Background Severe acute pancreatitis (SAP) is a systemic inflammatory disease, and it can often complicate into acute kidney injury (AKI) and acute lung injury/acute respiratory distress syndrome (ALI/ARDS). This study aimed to evaluate the clinical effectiveness of blood purification using a polymethylmethacrylate (PMMA) hemofilter.
Methods We retrospectively examined 54 patients, who were diagnosed with SAP according to the Japanese criteria from January 2011 to December 2019.
Results Of a total of 54 SAP patients, 26 patients progressively developed AKI and required continuous hemodialysis with a PMMA membrane hemofilter (PMMA-CHD). Acute Physiology and Chronic Health Evaluation (APACHE) II score and Sequential Organ Failure Assessment (SOFA) score were significantly higher in patients requiring PMMA-CHD than in patients not requiring hemodialysis. The lung injury scores were also significantly higher in patients requiring PMMA-CHD. Of the 26 patients, 16 patients developed ALI/ARDS and required mechanical ventilation. A total of seven patients developed severe ALI/ARDS and received additional intermittent hemodiafiltration using a PMMA hemofilter (PMMA-HDF). Although the length of intensive care unit stay was significantly longer in patients with severe ALI/ARDS, blood purification therapy was discontinued in all the patients. The survival rates at the time of discharge were 92.3% and 92.9% in patients with and without PMMA-CHD, respectively. These real mortality ratios were obviously lower than the estimated mortality ratios predicted by APACHE II scores.
Conclusions These finding suggest that the blood purification using a PMMA hemofilter would be effective for the treatment of AKI and ALI/ARDS in SAP patients.
Ariana Alejandra Chacón-Aponte, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, Tariq Janjua
Acute Crit Care. 2022;37(1):35-44. Published online February 11, 2022
The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.
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Background Overactivation of inflammatory cells, including macrophages and neutrophils, is associated with acute lung injury. BMS-470539 is a selective agonist of melanocortin 1 receptor, which triggers the inhibition of proinflammatory responses, suppressing neutrophil infiltration and protecting tissue. This study evaluated the effects of BMS-470539 on lipopolysaccharide-induced acute lung injury in a mouse model.
Methods Mice received a subcutaneous injection of saline or BMS-470539 (18.47 mg/kg) 1 hour before an intratracheal injection of saline or lipopolysaccharide (20 μg). Mice were sacrificed to analyze the severity of pulmonary edema (lung wet-to-dry weight [W/D] ratio) and inflammatory responses (level of leukocytes, polymorphonuclear neutrophils [PMNs] and tumor necrosis factor alpha [TNF-α] in bronchoalveolar lavage fluid [BALF]), and neutrophil infiltration (myeloperoxidase activity). TNF-α activation was also measured in neutrophils from bone marrow. Survival was investigated in a second-hit sepsis mouse model.
Results BMS-470539 improved sepsis-induced pulmonary edema, as demonstrated by a decreased W/D ratio (5.76%±0.83% to 3.81%±0.86%, P<0.05). The inflammatory response also improved, as shown by decreased levels of leukocytes (551±116 to 357±86×10²/mm³, P<0.05), PMNs (51.52%±16.23% to 18.41%±7.25%, P<0.01), and TNF-α (550±338 to 128±52 pg/ml, P<0.01) in the BALF. BMS-470539 also improved the inflammatory response, as shown by TNF-α levels (850±158 to 423±59 pg/ml, P<0.01) in neutrophils. BMS-470539 downregulated neutrophil infiltration in the lung (myeloperoxidase: 654±98 to 218±89 U/g, P<0.001). Lastly, BMS improved the survival rate (0% to 70%, P<0.01) in a mice multiple organ failure model.
Conclusions BMS-470539 improved lipopolysaccharide-induced acute lung injury and mortality in mice by affecting the inflammatory response.
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Since 2009, effective microorganisms (EMs) have been supplied by the local government to the citizens of Seongnam, Korea, for various environment-protective uses including manufacturing detergents, cosmetics and humidifier disinfectants. A 68-year-old man who had placed an EM blends into a humidifier for inhalation visited the emergency room with complaints of fever and dyspnea. He was in a shock state with hypoxia. Chest computed tomography revealed diffuse ground-glass opacities that were dominant in the bilateral upper lobes. Fiberoptic bronchoscopy with bronchoalveolar lavage and transbronchial lung biopsy was performed. Bronchoalveolar lavage fluid analysis and biopsy findings were consistent with alveolar hemorrhage. All microbiological and virological test results were negative. His symptoms and radiographic opacities had improved markedly after several days of conservative care, and he was discharged healthy after 1 week of hospital stay.
Background Mesenchymal stem cells (MSCs) attenuate injury in various lung injury models through paracrine effects. We hypothesized that intratracheal transplantation of allogenic MSCs could attenuate lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice, mediated by anti-inflammatory responses.
Methods Six-week-old male mice were randomized to either the control or the ALI group. ALI was induced by intratracheal LPS instillation. Four hours after LPS instillation, MSCs or phosphate-buffered saline was randomly intratracheally administered. Neutrophil count and protein concentration in bronchoalveolar lavage fluid (BALF); lung histology; levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and macrophage inflammatory protein-2; and the expression of proliferation cell nuclear antigen (PCNA), caspase-3, and caspase-9 were evaluated at 48 hours after injury.
Results Treatment with MSCs attenuated lung injury in ALI mice by decreasing protein level and neutrophil recruitment into the BALF and improving the histologic change. MSCs also decreased the protein levels of proinflammatory cytokines including IL-1β, IL-6, and TNF-α, but had little effect on the protein expression of PCNA, caspase-3, and caspase-9.
Conclusions Intratracheal injection of bone marrow-derived allogenic MSCs attenuates LPSinduced ALI via immunomodulatory effects.
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Background Flecainide is an antiarrhythmic agent that is used primarily in the treatment of cardiac arrhythmias. Some evidences also suggest that flecainide can participate in alveolar fluid clearance and inflammatory responses. This experiment was aimed to evaluate the effects of flecainide on sepsis induced acute lung injury in a rat model.
Methods Rats were treated with subcutaneous infusion of saline or flecainide (0.1 or 0.2 mg/kg/hr) by a mini-osmotic pump. Subcutaneous infusion was started 3 hours before and continued until 8 hours after intraperitoneal injection of saline or endotoxin. Animals were sacrificed for analyses of severity of acute lung injury with wet to dry (W/D) ratio and lung injury score (LIS) in lung and inflammatory responses with level of leukocyte, polymorphonuclear neutrophils (PMNs) and inteleukin-8 (IL-8) in bronchoalveolar lavages fluid (BALF).
Results Flecainide markedly improved dose dependently sepsis induced acute lung injury as analysed by W/D ratio (from 2.24 ± 0.11 to 1.76 ± 0.09, p < 0.05) and LIS (from 3 to 1, p < 0.05), and inflammatory response as determined by leukocyte (from 443 ± 127 to 229 ± 95, p < 0.05), PMNs (from 41.43 ± 17.63 to 2.43 ± 2.61, p < 0.05) and IL-8 (from 95.00 ± 15.28 to 40.00 ± 10.21, p < 0.05) in BALF.
Conclusions Flecanide improve sepsis induced acute lung injury in rats by controlling inflammatory responses.
Extracorporeal membrane oxygenation (ECMO) has been used successfully in critically ill patients with traumatic lung injury and offers an additional treatment modality. ECMO is mainly used as a bridge treatment to delayed surgical management; however, only a few case reports have presented the successful application of ECMO as intraoperative support during the surgical repair of traumatic bronchial injury. A 38-year-old man visited our hospital after a blunt chest trauma. His chest imaging showed hemopneumothorax in the left hemithorax and a finding suspicious for left main bronchus rupture. Bronchoscopy was performed and confirmed a tear in the left main bronchus and a congenital tracheal bronchus. We decided to provide venovenous ECMO support during surgery for bronchial repair. We successfully performed main bronchial repair in this traumatic patient with a congenital tracheal bronchus. We suggest that venovenous ECMO offers a good option for the treatment of bronchial rupture when adequate ventilation is not possible.
Although the incidence is not high in the general surgical population, pulmonary aspiration of gastric contents can result in serious long-term morbidity and mortality. We report a case of early use of extracorporeal membrane oxygenation (ECMO) to correct severe hypoxemia refractory to conventional mechanical ventilation in a patient with massive aspiration of gastric contents immediately followed by acute lung injury during general anesthesia induction.
A 64-year-old woman diagnosed with stomach cancer was scheduled for elective diagnostic laparoscopy. Although there was no sign of gastrointestinal tract obstruction and midnight Nil per Os (NPO) was performed before the operation, pulmonary aspiration occurred during the induction of anesthesia. Despite the endotracheal intubation with mechanical ventilation, severe hypoxemia with hypercapnea persisted. Medical team agreed with applying veno-venous (VV) ECMO, and her blood gas analysis results became stable. ECMO was weaned successfully 9 days after the first aspiration event had occurred. Based on this case, early application of extracorporeal life support can have survival benefits.
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Rupture limited to the lobar bronchus from blunt trauma is especially rare, and the symptoms are light so diagnosis is difficult. In a patient who visited the hospital complaining of shortness of breath after falling down, atelectasis continued in the chest x-ray. Four days after visiting the hospital, a left upper lobar bronchial rupture was diagnosed through a bronchoscopy and 3 dimensional chest computerized tomography. When diagnosis is delayed in the case of a rupture limited to the lobar bronchus, bronchial obstruction can occur from the formation of granulation tissue, so regular monitoring is important. Therefore, when atelectasis continues after blunt trauma, it is important to differentially diagnose a lobar bronchial rupture through tests such as bronchoscopy.
BACKGROUND Hypothermia is known to suppress inflammation in various experimental and clinical settings. We wanted to investigate how the suppressed inflammation by hypothermia is affected during rewarming. METHODS Mice were being assigned to normothermia (37degrees C) or hypothermia (32degrees C). After 30 minutes at the assigned temperature, lipopolysaccharide was administered intratracheally. The mice were then randomly grouped and subjected to 4 hours of normothermia (N), 24 hours of normothermia (NN), 4 hours of hypothermia (H), or 4 hours of hypothermia followed by normothermia for the next 20 hours (HN). In another experiment, other HN mice were treated with varying doses of anti-TNF-alpha or anti-IL-1beta antibodies (0, 6.25, 12.5, 25, and 50 microg/250 microl) immediately prior to rewarming. RESULTS The neutrophil counts of BAL fluid (x104/ml) were 23.0 +/- 13.1 in the N, 6.4 +/- 3.1 in the H (p = 0.002 vs N), 20.4 +/- 10.2 in the NN, and 49.7 +/- 21.0 in the HN (p = 0.005 vs H; p < 0.001 vs NN). Myeloperoxidase activity of the lung (unit/microg) was 6.7 +/- 2.9, 7.9 +/- 1.9, 17.8 +/- 4.0 (p < 0.001 vs N), and 12.9 +/- 5.9 (p = 0.034 vs H, p = 0.028 vs NN), respectively. Compared with control HN, total WBC and neutrophil counts of mice treated with anti-TNF-alpha antibody or anti-IL-1beta antibody prior to rewarming were lower at all tested doses. The combination of both anti-TNF-alpha or anti-IL-1beta antibodies was not increasingly reducing the neutrophilic sequestration. CONCLUSIONS Rewarming from induced hypothermia resulted in augmentation of neutrophilic sequestration of endotoxin-injured lung. Treatment with antibodies against TNF-alpha or IL-1beta prevented this rebound of neutrophilic infiltration.
Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortalities. Each type of blood product is likely to cause TRALI. Patients with TRALI present with dyspnea/respiratory distress and fever. The symptoms, signs and chest radiological findings in TRALI are similar to transfusion associated circulatory overload.
Therefore, it is difficult to distinguish such from circulatory overloads. We report a case of TRALI in a 49-year-old woman after stored packed red blood cell transfusion. The patient developed hypoxemia and pulmonary edema after packed red blood cell transfusion during postoperative period. The patient completely recovered after an oxygen support for 3 days.
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Acute respiratory distress syndrome (ARDS) is a common disorder associated with significant mortality and morbidity. The American-European Consensus Conference (AECC) definition of ARDS, established in 1994, has advanced the knowledge of ARDS by allowing the acquisition of clinical and epidemiological data, which in turn have led to improvements in care for patients with ARDS. However, after 18 years of applied research, a number of issues regarding various criteria of AECC definition have emerged. For these reason, and because all disease definitions should be reviewed periodically, the European Society of Intensive Care Medicine convened an international expert panel to revise the ARDS definition from September 30 to October 2, 2011, Berlin, Germany, with endorsement from American Thoracic Society and the Society of Critical Care Medicine.
This consensus discussion, following empirical evaluation and consensus revision, addressed some of the limitations of the AECC definition by incorporating current data, physiologic concepts, and clinical trials to develop a new definition of ARDS (Berlin definition). The Berlin definition should facilitate case recognition and better match treatment options to severity in both the research trials and clinical practice.
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Transfusion-related acute lung injury (TRALI) is a significant cause of iatrogenic injuries in patients. It is also the major cause of transfusion-associated fatalities.
Pathophysiologic mechanism is an implicated donor of HLA.
Neutrophil antibodies and biologic response modifiers are accumulated in the stored blood products. Pulmonary endothelial activation of the host may be the response from these mediators. Treatment is supportive and will be subjected to other forms of ALL/ARDS. Diverting donors at high risk for alloimmunization may decrease the incidence of such cases.
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BACKGROUND Pulmonary contusion is the most common pulmonary parenchymal injury in blunt chest trauma and may constitute a life-threatening thoracic injury. In this study, we evaluated the usefulness of high-frequency chest wall oscillation (HFCWO) therapy in patients with pulmonary contusion. METHODS Patients with lung contusion either received HFCWO therapy using the Vest system (Vest group; n = 18) or received conventional chest physiotherapy (non-Vest group; n = 23). The physiological parameters of the patients, length of stay in hospital and ICU, and the duration of mechanical ventilation were compared between the two groups. Variables, including pulmonary contusion score, percentage of patients receiving mechanical ventilation therapy, and PaO2/FiO2 ratio, were also analyzed. RESULTS The pulmonary contusion score was higher in the Vest group (p < 0.01), and mechanical ventilation was used more frequently in the Vest group (p = 0.027). Improvement in the PaO2/FiO2 ratio over the first 48 h did not differ between the Vest and Non-Vest groups. No significant differences in the physiological parameters, hospital and ICU stays, and duration of mechanical ventilation were observed between the two groups. CONCLUSIONS The therapeutic effect of the Vest system in patients with pulmonary contusion was similar to that of conventional chest physiotherapy. Therefore, the Vest system could be considered as an airway clearance technique in the management of patients with pulmonary contusion.
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Transfusion-related acute lung injury (TRALI) is a serious complication following the transfusion of blood products.
TRALI is under-diagnosed and under-reported because of a lack of awareness. TRALI occurs within 6 hours of transfusion in the majority of cases and its presentation is similar to other forms of acute lung injury. We report on the case of a 34-year-old pregnant woman who suffered from TRALI after transfusion during Cesarean section.
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A case of transfusion-related acute lung injury induced by anti-human leukocyte antigen antibodies in acute leukemia Sun Mi Jin, Moon Ju Jang, Ji Young Huh, Myoung Hee Park, Eun Young Song, Doyeun Oh The Korean Journal of Hematology.2012; 47(4): 302. CrossRef