Wednesday, August 6, 2014

Other Pulmonary Diseases

Other Pulmonary Diseases-

-Acute Respiratory Distress Syndrome-

-Acute Respiratory Distress Syndrome (ARDS) is a distinct type of hypoxemic respiratory failure

-When healthy lungs are disrupted by lung injury, infection, of fluid, there is a disruption of surfactant causing excess fluid in both the interstitial spaces and the alveoli

-The alveolar injury produces alveolar damage and causes release of inflammatory cytokines such as TNF and interleukins

-Damage of the capillary endothelium allows protein to escape from the vascular space.  The fluid then pours into the interstitial spaces and overwhelms the lymphatics

-As a result of this there is impairment of gas exchange, decreased lung compliance, and increase pulmonary artery pressure

-Possible etiologies of ARDS include:  sepsis, aspiration, pneumonia, trauma, burns, multiple blood transfusions, pancreatitis, drug overdose, near drowning, pulmonary contusion, smoke inhalation, CABG, pulmonary contusion, venous air embolism, drug reaction, amniotic fluid embolism, pulmonary edema, and BOOP

-Signs and symptoms of ARDS typically appear within 6-72 hours of the initial insult or injury and decline rapidly

-Patients typically present dyspnea, cyanosis, hypoxemia, diffuse crackles, tachycardia, diaphoresis, and accessory muscle use.  Patients are typically coughing and will have chest pain

-Patients typically are hypoxemic and a wide A-a gradient

-High FiO2 is needed to get desired oxygenation

-Chest X Ray typically shows bilateral alveolar infiltrates, and CT scan will show widespread patchy airspace opacities that are more apparent in dependent lung zones.  This will likely progress to a ground glass appearance

-Most patients require moderate to high concentration of inspired oxygen over the first several days.  The patients who survive will have better oxygenation and decrease in alveolar infiltrates which will allow ventilator weaning to begin

-Complications of ARDS are related to mechanical ventilation:  barotrauma, nosocomial pneumonia. May also have delirium, GI bleed due to stress, thrombosis, and catheter related infections

-Once the initial injury or insult is past or treated, the patients who respond can be weaned from the ventilator and FiO2 can be weaned

-Hyaline Membrane Disease-

-Hyaline membrane disease (HMD) is also known as Respiratory Distress Syndrome (RDS) or Infant Respiratory Distress Syndrome (IRDS)

-The pathophysiology behind HMD is that there is a deficiency of surfactant, usually due to prematurity, that reduces the alveolar surface tension, which decreases the pressure needed to keep the alveoli open, and maintain alveolar stability

-When the surfactant is deficient, the infant cannot generated the increased inspiratory pressure to keep the alveoli open, and results in alveolar collapse and diffuse atelectasis

-This subsequently leads to decreased lung capacity and low functional residual capacity.  Hypoxemia then results.  This may lead to right to left shunting and cause a further VQ mismatch

-Prior to exogenous surfactant administration, uncomplicated HMD typically progressed for 48-72 hours until there was production of endogenous surfactant

-Now with treatment with exogenous surfactant (Survanta), there is dramatic improvement of pulmonary function, and shortening of clinical course.  Use of CPAP has improved the clinical course of HMD

-Foreign Body Aspiration-

-Foreign body aspiration is can be potentially a life threatening event

-Foreign bodies are most likely to be aspirated into the right side secondary to the angle of the right mainstem bronchus

-Inorganic material such as glass or metal may cause little tissue inflammation but can result in direct airway injury if they are sharp

-Organic material such as nuts can cause significant inflammation and granulation tissue formation resulting in stenosis

-Aspiration of medications such as iron tablets in pill form can cause airway inflammation and ulceration

-X-Ray may confirm the presence of foreign body; however, direct visualization with bronchoscopy is need for definitive diagnosis and removal.

-In cases of life threatening aspiration initial support should focus on treating the airway and removing the obstruction.  If it is above the larynx may be able to be removed with forceps, if below the larynx will need bronchoscopy for removal.

Restrictive Pulmonary Disease

Restrictive Pulmonary Disease-

-Idiopathic Pulmonary Fibrosis-

-Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disorder of the lower respiratory tract that typically affects adults over the age of 40

-The pathogenies of IPF is unknown.  Certain risk facts include cigarette smoking, viral infection, environmental pollutants, chronic aspiration, genetic predisposition, and drugs

-Patients present with progressively worsening shortness of breath and eventually hypoxemia

-The severity of the disease is determined by pulmonary function testing

-Pulmonary function test usually demonstrate a reduction of the FVC and DLCO

-Advance disease is characterized clinically by dyspnea on mild exertion (less than 300 feet) and a requirement for supplemental oxygen at rest or exertion.  Extensive honeycombing is seen on imagine studies such as chest x ray or CT scan of chest

-The prognosis of IPF is poor.  Only 20-30 percent of all patients will survive greater than 5 years

-Elements of supportive care for IPF include eduction, supplemental oxygen if needed, pulmonary rehab, and vaccines against influenza and Streptococcus pneumoniae

-No medications have been show to slow lung damage

-Potential medication therapies include pirfenidone and phosphodiesterase inhibitors

-Lung transplantation is an option if patients with IPF meet certain conditions


-Coal workers pneumoconiosis comes from inhalation and deposition of silica free coal dust particles that induce the formation of coal macules in the alveoli

-Findings with pneumoconiosis give pigment and reticulin fibers that accumulate in the peri-hilar location.  Over time black amorphous masses develop and liquify in the center.  There is cavitation that results in ischemic necrosis

-On x ray you see rounded small nodular opacities less than 1 cm usually in the upper lobes.  Eventually there is a confluence of large opacities that lead to massive progressive fibrosis

-Findings of PFT's are similar to IPF.  There is a reduced FVC and DLCO.

-May have some improvement when the offending agents are removed

-Much like IPF, treatment is largely supportive


-Sarcoidosis is a multisystem granulomatous disorder of unknown etiology and is characterized by non-caseating granulomas in involved organs

-Sarcoidosis typically presents in young adults with pulmonary reticular opacities, bilateral hilar adenopathy, and skin, joint, or eye lesions

-The exact etiology and pathogenesis of sarcoidosis are unknown

-Sarcoidosis most often involves the lung (70 percent of the time)

-Diffuse interstitial lung disease is the classic type of lung development

-Common presenting symptoms of sarcoidosis are cough, dyspnea, chest pain, fatigue, malaise, fever, and weight loss

-Patients with lung parenchyma sarcoidosis typically will have crackles heard on lung exam.  Wheezing is heard when there is endobronchial involvement or traction bronchiectasis due to scarring

-Children with sarcoidosis usually do not become symptomatic

-Initial workup for suspected sarcoidosis patient should include:  CBC, BMP, tuberculin skin test, PA and lateral chest x ray, pulmonary function testing, EKG, and eye exam by an ophthalmologist

-Diagnosis is made my biopsy of involved organ.  Can do skin biopsy, or lung biopsy to confirm most commonly

-The majority of patients with pulmonary sarcoidosis have non progressive disease or experience spontaneous remission

-Oral glucocorticoids have been used for the relief of symptoms and control of potentially disabling respiratory impairment

Tuesday, August 5, 2014

Pulmonary Circulation

Pulmonary Circulation-

-Cor Pulmonale-

-Cor Pulmonale is the impaired function of the right side ventricle that comes from pulmonary hypertension and is associated with lung disease, vascular problems such as pulmonary artery hypertension, upper airway problems (obstructive sleep apnea), or chest wall impingement (kyphoscoliosis)

-Cor Pulmonale is mostly a complication of pulmonary hypertension

-Cor Pulmonale usually presents as  a slow insidious process.  It can also be acute though. 

-Common presenting symptoms of Cor Pulmonale include:  dyspnea on exertion, lethargy, exertional syncope, or exertional chest pain

-Anorexia can also come from RUQ pain secondary to passive congestion of the liver and bowel due to right ventricular dysfunction

-Common physical findings include:  increased intensity of the second heart sound, a narrowly split S2, a holosystolic murmur, and a diastolic pulmonary regurgitation murmur

-Right ventricle will become hypertrophied.  Will see elevated central venous pressure and elevated and may see jugular venous distention on both sides

-Patients with end stage cor pulmonale may develop signs of cardiogenic shock, hypotension, tachycardia, oliguria, and cool extremities.  Pulmonary edema is also a late stage finding

-Chest x ray usually demonstrates enlargement of central pulmonary arteries and may show loss of retrosternal space due to right ventricular hypertrophy

-EKG usually shows a right bundle branch block and right axis deviation.  

-ECHO usually shows an enlarged right ventricle 

-Right heart catheterization is the gold standard for diagnosis or cor pulmonale.  Findings will show right ventricular dysfunction, evidence of pulmonary artery hypertension, and no evidence of left heart disease

-Treatment of Cor Pulmonale is targeted at reduction of right ventricle afterload (reduction of pulmonary artery pressure), decrease of right ventricular pressure, and improvement of right ventricular contractility

-Right ventricular afterload can be helped by administering oxygen.  Treatment of pulmonary hypertension itself dose help right ventricular afterload

-Right ventricular pressure may be reduced by diuretic therapy

-Improvement of right ventricular contractility may be helped by dobutamine and milrinone.  Inhaled nitrous oxide may help also.  Oral digoxin should be avoided and can make worse

-Pulmonary Embolism-

-Pulmonary embolism refers to an obstruction of the pulmonary artery or one of its branches by material.

-The material causing the obstruction may be a thrombus, air, or fat that came from somewhere else in the body

-Pulmonary emboli can be classified by massive or submassive.

-Massive pulmonary emboli cause hypotension (SBP less than 90 mm Hg or a drop in SBP by 40 mm Hg in 15 minutes).  This is classified as a catastrophic entity that can result in right ventricular failure and then death

-All other pulmonary emboli that do not meet this definition are classified as submassive

-Saddle pulmonary emboli occur at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries

-Most of the  pulmonary emboli arise from the deep venous system of the lower extremities (approximately 80 percent)

-The remainder of pulmonary emboli arise from the upper extremities and pelvic veins (about 1 percent arise from the pelvic veins)

-Virchow's Triad describes the pathogenesis of thromboembolism
1.  Alterations of blood flow
2.  Vascular Endothelial Injury
3.  Alterations in the constituents of blood (inherited or acquired hypercoagulable states)

-Risk factors include:  more than 48 hours of immobilization in the last month, hospital admission in the last 3 months, surgery in the last 3 months, malignancy in the last 3 months, infection in the last 3 months, current hospitalization, trauma, recent major surgery, central venous catheter, immobilization, pregnancy, use of oral contraception, anti-phospholipid syndrome

-Other medical conditions predisposing to venous thromboembolism include:  Factor V Leiden, Prothrombin Mutation gene, Protein C and S deficiency, Anti-Thrombin III deficiency, and Dysfibrinogenemia

-Additional risk factors include obesity, HTN, and heavy cigarette smoking

-Signs and symptoms of pulmonary emboli include:  dyspnea at rest or with exertion, pleuritic pain, cough, orthopnea, tachypnea, jugular venous distention, S3 gallop, and tachycardia

-Diagnosis is made by CTA of Chest or Ventilation Perfusion (V/Q) scan of the lungs

-Anti-coagulation is the mainstay of treatment with pulmonary emboli.  Can also be treated with embolectomy.  Insertion of inferior vena cava filter can help from recurrent DVT migrating to the lungs but not 100 percent.

-If patient is hemodynamically unstable, thrombolytic therapy should be instituted

-Compared to IV unfractionated heparin, low molecular weight heparin has lower mortality and fewer recurrent thromboembolic events, and less bleeding

-Subcutaneous unfractionated heparin and low molecular weight heparin have similar effects on mortality and morbidity

-IV unfractionated heparin is the only anticoagulant that has been compared in clinical trials to no treatment.  The majority of the data show either equivalent or slightly superior efficacy of low molecular weight heparin

-IV heparin is still the preferred agent when there is persistent hypotension, increased risk of bleeding, and thrombolysis is being considered.

-The antidote for heparin is protamine sulfate

-Once the PTT is greater than 55 seconds, oral anticoagulation such as warfarin can be introduced.  The goal INR is 2-3.

-Pregnant patients will need to be on lovenox as opposed to warfarin because of warfarin crossing the placental barrier

-Treatment for 3-6 months is recommended for the first episode of PE when there is a reversible risk factor

-The second pulmonary embolus should have lifelong anticoagulation

-Pulmonary Hypertension-

-Pulmonary hypertension is defined as a mean arterial pulmonary pressure over 25 mm Hg.

-Normal pulmonary artery systolic pressure is 15-30 mm Hg, and normal pulmonary artery diastolic pressure is 4-12 mm Hg.

-The pathogenesis of pulmonary hypertension is multifactorial.  Largely a proliferative vasculopathy of the small muscular pulmonary arterioles

-Pulmonary hypertension can present with exertional dyspnea, atypical chest pain, and unexplained syncope.  Non specific symptoms such as exertional dyspnea and fatigue can manifest itself.  Peripheral edema may be present.

-If a patient is suspected of pulmonary hypertension, right heart catheterization which is the gold standard for diagnosis should be performed

-ECHO often times will provide evidence suggestive of pulmonary hypertension.  If left heart disease is present, it may be sufficient enough to explain pulmonary hypertension.

-Patient should also have pulmonary function tests, overnight pulse oximetry, VQ scan, ANA, HIV serology, and LFT's to exclude other pathology of symptoms

-For patients with idiopathic pulmonary hypertension additional genetic and catheterization criteria need to be performed to exclude other causes of heart failure such as left heart disease, lung disease, or thromboembolic disease

-Patients should undergo an invasive hemodynamic assessment prior to the initiation of advanced therapy.  Vasoreactivity test should be performed as part of their work up.

-Patients with a positive vasoreactivity test should be given a trial of oral calcium channel blocker therapy.

-If negative vasoactive response, means patient has class II-IV pulmonary hypertension.  Need to institute prostanoids such s prostacyclin, treprostinil.  Endothelial receptor antagonists are another option.

-If refractory to above or there is deterioration need to consider combination therapy.

-If that fails, need to consider atrial septostomy or lung transplant

Monday, August 4, 2014

Pleural Diseases

Pleural Diseases-

-Pleural Effusion-

-A pleural effusion is an accumulation of fluid between the lung and chest wall in the pleural space

-Pleural effusion can be transudative or exudative

-Transudate pleural effusion result from imbalances in the hydrostatic and oncotic pressures in the chest.  Common conditions responsible for this include CHF and nephrosis

-Exudate pleural effusions can result from disease in virtually any organ.  Common mechanisms are infection, malignancy, immunologic reactions, lymphatic problems, non infectious inflammation, iatrogenic causes, and movement of fluid from below the diaphragm

-Exudative pleural effusion most commonly result from lung inflammation or impaired lymphatic drainage from the pleural space

-Light's Rule for determining if pleural effusion is transudative or exudative (if one of the three is true, the fluid is exudative)
1.  Pleural fluid protein/serum protein ratio greater than 0.5
2.  Pleural fluid LDH/serum LDH ratio greater than 0.6
3.  Pleural fluid LDH greater than two thirds the upper limits of the labs normal serum LDH

-Indications for Thoracocentesis:
1.  Pleurisy
2.  Fever
3.  Bilateral pleural effusions that are markedly disparate sizes
4.  Absence of cardiomegaly on chest x ray
5.  ECHO not consistent with heart failure
6.  BNP levels not consistent with heart failure
7.  An A-a gradient larger than expected with heart failure
8.  The effusion does not resolve with diuresis

-Conditions that can be diagnosed by pleural fluid:
1.  Empyema
2.  Malignancy
3.  TB
4.  Fungal infection
5.  Chylothorax
6.  Cholesterol effusion
7.  Urinothorax
8.  Esophageal rupture
9.  Hemothorax
10. Extravascular migration of CVP catheter
11. Lupus
12. Rheumatoid disorders

-Exudative pleural effusions can be difficult to perform a thoracocentesis.  Sometimes require a VATS  (Video Assisted Thoracoscopy) for therapeutic removal of fluid.  May get some useful diagnostic information front the thoracocentesis.  The yield for producing malignant cells is low if cancer is suspected.


-A pneumothorax is an accumulation of air that causes a positive pressure in the pleural space.

-Pneumothoraces can be spontaneous or primary or from secondary causes

-Spontaneous pneumothorax usually occurs when the patient is at rest.  Presenting history and physical exam findings include decreased chest excursion on the affected side, diminished breath sounds on the effected side, and hyperresonant percussion on the effected side due to the increase in accumulation of air.  Patients may also complain of pain on that side. Subcutaneous emphysema may also be present.

-Evidence of hemodynamic compromise such as tachycardia, hypotension, labored breathing suggest the pneumothorax is under tension and warrants emergency decompression

-Findings on chest x ray for a pneumothorax include:  a white visceral line on the chest x ray where there is no pulmonary vessels beyond the pleural edge

-Findings suggesting tension pneumothorax on chest x-ray include tracheal deviation to the contralateral side.

-Risk factors for spontaneous pneumothorax include:  smoking, family history, Marfan's Syndrome, homocystinuria, and thoracic endometriosis

-Secondary Pneumothorax comes from a complication of an underlying lung disease

-Common causes of secondary pneumothorax include:  COPD, cystic fibrosis, primary or metastatic lung disease,  or necrotizing pneumonia

-Pneumothoraces can also come from blunt force trauma or barotrauma

-Treatment options include:  observation, supplemental oxygen, needle aspiration of air, chest tube insertion, and thoracoscopy

-Observation is appropriate for those patients who have stable vital signs, having their first spontaneous pneumothorax, and is small (less than 15%)

-Patients who are stable having their first spontaneous pneumothorax should undergo needle aspiration if it is greater than 15 percent.  If they fail, a chest tube should be inserted.

-Proper landmarks for needle aspiration is the second or third intercostal space in the mid-clavicular line

-Proper placement of the chest tube is the forth or fifth intercostal space in the anterior auxiliary line.

-Careful attention should be made to the neurovascular bundle beneath each rib.   The needle/tube should be inserted just above the rib below.

-A chest x ray should be taken after placement to ensure re-expansion

Monday, July 28, 2014

Obstructive Pulmonary Disease

Obstructive Pulmonary Disease-


-The classic signs of symptoms of asthma are intermittent dyspnea, cough and wheezing.  It can be considered a chronic inflammatory disorder of the airways.

-Reactive airway disease is a term that describes some to the features of asthma

-Some common triggers of asthma include:  allergens, exercise and  viral infections

-Symptoms of asthma are episodic

-Patients usually have a history or family history of atopy (atopic dermatitis, allergic rhinitis, and conjunctivitis)

-Physical exam may real nasal polyps or pale swollen nasal cavities with allergic rhinitis

-May have episodic wheezing and coughing

-Spirometry reveals a obstructive pattern which shows a reduction of the FEV1 to FVC

-If the FEV1/FVC is less than 0.70 airflow obstruction is present

-A key characteristic of asthma is reversibility.  Acute reversibility is assessed after administration of short acting bronchodilator after 10-15 minutes.  An increase of the FEV1 by 12 percent or more, with an absolute increase of at least 200 mL in the FEV1, indicates reversibility.

-Bronchoprovocation testing is useful for those who have normal spirometry prior to testing.  Administration of a methacholine is used to stimulate bronchoconstriction

-Peak expiratory flow is a test that can be done in a doctors office.  A reduced PEF that increases by 20 percent 10-20 percent after administration of quick acting bronchodilator implies the presence of asthma

-Chest X Ray is indicated with the following:  fever, chronic purulent sputum production, persistent localized wheezing, hemoptysis, weight loss, clubbing, inspiratory crackles, significant hypoxemia, and moderate or severe airflow obstruction that does not reverse with bronchodilators

-Wheezing can also be caused by luminal narrowing in the respiratory tract including glottis, trachea, and bronchi, as well as vocal cord dysfunction.

-Cough can also be caused by rhinitis, sinusitis, GERD, post viral tussive syndrome, and eosinophilic bronchitis, Bordetella pertussis, and cough induced by ACE inhibitors

-Dyspnea can also be caused by COPD, heart failure, pulmonary hypertension, pulmonary embolism, and sarcoidosis

-Asthma has 3 classifications based on:
1. Reported daytime and night time symptoms and exercise limitations over the previous 2-4 weeks
2. Current values of peak expiratory flow or FEV1/FVC
3. Number of exacerbations requiring oral glucocorticoids in the last year

-Intermittent asthma is characterized by symptoms occurring 2 or fewer times a week, two or few nocturnal a wakings, beta 2 agonist to relieve symptoms less than 2 a week, no interference with normal activities, PEF and FEV1 measurements when asymptomatic are normal, or one or less exacerbations requiring oral glucocorticoids in the last year.

-Mild asthma is characterized by normal FEV1 and peak flow measurements and the presence of the following:  symptoms more than 2 days a week, 3-4 nocturnal a wakings per month due to asthma, use of beta 2 agonists more than 2 times per week, minor interference with normal activities, and two or more exacerbations requiring oral glucocorticoids per year

-Moderate asthma is characterized by the following:  daily symptoms of asthma, nocturnal awakenings more than once a week, daily need for short term beta two agonists for symptom relief, more than minor limitation in normal activity, and a FEV1 between 60-80 percent of predicted

-Severe asthma is those patients that require high lose inhaled steroids or near continuous oral glucocorticoid treatment to maintain control of their asthma

-A cornerstone to asthma therapy is trigger avoidance

-Short term beta agonists have a rapid onset within 5 minutes and have a duration of 4-6 hours.  Patients should take their short term beta agonists 10-20 minutes prior to exposure of trigger such as exercise

-Ipatroprium is less effective than beta agonists in the treatment of asthma.  It is an anti-cholinergic

-Cromolyn Sodium aerosol helps prevent mast cell degranulation.  Not to used in an acute attack.  Should be used as a maintenance medication if necessary.  Not as widely used as once was.

-Inhaled glucocorticoids reduces the frequency of symptoms and the need for inhaled bronchodilators.  They are indicated for all patients with asthma

-Long acting beta agonists have a duration of action of at least 12 hours.  Should only be given in combination therapy in combination with an inhaled steroids

-Leukotriene inhibitors (Singulair and Accolate) inhibit potent chemical mediators in asthma.  These are preventive agents only.  Not to be used in an acute attack

-Theophylline is an alternative sustained released bronchodilator was used as a controller for persistent asthma.  It is no longer preferred because of side effects and blood levels must be monitored to avoid toxicity


-Bronchiectasis has inflamed and easily collapsible airways, and obstruction to airflow.  The diagnosis is made clinically by the basis of chronic daily cough with viscid sputum production, and the presence of bronchial wall thickening and luminal dilation on CT scan of the chest

-Induction of bronchiectasis includes an infectious insult, impaired drainage, airway obstruction, or a defect in host defense

-Numerous etiologies that cad induce or contribute to the pathophysiologic process that result in bronchiectasis:  foreign body aspiration, defective defense hosts, cystic fibrosis, Young's Syndrome, rheumatic disease, dyskinetic cilia, allergic bronchopulmonary aspergillosis, and cigarette smoking

-PFT's may demonstrate an obstructive pattern

-Deciding if a patient has an acute exacerbation upon systemic changes rather than any specific lab feature.

-Acute bacterial infections are usually manifested by increased production of sputum that is more viscous and darker in color

-Fever and chills is generally absent in acute attacks

-Chest X-Ray should be performed with patients with respiratory distress

-Frequently common organisms colonized with bronchiectasis include:  H. Influenzae, M. Catarrhalis, S. Aureus, and Pseudomonas

-Most afebrile stable patients can be treated as an outpatient

-Indications for inpatient treatment include:  respiratory rate greater than 25 breaths per minute, Temp over 38 degrees C, hypoxemia, or failure to improve after oral antibiotics

-Two organisms difficult to eradicate with bronchiectasis include mycobacterium avium complex and aspergillus species

-Macrolides can be used for those who have recurrent infections

-Bronchodilators and steroids should be used for symptomatic control

-Yearly influenza vaccine is recommended for patients with bronchiectasis

-Pulmonary rehabilitation has been shown to be benefit of patients with bronchiectasis

-Resection of the disease portion of the lung can be used in severe instances when appropriate

-Chronic Bronchitis-

-Chronic bronchitis is defined as a chronic productive cough for 3 months in each of two successive years for whom all other causes of chronic cough have been rule out

-Chronic bronchitis is often due to smoking

-Patients can also get chronic bronchitis from breathing toxic gas or fumes.

-Symptoms of chronic bronchitis include fatigue, productive cough, shortness of breath, and chest tightness

-Should have an X-Ray to exclude other causes of chronic cough such as pneumonia, lung cancer, or bronchiectasis

-Chronic bronchitis is managed with bronchodilators and steroids for symptomatic relief.  Oxygen may be needed for those with chronic hypoxemia.  Pulmonary rehabilitation has been shown to be helpful

-Cystic Fibrosis-

-Cystic fibrosis is an exocrine and endocrine disorder.  CF is caused by mutations in the transmembrane conductance regulator gene.

-Pulmonary disease is the leading cause of morbidity and mortality in patients with CF

-Ivacaftor is a small molecular weight oral drug used to treat patients who have a mutation in at least one of the CF transmembrane conductance regulator genes

-The course of CF is characterized by chronic infection with multiple organisms causing a gradual decline in pulmonary function, with period acute exacerbations that show increase sputum production, and shortness of breath

-Azithromycin is recommended for empiric treatment for those patients with CF

-Chronic treatment with nebulizer antibiotics to target pseudomonas with tobramycin appears to improve lung function

-There is limited evidence to guide decisions about use of beta 2 agonists.  There is limit evidence to suggest they decree the frequency of exacerbations or the quality of life.  Only beneficial as rescue medications

-Anticholinergic agents such as ipatroprium can induced bronchodilation following administration in patients with CF

-The endonuclease DNase can decrease the viscosity of purulent CF sputum by cleaving strands of denatured DNA that are released by neutrophils

-Hypertonic saline has been shown to be beneficial in patients over 14 years of age.  It has been shown to hydrate inspissated mucus that is present in the airways of patients with CF

-Mucomyst has not been shown to be beneficial in CF

-Chest Physiotherapy remains a pillar of those CF patients that continuously produce sputum

-Macrolide therapy is found to be beneficial for those with CF who have bronchitis

-High dose ibuprofen has been shown to be of value in patients with mild CF disease because of anti-inflammatory properties

-Influenza vaccine, the pneumococcal vaccine and synagis vaccine is recommended for patients with CF

-BiPAP has been used to be beneficial in patients with CF the have retained CO2 levels

-Lung transplantation in CF usually requires transplanting both lungs

-Gastrointestinal manifestations of CF can be broken down into intestinal, pancreatic, and hepatobiliary manifestation

-Intestinal pathology includes:  GERD, meconium ileus, distal intestinal obstruction, intussusception, small intestinal bacterial overgrowth, constipation, and rectal prolapse

-Pancreatic insufficiency is present from birth in patients with CF.  Insufficient secretion of enzymes leads to malabsorption of fat (with steatorrhea) and protein.  The fat malabsorption can lead to deficiencies of fat soluble vitamins A, D, E and K.  Patients with CF are prone to chronic pancreatitis

-Hepatobiliary manifestations include asymptomatic liver disease.  Usually found at autopsy.  Antemortum elevations of alkaline phosphatase is usually found in about 10 percent of the patients with CF

-The mainstay of treatment of pancreatic insufficiency is pancreatic enzyme replacement therapy


- COPD has subtypes which include chronic bronchitis, chronic obstructive asthma, and emphysema

-Emphysema is abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspaces walls, without fibrosis

-Exclusion of fibrosis is necessary to distinguish alveolar destruction due to emphysema from that due to interstitial pneumonia

-It is common for emphysema patients to have moderate to severe airway obstruction

-Many subtypes of emphysema including:  proximal acinar, panacinar, and distal acinar

-Emphysema can have variable ways of presenting.  Patients may present with a sedentary lifestyle and avoid exertional activity.  Patients present with respiratory symptoms and chronic cough, and patients present with increased cough, wheezing and purulent sputum

-Physical exam reveals prolonged expiatory phase, hyperinflation, and increased resonance to percussion.  May have decreased breath sounds, wheezing, or crackles in the lung bases.  Heart sounds maybe distant.  Patients may tripod or have pursed lipped breathing.  Clubbing is uncommon with COPD patients

-Spirometry shows a decreased FEV1/FVC that sides not improve with bronchodilator therapy (if does not have asthma component)

-Lung volumes and capacities are increased with COPD

-ABG's may demonstrate low Pa02, chronic PaCO2 retention, and metabolic compensation with increased HCO3

-Treatment is symptomatic similar to asthma.  Beta 2 agonists for acute rescue relief. Anticholinergics such as ipatroprium are effective.  Combination long term beta agonists with combination inhaled steroids can be used.  Glucocorticoids are given during exacerbations

-Alpha 1 Antitrypsin Deficiency (AAT)- is associated with pulmonary emphysema and several forms of liver disease, cirrhosis, neonatal hepatitis, and hepatocellular carcinoma.

-The discovery of AAT protein has allowed for replacement therapy.  IV augmentation of AAT protein is currently most direct efficiency of elevating AAT levels in the plasma and lungs

Neoplastic Disease

Neoplastic Disease-

-Carcinoid Tumors-

-Carcinoid lung tumors (such as bronchial) are uncommon and characterized by neuroendocrine differentiation and relatively indolent clinical behavior

-Were originally called bronchial adenomas

-Carcinoid tumors are considered malignant tumors with the potential to metastasize

-Bronchial carcinoid tumors derive from neuroendocrine cells that have migrated from the embryologic neural crest

-Bronchial carcinoid tumors are the most common primary lung neoplasm in children and usually present in late adolescence

-It is unclear if there is a correlation between smoking and bronchial carcinoid tumors

-Ten percent of neuroendocrine tumors have hereditary origin

-The majority of tumors arise in the proximal airways and are symptomatic from an obstructing tumor mass or bleeding due to hypervascularity

-The majority of carcinoid tumors will have an abnormal chest x ray

-Carcinoid tumors can produce vasoactive substances such as serotonin and other bioactive amines.  Symptoms of carcinoid crisis include cutaneous flushing, diarrhea, bronchospasm, and may cause venous telangectasia

-The best way to diagnose carcinoid tumors of the lung are by CT scan and confirmation by bronchoscopy with biopsy

-PET scanning is helpful for staging of carcinoid tumors

-Patients with typical or atypical bronchial carcinoid tumors, surgical resection is the best treatment for those who can tolerate it.  Endobronchial management for resection is an option if those cannot tolerate the procedure of resection

-Radiation therapy can provide some palliation if not resectable but is not curative for carcinoid tumors

-Chemotherapy has shown minimal activity for carcinoid tumors in the lung

-Lung Cancer-

-Lung cancer is the most leading cause of cancer deaths worldwide

-Lung cancer, also known as bronchogenic carcinoma, is the group of malignancies that originate from from the lung parenchyma

-Ninety five percent of all lung cancers are either small cell carcinoma or non small cell carcinoma

-The other 5 percent of cell types arise from the lung.  This become important for staging, treatment and prognosis

-Risk factors for lung cancer:  smoking, second hand smoke, asbestos or radon exposure, formaldehyde exposure, radiation exposure, various benign inflammation and lung disease, COPD, genetic factors, and dietary factors

-Four types of lung cancer:  adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and small cell carcinoma

-Adenocarcinoma is the most common type of lung cancer

-Most common symptoms of lung caner include:  cough, weight loss, dyspnea, chest pain, hemoptysis, bone pain, and hoarseness

-Complications of lung cancer include superior vena cava syndrome and pancoast syndrome

-The most frequent sites of distant metastasis include:  liver, bone, adrenal glands, and brain

-Cancer is staged using the TMN system

-Paraneoplastic effects of the tumor are:  hypercalcemia, SIADH secretion, and neurologic symptoms, anemia, leukocytosis, thrombocytosis, eosinophilia, hypercoagulable disorders, hypertrophic osteoarthropathy, dermatomyositis, and Cushing's syndrome

-Need to biopsy lesion to get tissue type to help determine treatment either by bronchoscopy or by CT guided biopsy.

-Ultimate goal of lung cancer treatment is resection if possible and appropriate

-Treatment will can involve surgery, chemotherapy, or radiation therapy or any combination of those

-Pulmonary Nodules-

-Pulmonary nodules are defined as a single lesion measuring less than 30 mm and well circumscribed radiographic lesion surrounded by lung parenchyma.

-Pulmonary lesions measuring greater than 30 mm are considered masses

-Spiculated nodules are said to have malignant characteristics

-Common causes of malignant pulmonary nodules are lung cancer, lung metastasis, and carcinoid tumors

-Common causes of benign pulmonary nodules include hamartoma, infectious causes, vascular AV malformations, and inflammatory lesions (Wegner's Granulomatosis)

-For nodules less than 4 mm, CT scans are not required to monitor

-Nodules 4 mm-6 mm should have a CT scan at 12 months in low risk individuals and follow up at 18-24 months in a high risk individual

-Nodules 6-8mm should have a CT scan at 6-12 months, and repeat scan at 18-24 months in low risk individuals and in high risk individual repeat at 3-6 months, 9-12 months, and at 24 months

-Multiple nodules should be worked up for malignancy in a smoker but are likely benign

-Non surgical biopsy such as CT guided biopsy or bronchoscopy is indicated in patients with intermediate risk

-Surgical excision is the gold standard for treatment for malignant pulmonary nodules

Monday, July 14, 2014

Infectious Disorders

Infectious Disorders-

-Acute Bronchitis-

-Acute Bronchitis is generally viewed as a self limiting condition, due to upper airway infection

-Patients usually present with a productive cough lasting more than 5 days but less than 3 weeks

-Chronic bronchitis is a productive cough for most the days for at least 3 months in each of two successive years

-Acute Bronchitis is generally caused by a virus

-Usual causes of acute bronchitis are influenza A and B, parainfluenza, coronavirus, rhinovirus, RSV, and human metapneumovirus.

-It has been suggested that bacterial pathogens that cause pneumonia (Strep Pneumoniae, Haemophilus Influenza, Staph Aureus, Moraxella Catarrhalis) can cause bronchitis, but there have been no studies to prove this

-Other organisms that rarely cause acute bronchitis include:  mycoplasma pneumoniae, Bordetella Pertussis, Chlamydophilia Pneumoniae

-Symptoms are productive cough, wheezing and may have an associated fever.

-Treatment is directed a symptom control.  Albuterol for wheezing and prednisone as needed for an adjunct.

-Indications for chest x ray include a HR greater than 100, RR greater than 24,  temperature greater than 38 degrees C, or oxygen saturation less than 94% on room air on healthy adults

-Acute Bronchiolitis-

-Acute Bronchiolitis is defined as a syndrome that occurs in children less than 2 years of age and presents as rhinorrhea followed by lower respiratory infection with inflammation that results in wheezes and/or crackles

-Acute Bronchiolitis typical is caused by viral pathogens but on occasion can be caused by Mycoplasma Pneumoniae

-Risk factors for developing severe disease with bronchiolitis include:  prematurity, age less than 12 weeks, chronic pulmonary disease, congenital and anatomic defects of the airways, congenital heart disease, immunodeficiency, and neurologic disease

-Indications for Hospitalization of Acute Bronchiolitis patients:
1.  Signs of respiratory distress nasal flaring, retractions, grunting, RR>70, dyspnea or cyanosis
2.  Toxic appearance, poor feeding, lethargy
3.  Apnea
4.  Hypoxemia
5.  Parents who are unable to care for the child at home

-Management includes management of hydration and oxygenation.  Bronchodilator therapy and glucocorticoids are indicated if wheezing.  Nasal suctioning is also helpful

-As a rule of thumb, antibiotics generally are not indicated in the treatment of acute bronchiolitis

-Acute Epiglottitis-

-Epiglottis is inflammation of the epiglottis and adjacent supraglottic structures

-Infectious epiglottitis is cellulitis of the epiglottis and its adjacent structures.  It can result from direct invasion or from bacteremia

-Once the infection begins, swelling rapidly progresses to involve the entire supraglottic larynx and swelling is halted by the tightly bound epithelium at the level of the vocal cords

-Airway obstruction can result in cardiopulmonary arrest

-Epiglottis can be caused by bacteria, viral, or fungal etiologies

-The most common pathogen of epiglottis is Haemophilus Influenza Type B (HIB)

-We have seen a dramatic decreased in the frequency of epiglottis because of the HIB vaccine

-In immunocompromised patients candidia or pseudomonas can cause epiglottitis

-Other non infectious etiologies include:  thermal injury, foreign body ingestion, and caustic ingestion

-Clinical symptoms include:  respiratory distress, signs of upper airway obstruction, stridor, sitting in the tripod or sniffing position, and drooling.

-Fever, severe sore throat, odynophagia, and drooling are common

-Chest x ray or soft tissue neck may reveal a "thumb print" sign

-Labs should be deferred until the airway is secured.  Labs should include CBC and Blood Culture

-Two main parts of management of epiglottis include securing the airway and instituting antibiotics.  Recommended empiric treatment includes third generation cephalosporins with clindamycin or vancomycin.


-Croup is also known as laryngotracheobronchitis (LTB)

-Croup presents clinically with inspiratory stridor, bark cough, and a hoarse voice.

-Most common ages afflicted are between the ages of 6 months and 3 years of age

-Most common offending organism is the parainfluenza virus

-Typically presents acutely rather than slow onset

-The mainstays of treatment of croup are glucocorticoids and racemic epinephrine

-The Wrestly Croup Score determines treatment and it is based on physical exam

-Severe croup can progress to respiratory failure where there is fatigue, listlessness, marked retractions, decreased breath sounds, decreased LOC, cyanosis, pallor, and tachycardia disproportionate to fever.   Rarely this patients may need mechanical ventilation.  Capillary blood gas should be obtained

-Mild Croup can be treated at home.  Cool mist can provide symptomatic relief

-Children have a tendency to get worse at night.  If the child looks bad or may need admission, consider admission especially if in night or evening hours

-Indications for admission of Croup patients include:  need for racemic epinephrine continuously, need for oxygen, moderate retractions, degree of response to initial therapy, if they look toxic, poor oral intake, if less than 6 months, return visit in 24 hours, poor parenteral care at home

-Usually resolves itself within 3-7 days


-Influenza is an acute respiratory illness caused by the Influenza A and B viruses

-Transmission of the virus is by respiratory secretions

-Generally speaking, viral shedding can be detected 24-48 hours before the onset of symptoms, but much lower during the symptomatic period of the illness

-Uncomplicated influenza presents with fever, headache, myalgias, nasal congestion, non productive cough, and sore throat.  Physical exam is usually unremarkable

-Pneumonia is the most common complication of influenza

-Myositis and rhabdomyolysis are also complications of influenza

-CNS complications of influenza include:  encephalopathy, encephalitis, transverse myelitis, aseptic meningitis, and Guillain Bare Syndrome

-Two classes of antiviral drugs available for treatment of influenza-
1.  Neuraminidase inhibitors such as zanamivir and oseltamivir are active against influenza A and B
2.  The adamantanes such as amantadine and rimantadine that are active against influenza A

-These agents can shorten the duration of the illness 12 hours to 3 days.  Most studies have shown benefit when instituted 24-48 hours from the onset of symptoms

-Institution of any antivirals is recommended when:  illness requiring hospitalization, age over 65, pregnant women or post partum less than 2 weeks, or progressive, severe or complicated illnesses-High priority age groups for influenza vaccine:  pregnancy, immunocompromised patients, healthcare workers and household contacts


-Pertussis is known as the whooping cough

-The organism that causes pertussis is Bordetella Pertussis

-Usually affect children less than 10 years and presents with a prolonged cough, inspiratory whoop, paroxysmal cough, and post-tussive emesis

-Since the pertussis vaccine, more than half of the cases occur in adolescents and adults

-Incubation stage is following exposure is typically 7-10 days but may be 3 weeks or longer

-3 Phases in Pertussis:  Catarrhal phase, paroxysmal stage, and convalescent stage

-Catarrhal phase:  earliest and lasts 1-2 weeks.  Presents with malaise, rhinorrhea, and mild cough.  Mild temperature may be present.  May have some conjunctivitis and excessive lacrimation

-Paroxysmal phase:  begins in the second week of the illness.  Hallmark symptom is paroxysmal cough, in a series of severe, vigorous coughs that occur during a single inspiration.  This is when the whooping sound is evident

-Convalescent phase-is characterized by a gradual reduction of frequency of the coughing.  Usually lasts 1-2 weeks

-Complications of this illness include pneumonia, otitis media, subconjunctival hemorrhage, rib fractures, lumbar strain and urinary incontinence

-Most morbidity and mortality occur with infants and young children

-Bacterial culture and PCR are most useful clinical tools for confirmation of pertussis

-Macrolides are effective in eradicating pertussis, bactrim is an alternative treatment for those with macrolide allergy


-Pneumonia is defined as an infection of the lung parenchyma that is acute

-3 Categories of Pneumonia-
1.  Community Acquired Pneumonia (CAP)- Acquired in the Community.  Not acquired in hospital or health care setting

2.  Hospital (Nosocomial) Acquired Pneumonia-aquired in the hospital

3. Healthcare Acquired Pneumonia (HCAP)-aquired in a nursing home, ambulatory surgical center or other health care facility (within 90 days of discharge from an acute or chronic care facility)

-Pathogenesis of pneumonia microaspiration of organisms in the lower respiratory tract

-Common clinical features is fever, pleuritic chest pain, dyspnea, sputum production.  Rigors may also be present

-Chest auscultation reveals audible rales in the majority of the patient.

-Laboratory evaluation usually reveals leukocytosis with WBC between 15,000-30,000.  Leukopenia implies poor prognosis

-The presence of an infiltrate on Chest X Ray is the gold standard for diagnosis of pneumonia.

-More than 100 organisms (bacteria, virus, and fungi, and parasites) can cause community acquired pneumonia

-Most common typical organisms causing community acquired pneumonia include:  Strep Pneumonia, H. Influenza, S. Aureus, Group A Streptococci, Moraxella Catarrhalis, anaerobes, and gram negative bacteria.

-Atypical Organisms include:  Mycoplasma pneumonia, Chlamydia pneumonia, Legionella, and C. Psittaci

-The most common organism causing community acquired pneumonia is Streptococcus Pneumonia

-Common viruses causes pneumonia include influenza virus, parainfluenza virus, respiratory syncytial virus, adenovirus, and coronavirus

-Fungi that cause community acquired pneumonia (usually in a immunocompromised patient) include Cryptococcus, Histoplasma Capsulatum, and Coccidioides

-Indications for hospitalization and severity of illness can be determined by the pneumonia severity index (PSI)

-Variables in PSI include:  sex (male is worse), age, nursing home resident, comorbid illness (neoplastic disease, liver disease, heart failure, cerebrovascular disease, and renal disease), altered mental status, respiratory rate over 30, systolic blood pressure under 90 mmHg, temperature under 35 or over 40 degrees C, pulse over 125, arterial pH less than 7.35, BUN greater than 30, Sodium less than 130, blood sugar greater than 250, hematocrit less than 30, Pa02 less than 60, and pleural effusion

-Risk factors for antibiotic resistance include:  age over 65, beta lactam, macrolide, or fluoroquinolone therapy within the past 3-6 months, alcoholism, medical comorbidity, immunosuppressive illness or therapy, or exposure to child in a daycare center

-For CAP outpatient treatment a macrolide or doxycycline is recommended.

-If there is a presence of comorbid problems, outpatient treatment with a fluoroquinolone, or beta-lactam should be used ouse a macrolide

-Inpatient non ICU patients with CAP a respiratory fluoroquinolone or a beta lactam should be used plus a macrolide

-ICU patients with CAP a beta-lactam plus azithromycin or a beta lactam plus a respiratory fluoroquinolone or a respiratory fluoroquinolone plus aztreonam

-If patients are at risk for pseudomonas an anti-pseudomonal beta-lactam plus cipro should be used with CAP.  Another option is a beta lactam, plus aminoglycoside, plus azithromycin

-Hospital acquired pneumonia (HAP) occurs 48 hours or more after admission and did not appear to be incubating at time of admission

-Ventilator associated pneumonia (VAP)- develops more than 48-72 hours after intubation

-Common pathogens causing HAP, VAP, and HCAP include escherichia coli, klebsiella pneumonia, enterobacter, pseudomonas, acinetobacter, staphylococcus aureus, MRSA, and streptococcus

-Recommendations for HAP, VAP, and HCAP for no known risk factors for multiple drug resistance pneumonia:  Ceftriaxone 2 grams daily, Unasyn 3.0 grams IV Q6, Levofloxacin or Avelox 400 mg IV or Ertapenem 1 gram IV daily

-If there is MDR risk factors above therapy plus one of the following for HAP, VAP, and HCAP cefepime, ceftazidime, meropenem, or zosyn

-If MRSA is suspected need to add Vancomycin, Linezolid, and Telavancin

-Three most common causes of fungal pulmonary pneumonia are:  pneumocystis, aspergillus and cryptococcus pneumonia

-Pneumocystis is seen in transplant patients, HIV patients

-Pneumocystis is highly associated with cytomegalovirus infections

-Aspergillus can be present as a primary infection acquired from a nosocomial or environmental source or failure to already present in airways that are damaged by surgery or underlying source.

-Cryptococcus infections are appreciate when there is an asymptomatic pulmonary nodule or lymph node enlargement that occurs on a routine chest radiograph

-A large percentage of patients with cryptococcus infections are organ transplant recipients

-Candidia pneumonia is extremely rare

-Cytomegalovirus is the most common virus of concern with immunocompromised patients

-Slow or incomplete resolution of pneumonia despite treatment is common causing a high amount of pulmonary consults

-There are mechanical processes such as malignancy that can give the presence of an infiltrate

-Slow resolution is defined as radiographic abnormalities for 1 month after clinical improvement of the patient

-Bronchiolitis Obliterans Organizing Pneumonia (BOOP)- is a type of interstitial lung disease that affects distal bronchioles, respiratory bronchioles, alveolar ducts, and alveolar walls.  The area of injury is the alveolar wall

-Often need steroids and other interventions with traditional antibiotics to get condition to improve

-Respiratory Syncytial Virus (RSV) Infection-

-RSV infection causes acute respiratory illness in patients of all ages.  In children, RSV usually results in a lower respiratory tract infection such as bronchiolitis

-In the Northern Hemisphere, RSV season is generally considered to be between November and April with a peak in January

-Risk factors for lower respiratory tract disease:  infants less than 6 months of age, infants with bronchopulmonary dysplasia (BPD), premature infants greater than 35 weeks, infants with congenital heart disease, secondhand smoke, immunocompromised patients, asthma, residence of at an altitude over 2500 m, elderly patients.

-Transmission of RSV is by inoculation with nasopharyngeal or ocular mucous membranes after contact with virus containing hosts

-Incubation period is usually 6 days

-Almost all patients have been infected by the age of 3 but previous infection does not convey protection against recurrent infection

-RSV usually presents with cough, wheezing, purulent nasal drainage.  Can have dyspnea, fever, and hypoxemia and signs of respiratory distress

-Clinical manifestations can include:  apnea, comorbid bacterial infection, and can be associated with SIADH

-RSV is also likely to have more ear and sinus involvement than other viruses

-Diagnosis of RSV is generally suspected in patients with clinical symptoms during the correct season.  Confirmed with nasal secretions and lab evaluation.  Chest x ray may show bronchiolitis or pneumonia

-Can have concomitant bacterial infection, especially with pneumonia

-Treatment of RSV is largely supportive.  Bronchodilators are indicated for children with wheezing or respiratory distress.  Corticosteroids are recommended for children with RSV bronchiolitis or pneumonia

-Ribavirin aerosolized is not recommended for adults, children and infants with RSV causing lower respiratory tract infection

-Oxygen may need to be given for hypoxemia, and rarely some infants may require mechanical ventilation

-Synagis is a human monoclonal antibody against RSV F glycoprotein is for use in children younger than 24 months with BPD, preterm birth less than 35 weeks, or hemodynamically significant congenital heart disease


-Tuberculosis (TB) is caused by the organism Mycobacterium Tuberculosis

-Signs and symptoms of TB include fever, productive cough, retrosternal pain, pleuritic pain, arthralgias, pharyngitis, and enlarged bronchial lymph nodes.

-90 percent of patients with normal immunity control further replication and enter a latent phase of TB

-The other 10 percent of patients develop TB pneumonia seeding near hilum, get hilar lymphadenopathy, may get cervical lymphadenopathy, meningitis, pericarditis, or get miliary dissemination

-Symptoms of reactivated TB include cough, hemoptysis, weight loss, fatigue, chest pain, dyspnea, and night sweats

-Findings on chest x ray with reactivation of disease include upper lobe cavitary lesions, hilar lymphadenopathy, and solitary nodules

-CT scans of the Chest is more sensitive for diagnosis the chest x-rays for TB

-Complications of TB include hemoptysis, pneumothorax, sepsis, bronchiectasis, extensive pulmonary destruction including gangrene, malignancy, and chronic pulmonary aspergilliosis

-Two tests available to for diagnosing latent TB infection:  tuberculin skin test (TST) and interferon gamma release assay

-Indications for testing for latent TB include:  close contacts of patients with active TB, casual contact of patients with highly contagious active TB, and healthcare workers and other occupations where there is a high risk of exposure with untreated contagious active TB (prisoners and homeless shelters)

-TST is used to show those that have been sensitized to mycobacterial antigens

-Induration for TST should be reassessed in 48-72 hours because is mediated by T Lymphocytes from a delayed hypersensitivity

-Interpretation of the test is as follows:  greater than 5 mm induration is positive in HIV patients, close contact with an active case, abnormal chest x ray with findings of old TB, and immunosuppressed patients.  Greater than 10 mm of induration is positive in patients with increase risk of reactivation, children less than 4 years, foreign born patients, residents and employees of high risk settings.  Greater than 15 mm of induration is considered positive in healthy people with a truly low likelihood of true TB infection

-To diagnose active TB, clinical manifestations must be present.  Generally a cough greater than 2-3 weeks, night sweats, weight loss, and lymphadenopathy.  History of prior positive TST, and radiographic features and labs consistent with TB.  It is recommended that the patient have at least three sputum specimens for acid fast bacillus (AFB)

-Patient should be respiratory isolation while being ruled out.  Positive patients need to be reported to the local health department.

-Four drugs are used in the initial treatment o f active TB because of concern INH resistance.  The 4 drugs are INH, rifampin, ethambutol, and pyrazinamide

-Duration of initial treatment lasts usually for 8 weeks.  If culture and sensitive implicate sensitivity to one of the 4 agents, then ethambutol can usually be discontinued

-The continuation phases is administered for 4-7 months and usually consists of INH and Rifampin

-Hepatotoxicity needs to be monitored

-Need to reassess sputum culture after treatment to determine if there is treatment failure