ACUTE RESPIRATORY DISTRESS SYNDROME AS A COMPLICATION OF VIRAL PNEUMONIA — CASE REPORT

ARDS is a life-threatening condition that requires monitoring in intensive care units. There is no specific treatment. We present a 49 year-old female patient with ARDS and its complications, ventilation assisted pneumonia (VAP) andbilateral pneumothorax.Good knowledge of the process can help to choose the appropriate treatment and to prevent or to recognize possible complications. Adequate oxygen therapy takes important place in treatment of these patients.


INTRODUCTION
The definition of ARDS was given in 2011 by The European Society of Intensive Care Medicine, supported by The American Thoracic Society and the Society of Critical Care Medicine and it is known as the Berlin Definition.According to it, ARDS is defined by time (one week from a clinical insult or a worsening of the chronic condition); radiographic changes (bilateral shadows, not fully explained by effusion, consolidation, atelectases); presence of lung edema in the absence of left heart failure and PaO2 / FIO2 ratio with a minumum of 5 cm 2 H20 continuous positive airway pressure (CPAP).By definition, 3 ARDS categories have been identified.Subtypes are based on the degree of hypoxemia: mild (PaO2 / FIO2 £ 300 mm Hg), moderate (PaO2 / FIO2 £ 200 mm Hg), and severe (PaO2 / FIO2 £ 100 mm Hg) (1,2).ARDS implies diffuse alveolar injury (DAD) and injury to the capillary endothelium in the lungs.Injuries of the capillary endothelium and alveolar epithelium lead to impaired fluid transport through alveoli and fluid accumulation rich in proteins within the alveoli, eventually leading to diffuse alveolar injury, with the release of proinflammatory cytokines, such as Tumor Necrosis Factor (TNF), IL-1 and IL-6 (3).Neutrophils are activated, releasing toxic mediators, proteases and free radicals (4).Abnormalities of transcription factors, including NF-cap B needed for gene transcription for many pro inflammatory mediators, are present in ARDS (5).Endothelin-1, angiotensin-2 and phospholipase A-2 also significantly increase vascular permeability.
The loss of epithelial integrity in ARDS has many consequences.First, under normal conditions, the epithelial barrier is much less permeable than the endothelial.Thus, epithelial injury contributes more to alveolar leakage.Secondly, the loss of epithelial integrity and injuries of epithelial cells type II impairs normal fluid and ion exchange, leading to edema within the alveolar space.Thirdly, pneumocyte type II injury reduces the production of surfactants leading to known abnormalities.Fourth, loss of the epithelial barrier can lead to septic shock in patients with bacterial pneumonia.Finally, if the injury of the alveolar epithelium is serious, the inability to regenerate ultimately leads to fibrosis.The fibrosis process was stimulated by interleukin (IL) -1.Progression to fibrosis can be predicted by the increased values of procollagen peptide III (PCP-III) in the sample obtained by BAL.The diseases most commonly associated with ARDS can be both lungs and systemic (Table 1).Mycobacteria pneumoniae, although associated with unilateral pneumonia, can also lead to changes that correspond to acute respiratory distress syndrome (6,7).
The main symptoms include breathing difficulties (dyspnoea), rapid breathing (tachypnoea), and extremely deep breathing (hyperventilation) and reduced oxygen levels in the circulation (hypoxemia it occurs 24 to 48 hours after the onset of the underlying disease or worsening of the existing one.One of the most significant characteristics of ARDS is that there is hypoxemia refractor to oxygen therapy, and therefore patients are subjected to mechanical ventilation.One of the most common complications of mechanical ventilation is bacterial pneumonia, which is usually caused by gram negative bacteria (P.aeruginosa, Acinetobacter baumannii, and Stenotrophomonas maltophilia) (40%), then Enterobacteriaceae (29%) and MRSA (21% ) In the laboratory tests we often find an increased number of white blood cells, which speaks for pneumonia or sepsis.Acido base status may show reduced H < 7.4.On the RTG image of the lung we find the presence of edema.CT may sometimes be needed, but usually a RTG record is sufficient.Ultrasound of the heart helps to exclude heart problems.Monitoring with arterial pulmonary catheter excludes the existence of pulmonary hypertension.Bronchoscopy can be considered if there is a need for evaluation of lung condition.

CASE REPORT
A 49 years old female was admitted to the Clinical Hospital Center of Montenegro pulmology department through Emergency Center due to choking, dry cough, weakness and fatigue, elevated body temperature.The illness started seven days before with mentioned problems that intensified by time, after which she was admitted to the General Hospital Berane.During treatment in the Berane General Hospital, a PCR test for influenza A and B was performed.The findings were sent for analysis to the Public Health Institute.Lung RTG was performed and bilateral pneumonia was noticed.In past medical history she reported diabetes mellitus type 2 with metformin therapy.
On admission to the Emergency Center, she was conscious, oriented, mobile.Discrete dyspnoea atrest was present, tachycardia, temperature 38.3 °C, cyanotic lips, dry plated tongue with herpetic changes in the labial region.The conclusion was that she leaves the-impression of a medium sick patient.A skin was of a reduced turgor, with no signs of hemorrhagic syndrome.Auscultatory fine crackels were heard at basal parts of lung.In the obtained laboratory tests, the increase in inflammatory parameters with elevated values of D dimer and liver function parameters were verified (WBC 14.After receiving the patient, an anesthesiologist was consulted, the patient was intubated and connected to mechanical ventilation A / C f12, FiO2 0.5.In the further course of the day, the patient was monitored by anesthetist for control of the respiratory pattern.The mode of mechanical ventilation was changed on several occasions depending on the condition of the patient (A/C, BiLevel, spontaneous).A therapy was given by pulmologists (corticosteroids, theophylline preparations, bronchodilatators, oseltamivir, combination of antibiotics for parenteral administration, antimycotics).
Subsequently, the arrival of the medical documentation from Publich Health Institute, a throat swab confirmed the presence of Influenza A, Real Time PCR was positive, as well.
The applied therapy led to a decrease in the value of CRP while maintaining high values of leukocytes.In the longer course of the treatment, a bronchoscopy was repeatedly made, respiratory tract toilete was done, and large amount of dense bleeding content was aspirated.BAL has been taken.Microbiological analysis showed the presence of Acinetobacter spp, which was accompanied bynew increase of inflammatory parameters (CRP, Le).The therapy included the antibiotic Collistin, due to the resistance of the bacterium to the standard antibiogram.Controlled MSCT lung arteries weremade-no signs of thrombotic changes.There were signs of bronchopneumonia on both sides.
Due to the need for further respiratory support, a tracheostomy has been done on the twelfth day of intubation.The day after tracheotomy at the control RTG, a pneumothorax on the leftside was diagnosed.A chest surgeon was consulted and a thoracic drain was placed.Two days after due to repeated pain in the chest and ab-domen, a new RTG of the lung was made which diagnosed the existence of a right-sided pneumothorax and the thoracic drain was placed in the right pleural space.The patient's condition was gradually improving (ABB: p CO2 5.5, p O2 7.2, CRP 56.4), and on the seventh day after the placement of the thoracic drains, the patient was extubated.Serial lung radiographs were obtained which showed re-expansion of both lungs.On the 11th day after the placement of the first thoracic drain, the left thoracic drain was removed, and the right one two days later.The patient was then transferred into the pulmonology department for further monitoring where oral antibiotic therapy continued during the next two weeks, as well as other supportive therapy.The patient was discharged in good general condition, hemodynamically stable for further ambulatory monitoring.

DISCUSSION AND CONCLUSION
People in whom ARDS is recognized often require treatment in intensive care units.There is no specific therapy.The treatment is primarily supportive.Mechanical respiration and adequate use of oxygen play a major role.A key advancement in therapy is the knowledge that lung transduction with positive pressure can exacerbate the existing condition.This attitude has contributed to the development of a new strategy in the treatment of mechanical ventilation using small breathing volumes (6ml/kg) in combination with positive pressure at the end of the expiry (PEEP).Appropriate oxygen therapy in other medical conditions can also prevent secondary development of ARDS.Determan and associates performed a controlled randomized study with 150 patients that compared the use of small breathing volumes versus standard patients with critical illness and pointed to reduced production of inflammatory cytokines in patients treated with low air volume (8).Then, there are also adequate nutrition and hydration.Antibiotic therapy is mandatory, most often ex-iuvantibus.Corticosteroids are occasionally administered to resolvethe primary condition, otherwise their use is controversial.Correction of acid base status and other therapies (diuretics, analgetics, anxiolytics, antihypertensives) is regulated as needed.If the recovery does not occur in the first seven days, there is a greater likelihood that progressive lung injury will develop followed by inflammation of the interstitium, and later fibrosis.
Our patient is just an example of this treatment.Complications such as ventialtion-assisted pneumonia and bilateral pneumothorax have prolonged her healing.According to the International Nosocomial Infection Control Consortium (INICC), the frequency of VAP is 13.6 versus 1.000 days spent on ventilation sup-Figure 2 -CT of patient's lungs arteries port, although the incidence varies depending on the hospital groups and hospital conditions, so that the frequency of VAP ranges between 13-51 and 1000 days spent on ventilation.Patients who survive the ARDS episode usually have lasting effects that are reflected in reduced HRQOL (health related quality of life).Usually we talk about neurocognitive impairment and psychiatric illness.Proper treatment certainly reduces this risk (9,10).
3, Hgb 124, PLT 331, CRP 147.6, AST 142, ALT 240, GGT 227, LDH 751, CK 68, K 3.8, Na 137, D dimer >36.436).The performed ABB showed a global respiratory insufficiency, metabolic compensated (p H 7.43, p CO2 6.1, p O2 5.1, HCO3 28.4,hco3 STD 26.1, BE 5.3, with O2 84%).On the performed RTG recording of the lungs in the UC, the bilateral shading of the lower and middle lung fields was described.CT of lung arteries excluded the presence of lung thromboembolism and described the consolidation of the lung parenchyma starting from lung apexand going through the middle and dorsobasal segments with the manifestation of typical signs of pulmonary edema.Hospital treatment was indicated Soon after the admission to the pulmonary department, the patient's condition worsened.Central cyanosis occurred and repeated ABB showed: p H 7.51, p CO2 5.3, p O2 3.8, HCO3 30.4,BE 8.2, SaO2 63.5,

Table 1 .
ARDS related diseases and conditions