January 24, 2011.  Always look for clubbing  Suprasternal and intercostal retractions may be...

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Transcript of January 24, 2011.  Always look for clubbing  Suprasternal and intercostal retractions may be...

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  • January 24, 2011
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  • Always look for clubbing Suprasternal and intercostal retractions may be normal following exercise Subcostal retractions always pathologic Accessory muscles Respiratory alternans- alternating abdominal and chest expansion Respiratory muscle fatigue
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  • 1-2 months of age Afebrile pneumonitis Congestion, wheezing, fine diffuse crackles Paroxysmal, staccato cough Inclusion conjunctivitis in 50% CBC may have eosinophil predominance
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  • Which CBC results support the diagnosis of Bordetella pertussis? A.High white count with lymphocytosis B.High white count with eosinophilia C.High white count with high bands D.Low white count
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  • 3 Phases Catarrhal Paroxysmal Severe paroxysmal coughing episodes Followed by cyanosis and apnea Inspiratory whoop Convalescent Apnea may be presenting sign CXR nonspecific Elevated WBCs with lymphocytosis
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  • Dx with PCR Treat only to reduce spread Macrolide (treat contacts also) Tdap vaccine Adults 19-64 years old, one Tdap At least 2 years after Td
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  • You diagnose a 4 year old patient with 3 rd episode of pneumonia. A dense, opaque area has been seen on CXR in same location all three times. What is most likely diagnosis? APulmonary Sequestration BBronchogenic cyst CCongenital Cystic Adenomatoid Malformation DRetained foreign body
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  • Think of underlying structural defect!!
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  • Bronchopulmonary Sequestration Bronchogenic Cyst Congenital Cystic Adenomatoid Malformation
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  • Portion of lungs perfused by systemic arteries Lacks normal connection with tracheobronchial tree Intralobar: Most common lower lobes Anywhere in thorax Extralobar: Subdiaphragmatic or retroperitoneal Associated with other anomalies
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  • Occur any point along the tracheobronchial tree Centrally located Does not communicate, fluid fill with wall composed of tissue resembling large airways Typically present 2 nd decade of life with recurrent wheezing, cough, pneumonia
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  • Previously known as Congenital Cystic Adenomatoid Malformation (CCAM) Hamartomatous lesion Cystic and adenomatous elements Resp distress, recurrent PNA, asymptomatic Surgical resection is symptomatic Controversial if asymptomatic
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  • A 21year old patient is in the ER for pneumonia, which has been recurrent. He has also been treated multiple times for chronic sinusitis. He has required multiple sets of ear tubes for OM, even as an adolescent. He has been married for a year, and has been trying unsuccessfully to have a child. On review of systems, he has had normal growth and development, no bowel or bladder complaints. On exam: bibasilar crackles and ronchi, nasal discharge, nasal polyps. CV exam normal. What is the most likely underlying diagnosis A. Cystic Fibrosis B. Kartagener Syndrome (Primary ciliary dyskinesia) C. Aquired ciliary dyskinesia D. Lymphocytic interstitial pneumonitis
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  • Triad: situs inversus, sinusitis, bronchiectasis Situs inversus in only 50% Recurrent OM Nasal polyposis Recurrent Pneumonia Infertility
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  • Far more common May follow LRTI Adeno Mycoplasma RSV Influenza Need bx of resp epithelium for confirmation
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  • Potentially fatal Associated with: Cardiac dz Glomerulonephritis (Goodpasture syndrome) Infantile hypersensitivity to cows milk Collagen vascular diseases Idiopathic
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  • Dyspnea, cough, hemoptysis, cyanosis, fever, iron-def anemia Hematemasis or melena May develop jaundice or clubbing CXR: variable Transient infiltrates Similar to miliary TB
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  • Dx: hemosiderin-laden macrophages (suggestive) Lung bx definitive
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  • School age children and adults May imitate viral URI Progress to lower resp tract Persistent Cough variable, may become productive May progress to consolidation Lower lobes Physical findings minimal (crackles/wheezing) Mycoplasma PCR available Primarily clinical diagnosis
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  • Usually following LRTI May persist for weeks or months Loud honking barking Disturbing to family members, classmates Always disappears with sleep Worse with: Stress Attention to cough Extensive evaluation may exacerbate problem
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  • Most common cause of inspiratory stridor kids Acute viral illness Parainfluenza Almost any viral resp illness Clinical findings Coryza 1-2 days Harsh cough Hoarseness stridor
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  • Mostly self limited Airway obstruction possible Treatment Dexamethasone Racemic Epi nebs (vaponeb) Warm or cool humidified air: no significant benefit
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  • Child treated for croup returns 3 days later looking toxic, stridor has returned Bacterial Tracheitis
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  • An 12 month old has been having daily stridor and intermittent ronchi. Mom was told that her child has laryngomalacia. What is your diagnosis? A. Laryngomalacia B. Laryngeal web C. Hemangioma D. Chronic aspiration E. Vascular ring
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  • Congenitally floppy glottis Symptoms Stridor usually by 1 st week of life Varies with activity May be biphasic Worse supine Usually self limited Improvement at 6-10 months of age
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  • Diagnosis Clinical Airway flouro or direct visualization if concerned Treat for GE Reflux Refer to ENT if failure to thrive or other complications
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  • Congenital Improves with age Acquired Endotracheal intubation Problematic May require tracheostomy
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  • Laryngeal papillomatosis Rare Life threatening Presents in first decade Vocal cords or entire tracheobronchial tree Clinical features Hoarseness Stridor Brassy cough
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  • Hemangiomas Stridor, brassy cough Cutaneous hemangiomas may offer clues Now treated with beta-blockers
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  • Laryngeal webs, cysts, laryngoceles Uncommon Clinical manifestations Resp distress Feeding difficulties Stridor Cyanosis
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  • Clinical Findings Weak or absent cry Hoarseness Insp stridor with/without distress Feeding difficulties Diagnosis Flexible bronchoscopy
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  • Unilateral Causes Cardiomegaly Vascular ring May be subltle Bilateral Causes Hydrocephalus Myelomeningocele Arnold-chiari malformation
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  • A 13 year old athlete has had wheezing and shortness of breath at multiple track meets this season. A. PFTs consistent with asthma B. PFTs consistent with restrictive lung disease C. PFTs consistent with vocal cord dysfunction D. Normal PFTs
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  • Often mistaken for exercise-induced asthma Many have BOTH Vocal cords adduct during inspiration Psychogenic origin Highly pressured adolescent female athlete Competitive event Sensation of dyspnea trouble getting air IN Localized to throat
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  • Diagnosis Clinical suspicion PFTs Flexible nasolaryngoscopy Treatment Speech therapists, breathing exercises Psychology may be needed
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  • Increased wheezing in previously well controlled asthmatic or CF patient Insidious presentation Low-grade fevers Fatigue Weight loss Productive cough Physical Wheeze Bibasilar crackles clubbing
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  • Imaging Consolidation or atelectasis Dilated bronchi radiating from hila Diagnosis Skin prick to Aspergillus fumigatus antigen Elevated total and specific IgE Isolation of A.fumigatus from sputum Worsened PFTs (obstruction)
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  • Recurrent wheezing or stridor CXR: Right sided aortic arch Tracheal deviation to the Left Barium swallow Inexpensive screening test MRI Delineates airway and vascular anatomy Necessary prior to surgery
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  • Dont forget about Goiter Mediastinal mass
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  • CXR: Large, hyperlucent area Few bronchovascular markings Compression atelectasis of adjacent lobes LUL most common Middle lobe also seen Treatment Conservative if infant thriving Resection for prolonged resp distress, recurrent infxn
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  • Any resp infection may cause severe illness May develop Chronic resp insufficiency Pulmonary HTN Cor pulmonale Most continue with reactive airways
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  • Bronchioles become inflamed/fibrosed Non-reversible obstructive lung disease Causes Idiopathic Post adenoviral Toxic inhalation Conjunction with other diseases (rheumatoid arthritis) Post-transplant
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  • CXR: hyperinflation decreased vascularity increased interstitial markings areas of atelectasis and consolidation PFTs: fixed lower airway obstruction Prognosis is poor