Tickets details
What kind of tickets do you mean?
- Travel or flight tickets
- Event or concert tickets
- Support or service tickets
- Ticket booking details you want me to organize
Rickets
Reading File
Finding Sources
Searching PubMed
rickets AND treatment
Searching the Web
WHO rickets vitamin D calcium diagnosis treatment children guideline
Rickets is a childhood disorder in which growing bones do not mineralize properly, causing soft, weak bones and possible deformities.
- Most common cause: vitamin D deficiency and/or too little calcium intake.
- Signs: delayed growth, bone pain, muscle weakness, widened wrists/ankles, bowed legs, frontal bossing, or a “rachitic rosary” along the ribs.
- Diagnosis: clinical assessment, blood tests such as calcium, phosphate, alkaline phosphatase and 25-hydroxyvitamin D, plus X-rays of the wrist or knee.
- Treatment: depends on the cause. Nutritional rickets is generally treated with vitamin D plus adequate calcium, while renal, genetic, or phosphate-wasting rickets needs specialist-directed treatment. The global consensus guidance recommends vitamin D with calcium for nutritional rickets, but children should be assessed before treatment because the correct regimen varies by age and cause.
If this concerns a child with seizures, severe weakness, difficulty breathing, or painful fractures, seek urgent medical care.
Mbbs theory
Reading File
Finding Sources
Finding Sources
Searching PubMed
rickets AND treatment
Searching the Web
Global Consensus Recommendations Prevention Management Nutritional Rickets diagnosis treatment calcium 500 mg vitamin D 2000 IU
Searching Images
rickets wrist radiograph metaphyseal cupping fraying widening
Educational composite image illustrating the clinical and radiological manifestations of nutritional rickets and subsequent recovery. The top panel features a pediatric growth chart (Birth to 36 months) documenting length and weight percentiles. It shows an initial period of growth failure followed by significant catch-up growth following therapeutic intervention with vitamin D and calcium. The bottom-left panel is a diagnostic radiograph of a pediatric hand and wrist, demonstrating classic rachitic changes including metaphyseal fraying and cupping of the distal radius and ulna, along with similar fraying at the distal aspects of the second through fifth metacarpals. The bottom-right panel displays a radiograph of the lower extremities, showing bilateral metaphyseal widening, cupping, and fraying at the distal femurs and proximal/distal tibiae. These findings are characteristic of impaired mineralization at the growth plates. The material serves as an educational resource for pediatric endocrinology and radiology, focusing on the diagnosis of metabolic bone disease and the monitoring of treatment efficacy in nutritional rickets.
Anteroposterior (AP) pediatric wrist radiograph demonstrating classic radiological signs of rickets, specifically metabolic bone disease of prematurity (MBDP). The primary findings are located at the distal metaphyses of the radius and ulna. These include significant metaphyseal widening (splaying), fraying (loss of sharp cortical definition), and cupping of the metaphyseal margins. The growth plates (physes) appear abnormally widened. The carpal centers are not yet ossified, consistent with neonatal or early infant developmental age. These skeletal changes reflect inadequate mineralization of the osteoid at the zone of provisional calcification. The image serves as a key diagnostic reference for identifying rickets-like changes in a clinical pediatric or neonatal setting.
This composite figure presents clinical and radiological findings in a pediatric patient with Hereditary Vitamin D-Resistant Rickets (HVDRR). The left panel is a clinical photograph of an infant showing near-total alopecia, a hallmark feature of certain VDR gene mutations. Panels (a) and (b) are diagnostic radiographs of the wrist and distal forearm. Radiograph (a) demonstrates classic baseline rachitic changes, including significant cupping, fraying, and widening of the distal radial and ulnar metaphyses, alongside generalized osteopenia and an obscured provisional zone of calcification. Radiograph (b) shows the same anatomical region following medical management with high-dose calcitriol, calcium, and cinacalcet. This follow-up image exhibits marked interval improvement, characterized by increased bone density (remineralization) and a significant reduction in metaphyseal fraying and cupping, indicating partial healing of the skeletal rickets. The series serves as an educational comparison of disease manifestation and therapeutic response in metabolic bone disease.
Reading File
Reading File
Reading File
Reading Web Page
https://pmc.ncbi.nlm.nih.gov/articles/PMC4880117
Rickets
Definition
Rickets is a disorder of the growing skeleton in children caused by defective mineralization of osteoid and the growth plate. It leads to soft bones, growth failure, skeletal deformity, and muscle weakness.
The corresponding disorder after epiphyseal closure in adults is called osteomalacia. The usual underlying abnormalities are vitamin D deficiency or phosphate depletion. Tietz Textbook of Laboratory Medicine, 7th Edition, p. 2195.
Etiology
1. Nutritional rickets, most common
- Vitamin D deficiency
- Inadequate dietary calcium intake
- Limited sunlight exposure
- Exclusive breast-feeding without vitamin D supplementation in an at-risk infant
2. Defective vitamin D absorption or metabolism
- Malabsorption: celiac disease, chronic diarrhea, pancreatic insufficiency
- Chronic liver disease
- Chronic kidney disease, with impaired formation of active vitamin D
- Drugs increasing vitamin D metabolism, for example anticonvulsants
3. Vitamin D dependent or resistant rickets
- Vitamin D-dependent rickets type 1: deficiency of renal 1-alpha-hydroxylase, CYP27B1 mutation
- Vitamin D-dependent rickets type 2: vitamin D receptor resistance
- X-linked hypophosphatemic rickets: renal phosphate wasting, commonly due to a PHEX mutation
4. Other phosphate-wasting states
- Renal tubular acidosis
- Fanconi syndrome
- Hereditary hypophosphatemic rickets
- Tumor-induced phosphate wasting, rare in children
Causes include vitamin D deficiency, calcium deficiency, hypophosphatemia, Fanconi syndrome, malabsorption, renal tubular acidosis, and inherited vitamin D or phosphate disorders. Rheumatology, 2-Volume Set, Box 204.1, p. 204.
Pathogenesis of nutritional rickets
- Vitamin D deficiency or low calcium intake reduces intestinal calcium absorption.
- Serum calcium is initially maintained by increased parathyroid hormone, PTH.
- PTH increases bone resorption and urinary phosphate loss.
- Hypophosphatemia and inadequate calcium-phosphate product prevent mineralization of osteoid and the growth plate.
- The growing metaphyses become widened, irregular, cupped, and frayed.
- Weight bearing on soft bones produces deformities such as bow legs or knock knees.
Clinical features
General
- Irritability, sweating, poor growth
- Delayed motor milestones
- Hypotonia and proximal muscle weakness
- Bone pain, especially in lower limbs
- Growth retardation and short stature
Skull
- Craniotabes, soft occipital or parietal bones
- Frontal bossing
- Delayed closure of anterior fontanelle
- Delayed dentition and enamel defects
Chest
- Rachitic rosary: prominent costochondral junctions
- Harrison sulcus
- Pigeon chest deformity
Limbs
- Widening of wrist and ankle
- Bow legs, genu varum, or knock knees, genu valgum
- Coxa vara
- Bone tenderness
- Pathological fractures may occur in severe disease
Spine and pelvis
- Kyphosis or scoliosis
- Pelvic deformity in longstanding disease
Neuromuscular manifestations of hypocalcemia
- Tetany
- Carpopedal spasm
- Seizures
- Laryngospasm, rarely
Orthopedic descriptions include short stature, varus limb angulation, bone pain, rachitic rosary, bowing of long bones, ligamentous laxity, and dorsal kyphosis. Miller’s Review of Orthopaedics, 9th Edition, p. 322.
Investigations
Biochemical tests
| Test | Typical nutritional vitamin D-deficiency rickets |
|---|---|
| Serum calcium | Normal or low |
| Serum phosphate | Low |
| Alkaline phosphatase, ALP | Markedly raised |
| 25-hydroxyvitamin D | Low |
| Parathyroid hormone, PTH | Raised |
| Serum magnesium | May be low |
| Renal function, liver function | To identify secondary causes |
If hypophosphatemia persists despite adequate vitamin D status, evaluate for renal phosphate wasting. Useful tests include urinary phosphate, tubular maximum phosphate reabsorption, renal function, acid-base status, and, where appropriate, FGF-23 and genetic testing.
X-ray findings
X-ray of the wrist and knee is most useful.
- Generalized osteopenia
- Widening of growth plate
- Metaphyseal cupping, fraying, and splaying
- Delayed ossification of epiphyses
- Bowing of long bones
- Looser zones or pseudofractures in severe disease
Classic radiographic findings include physeal cupping and widening, long-bone bowing, and Looser lines. Miller’s Review of Orthopaedics, 9th Edition, p. 322.
Differential diagnosis
- Physiological genu varum or genu valgum
- Blount disease
- Skeletal dysplasia
- Osteogenesis imperfecta
- Hypophosphatasia
- Renal osteodystrophy
- Hypophosphatemic rickets
- Metaphyseal dysplasia
Management
A. Nutritional rickets
Treat with vitamin D plus adequate calcium, not vitamin D alone.
A commonly cited consensus approach is:
| Age | Vitamin D daily for 90 days | Maintenance |
|---|---|---|
| <3 months | 2,000 IU/day | 400 IU/day |
| 3-12 months | 2,000 IU/day | 400 IU/day |
| 1-12 years | 3,000-6,000 IU/day | 600 IU/day |
| >12 years | 6,000 IU/day | 600 IU/day |
- Ensure calcium intake of about 500 mg/day through diet or supplementation in most children with nutritional rickets.
- Oral treatment is generally preferred.
- Reassess clinical status, calcium, phosphate, ALP, and vitamin D response after about 3 months.
- Continue maintenance vitamin D and improve dietary calcium intake.
The global rickets consensus recommends at least 2,000 IU/day vitamin D for at least 3 months with calcium intake or supplementation, and age-specific higher doses for older children.
B. Treat the specific cause
- Chronic kidney disease: active vitamin D analogues, phosphate management, and renal specialist care.
- Vitamin D-dependent rickets: calcitriol or alfacalcidol with calcium, under pediatric endocrinology supervision.
- Hypophosphatemic rickets: phosphate replacement plus active vitamin D, or targeted therapy such as burosumab in selected X-linked hypophosphatemia cases.
- Malabsorption or liver disease: higher or modified vitamin D treatment and management of the underlying illness.
C. Orthopedic care
- Most deformities improve after medical correction if treatment is early.
- Bracing is usually not required for early, mild deformity.
- Persistent severe deformity after metabolic healing may need guided growth or corrective osteotomy.
Prevention
- Promote adequate maternal vitamin D and calcium nutrition.
- Exclusive breast-fed infants should receive routine vitamin D supplementation according to local pediatric guidance.
- Ensure age-appropriate dietary calcium.
- Encourage safe sunlight exposure where appropriate.
- Screen high-risk groups: darker skin, low sun exposure, malabsorption, chronic liver or kidney disease, anticonvulsant therapy, and poor dietary intake.
MBBS exam conclusion
Rickets is a preventable metabolic bone disease of childhood, most often due to vitamin D deficiency and/or low calcium intake. Early recognition through clinical signs, biochemical testing, and wrist X-ray permits effective treatment and prevents permanent skeletal deformity.
Bronchitis and litis
Reading File
Finding Sources
Finding Sources
Searching PubMed
acute bronchitis AND management
Searching the Web
acute bronchitis acute laryngitis adult management antibiotics guideline CDC
Bronchitis and Laryngitis - MBBS Theory Notes
1. Acute Bronchitis
Definition
Acute bronchitis is an acute inflammation of the large airways (bronchi), usually caused by a viral respiratory infection, with cough but without pneumonia.
Etiology
Viral causes, most common:
- Influenza virus
- Parainfluenza virus
- Rhinovirus
- Coronavirus
- RSV
- Adenovirus
Less common bacterial causes:
- Mycoplasma pneumoniae
- Chlamydophila pneumoniae
- Bordetella pertussis
Clinical features
- Cough, initially dry and later with sputum
- Cough usually lasts 1-3 weeks and may persist up to 4 weeks
- Low-grade fever
- Malaise, sore throat, coryza
- Chest discomfort or burning sensation
- Rhonchi or wheeze may be heard
- Mild dyspnea can occur
Important: Yellow or green sputum alone does not prove bacterial infection.
Diagnosis
It is mainly a clinical diagnosis. Rule out pneumonia, asthma exacerbation, COPD exacerbation, COVID-19, and pertussis.
Chest X-ray is considered if pneumonia is suspected, for example:
- Fever 38°C or more
- Respiratory rate 24/min or more
- Pulse 100/min or more
- Focal crepitations, bronchial breathing, or signs of consolidation
- Elderly, immunocompromised, or seriously ill patient
Treatment
- Rest and adequate fluids
- Antipyretic or analgesic: paracetamol
- Honey may help cough in children over 1 year and adults
- Short-term bronchodilator only if wheeze or bronchospasm is present
- Antitussives may be used selectively for troublesome dry cough
Antibiotics are not routinely indicated, because most cases are viral. They may be considered when pertussis is suspected or there is evidence of a specific bacterial infection. The CDC outpatient guidance advises against routine antibiotics for uncomplicated acute bronchitis.
Complications
- Secondary bacterial pneumonia, uncommon
- Exacerbation of asthma or COPD
- Persistent post-infectious cough
2. Laryngitis
Definition
Laryngitis is inflammation of the larynx, including the vocal cords, leading mainly to hoarseness or loss of voice.
Types
- Acute laryngitis
- Chronic laryngitis
Causes
Acute laryngitis
- Viral upper respiratory infection, most common
- Excessive voice use or shouting
- Smoking and inhaled irritants
- Gastroesophageal reflux
- Rarely bacterial or fungal infection
Chronic laryngitis
Symptoms persisting for more than 3 weeks suggest chronic laryngitis. Causes include:
- Smoking
- Chronic voice abuse
- Laryngopharyngeal reflux
- Chronic sinus or respiratory infection
- Tuberculosis, fungal infection, or syphilis, less common
- Laryngeal malignancy, especially in smokers
Clinical features
- Hoarseness of voice
- Aphonia, loss of voice
- Sore throat or throat irritation
- Dry cough
- Frequent throat clearing
- Pain on speaking
- Low-grade fever and coryza in viral cases
Diagnosis
Usually clinical.
Laryngoscopy is indicated if:
- Hoarseness persists beyond 3 weeks
- Recurrent episodes occur
- There is smoking history
- Dysphagia, neck mass, hemoptysis, weight loss, or ear pain is present
- Malignancy or vocal-cord lesion is suspected
Management
Acute laryngitis
- Voice rest: avoid shouting and whispering
- Warm fluids and hydration
- Avoid smoking, alcohol, dust, and irritants
- Steam or humidification may provide symptomatic relief
- Treat reflux if present
- Paracetamol or NSAID for pain and fever, when appropriate
Routine antibiotics are generally not indicated because acute laryngitis is usually viral. A Cochrane review found no meaningful objective benefit that would justify routine antibiotic use.
Chronic laryngitis
- Stop smoking
- Voice hygiene and speech therapy when indicated
- Treat reflux disease
- Investigate persistent hoarseness with laryngoscopy
- Treat specific infections or lesions according to the cause
Differences between acute bronchitis and laryngitis
| Feature | Acute bronchitis | Acute laryngitis |
|---|---|---|
| Site | Bronchi | Larynx and vocal cords |
| Main symptom | Cough | Hoarseness |
| Sputum | May be present | Usually absent or minimal |
| Voice change | Usually absent | Characteristic |
| Common cause | Viral lower respiratory infection | Viral upper respiratory infection or voice strain |
| Main treatment | Supportive cough care | Voice rest and supportive care |
| Antibiotics | Usually not required | Usually not required |
Red-flag symptoms
Urgent assessment is needed for stridor, difficulty breathing, cyanosis, high fever with toxicity, coughing blood, chest pain, confusion, inability to swallow saliva, or persistent hoarseness with weight loss or neck swelling.
Bronchiolitis
Reading File
Finding Sources
Finding Sources
Searching PubMed
bronchiolitis AND treatment
Searching the Web
NICE bronchiolitis children diagnosis management oxygen hydration no antibiotics bronchodilators guideline
Searching Images
infant bronchiolitis chest radiograph hyperinflation peribronchial thickening
Bronchiolitis - MBBS Theory Notes
Definition
Acute bronchiolitis is an acute viral infection of the small airways, bronchioles, causing inflammation, edema, increased mucus secretion, and bronchiolar obstruction. It occurs mainly in children below 2 years, especially infants.
Etiology
Common viral causes
- Respiratory syncytial virus, RSV - most common
- Rhinovirus
- Parainfluenza virus
- Influenza virus
- Adenovirus
- Human metapneumovirus
- Coronavirus
Transmission occurs through respiratory droplets, contact with secretions, and contaminated hands or surfaces.
Risk factors for severe disease
- Age less than 3 months
- Prematurity
- Congenital heart disease
- Chronic lung disease of prematurity
- Neuromuscular disease
- Immunodeficiency
- Poor feeding or dehydration
- Exposure to tobacco smoke
Pathogenesis
- Virus infects bronchiolar epithelial cells.
- There is epithelial necrosis, edema of the bronchiolar wall, mucus hypersecretion, and cellular debris.
- Narrow infant bronchioles become partially or completely obstructed.
- Partial obstruction produces air trapping and hyperinflation.
- Complete obstruction may lead to atelectasis.
- The child develops tachypnea, wheeze, crackles, increased work of breathing, and hypoxemia.
Clinical features
Typical progression
Initially, the infant has symptoms of an upper respiratory infection for 1-3 days:
- Rhinorrhea
- Nasal blockage
- Mild fever
- Cough
- Poor feeding
This is followed by lower respiratory symptoms:
- Tachypnea
- Wheeze
- Fine inspiratory crackles
- Chest retractions
- Nasal flaring
- Grunting
- Difficulty feeding
- Apnea, especially in young or premature infants
- Cyanosis in severe disease
Physical examination
- Tachypnea
- Subcostal and intercostal retractions
- Hyperinflated chest
- Diffuse wheeze
- Fine crackles
- Prolonged expiration
- Reduced air entry in severe disease
- Signs of dehydration
Diagnosis
Bronchiolitis is primarily a clinical diagnosis in a child under 2 years with coryza followed by cough, tachypnea, wheeze or crackles, and respiratory distress.
Investigations
Routine tests are not needed in typical mild bronchiolitis.
Investigations may be required in severe, atypical, or hospitalized cases:
| Investigation | Finding or purpose |
|---|---|
| Pulse oximetry | Detect hypoxemia |
| Chest X-ray | Not routine. May show hyperinflation, peribronchial thickening, patchy atelectasis |
| Viral testing | Usually not required, may help cohort hospitalized patients |
| Blood gas | Severe respiratory distress, suspected respiratory failure |
| CBC, CRP, blood culture | Only if bacterial infection or sepsis is suspected |
Chest X-ray changes can resemble pneumonia, so X-ray should not be routinely obtained in uncomplicated bronchiolitis.
Severity assessment
Features suggesting severe bronchiolitis
- Apnea
- Cyanosis
- Severe chest recession, grunting, or exhaustion
- Respiratory rate more than 70/min
- Inability to feed or markedly reduced intake
- Clinical dehydration
- Persistent oxygen saturation below local threshold, commonly <90-92%
- Altered sensorium or poor responsiveness
Management
A. Mild disease - home care
- Nasal saline drops and gentle suction if nasal secretions interfere with feeding
- Continue breastfeeds or give small frequent feeds
- Maintain hydration
- Antipyretics such as paracetamol for fever or discomfort
- Avoid tobacco smoke exposure
- Educate parents about danger signs and when to return
B. Indications for hospital admission
- Apnea or a history of apnea
- Significant respiratory distress
- Hypoxemia
- Inadequate oral intake or dehydration
- Young infant, especially under 3 months
- Prematurity or serious comorbidity
- Caregiver unable to safely observe the child at home
C. Hospital management
Treatment is mainly supportive:
- Oxygen for persistent hypoxemia
- Nasal suction when secretions impair breathing or feeding
- Nasogastric fluids or intravenous fluids if oral intake is inadequate
- High-flow nasal oxygen or CPAP for worsening respiratory distress
- Mechanical ventilation if impending or established respiratory failure
The NICE bronchiolitis guideline provides current recommendations for assessment, oxygen thresholds, admission, and discharge decisions.
Treatments not routinely recommended
The following are generally not used routinely in typical bronchiolitis:
- Antibiotics, unless bacterial infection is suspected
- Salbutamol or other bronchodilators
- Nebulized adrenaline
- Corticosteroids
- Chest physiotherapy
- Hypertonic saline in routine emergency treatment
- Montelukast
Beta-adrenergic agents and nebulized epinephrine are not recommended for routine RSV bronchiolitis management. Red Book 2021: Report of the Committee on Infectious Diseases, RSV section.
Complications
- Apnea
- Respiratory failure
- Dehydration
- Secondary bacterial infection, uncommon
- Atelectasis
- Rarely, pneumothorax
- Recurrent wheeze after an episode, though bronchiolitis itself does not equal asthma
Differential diagnosis
- Bronchial asthma or viral-induced wheeze
- Pneumonia
- Foreign body aspiration
- Congestive cardiac failure
- Pertussis
- Congenital heart disease
- Sepsis
- Gastroesophageal reflux with aspiration
Bronchiolitis versus bronchitis
| Feature | Bronchiolitis | Acute bronchitis |
|---|---|---|
| Main site affected | Bronchioles, small airways | Bronchi, large airways |
| Usual age group | Infants and children <2 years | Older children and adults |
| Common cause | RSV and other respiratory viruses | Usually respiratory viruses |
| Main symptoms | Tachypnea, wheeze, crackles, retractions, feeding difficulty | Cough, sputum, mild fever |
| Treatment | Supportive care, oxygen/fluids if required | Symptomatic treatment |
| Antibiotics | Usually not indicated | Usually not indicated |
Short exam answer
Bronchiolitis is an acute viral lower respiratory tract infection affecting bronchioles, predominantly in infants below 2 years. RSV is the commonest cause. The condition presents with coryza, cough, tachypnea, wheeze, crackles, chest retractions, and feeding difficulty. Diagnosis is clinical. Management is supportive with oxygen for hypoxemia, hydration, and nasal clearance. Routine antibiotics, bronchodilators, corticosteroids, and nebulized adrenaline are not recommended.
Salbutamol receipe details child <4 yr
Reading File
Finding Sources
Finding Sources
Searching PubMed
preschool asthma AND salbutamol
Searching the Web
GINA 2025 children 5 years and younger salbutamol dose spacer acute wheeze
Salbutamol for a child under 4 years
Salbutamol is a short-acting bronchodilator used for wheeze/asthma-type bronchospasm. It should not be routinely used for bronchiolitis, where it usually does not improve outcomes.
Preferred route: inhaler with spacer and face mask
Use a salbutamol metered-dose inhaler, MDI, 100 micrograms per puff, with a valved spacer and well-fitting mask.
For an acute wheezing episode in a child aged 0-4 years:
- Give 4 puffs, one puff at a time through the spacer.
- Let the child take 5-6 normal breaths after each puff.
- For moderate or severe wheeze, it may be repeated every 20 minutes, up to 3 doses in the first hour, while obtaining medical assessment.
- If the child improves, further use must follow a clinician-provided asthma/wheeze action plan.
The current GINA guidance for young children prefers MDI plus spacer over nebulization and uses 4 or more puffs as initial treatment.
Nebulized salbutamol
This should generally be given in a clinic, emergency department, or under explicit medical instruction.
- 2.5 mg nebulized salbutamol is the standard acute dose for children aged 5 years and younger in GINA guidance.
- It may be repeated every 20 minutes up to 3 times in the first hour for moderate/severe exacerbation, with reassessment.
Do not confuse 2.5 mg with 0.25 mg. GINA specifically corrected a previous dose error and confirms that 2.5 mg is the appropriate nebulized dose for this age group.
Side effects
- Fast heartbeat or palpitations
- Tremor or shakiness
- Excitability, restlessness
- Headache
- With repeated high doses: low potassium and, rarely, abnormal heart rhythm
Seek urgent medical care now if the child has
- Blue lips, pauses in breathing, drowsiness, or exhaustion
- Severe chest indrawing/retractions, grunting, or inability to speak/cry/feed
- No improvement after initial salbutamol doses
- Need for 4 puffs again within 4 hours, or repeated need for salbutamol
- First episode of wheeze in an infant, particularly below 1 year
Important: If you mean bronchiolitis in an infant, use supportive care and medical review rather than starting salbutamol without a pediatrician's advice.
This is a shared conversation. Sign in to Orris to start your own chat.