RS - Upper Respiratory Tract Infections Medical Notes PDF

Summary

This document appears to be a medical textbook or revision notes covering various upper respiratory tract infections, including otitis media, sinusitis, and rhinitis. The notes discuss the etiology, signs, symptoms, diagnosis, management, and complications of these conditions, often in a bullet-point format.

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38 Upper respiratory tract infections Otitis media It is common between 6 months- 3 years of age Definitions:  Acute otitis media: Inflammation of the middle ear with rapid onset of symptoms  Recurrent otitis media: 3 new AOM episod...

38 Upper respiratory tract infections Otitis media It is common between 6 months- 3 years of age Definitions:  Acute otitis media: Inflammation of the middle ear with rapid onset of symptoms  Recurrent otitis media: 3 new AOM episodes within 6 months or 4 episodes/year  Chronic otitis media: Persistent ear discharge for > 6 weeks (or > 2 weeks as WHO classification) Acute otitis media: Etiology:  Bacteria: 1. S. Pnemoniae 2. H. influenza 3. Group A strept 4. Moraxella catarrhalis 5. Staphylococcus Aureus 6. Pseudomonas aeruginosa  Viruses: It causes Eustachian tube obstruction, followed by 2ry bacterial infection WHO classification of ear infection by IMNCI Symptoms& signs Classification Tender swelling behind the ear Mastoiditis Pus is seen or reported for less than 2 weeks Acute otitis media Or Ear pulling& irritability in infants or severe ear pain Pus is seen or reported for more than 2 weeks Chronic otitis media Predisposing factors: Younger age Air pollution Passive smoking Structural defect Immunodeficiency Low socioeconomic class Sibling with recurrent AOM Clinical picture:  Asymptomatic  Infants: Fever, irritability, ear pulling +/- diarrhea& vomiting  Children: Fever& Pain of one or both ears +/- ear discharge 39 Investigations:  Otoscopy  Erythema of tympanic membrane  Opacification of tympanic membrane  Scar or perforation of tympanic membrane  Culture of the ear discharge if it is present Complications: Turbid exudate  Mastoditis  Hearing loss  Facial paralysis  Trauma of middle ear  Sigmoid sinus thrombosis Serous exudate  Meningitis& brain abscess Turbid ear-drum Management:  Drying  Analgesia  Antibiotics:  Amoxicillin Tympanostomy  Amoxicillin-clavulanic acid  Cefaclor or Cefuroxime or Cefixime  Trimethoprim-sulfamthoxazole  In case of penicillin allergy: Erythromycin  In case of penicillin resistant: Ceftriaxone IM  In case of deterioration: Tympanocentesis for relieve& C/S 40 Acute Sinusitis Microrganism:  S pneumonia  Other streptococci  H influenzae  Less commonly, S aureus and Moraxella catarrhalis. Clinical picture:  Fever.  Headache.  Hyposmia.  Expectoration.  Nasal obstruction.  Unilateral purulent nasal drainage.  The maxillary sinusitis is the most common.  Maxillary sinusitis may result from dental infection.  Unilateral facial fullness, pressure and tenderness over the cheek.  Removal of the diseased tooth or drainage of the periapical abscess resolves the sinus infection. Management:  Nonsteroidal anti-inflammatories for pain  Oral decongestant eg, oral pseudoephedrine  Nasal decongestant e.g. oxymetazoline, or xylometazoline  Antibiotic therapy: Amoxicillin, Trimethprim, Deoxycycline , Levofloxacin& Augmentin Complications:  Orbital abscess  Orbital cellulitis  Osteomyelitis  Intracranial extension  Cavernous sinus thrombosis RT maxillary sinusitis 41 Rhinitis Viral rhinitis (Common Cold-Coryza) Microorganisms: Rhinoviruses, adenoviruses, and other viruses Clinical picture:  Hyposmia.  Clear rhinorrhea.  Nasal congestion.  Associated symptoms: malaise, headache, and cough. Examination:  Erythematous, engorged nasal mucosa.  Absence of intranasal purulence. Complications: Exacerbation of more serious conditions, such as acute bacterial sinusitis, acute otitis media, asthma and cystic fibrosis exacerbation and bronchitis Management:  Zinc lozenge within the first 24–48 hours  Oral decongestants (pseudoephedrine 120 mg twice daily)  Nasal sprays such as oxymetazoline or phenylephrine They should not be used for more than a few days at a time, since prolonged use leads to rhinitis medicamentosa. Allergic rhinitis Clinical picture:  Sneezing  Tearing  Eye irritation  Nose pruritus  Palate pruritus  Clear recurrent rhinorrhea  Associated symptoms: cough, bronchospasm, eczematous dermatitis. Environmental allergen IgE: Pollens and spores. Flowering shrub and tree pollens are most common in the spring, flowering plants and grasses in the summer, and ragweed and molds in the fall. Dust, household mites, air pollution, and pets. Management:  Antihistamines  Intranasal Corticosteroids  Adjunctive Treatment Measures 42 Epistaxis Clinical picture:  Bleeding from unilateral anterior nasal cavity most common.  Most cases successfully treated by direct pressure on the bleeding site for 15 minutes.  Topical sympathomimetics and various nasal tamponade methods are usually effective.  Posterior, bilateral, or large volume epistaxis should be triaged immediately to a specialist in a critical care setting Predisposing factors:  Trauma  Rhinitis  Hypertension  Telangiectasia  Antiplatelet drugs  Supplemental nasal oxygen  Dryness of the nasal mucosa  Deviation of the nasal septum  Hereditary or acquired hemorrhagic disease Treatment of anterior epistaxis:  Direct pressure on the site by compression  Venous pressure is reduced in the sitting position  Slight leaning forward lessens the swallowing of blood.  Short-acting topical nasal decongestants eg, oxymetazoline  Cauterized with silver nitrate, diathermy, or electrocautery. Treatment of posterior epistaxis:  It is pathological  Posterior nasal pack  Treatment of the cause 43 Acute tonsillitis& pharyngitis  It is the commonest disorder of URT  It may be caused by viral or bacterial  The most important organism is GAS Epidemiology:  It is uncommon in infants  It is common in winter& early spring  Pharyngitis common in < 2 years old is viral  Tonsillitis common at age 5 - 15 years of age WHO classification of throat problem by IMNCI Fever OR sore throat and 2 of the following: Streptococcal sore throat Red(congested) throat White or yellow exudate on tonsils or throat Enlarged tender anterior lymph node enlargement Insufficient criteria to say strept. Sore throat Non streptococcal sore throat Clinical picture:  Fever is > 38.5 C  Painful swallowing  Young: fever, cough, vomiting and abdominal pain  Older: Fever, cough, sore throat, headache, malaise  Congested enlarged tonsils +/- yellow exudates with tender anterior cervical lymph node enlargement Investigations:  Leukocytosis  Culture/ Sensitivity Differential diagnosis: Other organisms:  Viruses: adenovirus, rhinovirus, enterovirus, parainfluenza virus, herpes simplex, EBV  Bacteria: mycoplasma pneumonia, corynebacterium diphtheria, B-hemolyticstrept. Complications: Local Systemic AOM Scarlet fever Sinusitis Acute rheumatic fever Peri-tonsillar abscess Acute glomerulonephritis Retropharyngeal abscess Rheumatic heart disease Suppurative cervical lymphadenitis Wide spread: meningitis, pneumonia, carditis … 44 Management:  Penicillin V orally for 10 days In case of non compliance: Benzathine penicillin single IM inj  600.000 IU for children < 25 Kg  1.200.000 IU for children > 25 Kg In case of allergy: Macrolides& Cephalosporins In case of >3 documented infections in 6 months: Give daily penicillin in winter  Tonsillectomy if continue to have: Frequent episodes > 6 times/year or upper airway obstruction& sleep disorders  Do not do tonsillectomy unless it HARMS the patient H Hypertrophy with change voice A Abscess peritonsillar R Recurrent sore throat M Malignancy is suspected S Seizures (febrile due to tonsillitis) Adenoid hypertrophy Definition: Upper airway obstruction (posterior nasal pharynx) Clinical picture:  Mouth breathing  Adenoid face  Snoring Indications of adenoidectomy:  Loud snoring  Nasal obstruction  Chronic mouth breathing  Chronic nasal infection  Chronic sinus infections  Recurrent otitis media  Chronic otitis media  Upper airway obstruction. Adenoid X-ray 45 Acute epiglottitis Epidemiology:  It occurs in winter  Affects < 2 years old  Peak is 2-5 years of age  Organism is Hemophilus influenza type b Pathogenesis: Infection  Inflammation  Edema Clinical picture:  URTI Epiglottitis S&S: 5Ds  Sudden onset of high grade fever  Distress  Moderate to severe respiratory distress  Dyspnea  Stridor = harsh musical inspiratory sound  Drooling  Drooling of saliva due to dysphagia  Dysphagia  Irritability& restlessness due to SOB  Dysphonia  Sits with leaning forward (tripoid position) Investigations:  CBC & CRP  Neck x-ray: thumb sign  Laryngoscopy: congested edematous epiglottis Differential diagnosis:  Croup Management: Thumb sign in lat. Neck A. If patient is alert& able to maintain airway so, leave him in X-ray position of comfort Transport to OT for airway management immediately  Secure the airway  Nasotracheal intubation  Ventilation, throat swab for C/S  IV Fluids& electrolytes support  IV ceftriaxone 100 mg/kg/day for 10 days B. If patient is not alert& with S&S of respiratory failure, begin bag-mask ventilation. So, attempt intubation, laryngeal mask, cricothyrotomy or tracheostomy emergently 46 Croup (Acute laryngotracheobronchitis) It consists of the triad:  Stridor, hoarse voice& barking cough Epidemiology: Children < 4 years old More common boys in winter Etiology:  Influenza virus  Parainfluenza virus Pathogenesis: Steeple sign in the airway  Infection in nasopharynx  It extend to larynx& trachea  Infection  Inflammation  Edema  Narrowing of airway Clinical picture:  Gradual course  Worse at night  Duration is 3-7 days  Child has cold, cough  Coryza& low grade fever  Croupy cough, stridor, distress Investigations:  CBC & CRP Narrowing of airway  X-ray of neck& chest: steeple sign Complications: Croup features: 6 Ss  Secondary infection  Stridor  Respiratory failure& hypoxia  Seal-bark cough Management:  Subglottic edema  Cold mist therapy  Steroid treatment  Racemic Epinephrine nebulizer SOS  Steamed epinephrine  Dexamethasone 0.6 mg/kg/day oral or IM  Steeple sign in the X-ray Causes of srtidor: FATHER  Foreign body aspiration  Anaphylaxis Common causes of stridor Acute Chronic  Tracheal obstruction Croup GERD  Hypersensitivity Epilglottits Laryngeomalacia  Epiglottitis Anaphylaxis Anatomical disorder  Retropharyngeal abscess Foreign body aspiration Benign or malignant mass 47 Types of stridor:  Inspiratory stridor: Obstruction at the level of vocal cords  Expiratory stridor: Obstruction at the level of trachea=wheezing  Biphasic stridor: Supra-glottic & sub-glottis obstruction Grades of stridor:  Grade I: During crying or exercise  Grade II: During rest Infants 60 c/m  RR & chest Severe pneumonia  Dullness to percussion neonate indrawing  Abnormal vocal fremitus RR> 50 c/m  RR Pneumonia  Decreased air entry infant Non of the above No pneumonia,  Bronchial breathing RR < 40 c/m Cough or cold Child  Crepitation  Wheezing Differential diagnosis:  Atelectasis  Gastric aspiration  Congestive heart failure  Foreign body aspiration  Congenital malformations  Pulmonary hemosiderosis  Tumors such as metastasis  Chronic interstitial lung diseases Investigations:  Chest X-ray: (lateral and frontal views)  Patchy infiltrates or unilateral infiltrate  Atelectasis, hilar adenopathy, or pleural effusion in complicated cases.  Others like CBC, CRP, S. E, LFT& KFT are not conclusive. Complications:  Heart failure& respiratory failure.  Local spread: Effusion, empyema& lung abscess.  Distant spread: meningitis, otitis media, sinusitis& liver abscess. 53 Management: Supportive:  IV fluids  Antipyretic  Oxygen therapy Specific:  Empiric antibiotics according to suspected organism. Indication of hospital admission:  Vomiting  Young age Bronchopneumonia  Feeding difficulty  Breathing difficulty  Non family compliance  Failure of oral antibiotic  Other illness or complication Antibiotic guidelines:  Pneumonia without distress or complications: Pleural effusion Treated by: oral amoxicillin, Augmentin, Cefuroxime  Pneumonia caused by pneumococcus: It is very common It causes lobar pneumonia Treated by: Penicillin, Ceftriaxone, Cefotaxime  Pneumonia caused by staphylococcus: Lobar pneumonia It comes after infancy It is acute, fatal, causes pneumatocele. Treated by: Vancomycin, Lincomycin, Cephradine  Pneumonia caused by haemophilus: It is usually insidious It causes pleural effusion Cefotaxime, Ceftriaxone, Ampicillin  Pneumonia caused by Chlamydia& Mycoplasma: Treated by: Macrolide: Azithromycin, Clarithromycin, Erythrmoycin 54 Aspiration pneumonia Risk factors: Seizures Altered consciousness Gastro-esophageal reflux Neuromuscular disease affects swallowing Nasogastric, endotracheal, or tracheostomy tubes Anatomic abnormalities e.g. cleft, TEF, vocal cord paralysis Clinical picture:  Chocking, Coughing & Cyanosis.  Right upper lobe in the supine patient.  Right lower lobe in the recumbent position.  In patients with chronic aspiration, diffuse wheezing may occur.  Generalized rales. And may not develop acute febrile pneumonia. Differential diagnosis:  Immunodeficiencies, ciliary dysfunction, or foreign body. Investigations: Upper right lobe  CBC, CRP, C/S consolidation in infant  CXR: consolidation in upper right lobe in infants.  Consolidation in lower right lung in children. Complications:  Acute aspiration  empyema or lung abscess.  Chronic aspiration  bronchiectasis. Management:  Good supportive care: Lower right lobe  Oxygen, hydration, bed rest& chest physiotherapy consolidation in child  In general, clindamycin is appropriate initial coverage.  Low dose steroid IV or inhalation as anti-inflammatory. 55 Lung abscess Definition: Necrosis of pulmonary tissue& formation of cavity containing necrotic debris. Risk factors:  Malnutrition  Severe infections  Recurrent aspiration  Blunt trauma to chest  Immunocompromised patient Micro-organism:  Mycobacterium  Aspergillus  Cryptococcus  Histoplasma Lung abscess  Blastomyces  Actinomyces Clinical picture:  High fever, malaise, cough and weight loss are often present. Complications:  Septicemia.  Distant spread.  Mediastinal shift.  Tension pneumothorax.  Spontaneous rupture can occur. Investigations:  CBC, CR, C/S  Chest X-ray: Air-fluid levels can be present. Left middle lobe air fluid Single or multiple thick-walled lung cavity. level of lung abscess Lower part of apical segment is the most common site. Management: Supportive:  Bed rest, IVF, oxygen, expectorant& antipyretic. Specific:  Coverage for anaerobic and gram-negative organisms.  Clindamycin& cephalosporin for 3 weeks or more.  Surgical drainage of the abscess by chest tube. 56 Pleural effusion& Empyema Definition:  Effusion is non-purulent fluid in the pleural space  Empyema is purulent fluid in the pleural space Etiology of pleural effusion:  Pneumonia:  Staph. aureus  Strept. pneumonia  Gram negative bacilli  Tuberculous pleuritis  Thoracic trauma Rt pleural effusion: C-shape  Severe sepsis Parapneumonic Effusion causes: H3 C3 I3  Heart failure, Hypoproteinemia& Hypothyroidism  Constrictive pericarditis, Connective tissue disease& Consumption of TB  Infection, Infarction& Inflammation of abdomen Clinical picture:  Signs of pneumonia: fever, tachypnea, and cough  Chest pain, dullness to percussion, decreased breath sounds Investigations:  Chest X-ray: Homogeneous density that obscures cardiophrenic angle first then costophrenic angle.  Large effusions cause mediastinum shift to the contralateral side  Thoracentesis reveals findings that detect the cause Types of pleural effusion Transudate Exudate Congestive heart failure Tuberculosis Constrictive pericarditis Parapneumonic cause Cirrhosis liver Malignancy Nephrotic syndrome Collagen vascular disease Myxedema Radiation pleuritis Management: Supportive Specific Oxygen Appropriate empiric intravenous antibiotics Hydration Adequate drainage of the fluid remain the mainstay of therapy Antipyretic Evidence of early decortication using the thoracoscopic techniques 57 Lower airway diseases Laryngeomalacia Definition:  Floppy larynx  It is the most common cause of inspiratory stridor in infants.  It is aggravated by swallowing problems and gastro- esophageal reflux.  Hoarseness suggests vocal cord involvement. Clinical picture  Chronic stridor decreases during sleep.  Children with upper airway obstruction have suprasternal Management:  ENT consultation if not improved spontaneously at 1.5 years old. Or the patient has distress and interfere with feeding or breathing. Tracheomalacia Definition:  It is a floppy trachea due to lack or damage of cartilage.  With excessive collapse of the trachea during expiration. Types:  Congenital (tracheoesophageal fistula or bony dysplasia syndromes)  Acquired (long-term mechanical ventilation) Differential diagnosis:  Extrinsic tracheal compression by masses or vascular structures  Viral infections exacerbate tracheomalacia giving sound of: Wheezing as bronchial asthma or croup or severe brassy cough Investigations:  CXR: narrow ragged trachea or membrane. Management:  Tracheomalacia improves with airway growth.  The lumen increases in diameter and the tracheal wall becomes firm.  Tracheostomy tubes to give continuous positive airway pressure (CPAP) 58 Foreign body aspiration It could go to the esophagus or to the trachea. Clinical picture:  Witnessed aspiration  Menomenic: 3 Cs : Chocking, Coughing& Cyanosis  Most of cases have expelled immediately the foreign body  Some aspirate it and the clinical picture depend on the site of lodge and if the obstruction is complete or partial. Localized wheezing and unilateral absence of breath sounds. Alternatively, recurrent or persistent pneumonia in the same region.  Stridor and rarely bloody sputum. Or SABA resistant wheezing  Persistent atelectasis& chronic cough. Obstruction Larynx Trachea Bronchus Partial Stridor Metallic cough Wheezing Hoarse Aphonia Complete Suffocation SOB Pneumonia, Lung abscess Cyanosis Lung collapse, Bronchiectasis Atelectasis Clinical picture:  Under 4 years of age  It leads to death or may  Pass through right bronchus  Some FB are not radio-opaque  The most common aspirate is food as nuts or toys  The coins are more common to lodge in the esophagus  The batteries are rare but bad because it leads to injury, fibrosis& stricture. Investigations:  CXR: Radiopaque objects can be seen Focal air trapping, especially on expiratory views  Bronchoscopy: Rigid or flexible bronchoscopy to see& remove the foreign body Management:  If patient is alert& able to maintain airway: Oxygen& comfortable position  If patient has complete airway obstruction: Infants: 5 back blows followed by 5 chest thrusts Child: 5 abdominal thrusts  If basic life support fails: Begin bag-mask ventilation Perform laryngoscopy to remove the FB with Magill forceps  If upper airway obstruction persists: Consider intubation, cricothyrotomy, tracheostomy or heliox 59 Emphysema Definition: It is a condition due to disruption or destruction of alveolar septa. It refers to hyperinflation or to leakage of air into the pulmonary interstitial spaces. Causes:  α1-antitrypsin deficiency  Mechanical ventilation  Airway obstruction  Congenital Clinical picture:  Asymptomatic  Shortness of breath due to the original pathology that leads to emphysema. Management: Depends on the respiratory distress degree  Mild: no treatment, Moderate: resection, Severe: lobectomy. Primary ciliary dyskinesia (PCD, immotile cilia syndrome) Pathogenesis:  Cilia fail to beat normally.  Secretions accumulate in the airways  Endobronchial infection results with chronic infection.  If infection untreated, it leads to bronchiectasis by early adulthood. Clinical picture:  Recurrent otitis media, chronic sinusitis, and bronchiectasis.  Kartagener syndrome; the triad of situs inversus, pansinusitis, and bronchiectasis. Investigations:  Chest X-ray  Scrapings/biopsy of nasal or airway epithelium Management:  Chest physiotherapy.  Prompt treatment of bacterial infections.  However, the course of the disease tends to be slowly progressive. 60 Pulmonary edema Definition: It is the seepage of fluid into the alveolar and interstitial spaces. Pathogenesis: Hydrostatic pressure  Alveolar fluid  Plasma oncotic pressure  Left ventricular function  pulmonary venous hypertension   capillary hydrostatic pressure  fluid moves into the interstitial space and alveoli.  intrapulmonary shunting (alveolar units that are perfused but not ventilated).  Decreased ventilation (hypercarbia) is a late finding. Causes:  Excessive swing in intrathoracic pressure as tracheal foreign body aspiration  Upper airway obstruction by hypertrophied tonsils and adenoids.  Heart failure from left ventricular or biventricular dysfunction.  Decreased serum oncotic pressure (hypoalbumenemia),  After CNS injury (neurogenic pulmonary edema).  (High altitude pulmonary edema)  After volume overload by IVF Clinical picture:  Dyspnea& tachypnea.  Cough (with frothy, pink-tinged sputum).  Moreover, SOB, hypoxemia, and diffuse inspiratory crackles. Investigations:  Diffuse hazy infiltrates, classically in a perihilar pattern  As butter fly in appearance. +/- obscured by pneumonia. Management:  Upright posture.  Given supplemental O2.  Diuretic therapy like Lasix.  Rapidly acting IV inotropic agents.  It is helpful in cardiogenic pulmonary edema.  Continuous positive airway pressure (CPAP) or  Positive pressure ventilation by high (PEEP). 61 Pulmonary arterial hypertension (PAH) Types:  Primary  Secondary Causes:  Chronic hypoxia  Chronic lung disease  Exposure to high altitude  Upper airway obstruction  Pulmonary thromboembolism  Autoimmune diseases (Scleroderma).  Excessive pulmonary blood flow due to left-to-right cardiac shunt. Pathogenesis: Prolonged PAH, irreversible changes in the intima and media of the pulmonary arterioles. Complications: Pulmonary arterial hypertension strains the right side of the heart  dilation of the right ventricle  right ventricle hypertrophy  right-sided heart failure leads to hepatic congestion  fluid retention, and  tricuspid insufficiency. Clinical picture:  Accentuated pulmonary component of the second heart sound  +/- Cyanosis relieved by oxygen Investigations:  CXR: Right ventricle hypertrophy  Echo:  Tricuspid valve insufficiency  Right ventricle hypertrophy  D-shaped right ventricle Management:  Treat the cause.  Relieve hypoxia by O2.  Correct left to right shunt.  Treat heart failure by diuretics.  Vasodilator therapy e.g. sildenafil.  Inhaled nitric oxide can be used short term.  Lung or heart lung transplantation in idiopathic PAH. 62 Tuberculosis Definition: A. Tuberculosis infection: The patient has the microorganism B.Tuberculosis disease: The patient has S&S of the disease Types:  Pulmonary  Extra-pulmonary Extra-pulmonary:  Lymphatic  Intestinal  Peritoneal  Pericardial  Neurological  Disseminated  Musculoskeletal Primary T.B.: Primary complex  Primary complex:  AFB is taken to the regional LN  Basic lesion formed Ghon’s focus  Progressive primary complex: Extension of the infection in the same region Secondary T.B.: Active T.B. after 1ry infection or disease due to endogenous spread Etiology: Mycobacterium Tuberculosis Non motile non spore forming bacilli Its cell wall is lipid, for that reason it resists acid& complement& AB. So, it Can survive for longer times Epidemiology: 90% of children are infected 1/3 cases are diseased Transmission: By droplets From person to person Primary complex& Lt Cavity From adult has cavitary lesion 63 Predisposing factors of transmission:  Sputum for AFB is +ve  Upper lobe infiltrate  Copious sputum  Severe cough Pathogenesis:  Local inflammation  Ghon’s focus  alveolar multiplication  hilar LNE AFB spread by blood to body& lung  cell mediated immunity after 1 month  fibrosis, calcification& central necrosis  AFB remain viable for years  Calcification disappear in 3-5 years Possibilities: 1. Ghon ‘s focus compress bronchi  hyperinfalted lung 2. Central caseation rupture to lung  pneumonia 3. Cavitary formation due to liquefaction  open to bronchus 4. Lympho-hematogenous spread causing   Miliary TB  Meningeal TB  Dissiminated TB In 3-6 months after infection Primary complex Clinical picture: Most of them are subclinical detected by TST If S&S developed +/- CXR findings, it is called overt primary tuberculosis. Symptoms:  Night fever  Night sweats  Loss of weight  Loss of appetite  Chronic dry cough > 2 wks  Fatigue, malaise& irritability Cavity in upper left Investigations:  CBC:  Hb,  lympho &ESR  CXR: Consolidation, effusion& cavity  Tuberculin skin test: TST  AFB smear  AFB PCR  AFB C/S Miliary tuberculosis 64  CXR: *Ghon’s focus *Emphysema *Pleural effusion *Bronchopneumonia *Collapse& bronchiectasis  Tuberculin skin test:  Detects delayed hypersensitivity reaction in 72 hours as maximum  1 IU of PPD intradermally in the forearm  +ve response is : 10 mm red induration  -ve response is: < 5 mm induration  Doubtful: 5-10 mm induration  15 mm is patient Tuberculin skin test Causes of positive TST:  BCG has been given  Active tuberculosis  Past tuberculosis  Subclinical  TST Causes of true negative TST: TST indration  Patient hasn’t TB  Patient hasn’t BCG vaccine Causes of false negative TST:  Incubation  Malnutrition  Chemotherapy  Steroid therapy AFB smear  False technique  Immune deficiency  Miliary tuberculosis  Measles or whooping cough  AFB smear:  Difficult to have AFB in children sputum  Morning gastric aspiration for AFB  It needs at least 3 successive days  The AFB culture needs 4-6 weeks  Sensitivity needs 2-4 wks  Biopsy:  LNE, mass& pleura. 65  Aspiration:  Pleural fluid& peritoneal fluid.  PCR:  DNA testing of organism Reactivation of post primary TB: Healed lesion form Simon foci  or it caseate& liquefy  cavity Complications of reactivation of TB:  Severe pulmonary disease  Pulmonary hemorrhage  Bronchial ulceration  Pneumothorax  Empyema Extrapulmonary TB: Pericardial disease:  Pericarditis due to direct spread or invasion  There is sero-fibrinous or hemorrhagic fluid  Over many years it leads to constrictive pericarditis Skeletal tuberculosis:  Invasion of metaphysis Abdominal TB  Granulation& destruction  The vertebrae is the commonest site Abdominal TB:  Ingestion of milk  Chronic enteritis Cold abscess of LN  Mesentric adenitis  Generalized peritonitis  Paracentesis is usually diagnostic Superficial LNE:  Scrofula  It appears 6 - 9 months Scrofula (TB sinus)  It follows upper lobe infection  It occurs in the submandibular LN  In the start it is firm but it gets larger& extend to adjacent LN& skin which gets shiny. Then it opened to drain the pus from the caseating LN which is called sinus CNS TB:  Meningeal  Brain abscess  Spinal abscess: all are discussed later 66 Perinatal TB:  Mother transmit AFB to her fetus through placenta to umbilical vein to lungs  If the mother is the contact , give the neonate INH for 3 months. After that mantoux test is done  If it is +ve, give ATT. But if it is –ve, give BCG vaccine  If the mother is open case after delivery, isolation of neonate for 2 weeks till maternal sputum for AFB is –ve. Then do all the previous steps. Management: Supportive, specific& prevention Indication for hospitalization:  CNS TB  Miliary TB  Young infant  Surgical intervention Supportive:  Antipyretic  Antibiotic  Feeding Specific: ATT- DOT (anti-tuberclosis therapy): Treatment of tuberculosis: Must be combination to prevent resistance STRIPE  INH: Isoniazide 10 mg/kg/day PO  Streptomycin  Rif: Rifampicin 20 mg/kg/day PO  Rifampicin  PZM: Pyrazinamide 30 mg/kg/day PO  Isoniazid  STP: Streptomycin 40 mg/kg/day IM  Pyrazinamide  ETB: Ethambutol 10 mg/kg/day PO  Ethambutol / Ethionamide  DOT: Direct observation therapy Duration: Anti TB side effects A. Induction phase:  2 months  INH, Rif, PZM: for simple  INH, Rif, PZM, ETB: > 2 systems or severe B. Maintenance phase:  4 months in pulmonary& abdominal  6 months in reactivation& CNS, CVS  12 months in MSS  INH, Rif 67 Corticosteroids:  Endobronchial  Neurological  Peritoneal  Pericardial  Pleural  Miliary Predenisolone 1-2 mg/kg/day for 4 weeks& gradual tapering of the dose over weeks Prevention:  Primary: Prevents establishment of infection by BCG vaccination  Secondary: Prevents establishment of disease after infection occurs by INH 68 Bronchial asthma Definition: Reversible lower airway obstruction due to hyper-reactivity to variant stimuli. Pathogenesis: A. Airway hyper-reactivity B. Bronchoconstriction C. Chronic inflammation Risk factors:  Bottle-feeding Trigger factors of asthma:  Genetic predisposition  Change in weather  Other allergy e.g. Rhinitis, Eczema, Urticaria& food allergy  Emotional stress Clinical picture:  Viral infection History:  Chemicals  Night or early morning cough  Exercise  Dry cough > 2 weeks  Animals  Tightness of chest  Pollens  Seasonal cough  Smoke  Drugs  Wheezy chest  Allergens  Dyspnea  Presence of other allergy  Family history of allergy  Respond to SABA Chemicals Dust Genetic Food Alcohol Virus Dandruff Smoke Examination  Irritable  Respiratory distress  Prolonged expiration  +/- Wheezing in moderate  Silent chest in severe attack  Lethargy in respiratory failure Investigations:  CXR: Hyper-inflated chest +/-  Pneumonia  Lung collapse  Pneumothorax  CBC: may be eosinophilia  May be hyper Ig E  Spirometery: FEV is high  Peak expiratory flow meter 69 Differential diagnosis of wheezy chest:  Bronchiolitis.  Cystic fibrosis.  Bronchomalacia.  Foreign body aspiration.  Severe congestive heart failure.  Gastroesophageal reflux disease.  Airway compression by LN or mass. Management:  Prevention by avoid triggers.  Treat the attack by rapid acting drugs.  Maintain airway stability by long acting drugs. Treat the attack by:  SABA: short acting β₂ agonist e.g. Salbutamol, Albuterol  Anticholinergic: Ipratropium bromide nebulizer& inhaler  Systemic steroid: predenisolone, methylpredenisolone Maintain airway stability by:  Inhaled steroids e.g. Beclomethasone, Budesonide, Fluticasone, Triamcinolone& Momentasone  LABA: long acting β₂ agonist e.g. Salmetrol, Formetrol  Leukotriene receptor antagonist e.g. Montelukast, Zafirlukast & Zileuton.  Theophylline used as treat& prevent the attack  Sodium cromoglycate is not effective as previous medicines Clinical assessment of severity of asthma in E/R Mild/Moderate Severe Life threatening SpO2 > 92% SpO2 < 92% SpO2 < 90% PEFR > 70 % PEFR > 50 % PEFR < 35 % RR < 30 c/m (over 5 y) RR > 30 c/m (over 5 y) Cyanosis < 40 c/m (under 5 y) > 40 c/m (under 5 y) No or minimal accessory Use of minimal accessory Poor respiratory effort respiratory muscles use respiratory muscles Normal feeding Too SOB to feed or speak Agitation/lethargy Speak sentences Speak phrases Speak words May be wheezing by Audible wheezing Silent chest stethoscope SpO2 > 95% SpO2 < 95% SpO2 < 90% 70 Pulmonary index score Score RR Wheezing Insp./Exp Accessory muscles O2 saturation 0 < 20 c/m None 2:1 None > 95 % 1 21-35 c/m End expiration 1:1 Mild 93-95 % 2 36-50 c/m Entire expiration 1:2 Moderate 90-92 % 3 > 50 c/m Inspiration& 1:3 Severe < 90 % expiration Total score for > 6 years old is 0-15:  Mild asthma < 7  Moderate 7-11  Severe asthma > 11 Mild asthma management:  Salbutamol nebulizer by: metered dose inhaler MDI: ¼ puffs/kg every 20 min for 3 doses then every 1-4 hours as needed or by: continuous nebulizer 0.5 mg/kg/hr  Systemic steroids: prednisolone orally 2 mg/kg/day for 5 days or  Dexamethasone 0.6 mg/kg/day PO or IM or IV for 1-2 days Moderate asthma management:  Oxygen inhalation  Salbutamol+Ipratrobium same previous dose every 20 min. as needed then  Systemic steroid: Methylprednisolone 2 mg/kg/dose IV or IM then 2 mg/kg/day  Magnesium sulfate 25-775 mg/kg/dose IV infusion over 20 min if no improvement Severe asthma management:  Oxygen inhalation.  Salbutamol+Ipratropium bromide nebulizer  Parenteral β₂ agonist: adrenaline 0.01 mg/kg/dose IM or SC slowly every 20 min for 3 doses  If improved, continue treatment as moderate. If no improvement, give the following:  Methylprednisolone infusion over 20 min. as loading dose then maintenance dose  Continuous salbutamol or terbutaline nebulizer or intermittent every 30-40 min.  Magnesium sulfate IV infusion  Aminophylline 5mg/kg/dose IV infusion as loading dose then 1 mg/kg/hr IV infusion Discharge home:  Clinical improvement within 2 hours  Oxygen saturation > 94 % without oxygen  Patient can take oral medications at home.  Access to medicine or medical center & appropriate follow up.  Precise patient education about his disease, routine emergency management. 71 Classification of asthma severity long term asthma management Intermittent Mild persistent Moderate Severe persistent persistent Daytime S&S < 1/week >1 day/week Daily Daily Nocturnal S&S 2/month >1/week Frequent Need for drugs 2 days/week >2 days/week extreme activity limitation lung function >80% > 80% 60-80 % < 60% test:: PEFR, FEV Step down if controlled for 3 months Step up if not controlled in 1 month Step 2: Low dose ICS (inhaled corticosteroids) or montelukast Step 3: Medium dose ICS or low dose ICS+Montelukast or low dose ICS+LABA Step 4:Medium dose ICS+Montelukast or Mdedium dose ICS+LABA Step 5: High dose ICS+Montelukast or high dose ICS+LABA Step 6: Lowest dose oral GCC+ High dose ICS+Montelukast or High dose ICS+LABA Management of asthma: ASTHMA Wheezing causes: ASTHMA  Adrenergic β₂ agonist Albuterol  Asthma  Systemic steroids  Small airway disease  Theophylline  Tracheal obstruction  Hydration  Heart failure  Mask oxygen  Mediastinal mass  Anticholinergic/Antibiotics  Anaphylaxis 72 Indications of tonsillectomy: HARMS  Hypertrophy  Abscess  Recurrent sore throat > 6/year  Malignancy is suspected  Seizures (febrile due to tonsillitis Causes of breathing difficulty: BREATH  Bacterial (pneumonia, endocarditis)  Embolism (pulmonary)  Airway obstruction/ Acute coronary syndrome  Tension pneumothorax  Heart failure  Edema/ Effusion/ Electrical arrhythmia Causes of dyspnea: 7 P  Pneumonia  Pump failure  Pneumothorax  Pleural effusion  Pulmonary embolism  Possible foreign body aspiration  Pulmonary bronchoconstriction Causes of chronic cough: SAVE LIVES  Somatic cough (psychogenic cough)  Asthma/ ACE inhibitor/ Aspiration  Very dilated bronchi (bronchiectasis)  Eosinophilic bronchitis  Laryngeal reflux GERD/ Lung cancer  Infection (LRTI)  Variable disorders of URT  Esophageal reflux  S&S of CHF/ Smoke Causes of chronic cough: CRADLE  Cystic fibrosis  Rings, slings  Aspiration  Dyskinetic cilia  Lung malformation  Edema 73 Clinical picture of FB aspiration: 3 C  Chocking  Coughing  Cyanosis COPD types: ABCDE  Asthma  Bronchiectasis  Chronic bronchitis  Dyspnea  Emphysema Causes of hemoptysis: CAVITATES  Congestive heart failure  Airway disease  Vascular malformation  Infection (TB)  Trauma  Anticoagulant  Tumor  Embolism  Stomach related Clubbing causes: CLUBBING  Cyanotic heart disease  Lung cancer, Lung abscess  Ulcerative colitis  Bronchiectasis  Benign mesothelioma  Infective endocarditis  Neurogenic tumors  Gastrointestinal disease Causes of acute stridor in children: FATHER  Foreign body aspiration  Airway burns  Tracheitis& trauma  Hypersensitivity  Epiglottitis  Retropharyngeal abscess 74 Causes of acute stridor with fever: ABCDE  Abscess  Bacterial tracheitis  Croup  Diphtheria  Epiglottitis Croup features: 6 S  Stridor  Seal-bark cough  Subglottic swelling  Steroid treatment  Steamed epinephrine  Steeple sign in X-ray Epiglottitis picture: 5 D  Distress  Dyspnea  Drooling  Dysphagia  Dysphonia Respiratory causes of finger clubbing: ABCDEF  Abscess  Bronchiectasis  Cancer  Decrease oxygen  Empyema  Fibrosing alveolitis History taking in bronchiolitis: WARD  Wheezing  Apnea  Respiratory distress  Difficult feeding Pathogenesis of ARDS: ARDS  Assault to pulmonary  Respiratory distress  Decrease lung compliance  Severe respiratory failure 75 Pneumonia complications: DON’T SLAP HER  Septicemia  Lung abscess  ARDS  Parapneumonic effusion  Hypotension  Empyema  Respiratory failure Para-pneumonic Effusion causes: H3 C3 I3  Heart failure/ Hypoproteinemia/ Hypothyroidism  Constrictive pericarditis/ Connective tissue disease/ Consumption of TB  Infection/ Infarction/ Inflammation of abdomen Pathogenesis of bronchial asthma: ABC  Airway hyper-reactivity  Bronchoconstriction  Chronic inflammation Wheezing causes: ASTHMA  Asthma  Small airway disease  Tracheal obstruction  Heart failure  Mediastinal mass  Anaphylaxis Risk factors of bronchial asthma: FEAR UP  Family history  Eczema  Acid reflux  Rhinitis  Urticaria  Polyps nasal Management of asthma: ASTHMA  Adrenergic beta2 agonist Albuterol  Systemic steroids  Theophylline  Hydration  Mask oxygen  Anticholinergic/Antibiotics 76 Acute asthma attack picture: SHOCK  Silent chest  Hypotension  One third PFR  Cyanosis  Konfusion Management of severe asthma: ASTHMA  Adrenergic beta2 agonist/Adrenaline  Systemic steroids IV  Theophylline  Hydration  Mask oxygen/Magnesium sulfate  Anticholinergic/Antibiotics Apical lung disease causes: CARPETS  Cystic fibrosis  Ankylosing spondylitis  Radiation pneumonitis  Pneumoconiosis  Eosinophilic pneumonitis  Tuberculosis  Sarcoidosis Treatment of tuberculosis: STRIPE  Streptomycin  Rifampicin  Isoniazid  Pyrazinamide  Ethionamide/Ethambutol Drugs that can stop breathing: STOP  Sedatives& hyponotics  Trimethoprim  Opiates  Polymexins 77 A sick airway causes: A SICK AIRWAY  Airway lesion or obstruction  Sequestration  Immune deficiency syndrome  Cystic fibrosis  Kartagener syndrome  Allergic Aspergellosis  Infection TB  Reflux  recurrent aspiration  William cambel & Mounier  Alpha-I antitrypsin deficiency  Yellow nail syndrome Intervention in COPD: ABCDEF  Aminophylline  Bronchodilators  Chest physiotherapy  Deliver oxygen at 2- L/m  Expectorants  Force fluids