PULMONARY EMERGENCIES

Summer 2009

Topics

•Asthma•COPD•Pulmonary Embolism•Pneumonia•Pneumothorax

Asthma

Asthma is a chronic inflammatory disorder characterized by

increased responsiveness of the airways to multiple stimuli.

AsthmaAsthmaAffects approximately 4 to 5 percent of the population in the United States.

It is the most common chronic disease of childhood.

About one-half of cases of asthma develop before the age of 10 and another one-third before the age of 40.

The 2:1 male to female preponderance of asthma in childhood equalizes by age 30.

AsthmaAsthma

Relevant HistoryRelevant History

•The possible cause of exacerbation

•Previous ICU admission for asthma

•Previous intubations

•Length of recent steroid use

•Frequency of asthma medications

AsthmaAsthmaClinical Clinical

PresentationPresentationMost common symptoms

•Dyspnea or chest tightness

•Wheezing

•Cough

AsthmaAsthma

Clinical Clinical PresentationPresentationSevere Asthma

•Tripod position and gasping for air•Audible wheezes with prolonged

expiration•Accessory muscle use•Tachycardia•Tachypnea•Hypertension•Hypoxia

AsthmaAsthma

Clinical Clinical PresentationPresentation

Indication of severe bronchospasmIndication of severe bronchospasm

• Cyanosis and Diaphoresis

• Pulses paradoxus of >20mmHg or more

Indication of hypercapniaIndication of hypercapniaAltered mental statusTremorApnea

AsthmaAsthma

EvaluationEvaluationPeak flowPulse ox for O2 saturationABG to assess for:

Hypercapnia Respiratory acidosis

CXREKG

AsthmaAsthma

TreatmentTreatmentThe goal of treatment of acute asthma

in the ED is to:Reverse airflow obstruction rapidly

by repetitive or continuous administration of inhaled 2 agonists

Ensure adequate oxygenation

Relieve inflammation

AsthmaAsthma

TreatmentTreatmentOxygenAlbuterol nebulizedAtrovent nebulizedSystemic corticosteroidsTerbutaline sulfateEpinephrineMagnesium sulfate

AsthmaAsthma

TreatmentTreatmentIndications for mechanical ventilationIndications for mechanical ventilation

HypoxiaSevere hypercapniaAltered mental statusExhaustionWorsening acidosis

COPD

The American Thoracic Society (ATS) defines COPD as a disease

state characterized by the presence of airflow obstruction

due tochronic bronchitis or emphysema

COPD• In North America, COPD is rare in persons

younger than age 40

• Common among older individuals– prevalence of approximately 10 percent in those

aged 55 to 85 years.

• In the United States, COPD is– The fourth most common cause of death– The third most common cause of hospitalization– The only leading cause of death increasing in

prevalence.

Risk factorsRisk factors

• Cigarette smoking(80-90% )

1-antitrypsin deficiency

Treatment for Treatment for COPD ExacerbationCOPD Exacerbation

• The first goal in the treatment of COPD is to correct or preventlife-threatening hypoxemia.

COPD ExacerbationCOPD ExacerbationTreatmentTreatment

OxygenNasal cannula if needed

Albuterol nebulizedAtrovent nebulizedSystemic corticosteroids

Not for mild or moderate

Antibiotic choices include:MacrolidesTrimethoprim-sulfamethoxazoleFluoroquinolones

COPD ExacerbationCOPD ExacerbationAdmission CriteriaAdmission Criteria

Failure to improve adequately inspite of therapy

Deterioration in condition in spite of therapy

H/o significant comorbid illnesses

Patients without an intact social support system at home.

Pneumothorax• Pneumothorax occurs when air enters

the potential space between the visceral and parietal pleura.

• The cause may be:– Spontaneous– Penetrating trauma

• Iatrogenic pneumothorax

– Blunt trauma

PneumothoraxFour causes of iatrogenic pneumothoraxFour causes of iatrogenic pneumothorax

• CVP line placement• Thoracentesis• Intercostal nerve block• Mechanical ventilation

SPONTANEOUS PNEUMOTHORAX

• Primarily a disease of male smokers who have larger height-to-weight ratios.

• Three peaks:

– among neonates • (due to hyaline membrane disease or aspiration)

– among 20- to 40year-olds • (such cases tend to be primary)

– among those older than age 40 • (typically secondary cases)

SPONTANEOUS PNEUMOTHORAX

• Secondary causes– COPD– Asthma Cystic fibrosis– Interstitial lung disease– Cancer– Pneumocystis carinii pneumonia

Thoracocentesis at the 7th intercostal, midthoracic space

PNEUMOTHORAX

• Symptoms– Pleuritic chest pain– Dyspnea

• Signs– Decreased breath sounds– Tachypnea

PNEUMOTHORAX

Gold standard for diagnosis

•CXR (PA) expiratory

TreatmentTreatment goals are:

• the elimination of intrapleural air• optimization of pleural healing• prevention of recurrences.

Treatment• O2• Observation over 6hours if small and

asymptomatic ( < 20%)• Thoracostomy

If tensionIf tension• Needle thoracostomy• Then tube thoracostomy

Pneumonia

Pneumonia

• Community-acquired pneumonia is a common medical problem, accounting for about 4million cases and 1 million hospitalizations per year in the U.S.

• Pneumonia is the 6th leading cause of death in the U.S.

Pneumonia

• Pneumococcus is the most common cause of bacterial pneumonia

• Some other causes of include: E. coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Staph aureus, H. influenzae, and group strep A.

• Legionella species and anaerobes are less frequent.

Pneumonia

• Mycoplasma, Chlamydia , and respiratory are grouped into atypical pneumonia.

• Pneumocystis carinii pneumonia (PCP) is a common complication of HIV infection.

• Aspiration pneumonia occurs more frequently in alcoholics and patients with seizures, stroke, or other neuromuscular disorders.

Pathophysiology

• Pneumonia is an infection of the alveolar or gas exchange portions of the lung. Some forms of pneumonia produce an intense inflammatory response within the alveoli that leads to filling the air space with organisms, exudates, and WBCs.

• Patients at most risk for pneumonia include those with predisposition to aspiration, impaired mucociliary clearance, or risk of bacteremia.

Clinical features

• Bacterial pneumonia generally presents as fever, dyspnea, cough, pleuritic ches pain, and sputum production

• Pneumococcal pneumonia classically presents abruptly with fever, rigors, and rusty brown sputum.

• Pleural effusion occurs in 25% of patients.

Clinical features

• H. Influenzae is more common in smokers and the elderly.

• Reveals rales and ronchi on examinmation without signs of consolidation.

• Legionella is spread through aerolized water droplets rather than by person-to-person contact.

• Presents with F/C malaise, dyspnea, and nonproductive cough.

Clinical features

• Legionella commonly presents with GI symptoms e.g. Anorexia, nausea, vomiting and diarrhea. Mental status changes may also be present.

• Begins with findings of patchy bronchopneumonia and progresses to signs of frank consolidation, other common signs relative bradycardia and confusion.

Clinical features

• Staph aureus frequently follows a viral respiratory illness , especially influenzae and the measles.

• Klebsiella exhibit signs of consolidation including bronchial breath sounds, egophony, increased tactile fremitus, and dullness to percussion. A pleural friction rub and cyanosis may be present.

Clinical features

• Mycoplasma, Chlamydia, and viral pneumonias present w/ fever/chills, malaise, dyspnea and nonproductive cough.

• Mycoplasma , Chlamydia, and viral pneumonia may exhibit fine rales, rhonchi, or normal breath sounds.

• Bullous myringitis, when present is pathognomonic for Mycoplasma infection.

Clinical features

• Empyemas are most common w/ S. aureus, Klebsiella, and anaerobic infections.

• Aspiration pneumonitis depends on the volume and pH of the aspirate, the presence of particulate matter in the aspirate, and bacterial contamination.

• Acid aspiration results in rapid onset of symptoms of tachypnea, tachycardia, and cyanosis.

Clinical features

• Acid aspiration often progresses to frank pulmonary failure, most other cases of aspiration pneumonia progress more insidiously.

• Physical signs develop over hours and include rales, ronchi, wheezing, and copious frothy or bloody sputum.

• RLL is most commonly involved.

Diagnosis and differential

• DDX: acute tracheobronchitis, pulmonary embolus or infarction, COPD exacerbation, pulmonary vasculitides, including Good-pasture’s disease and Wegener’s granulomatosis; bronchiolitis obliterans; and endocarditis.

Diagnosis and differential

• The diagnosis is suspected based on a constellation of symptoms and signs, but individual symptoms and clinical findings lack accuracy for precise diagnosis.

• CXR• WBC w/diff, pulse ox, blood cx, pleural

fluid examination, ABG(ill-appearing patients)

Diagnosis and differential

• Sputum gram’s stain rarely changes therapy.

• LFTs, serum chemistry, serologic testing for mycoplasma, urine antigen for legionella species.

• Most patients do not require identification of a specific organism.

Treatment

• The ED treatment and disposition depends primarily on the severity of the clinical presentation and X-ray findings.

• O2 prn• Antibiotics treatment should be

initiated.

Treatment

• Outpatient treatment is standard in healthy patients who are nontoxic and without comorbid disease. Antibx include zithromax, biaxin, cefpodoxime, augmentin, or doxycycline.

• Oral fluroroquinolones are highly effective ; however, the CDC recommends reserving them for those who cannot tolerate or have failed other agents.

Treatment

• For outpatient management of patients <60 years old or those w/comorbid diseases, levaquin is a good choice as a single agent.

• Augmentin or biaxin in combination w/ either cefuroxime or augmenting are excellent drug regimens.

• Close follow-up is necessary to monitor response to therapy.

Treatment

• Hospital admission should be reserved for patients at the extremes of life, immunocompromised patients , pregnant women, and those with clinical signs of hypoxemia (respiratory rate >30breaths/min, HR >125bpm, SBP <90mm Hg, hypoxemia, altered mental status or volume depletion)

Treatment

• Serious comorbid). condions (eg, neoplastic disease, renal failure, diabetes, cardiac disease, or debilitated state

• Patients requiring admission generally receive empiric antibiotic therapy.

• Recommended treatment include ceftriaxone, levaquin, cefotaxime, ampicillin-sulbactum, piperacillin-tazobactam, or cefepime.

Treatment

• Patients at high risk for gram-negative pneumonia or Legionella (eg, alcoholics, diabetics, and institutionalized or intubated patients)

• Should be treated w/levaquin as monotherapy or w/ a combination of a macrolide such as erythromycin and either ampicillin-sulbactam or ceftriaxone.

Treatment

• If Pseudomonas is suspected double coverage w/ antipseudomonal penicillin or cephalosporin plus either an antipseudomonal aminoglycoside or a fluoroquinolone is recommended.

• Local antibiotic sensitivities and resistance patterns, as well as local standards of care, should help determine final antibx choice.

Treatment

• Aspiration pneumonitides require a different approach.

• Witnessed aspirations should be tx’d w/immediate tracheal suctioning, and pH of aspirate ascertained

• Bronchoscopy is indicated for the removal of large particles and further clearing of airways.

Treatment

• Patients requiring intubation should also receive positive end-expiratory pressure.

• O2 should be administered, but steroids and prophylactic antibx are of no value and should be withheld.

• For patients at risk for aspirtion and for those that present w/ signs & symptoms of infection, antibiotics are indicated.

Treatment

• Levaquin or rocephin are sufficient for most cases of aspiration.

• In cases of severe periodontal dz., putrid sputum, or alcoholism, consider piperacillin-tazobactam or impenem or a fluoroquinolone plus clindamycin.

Treatment

• Failure of outpatient therapy generally requires hospital admission and broader-spectrum IV antibx.

• Patients w/hypoxemia despite O2 therapy or those with impending respiratory failure should be tx’d w/ endotracheal intubation and mechanical ventilation.

DEFINITIONTHROMBOEMBOLISMTHROMBOEMBOLISM

A condition in which a blood vessel is blocked by an embolus carried in the bloodstream from the site of formation of the clot, usually from a peripheral vein.

.

DEFINITIONPULMONARY THROMBOEMBOLISMPULMONARY THROMBOEMBOLISM

The blockage of a pulmonary artery by foreign matter such as fat, air, tumor tissue or thrombus that usually arises from a peripheral vein.–Mostly form in the deep vein of the thigh.

PTEPTE• Thromboembolism

– Arise from right side of the heart.– Arise from thrombus in venous circulation.

• Tumor emboli - arise from tumors that invade the venous circulation.

• Other sources– Fat.– Air.– Bone marrow.– Foreign IV material.

Predisposing factors

Symptoms & signsSymptoms & signs

• Clinical findings in acute PTE depend on – The size of the embolus.– The patient’s preexisting cardiopulmonary

status.• No single symptom or sign or

combination of clinical findings is pathognomonic of PTE.

• Massive PE results in– Acute Rt side ventricular failure.– Systemic hypotension.

SymptomsSymptoms

•Dyspnea.•Pleuritic chest pain.•Hemoptysis.•Cough.•Chest pain.•Anxiety.•Sweats.•Syncope.

Classic triad

SIGNSSIGNS

• Tachypnea.• Tachycardia.• Crackles.• Accentuated pulmonary component

of second heart sound.• Low grade fever.• Cardiac arrhythmias.

– Atrial arrythmias.• Cyanosis.

Symptoms & signsSymptoms & signs

Small embolism distally near the pleura. – Dyspnea (most common symptom).– Tachypnea (most frequent sign)– Pleuritic pain. – Cough, or hemoptysis. – Syncope.

Massive PTE– Dyspnea. – Tachypnea– Syncope.– Hypotension.– Cyanosis.

DDXDDX

• Pneumonia, bronchitis, COPD exacerbation.• Myocardial infarction, unstable angina.• Pneumothorax.• Rib fracture.• Congestive heart failure.• Asthma.• Pericarditis.• Primary pulmonary hypertension.• Costochondritis, ``musculoskeletal pain,'' • Anxiety.• Cellulitis or lymphangitis.• Ruptured baker’s cyst.• Muscle strain or rupture.

Key testsKey tests

ABGABG – Acute respiratory alkalosis due hyperventilation.– Po2 <80 mm Hg. Pco2 due to tachypnea.

EKGEKG is abnormal but non diagnostic.– Tachycardia.– Non-specific ST-T changes.–S1Q3, T wave inversion in V1-3–Rt. axis deviation.–Rt. bundle branch block.

Imaging Imaging

• CXR– Usually abnormal but no pathognomonic

findings.• Lung scan • Lower extremity evaluation by

ultrasound.• Pulmonary arteriography (Gold standard)• Echocardiography.• D-Dimer

TREATMENTTREATMENT• IV fluids• Intravenous heparin.• Warfarin beginning day one or day

two of – IV heparin for long term therapy

• Therapy for least three months. – Warfarin dose adjusted to prolong

prothrombin time to an INR of 2.5 (range 2.0 to 3.0).