Should an emergency physician be a "surgeon" in a rural area? A case of blunt cardiac rupture successfully treated by an emergency physician.

Objective: Blunt cardiac rupture is a life-threatening injury that requires surgical repair by cardiovascular or trauma surgeons. We report a case of blunt cardiac rupture in a rural area in which emergency physicians performed emergency department thoracotomy and surgical repair to save the patient's life. Patient and Methods: This case involved an 18-year-old female who was injured in a traffic accident and underwent emergency thoracotomy and surgical repair. Results: The patient's left thorax was deformed, and sonographic assessment revealed pericardial effusion. She experienced cardiopulmonary arrest 13 min after hospital arrival. An emergency physician performed an emergency department thoracotomy. The clots were removed from the surface of the left ventricle, followed by wound compression to control bleeding from the ruptured left ventricular wall. After the recovery of spontaneous circulation, the emergency physician sutured the ruptured heart. The patient survived with good neurological function. Conclusion: In rural areas, blunt cardiac rupture may require emergency department thoracotomy and cardiac repair by emergency physicians. The establishment of educational systems that include continuous education on trauma surgical procedures and consensus guidelines is needed to assist rural emergency physicians in performing surgical procedures.

Successful Treatment of Sepsis-Induced Cardiomyopathy with Intra-Aortic Balloon Pumping: A Case Report and Literature Review.

BACKGROUND Sepsis-induced cardiomyopathy is cardiac dysfunction in sepsis that sometimes results in reduced cardiac output. Inotropic agents are recommended in patients with sepsis and cardiac dysfunction. Here, we present a case of sepsis-induced cardiomyopathy that was resistant to inotropes and was successfully treated with intra-aortic balloon pumping (IABP). We also reviewed the literature on similar cases of sepsis-induced cardiomyopathy treated with IABP. CASE REPORT A 40-year-old woman with fever and hypotension was admitted to a university hospital. Laboratory test results showed elevated inflammatory markers and cardiac markers, such as creatinine kinase-MB and troponin T. Echocardiography revealed severe left ventricular hypokinesis, and cardiac monitoring revealed a low cardiac output. The patient received antimicrobials, vasopressors, and dobutamine; however, her circulatory status did not respond to these treatments. IABP was introduced 7 h after admission and dramatically increased her blood pressure and cardiac output, resulting in the reduction of vasopressor and dobutamine doses. The patient survived without any IABP-related complications. The literature review of 11 cases of sepsis-induced cardiomyopathy treated with IABP shows consistent results with the presented case in terms of positive effects of IABP on circulatory status and cardiac function, resulting in a reduction of inotropes. CONCLUSIONS Some sepsis-induced cardiomyopathy cases with reduced left ventricular function may not respond to inotropes. IABP would be a treatment option for these patients because of its positive effects on cardiac and circulatory functions.

Metolachlor Poisoning with Lactic Acidosis Improved by Thiamine Administration: A Case Report.

BACKGROUND Metolachlor is a chloroacetamide herbicide that is extensively used worldwide. Ingestion of metolachlor causes acute toxicity via the generation of methemoglobin. Elevated levels of methemoglobin inhibit the transport of oxygen to tissue, causing hypoxia and lactic acidosis. A common treatment approach has been to reduce methemoglobin by administration of methylene blue. Herein, we present a case of metolachlor poisoning causing lactic acidosis that was treatable by thiamine administration, in which the methemoglobin level was not elevated. CASE REPORT A 61-year-old man was admitted to the emergency room with seizures and impaired consciousness after the ingestion of metolachlor (250 mL, 83%) with the intent to commit suicide. The patient's methemoglobin and lactate levels on admission were 0.9% and 11.8 mmol/L, respectively. After admission, the levels of lactate decreased gradually; however, they increased 13 h after admission. There was no evidence of heavy alcohol consumption, hyponutrition, or chronic thiamine deficiency. We initially administered a thiamine bolus (100 mg), which immediately improved his consciousness, followed by continuous administration of the same substance (1500 mg/day). The patient's consciousness improved, and was discharged from the intensive care unit on day 4. CONCLUSIONS Metolachlor can cause metabolic dysfunction and lactic acidosis without an increase in methemoglobin. Moreover, thiamine administration may be beneficial for patients with metolachlor intoxication exhibiting symptoms of elevated lactate levels, impaired consciousness, and lack of elevated methemoglobin levels.

Acquired Thrombotic Thrombocytopenic Purpura Without Anti-ADAMTS13 Antibody Caused by Influenza A (H1N1) Virus Successfully Treated by Plasma Exchange: A Case Report.

BACKGROUND Thrombotic microangiopathy, characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage by microvascular thrombosis, has a high mortality rate; therefore, early diagnosis and treatment are important. Thrombotic thrombocytopenic purpura is caused by a deficiency of a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13 (ADAMTS13), and results in thrombotic microangiopathy. Influenza virus causes thrombotic thrombocytopenic purpura by inducing immunoglobulin G autoantibodies against ADAMTS13. We report a rare case of thrombotic thrombocytopenic purpura caused by influenza A without anti-ADAMTS13 antibody that was treated by plasma exchange. CASE REPORT A 57-year-old woman was admitted to our hospital because of hypoxemia. We diagnosed pneumonia and disseminated intravascular coagulation. Despite treatment, she developed thrombocytopenia, and we diagnosed thrombotic microangiopathy and started plasma exchange. With a PLASMIC score of 6 points and neuropsychiatric symptoms, we strongly suspected thrombotic thrombocytopenic purpura and started rituximab. However, ADAMTS13 activity by FRETS-VWF73 assay was 65%, and anti-ADAMTS13 antibody was negative. After 4 plasma exchanges and 2 rounds of rituximab, platelet numbers and lactate dehydrogenase and creatinine concentrations normalized on the 16th day of hospitalization. Subsequently, influenza A (H1N1) was identified in a nasopharyngeal swab collected on admission. Plasma enzyme-linked immunosorbent assay testing for chromogenic ADAMTS13 activity showed a significant decrease (<0.5%). Therefore, we diagnosed thrombotic thrombocytopenic purpura caused by influenza A without anti-ADAMTS13 antibody. CONCLUSIONS We present a rare case of thrombotic thrombocytopenic purpura without anti-ADAMTS13 antibody caused by influenza A virus successfully treated by plasma exchange. Influenza A may reduce ADAMTS13 activity without inducing autoantibodies.

Complement Activation in Human Sepsis is Related to Sepsis-Induced Disseminated Intravascular Coagulation.

INTRODUCTION: In human sepsis, little is known about the relationships between complement activation and the clinical characteristics of sepsis, including disseminated intravascular coagulation (DIC), interventions, and prognosis. PATIENTS AND METHODS: Adult patients with sepsis admitted from November 2016 to December 2018 were included. We used the plasma levels of soluble C5b-9 (SC5b-9) as a marker of complement activation. We compared the clinical characteristics and complement components between patients with and without DIC. We also compared the clinical characteristics and each DIC parameter across quartile groups for the SC5b-9 value. RESULTS: Forty-nine sepsis patients were eligible. Thirty-four patients developed DIC, and eight patients died. The median (interquartile range) SC5b-9 value was 342 (261-501) ng/mL. Compared with patients without DIC, patients with DIC showed lower C3 levels (mean, 95.7 vs. 70.4 mg/dL, P < 0.01) and higher SC5b-9 levels (median, 287 vs. 400 ng/mL, P = 0.01). Patients were stratified by SC5b-9 quartile (ng/mL: low: < 260, moderate: 260-342, high: 343-501, highest: > 501). The mean Sequential Organ Failure Assessment score varied across these groups (P = 0.02). In the high and highest groups, many more patients received vasopressors and developed DIC. In the highest group, the coagulation parameters were severe, and thrombocytopenia was prolonged. In-hospital mortality tended to be high (33%) in the highest group. CONCLUSIONS: The degree of complement activation is related to DIC, severity, intensive interventions, and mortality. Further studies are needed to confirm the usefulness of SC5b-9 for stratifying sepsis patients.

Four-point probe resistance measurements using PtIr-coated carbon nanotube tips.

We performed four-terminal conductivity measurements on a CoSi2 nanowire (NW) at room temperature by using PtIr-coated carbon nanotube (CNT) tips in a four-tip scanning tunneling microscope. The physical stability and high aspect ratio of the CNT tips made it possible to reduce the probe spacing down to ca. 30 nm. The probe-spacing dependence of resistance showed diffusive transport even at 30 nm and no current leakage to the Si substrate.