bubble_chart Overview

Primary pulmonary tuberculosis (primary pulmonary tuberculosis) is the primary infection caused by the initial invasion of Mycobacterium tuberculosis into the lungs. It is a common clinical type of pediatric pulmonary tuberculosis, including the primary complex and bronchial lymph node tuberculosis (also known as hilar lymph node tuberculosis). The former involves the simultaneous presence of three pathological components: the primary pulmonary lesion, lymphangitis, and bronchial lymphadenitis. The latter is characterized by significantly enlarged bronchial lymph nodes, while the primary pulmonary lesion may be too small or already absorbed to be detected by X-ray examination. Therefore, there is no fundamental difference between the two; they are essentially two manifestations of the same disease process.

Primary pulmonary tuberculosis is the initial infection site, which absorbs relatively quickly and generally has a good prognosis. However, the residual bacteria in the lymph nodes can become the source of subsequent secondary pulmonary tuberculosis. Additionally, it may worsen during infancy and early childhood, so it should not be overlooked.

bubble_chart Etiology

After the bacillus initially invades the lungs through the respiratory tract, it forms a primary lesion, mostly located at the base of the upper lobe or the upper part of the lower lobe of the lung, particularly in the right lung. The lesion is usually single, though sometimes there may be two or more, often close to the pleura. Therefore, during primary infection, the pleura is easily affected. The primary lesion manifests as a localized pulmonary inflammation dominated by exudation, followed by caseous necrosis at the center, subsequent proliferative nodules, and gradual formation of a fibrous capsule. During the formation of the primary lesion, the bacteria travel along the lymphatic vessels to the mediastinal lymph nodes at the hilum of the lung, causing lymphangitis and lymphadenitis. At this stage, the body is in a hypersensitive state, and the inflammatory reaction and caseous necrosis progress rapidly, leading to significant swelling of the lymph nodes. The tracheal and bronchial lymph nodes are interconnected by lymphatic vessels. If subcutaneous node inflammation occurs, not only the lymph nodes on the same side as the pulmonary lesion will swell, but the contralateral lymph nodes may also become infected. Sometimes, one lymph node lesion may have already hardened, while another remains active. When the body's immunity declines, subcutaneous node lymph nodes may rupture and disseminate. The healing process of intrathoracic lymph node subcutaneous nodes generally takes longer than that of the primary pulmonary lesion, which is why bronchial lymph node subcutaneous nodes are far more common than primary complex.

Primary pulmonary subcutaneous nodes need to be differentiated from the following diseases:

1. Patients with tracheitis subcutaneous node disease may exhibit symptoms similar to tracheitis, such as cough and sputum production, but children with tracheitis do not show subcutaneous node toxic symptoms. The OT test and X-ray examination can aid in differentiation.
2. Children with bronchial lymph node subcutaneous nodes may exhibit spasmodic paroxysmal cough symptoms similar to whooping cough. However, children with whooping cough have a history of whooping cough exposure, elevated total white blood cell count with a significant increase in lymphocytes, often exceeding 60%. Additionally, subcutaneous node exposure history, OT test, and chest X-ray examination can assist in differentiation.
3. The pulmonary X-ray shadows of mycoplasma pneumonia sometimes resemble those of tumor-like bronchial lymph node subcutaneous nodes. However, this condition tests positive for cold agglutination and lacks signs of bronchial lymph node subcutaneous nodes.
4. Pulmonary X-ray shadows of cervical malignancy with cachexia should be differentiated from bronchial lymph node subcutaneous nodes. In cervical malignancy with cachexia, the hilar lymph nodes exhibit bilateral symmetrical enlargement, smooth margins, and bulging into the lungs. This condition affects systemic lymph nodes and progresses rapidly. Bone marrow smear examination may reveal poorly differentiated reticular cells, lymphocytes, or multinucleated giant cells.

bubble_chart Clinical Manifestations

Most cases of this disease are mild, especially in older children, who may have no obvious symptoms and are only discovered during chest X-ray examinations. Slightly more severe cases also have a slow onset, presenting with varying degrees of subcutaneous node poisoning symptoms, such as prolonged irregular low-grade fever, loss of appetite, weight loss, night sweating, and fatigue. In younger children, the condition is often slightly more severe, manifesting as acute fever with temperatures reaching around 39°C, persisting for 2–3 weeks before turning into a low-grade fever that lingers, often misdiagnosed as common cold or cold-damage disease. When bronchial lymph nodes are significantly enlarged, compression symptoms may occur. Commonly, due to enlarged lymph nodes at the bronchial intersection, whooping cough-like spasmodic cough may appear. Compression of the bronchus or bronchial perforation can lead to asthma, expiratory or inspiratory dyspnea, and sometimes lung qi swelling or atelectasis. If a large amount of caseous material suddenly ruptures into the bronchus, it can cause paroxysmal coughing, wheezing, inspiratory dyspnea, cyanosis, or even suffocation. If deficient and not treated promptly, it can be fatal.

Physical examination may reveal generalized superficial lymphadenopathy. Lung signs are mostly inconspicuous, with a few cases exhibiting minor dry or moist rales. In cases complicated by atelectasis, corresponding chest wall percussion may show dullness, and auscultation may reveal diminished breath sounds or tubular breathing sounds. Children in a highly hypersensitive state may develop herpetic conjunctival membrane inflammation or cutaneous nodular erythema.

bubble_chart Auxiliary Examination

1. X-ray examination:
   (1) Primary complex: The primary lesion in the lung is mostly located in the middle and lower lung fields, appearing as an exudative lesion with indistinct margins. In infants and young children, extensive infiltration around the primary lesion is often observed, sometimes even involving an entire lobe, accompanied by pleural reaction. The hilar lymph nodes appear as a mass-like shadow. Between the primary lesion and the hilar lymph nodes, linear shadows of lymphangitis often connect them, forming a dumbbell-shaped bipolar shadow.
   (2) Bronchial lymph node subcutaneous node: Enlarged bronchial lymph nodes appear as round, mass-like shadows. Those with clear margins are classified as the tumor type, while those with indistinct margins extending into the lung fields are classified as the infiltrative type.
2. Peripheral blood examination: Grade I anemia may be detected, and both the white blood cell count and neutrophil count may increase. The erythrocyte sedimentation rate (ESR) is elevated during the active phase.
3. Peripheral lymph node aspiration smear or lymph node biopsy may reveal subcutaneous node nodules and caseous necrosis.

bubble_chart Diagnosis

Early diagnosis is a crucial factor in determining prognosis. A detailed history should be obtained regarding the child's BCG vaccination, exposure to subcutaneous node disease, and other infectious diseases such as measles and whooping cough. For children presenting with prolonged low-grade fever, night sweats, weight loss, mild cough, poor appetite, and fatigue, an OT test and chest X-ray should be performed immediately. Based on the comprehensive analysis of the physical examination findings, a definitive diagnosis can then be made.

bubble_chart Prognosis

The prognosis of primary complex is generally good. The primary lesion begins to resolve or form indurations within 3 to 6 months after onset and usually heals completely or leaves calcified foci within 2 years. The course of bronchial lymph node tuberculosis is longer. With proper treatment, most lesions undergo fibrosis or form calcified indurations. However, Mycobacterium tuberculosis within the lesions may survive for a long time, becoming latent foci for secondary tuberculosis in adults. When the body's immunity declines, the lesions may reactivate, leading to progression or worsening of the disease.