Disseminated pulmonary tuberculosis: symptoms

Various pathomorphological changes and pathophysiological disorders that occur with disseminated tuberculosis cause characteristic symptoms of disseminated pulmonary tuberculosis.

Acute disseminated (miliary) pulmonary tuberculosis usually develops within 3-5 days, reaching full severity by the 7-10th day of the disease. The following symptoms of disseminated pulmonary tuberculosis appear first: weakness, increased sweating, worsening of appetite, fever, headache, and sometimes dyspepsia. The body temperature rises rapidly to 38-39 ° C; note a fever of a hectic type. The increase in intoxication and functional disorders is accompanied by loss of body weight, adynamy, increased sweating, deafness or temporary loss of consciousness, delirium, tachycardia and acrocyanosis. A characteristic clinical symptom of disseminated pulmonary tuberculosis is dyspnea. Perhaps the appearance of a cough, often dry, sometimes with the allocation of scanty mucous sputum. In some cases, on the front surface of the chest and upper abdomen appears a delicate rosaceous rash, caused by the development of toxic-allergic thrombovasculitis.

Over the entire surface of the lungs determine the tympanic percussion sound, listen to weakened or hard breathing, a small amount of dry or small bubbling rales. Often noted increase in the liver and spleen, sometimes a moderate swelling of the abdomen.

The 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 departments.

Asphyxia shortness of breath, increasing tachycardia, acrocyanosis, as well as dry coughing caused by the precipitation of miliary foci in the bronchial mucosa, allow to diagnose 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 is rapidly progressing and often acquires a complicated course. Increasing tuberculosis intoxication and respiratory failure lead to death usually in the first 2 months of the disease.

Subacute disseminated pulmonary tuberculosis usually develops gradually, within a few weeks and has no bright manifestations. Despite the considerable length of the lesion, the patient's well-being can be good. And the general condition is satisfactory. Typically, the discrepancy between the low severity of clinical manifestations and the multiple nature of lung damage. In patients, we disseminate disseminated tuberculosis with marked vegetative-vascular dystonia, psychoemotional lability, and a peculiar euphoria, manifested in a biased evaluation of one's condition.

At the onset of the disease, the most frequent symptoms are general weakness, increased fatigue, decreased efficiency, irritability, sweating, worsening of appetite, a gradual decrease in body weight. Sometimes subfebrile body temperature, a slight dyspnea and a recurring productive cough are noted. In the future, often pain in the side or perspiration and pain in the throat when swallowing, hoarse voice. 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 - tuberculosis of the larynx.

In an objective examination, in patients with subacute disseminated tuberculosis, persistent red dermographism, a relatively symmetrical shortening of percussion sound and unstable dry wheezes in the interscapular space above the foci of foci of foci can be detected. Sometimes wet small bubbles are heard, and in the formation of cavities of decay - and medium bubbling rales.

With slow progression, subacute disseminated pulmonary tuberculosis is gradually transformed into chronic disseminated tuberculosis.

Symptoms of disseminated pulmonary tuberculosis depend on the phase of the tuberculosis process and its prescription. When the process is aggravated, symptoms of intoxication and cough, more often dry, sometimes with a small amount of sputum, are observed. When the inflammatory reaction subsides, the disease proceeds almost asymptomatically. However, after a while the process becomes aggravated again.

Dyspnoea is considered the most constant clinical symptom of chronic disseminated tuberculosis. Its development is associated with a gradual increase in diffuse fibrosis and emphysema. With an exacerbation of the tuberculosis process and an increase in intoxication, the manifestation of dyspnea also increases. Often, patients are noted for various neurotic reactions caused by functional changes in the central and autonomic nervous system. Endocrine disorders are possible, especially hyper- or hypothyroidism.

Fibrotic changes in the upper lobes of both lungs, bronchial deformities and chronic bronchitis cause a shortening of percussion sound over the upper sections of the chest, the appearance of dry wheezes. During the period of exacerbation, you can listen to numerous wet rales. Above the lower sections of the chest in connection with emphysema, a tympanic percussion sound is revealed and a weakened vesicular breath is heard. Caverns with chronic disseminated tuberculosis are often "mute", i.e. With percussion and auscultation they are not detected.

Without treatment, chronic disseminated tuberculosis gradually progresses and is transformed into fibrous-cavernous tuberculosis. Etiotropic treatment usually leads to partial resorption of tuberculosis foci. Most foci are densified and encapsulated, and diffuse fibrotic changes in the lungs become more pronounced over time.

[1], [2], [3], [4]

Complications of disseminated tuberculosis

Complications of disseminated pulmonary tuberculosis: caseous pneumonia, hematogenous dissemination. Formation of multiple caverns in the lungs followed by bronchogenic dissemination.

[5], [6], [7], [8], [9], [10]