Foxtail millet-sized subcutaneous nodules (miliary tuberculosis), also known as hematogenous disseminated subcutaneous nodules, are often the result of the deterioration of primary complex. They are classified into three types: acute, subacute, and chronic. Acute foxtail millet-sized subcutaneous nodules occur when a large number of tuberculosis bacteria suddenly enter the bloodstream while the child's immunity is compromised, leading to acute hematogenous dissemination. This typically happens within six months of the primary infection. When tuberculosis bacteria enter the bloodstream through the pulmonary vein, they travel via the left heart and main artery to spread throughout the body, causing systemic foxtail millet-sized subcutaneous nodules. If the bacteria enter the bloodstream through the pulmonary artery or bronchial veins, they disseminate within the lungs, resulting in pulmonary foxtail millet-sized subcutaneous nodules. Subacute and chronic hematogenous disseminated subcutaneous nodules are caused by repeated, small amounts of tuberculosis bacteria entering the bloodstream. The acute type is more common in children.

bubble_chart Diagnosis

(1) Acute miliary tuberculosis

1. Clinical symptoms: Most cases have an acute onset. (1) Local respiratory symptoms: Dyspnea, cyanosis, and severe cough appear at the onset, with occasional blood streaks in the sputum. (2) Systemic symptoms: Similar to those of cold-damage disease or sepsis, such as high fever (39–40°C), lethargy, and delirious speech. (3) Over 50% of children exhibit symptoms of tuberculous meningitis concurrently, including severe headache, vomiting, and impaired consciousness. In infants, due to the buffering effect of the anterior fontanelle, intracranial pressure-related headache and vomiting are often less severe.
2. Signs: (1) Lung signs are disproportionate to dyspnea and cyanosis; percussion reveals no dullness, and auscultation may detect a few fine moist rales. (2) Fundus examination may show retinal central artery pulsation and choroidal tubercles, appearing as white nodules the size of millet grains. This finding has specific diagnostic significance. (3) Hepatosplenomegaly and superficial lymphadenopathy. (4) In cases of tuberculous meningitis, signs such as neck stiffness, positive Kernig's sign, hyperactive tendon reflexes, and optic disc edema may occur.
3. Laboratory tests: Increased erythrocyte sedimentation rate. Peripheral blood shows reduced total white blood cell count and lymphocyte proportion, with a left shift and monocytosis. Tubercle bacilli are rarely found in sputum. In tuberculous meningitis, intracranial pressure is elevated, cerebrospinal fluid (CSF) shows increased cell count (mostly lymphocytes), elevated protein, and decreased glucose and chloride levels. Acid-fast staining of CSF after 24-hour sedimentation may reveal tubercle bacilli. 4. OT or PPD test: About one-third of children with acute miliary tuberculosis show no reaction due to low immunity. A positive result does not rule out the diagnosis. 5. X-ray examination: Chest fluoroscopy may not detect pulmonary granular shadows; radiography is necessary. In the first 1–2 weeks, lesions are too small, showing only increased lung markings. After 2 weeks, uniform miliary shadows appear, denser in the hilar and upper-middle lung fields and sparser in the lower fields.

1. Clinical symptoms: Onset is more gradual. Systemic symptoms are milder than in acute miliary tuberculosis, typically presenting as general tuberculous toxemia, such as low-grade fever, night sweats, fatigue, weight loss, and poor appetite. Cough may vary from mild to severe, with possible hemoptysis. Chronic hematogenous disseminated tuberculosis may also show no obvious systemic symptoms or intermittent symptoms lasting years.
2. Signs: Mild cases may show no significant signs. Larger pulmonary lesions may present with fine crackles. Pleurisy may cause dullness on percussion and reduced breath sounds. Extrapulmonary tuberculosis (e.g., bone/joint or genitourinary tuberculosis) may present with corresponding signs.
3. Laboratory tests: Similar to acute miliary tuberculosis; tubercle bacilli may be found in sputum.
4. X-ray examination: Variable-sized punctate shadows are seen in the lung fields, distributed asymmetrically in the upper lungs (less uniform than in acute miliary tuberculosis). Lesions vary in shape and nature, including nodular proliferative foci, exudative fuzzy shadows, fibrosis, or calcification, possibly with fusion and thin-walled cavities. Upper lung field lesions are older, while lower field lesions are fresher, often asymmetrical.

bubble_chart Treatment Measures

﹝Treatment﹞

(1) General therapy is the same as for primary pulmonary subcutaneous node, but absolute bed rest is required. (2) Immediately use anti-subcutaneous node drugs, and two or more bactericidal drugs must be used. The treatment is divided into two stages.

1. **Intensive treatment phase**: Depending on the condition, the following options may be selected: (1) INH + RFP: 10mg/(kg·d) each, orally (INH can be administered intravenously initially), for 3 months. (2) INH + RFD: INH 15–20mg/(kg·d) (maximum not exceeding 400mg/d) orally or intravenously; RFD 3–4mg/(kg·d) orally, for 3 months. (3) INH + SM: INH dose as above, for 3 months; SM 20mg/(kg·d) (maximum 0.75g/d) intramuscularly, for 2–3 months. (4) INH + EBM: INH dose as above; EBM 15–20mg/(kg·d) orally, for 3 months. (5) INH + SM + PAS: INH dose as above, orally or partially intravenously for 3 months; SM 20mg/(kg·d) intramuscularly for 2–3 months (every other day in the 2nd month, twice weekly in the 3rd month); PAS 200–300mg/(kg·d) (maximum dose 8g/d) orally for 3 months. (6) INH + SM + EBM: INH and SM doses as above; EBM dose as above, orally, for 3 months. **Consolidation treatment phase**: (1) For severe cases, INH + RFD may be used: INH dose as above, from the 4th to 18th month, or up to 24 months if necessary; RFD daily dose as above, from the 4th to 6th month. (2) For moderate cases, INH + EMB may be used: INH dose as above, from the 4th to 18th month; EMB dose as above, from the 4th to 12th month. (3) **Use of adrenal corticosteroids**: For severe toxic symptoms such as high fever, dyspnea, or cyanosis, prednisone 1–2mg/(kg·d) may be used concurrently with sufficient anti-subcutaneous node drugs. The course lasts 1–3 months to alleviate symptoms. In summary, anti-subcutaneous node drugs must be used in sufficient doses, and the treatment course must be adequate. If ineffective, the regimen should be adjusted promptly. When using two or more hepatotoxic drugs such as INH and RFP, the dose should be reduced to 10mg/(kg·d), and liver protection measures should be taken. If liver dysfunction occurs, switch medications and monitor for auditory nerve damage caused by SM.

AD

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bubble_chart Differentiation

(1) Pneumonia presents with fever, cough, and wheezing, with medium to fine crackles audible in the lungs. X-ray findings vary depending on the lesion, showing large or patchy shadows or merely thickened lung markings without shadows. Persistent pneumonia should be differentiated from pulmonary subcutaneous nodules, especially fungal pneumonia, where lung signs are subtle. Chest X-rays may reveal dense punctate shadows resembling foxtail millet-sized pulmonary subcutaneous nodules, but a history of prolonged antibiotic use is common. Concurrent fungal infections in the digestive tract and a negative PPD test can aid in differentiation. (2) Cold-damage disease is common in summer and autumn, characterized by high fever, relative bradycardia, leukopenia, and eosinophil depletion. Positive cultures for cold-damage bacilli and a positive Widal reaction confirm the diagnosis. Acute foxtail millet-sized subcutaneous nodules in cold-damage disease are often misdiagnosed as cold-damage disease itself, though the reverse misdiagnosis is rare. This type presents abruptly with persistent high fever, headache, poor appetite, thick tongue coating, and grade I splenomegaly, but also features rapid pulse, profuse sweating, tachypnea, and grade I cyanosis. After two weeks, small nodular shadows may appear on X-rays, along with nodules on the choroid membrane of the fundus. (3) Sepsis begins acutely with chills followed by high fever, typically of the remittent type. It usually involves a primary suppurative focus and symptoms of toxic infection, such as petechiae on the skin and mucous membranes, jaundice, hepatosplenomegaly, leukocytosis with a marked left shift, and toxic granules in neutrophils. Septic shock and DIC may occur. A positive blood culture confirms the diagnosis. The PPD test is negative, and X-rays show no abnormalities unless the primary infection is pneumonia. (4) Histiocytosis presents with irregular fever, recurrent foxtail millet-sized hemorrhagic papules or seborrheic rashes with central crusting and scaling, along with hepatosplenomegaly and lymphadenopathy. Chest X-rays may show reticular and speckled shadows, and some cases exhibit localized skull defects. Pressed smears of opened rashes stained with Wright's stain reveal histiocytic infiltration. (5) Idiopathic pulmonary hemosiderosis is characterized by the deposition of hemosiderin in the lungs and a history of recurrent hemoptysis. Main symptoms include episodic pallor, weakness, low-grade fever, and cough, sometimes with small amounts of fresh blood. Dyspnea, cyanosis, palpitations, and tachycardia may occur suddenly and repeatedly, potentially leading to heart failure. Chest X-rays show scattered, diffuse small speckled shadows in the lung fields. Macrophages containing hemosiderin can be found in sputum or gastric fluid, accompanied by hypochromic microcytic anemia.