Consolidation

Published on 02/04/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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103 Consolidation

Instruction

Examine this patient’s chest.

Salient features

History

• Abrupt onset of symptoms

• Cough with purulent sputum

• Fever with sweating or rigors

• Pleuritic chest pain (p. 355)

• Shortness of breath

• Haemoptysis

• Nausea, vomiting, diarrhoea (consider legionella infection)

• Mental status changes (especially in the elderly).

Examination

• Purulent sputum (if bacterial in aetiology)

• Tachypnoea

• Reduced movement of the affected side

• Trachea central

• Impaired percussion note

• Bronchial breath sounds

• Crackles.

Diagnosis

This patient has left lower lobe consolidation with purulent sputum (lesion) indicating a bacterial pneumonia (aetiology) and her CURB65 score is zero (functional status).

Questions

What is the aetiology?

• Bacterial pneumonia

• Bronchogenic carcinoma

• Pulmonary infarct.

How would you investigate suspected bacterial pneumonia?

• FBC, serum urea, electrolytes and liver function tests

• Sputum and blood cultures

• Arterial blood gases

• Chest radiography (Fig. 103.1)

• Test for Legionella (culture, direct fluorescent-antibody test or urinary antigen assay), mycoplasma immunoglobulin M

• Consider serological testing for HIV (for patients 15–54 years, particularly when there is lymphopenia or a low CD4 cell count).

image

Fig. 103.1 Air bronchograms in a collapsed and consolidated right lower lobe.

(With permission from Adam et al. 2008.)

Advanced-level questions

How do you determine the severity?

Using the CURB65 severity score, 1 point for each feature present:

• Confusion

• Urea> 7 mmol/l

• Respiratory rate ≥30/min

• BP (systolic <90 mmHg or diastolic ≤60 mmHg)

• Age ≥65 years.

The prognosis based on CURB65 score:

4 or 5: assess with specific consideration to the need for transfer to a critical care unit

≥3: high risk of death

2: moderate risk of death; considered for short-stay inpatient treatment or hospital-supervised outpatient treatment

0 or 1: low risk of death; may be suitable for therapy at home.

The CURB65 severity score should be interpreted in context of the overall clinical picture.

What are the causes of a poorly resolving or recurrent pneumonia?

• Carcinoma of the lung

• Aspiration of a foreign body

• Inappropriate antibiotic

• Sequestration (rare; suspect if left lower lobe is involved).

What do you know about atypical pneumonias?

Typical pneumonia is caused by the pneumococcus (Streptococcus pneumoniae), whereas atypical pneumonia is that not resulting from pneumococcus infection; it may be caused by Mycoplasma, Legionella, Chlamydia, Coxiella spp. The clinical picture in atypical pneumonia is dominated by constitutional symptoms, such as fever and headache, rather than respiratory symptoms.

What do you know about mycoplasma pneumonia?

Mycoplasma pneumoniae is an important cause of atypical pneumonia. It is important community-acquired pneumonia and epidemics are seen every 4 years or so. Its incubation is 2–3 weeks and it is usually seen in children and young adults. Reinfection can occur in older patients with detectable M. pneumoniae antibody. Like all other pneumonias, mycoplasma pneumonia is common in winter months.

What are the extrapulmonary manifestations of mycoplasma pneumonia?

• Arthralgia and arthritis

• Autoimmune haemolytic anaemia

• Neurological manifestations involving both central and peripheral systems

• Pericarditis, myocarditis

• Hepatitis, glomerulonephritis

• Non-specific rash, erythema multiforme and Stevens–Johnson syndrome

• Disseminated intravascular coagulation (DIC).

What are the complications of pneumonia?

• Septicaemia

• Lung abscess

• Empyema

• Adult respiratory distress syndrome

• Multiorgan failure, renal failure

• Haemolytic syndrome

• Death.

Which antibiotics would you use in a patient with community-acquired pneumonia where the pathogen is not known?

The British Thoracic Society recommends that empirical therapy ‘should always cover’ S. pneumoniae. The preferred regimen is amoxicillin or pencillin; when Legionella sp. or M. pneumoniae is specifically suspected, erythromycin should be given, and antibiotics directed against Staphylococcus aureus should be considered during epidemics of influenza.

What are the poor prognostic factors in patients with community-acquired pneumonia?

• Age >65 years

• Coexisting conditions such as cardiac failure, renal failure, COPD, malignancy

• Clinical features: respiratory rate >30 breaths/min, hypotension (systolic BP <90 mmHg or diastolic BP <60 mmHg), temperature >38.3°C, impaired mental status (stupor, lethargy, disorientation or coma), extrapulmonary infection (e.g. septic arthritis, meningitis)

• Investigations: haematocrit <30%, white cell count <4 or >30 × 106 cells/l, azotaemia, arterial blood gas <60 mmHg while breathing room air, chest radiograph showing multiple lobe involvement, or rapid spread or pleural effusion

• Microbial pathogens: S., Legionella sp., S. pneumoniae.

What do you know about Panton–Valentine leukocidin-producing Staphylococcus aureus?

Panton–Valentine leukocidin-producing S. aureus (PVL-SA) infection causes very severe pneumonia, resulting in rapid lung cavitation and multiorgan failure. Affected patients often require admission to the critical care unit. In patients with suspected necrotizing pneumonia, the antibiotic regimen should include include a combination of intravenous linezolid 600 mg twice daily, intravenous clindamycin 1.2 g four times a day and intravenous rifampicin 600 mg twice daily in addition to the initial empirical antibiotic regimen. As soon as PVL-SA infection is either confirmed or excluded, antibiotic therapy should be narrowed accordingly.

What do you know about pulmonary eosinophilic disorders?

Crofton et al. (1952) described five classes of pulmonary eosinophilic disorder (Thorax 1952;7:1–35).

Löffler syndrome. This is characterized by transient pulmonary infiltrates and peripheral eosinophilia. It is associated with parasitic infections, drug allergies and exposure to inorganic chemicals such as nickel carbonyl. The course is benign and respiratory failure almost unknown.

Eosinophilia in asthmatics. The most common cause is allergic bronchopulmonary aspergillosis. This condition is benign but chronic.

Tropical eosinophilia. This is secondary to filarial infection (Wuchereria bancrofti or W. malayi brugi).

Churg–Strauss syndrome. Diagnosis requires four of the following features: asthma; eosinophilia >10%, mononeuropathy or polyneuropathy; paranasal sinus abnormality; non-fixed pulmonary infiltrates visible on chest radiographs; and blood vessels with extravascular eosinophils found on biopsy.

Chronic eosinophilic pneumonia. This chronic debilitating illness is characterized by malaise, fever, weight loss and dyspnoea. The chest radiograph shows a peripheral alveolar filling infiltrate predominantly in the upper lobes (the ‘photographic negative’ of pulmonary oedema).

What do you know about bronchopulmonary sequestration?

It is an uncommon congenital lesion in which a portion of non-functioning lung tissue is detached from the normal lung and supplied by an anomalous systemic artery, usually arising from the aorta or one of its branches. The tissue has no communication with the bronchopulmonary tree. Two types of sequestration have been described: extralobar and intralobar. An extralobar sequestration has its own pleural lining, which separates it from the remaining lung tissue, and the intralobar type shares its pleura with the adjacent normal lung. Patients usually present in childhood with cough and recurrent pneumonia, and occasionally present with haemoptysis.

What is the pathogenesis of ventilator-acquired pneumonia?

Hospital-acquired pneumonia. Micro-aspiration is the primary route of bacterial entry into the lower respiratory tract. Risk factors include sedation, intubation for operative procedures, vomiting and impaired swallowing.

Ventilator-associated pneumonia. Leakage of bacteria and oral secretions around the endotracheal cuff, inhalation of contaminated aerosols, or reflux of contaminated ventilator tubing condensate are the primary routes of bacterial entry into the lower respiratory tract. Promising biomarkers include procalcitonin, C-reactive protein and soluble triggering receptor expressed on myeloid cells (sTREM-1).

Outcomes. The ‘battlefield’ between the pathogens entering the lower respiratory tract and the host defences determines possible outcomes: colonization, tracheobronchitis or hospital/ventilation-acquired pneumonia.

What do you understand by the term healthcare-associated pneumonia?

Pneumonia acquired in the community by patients who have had direct or indirect contact with a healthcare or long-term care facility and are subsequently hospitalized. These patients are more likely to have a coexisting illness and to receive ineffective empirical antibiotic therapy and are at greater risk for mortality than patients who have true community-acquired pneumonia. Therefore, a broader spectrum of antibiotics (especially against Psudomonas aeruginosa, other multidrug-resistant Gram-negative bacilli, and drug-resistant S. aureus) may be needed.

Further reading

Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med. 1995;333:1618-1624.

British Thoracic Society. Guidelines for the management of community-acquired pneumonia in adults admitted to hospital. Br J Hosp Med. 1993;49:346-350.

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