[
  {
    "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. Enteral feeding is started 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, chronologic age is always corrected for degree of prematurity when assessing growth and [[10|developmental milestones]], and longer well-child visits are planned to properly evaluate nutritional status, developmental trajectory, and family coping. Proactive - not just reactive - screening is done 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. Growth parameters, especially head circumference, are tracked as an early marker of nutritional adequacy and neurodevelopmental risk. Given the described association between preterm/low birth weight and later hypertension, blood pressure monitoring is considered for incorporation 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, referral is made for a comprehensive ophthalmic evaluation including cycloplegic retinoscopy rather than relying on instrument-based (autorefractor) screening alone, since autorefraction can overestimate myopia in children. Referral is prioritized 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, prompt correction with glasses is arranged 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. Contact lenses are reserved for very high or markedly asymmetric refractive errors or for adolescents who decline glasses. Referral for off-label laser refractive surgery is considered only 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. Consistent follow-up is arranged for any child treated for amblyopia or anisometropia 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": "The diagnosis is confirmed using the 48-hour onset criterion plus tragal/auricular traction tenderness, and the canal is gently debrided both to confirm the diagnosis directly and to allow topical medication to reach the inflamed skin. First-line topical combination antibiotic-corticosteroid drops (polymyxin/neomycin or a fluoroquinolone) are started for uncomplicated cases, and oral analgesia is added given how painful this condition typically is. If canal swelling is too severe for drops to penetrate proximally, a wick is placed — and referral to ENT is made if the swelling is severe enough that the tympanic membrane cannot be visualized, since these patients need specialist canal management and a temporary wick.\n\nEscalation to oral ciprofloxacin is made for cases not responding to topical therapy or when [[353|cellulitis]] has spread beyond the external canal, and evaluation for malignant otitis externa with imaging is performed in any diabetic or immunosuppressed patient who has disproportionate pain, otorrhea, or new cranial nerve findings — this population should not be managed with topical therapy alone. If drainage persists beyond 2 weeks despite appropriate treatment, referral to otolaryngology is made; if it persists beyond 6 weeks, evaluation for cholesteatoma is undertaken; and if it persists beyond 3 months despite multiple antibiotic courses, MRSA is considered the likely organism and antimicrobial coverage is adjusted accordingly.\n\nFor prevention, families are counselled to dry the ear canal after swimming and to avoid cotton swabs and other objects that disrupt the protective cerumen layer or cause canal trauma, and drying drops (e.g., dilute acetic acid or alcohol-based solutions) are considered 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": "Every newborn receives screening in the first few days of life, and testing is specifically repeated 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 — PKU is considered even if newborn screening was reportedly normal or is pending, and plasma phenylalanine and phenylalanine:tyrosine ratio testing is pursued; 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, a phenylalanine-restricted diet with a phenylalanine-free medical formula is initiated as soon as possible, and referral is made 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. Continued breastfeeding is supported if the family wishes, but only with close specialty clinic oversight to balance breast milk's phenylalanine content against formula and dietary needs. Families are counselled explicitly that aspartame-containing products must be avoided completely, since this common sweetener is a hidden phenylalanine source.\n\nClassic PKU is differentiated 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, strict return to (or maintenance of) phenylalanine restriction before and throughout pregnancy is emphasized, since maternal PKU can cause fetal harm irrespective of the fetus's own genetic status. Treated children are monitored 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, thorough irrigation is performed, [[266|tetanus]] prophylaxis is updated as indicated by the child's immunization history, and a course of antibiotics is considered per local practice; families are counselled that the majority of these wounds heal without complication using this approach. Whether the puncture occurred through a shoe, particularly a sneaker, is specifically asked about, since this raises specific concern for Pseudomonas infection and should influence empiric antibiotic selection if infection develops. A plain radiograph is obtained 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, ultrasound, CT, or MRI is pursued, since organic material is often radiolucent.\n\nPrompt reassessment is warranted if [[353|cellulitis]] develops after a puncture wound — treatment is with IV antibiotics, with surgical drainage added if an abscess forms — and the workup is escalated 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, ultrasound is used to confirm a drainable collection when exam is unclear, I&D is performed for mild-to-moderate disease, and TMP-SMX is added or IV vancomycin with I&D is used based on abscess size, extent of cellulitis, and systemic signs (fever, hypotension) or immunocompromise.\n\nFor animal or human bite puncture wounds, wound severity and location are assessed (hand/face carry higher risk), and amoxicillin-clavulanate prophylaxis is given 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 — prophylaxis should not be withheld 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, school refusal is first distinguished from truancy and from ordinary illness-related absenteeism: confirmation that the parent is aware the child is at home rules out truancy, and the characteristic pattern of somatic symptoms confined to weekday, term-time mornings that resolve by midday, without underlying organic explanation, is sought. A sensitive, holistic history-taking approach is used — the first conversation itself begins building the therapeutic alliance needed to shift the family away from avoidant behavior — and child-related factors (age-appropriate fears, temperament, academic performance), family factors (parental illness, family stress, overdependency dynamics), and school factors (bullying, violence, academic pressure) are systematically explored rather than assuming a single cause.\n\nBullying (traditional and cyber) and violence or fear of violence at school are always asked about directly, given how commonly these contribute to school-associated refusal and how serious the downstream emotional consequences can be. Screening is done 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. Suicidal ideation is asked about directly given documented cases among school refusers, and any positive response is treated as requiring immediate, serious follow-up rather than downplaying it as anxiety.\n\nManagement is tailored to age and underlying dynamic: for a younger child with separation-anxiety-driven refusal, work is directed toward gently increasing tolerance of separation from parents (for example, practicing overnight stays with relatives or friends) while a prompt, early return to school rather than prolonged time at home is arranged, since delay tends to entrench the avoidance pattern. The family and the school are engaged collaboratively in a shared plan, cognitive-behavioral therapy and relaxation techniques are involved, and, when an anxiety or depressive disorder is present, SSRIs are considered as part of a comprehensive treatment plan. Physician involvement itself is framed 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 families are counselled 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": "Hypoglycemia is treated 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 are 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": "Hypoglycemia is suspected in any infant or child with autonomic signs (shakiness, sweating, pallor, dizziness) or neuroglycopenic signs (irritability, lethargy, confusion, seizures); 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), a critical sample is obtained 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": "Examination is performed in a warm room with warm hands. Inspection for scrotal asymmetry is done - a hypoplastic hemiscrotum suggests the testis has never descended. With the child supine or sitting, an attempt is made to guide the testis down the inguinal canal into the scrotum. If successful, it is held in the scrotum for 30 seconds to fatigue the cremaster: a retractile testis remains down, a true undescended testis springs back up. Scrotal ultrasound has no role in locating a non-palpable testis - it does not change management and is reserved for a painful or mass-like scrotum. If the testis has not descended by 6 months of age (corrected for gestational age), referral for surgery is made 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": "An intranasal speculum exam is performed 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, re-examination is planned 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, evaluation starts 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. Examination is done for craniotabes, frontal bossing, delayed fontanel closure, rachitic rosary, Harrison groove, and widened wrists and ankles, and hypocalcemic signs — tetany, seizures, or stridor from laryngeal spasm — are checked for. Diagnosis is confirmed 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, calcium, phosphorus, and alkaline phosphatase are monitored weekly and serum bicarbonate is checked periodically, since [[387|metabolic acidosis]] promotes bone dissolution. At least one screening radiograph for rickets is obtained at 6-8 weeks of age in high-risk infants, with additional films as clinically indicated. For prevention, breastfed infants are given 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": "Vitamin D deficiency is considered 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. Screening is done with serum 25-hydroxyvitamin D: a level under 15 ng/mL defines deficiency and 15-20 ng/mL defines insufficiency. The classic pattern of low-normal or low calcium, low phosphate, high alkaline phosphatase, and high PTH is expected 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, management is nonoperative 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. CT findings are used to guide the timing of safe return to usual activity, and follow-up imaging is not routinely ordered once the child is stable. Laparotomy is reserved for the rare child who is not hemodynamically stable, and splenic repair is preferred 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). Prophylactic penicillin or amoxicillin is started, especially in children under 5 years of age, and pneumococcal conjugate, Hib, and meningococcal vaccines are kept up to date. Families are counselled 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, any cast or splint is removed or split immediately, and the affected extremity is elevated only to the level of the heart — not above it, since elevation above heart level reduces tissue perfusion and worsens ischemia. Urgent orthopedic consultation is obtained without delay; definitive treatment is prompt, wide fasciotomy of the affected compartments. All children with an open fracture, or with a diagnosis of or concern for compartment syndrome, are admitted 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": "Compartment syndrome is suspected 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, the \"3 As\" — anxiety, agitation, and an escalating analgesia requirement — are relied on rather than the classic \"5 Ps\", since paresthesia, pallor, pulselessness, and paralysis are late findings and a child may show only a single sign. Examination is done for pain with passive stretch of the toes or fingers, and for a tense, non-compressible, swollen compartment. Orthopedics is consulted urgently for any such concern, and compartment pressure measurement is obtained 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": "Herpes zoster is suspected 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. Risk factors that raise suspicion and prognosis are asked about: 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). An ophthalmologic examination is performed 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": "Otolaryngology (and, where available, a pediatric anesthesiologist and pediatric surgeon or otolaryngologist) is involved 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. Intubation is typically needed for about 2-3 days given the usually rapid response to antibiotics. Broad-spectrum antibiotics are started 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- Agitating the child or manipulating the oropharynx outside a controlled setting is avoided - this can precipitate sudden, complete airway obstruction.\n- Management: the airway is secured (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": "Epiglottitis is suspected 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. The child is not agitated, the oropharynx is not examined with a tongue depressor, the child is not placed supine, and the child is not sent alone for imaging: any of these can precipitate sudden, complete airway obstruction. The child is kept calm, ideally in a caregiver's lap, while care moves 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, it is noted 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. A standardized neurological examination (per the International Standards for Neurological and Functional Classification of SCI, applicable from age 6) is performed 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. Local spinal pain or torticollis is specifically watched for. The back is examined by logrolling, and hair, collars, and splints are checked underneath. Corticosteroids are not given for acute spinal cord injury — this is no longer recommended. MRI is obtained 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, priority is given to avoiding secondary and iatrogenic injury: impaired systemic function is supported, the spine is stabilized (surgically if indicated, recognizing this may limit subsequent MRI assessment), and emergent decompression is pursued for any cord impingement. Management is 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, birth-related cervical spinal cord injury is considered and spinal shock (flaccid extremities, diaphragmatic breathing, distended bladder, paralyzed abdominal movements) is watched for; treatment here is supportive. Families are counselled early that neurologic status at presentation — intact/incomplete versus complete injury — is the strongest predictor of eventual recovery, and acute inpatient rehabilitation addressing mobility, skin and pressure-ulcer prevention, thermoregulation, and stress-ulcer prophylaxis is planned."
  },
  {
    "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. The individual risk factors identified on screening (weight/adiposity, blood pressure, dyslipidemia, hyperglycemia) are treated 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": "Every child with syncope is evaluated 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. Specific inquiry is made 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 is made of 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. Any child with an abnormal cardiac exam is referred 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": "Cardiac evaluation (echocardiography, further rhythm monitoring, specialist referral) is reserved 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": "Treatment is with cool compresses and oral analgesics; topical anesthetics are avoided, as they 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. The visit is used 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. Routine doxycycline prophylaxis is not offered after an isolated tick bite, since the risk of infection is low and effectiveness unproven; prevention counseling is given instead — 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. Confirmed ehrlichiosis or anaplasmosis is reported 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. 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. 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."
  },
  {
    "article_id": 337,
    "article_title": "Thyroid Nodule",
    "section_id": "dc1e7d892fbc42c09e24464fe48b33f8",
    "section_title": "Red Flags and Syndromic Considerations",
    "variant": "clinical",
    "imperatives": 2,
    "content": "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. 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 - 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": "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. 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."
  },
  {
    "article_id": 338,
    "article_title": "Toxic Ingestion",
    "section_id": "975ae4c813274cdcbe27d194ef772854",
    "section_title": "Bedside assessment of a possible ingestion",
    "variant": "clinical",
    "imperatives": 1,
    "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. 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. 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": "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. 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."
  },
  {
    "article_id": 339,
    "article_title": "Tinea Capitis",
    "section_id": "02469975b4a24581bd592f3f84513a13",
    "section_title": "Treating Tinea Capitis",
    "variant": "clinical",
    "imperatives": 3,
    "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 counselled 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": "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. 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."
  }
]