Serofibrinous Pleurisy

Description, Pathological Anatomy, Physical Exam, Clinical Forms, Complications, Therapy.

It is an acute inflammation of the pleura characterised by the presence of exudate in the pleural cavity. Pulmonary tuberculosis is the most common cause (50%). It is most common in people between the ages of 16 and 35. The violent response of serous pleura to tuberculosis is due to an allergic mechanism. The disease is often the first clinical manifestation of tuberculosis, occurring in the weeks or months following primary infection.

Pleural touching occurs through the hematogenous pathway and especially through contiguity from a lung or lymph node. A favourable role is played by the season (March-May), cold, humidity and diseases that lower body resistance.

Pathological anatomy

Serofibrinous Pleurisy is usually preceded by pleurisy. The pleura is edematous, erythematous and covered by fibrin deposits. If the process progresses, the exudate (a clear, yellow liquid) is formed. Pleural effusions lose their gloss and are covered by fibrin membranes under which are found fibrin tubers. The inflammatory process can be cured without sequelae.

Sometimes pleural effusions join together to form pleural symphysis that may be partial or total (fibrothorax).

Onset is brutal in more than half of the cases, with intense chest pain, sometimes irradiated in the abdomen or shoulder, exaggerated by the respiratory movements and calmed by the chest immobilisation or the build-up of the fluid, with repeated chills and fever that in 2-3 days can exceed 39 degrees.

Sometimes onset is progressive with signs of bacillary impregnation, with progressive fever.

Sometimes it is latent, the exudation being noisy and accidentally discovered.

In the status period (5 days to 3 weeks) the fever is constant (39-40) less irregularly, and the chest pain is diminished or disappeared. Can appear dizziness, dry and tiring coughing, paleness.

Physical examination

It describes the signs of the pleuretic syndrome: veneering of the affected chest, ablation of vocal vibrations and vesicular murmur, chelation and pleuretic bloating.

The exploratory puncture specifies the nature of the liquid, which is a rich albumin exudate, with the positive Rivalta reaction, containing many lymphocytes. Bacillus Koch is exceptional.

The radiological examination specifies the existence and volume of the liquid collection, the exudate appearing as an intense and homogeneous basal opacity with the imprecisely defined superior part.

Clinical forms

  • Tuberculous serotype pleurisy is the most common form and occurs in adolescents and young adults. It is preceded by a primary infection or signs of bacillary impregnation. The onset is progressive.
  • Pleurisy that accompanies or follows bacterial pneumonia occurs either in the first half of the evolution of the pneumonic process or in the craving of pneumonia. The exudate is rich in polynuclear, it can resorb spontaneously, but sometimes it tends to evolve towards empyema.
  • Rheumatism pleurisy occurs in children and adolescents. It coexists with acute polyarticular rheumatism. The exudate is low and contains a lot of fibrin, albumin and endothelial cells.
  • Neoplastic pleural effusion usually occurs in patients over 50 years of age. Evolves afebrile, the fluid recovers after evacuation and presents neoplastic cells. It can often be haemorrhagic.

Complications

Sudden death, loss of other serous, pulmonary tuberculosis, pleural symphysis.

A positive diagnosis is suggested by a feverish condition accompanied by chest pain and dry cough.

Therapy

Hygiene-dietetic  serofibrinous  pleurisy treatment includes bed resting throughout the fever, with the resumption of normal activities after at least six months of afebrility. The room should be warm and well ventilated. The diet will be high in calories and vitamins.

Etiological serofibrinous pleurisy treatment consists of the administration of tuberculostatics in double or triple combination. The duration of treatment should be approximately two years.

Pathogenic serofibrinous pleurisy treatment includes the administration of cortico-hormones, using the anti-inflammatory effect of cortisone and its derivatives.

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