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Pulmonology Pulmonology Presentation Transcript

  • Respiratory diseases Archer Online USMLE Reviews www.ccsworkshop.com All Rights reserved
  • URTIs
  •        Allergic Rhinitis Hay fever Onset under age 30 Peak incidence – childhood & adolescence Most common chronic disease in the USA and significantly affects quality of life Pathophysiology : Type I hypersensitivity reaction to allergens Common allergens : Seasonal Allergens: Tree pollen (early spring), Grass pollen (late spring) and Outdoor Molds (summer and fall) ) , Perennial : Dust mites and Animal dander Irritant: Cigarette Smoke Associated conditions :  Atopy : Eczematous Dermatitis , Allergic Rhinitis and Asthma  Allergic Triad : Aspirin Allergy, Nasal Polyp and Asthma
  • Allergic Rhinitis Symptoms: Specific : Sneezing, Rhinorrhea, Nasal congestion and Pruritus of the nose, eyes, and throat , Eye Tearing and Conjunctival discharge Symptoms due to Chronic Nasal Obstruction: Mouth Breathing, Snoring, Anosmia, Cough, Headache and Halitosis Signs : * Look for antihistamine induced Hypertension in these guys *Nose exam : pale blue and boggy mucosa, clear discharge *Face exam: “Allergic Shiners”  bluish purple rings arround both eyes due to chronic mid face venos congestion “ Dennie’s Lines:  Skin folds under the eyes “ Allergic Salute:  transverse nasal crease from chronic rubbing *Sinuses: r/o sinusitis  purulent discharge, tenderness and impaired transillumination
  • Allergic Rhinitis    Diagnosis : * Skin testing  Gold Standard * RAST  use this if unable to do a skin test or if its contraindicated * CBC  may show eosinophilia * IgE levels are elevated D/D : 1) Nasal causes of Rhinitis : Nonallergic rhinitis ( eosinophila synd), Nasal polyps, Vasomotor rhinitis, infectious rhinitis, Rhinitis medicamentosa 2) Medications: Aspirin, Clonidine, Hydralazine, Labetalol, propranolol, tearazosin, OC pills Management  Do Skin test / RAST and find the responsible Allergen. Advise the pt to avoid the allergen. “Avoid pets in the bed if its found to be animal dander”  Intranasal Steroids ( are the drug of choice for pts with chronic symptoms. Can be used prn but most effective when used as maintainance therapy  fluticasone, beclomethasone) , Antihistamines ( cetrizine, loratidine) , Saline nasal drops , decongestants ( pseudoephedrine), nasal cromolyn
  • Allergic Rhinitis Antihistamines vs. Nasal Corticosteroids. The majority of studies favor the use of intranasal corticosteroids over sedating or nonsedating antihistamines for relief of symptoms of nasal allergy. These results are true for seasonal and perennial allergic rhinitis. ( antihistamines are used for immediate symptom relief) Immunotherapy: Immunotherapy is indicated in patients who present with any of the following characteristics:  Insufficient control by pharmacotherapy;  Insufficient control of symptoms;  A desire not to take medication;  Medication produces undesirable side effects; and  A desire to avoid long-term pharmacotherapy (with intranasal steroids)
  • Case Study  You are treating an 18-year-old white male college freshman for allergic rhinitis. It is September and he tells you that he has severe symptoms every autumn, which impair his academic performance. He has a strongly positive family history of atopic dermatitis. Which one of the following medication is considered optimal treatment for this condition?  Intranasal glucocorticoids Intranasal cromolym sodium Intranasal decongestants Intranasal antihistamine   
  • Ans  Topical intranasal glucocorticoids are currently believed to be the most efficacious medications for the treatment of allergic rhinitis. They are far superior to oral preparations in terms of safety.  Cromolyn sodium is also an effective topical agent for allergic rhinitis; however, it is more effective if started prior to the season of peak symptoms.  Because of the high risk of rhinitis medicamentosa with chronic use of topical decongestants, these agents have limited usefulness in the treatment of allergic rhinitis.  Some of the newer oral antihistamines have been found to be comparable in efficacy to intranasal steroids, but their use slightly increases the incidence of adverse effects and drug interactions. They are not as useful for congestion as they are for sneezing, pruritis, and rhinorrhea. Newer agents are relatively free of sedation. Overall, they are not as effective as topical glucocorticoids. Azelastine , an intranasal antihistamine, is effective in controlling symptoms but can cause somnolence and has a very bitter taste.
  • Vasomotor Rhinitis Diagnosis of exclusion  Symptoms similar as Allergic Rhinitis  has rhinorrhea, congestion, nasal obstruction ( normal nasal exam, normal Ig E and Normal skin test/ RAST )  No specific test is available to diagnose vasomotor rhinitis  First exclude allergic rhinitis as the cause of symptoms by using conventional skin testing or by evaluation for specific IgE antibodies to known allergens.  Rx: Stepwise Approach ( next slide )  Pregnancy Step 1: Nasal Saline Step 2: Intranasal Atrovent (Pregnancy Category B)  Traditional oral antihistamines have no established beneficial effect in patients with vasomotor rhinitis and may be associated with sedation. Newer, less-sedating antihistamines also have no proven effectiveness for vasomotor rhinitis, and their administration delays proper treatment while incurring significant cost and burden to the health care system. Topical antihistamines are used as first choice if symps are rhinorrhea, sneezing, post nasal drip
  • Rhinitis Medicamentosa Pathophysiology  Associated with topical agent use >5-7 days  Tachyphylaxis associated with medications   Nasal Decongestants (Afrin, Neo-Synephrine) Other associated medications     Reserpine Oral Contraceptive pills Inderal Aldomet Symptoms  Rebound nasal Congestion after nasal Decongestant Signs  Fiery red edema at nasal mucosa Management  Intranasal Steroid  Withdrawal of nasal Decongestant
  • Acute & Chronic Sinusitis Criteria for diagnosis:  Maxillary toothache  Purulent nasal secretion  History of colored Nasal discharge  Poor response to nasal Decongestants  Abnormal Sinus Transillumination If 4 or more criteria +  diagnosis is definite If 2 or 3 crieria +  Diagnosis is intermediate  recommended initial study Sinus CT If less than 2 criteria  negative for sinusitis  Most common is maxillary sinusitis. Next common is Frontal. Ethmoids are most commonly affected in children. Spenoids has highest risk of intracranial spread  Symptoms may last as long as 4 weeks in acute sinusitis, Symptoms b/w 4-8 weeks is subacute ans symptoms persisting > 8 weeks is chronic sinusitis. In recurrent sinusitis, there are 3 or more episodes of acute sinusitis per year, and different episodes may be caused by different organisms.  Signs  Diagnostic tests  Step wise Treatment  Complications
  • Acute & Chronic Sinusitis Signs : Nasal Mucosa erythema and boggy due to edema   Contrast with Allergic Rhinitis (pale, boggy mucosa) Nasal exam to view pus discharge from lateral wall Instruments Nasal speculum (minimal visualization) , Flexible Nasolaryngoscopy      Middle Meatus (hiatus semilunaris)  Drains Maxillary, Frontal, and Anterior Ethmoid  Consider local Topical Decongestant application Superior Meatus (Rarely discharge is seen)  Drains posterior ethmoid sinus Turbinates enlarged Sinus tenderness to percussion Sinus Transillumination in darkened room  Frontal and maxillary sinus
  • Acute & Chronic Sinusitis  Symptoms suggesting bacterial etiology  Symptoms persist beyond 10 to 14 days, Remember that under 10 days, viral sinusitis predominates,  By day 10, 40% of sinusitis resolves spontaneously  0.5% of viral URIs develop into bacterial sinusitis  Symptoms worsen after 5-7 days ( “double” sickening)  purulent nasal discharge  “Unilateral” maxillary sinus tenderness  Maxillary tooth or facial pain (esp. if unilateral)
  • Acute & Chronic Sinusitis    Don’t culture nasal swabs  not cost effective Diagnosis is clinical in Acute Sinusitis Indications for Imaging   Complicated sinusitis , Chronic or recurrent sinusitis , Sinusitis refractory to maximal medical therapy Imaging is not needed in routine cases  Empiric therapy for 1-2 courses is appropriate 1. Sinus X-Ray (Sinus CT preferred)  Plain radiographic signs consistent with sinusitis include greater than 6 mm of mucosal thickening in adults and 4 mm in children, greater than 33% loss of air space volume in the maxillary sinuses, or opacification–airfluid levels.   Single Waters' View X-Ray is sufficient Indication (rarely indicated unless CT not available)   Sinus CT (gold standard) Indications       Complicated Acute Sinusitis & Suspected Chronic Sinusitis Osteomeatal complex occlusion Complicated acute sinusitis  orbital cellulitis etc Chronic Sinusitis Recurrent Sinusitis Allergic Fungal Sinusitis Sinus MRI   No advantage over Sinus CT (and more false positives) Indications : Suspected neoplasm and Fungal Sinusitis
  • Acute Sinusitis - Complications Unless severe symptoms of acute sinusitis develop, such as fever, facial pain or tenderness, or periorbital swelling, antibiotics should be withheld for 10 to 14 days.  Complications : Orbital Cellulitis, Meningitis, Extradural abscess , Subdural abscess , Brain abscess , Osteomyelitis and Cavernous Sinus Thrombosis  Symptoms: Red Flag (consider immediate ENT referral)  High Fever over 102.2 F (39 C) or peristent fever  Visual complaints (e.g. Diplopia)  Periorbital edema or erythema ( check for EOMs  ?pain)  Mental status changes  Severe facial or dental pain  Infraorbital hypesthesia  consider referral in immunodeficiency or if persistent symptoms despite treatment 
  • Sinusitis - Treatment General Measures  Symptomatic relief : Warm, moist compresses over sinuses , Tylenol  Nasal Saline spray (2% buffered saline)       Systemic Decongestant: Pseudoephedrine Mucolytic : Guaifenesin (e.g. Mucinex) 600 to 1200 mg PO bid  there is no evidence that mucolytics are useful adjuncts Topical Decongestant (Maximum of 3 days of use)   Oxymetazoline or Phenylephrine (Neo-Synephrine) Intranasal Steroid (treat for 3-6 weeks minimum)    Effective Decongestant Also use as pretreatment prior to Intranasal Steroid Effective in recurrent Sinusitis when used daily Chronic Sinusitis Nasal Polyp Avoid Antihistamines!!  Dries secretions and Impedes osteomeatal complex drainage
  • Sinusitis - Treatment ANTIBIOTICS:  Indicated only in acute bacterial Sinusitis  Protocol Antibiotic course  Minimum course: 10-14 days Longer course for persistent symptoms: 28 days  Change antibiotic if no improvement in 3 days REMEMBER THAT Beta-lactamase resistance in acute cases: <30% , Betalactamase resistance in chronic cases: 40-50%  First-Line  Indications to start on first-line agents Mild to moderate symptoms , No daycare exposure & No recent antibiotic use  Amoxiicillin  Disadvantages: Misses Beta-lactamase producers : Haemophilus Influenzae , Moraxella catarrhalis & Penicillin Resistant Pneumococcus (increasing)  Trimethoprim Sulfamethoxazole (Bactrim) No longer recommended as first-line agent , Higher resistance rate than other agents  Disadvantages : Misses Staphylococcus , Risk of Toxic Epidermal Necrolysis& Risk of Steven's Johnson Syndrome
  • Sinusitis - Treatment   Second-Line  Indications to start on second-line agents : Severe symptoms Daycare exposure , Recent antibiotic use  Amoxicillin-Clavulanate (Augmentin ) or Cefuroxime (Zinacef) , Cefpodoxime  Avoid Cefixime ( poor Gram + coverage ) Third Line recommendation If no improvement with above a) Consider adding Flagyl to second-line agents b) Consider second-line agent for longer course (4 week) c) Switch to Fluoroquinolone (avoid under 16 yrs of age ), Moxifloxacin or Gatifloxacin (Tequin)
  • Sinusitis - Treatment Management : Penicillin or Cephalosporin Allergy  Macrolide antibiotics (High bacterial resistance rate)  Erythromycin , Azithromycin (Zithromax) or Clarithromycin (Biaxin)  Trimethoprim-Sulfamethoxazole (Bactrim)  Increasing bacterial resistance, So other agents are preferred for Sinusitis  Clindamycin  Consider in combination with Rifampin if severe , Poor efficacy against Gram Negative Bacteria  Fluoroquinolones ( avoid under age 16 years )
  •  Sinusitis - Treatment “Unless severe symptoms of acute sinusitis develop, such as fever, facial pain or tenderness, or periorbital swelling, antibiotics should be withheld for 10 to 14 days. Although the primary therapy for acute bacterial sinusitis is antibiotics, increasing resistance to penicillin may days. necessitate the use of alternative antibiotics. The choice of antibiotics is based on predicted efficacy, cost, and adverse effects. A 10- to 14day course is generally adequate for acute disease, but shorter courses may be indicated for newer antibiotics. If there is no improvement in 3 to 5 days, an alternative antibiotic should be considered” ( guidelines, journal of clinical immunology, 2006) considered”      Primary therapy for acute bacterial sinusitis is antibiotics with a 10to 14-day course considered adequate. Amoxicillin is a drug of choice with trimethoprim-sulfamethoxazole an alternative. If no response occurs within 3 to 5 days, a change to high-dose amoxicillin-clavulanate, cephalosporins, or macrolides may be indicated. In areas of high antibiotic resistance or with failure to improve after 21 to 28 days, broad spectrum single agents should be considered, such as amoxicillin-clavulanate, cefuroxime, or cefpodoxime, or use of anaerobic coverage, such as clindamycin or metronidazole. Nasal corticosteroids are indicated in acute and chronic sinusitis and short-term adjunct oral steroids may be used after failure of response or when nasal polyps are present. Saline nasal sprays may help to reduce crusting!!
  • Acute Pharyngitis      Symptoms: Sore throat , Dysphagia & Odynophagia (pain with swallowing) Generalized symptoms : Fever, Chills, Malaise, Headache , Abdominal Pain , Nausea or Vomiting Symptoms suggestive of viral illness: Coryza, Conjunctivitis & Hoarseness Signs Viral  Non-exudative pharyngeal erythema        Exception: Tonsillar exudate in Mononucleosis (EBV) Vesicular OR ulcerative oral lesions Conjunctivits in Adenovirus and Kawasaki Disease Group A Streptococcus and other bacteria  clues are Enlarged tonsils with or without exudate , Petechiae on Soft Palate (pathognomonic) , Erythema , Tender cervical Lymphadenopathy  Strawberry Tongue (in Scarlet Fever) Peritonsillar Cellulitis or Peritonsillar Abscess  Suspect Unilateral erythema of Soft Palate , Uvula deviated , Dysphagia, Odynophagia & Fever Diphtheria  Suspect when Gray membranous exudate covers tonsils and pharynx or Exudate bleeds easily on removal Kawasaki Disease  Suspect when Pharyngitis with strawberry Tongue in age <5 years , Non-purulent Conjunctivitis (also in Adenovirus) & Palmar erythema and cracked red lips after 3 days
  • STREP THROAT Acute Pharyngitis caused by Group A beta hemolytic streptococci.  Most common in children 5-12 yr old  Infectivity  Decreases 1-3 days after antibiotic started  Return to School and day care recommendations  Child should receive Antibiotics for minimum of 24 hours and Afebrile 
  • Complications  Non-suppurative    Strep Throat Rheumatic Fever  we Rx Strep Throat to prevent this. ABX Rx does not prevent PSGN Acute Post-Streptococcal Glomerulonephritis ( PSGN) Suppurative          Peritonsillar Abscess Suppurative Otitis Media Cervical lymphadenitis Acute Sinusitis Mastoiditis Meningitis Bacteremia Endocarditis Pneumonia
  • Strep Throat – Strep Score Original Criteria (interpretation below based on these)  1 point for each  Tonsillar exudate  Tender, anterior cervical adenopathy  Cough absent  Fever present  Modifiers : Age younger than 15 years: +1 point, Age 15 to 45 years: 0 points & Age over 45 years: -1 points ER and OP probability:  Score 0: Streptococcus probability 1% (3% in ER)  Score 1: Streptococcus probability 4% (8% in ER)  Score 2: Streptococcus probability 9% (18% in ER)  Score 3: Streptococcus probability 21% (38% in ER)  Score 4: Streptococcus probability 43% (63% in ER)
  • Strep throat (?) - Approach Strep Score 4 (or Strep Score 2 if patient unreliable)  Treat with antibiotics Strep Score 2 to 3: Perform rapid antigen test     Antigen test positive: Treat with antibiotics Antigen test negative: Throat Culture (Requires 24 hour minimum for adequate growth ) most specific (99%). Sensitivity 90%. Not recommended as primary test due to 24 hour delay . Remember that –ve Rapid strep does not rule out Strep throat Strep Score 0 to 1   Provide Pharyngitis Symptomatic Treatment  salt water gargles, sucking candies, ibuprofen
  • Strep throat - Antibiotics     Penicillin is the first choice ( coz its strep)  penicillin VK 500 mg  If using this standard course duration is 10 days. Alternatively use Amoxicillin 500 bid in adults/ 10 days Alternative antibiotics : Five days of alternative antibiotics effective Amoxicillin Clavulanate (Augmentin) , Ceftibuten, Cefuroxime, Clarithromycin or Erythromycin estolate ( for pen allergic pts) Non-Compliant pts  single dose benzathine penicllin IM Recurrent Strep Throat  Cephalosporins are choice ( Keflex  cephalexin 500 bid) or can use Augmentin
  • Etiologies for recurrent Streptococcal Pharyngitis Poor Compliance with oral medications (most common)      Day 3: 50% stopped antibiotics Day 6: 70% stopped antibiotics Day 9: 80% stopped antibiotics Families reporting taking all the medication: 80% Repeat exposure in crowded conditions   School , Daycare & Home or workplace Eradicated protective throat flora by prior antibiotic    a-hemolytic Streptococcus is protective normal flora Cephalosporins apparently do less harm Selected beta-lactam resistance by prior antibiotic   Consider Augmentin for 10 day course Suppressed Immune response from prior antibiotics Antibiotic Resistance     Penicillin resistance is infrequent in strep throat Macrolide (Erythromycin, Biaxin, Zithromax)    Resistance 2-8% in U.S. Chronic Pharyngeal Carriage of Streptococcus pyogenes Consider Pharyngitis due to another cause
  • School Attendance ADVISE TO PARENTS!! High Yield!
  • Contraindications to school attendance  Infectious  Fever  Vomiting or dehydration Indications for school return in viral infection  Viral infection examples : Influenza, Rhinovirus (Common Cold) , Fifth Disease, Hand Foot and Mouth Disease  Indications to return to school  No fever and Child must practice good hygiene (i.e. hand washing) Indications for school return in bacterial infection  Bacterial infection examples: Impetigo, Bacterial Conjunctivitis, Streptococcal Pharyngitis (Strep Throat)  Indications to return to school  after Antibiotics for 24 hours Indications for school return in specific conditions  Chicken Pox  All lesions have crusted over  Head Lice  After anti-lice shampoo and manual nit removal  Pinworm  Day after Pyrantel, Mebendazole, or Albendazole  Vomiting  24 hours after last Emesis Conditions allowing immediate school return  Viral Conjunctivitis (Pink Eye)  Otitis Media (ear infection)
  • LRTIs
  • Acute Bronchitis   Usually viral Treat with antibiotics if second sickening or if associated with COPD exacerbation
  • Pneumonia  Community Acquired Pneumonia  Typical etiology : S.pneumoniae. Others: H.influezae, M.catarrhalis  Atypical pneumonia : Legionella, mycoplasma, chlamydia  Health care associated  - Nursing home acquired, - Hospl acquired , Ventilator associated
  • Severe Pneumonia CURB 65 predicts highly severe pneumonia  RR>30  DBP<60mmhg  BUN>20  CONFUSION  Age>65 yrs 
  • Whether to admit?  Most Pneumonias are treated as Outpatient  Admission is required if:  Those with underlying immunosuppression ( chemotherapy, HIV)  Elderly patients > 65 yrs  Pts with altered mental status  Those with hemodynamic ( shock) or respiratory compromise ( tachypnea, respiratory failure)  Pts with poor social support ( homeless) or without ability to self supervise
  • Where to Admit? Admission to ICU is needed if: LOOK AT VITALS!  Hypotension (SBP<90)  Hemodynamic Instability/ Shock (map<60)  Hypoxemia<60  Organ failure ( ARF etc)  Impending respiratory failure that may require mechanical ventilation ( persistent tachypnea, desaturation etc)  Deteriorating comorbid illness ( CHF, renal failure etc)  Heart failure, severe copd exacerbation, Diabetic complications (?DKA) 
  • Community acqd   Outpatient  Rx with Macrolide ( azithromycin) or newer Quinolones Inpatient  Rx with Ceftriaxone + macrolide or Fluoroquniolone alone
  • Health Care Associated Pneumonia    Either NH associated or hospital acquired NH associated pneumonia may have MRSA and Gram –ve bacteria as etiologies ( E.coli, proteus, klebsiella)  so emperically Rx with Vanco +Zosyn (pip/tazo) before sputum culture results are available. Once Cx and sensitivity are obtained d/c the antibiotic that’s not needed Hospital acquired pneumonia is the one that develops 48 hrs after hospitalization  has a different spectrum of bacteria ( MRSA + resistant gram –ves)  initially can start VANCO + Zosyn before cx results are available. If severe, use imipenem instead of Zosyn (pip/tazo)
  • VAP    Ventilator Acquired Pneumonia  Pneumonia that develops 48 hrs after intubation  diagnosed by c/f like fever, leucocytosis, newly developed CXR infiltrates and purulent ET tube secretions  the spectrum of bacteria here is more resistant i.e; MRSA+ Resistant gram –ves including P.aeruginosa  start emperical VANCO+Imipenem ( do not take chance with resistance here) Culture ET secretions, Get a CXR Bronchoscopy may be required in pts showing no response and also to differentiate b/w colonization vs. Infection  Recovery of bacteria in high concentrations from bronchoalveolar lavage (BAL) >10,000 col/ml helps in differentiation of non infectious from infectious causes of pulmonary infiltrates ( i.e; if the colonies are this high think of infection other wise think of non infectious cause like ARDS, CHF etc for explaining these pulmonary infiltrates in vent patients)
  • PCP       • • Pneumocystis Carinii pneumonia  Seen in immunocompromised pts Pts who are HIV,{CD4< 200} Immunocompromised and pts on high dose steroids ( prednisone>20mg/d), Symps: dry cough, fever, chills, sob, chestpain Needs high suspicion for diagnosis  LDH will help when in doubt, Gallium scan will help too CXR  Interstitial infiltrates, LDH high, Ground glass appearance on CT scan, Sputum for silver staining,  if sputum –ve, bronchoscopy needed for diagnosis where you do Bronchoalveolar lavage – silver staining Get an ABG Rx  Simple pcp  oral bactrim Severe pcp  iv bactrim + steroids ( make sure u give enough i.e; prednisone 40mg bid or solumedrol 30mg iv bid  Po2 < 70mm hg/ increased A-a > 35are indication for steroid Rx) Sulfa allergy  aerosolized pentamidine
  • Case Study       A 36-year-old woman is admitted to the medical intensive care unit because of respiratory depression resulting from a barbiturate overdose. She is intubated and mechanical ventilation is begun. Physical examination, except for her comatose condition, is unremarkable. Chest radiography and arterial blood gases are within normal limits. Which of the following will minimize her risk of developing a nosocomial infection? ( A ) Ventilator tubing changes every 12 hours ( B ) Elevation of the head of the bed to 45 degrees ( C ) Ceftriaxone, intravenously ( D ) Oropharynx polymyxin B spray every 8 hours ( E ) Enteral feedings by nasogastric tube
  • Ans.B   Patients who are mechanically ventilated in the supine position have an approximately six fold increased risk of developing pneumonia compared with patients maintained in a semirecumbent position. Elevation of the patient's head to 45 degrees may reduce aspiration and nosocomial pneumonia. Nosocomial pneumonia is a major cause of morbidity and mortality in mechanically ventilated patients.
  • Case Study  A 21-year-old woman with cystic fibrosis diagnosed at 6 months of age is evaluated because of increased dyspnea, blood-streaked purulent sputum, decreased energy, and a 1.8-kg (4-lb) weight loss of 4 weeks’ duration. She was last treated with intravenous antibiotics 12 months ago. Her sputum cultures repeatedly grow a mucoid strain of Pseudomonas aeruginosa. Her forced expiratory volume in 1 second (FEV1) has decreased by 400 mL in 6 months and is now 47% of predicted. Chest radiography shows diffuse bronchiectatic changes but no consolidation. She takes replacement pancreatic enzymes, albuterol nebulization three times daily, inhaled recombinant human Dnase once daily,and uses a flutter device to aid expectoration. Which of the following is the best management option at this time?  ( A ) Tobramycin, inhaled, twice daily ( B ) Increase Dnase, albuterol nebulizations, and chest physiotherapy ( C ) Piperacillin and tobramycin, intravenously ( D ) Ciprofloxacin, orally, and tobramycin, inhaled, twice daily ( E ) Bronchoscopy    
  • Ans.C   Patients with cystic fibrosis and a bronchitic exacerbation of chronic bronchiectasis with Pseudomonas aeruginosa require intravenous antibiotics with two antipseudomonal agents for 2 to3 weeks. The use of aerosolized tobramycin is indicated for patients with chronic Pseudomonas colonization and is associated with long-term improvement in forced expiratory volume in 1 sec (FEV1) of about 10%, as well as decreased need for hospitalization and intravenous antibiotics, but it is not sufficient for an exacerbation.
  • Pulmonary Embolism       Causes Clinical features  chestpain, sob, cough, leg swelling EKG – Sinus tachy, S1Q3T3 ABGs – resp alkalosis Diagnosis  v/q, d-dimer, high resolution CT (Spiral CT scan) ( Serum D-dimer < 500ng/ml Treatment – if shock or if no shock , if anticoagulation is contraindicated
  • PE on EKG  Pulmonary embolism (acute cor pulmonale) : Look for new signs of new signs of tachycardia; complete or incomplete RBBB; the S1Q3T3 pattern; and/or right axis shift. There may be inferior or RV injury patterns. The most common cause of an S1Q3T3 pattern is a completed inferior MI.  Get a Right sided EKG.
  • PE on CXR    Initial CxR may be NORMAL. ( PIOPED study showed that only 12% of CXRs in pts with angiographically proven PE were interpreted as normal) May show – Collapse, atelectasis, consolidation, small pleural effusion, elevated diaphragm. Pleural based opacities with convex medial margins are also known as a Hampton's Hump
  • Hampton's Hump  Pleural based opacities with convex medial margins are also known as a Hampton's Hump. This may be an indication of lung infarction. However, that rate of resolution of these densities is the best way to judge if lung tissue has been infarcted. Areas of pulmonary hemorrhage and edema resolve in a few days to one week. The density caused by an area of infarcted lung will decrease slowly over a few weeks to months and may leave a linear scar
  • PE on CXR  Westermark sign – Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels, often with a sharp cut off.
  • Pulmonary Embolism with Infarction       Consolidation Cavitation Pleural effusion (bloody in 65%) No air bronchograms “Melting” sign of healing Heals with linear scar
  • Case Study       A 56-year-old man is evaluated in the emergency department because of progressive swelling of the right lower extremity during the previous 5 days and right-sided pleuritic chest pain and dyspnea beginning 1 to 2 hours ago.On physical examination, his temperature is 38.2 °C (100.8 °F), pulse rate is 105/min, respiration rate is 28/min, and blood pressure is 160/80 mm Hg. Cardiac and pulmonary examinations are unremarkable. Arterial blood gases with the patient breathing room air are PO2, 78 mm Hg; PCO2, 30 mm Hg; and pH, 7.48.Electrocardiography shows sinus tachycardia and nonspecific ST-T wave changes, and chest radiography is normal.Ventilation-perfusion scanning shows two unmatched segmental defects. The D-dimer value is three times the upper limit of normal. Which of the following is the most appropriate course of action? ( A ) Heparin ( B ) Helical computed tomography with contrast ( C ) Noninvasive studies of the lower extremities ( D ) Pulmonary angiography
  • Key Point In patients with a high pretest probability of pulmonary embolism and high-probability ventilation-perfusion scanning, additional diagnostic testing is not necessary before initiating therapy.
  • Pneumothorax     Causes – Trauma, bulla rupture, necrotizing pneumonia Clinical features  chest pain, dyspnea, shock Ventilator associated Pneumothorax ? sudden hypotension while on vent  look at peak and plateau pressures Treatment  needle thoracentesis, needle thoracostomy, tube thoracostomy
  • ARDS     Diffuse pulmonary capillary damage leading to increased permeability of alveolar capillaries  pulm edema Criteria  1) There should be a cause 2) PO2/Fio2 ( in liter) Ratio, Po2/Fio2 < 300  ALI, <200 ARDS 3) B/L CXR infiltrates 4) Should not be due to CHF; Clues: 2D ECHO EF Good/ no diastolic dysfunction. If in doubt whether CXR infiltrates are due to CHF or ARDS  measure PCWP ( Swan Ganz insertion ) Ventilation strategies  Low Vt ( 6cc/kg) (  prevent overdistension injury) and High PEEP strategy ( reduce derecruitment injury) Causes  TTP, Sepsis, Shock, Aspiration pneumonia, chemical pneumonitis, Drugs like Heroin, Pancreatitis, Burns, Drowning
  • Case Study        A 58-year-old man is admitted to the intensive care unit with increasing dyspnea after developing influenza symptoms 3 days previously. On physical examination, his temperature is 39.1 °C (102.3 °F), pulse rate is 110/min, and bloodpressure is 135/83 mm Hg. He weighs 73 kg (161 lb). He is using accessory muscles of respiration, and he has finecrackles throughout all lung fields. Cardiac examination is unremarkable, and no edema is noted. Chest radiographyshows diffuse infiltrates throughout both lungs with patchy areas of consolidation. The patient has a history of moderate obstructive lung disease secondary to smoking. Several months before hospitalization his forced expiratory volume in 1sec (FEV1) was 53% of predicted, and he had normal oxygen saturation and no hypercapnia.Shortly after hospitalization, he is intubated because of increasing hypoxemia and hypercapnia. Subsequent arterial blood gases with the patient breathing 100% oxygen and 10 cm H2O of positive end-expiratory pressure are PO2, 68mm Hg; PCO2, 65 mm Hg; pH, 7.23; and bicarbonate, 26 meq/L. Tidal volume is 450 mL, respiration rate is 25/min,inspiratory flow rate is 100 L/min, and inspiratory/expiratory ratio is 1:5. Peak airway and plateau ventilatory pressures are 48 cm H2O and 32 cm H2O. Which of the following is the best option? ( A ) Increase the tidal volume ( B ) Increase the respiration rate ( C ) Increase the positive end-expiratory pressure ( D ) Decrease the positive end-expiratory pressure ( E ) Administer sodium bicarbonate, intravenously
  • Key Points   Ans. E In patients with acute respiratory distress syndrome, mortality was significantly improved by ventilating patients with tidalvolumes of 6 mL/kg of ideal body weight and keeping plateau ventilatory pressure at =30 cm H2O.  If changes in respirator settings required to prevent hypercapnia have associated untoward effects, it is reasonable to allow arterial PCO2 to rise and, if necessary, prevent acidemia by administration of buffer  as in this case!! ( don’t increase tidal volume here  low Vt is good for this  remember Permissive Hypercapnia)  Increasing PEEP is not good here. Raising PEEP is undesirable because this will narrow the pressure difference between the plateau ventilatory pressure and the PEEP, decreasing the pressure available to deliver the tidal volume. This will reduce the tidal volume and exacerbate hypercapnia. PEEP should remain unchanged because the patient has acceptable oxygenation with the present setting. The level of PEEP cannot be reduced since reduction likely will lead to unacceptable hypoxemia. The patient is barely at an acceptable level without any reduction.  Increasing the respiration rate likely will increase auto-positive end-expiratory pressure (PEEP) in this patient with chronic obstructive pulmonary disease ( they have proloned expiration!) by “breath stacking,” that is, delivering the next breath before the previous breath is completely expired.This will also raise the plateau ventilatory pressure above a desirable range.
  •       Case Study A 57-year-old man with severe chronic obstructive pulmonary disease is hospitalized with respiratory distress of 12 hours’ duration. Arterial blood gases with the patient breathing 35% oxygen through a face mask are PaO2, 50 mm Hg; PaCO2, 70 mm Hg; and pH, 7.24. When seen as an outpatient 1 month previously, his arterial blood gases while breathing room air were PaO2, 58 mm Hg; PaCO2, 50 mm Hg; and pH, 7.37. Despite maximal therapy, mechanical ventilation is required. During controlled breaths, his peak airway pressure is 25 cm H2O, and plateau ventilatory pressure is 12 cm H2O. The arterial blood gases are checked after 1 hour. Which of the following is the most desirable set of arterial blood gas values? ( A ) Pa O2, 50 mm Hg; PaCO2, 45 mm Hg; pH, 7.44; FIO2, 0.3 ( B ) Pa O2, 65 mm Hg; PaCO2, 52 mm Hg; pH, 7.38; FIO2, 0.4 ( C ) Pa O2, 65 mm Hg; PaCO2, 40 mm Hg; pH, 7.48; FIO2, 0.4 ( D ) Pa O2, 90 mm Hg; PaCO2, 60 mm Hg; pH, 7.32; FIO2, 0.5 ( E ) Pa O2, 133 mm Hg; PaCO2, 55 mm Hg; pH, 7.41; FIO2, 0.6
  • Ans.B   When instituting mechanical ventilation in a patient with chronic hypercapnia, it is critical to avoid the development of respiratory alkalemia secondary to overventilation, and ventilator settings should have pH as a target, rather than PaCO2. When seen 1 month before hospitalization, the patient had chronic carbon dioxide retention. When instituting mechanical ventilation in a patient with hypercapnia, it is critical to avoid the development of respiratory alkalemia secondary to overventilation. Severe alkalosis in this setting may result in cardiovascular instability, arrhythmias, andseizures. Ventilator settings should have pH as a target, rather than PaCO2.
  • Acute Pulmonary Edema   Treatment  morphine, loop diuretics in LVF, Ventilation strategies in ARDS and Hemodialysis when indicated Causes  ARDS, Acute LVF, Fluid Overload, Missing Hemodialysis
  •         A 58-year-old man is admitted to the intensive care unit with increasing dyspnea after developing influenza symptoms 3 days previously. On physical examination, his temperature is 39.1 °C (102.3 °F), pulse rate is 110/min, and blood pressure is 135/83 mm Hg. He weighs 73 kg (161 lb). He is using accessory muscles of respiration, and he has fine crackles throughout all lung fields. Cardiac examination is unremarkable, and no edema is noted. Chest radiography shows diffuse infiltrates throughout both lungs with patchy areas of consolidation. The patient has a history of moderate obstructive lung disease secondary to smoking. Several months before hospitalization his forced expiratory volume in 1 sec (FEV1) was 53% of predicted, and he had normal oxygen saturation and no hypercapnia. Shortly after hospitalization, he is intubated because of increasing hypoxemia and hypercapnia. Subsequent arterial blood gases with the patient breathing 100% oxygen and 10 cm H2O of positive end-expiratory pressure are PO2, 68 mm Hg; PCO2, 65 mm Hg; pH, 7.23; and bicarbonate, 26 meq/L. Tidal volume is 450 mL, respiration rate is 25/min, inspiratory flow rate is 100 L/min, and inspiratory/expiratory ratio is 1:5. Peak airway and plateau ventilatory pressures are 48 cm H2O and 32 cm H2O. Which of the following is the best option for improving this patient’s acid–base disorder? ( A ) Increase the tidal volume ( B ) Increase the respiration rate ( C ) Increase the positive end-expiratory pressure ( D ) Decrease the positive end-expiratory pressure ( E ) Administer sodium bicarbonate, intravenously
  • Ans.   In patients with acute respiratory distress syndrome, mortality was significantly improved by ventilating patients with tidalvolumes of 6 mL/kg of ideal body weight and keeping plateau ventilatory pressure at =30 cm H2O. If changes in respirator settings required to prevent hypercapnia have associated untoward effects, it is reasonable to allowarterial PCO2 to rise and, if necessary, prevent acidemia byadministration of buffer.
  • COPD
  • COPD – Screening with Spirometry     Consider screening smokers or former smokers with certain clinical characteristics for COPD with pulmonary function testing. In patients who smoke or have smoked, consider obtaining screening spirometry readings to document obstruction if they give a history of cough or sputum production or have findings compatible with emphysema on chest x-ray. Obtain spirometry readings if the patient has limiting symptoms such as dyspnea inappropriate to the level of activity, frequent episodes of acute bronchitis related to upper respiratory tract infections (i.e., a possible acute exacerbation), difficulty sleeping due to cough and dyspnea, and general diminished activity levels and energy from difficulty in breathing. If the patient has no other clinical characteristics for COPD, but has a significant history of smoking, consider obtaining spirometry readings because significant pulmonary function impairment may still be present.
  •    COPD Exacerbations COPD – Chr.bronchitis, Emphysema – blue bloaters, Pink puffers COPD exacerbations  History, Clinical exam, get pulse ox, Mild, Moderate, Severe  classify depending on 3 criteria (Increase in amount of sputum, Increased sputum purulence, worsening dyspnea)  Mild exacerbation ( 1 of above criteria)  use simple antibiotics like Bactrim or Doxycycline  Moderate exacerbation ( 2 of above criteria) use 2nd line Antibiotics like quinolones, b-lactam/clavulanate ( Augmentin)  Severe Exacerbation ( 3 of above criteria)  Look at the ABGs, o2 inhalation, nebulizer with ipratropium + albuterol  caution with o2, o2 inhalation only as much as to maintain sao2>90%.  If no response , non invasive ventilation ( positive pressure ventilation, BIPAP)  Pt must be cooperative for this  if altered mental status, no response with non invasive ventilation  Intubate and ventilate. Remember to get ABGs after u place a COPD guy on oxygen Beware of posthypercapnic alkalosis  if develops, acetazolomide COPD exacerbation  ? Ask urself secondary to what  Acute bronchitis, pneumonia  use of antibiotics in COPD exacerbations Steroids is a MUST  methylprednisolone high doses 125mg q6hrs, then tapering steroids    
  • When To Admit? Indications for hospitalization of patients with COPD:  Patient has acute exacerbation plus one or more of the following:             Inadequate response of symptoms to outpatient management Inability to walk between rooms (patient previously mobile) Inability to eat or sleep due to dyspnea Conclusion by family, physician, or both that patient cannot manage at home and supplementary home care resources are not immediately available Presence of a high-risk comorbid condition, pulmonary (e.g., pneumonia) or nonpulmonary Prolonged, progressive symptoms before emergency department visit Altered mentation Worsening hypoxemia New or worsening hypercarbia Patient has new or worsening cor pulmonale unresponsive to outpatient management A planned invasive surgical or diagnostic procedure requires analgesics or sedatives that may worsen pulmonary function Comorbid conditions (e.g., steroid myopathy or vertebral compression fractures) have worsened pulmonary function
  • Where To Admit?  Admit patients with COPD to an intensive care unit if they meet specific criteria.     Confusion, lethargy, or respiratory muscle fatigue Persistent or worsening hypoxemia despite supplemental O2 or severe or worsening of respiratory acidosis (pH 7.30); use of supplemental oxygen should be at the lowest flow rate to raise PaO 2 >60 or SaO 2 >90% to avoid hyperoxic hypercapnia Need for assisted mechanical ventilation, whether through means of tracheal intubation or noninvasive techniques Severe dyspnea that responds inadequately to initial emergency room therapy
  • COPD – Home Oxygen Therapy At discharge, evaluate pt for home 02 therapy. Especially at nights when pts may desaturate ( acidosis at nights shifts curve to right). Goal maintain sao2 90 or po2 60  Indications :  Po2<55 or sao2 <85%  Po2 b/w 56 to 59 if corpulmonale or polycythemia ( erythrocytosis) (  these suggest evidence of hypoxia) 
  • Lung Volume Reduction Surgery  Consider LVRS for patients whose initial clinical criteria include:        CT scan evidence of bilateral emphysema Prerehabilitation postbronchodilator TLC and residual volume >/= to 100% and 150% predicted, respectively Maximum FEV1 </= 45% predicted PaCO2 </= 60 mm Hg PaO2 >/= 45 mm Hg Completion of a pulmonary rehabilitation program Do not consider LVRS for patients whose clinical criteria include:   FEV1 less than or equal to 20% predicted ( very low for surgery) and either homogenous emphysema or carbon monoxide diffusing capacity less than or equal to 20% predicted (DLCO) Non-upper-lobe emphysema and high baseline exercise capacity
  • Interpretation of PFT’S Restrictive vs. Obstructive  FEV1 to FVC Ratio (Normally over 75%)  Not useful if both FEV1 and FVC are normal  Obstructive lung: Moderately to severely decreased  Restrictive lung: Normal or increased Reversibility:  Bronchodilator response (Significant values)  Response suggests reversible component if  FVC or FEV1 improves by 12 to 15% over baseline  FVC or FEV1 increases by at least 200 ml  FEF25-75 improves by 15 to 25% over baseline 
  • COPD Outpatient Rx     By MDIs  Ipratropium all the time ( q6hrs) + albuterol as needed. Can use tiotropium because its long acting Evaluate for home o2 therapy Steroids/ antibiotics in acute exacerbations only.  ( unlike in Asthma, steroids are not a part of chronic therapy in COPD) MDIs deliver only fixed dose of drug. Nebulizers deliver larger dose of drug  so in exacerbation u start with nebulizer if MDIs don’t work
  • COPD with Asthma  Asthma may be present in about 10% of cases of COPD; however, reversibility of FEV1 alone should never be used to make a diagnosis of asthma in the absence of other supporting evidence such as a childhood history of asthma, atopic symptoms, blood or sputum eosinophilia, or onset of symptoms before substantial history of cigarette smoking
  • COPD in the Young
  •        A 38-year-old man is evaluated because of a morning cough productive of clear sputum, chest tightness, and shortness of breath when walking. He has smoked two packs of cigarettes per day since his teenage years and says that previous chest radiography showed "early emphysema." He is a baker but notes no improvement in symptoms when on vacation. His wife has three indoor cats, and he has an outdoor dog. The patient has normal vital signs. The chest is hyperresonant to percussion, breath sounds are decreased in intensity, and expiration is prolonged. Pulmonary function tests show forced expiratory volume in 1 sec (FEV1) is 45% of predicted, forced vital capacity (FVC) is 65% of predicted, total lung capacity (TLC) is slightly increased (120% of predicted), and diffusing lung capacity for carbon monoxide (DLCO) is moderately reduced (60% of predicted). Chest radiography shows hyperinflation with a suggestion of several small bullae in the lower lung fields. Which of the following tests is indicated? ( A ) Sputum Gram stain and culture ( B ) Methacholine inhalation challenge test ( C ) Skin tests for allergens and serum precipitins to wheat extract ( D ) Measurement of serum a 1-antitrypsin level ( E ) Esophageal pH monitoring for 24 hours
  •   Severe chronic obstructive pulmonary disease in young persons is suggestive of a1antitrypsin deficiency, and an a1-antitrypsin level should be measured. Smoking is an important precipitating factor and also increases progression
  • Case Study        A 67-year-old man with longstanding chronic obstructive pulmonary disease (COPD) is hospitalized with a 1-week history of increasing cough productive of large amounts of purulent sputum, low-grade fever, lethargy, and shortness ofbreath.On physical examination, his vital signs are normal except for a temperature of 38.2 °C (100.7 °F) and a pulse rate of 108/min. The neck veins are not distended. The anterior–posterior chest dimension is increased and is hyperresonant to percussion, breath sounds are reduced, and expiration is prolonged.Arterial blood gases are normal except for a PO2 of 62 mm Hg with the patient breathing 28% oxygen through a venturi mask. Chest radiography shows changes compatible with COPD but no acute process.In the emergency department, treatment with inhaled bronchodilators and antibiotics was begun. Which of the following options is the best choice? ( A ) Add inhaled fluticasone, every 12 hours ( B ) Add methylprednisolone, 500 mg intravenously once ( C ) Add methylprednisolone, 125 mg intravenously every 6 hours for 3 days, then taper over 2 weeks (D) No need to add steroids in this patient E) Intubate the patient
  • Key Point Patients with exacerbations of chronic obstructive pulmonary disease (COPD) who receive intravenous corticosteroids and a tapering dose of prednisone over 2 weeks experience shorter hospitalization and less treatment failures. Two weeks of tapering prednisone is just as effective as 8 weeks in treating exacerbations of COPD.
  •            A 57-year-old man with severe chronic obstructive pulmonary disease is hospitalized with respiratory distress of 12 hours’ duration. Arterial blood gases with the patient breathing 35% oxygen through a face mask are PaO2, 50 mm Hg; PaCO2, 70 mm Hg; and pH, 7.24. When seen as an outpatient 1 month previously, his arterial blood gases while breathing room air were PaO2, 58 mm Hg; PaCO2, 50 mm Hg; and pH, 7.37. Despite maximal therapy, mechanical ventilation is required. During controlled breaths, his peak airway pressure is 25 cm H2O, and plateau ventilatory pressure is 12 cm H2O. The arterial blood gases are checked after 1 hour. Which of the following is the most desirable set of arterial blood gas values? ( A ) Pa O2, 50 mm Hg; PaCO2, 45 mm Hg; pH, 7.44; FIO2, 0.3 ( B ) Pa O2, 65 mm Hg; PaCO2, 52 mm Hg; pH, 7.38; FIO2, 0.4 ( C ) Pa O2, 65 mm Hg; PaCO2, 40 mm Hg; pH, 7.48; FIO2, 0.4 ( D ) Pa O2, 90 mm Hg; PaCO2, 60 mm Hg; pH, 7.32; FIO2, 0.5 ( E ) Pa O2, 133 mm Hg; PaCO2, 55 mm Hg; pH, 7.41; FIO2, 0.6
  • Q        65 Y/O comes with cough and exertional sob of several month duration. He has smoked for 35 years. On physical examination, he is sweating, ruddy, and cyanotic. His pulse rate is120/min and regular, respiration rate is 30/min and labored, and blood pressure is 150/90 mm Hg. The neck veins are distended to the angle of the jaw when sitting upright. The chest shows hyperinflation, prolonged expiration, wheezing, and crackles at each posterior base. The pulmonic sound is increased, and there is a summation gallop. An enlargedand tender liver edge is felt 2 cm below the costal margin. He has marked dependent edema up to the knees.The hematocrit is 55%, and leukocyte count is 8000/μL. Arterial blood gases with the patient breathing room air arePaO2, 47 mm Hg; PaCO2, 50 mm Hg; and pH, 7.30. Spirometry performed 2 years earlier showed a forced expiratoryvolume in 1 sec (FEV1) of 0.65 L and a forced vital capacity (FVC) of 3.05 L. Chest radiography shows hyperinflation, clear lung fields, and biventricular enlargement. Ventilation-perfusion lung scanning shows multiple matched fillingdefects that are not segmental. Doppler studies of the legs are negative.After treatment of the patient’s acute condition, which of the following is the best long-term therapy for this patient? ( A ) Nifedipine ( B ) Warfarin ( C ) Bosentan ( D ) Oxygen ( E ) Phlebotomy
  • Case Study  A 65-year old male hospital in-patient has smoked cigarettes since he was 18 years old. He has a chronic cough and marked sputum production. When his doctor starts to give him the usual talk about losing weight, he explains that since he has about fifty pounds to lose, he has tried to exercise, but is unable to because of shortness of breath with any activity. Upon further questioning, he comments that his symptoms have been present for a very long time, but he was hospitalized due to a marked exacerbation of his complaints. On auscultation, rhonchi and wheezes are heard.His laboratory results are as follows:  pCO2 60 mm Hg(35-45 mm Hg) pH 7.34( 7.35-7.45) bicarbonate 31 mEq/L( 24 mEq/L) Na+ 140 mEq/L( 135-145 mEq/L) K+ 4.0 mEq/L( 3.5-5.5 mEq/L) Cl-100 mEq/L(98-109 mEq/L) What is the primary disorder?       a) metabolic acidosis with a normal anion gap b) metabolic acidosis with an elevated anion gap c) metabolic alkalosis d) respiratory acidosis e) respiratory alkalosis
  • Ans.D  This patient has symptoms and signs of chronic obstructive pulmonary disease, specifically chronic bronchitis. Symptoms and signs include cough, sputum production and dyspnea with exertions. Patients tend to be stocky or overweight, as the case here. Auscultation will reveal wheezes and rhonchi. This patient is retaining CO2, since his pCO2 is elevated. CO2 is in equilibrium with carbonic acid. An increase in CO2 will shift the Henderson Hasselbalch equation to the left, resulting in acidosis. Since the cause of the primary problem is respiratory, e.g. retention of CO2, this is a respiratory acidosis. This is reflected in the pH being reduced as well.Metabolic acidosis (choice a, choice b) is incorrect because the primary problem is not due to a administration of acid, excess metabolic acid formation, or loss of base. Although the bicarbonate level is abnormal in this patient, that is due to metabolic compensation for the respiratory acidosis. Alkalosis (choice c, choice e) are incorrect because his pH is acidotic. Although compensatory mechanisms can bring the pH towards the normal range, compensatory mechanisms will never overshoot.
  •       A 54-year-old man is hospitalized because of severe shortness of breath, ankle swelling, and confusion of 5 days’ duration. He has smoked for 35 years. On physical examination, he is sweating, ruddy, and cyanotic. His pulse rate is 120/min and regular, respiration rate is 30/min and labored, and blood pressure is 150/90 mm Hg. The neck veins are distended to the angle of the jaw when sitting upright. The chest shows hyperinflation, prolonged expiration, wheezing, and crackles at each posterior base. The pulmonic sound is increased, and there is a summation gallop. An enlarged and tender liver edge is felt 2 cm below the costal margin. He has marked dependent edema up to the knees. The hematocrit is 55%, and leukocyte count is 8000/μL. Arterial blood gases with the patient breathing room air are PaO2, 47 mm Hg; PaCO2, 50 mm Hg; and pH, 7.30. Spirometry performed 2 years earlier showed a forced expiratory volume in 1 sec (FEV1) of 0.65 L and a forced vital capacity (FVC) of 3.05 L. Chest radiography shows hyperinflation, clear lung fields, and biventricular enlargement. Ventilationperfusion lung scanning shows multiple matched filling defects that are not segmental. Doppler studies of the legs are negative. After treatment of the patient’s acute condition, which of the following is the best long-term therapy for this patient? ( A ) Nifedipine ( B ) Warfarin ( C ) Bosentan ( D ) Oxygen ( E ) Phlebotomy
  • Ans. D  In patients with cor pulmonale caused by chronic hypoxemia, oxygen therapy is the treatment of choice; it may decrease the heart failure and polycythemia seen in this condition.
  • Asthma   Classification: Management Grouping Mild Intermittent Asthma   Mild Persistent Asthma    Daily symptoms with daily Beta Agonist use Severe Persistent Asthma   Frequent exacerbations (>twice weekly, but not daily) Moderate Persistent Asthma   Occasional exacerbations (Less than twice per week) Continuous Symptoms and frequent exacerbations Treatment  short acting MDIs as needed, long acting bronchodilators ( once asthma becomes moderate to severe add these as adjuncts to inhaled steroids), inhaled steroids ( first line agent in all persistent asthmas) , systemic steroids, monteleukast ( add this as adjunct in moderate to severe asthma) Status asthmaticus
  • Asthma Examples of different therapeutic approaches:  Mild Intermittent: use only prn albuterol; if related to exercise, use albuterol one-half hour prior to exercise; also used: cromolyn one half-hour prior to exercise.  Mild Persistent: daily: low dose inhaled steroids; and use albuterol intermittently as needed. May use inhaled cromolyn.  Moderate Persistent: use peak flow meter daily; use med dose inhaled steroid or low dose steroids plus serevent or singulair. Others switch to Advair. PO steroids prn.  Severe Persistent: use peak flow meter daily; po steroids as needed. Daily meds to include high dose inhaled steroids, singulair, serevent or possibly Advair.
  • Classification:   Mild  Mild  Mod  Intermitt Persist Persist Severe Persistent ent ent ent Sym < 2 /  ptom week s > 2 /  week Daily Continual Night  < 2 /  sx month > 2 /  month > 1 /  week Frequent FEV 1 > 80%  >  predicte 80%pre 60-80% < 60% d dicted Peak  flow  < 20% Varia bility 20-30% > 30 % > 30%
  • Management  of different categories of  Asthma: Mild    Intermitte nt Peak Flow Meter         Mild  Persistent Mod  Persistent Severe Persistent          X       X Preventive Meds (daily): --Inhaled Cromolyn   X (X)   --Inhaled Steroids   X (low  dose) X (med  dose) X (high dose) --Po Singulair   X X X --Advair Diskus  ( Salmetrol/  Fluticasone)     X X --Serevent  ( Salmetrol)     X X --Albuterol X X X X --Po Prednisone prn Prn Prn prn  Skin Testing:  Allergy Evaluation    Consider  Consider  Consider Rescue Medications
  • Case Study       A 68-year-old man with asthma is evaluated because he needs to use his albuterol inhaler at night once or twice a week after waking up with chest tightness. His forced expiratory volume (FEV) is 2.18 L (65% of predicted) before and 2.62 L(82% of predicted) after inhaled albuterol. Current medications include inhaled fluticasone, 440 μg twice daily, and an albuterol metered-dose inhaler as needed. Which of the following should be done next to better control his symptoms? ( A ) Increase fluticasone to 880 μg twice daily ( B ) Add salmeterol ( C ) Add prednisone ( D ) Add allergen immunotherapy ( E ) Add a long-acting theophylline at bedtime
  • Key Point In patients with moderate-to-severe asthma not responding to adequate doses of a short-acting ß-agonist and inhaled corticosteroids, the next step is addition of a long-acting ß-agonist.
  • Case Study       A 25-year-old woman is evaluated because of a 3-year history of a nonproductive cough. The cough is aggravated by bicycle riding and occasionally awakens her from sleep. During the past year, she experienced two episodes of bronchitis followed by a dry cough persisting for 2 months. The cough worsened when she visited her sister in Alaska. She has seasonal symptoms of watery, runny nose and sneezing. There is no postnasal discharge, nasal congestion, heartburn, weight loss, or night sweats. She does not smoke. Her physical examination and chest radiography are normal. Spirometry shows forced expiratory volume in 1 sec (FEV1) 3.29 L; forced vital capacity (FVC), 4.13 L; and FEV1/FVC ratio of 79%. Which of the following is the best next management step? ( A ) Chest computed tomography ( B ) Bronchoscopy ( C ) Methacholine inhalation challenge testing ( D ) Observation and reassurance ( E ) Therapeutic trial of a proton pump inhibitor
  • Cough Variant Asthma Cough-variant asthma is nonproductive, provoked by exercise and cold air, disturbs sleep, and worsens after a lower respiratory tract infection. The inhalation of methacholine produces airway obstruction in most patients with asthma; less than 10% of normal persons have positive responses ( false +ves) .
  • Case Study       A 45-year-old woman is evaluated because of dyspnea during exercise that began when she started an aerobics class. She has dyspnea, chest tightness, and a nonproductive cough after 15 minutes of vigorous step exercises. The symptoms worsen slightly when she stops, then gradually abate. She has a 5-pack-year smoking history but quit 10 years ago. The physical examination, chest radiography, and electrocardiography are all normal. Spirometry shows forced expiratory volume in 1 sec (FEV1), 2.72 L (83% of predicted); forced vital capacity (FVC), 3.2 L(86% of predicted); and FEV1/FVC ratio of 85%. Postexercise spirometry shows FEV1, 2.04 L (25% drop from baseline),and FVC, 3.00 L (2% drop from baseline). Which of the following management options should be done next? ( A ) Reassure the patient ( B ) Prescribe an albuterol inhaler 15 minutes before exercise ( C ) Perform an exercise stress test ( D ) Measure lung volumes and diffusing capacity ( E ) Perform high-resolution computed tomography of the chest
  • Ans.b  For patients with exercise-induced asthma, an inhaled ß-agonist should be prescribed before exercise.
  • Case Study  WHEN CONSIDERING THE DRUG TREATMENT OF ASTHMA WITH INHALER DEVICES A. The incidence of oral candidiasis is increased by the use of spacer devices. B. Salmeterol is indicated for p.r.n. usage. C. Intermittent terbutalin has been shown to lead to long term worsening of asthma. D. Steroid dosage of 600mg daily has been shown to be associated with adrenal suppression in adults. E. Sodium cromoglycate is of no proven value in treating acute asthmatic attacks
  • Ans.E  Spacer devices decrease the incidence of oral candidiasis by preventing the deposition in the mouth. Salmeterol is a long acting beta antagonist, its action is slow in onset and therefore it should be given regularly rather than p.r.n. The Committee on Safety of Medicines has reported that salbutamol and terbutaline have not been shown to lead to a worsening of mild asthma. In adults an inhaled dosage of steroid of 1,500 micrograms daily is associated with adrenal suppression . Sodium cromoglycate is of no value in and acute attack and is only indicated for prophylaxsis.
  • OSA       Check for symptoms of excessive daytime sleepiness Diagnose by sleep study. Obesity – neck circumference > 17cm important predictor. Check local anatomy, Throat crowding, secondary factors (thyroid, cushings) causing obesity. Obesity Hypoventilation syndrome Rx – c-pap at nights
  • Q       A 43-year-old man is evaluated because of uncontrolled hypertension, documented in and outside of the office, despite moderate doses of hydrochlorothiazide and enalapril. For the past 6 months he has noted increased fatigue and irritability that he attributes to personal problems at work. He admits to difficulty concentrating at work. He has two beers before bed to fall asleep. He is a salesman, smokes one pack of cigarettes per day, and lives alone. His neck circumference is 17.5 in. On physical examination, he has a ruddy complexion, body mass index is 32, and blood pressure is 158/88 mm Hg. Jugular venous distention cannot be evaluated because of obesity. An S4 is present. The remainder of the examination is normal. A complete blood count, serum electrolytes, serum creatinine, blood urea nitrogen, electrocardiography, and chest radiography are normal. Which of the following is most likely to establish a diagnosis? ( A ) Ambulatory blood pressure monitoring ( B ) Pulmonary function studies ( C ) Polysomnography ( D ) Arterial blood gases and blood volume determination
  • Q2       A 58-year-old man is evaluated because of daytime sleepiness. He is requesting an evaluation at this time because last week he fell asleep while driving and had a minor accident. He is a lifetime nonsmoker and is otherwise healthy. On physical examination, his body mass index is 26. There are no obvious abnormalities of his oropharynx. Chest and cardiac examinations are normal. There is no peripheral edema. Chest radiography and electrocardiography are normal. Overnight polysomnography for 6 hours of sleep shows 60 episodes of apnea (cessation of airflow for more than 10 seconds) per hour accompanied by frequent oxygen desaturation below 85%. There is evidence of rib cage and abdominal motion during the apneic periods. Which of the following is the most appropriate form of therapy for this patient? ( A ) Nasal continuous positive-airway pressure ( B ) Uvulopalatopharyngoplasty ( C ) Progesterone ( D ) Mandibular repositioning device ( E ) Nocturnal supplemental oxygen by nasal cannula
  • Ans. A    Nasal continuous positive-airway pressure (CPAP) is the standard initial treatment for patients with symptomatic moderate-to-severe obstructive sleep apnea syndrome. It works by splinting the upper airway in an open position. Surgical procedures such as uvulopalatopharyngoplasty (UPPP) and tracheostomy are best considered in severely ill patients for whom more conservative measures such as nasal CPAP are ineffective. Although tracheostomy cures obstructive sleep apnea, it carries associated complications and is poorly accepted by patients. UPPP, whether performed with conventional or laser surgery, has variable long-term results and also has associated complications.
  • Restrictive Diseases - Sarcoidosis Pathophysiology  Noncaseating granuloma formation  Idiopathic  underlying genetic predisposition   Precipitated by trigger  Infection (e.g. Mycobacteria, Borrelia Burgdorferi), Environmental exposure (e.g. Beryllium, Aluminum) Common involvement sites (affects all organ systems)        Lungs (>90%): Interstitial Lung Disease Lymphadenopathy: Hilar adnenopathy (>95%) Liver (50-80%) : Hepatic Granulomas (86%), Increased Alkaline Phosphatase Spleen Skin lesions (25%) Eyes : Anterior Uveitis ( also in Spondyloarthropathy) , Posterior Uveitis, Heart (5%)   Tachyarrhythmias Cardiomyopathy ERYTHEMA NODOSUM SUGGESTS BETTER PROGNOSIS  Associated with acute arthritis (Lofgren's Syndrome) - Not associated with chronic arthritis  Most common associated nonspecific skin sign 
  • Sarcoidosis Diagnosis  Pulmonary Function Testing   Serum Angiotensin-converting enzyme (Serum ACE)   Findings consistent with Interstitial Lung Disease Increased in 50-80% of Sarcoidosis patients Biopsy or Cytology (Gold standard)  Finding   Discrete noncaseating epithelioid granuloma Biopsy sites      Transbronchial lung biopsy (preferred site) Bronchoalveolar lavage (CD4-CD8 ratio >3.5) Skin biopsy of lesion Palpable peripheral lymph node biopsy Salivary Gland biopsy
  • Sarcoid - lung Radiology: Chest XRay (abnormal in 90% of cases)  Type 0: No abnormality (<10% of cases)  Type I: Lymphadenopathy alone (43% of cases)     Type II: Adenopathy and Infiltrates (24% of cases)     Bilateral hilar Lymphadenopathy Mediastinal Lymphadenopathy Right paratracheal Lymphadenopathy Lymphadenopathy as in Type I Chest XRay findings Parenchymal infiltrates Symptomatic respiratory disease presentation Type III: Infiltrates alone (13% of cases)  Parenchymal infiltrates
  • Sarcoidosis - Treatment    Cutaneous  for Erythema nodosum use NSAIDS, For sarcoid lesions use intralesional Corticosteroids For uveitis  topical CS, Systemic CS if refractory For pulmonary sarcoidosis stage 2 or 3  Indications : Dyspnea , Persistent cough and Widespread debilitating disease  systemic CS/ AZA
  • Sarcoidosis - Prognosis Prognosis  Overall mortality (from respiratory failure): 1-5%  Factors suggestive of worse prognosis     Onset after age 40 years Black race Chronic Hypercalcemia Specific higher risk organ involvement       Neurologic involvement Cardiac involvement Eye involvement (Chronic Uveitis) Renal involvement (Nephrocalcinosis) Cystic bone lesions Progressive pulmonary fibrosis
  • Idiopathic Pulmonary Fibrosis     CXR – Picture Physical – chest bibasal creps HRCT confirmatory Not responsive to steroids
  • TB - Screening    Screen for LTBI in persons at increased risk of recent infection, including immigrants within the last 5 years from high prevalence countries; pre- and postexposure in travelers visiting countries with a high prevalence of TB; those in recent contact with a case of infectious TB; health care workers with potential exposure to mycobacteria; and residents and employees of high-risk congregate settings where local epidemiology indicates a high rate of TB. Screen for LTBI in persons with conditions associated with an increased risk of developing active TB, including HIV infection, diabetes, silicosis or exposure to silica dust, low body weight, chronic renal failure or hemodialysis, gastrectomy, jejunoileal bypass, cirrhosis of the liver, organ transplantation, anticancer chemotherapy and other immunosuppression (e.g., TNF-α antagonists), malignant head or neck carcinoma, or fibrotic changes on CXR film compatible with previous TB. Screen children and adolescents for LTBI who have risk factors for development of active disease (e.g., HIV), have been exposed to adults at high risk for TB, or have been adopted from abroad, especially if they were born in countries with endemic TB.
  • TB - Screening   PPD test is used for screening and its sensitivity approaches 100% in pts with normal immunity. As an alternative to the PPD, consider using a wholeblood IFN-γ assay such as QuantiFERON-TB Gold, recognizing its limitations in children and immunocompromised patients and that all currently available studies on the sensitivity and specificity of this test are limited by the lack of an eternal “gold standard” for the diagnosis of tuberculous infection, but that there is good reason to believe that the QuantiFERON-TB Gold test is superior to the TST in BCG-vaccinated individuals because it employs the ESAT-6 antigen that is lacking in BCG
  • TB and PPD Interpretation: PPD under 5 mm  Negative  Observe Patient Interpretation: PPD 5 mm or greater  Positive if      HIV Infection Tuberculosis contact Immunosuppressed (e.g. HIV, Prednisone >15 mg qd) Abnormal finding on Chest XRay Management   Chest XRay and exam for disseminated disease If cxr –ve INH for 9 mos
  • TB and PPD Interpretation: PPD 10 mm or greater  Positive if           Health care workers New immigrant within last 5 years Intravenous Drug Abuse Homeless Under 4 years old Malnutrition Diabetes Mellitus Silicosis Tuberculosis endemic to region Management  Chest XRay and exam for disseminated disease
  • TB and PPD Interpretation: PPD 15 mm or greater  Positive in all persons  Management Chest XRay and exam for disseminated disease  INH 9 mos if no active disease ( i.e; you are treating Latent TB)  If active disease  First step Sputum for AFB smear x 3, Sputum for AFB cx and Sensitivity; isolate the patient, isolate organism for susceptibility testing  start emperic multi drug regimens HRZE  For failure/ resistant TB  SHRZE  Sputum –ve pts can be taken off Isolation. 
  • Latent TB – Imp Points In case of patients who are TB contacts:  Do PPD test and if –ve repeat another after 8-12 wks  Begin latent TB therapy in contacts such as children and patients with HIV even if the initial skin test is negative.  If the second test is also negative, stop medication in immunocompetent individuals. If a known high-risk TB exposure has occurred in a patient with HIV infection, continue LTBI treatment for the full period, regardless of TST results. 
  • Tuberculosis & PPD – Imp Points     PPD skin test Next step if ppd +ve ( Latent TB) INH rx When screening for LTBI in TB contacts, if the initial PPD result is negative a second PPD should be done 8 to 12 weeks after the last known exposure ( In a review of literature, several studies support a maximum interval of 8 weeks from initial infection to development of a delayed-type hypersensitivity reaction. A Tuberculin Skin Test > 8 weeks from last exposure is recommended. )
  • Tuberculosis & PPD – Imp Points Do not do a Tuberculin Skin Test on any patient  with a history of severe blistering reactions  with previously documented active TB, With a history of treatment for TB, With a documented previous positive TST result  because the TST remains positive in most of these patients  Do not use TST to see if it turns –ve to monitor the success of your treatment  that wont happen  TST remains +ve even after therapy. 
  • Tuberculosis & PPD – Imp Points  Delay the PPD Test for 4 to 6 weeks after a major viral illness such as measles, mumps, rubella, or influenza, because cutaneous anergy can develop, leading to a false-negative TST result.  Do periodic serial PPD screening in persons with ongoing exposure to TB ( Health Care Workers, Residents)  q1year is good enough!
  • Chronic Cough
  • Common Causes of Chronic Cough        Smoker’s cough Chronic bronchitis due to smoking Post-nasal drip Post-infectious Viral Bacterial—Bordetella pertussis, Mycoplasma, Chlamydia ( tracheobronchitis) Gastroesophageal reflux disease Asthma Angiotensin converting enzyme inhibitors
  • Less Common Causes of Chronic Cough              Infectious causes Tuberculosis—typical or atypical,  Fungal Endobronchial lesions  Benign — bronchial adenoma, carcinoid tumor  Malignant — bronchogenic carcinoma, metastatic cancer Foreign body Interstitial lung diseases  Hypersensitivity pneumonitis  Bronchiolitis obliterans with organizing pneumonia, ( BOOP)  Sarcoidosis  Chronic interstitial pneumonia Chronic aspiration Masses in the neck/thyroid disorders Hair impinging on the tympanic membrane Bronchiectasis Occult congestive heart failure Disorders of the pleura, pericardium, diaphragm Psychogenic/habitual cough Occupational bronchitis Enlarged tonsils or uvula
  • History       The cause(s) of chronic cough may become apparent after taking a careful history. Is the symptom a cough or “hawking” or clearing the throat?  It helps to have the patient act out the cough to distinguish true cough from throat clearing. Is the cough dry or productive? If so, what is produced? Are systemic symptoms such as fever, night sweats or weight loss present? A detailed history of the work and home environment should be taken with emphasis on possible exposure to noxious inhalants or allergens. The history should include the time and circumstances of onset, frequency, and aggravating and relieving factors. Patients with asthma may note worsening of cough on exposure to cold air, irritants or allergens. Is there an allergic history? Does the patient wheeze with cough?
  • HISTORY      Is the cough accompanied by dyspnea? If so, congestive heart failure or interstitial lung disease may be suspected. Is the cough related to time of day, eating or position?  A nocturnal cough may be associated with asthma, post-nasal drip, congestive heart failure or gastroesophageal reflux disease (GERD). Half of the patients with GERD have none of the classic symptoms. Does the patient cough while eating? Chronic aspiration is common in the elderly patient, especially following stroke. Is the patient on angiotensin converting enzyme inhibitors or other drugs that may predispose to cough or asthma? Do not overlook ophthalmic preparations. Beta blocker eye drops may precipitate asthma.
  • Physical      The physical examination may provide clues to the causes of cough. Examination of the upper airways may show nasal mucous membrane swelling, post-nasal drip or nasal polyps. The finding of wheezes, rhonchi or crackles may indicate asthma, bronchitis, COPD, interstitial lung disease or congestive heart failure. The finding of unilateral wheezing may be due to an endobronchial lesion or foreign body. Masses in the neck, including thyroid enlargement, can compress the trachea and cause cough.
  • Diagnostic Tests          The work-up for chronic cough should begin with standard posterior- anterior and lateral chest x-rays  these often reveal the presence of underlying infectious or neoplastic causes of chronic cough. Spirometric studies before and after bronchodilator administration may reveal reversible airways obstruction (asthma). In patients with normal base-line spirometry  methacholine inhalation challenge (MIC) is indicated to rule out asthma that presents primarily with cough. ( COUGH VARIANT ASTHMA) Computerized tomograms (CT) of the sinuses are superior to plain x-rays in identifying sinusitis. High-resolution or spiral CT scans of the thorax may reveal subtle changes consistent with cough due to chronic interstitial pneumonia or bronchiectasis. The finding of a reduced single breath diffusing capacity (DLCO) may suggest interstitial lung disease. Barium esophagograms and upper gastrointestinal endoscopy have a low sensitivity (48%) and specificity (76% ) for identifying GERD as the culprit in chronic cough  monitoring the esophageal pH for 24 hours is the gold standard. ( If cough is the only symptom of GERD it gets difficult to diagnose  so, 24hr Ph monitoring) In patients suspected of having chronic aspiration, a video swallowing study with a speech therapist in attendance should be performed. ( SWALLOW EVALUATION) A systematic approach to the work-up of a patient with nondrug-related chronic cough is presented in THE NEXT SLIDE. If you suspect Drug related cough  stop the drug and observe
  • Chronic Cough Post-nasal Drip Syndrome  Post-nasal drip syndrome is said to be one of the most common causes of chronic cough and is caused by a variety of conditions including vasomotor rhinitis, allergic rhinitis, nasal polyps and chronic sinusitis.  The diagnosis is made on clinical grounds.  Patients may complain of a tickle or drainage of liquid in the back of the throat.  On examination, cobblestoning of the nasal or oropharygeal mucosa may be observed. In many patients cough may be the only symptom of post-nasal drip syndrome.  Confirmation of the diagnosis may depend on the resolution of symptoms after treatment with antihistamines and intranasal or systemic corticosteroids.
  • Chronic Cough Asthma & Cough-variant Asthma  Typically, asthma patients complain of episodic wheezing, cough, chest tightness and dyspnea and demonstrate reversible obstructive air flow.  In so called cough-variant asthma  a dry cough, particularly at night, is the only symptom and routine spirometry is normal.  Diagnosis : Spirometry is normal in cough variant type  The diagnosis is often made on the basis of a favorable clinical response to empirically administered beta2-agonist bronchodilators and inhaled corticosteroids, and a positive bronchoprovocation test using methacholine inhalation challenge (MIC)  A positive MIC test, defined as a 20% or greater decrease in the FEV1 after MIC, indicates bronchial hyperreactivity but not necessarily asthma. For example, bronchial hyperreactivity may follow viral respiratory tract infections and persist for as long as 6 weeks. Because MIC has a positive predictive value of from only 60% to 80%, Irwin and colleagues advise that a positive test must be correlated with favorable response to therapy before concluding that a patient has cough-variant asthma.
  • Chronic Cough Gastroesophageal Reflux-related Chronic Cough  GERD is a very common problem. Surveys of the general population have led to estimates that 10% of the adult population of the United States have daily heartburn and a third have intermittent symptoms; moreover, GERD has been shown to cause 10% to 40% of cases of chronic cough  Cough in GERD is triggered by reflux of acid into the distal esophagus and stimulation of an esophageal-tracheobronchial reflex. Cough is not dependent on aspiration into the larynx or tracheobronchial tree.  Proving the relationship of chronic cough to GERD can be difficult. The lack of typical symptoms of reflux and negative endoscopic and radiographic studies do not rule it out.  The 24-hour esophageal pH monitoring test has become the gold standard for diagnosis and has both a sensitivity and specificity approaching 90%.  Correlation of the results of pH monitoring with response to therapy adds to the reliability of the test.  If GERD is the sole cause of chronic cough, aggressive anti-reflux therapy should eliminate the cough in nearly all cases. One study reported 100% success. Treatment involves the use of dietary, mechanical and drug therapy. Drug therapy should be initiated with proton pump inhibitors for GERD.
  • Chronic Cough Post-infectious Cough  Patients who have had recent viral respiratory tract infections may have prolonged cough that is refractory to treatment. Airway hyperresponsiveness can be demonstrated by MIC testing in some cases. Treatment with bronchodilators and inhaled or systemic corticosteroids in moderate to high doses may help relieve symptoms. The cough can be selfperpetuating and cause continuing trauma to the airways, and in these cases, prolonged suppression with narcotics may eventually allow resolution.  Bordetella pertussis (the cause of whooping cough) infection in adults should be included in the differential diagnosis of chronic cough. In one series of 75 patients with chronic cough lasting longer than 2 weeks, 21% had pertussis.
  • Chronic Cough Angiotensin Converting Enzyme Inhibitor Cough  Angiotensin converting enzyme inhibitor (ACEI) drugs are frequently used in the treatment of hypertension, congestive heart failure and myocardial infarction. Ten to 20% of patents taking ACEI drugs develop cough. There is no evidence at this time that any one ACEI drug is less likely to cause cough than another. In spite of this well-documented side effect, referrals to a specialist for evaluation of chronic cough still occur frequently. Many of these patients have had extensive and costly work-ups and treatment with a variety of medications, including antihistamines, antibiotics, cough suppressants and corticosteroids, without relief.  Clinically, the cough may begin from as early as 3 weeks to as long as a year after starting treatment. The severity of the cough can vary from a mild tickle in the throat to a severe hacking, debilitating cough that interferes with sleep, work and social function. It is frequently worse at night and in the supine position.  When the ACEI drug is discontinued, the cough usually abates in 2 weeks but may persist for months.  Angiotensin ll receptor antagonists have not been associated with an increased incidence of cough.
  • Chronic Cough Less Common Causes of Cough  Chronic cough may be the presenting complaint in patients who ultimately prove to have tumors, both benign and malignant, sarcoidosis or other infiltrating lung diseases; all these conditions require special investigations to make the diagnosis.  Psychogenic or habitual cough does exist but patients should not be put in this category without an exhaustive work-up, failure of empirical therapy and prolonged follow up.
  • Chronic Cough Symptomatic Treatment  The treatment of cough is effective only if directed at the cause, but patients should be offered symptomatic relief while awaiting the results of specific therapy. Expectorants such as iodides and guaifenesin, hydration, inhaled steam, cough lozenges and hard candies are helpful. Dextromethorphan and codeine are effective cough suppressants. When to Refer  When the patient with chronic cough remains symptomatic despite evaluation and treatment for 6 to 8 weeks, the primary care physician should consider referral to a specialist. In difficult cases referral to a pulmonologist for evaluation, therapy and for specific testing such as fiberoptic bronchoscopy and MIC is recommended. Referral for upper gastrointestinal endoscopy and 24-hour pH monitoring may be indicated to rule out cough due to GERD. Referral to an allergist may be indicated for allergy testing and subsequently for immunotherapy if the patient is sensitive to an unavoidable antigen. Medicolegal Issues  One of the most common reasons patients file suit is for failure to diagnose cancer.  Even though bronchogenic carcinoma is an uncommon cause of chronic cough in the context of a normal chest x-ray, it must not be overlooked .  Failure to diagnose tuberculosis is another cause of litigation but again would be an unlikely cause of chronic cough with normal chest roentgenograms .
  • Solitary Pulmonary Nodule
  • Characteristics of Solitary Pulmonary Nodules Variable Benign Malignant Age < 30 years > 50 years Calcificati Popcorn, dense, None or minimal on concentric Nodule edge Smooth, round Irregular, spiculated Smoking history Never smoked > 20 pack-years Size of diameter < 1.5 cm > 1.5 cm
  • X-ray Characteristics of SPN  Benign nodule charecterestics : the presence of calcification, which can be a diffuse speckled, or “popcorn,” pattern, typical of a hamartoma, or a large central nidus or concentric calcification typical of a granuloma.  The second important factor distinguishing a malignant from a benign nodule is the growth rate. Since the “doubling time” of a lung cancer ranges from 15 to 450 days, the nodule that does not increase in diameter over a two year period can be considered benign. Any lesion that increases in size over a two year period of observation, or less, must be considered malignant until proven otherwise. One exception is a nodule doubling in less than 20 days, which usually suggests an acute inflammatory process.  The third important characteristic is the appearance of the nodule’s edge. Benign lesions have smooth rounded edges, whereas the incidence of neoplasm increases dramatically in lesions with irregular, spiculated borders. An increasing incidence of malignancy occurs, ranging from 2093%, depending on the degree of border irregularity
  • Diagnosis     The first step in evaluating a SPN is to try to obtain old chest x-rays for comparison  If this is not possible, and the nodule does not have a classic, calcified appearance typical of a granuloma or hamartoma, then further testing or a period of careful observation must be undertaken. A CT scan can help distinguish the pattern of calcification, and classify lesions as “indeterminate” based on the presence of stippled or eccentric calcification and medium density, or “benign” based on the presence of fat density typical of a hamartoma. The most common CT finding in early stage adenocarcinoma and squamous cell carcinoma of the lung is that of a solitary pulmonary nodule which enhances after administration of IV contrast. In small cell carcinoma, however, hilar and mediastinal adenopathy secondary to metastases is the most common CT presentation. The presence of irregular margins, associated air bronchogram, convergence of the surrounding structure, or the involvement of three or more blood vessels is more likely in malignant lesions. If a period of observation is chosen, chest x-rays, and possibly serial CT scans, should be done at 3-month intervals over at least a two year period to determine if any change in the size of the nodule has occurred. An increase in the diameter of the nodule by 25% indicates a doubling of the mass volume a sign of malignancy.
  • Diagnosis - PET  Because of the difficulty with noninvasive diagnosis of the SPN, new radiologic techniques are being studied, including positron emission tomography imaging (PET), which is able to distinguish benign from malignant pulmonary nodules by measuring 18-fluorodeoxyglucose (FDG), and by showing increased FDG uptake and retention in malignant cells. PET scanning is a valuable, noninvasive tool with a 95% sensitivity for identifying malignancy and a specificity of 85% or greater. However, false positive results may be obtained in lesions containing an active inflammatory process (for example a reactive lymphadenopathy), and this diagnostic modality is not generally available.
  • SPN When to Refer  Once the decision has been made that the patient’s SPN may represent a malignancy, a histologic diagnosis is needed. If the patient’s SPN has characteristics strongly suggesting malignancy, and there are no contraindications to surgery, refer to a thoracic surgeon.  In most other circumstances refer to a pulmonologist for further workup. Diagnostic procedures may include: fiberoptic bronchoscopy aided by fluoroscopy, or CT-guided transthoracic fine needle aspiration. The yield of these procedures in the diagnosis of the small solitary pulmonary nodule (< 1.5 cm in diameter) is about 40% for fiberoptic bronchoscopy, and 50% for fine needle aspiration. The incidence of pneumothorax requiring chest tube insertion from bronchoscopic transbronchial biopsy is about 5% and from needle aspiration about 25%, depending on patient characteristics and variation of local physician technique.  Thoracoscopic resection or thoracotomy is needed for diagnosis in about 20% of patients, in whom the less invasive techniques were not successful.
  •       A 43-year-old woman is evaluated because of an abnormal chest radiograph taken before an elective hysterectomy for fibroids. She has no previous history of pulmonary disease. Her cardiac and pulmonary review of systems is unremarkable. The patient smoked one pack of cigarettes per day from age 16 to 33 years, but has not smoked since then. On physical examination, her blood pressure is 120/60 mm Hg and the lung fields are clear. The remainder of the examination is unremarkable. Her laboratory evaluation, including a complete blood count and chemistry profile, is normal. Spirometry shows forced expiratory volume in 1 sec (FEV1), 2.72 L (84% of predicted); forced vital capacity (FVC), 3.68 L (98% of predicted); and FEV1/FVC ratio of 74%. Chest radiography shows an approximately 1-cm nodule in the left lower lobe periphery. There are no previous radiographs. High-resolution helical computed tomography (CT) of the 1.2-cm lesion in the left lower lobe is shown. The full chest CT shows no evidence of mediastinal adenopathy. Which of the following is the best management option? ( A ) Bronchoscopy with transbronchial biopsies ( B ) No further studies are needed ( C ) Repeat high-resolution CT in 3 months ( D ) Resection of the lesion with video-assisted thoracoscopic surgery ( E ) Percutaneous fine needle aspiration of the lesion
  •   The likelihood of a solitary pulmonary nodule being malignant substantially decreases if the lesion is small (approximately 1cm), has smooth borders, is located in a lower lobe, and, most importantly, has central calcification. Observation at 3 month intervals for 2 years to ensure stability of the finding is sufficient!!
  • Pleural Effusions
  • EFFUSIONS     EXUDATES: pleural fluid [protein] / plasma [protein] > 0.5 and/or pleural fluid [LDH] / plasma [LDH] > 0.6 and/or pleural fluid LDH >200 or >2/3 of serum LDH TRANSUDATES – Nephrotic syndrome, CHF, Atelectasis, Cirrhosis (Hydrothorax) EMPYEMA Diagnosis  By thoracentesis. Except in known CHF, must be done in all pleural effusions.
  •  A 56-year-old man with chronic alcoholism is evaluated because of fatigue, decreased appetite, and episodes of sweating. He has a cough productive of purulent, foul-smelling grayish-green sputum and describes heaviness in the right lower chest. The patient has reduced his activity, but only missed 2 days of work as a painter because of his illness. On physical examination, his temperature is 37.4 °C (99.3 °F), pulse rate is 84/min, respiration rate is 14/min, and blood pressure is 132/85 mm Hg. There is dullness to percussion at the right lateral and posterior lung base associated with decreased breath sounds. Chest radiography shows a large right-sided pleural effusion and a small parenchymal infiltrate. The effusion did not layer along the chest wall in a lateral decubitus film. A thoracentesis is performed, and the leukocyte count is 32,500/μL with83% neutrophils, the pH is 7.12, and glucose is 25 mg/dL. The fluid is sent for culture, and antibiotics are begun.  Which of the following should be done next to manage the pleural fluid? ( A ) Insertion of a pigtail catheter into the pleural space ( B ) Insertion of a large-bore chest tube ( C ) Repeat thoracentesis if the pleural effusion does not improve in 48 hours ( D ) Open surgical decortication ( E ) Reevaluation of the pleural effusion in 7 days     
  • Ans.  Frankly purulent pleural fluid, pleural fluid pH <7.20, and,possibly, loculated collections of fluid are indications for chest tube drainage