Complications
Pleural effusion can be classified into three stages: exudative (a simple parapneumonic effusion); fibrinopurulent (complicated parapneumonic effusion); organising (with features of fibroblastic activity and peel formation).[2]
Suspect effusion if auscultation reveals absent or severely decreased breath sounds with a dull percussion note.[2][3][9] Fremitus is reduced in pleural effusion.[2]
If parapneumonic effusion is suspected in a child with CAP, order chest x-rays to confirm the presence of pleural fluid.[1][19] Signs of parapneumonic effusion include blunting of the costophrenic angle and a rim of fluid ascending the lateral chest wall (meniscus sign). Large effusions can appear as a complete white-out.[2] If the chest radiograph raises suspicion of effusion, chest ultrasound is recommended for confirmation.[2][19]
Small parapneumonic effusions often resolve with a prolonged course of antibiotic therapy, preventing progression to empyema.[2][19] Large effusions and empyemas may require percutaneous aspiration, fibrinolytics, surgical drainage, or thoracoscopy.[19]
Pleural drainage, ideally ultrasound-guided, should be done if effusions are symptomatic (e.g. respiratory distress) or contain loculations.[1][2]
Empyema is an advanced stage of parapneumonic effusion, with a complicated outcome. In empyema, effusions are initially exudative; without treatment they become fibro-purulent, loculated, and infected. Ongoing fibroblastic growth causes a thick peel to form over the visceral pleura, preventing lung expansion.[3]
Suspect empyema if fever persists beyond 7 days or does not start settling after 48 hours of adequate antibiotic therapy.[3][9] Chest radiography will reveal fluid in the pleural space, and ultrasound can be used to establish the extent of fluid.
Children with empyema should be referred to a centre with expertise in the management of complicated CAP.[2][3] Non-operative intervention with fibrinolytics is the recommended first-line option in complicated parapneumonic effusion and empyema.[75][76] Information from pleural space imaging and drainage should guide the decision on whether to administer intrapleural fibrinolytics. Fibrinolytics are often administered.[2][77] Video-assisted thoracoscopic surgery (VATS) is reserved for children who do not respond to non-operative interventions (e.g., persistent fever, sepsis, or respiratory distress, or when repeat imaging shows persistent or increasing intrapleural collections or an organising phase with peel formation).[1][2][75] VATS is associated with a slightly shorter length of stay and reduced need for re-intervention compared with chest drain plus fibrinolytic therapy.[2][78] However, it is not widely available.
Necrotising pneumonia is characterised by extensive destruction and liquefaction of pulmonary tissue, despite antibiotic treatment.[2] Its precise pathophysiology remains unclear.[2]
The initial stage involves consolidation with necrosis. This progresses to cavitation (pneumatoceles), which is usually peripheral and limited to a single lobe. Cavities then coalesce to form large cysts with air-fluid levels, mimicking a lung abscess.[2] Rupture of the cysts into the pleural space can create a bronchopleural fistula.[2]
Necrotising pneumonia is often associated with Staphylococcus aureus strains that produce Panton-Valentine leukocidin (PVL) toxin, with a high risk of mortality.[2][9] A previous viral respiratory infection can increase the risk for developing necrotising pneumonia.
Children with necrotising pneumonia are usually unwell with a high fever, cough, tachypnoea, hypoxia, mild anaemia, and hypoalbuminemia.[2][3]
Suspicion of necrotising pneumonia may be raised by the chest x-ray findings, and the diagnosis can be confirmed by computed tomography (CT) scan.[2] Note that the initial phase of necrotising pneumonia is difficult to detect on chest x-ray because fluid-filled cavitary lesions have the same density as adjacent consolidated lung. On chest CT, necrotising pneumonia will show as a rapid transition from a thin-walled fluid-filled compartment to cavitation. Lung abscess will show as a thick-walled compartment with fluid, with or without air.[2]
Referral to a tertiary centre with specific expertise in management of complicated CAP is recommended.[2][3]
The onset of influenza-like symptoms, haemoptysis, erythematous rash, and declining peripheral white blood cell counts are signs of possible deterioration.[2] Intensive care unit (ICU) care is frequently needed.[1] Affected children may experience respiratory distress, septic shock, multi-organ involvement, or acute respiratory distress syndrome requiring circulatory and ventilatory support and sometimes extracorporeal membrane oxygenation.[2]
In children with necrotising pneumonia, chest drains are only used if the child also has a large empyema because of the high risk of bronchopleural fistula.[2] Intrapleural fibrinolytics should be avoided because the breakdown of fibrin may result in air leaks from peripheral necrotic parts of the lung.
Lung abscess is a rare complication of CAP, but the risk is higher in children with a pre-existing congenital cystic lung malformation or immunodeficiency.[2]
Progression from disease onset is usually slow, resulting in a single, thickly walled cavity containing purulent material.[2] Pneumothorax, bronchopleural fistula, lung compression, and mediastinal shift can complicate lung abscess.
Children with lung abscesses usually present with protracted low-grade fever and cough. Chest pain, dyspnoea, sputum production, and occasionally haemoptysis may also be present.[2] On chest x-ray, the abscess may show as a well-defined, thick-walled cavity, often containing an air-fluid level. However, abscesses can be difficult to distinguish from consolidation.
In most cases, a prolonged course of appropriate antibiotics is effective.
In children with lung abscesses resistant to antibiotic treatment, a combination of image-guided drainage of the cavitation through a pigtail catheter together with systemic antimicrobial therapy can be used.[2]
Sepsis in children often presents initially with non-specific symptoms, especially in younger age groups. The diagnosis should be considered in any child with a suspected infection who has signs of a systemic response, which may be indicated by a change in physiological observations (e.g., abnormal core temperature, tachycardia or bradycardia, tachypnoea), an altered mental state, or a change in the child's normal behaviour.[79][80] Older children may present with a clearer focus of infection.
Progression to organ failure and shock can occur very rapidly, so early recognition and treatment is crucial. Vasoconstrictive shock is characterised by constricted systemic vasculature, resulting in cold peripheries, prolonged capillary refill time, increased core-toe temperature gap, and weak pulses. Blood pressure is usually preserved but the patient is typically tachycardic.[81] In vasodilatory shock, capillary refill time is brisk and pulses are usually full or bounding. Pulse pressure is high (due to a low diastolic blood pressure) and the patient is usually tachycardic.[81]
Use of care bundles is recommended to ensure prompt and appropriate management of sepsis. These encompass blood cultures, administration of supplementary oxygen if needed, prompt use of intravenous antibiotics, consideration of fluid resuscitation, and use of vasoactive/inotropic support if required to restore normal physiological parameters.[82]
Atelectasis is the partial or complete collapse of a lung. It can occur secondary to mucus plugging in CAP, and it can be due to alveolar deflation as well as accumulation of alveolar fluids.
Flexible bronchoscopy has been shown to be beneficial in persistent atelectasis associated with CAP.[83]
ARDS is a non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness, and presents with a severe hypoxaemia refractory to supplemental oxygen therapy that usually occurs within 72 hours of an acute inflammatory lung condition. Diagnosis is based on fulfilling three main criteria: acute onset (within 1 week); bilateral opacities on chest x-ray or CT, or bilateral B lines and/or consolidations on ultrasound not fully explained by effusions, atelectasis, or nodules/masses; PaO₂/FiO₂ (arterial to inspired oxygen) ratio ≤300 or SpO₂/FiO₂ (pulse oximetric saturation to inspired oxygen) ratio ≤315.[84]
Mortality rates range from 10% to 90%.[85]
SIADH is characterised by excessive release of antidiuretic hormone from the posterior pituitary gland leading to euvolaemic, hypotonic hyponatraemia.[86] Clinically, the patient shows neurological symptoms with altered mental state and sometimes seizures.[87] The mainstay of management is to remedy hyponatraemia with salt administration and/or fluid restriction.
HUS is a very rare complication of CAP. It is usually associated with Streptococcus pneumoniae serotype 3 in patients with parapneumonic effusion.[2] The majority of cases occur in children <2 years old.[88]
Suspect HUS in cases of CAP associated with anaemia, thrombocytopenia, and renal dysfunction (anuria).[9] In most cases (75%), these patients require dialysis.[2]
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