[
  {
    "article_id": 237,
    "article_title": "Bacterial Gastroenteritis",
    "section_id": "f33dbc4817554d7b93bca60f53034e08",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 4,
    "content": "**Assessment and Initial Management**\n\nDehydration and shock are rapidly assessed, particularly in infants who can deteriorate quickly. Hypoglycemia, which is common in young infants, is checked for. A history of bloody diarrhea (suggests bacterial infection) and recent antibiotic use (suggests *C. difficile*) is obtained.\n\n**Fluid Resuscitation**\n\nFluid resuscitation is the cornerstone of treatment. In infants, this may improve clinical appearance and clarify whether dehydration is the primary diagnosis.\n\n**Diagnostic Testing**\n\nStool culture is sent for bacterial identification (results in several days). Rapid PCR detection of gastrointestinal pathogens is considered if available. Complete blood count is obtained; bandemia with normal WBC count suggests *Shigella*. For suspected *Vibrio* infection, the laboratory is notified so special identification techniques can be employed.\n\n**Antibiotic Treatment**\n\nAntibiotics are indicated for:\n- *Salmonella* (nontyphi): Ceftriaxone or azithromycin if bacteremic, <3 months old, or immunocompromised (including children with hemoglobinopathies)\n- *Shigella*: Azithromycin or ceftriaxone daily for 3 days\n- *Giardia*: Metronidazole 15 mg/kg/day divided into three daily doses for 5 days (maximum 750 mg/day)\n\nFor invasive disease from susceptible strains, an expanded-spectrum cephalosporin, azithromycin, or fluoroquinolone is used.\n\n**Monitoring and Disposition**\n\nTransfer to ICU is indicated for decompensated shock unresponsive to fluid boluses, concern for acute adrenal insufficiency, [[241|diabetic ketoacidosis]], increased intracranial pressure, or [[100|myocarditis]].\n\nDischarge is appropriate when dehydration has resolved, oral intake is adequate to maintain hydration, and oral antibiotics (if indicated) are tolerated.\n\n**Specialist Consultation**\n\n- **Gastroenterology**: Persistent diarrhea >14 days, significant GI bleeding, or suspected [[254|inflammatory bowel disease]]\n- **Infectious disease**: Unusual or resistant pathogen, multiple *C. difficile* recurrences\n- **Surgery**: Possible [[193|acute abdomen]]"
  },
  {
    "article_id": 238,
    "article_title": "Bacterial Meningitis",
    "section_id": "23b4c43309f04f6ca7b05094c552ac2e",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "**Immediate Actions**\n\n1. **The clinical picture is recognised**: Fever with irritability, vomiting, altered sleep, or paradoxical irritability (worsens with handling). Bulging fontanelle in infants. [[315|Seizures]] in 20% of cases.\n\n2. **Neuroimaging before lumbar puncture is decided upon**: CT scan is performed prior to lumbar puncture if the child has coma, recent CNS trauma, focal neurological deficit, papilledema, or cerebrospinal fluid shunt. Neuroimaging is also considered in immunocompromised children.\n\n3. **Antibiotics are started immediately** (lumbar puncture results are not awaited):\n   - **Vancomycin**: 60 mg/kg intravenously\n   - **Ceftriaxone**: 100 mg/kg intravenously, up to 2 g, every 12 hours\n\n4. **Lumbar puncture is performed** (once safe to do so) and cerebrospinal fluid is sent for:\n   - Gram stain\n   - Culture and sensitivities\n   - Cell count with differential\n   - Protein\n   - Glucose\n   - Opening pressure measurement\n\n5. **Cerebrospinal fluid findings are interpreted**:\n   - WBC count typically >1,000/μL with neutrophil predominance\n   - Glucose <40 mg/dL\n   - Protein >100 mg/dL\n   - Opening pressure may be >25 cm H₂O in older children\n   - Absence of organism on Gram stain does not exclude bacterial [[147|meningitis]]\n\n**Ongoing Management**\n\n6. **Antibiotics are adjusted based on susceptibilities** once available:\n   - For susceptible organisms: aqueous penicillin G 250,000 U/kg per day divided every 4 hours OR ampicillin 300 mg/kg per day divided every 6 hours\n   - For penicillin- and cephalosporin-resistant *S. pneumoniae*: vancomycin and ceftriaxone are continued; rifampin may be added\n\n7. **Adjunctive dexamethasone is added**:\n   - Dose: 0.15 mg/kg per dose intravenously\n   - Frequency: every 6 hours\n   - Duration: 2 days\n   - Timing: begins with the first dose of antibiotic\n   - Benefit: reduces [[248|hearing loss]] and short-term neurological sequelae\n\n8. **Antibiotic therapy is continued**:\n   - Neonates: 3 weeks\n   - Older children: 7–10 days (may extend longer)\n\n9. **Infection control**:\n   - Droplet precautions for meningococcal [[147|meningitis]]\n   - Standard precautions for other bacterial causes\n\n10. **Supportive care**: Raised intracranial pressure, electrolyte imbalances, and [[315|seizures]] are managed as needed. Intensive care unit admission is considered for close initial monitoring."
  },
  {
    "article_id": 240,
    "article_title": "Brain Death",
    "section_id": "94ec5456264f477daef0bd31b08af25c",
    "section_title": "Clinical Assessment and Documentation",
    "variant": "clinical",
    "imperatives": 1,
    "content": "**Step 1: Verify Prerequisites**\n\nBefore the brain death examination begins, the following prerequisites are confirmed:\n- Known catastrophic brain injury from recognised aetiology ([[272|traumatic brain injury]], anoxic brain injury, intracranial infection, [[338|toxic ingestion]], or other specified cause)\n- Blood pressure normal for age\n- Core temperature >35°C\n- Serum electrolytes normal\n- Blood glucose normal\n- No sedating medications or muscle relaxants on board\n- Sufficient time elapsed for clearance of any sedating drugs or toxins\n- Reversible causes of coma excluded through review of medical history, neuroimaging, EEG, and laboratory data\n\n**Step 2: First Clinical Examination**\n\nA comprehensive neurologic examination is performed, documenting:\n- Deep coma: unresponsiveness to tactile, auditory, and visual stimulation (excluding spinally mediated reflexes)\n- Absent brainstem reflexes: all cranial nerve reflexes are tested as per institutional protocol\n- Apnea: absence of respiratory effort with adequate respiratory stimulus\n- Any motor movements are confirmed as spinally mediated; ancillary testing is used if the distinction is unclear\n\n**Step 3: Observation Period**\n\n- Term newborns (37 weeks gestational age) to 30 days old: at least 24 hours are observed before the second examination\n- Children 31 days to 18 years old: at least 12 hours are observed before the second examination\n- The observation interval may be shortened if an ancillary study (EEG or other) is consistent with brain death\n\n**Step 4: Second Clinical Examination**\n\nThe complete neurologic examination is repeated, with the same findings as the first examination.\n\n**Step 5: Documentation**\n\nThe institutional brain death checklist is used to document:\n- Irreversible and identifiable cause of coma\n- Correction of confounding conditions\n- Completion of all components of neurologic examination\n- Timing of both examinations and observation interval\n- Results of any ancillary testing performed\n- Names and credentials of examining physicians\n\n**Note on Ancillary Testing**\n\nAncillary tests such as EEG may be used if the patient cannot tolerate portions of the clinical examination (particularly apnea testing) or is very young, especially under 1 year of age."
  },
  {
    "article_id": 241,
    "article_title": "Diabetic Ketoacidosis",
    "section_id": "ea656d64bd9541d98f97de7084f3d7b1",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 5,
    "content": "**Initial Assessment and Investigations**\n\n1. Pediatric endocrinology and/or pediatric intensive care is consulted early\n2. Height and weight are obtained (compared to premorbid weight)\n3. Severity of [[99|dehydration]] and level of consciousness are assessed\n4. Essential investigations are performed:\n   - Blood glucose\n   - Blood ketones\n   - Urea and electrolytes, creatinine\n   - Blood gas analysis\n   - Blood and urine cultures (to identify infection)\n   - Cardiac monitor (assess for T-wave changes of hypokalaemia)\n\n**Treatment Goals**\n\n- Circulating volume is restored\n- Metabolic derangements are corrected\n- Treatment complications (hypokalemia, cerebral edema) are avoided\n- The underlying cause (infection, insulin pump malfunction, etc.) is identified and treated\n\n**Monitoring for Complications**\n\nCerebral edema, which typically presents 4–12 hours after treatment initiation, is watched for. High vigilance is maintained in patients with risk factors: elevated blood urea nitrogen, low CO₂ tension, age under 3 years, new-onset diabetes, or failure of serum sodium to rise steadily during hyperglycemia correction."
  },
  {
    "article_id": 242,
    "article_title": "Duchenne Muscular Dystrophy",
    "section_id": "2207461fd3ae43ef8f258b9c9a457202",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 6,
    "content": "**Diagnosis**\n\n1. Serum creatine kinase level is obtained (marked elevation, 10–10,000 times normal, is expected)\n2. Genetic testing is performed on peripheral blood (detects mutations in ~70% of cases)\n3. If genetic testing is negative, muscle biopsy with dystrophin analysis is arranged\n4. Intellectual function is assessed and screening is performed for [[114|learning disability]], ADHD, and [[117|autism spectrum disorder]]\n\n**Pharmacological Management**\n\nSystemic corticosteroids are indicated to slow disease progression and maintain strength. Specific dosing regimens are not detailed in the available passages.\n\n**Monitoring and Complications**\n\n- Respiratory complications after loss of ambulation, including [[224|scoliosis]], ineffective cough, and sleep-disordered breathing, are monitored for\n- Cardiac function is assessed regularly given the high incidence of cardiomyopathy and dysrhythmias\n- Diaphragm function is evaluated, as weakness is common\n- Multidisciplinary care is provided, addressing neuromuscular, respiratory, cardiac, orthopedic, endocrine, gastrointestinal, and nutritional needs\n- Psychosocial support and transition planning are coordinated across the lifespan"
  },
  {
    "article_id": 244,
    "article_title": "Febrile Neutropenia",
    "section_id": "7e750cc675d0491a85924e279f878c93",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 2,
    "content": "- Neutropenia is ANC <1500/μL; severe neutropenia is <500/μL\n- Febrile neutropenia is fever (≥38.3°C single reading or ≥38.0°C for 1 hour) with ANC <500/μL\n- Fever may be the only sign of life-threatening infection; clinical signs of infection are often diminished\n- Approximately 50% of febrile neutropenic patients have documented infections; 1 in 5 with profound neutropenia (ANC <100/μL) develop [[350|bacteremia]]\n- Blood cultures, urine cultures, and cultures from identified infection sites are obtained before antibiotics are started\n- Broad-spectrum IV antibiotics are started within 1 hour of arrival; culture results are not awaited\n- High-risk patients (anticipated neutropenia >7 days, clinically unstable, or comorbidities) require hospitalisation and IV antibiotics\n- If fever persists >3–5 days on antibiotics, empiric antifungal coverage for *Candida* and *Aspergillus* is added\n- *Staphylococcus aureus* and gram-negative organisms are common causative pathogens\n- Treatment continues until fever resolves and neutrophil count rises"
  },
  {
    "article_id": 244,
    "article_title": "Febrile Neutropenia",
    "section_id": "f72ed46188374292aee69b7251880b0a",
    "section_title": "Management at the Bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "**Initial Assessment and Culture**\n\n1. Blood cultures, urine cultures, and cultures from any identified infection sites (abscess, [[353|cellulitis]], etc.) are obtained\n2. Cerebrospinal fluid is examined if CNS infection is suspected\n3. Antibiotics are not delayed while culture results are awaited\n\n**Antibiotic Initiation**\n\nBroad-spectrum intravenous antibiotics are started within 1 hour of patient arrival. For high-risk patients (anticipated neutropenia >7 days, clinically unstable, or with comorbidities), empiric monotherapy is used with one of the following:\n\n- Piperacillin/tazobactam\n- Carbapenem\n- Ceftazidime\n- Cefepime\n\nFor ill-appearing patients or those with poor marrow function (congenital neutropenias, bone marrow failure syndromes), an example initial regimen may include ceftriaxone, vancomycin, and metronidazole. If abdominal pain is present, anaerobic coverage is ensured.\n\n**Special Considerations**\n\n- For soft tissue infections, a semisynthetic penicillin and aminoglycoside or vancomycin may be added to cover for MRSA\n- With evidence of [[226|sepsis]], double coverage for gram-negative organisms is added in addition to vancomycin\n- For patients in shock, fungal coverage is considered\n\n**Ongoing Management**\n\n- Antibiotics are continued until fever resolves and neutrophil count rises\n- If fever persists for more than 3–5 days despite broad-spectrum antibiotics, empiric antifungal coverage is added\n- Low-risk, well-appearing patients with normal marrow function and reassuring vital signs may be managed as outpatients following an initial antibiotic dose, with close observation and follow-up\n\n**Transfusion Support**\n\nPatients receiving immunosuppressive therapy should receive irradiated blood products to prevent graft-versus-host disease and leukoreduced blood products to prevent transfusion-associated reactions and infections."
  },
  {
    "article_id": 245,
    "article_title": "Gastroesophageal Reflux",
    "section_id": "3356818d9c0b4e06817b5cc103ed1863",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 5,
    "content": "**Initial Assessment**\n\nA history of symptom onset, frequency, and character is obtained. Whether regurgitation or vomiting is present is determined. Respiratory symptoms (cough, wheezing, hoarseness, apnea), failure to thrive, poor weight gain, and irritability are assessed. History of reflux in infancy and reactive airway disease is evaluated.\n\nRegurgitation episodes need not be present for GERD diagnosis.\n\n**Nonpharmacologic Management (First-line)**\n\nFor infants and young children:\n- Feed volumes are reduced\n- Feeds are thickened\n- The infant is positioned after feeds\n\nFor older children:\n- Foods that exacerbate symptoms are avoided\n- Small, frequent meals are recommended\n\nParental education, guidance, and support are provided, particularly regarding choking after spitting up.\n\n**Pharmacologic Management**\n\nIf nonpharmacologic measures are insufficient:\n- Proton pump inhibitors are initiated (specific dosing not provided in source material)\n- Prokinetic drugs are considered if gastroparesis is associated\n\nProton pump inhibitor therapy is often adequate for symptom control.\n\n**Surgical Management**\n\nFundoplication is rarely indicated and reserved for medically refractory cases of GERD. Alternative causes of recurrent vomiting are excluded before surgery is considered.\n\n**Follow-up Considerations**\n\nPatients with esophageal atresia and tracheoesophageal fistula require long-term follow-up due to increased risk of Barrett esophagus and esophageal cancer."
  },
  {
    "article_id": 246,
    "article_title": "Growth Failure",
    "section_id": "eded775f4f4f4e4eae8f630091343157",
    "section_title": "Evaluation and management at the bedside",
    "variant": "clinical",
    "imperatives": 3,
    "content": "Careful, accurate anthropometry is performed at every visit: length/height, weight, and head circumference are weighed and measured with consistent technique, and plotted on the appropriate growth chart (WHO for children under 2 years). The defining patterns are specifically sought - weight-for-age below the 3rd-5th percentile, weight-for-length below the 5th percentile, or crossing of two or more major percentile lines - and correction is made for prematurity where relevant (weight to 24 months, head circumference to 18 months, length/height to 40 months).\n\nBecause the underlying problem is almost always undernutrition, the history and exam are structured to sort the child into one (or more) of four functional categories: inadequate intake (feeding technique, access to food, formula preparation errors, oral-motor or behavioral feeding problems), excessive losses (vomiting, diarrhea, malabsorption), ineffective use of calories (metabolic disease), or increased requirement (chronic illness, congenital heart disease, chronic infection). A thorough psychosocial assessment of the family is a required part of the work-up in every case, not only when a nonorganic cause is suspected, since organic and nonorganic contributors commonly overlap. Escalation to subspecialty or hospital-based evaluation is reserved for children with severe or rapidly progressive growth deceleration, suspected serious organic disease, or when outpatient nutritional intervention and follow-up have failed - re-measurement and re-plotting of growth parameters over time is the key tool for judging whether an intervention is working."
  },
  {
    "article_id": 246,
    "article_title": "Growth Failure",
    "section_id": "e459aa3569f44206b2624927b6f7814b",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 1,
    "content": "- Growth failure (old term \"[[104|failure to thrive]]\") is a descriptive sign, not a diagnosis - the underlying cause is [[214|malnutrition]] in nearly all cases\n- Common anthropometric criteria: weight-for-age below the 3rd-5th percentile, weight-for-length below the 5th percentile, or downward crossing of 2 or more major percentile lines\n- Also defined as no growth for 2 consecutive months if under age 6 months, or no growth for 3 consecutive months if over age 6 months\n- Affects mainly infants and toddlers, most sources scope it to children under 3-5 years of age\n- Prevalence is about 5-10% in Western primary care populations, roughly 8% by one estimate, with 1% of tertiary-center hospital admissions attributable to it\n- Traditionally split into organic (identifiable medical illness) and nonorganic/psychosocial causes; nonorganic causes account for up to 80% of cases and the two often coexist\n- Weight is affected earlier and more severely than length; head circumference is relatively spared until undernutrition is prolonged\n- WHO growth charts (not CDC) are used for children under 2 years - they flag fewer children as underweight\n- When correcting for prematurity, weight is adjusted until 24 months, head circumference until 18 months, and length/height until 40 months of age\n- Distinguished from constitutional growth delay, where weight and height dip in infancy, track along a lower percentile through childhood, then show a growth spurt in late adolescence reaching a normal adult height"
  },
  {
    "article_id": 248,
    "article_title": "Hearing Loss",
    "section_id": "9edea285cbaa4c818e8e6887fcfeb568",
    "section_title": "Evaluation and referral",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In a newborn who fails hearing screening (OAE and/or ABR), prompt referral is made to a multidisciplinary center for audiology, otolaryngology, and speech pathology evaluation and treatment; a genetics consultation is added, since roughly half of sensorineural hearing loss has a genetic etiology and genetics can clarify diagnosis, prognosis, and associated risks. If auditory neuropathy is suspected, ABR is the appropriate screening/diagnostic modality rather than OAE alone. For a child old enough to cooperate (generally by age 4), pure tone audiometry with air and bone conduction is obtained to characterize the type and degree of loss. Hearing testing is ordered in any child with [[378|language delay]], learning problems, or suspected hearing loss, including after episodes of [[4|acute otitis media]] or [[258|[[160|otitis media]] with effusion]], since the associated conductive loss (typically 15–40 dB, average ~27 dB) can otherwise go unrecognized and compound developmental risk. In counseling families, it is emphasized that intervention initiated within the birth-to-3-year window has the greatest capacity to prevent downstream speech, language, academic, and social-emotional consequences, and families are directed to family-facing resources (e.g., the AAP Early Hearing Detection and Intervention program, babyhearing.org) for education and support during the diagnostic and intervention process."
  },
  {
    "article_id": 250,
    "article_title": "Hypoxic-Ischemic Encephalopathy",
    "section_id": "e7d1df943f734f7b8de26677829cd672",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Therapeutic hypothermia has become the standard of care for moderate or severe neonatal HIE in the UK and many other countries and should be considered promptly once the diagnosis is suspected in an infant meeting perinatal-event, examination, Apgar, and blood-gas-acidosis criteria. Because much of the ultimate brain injury occurs during the secondary, reperfusion phase rather than the initial insult, early recognition and supportive stabilization matter: respiration is supported (these infants may be unable to sustain spontaneous respiration in severe disease), blood pressure/cardiac output is supported given the risk of myocardial dysfunction and hypotension, and the metabolic derangements that commonly accompany HIE — hypoglycemia, [[368|hypocalcemia]], and [[170|hyponatremia]] — are corrected. Seizures are monitored for and managed, and coexisting multi-organ dysfunction (renal failure, DIC, persistent pulmonary hypertension of the newborn) is evaluated for, since these commonly accompany severe encephalopathy. Staging severity (e.g., by the Levene system — consciousness, tone, presence/duration of seizures, ability to suck or sustain respiration) helps track clinical trajectory. Long-term follow-up is essential given the substantial risk of neurologic disability after moderate-to-severe HIE."
  },
  {
    "article_id": 251,
    "article_title": "Intimate Partner Violence",
    "section_id": "21bb8369346a49edaf228037eeaa1ba4",
    "section_title": "Approach when IPV is identified",
    "variant": "clinical",
    "imperatives": 2,
    "content": "When a screening tool is positive, privacy and safety are ensured before proceeding further — IPV is never discussed in front of the partner, and removing children from the room is considered. The circumstances are clarified. A reflect–empathize–teach–offer approach is used: what was heard is reflected back (\"It looks like you've had some tough experiences with your partner\"); blame is removed through empathy (\"The violence is not your fault. You do not deserve to be hurt this way.\"); why help matters is explained (violence usually continues and worsens, it is a crime, and children can be hurt emotionally and physically by exposure); and intervention is offered, connecting the patient with community resources and options. State-specific mandatory reporting rules are noted — in some states, a child's exposure to IPV is itself considered maltreatment and must be reported to CPS.\n\nFor an adolescent, IPV is screened for at every health visit given how common and under-disclosed it is, and the warning signs above (avoidance of primary care, frequent ED visits, unexplained injuries, an overly attentive partner) are actively looked for. Findings are documented thoroughly, including any injury without a consistent explanation or bruising at different stages of healing. When wounds are treated, poor healing and signs of infection are monitored for as medically indicated. Care is coordinated around identified [[94|mental health]] needs (depression, anxiety, PTSD symptoms) with therapy modalities shown to help, and social work/behavioral health and community domestic-violence resources are involved as part of the ongoing management and follow-up plan."
  },
  {
    "article_id": 252,
    "article_title": "Hepatitis B",
    "section_id": "6bc4cf90bcd14aeaad71a8027c4b3697",
    "section_title": "Perinatal and postexposure management at the bedside",
    "variant": "clinical",
    "imperatives": 1,
    "content": "For every newborn of an HBsAg-positive (or HBsAg-status-unknown) mother, hepatitis B vaccine is given within 12 hours of birth AND HBIG 0.5 mL IM at a different anatomic site, and the vaccine series is completed with doses 2 and 3 by 6 months of age. Breastfeeding initiation is not delayed to wait for immunization. The infant is tested for HBsAg and anti-HBs after completion of the series to confirm protection and rule out infection.\n\nFor a needlestick or other percutaneous/permucosal exposure, the exposed person's vaccination/response status and the source's HBsAg status are established first. For an unimmunized exposed person with an HBsAg-positive source, HBIG 0.06 mL/kg (max 5 mL) IM is given and the vaccine series is started. For an unimmunized person with an HBsAg-negative or untested/unknown source, the vaccine series is started alone. For someone previously immunized and known to have responded, no treatment is needed. For someone previously immunized but a documented inadequate responder (anti-HBs <10 mIU/mL) with an HBsAg-positive source, HBIG is given immediately, and either HBIG is repeated in 1 month or reimmunization is begun. After any acute infection, HBsAg and HBV DNA are rechecked several months later to confirm resolution rather than progression to chronic infection."
  },
  {
    "article_id": 253,
    "article_title": "Hypoplastic Left Heart Syndrome",
    "section_id": "f1d6a820bb1b46b3a63d440a06044cf7",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 3,
    "content": "HLHS is suspected in any neonate who develops sudden poor perfusion, cyanosis with a grayish hue, weakening pulses, or cardiogenic shock in the first days of life, particularly if antenatal ultrasound was not performed or was normal - the clinical deterioration typically coincides with ductal closure. Confirmation is made with echocardiography, looking for a small, apex-forming-failing left ventricle, aortic/mitral valve hypoplasia or atresia, a diminutive ascending aorta, and a left-to-right bowing, pressure-restrictive atrial septum.\n\nOnce suspected or confirmed, initial stabilization centers on maintaining ductal patency and balancing the pulmonary and systemic circuits. Ventilation is titrated to keep PCO2 around 45-50 mmHg, and supplemental oxygen is avoided when systemic saturation is running 70-80%, since oxygen acts as a pulmonary vasodilator and can divert flow away from the systemic circulation, worsening perfusion. If the atrial septum is restrictive on echo, escalation to catheter-based intervention follows - Rashkind balloon atrial septostomy, septal balloon dilation, or rarely blade septostomy - to relieve pulmonary venous congestion. Definitive care requires transfer to a center capable of staged single-ventricle surgical palliation."
  },
  {
    "article_id": 256,
    "article_title": "Osgood-Schlatter Disease",
    "section_id": "05fed3425ae846cc8086fede33438115",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Osgood-Schlatter disease is diagnosed clinically in an adolescent runner/jumper with gradual-onset pain and swelling localized to the tibial tubercle, worsened by quadriceps loading and relieved by rest - radiographs are not required but are reasonable if there is concern for an acute avulsion fracture, neoplasm, or if the presentation is atypical (e.g., acute onset with severe disability, which points instead toward a traumatic avulsion).\n\nTreatment starts with conservative, symptomatic measures: activity modification (reducing but not necessarily fully stopping sport, guided by symptom severity), NSAIDs for pain, ice after activity, and a protective pad over the tibial tubercle for athletes returning to contact or kneeling activities. Quadriceps and hamstring stretching and physical therapy are added. The family is counselled explicitly that this is self-limited but slow - resolution commonly takes 12-18 months and symptoms typically settle around age 14-15 as the tibial tubercle apophysis closes - so the goal is symptom control and continued function rather than a quick fix. Escalation to bracing/casting or surgical referral is reserved for the rare case with a suspected patellar tendon avulsion, rupture, or growth arrest with recurvatum deformity."
  },
  {
    "article_id": 257,
    "article_title": "Obesity",
    "section_id": "8660409bc69f448880523041839166e5",
    "section_title": "Management approach",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Severity is assessed using BMI percentile for age and sex together with the presence of current morbidities — a child with BMI above the 95th percentile, or above the 85th percentile with an obesity-related comorbidity (especially with a family history of such comorbidities), is considered to have severe obesity and is evaluated accordingly. The comorbidities associated with pediatric obesity are actively screened for: blood pressure is checked with an appropriately sized cuff, and evaluation is made for type 2 diabetes, dyslipidemia, nonalcoholic fatty liver disease, [[311|obstructive sleep apnea]], and orthopedic complaints as clinically indicated.\n\nCounseling is delivered as a family intervention rather than targeting the child alone: the plan is framed around small, sustainable changes in diet and physical activity, it is emphasized that these changes take time to produce visible results, and the fact that the whole family benefits from adopting a healthier lifestyle together is normalized. Patience and honesty with the family are maintained, and room is created to discuss the emotional and psychological aspects of weight, diet, and exercise, since stigma and psychological morbidity are recognized complications in their own right, particularly in severe obesity. For children with severe obesity who do not respond to behavioral and family-based measures, especially those with significant comorbidities, referral is made for consideration of metabolic and bariatric surgery."
  },
  {
    "article_id": 258,
    "article_title": "Otitis Media With Effusion",
    "section_id": "bbf416ffc54e4385abdf2a1ebe6f9c81",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "The diagnosis is confirmed with pneumatic otoscopy and tympanometry rather than treating empirically — decreased/immobile TM mobility (tympanometry type B) is sought without the acute inflammatory signs (otalgia, fever, red/bulging TM) that would instead point to AOM. Once OME is confirmed, antibiotics are not prescribed. In an otherwise healthy child with no risk factors, the appropriate initial step is watchful observation, since most OME clears spontaneously within about 3 months.\n\nIf effusion persists beyond 3 months, a hearing test is obtained; if it persists 3–6 months, or is bilateral, a hearing test is arranged and referral for ENT consultation is made, since untreated persistent effusion risks conductive [[248|hearing loss]] that can affect behavior and delay speech/language development. Prompt referral (rather than waiting through the usual observation period) is made for children who are otitis-prone or who carry additional risk for developmental impact — permanent hearing loss independent of OME, suspected or diagnosed speech/[[378|language delay]], [[117|autism spectrum disorder]] or other pervasive developmental disorders, Down syndrome or craniofacial disorders, blindness or uncorrectable [[343|visual impairment]], cleft palate, or developmental delay — since these children have less capacity to compensate for even mild, fluctuating hearing loss. When surgery is indicated, tympanostomy tube insertion is the preferred procedure; adenoidectomy is reserved for children with a separate indication such as nasal obstruction or chronic adenoiditis, and medical management of the mucosal disease is continued alongside any surgical intervention until the condition resolves."
  },
  {
    "article_id": 259,
    "article_title": "Patent Ductus Arteriosus",
    "section_id": "9058fb9c21014b5a9ee6975cfe05ba9d",
    "section_title": "Management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Not all PDAs require closure, and the optimal approach among conservative, prophylactic, and symptomatic treatment strategies remains unsettled given a paucity of large randomized trials. For asymptomatic or borderline cases, supportive/conservative management includes a thermoneutral environment, maintaining hematocrit above 35% (increases pulmonary vascular resistance), higher positive end-expiratory pressure with a shorter inspiratory time, and moderate fluid restriction (110–130 mL/kg/day). Loop diuretics are avoided, since they promote ductal patency via vasodilatory prostaglandin E2 release and add side effects; thiazide diuretics are used instead if a diuretic is needed. Watchful expectancy is reasonable for a hemodynamically significant PDA in an infant who remains on the ventilator beyond the first week of life, since prophylactic and symptomatic pharmacologic approaches are not clearly superior in this setting.\n\nFor medical closure, indomethacin 0.2 mg/kg IV every 12 hours for 3 doses closes a clinically significant ductus in about two-thirds of cases; if it reopens or fails to close fully, a second course can be given, or surgical ligation considered if the infant remains symptomatic. In extremely low-birth-weight infants (<1000 g) at very high risk for a symptomatic ductus, a prophylactic regimen of indomethacin 0.1 mg/kg every 24 hours for 3–5 days starting on day 1 of life may be used, which may reduce severe [[299|intraventricular hemorrhage]], though without demonstrated mortality or neurodevelopmental benefit. The most common side effect, transient oliguria, is managed with fluid restriction until urine output recovers; indomethacin is avoided if the infant is hyperkalemic or has a creatinine above 2 mg/dL. Ibuprofen and acetaminophen are alternative medical options used successfully in many cases. Catheter-based (percutaneous) PDA closure is increasingly favored for infants weighing more than 1 kg. Surgical ligation is reserved for infants who fail prior medical/catheter therapy and remain symptomatic, or when the ductus diameter exceeds 1.5–2 mm.\n\nIn full-term infants, the PDA is structurally different and indomethacin is usually ineffective — close monitoring is maintained and surgical ligation is considered at the earliest signs of significant [[285|congestive heart failure]]. Even without overt heart failure, ligation before age 1 year is recommended in full-term infants with a persistent PDA to prevent endocarditis and pulmonary hypertension."
  },
  {
    "article_id": 260,
    "article_title": "Patellofemoral Pain Syndrome",
    "section_id": "18f376c3e00c4d0f8fba7a166ac6a224",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "In an adolescent, especially a female athlete or runner, presenting with gradual-onset anterior/peripatellar knee pain worsened by stairs, squatting, running, or prolonged sitting with the knee flexed, and relieved by extension or walking, a focused exam is performed: a medially displaced patella, tenderness of the patellar articular surface with the knee extended, crepitus, and a positive patellar stress/compression test are checked for, while red flags that argue against PFPS are specifically looked for - significant effusion, true mechanical locking, or joint-line tenderness (which point toward a meniscal tear or other internal derangement warranting MRI rather than a PFPS diagnosis).\n\nIf the presentation is classic, treatment is empiric, without radiographs: ice, relative rest/activity modification, NSAIDs for pain, and referral to a physical therapy program targeting the quadriceps (with attention to vastus medialis strengthening), hamstrings, and hip abductors/external rotators. The patient is counselled on any recent training changes (volume, surface, footwear) that may have precipitated the episode, and these are addressed as part of the return-to-activity plan. Radiographs or further imaging are reserved for atypical presentations - significant swelling, mechanical symptoms, trauma, or failure to improve with a reasonable trial of conservative therapy."
  },
  {
    "article_id": 261,
    "article_title": "Pyelonephritis",
    "section_id": "129233a84b604ea7b28a50cd1f07c081",
    "section_title": "Diagnostics",
    "variant": "long",
    "imperatives": 1,
    "content": "A urinalysis and urine culture are obtained before antibiotics are started; in a child too young to provide a reliable clean-catch specimen, urine is collected via straight catheterization. Significant bacteriuria in infants and children is generally defined as at least 50,000 CFU/mL of a single urinary pathogen, with a transition zone of 10,000–100,000 CFU/mL where the likelihood of true pyelonephritis versus asymptomatic bacteriuria increases. Imaging is used selectively and sequenced to limit radiation exposure: renal ultrasonography detects hydronephrosis or bladder/urinary tract anomalies and can be performed even during acute treatment; a micturating cystourethrogram (VCUG) is used to diagnose and grade [[271|vesicoureteral reflux]] and define bladder/urethral anatomy, typically performed 2–4 weeks after UTI treatment; DMSA scintigraphy detects cortical renal scarring (regions of decreased uptake with loss of contour or cortical thinning) and is deferred 3–4 months after treatment specifically to distinguish permanent scarring from reversible acute pyelonephritic changes. On CT, pyelonephritis appears as foci of diminished cortical enhancement; on ultrasound, altered cortical echogenicity with adjacent perinephric fluid may be seen."
  },
  {
    "article_id": 261,
    "article_title": "Pyelonephritis",
    "section_id": "2714af07312c45f18e97439c9e0e7f79",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 1,
    "content": "- Pyelonephritis is upper [[8|urinary tract infection]] with renal parenchymal involvement; without parenchymal involvement the term pyelitis applies instead. It is the most common [[278|bacterial infection]] in febrile infants under 24 months without an obvious source.\n- Young children present atypically: vague abdominal discomfort rather than classic adult flank pain; fever may be the only sign. It is considered for a temperature ≥39°C (102.2°F) without another source lasting more than 48 hours in infants. Newborns may show only poor feeding, irritability, jaundice, or weight loss. All neonatal UTIs are considered pyelonephritis.\n- Higher-risk groups: infants younger than 6 months, females, uncircumcised males, and children with obstructive urologic abnormalities or bladder/bowel dysfunction.\n- On exam, pyelonephritis typically causes a high fever (≥39.4°C/103°F) with costovertebral angle tenderness on gentle percussion; urinalysis and culture are obtained before antibiotics are started, via straight catheterization if the child cannot provide a clean catch.\n- Significant bacteriuria in infants/children is generally defined as ≥50,000 CFU/mL of a single urinary pathogen (the transition range where pyelonephritis becomes more likely than asymptomatic bacteriuria is 10,000–100,000 CFU/mL).\n- Outpatient oral therapy: cephalexin or cefadroxil if tolerating PO. Inpatient IV therapy: ceftriaxone 50 mg/kg/day (max 2 g/day) or cefotaxime 150 mg/kg/day divided q8h (max 6 g/day), since most E. coli are ampicillin-resistant; ciprofloxacin (IV 18–30 mg/kg/day divided q8h, max 1.2 g/day, or oral 20–30 mg/kg/day divided q12h, max 1.5 g/day) is added if increased Pseudomonas risk; ampicillin 100 mg/kg/day divided q6h (max 4 g/day) is added if Enterococcus risk or gram-positive rods on Gram stain.\n- Standard treatment duration is 7 days, with up to 14 days considered if not improving after 3 days of therapy; transition to oral antibiotics occurs once clinically improved.\n- Imaging: renal ultrasound detects hydronephrosis/anatomic anomalies and can be done even during UTI treatment; micturating cystourethrogram (VCUG) for VUR diagnosis/grading is done 2–4 weeks after UTI treatment; DMSA scan for renal scarring is done 3–4 months after treatment to distinguish permanent scars from reversible acute changes.\n- Recurrent or unusual pyelonephritis with a renal mass, weight loss, and minimal urinary symptoms should raise concern for xanthogranulomatous pyelonephritis, associated with renal calculi, obstruction, and Proteus or E. coli infection, which usually requires total or partial nephrectomy."
  },
  {
    "article_id": 261,
    "article_title": "Pyelonephritis",
    "section_id": "0ebe1efb3a2947738921295c09efec93",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 3,
    "content": "Vital signs (including temperature and blood pressure) and weight are assessed, the abdomen is examined for tenderness or a mass, the costovertebral angle is gently percussed for tenderness, and the external genitalia are examined for anatomic anomalies or irritation. A urinalysis and culture are obtained before any antibiotic is given — straight catheterization is used if the child cannot give a reliable clean-catch sample — and bacteriuria of at least 50,000 CFU/mL of a single pathogen is treated as significant.\n\nTherapy is chosen by clinical severity and risk factors. If the child tolerates oral intake and has no complicating risk factors, oral cephalexin or cefadroxil is used. If the child needs inpatient IV therapy, ceftriaxone 50 mg/kg/day (max 2 g/day) or cefotaxime 150 mg/kg/day divided every 8 hours (max 6 g/day) is started — ampicillin alone is not relied on given high rates of E. coli resistance. IV ciprofloxacin 18–30 mg/kg/day divided q8h (max 1.2 g/day) is added for Pseudomonas risk (prior Pseudomonas UTI, chronic catheter, neurogenic bladder), and ampicillin 100 mg/kg/day divided q6h (max 4 g/day) is added empirically if there is an Enterococcus risk factor (GU instrumentation, renal anomaly) or gram-positive rods on Gram stain. Treatment is given for 7 days total, extending to as long as 14 days if the child has not improved by day 3, with a switch to oral therapy once clinically improving.\n\nFollow-up imaging is sequenced to answer specific questions while minimizing radiation: a renal ultrasound is obtained (even during acute treatment) to look for hydronephrosis or structural anomalies; if reflux is a concern, a VCUG is obtained 2–4 weeks after treatment completes; if scarring is a concern, a DMSA scan is obtained 3–4 months after treatment (not sooner, to avoid mistaking reversible acute changes for permanent scarring). If a child instead presents with a renal mass, weight loss, and minimal urinary symptoms, xanthogranulomatous pyelonephritis is considered and urology is involved, since this typically requires nephrectomy rather than antibiotics alone."
  },
  {
    "article_id": 262,
    "article_title": "Pyloric Stenosis",
    "section_id": "e969883b690946ad9a7b8ae469b4f8aa",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "In a 2-8-week-old infant with progressive, nonbilious, projectile vomiting who remains hungry after vomiting, examination is performed for an epigastric \"olive\" mass and visible peristaltic waves, and a basic metabolic panel is sent looking for hypochloremic, hypokalemic metabolic alkalosis. The diagnosis is confirmed with abdominal ultrasound (pyloric channel length >18 mm, wall thickness >4 mm per ACR criteria); if the study is negative or equivocal but suspicion remains high, it is repeated in about a week rather than ruling out the diagnosis on one negative scan.\n\nOnce confirmed, this is not a surgical emergency - stabilization comes first. Dehydration is corrected with isotonic fluids, and hypokalemia and metabolic alkalosis are specifically corrected before proceeding to the operating room, since anesthesia in an alkalotic, hypokalemic infant carries risk (including apnea). Once fluids and electrolytes are normalized, pyloromyotomy (open or laparoscopic) is arranged - it is curative with mortality under 0.5%. Advancement to full oral feeds occurs relatively quickly postoperatively per surgical team protocol. The differential is kept in mind if the clinical or lab picture doesn't fit cleanly: acidosis rather than alkalosis should prompt evaluation for adrenal insufficiency or an inborn error of metabolism rather than assuming pyloric stenosis."
  },
  {
    "article_id": 263,
    "article_title": "Tension Headache",
    "section_id": "156384a4e51249f4a86c389f6c020164",
    "section_title": "Approach at the bedside",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In a child or adolescent presenting with recurrent bilateral, dull, pressing headache that worsens through the day, is not aggravated by routine activity, and lacks significant nausea/vomiting or more than one of photophobia/phonophobia, the ICHD-3 frequency classification (infrequent episodic, frequent episodic, or chronic) is applied to characterize the headache and guide counseling and follow-up. Examination is performed specifically for pericranial muscle tenderness on palpation, which supports the diagnosis, and a careful history is taken for red flags that would point toward a secondary cause instead - progressive course, nausea/vomiting/ataxia/visual changes (concerning for a mass lesion), abnormal eye movements or focal weakness (concerning for hemorrhage), fever or meningeal signs (concerning for CNS infection), or a history of trauma.\n\nThe frequency and type of any headache medications being used are specifically asked about, since frequent use of simple analgesics, NSAIDs, triptans, or opioids can itself cause medication-overuse headache and should be addressed as part of management. If the headache began abruptly and has been present daily since within 3 days of onset, new daily persistent headache (NDPH) is considered rather than standard TTH, since this distinct entity is defined specifically by that abrupt onset pattern. Headache frequency is documented systematically at follow-up, since crossing the threshold of more than 15 days per month for 3 months redefines the headache as chronic and may change the management approach."
  },
  {
    "article_id": 264,
    "article_title": "Respiratory Failure",
    "section_id": "4762d91e11b3416582f7f8f61ab56eac",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 1,
    "content": "- Respiratory failure = oxygenation and/or ventilation insufficient to meet the body's metabolic demands; it is often the end stage of [[151|respiratory distress]] if not intercepted early.\n- Conceptually it results from a \"respiratory balance\" failure: ventilatory muscle power and central respiratory drive must overcome the respiratory load — failure occurs when muscle power/central drive falls and/or load rises enough that adequate ventilation cannot be sustained.\n- Formal criteria (2 clinical + 1 laboratory finding suggest respiratory failure): clinical — tachypnea/bradypnea/apnea/irregular respirations, pulsus paradoxus >30 mm Hg, stridor/wheeze/grunting, severe retractions with accessory muscle use, cyanosis in 40% O2, altered consciousness, weak/absent cough or gag, poor muscle tone; laboratory — PaO2 <60 mmHg in 60% O2, PaCO2 >60 mmHg and rising, pH <7.3.\n- Infants/toddlers are physiologically predisposed: proportionally large tongue, narrow subglottic airway, small/compliant airways, fewer alveoli, more compliant chest wall, more fatigable respiratory muscles, and an immature respiratory center.\n- Site of pathology predicts the physical exam pattern: extrathoracic airway obstruction produces stridor with markedly increased retractions; intrathoracic (extrapulmonary or intrapulmonary) obstruction produces wheezing; alveolar/interstitial disease produces grunting and crackles with the most severe tachypnea and retractions.\n- Etiologies span 5 categories: upper airway obstruction (adenotonsillar hypertrophy, choanal atresia, croup, [[331|epiglottitis]], foreign body, retropharyngeal abscess), lower airway obstruction ([[107|asthma]], [[3|bronchiolitis]], bacterial tracheitis), parenchymal lung disease (ARDS, aspiration, [[150|pneumonia]], pulmonary contusion), pulmonary edema (heart failure), neuromuscular weakness (botulism, Guillain-Barré, muscular dystrophy, [[332|spinal cord injury]], SMA), and thoracic mass effect (effusion/empyema, [[396|pneumothorax]], tumor, ascites).\n- Spirometry distinguishes restrictive from obstructive disease: both reduce FEV1 and vital capacity, but the FEV1/vital-capacity ratio stays normal in restrictive disease and falls in obstructive disease; obstructive disease also causes air trapping with elevated functional residual capacity and residual volume.\n- In [[184|cystic fibrosis]], about 90% of patients ultimately die of respiratory failure, often precipitated by a pulmonary exacerbation, hemoptysis, pneumothorax, or nonpulmonary surgery; noninvasive ventilation is increasingly used to rest respiratory muscles in this population.\n- Supplemental oxygen is given cautiously in chronic CO2 retainers (e.g., advanced CF), since it can suppress hypoxic ventilatory drive.\n- Acute respiratory failure from a severe infectious illness can be recovered from fully with aggressive treatment — intensive antibiotics, postural drainage, oxygen, and ventilatory support as needed continued for 1–2 weeks after the patient returns to baseline."
  },
  {
    "article_id": 265,
    "article_title": "Small For Gestational Age",
    "section_id": "c1b474a8481946de9ad31f1c18a7518c",
    "section_title": "Follow-up and management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "When an SGA infant is identified, investigation is made for the underlying category of cause — maternal, placental, or fetal — since this shapes counseling and follow-up; congenital (TORCH) infection and chromosomal/dysmorphic causes should be considered, particularly with symmetric growth restriction (weight, length, and head circumference all reduced together). All four anthropometric measures (weight, length, head circumference, ponderal index) are assessed rather than weight alone, since the pattern of restriction points toward different causes and prognoses.\n\n[[97|Neonatal hypoglycemia]] is screened for and monitored, since SGA infants are at particular risk through a primary glycogen storage deficit distinct from the mechanisms seen in AGA or LGA infants. For long-term growth, families are reassured that the majority of SGA children — 85–90% — catch up to their genetic height potential by age 4 years; for the minority who do not catch up spontaneously, growth hormone therapy has been shown to be of benefit and should be considered. When any child is later evaluated for [[103|short stature]], the pregnancy and delivery history is always reviewed, since an evaluation for short stature is considered incomplete without this context."
  },
  {
    "article_id": 267,
    "article_title": "Thermal Burns",
    "section_id": "dfe06d286c47492c9f0ca50e0b3ad854",
    "section_title": "In short",
    "variant": "short",
    "imperatives": 1,
    "content": "- Burns are classified by depth: first-degree (superficial, epidermis only — erythematous, painful, dry, heals within 2 weeks, no scarring); second-degree/partial-thickness (superficial: pink, moist, painful, heals <3 weeks; deep: paler, drier, less painful from nerve destruction, often speckled from thrombosed vessels, heals >3 weeks with scarring, may need grafting); third-degree/full-thickness (destroyed dermis, insensate, yellowish/depressed appearance).\n- Mechanisms: scalds (hot liquid/steam), contact (hot objects), flame, chemical (strong acid/alkali), and electrical.\n- Water-temperature/time-to-full-thickness-burn relationship: 120°F takes about 10 minutes, 130°F about 30 seconds, 140°F about 5 seconds, 150°F about 2 seconds, 158°F about 1 second — a normal child's withdrawal reflex from water above 120°F should leave only superficial fingertip/toe burns, so a full-thickness immersion burn is rarely accidental.\n- Fluid resuscitation for significant burns uses the Parkland formula: IV fluid (mL) = weight (kg) × %TBSA burned × 4; give half in the first 8 hours and the remaining half over the next 16 hours, in addition to maintenance fluids.\n- Burn center referral criteria: partial-thickness burns >10% TBSA, full-thickness burns >5% TBSA, any third-degree burn, electrical burns (high-tension wires or lightning), chemical burns, [[190|inhalation injury]] regardless of TBSA, burns of the face/hands/feet/perineum/genitals/major joints, inadequate home/social environment, suspected abuse or neglect, preexisting conditions complicating recovery, and associated injuries (e.g., fractures).\n- Prevention measures shown to help: flame-retardant clothing, smoke detectors, setting water heater thermostats to 48.9°C (120°F), and prohibiting cigarette smoking around children.\n- With dedicated burn-center care, survival of at least 80% is achievable even with burns covering 90% of total body surface area (TBSA) in children and young adults; death is more likely when irreversible anoxic brain injury occurred at the time of the burn.\n- Inhalation injury is assessed for with any thermal burn — exposure to toxic gases (carbon monoxide, hydrogen cyanide) and direct airway injury from high-temperature gas, steam, or hot liquid inhalation; for chemical burns, the causative agent is identified and irrigation is performed promptly, with ophthalmology consulted urgently for any chemical eye burn.\n- Cigarette burns are the most common thermal injury to the cornea in childhood, typically in 2-4 year olds, usually when a toddler runs into a cigarette held at eye level by an adult; the eyelid-closure reflex and Bell phenomenon usually limit corneal damage.\n- Emergency triage stratifies by severity: critical/resuscitation-room criteria include inhalational injury, [[142|altered mental status]], burns >25% TBSA, and facial burns with singed nasal hairs or hoarse voice; acute-level criteria include any full-thickness burn, partial-thickness burns >15% TBSA, and burns to the face or genitalia."
  },
  {
    "article_id": 267,
    "article_title": "Thermal Burns",
    "section_id": "f6a3209f02c947adb5df5101011e50e9",
    "section_title": "Initial management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "Burn depth and TBSA are estimated immediately, and assessment is made for [[190|inhalation injury]] (toxic gas exposure — carbon monoxide, hydrogen cyanide — and direct thermal airway injury) with any significant thermal burn, since this can dictate airway management ahead of the skin injury itself. For chemical burns or IV extravasation, the causative agent is identified and irrigation is performed promptly; ophthalmology is involved emergently for any chemical or thermal burn to the eye.\n\nIV fluid resuscitation is calculated using the Parkland formula for significant burns: fluid volume (mL) = weight (kg) × %TBSA burned × 4, with half given over the first 8 hours post-injury and the remainder over the next 16 hours, in addition to maintenance fluids. Triage proceeds by severity: the resuscitation room is used for inhalational injury, altered mental status, chest pain/arrhythmia, or major associated trauma; critical-level treatment is given for facial burns with singed nasal hairs or hoarse voice, burns over 25% TBSA, or electrical burns with loss of consciousness or seizure; acute-level treatment is given for any full-thickness burn, partial-thickness burns over 15% TBSA, or burns involving the face or genitalia.\n\nReferral to a dedicated burn center is made for partial-thickness burns over 10% TBSA, full-thickness burns over 5% TBSA, any third-degree burn, electrical burns from high-tension wires or lightning, chemical burns, any inhalation injury regardless of TBSA, burns involving the face, hands, feet, perineum, genitals, or major joints, burns in a child with a preexisting condition that could complicate recovery, associated injuries such as fractures, an inadequate home or social environment, or any suspicion of abuse or neglect — including immersion burns with a sharp demarcation line inconsistent with a normal withdrawal reflex. Burns are reassessed serially, since apparent depth can worsen with secondary infection, trauma, or hypoperfusion, and edema can initially mask a full-thickness injury as superficial."
  },
  {
    "article_id": 269,
    "article_title": "Tic Disorder",
    "section_id": "039a0eeae499461aa2aa7a4ab1976d72",
    "section_title": "Approach at the bedside",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In a school-age child brought in for repetitive blinking, sniffing, throat clearing, or similar movements, a history is taken focused on onset, waxing/waning course, suppressibility, presence of a premonitory urge, and whether both motor and vocal tics are present and for how long - this determines whether the picture fits transient tic disorder (4 weeks to 1 year), chronic tic disorder (motor or vocal, >1 year), or Tourette syndrome (both motor and vocal, >1 year). A neurologic exam is performed, which should be normal aside from the tics; neuroimaging is not indicated for a typical presentation.\n\nScreening for common comorbidities is performed specifically at the same visit - ADHD and OCD are present in about half of Tourette syndrome patients, and anxiety, depression, and learning difficulties are also common - since these comorbidities, not tic severity itself, are usually the bigger driver of functional impairment and should be actively treated. For most children with mild tics and no significant distress, reassurance and education alone are appropriate; over-medicalizing a transient, self-limited presentation is avoided. If tics are causing meaningful distress or impairment, an alpha-2 agonist (clonidine or guanfacine) is used as first-line pharmacotherapy, paired with behavioral therapy. If a child on stimulant medication for ADHD develops new tics, the family is reassured that this reflects unmasking of an underlying predisposition rather than a medication-caused tic disorder - this is a common point of parental concern worth addressing directly."
  },
  {
    "article_id": 270,
    "article_title": "Type 1 Diabetes",
    "section_id": "b5a3a1be841e4c40b9745701aaf79468",
    "section_title": "Approach at diagnosis and initial management",
    "variant": "clinical",
    "imperatives": 1,
    "content": "In a child presenting with polydipsia, polyuria, and weight loss (with or without overweight/obesity - obesity does not rule out T1D), the diagnosis is confirmed using ADA criteria: fasting glucose ≥126 mg/dL, 2-hour OGTT glucose ≥200 mg/dL, random glucose ≥200 mg/dL with classic symptoms, or HbA1c ≥6.5%. DKA is assessed for at presentation given its associated morbidity and mortality, and ketosis alone does not distinguish T1D from type 2 diabetes - about a third of adolescents ultimately diagnosed with type 2 diabetes present with ketones and about 6% present in DKA. If the type of diabetes is unclear (e.g., an overweight or obese adolescent with new hyperglycemia), pancreatic autoantibodies (islet cell antigen 512, insulin, GAD, ZnT8) are sent to help confirm an autoimmune process, and monogenic diabetes is kept on the differential if there is an autosomal dominant family history, early onset, non-obese phenotype, or preserved C-peptide.\n\nOnce T1D is confirmed, insulin therapy is initiated - either a basal-bolus regimen (long-acting basal insulin such as glargine or detemir, plus short-acting boluses for meals and correction) or an insulin pump - alongside structured diabetes education covering nutrition, exercise, and self-monitoring of blood glucose. If the family is using a fixed-dose (non-analog basal) regimen, counseling covers eating at consistent times aligned with the insulin's peak action; if using a pump or long-acting basal analog, more flexible meal timing is possible. The long-term treatment target of HbA1c below 6.5% (48 mmol/mol) is set to reduce the risk of long-term vascular complications, and a team approach (medical, nutritional, and psychosocial support) is built given the lifelong self-management burden T1D places on the child and family."
  },
  {
    "article_id": 271,
    "article_title": "Vesicoureteral Reflux",
    "section_id": "4c60fc5385d6448e9ad6e31f263f7f22",
    "section_title": "Approach at the bedside",
    "variant": "clinical",
    "imperatives": 4,
    "content": "VUR is suspected in a child presenting with a febrile urinary tract infection (especially a girl, given the roughly 30% prevalence of VUR in this group) or in an infant found to have antenatal hydronephrosis (5-15% will have VUR). Confirmation and grading are made with a voiding cystourethrogram, using the International Reflux Study grading system (I-V) to communicate severity, and a radionuclide cystogram is considered for lower-radiation follow-up imaging once the initial diagnosis and anatomy are established.\n\nFor most children, particularly those with lower-grade reflux diagnosed at a younger age, a reasonable approach is expectant management: antibiotic prophylaxis to reduce febrile UTI risk while spontaneous resolution is watched for, which occurs in about 80% of primary VUR cases as the ureterovesical junction matures. Surgical correction (open or endoscopic) is reserved for higher-grade reflux, breakthrough febrile infections despite prophylaxis, or reflux that persists without improvement over serial follow-up. Families are counselled that the goal of management is preventing recurrent [[261|pyelonephritis]] and renal scarring - since scarring, not the reflux itself, is what drives the downstream risk of hypertension and [[284|chronic kidney disease]] - so prompt treatment of any febrile UTI in a child with known VUR is a priority regardless of which management strategy (prophylaxis vs. surgery) is chosen."
  },
  {
    "article_id": 272,
    "article_title": "Traumatic Brain Injury",
    "section_id": "9544cd74a3f846039cad8640b43daa89",
    "section_title": "Management at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Any patient with altered memory, alertness, irritability, new seizures, or unexplained poor feeding/emesis after a plausible mechanism is treated as having possible TBI until proven otherwise. The systemic factors that drive secondary injury are identified and corrected as a priority — hypoxia, hypotension, hypoglycemia, and hyperthermia — since these are directly actionable and worsen brain injury independent of the primary insult. The Cushing triad (bradycardia, hypertension, apnea) is not relied on to recognize rising intracranial pressure, since it appears late and is often incomplete; nonspecific changes in mental status are treated as a possible early warning sign instead.\n\nFollow-up imaging is obtained within 12 hours of presentation in a child with an identified traumatic intracranial injury, specifically to catch progression of contusion/hemorrhage and early radiographic signs of worsening cerebral edema (sulcal effacement at the vertex, smaller basal cisterns) before clinical deterioration occurs — by the time clinical signs of herniation or rising ICP appear, the window to interrupt progressive injury has narrowed considerably. For severe TBI requiring ICU-level care, tiered guideline-based management is followed: systemic derangements are corrected first, and escalation to second-tier therapies for refractory intracranial hypertension occurs only when first-tier measures are inadequate, with advanced monitoring used to guide these interventions when available.\n\nWhen evaluating any infant or young child with TBI, especially with a mechanism that seems inconsistent with the severity of injury, an ophthalmologic exam for retinal hemorrhages and a skeletal survey for occult fractures are added to evaluate for inflicted injury, and child protective services and law enforcement are involved promptly if abuse is suspected — outcomes tend to be worse in this population, and early recognition protects both the current patient and any siblings. On longer-term follow-up, growth is monitored and screening is performed for hypopituitarism symptoms in children recovering from significant TBI, since endocrine dysfunction can emerge post-injury and may improve substantially after the first year if identified and managed."
  },
  {
    "article_id": 273,
    "article_title": "Acute Gastroenteritis",
    "section_id": "ddb4ab6e20fe46d4bddddbc372b5a974",
    "section_title": "Approach at the bedside",
    "variant": "clinical",
    "imperatives": 2,
    "content": "In a child presenting with vomiting and/or three or more loose stools per day, the central clinical task is assessing the degree of dehydration, since this - not the specific pathogen - drives management decisions and correlates with illness severity; hydration status is reassessed at follow-up to confirm rehydration efforts are working. For a well-appearing child with a typical, self-limited-appearing presentation (fever, crampy pain, watery diarrhea, hyperactive bowel sounds, no blood), no laboratory testing is routinely needed and supportive care with attention to rehydration is appropriate.\n\nFeatures that should prompt reconsideration of a bacterial cause and possibly further workup are specifically looked for: hematochezia, high fever in an older child, or recent international travel to a developing country. Recent shellfish consumption is asked about if the presentation is unusual or severe, since this points to Vibrio, particularly in a patient with underlying liver disease, low gastric acidity, or [[122|immunodeficiency]] who would be more susceptible. Persistent high fever and lethargy are red flags for more severe or systemic illness rather than routine viral AGE and warrant closer evaluation. Families are counselled on the expected self-limited course of viral AGE, the importance of monitoring hydration status at home, and when to seek reassessment (worsening dehydration, persistent high fever, lethargy, or blood in the stool)."
  },
  {
    "article_id": 275,
    "article_title": "Achondroplasia",
    "section_id": "22f26ea0dd2f4e9da15230ef74462968",
    "section_title": "Health supervision and monitoring",
    "variant": "clinical",
    "imperatives": 2,
    "content": "Children with achondroplasia require structured, condition-specific health supervision rather than standard well-child monitoring alone, per American Academy of Pediatrics guidance developed and twice revised specifically for this population. Achondroplasia-specific growth curves are used rather than standard population curves to track height, weight, and head circumference, and weight-for-height is monitored carefully given how common and disabling obesity becomes in older children with this condition.\n\nProactive screening is performed for the serious but less common complications rather than waiting for symptoms: infants are assessed for risk of cervicomedullary-junction compression, since this is a recognized cause of increased infant mortality in achondroplasia; hydrocephalus is monitored for; and the thoracolumbar spine is evaluated for kyphosis, with positioning guidance intervening early since fixed, angular kyphosis is considered probably preventable if caught before it becomes structural (most infantile gibbus resolves spontaneously by walking age without intervention). [[311|Obstructive sleep apnea]] and, less commonly, central sleep apnea are screened for, and hearing screening is arranged given the frequency of middle-ear dysfunction and associated [[248|hearing loss]] in this population. If surgery is needed for any reason, a team experienced in the specific perioperative considerations for skeletal dysplasia is involved, given the airway and cervicomedullary risks described above. Families are reassured that cognitive development and life expectancy are generally normal, while being clear and proactive about the orthopedic, respiratory, and neurologic surveillance this condition specifically requires."
  }
]