Negative Intrapleural Pressure Research Articles

Re-expansion Pulmonary Edema

Re-expansion pulmonary edema (RPE) is a rare complication of pleural puncture (thoracentesis) and chest tube insertion. The incidence of RPE is low (1%), but mortality can be up to 20%. The main pathophysiological mechanism is pulmonary edema due to increased permeability and increased hydrostatic pressure in the pulmonary capillaries. Risk factors include duration of lung collapse (>3 to 7 days), size of pneumothorax (>30%), volume of aspirated air or fluid (>1.5 to 3 L), excessive negative intrapleural pressure, diabetes mellitus, and chronic hypoxemia. Prevention includes limiting the volume of aspirated air or fluid (<1.5 L), air or fluid evacuation in a controlled manner, and preventing excessive negative intrapleural pressure. Treatment is supportive care through cardiovascular and respiratory monitoring, oxygen and decubitus positioning.

C11 LARGE PLEURAL AND PERICARDIAL EFFUSION: WHICH DRAIN FIRST?

Abstract Introduction Large pleural and pericardial effusion is a common finding in lung cancer patients. However, a chronic large pleural effusion and the “lung entrapment” fenomenon, due to the neoplastic lung infiltration, could precipitate the re–expansion pulmonary edema (REPO) after the thoracentesis procedure. REPO is a rare and potentially life–threatening complication after large volume thoracentesis. It is characterized by alveolar infiltration in the reexpanded lung.Indeed, in the presence of “lung entrapment”, REPO development could be due not only to and excessive fluid removal, but also to the development of an excessively negative intrapleural pressure (< – 20 mmHg). As the REPO is often associated to an hemodynamic impairment, in patients with concomitant severe pericardial effusion, this condition could cause cardiac tamponade and the optimal therapeutic approach could be challenging.In this perspective, the decision on the effusion to be drained first, in this population, is not always straightforward.Case report In a 62 years –old woman with severe respiratory failure, a chest CT scan showed a massive left –sided pleural effusion with a complete collapse of the left lung, a severe pericardial effusion (35 mm) and the presence of malignant mediastinal nodes. (Figure 1).In the ICU a left thoracentesis was performed, with an early drainage of 1400 ml, the drain was then clamped. 30 minutes later, the patient developed a severe acute respiratory failure. An urgent chest x ray revealed an ipsilateral pulmonary oedema (Figure2). The patient was then treated with respiratory support with cPAP and intravenous diuretic therapy. Afterward, a rapid hemodynamic derangement occurred, with cardiac tamponade. An emergency echoguided pericardiocentesis was then performed followed by an immediate recovery. A repeated thorax CT scan revealed an advanced pulmonary tumor (Figure 3). Discussion In this case all the risk factors for REPO were coexistent: chronic pleural effusion and lung cancer. In addition, the large pericardial effusion represented a complicating factor in this situation as both the cPAP and the REPO’s hypovolemia may have brought to a clinical tamponade. In this context, where a neoplastic severe pleural and pericardial effusions are coexistent, it is essential to know which possible complications may occur after a large volume thoracentesis in order to prevent a high risk urgent pericardial drainage in patient with severe respiratory distress.

Trapped lung: a review of literature and recent cases

A trapped lung, one that cannot expand due to a restrictive fibrous visceral pleural peel, is caused by malignancy, chest trauma, thoracic surgery, complicated infection, and autoimmune conditions. Suspicion for and evaluation of this condition should be considered early on in a patient with history of the above conditions that presents with a chronic pleural effusion of stable volume. Diagnosis is reached with pleural fluid analysis, manometry that shows negative intrapleural pressure that is further reduced with fluid aspiration, and imaging that shows a chronic effusion and pleural thickening. Treatment is dependent on symptomatology and overall patient condition, and ranges from observation to fluid removal, fibrinolytic therapy, talc pleurodesis, indwelling pleural catheter, and surgical decortication. A review of English literature from the last 10 years including case reports, case series, and observational reviews was conducted. A majority of these patients presented with trapped lung due to malignancy, infection, or autoimmune conditions. Treatment varied depending on the cause of the trapped lung, underlying conditions, and patient preference; a majority of these patients received either pleurodesis, intrapleural fibrinolytic therapy, or surgical decortication.

Negative-pressure pulmonary edema and alveolar hemorrhage are potentially life-threatening complications of upper airway obstruction

Negative pressure pulmonary edema and alveolar hemorrhage are potentially life-threatening complications after relief of upper airway obstruction. The laryngeal-pharyngeal obstruction results in high negative intrapleural pressures. The increased intrapleural pressures affect the integrity of the alveolo-capillary membrane due to various factors. This review describes clinical symptoms, etiologic factors, pathophysiology and treatment strategies associated with each of these factors. The aim of this review is to equip clinicians with the knowledge base necessary to identify patients at increased risk for negative pressure pulmonary edema and alveolar hemorrhage.

The effects of chest drainage on pressure-controlled ventilation

BackgroundThe use of pressure-controlled ventilation (PCV) for anesthesia management is becoming more commonly used. Chest drainage is commonly performed after thoracic surgery, and the negative pressure it generates might affect the transpulmonary pressure (TPP). In the present study, we investigated how chest drainage could affect ventilating conditions during PCV.MethodsWe created a hand-made simple thoracic and lung model, which was connected to an anesthesia machine. The tidal volume (TV) was measured with positive end-expiratory pressure (PEEP) 0 and no chest drainage (baseline), followed by 10 cmH2O PEEP/no drainage, 10 cmH2O PEEP/drainage with − 10 cmH2O and 10 cmH2O PEEP/drainage with − 20 cmH2O. Finally, TV with 20 cmH2O and 30 cmH2O PEEP/no drainage was measured. Driving (inspiratory) pressure was maintained at 20 cmH2O during the whole experiment.ResultsTV was significantly increased by applying 10 cmH2O PEEP compared with baseline, further increased by applying − 10 cmH2O by drainage, similar to the value with PEEP 20 cmH2O with no drainage (end-tidal TPP of 20 cmH2O for both). TV decreased to < 50% of the baseline by applying 10 cmH2O PEEP with − 20 cmH2O by drainage, which was similar to that with 30 cmH2O PEEP with no drainage (end-tidal TPP of 30 cmH2O for both).ConclusionsTV was maintained at similar levels with the same TPP, regardless of PEEP or negative pressure by chest drainage change, suggesting that negative intrapleural pressure by the chest tube drainage system might mimic PEEP from the point of TV.

A case requiring re-thoracotomy due to a significant reduction of tidal volume after commencement of chest tube drainage under pressure control ventilation following lower lobectomy

BackgroundThe use of pressure-controlled ventilation (PCV) during one lung ventilation (OLV) has been popular to avoid high airway pressure. We experienced a case of a significant reduction of tidal volume (TV) after commencement of chest tube drainage under PCV following lower lobectomy, which required re-thoracotomy to evaluate the degree of air leak.Case presentationA 70-year-old man was scheduled for a lower lobectomy. OLV was managed by PCV. The driving pressure was set at 15–20 cmH2O with 4 cmH2O of positive end-expiratory pressure (PEEP). A chest drainage tube was placed after completion of lobectomy. To switch OLV to two lung ventilation (TLV), PCV settings were changed to the driving pressure at 10 cmH2O with 4 cmH2O of PEEP, which generated 450 ml of TV. Immediately after applying drainage (−10 cmH2O), TV decreased down to 250 ml. To maintain 450 ml of TV, PCV was switched to volume-controlled ventilation with 450 ml of TV, which raised the plateau pressure close to 24 cmH2O. Re-thoracotomy was done; however, significant findings were not detected.ConclusionsWe experienced a case of a significant reduction of TV immediately after chest tube drainage following lower lobectomy. Probably, negative intrapleural pressure increased the residual volume, which might have significantly affected the limited lung volume after lobectomy, resulting in decreasing TV during PCV.

Intraoperative pleural rent during kyphosis surgery: Monitor tells before surgeons!!

Dear Editor, Spine surgery is a complex surgery associated with complications even in the most experienced hands.[1] One of the known complications is intraoperative pleural injury especially with thoracic spine involvement.[2] We are reporting an intraoperative incident during thoracolumbar kyphosis correction surgery of a 13-year old female child (weighing 30 kg, 140 cm height) who underwent surgery involving fifth thoracic to second lumbar vertebral levels by posterior instrumentation. Kyphosis angle was 15° with no other systemic illness. After adequate fasting, child was shifted to OT and standard anesthesia monitors were attached. She was induced intravenously after securing an intravenous (i.v.) cannula and positioned prone after securing 6.5mm cuffed endotracheal tube. Initially during surgery, baseline ventilatory parameters were peak airway pressures of 18 to 19cm H2O and pulmonary compliance of 17ml/cm H2O. After 2 h of surgery, there was a sudden decrease in peak airway pressures (from 19 to 8cm H2O) and a marked increase in lung compliance (recorded in Dräger Primus anesthesia workstation) (from 17.2 to 48ml/cm H2O) [Figure 1a and b]. A fall in central venous pressure (CVP) from 9 to 5mmHg was noticed without significant blood loss and with adequate volume replacement [Figure 2a and b].Figure 1: Intraoperative trends of peak airway pressure and compliance (a) after repair of one-sided pleural rent with normalized parameters and (b) at the time of pleural rent on other side showing fall in airway pressures and increase in complianceFigure 2: Intraoperative central venous pressure (CVP) trends (a) after repair of one-sided pleural rent and (b) at the time of pleural rent on other side showing fall in CVPConsidering close proximity of surgical field to pleura and nature of event, we suspected pleural injury possibly pleural rents. The relationship between transmural pressure and lung’s volume is defined by compliance. Our lungs have an inherent tendency to collapse, whereas chest wall has tendency to expand. These two opposing forces create a negative intrapleural pressure. For lung expansion, positive transmural pressure is required (intra-alveolar pressure > intrapleural pressure).[3] The compliance curve is steeper at lower lung volumes and plateaus as volume increases meaning easier expansion of lung at lower lung volume when pulmonary compliance is high. This physiological phenomenon was clearly seen in our intraoperative findings. Fall in peak airway pressures and dramatically increased compliance. It normalised within a few minutes. [Figure 1a] picture after sealing of pleural rent. Again after a few minutes peak pressures dropped from 19 to 8cm H2O and lung compliance increased from 17.2 to 48ml/cm H2O [Figure 1b]. The operating surgeon figured out the cause and repaired the pleural rent bilaterally. Due to rent in pleura, there was a loss of intrapleural pressure and the lungs that have a tendency to collapse showed an increased compliance due to markedly decreased lung volume, which normalised after repair and similar thing happened on the other side, [Figure 1b]. A fall in CVP was also noticed due to fall in intrathoracic pressure to 5mmHg [Figure 2b], which returned to baseline (9mmHg) after pleural repair [Figure 2a]. Our case, had an open pneumothorax due to large pleural rent as opposed to tension pneumothorax associated to a ball-valve mechanism in literature.[4,5] Timely diagnosis and repair of pleural rent can prevent post-operative pneumothorax. Therefore, ventilatory parameters monitored by advanced anesthesia workstations can guide for early detection and immediate repair of large pleural rents even if it goes undetected by surgical team. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

RARE BACTERIAL EMPYEMA AFTER A BLUNT TRAUMA

TOPIC: Disorders of the Pleura TYPE: Medical Student/Resident Case Reports INTRODUCTION: Pleural effusion (PE) is an accumulation of excess fluid in the pleural space. PE is classified as transudative or exudative. Transudative pleural effusion can result from: increased hydrostatic pressure, decreased oncotic forces or increased negative intrapleural pressure. On the other hand, exudative pleural effusion result from increased capillary permeability and impaired lymphatic drainage caused by inflammatory processes. Parapneumonic effusions such as empyema are related to pneumonia in 20-40%. ß hemolytic Lancefield group A streptococcus pyogenes (GAS) is a common cause of upper respiratory tract and cutaneous infections which commonly is related to streptococcal toxic shock syndrome. GAS is an uncommon pathogen with 1.14 per 100,000 habitants associated to bacterial pneumonia, however the prevalence of GAS associated to empyema is only 0.7%. CASE PRESENTATION: Case of 46-year-old man with history of IVDA who arrived to urgency room due to shortness of breath, dry cough and left pleuritic chest pain of 3 weeks of evolution. He had a chest trauma as a pedestrian 2 weeks prior arrival. He denied fever, night sweats, hemoptysis, palpitations, or weight changes. Vitals signs were remarkable for tachycardia, tachypnea and decreased peripheral oxygen saturation. Physical examination was remarkable for bilateral decreased breath sounds and left side dullness to percussion. ABG's with oxygen supplementation revealed hypercapnia 57.3 mmHg with elevated A-a gradient 66.3 mmHg. CBC showed leukocytosis with left shifting. Chemistry panel was remarkable for metabolic alkalosis 31 mmol/L and lactate dehydrogenase was elevated 615 IU/L. Chest X-Ray showed left sided white lung, followed by a chest CT with bilateral pleuro-parenchyma fibrotic changes, bullae formation, centrilobular emphysema, patchy ground glass appearance at both lung fields and decreased right lung volume with ipsilateral displacement of the heart and mediastinal structures with large, multiloculated left pleural effusion with increased density. Left side thoracentesis performed collecting 120ml of purulent fluid, elevated WBC 150,000 with PMN 65% and gram stain positive. Chest tube was placed and drain 1400ml of brown-yellow purulent fluid and pleural culture showed growth of streptococcus pyogenes group A. Patient started on directed IV antibiotic therapy. DISCUSSION: Empyema is an accumulation of excess pus in pleural space. The M protein, the major virulence factor, is a macromolecule incorporated in fimbriae present on the cell membrane projecting on the bacterial cell wall. It is the primary cause of antigenic shift and antigenic drift among GAS. CONCLUSIONS: We expect to contribute awareness and knowledge to the medical field to always include empyema in the working diagnosis of all patients with progressive dyspnea after blunt trauma. REFERENCE #1: Sakai T, Taniyama D, Takahashi S, Nakamura M, Takahashi T. Pleural empyema and streptococcal toxic shock syndrome due to Streptococcus pyogenes in a healthy Spanish traveler in Japan. IDCases. 2017;9:85-88. Published 2017 Jun 27. doi:10.1016/j.idcr.2017.06.006 REFERENCE #2: Shebl E, Paul M. Parapneumonic Pleural Effusions And Empyema Thoracis. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534297/ REFERENCE #3: Tamayo E, Montes M, Vicente D, Pérez-Trallero E. Streptococcus pyogenes Pneumonia in Adults: Clinical Presentation and Molecular Characterization of Isolates 2006-2015. PLoS One. 2016;11(3):e0152640. Published 2016 Mar 30. doi:10.1371/journal.pone.0152640 DISCLOSURES: No relevant relationships by Maria Betancourt, source=Web Response No relevant relationships by Marlene Farinacci Vilaro, source=Web Response No relevant relationships by Kyomara Hernandez-Moya, source=Web Response No relevant relationships by Arnaldo Nieves-Ortiz, source=Web Response No relevant relationships by Ivanisse Ortiz Velez, source=Web Response No relevant relationships by Neshma Roman-Velez, source=Web Response

Work in progress report of a multicentre retrospective observational study to evaluate the association between the airflows and the intrapleural pressures digitally recorded after video-assisted lobectomy.

Digital chest drainage systems allow real-time and continuous monitoring and recording of air leak flow rate and intrapleural pressure (IPP) from the immediate postoperative period to the chest drainage removal. A multicentre retrospective observational analysis of consecutive patients undergoing pulmonary lobectomy for lung cancer was performed to evaluate the association between the airflow and IPP digitally recorded during the immediate postoperative period after video-assisted thoracic surgery (VATS) lobectomy for lung cancer. Here, we present a work in progress report. All patients treated with VATS lobectomies for lung cancer were included. Multiple airflow measurements and minimum and maximum IPP through the chest tubes were digitally monitored and recorded using microelectronic mechanical sensor technology. The PALs were defined as an air leak lasting >5 days from the conclusion of the surgical procedure. The cessation of air leaks was defined as an airflow <10 ml/min during 6 consecutive hours. This analysis comprised 76 patients who underwent VATS lobectomy for lung cancer. Nineteen patients (25%) showed prolonged air leaks (PAL) (≥5 days). The operative time was higher in the PAL group (mean difference = 44 min) without a statistically significant difference. Before the 7th postoperative hours, there were no statistically significant differences in IPPs. Patients with PAL showed less negative IPP in the first 24 postoperative hours. Therefore, the 7th-24th postoperative hours were critical in PAL prediction since the mechanism for PAL seems to develop after the 7th postoperative hour.

Bronchopleural Fistula in the Mechanically Ventilated Patient: A Concise Review

To describe the physiology of air leak in bronchopleural fistula in mechanically ventilated patients and how understanding of its physiology drives management of positive-pressure ventilation. To provide guidance of lung isolation, mechanical ventilator, pleural catheter, and endobronchial strategies for the management of bronchopleural fistula on mechanical ventilation. Online search of PubMed and manual review of articles (laboratory and patient studies) was performed. Articles relevant to bronchopleural fistula, mechanical ventilation in patients with bronchopleural fistula, independent lung ventilation, high-flow ventilatory modes, physiology of persistent air leak, extracorporeal membrane oxygenation, fluid dynamics of bronchopleural fistula airflow, and intrapleural catheter management were selected. Randomized trials, observational studies, case reports, and physiologic studies were included. Data from selected studies were qualitatively evaluated for this review. We included data illustrating the physiology of driving pressure across a bronchopleural fistula as well as data, largely from case reports, demonstrating management and outcomes with various ventilator modes, intrapleural catheter techniques, endoscopic placement of occlusion and valve devices, and extracorporeal membrane oxygenation. Themes related to managing persistent air leak with mechanical ventilation were reviewed and extracted. In case reports that demonstrate different approaches to managing patients with bronchopleural fistula requiring mechanical ventilation, common themes emerge. Strategies aimed at decreasing peak inspiratory pressure, using lower tidal volumes, lowering positive end-expiratory pressure, decreasing the inspiratory time, and decreasing the respiratory rate, while minimizing negative intrapleural pressure decreases airflow across the bronchopleural fistula. Mechanical ventilation and intrapleural catheter management must be individualized and aimed at reducing air leak. Clinicians should emphasize reducing peak inspiratory pressures, reducing positive end-expiratory pressure, and limiting negative intrapleural pressure. In refractory cases, clinicians can consider lung isolation, independent lung ventilation, or extracorporeal membrane oxygenation in appropriate patients as well as definitive management with advanced bronchoscopic placement of valves or occlusion devices.

An alternative explanation for the phasic variations in venous flow

BackgroundPhasic venous flow variation with respiration is surrounded by controversy and not well understood. The current concept assigns a major role to the “abdominal pump.” According to this model, inspiratory increases in abdominal pressure compress the vena cava, increasing its internal venous pressure and propelling blood upstream. Some have assigned a secondary role to the “thoracic pump,” with the negative intrapleural pressure aiding blood flow toward the heart. The aim of the present study was to examine the phasic changes in flow, pressure, and volume in the central veins and named tributaries. MethodsCaliber area changes were measured using intravascular ultrasonography in 37 patients undergoing iliac vein stenting. The pressure was measured in 48 patients using transducer tip catheters with electronic zero calibration. Duplex ultrasound flow in the head and neck and truncal and limb veins during inspiration and expiration was measured in 15 normal volunteers. ResultsThe caliber of the abdominal inferior vena cava had increased by 32% and its lateral pressure had decreased significantly during inspiration. Intravenous pressure in the central veins of the chest and right atrium was positive at 6 to 14 mm Hg. Negative pressures were rarely seen and then only transiently. The internal jugular vein displayed little phasic variation. The upper limb veins displayed weak inspiratory phasicity. Phase polarity was reversed in the lower limbs, with near flow stoppage during inspiration. ConclusionsThese observations conflict with the current notions of venous flow phasicity, which are based on push–pull pressure changes in the abdominal and thoracic veins. The paradoxical inspiratory inferior vena cava caliber increase probably explains the concurrent pressure decrease. Sustained negative pressures in the thoracic central veins and right atrium did not occur. We have proposed an alternate hypothesis for venous flow phasicity based on alternate stretching and relaxation of the mobile section of the great veins with respiratory movement.

Intrathoracic Migration of Abdominal Viscera in Pregnancy

A 28-year-old primiparous woman presented to the emergency department at 36 weeks of gestation for abdominal pain and dyspnea. She underwent uneventful sleeve gastrectomy 2 years previously. Physical examination showed abdominal diffuse tenderness with sparse abdominal metallic sounds, which were also present on the whole left chest with abolished breath sound. Results of the obstetric examination and fetus ultrasound examination were normal. An urgent low-dose computed tomography scan showed the small and large bowel in the left thoracic cavity, with contralateral mediastinal shift (Figure 1). A median laparotomy was performed, allowing delivery of a live-born neonate. Inspection of the left diaphragm showed the presence of a 3-cm diaphragmatic tear near but independent from the esophageal hiatus. Abdominal reintegration of the bowel was performed. The diaphragmatic tear was repaired with direct not absorbable sutures. Postoperative recovery of the patient and baby were uneventful. During pregnancy the growth of uterus increases intraabdominal pressure, and congenital or acquired minor resistance sites, or both, are stretched and under tension.1Paramore R.H. The intra-abdominal pressure in pregnancy.Proc R Soc Med. 1913; 6: 291-334PubMed Google Scholar In our case, we hypothesize that the diaphragmatic tear was acquired during the previous operation for gastric volume reduction and that the increasing of intraabdominal pressure during pregnancy led to its enlargement. As usual, in the presence of diaphragmatic holes, negative intrapleural pressure facilitates intrathoracic migration of abdominal organs.2Hood R.M. Traumatic diaphragmatic hernia.Ann Thorac Surg. 1971; 12: 311-324Abstract Full Text PDF PubMed Scopus (118) Google Scholar Fortunately, few dozen of cases of such a dramatic event are present in medical literature.3Reddy M. Kroushev A. Palmer K. Undiagnosed maternal diaphragmatic hernia–a management dilemma.BMC Pregnancy Childbirth. 2018; 18: 237Crossref PubMed Scopus (7) Google Scholar

Protocolo diagnóstico y terapéutico del neumotórax

Pneumothorax is defined as the presence of air in the pleural space, modifying negative intrapleural pressures and causing total or partial lung collapse. Incidence of pneumothorax varies according with its classification, however the rate is higher in males. Mortality rate is highly variable too (depending on patient characteristics –cardiopulmonary reserve– and pneumothorax type). Diagnosis of pneumothorax is mainly based on chest X-ray. Management requires general treatment measures as well as air- evacuation techniques

Apnea causes microvascular perfusion maldistribution in isolated rat lungs.

Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously breathing rats exposed to five episodes of obstructive apnea. We quantified microvascular perfusion by analyzing trapping patterns of 4 μm diameter fluorescent latex particles infused into the pulmonary circulation after the last episode. We could not determine if the perfusion maldistribution was due to the effects of large subatmospheric intrapleural pressures during apnea, or to precapillary OSA hypoxic vasoconstriction. To address this, we repeated these studies using isolated, buffer‐perfused rat lungs (P pulm art, 10 cm H2O) ventilated in a chamber (−5 to −15 cm H2O, 25 breaths/min; P trachea = 0). We simulated apnea by clamping the trachea and cycling the chamber pressures between −25 and −35 cm H2O for five breaths. After five apnea episodes, we infused 4 μm diam. fluorescent latex particles into the pulmonary artery. The number of particles recovered from the venous effluent was 74% greater in nonapneic isolated lungs compared to apneic lungs (P ≤ 0.05). Apneic lungs also had perfusion maldistributions that were 73% greater than those without apnea (P ≤ 0.05). We conclude that simulated apnea in isolated, perfused rat lungs produces significantly greater particle trapping and microvascular perfusion maldistribution than in nonapneic isolated lungs. We believe these effects are due to the large, negative intrapleural pressures produced during apnea, and are not due to hypoxia.

Edema de reexpansión pulmonar “REPE” intraoperatorio tras toracoscopia mediante ventilación unipulmonar

El “REPE” (Re-expansion Pulmonary Edema) es una complicación poco común que puede ocurrir después del drenaje rápido de un neumotórax o de abundante líquido pleural (1,2). La incidencia en adultos es del el 0-1%. Su mortalidad puede alcanzar el 20% (1,3). Las hipótesis propuestas para el desarrollo de dicha entidad incluyen, el aumento de la permeabilidad de la microvasculatura pulmonar, cambios en el flujo linfático, disminución de la producción de surfactante y aumento de la presión hidrostática del flujo vascular del pulmón reexpandido (4). Se caracteriza por el desarrollo agudo de hipoxemia refractaria al oxígeno y la aparición de infiltrados alveolares intersticiales en un plazo de 24 horas tras el drenaje (5). Son factores de riesgo de REPE: la edad comprendida entre los 20 y 40 años, la duración del colapso pulmonar mayor de 72 horas, la aplicación de altas presiones negativas durante la toracocentesis (20 cm H2O), una rápida reexpansión tras drenajes de altos volúmenes de líquido pleural (&gt; 1.5 L) o la existencia de factores predisponentes para el edema pulmonar (hipoalbuminemia, estasis en la circulación pulmonar). ABSTRACT Intraoperative reexpansion pulmonary edema “REPE” following thoracoscopy by one lung ventilation The sudden pulmonar expansion which has remained collapsed among different hours or days, likewise the fast pneumothorax or pleural effusion drainage, can cause a flash or acute edema on the affected lung. It is believed that the rexpansive pulmonary syndrome (REPE), is caused due to an increment in the capillary permeability after being exposed the affected lung to high negative intra-pleural pressure. The ocurrence of REPE is a rare event with most cohort studies reporting an incidence of between 0%- 1%. It may extend with hypoxaemia, hypotension and even cardiac arrest. The treatment of these patients include mechanical ventilation with optimal PEEP levels, the use of vasopressors and an intesive electrolyte resuscitation. We expose the case of a 16 year old patient with mediastinal mass diagnosis and massive left-pleural effusion, where after a thorascocopy for biopsy and pleuritic drainage, it is observed a reexpansion pulmonary edema with respiratory repercussion, haemodynamics and the requirement of endotracheal reintubation.

ISOLATED CHYLOTHORAX IN LIVER CIRRHOSIS

SESSION TITLE: Disorders of the Pleura SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 pm - 02:15 pm INTRODUCTION: Hepatic hydrothorax, commonly seen in cirrhotic portal hypertension occurs from the movement of ascitic fluid into the pleural space across microscopic defects in the diaphragm due to the negative intrapleural pressure. Liver cirrhosis causing chylothorax is extremely rare accounting for only about 1% cases. CASE PRESENTATION: We present a 43-year-old female with recurrent hepatic hydrothorax from decompensated alcoholic cirrhosis complicated by hepatic encephalopathy. She was admitted to the intensive care unit for airway monitoring. Patient was evaluated by Hepatology in the past and deemed not a liver transplant candidate due to severe malnutrition. She gets frequent thoracentesis and paracentesis that have been reported as yellow or straw colored. She has not had any thoracic or abdominal surgeries. We performed a diagnostic thoracentesis to rule out infection, as she had no ascitic fluid noted on ultrasound examination. The fluid appeared milky yellow and thick (Fig2). A pigtail catheter was then placed for drainage with concern for empyema (Fig3). Pleural fluid studies revealed a transudative fluid with 60 white cells and negative gram stain and culture. The triglyceride level was 149 mg/dl and cholesterol was 16 mg/dl. Ratio of Pleural fluid to serum triglyceride was 1.2 confirming chylothorax. Subcutaneous octreotide was started to reduce the portal hypertension and potentially reduce splanchnic lymphatic pressures. Patient was not a candidate for TIPS due to hepatic encephalopathy and high bilirubin. CT chest did not show lymphadenopathy or lung parenchymal abnormality. The chest tube was removed after a few days once the drainage slowed. DISCUSSION: Chylothorax is defined as pleural fluid triglyceride level >110mg/dl and cholesterol <200mg/dl, with the ratio of pleural fluid to serum triglyceride more than 1. Pseudochylothorax develops due to long-standing exudative effusions and will have pleural fluid cholesterol levels >200mg/dl. Chylothorax occurs most commonly due to malignant obstruction of the thoracic duct and only 1% of cases due to cirrhosis. The mechanism in cirrhosis is thought to be portal hypertension resulting in high pressures in the splanchnic lymphatic vessels. This causes rupture of lymphatics and leakage of chylous fluid in the peritoneal space. Chylothorax is usually exudative but is transudative in the setting of cirrhosis, nephrotic syndrome and heart failure. Chylous ascites is managed conservatively with a low-fat diet that contains more medium chain triglycerides. Total parenteral nutrition is an alternative in resistant cases. TIPS is an effective treatment in patients who don’t improve with conservative measures. CONCLUSIONS: Isolated chylothorax without chylous ascites has not been previously reported in literature, as was seen in our patient. Low fat diet and measures to reduce portal hypertension can be attempted to resolve the chylothorax. Reference #1: Romero S, Martín C, Hernandez L, et al. Chylothorax in cirrhosis of the liver: analysis of its frequency and clinical characteristics. Chest. 1998;114(1):154-9. Reference #2: Valdes L, Alvarez D, Pose A, Valle JM. Cirrhosis of the liver, an exceptional cause of chylothorax: two cases. Respir Med. 1996;90(1):61-2. Reference #3: McGrath EE, Blades Z, Anderson PB. Chylothorax: Aetiology, diagnosis and therapeutic options. Respir Med. 2010; 104 (1): 1-8. DISCLOSURES: No relevant relationships by Sabin Bista, source=Web Response No relevant relationships by Deepak Chandra, source=Web Response No relevant relationships by Navin Victor, source=Web Response

Fluid Balance Is Associated with Clinical Outcomes and Extravascular Lung Water in Children with Acute Asthma Exacerbation.

The effects of fluid administration during acute asthma exacerbation are likely unique in this patient population: highly negative inspiratory intrapleural pressure resulting from increased airway resistance may interact with excess fluid administration to favor the accumulation of extravascular lung water, leading to worse clinical outcomes. Investigate how fluid balance influences clinical outcomes in children hospitalized for asthma exacerbation. We analyzed the association between fluid overload and clinical outcomes in a retrospective cohort of children admitted to an urban children's hospital with acute asthma exacerbation. These findings were validated in two cohorts: a matched retrospective and a prospective observational cohort. Finally, ultrasound imaging was used to identify extravascular lung water and investigate the physiological basis for the inferential findings. In the retrospective cohort, peak fluid overload [(fluid input - output)/weight] is associated with longer hospital length of stay, longer treatment duration, and increased risk of supplemental oxygen use (P values < 0.001). Similar results were obtained in the validation cohorts. There was a strong interaction between fluid balance and intrapleural pressure: the combination of positive fluid balance and highly negative inspiratory intrapleural pressures is associated with signs of increased extravascular lung water (P < 0.001), longer length of stay (P = 0.01), longer treatment duration (P = 0.03), and increased risk of supplemental oxygen use (P = 0.02). Excess volume administration leading to fluid overload in children with acute asthma exacerbation is associated with increased extravascular lung water and worse clinical outcomes.

A pleural vacuum relief device for pleural drain unit use in the hyperbaric environment.

When a standard water-seal pleural drain unit (PDU) is used under hyperbaric conditions there are scenarios where excessive negative intrapleural pressure (IPP) and/or fluid reflux can be induced, risking significant morbidity. We developed and tested a pleural vacuum relief (PVR) device which automatically manages these risks, whilst allowing more rapid hyperbaric pressure change rates. The custom-made PVR device consists of a one-way pressure relief valve connected in line with a sterile micro filter selected for its specific flow capacity. The PVR device is designed for connection to the patient side sampling port of a PDU system, allowing inflow of ambient air whenever negative pressure is present, creating a small, controlled air leak which prevents excessive negative pressure. The hyperbaric performance of a Pleur-Evac A-6000 intercostal drain was assessed with and without this added device by measuring simulated IPP with an electronic pressure monitor connected at the patient end of the PDU. IPP readings were taken at 10, 15, 20 and 30 cmH₂O of suction (set on the drain unit) at compression rates of 10, 30, 60, 80, 90 and 180 kPa·min⁻¹ to a pressure of 280 kPa. At any compression rate of > 10 kPa·min⁻¹, the negative IPP generated by the Pleur-Evac A-6000 alone was excessive and resulted in back flow through the PDU water seal. By adding the PVR device, the generated negative IPP remains within a clinically acceptable range, allowing compression rates of at least 30 kPa·min⁻¹ with suction settings up to -20 cmH₂O during all phases of hyperbaric treatment. The PDU PVR device we have developed works well, minimising attendant workload and automatically avoiding the excessive negative IPPs that can otherwise occur. This device should only be used with suction.

Laringeal maske kullanımı sırasında negatif basınçlı pulmoner ödem: Olgu sunumu

Negative pressure pulmonary edema (NPPE), a non-cardiogenic pulmonary edema, develops due to airway obstruction. Young, healthy, male patients, who have a lot of muscle mass that can lead to produce high negative intra-pleural pressure (athletes pulmonary edema syndrome, APS), are under the risk of developing NPPE. Usually, NPPE develops after extubation in patients who undergo endotracheal intubation however; there are some case reports showing that it can develop after laryngeal mask application (LMA) even in a less manner. The most possible reasons lead to airway obstruction during LMA use are biting of laryngeal mask tube, misplacement of tube, and laryngospasm. This case report presents a patient who undergoes LMA and develops NPPE due to laryngospasm during recovery from anesthesia.

Rib fracture management

### Key points Trauma is a major cause of morbidity and mortality worldwide, and the leading cause of death in the first four decades of life. Rib fractures are very common and are detected in at least 10% of all injured patients, the majority of which are as a consequence of blunt thoracic trauma (75%) with road traffic collisions being the main cause. The remaining 25% are due to penetrating injuries. Rib fractures are associated with significant morbidity, with patients frequently requiring admission to the intensive care unit (ICU), and mortality rates as high as 33%.1 This morbidity and mortality associated with rib fractures is caused by three main problems: hypoventilation due to pain, impaired gas exchange in damaged lung underlying the fractures, and altered breathing mechanics. Pain associated with rib movement reduces the tidal volume and predisposes to significant atelectasis. This can further lead to retention of pulmonary secretions and pneumonia. An injury severe enough to fracture ribs, especially if so significant as to cause a flail segment, will invariably cause a substantial contusion to the underlying lung. The lung becomes oedematous with varying degrees of haemorrhage and necrosis. The damaged lung is poorly compliant and will not take part in gas exchange, leading to intrapulmonary shunting and a decrease in P a O 2 . In the presence of a flail segment, the generation of negative intrapleural pressure produces paradoxical movement of the flail, causing it to move inward, while the rest of …