
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Disseminated pulmonary tuberculosis - Symptoms
Medical expert of the article
Last reviewed: 04.07.2025
Various pathomorphological changes and pathophysiological disorders that occur with disseminated tuberculosis cause the characteristic symptoms of disseminated pulmonary tuberculosis.
Acute disseminated (miliary) pulmonary tuberculosis usually develops over 3-5 days, reaching full expression by the 7th-10th day of the disease. The following symptoms of disseminated pulmonary tuberculosis appear first: weakness, increased sweating, loss of appetite, increased body temperature, headache, and sometimes dyspeptic disorders. Body temperature quickly rises to 38-39 °C; hectic fever is noted. The increase in intoxication and functional disorders is accompanied by weight loss, adynamia, increased sweating, confusion or temporary loss of consciousness, delirium, tachycardia, and acrocyanosis. A characteristic clinical symptom of disseminated pulmonary tuberculosis is dyspnea. Cough may appear, often dry, sometimes with the release of scanty mucous sputum. In some cases, a delicate roseola rash appears on the anterior surface of the chest and upper abdomen, caused by the development of toxic-allergic thrombovasculitis.
A tympanic percussion sound is detected over the entire surface of the lungs, weakened or harsh breathing, a small amount of dry or fine-bubble wheezing are heard. Enlargement of the liver and spleen is often noted, sometimes moderate abdominal distension.
Sharply expressed symptoms of intoxication with deep functional disorders of the central nervous system resemble typhoid fever and are the basis for diagnosing the typhoid form of miliary tuberculosis. Such patients are often initially hospitalized in general infectious diseases departments.
Asphyxial dyspnea, increasing tachycardia, acrocyanosis, and dry, hacking cough caused by the rash of miliary foci in the bronchial mucosa allow diagnosing the pulmonary form of miliary tuberculosis. Patients with this form of tuberculosis are often hospitalized in therapeutic departments, assuming a nonspecific etiology of the inflammatory process in the lungs.
Without etiotropic treatment, miliary tuberculosis progresses rapidly and often becomes complicated. Growing tuberculosis intoxication and respiratory failure usually lead to death in the first 2 months of the disease.
Subacute disseminated pulmonary tuberculosis usually develops gradually, over several weeks, and has no obvious manifestations. Despite the significant extent of the lesion, the patient may feel good, and the general condition may be satisfactory. Typically, there is a discrepancy between the low severity of clinical manifestations and the multiple nature of lung damage. Patients with subacute disseminated tuberculosis experience pronounced vegetative-vascular dystonia, psychoemotional lability, and a kind of euphoria, manifested in an objective assessment of their condition.
At the onset of the disease, the most common symptoms are general weakness, increased fatigue, decreased performance, irritability, sweating, loss of appetite, and gradual weight loss. Sometimes subfebrile body temperature, slight shortness of breath, and periodically occurring productive cough are noted. Later, pain in the side or a sore throat when swallowing, hoarseness of the voice often appear. These symptoms of disseminated pulmonary tuberculosis usually indicate the development of typical complications of disseminated tuberculosis. Pain in the side indicates the possible occurrence of pleurisy, and changes in the upper respiratory tract indicate tuberculosis of the larynx.
During an objective examination of patients with subacute disseminated tuberculosis, persistent red dermographism, relatively symmetrical shortening of the percussion sound and inconstant dry rales in the interscapular space above the areas of accumulation of foci can be detected. Sometimes, moist fine-bubble rales are heard, and when cavities of decay are formed, medium-bubble rales are also heard.
With slow progression, subacute disseminated pulmonary tuberculosis gradually transforms into chronic disseminated tuberculosis.
Symptoms of disseminated chronic pulmonary tuberculosis depend on the phase of the tuberculosis process and its duration. When the process worsens, symptoms of intoxication and cough are observed, often dry, sometimes with a small amount of sputum. When the inflammatory reaction subsides, the disease proceeds almost asymptomatically. However, after some time, the process worsens again.
The most constant clinical symptom of chronic disseminated tuberculosis is considered to be dyspnea. Its development is associated with a gradual increase in diffuse fibrosis and emphysema. With an exacerbation of the tuberculosis process and increased intoxication, the severity of dyspnea also increases. Patients often experience various neurotic reactions caused by functional changes in the central and autonomic nervous system. Endocrine disorders are possible, especially hyper- or hypothyroidism.
Fibrous changes in the upper lobes of both lungs, deformation of the bronchi and chronic bronchitis cause a shortening of the percussion sound over the upper sections of the chest, the appearance of dry wheezing. During an exacerbation, numerous moist rales can be heard. Over the lower sections of the chest, due to emphysema, a tympanic percussion sound is detected and weakened vesicular breathing is heard. Caverns in chronic disseminated tuberculosis are often "silent", i.e. they are not detected by percussion and auscultation.
Without treatment, chronic disseminated tuberculosis gradually progresses and transforms into fibrous-cavernous. Etiotropic treatment usually leads to partial resorption of tuberculosis foci. Most foci become denser and encapsulated, and diffuse fibrous changes in the lungs become more pronounced over time.