bubble_chart Overview

Acute pneumonia is a common disease in childhood, with severe pneumonia being one of the leading causes of death in infants and young children. In recent years, the integration of Chinese and Western medicine has significantly reduced the mortality rate. Clinically, it is often classified based on pathology, etiology, condition, and course of the disease. Acute bronchopneumonia is most common in infants and young children. This section mainly discusses bronchopneumonia in children.

bubble_chart Etiology

(1) Disease Cause

Pathogenic viruses are the main causative agents of this disease. In the past, adenovirus types 3 and 7 were common in northern China, with type 7 often leading to severe pneumonia. Recently, adenovirus infections have shown a declining trend, while respiratory syncytial virus has risen to the top. Other viruses such as parainfluenza virus, influenza virus, and rotavirus have also been reported to cause pneumonia.

Many bacteria can cause bronchopneumonia, often secondary to viral infections, though some cases are primarily bacterial. Common bacteria include pneumococcus, Staphylococcus aureus, hemolytic streptococcus, and large intestine bacillus. Haemophilus influenzae can also cause pneumonia, while other bacterial infections are rare.

Mycoplasma pneumoniae pneumonia is more common in older children, while fungal pneumonia is more likely to occur in infants and young children who have long-term misuse of antibiotics or adrenal corticosteroids, as well as in malnourished patients.

(2) Predisposing Factors

1. Physiological and anatomical factors of the pediatric respiratory tract: The nasopharynx, trachea, and bronchi are narrow, mucus secretion is low, ciliary movement is poor, lung tissue differentiation is incomplete, elastic fibers are underdeveloped, compensatory capacity is weak, alveoli are few, and interstitial tissue is highly developed. As a result, there is less air and more blood in the lungs. These characteristics are more pronounced in infants. Coupled with an underdeveloped immune system, they are more susceptible to bronchopneumonia.

2. Disease impact: The overall health condition of the body is closely related to the occurrence of pneumonia. Particularly in cases of malnutrition, rickets, anemia, congenital heart disease, or cerebral dysplasia—conditions where the body's resistance and immunity are low—pneumonia is more likely to develop.

3. Environmental factors: Sudden climate changes, poor ventilation in living spaces, and air pollution, among others.

bubble_chart Pathogenesis

(1) Infection and Toxemia Can cause high fever, listlessness, loss of appetite, and damage to other organ systems.

When inflammation spreads downward through the bronchi and bronchioles to the alveoli, pneumonia develops. At this time, the bronchial mucosa is often inflamed and edematous, narrowing the bronchial lumen. The alveolar walls thicken due to congestion, and the alveolar spaces fill with inflammatory exudate, impairing ventilation and increasing gas diffusion resistance. The accumulation of secretions in the small bronchial lumens, combined with poor ciliary development and motility, weakens the ability to clear secretions, further narrowing or even obstructing the small airway lumens. This leads to obstructive lung qi distension or localized atelectasis, exacerbating ventilation and gas diffusion disorders, ultimately resulting in hypoxia and carbon dioxide retention, which affect systemic metabolic processes and the function of vital organs.

(2) Hypoxemia When the entry of air into the alveoli and the diffusion of oxygen from the alveoli to the bloodstream are impaired, blood oxygen levels decrease. The partial pressure of oxygen (PaO2) and oxygen saturation (SaO2) drop. When SaO2 falls below 85%, it is termed hypoxemia. When reduced hemoglobin exceeds 5.0 g/dL (50 g/L), cyanosis appears. If carbon dioxide elimination is also severely impaired, respiratory failure is likely to occur.

(3) Cardiovascular System Hypoxemia and carbon dioxide retention can cause reflexive contraction of pulmonary small stirred pulse, increasing pulmonary circulation pressure and forming pulmonary stirred pulse hypertension, thereby加重ing the right heart's workload. Additionally, pathogen toxins can act on the myocardium, causing toxic myocarditis. Pulmonary stirred pulse hypertension and toxic myocarditis are major predisposing factors for heart failure. Severe pneumonia can lead to microcirculatory disorders. Due to severe hypoxia, acidosis, and the effects of pathogen toxins, micro stirred pulse spasms may occur, causing blood stasis, slowed blood flow, opening of arteriovenous shunts, and impaired material exchange between blood and cells. Cells become hypoxic, and carbon dioxide cannot be eliminated. In the advanced stage, capillaries dilate, blood flow slows, arteriovenous shunts open, and material exchange between blood and cells is impaired. Cells remain hypoxic, and carbon dioxide cannot be expelled. In the advanced stage, capillaries dilate, blood flow stagnates, and fluid leaks from vessels into interstitial spaces, causing tissue edema. Blood thickens, effective circulating volume decreases, and venous return to the heart declines, reducing cardiac output and leading to shock or worsening heart failure. Microcirculatory disorders can also induce shock.

(4) Nervous System Hypoxia and carbon dioxide retention can dilate cerebral capillaries, increase blood-brain barrier permeability, and disrupt brain cell metabolism. The sodium pump fails, preventing sodium excretion and potassium retention, leading to intracellular sodium and water retention in brain cells. This causes cerebral edema or even brain herniation, which can suppress the respiratory center, resulting in central respiratory failure and worsening pneumonia.

(5) Acid-Base Imbalance Severe hypoxia disrupts aerobic metabolism, increasing acidic metabolic byproducts. In pneumonia, factors such as high fever, reduced food intake, starvation, and dehydration often lead to metabolic acidosis. Concurrently, carbon dioxide retention can cause respiratory acidosis. Thus, severe pneumonia often involves varying degrees of both metabolic and respiratory acidosis.

(6) Gastrointestinal Dysfunction Hypoxemia and pathogen toxins can disrupt gastrointestinal function, increasing capillary permeability and causing gastrointestinal bleeding or even toxic intestinal paralysis.

bubble_chart Clinical Manifestations

Due to differences in pathogens and host responses, the clinical manifestations vary in severity.

(1) Mild Bronchopneumonia The onset may be acute or gradual, often preceded by upper respiratory infection symptoms, but it can also occur suddenly.

1. Fever Most cases present with high fever, around 39-40°C, irregular and variable in pattern, often remittent. Infants with rickets or malnutrition may not exhibit high fever; newborns with pneumonia may even show hypothermia.

2. Cough This is an early symptom, starting as frequent, irritating dry cough, followed by phlegmy sounds in the throat. Coughing may be accompanied by vomiting or choking during feeding.

3. Shallow and rapid breathing, flaring nostrils, and grade I cyanosis around the mouth or nails in some children.

4. Pulmonary signs Early signs are subtle, with only coarse or slightly diminished breath sounds. After a few days, medium or fine moist rales may be heard, especially fine moist rales, which are more prominent at the lung bases and paravertebral regions, becoming clearer at the end of deep inspiration. When large areas of the lungs become consolidated, increased vocal fremitus, dullness on percussion, diminished breath sounds, or tubular breath sounds may appear as signs of lung consolidation.

Apart from respiratory symptoms, children may also experience lethargy, dysphoria, restlessness, poor appetite, chills, diarrhea, and other systemic symptoms. With timely and appropriate treatment, recovery usually occurs within two weeks.

(2) Severe Pneumonia In addition to worsening symptoms of mild pneumonia, persistent high fever and severe systemic toxic symptoms are present, along with damage to other organ functions.

1. Respiratory symptoms Children exhibit shallow, rapid breathing, with rates exceeding 80 breaths per minute, pronounced nasal flaring, and marked retractions at the suprasternal, supraclavicular, intercostal, and subxiphoid regions during respiration, known as "three depressions." Severe cases may develop head-nodding respiration or expiratory groaning, with obvious cyanosis of the face and extremities, or even pallor or grayish complexion. Dense fine moist rales can be heard in both lungs.

2. Circulatory symptoms Infants with pneumonia often experience cardiac insufficiency, manifested as: (1) Sudden worsening of dyspnea, with respiratory rates exceeding 60 breaths per minute, unexplained by respiratory disease alone. (2) Sudden dysphoria, restlessness, pallor, or cyanosis unrelieved by oxygen or sedatives. (3) Sudden tachycardia, exceeding 160 bpm in infants or 180 bpm in newborns, unexplained by fever or hypoxia. (4) Muffled heart sounds, gallop rhythm, or cardiomegaly. (5) Rapid liver enlargement (>1.5 cm in a short time) with soft texture. (6) Sudden increase in lung rales, possibly accompanied by jugular vein distension, facial or limb edema, and oliguria.

3. Neurological symptoms (1) Dysphoria, drowsiness, staring, strabismus, or upward gaze. (2) Lethargy, unconsciousness, or convulsions. (3) Bulbar conjunctival edema. (4) Pupillary changes, sluggish or absent light reflex. (5) Irregular breathing patterns. (6) Bulging anterior fontanelle, meningeal irritation signs. Cerebrospinal fluid pressure is elevated, but other parameters are normal, indicating toxic encephalopathy. Severe cases may develop higher intracranial pressure, leading to brain herniation.

4. Digestive symptoms Children may exhibit decreased appetite, vomiting, diarrhea, abdominal distension, and fullness. Severe cases may vomit coffee-ground material or have hematochezia, with absent bowel sounds, toxic intestinal paralysis, or toxic hepatitis.

5. Metabolic acidosis, respiratory acidosis, or mixed acidosis may occur. Additionally, DIC may develop.

(3) Clinical Features of Different Types of Pneumonia

1. Neonatal Pneumonia

Neonatal pneumonia is a common condition and a significant cause of neonatal mortality.

Clinical manifestations vary depending on the disease cause. Aspiration pneumonia presents with varying degrees of dyspnea and cyanosis. Infectious neonatal pneumonia is divided into intrauterine infection and postnatal infection, with the latter being more common. General symptoms include poor responsiveness or irritability, drowsiness or restless sleep, refusal to feed or poor feeding, fever or hypothermia, pale or grayish complexion, and cold extremities or mottled skin. Respiratory symptoms are often inconspicuous, but may include cough, frothing at the mouth, perioral cyanosis, and tachypnea. In severe cases, nasal flaring, retractions, head nodding, and expiratory grunting may occur. Only some patients may exhibit crepitations or fine moist rales on lung auscultation. Dullness on percussion suggests complicating empyema, while sudden cyanosis or dyspnea may indicate pneumothorax.

Although neonatal pneumonia has various types, the treatment principles and methods are similar. However, the condition changes rapidly and requires close observation.

2. Staphylococcus aureus pneumonia

It is caused by the hematogenous spread of a local Staphylococcus aureus infection in the body, leading to pulmonary infection. The pathological changes are characterized by widespread hemorrhagic necrosis and multiple small abscesses. The clinical manifestations are severe and are most common in infants under 1 year of age. After respiratory or skin infections, there is a sudden persistent high fever, while older children may have prolonged high fever, and newborns may exhibit low-grade fever, no fever, or even hypothermia. The onset is acute, with early respiratory symptoms, rapid progression of pneumonia, and mottled skin with measles-like or scarlet-like rashes. Vomiting, diarrhea, abdominal distension, and fullness (drum-like) may occur. The child may be dysphoric or drowsy, and in severe cases, convulsions or shock may occur. Lung signs appear early, and the clinical symptoms may not match the chest X-ray findings. Initially, the clinical symptoms are severe, but X-ray signs are minimal. As the clinical symptoms improve, pulmonary bullae may appear on X-ray. The disease progresses rapidly, and within hours, lung abscesses, pulmonary bullae, empyema, or pyopneumothorax may develop. In severe cases, mediastinal emphysema, subcutaneous emphysema, or bronchopleural fistula may occur.

The total white blood cell count is 20–30×10^9/L, with neutrophils accounting for 0.9 and toxic granules present. If the total white blood cell count is below 0.5×10^9/L, the prognosis is poor.

The detection of Staphylococcus aureus is definitive for diagnosis. Positive results can be obtained from cultures of skin or tissue abscess puncture fluid, blood, or pleural puncture fluid. Blood cultures should be performed before antibiotic use, with a positive rate of about 10–30%. Treatment: Selecting effective antibiotics, oxygen therapy, and supportive care are crucial for prognosis. Complications such as pulmonary emphysema, lung abscess, empyema, or pyopneumothorax worsen the prognosis. Infants are prone to tension pneumothorax or pyopneumothorax, which carry a more severe prognosis.

3. Adenovirus Pneumonia

The clinical features of this disease include severe illness, slow recovery, and a relatively high mortality rate, though its incidence has declined in recent years. It often occurs in winter and spring, especially winter, and is common in infants aged 6 months to 2 years. Most cases have an acute onset, with body temperature rising to 39–40°C within 1–2 days and remaining persistently high. The fever duration is long: 7–11 days in mild cases and 10–20 days in severe cases before returning to normal; in a few cases, it may last 3–4 weeks. Neurological symptoms appear 3–4 days after fever onset: lethargy, drowsiness, sometimes dysphoria, and in severe cases, convulsions or unconsciousness. Some children may exhibit head tilting and neck stiffness, but cerebrospinal fluid is normal, with no meningeal irritation signs. Respiratory symptoms include unilateral conjunctival congestion in the early stage, pharyngeal congestion, tonsillar swelling, and frequent cough. Dyspnea and cyanosis appear 3–6 days later, gradually worsening with nasal flaring, three depressions sign, and wheezing. In the initial stage, the lungs may only show coarse breath sounds and dry rales, with wet rales appearing 3–4 days after onset. Dullness on percussion is accompanied by diminished breath sounds, and sometimes tubular breath sounds may be heard. Severe cases may have pleural reactions or pleural effusion. Pale complexion is common, and in severe cases, the complexion may turn gray. Heart rate ranges from 160–180 beats/min, sometimes exceeding 200 beats/min. Electrocardiogram shows tachycardia, T and ST segment changes, low voltage, and occasionally first- or second-degree atrioventricular block. Rarely, pulmonary P waves may appear, and in severe cases, heart failure may occur. Digestive symptoms include decreased appetite, vomiting, and grade I diarrhea.

Chest X-ray in the early stage shows increased and blurred lung markings. By days 4–5 of the illness, patchy lesions of varying sizes appear, mostly in the lower lobes of both lungs and the right upper lobe. By days 6–11, the lesions increase and spread widely, merging into large infiltrates, though not confined to a single lobe. Unilateral pleural effusion may occur.

4. Respiratory Syncytial Virus Pneumonia (Respiratory Syncytial Virus Pneumonia)

This disease is more common in infants under 1 year of age, especially in babies within 6 months, and newborns can also be affected. In recent years, the incidence in China has risen significantly, ranking first among viral pneumonias in children, with a higher prevalence in winter and spring, and it can be epidemic.

The pathological changes mainly consist of interstitial infiltration dominated by mononuclear cells, including lymphocytes, plasma cells, and macrophages. The alveoli are filled with edema fluid, and pulmonary hyaline membranes may form. The small bronchi are obstructed by mucus, fibrin, and necrotic epithelial cells, leading to pulmonary emphysema and atelectasis.

Respiratory syncytial virus pneumonia is clinically characterized by paroxysmal wheezing and widespread wheezing sounds in both lungs. Generally, after infection with the syncytial virus, following a 3–5 day incubation period, upper respiratory symptoms such as cough and stuffy nose appear. Fever is usually mild or even absent, though some patients may have high fever. The febrile course lasts 4–10 days in most cases, with a few persisting beyond 10 days. The child exhibits cough, dyspnea, nasal flaring, cyanosis, and marked intercostal retractions. Paroxysmal wheezing is common, with shallow and rapid breathing during episodes, accompanied by expiratory moaning and wheezing, pale complexion, and forehead sweating. Lung percussion reveals hyperresonance, auscultation shows diminished breath sounds, and diffuse wheezing with medium to fine moist rales. The liver and spleen are often pushed below the costal margin due to pulmonary emphysema. Wheezing leads to decreased PaO2 and SaO2 and increased PaCO₂, resulting in respiratory acidosis. Severe cases may complicate with respiratory failure, heart failure, or even fatal asphyxia, particularly in children with congenital heart disease, who have a high mortality rate.

X-ray findings mainly show interstitial pneumonia, pulmonary emphysema, and alveolar lesions, mostly appearing as small patchy shadows, with some forming larger shadows that may merge with blurred edges. The peripheral lung fields show increased transparency, possibly accompanied by local atelectasis or focal emphysema.

Respiratory syncytial virus can cause pneumonia as well as bronchiolitis, and distinguishing between the two is challenging.

5. Mycoplasma Pneumonia

The primary pathogen of this disease is Mycoplasma pneumoniae, transmitted via droplets, with patients and convalescent carriers as the source of infection. It occurs year-round but is more common in cold seasons. The affected age group is mostly 5–9 years, followed by 10–14 years.

Clinical manifestations: The incubation period is 2–3 weeks, with varied clinical presentations. The onset is generally not acute, with temperatures ranging from 37.5–41°C, which may be continuous, remittent, or only low-grade or even absent. Persistent paroxysmal severe cough is a prominent feature. Patients expectorate mucoid sputum, and a few may have sputum streaked with blood. Some children experience widespread chest pain. Symptoms such as fear of cold, headache, and anorexia are common. Dyspnea is usually absent, though infants may exhibit signs of bronchiolitis. Chest signs are unremarkable, and X-ray findings are disproportionate to the signs. Lung shadows may appear patchy, cloudy, reticular, miliary, or interstitial. 20% of children have small pleural effusions, transient atelectasis, or emphysema. The course lasts 3–4 weeks, with slow resolution, sometimes extending for months to a year, and may even lead to reduced lung function. Recurrences are common. Cold agglutinin tests aid in etiological diagnosis. Erythromycin and tetracycline are effective treatments.

bubble_chart Diagnosis

The diagnosis of bronchopneumonia is not difficult based on medical history, clinical manifestations, and X-ray examination. What is important is to further determine the severity (mild or severe) and etiological diagnosis to guide correct and effective treatment.

(1) Establishing the diagnosis of pneumonia

The diagnosis of pneumonia is primarily based on clinical manifestations such as cough, fever, rapid breathing, and fine moist rales in the lungs, combined with chest X-ray findings.

(2) Determining the severity of pneumonia

Timely and accurate diagnosis of the condition is of great clinical significance for reducing the mortality rate of pediatric pneumonia and minimizing sequelae. The key lies in carefully taking the medical history, thoroughly collecting and analyzing examination data from various systems, including selecting some necessary laboratory tests, to assess whether there is concurrent damage or failure of organ functions. The clinical diagnostic criteria for mild and severe pneumonia are as follows:

1. Mild type: Mainly characterized by respiratory symptoms, without respiratory failure or significant damage or failure of other organs or systems.

2. Severe type: In addition to respiratory symptoms, concurrent conditions such as heart failure, respiratory failure, disseminated intravascular coagulation, hyperpyrexia or hypothermia, toxic encephalopathy, toxic intestinal paralysis, or damage to liver and kidney function. Pneumonia in children with congenital heart disease, malnutrition, or newborns is also classified as severe.

(3) Etiological diagnosis

1. In the absence of laboratory diagnostic methods, the etiology of pneumonia is estimated mainly through comprehensive analysis of clinical manifestations, signs, X-ray changes, the presence of complications, and response to treatment. The following tests may provide some reference value in distinguishing bacterial from viral infections.

(1) White blood cell count: In bacterial pneumonia, the total white blood cell count increases, approximately 15–20×10⁹/L. Neutrophils may increase with a left shift and toxic granules in the cytoplasm. The positive rate and score of alkaline phosphatase activity are both elevated, with scores often exceeding 200. However, in severe cases of Staphylococcus aureus pneumonia or Haemophilus influenzae pneumonia, the total white blood cell count may sometimes decrease. In viral pneumonia, the white blood cell count is normal or reduced, with an increased proportion of lymphocytes and no elevation in neutrophils. The alkaline phosphatase activity score is below 60.

(2) C-reactive protein test (CRP): In recent years, rocket electrophoresis has been used to measure serum CRP levels, with a normal value of <10000μg/L，在細菌性感染、敗血症等此值上升，升高與感染的嚴重程度呈正比。當治療有效時下降，治療無效時繼續上升。病毒及支原體感染時不增高。本法對細菌性及排除病毒性或支原體肺炎有價值，在區別新生兒病毒或細菌性肺炎時有幫助。

2. Laboratory etiological tests

(1) Cellular etiological tests: These remain challenging to date. Throat swab bacterial cultures do not represent the causative agents of pneumonia. Quantitative bacterial cultures of suctioned sputum from the larynx under negative pressure have some significance in the etiological diagnosis of pneumonia and can guide antibiotic selection based on drug sensitivity tests. Currently, research is being conducted domestically and internationally on rapid bacterial diagnosis. Methods such as counterimmunoelectrophoresis and ELISA have been used for rapid diagnosis of infections caused by Streptococcus pneumoniae, β-hemolytic Streptococcus, and Haemophilus influenzae, and can differentiate these from carriers.

(2) Viral etiological tests

Traditional diagnostic methods involve isolating viruses from nasopharyngeal secretions or other specimens and detecting paired serum-specific antibodies, which can only provide retrospective diagnoses. In recent years, significant progress has been made both domestically and internationally in the rapid diagnosis of respiratory viral infections. Domestically, test kits for adenovirus, respiratory syncytial virus, influenza virus, parainfluenza virus, and others have been developed. These kits can directly detect viral antigens in nasopharyngeal secretions or specific IgM in acute-phase serum using indirect immunofluorescence, A-PAAP, or ELISA methods, yielding favorable results. The detection results can be reported within hours, offering advantages of speed, sensitivity, and specificity. Notably, the A-PAAP and ELISA methods require only an ordinary microscope or an ELISA reader, making them easy to popularize and promote in primary healthcare facilities.

bubble_chart Treatment Measures

This disease should be treated with reasonable comprehensive measures. Actively control infection, maintain respiratory tract patency, correct hypoxia, prevent complications, and enhance the body's resistance to promote recovery.

(1) General Nursing and Supportive Therapy

1. The room temperature should be maintained at around 20°C, with a relative humidity of 55–65%, to prevent respiratory secretions from drying out and becoming difficult to expectorate. In winter, open windows regularly for ventilation, 30 minutes each time, three times a day, avoiding drafts. Ensure adequate rest and implement strict respiratory isolation measures to prevent cross-infection. Closely monitor changes in the condition and provide timely corresponding treatment. For children with a grayish complexion, perioral cyanosis, dysphoria, or drowsiness, pay attention to changes in heart sounds and heart rate, and observe for signs of myocarditis. If cyanosis worsens after feeding or crying and does not improve with oxygen therapy, promptly investigate the cause and provide appropriate treatment.
2. Pay attention to nutrition and hydration; breastfeeding is preferred. For formula-fed infants, adjust the milk volume and concentration based on digestive function and condition. For those with diarrhea, provide skimmed milk. For toddlers or older children, offer a light, easily digestible diet rich in vitamins. During the convalescence stage, provide nutrient-dense, high-calorie foods. For critically ill children unable to eat, administer intravenous fluids to supplement calories and hydration, with a daily fluid volume of 60–80 ml/kg. Whole blood or plasma transfusions may be given if necessary. For children with rickets, vitamin D₃ therapy should be administered.
3. Maintain respiratory tract patency by promptly removing nasal crusts, nasal secretions, and respiratory mucus. Improve ventilation, increase alveolar ventilation, correct hypoxia, and reduce CO₂ retention. For thin and copious sputum, repeatedly reposition and pat the back to facilitate expectoration. Oral expectorants such as ammonium chloride mixture (1 ml per year of age, three times daily) may also be given. For thick, sticky sputum that is difficult to expectorate, suction or ultrasonic nebulization may be used. The nebulization solution consists of 30 ml of saline or distilled water, 20,000 U of gentamicin, 5 mg of α-chymotrypsin, and 1 mg of dexamethasone. Each inhalation lasts 10–15 minutes, administered 2–3 times daily.

(2) Application of Anti-Infective Drugs Select appropriate anti-infective drugs based on age, severity of the condition, previous medication use, and drug sensitivity test results.

1. Selection of Antibiotics
   1. For Gram-positive coccal lung infections: Penicillin remains the first choice for pneumococcal pneumonia. Generally, high-dose penicillin is administered intravenously. For those allergic to penicillin, switch to erythromycin. For staphylococcal pneumonia, start with β-lactamase-resistant drugs such as new penicillin II, cephalosporin I, or third-generation cephalosporins intravenously. The treatment course lasts 3–6 weeks, as stopping too early may lead to relapse. For anaerobic pneumonia, piperacillin and metronidazole are effective.
   2. For Gram-negative bacillary lung infections, ampicillin or aminoglycoside antibiotics are generally used. For Pseudomonas aeruginosa pneumonia, ceftazidime or ceftriaxone may be used.
   3. For mycoplasma pneumonia, erythromycin is commonly used, with a recommended treatment course of two weeks.
   4. For pneumonia with unidentified bacteria, broad-spectrum antibiotics should be selected based on the condition, with combination therapy (one of which should target Gram-negative bacteria). Once the bacteria are identified, adjust to the corresponding sensitive antibiotics. For severe pneumonia, antibiotics should primarily be administered intravenously.
2. Application of Antiviral Drugs

   Interferon: For children under 5 years, 100,000 U intramuscularly once daily; for those over 5 years, 200,000 U intramuscularly once daily, for a course of 2–3 days. Alternatively, interferon may be administered as nasal drops (10,000 U/ml, 1–2 drops per nostril, 15–30 minutes per session, reduced to 3–4 times daily after fever subsides) or via ultrasonic nebulization.

   Ribavirin Ultrasonic nebulization is the main route of administration, dose: 10mg for children under 2 years old, 20-30 mg for those over 2 years old, dissolved in 30 ml of distilled water until nebulization is completed, twice daily for 5 to 7 consecutive days. Alternatively, a 0.5% solution can be used for nasal drops every 1 to 2 hours.

(3) Oxygen therapy:

Common clinical oxygen delivery methods include:

1. **Shallow nasal catheter or stuffy nose method**: The catheter tip is placed in the nasal vestibule and secured with adhesive tape. This method is simple, relatively safe, and commonly used. For newborns and infants, the oxygen flow rate is 0.5–1 L/min.
2. **Fistula disease bucket method**: The entire fistula disease bucket is placed over the nose, with its edges slightly spaced from the facial skin. It is difficult to secure for infants and young children, and most of the oxygen is lost, resulting in minimal inhalation and poor efficacy. However, this method is suitable for children with extreme dysphoria or restlessness who cannot tolerate the nasal catheter method.
3. **Headbox method**: A rigid plastic headbox is used with an oxygen flow rate of 3–5 L/min. It is best administered through a nebulizer. The headbox size is approximately 40×40×40 cm; smaller sizes may lead to CO₂ retention.
4. **Mask nebulized oxygen delivery**: Oxygen is delivered through a nebulizer mask. For children, the flow rate is 3–5 L/min, with an oxygen concentration of 40–60%. Since oxygen passes through the nebulizer, some mist can reach the small bronchi. The high humidity prevents oxygen dryness, dilutes sputum for easier expectoration, and helps maintain airway patency.
5. **Positive pressure oxygen delivery**: For critically ill children with respiratory failure, mechanical ventilation with positive pressure oxygen is required. Depending on the child’s condition, continuous positive airway pressure (CPAP), intermittent positive pressure breathing (IPPB), or positive end-expiratory pressure (PEEP) may be used. High-frequency ventilation is also an option.

   **High-concentration (>60%) prolonged oxygen therapy** can damage the brain, heart, lungs, kidneys, and other organs. In the lungs, it may cause interstitial edema, alveolar epithelial hyperplasia, pulmonary hyaline membrane formation, and pulmonary hemorrhage. In premature infants and newborns, it may lead to retrolental fibroplasia, affecting vision. Care must be taken to prevent oxygen toxicity during oxygen administration.

**(4) Symptomatic Treatment**

1. **Fever reduction and sedation**: Physical cooling methods are generally used first, such as cold compresses on the occiput or lukewarm sponge baths. If the temperature does not decrease, medication may be administered, such as APC at 5–10 mg/kg per dose. For specific cases, chlorpromazine and promethazine may be given intravenously or intramuscularly to maintain the temperature below 38°C, allowing the child to rest quietly. For convulsions, 10% chloral hydrate may be administered rectally at 60 mg/kg per dose. If ineffective, diazepam may be given intramuscularly or intravenously at 0.3 mg/kg per dose.
2. **Resolving phlegm and relieving cough (antiasthmatic)**: For thick sputum that is difficult to expectorate, pediatric ammonium chloride mixture may be administered orally at 1 mL/year of age per dose, three times daily. Bisolvon may be given at 0.7 mg/kg daily, divided into three doses. For severe thick sputum and cough, ultrasonic nebulization may be used. For severe wheezing, Kechuanning may be given orally at 1 mL/year of age, three times daily. Alternatively, 654-2 may be administered orally at 0.5 mg/kg daily, every 12 hours. For severe cough, vitamin K1 may be given intramuscularly or intravenously at 1 mg/kg per dose.

**(5) Management of Major Organ Damage**

1. **Treatment of heart failure**: In addition to oxygen therapy, resolving phlegm and relieving cough, and sedation, cardiac glycosides should be administered. Diuretics may be added if necessary. Commonly used digitalis preparations include:
   1. **Strophanthin K**: The digitalizing dose is 0.007–0.01 mg/kg, slowly injected intravenously with 20 mL of 25% glucose. Depending on the condition, half the dose may be repeated after 6–8 hours until heart failure is corrected.
   2. **Cedilanid**: The digitalizing dose is 0.03–0.04 mg/kg for children under 2 years old and 0.02–0.03 mg/kg for those over 2 years old. Half the digitalizing dose is given initially, and the remainder is divided into two doses, administered every 12 hours with glucose via slow intravenous injection.
   3. Digoxin: Oral digitalization dose: For children under 2 years old, 0.04～0.05 mg/kg; for those over 2 years old, 0.03～0.04 mg/kg. The first dose should be half of the calculated amount. The remaining dose is divided into two portions, administered every 6 to 8 hours. The maintenance dose is one-fourth of the digitalization dose and can be divided into two oral doses. The intravenous dose is calculated as three-fourths of the oral dose. Do not administer concurrently with calcium preparations.
   When using Rehmannia preparations to correct heart failure, phentolamine can be added. The primary effects of phentolamine are to reduce resistance in small stirred pulses, dilate the venous system, alleviate cardiac preload and afterload, improve cardiac function, reduce pulmonary stirred pulse hypertension, pulmonary static blood, and pulmonary edema; increase glomerular filtration rate and blood flow, and protect the kidneys. The dose is 0.5～1 mg/kg per administration, added to 20 ml of glucose and injected intravenously over 10～15 minutes or infused through a Murphy drip. Repeat every 2 to 6 hours based on the condition. This medication also improves gastrointestinal microcirculation, enhances intestinal motility, and is effective in treating abdominal distension and fullness. The drawbacks include increased heart rate and sudden hypotension, so close monitoring is required.

   For acute heart failure in children, especially those accompanied by pulmonary edema, potent diuretics combined with Rehmannia preparations have been increasingly used in recent years. Furosemide is commonly administered at a dose of 1mg/kg per dose, which may be repeated once after 2 hours if necessary.

2. Treatment of pneumonia complicated by respiratory failure: The key lies in addressing the primary disease and precipitating factors (such as toxicity, pulmonary edema, etc.), with a focus on improving respiratory function, increasing PaO₂ and SO₂, and enhancing ventilation to reduce PaCO₂. Respiratory stimulants are one component of comprehensive treatment but should not be overly relied upon due to their transient efficacy. Commonly used drugs include lobeline, nikethamide, cytisine, and pentylenetetrazol, or a respiratory triple combination of lobeline 3mg, dimefline 8mg, and nikethamide 0.75g or methylphenidate 10mg in 10% glucose solution 250ml administered intravenously. Close monitoring is essential during use to prevent overdose-induced convulsions. Management of cerebral edema is discussed in the following section.
3. Treatment of toxic encephalopathy

   First, ensure airway patency, improve ventilation, and provide oxygen. In cases of airway obstruction or respiratory failure, perform tracheostomy and use a ventilator early to alleviate cerebral edema and reduce intracranial pressure:

   1. Mannitol: Dose 1–2g/kg per administration, given intravenously over 15–30 minutes or rapidly infused, every 4–8 hours. For cerebral herniation, the initial dose is 2g/kg intravenously, repeated once after 1–2 hours. Gradually extend the interval as the condition improves until discontinuation. Prolonged use may cause hematuria; it is best to administer dehydrating agents only after diuretics and cardiotonics have increased urine output and improved cardiac function.
   2. Diuretics: Systemic dehydration through diuresis can help reduce intracranial pressure. Furosemide is commonly used, with dosage and administration as previously described. During dehydration therapy, strict recording of intake and output is necessary, adhering to the principle of balancing rehydration and dehydration, ideally maintaining the child in grade I dehydration.
   3. Use of vasodilators: Vasodilators relieve cerebrovascular spasm, improve cerebral microcirculation, thereby reducing cerebral edema and ensuring hypertonic dehydrating agents reach brain tissue to take effect. Common drugs include: A. 654-2: Dose 1–2mg/kg every 10–15 minutes, reduced to 0.5–1mg/kg every 2–4 hours once stabilized, administered intravenously. B. Scopolamine: 0.02–0.04mg/kg every 30 minutes, added to 5% glucose 10–20ml for intravenous injection. Facial flushing and improved respiration indicate the need to extend intervals or reduce infusion speed. Intracranial pressure typically improves within 1–2 hours. Reduction in respiratory secretions and pulmonary rales may also occur. Phenoxybenzamine and dexamethasone can reduce vascular and blood-brain barrier permeability, increase renal blood flow, and inhibit posterior pituitary secretion of antidiuretic hormone, aiding in diuresis and preventing cerebral edema. Dexamethasone is commonly dosed at 0.15–0.25mg/kg every 6 hours intravenously, tapered or discontinued after 2–3 days. Its effects are slower but sustained, without rebound.
   4. Drugs to promote brain cell recovery: Commonly used agents include adenosine triphosphate (ATP), coenzyme A, cytochrome C, glutamic acid, γ-aminobutyric acid, meclofenoxate, antiradon, and vitamins B1 and B6. Citicoline is particularly effective in improving consciousness, regulating cerebrovascular tone, and promoting patient awakening.
4. Treatment of toxic intestinal paralysis

   Severe pneumonia is prone to cause abdominal distension and fullness, which is more common in infants and young children. It is advisable to first use diluted soap (2%) for enema and retain the catheter for gas expulsion. If ineffective, neostigmine can be used, with a dosage of 0.03–0.04 mg/kg per dose for infants and young children, administered intramuscularly or subcutaneously, but not for those with wheezing. At the same time, apply Knotty Pine Wood oil to the abdomen, and insert a rectal tube for gas expulsion 15–20 minutes after injection. This can be done 3–4 times a day. For severe abdominal distension and fullness, gastrointestinal decompression can be performed to remove gastrointestinal contents and gas. For abdominal distension and fullness caused by hypokalemia, oral administration of 10% potassium chloride solution at 0.5 mg/kg, 3–4 times daily, can be given. In recent years, phentolamine has shown relatively good efficacy in treating abdominal distension and fullness, with the dosage as mentioned above.

(6) Application of adrenal cortex hormones

Generally, pneumonia does not require the use of adrenal corticosteroids. For severe pneumonia cases accompanied by high fever, toxic encephalopathy, shock, severe wheezing, pleural effusion, and other symptoms, adrenal corticosteroids may be added for short-term use alongside adequate and effective antibiotics. Attention should be paid to side effects such as stress-induced gastrointestinal bleeding and reduced antimicrobial capacity. Hydrocortisone can be administered intravenously at 5–10 mg/kg per day, or dexamethasone at 0.25–0.5 mg/kg per day intravenously, or prednisone orally at 5 mg/kg per day. Typically, the treatment lasts 3–5 days and can be discontinued once symptoms improve.

(7) Management of complications.

For children with concurrent lung abscess, infection control is crucial. Antibiotics should be selected based on sputum, pus, or blood culture results, and blood or plasma transfusions may be provided for support. Oxygen therapy should be administered to those with breathing difficulties. If sputum is too thick, oral or injectable trypsin may be used to dilute it, along with postural drainage. For older children with poor pus expulsion, bronchoscopic suction may be considered as appropriate. For empyema or pyopneumothorax, if the amount of pus or gas is small, repeated punctures may be performed; if the amount is large, closed thoracic drainage should be promptly performed to expel pus and release gas. For ruptured pulmonary bullae, gas should be aspirated promptly. (8) Physical therapy. During the convalescence stage of pneumonia, if lung rales persist, methods such as ultrashort-wave therapy may be used to promote inflammation absorption. However, this is contraindicated in cases complicated by heart failure.

bubble_chart Differentiation

1. Bronchitis: Systemic symptoms are mild, generally without dyspnea or hypoxia. Dry rales and medium coarse moist rales can be heard in the lungs, which are not fixed and often disappear with cough or changes in body position.
2. Acute miliary pulmonary tuberculosis: Children with sudden onset often present with systemic toxic symptoms such as high fever, chills, general malaise, tachypnea, and cyanosis, resembling bronchitis. However, there are often no obvious signs in the lungs, or fine moist rales scattered across both lungs, mostly detected at the end of inspiration. X-ray findings also share similarities with bronchopneumonia. Differentiation can be made based on the history of tuberculosis exposure, clinical symptoms, positive tuberculin test, increased erythrocyte sedimentation rate, detection of tuberculosis bacteria in sputum or gastric lavage fluid, and characteristic X-ray follow-up observations.
3. Caseous pneumonia: This condition mostly occurs in children who are weak or have low resistance. X-rays show dense consolidation in a lung segment or even a large part of a lobe, with a relatively blurred outline. Typically, more translucent liquefaction areas or even translucent cavities can be seen. The combination of disease history and tuberculin test makes it easy to differentiate from bronchopneumonia.
4. Bronchial foreign body: There is a history of foreign body aspiration or choking cough. Clinical severity varies, and the duration of the illness differs. Prolonged cases with secondary infections may present with recurrent fever, cough, and moist rales in the lungs, resembling pneumonia. Sometimes, tracheal slapping sounds heard during auscultation can aid in diagnosis, but confirmation relies on fiberoptic bronchoscopy.
5. Bronchiolitis: It closely resembles acute pneumonia, but this disease is primarily characterized by wheezing and breathlessness. Widespread wheezing and fine moist rales can be heard in both lungs. Severely ill children show obvious hypoxia, and X-rays only reveal increased lung transparency, diaphragmatic depression, and transient emphysema-like changes, with a few children showing minor spotty shadows.