The platelet count nadir was 0.24??109/L after one week of heparin therapy and the 4T’s score was 5 points concerning for heparin-induced thrombocytopenia (HIT), so heparin was changed to Argatroban hydrate (target APTT 40C60sec). Rabbit Polyclonal to MAN1B1 disease, Anti-glomerular basement membrane disease; DAH, Diffuse alveolar hemorrhage; BAL, Brochoalveolar Treprostinil sodium lavage; HIT, Heparin-induced thrombocytopenia; ER, Emergency room Abbreviations VV-ECMOVeno-venous extracorporeal membrane oxygenationanti-GBM diseaseAnti-glomerular basement membrane diseaseDAHDiffuse alveolar hemorrhageBALBronchoalveolar lavageEREmergency roomHITHeparin-induced thrombocytopenia 1.?Intro DAH is a clinical syndrome in which alveolar capillaries and pulmonary small arteries and veins are damaged, and alveolar spaces are filled with blood. DAH is definitely a rare condition with multiple etiologies. Supportive care, prompt analysis, and specific therapy is required. Mortality rates have been reported as high as 25C50% [1], despite ventilator and supportive ICU care in some cases. A limited number of cases using VV-ECMO for anti-GBM disease are reported [2,3]. Here, we statement a rare case of successful VV-ECMO without bleeding complications for hypoxemic respiratory failure caused by diffuse alveolar Treprostinil sodium hemorrhage caused by isolated pulmonary anti-GBM disease. VV-ECMO can be used like a supportive treatment until definitive analysis and effects of specific curative treatment are effective. 2.?Case statement A 34-year-old woman developed acute onset of dyspnea over 24 hours. She complained to her spouse Treprostinil sodium that small blood is combined in her sputum and that she experienced respiratory discomfort beginning the previous day time. She offered to a primary care physician with top respiratory symptoms and began therapy with an inhaled beta agonist and symptomatic treatment for suspected asthma. The following day, progressive symptoms prompted demonstration to an emergency space (ER). Percutaneous oxygen saturation (SpO2) was 68% (space air flow) and chest X-ray showed bilateral diffuse consolidation, and she was transferred to our higher-level acute care hospital. Physical examination in our ER revealed an alert patent in respiratory stress with blood pressure 140/78?mm Hg, pulse 110 beats/min, respiratory rate was 28 breaths/min, SpO2 90% on 10L/min non-rebreathing face mask, with bilateral coarse crackles on auscultation. Chest X-ray shown bilateral diffuse consolidation and CT scan shown bilateral floor glass shadow with consolidation. She was intubated for acute hypoxic respiratory failure and bronchoscopy shown bilateral diffuse airway hemorrhage suggesting DAH (Fig. 1), but bronchoalveolar lavage (BAL) was not performed due to her severe hypoxia. Open in a separate window Fig. 1 Non-contrast CT of the lung shows diffuse floor glass shadow and bronchoscope shows diffuse alveolar hemorrhage. On admission, initial investigation revealed the following: hemoglobin (Hb): 11.2 g/dL; white cell count: 2.3??109/L; neutrophils: 1.0??109/L, platelet: 3.0??109/L; C reactive protein: 7.2 mg/dL; blood urea nitrogen: 10.8 mg/dL; sCr: 0.53 mg/dL; international normalized percentage of prothrombin time: 0.9; Treprostinil sodium triggered partial thromboplastin time: 24 sec; immunoglobulin (Ig) G: 1301 mg/dL; IgA: 202 mg/dL; IgM: 71 mg/dL; C3: 59.4 mg/dL; and C4: 29.5 mg/dL. Test results for ANCA, blood culture, urine tradition, sputum tradition, T-SPOT, urinary protein, urinary occult blood were all negative; however, anti-GBM antibodies were recognized at a level of 6.7 enzyme-linked immunosorbent assay unit (EU). The patient was diagnosed with isolated pulmonary anti-GBM disease without renal involvement, based on serological and urinary findings. Severe respiratory failure progressed despite administration of pulse-dosed methylprednisolone (1g/day time, 3 days). The PaO2/Fio2 percentage was 50 with optimized ventilator establishing and prone position on 12hrs after hospitalization and veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated. VV-ECMO system parts and technique utilized the following: Pump (JMS Blend Circulation), Oxygenator (Bio Cube 6000), right internal jugular vein drainage cannula (MAQUET HLS cannula 23Fr 38cm), right femoral vein return cannula (MAQUET HLS cannula 19Fr 23cm). Initial ECMO establishing with heparin as anticoagulant included; ECMO Circulation4.5 L/min; ECMO RPM4500?rpm; FIO21.0; Sweep gas5 L/min, target APTT-R1.5C2.5. Anti-GBM antibody positive results were reported on hospital day 4; plasma exchange was initiated for 4 days and methyl prednisolone was decreased to 60mg/day time. Rituximab 375mg/m2 IV was given on hospital day time 8. The platelet count nadir was 0.24??109/L after one week of heparin therapy and the 4T’s score was 5 points concerning for heparin-induced thrombocytopenia (HIT), so heparin was changed to Argatroban hydrate (target APTT 40C60sec). Thereafter, the test revealed that HIT antibodies were positive. On hospital day time 12 respiratory failure was improving. The PaO2/Fio2 percentage was 350, and VV-ECMO was discontinued, the patient was extubated on hospital day time 18 and remaining the ICU and was discharged on hospital days 20 and 45 respectively. (Fig. 2). Open.