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Board Review: Pulm and
Critical Care
Carrie Clark DO
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Respiratory Physiology
īŽ

A-a gradient
īŽ

=PAO2-PaO2
īŽ

PAO2 value from alveolar gas equation
īŽ

īŽ

Alveolar gas equation: PAO2=150-(1.25xPaCO2) (at sea level
and room air)

PaO2 obtained from ABG
+

Hypoxemia
īŽ

Defined as PaO2<60mmHg

īŽ

Etiology
īŽ

īŽ

V/Q mismatch
īŽ Airspace not being perfused OR perfused areas not being ventilated
īŽ Etiologies: asthma, COPD, PE, interstitial lung disease
īŽ Management: oxygen and treat underlying cause
Shunting
īŽ Decreased diffusion of oxygen
īŽ Etiologies: alveolar collapseīƒ ARDS, also from alveolar filling
(pneumonia, pulmonary edema)
īŽ Management: does NOT respond well to oxygenīƒ  responds better
to PEEP
+

Hypoxemia
īŽ

Decreased diffusion
īŽ

īŽ

īŽ

Etiologies: thickening of alveolar/capillary interface (commonly
interstitial lung disease)
Management: responds to O2

Hypoventilation
īŽ

īŽ

īŽ

Lack of respiratory effort resulting in low PaO2 and high PaCO2,
commonly from drug overdose
Normal A-a gradient

High Altitude
īŽ

Decrease in partial pressure of available O2

īŽ

Normal A-a gradient
+

Critical Care: ARDS
īŽ

Acute onset of alveoli edema caused by capillary membranes
injury and increased permeability
īŽ

Sepsis, acute pulmonary infection, DIC, shock lung, freebase
cocaine smoking

īŽ

You will see bilateral infiltrates on chest x-ray

īŽ

Ratio of PaO2/FiO2<200mmHg

īŽ

Symptoms: respiratory distress, hypoxemia unresponsive to
increasing supplemental O2

īŽ

Onset is often within the first 2 hours of inciting event, but it can
be delayed as long as 1-3 days
+

Critical Care: ARDS
īŽ

Management
īŽ

35-50% mortality

īŽ

Treat underlying disease

īŽ

Mechanical ventilation with PEEP
īŽ

Use low tidal volumes to prevent barotrauma

Steroids NOT shown to be beneficial
+

Disorders of Pleura, Mediastinum
and Chest Wall
īŽ

Mediastinitis

īŽ

Pneumomediastinum

īŽ

Pleural Effusion

īŽ

Pneumothorax
+

Mediastinitus
īŽ

Inflammation of the mediastinum

īŽ

Etiology
īŽ

īŽ

īŽ

Mixed organisms but most commonly Streptococcus and
Bacteroides
Esophageal rupture most common cause (foreign body ingestion or
stuck fish bone may accompany history or esophageal inj)

Risk Factors
īŽ

īŽ

Immunocompromise and diabetes, drug abuse

Symptoms
īŽ

Fever, dyspnea, pleuritic, retrosternal chest pain, sub-q emphysema
of neck and chest
+

Mediastinitis
īŽ

Diagnosis
īŽ
īŽ

Soft tissue x-ray of the neck may show precervical or
retropharyngeal air/edema

īŽ

īŽ

A CXR may show a widened mediastinum

CT should be performed to further evaluate soft tissue spaces

Management
īŽ

Broad-spectrum antibiotic therapy

īŽ

ENT and cardiothoracic consult
+

Pneumomediastinum
īŽ

Etiology
īŽ

Spontaneousīƒ extremely rare, blunt chest trauma, endoscopy,
obstructive lung disease

īŽ

Considerer Boerhaave syndrom if h/o vomiting

īŽ

Valsalva maneuver (foreceful cough against a closed glottis,
consitpation)
īŽ

īŽ

Observed in crack cocaine users

Symptoms
īŽ

Chest pain and dyspnea

īŽ

Signs: sub-q emphysema and Hamman sign (crunching, rasping
sound, synchronous with heartbeat)

īŽ

Decreased cardiac output if tension pneumomediastinum is present
+

Pneumomediastinum
īŽ

Diagnosis
īŽ

īŽ

Esophagogramīƒ perform in right lateral decubitus position, use a
water-soluble contrast, if clinical suspicions remain high and the
initial study is negative, repeat study with oral barium contrast

īŽ

Esophagoscopyīƒ for suspected esophageal rupture in acute
traumatic rupture

īŽ

īŽ

CXRīƒ reveals free air within the mediastinum, air posterior to
sternum and posterior to the heart on lateral film

Bronchoscopyīƒ for suspected bronchotracheal tree rupture

Management
īŽ

Should be admitted and observed for signs of serious complications

īŽ

Broad-spectrum antibiotics for suspected esophageal rupture
+

Pleural Effusion
īŽ

Collection of fluid within pleural space

īŽ

Epidemiology
īŽ

īŽ

īŽ

CHF is the most common cause followed by malignancy, bacterial
pneumonia, and PE
TB is the most common etiology of pleural effusion in developing
countries

Etiology
īŽ

Transudativeīƒ CHF, cirrhosis with ascites, nephrotic syndrome, PE

īŽ

Exudativeīƒ Cancer, infectious (pneumonia, empyema, abscess,
TB), inflammatory (SLE, pancreatitis, RA, and PE
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Pleural Effusion
īŽ

Symptoms
īŽ

īŽ

Dyspnea and pleuritic chest pain, decreased breath sounds on
auscultation, dullness to percussion

Diagnosis
īŽ
īŽ
īŽ

CXR: AP XR demonstrates effusion when pleural fluid volume
approaches 150cc
CT or US most sensitive
Thoracentesis necessary when etiology is unclear
īŽ Light criteriaīƒ a single positive criterion is enough to classify the fluid
as an exudate
īŽ Glucoseīƒ low pleural fluid levels (<25)=RA, TB, empyema, and
malignancies
īŽ pHīƒ low pH=inflammatory and infiltrative processes (empyema,
malignancies, TB, esophageal rupture)
īŽ Amylaseīƒ high amylase (>200) pancreatitis, malignancy, rupture
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Pleural Effusion
īŽ

Light Criteria

Transudate

Exudate

Pleural and
serum Protein

<0.5

>0.5

Pleural and
serum LDH

<0.6

>0.6

Pleural LDH

<200

>200
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Pleural Effusion
īŽ

Management
īŽ

Treat underlying cause

īŽ

Therapeutic thoracentesis for patients dyspneic at rest

īŽ

Thoracotomy tube placement for empyema
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Pneumothorax
īŽ

Etiology
īŽ

īŽ

īŽ

Spontaneousīƒ no underlying lung disease
īŽ Male:female 6:1
īŽ Young, tall, thin
īŽ Smoking 20:1
īŽ Valsalva
īŽ Ruptured bleb
īŽ Many recur (20-50%)
Secondary-caused by underlying lung disease
īŽ Asthma, COPD, neoplasm
īŽ Marfan, Ehlers Danlos, Cystic fibrosis
īŽ Penumonia, especially with abscess or cavitation
īŽ HIV-PCP
Tension pneumo
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Pneumothorax
īŽ

Symptoms
īŽ
īŽ
īŽ
īŽ

īŽ

Dyspnea and pleuritic chest pain
Decreased breath sounds and hyperresonace to percussion
JVD and hypotension
Tracheal deviation away from affected side

Diagnosis
īŽ

īŽ

Pneumothorax
īŽ CXR for simple pneumothorax (end expiratory for highest sensitivity)
īŽ CT test of choice for supine trauma patient
Tension pneumo
īŽ Clinical diagnosis
īŽ Tracheal deviation away from affected lung
īŽ Hypotension
īŽ Do NOT wait for x-rays before treating
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Pneumothorax
īŽ

Management
īŽ

Small, stable ptx (<10%)
īŽ
īŽ

Reabsorb 5-7% per day

īŽ

īŽ

100% O2
Stable patient with a small ptx can be discharged with next day
follow up after 6 hours observation and stable x-ray

Large ptx
īŽ
īŽ

īŽ

100% O2
Tube thoracostomy

Tension ptx
īŽ

Immediate decompression followed by chest tube
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Noncardiogenic Pulm Edema
īŽ

Definition: radiographic evidence of alveolar fluid accumulation
without hemodynamic evidence of a cardiogenic etiology (ie
pulmonary capillary wedge pressure <18mmHg)

īŽ

Etiology
īŽ

ARDS

īŽ

High-altitude pulmonary edema

īŽ

Reexpansion pulmonary edema
īŽ
īŽ

īŽ

Large volume thoracentesis (>1L)
Rapid lung re-expansion of ptx, especially when it has been
collapsed for >3 days

Drug induced (meprobamate, opiates, naloxone, PCP, Salicylate)
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Obstructive Lung Disease
īŽ

Asthma and reactive airway disease

īŽ

COPD

īŽ

Cystic Fibrosis
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Asthma and reactive airway disease
īŽ

Chronic inflammatory disorder of the small airways characterized
by reversible obstruction

īŽ

Etiology and patho
īŽ
īŽ

īŽ
īŽ

īŽ

Airway inflammation/bronchial wall edema leading to decreased airway
diameter
Airway hyperreactivity, smooth muscle contraction
Secretions forming mucous plugs
Chronic inflammation leads to lung remodeling

Symptoms
īŽ
īŽ

īŽ

Dyspnea with or without cough
Prolonged expiratory phase with predominantly exp wheezing
Severe exacerbations may present with absence of wheezing, inability
to speak, pulses paradoxus and hypoxia
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Asthma and reactive airway disease
īŽ

History associated with higher mortality
īŽ

>2 hospitalizations during past year

īŽ

>3 ED visits during past year

īŽ

Prior intubation or ICU admission

īŽ

Use of 2 or more adrenergic canisters per month

īŽ

Current use of systemic steroids or recent withdrawal

īŽ

Low socioeconomic class
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Asthma and reactive airway disease
īŽ

Diagnosis
īŽ

īŽ

Bedside spirometryīƒ peak flow to monitor response to beta-agonist
treatment
īŽ Peak flow <50% indicates severe exacerbation

Treatment
īŽ
īŽ
īŽ
īŽ

Oxygen to keep O2>88%
Beta agonistsīƒ relaxation of bronchial smooth muscle
Epinephrine (1:1000)īƒ reserved for severe exacerbations, is
administered sub-q 0.3 q20-30 minutes up to three doses
Terbutalineīƒ  reserved for severe exacerbations given SC 0.25mg
every 20-30 min up to three doses
īŽ Longer duration of action than epinephrine
+

Treatment cont.
īŽ

Corticosteriodsīƒ used in both acute and chronic setting to
prevent late phase inflammatory response
īŽ

Oral dosing as effective as IV administration

īŽ

Magnesiumīƒ benefit in severe exacerbation

īŽ

Mechanical ventilationīƒ 
īŽ

Avoid air-trapping or auto-peep

īŽ

Smaller tidal volumes

īŽ

Keep rate low

īŽ

Consider increasing peak inspiratory flowīƒ longer expiratory time
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Treatment cont
īŽ

When treating pregnant asthmaticsâ€Ļ
īŽ

Fetus more susceptible to hypoxia than mother

īŽ

No contraindications to use of beta agonists, corticosteroids and
anticholinergics

īŽ

Chronic steroids may result in lower birth weights

īŽ

Epinephrine is teratogenic during first trimester and associated with
preterm delivery
+

COPD
īŽ

Progressive partially reversible limitation of airflow

īŽ

Caused by two processesīƒ chronic bronchitis and
emphysema, which occur together in most patients

īŽ

Epidemiology
īŽ

īŽ

The single most important risk factor for COPD is smoking

Etiology
īŽ

80% of acute COPD exacerbations are of infectious origin
īŽ

Streptococcus pneumoniae, Haemophilus influenzae, or
moraxella catarrhalis
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COPD
īŽ

Signs and symptoms
īŽ
īŽ

īŽ

Dyspnea on exertion, tachypnea, cyanosis, agitation, apprehension,
and hypertension are indicative of hypoxia
Wheezing, rales, rhonci, prolonged expiratory phase, pursed-lip
breathing and clubbing of digits

Diagnosis
īŽ
īŽ
īŽ
īŽ

Elevated hematocrit 2/2 chronic hypoxia
ABG: mild to moderate hypoxemia without hypercapnea in early
stages
CXRīƒ hyperinflation, flattened diaphragm, long narrow heart
shadow
EKGīƒ a-fib, multifocal atrial tachycardia, cor-pulmonale (tall pwaves), right axis deviation and right ventricle hypertrophy
+

COPD
īŽ

Management
īŽ

Supplemental oxygen reduces mortality in patients with advanced
COPD with room air O2 saturaion <88%

īŽ

Nebulized anticholinergics

īŽ

Bronchodilators

īŽ

Antibiotics
īŽ

First line choices include amoxicillin, cefaclor, fluoroquinolones, or
bactrim

īŽ

Gram-negative infections more likely in those with frequent
exacerbation and need a third-generaltion cephalosporin

īŽ

corticosteroid
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Cystic Fibrosis
īŽ

Most common in Europeans and Ashkenazi Jews

īŽ

Autosomal recessive mutation
īŽ

īŽ

īŽ

Abnormalities in chloride transport in exocrine tissues leads to
multiorgan involvement
Thick, viscous secretions in lungs, intestine, pancreas, and
reproductive tract

Symptoms and signs
īŽ

Respiratory manifestationsīƒ most common, exacerbations
characterized by increased cough, sputum production, decreased
lung function
+

CF symptoms and signs cont.
īŽ

Undiagnosed patients may present with failure to thrive chronic
cough, repeated pulmonary or sinus infections, chronic
diarrhea from pancreatic insufficiency

īŽ

Alternative presentations
īŽ

Increased salt content in sweat gland secretion

īŽ

Meconium ileus in neonates

īŽ

Steatorrhea from pancreatic enzyme insufficiency

īŽ

Intestinal obstruction

īŽ

Spontaneous pneumo

īŽ

Chronic pancreatitis

īŽ

Hepatobiliary disease
+

CF diagnosis
īŽ

Electrolytes
īŽ

īŽ

Hyponatremia and alkalosis

CXR
īŽ

Bronchiolar thickening, hyperinflation, and patchy, diffuse infiltrates

īŽ

Newborn screening

īŽ

Chloride sweat testing or genetic testing
+

CF Management
īŽ

Broad-spectrum antibiotics
īŽ

Cover Staph aureus, H. flu, and double cover Pseudomonas

īŽ

Chronic colonization with pathologic bacteria and chronic antibiotic
use leads to resistant organisms requiring intravenous vanco,
tobramycin, meropenem, cipro, and piperacillin

īŽ

Mucolytics

īŽ

Bronchodilators

īŽ

Aggressive chest physiotherapy

īŽ

Provide O2

īŽ

Consult Pulm
+

Restrictive Lung disease
īŽ

Loss of lung compliance resulting in volumes loss
īŽ

Interstitial Lung Disease
īŽ

īŽ

Idiopathic pulmonary fibrosis

Sarcoidosis
+

ILD
īŽ

ILD
īŽ

īŽ

Restrictive pulmonary dysfunctions with the common end-point of
interstitial collagen deposits and scarring

Idiopathic pulmonary fibrosis
īŽ

50% of ILDs

īŽ

Likely autoimmune

īŽ

Symptoms and signsīƒ dyspnea, cough, fine dry crackles, clubbing
of fingers

īŽ

Diagnosisīƒ CXR has honeycombed lungs, CTīƒ ground glass
opacity

īŽ

Management īƒ corticosteroids, immune modulators, lung transplant
+

Sarcoidosis
īŽ

Epidemiology
īŽ
īŽ

īŽ

African americans>caucasians
females>males

Etiologyīƒ typical finding includes non-caseating granuloma,
which is composed of T-helper cells and other inflammatory
cells
+

Sarcoidosis
īŽ

Symptoms and Signs
īŽ

Most patients are asymptomatic

īŽ

Disease is fatal in 10% of patients because of extensive organ
involvement

īŽ

Constitutional symptomsīƒ fever, fatigue, weight loss, polyarthritis,
myositis

īŽ

Pulm symptomsīƒ cough, hemoptysis, shortness of breath with
exertion

īŽ

Neuroīƒ bells palsy, seizures

īŽ

Skin lesionsīƒ plaques, subcutaneous nodules, erythema nodosum

īŽ

Cardiacīƒ arrhythmias, CHF

īŽ

Lympthadenopathy

īŽ

Ophthalmologicīƒ uveitis, or conjunctivitis
+

Sarcoidosis
īŽ

Diagnosis
īŽ

CXR
īŽ
īŽ

Stage 1īƒ hilar adenopathy

īŽ

Stage 2īƒ Hilar adenopathy and parenchymal involvement

īŽ

Stage 3īƒ parenchymal involvement without adenopathy

īŽ
īŽ

Stage 0īƒ no findings

Stage 4īƒ pulmonary fibrosis

Lab studies
īŽ

Leukocytosis, elevated ESR or serum ACE, hypercalcemia or
hyperphosphatemia, elevated CK and CK-MB with cardiac
involvement

īŽ

Gallium 67īƒ used to detect extrapulmonary sarcoidosis

īŽ

Biopsy of involved organ is most useful for diagnosis
+

Sarcoidosis
īŽ

Management
īŽ

Cardiac monitoring

īŽ

Consider steroids or cytotoxic medications

īŽ

Lung transplantation for patients with severe refractory disease
+

Thromboembolic Disease
īŽ

DVT

īŽ

PE
+

DVT
īŽ

Risk factors
īŽ

Previous thrombosis

īŽ

Vascular endothelial damage
īŽ

īŽ

Trauma, sugery (especially ortho), smoking

Hypercoagulability
īŽ
īŽ

Factor V Leiden (most common hereditary hypercoagulability

īŽ

Antithrombin III deficiency

īŽ
īŽ

Protein C or S deficiency

Oral contraceptives or 3rd trimester pregnancy

Immobilization or low cardiac output
īŽ

Long periods of sitting, CHF
+

DVT
īŽ

Signs and Symptoms
īŽ

Pain, warmth and edema

īŽ

Discoloration of affected extremity

īŽ

Palpable cord of a thrombosed vein
+

DVT
īŽ

Diagnosis
īŽ

CT angiography

īŽ

Doppler ultrasonography
īŽ

īŽ

Limitationsīƒ operator dependent, cannot distinguish between old
and new clot, not accurate in detecting DVT in the pelvis or the
small vessels of the calf

Management
īŽ

Anticoagulationīƒ unfractionated low-molecular weight heparin or
warfarin therapy

īŽ

Filter placement for patients with failure of anticoagulation or
contraindication to anticoagulation
+

Pulmonary Embolus
īŽ

Risk factor are the same as for DVTīƒ  60% of patients with a
DVT have a PE

īŽ

Symptoms and signs
īŽ

Sudden-onset dyspnea, tachypnea, tachycardia, pleuritic pain,
hemoptysis, syncope, cough, and wheeze
+

PE diagnosis
īŽ

ECG
īŽ

īŽ

Nonspecific ST-T wave changes and/or sinus tach are most common, S1Q3T3,
precordial flipped T waves

CXR
īŽ
īŽ
īŽ

Findings are abnormal but nonspecific, pleural effusion, elevated hemidiaphragm
secondary to atelectasis and noninfectious infiltrates
Westermark signīƒ abrupt cut-off of vascular markings
Hamptom humpīƒ pleural based wedge-shaped infarct

īŽ

CT pulm angiography

īŽ

VQ scanīƒ useful in severe contrast allergies
īŽ

A normal scan is sufficient to exclude PE in patient with low pretest probability

īŽ

Echoīƒ may reveal evidence of right heart strain

īŽ

Pulmonary angiographyīƒ the gold standard for diagnosing PE (used
infrequently because of noninvasive CT scans
+

PE management
īŽ

Supplemental O2

īŽ

Hemodynamic support

īŽ

Anticoagulation

īŽ

Thrombolytic
īŽ

Indicated in patients with associated hemodynamic instability

īŽ

Surgical Embolectomy

īŽ

IVC filter for anticoagulation failure or contraindication
+

Pulmonary Infections
īŽ

Pneumonia
īŽ
īŽ

īŽ

Bacterial
viral

Tuberculosis
+

Bacterial Pneumonia
īŽ

Etiology
īŽ

Typical Pneumonia
īŽ

īŽ

S. pneumoniae, H. influenzae, and Staph (S. Pneumo most
common)

Atypical Pneumonia
īŽ

Influenza virus, mycoplasma, chlamydia, legionella, and
adenovirus

īŽ

IV drug usersīƒ S. aureus

īŽ

Alcoholism, diabetes, and COPDīƒ K, Pneumoniae

īŽ

Asthmaticsīƒ H. Flu

īŽ

Hospital acquired pneumoniaīƒ pseudomonas aeruginosa
+

Bacterial Pneumonia
īŽ

Symptoms and signs
īŽ

Chest pain

īŽ

Productive cough
īŽ

Klebsiellaīƒ currant jelly

īŽ

S. Pneumoniaeīƒ bloody or rusty colored

īŽ

Aspirationīƒ foul-smelling sputum

īŽ

Chlamydiaīƒ staccato cough

īŽ

Rigorsīƒ particularly associated with S. Pneumonia

īŽ

Diarrhea and GI upset with Legionella

īŽ

Bullous myringitis with Mycoplasma pneumoniae

īŽ

Pleural rubs
+

Bacterial Pneumonia
īŽ

Diagnosisīƒ Chest radiography
īŽ

Bilateral diffuse infiltrates consistent with atypical infections (M.
Pneumoniae, P. Carinii, C. Psittaci)

īŽ

Abscess and bulging lung fissures are indicative of infections
caused by Klebsiella and S. aureus

īŽ

Pleural effusions and empyema associated with cavitary lesions are
seen with s. aureus and M. tuberculosis

īŽ

Upper lung fieldsīƒ K. Pneumoniae

īŽ

Lower lung fieldsīƒ L. Pneumoniae

īŽ

Miliary patternīƒ M. Tuberculosis
+

Bacterial Pneumonia
īŽ

Laboratory studies
īŽ

Hyponatremia and hypophosphatemia associated with L.
Pneumophila

īŽ

Sputum samples for gram stain and culture are accurate about 50%
of the time
īŽ

Adequate sputum contains <10 epithelial cells, >25 WBC per low
power field and remain uncontaminated from oral flora

īŽ

Mycoplasma and Chlamydia immunoglobulin M antibodiesīƒ  a
rise in antibody titer of 1:128 confirms the diagnosis
+

Bacterial Pneumonia
īŽ

Management
īŽ

Community-acquired pneumonia
īŽ
īŽ

īŽ

Pneumonia severity index score helps determine risk
Admit if total score >90 points and consider ICU for >130

Hospital-acquired pneumonia
īŽ
īŽ

īŽ

Double-drug coverage for Pseudomonas

Optimal combinations include cefipime plus levofloxacin,
aztreonam, meropenem, or aminoglycoside

Aspiration pneumonia
īŽ

Intubation should be considered in any patient who is unable to
protect airway, add anaerobic coverage
+

Types of Bacterial Pneumonia
īŽ

Bordetella Pertussis (whopping cough)
īŽ

īŽ

Summer and fall months, neither active disease nor vaccination
provides lifelong immunity

Symptoms and signsīƒ 3 stages, each lasting about 2 weeks
īŽ

Catarrhal
īŽ

īŽ

Paroxysmal
īŽ

īŽ

Most infectious during this time, symptoms indistinguishable from
a URI
Coughing episodes followed by an inspiratory “whoop” , posttussive exhaustion and emesis

Convalescent
īŽ

Chronic cough that can last several months

īŽ

Complications include mucous plug, secondary bacterial infection,
ruptured diaphragm, hernia, and rectal prolapse
+

Pertussis
īŽ

Diagnosis
īŽ
īŽ

īŽ

Degree of lymphocytosis correlates with severity of disease
Definitive diagnosis is made via nasopharyngeal culture

Treatment
īŽ

Erythromycin x14 days

īŽ

Consider prophylaxis with erythromycin for close contacs

īŽ

Consider hospitalization for infants <6 months, premature infants,
and those with significant comorbitites
+

Mycoplasma Pneumonia
īŽ

Most common atypical

īŽ

14-day incubation period

īŽ

More common in young adults

īŽ

CXR may show interstitial pattern or patchy infiltrate

īŽ

Treat with macrolide antibiotic

īŽ

Associations
īŽ
īŽ
īŽ
īŽ

Bullous myringitis
Meningitis and encephalitis
Erythema multiforme
Guillain-Barre
+

Chlamydia Pneumonia
īŽ

Obligate intracellular parasite

īŽ

Infants
īŽ
īŽ
īŽ
īŽ
īŽ

Acquired at birth
50% conjunctivitis
Tachypnea
May be afebrile
CXR shows hyperinflation and diffuse infiltrates

īŽ

Common in young adults complaining of hoarseness, cough, and
persistent malaise

īŽ

Staccato cough

īŽ

Treat with macrolide
+

Legionella Pneumonia
īŽ

Airborne and associated with water sources

īŽ

Classically associated with recent air travel

īŽ

No person to person transmission

īŽ

Symtpoms and signs
īŽ

īŽ

Pleuritic chest pain, relative bradycardia, GI symtpoms

Diagnosis
īŽ

Labs may reveal hyponatremia and hypophosphatemia

īŽ

Chest x-ray may show alveloar infiltrates or consolidation that my
progress to hilar adenopathy and pleural effusion

īŽ

Treat with erythromycin for 3 weeks
+

Tuberculosis
īŽ

Leading cause of death worldwide

īŽ

Humans are sole reservoir

īŽ

TB can remain dormant for years in granulomas

īŽ

Risk factors
īŽ

Immunocompromised (HIV, malignancy, DM, extremes of age)

īŽ

Close contacts or occupational exposure

īŽ

Medically underserved, low-income populations
+

TB symptoms and signs
īŽ

Primary TB
īŽ

Only 10% of exposed individuals develop primary TB

īŽ

Constitutional symptoms
īŽ

Coughīƒ most common symptoms of pulmonary TB

īŽ

Initially nonproductive or nonspecific sputum

īŽ

Hemoptysis may be presenting complaint

īŽ

Pleuritic chest pain

īŽ

Night sweats

īŽ

“classic” presentation is uncommon
+

TB
īŽ

Postprimary TB (reactivation TB)
īŽ

Lifetime risk in immunocompetent individual is 10% to 15%

īŽ

In HIV-positive patients
īŽ

37% with disease in 6 months

īŽ

10% incidence of disease per year

īŽ

Signs and symptoms similar to primary TB
+

TB extrapulmonary
īŽ

Lymphadenitis (scrofula)
īŽ

īŽ

Pleural effusion
īŽ

īŽ

Pott’s disease (spinal)īƒ spinal cord injury possible, lumbar infection may lead to
psoas abscess

acute disseminated
īŽ

īŽ

Small and unilateral, diagnosis through pleurocentesis

Bone and joint infection
īŽ

īŽ

Most common EPTB, enlarging, painless, erythematous firm mass near cervical
nodes, do NOT I and D

Generalized systemic illness, typically in elderly and HIV patients, fever, weight
loss, anorexia, weakness, SIADH is common, often associated with meningitis

CNS
īŽ
īŽ

6% of cases, peak in newborn to 4 years, SIADH, tuberculosis meningitis
CSF analysisīƒ lowest glucose CSF levels of any meningitis
+

TB diagnosis
īŽ

TB skin testingīƒ read 48-72 hours later, induration not
erythema
īŽ

15mm in low-risk, immunocompetent patients

īŽ

10mm in high-risk immunocopetent patients

īŽ

5mm in HIV, Close contacts infectious TB, abnormal CXR,
immunocompromised from steroids
+

TB medical therapy
īŽ

Latent TBīƒ infections without active disease,
chemoprophylaxis with isoniazid for 9 months

īŽ

Active TBīƒ treated for 6 months, 4 drugs until resistance
pattern determined, after 2 months may discontinue
pyrazinamide if TB isolates do not demonstrate resistance

īŽ

Extrapulmonary TB->treat for 6 months
īŽ

CNS infection (tuberculous meningitis) is the exception, requires 912 months of treatment

īŽ

Consider steroids for CNS and pericardial TB
+

Treatment of TBīƒ drugs
īŽ

First line agents
īŽ

Isoniazid (INH)
īŽ
īŽ

īŽ

8% resistance rate

Prevent INH-related seizures: supplement with pyridoxine (B6)

Rifampin
īŽ
īŽ

īŽ

Orange discoloration of bodily fluids
Oral contraception failure

Pyrazinamide (PZA)
īŽ

īŽ

Hepatotoxicity, polyarthralgias

Ethambutol (ETH)
īŽ

Prevents emergence of RIF resistance

īŽ

Retrobulbar neuritisīƒ decreased visual acuity or red/green color
blindness
+

Treatment cont.
īŽ

Noncompliant patients
īŽ

īŽ

Court-ordered directly observed therapy (DOT)

īŽ

īŽ

Uncooperative and potentially infectious patients may be compelled
to comply
Incarceration as last resort

In pregnancy
īŽ

INH, RIF, ETH cross placenta and are safe
+

Viral Pneumonia
īŽ

Influenza

īŽ

Varicella

īŽ

Cytomegalovirus

īŽ

hantavirus
+

influenza
īŽ

Often associated with bacterial superinfection (s. aureus)

īŽ

Diagnosis: nasopharyngeal swab culture for influenza aid
diagnosis

īŽ

CXR shows diffuse bilateral infiltrates
+

Varicella
īŽ

Symptoms and signs: pneumonia may present with chest pain
and hemoptysis preceded by a rash

īŽ

More severe in adults

īŽ

Managementīƒ mandates admission for treatment with
acyclovir
+

cytomegalovirus
īŽ

Most common in solid organ transplant and bone marrow
transplant recipients

īŽ

Often presents simultaneously with pneumocystis pneumonia

īŽ

Management
īŽ

īŽ

IV ganciclovir or foscarnet plus immunoglobulin therapy

CXR
īŽ

Bilateral interstitial pattern
+

Hantavirus
īŽ

Aerosolized contaminated material from rodent feces or urine
īŽ

Southwest US

īŽ

Symptoms and signsīƒ flu-like symtpoms that progress to
respiratory distress and shock

īŽ

Diagnosisīƒ CXR reveals bilateral infiltrates
+

Fungal Pneumonia
īŽ

Histoplasma capsulatum, blastomyces dermatitides and
coccidioides present in the soil in various geographic areas of
the US
īŽ

Histoplasma capsulatum in the mississippi and Ohio River valleys

īŽ

Coccidioides immitis in desert areas of the Southwest

īŽ

Symptoms and signs vary from acute or chronic pneumoina to
asymptomatic granulomas on CXR

īŽ

Diagnosisīƒ hilar adenopathy
EM Board Review Pulmonary & Critical Care...Carrie Clark

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EM Board Review Pulmonary & Critical Care...Carrie Clark

  • 1. + Board Review: Pulm and Critical Care Carrie Clark DO
  • 2. + Respiratory Physiology īŽ A-a gradient īŽ =PAO2-PaO2 īŽ PAO2 value from alveolar gas equation īŽ īŽ Alveolar gas equation: PAO2=150-(1.25xPaCO2) (at sea level and room air) PaO2 obtained from ABG
  • 3. + Hypoxemia īŽ Defined as PaO2<60mmHg īŽ Etiology īŽ īŽ V/Q mismatch īŽ Airspace not being perfused OR perfused areas not being ventilated īŽ Etiologies: asthma, COPD, PE, interstitial lung disease īŽ Management: oxygen and treat underlying cause Shunting īŽ Decreased diffusion of oxygen īŽ Etiologies: alveolar collapseīƒ ARDS, also from alveolar filling (pneumonia, pulmonary edema) īŽ Management: does NOT respond well to oxygenīƒ  responds better to PEEP
  • 4. + Hypoxemia īŽ Decreased diffusion īŽ īŽ īŽ Etiologies: thickening of alveolar/capillary interface (commonly interstitial lung disease) Management: responds to O2 Hypoventilation īŽ īŽ īŽ Lack of respiratory effort resulting in low PaO2 and high PaCO2, commonly from drug overdose Normal A-a gradient High Altitude īŽ Decrease in partial pressure of available O2 īŽ Normal A-a gradient
  • 5. + Critical Care: ARDS īŽ Acute onset of alveoli edema caused by capillary membranes injury and increased permeability īŽ Sepsis, acute pulmonary infection, DIC, shock lung, freebase cocaine smoking īŽ You will see bilateral infiltrates on chest x-ray īŽ Ratio of PaO2/FiO2<200mmHg īŽ Symptoms: respiratory distress, hypoxemia unresponsive to increasing supplemental O2 īŽ Onset is often within the first 2 hours of inciting event, but it can be delayed as long as 1-3 days
  • 6. + Critical Care: ARDS īŽ Management īŽ 35-50% mortality īŽ Treat underlying disease īŽ Mechanical ventilation with PEEP īŽ Use low tidal volumes to prevent barotrauma Steroids NOT shown to be beneficial
  • 7. + Disorders of Pleura, Mediastinum and Chest Wall īŽ Mediastinitis īŽ Pneumomediastinum īŽ Pleural Effusion īŽ Pneumothorax
  • 8. + Mediastinitus īŽ Inflammation of the mediastinum īŽ Etiology īŽ īŽ īŽ Mixed organisms but most commonly Streptococcus and Bacteroides Esophageal rupture most common cause (foreign body ingestion or stuck fish bone may accompany history or esophageal inj) Risk Factors īŽ īŽ Immunocompromise and diabetes, drug abuse Symptoms īŽ Fever, dyspnea, pleuritic, retrosternal chest pain, sub-q emphysema of neck and chest
  • 9. + Mediastinitis īŽ Diagnosis īŽ īŽ Soft tissue x-ray of the neck may show precervical or retropharyngeal air/edema īŽ īŽ A CXR may show a widened mediastinum CT should be performed to further evaluate soft tissue spaces Management īŽ Broad-spectrum antibiotic therapy īŽ ENT and cardiothoracic consult
  • 10. + Pneumomediastinum īŽ Etiology īŽ Spontaneousīƒ extremely rare, blunt chest trauma, endoscopy, obstructive lung disease īŽ Considerer Boerhaave syndrom if h/o vomiting īŽ Valsalva maneuver (foreceful cough against a closed glottis, consitpation) īŽ īŽ Observed in crack cocaine users Symptoms īŽ Chest pain and dyspnea īŽ Signs: sub-q emphysema and Hamman sign (crunching, rasping sound, synchronous with heartbeat) īŽ Decreased cardiac output if tension pneumomediastinum is present
  • 11. + Pneumomediastinum īŽ Diagnosis īŽ īŽ Esophagogramīƒ perform in right lateral decubitus position, use a water-soluble contrast, if clinical suspicions remain high and the initial study is negative, repeat study with oral barium contrast īŽ Esophagoscopyīƒ for suspected esophageal rupture in acute traumatic rupture īŽ īŽ CXRīƒ reveals free air within the mediastinum, air posterior to sternum and posterior to the heart on lateral film Bronchoscopyīƒ for suspected bronchotracheal tree rupture Management īŽ Should be admitted and observed for signs of serious complications īŽ Broad-spectrum antibiotics for suspected esophageal rupture
  • 12. + Pleural Effusion īŽ Collection of fluid within pleural space īŽ Epidemiology īŽ īŽ īŽ CHF is the most common cause followed by malignancy, bacterial pneumonia, and PE TB is the most common etiology of pleural effusion in developing countries Etiology īŽ Transudativeīƒ CHF, cirrhosis with ascites, nephrotic syndrome, PE īŽ Exudativeīƒ Cancer, infectious (pneumonia, empyema, abscess, TB), inflammatory (SLE, pancreatitis, RA, and PE
  • 13. + Pleural Effusion īŽ Symptoms īŽ īŽ Dyspnea and pleuritic chest pain, decreased breath sounds on auscultation, dullness to percussion Diagnosis īŽ īŽ īŽ CXR: AP XR demonstrates effusion when pleural fluid volume approaches 150cc CT or US most sensitive Thoracentesis necessary when etiology is unclear īŽ Light criteriaīƒ a single positive criterion is enough to classify the fluid as an exudate īŽ Glucoseīƒ low pleural fluid levels (<25)=RA, TB, empyema, and malignancies īŽ pHīƒ low pH=inflammatory and infiltrative processes (empyema, malignancies, TB, esophageal rupture) īŽ Amylaseīƒ high amylase (>200) pancreatitis, malignancy, rupture
  • 14. + Pleural Effusion īŽ Light Criteria Transudate Exudate Pleural and serum Protein <0.5 >0.5 Pleural and serum LDH <0.6 >0.6 Pleural LDH <200 >200
  • 15. + Pleural Effusion īŽ Management īŽ Treat underlying cause īŽ Therapeutic thoracentesis for patients dyspneic at rest īŽ Thoracotomy tube placement for empyema
  • 16. + Pneumothorax īŽ Etiology īŽ īŽ īŽ Spontaneousīƒ no underlying lung disease īŽ Male:female 6:1 īŽ Young, tall, thin īŽ Smoking 20:1 īŽ Valsalva īŽ Ruptured bleb īŽ Many recur (20-50%) Secondary-caused by underlying lung disease īŽ Asthma, COPD, neoplasm īŽ Marfan, Ehlers Danlos, Cystic fibrosis īŽ Penumonia, especially with abscess or cavitation īŽ HIV-PCP Tension pneumo
  • 17. + Pneumothorax īŽ Symptoms īŽ īŽ īŽ īŽ īŽ Dyspnea and pleuritic chest pain Decreased breath sounds and hyperresonace to percussion JVD and hypotension Tracheal deviation away from affected side Diagnosis īŽ īŽ Pneumothorax īŽ CXR for simple pneumothorax (end expiratory for highest sensitivity) īŽ CT test of choice for supine trauma patient Tension pneumo īŽ Clinical diagnosis īŽ Tracheal deviation away from affected lung īŽ Hypotension īŽ Do NOT wait for x-rays before treating
  • 18. + Pneumothorax īŽ Management īŽ Small, stable ptx (<10%) īŽ īŽ Reabsorb 5-7% per day īŽ īŽ 100% O2 Stable patient with a small ptx can be discharged with next day follow up after 6 hours observation and stable x-ray Large ptx īŽ īŽ īŽ 100% O2 Tube thoracostomy Tension ptx īŽ Immediate decompression followed by chest tube
  • 19. + Noncardiogenic Pulm Edema īŽ Definition: radiographic evidence of alveolar fluid accumulation without hemodynamic evidence of a cardiogenic etiology (ie pulmonary capillary wedge pressure <18mmHg) īŽ Etiology īŽ ARDS īŽ High-altitude pulmonary edema īŽ Reexpansion pulmonary edema īŽ īŽ īŽ Large volume thoracentesis (>1L) Rapid lung re-expansion of ptx, especially when it has been collapsed for >3 days Drug induced (meprobamate, opiates, naloxone, PCP, Salicylate)
  • 20. + Obstructive Lung Disease īŽ Asthma and reactive airway disease īŽ COPD īŽ Cystic Fibrosis
  • 21. + Asthma and reactive airway disease īŽ Chronic inflammatory disorder of the small airways characterized by reversible obstruction īŽ Etiology and patho īŽ īŽ īŽ īŽ īŽ Airway inflammation/bronchial wall edema leading to decreased airway diameter Airway hyperreactivity, smooth muscle contraction Secretions forming mucous plugs Chronic inflammation leads to lung remodeling Symptoms īŽ īŽ īŽ Dyspnea with or without cough Prolonged expiratory phase with predominantly exp wheezing Severe exacerbations may present with absence of wheezing, inability to speak, pulses paradoxus and hypoxia
  • 22. + Asthma and reactive airway disease īŽ History associated with higher mortality īŽ >2 hospitalizations during past year īŽ >3 ED visits during past year īŽ Prior intubation or ICU admission īŽ Use of 2 or more adrenergic canisters per month īŽ Current use of systemic steroids or recent withdrawal īŽ Low socioeconomic class
  • 23. + Asthma and reactive airway disease īŽ Diagnosis īŽ īŽ Bedside spirometryīƒ peak flow to monitor response to beta-agonist treatment īŽ Peak flow <50% indicates severe exacerbation Treatment īŽ īŽ īŽ īŽ Oxygen to keep O2>88% Beta agonistsīƒ relaxation of bronchial smooth muscle Epinephrine (1:1000)īƒ reserved for severe exacerbations, is administered sub-q 0.3 q20-30 minutes up to three doses Terbutalineīƒ  reserved for severe exacerbations given SC 0.25mg every 20-30 min up to three doses īŽ Longer duration of action than epinephrine
  • 24. + Treatment cont. īŽ Corticosteriodsīƒ used in both acute and chronic setting to prevent late phase inflammatory response īŽ Oral dosing as effective as IV administration īŽ Magnesiumīƒ benefit in severe exacerbation īŽ Mechanical ventilationīƒ  īŽ Avoid air-trapping or auto-peep īŽ Smaller tidal volumes īŽ Keep rate low īŽ Consider increasing peak inspiratory flowīƒ longer expiratory time
  • 25. + Treatment cont īŽ When treating pregnant asthmaticsâ€Ļ īŽ Fetus more susceptible to hypoxia than mother īŽ No contraindications to use of beta agonists, corticosteroids and anticholinergics īŽ Chronic steroids may result in lower birth weights īŽ Epinephrine is teratogenic during first trimester and associated with preterm delivery
  • 26. + COPD īŽ Progressive partially reversible limitation of airflow īŽ Caused by two processesīƒ chronic bronchitis and emphysema, which occur together in most patients īŽ Epidemiology īŽ īŽ The single most important risk factor for COPD is smoking Etiology īŽ 80% of acute COPD exacerbations are of infectious origin īŽ Streptococcus pneumoniae, Haemophilus influenzae, or moraxella catarrhalis
  • 27. + COPD īŽ Signs and symptoms īŽ īŽ īŽ Dyspnea on exertion, tachypnea, cyanosis, agitation, apprehension, and hypertension are indicative of hypoxia Wheezing, rales, rhonci, prolonged expiratory phase, pursed-lip breathing and clubbing of digits Diagnosis īŽ īŽ īŽ īŽ Elevated hematocrit 2/2 chronic hypoxia ABG: mild to moderate hypoxemia without hypercapnea in early stages CXRīƒ hyperinflation, flattened diaphragm, long narrow heart shadow EKGīƒ a-fib, multifocal atrial tachycardia, cor-pulmonale (tall pwaves), right axis deviation and right ventricle hypertrophy
  • 28. + COPD īŽ Management īŽ Supplemental oxygen reduces mortality in patients with advanced COPD with room air O2 saturaion <88% īŽ Nebulized anticholinergics īŽ Bronchodilators īŽ Antibiotics īŽ First line choices include amoxicillin, cefaclor, fluoroquinolones, or bactrim īŽ Gram-negative infections more likely in those with frequent exacerbation and need a third-generaltion cephalosporin īŽ corticosteroid
  • 29. + Cystic Fibrosis īŽ Most common in Europeans and Ashkenazi Jews īŽ Autosomal recessive mutation īŽ īŽ īŽ Abnormalities in chloride transport in exocrine tissues leads to multiorgan involvement Thick, viscous secretions in lungs, intestine, pancreas, and reproductive tract Symptoms and signs īŽ Respiratory manifestationsīƒ most common, exacerbations characterized by increased cough, sputum production, decreased lung function
  • 30. + CF symptoms and signs cont. īŽ Undiagnosed patients may present with failure to thrive chronic cough, repeated pulmonary or sinus infections, chronic diarrhea from pancreatic insufficiency īŽ Alternative presentations īŽ Increased salt content in sweat gland secretion īŽ Meconium ileus in neonates īŽ Steatorrhea from pancreatic enzyme insufficiency īŽ Intestinal obstruction īŽ Spontaneous pneumo īŽ Chronic pancreatitis īŽ Hepatobiliary disease
  • 31. + CF diagnosis īŽ Electrolytes īŽ īŽ Hyponatremia and alkalosis CXR īŽ Bronchiolar thickening, hyperinflation, and patchy, diffuse infiltrates īŽ Newborn screening īŽ Chloride sweat testing or genetic testing
  • 32. + CF Management īŽ Broad-spectrum antibiotics īŽ Cover Staph aureus, H. flu, and double cover Pseudomonas īŽ Chronic colonization with pathologic bacteria and chronic antibiotic use leads to resistant organisms requiring intravenous vanco, tobramycin, meropenem, cipro, and piperacillin īŽ Mucolytics īŽ Bronchodilators īŽ Aggressive chest physiotherapy īŽ Provide O2 īŽ Consult Pulm
  • 33. + Restrictive Lung disease īŽ Loss of lung compliance resulting in volumes loss īŽ Interstitial Lung Disease īŽ īŽ Idiopathic pulmonary fibrosis Sarcoidosis
  • 34. + ILD īŽ ILD īŽ īŽ Restrictive pulmonary dysfunctions with the common end-point of interstitial collagen deposits and scarring Idiopathic pulmonary fibrosis īŽ 50% of ILDs īŽ Likely autoimmune īŽ Symptoms and signsīƒ dyspnea, cough, fine dry crackles, clubbing of fingers īŽ Diagnosisīƒ CXR has honeycombed lungs, CTīƒ ground glass opacity īŽ Management īƒ corticosteroids, immune modulators, lung transplant
  • 35. + Sarcoidosis īŽ Epidemiology īŽ īŽ īŽ African americans>caucasians females>males Etiologyīƒ typical finding includes non-caseating granuloma, which is composed of T-helper cells and other inflammatory cells
  • 36. + Sarcoidosis īŽ Symptoms and Signs īŽ Most patients are asymptomatic īŽ Disease is fatal in 10% of patients because of extensive organ involvement īŽ Constitutional symptomsīƒ fever, fatigue, weight loss, polyarthritis, myositis īŽ Pulm symptomsīƒ cough, hemoptysis, shortness of breath with exertion īŽ Neuroīƒ bells palsy, seizures īŽ Skin lesionsīƒ plaques, subcutaneous nodules, erythema nodosum īŽ Cardiacīƒ arrhythmias, CHF īŽ Lympthadenopathy īŽ Ophthalmologicīƒ uveitis, or conjunctivitis
  • 37. + Sarcoidosis īŽ Diagnosis īŽ CXR īŽ īŽ Stage 1īƒ hilar adenopathy īŽ Stage 2īƒ Hilar adenopathy and parenchymal involvement īŽ Stage 3īƒ parenchymal involvement without adenopathy īŽ īŽ Stage 0īƒ no findings Stage 4īƒ pulmonary fibrosis Lab studies īŽ Leukocytosis, elevated ESR or serum ACE, hypercalcemia or hyperphosphatemia, elevated CK and CK-MB with cardiac involvement īŽ Gallium 67īƒ used to detect extrapulmonary sarcoidosis īŽ Biopsy of involved organ is most useful for diagnosis
  • 38. + Sarcoidosis īŽ Management īŽ Cardiac monitoring īŽ Consider steroids or cytotoxic medications īŽ Lung transplantation for patients with severe refractory disease
  • 40. + DVT īŽ Risk factors īŽ Previous thrombosis īŽ Vascular endothelial damage īŽ īŽ Trauma, sugery (especially ortho), smoking Hypercoagulability īŽ īŽ Factor V Leiden (most common hereditary hypercoagulability īŽ Antithrombin III deficiency īŽ īŽ Protein C or S deficiency Oral contraceptives or 3rd trimester pregnancy Immobilization or low cardiac output īŽ Long periods of sitting, CHF
  • 41. + DVT īŽ Signs and Symptoms īŽ Pain, warmth and edema īŽ Discoloration of affected extremity īŽ Palpable cord of a thrombosed vein
  • 42. + DVT īŽ Diagnosis īŽ CT angiography īŽ Doppler ultrasonography īŽ īŽ Limitationsīƒ operator dependent, cannot distinguish between old and new clot, not accurate in detecting DVT in the pelvis or the small vessels of the calf Management īŽ Anticoagulationīƒ unfractionated low-molecular weight heparin or warfarin therapy īŽ Filter placement for patients with failure of anticoagulation or contraindication to anticoagulation
  • 43. + Pulmonary Embolus īŽ Risk factor are the same as for DVTīƒ  60% of patients with a DVT have a PE īŽ Symptoms and signs īŽ Sudden-onset dyspnea, tachypnea, tachycardia, pleuritic pain, hemoptysis, syncope, cough, and wheeze
  • 44. + PE diagnosis īŽ ECG īŽ īŽ Nonspecific ST-T wave changes and/or sinus tach are most common, S1Q3T3, precordial flipped T waves CXR īŽ īŽ īŽ Findings are abnormal but nonspecific, pleural effusion, elevated hemidiaphragm secondary to atelectasis and noninfectious infiltrates Westermark signīƒ abrupt cut-off of vascular markings Hamptom humpīƒ pleural based wedge-shaped infarct īŽ CT pulm angiography īŽ VQ scanīƒ useful in severe contrast allergies īŽ A normal scan is sufficient to exclude PE in patient with low pretest probability īŽ Echoīƒ may reveal evidence of right heart strain īŽ Pulmonary angiographyīƒ the gold standard for diagnosing PE (used infrequently because of noninvasive CT scans
  • 45. + PE management īŽ Supplemental O2 īŽ Hemodynamic support īŽ Anticoagulation īŽ Thrombolytic īŽ Indicated in patients with associated hemodynamic instability īŽ Surgical Embolectomy īŽ IVC filter for anticoagulation failure or contraindication
  • 47. + Bacterial Pneumonia īŽ Etiology īŽ Typical Pneumonia īŽ īŽ S. pneumoniae, H. influenzae, and Staph (S. Pneumo most common) Atypical Pneumonia īŽ Influenza virus, mycoplasma, chlamydia, legionella, and adenovirus īŽ IV drug usersīƒ S. aureus īŽ Alcoholism, diabetes, and COPDīƒ K, Pneumoniae īŽ Asthmaticsīƒ H. Flu īŽ Hospital acquired pneumoniaīƒ pseudomonas aeruginosa
  • 48. + Bacterial Pneumonia īŽ Symptoms and signs īŽ Chest pain īŽ Productive cough īŽ Klebsiellaīƒ currant jelly īŽ S. Pneumoniaeīƒ bloody or rusty colored īŽ Aspirationīƒ foul-smelling sputum īŽ Chlamydiaīƒ staccato cough īŽ Rigorsīƒ particularly associated with S. Pneumonia īŽ Diarrhea and GI upset with Legionella īŽ Bullous myringitis with Mycoplasma pneumoniae īŽ Pleural rubs
  • 49. + Bacterial Pneumonia īŽ Diagnosisīƒ Chest radiography īŽ Bilateral diffuse infiltrates consistent with atypical infections (M. Pneumoniae, P. Carinii, C. Psittaci) īŽ Abscess and bulging lung fissures are indicative of infections caused by Klebsiella and S. aureus īŽ Pleural effusions and empyema associated with cavitary lesions are seen with s. aureus and M. tuberculosis īŽ Upper lung fieldsīƒ K. Pneumoniae īŽ Lower lung fieldsīƒ L. Pneumoniae īŽ Miliary patternīƒ M. Tuberculosis
  • 50. + Bacterial Pneumonia īŽ Laboratory studies īŽ Hyponatremia and hypophosphatemia associated with L. Pneumophila īŽ Sputum samples for gram stain and culture are accurate about 50% of the time īŽ Adequate sputum contains <10 epithelial cells, >25 WBC per low power field and remain uncontaminated from oral flora īŽ Mycoplasma and Chlamydia immunoglobulin M antibodiesīƒ  a rise in antibody titer of 1:128 confirms the diagnosis
  • 51. + Bacterial Pneumonia īŽ Management īŽ Community-acquired pneumonia īŽ īŽ īŽ Pneumonia severity index score helps determine risk Admit if total score >90 points and consider ICU for >130 Hospital-acquired pneumonia īŽ īŽ īŽ Double-drug coverage for Pseudomonas Optimal combinations include cefipime plus levofloxacin, aztreonam, meropenem, or aminoglycoside Aspiration pneumonia īŽ Intubation should be considered in any patient who is unable to protect airway, add anaerobic coverage
  • 52. + Types of Bacterial Pneumonia īŽ Bordetella Pertussis (whopping cough) īŽ īŽ Summer and fall months, neither active disease nor vaccination provides lifelong immunity Symptoms and signsīƒ 3 stages, each lasting about 2 weeks īŽ Catarrhal īŽ īŽ Paroxysmal īŽ īŽ Most infectious during this time, symptoms indistinguishable from a URI Coughing episodes followed by an inspiratory “whoop” , posttussive exhaustion and emesis Convalescent īŽ Chronic cough that can last several months īŽ Complications include mucous plug, secondary bacterial infection, ruptured diaphragm, hernia, and rectal prolapse
  • 53. + Pertussis īŽ Diagnosis īŽ īŽ īŽ Degree of lymphocytosis correlates with severity of disease Definitive diagnosis is made via nasopharyngeal culture Treatment īŽ Erythromycin x14 days īŽ Consider prophylaxis with erythromycin for close contacs īŽ Consider hospitalization for infants <6 months, premature infants, and those with significant comorbitites
  • 54. + Mycoplasma Pneumonia īŽ Most common atypical īŽ 14-day incubation period īŽ More common in young adults īŽ CXR may show interstitial pattern or patchy infiltrate īŽ Treat with macrolide antibiotic īŽ Associations īŽ īŽ īŽ īŽ Bullous myringitis Meningitis and encephalitis Erythema multiforme Guillain-Barre
  • 55. + Chlamydia Pneumonia īŽ Obligate intracellular parasite īŽ Infants īŽ īŽ īŽ īŽ īŽ Acquired at birth 50% conjunctivitis Tachypnea May be afebrile CXR shows hyperinflation and diffuse infiltrates īŽ Common in young adults complaining of hoarseness, cough, and persistent malaise īŽ Staccato cough īŽ Treat with macrolide
  • 56. + Legionella Pneumonia īŽ Airborne and associated with water sources īŽ Classically associated with recent air travel īŽ No person to person transmission īŽ Symtpoms and signs īŽ īŽ Pleuritic chest pain, relative bradycardia, GI symtpoms Diagnosis īŽ Labs may reveal hyponatremia and hypophosphatemia īŽ Chest x-ray may show alveloar infiltrates or consolidation that my progress to hilar adenopathy and pleural effusion īŽ Treat with erythromycin for 3 weeks
  • 57. + Tuberculosis īŽ Leading cause of death worldwide īŽ Humans are sole reservoir īŽ TB can remain dormant for years in granulomas īŽ Risk factors īŽ Immunocompromised (HIV, malignancy, DM, extremes of age) īŽ Close contacts or occupational exposure īŽ Medically underserved, low-income populations
  • 58. + TB symptoms and signs īŽ Primary TB īŽ Only 10% of exposed individuals develop primary TB īŽ Constitutional symptoms īŽ Coughīƒ most common symptoms of pulmonary TB īŽ Initially nonproductive or nonspecific sputum īŽ Hemoptysis may be presenting complaint īŽ Pleuritic chest pain īŽ Night sweats īŽ “classic” presentation is uncommon
  • 59. + TB īŽ Postprimary TB (reactivation TB) īŽ Lifetime risk in immunocompetent individual is 10% to 15% īŽ In HIV-positive patients īŽ 37% with disease in 6 months īŽ 10% incidence of disease per year īŽ Signs and symptoms similar to primary TB
  • 60. + TB extrapulmonary īŽ Lymphadenitis (scrofula) īŽ īŽ Pleural effusion īŽ īŽ Pott’s disease (spinal)īƒ spinal cord injury possible, lumbar infection may lead to psoas abscess acute disseminated īŽ īŽ Small and unilateral, diagnosis through pleurocentesis Bone and joint infection īŽ īŽ Most common EPTB, enlarging, painless, erythematous firm mass near cervical nodes, do NOT I and D Generalized systemic illness, typically in elderly and HIV patients, fever, weight loss, anorexia, weakness, SIADH is common, often associated with meningitis CNS īŽ īŽ 6% of cases, peak in newborn to 4 years, SIADH, tuberculosis meningitis CSF analysisīƒ lowest glucose CSF levels of any meningitis
  • 61. + TB diagnosis īŽ TB skin testingīƒ read 48-72 hours later, induration not erythema īŽ 15mm in low-risk, immunocompetent patients īŽ 10mm in high-risk immunocopetent patients īŽ 5mm in HIV, Close contacts infectious TB, abnormal CXR, immunocompromised from steroids
  • 62. + TB medical therapy īŽ Latent TBīƒ infections without active disease, chemoprophylaxis with isoniazid for 9 months īŽ Active TBīƒ treated for 6 months, 4 drugs until resistance pattern determined, after 2 months may discontinue pyrazinamide if TB isolates do not demonstrate resistance īŽ Extrapulmonary TB->treat for 6 months īŽ CNS infection (tuberculous meningitis) is the exception, requires 912 months of treatment īŽ Consider steroids for CNS and pericardial TB
  • 63. + Treatment of TBīƒ drugs īŽ First line agents īŽ Isoniazid (INH) īŽ īŽ īŽ 8% resistance rate Prevent INH-related seizures: supplement with pyridoxine (B6) Rifampin īŽ īŽ īŽ Orange discoloration of bodily fluids Oral contraception failure Pyrazinamide (PZA) īŽ īŽ Hepatotoxicity, polyarthralgias Ethambutol (ETH) īŽ Prevents emergence of RIF resistance īŽ Retrobulbar neuritisīƒ decreased visual acuity or red/green color blindness
  • 64. + Treatment cont. īŽ Noncompliant patients īŽ īŽ Court-ordered directly observed therapy (DOT) īŽ īŽ Uncooperative and potentially infectious patients may be compelled to comply Incarceration as last resort In pregnancy īŽ INH, RIF, ETH cross placenta and are safe
  • 66. + influenza īŽ Often associated with bacterial superinfection (s. aureus) īŽ Diagnosis: nasopharyngeal swab culture for influenza aid diagnosis īŽ CXR shows diffuse bilateral infiltrates
  • 67. + Varicella īŽ Symptoms and signs: pneumonia may present with chest pain and hemoptysis preceded by a rash īŽ More severe in adults īŽ Managementīƒ mandates admission for treatment with acyclovir
  • 68. + cytomegalovirus īŽ Most common in solid organ transplant and bone marrow transplant recipients īŽ Often presents simultaneously with pneumocystis pneumonia īŽ Management īŽ īŽ IV ganciclovir or foscarnet plus immunoglobulin therapy CXR īŽ Bilateral interstitial pattern
  • 69. + Hantavirus īŽ Aerosolized contaminated material from rodent feces or urine īŽ Southwest US īŽ Symptoms and signsīƒ flu-like symtpoms that progress to respiratory distress and shock īŽ Diagnosisīƒ CXR reveals bilateral infiltrates
  • 70. + Fungal Pneumonia īŽ Histoplasma capsulatum, blastomyces dermatitides and coccidioides present in the soil in various geographic areas of the US īŽ Histoplasma capsulatum in the mississippi and Ohio River valleys īŽ Coccidioides immitis in desert areas of the Southwest īŽ Symptoms and signs vary from acute or chronic pneumoina to asymptomatic granulomas on CXR īŽ Diagnosisīƒ hilar adenopathy