Acute pancreatitis is one of the most common diseases of the pancreas. Although the incidence of acute pancreatitis is increasing, the mortality is decreasing. In general, most of fatal cases occur within 2 weeks after admission due to multi-organ failure. Initial medical treatment of acute pancreatitis is important in order to improve the prognosis of the patients with acute pancreatitis. Essential treatment in this early period includes intravenous hydration, paint control, enteral nutrition, and antimicrobial therapy. Although aggressive intravenous hydration with lactated Ringer's solution can improve mortality rates and decrease the development of systemic inflammatory response syndrome in the patients with acute pancreatitis, fluid overload can induce pulmonary edema, increase of the extra-pancreatic fluid collection, intra-abdominal compartment syndrome, sepsis, and increase of the mortality. Therefore, goal-directed therapy, utilizing various parameters to guide fluid administration, reduces the risk of persistent single or multiple organ system failure, infected pancreatic necrosis or mortality from acute pancreatitis. Initiation of early oral feeding is recommended, beginning within 24 hours for mild acute pancreatitis. Enteral nutritional support is favored over parental nutrition in severe acute pancreatitis. Recent guidelines do not support the use of prophylactic antibiotics to prevent infection in necrotizing acute pancreatitis and severe acute pancreatitis.
Anti-Bacterial Agents ; Compartment Syndromes ; Enteral Nutrition ; Humans ; Incidence ; Mortality ; Necrosis ; Nutritional Support ; Paint ; Pancreas ; Pancreatitis ; Parents ; Prognosis ; Pulmonary Edema ; Sepsis ; Systemic Inflammatory Response Syndrome

Thirty years have passed since the Korean Association of Pediatric Allergy and Respiratory Disease was founded. There have been great changes in the pattern of respiratory diseases in Korean children during the last 30 years with economic development in the country. Pneumonia remains the leading cause of childhood morbidity, despite advances in the prevention and management. The incidence and mortality of pneumonia caused by typical bacterial pathogens have been reduced. However, the predominance of Mycoplasma pneumoniae or virus-associated diseases is emerging, which suggests that novel diagnostic and therapeutic strategies are needed. Viral bronchiolitis is one of the most substantial health burdens for infants and young children worldwide. Although respiratory syncytial virus is the most common pathogen, molecular diagnostic techniques have identified many other viruses including human rhinovirus causing bronchiolitis. Bronchiectasis is a chronic respiratory condition characterized by chronic infection, airway inflammation, and progressive lung function decline. Research into the interactions between early life respiratory infections and development of bronchiectasis is imperative to halt the disease in its origin and improve adult outcomes. Acute respiratory distress syndrome (ARDS) is a severe, life-threatening lung disease with diffuse inflammatory lung injury leading to pulmonary edema and hypoxia. Although many modalities to treat ARDS have been studied, supportive therapies and lung protective ventilator support remains the mainstay. This review focuses on the current trends in research on these childhood respiratory diseases through literature review and aims to investigate the impact of Korean study results in this field.
Adult ; Anoxia ; Bronchiectasis ; Bronchiolitis ; Bronchiolitis, Viral ; Child ; Economic Development ; Humans ; Hypersensitivity ; Incidence ; Infant ; Inflammation ; Korea* ; Lung ; Lung Diseases ; Lung Injury ; Molecular Diagnostic Techniques ; Mortality ; Mycoplasma pneumoniae ; Pneumonia ; Pneumonia, Mycoplasma ; Pulmonary Edema ; Respiratory Distress Syndrome, Adult ; Respiratory Syncytial Viruses ; Respiratory Tract Infections ; Rhinovirus ; Ventilators, Mechanical

Mortality rate for pulmonary embolectomy in critically ill patients still ranges from 30% to 45%. The causes of death in these patients are persistent pulmonary hypertension, pulmonary edema, and massive pulmonary hemorrhage. Residual thrombus and air trapping in peripheral pulmonary artery during pulmonary embolectomy can cause intractable right heart failure and persistent pulmonary hypertension. We report a successful extraction of residual thrombus and air bubbles during pulmonary embolectomy by retrograde pulmonary perfusion. Use of this technique could decrease morbidity and mortality from persistent right heart failure after pulmonary embolectomy in critically ill patients.
Cause of Death ; Critical Illness ; Embolectomy* ; Heart Failure ; Hemorrhage ; Humans ; Hypertension, Pulmonary ; Mortality ; Perfusion* ; Pulmonary Artery ; Pulmonary Edema ; Pulmonary Embolism* ; Thoracic Surgery ; Thrombosis

Data reported recently suggest that acute kidney injury (AKI) is a systemic disease that adversely affects the function of other organs-including the heart, lung, liver, brain and immune system-which is related to the high mortality rate of affected patients. Kidney and lung function are closely related in both health and disease. Data support deleterious bidirectional crosstalk between the lung and kidney. AKI is a common complication in patients with acute respiratory distress syndrome, and has been reported to exert adverse effects on the lungs. Mortality rates for AKI combined with acute lung injury (ALI) can be up to 80% in critically ill patients. Although AKI-associated ALI presents clinically as increased pulmonary edema, the mechanism of AKI-associated ALI extends beyond simple volume overload. Data from animal studies suggest that AKI-induced pulmonary edema is related to both cardiogenic edema (due to elevated hydrostatic pressure) and non-cardiogenic edema (due to pulmonary endothelial and epithelial cell injury caused by inflammation, oxidative stress, and apoptosis). ALI with mechanical ventilation causes a decline in renal hemodynamic function and apoptosis. Elucidation of the mechanisms of kidney-lung crosstalk would facilitate development of effective therapies and reduce the mortality rate of AKI combined with respiratory failure.
Acute Kidney Injury ; Acute Lung Injury ; Animals ; Apoptosis ; Brain ; Critical Illness ; Edema ; Epithelial Cells ; Heart ; Hemodynamics ; Humans ; Inflammation ; Kidney* ; Liver ; Lung* ; Mortality ; Oxidative Stress ; Pulmonary Edema ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Respiratory Insufficiency

Pulmonary edema is a major cause of mortality due to acute lung injury (ALI). The involvement of protein kinase C-delta (PKC-delta) in ALI has been a controversial topic. Here we investigated PKC-delta function in ALI using PKC-delta knockout (KO) mice and PKC inhibitors. Our results indicated that although the ability to produce proinflammatory mediators in response to LPS injury in PKC-delta KO mice was similar to that of control mice, they showed enhanced recruitment of neutrophils to the lung and more severe pulmonary edema. PKC-delta inhibition promoted barrier dysfunction in an endothelial cell layer in vitro, and administration of a PKC-delta-specific inhibitor significantly increased steady state vascular permeability. A neutrophil transmigration assay indicated that the PKC-delta inhibition increased neutrophil transmigration through an endothelial monolayer. This suggests that PKC-delta inhibition induces structural changes in endothelial cells, allowing extravasation of proteins and neutrophils.
Acute Lung Injury* ; Animals ; Capillary Permeability* ; Endothelial Cells ; Lung ; Mice ; Mortality ; Neutrophils ; Protein Kinase C-delta* ; Protein Kinases* ; Pulmonary Edema

Development of transfusion-related acute lung injury (TRALI), a non-cardiogenic pulmonary edema, after blood transfusion, is a rare but potentially leading cause of mortality from blood transfusion. We report on a case of TRALI in a 51-year male with acute calculous cholecystitis and liver cirrhosis. As preoperative treatment, he was given ten units of fresh frozen plasma (FFP) for 3 days before the operation. During the transfusion of the 10th unit of FFP, he experienced a sudden onset of hemoptysis, tachypnea, tachycardia, and cyanosis. Bilateral pulmonary infiltration not observed on the chest X-ray at the visit was newly developed. There was no evidence of volume overload but severe hypoxemia. Blood transfusion was stopped and he recovered fully after 8 days of oxygen therapy through a nasal cannula. Although HLA and HNA antibodies were not detected in the donor's blood, HLA antibodies (A2, B57, B58) were detected in the patient's blood. We reported this meaningful case of TRALI that occurred after transfusion of only fresh frozen plasma which did not contain human leukocyte antibody in a patient with HLA antibody.
Acute Lung Injury* ; Anoxia ; Antibodies ; Blood Transfusion ; Catheters ; Cholecystitis ; Cyanosis ; Hemoptysis ; Humans ; Leukocytes ; Liver Cirrhosis ; Male ; Mortality ; Oxygen ; Plasma* ; Pulmonary Edema ; Tachycardia ; Tachypnea ; Thorax

BACKGROUND: Patients on dialysis undergoing surgery belong to a high-risk group. Only a few studies have evaluated the outcome of major thoracic surgical procedures in dialysis patients. We evaluated the outcomes of pulmonary resection for non-small cell lung cancer (NSCLC) in patients on hemodialysis (HD). METHODS: Between 2008 and 2013, seven patients on HD underwent pulmonary resection for NSCLC at our institution. We retrospectively reviewed their surgical outcomes and prognoses. RESULTS: The median duration of HD before surgery was 55.0 months. Five patients underwent lobectomy and two patients underwent wedge resection. Postoperative morbidity occurred in three patients, including pulmonary edema combined with pneumonia, cerebral infarction, and delirium. There were no instances of in-hospital mortality, although one patient died of intracranial bleeding 15 days after discharge. During follow-up, three patients (one patient with pathologic stage IIB NSCLC and two patients with pathologic stage IIIA NSCLC) experienced recurrence and died as a result of the progression of the cancer, while the remaining three patients (with pathologic stage I NSCLC) are alive with no evidence of disease. CONCLUSION: Surgery for NSCLC in HD patients can be performed with acceptable perioperative morbidity. Good medium-term survival in patients with pathologic stage I NSCLC can also be expected. Pulmonary resection seems to be the proper treatment option for dialysis patients with stage I NSCLC.
Carcinoma, Non-Small-Cell Lung* ; Cerebral Infarction ; Delirium ; Dialysis ; Follow-Up Studies ; Hemorrhage ; Hospital Mortality ; Humans ; Lung Neoplasms ; Pneumonia ; Prognosis ; Pulmonary Edema ; Pulmonary Surgical Procedures ; Recurrence ; Renal Dialysis* ; Renal Insufficiency, Chronic* ; Retrospective Studies ; Thoracic Surgery ; Thoracic Surgical Procedures

Streptococcus pneumoniae (S. pneumoniae, also known as pneumococcus) infections are major causes of death worldwide. Despite the development and use of effective antibiotics, high, early mortality due to pneumococcal infections has not been decreased for the last few decades. Recent study found a deadly hemorrhagic acute lung injury (ALI) as a major cause of death at the early stage of severe pneumococcal infections. Interleukin (IL)-1beta was known to play critical roles not only for the development of ALI but also resolution of it. The role of IL-1beta on the pathogenesis of pneumococcal ALI, however, has not been well understood yet. This study aims to investigate the role of IL-1beta on the development of pneumococcal ALI and subsequent death. IL-1beta expression was upregulated in the lungs of pneumococcal ALI in wild-type (WT) mice, but not in the plasma. Despite an increased expression of pulmonary IL-1beta, no inflammatory cell infiltration into airway has been observed. Upregulation of IL-1beta expression was indeed dependent on pneumococcal cytoplasmic toxin pneumolysin and its cell surface receptor Toll-like receptor 4. Deficiency of IL-1R1, a cell surface receptor of IL-1beta, resulted in a markedly reduced hemorrhagic pulmonary edema and early death in pneumococcal ALI. Finally, IL-1beta neutralization in WT mice protects against pulmonary hemorrhagic edema and death. These data suggest that pulmonary expression of IL-1beta exacerbates pneumolysin-induced ALI and death by promoting alveolar hemorrhagic edema.
Acute Lung Injury* ; Animals ; Anti-Bacterial Agents ; Cause of Death ; Cytoplasm ; Edema ; Interleukin-1beta* ; Interleukins ; Lung ; Mice ; Mortality ; Plasma ; Pneumococcal Infections ; Pneumonia ; Pulmonary Edema ; Streptococcus pneumoniae ; Toll-Like Receptor 4 ; Up-Regulation

Paraquat poisoning can cause severe multiple organ failure involving the kidneys, liver, lungs, adrenals, and central nervous system. The toxic effect of paraquat on the lung manifests as pulmonary edema, hypoxia, respiratory failure, and pulmonary fibrosis. However, optimal guidelines for treatment of lung fibrosis following paraquat ingestion are not available. We experienced two cases, a 45-year-old Korean male and a 66-year-old Korean male, who visited the emergency center because of paraquat poisoning. They initially received methylprednisolone pulse therapy and cyclophosphamide. Then they experienced pulmonary fibrosis approximately 10 days after admission during renal recovery. Although steroid pulse therapy with cyclophosphamide was reported to reduce mortality due to paraquat poisoning, the side effects of cyclophosphamide treatment were concerning in our patients, who had already received cyclophosphamide. Therefore, we decided to repeat steroid pulse therapy without cyclophosphamide. Fortunately, pulmonary fibrosis in these two patients resolved after repeated steroid pulse therapy. Thus, steroid pulse therapy alone could benefit patients with lung fibrosis, who have already received steroid and cyclophosphamide treatment. Herein, we report on two cases of pulmonary fibrosis due to paraquat poisoning that were treated successfully with repeated steroid pulse therapy.
Aged ; Anoxia ; Central Nervous System ; Cyclophosphamide ; Eating ; Emergencies ; Fibrosis ; Humans ; Kidney ; Liver ; Lung ; Male ; Methylprednisolone ; Middle Aged ; Mortality ; Multiple Organ Failure ; Paraquat* ; Poisoning* ; Pulmonary Edema ; Pulmonary Fibrosis* ; Respiratory Insufficiency ; Steroids

BACKGROUND: Stress-induced cardiomyopathy (SCM) is characterized by apical ballooning on echocardiography, but some of SCM patients show non-apical involvement and their characteristics are not well defined. METHODS: We investigated 56 patients that were diagnosed as SCM and divided them into 2 groups: apical ballooning syndrome (ABS, n = 49, 87.5%) and non-apical ballooning syndrome (N-ABS, n = 7, 12.5%) groups. Patients with N-ABS were significantly younger than those of the ABS group (52 +/- 11 vs. 73 +/- 10 years, p < 0.001). RESULTS: Types of preceding stressors and clinical presentation including chest pain, pulmonary edema, cardiogenic shock and in-hospital mortality were comparable between the two groups. In the N-ABS group, wall motion score index was significantly lower than in the ABS group (1.61 +/- 0.35 vs. 1.93 +/- 0.31, p = 0.016). On electrocardiogram (ECG), T-wave inversion (57.1% vs. 95.8%, p < 0.001) were less frequent in the N-ABS than in the ABS group. Furthermore, maximum QT and corrected QT (QTc) intervals in the N-ABS patients were significantly shorter than the ABS patients (QT, 419.9 +/- 66.1 vs. 487.3 +/- 79.6 ms, p = 0.038; QTc, 479.0 +/- 61.9 vs. 568.0 +/- 50.5 ms, p < 0.001). CONCLUSION: Patients with the N-ABS showed not only atypical echocardiographic findings, but also atypical clinical and ECG manifestations. Integrated consideration is needed to reach a diagnosis of the non-apical subtype of SCM.
Chest Pain ; Echocardiography ; Electrocardiography ; Hospital Mortality ; Humans ; Pulmonary Edema ; Shock, Cardiogenic ; Takotsubo Cardiomyopathy*