Symptoms of Kashiwa pneumonia

Symptoms of Kashiwa pneumonia

Many people may not be so clear about the disease of Pneumonia, because the incidence of this disease is relatively not that high now. It is just a relatively chronic disease. If it is just at the beginning of the disease, people will not pay too much attention to this problem. After all, the symptoms are not so obvious, and there will not even be any coughing. You can only feel that your blood pressure has increased.

Chronic pneumonia is characterized by periodic relapses and exacerbations that occur in waves. Symptoms vary depending on the stage of the disease, age and individual. During the resting period, the body temperature is normal, there are no obvious signs, and there is almost no cough, but the patient is prone to shortness of breath when running and climbing stairs. During the exacerbation phase, there is often pulmonary insufficiency, cyanosis and dyspnea, and external respiratory dysfunction such as hyperventilation due to reduced vital capacity and respiratory reserve and shortened breath-holding time. After worsening, the condition improves very slowly, with frequent coughing up sputum, and even facial edema, cyanosis, chest deformation, and clubbing of fingers and toes. Due to emphysema and pulmonary insufficiency, the pulmonary circulation resistance increases, the pulmonary artery pressure increases, and the burden on the right heart increases, which may lead to cor pulmonale within six months to two years. There may also be liver dysfunction. White blood cell count increased and erythrocyte sedimentation rate moderately increased.

Chest X-rays show that the lung texture in the middle and lower fields of both lungs and the hilar area may be honeycombed, with alveolar emphysema, and may be accompanied by substantial inflammatory lesions. The shadows at the hilum of both sides can be seen to increase symmetrically. As the disease progresses, X-ray signs of cor pulmonale such as bronchiectasis, right ventricular hypertrophy and protrusion of the pulmonary artery segment may also occur. In patients with cor pulmonale, the electrocardiogram shows clockwise rotation, tall and sharp P waves, and most QRS complexes show changes such as right ventricular hypertrophy pattern.

A disease course of more than 3 months is considered chronic pneumonia. The mortality rate of acute pneumonia in children has been decreasing in recent years, but children with severe pneumonia sometimes do not recover completely, and relapse and development of chronic pneumonia are not uncommon. Therefore, it is very important to prevent and treat chronic pneumonia in a timely manner.

The factors that contribute to chronic pneumonia include the following: ① When children with malnutrition, rickets, congenital heart disease or tuberculosis develop pneumonia, the course of the disease is likely to be prolonged. ②Viral infection causes interstitial pneumonia, which can easily develop into chronic pneumonia. The Capital Institute of Pediatrics followed up 103 cases of adenovirus pneumonia 1 to 5 years after the onset of the disease and found that 30.1% showed chronic pneumonia and atelectasis of varying severity on X-ray examination, and some children also had bronchiectasis. Thirteen cases of measles complicated with adenovirus pneumonia were followed up 2 to 3 years after onset of the disease, of which 6 had developed chronic pneumonia. ③Recurrent upper respiratory tract infections or bronchitis and chronic sinusitis are all causes of chronic pneumonia. ④ Foreign objects that penetrate deep into the bronchi, especially those that lack irritation and do not cause initial acute fever (such as date pits, etc.), can be ignored and remain in the lungs for a long time, forming chronic pneumonia. ⑤ Children with immunodeficiency, including humoral and cellular immunity deficiency, complement deficiency and leukocyte phagocytic function deficiency can all suffer from repeated attacks of pneumonia, which may eventually become chronic. ⑥ Primary or secondary abnormalities in the morphology and function of respiratory cilia can cause chronic lung inflammation.

Inflammatory lesions can invade bronchi, alveoli, interstitial tissues and blood vessels at all levels. Especially in the inflammation of interstitial tissue, each attack progresses, causing the destruction of the elastic fibers of the bronchial wall, and eventually leading to stenosis of the lumen due to fibrosis. At the same time, atelectasis occurs due to the blockage of the lumen by secretions, eventually leading to bronchial dilatation. Due to the destruction of the bronchial walls and alveolar walls, air spreads through the lymphatic vessels and enters the tissue spaces, forming interstitial emphysema. Local blood vessels and lymphatic vessels also undergo proliferative inflammation, with thickening of the vessel walls and narrowing of the lumen.

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