaluation and, typically, nasotracheal intubation in the operating room; tracheostomy is used less often. Direct visualization/instrumentation should be performed only in this controlled setting because of the risk of triggering complete obstruction. Expect intubation to be needed for about 2-3 days given the usually rapid response to antibiotics. Start broad-spectrum antibiotics promptly - vancomycin plus cefotaxime, or ceftriaxone/cefotaxime - to cover H. influenzae, S. pneumoniae, group A streptococcus, and S. aureus. Because occult H. influenzae [[350|bacteremia]] leads to meningitis or another deep/focal infection in 30-50% of cases, adequate systemic antibiotic treatment of the underlying infection is essential alongside airway management."
  },
  {
    "article_id": 331,
    "article_title": "Epiglottitis",
    "section_id": "903ade6ddb3d4a5fba7013e53fe40ff3",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 1,
    "content": "- Epiglottitis (supraglottitis) is a life-threatening, rapidly progressive inflammation of the epiglottis and surrounding supraglottic structures, classically caused by Haemophilus influenzae type B (Hib).\n- Peak age is 1-8 years (most sources say 2-7 years), though it can occur at any age; onset is abrupt, typically presenting within 6-24 hours of first symptoms.\n- Since Hib vaccination, incidence has fallen dramatically - as low as 0.02 per 100,000 in Western countries - and today's cases are more often Streptococcus pneumoniae, group A streptococcus, or Staphylococcus aureus, with sporadic Hib cases in unimmunized children or vaccine failures.\n- Classic triad: drooling, dysphagia, and (respiratory) distress, with high fever and a toxic, anxious appearance; the child often sits upright leaning forward or in a tripod position (upright, neck extended, mouth open).\n- Unlike croup, there is no preceding viral prodrome or barky cough, and the voice may be muffled (\"hot potato\" voice); stridor, when present, is typically quiet and not always prominent.\n- Lateral neck radiograph may show the \"thumbprint sign\" (enlarged, thickened epiglottis and aryepiglottic folds) with occasional mild subglottic narrowing, but direct instrumentation/visualization should only be attempted in a controlled operative setting given the risk of precipitating airway obstruction.\n- Do not agitate the child or manipulate the oropharynx outside a controlled setting - this can precipitate sudden, complete airway obstruction.\n- Management: secure the airway (endotracheal or nasotracheal intubation, rarely tracheostomy), typically for 2-3 days until inflammation subsides, plus broad-spectrum antibiotics such as vancomycin and cefotaxime (or ceftriaxone/cefotaxime).\n- Occult H. influenzae [[350|bacteremia]] can lead to [[147|meningitis]] or other focal infection in 30-50% of cases, underscoring the need for prompt antibiotic treatment of the underlying infection."
  },
  {
    "article_id": 331,
    "article_title": "Epiglottitis",
    "section_id": "dc649daf4a9740758952a0cc715dbd17",
    "section_title": "Recognizing and Stabilizing the Child with Epiglottitis",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Suspect epiglottitis in a toxic-appearing, febrile child aged roughly 1-8 years with the triad of drooling, dysphagia, and respiratory distress, especially when sitting upright, leaning forward, or tripoding, with no preceding viral prodrome, no barky cough, and no hoarseness - features that separate it from croup. Do not agitate the child, attempt to examine the oropharynx with a tongue depressor, place the child supine, or send the child alone for imaging: any of these can precipitate sudden, complete airway obstruction. Keep the child calm, ideally in a caregiver's lap, and move directly toward definitive airway management. If a lateral neck radiograph is obtained, it should not delay this process; a thumbprint sign supports the diagnosis but a normal or unobtainable film does not exclude it in a clinically classic presentation. A skilled provider should stay with the patient at all times until the airway is visualized and secured."
  },
  {
    "article_id": 332,
    "article_title": "Spinal Cord Injury",
    "section_id": "2f4e95a7f96a4df58a5e487fdfadd7a6",
    "section_title": "Bedside evaluation of the child with possible SCI",
    "variant": "clinical",
    "imperatives": 3,
    "content": "In any child with a significant mechanism of injury (motor vehicle crash, fall, sports injury, or assault) or clinical findings suggesting SCI, remember that in children under 5 injury more often localizes to the upper cervical spine (occiput to C3), while adolescents pattern more like adults, with lower cervical or thoracolumbar fracture-dislocation. Perform a standardized neurological examination (per the International Standards for Neurological and Functional Classification of SCI, applicable from age 6) rather than relying on imaging alone: a normal X-ray and initial exam do not exclude SCI, since children are prone to SCIWORA and can have neurologic deficits with delayed onset up to 4 days after injury. Watch specifically for local spinal pain or torticollis. Logroll to examine the back, and look under hair, collars, and splints. Do not give corticosteroids for acute spinal cord injury — this is no longer recommended. Obtain MRI whenever there is real concern for cord injury."
  },
  {
    "article_id": 332,
    "article_title": "Spinal Cord Injury",
    "section_id": "8f67baedd71647d4b4123068509addf5",
    "section_title": "Managing the confirmed injury",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Once SCI is identified, prioritize avoiding secondary and iatrogenic injury: support impaired systemic function, stabilize the spine (surgically if indicated, recognizing this may limit subsequent MRI assessment), and pursue emergent decompression for any cord impingement. Manage as an interdisciplinary team from the outset — neurosurgery, critical care/trauma surgery, neurology, physical medicine and rehabilitation, and allied therapies. In a neonate with severe respiratory compromise and profound hypotonia after a breech or forceps delivery, consider birth-related cervical spinal cord injury and watch for spinal shock (flaccid extremities, diaphragmatic breathing, distended bladder, paralyzed abdominal movements); treatment here is supportive. Counsel families early that neurologic status at presentation — intact/incomplete versus complete injury — is the strongest predictor of eventual recovery, and plan for acute inpatient rehabilitation addressing mobility, skin and pressure-ulcer prevention, thermoregulation, and stress-ulcer prophylaxis."
  },
  {
    "article_id": 333,
    "article_title": "Metabolic Syndrome",
    "section_id": "ea700dc461884fdeb79bf2db3156f22f",
    "section_title": "Managing Identified Risk Factors",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Because the component risk factors share a common pathophysiologic root in [[373|insulin resistance]] and adipose tissue dysfunction, first-line management of each is largely the same: lifestyle modification. Treat the individual risk factors identified on screening (weight/adiposity, blood pressure, dyslipidemia, hyperglycemia) rather than withholding intervention while waiting for a formal syndrome diagnosis, since early treatment of this risk clustering is the actionable target in pediatric care."
  },
  {
    "article_id": 334,
    "article_title": "Syncope",
    "section_id": "159b005c5c254b5fb5b0951ff0ad38ac",
    "section_title": "Bedside history and examination",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Evaluate every child with syncope with a comprehensive medical and family history, thorough physical examination, and a 12-lead ECG — this combination identifies most patients with a life-threatening cause, while routine blood testing and imaging add little and are not recommended routinely. Specifically ask about syncope occurring while recumbent or during exercise, associated chest pain or palpitations, personal history of repaired or unrepaired heart disease, and family history of unexplained death, [[291|drowning]], [[146|hypertrophic cardiomyopathy]], [[213|long QT syndrome]] or other arrhythmias, or pacemaker placement. Note whether there was a typical vasovagal prodrome (diaphoresis, warmth, pallor, lightheadedness) and a recognizable trigger (prolonged standing, heat, crowding, pain, emotional distress, position change) — syncope without a prodrome is a concerning feature. Refer any child with an abnormal cardiac exam for urgent cardiac evaluation."
  },
  {
    "article_id": 334,
    "article_title": "Syncope",
    "section_id": "4d3b81f1f608435ba2b435c4a8d3b856",
    "section_title": "Deciding on further workup and disposition",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Reserve cardiac evaluation (echocardiography, further rhythm monitoring, specialist referral) for children with high-risk features: early sudden cardiac death in the family, known or suspected heart disease, congenital cardiac abnormality, exercise-induced syncope, syncope without a prodrome, or an abnormal ECG. In their absence, and with a history consistent with reflex (vasovagal/situational) syncope, observation until the patient returns to baseline, followed by education and reassurance, is appropriate, since recurrence is common but the overall prognosis is benign. Most patients can be discharged home after this evaluation without further testing."
  },
  {
    "article_id": 335,
    "article_title": "Sunburn",
    "section_id": "6c158dd1cba4484c83159b9c6bc0b78b",
    "section_title": "Managing Acute Sunburn",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Treat with cool compresses and oral analgesics; avoid topical anesthetics, which are relatively ineffective for sunburn and can themselves cause a contact dermatitis. Once peak erythema is reached (roughly 24 hours after exposure), a bland emollient such as plain petrolatum can be used through the desquamative (peeling) phase. Use the visit as an opportunity for prevention counseling, since instruction about preventing future sunburns should be delivered at the time of the burn itself."
  },
  {
    "article_id": 336,
    "article_title": "Tick-Borne Illness",
    "section_id": "97d30f5bc7ff41869a16841e129f9b21",
    "section_title": "Management and prevention counseling",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Treatment for tick-borne rickettsial illness is supportive, avoiding analgesics that impair platelet function because of the bleeding risk from vasculitis. Do not offer routine doxycycline prophylaxis after an isolated tick bite, since the risk of infection is low and effectiveness unproven; instead counsel on prevention — avoiding densely vegetated or brushy areas, using repellents and protective clothing, and checking for and promptly removing attached ticks, since attachment for 6 hours or more is associated with transmission. Report confirmed ehrlichiosis or anaplasmosis to the local or state health department, as these are notifiable diseases."
  },
  {
    "article_id": 337,
    "article_title": "Thyroid Nodule",
    "section_id": "4f82417788804a6c9c11666bcb8f3a88",
    "section_title": "Initial Work-Up of a Pediatric Thyroid Nodule",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Every thyroid nodule identified in a child merits complete evaluation, given the higher relative malignancy risk compared with adults. Start with a serum TSH and a neck ultrasound. If TSH is low, obtain radionuclide scintigraphy to assess for an autonomous (hyperfunctioning) nodule; these are generally benign and usually do not need biopsy. If TSH is normal or elevated, proceed with ultrasound characterization of the nodule and gland; refer for ultrasound-guided fine-needle aspiration biopsy if the nodule is sonographically suspicious or 1 cm or larger. Take a history 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. Arrange urgent outpatient follow-up with a specialist experienced in pediatric thyroid nodules for any child in whom a nodule is found, since same-visit reassurance is not appropriate even for an asymptomatic, incidentally discovered nodule."
  },
  {
    "article_id": 337,
    "article_title": "Thyroid Nodule",
    "section_id": "dc1e7d892fbc42c09e24464fe48b33f8",
    "section_title": "Red Flags and Syndromic Considerations",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Treat the following 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. Check a calcitonin level and consider RET genetic testing when there is a family history of medullary thyroid carcinoma, pheochromocytoma, hyperparathyroidism, or mucosal neuromas suggestive of MEN-2A or MEN-2B - 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."
  },
  {
    "article_id": 338,
    "article_title": "Toxic Ingestion",
    "section_id": "9695dc25742548f7b7c41e652434ff6d",
    "section_title": "Assessing severity and risk",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Weigh the type of exposure 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. Consider the classically lethal-in-small-dose pharmaceutical categories specifically — antimalarials, beta-blockers, calcium channel blockers, camphor, antidiarrheals, salicylates, opioids, and tricyclic antidepressants — since these carry disproportionate risk even in small quantities. A slower-onset coma, or one preceded by delirium or abnormal behavior, favors a toxic cause over trauma. Remember the classic accidentally-attractive agents — iron tablets resembling candy, and high-ethanol mouthwash without child-safety packaging — when taking an exposure history in a toddler."
  },
  {
    "article_id": 338,
    "article_title": "Toxic Ingestion",
    "section_id": "975ae4c813274cdcbe27d194ef772854",
    "section_title": "Bedside assessment of a possible ingestion",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Approach 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 — with toxic ingestion on the differential, especially if the presentation does not fit a recognizable clinical syndrome. Start 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, also screen for metabolic derangements — hypoglycemia, [[170|hyponatremia]], hyperammonemia — that can accompany or mimic ingestion. Initial emergency management in any responsive patient prioritizes airway, breathing, and circulation."
  },
  {
    "article_id": 339,
    "article_title": "Tinea Capitis",
    "section_id": "5b8429a2c1724d00b73969eeed830801",
    "section_title": "Recognizing and Confirming Tinea Capitis",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Suspect tinea capitis 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 - consider it even when classic crusting or redness is absent. Perform a mycologic examination looking for T. tonsurans, the cause of up to 95% of US cases; ask about contact with kittens or puppies if M. canis (zoophilic) is suspected, and about contact with other affected children, shared combs/hats/hairbrushes, or affected family members 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, consider screening close contacts when a child has recurrent infection."
  },
  {
    "article_id": 339,
    "article_title": "Tinea Capitis",
    "section_id": "02469975b4a24581bd592f3f84513a13",
    "section_title": "Treating Tinea Capitis",
    "variant": "clinical",
    "imperatives": 3,
    "content": "Do not use topical antifungals alone - they cannot penetrate the hair shaft and will not clear the infection. Start oral griseofulvin (first-line) for at least 8 weeks in children over 2 years of age, advising administration with fatty food to improve absorption; oral terbinafine for 2-6 weeks is an alternative in children over 4 years. In children under 2 years, use oral fluconazole; 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. Manage a kerion 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. Counsel families about hygiene measures and shared-object precautions (combs, hats, brushes, bedding) to reduce spread to other household members and contacts."
  },
  {
    "article_id": 340,
    "article_title": "Varicella Zoster",
    "section_id": "a23492a2173e4905aa933a5f3bc8ddad",
    "section_title": "Isolation, treatment, and high-risk exposures",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Keep a child with varicella in isolation until all lesions have crusted, or a minimum of 5 days if crusting is earlier; in a healthcare setting, place an exposed, susceptible contact 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; reserve acyclovir/valacyclovir for adolescents, unvaccinated children 12 years or older, those with chronic skin or lung disease, and immunocompromised children, since these agents shorten disease duration. Ask about the timing of any maternal varicella exposure during pregnancy or around delivery: 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."
  }
]