Acute miliary tuberculosis of the lung (acute hematogenous disseminated pulmonary tuberculosis) is the result of the progression and deterioration of primary pulmonary tuberculosis. It is mainly seen in children, especially infants and young children. It is often triggered within 6 months after the primary infection due to conditions such as measles, whooping cough, or malnutrition. The disease is usually severe with a high mortality rate, but if diagnosed early and treated promptly, it can still be cured. If treatment is incomplete, it often leads to serious complications of tuberculosis and becomes the source of extrapulmonary tuberculosis.

bubble_chart Etiology

This condition is primarily caused by caseous lesions in intrathoracic lymph nodes or primary foci rupturing into blood vessels, allowing a large number of subcutaneous node bacilli to enter the bloodstream simultaneously or within a short period, leading to hematogenous dissemination. If bacteria spread from the pulmonary stirred pulse, only the lungs are affected, resulting in foxtail millet-sized pulmonary subcutaneous nodes. If bacteria enter the pulmonary veins, they disseminate through systemic circulation to major organs such as the lungs, brain, meninges, liver, spleen, kidneys, intestines, and peritoneum, causing systemic foxtail millet-sized subcutaneous nodes. The subcutaneous node bacilli disseminated to these organs form uniformly distributed, grayish-white or grayish-yellow, foxtail millet-sized nodules in the interstitial tissue. In the lungs, subcutaneous node nodules are more prevalent in the upper lobes than the lower lobes, which contrasts with the distribution of bronchopneumonia lesions. The severity of foxtail millet-sized pulmonary subcutaneous node disease is related to the number of bacteria entering the bloodstream, the frequency and speed of dissemination, and the host's immune status.

The onset can be acute or insidious, with acute onset being more common. Infants and young children often experience sudden high fever, accompanied by night sweating, loss of appetite, cough, pale complexion, shortness of breath, and cyanosis. Pulmonary signs are often inconspicuous, and only in the advanced stage can dry rales or a small amount of moist rales be heard. Some cases present with acute pulmonary symptoms and signs, where fine moist rales may be heard in the lungs, leading to misdiagnosis as pneumonia. Sometimes, the child may have persistent high fever or remittent fever, accompanied by loss of appetite, fatigue, hepatosplenomegaly, or even jaundice, which can easily be confused clinically with cold-damage disease or sepsis. More than 50% of children show signs of subcutaneous nodular meningoencephalitis at the initial stage of the disease.

Symptoms in infants are often atypical, mainly manifesting as general toxic symptoms such as fever, loss of appetite, emaciation, and fatigue, often misdiagnosed as grade III malnutrition.

In children with systemic miliary subcutaneous nodular disease, fundus examination may reveal choroidal subcutaneous nodules distributed around the central retinal artery branches.

bubble_chart Auxiliary Examination

1. X-ray examination: 1-3 weeks after onset, chest X-rays reveal uniformly sized and evenly distributed foxtail millet-like shadows densely scattered in both lung fields. Due to the fine nature of the lesions, these shadows are generally not detectable under fluoroscopy.
2. The total white blood cell count and neutrophils increase, with a left shift in nuclear morphology and monocytosis. Sometimes, a leukemoid reaction may occur.
3. Erythrocyte sedimentation rate (ESR) accelerates.
4. In severe cases, the OT test may show weakly positive or negative results, turning positive as the condition improves.
5. Subcutaneous node bacilli can be found in sputum or gastric lavage fluid.

bubble_chart Diagnosis

The diagnosis is primarily based on clinical manifestations, hepatosplenomegaly, a positive OT test, and a history of subcutaneous node contact. Suspected cases should undergo laboratory tests and chest X-rays. Chest radiography often plays a decisive role in the diagnosis.

bubble_chart Treatment Measures

1. General therapy and the application of adrenal cortical hormones.
2. Anti-subcutaneous node drug therapy: Same as subcutaneous node meningoencephalitis.

bubble_chart Differentiation

1. Bronchopneumonia: The onset is acute, and the more severe the hypoxia symptoms, the more fine moist rales are heard in the lungs. The rales are often bilaterally symmetrical and predominantly located in the back. In cases of miliary pulmonary or subcutaneous nodules, symptoms of subcutaneous nodule poisoning are present, but lung signs are not obvious. OT testing and X-ray examination aid in differentiation.
2. Cold-damage disease: It is more common in summer and autumn. Pay attention to inquiring about contact history and usual dietary hygiene habits. In infants and young children with cold-damage disease, toxic symptoms are milder, with digestive symptoms being predominant. Blood, stool, and urine cultures, as well as the Widal test, assist in diagnosis.
3. Septicemia: There is often a primary infection focus. Early blood culture can clarify the pathogenic diagnosis.
4. Leukemia: There is irregular fever, anemia, enlargement of superficial lymph nodes, liver, and spleen, and an often elevated total white blood cell count in peripheral blood, with immature white blood cells frequently observed. Bone marrow smear examination can confirm the type of leukemia.