Use of venovenous extracorporeal membrane oxygenation for perioperative management of acute respiratory distress syndrome caused by fat embolism syndrome: A case report and literature review.

INTRODUCTION: Fat embolism syndrome (FES) is a known complication of long bone fracture and can affect multiple organs. The organ most commonly affected with FES is the lung. Severe cases of FES from long bone fracture can cause acute respiratory distress syndrome (ARDS). Although the treatment of ARDS remains challenging, it is reported that a lung protection strategy and prone positioning are effective. In addition, early fixation is reported to be beneficial in respiratory failure due to FES, though it may exacerbate respiratory failure during the perioperative period. We report the use of venovenous extracorporeal membrane oxygenation (VV-ECMO) for the successful perioperative management of a patient diagnosed with ARDS due to FES. PATIENT CONCERNS: A 24-year-old man injured in a traffic accident was brought to our emergency department due to shock and consciousness disorder. DIAGNOSIS: After examining the patient, we noted bilateral pneumothorax, liver and spleen injuries, and multiple long bone fractures. Four days after admission, he was diagnosed with FES due to a prolonged consciousness disorder, progressive hypoxia with diffuse lung damage, and cutaneous and mucosal petechiae. INTERVENTION: As respiratory failure progressed, VV-ECMO was initiated on the 6th day. To improve the respiratory failure caused by ARDS, prone position therapy was necessary. Thus, we performed osteosynthesis on the 9th day under ECMO. Prone position therapy was started after surgery. OUTCOMES: Subsequently, his respiratory condition and chest radiographs improved steadily. VV-ECMO was discontinued on the 17th day and the ventilator was removed on the 28th day. His consciousness levels improved without residual central nervous system complications. CONCLUSION: Our study reveals the successful improvement of FES-induced ARDS by osteosynthesis and prone positioning under VV-ECMO. This strategy prioritizes supportive treatment over pharmacologic interventions.

Brain perivascular macrophages contribute to the development of hypertension in stroke-prone spontaneously hypertensive rats via sympathetic activation.

Hypertension is associated with systemic inflammation. The activation of the sympathetic nervous system is critically involved in the pathogenesis of hypertension. Brain perivascular macrophages (PVMs) can be affected by circulating inflammatory cytokines, and the contribution of brain PVMs to sympathoexcitation has been demonstrated in a heart failure model. We thus investigated whether brain PVMs contribute to the development of hypertension through sympathoexcitation. Stroke-prone spontaneously hypertensive rats (SHRSP) developed hypertension over an 8-week period from 4 to 12 weeks of age. The number of brain PVMs and plasma interleukin-1ß levels significantly increased at the ages of 8 and 12 weeks in SHRSP compared with normotensive Wistar-Kyoto rats (WKY). To determine the contribution of brain PVMs to blood pressure elevation, we intracerebroventricularly injected liposome-encapsulated clodronate, which eliminates macrophages by inducing apoptosis, into 8-week-old rats; we then assessed its effects in 10-week-old rats. Clodronate treatment attenuated the increase in mean blood pressure in SHRSP but not in WKY. Clodronate treatment reduced the depressor effect of hexamethonium, an index of sympathetic activity; it also reduced neuronal activity in sympathetic regulatory nuclei such as the hypothalamic paraventricular nucleus and rostral ventrolateral medulla and reduced the expression of cyclooxygenase-2 and prostaglandin E2, a downstream pathway in activated macrophages, in SHRSP but not in WKY. Furthermore, clodronate treatment attenuated the increase in blood pressure and renal sympathetic nerve activity in response to an acute intravenous injection of interleukin-1ß in WKY. In conclusion, brain PVMs contribute to the development of hypertension via sympathetic activation. PVMs may be activated by increased levels of circulating interleukin-1ß.

A case of coronary subclavian vertebral steal syndrome successfully treated with stenting to the stenosis of left subclavian artery.

Coronary subclavian vertebral steal syndrome (CSVSS) is a rare but important complication of coronary artery bypass graft surgery (CABG) when an internal mammary artery (IMA) is used. This syndrome is defined as a retrograde flow from coronary artery via the IMA and the vertebral artery to the subclavian artery due to a proximal subclavian artery stenosis. We describe a case of a 64-year-old female who underwent CABG, complaining of dyspnea and chest pain by exercise of left arm, and dizziness when she turned her face to the left. Her blood pressure was 113/69 mmHg in the left arm and 137/84 mmHg in the right arm. Coronary angiography revealed retrograde flow from the left anterior descending (LAD) artery to the left IMA. Aortography showed that the ostium of the left subclavian artery had a severe stenosis and that the left vertebral artery was visualized retrogradely. Thereby, the diagnosis of CSVSS was made. The stenosis of the left subclavian artery was successfully treated with a percutaneous transluminal angioplasty and stent implantation, resulting in the restoration of antegrade flow from the left IMA to the LAD artery and from the left subclavian artery to the left vertebral artery. She was discharged with no chest pain and dizziness. .

A case of Kounis syndrome associated with transcatheter arterial chemoembolization for hepatocellular carcinoma.

Kounis syndrome, which is known as allergic angina and allergic myocardial infarction today, was described as the coexistence of acute coronary syndrome with allergic reactions in 1991 by Kounis and Zavras. We report a case of a 79-year-old man with hypertension, hepatocellular carcinoma (HCC), and no allergic history. He had received transcatheter arterial chemoembolization (TACE) for treatment of HCC five times without allergic reactions. At the sixth time of TACE, he presented an anaphylactic reaction such as systemic erythema and severe arterial hypotension. Simultaneously, he complained of anterior chest pain and electrocardiogram showed significant ST segment elevation in inferior leads, indicating inferior myocardial infarction. Emergency coronary angiography, however, did not demonstrate any organic stenoses or occluded lesions of the coronary arteries. We made the diagnosis of Kounis syndrome associated with TACE. Although Kounis syndrome is a rare condition, physicians should be aware of possible co-occurrence of anaphylactic reactions and acute coronary syndrome. .