Other Causes of Hemoptysis

June 5, 2024
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Patients’ Management in Pneumonia by General Practitioner of Family Medicine: diagnosis, patient’s referral arrangement, protocols of non-hospital pneumonia treatment. Rational antibiotic therapy and  its complications. Rehabilitation and Prophylactic Medical Examination in Pneumonia Patients.Health resort treatment and forms of its assignment. Medical and Labour Expert Examination

Community-acquired pneumonia (CAP) is one of the most common infectious diseases addressed by clinicians. CAP is an important cause of mortality and morbidity worldwide.

Pneumonia

Pathophysiology: CAP usually is acquired by inhalation or aspiration of pulmonary pathogenic organisms into a lung segment or lobe. Less commonly, CAP may result from a secondary bacteremia from a distant source, such as CAP secondary to Escherichia coli urinary tract infection and/or bacteremia. CAP due to aspiration of oropharyngeal contents is the only form of CAP with multiple pathogens.

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Frequency:

  • In the US: Elderly individuals and patients with chronic obstructive pulmonary disease (COPD), such as chronic bronchitis (not emphysema), most frequently are admitted to the hospital for CAP. CAP is a common cause of hospital admission, but statistics for patients treated for CAP in the ambulatory setting are difficult to obtain. Overall, incidence of CAP in 1994 was 170 cases per 10,000 individuals.

  • Internationally: Prevalence of zoonotic CAPs is higher internationally than in the United States.

Mortality/Morbidity:

  • Patients with severe CAP invariably have severe cardiopulmonary disease or diminished or absent splenic function.

  • Mortality and morbidity rates are highest in elderly patients.

Race:

  • All races are affected equally.

Sex:

  • No sex-related differences exist.

Age:

CLINICAL

  • CAP is particularly common in elderly adults, with an incidence rate in the United States of 280 cases per 10,000 individuals older than 65 years.

History: Patients with CAP due to typical bacterial pathogens present with a variety of pulmonary symptoms, while those with CAP due to atypical pathogens present with a variety of both pulmonary and extrapulmonary symptoms.

  • Typically, patients with bacterial CAP present with variable degrees of fever, usually with a productive cough and often with pleuritic chest pain.

  • Clinical presentation in patients with CAP due to atypical pathogens usually is less acute than in those with typical bacterial pathogens.

  • CAP due to atypical pathogens may have one or more extrapulmonary features, which is a clue to their presence.

  • Patients with Legionella infections may have a productive or nonproductive cough. In contrast, patients with pneumonia due to Mycoplasma pneumoniae or Chlamydia pneumoniae usually present with a nonproductive cough.

  • With the exception of Legionella infections, chest pain usually is not a feature of nonzoonotic atypical pathogens causing CAP.

Physical:

  • With typical bacterial CAP, abnormal physical findings are confined to the chest.

  • Rales are heard upon auscultation of the chest over the involved lobe or segment. If consolidation is present, an increase in tactile fremitus, bronchial breathing, and E to A change may be present.

  • Patients with pleural effusion (usually due to Haemophilus influenzae) have signs of pleural effusion if it is large enough to be detected during the physical examination.

  • Patients with pleural effusion have decreased tactile fremitus and dullness upon chest percussion.

  • Purulent sputum is characteristic of pneumonia caused by typical bacterial pathogens and usually is not a feature of atypical pathogens, with the exception of Legionnaires disease.

  • Blood-tinged sputum may be found with pneumococcal infections, Klebsiella pneumonia, or Legionella pneumonia.

  • Legionella pneumonia, Q fever, and psittacosis are atypical pneumonias that may present with signs of consolidation.

  • Consolidation is not a feature of pneumonia caused by M pneumoniae or C pneumoniae.

  • Pleural effusion in a patient with CAP and extrapulmonary manifestations should suggest the presence of Legionella species. Pleural effusion with an appropriate epidemiologic history, such as contact with a rabbit or deer, may suggest the presence of tularemia.

  • Patients presenting with acute heart failure, such as acute myocardial infarction without preexisting congestive heart failure (CHF), often have normal cardiac silhouettes, bilateral symmetric moist rales, and an S3 gallop rhythm present upon auscultation.

  • Severe CAP is caused by the same spectrum of pathogens as mild or moderately severe CAP.

    • Severity of CAP is determined by the preexisting function of the heart, lungs, and spleen.

    • Host factors, not different or more virulent pathogens, make CAP mild or severe.

Causes:                                                   Table 1. Respiratory Pathogens and Nonpathogens in Community-acquired Pneumonia

Typical Bacterial Pathogens in CAP (approximately 85%)

Streptococcus pneumoniae
Penicillin-sensitive S pneumoniae
Penicillin-resistant S pneumoniae
H influenzae
Ampicillin-sensitive H influenzae
Ampicillin-resistant H influenzae
Moraxella catarrhalis
(all strains penicillin resistant)

Atypical Respiratory Pathogens in CAP (approximately 15%)

Legionella species
Mycoplasma species
C pneumoniae

Rare Bacterial Pathogens in CAP

Klebsiella pneumoniae – Only in those with chronic alcoholism
Staphylococcus aureus – Postviral influenza setting
Pseudomonas aeruginosa – Only in patients with cystic fibrosis or bronchiectasis


Nonpulmonary Pathogens in Pneumonia

Nonaeruginosa pseudomonads
Stenotrophomonas (Xanthomonas) maltophilia
Citrobacter freundii
Burkholderia (Pseudomonas) cepacia
Citrobacter koseri

Enterobacter species
Flavobacterium species
Enterobacter cloacae
Flavobacterium meningisepticum
Enterobacter agglomerans
Enterococcus
species

 

  • Typical bacterial pathogens

Click to see larger pictureTypical bacterial pathogens causing CAP are S pneumoniae, H influenzae, and M catarrhalis.

      • In patients with chronic bronchitis who develop CAP requiring hospitalization, M catarrhalis is particularly common.

      • S pneumoniae remains the most common agent responsible for CAP.

    • Importantly, S aureus, K pneumoniae, and P aeruginosa are not causes of CAP in typical hosts.

      • S aureus causes CAP in the setting of postviral influenza.

      • K pneumoniae occurs primarily in persons with chronic alcoholism.

      • P aeruginosa is a cause of CAP in patients with bronchiectasis or cystic fibrosis.

    • Other gram-negative pathogens rarely cause CAP.

    • Aspiration pneumonia is caused by the aspiration of oropharyngeal secretions into the lung. The extent of aspiration and lobar distribution of the infiltrates depends on the patient’s position at the time of aspiration.

    • Nearly all cases of CAP are due to a single pathogen. Exceptions certainly occur, but they are rare.

    • Aspiration pneumonia is the only form of CAP caused by multiple pathogens.

  • Atypical pathogens

    • Atypical pneumonias can be divided into zoonotic and nonzoonotic atypical pathogens.

    • Zoonotic atypical pathogens causing CAP include Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever).

      • Contact with the appropriate vector is required for these zoonotic pathogens to cause CAP.

      • The appropriate epidemiologic questions for patients with Q fever include recent close contact with a parturient cat or sheep.

      • Patients who are suspected of having psittacosis have a history of recent close contact with psittacine birds.

      • Patients with tularemia have a history of recent close contact with deer or rabbits or recently have been bitten by a tick or deer fly.

    • Nonzoonotic atypical pneumonias are caused by Legionella species, M pneumoniae, or C pneumoniae.

    • The pattern of extrapulmonary findings, not individual findings, allows the clinician to differentiate between typical and atypical pneumonias.

    • Typical bacterial pneumonias have few, if any, extrapulmonary findings. Each atypical pathogen has its own distribution pattern of extrapulmonary organ involvement, which permits an accurate and rapid presumptive clinical diagnosis.

Table 2.                                  Differential Diagnostic Features of the Atypical Pneumonias

 

Zoonotic Atypical Pneumonias

Nonzoonotic Atypical Pneumonias

Key Characteristics

Psittacosis

Q Fever

Tularemia

Mycoplasma
Pneumonia

Legionnaires
Disease

Chlamydia
Pneumonia

Symptoms

 

Mental confusion

±

+

Prominent headache

+

+

Meningismus

+

±

Myalgias

+

+

+

+

Ear pain

±

Pleuritic pain

±

+

Abdominal pain

+

Diarrhea

±

+

Signs

 

Rash

±
(Horder spots)

±
(erythema multiforme)

±

Raynaud phenomenon

±

Nonexudative pharyngitis

+

±

+

+

Hemoptysis

+

+

Lobar consolidation

±

±

±

±

±

Cardiac involvement

±
(endocarditis)

±
(myocarditis)

 

±
(myocarditis/
heart block/
pericarditis)


(endocarditis,
myocarditis)

 

Splenomegaly

+

+

Relative bradycardia

+

±

+

Chest Film

 

Infiltrate

Patchy/
consolidation

Patchy/
consolidation

“Ovid
bodies”

Patchy

Patchy/
consolidation

Single
“circumscribed”
lesions

Bilateral hilar adenopathy

+

Pleural effusion

+
(bloody)

±
(small)

±
(small/
moderate)

±

    • Legionella species are the most important atypical pathogen causing CAP.

    • Although Q fever and psittacosis are associated with relative bradycardia, these zoonotic pneumonias may be excluded by a negative epidemiologic vector contact history.

    • If psittacosis and Q fever are eliminated from the diagnostic consideration by history, then relative bradycardia in a patient with CAP should suggest Legionnaires disease.

      • Because Legionella pneumonia has its own characteristic pattern of organ involvement, it is readily distinguished from other typical and atypical pathogens.

      • Some signs and symptoms are more important than others and can be expressed in a weighted diagnostic point system, which is highly accurate in assisting the clinician with determining a clinical diagnosis of Legionnaires disease.

Table 3.                    Relative Bradycardia

Determination and Evaluation of Relative Bradycardia

Inclusive criteria

Patient must be an adult, ie, >12 years

Patient must have a temperature >101°F

Pulse must be taken simultaneously with the temperature elevation

Exclusive criteria

Patient has normal sinus rhythm without arrhythmia, second-degree/third-degree heart block, or pacemaker-induced rhythm

Patient must not be on beta-blocker medication

Appropriate Temperature-Pulse Relationships (temperature and corresponding pulse [beats/min])

41.1°C/106°F = 150/min
40.6°C/105°F = 140/min
40.0°C/104°F = 130/min
39.5°C/103°F = 120/min
38.9°C/102°F = 110/min

Causes of Relative Bradycardia

Infectious causes

Legionella species
Psittacosis
Q fever
Typhoid fever
Typhus
Malaria
Babesiosis
Leptospirosis
Yellow fever
Dengue fever
Rocky Mountain spotted fever
Tularemia
Salmonella infections

Noninfectious causes

Beta-blockers
CNS lesions
Lymphomas
Factitious fever
Drug fever

    • Another clue to Legionnaires disease is the lack of response to beta-lactam antibiotic treatment in a patient with CAP and relative bradycardia. If other causes of relative bradycardia are excluded, this is a clue because it is a constant early finding in Legionnaires disease.

Table 4.                                  Weighted Diagnostic Point System

Findings

Qualifying Conditions

Point Score

Clinical

Acute onset

+1

Mental confusion/
encephalopathic

Acute onset

+2

Lethargy

Acute onset

+3

Ear pain

Acute onset

-3

Nonproductive cough/
sore throat

Acute onset

-3

Hoarseness

Acute onset

-3

Sputum

Purulent

-2

Hemoptysis

Mild/moderate

-1

Chest pain

Pleuritic

-2

Loose stools/diarrhea

Not secondary to erythromycin/
diarrhea-causing drugs

+3

Abdominal pain

With or without diarrhea

+5

Relative bradycardia

Adults with temperature ³102°F, no beta-blockers,
pacemaker, or arrhythmias

+5

Lack of response to
to beta-lactam therapy

After 72 hours

+5

Acute renal failure

Excluding other causes

+1

Laboratory

Low sodium

 

+4

Low phosphate ion level

Excluding other causes of
hypophosphatemia

+4

Elevated serum glutamic-oxaloacetic transaminase/serum glutamic-pyruvic transaminase

Excluding preexisting/other causes of elevated serum transaminases

+4

Elevated total bilirubin

 

+2

Elevated cold agglutinin titer ³1:64

 

-3

Elevated creatinine

Excluding preexisting/other causes of elevated serum transaminases

+1

Microscopic hematuria

Otherwise unexplained

+2

Diagnostic Point Score

Legionella

Legionella

Legionella

Highly probable

Probable

Unlikely

>10

5-10

<5

 

    • In typical hosts, CAP does not present with shock. If CAP presents with shock, look for impaired or absent splenic function. Disorders associated with impaired splenic function include those listed in Table 5.

Table 5.                   Differential Diagnosis of Severe Community-acquired Pneumonia Presenting with Shock

 

Chronic alcoholism
Amyloidosis
Chronic active hepatitis
Fanconi syndrome
Hyposplenism of elderly patients
Immunoglobulin A (IgA) deficiency
Intestinal lymphangiectasia
Myeloproliferative disorders
Waldenstr
цm macroglobulinemia
Non-Hodgkin lymphoma
Celiac disease
Regional enteritis
S
йzary syndrome

Congenital asplenia
Splenectomy
Sickle cell trait/disease
Splenic infarcts
Splenic malignancies
Steroid therapy
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic mastocytosis
Systemic necrotizing vasculitis
Thyroiditis
Pulmonary embolism
Congestive heart failure or acute myocardial infarction

      • If CAP presents with shock in the absence of conditions associated with hyposplenism, look for mimics of pneumonia that present with pulmonary infiltrates on chest films, fever, leukocytosis, and hypotension, such as acute myocardial infarction or acute pulmonary embolism.

      • If CAP presents with shock and without evidence of hyposplenia, acute myocardial infarction, or acute pulmonary embolism, consider an exacerbation of preexisting cardiopulmonary disease that presents with hypotension and coronary insufficiency with hypoxemia or emphysema.

WORKUP

Imaging Studies

  • Chest radiography

    • Air bronchograms may be observed in the presence of S pneumoniae. Frank consolidation and air bronchograms have been associated with a higher incidence of bacteremia.

    • Cavitary lesions and bulging lung fissures may be observed with Klebsiella pneumoniae infection.

    • Cavitation and associated pleural effusions are observed in cases of S aureus infection, anaerobic infections, gram-negative infections, and tuberculosis.

    • Legionella has a predilection for the lower lung fields. A radiograph depicting bilateral lower lobe pneumonia is shown below.

    •  

Bacterial pneumonia. Lateral image in a patient w...

Bacterial pneumonia. Lateral image in a patient with bilateral lower lobe pneumonia. Note the spine sign, or loss of progression of radiolucency of the vertebral bodies.

    • Klebsiella has a tendency to occur in the upper lobes. A radiograph depicting right upper lobe pneumonia is shown below.

 

Bacterial pneumonia. Lateral image in a patient w...

Bacterial pneumonia. Lateral image in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD).

    • A radiograph of right middle lobe pneumonia is shown below.

 

Bacterial pneumonia. Early right middle lobe pneu...

Bacterial pneumonia. Early right middle lobe pneumonia.

  • In unclear cases, high-resolution CT scanning of the lungs may aid in the diagnosis.

Other Tests

  • Sputum examination may be performed.

    • An adequate specimen must have fewer than 10 oral squamous epithelial cells per low-power field.

    • The WBC count should be more than 25 per low-power field.

    • A single predominant microbe should be noted at Gram staining, although mixed flora may be observed with anaerobic infections.

    • Often, patients cannot produce an adequate specimen. Many specimens produced are so contaminated by oral materials that they are unusable.

    • Cultures of the sputum have similar limitations. To be accurate, only specimens that have been examined microscopically and that have satisfied the criteria above should be submitted for culturing.

  • Blood cultures have limited value.

    • Positive findings correlate well with the causative agent.

    • Findings are positive in approximately 40% of cases. (This rate is true even in pneumococcal pneumonia, which has the highest association with positive culture findings.)

    • Cultures require 24 hours (minimum) to incubate.

    • Findings probably have minimal clinical effect in treating bacterial pneumonia.

  • Urine assays are available for the rapid detection of Legionella and pneumococcal antigens. These fast card-type assays have been developed recently, may be performed at the bedside, and may be useful in unclear cases or when the choices for antimicrobial therapy are limited.

  • An elevated international normalized ratio has been associated with more severe illness. This finding may herald the development of disseminated intravascular coagulation.

  • An elevated C-reactive protein level may be predictive of more serious disease.7 It is has not been clearly shown to differentiate bacterial versus viral illness.

Procedures

  • Bronchoscopy

  • Transtracheal aspiration for culturing

  • Thoracentesis

 

Lab Studies:

  • Send the sputum of patients with CAP for a Gram stain and/or culture. Many patients, especially elderly patients, may not be able to produce an adequate suitable sputum sample.

    • Patients with Legionnaires disease and purulent sputum show few or no predominant organisms after the Gram stain.

    • Do not send the sputum of patients with COPD (eg, chronic bronchitis) for Gram stain or culture because these patients invariably demonstrate a mixed or normal flora.

  • Obtain 2 or 3 sets of blood cultures from all patients with CAP upon admission because some typical bacterial pathogens, such as S pneumoniae and H influenzae, frequently are associated with positive blood cultures. M catarrhalis bacteremia is unusual.

  • Presentation with CAP and extrapulmonary findings is suggestive of the presence of atypical pathogens. Workup should include serum transaminase levels, serum phosphorous levels, urinalysis, and cold agglutinin titers.

    • Otherwise unexplained early, transient, and slight increases in serum transaminases in a patient with CAP suggest the presence of psittacosis, Q fever, or pneumonia caused by Legionella species.

    • Otherwise unexplained hypophosphatemia in a patient with CAP suggests Legionnaires disease.

    • Otherwise unexplained microscopic hematuria in a patient with CAP also suggests Legionnaires disease.

  • Low titer cold agglutinin elevations occur in a variety of viral and neoplastic illnesses. In patients with Mycoplasma-associated pneumonia, 75% develop transient elevations of cold agglutinins early in the course of the illness.

    • A negative cold agglutinin titer does not exclude the presence of Mycoplasma species.

    • A moderately elevated cold agglutinin titer effectively rules out Legionella pneumonia. Because low titer elevations of cold agglutinins are not specific, the diagnosis of Mycoplasma pneumonia is likely only if the cold agglutinin titer is highly elevated (>1:64) in a patient with CAP.

    • In a patient with CAP, the higher the cold agglutinin titer is (>1:64), the more likely the cold agglutinins are due to Mycoplasma species.

  • If a patient is suspected of having Legionella pneumonia, direct fluorescent antibody (DFA) testing of the sputum can assist in making the diagnosis if obtained early and before antimicrobial treatment. Antimicrobial treatment rapidly decreases the sputum yield of DFA testing.

  • Send serology if zoonotic atypical pathogens are suspected because isolation and culture are difficult and dangerous for microbiology personnel. A diagnosis of zoonotic pathogen-associated pneumonia is based on a 4-fold or greater increase in titers between acute and convalescent serum specimens.

  • Order immunoglobulin M (IgM) and immunoglobulin G (IgG) titers for C pneumoniae and M pneumoniae if they are a diagnostic possibility. An increase in the IgG titer for either organism suggests past exposure and does not indicate the diagnosis of acute infection. An increase in the IgM titer for either pathogen allows the clinician to make the diagnosis in a patient with CAP.

  • Order Legionella serologies if Legionella pneumonia is suggested based on the pattern of extrapulmonary findings. If acute titers are negative, this does not rule out Legionnaires disease because titers may not rise for 6-8 weeks. The finding of an initially high Legionella titer is unusual, and clinical diagnosis rests on demonstrating a 4-fold or greater increase between acute and convalescent titers.

  • The Legionella urine antigen test is only applicable for the Legionella pneumophila serogroup type I, which accounts for approximately 80% of infections. The urinary antigen test for Legionella species infections remains positive for long periods but may be negative early in the infection.

  • If C pneumoniae is suspected, order specific pneumonia IgM and IgG titers. Do not order chlamydial titers without specifying the species.

  • Approach CAP in patients with HIV as follows:

    • The pathogen causing CAP in patients with HIV is determined by the CD4 count. The differential diagnosis of the pathogen is determined by assessing the CD4 count and the chest x-ray appearance in the patient with HIV.

    • Patients with HIV and normal or slight decreases in their CD4 count with focal infiltrates have approximately the same pathogen distribution as typical hosts. Patients with nonfocal infiltrates or hypoxemia may have Pneumocystis carinii pneumonia when the CD4 count is decreased appropriately.

    • Patients with HIV, very low CD4 counts, and focal infiltrates commonly have tuberculosis, which is easily diagnosed using an acid-fast bacillus smear of sputum.

Imaging Studies:

  • Order a chest x-ray in all patients suspected of having CAP.

    • Obtain a chest x-ray to exclude conditions that mimic CAP and to confirm the presence of an infiltrate compatible with the presentation of CAP.

    • Patients presenting very early with CAP may have negative findings on chest x-ray. In these patients, repeat the chest x-ray within 24 hours.

    • Chest x-ray assists with the differentiation of viral pneumonias from nonviral pneumonias. Viral pneumonias have few or no infiltrates on chest x-ray, but, when present, infiltrates almost always are bilateral, perihilar, symmetric, and interstitial. Bacterial pneumonias have a predominantly focal segmental or lobar distribution.

    • In contrast, typical or atypical pathogens produce a lobar or segmental pattern on chest x-ray, with or without consolidation or pleural effusion.

    • Chest x-ray findings should be negative in patients with asthma who do not have CAP. Chest x-ray findings also are negative in patients with chronic bronchitis.

    • The infiltrates observed with CHF appear as increased interstitial markings and vascular redistribution to the upper lobes. Usually, cardiomegaly is present in patients with preexisting heart failure.

    • Rapid cavitation is not a feature of CAP. Aspiration pneumonitis may develop cavitation 1 week after aspiration. Findings of cavitation are not present on the initial chest x-ray in patients with CAP due to aspiration.

  • Serial chest x-rays can be used to observe the progression of CAP.

    • Rapidly progressive asymmetric infiltrates suggest the possibility of Legionnaires disease.

    • The appearance of chest x-ray findings worsens over a short period and requires a long time to improve. Clinical resolution occurs long before radiologic resolution.

  • Obtain a CT scan of the chest when an underlying bronchogenic carcinoma is suggested or if any abnormalities exist that are not consistent with the diagnosis of pneumonia only.

Procedures:

  • Transtracheal aspiration (TTA) is a potentially hazardous procedure and offers no additional diagnostic information in patients with CAP.

  • Transthoracic fine-needle aspiration of the infiltrate can be performed and is less hazardous than TTA; however, transthoracic fine-needle aspiration offers no additional information beyond that obtainable by other available diagnostic measures. This procedure is most useful to assess the cause of noninfectious-associated infiltrates that are not responding to antibiotic treatment.

Histologic Findings: Lung sections with typical bacterial pneumonias show the progression from red hepatization to white hepatization during the resolution process. The lung is repaired after bacterial pneumonia is complete and the infectious process resolves.

 

TREATMENT

Medical Care:

Table 6.                            Empiric Therapeutic Approach to Community-acquired Pneumonia in Patients with HIV

CAP with the Following:
Chest x-ray: Focal infiltrate
CD4:
³200 cells/mm3

CAP with the Following:
Chest x-ray: Focal infiltrate
CD4: Very low (
£200 cells/mm3)

Most Likely Pathogen
S pneumoniae
H influenzae
M legionella
Salmonella
C pneumoniae

Most Likely Pathogen
Those causing tuberculosis
Mycobacterium avium-intracellulare

Optimal Empiric Therapy
Extrapulmonary findings
(atypical pathogens):
Levofloxacin
or
Doxycycline

No Extrapulmonary findings
(typical bacteria):
Ceftriaxone
or
Third-generation cephalosporins
or
Cefepime
or
Levofloxacin

Features of both typical and atypical:
Levofloxacin

Optimal Empiric Therapy
Tuberculosis: Isoniazid, ethambutol, rifampin, pyrazinamide
Mycobacterium avium-intracellulare: Azithromycin
+
Ethambutol
±
Rifampin
or
Azithromycin
+
Ethambutol
+
Levofloxacin

  • Hospitalize patients with CAP who are moderately to severely ill. Factors that predict risk for increased mortality in patients with CAP have been studied and include older age, significant comorbidities, increased respiratory rate, hypotension, fever, multilobar involvement, anemia, and hypoxia, to name a few.

  • Patients with severe CAP require admission to an intensive care unit (ICU). Oxygen and/or ventilatory support may be required.

  • Because the severity of CAP frequently is due to underlying severe cardiopulmonary disease, direct medical efforts at supporting cardiopulmonary function while treating the patient with antibiotics for CAP.

  • Patients admitted with severe CAP and hypotension or shock often are hypotensive because of an acute pulmonary or cardiac insult such as pulmonary embolism or acute myocardial infarction.

  • If no acute cardiopulmonary explanation can be found (eg, exacerbation of severe underlying lung disease, exacerbation of preexisting CHF), the patient with shock likely has diminished or absent splenic function.

    • Many underlying conditions are associated with diminished splenic function that may present as severe CAP.

    • An abdominal scar resulting from abdominal trauma or lymphoma staging is an obvious manifestation of possible asplenia.

    • Investigate for the disorders associated with hyposplenic function as indicated in.

    • Hyposplenism may be inferred from the presence of Howell-Jolly bodies in the peripheral blood smear in a patient presenting with CAP who is in shock. The first step in treating a patient in shock is effective intravascular volume replacement. If aggressive intravascular replacement is inadequate, then pressors may be added. Do not administer pressors before adequate volume replacement because effective intracirculating intravascular volume decreases and the blood pressure drops further.

  • Treatment of penicillin-resistant pneumococcal pneumonia is as follows:

    • The overuse of beta-lactam and macrolide antibiotics probably has caused a gradual increase in the S pneumoniae minimal inhibitory concentration (MIC). This relative increase in the MIC (ie, intermediate resistance or relative resistance) can be overcome by using full recommended doses of beta-lactams.

    • In most cases of penicillin-resistant S pneumoniae, treatment remains penicillin. Most strains have increased MICs but still are susceptible and are not clinically resistant to penicillin.

    • Penicillin resistance is classified according to MICs. Breakpoints are as follows:

      • Sensitive – Equal to or less than 0.6 mcg/mL

      • Intermediate resistance – 0.1-1 mcg/mL

      • Highly resistant – Equal to or greater than 2 mcg/mL (fortunately, few highly penicillin-resistant pneumococci exist)

    • Strains of pneumococci that are highly resistant to penicillin may be treated with levofloxacin, the only quinolone indicated for the treatment of highly penicillin-resistant S pneumoniae. Alternatively, vancomycin, clindamycin, or linezolid may be used.

    • The use of non-C cell-wall active agents against S pneumoniae, such as doxycycline or levofloxacin, should decrease penicillin resistance among pneumococci.

    • The widespread use of macrolides, such as trimethoprim-sulfamethoxazole (TMP-SMX) and tetracycline (excluding doxycycline), has been associated with H influenzae resistance.

    • Most oral cephalosporins, except cefprozil, have been associated with increased S pneumoniae resistance.

    • Worldwide, the unrestricted use of levofloxacin since 1993 has not resulted in any increase in S pneumoniae resistance, although one study in Canada demonstrated an increase in fluoroquinolone resistance in its pneumococcal isolates from 1993-1998.

  • Use of intravenous-to-oral switch programs is as follows:

    • Most patients admitted to the hospital with CAP are treated with empiric intravenous antibiotic therapy. Unless these patients are acutely ill in the ICU or are unable to absorb medication from the gastrointestinal tract, patients may be switched to equivalent oral therapy to complete a 2-week course of therapy after 48 hours.

    • Candidate agents for intravenous-to-oral (IV-to-PO) switch programs have the same spectrum as intravenous agents, excellent bioavailability, few adverse effects, low resistance potential, and relatively low cost. Ideal agents for IV-to-PO switch programs include levofloxacin and doxycycline.

    • Other agents that may be used if S pneumoniae is not the etiologic agent include azithromycin or clarithromycin.

Table 7.                        Community-acquired Pneumonia: Therapeutic Principles

Pathogens

§             Single pathogens cause CAP.

§             Multiple pathogens rarely, if ever, cause CAP.

§             Rarely, if ever, is CAP caused by more than 1 typical or 2 atypical organisms or multiple typical/atypical organisms. Studies describing multiple pathogens are flawed and demonstrate one organism microbiologically with serologic evidence of prior exposure to the other pathogen. Clinical experience has demonstrated this principle for decades.

§             The only cause of multiple-pathogen pneumonia is aspiration pneumonia.

Comorbid conditions

§             Comorbid conditions do not affect selection of antimicrobial therapy.

§             Monotherapy is as effective as multiple-drug therapy.

§             The addition and/or change of antibiotics because of severity of illness and/or comorbidities is not rational.

§             Antimicrobial therapy is directed against the pathogen, not against the comorbid factors.

§             Comorbidity is an important prognostic factor and contributes to the severity index, but it has no place in antibiotic selection.

Severity

§             The severity of CAP is determined by underlying conditions of the lungs, heart, and spleen.

§             Do not change antibiotics or use additional antibiotics to treat severe CAP.

§             Additional antibiotics do not affect the pulmonary, cardiac, or splenic dysfunction that determines clinical severity.

§             CAP presenting with hypotension and/or shock is due to underlying lung disease, cardiac disease, acute myocardial infarction, or an exacerbation of CHF.

§             Antibiotic monotherapy is the same for mild, moderate, or severe CAP.

Appropriate empiric coverage

§             No need exists to cover S aureus, Klebsiella species, or P aeruginosa in CAP (most CAP regimens include K pneumoniae coverage).

§             No need exists to cover oral anaerobes in community-acquired aspiration pneumonia.

§             Virtually all antibiotics used to treat community-acquired aspiration pneumonia are highly effective against oral anaerobes. B fragilis coverage with metronidazole or clindamycin is unnecessary.

§             Coverage should include the typical (S pneumoniae, H influenzae, M catarrhalis) and atypical (Legionella and Mycoplasma species, C pneumoniae) pathogens.

§             Nursing home–acquired pneumonia (NHAP) should be treated as CAP. NHAP pathogens most closely resemble CAP and not hospital-acquired pathogens, eg, P aeruginosa.

Therapeutic considerations

§             Monotherapy coverage of both typical and atypical pathogens in CAP is preferred to double-drug therapy.

§             Monotherapy is less expensive and as effective as double-drug regimens.

§             Avoid empiric macrolide monotherapy because approximately 25% of S pneumoniae are naturally resistant to all macrolides.

§             Preferred monotherapy for CAP includes doxycycline or levofloxacin.

§             This is the least expensive way to optimally treat CAP.

§             No increased resistance is noted with extensive use.

§             No serious adverse effects are noted.

§             It is well tolerated in both PO/IV forms.

§             It is ideal for IV-to-PO switch monotherapy from patient compliance, safety, and cost perspectives.

§             In patients with CAP who are able to take PO medication, switch from IV to PO after 48 hours, using an antibiotic with the appropriate spectrum, high bioavailability, few adverse gastrointestinal effects, little or no resistance potential, and relatively low cost (eg, doxycycline, levofloxacin).

Penicillin-resistant S pneumoniae

§             Most penicillin resistance is “relative resistance” and is readily treatable with penicillin and/or beta-lactams.

§             Most highly penicillin-resistant S pneumoniae (MIC >2 mcg/mL) also may be treated with beta-lactams. Alternately, doxycycline, clindamycin, or levofloxacin may be used.

§             Vancomycin rarely, if ever, is needed. Very highly penicillin-resistant S pneumoniae (MIC >2 mcg/mL) remains a rare cause of CAP.

Table 8.                                  Empiric Therapy of Hospitalized Patients with Community-acquired Pneumonia

Suboptimal regimens

Monotherapy

Ceftriaxone

§             Covers typical pathogens, misses atypical pathogens

§             Adverse effects – Diarrhea not caused by C difficile, pseudobiliary lithiasis

§             Moderately expensive

§             1 g (IV) q24h

§             $27 (antibiotic cost) + $10 (IV charge) = $37/d (cost to institution)

Azithromycin

§             Misses approximately 25% of S pneumoniae, should not be used alone, covers atypical pathogens

§             Adverse effects – Nausea, vomiting, diarrhea not caused by C difficile

§             Very low serum levels – Slow onset/delayed therapeutic effect

§             Moderately expensive – $20 (antibiotic cost) + $10 (IV charge) = $30/d (cost to institution)

Combination therapy

Ceftriaxone plus erythromycin – Most expensive regimen

§             Covers typical and atypical organisms

§             Adverse effects – Nausea, vomiting, diarrhea not caused by C difficile, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis

§             Most expensive combination

Ceftriaxone 1 g IV q24h = $37/d plus
erythromycin 1 g IV q6h = $50/d
Total cost = $87/d (cost to institution)

§             IV-to-PO switch therapy – Disadvantage of double-drug therapy (relatively expensive/inconvenient)

Ceftriaxone plus azithromycin – Very expensive regimen

§             Covers typical and atypical pathogens

§             Adverse effects – Nausea, vomiting, diarrhea not caused by C difficile, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis

Ceftriaxone 1 g IV q24h = $37/d
plus azithromycin 500 mg IV q24h = $30/d
Total cost = $67/d (cost to institution)

§             IV-to-PO switch therapy – Disadvantage of double-drug therapy (relatively expensive/inconvenient)

Optimal regimens

Monotherapy

Doxycycline

§             Effective against all typical penicillin-resistant S pneumoniae/atypical pathogens

§             Adverse effects

§             PO – Gastrointestinal upset

§             IV – Phlebitis if volume/diluent inadequate

§             Inexpensive

200 mg IV q12h
$5 (antibiotic cost) + $20 (IV charge) = $25/d (cost to institution)

§             IV-to-PO switch therapy – Excellent bioavailability (eg, >9%)

§             Most inexpensive regimen – Compliance advantages of monotherapy

100 mg PO q12h = $6.44 (brand)
100 mg PO q12h = $0.20 (generic)

Levofloxacin

§             Highly active against all typical highly penicillin-resistant S pneumoniae/atypical pathogens

§             Inexpensive

500 mg IV q24h
$22 (antibiotic cost) + $10 (IV charge) = $32/d (cost to institution)

§             Adverse effects – None

§             No rationale for adding other coverage in typical and/or compromised hosts with severe CAP

§             IV-to-PO switch

§             Excellent bioavailability (eg, 99-100% compliance advantages of monotherapy)

§             Relatively inexpensive

500 mg PO q24h = $5.11/d

§             Intravenous administration of antibiotics – $10/dose (versus national average) cost to the institution

Consultations: Patients with severe CAP should have the benefit of an infectious disease specialist to assist in the underlying explanation for severe CAP.

Diet: Diet is as tolerated.

Activity: Patients with mild CAP may be treated in the ambulatory setting. Guide activity with common sense.

MEDICATION

         Before the role of atypical pathogens was appreciated, most patients with CAP were treated with a parenteral beta-lactam antibiotic. Approximately 15% of patients with possible atypical pneumonias were treated empirically with erythromycin or doxycycline.

Approximately 85% of CAP cases are caused by typical pathogens, such as S pneumoniae, H influenzae, or M catarrhalis, and 15% are due to the nonzoonotic atypical pathogens, such as Legionella species, Mycoplasma species, or C pneumoniae. Atypical pathogens, such as Legionella species, were found to be important causes of CAP. Because clinicians could not differentiate typical and atypical pneumonias on clinical grounds, combination therapy with a beta-lactam, such as ceftriaxone, in addition to erythromycin to cover both typical and atypical pathogens, became popular.

Even though clinically differentiating the typical from the atypical pneumonias with a reasonable degree of certainty is possible, many clinicians empirically treat patients with CAP for both atypical and typical pathogens. Presently, a preferred therapeutic approach to CAP is monotherapy with a respiratory quinolone such as levofloxacin.

Severity of CAP determines the route of antibiotic administration (ie, PO for mild cases, IV for moderate-to-severe cases), predicts the necessity of admission to an ICU, predicts the duration of hospital stay, and contributes to the prognosis.

Because patients with CAP have the same pathogen distribution regardless of clinical severity, the empiric antibiotic treatment for CAP is the same, regardless of severity.

Because the severity of CAP is determined by impaired cardiopulmonary or splenic function, using different antibiotics for severe or less severe cases of CAP or adding additional antibiotics because the patient has severe CAP is not logical. Antimicrobial therapy is directed against the microorganism and does not improve cardiopulmonary or splenic function, regardless of the degree of severity.

Drug Category: Antibiotics — Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Drug Name

Levofloxacin (Levaquin) — Second-generation quinolone. Acts by interfering with DNA gyrase in bacterial cells. Bactericidal. Highly active against gram-negative and gram-positive organisms, including P aeruginosa.

Adult Dose

500 mg/d PO/IV for 7-14 d

Pediatric Dose

<18 years: Not recommended
>18 years: Administer as in adults

Contraindications

Documented hypersensitivity

Interactions

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 1-2 h before or after taking fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations

Pregnancy

C – Safety for use during pregnancy has not been established.

Precautions

Adjust dose in renal function impairment

 

Drug Name

Gemifloxacin (Factive) — Fluoroquinolone antibiotic with wide range of activity against gram-negative and gram-positive organisms. Acts by inhibiting both DNA gyrase and topoisomerase IV (TOPO IV), which are essential for bacterial growth. Because of this dual mechanism, MIC values remain in the susceptible range for some double mutants (eg, Streptococcus pneumoniae).
Indicated for mild-to-moderate CAP caused by S pneumoniae (including penicillin-resistant strains; MIC value for penicillin >2 mg/mL), Haemophilus influenzae, Moraxella catarrhalis, Mycoplasma pneumoniae, Chlamydia pneumoniae, or Klebsiella pneumoniae.

Adult Dose

320 mg PO qd for 7 d

Pediatric Dose

<18 years: Not established
>18 years: Administer as in adults

Contraindications

Documented hypersensitivity to gemifloxacin or other fluoroquinolones

Interactions

Coadministration with antacids and divalent or trivalent cations (eg, aluminum, magnesium, iron) significantly reduces absorption (administer 3 h before or 2 h after gemifloxacin); sucralfate decreases absorption and should be administered 2 h following gemifloxacin; may increase QT interval prolongation risk if coadministered with class IA (eg, quinidine, procainamide) or class III antiarrhythmic agents (sotalol, amiodarone), or other drugs known to prolong QT interval (eg, erythromycin, antipsychotics, antidepressants)

Pregnancy

C – Safety for use during pregnancy has not been established.

Precautions

Decrease dose by 50% with CrCl <40 mL/min; may prolong QT interval; may cause maculopapular rash

 

Drug Name

Ceftriaxone (Rocephin) — Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell-wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Adult Dose

2 g IV q12-24h; not to exceed 4 g/d

Pediatric Dose

Neonates >7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 100 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d

Contraindications

Documented hypersensitivity

Interactions

Probenecid may decrease clearance, causing an increase in ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Pregnancy

B – Usually safe but benefits must outweigh the risks.

Precautions

Pseudobiliary lithiasis (sludge in gallbladder) can lead to cholecystectomy; use has been associated with diarrhea that is not caused by C difficile; caution in breastfeeding and in those with penicillin allergy

 

Drug Name

Azithromycin (Zithromax) — Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing arrest of RNA-dependent protein synthesis.

Adult Dose

500 mg IV q24h for 3 d, then 500 mg/d PO for 7-10 d

Pediatric Dose

<6 months: Not established
>6 months:
Day mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Interactions

May cause QT prolongation with cisapride, itraconazole, sparfloxacin, and other medications (probably very rare); may increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Pregnancy

B – Usually safe but benefits must outweigh the risks.

Precautions

Site reactions can occur with IV route; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function or prolonged QT intervals; caution in patients who are hospitalized, elderly, or debilitated; misses 25% of S pneumoniae

 

Drug Name

Doxycycline (Vibramycin) — Much more active than tetracycline against many pathogens. Different adverse effect profile and pharmacokinetics than tetracycline. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing arrest of RNA-dependent protein synthesis.

Adult Dose

100-200 mg PO/IV q12h

Pediatric Dose

<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO/IV in 1-2 divided doses; not to exceed 200 mg/d

Contraindications

Documented hypersensitivity; avoid in pregnancy and children <8 y

Interactions

Bioavailability minimally decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate

Pregnancy

D – Unsafe in pregnancy

Precautions

Rarely, if ever, causes photosensitivity; use during tooth development (last one half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

 

FOLLOW-UP

Further Inpatient Care:

  • Patients with severe cardiopulmonary disease or hyposplenic dysfunction have a prolonged course that may require transfer to a subacute unit with less intensive care.

Further Outpatient Care:

  • Monitor patients with mild CAP treated on an outpatient basis to be sure that they are compliant with their medications and that they are improving. After 1 week, a repeat visit and chest x-ray is advisable. As long as the patient is improving and parapneumonic complications are not evident, a posttherapy chest x-ray is not needed.

In/Out Patient Meds:

  • Most patients with CAP who are admitted to the hospital are treated intravenously for 2 days and then complete a 12-day course of therapy for a total of 14 days of combined intravenous and oral therapy.

  • Patients who are severely ill or are unable to tolerate or absorb medications administered orally require a longer duration of intravenous therapy before switching to an oral antibiotic.

  • Mild to moderately ill patients with CAP may be treated entirely via the oral route, either as an inpatient or an outpatient. Patients receiving oral antibiotics may be admitted for hospital services, such as pulmonary toilet and additional diagnostic tests, that are not obtainable on an outpatient basis.

  • If patients are switched to an oral regimen and are doing well, earlier discharge from the hospital is possible. The oral therapy regimen can be completed at home.

  • Most typical hosts with CAP may be treated with a total 14-day course of medication. Very healthy young adults and children may be treated for shorter periods of time. Patients who are debilitated (eg, those with underlying disorders, compromised hosts) may require longer periods of treatment that are based on clinical response.

  • IV-to-PO switch therapy is optimal with a single agent that has an appropriate spectrum, has excellent bioavailability, is well tolerated, has a low resistance potential, and is relatively inexpensive.

Deterrence/Prevention:

  • Pneumococcal vaccines prevent pneumococcal bacteremia but not necessarily pneumococcal pneumonia.

  • Nonleukopenic compromised hosts, such as those with rheumatoid arthritis, SLE, or alcoholism, may not develop an antibody response to the pneumococcal vaccine and, therefore, may remain susceptible to pneumococcal pneumonia. The same is true concerning the use of the Haemophilus vaccine.

Complications:

  • Infections caused by S pneumoniae may be complicated by a pleural effusion and/or empyema. Cavitation is not a feature of pneumococcal pneumonia. Bacteremia is part of the disease process and is not a complication of pneumococcal pneumonia.

  • Infections caused by K pneumoniae, occurring only in patients with chronic alcoholism, also may be complicated by empyema. Cavitation from Klebsiella species is a normal part of the disease process and should not be viewed as a complication. Bacteremia is part of the disease process and is not a complication of Klebsiella pneumonia.

  • Pleural effusion with H influenzae is part of the disease process and should not be viewed as a complication.

  • M catarrhalis usually is not associated with bacteremia, pleural effusions, or empyema; however, M catarrhalis causing CAP in a patient with advanced lung disease may prove fatal because of the underlying pulmonary condition of the host.

  • Consider extrapulmonary manifestations associated with M pneumoniae as part of the disease process and not as complications. Following an infection with M pneumoniae, patients may develop short-term or permanent asthma.

  • As with Mycoplasma-associated pneumonia, Chlamydia-associated pneumonia may be followed or complicated by short-term or long-term bronchospasm. A theory has been suggested that upper respiratory tract infections with C pneumoniae infections may be associated with acute coronary events or coronary artery disease.

Prognosis:

  • Severity and prognosis of CAP depends primarily on host factors, such as the status of the cardiopulmonary system and splenic function. Obviously, when all other factors are equal, patients who are older do not fare as well as younger adults.

  • Patients with impaired splenic function may develop overwhelming pneumococcal sepsis and experience a fatal outcome in 12-24 hours, regardless of the antimicrobial regimen used.

  • Prognostic factors that predict a bad outcome include preexisting lung disease, underlying cardiac disease, advanced age, multilobar involvement, and delay in the initiation of appropriate antimicrobial therapy.

Patient Education:

  • Remind patients to comply with the medication even after they experience clinical improvement. Except in patients with heart failure, adequate hydration and preservation of the cough reflex during the convalescent period are important.

 

 

Hemoptysis or haemoptysis is the expectoration (coughing up) of blood or of blood-stained sputum from the bronchi, larynx, trachea, or lungs (e.g., in tuberculosis or other respiratory infections or cardiovascular pathologies).

 

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Differential diagnosis

There are many conditions involving Hemoptysis, including but not limited to bronchitis and pneumonia most commonly, but also lung neoplasm (in smokers, hemoptysis is often persistent), aspergilloma, tuberculosis, bronchiectasis, coccidioidomycosis, pulmonary embolism, pneumonic plague, and Cystic Fibrosis. Rarer causes include hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome), or Goodpasture’s syndrome and Wegener’s granulomatosis. In children, hemoptysis is commonly caused by the presence of a foreign body in the respiratory tract. The condition can also result from over-anticoagulation from treatment by drugs such as warfarin.

Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such secretions can be a sign of nasal or sinus cancer, but also a sinus infection). Extensive non-respiratory injury can also cause one to cough up blood. Cardiac causes like congestive heart failure and mitral stenosis should be ruled out.

 

Нормальное кровохарканье!

 

The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-colored blood comes from the gastrointestinal tract. Sometimes hemoptysis may be rust-colored.

·         Lung cancer, including both non-small cell lung carcinoma and small cell lung carcinoma.

·         Sarcoidosis

·         Aspergilloma

·         Tuberculosis

·         Histoplasmosis

·         Pneumonia

·         Foreign body aspiration and aspiration pneumonia

·         Goodpasture’s syndrome

·         Wegener’s granulomatosis

·         Bronchitis

·         Bronchiectasis

·         Pulmonary embolism

·         Anticoagulant use[

·         Trauma

·         Lung abscess]

·         Mitral stenosis

·         Tropical eosinophilia

·         Drug induced

·         Bleeding disorders

·         Hughes-Stovin Syndrome and other variants of Behçet’s disease

Diagnostic approach

 

Diagnostic approach to solving the puzzle of hemoptysis.

·         Past history, history of present illness, family history

·         history of tuberculosis, bronchiectasis, chronic bronchitis, mitral stenosis, etc.

·         history of smoking, occupational diseases by exposure to silica dust, etc.

·         Blood

·         duration, frequency, amount

·         Amounts of blood: large amounts of blood, or is there blood-streaked sputum

·         Probable source of bleeding: Is the blood coughed up, or vomited?

·         Bloody sputum

·         color, characters: blood-streaked, fresh blood, frothy pink, bloody gelatinous.

·         Accompanying symptoms

·         fever, chest pain, coughing, purulent sputum, mucocutaneous bleeding, jaundice.

·         Imaging examination

·         chest X-ray, CT scan and 3D reconstruction images or CT virtual bronchoscopy, bronchial angiography.

·         Laboratory tests

·         blood test: WBC

·         Sputum: cells and bacterial examinations, sputum culture

·         Bronchial fiber endoscopy[

Treatment

Treatment depends largely upon the underlying cause. Many modalities of treatment can be used, like, iced saline, or topical vasoconstrictors, such as adrenalin or vasopressin can be used. Selective bronchial intubation can be used to collapse lung in which the hemorrhage is occurring, also endobronchial tamponade can be used. Laser photocoagulation can be used to stop bleeding during bronchoscopy. Angiography of bronchial arteries can be performed to locate the bleeding, and it can often be embolized. Surgical option is usually the last resort, and can involve,lobectomy or pneumonectomy. Non–Small-Cell Lung Cancer can also be treated with Erlotinib or Gefitinib

Hemoptysis, the act of coughing up blood, is an important symptom since it frequently reflects serious underlying lung disease. Because many of the lung conditions that are heralded by hemoptysis are treatable, the symptom requires systematic and thorough evaluation to discover its etiology. A possible exception is mild hemoptysis occurring in a patient with chronic bronchitis during an acute exacerbation. Hemoptysis in this situation is common, usually mild, and self-limited. Therefore, it may be observed without further work-up. However, if the hemoptysis is substantial, persistent, or recurrent then further evaluation is indicated, particularly since patients with chronic bronchitis related to smoking are at high risk for lung cancer.

I.                        Causes

A.  Non-respiratory tract sources (Differential Diagnosis)

1.     Nasopharyngeal source of bleeding

2.     Upper Gastrointestinal Bleeding

B.   Common Causes of respiratory tract bleeding

1.     Infection (60-70% ofHemoptysis)

     2. Acute Bronchitis (26% of Hemoptysis)

     С. Pneumonia (10% ofHemoptysis)

1. Staphylococcus aureus

             i.      Pseudomonas aeruginosa

b.                      Tuberculosis (8% of Hemoptysis)

c.                       Fungal organisms (e.g. Aspergillosis)

d.                      Influenza

1.                                         Lung Cancer (23% of Hemoptysis)

a.                Hemoptysis is rarely due to metastases

C.              Less common causes of respiratory tract bleeding

1.                                         Cardiovascular causes

a.                Pulmonary venous Hypertension

                   i.                       Congestive Heart Failure

                 ii.                       Severe Mitral Stenosis

b.                Pulmonary Embolism

c.                 Arteriovenous malformation

1.                                         Pulmonary causes

a.                Bronchiectasis

b.                Airway trauma or foreign body (esp. children)

c.                 Lung Abscess

d.                Goodpasture’s Syndrome

e.                 Wegener’s Granulomatosis

f.                  Lupus pneumonitis

   II.            Causes: Blood streaked Sputum

A.  Upper respiratory inflammation

1.     Nose or nasopharynx

2.     Gums

3.     Larynx

B.  Severe coughing paroxysms

C.  Trauma

III.            Causes: Pink Sputum

A.  Blood and secretions mix in alveoli, small bronchioles

B.  Conditions associated with pink Sputum

1.     Pneumonia

2.     Pulmonary edema

IV.            Causes: Heavy Bleeding into respiratory tree

A.  Pulmonary Tuberculosis

B.  Lung Abscess

C.  Bronchiectasis

D.  Pulmonary infarction

E.   Pulmonary Embolism

F.   Bronchogenic Carcinoma

G.  Broncholithiasis

H.  Mitral Stenosis

I.      Actinomycosis Lung Abscess

J.     Blastomycosis Lung Abscess

 

Sources

The first step in the evaluation of hemoptysis is to decide if it is really hemoptysis—that is, is the blood coming from the bronchial tree or lungs or from some other site? In most cases, history will suggest that blood is actually being coughed up from the airways or lungs, but it may be difficult at times to distinguish blood being coughed up from the respiratory system from blood coming from two other sites: bleeding in the upper respiratory tract, in the nasopharynx or sinuses, or blood originating in the gastrointestinal tract that was regurgitated or vomited. A history of frequent nosebleeds, hoarseness, or some other change in the voice or history of mouth lesions might suggest bleeding from the upper respiratory tract. If bleeding is not clearly from the lungs then a thorough examination of the upper respiratory system is indicated. If the source remains equivocal, i.e., no abnormality in the upper respiratory tract is found on initial examination and no source is found after further pulmonary work-up as described below, then an examination by an otolaryngology specialist may be warranted. Hematemesis occasionally may be difficult to distinguish from hemoptysis; moreover, blood from a respiratory source may be swallowed and may present as coffee-ground emesis. Gastrointestinal symptoms suggest an upper GI work-up when the bleeding source is unclear.

The second question to be asked is whether the bleeding is massive (or life-threatening), which if present changes the approach to management as well as affecting the differential diagnosis. Massive or life-threatening hemoptysis has usually been defined by the rate of bleeding, defined as greater than 200 ml per day by various authors. The bleeding rate is critical since the problem with massive hemoptysis is not exsanguination but asphyxiation from blood that floods alveoli or clots that functionally obstruct airways. Thus, any amount of bleeding at a high rate, even over a short period of time, should be managed as being potentially life-threatening. The approach to massive hemoptysis is described in more detail below.

Differential Diagnosis

The differential diagnosis of hemoptysis is shown in Table 1. The most common causes are bronchitis, lung cancer, pneumonia, lung abscess, tuberculosis, bronchiectasis, and pulmonary thromboembolism. The prevalence of these disorders in causing hemoptysis appears to be changing and varies considerably in different series. In North America, tuberculosis (both active and inactive) and bronchiectasis appear to be decreasing as a cause of hemoptysis whereas they are still extremely frequent causes of hemoptysis in many other parts of the world. In many (but not all) series, a significant proportion of cases remain undiagnosed despite extensive work-up.

Use of anticoagulants or fibrinolytics

Conditions that cause massive hemoptysis are generally inflammatory disorders which erode into the bronchial circulation. Because the bronchial circulation is under systemic vascular pressure, the bleeding is likely to be more severe than if the source of bleeding were the pulmonary circulation. Thus, causes of massive hemoptysis consist mainly of suppurative or chronic infections or conditions complicated by infection (lung abscess, tuberculosis, bronchiectasis, or cystic fibrosis), but also include lung cancer.

Evaluation of Hemoptysis

The initial evaluation in all patients consists of a careful history, physical examination, and upright postero-anterior and lateral chest x-rays. The history should elicit and detail any acute or chronic pulmonary symptoms, including cough, sputum production, shortness of breath or wheezing, and any previous history of lung disease. Systemic symptoms such as fever, sweats, weight loss, and malaise may reflect ongoing inflammation or reflect a catabolic process related to cancer or chronic infection. The history should uncover symptoms associated with the specific causes in the differential diagnosis including symptoms of heart disease (especially mitral stenosis), vasculitis, and with particular attention given to pulmonary thromboembolism. In considering pulmonary thromboembolism, in addition to the acute onset of pulmonary symptoms and any leg symptoms reflecting possible deep venous thrombosis, the most important part of the history focuses on asking about possible risk factors for deep venous thrombosis.

Physical examination includes auscultation, listening for generalized wheezing (COPD/asthma), localized wheezing (local bronchial obstruction), or diffuse or localized crackles or rhonchi which may reflect infectious or inflammatory processes including lung abscess, pneumonia, and bronchiectasis. A careful cardiovascular examination should be done, particularly looking for congestive heart failure, evidence of mitral stenosis and signs of deep venous thrombosis. It is important to recognize that signs of deep venous thrombosis are lacking in at least half of the cases in which deep venous thrombosis is eventually proven. A negative result of the examination, therefore, clearly does not rule out deep venous thrombosis or the possibility of pulmonary thromboembolism.

A complete blood count and coagulation studies should be ordered. A posteroanterior and lateral chest x-ray should be routinely obtained. The chest x-ray may be very helpful in suggesting a source of the hemoptysis, such as pulmonary inflammatory disease or cancer. If the chest x-ray is abnormal, it will often suggest subsequent steps in the work-up. Sputum cytology on expectorated sputum should be obtained in any patient at significant risk for lung cancer based on epidemiologic considerations, whether or not the chest x-ray is suspicious for cancer. This includes all patients with chronic obstructive pulmonary disease.

If the chest x-ray is negative or unrevealing it does not rule out important disease as a cause of hemoptysis. Therefore, one must make a clinical decision about how much further to go in the evaluation. This decision should be individualized according to each clinical situation and the availability of diagnostic facilities and subspecialty consultation. Generally, computed tomography (CT) of the chest is the preferred next study since it is noninvasive, can detect small cancers in the bronchial tree and lung parenchyma, and can diagnose bronchiectasis. Chest CT might also provide information useful to the bronchcoscopist if bronchoscopy becomes a consideration. Three forms of chest CT are available that might be helpful in diagnosing the cause of hemoptysis: chest CT with contrast; high resolution chest CT; and spiral CT of the chest. Each has its advantages for diagnosing some of the conditions in the differential diagnosis. Consultation may be indicated to determine which form of chest CT should be ordered for evaluation of a given patient.

Specialized Work-Up

Fiberoptic bronchoscopy is generally the next study to be considered. The decision to perform bronchoscopy should be made in consultation with a pulmonologist. Fiberoptic bronchoscopy may identify an endobronchial lesion, most often lung cancer, as the cause for hemoptysis and can help localize the lobe or segment from which the blood is coming. The combination of fiberoptic bronchoscopy and chest CT has been shown to give a higher yield of specific diagnoses than either test alone.

Fiberoptic bronchoscopy is indicated in certain categories of patients: those in whom the diagnosis is not evident from history, physical examination, chest x-ray, or chest CT; those with significant bleeding (greater than 30 ml per day) or in whom hemoptysis persists for longer than one week; and those who have systemic symptoms suggesting cancer or who are at particularly high risk for lung cancer, especially cigarette smokers over the age of forty. If none of these conditions is present, then the chance of finding lung cancer on bronchoscopy is very low and a decision to observe the patient should be considered.

If suspicion of pulmonary embolus is moderate, particularly if risk factors exist for deep venous thrombosis and pulmonary thromboembolism, then a ventilation/perfusion lung scan should be obtained.

Therapy

The therapy of hemoptysis consists of that treatment appropriate for the underlying disease process, for example, antibiotic therapy for infectious etiologies. Otherwise, the treatment is nonspecific. The exception to this is when massive hemoptysis is present.

Management of Massive Hemoptysis

When the rate of bleeding qualifies as massive hemoptysis (a rate of greater than 200 ml per day) the situation should be considered to be a medical emergency requiring referral for immediate diagnostic and therapeutic steps. The treatment of massive hemoptysis includes consideration of either surgical removal of the bleeding site or bronchial angiography with embolization of the bleeding site when feasible. Although there is some debate regarding the role of bronchial embolization, with some authors suggesting it be performed in all cases, the standard management for life-threatening bleeding due to localized disease in a patient with good pulmonary reserve is usually surgical resection. If emergent surgery is being considered, the diagnostic goal consists of localizing the bleeding site, first, as to which lung is bleeding and then, if possible, as to which lobe or segment contains the bleeding source. Bronchial arterial embolization is usually indicated in patients with nonlocalized disease and/or limited breathing reserve to preserve pulmonary parenchyma and function. Localization can also be helpful when bronchial embolization is being considered because it permits selective bronchial angiography to be undertaken, which markedly shortens the angiographic procedure. Bronchoscopy, either fiberoptic or rigid bronchoscopy, should be performed as soon as possible in an attempt to localize the site of bleeding within the lung. Localization of the bleeding source is much more successful if some degree of active bleeding is still occurring.

If the lung from which the bleeding is occurring is suspected (e.g., based on the chest x-ray or the patient’s subjective impression), the patient should be positioned with the affected lung placed in a dependent position to prevent drainage of blood into the contralateral lung. The patient may be lightly sedated or tranquilized to diminish cough, but the state of consciousness should not be impaired such that the patient is unable to cough and maintain a clear airway. Once it is decided that surgery is indicated, then control of the airways should be obtained. Ideally, a double lumen tube should be inserted. However, if the required experience is not available, a standard endotracheal tube should be placed. If the bleeding is suspected to be from the left lung then the tube can be placed in the right mainstem bronchus and the right lung ventilated while the patient is prepared for emergent surgery.

When to Refer

Indications for referral to subspecialists for evaluation of hemoptysis include the following:

  • Consideration of CT scan (to help determine type)

  • Consideration of bronchoscopy (see indications above)

  • Presence of massive or life-threatening hemoptysis

  • Persistent or recurrent undiagnosed hemoptysis.

Medicolegal Concerns

The biggest concern for liability on the part of the physician in evaluation of hemoptysis is failure to diagnose lung cancer. A less frequently occurring situation is the failure to diagnose pulmonary thromboembolism. Because these clinical situations have differing concerns they will be treated separately.

Eventual diagnosis of lung cancer when the patient presented earlier with hemoptysis is a cause for malpractice litigation. Two considerations allow appropriate evaluation while protecting the physician from risk. The first is to recognize the patient at risk for lung cancer from demographic data and smoking history, and include a sputum cytology (and, if warranted clinically, fiberoptic bronchoscopy) in the initial work-up. The second is to clearly record the advice given to the patient with suspected bronchitis and mild hemoptysis that stops spontaneously to return for further evaluation should hemoptysis recur.

Hemoptysis is an infrequent but important symptom in pulmonary thromboembolism. The liability here is failure to consider pulmonary thromboembolism and to order appropriate tests when hemoptysis is associated with other acute symptoms (including shortness of breath and/or pleuritic chest pain) in a patient at risk for deep venous thrombosis.

Summary

There are several important steps in evaluation of the patient with hemoptysis. First, it should be determined whether the bleeding represents true hemoptysis or whether the source of bleeding is in the upper airway or in the gastrointestinal tract. Second, the significance of the bleeding should be evaluated, specifically ascertaining whether life-threatening bleeding is present. Third, a differential diagnosis based on the initial history should be developed; this will help focus subsequent questioning, physical examination, and laboratory studies on likely sources of bleeding for the specific clinical situation. A chest x-ray should be obtained. If history, physical examination, and a chest x-ray do not reveal the source of bleeding, then a chest CT should be considered. Patients who are candidates for bronchoscopy include those with bleeding of more than 30 ml per day, hemoptysis which has been persistent for one week, and patients at high risk for lung cancer, particularly cigarette smokers older than forty years of age. Massive or life-threatening hemoptysis (bleeding at a rate of greater than 200 ml per day) constitutes an emergency with the major diagnostic objective being localizing the source of the bleeding so that emergent surgery to remove the bleeding site can be carried out. Bronchial arteriography and embolization should be considered in patients with poor pulmonary reserve due to pre-existing lung disease.

 

Verview of Hemoptysis

Hemoptysis (which is pronounced he-MOP-tis-is) is coughing up blood from the respiratory tract. Blood can come from the nose, mouth, throat, the airway passages leading to the lungs, or the lungs. The word “hemoptysis” comes from the Greek “haima,” meaning “blood,” and “ptysis,” which means “a spitting”.

Blood-tinged mucus in a healthy nonsmoker usually indicates a mild infection. Indeed, the most common cause for coughing up blood is the least serious—a ruptured small blood vessel caused by coughing and/or a bronchial infection.

In patients with a history of smoking and those who are otherwise at risk for lung disease, however, hemoptysis is often a sign of serious illness. Serious conditions that can cause hemoptysis include bronchiectasis (chronic dilation and infection of the bronchioles and bronchi), pulmonary embolus (a clogged artery in the lungs that can lead to tissue death), pneumonia (a lung infection), and tuberculosis.

Hemoptysis can also result from inhaling a foreign body (e.g., particle of food) that ruptures a blood vessel. Whatever the suspected cause, hemoptysis should always be reported to a physician.

Hemoptysis refers specifically to blood that comes from the respiratory tract. Blood also may come from the nose, the back of the throat, or part of the gastrointestinal tract. When blood originates outside of the respiratory tract, the condition is known as“pseudohemoptysis.” Vomiting up blood, medically known as hematemesis, is one type of pseudohemoptysis. Differentiating between hemoptysis and hematemesis is an integral part of diagnosis. Since they involve different parts of the body, treatments and prognose (prospect of recovery) are not the same.

Classifying hemoptysis as mild or massive (some practitioners classify it as trivial, moderate, or massive) is difficult because the amount of blood is often hard to accurately quantify. Life-threatening, “massive” hemoptysis, which requires immediate medical attention, is differentiated from less severe cases.

Massive Hemoptysis

Hemoptysis is considered massive, or major, when there is so much blood that it interrupts breathing (generally more than about 200-240 mL, or about 1 cup, in 24 hours). Massive hemoptysis is a medical emergency: the mortality rate for patients with massive hemoptysis can be as high as 75%. Most patients who die from hemoptysis suffer from asphyxiation (lack of oxygen) due to too much blood in the airways.

Mild Hemoptysis

If there is a small amount of blood or sputum streaked with blood, the spitting is considered mild hemoptysis. In 60% to 70% of mild hemoptysis cases, the underlying disorder is benign and disappears on its own without causing serious problems or permanent damage.

Even mild hemoptysis can result in critical breathing problems, depending on the underlying cause for the bleeding. Additionally, hemoptysis tends to occur intermittently and recur sporadically, and there is no way to predict if patients with mild hemoptysis are at risk for massive hemoptysis. Diagnosis is important to prevent a more serious condition.

Causes of Hemoptysis

There are many underlying disorders that can cause hemoptysis (coughing up blood), ranging from heart problems to trauma to infections to lung disease. Worldwide, tuberculosis is the most common cause of hemoptysis. In industrialized countries, the most common causes are bronchitis, bronchiectasis, andbronchogenic carcinoma.

In patients with AIDS, the most common cause of hemoptysis is pneumonia. In about 15% to 30% of cases, the underlying problem is never found—undiagnosed hemoptysis is commonly referred to as idiopathic hemoptysis.

Tuberculosis and Other Mycobacterial Infections

A mycobacterium is a type of bacteria that causes a variety of infections, including tuberculosis. A mycobacterial infection can destroy pulmonary tissue, usually by forming cavities in the airway walls.

The hemoptysis that results is usually mild to moderate and may be associated with other symptoms, including unexplained weight loss, cough, purulent sputum (thick, opaque, yellowish white discharge), and a history of mycobacterial exposure. A chest x-ray usually shows signs of infection, including a visible cavity, and the mycobacterium should be microscopically visible in the patient’s sputum.

Bronchitis

Bronchitis is an inflammation and swelling of the bronchi that can be acute orchronic. It is a very common cause of hemoptysis that results from recurrent coughing that irritates and eventually breaks down the mucosal lining of the airways.

The hemoptysis is usually mild and often associated with a purulent sputum (thick, opaque, yellowish-white discharge), low-grade fever and occasionally, wheezing. Usually the sputum is examined under the microscope to look for the pathogenic culprit. A chest x-ray is usually normal. The patient is usually prescribed cough suppressants and antibiotics.

Bronchiectasis

Bronchiectasis is a chronic dilation and consequent infection of the bronchioles and bronchi that results from obstruction in the bronchi. The dilation results from damage to the surrounding supportive tissue and is usually a result of infection or fibrosis (the abnormal formation of scar tissue).

Cystic fibrosis is an example of a disease that leads to bronchiectasis. In addition to hemoptysis, patients with bronchiectasis often have a severe cough and chronic purulent sputum (thick, opaque, yellowish white discharge).

LUNG CANCER

Bronchogenic carcinoma is cancer that originates in the lining of the bronchi. About 90% of lung cancers are bronchogenic. The other 10% begin in the bronchioles, alveoli, or trachea. Bronchogenic carcinoma is a less common cause of hemoptysis than bronchitis or bronchiectasis, but is an important one.

Most cases of bronchogenic carcinoma occur in smokers. If the disease is advanced, patients may experience unaccountable weight loss and various other common symptoms of lung cancer.

A chest x-ray can reveal the location of the neoplasm (tumor), and cancerous cells can often be detected in microscopic examination of the patient’s sputum. The diagnosis sometimes cannot be confirmed until the tissue is biopsied.

About 7% of patients with bronchogenic cancer are initially diagnosed because of hemoptysis. About 20% of patients with bronchogenic cancer experience hemoptysis at some point. The bleeding results from necrosis of the tumor (death of the cells that make up the tumor), the rupture of small blood vessels in the area, or the tumor invading one of the pulmonary blood vessels. Massive bleeding can occur if the tumor erodes into one of the large pulmonary vessels.

Hemoptysis can also result from metastatic cancer to the lungs (especially breast, kidney, colon, and esophageal metastases). The cancer causes bleeding in much the same way that bronchogenic carcinoma causes bleeding.

Pneumonia

Pneumonia is a lung infection caused by a number of different microorganisms. When a healthy person inhales one of these microbes, the immune system responds and prevents the microbe from reproducing and causing infection. But, in people with weakened immune systems (e.g., patients with AIDS), the microbes settle in the lungs, where they grow and multiply.

As the lung tissue tries to protect itself, the lungs fill with liquid and pus. In addition to hemoptysis, other symptoms include a high fever, cough, and chest pain.

Other Causes of Hemoptysis

Hemoptysis Other Causes

Other causes for hemoptysis include pulmonary infarction or embolism, various heart problems, vascular disorders, pulmonary AVM , and trauma.

Pulmonary Infarction or Embolism & Hemoptysis

A pulmonary embolism is the sudden closure of a pulmonary artery due to a blood clot or presence of foreign material. Pulmonary infarction is the death of lung tissue due to the lack of oxygen resulting from a single embolism or several recurrent embolisms. Pulmonary embolism can be massive, resulting in death or severe shock; or it can be relatively mild.

Infarction is a relatively uncommon cause of hemoptysis. Associated symptoms include chest pain (pleuritic chest pain in particular, meaning the pain is felt as the patient breathes in and out), cough, low-grade fever, tachypnea (rapid breathing), tachycardia (rapid heartbeat), and dyspnea (shortness of breath, even without exertion).

The chest x-ray of a patient with a pulmonary infarction or embolism is usually normal, but there may be a couple of distinguishing features.

Heart Problems & Hemoptysis

Mitral stenosis (a narrowing of the mitral valve that leads into the left ventricle) can lead to very mild hemoptysis—pink, frothy sputum with mild traces of blood. Other symptoms associated with left ventricular failure include orthopnea (difficulty breathing when lying down), paroxysmal nocturnal dyspnea (PND; a shortness of breath that appears suddenly at night, usually waking a person from sleep), and shortness of breath while exercising.

Coagulopathy & Hemoptysis

A coagulopathy (also known as a hypercoagulable state) is any disease that affects coagulability—the ability to of the blood to clot. In a patient with coagulopathy, clots cannot form after even mild trauma to the mucosal lining of the respiratory airways, leading to mild hemoptysis.

Other signs of coagulopathy include epistaxis (nosebleed), purpura (appearance of lesions, or bruises, on the skin due to broken blood vessels), menorrhagia (excessively long or heavy periods), and hematuria (blood in the urine).

Anticoagulants & Hemoptysis

Anticoagulants are drugs commonly prescribed to prevent the formation of blood clots. They are often used to treat thromboembolic disorders (blood clot disorders; a thrombus is a clot and an embolism is the sudden closure of an artery due to a clot). Hemoptysis sometimes develops in people who take anticoagulant medication.

Drug Use & Hemoptysis

In addition to anticoagulants, a variety of other drugs including aspirin, cocaine, and penicillamine (a drug used to treat lead poisoning and other disorders) are known to cause hemoptysis.

Catamenial Hemoptysis

Catamenial hemoptysis is menstrual-related hemoptysis. It is also known as pulmonary endometriosis. Endometriosis is the development of cells outside of the uterus that normally grow only inside the uterus—the same cells that are shed monthly during menstruation. Researchers do not know how or why endometriosis occurs.

Usually the abnormal cell growth occurs in other areas of the reproductive tract, but sometimes it occurs in the liver, lung, and even the brain. Endometriosis in the lungs results in catamenial hemoptysis. It is very rare and usually treated using hormones.

Cryptogenic Hemoptysis

About 15% to 30% of hemoptysis cases go undiagnosed and the underlying cause is never determined. This is true even after extensive diagnostic tests, including a bronchoscopy. Usually the hemoptysis is mild and attributed to bronchial inflammation, and the prognosis (final outcome) for most patients is good.

Iatrogenic Hemoptysis

An iatrogenic condition occurs as a result of the activity of a physician or surgeon. Iatrogenic hemoptysis can occur following a biopsy of lung tissue taken during a bronchoscopy. Usually the bleeding stops on its own, but sometimes it can be severe.

Aspergillosis & Hemoptysis

Aspergillosis is a lung infection caused by the fungus Aspergillus fumigatus. It is rare, except in patients with compromised immune systems. The fungus usually grows to form a ball (known as an aspergilloma) that can invade the blood vessels in the area, causing massive hemoptysis and major damage. A chest x-ray is usually diagnostic, and treatment usually involves surgically removing the lesion.

Lung Abscess & Hemoptysis

A lung abscess is an accumulation of pus (a fluid product of inflammation and infection) in the lungs that can cause hemoptysis.

Arteriovenous Malformation (AVM) & Hemoptysis

AVM is a congenital (present at birth) childhood disease characterized by the presence of abnormal arteries and veins throughout the lungs. The abnormalities cause internal damage to the lungs and eventually cause loss of function.

Idiopathic Pulmonary Hemosiderosis & Hemoptysis

Idiopathic pulmonary hemosiderosis is a rare childhood disease that leads to the deposition of hemosiderin (an iron byproduct of hemoglobin) in the lungs. It is believed to be an autoimmune disease, meaning that the body mistakenly attacks its own healthy tissue, causing damage. Patients suffer repeated sudden attacks of hemoptysis and dyspnea (difficult breathing).

Goodpasture’s Syndrome & Hemoptysis

Goodpasture’s syndrome also involves an accumulation of iron in the lungs. Goodpasture’s also involves the kidneys, and most patients die from kidney failure several months after being diagnosed.

Trauma & Hemoptysis

Trauma to the chest, such as from a car accident or other injury, can cause hemoptysis immediately following the incident or later.

Wegener’s Granulomatosis & Hemoptysis

Wegener’s granulomatosis is an autoimmune disease, meaning that the body attacks its own healthy, normal tissue, causing damage. Wegener’s is very rare and is characterized by inflammation.

Signs and Symptoms of Hemoptysis

Hemoptysis is a symptom of many different underlying disorders, from cancer to a mild bronchial infection. In addition to coughing up blood and depending on what is causing the bloody sputum, a patient may notice other symptoms including the following:

  • Chest pain

  • Dyspnea (shortness of breath, even without exercise)

  • Fever

  • Nausea

  • Tachypnea (rapid breathing)

  • Vomiting

Even without other symptoms, anyone who coughs up blood should contact his or her physician or health care practitioner. In most cases, hemoptysis is symptomatic of a mild bronchial infection, it can be a sign of a more serious illness.

Patients are ofteot sure if the blood is from the respiratory tract or not. There is a big difference, in terms of prognosis (final outcome and expected recovery) and treatment, between hemoptysis and hematemesis (vomiting blood).

Signs of hemoptysis include:

  • Any respiratory symptoms, such as a cough

  • Bright red blood

  • Blood that has a liquid or clotted, frothy appearance

Signs of hematemesis include:

  • A history of excessive alcohol use or liver disease

  • Any esophogastric symptoms, such as nausea or vomiting

  • Brown or black blood

  • Blood that looks like coffee grounds

  • Dark-colored, tar-like stools (a condition known as melena)

Hemoptysis Diagnosis

An essential part of diagnosing hemoptysis is ruling out hematemesis (vomiting of blood) and other forms of pseudohemoptysis (blood in the sputum that originates outside of the respiratory tract). Blood can originate in the back of the mouth (an area known as the oropharynx) or in the gastrointestinal tract.

After confirmation of hemoptysis, diagnosis involves differentiating among the possible causes of the bleeding, from lung cancer to bronchitis. The diagnosis involves a detailed medical history, laboratory tests, and a chest x-ray.

It may also involve a bronchoscopy or CT scan, depending on the nature of the hemoptysis and likelihood of cancer. If the underlying cause may be related to a vascular disorder (a blood vessel disorder), a pulmonary angiography may be done.

Medical history
The first part of the diagnosis is a thorough medical history. A history of the symptoms can provide important clues about the source of the blood and whether the patient is experiencing hemoptysis or pseudohemoptysis.

The doctor will ask about any abnormalities, from vomiting to the color of stools. They will also ask the patient about the color and consistency of the blood.

The physician will ask questions to find clues about what is causing the hemoptysis and how serious the condition is. The first questions involve the patient’s history of smoking and other cancer-related risk factors.

Because bronchitis, bronchiectasis, and TB are some of the most common causes of hemoptysis, these are usually the first causes that a physician suspects and must confirm or eliminate in the diagnosis. If the hemoptysis is mild, it is an indication of chronic bronchitis and if it is massive, it is an indication of bronchiectasis or TB.

What does the blood look like?
Although the blood that comes from the respiratory tract is usually bright red and frothy, its appearance and consistency can vary considerably. Sometimes this variation can provide important clues about the underlying disorder.

For example, if the patient is coughing up purulent sputum (thick, opaque, yellowish-white discharge) mixed with blood, the physician will likely suspect an underlying pulmonary infection. If the patient is spitting up blood without pus, the doctor will probably examine the likelihood of TB, cancer, or pulmonary infarction. If the blood is foul-smelling, it may indicate a lung abscess or infection. If the patient is coughing up pink, frothy sputum, they may have pulmonary edema.

Pattern of bleeding
The pattern of bleeding can provide helpful clues about what is causing the hemoptysis. For example, patients with bronchitis or bronchiectasis usually have recurrent, brief episodes. If the bleeding occurs monthly, it may be menstrual-related, known as catamenial hemoptysis.

Other symptoms
It is helpful for the physician to know about other symptoms that accompany the hemoptysis. Unexplained weight loss prior to the hemoptysis episodes may be an indication of cancer. A history of night sweats, fever, and general ill health suggests TB.

Risk factors for causative conditions
Because of the seriousness of
lung cancer, patients with hemoptysis should be evaluated for the likelihood of bronchogenic carcinoma. Risk factors include the following:

  • Male

  • Over 40 years of age

  • History of smoking

  • Hemoptysis that has lasted longer than a week

  • Coughing up large amounts of blood (more than about 30 mL per episode)

If a patient is at risk for lung cancer, more invasive diagnostic tests, such as a bronchoscopy with biopsy, are indicated.

It is also helpful to evaluate risk factors for illnesses other than cancer. If, for example, the patient has traveled recently where there is an infectious agent (parasite, virus, fungus, bacteria) known to cause hemoptysis, this is helpful information to the physician. It is also important to know if the patient has experienced any trauma to the chest.

Diagnosis of Hemoptysis

Laboratory Tests for Hemoptysis

A variety of laboratory tests may be done to help in the diagnosis. They usually involve collecting bodily fluids (blood, urine, coughed-up sputum) and looking at them through a microscope or analyzing their components using specialized machinery.

Depending on the medical history and symptoms, laboratory tests might include a complete blood count (an analysis of the various components of the blood), a coagulation profile (an analysis of the clotting capabilities of the blood), an AFB smear (a test that looks for the presence of mycobacterium in the sputum), a sputum culture (a test for other signs of infection in the sputum), arterial blood gas studies (measuring the levels of oxygen and carbon dioxide in the blood), and urinalysis (a test that examines the urine).

If there is still any question about whether the patient is experiencing hemoptysis or hematemesis, these tests can confirm the diagnosis. For example, if the pH of the blood is alkaline, the patient likely has hemoptysis, and if the blood is acidic, the patient probably has pseudohemoptysis.

If alveolar macrophages (immune system cells in the alveoli—the lung’s first line of defense against the foreign particles in the air) are present in the sputum, the blood is likely hemoptysis, and if there are food particles, it is likely hematemesis.

Chest X-ray to Diagnose Hemoptysis

The chest x-ray is an integral part of the diagnosis and involves exposing the chest to radiation to produce an image of the lungs, heart, bones, and other tissue in the chest region. The radiologist (a physician trained to read and interpret x-ray images) can spot abnormalities that may be related to the hemoptysis.

Certain radiological features are helpful iarrowing the diagnostic choices or confirming a particular diagnosis. Many relatively mild causes of hemoptysis present with a clear chest x-ray. However, other diagnostic tests, including laboratory tests and possibly a bronchoscopy, may be indicated if the cause of the bleeding cannot be determined.

CT Scan to Diagnose Hemoptysis

A CT scan (also known as a “CAT” scan, computerized axial tomography) is a painless procedure that uses x-ray images with the aid of a computer to obtain 3-dimensional, cross-sectional pictures of the internal anatomy. A chest CT produces more detailed pictures than a normal chest x-ray and is more sensitive to abnormalities that may not be present on the chest x-ray.

Some physicians recommend CTs only when abnormalities show up on the chest x-ray or the patient is at risk for cancer. Because of its detailed sensitivity and diagnostic power, others think CTs should always be performed. Chest CT benefits vary and it is especially helpful for diagnosing bronchiectasis (see bronchiectasis). If a doctor suspects bronchiectasis (the patient is less than 40 years old and is not at risk for cancer), a chest CT may be indicated.

Fiberoptic Bronchoscopy (with or without biopsy) to Diagnose Hemoptysis

Bronchoscopy involves inserting a flexible tube through the mouth or nose, into the airway, and into the lungs. It enables the doctor to view the tissue inside the lungs (directly or on a monitor) and biopsy (collect a small sample) abnormal tissue for microscopic examination. The tissue is later examined under a microscope to confirm the diagnosis. The procedure is painless (patients are given relaxation medication and a local anesthetic) and takes from 15 minutes to an hour.

There are several different ways to biopsy the airway or lung tissue. If the abnormal area is on the wall of an airway, the tissue can be washed with a saline solution and suctioned, or it can be brushed with a soft brush. If the abnormal tissue is not easily accessible, a needle biopsy or a forceps biopsy is usually done.

A needle biopsy involves using a small needle to collect cells on the other side of the airway wall. A forceps biopsy involves using forceps to sample an area of tissue.

If the lesion or abnormal tissue is deep within the lung, a technique called fluoroscopy may be used during the bronchoscopy. Fluoroscopy involves using x-rays to examine tissue deep within the body and guide the biopsy. Once the biopsy is done, the tissue sample is sent to the laboratory for microscopic evaluation, the cells are observed, and abnormalities detected.

The decision to perform a bronchoscopy depends on several factors, including the patient’s risk factors for lung cancer, the timing of the procedure, and the risks associated with bronchoscopy. Patients should discuss the procedure thoroughly with the physician before making a decision.

There is general agreement that if potentially cancerous abnormalities are found on the chest x-ray, a patient with hemoptysis should have a bronchoscopy. A bronchoscopy allows the physician to examine the lung and bronchial tissue and collect samples of abnormal or potentially cancerous tissue.

About 30% to 60% of bronchogenic cancer patients have hemoptysis, so if the chest x-ray shows a potential malignancy (cancerous growth), the bronchoscopy is an important diagnostic tool.

There is controversy about whether a bronchoscopy is necessary if no abnormalities are detected on the chest x-ray. About 5% of hemoptysis patients who do not have bronchoscopies do have cancer. Certain risk factors for cancer may indicate the need for a bronchoscopy, including: the patient is male; older than 40 years old; has a history of smoking; has long-lasting hemoptysis (more than a week); and has spit up more than 30 mL of blood per episode.

If no abnormalities are seen on the chest x-ray and the patient is not at risk for lung cancer, is a bronchosocpy necessary or recommended? If the bleeding has been persistent, a bronchoscopy is probably a good idea. If the patient is not at risk for lung cancer, and the bleeding has not been persistent, a bronchoscopy most likely would prove unnecessary.

Some physicians think that it is very important that the bronchoscopy be done early on. It is usually easier to localize the source of the bleeding if the procedure is done less than 48 hours after the onset of bleeding. It is not clear that the timing of the bronchoscopy affects the clinical diagnosis, but an early bronchoscopy allows more immediate treatment.

As in any medical procedure, there are potential complications; but, the complications of this procedure are rare and usually minor. They include nosebleed, vocal cord injury, temporary lack of oxygen, heart injury (due to either the lack of oxygen or medication), bleeding from the site where the tissue is sampled, and a punctured lung.

Rigid Bronchoscopy to Diagnose Hemoptysis

Rigid bronchoscopy has largely been replaced by the newer, less invasive, easier fiberoptic techniques. It is still sometimes used for cases of massive hemoptysis, since the optics are better (providing better visibility through the blood) and the suction channel is better (making it easier to clean out the blood so the source of the bleeding can be seen and biopsied). A rigid bronchoscopy requires general anesthesia, meaning the patient is unconscious during the procedure.

Pulmonary Angiography to Diagnose Hemoptysis

Angiography is the use of x-rays to produce a picture called an “angiogram.” It requires injecting a radiopaque substance (a contrast agent, or dye, that is impenetrable to x-rays) into the blood vessels, making them easier to see than in a conventional x-ray. Angiograms are most commonly used to examine the coronary arteries in patients with coronary artery disease; but they can also be used to examine the lungs in patients with hemoptysis. The lungs receive their blood supply from the pulmonary arteries and the bronchial arteries.

In cases of bronchiectasis, a bronchial angiogram may be performed instead of, or as well as, a pulmonary angiogram. The technique is sometimes used to diagnose vascular causes of hemoptysis (i.e., causes related to abnormalities or blockage in the blood vessels).

Treatment

Treatment for hemoptysis depends on the cause and the quantity of blood. Infrequent, mild hemoptysis usually does not require specific, immediate treatment, but it should always be thoroughly investigated in case the underlying disorder is life threatening. There is no way to predict whether a patient with mild hemoptysis will experience massive, life-threatening hemoptysis, so it is very important that the underlying cause be determined and treated.

Massive, or major, hemoptysis is a medical emergency. Death can result, usually from asphyxiation (impaired gas exchange in the lungs, leading to a lack of oxygen and excess of carbon dioxide in the body). In massive hemoptysis, steps are usually taken to localize the source of the bleeding, control the bleeding, and assure that the patient is able to breathe.

Some methods of controlling bleeding include: Bronchial artery embolization, surgical resection, and bronchoscopic laser therapy.

For mild or moderate hemoptysis in patients who have chronic bronchitis, bronchiectasis, or tuberculosis, treatment usually involves antibiotics. For bronchogenic carcinoma, treatment depends on the stage of the cancer.

In the 20% to 30% of cases that do not have an indentifiable underlying cause, treatment should be fairly conservative and the hemoptysis carefully monitored for at least 2 or 3 years after the initial diagnosis. In 90% of patients who have a normal chest x-ray and bronchoscopy, the hemoptysis usually disappears within 6 months.

For chronic hemoptysis, the treatment is dependent on the symptoms and causes. Sometimes all that is necessary is switching antibiotics. In other instances, more aggressive treatment may be necessary.

Bronchial artery embolization involves injecting substances into the bloodstream to stop blood flow. It is a proven technique for stopping life-threatening massive hemoptysis and can have beneficial long term effects as well, although it is not always successful and is not without complications.

Surgical resection is the surgical removal of the abnormal tissue causing the hemoptysis. It is often recommended as an early treatment for hemoptysis caused by aspergilloma.

Bronchoscopic laser therapy involves using laser therapy during a bronchoscopy to remove tumors and lesions or widen airways.

All of these techniques have proved beneficial in controlling or curing hemoptysis due to bronchiectasis or other inflammatory disorders. The pros and cons of the various techniques depend on the skill of the doctor performing the procedure and the availability of the necessary equipment. The patient should discuss the various procedures thoroughly with their primary physician, thoracic surgeon, and radiologist.

Follow-Up for Hemoptysis

Follow-up depends on the cause and severity of the hemoptysis. Patients should discuss the need for return appointments with the physician.

If, for example, a mild case of hemoptysis due to bronchitis, TB, or bronchiecstasis becomes chronic after treatment with antiobiotics, a different antibiotic may be needed or more agressive treatment may be necessary.

If the underlying cause of the hemoptysis is unknown (cryptogenic hemoptysis), the hemoptysis should be carefully monitored for 2–3 years following initial treatment. This monitoring may involve routine chest x-rays.

 

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