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85 Cards in this Set
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Respiratory Tract Infection
Description Epidemiology—Pneumonia: More common in alcoholics, elderly, patients with chronic lung disease, chronic disease (cancer, dia- betes, immunocompromise, etc.). Pneumonia is either community acquired or hospital acquired (hospital acquired, defined as pneu- monia ≥ 48 hours after admission). Bronchitis may be bacterial or viral, and in adults is often from smoking (chronic bronchitis). Source of infection may be aspiration, inhalation, or hemato- logic/contiguous spread. Sinusitis has to be included within respi- ratory tract infection. It can be chronic as well as acute and can be seen in outpatient as well as inpatient population. Impact—Vast number of people affected, time lost from work, cost of prescription and over-the-counter (OTC) cough/cold prepa- rations, and mortality |
Prevention—Vaccination where indicated (children: diphtheria,
pertussis; susceptible adults: influenza, pneumococcal), and edu- cation (including hygiene, smoking cessation, etc.). Prevention of Complications in Human Immunodeficiency Virus (HIV)/ Acquired Immune Deficiency Syndrome (AIDS) Patients—Antiretroviral tharapy may reduce infection incidence. Trimethoprim– sulfamethoxazole for Pneumocystis carinii prophylaxis (aerosolized pentamidine if patient is allergic to sulfa drugs), isoniazid for re- active purified protein derivative (PPD) patients, hygiene, pa- tient education. |
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Chronic Bronchitis, Emphysema,
Larynx and Lung Carcinoma Description Epidemiology—In chronic bronchitis, emphysema, lung and larynx carcinoma, smoking is the major cause. Most common lung tu- mor type: adenocarcinoma. Most head/neck cancer is squamous cell, and alcohol is an additional risk factor. There is an in- creased risk of metachronous/synchronous head and neck can- cers. Impact—Vast morbidity/mortality and cost. |
Prevention—Patient education, including smoking cessation and
reduction in alcohol and environmental risks (nickel, arsenic, as- bestos, radiation, etc.). |
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Tuberculosis
Description Epidemiology—Most often due to Mycobacterium tuberculosis. Marked impact in underdeveloped areas, immunocompromised hosts (HIV+, cancer), and airborne transmission by prolonged close exposure. |
Prevention of active disease in patients with evidence of tubercular
infection (e.g., positive PPD) is now called “Treatment of latent TB infection” (LTBI). INH 10 mg/kg/day (up to a maximum of 300 mg/day) for 9 months is the recommended therapy for LTBI. |
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Occupational and Environmental
Pulmonary Disease and Asthma Description Epidemiology—Exposure to occupational and environmental toxins results in a wide range of pulmonary disorders (acute, firefight- ers smoke inhalation, or over many years, asbestosis-induced mesothelioma, berylliosis, and coal miner’s disease). Risk factors for occupational asthma includes atopy (allergic rhinitis, eczema), smoking, and genetic factors. Occupational factors in- clude type and intensity of offending agent (organic versus inor- ganic, high or low molecular weight, etc.). |
Prevention—Avoid exposure to offending agent, including
toxin/dust control, adequate ventilation, and mask/respirator protection, can also consider premedication depending on clini- cal scenario |
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Postoperative Pulmonary
Complications Description Epidemiology—Complications include atelectasis (most common), respiratory failure, pneumonia/aspiration, and hypoxemia. Risk Factors—Chronic obstructive pulmonary disease (COPD), obesity, smoking, arteriosclerotic cardiovascular disease (ASCVD), congestive heart failure (CHF), upper abdominal surgery, age > 70. Preoperative Assessment—History and physical examination for everyone; pulmonary function testing and/or arterial blood gas (ABG) in selected high-risk cases. |
Prevention—Chest physical therapy (CPT), incentive spirometry
(IS), deep breathing, early mobilization, and the use of perioperative nebulizer treatments with albuterol and/or ipratropium bromide (Atrovent). |
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Newborn Respiratory
Distress Syndrome Description Epidemiology—Lack of surfactant resulting in atelectasis. Other risk factors—Maternal diabetes, cesarean section delivery, male sex. |
Prevention—Avoid prematurity; betamethasone given 48–72 hours
before delivery in fetuses < 32 weeks, treatment with exogenous surfactant, check lecithin/sphingomyelin (L/S) ratio (over 2:1 is okay). |
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Pulmonary Aspiration
Description Prevent aspiration in high-risk patients (elderly, neurologic disor- ders, intubation/tracheostomy/sedated patients). |
Prevent and minimize symptoms with H2 antagonists, elevate head of bed, safe feed-
ing tube flow rates, cricoid pressure during intubation, preoperative and postoperative fasting. |
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Symptoms/Diagnosis
Rhinitis, sneezing, headache, malaise, and cough. Clinical diagnosis. |
Common Cold
Pathology/Treatment Rhinovirus commonly, many others possible (adenovirus, respiratory syncytial virus [RSV], influenza, etc.). Supportive treatment. |
SYMPTOMATIC TREATMENT
FOR VIRAL UPPER RESPIRATORY TRACT INFECTIONS •Keep well hydrated. •Acetaminophen/nonste- roidal anti-inflammatory drugs (NSAIDs) for fever, pain. •Warm salt water gargles for pharyngitis/laryngitis. •Pseudoephedrine or phenlylephrine for nasal congestion. •Guiafenesin for chest congestion. •Avoid aspirin in children. |
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Symptoms
Fever, dry/sore throat, headache, and cough. |
Pharyngitis
•Although viruses can be a common cause of pharyngitis, it is important to rule out bacterial infection, most commonly with group A Streptococcus (S. pyogenes). If present, it must be treated to prevent complications. •Clues to the presence of S. pyogenes include cervical lymphadenopathy, fever, pharyngeal and tonsillar exudates, and the absence of cough. However, rapid strep testing or routine throat culture are still used to diagnose S. pyogenes |
•Treatment is given to prevent complications (peritonsillar or retropharyngeal abscess,
meningitis, endocarditis, acute rheumatic fever, and glomerulonephritis). •Antibiotics include penicillin and erythromycin. •If viral etiology, supportive care only. Treatment Steps Supportive if viral SYMPTOMATIC TREATMENT FOR VIRAL UPPER RESPIRATORY TRACT INFECTIONS •Keep well hydrated. •Acetaminophen/nonste- roidal anti-inflammatory drugs (NSAIDs) for fever, pain. •Warm salt water gargles for pharyngitis/laryngitis. •Pseudoephedrine or phenlylephrine for nasal congestion. •Guiafenesin for chest congestion. •Avoid aspirin in children. |
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Symptoms/Diagnosis
Sore throat, halitosis, high fever. Diagnose clinically, throat culture. |
Tonsillitis
Pathology Group A, β-hemolytic strep is common; other bacterial/viral agents possible. |
Treatment Steps
Antibiotics as per culture report, symptomatic measures. SYMPTOMATIC TREATMENT FOR VIRAL UPPER RESPIRATORY TRACT INFECTIONS •Keep well hydrated. •Acetaminophen/nonste- roidal anti-inflammatory drugs (NSAIDs) for fever, pain. •Warm salt water gargles for pharyngitis/laryngitis. •Pseudoephedrine or phenlylephrine for nasal congestion. •Guiafenesin for chest congestion. •Avoid aspirin in children. |
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Symptoms
Dysphagia, fever, pain, trismus (hard to open mouth). Diagnosis History and physical exam (uvula displaced by peritonsillar mass/swelling), culture of aspirate. May be a complication of untreated strep throat. |
Peritonsillar Abscess
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Treatment Steps
1. Surgical drainage. 2. Antibiotics |
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Symptoms
White patch in mouth; removable. Dysphagia may be present if thrush is in posterior oropharynx and/or the esohagus. Diagnosis History and physical (bleeding surface after scraping plaque off), fungal culture, potassium hydroxide (KOH) prep. |
Thrush
Description Moniliasis. Pathology Excess Candida (C. albicans usually). Much more common in immunocompromised adults and infants. |
Treatment Steps
Antifungal (nystatin, fluconazole, etc. |
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SIGN OR SYMPTOM:
EPISTAXIS |
hink of: Common things
first—nose picking!; coagulopathies (or anticoagulation); other trauma besides nose manipulation; severe hypertension; dry mucosa; iatrogenic (e.g., nasogastric tube placement); arteriovenous malformations less frequently but need to think of it; Goodpasture’s, Wegener’s, and others less frequent such as ectopic pregnancy, etc. |
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Symptoms
Facial pain/pressure, fever, headache, referred pain (teeth). Diagnosis History and physical (sinus tender to percussion, purulent rhinitis, decreased transillumination), x-ray and computed tomography (CT) scan, culture from sinus. |
Sinusitis
Pathology Streptococcus and Haemophilus influenzae common; maxillary most common. Only maxillary and ethmoid sinuses are present in children. Ethmoid sinusitis more frequent in children. Cavernous sinus thrombosis: sinusitis complication (facial edema, meningitis, ophthalmoplegia). |
Treatment Steps
1. Antibiotics. 2. Decongestants (pseudoephedrine, phenylephrine). 3.Drainage with decongestants. Also use nasal saline spray. 4.Irrigation |
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Symptoms
Sneezing, itchy/watery eyes, nose blocked and/or runny Diagnosis History and physical (blue, boggy turbinates), allergy testing, nasal smear for eosinophils. |
Allergic Rhinitis
Vasomotor rhinitis: rhinitis and nasal vascular congestion, nonallergic, etiology unknown. |
Treatment Steps
1.Anti-inflammatory drugs (nasal corticosteroids, cromolyn sodium). 2.Antihistamines and/or decongestants. 3.Allergy shots in patients with severe recurrent disease not con- trolled on above treatment. |
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Description/Symptoms
Swollen mucosa/submucosa polypoid tissue. Nasal obstructive symptoms. Diagnosis History and physical examination (polyp: smooth, blue, wet appear- ance). |
Nasal Polyps
Pathology Associated with allergic rhinitis, cystic fibrosis, and asthma with as- pirin intolerance (asthma triad). |
In adults, part of triad
resulting in asthma. Childhood nasal polyps: rule out cystic fibrosis Treatment Steps Medical or surgical. |
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Symptoms
Cold symptoms at onset, then barking cough, slight fever, inspira- tory/expiratory stridor. |
Acute Laryngotracheobronchitis (Croup)
Description An acute viral illness seen in young children |
Diagnosis
History and physical examination, chest/lateral neck x-ray Treatment Steps 1. Humidification of air. 2. Racemic epinephrine. 3.Oxygen. 4.Steroids. 5.Supportive care (see Table 16–1). Outpatient Humidified air Oral hydration Fever control Plan for physician follow-up visit after phone communication Decadron (outpatient use may be appropriate if there is adequate follow-up care) Hospital Humidified air (if tolerated) and oxygena Racemic epinephrine or L-epinephrineb Decadron (0.6 mg/kg intramuscularly given once) Fever control Hydration Antiviral drugs for influenza A virus or respiratory syncytial virus |
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SIGN OR SYMPTOM:
WHEEZING |
hink of: All that wheezes
is not asthma! Asthma, congestive heart failure (CHF), airway hyperactivity (postinfectious), foreign object (especially in children), pseudoasthma (vocal cord dysfunction), and a few others that are not as common. |
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Description/Symptoms
Dangerous airway-compromising infection. Presents with high fever, respiratory obstruction, dyspnea, drooling, dysphagia, barking cough, inspiratory stridor |
Epiglottitis
Pathology Children ages 2–7, usually H. influenzae type b, supraglottic. Incidence of H. influenzae is decreasing since most children are immunized. Epiglottitis—examine epiglottis only with cardiorespiratory support team available, as examination may provoke laryngospasm/complete airway loss/cardiac arrest! |
Diagnosis
History and physical, cherry-red epiglottis, lateral neck x-ray, blood culture. A: Posteroanterior view of the upper airway shows the so-called “steeple” sign, the tapered narrowing of the immediate subglottic airway (arrows). B: On lateral neck x-ray, look for “thumb sign.” Lateral view of the upper airway shows good delineation of the supraglottic anatomy. The subglottic trachea is hazy and poorly defined (arrow) because of the inflammatory edema that has obliterated the sharp undersurface of the vocal cords and extends down the trachea in a diminishing manner. Treatment Steps 1. Antibiotics (cefuroxime [Zinacef]), or other third-generation cephalosporin. 2.Treat nonimmunized household contacts (usually with rifampin). |
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Diagnosis
History and physical exam, nasopharyngeal culture, leukocytosis. The cough in pertussis is distinctive. Patients often have paroxysms of cough. Patients make the posttussive “whooping” sound about 50% of the time. Coughing spells are often followed by posttussive emesis. |
Pertussis (Whooping Cough)
Symptoms Three stages of illness: Catarrhal stage (coryza, 1–2 weeks), paroxys- mal stage (coughing and inspiratory whoop, 2–4 weeks), convalescent stage weeks later Pathology Bordetella pertussis; infants under 2 years. |
Treatment Steps
1. Erythromycin will help in catarrhal stage. 2.Otherwise, supportive care. 3.Treat household contacts. |
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Symptoms
Persisting hoarseness; recurrent acute laryngitis episodes. |
Chronic Laryngitis
Pathology Chronic irritation (smoking, overuse of voice, reflux). |
Diagnosis
History and physical examination, laryngoscopy. Treatment Steps 1.Voice rest. 2.Speech therapy. 3.Steroids. 4.Treatment for reflux disease. |
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Symptoms/Diagnosis
Stridor, hoarseness, subcutaneous emphysema. Laryngoscopy for di- rect visualization |
Larynx and Pharynx Trauma
Pathology Injuries include thyroid cartilage fracture, contusions, arytenoid dis- location. |
Treatment Steps
1. Do not intubate. 2.Observation if stable. 3.Tracheotomy if airway obstruction. |
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children 1–3, night onset,
lasts few hours, usually viral, no fever. |
Spasmodic croup
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SIGN OR SYMPTOM:COUGH
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Causes of acute cough
(< 3 weeks’ duration) are viral or bacterial upper repiratory tract infections (e.g., common cold, acute bacterial sinusitis), allergic rhinitis, and environmental irritants. Most common causes of chronic cough (> 3 weeks’ duration) are postnasal drip, asthma, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, and drugs like angiotensin-converting enzyme inhibitors. |
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Description/Symptoms
Large airway inflammation/infection, causing productive cough, fever, mild shortness of breath. Often due to a viral infection. More likely bacterial in smokers/patients with COPD. |
Acute Bronchitis
Diagnosis History and physical, chest x-ray (CXR) should be clear, sputum cul- ture. (Presence of an infiltrate would lead to a diagnosis of pneumo- nia rather than bronchitis.) |
Treatment Steps
1.Antibiotics (if underlying COPD, Gram stain and culture of spu- tum are unnecessary and often misleading, because normal respi- ratory tract flora are often seen). 2.Otherwise supportive (hydration, expectorants, bronchodilators). |
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Symptoms/Diagnosis
Tachypnea, wheezing, fever, and cough. Diagnose clinically. Chest x-ray may show overinflation. |
Bronchiolitis
Description Lower respiratory tract infection, with small airway inflammation/obstruction. Pathology Viral (RSV common); affecting infants younger than 2 (not exclusive of pediatric patients), also seen (rarely) in adults. |
Treatment Steps
1.Ribavirin for RSV. 2. Oxygen. 3.Fluids |
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Symptoms
Typically, bacterial pneumonia is characterized by fever, cough pro- ductive of purulent sputum, and difficulty breathing. Exam often re- veals signs of consolidation (rhonchi). CXR often shows an infil- trate. Other symptoms may (or may not) exist based on the infectious organism causing the pneumonia. |
Pneumonia
3–1.General Facts Description Infection of the lower respiratory tract caused by a variety of differ- ent pathogens (bacterial, viral, fungal). |
Diagnosis
Initial treatment should start based on the history and physical, keeping in mind the patient’s medical history and what type of pneumonia is most likely in that particular patient Treatment Steps Guided by the specific etiology. |
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SCENARIOS FOR PNEUMONIA
•A young, otherwise healthy adult may have an atypical pneumonia |
Mycoplasma
pneumoniae |
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SCENARIOS FOR PNEUMONIA
•An elderly patient with COPD likely has a bacterial pneumonia, or, if in the winter |
influenza
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SCENARIOS FOR PNEUMONIA
An AIDS patient with a low CD4 count and subacute illness |
Pneumocystis carinii
pneumonia (PCP). |
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SCENARIOS FOR PNEUMONIA
patient whose mentation is altered (e.g., postop from anesthesia or other sedatives) or who has swallowing dysfunction from a stroke |
aspiration pneumonia.
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SIGN OR SYMPTOM:
HEMOPTYSIS |
First need to
figure out if it is true hemoptysis or if it is epistaxis or hematemesis. The most common causes of hemoptysis are bronchitis/bronchiectasis and carcinoma. One-third of the cases are due to unknown causes. Other less common causes are arteriovenous malformations, foreign bodies, mitrial stenosis, trauma, infections (like tuberculosis, aspergilloma), pulmonary embolism, and vasculitis/autoimmune diseases (Wegener’s granulomatosis, systemic lupus erythematosus (SLE), Goodpasture’s syndrome). |
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Symptoms
Influenza most commonly presents with the acute onset of malaise, myalgias, fever, chills, cough, and sore throat. In certain patients, pneumonia can develop. The pneumonia may be caused by the in- fluenza itself, a secondary bacterial pneumonia, or a mixed picture. |
Influenza and Pneumonia
Description Influenza is an acute respiratory infection caused by an RNA virus. Common types of the virus are types A and B. Typically, the strain of influenza varies from year to year, and vaccines are developed trying to anticipate the specific strains. |
Diagnosis
Throat or nasal swabs can confirm the presence of influenza (and specific type, A or B). CXR can reveal infiltrates/pneumonia Treatment Steps 1.Rest/fluids/symptomatic treatment with analgesics/antipyretics. 2.If the infection is discovered within the first 48 hours, treatment can begin with oseltamivir (Tamiflu) given for 5 days. This med- ication can also be given after close contact with an infected indi- vidual as prophylaxis. Amantadine can be used for prophylaxis and treatment of influenza A infections only. 3.Antibiotics often needed if pneumonia develops. |
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Description/Symptoms
often presents with a subacute onset, nonproductive cough, multiple extrapulmonary symptoms (headache, sore throat, gastrointestinal [GI] complaints), and minimal findings on exam. However, the x-ray often shows a diffuse or patchy, often bilateral infiltrate. |
Atypical Pneumonia
Pathology Classically due to Mycoplasma pneumoniae or Chlamydia pneumoniae and seen in young, otherwise healthy patients. Other, much less common organisms include Chlamydia psittaci, Coxiella burnetii, and Francisella tularensis. |
Diagnosis
Based on clinical picture and patient risk factors. Sputum culture may help with identifying specific pathogen. Treatment Steps Based on suspected pathogen. Antibiotics must cover these “atypi- cal” pathogens. Antibiotics include erythromycin, doxycycline, azithromycin, clarithromycin, levofloxacin, and tetracycline. |
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Description/Symptoms
Pneumonia caused by the aerobic, gram-negative bacillus Legionella species (Legionella pneumophila in 80–90% of cases). Risk factors in- clude smoking, elderly, and immunosuppressed patients. These include headache, diarrhea, high fever, lack of organisms on putum Gram stain despite multiple neutrophils, hyponatremia, ab- normal liver function tests (LFTs), and failure to respond to typical antibiotic therapy (β-lactam drugs). |
Legionella
Diagnosis A few aspects of the illness should raise suspicion for Legionella. These include headache, diarrhea, high fever, lack of organisms on sputum Gram stain despite multiple neutrophils, hyponatremia, ab- normal liver function tests (LFTs), and failure to respond to typical antibiotic therapy (β-lactam drugs). Special lab testing can be done for Legionella, which includes direct fluorescent antibody (DFA) staining of sputum, Legionella urine antigen testing, and serologies. |
Treatment Steps
Medications include those antibiotics active against “atypical” organ- isms (erythromycin, doxycycline, azithromycin, clarithromycin, levofloxacin, and tetracycline |
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Description/Symptoms
Presentation is consistent with typical bacterial pneumonia (see sec- tion II.B.3–1). Complications can include pleural effusion (transudative or empyema), meningitis. |
Pneumococcal Pneumonia
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Diagnosis
Clinical picture. Gram stain shows gram-positive diplococci Treatment Steps Most β-lactam antibiotics and fluoroquinolones are effective. Prevention with vaccination (see Table 16–2). |
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Description/Symptoms
common in in- fancy/early childhood or debilitated patients. The course is rapidly progressive with a relatively high mortality. After a short prodrome, patients have acute respiratory distress. |
Staphylococcal Pneumonia
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Diagnosis
Clinical setting, and organism seen on Gram stain and culture (Fig.16–2). Treatment Steps Aggressive supportive therapy. Vancomycin may be needed initially until the sensitivity of the organism is known. Vancomycin can be changed to an alternative antibiotic if the isolate is not methicillin- resistant S. aureus (MRSA) |
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Symptoms
Classically, patients have a subacute illness (lasting usually a few weeks) consisting of dry cough, fever, malaise, fever, weight loss, and dyspnea. Patients are very commonly hypoxemic. |
Pneumocystis carinii Pneumonia (PCP)
Description Pneumocystis carinii is a ubiquitous unicellular eukaryote, and differ- ing opinions exist as to whether it is classified as a protozoan or fun- gus. It is the most common opportunistic respiratory infection in patients infected with HIV, and can cause disease in other immunocompromised populations. PCP is an AIDS-defining illness. |
Diagnosis
CXR classically shows diffuse bilateral infiltrates (see Fig. 16–3). May be hard to diagnose in a patient with no prior diagnosis of HIV and who may not fully disclose all risk factors. In a patient who has never had PCP before, it is better to isolate the organism (which may require bronchoscopy and bronchoalveolar lavage) Treatment Steps Trimethoprim–sulfamethoxazole (Bactrim) is the standard of care. In patients with severe allergy, other options include pentamidine, dap- sone, and atovaquone. The use of steroids (prednisone) is somewhat controversial. It is thought that steroid treatment decreases inflamma- tion produced by the organism. It is usually reserved only for patients with HIV/AIDS who are hypoxemic. |
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Description/Symptoms
Pneumonia occurring when food or gastric aspirate enters the lung. Common scenarios include patients with stroke and dysphagia, and patients with altered sensorium (delirium, sedation). |
Aspiration Pneumonia
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Diagnosis
Clinical scenario. CXR classically shows right middle or lower lobe infiltrate. Treatment Steps Antibiotics used to cover gram-positive and anaerobic infections, in- cluding clindamycin and amoxicillin/clavulanate (Augmentin). |
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cause
of nosocomial pneumonia. Suspect in patients recently or fre- quently hospitalized or patients who live in nursing homes. |
Pseudomonas aeruginosa (and other gram-negative pathogens) un-
commonly cause pneumonia. |
An-
tipseudomonal antibiotics include piperacillin/tazobactam, cef- tazidime, and most aminoglycosides. P.aeruginosa is a common pathogen in patients with cystic fibrosis. |
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Causes of Pneumonia
However, three states (Arkansas, Okla- homa, and Missouri) account for more than 50% of all cases in the United States. Pulmonary tularemia has a high mortality rate |
rancisella tularensis is a gram-negative bacteria relatively uncom-
mon in the United States. |
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Causes of Pneumonia
Cattle, sheep, and goats are the reservoirs for the organisms and farmers and veteri- narians are at highest risk. |
Coxiella burnetii is the organism causing Q fever.
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Doxycycline is the treatment of choice.
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patients with community-acquired pneumonia who have had exposure to birds.
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Chlamydia psittaci is an obligate intracellular parasite that causes
psittacosis. |
Doxycycline is the treatment of choice.
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Symptoms
Asymptomatic, or weight loss, night sweats, cough, malaise, and hemoptysis. • Symptoms: Fatigue, weight loss, night sweats, fevers, productive cough. |
Tuberculosis
Description Mycobacterial infection due to Mycobacterium tuberculosis; pulmonary, genitourinary (GU), GI, bone, and meningitis may present. More common in HIV/AIDS patients, homeless persons. Diagnosis: History and physical, sputum sample (identify M. tuberculosis bacilli on acid-fast stain and culture). CXR, PCR, positive PPD. |
Diagnosis
History and physical, CXR, sputum culture and polymerase chain re- action (PCR) testing and smear for acid-fast bacilli, skin test, tissue/body fluid exam for M. tuberculosis. (See Fig. 16–4.) Treatment Steps 1. Start four drugs (isoniazid [INH] 300 mg daily plus rifampin 600 mg daily, pyrazinamide (PZA), and ethambutol) until culture sen- sitivities arrive. 2. Narrow treatment according to sensitivities to complete 6 months of treatment. 3. In HIV, follow strict culture sensitivities. Always monitor liver en- zymes and tailor drug therapy to individual case. 4. Other treatment modalities include DOT (direct observe therapy) for the poor compliance patient. Treatment: Most commonly use INH, rifampin, pyrazinamide, ethambutol, streptomycin (important to correlate with specific sensitivies and population group for choices of combination of 3–4 drugs and duration). •Prevention: Screening individuals via skin testing (PPD) and initiating treatment if skin test is positive. Renal TB—sterile pyuria. • INH—side effects include neuropathy from pyridoxine loss, and hepatitis. • Positive TB skin test (PPD) in person with history of bacillus Calmette–Guérin (BCG) vaccine does not necessarily indicate infection. CXR needed. |
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Symptoms
Asymptomatic, or nonproductive cough, myalgia, fever, chest pain, mild flulike presentation. |
Histoplasmosis
Description Most patients who are exposed to this soil mold (Histoplasma capsula- tum) are asymptomatic. Patients who develop clinical manifestations are often immunocompromised. Pathology Histoplasma is a soil mold. Bird/bat droppings in soil grow spores, which are inhaled. The endemic areas for H. capsulatum include most of the midwestern and south central United States (the Ohio, Missouri, and Mississippi River valleys). |
Diagnosis
History and physical, CXR (Fig. 16–5), serologic testing; in some cases, might need lung biopsy (see Fig. 16–6). Treatment Steps 1. In mild case no treatment indicated. 2. If more ill, then ketoconazole 400 mg/day, or amphotericin B. Progressive disseminated histoplasmosis: associated with AIDS, do blood/bone marrow culture and treat with amphotericin B. |
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Symptoms
Asymptomatic or flulike presentation, arthralgia, erythema no- dosum/multiforme rash. Can be difficult to differentiate from other respiratory infections |
Coccidioidomycosis
Description Infection with Coccidioides immitis; common Southwest U.S. mold. Diabetics and blacks tend toward progressive infection. |
Diagnosis
History and physical, serologic testing. Travel or residence in an en- demic area is important. CXR is nonspecific. Treatment Steps 1. If mild, no treatment or possibly oral fluconazole. 2. If severe, give amphotericin B. |
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Symptoms
Fever, cough, and dissemination in immunocompromised patients. Clinical picture can vary from minimal symptoms to acute respira- tory distress syndrome (ARDS) |
Cryptococcosis
Description Infection with Cryptococcus neoformans, an encapsulated yeast. Two principal sites of infection are lungs and central nervous system (CNS), causing meningitis. Pathology C. neoformans infection; in soil and pigeon droppings. Risk factors include AIDS and corticosteroid use. |
Diagnosis
Fungal culture, CXR. Treatment Steps Amphotericin B plus flucytosine for severe pulmonary disease. |
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Symptoms
Purulent/putrid sputum, cough, chest pain, fever. |
Lung Abscess
Pathology Anaerobic bacteria most often (bacteroides, peptostreptococcus). Risk factors: poor dentition and aspiration (CNS disease, overdose, alcoholism, etc.). |
Diagnosis
History and physical, CXR (cavities and air–fluid level), bronchoscopy/culture, CT scan, lung biopsy. Treatment Steps 1.Antibiotics penicillin G, 2 million units IV every 4 hours. 2.Clindamycin 600 mg every 6 hours. 3.Surgical drainage rarely. |
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Symptoms
Symptoms common to COPD, regardless of CB or emphysema, in- clude worsening dyspnea and progressive decrease in exercise toler- ance. (Other symptoms are more specific to each disorder; see be- low.) |
Chronic Obstructive Pulmonary Disease
(COPD)––General COPD in general refers to three disease processes: chronic bronchi- tis (CB), emphysema, and asthma. (However, other diseases can cause obstructive lung disease, including bronchiectasis, cystic fibro- sis, and allergic bronchopulmonary aspergillosis [ABPA].) OBSTRUCTIVE •FEV1 and FVC are both depressed. •Ratio of FEV1 to FVC is depressed. •In emphysema, DLCO is depressed. •FEV1 can determine severity of disease. FEV1 that is 60–70% of normal may be moderate chronic obstructive pulmonary disease (COPD), while FEV1 < 50% of normal is severe COPD. DEFINITIONS •FEV1: Amount of air exhaled in the first second of forced exhalation •FVC: Forced vital capacity (total volume of air exhaled from full lungs) •DLCO:Diffusion capacity, gives information on gas exchange at the level of the alveoli •TLC:Total lung capacity (volume of air in full lungs) •RV: Residual volume (volume of air left in lungs after full expiration) |
Diagnosis
In general, diagnosis is made based on the clinical scenario. Techni- cally, the diagnosis should be made with PFTs but often, prior to PFTs, the diagnosis is made clinically and empiric treatment is started. Treatment Steps From a medication standpoint, the two conditions are treated fairly similarly. 1.Inhaled medications: •Anticholinergics: Ipratroprium bromide (Atrovent) usually four times per day. Tiotropium (Spiriva) is newer and used once a day. •Ipratroprium or tiotropium is usually administered with a short-acting β-agonist (albuterol). •Long-acting β-agonist (salmeterol) used twice a day. •Corticosteroids (fluticasone, beclomethasone) •In an acute exacerbation, albuterol with atrovent is often given as a nebulized solution. 2.Theophylline is used in some patients but has multiple toxicities. 3.Acute exacerbations are treated with empiric antibiotics, which should provide broad-spectrum coverage (against pneumococcus, H. influenzae, Legionella species, and gram-negative enterics). Azithromycin, levofloxacin, and trimethoprim–sulfamethoxazole have all been used. 4.Concerns with hospitalization: ABGs can assess hypoxemia as well as retention of carbon dioxide (hypercapnia). Oxygen should be administered for hypoxemia. If initial treatment for the acute ex- acerbation does not improve hypercapnia, other methods may be needed (such as bilevel positive airway pressure [BiPAP] or intu- bation with mechanical ventilation). |
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Description/Symptoms
Classically, patients are referred to as “blue bloaters” and have pro- ductive cough and recurrent pulmonary infections. With further progression, respiratory and cardiac failure develop (cor pul- monale) with edema and weight gain. |
COPD––Chronic Bronchitis
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Diagnosis
In general, diagnosis is made based on the clinical scenario. Techni- cally, the diagnosis should be made with PFTs but often, prior to PFTs, the diagnosis is made clinically and empiric treatment is started. Treatment Steps From a medication standpoint, the two conditions are treated fairly similarly. 1.Inhaled medications: •Anticholinergics: Ipratroprium bromide (Atrovent) usually four times per day. Tiotropium (Spiriva) is newer and used once a day. •Ipratroprium or tiotropium is usually administered with a short-acting β-agonist (albuterol). •Long-acting β-agonist (salmeterol) used twice a day. •Corticosteroids (fluticasone, beclomethasone) •In an acute exacerbation, albuterol with atrovent is often given as a nebulized solution. 2.Theophylline is used in some patients but has multiple toxicities. 3.Acute exacerbations are treated with empiric antibiotics, which should provide broad-spectrum coverage (against pneumococcus, H. influenzae, Legionella species, and gram-negative enterics). Azithromycin, levofloxacin, and trimethoprim–sulfamethoxazole have all been used. 4.Concerns with hospitalization: ABGs can assess hypoxemia as well as retention of carbon dioxide (hypercapnia). Oxygen should be administered for hypoxemia. If initial treatment for the acute ex- acerbation does not improve hypercapnia, other methods may be needed (such as bilevel positive airway pressure [BiPAP] or intu- bation with mechanical ventilation). |
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Description/Symptoms
Patients are referred to as “pink puffers” and have a long history of progressive dyspnea. Cough is not a predominant symptom; it pre- sents late in the illness and is usually nonproductive. Patients are eventually cachexic, with a barrel chest. They often adopt the tripod position to facilitate breathing. Chest can be hyperresonant with dis- tant heart sounds. |
COPD––Emphysema
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Diagnosis
In general, diagnosis is made based on the clinical scenario. Techni- cally, the diagnosis should be made with PFTs but often, prior to PFTs, the diagnosis is made clinically and empiric treatment is started. Treatment Steps From a medication standpoint, the two conditions are treated fairly similarly. 1.Inhaled medications: •Anticholinergics: Ipratroprium bromide (Atrovent) usually four times per day. Tiotropium (Spiriva) is newer and used once a day. •Ipratroprium or tiotropium is usually administered with a short-acting β-agonist (albuterol). •Long-acting β-agonist (salmeterol) used twice a day. •Corticosteroids (fluticasone, beclomethasone) •In an acute exacerbation, albuterol with atrovent is often given as a nebulized solution. 2.Theophylline is used in some patients but has multiple toxicities. 3.Acute exacerbations are treated with empiric antibiotics, which should provide broad-spectrum coverage (against pneumococcus, H. influenzae, Legionella species, and gram-negative enterics). Azithromycin, levofloxacin, and trimethoprim–sulfamethoxazole have all been used. 4.Concerns with hospitalization: ABGs can assess hypoxemia as well as retention of carbon dioxide (hypercapnia). Oxygen should be administered for hypoxemia. If initial treatment for the acute ex- acerbation does not improve hypercapnia, other methods may be needed (such as bilevel positive airway pressure [BiPAP] or intu- bation with mechanical ventilation). |
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Symptoms
Symptoms of emphysema at early age (or in nonsmoker). |
α1-Antitrypsin Deficiency
Description A genetic defect resulting in depressed levels of α1-antitrypsin. The primary result is panacinar emphysema occurring at a young age. Hepatic cirrhosis can also develop. Pathology Excess elastase (without α1-antitrypsin to inactivate it), results in lung damage. |
Diagnosis
Clinical scenario. Can check serum levels of α1-antitrypsin. CXR (basal bullae, not only found at the bases), high-resolution CT scan of chest, and PFTs. Treatment Steps 1.Make sure patient quits smoking. 2.Treatment for emphysema (see above, section II.C.3). 3.Replacement therapy with purified human α1-antitrypsin. 4.Lung volume reduction surgery is sometimes done, as is lung transplantation. |
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Symptoms
Productive purulent cough, weight loss, hemoptysis, clubbing. |
Bronchiectasis
Description Bronchial infection/inflammation, resulting in bronchi dilation. |
Diagnosis
History and physical. Bronchography was the traditional technique for diagnosing bronchiectasis, but is no longer recommended. High-resolution CT scan of the chest is the diagnostic test of choice. Treatment Steps 1.Chest physical therapy. 2.Antibiotics. 3.Bronchodilators. 4.Surgery. |
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Symptoms
Wheezing, central bronchiectasis, productive cough. |
Allergic Bronchopulmonary Aspergillosis (ABPA)
Description ABPA is a hypersensitivity reaction to Aspergillus fungus; most commonly seen in patients with asthma and cystic fibrosis. DIAGNOSIS OF ABPA If six of seven criteria are met, almost 100% have ABPA: •History of asthma •Peripheral eosinophilia •Pulmonary infiltrates •Positive skin test to Aspergillus •High serum immunoglobulin E (IgE) •Positive IgE and IgG for Aspergillus •Central bronchiectasis |
Treatment Steps
Prednisone. New studies suggest some role of antifungals (itracona- zole) in selected patients with this disease. |
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Symptoms
Steatorrhea, cough, sputum production, diabetes |
Cystic Fibrosis (CF)
Description Autosomal recessive genetic disorder of exocrine gland function in- volving multiple organ systems. Pulmonary involvement exists in 90% of patients surviving the neonatal period. Pancreatic exocrine gland dysfunction also occurs. If azoospermia noted, or Pseudomonas aeruginosa in sputum, think cystic fibrosis |
Diagnosis
Clinical scenario, sweat chloride test (> 60 mEq/L of sweat chloride is diagnostic of CF) Treatment Steps Multidisciplinary approach: 1. Chest physical therapy. 2.Antibiotics. 3.Inhaled Dornase alfa (recombinant human DNAse––cleaves ex- tracellular DNA and thus decreases the viscosity of sputum). 4.Double lung transplantation (end-stage lung disease). |
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Description/Symptoms
Lung collapse (segment or lobe). Patients have shortness of breath, hypoxia, fever |
Atelectasis
Pathology Bronchi obstruction (frequently mucus/secretions plug). Most fre- quent postop pulmonary problem. Risk factors include COPD/ smoking, obesity, age > 70, and upper abdominal/thoracic surgery. |
Diagnosis
History and physical, CXR. Treatment Steps 1.Incentive spirometry. 2.Deep breathing exercises. 3.OOB (out of bed). 4.Chest physical therapy. 5.Continuous positive airway pressure (CPAP). 6.Bronchoscopy (if atelectasis is severe). |
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gastric aspiration, often
postop, may cause ARDS. |
Mendelson syndrome:
Most risky time for aspiration during surgery is during anesthetic induction. |
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Symptoms
Snoring, morning headaches, difficulty concentrating and decreased memory capability, obesity, daytime hypersomnolence, dry mouth in A.M., sensation of choking or gasping for air in the middle of the night, peripheral edema. Pauses in breathing while asleep |
LEEP-DISORDERED BREATHING
Background Abnormal ventilation in sleep is found by the presence of apneic and/or hypoxic events. Most commonly recognized sleep disordered breathing: obstructive sleep apnea (OSA), central sleep apena, and mixed events. There are other disorders of clinical importance but less frequently seen, such as primary alveolar hypoventilation and obesity hypoventilation syndrome. Etiology Not certain in all cases, but in OSA there is a true obstruction of the airway, usually at the level of the posterior pharynx. |
Diagnosis
History and physical. Polysomnography, overnight continuous pulse oximetry (helps, but not diagnostic). Treatment 1.Continuous positive airway pressure (CPAP). 2.Oral appliances. 3.Surgical intervention. 4.Weight reduction. 5.BiPAP in severe cases. 6.Tracheostomy. |
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Symptoms
Dyspnea; if massive, shock. |
Hemothorax
Description Blood in pleural space, usually caused by trauma or as a postproce- dural complication. |
Diagnosis
History and physical, decubitus film (can detect decrease in hematocrit if severe enough), true blood will clot unlike other bloody effusions. Treatment Steps 1. Very small—observe. 2. All others—chest tube (32–40 French with 20 cm water suction). 3. Possible thoracotomy (for continued bleeding > 200 mL/hour). |
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Symptoms
Asymptomatic, or exertional dyspnea, cough. Pathology Histologic hallmark—ferruginous bodies. Asbestosis may lead to mesothelioma and lung cancer. Additional risk if patient smokes. |
Asbestosis
Description An interstitial lung disorder caused by long-term exposure to asbestos |
Diagnosis
History and physical, CXR (pleural thickening/plaques, effusion, and opacities), pulmonary function testing (restrictive disease), lung biopsy. Treatment Steps 1. None. 2.Stop smoking. Prevention: in areas of known possible asbestos exposure (removal sites, industrial pipe maintenance, etc.), body suits and respirator masks (EPA [Environmental Protection Agency] approved) required as other government-regulated measurements are to be followed. |
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Symptoms
Asymptomatic or exertional dyspnea and cough. Diagnosis History and physical, CXR (upper lobe nodules and eggshell hilar node calcification). |
Silicosis
Description Silica-induced fibrosing lung disease; with increased risk of mycobacterial infections and lung cancer. Pathology Found with sandblasters/miners; TB and bacteria may coexist with silicosis. Silicosis may be acute, chronic, or accelerated in type. |
Treatment Steps
1.No specific treatment. 2.Annual screening for mycobacterial disease. |
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Symptoms
Asymptomatic, or fever, dyspnea, skin/eye/CNS/cardiac symptoms (erythema nodosum, iritis, arrhythmia, nerve palsy). Diagnosis History and physical, CXR (bilateral enlarged hilar adenopathy), biopsy, elevated angiotensin-converting enzyme, possibly elevated cal- cium, skin test anergy. Pulmonary function test. (See Cram Facts.) |
Sarcoidosis
Description Multisystem granulomatous disorder, commonly with pulmonary involvement. Pathology Etiology unknown; more common in blacks. Biopsy of an involved area (commonly skin or lung) that demonstrates noncaseating granulomas without acid-fast bacilli is the most definitive test |
Treatment Steps
Corticosteroids. Cutaneous sarcoid: chloroquine (Plaquenil). |
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Symptoms
Respiratory distress (cyanosis, grunting, tachypnea). Diagnosis History and physical, CXR (air bronchograms and fine reticular pat- tern). |
Newborn Respiratory Distress (Hyaline Membrane
Disease) Pathology Deficient surfactant, and high lung surface tension. |
Treatment Steps
1. Oxygen. 2.Mechanical ventilation. 3. CPAP. |
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tachypnea
without distress/ cyanosis, usually cesarean section baby |
Transient tachypnea of
the newborn |
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Symptoms
Dyspnea, tachypnea, tachycardia. |
Acute Respiratory Distress Syndrome (ARDS)
Description Acute lung damage syndrome, from increased pulmonary (alveolar) permeability Pathology Etiology includes infection, aspiration, shock, drugs, and multiple other conditions. ACUTE LUNG INJURY •Arterial hypoxemia (PaO2/FiO2 ratio, ≤ 300) •Pulmonary artery wedge pressure ≤ 18 mm Hg or no clinical evidence of left atrial hypertension, and •Bilateral infiltrates consistent with pulmonary edema on frontal CXR (infiltrates can be mild) ARDS •Same criteria as acute lung injury, but more severe hypoxemia (PaO2/FiO2, ≤ 200 |
Treatment Steps
1. Supportive. 2.Treat underlying etiology. 3.“Lung protective ventilation” with low tidal volumes (6 mL/kg ideal body weight). 4. Positive end-expiratory pressure (PEEP). |
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Symptoms
Dyspnea, hypoxemia (headache, confusion, tachycardia, shock) |
Acute and Chronic Respiratory Failure
Pathology Etiology includes ARDS, pulmonary edema, drugs, and neuromuscu- lar conditions. Reduced Po2 etiology: impaired diffusion, ventila- tion–perfusion mismatch, hypoventilation, right–left shunt, and re- duced inspired Po2. |
Diagnosis
History and physical, arterial blood gas (hypoxemia/hypercapnia). PFTs are useful in chronic respiratory disease but are not useful in the acute setting. Treatment Steps 1. Control airway. 2. Oxygen. 3.Improving ventilation by limiting sedation/discontinuing seda- tive medications. 4.More often ventilation assistance is needed with either noninasive ventilation (CPAP or BiPAP) or invasive ventilation (intubation with ventilator) |
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Symptoms
Chest pain, cough, hemoptysis, tachycardia/tachypnea, or nonspecific symptoms (apprehension). • Symptoms: sudden onset dyspnea, pleuritic chest pain, hemoptysis, palpitations, syncope, split S2 sound. • Diagnosis: history and physical, CXR, ventilation–perfusion scan, electrocardiogram (S1, Q3, T [V] 1–3), venous ultrasound of legs, pulmonary angiography, and arterial blood gas (respiratory alkalosis with or without significant hypoxia but increased A-a gradient). |
Pulmonary Embolism (PE)
Description Pulmonary thrombus, via the right side of the heart, from the venous system. • Etology: may vary. Venous stasis, venous thrombosis, hypercoagulable states (e.g., SLE, malignancies), protein C and S deficiency, oral contraceptives, antithrombin III deficiency, and others. Pathology Mostly from deep leg vein thrombi and pelvic venous system (less frequent etiology). |
Diagnosis
History (sudden onset!) and physical (fever, rales, or normal), arter- ial blood gas (increase A-a gradient), lung scan (ventilation–perfu- sion), CXR, electrocardiogram (ECG) with sinus tachycardia and/or S1, Q3, T3, pulmonary angiography (gold standard), search for deep vein thrombosis (DVT) in lower extremities Treatment Steps 1. Anticoagulation (heparin, then Coumadin). 2.Thrombolytic medication (use with massive PE and hypotension). 3. If cannot use anticoagulation, vena caval filter. Prevention impor- tant for high-risk groups (orthopedic surgery, pelvic/abdominal surgery associated with malignancy, surgery with history of DVT or PE). 4.Embolectomy (use in nonresponding shock case). 5.In pregnancy where Coumadin is contraindicated, need to use heparin subcutaneously until term is reached (keeping therapeu- tic partial thromboplastin time [PTT]). Anticoagulation: heparin 5,000–10,000 U (80 U/kg) bolus IV, then 1,000 U/hour (18 U/kg/hour IV), PTT (1.5–2 times control), duration 5–10 days. After 96 hours, start Coumadin (to maintain INR > 2.0). Continue Coumadin 3 months. Monitor platelet count: heparin-induced thrombocytopenia. |
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Symptoms
Chest pain, dyspnea, lethargy, syncope, and occasional hemoptysis. |
Pulmonary Hypertension
Description Elevated pulmonary artery pressure. Etiology Major etiology is hypoxia, but may also be from obstruction, shunts, or unknown etiology (primary pulmonary hypertension) |
Diagnosis
History and physical (shortened second heart sound split and louder P2, weak peripheral pulse/cold hands), ECG (right heart-strain pattern), CXR, polycythemia. Increase pulmonary artery pressures (PAP), pul- monary capillary wedge pressure (PCWP) is usually normal (increased PCWP in pulmonary hypertension from cardiac causes). Pulmonary function tests show normal lung volumes with low diffusion capacity. Treatment Steps 1. Oxygen. 2. Vasodilators. 3.Anticoagulation. 4.Calcium channel blockers. 5.Prostaglandins. |
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Symptoms
Dyspnea, weight gain, wheezing |
Cor Pulmonale
See also Chapter 1, section II.D. Description Right ventricular hypertrophy (RVH) secondary to pulmonary disease. |
Diagnosis
History and physical (cyanosis, edema, ascites, clubbing), ECG (RVH), CXR (large pulmonary artery [main and left/right descend- ing, and RVH]), echocardiogram. Treatment Steps 1. Oxygen. 2.Bronchodilators. 3.Diuretics. 4.Treat right heart failure. |
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Symptoms
Dyspnea, diaphoresis, anxiety, wheezing, tachycardia, cyanosis • Symptoms: Dyspnea, DOE (dyspnea on exertion), orthopnea, paroxysmal nocturnal dyspnea (PND) • Signs: Peripheral edema; rales/crackles; jugular venous distention (JVD); sometimes pink, frothy sputum • CXR: Bilateral infiltrates or “cephalization,” Kerley B lines • Echocardiogram: Useful in documenting depressed ejection fraction and valvular disease |
Pulmonary Edema
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Treatment Steps
1.Oxygen. 2.Diuretics. 3.Morphine sulfate. 4.Venodilators. 5.Dopamine if hypotensive |
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SIGN OR SYMPTOM:
ARRHYTHMIAS |
Think of: Important to
define if they are atrial or ventricular in origin. Think of cardiac ischemia, thyroid disease, medication- induced stress, drugs, post–myocardial infarction (MI) pulmonary embolism, mitral valve prolapse, panic attacks; other less frequent but you need to be aware of: Wolff–Parkinson–White, multifocal atrial tachycardia (MAT), and prolonged QT, just to mention a few. |
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Symptoms
Hemoptysis, glomerulonephritis, anemia, chills/fever/chest pain. Diagnosis Clinical scenario, anti–GBM antibodies, renal biopsy. |
Goodpasture’s Syndrome
Description An autoimmune disorder characterized by antiglomerular basement membrane antibodies (anti-GBM), causing diffuse pulmonary hemorrhage and glomerulonephritis. (See also Chapter 7.) |
Treatment Steps
1. Prednisone. 2. Cyclophosphamide. 3. Plasmapheresis. |
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Symptoms
Cough, dyspnea, lethargy, conjunctivitis, glomerulonephritis, fever, purulent sinusitis. |
Wegener’s Granulomatosis
Description Necrotizing upper and lower pulmonary granulomatous vasculitis with glomerulonephritis. |
Diagnosis
Clinical scenario, lung or renal biopsy. Treatment Steps 1. Cyclophosphamide. 2. Corticosteroids. Attention: There are other types of vasculitis but these are the most frequently asked in test questions. Be aware of the others. |
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1.Pleural protein to serum protein ratio > 0.5.
2.Pleural LDH to serum LDH > 0.6. 3.Pleural LDH > 2 ⁄3 upper serum LDH. protein and LDH numbers above the transudate values. Empyema or complicated parapneumonic effusions (LDH > 1,000 or pH of fluid < 7.20 and/or decrease glucose concentration |
Noted in infections, malignancy, and trauma.
Exudates: empyema, parapneumonic effusions, malignancies, TB, Meigs’ syndrome, pancreatic disease, sarcoidosis, connective tissue disease, Dressler syndrome, |
Criteria suggesting need for aggressive treatment of pleural effusion:
1.Pleural LDH > 1,000. 2.Pleural pH < 7.2. 3.Bacteria present on pleural fluid stain. |
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pleural
fluid protein divided by serum protein under 0.5 and pleural lactic dehydrogenase (LDH) divided by serum LDH under 0.6 |
Noted in CHF, and renal/liver
disease. Transudates: CHF, pulmonary emboli, nephrotic syndrome, ascites, myxedema, peritoneal dialysis, severe atelectasis, and superior vena cava syndrome. |
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Description/Symptoms
Pleural inflammation, causing inspiratory pain (usually unilateral, and of rapid onset), dyspnea. Clinical diagnosis |
Pleurisy
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Treatment Steps
1.Indomethacin. 2.Intercostal nerve block. |
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Symptoms
May be asymptomatic or present as per primary etiology, also dysp- nea, pleuritic chest pain |
Pleural Effusion
Diagnosis History and physical, CXR (lateral decubitus film), pleural fluid exam. (See Differential Diagnosis and Cram Facts.) Pathology Increased capillary permeability or hydrostatic pressure, or de- creased lymph drainage or oncotic pressure. |
Treatment Steps
Treat primary etiology. |
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Pleurodynia
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epidemic
infection in young people, coxsackie B virus, |
supportive treatment.
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Intubation
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ndotracheal tube: via oral or nasal route, with posi-
tion confirmed by x-ray and auscultation (where available, also can use CO2 detector for airway as an aid to confirm position). Nasal tube is more difficult to suction through than oral tube (and has increased infection risk after 5 days). |
Endotracheal intu-
bation may be maintained without time limit (in prolonged intu- bations or recurrent intubations watch for tracheostenosis, also watch for increased balloon pressures and tracheal trauma). If long-term ventilation is needed, tracheostomy is considered. |
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Tracheostomy
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easier to suction through than oral tube. More
comfortable to patients for prolonged/extended periods of time. Air must be humidified. |
As all tubes, bypass normal nose/upper
airway humidification. Same precautions as above. |
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Assisted ventilation
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decision to intubate is clinical in nature. Clin-
ical signs to look for: paradoxical respirations, increased JVD, pul- sus paradoxicus, and increased lethargy or severe confusion. ABG is also very useful in documenting the severity of hypoxemia or hypercapnia. |
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IMV
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delivers set respiratory rate per minute with set tidal volume
with each of those breaths. In between machine breaths, pa- tient can generate his/her own breaths with tidal volume de- termined by patient’s effort, allowing for patient’s own mus- cles to be exercised. |
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A/C
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patient receives set rate per minute with set volumes
with each breath. Any extra breaths generated by the patient, in addition to the ones already set, will be assisted (the ma- chine will complete/supplement each breath [volume]) for patient |
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PEEP added to A/C or
IMV to produce constant positive ventilation pressure; |
ost useful for
pulmonary edema, ARDS, or other conditions in which Oxygenation is pooR, with settings of 3–20 cm water. |
• Complications of
PEEP—reduced cardiac output and pneumothorax. • Ventilator problem— disconnect patient from machine, and ventilate by bag. Hard to ventilate: suction patient, and rule out pneumothorax, tube position problem, or obstruction. Treat as indicated. |
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Symptoms
Hemoptysis, hypoxia, dyspnea, lethargy, wheezing. |
Massive Hemoptysis
Description Blood flow of 200–600 mL into the pulmonary system within 24 hours Pathology Bronchiectasis, TB, vasculitis, fungal cavitations, abscess, and coagulopathies most commonly |
Diagnosis
History and physical exam, CXR and lab, bronchoscopy Treatment Steps 1.Oxygen. 2.Fluids. 3.Bronchoscopy. 4.Correct coagulopathy. 5.A-gram embolization. 6.Surgery. |
