Introduction: Systemic capillary leak syndrome (SCLS) is an increasingly recognized rare syndrome. Its diagnosis is suggested by the occurrence of edema with arterial hypotension, hemoconcentration, and paradoxical hy...Introduction: Systemic capillary leak syndrome (SCLS) is an increasingly recognized rare syndrome. Its diagnosis is suggested by the occurrence of edema with arterial hypotension, hemoconcentration, and paradoxical hypoalbuminemia. SCLS can be idiopathic (Clarkson syndrome) or secondary. Secondary SCLS (SSCLS) is mainly triggered by infections (especially viruses), drugs (antitumor therapy), malignancies, and inflammatory diseases. We report a case of systemic capillary leak syndrome secondary to the COVID-19 infection. Observation: A 74-year-old chronic smoker with no particular history was initially admitted to the intensive care unit (ICU) with a picture of respiratory distress secondary to a COVID-19 infection with favorable evolution, hence his transfer to the emergency services. On Day 8 of hospitalization, following the installation of arterial hypotension, not responding to filling, associated with hypoalbuminemia, and generalized edematous syndrome, and in the absence of any other explanation for this clinical picture, a SCLS secondary to COVID-19 infection was suggested. On the balance sheet, after the discovery of acute renal failure, serum creatinine went from 7.9 mg/l to 16.6 mg/l with microalbuminuria at 420 mg/24h and leukocyturia at 20 elements/mm<sup>3</sup> without germ-evoked tubulointerstitial nephritis (TIN) secondary to a viral infection with COVID-19. The evolution was marked by the spontaneous regression of the edema and the normalization of the blood pressure figures. Discussion: The classic triad combining hypotension, hemoconcentration, and hypoalbuminemia suggests the diagnosis of SCLS once all other causes of shock have been ruled out. Hemoconcentration is less constant in SSCLS than in ISCLS. This is the case with our patient. The exact pathophysiological process of SCLS is largely unknown. Viral infections are the most common infectious cause of SCLS. The kidneys are the second-most common organs affected by the SARS-Cov-2 coronavirus infection. The presence of nephritis can be used as an indicator of SCLS, which can be a predictor of serious complications such as fluid overload, respiratory failure, and the need for ICU admission. Conclusion: In the event of COVID-19 infection, the appearance of hypotension and hypoalbuminemia with the gradual onset of generalized edema should suggest SCLS. The establishment of close monitoring is mandatory, given the risk of fatal evolution. Fortunately, for our patient, the evolution was favorable.展开更多
文摘Introduction: Systemic capillary leak syndrome (SCLS) is an increasingly recognized rare syndrome. Its diagnosis is suggested by the occurrence of edema with arterial hypotension, hemoconcentration, and paradoxical hypoalbuminemia. SCLS can be idiopathic (Clarkson syndrome) or secondary. Secondary SCLS (SSCLS) is mainly triggered by infections (especially viruses), drugs (antitumor therapy), malignancies, and inflammatory diseases. We report a case of systemic capillary leak syndrome secondary to the COVID-19 infection. Observation: A 74-year-old chronic smoker with no particular history was initially admitted to the intensive care unit (ICU) with a picture of respiratory distress secondary to a COVID-19 infection with favorable evolution, hence his transfer to the emergency services. On Day 8 of hospitalization, following the installation of arterial hypotension, not responding to filling, associated with hypoalbuminemia, and generalized edematous syndrome, and in the absence of any other explanation for this clinical picture, a SCLS secondary to COVID-19 infection was suggested. On the balance sheet, after the discovery of acute renal failure, serum creatinine went from 7.9 mg/l to 16.6 mg/l with microalbuminuria at 420 mg/24h and leukocyturia at 20 elements/mm<sup>3</sup> without germ-evoked tubulointerstitial nephritis (TIN) secondary to a viral infection with COVID-19. The evolution was marked by the spontaneous regression of the edema and the normalization of the blood pressure figures. Discussion: The classic triad combining hypotension, hemoconcentration, and hypoalbuminemia suggests the diagnosis of SCLS once all other causes of shock have been ruled out. Hemoconcentration is less constant in SSCLS than in ISCLS. This is the case with our patient. The exact pathophysiological process of SCLS is largely unknown. Viral infections are the most common infectious cause of SCLS. The kidneys are the second-most common organs affected by the SARS-Cov-2 coronavirus infection. The presence of nephritis can be used as an indicator of SCLS, which can be a predictor of serious complications such as fluid overload, respiratory failure, and the need for ICU admission. Conclusion: In the event of COVID-19 infection, the appearance of hypotension and hypoalbuminemia with the gradual onset of generalized edema should suggest SCLS. The establishment of close monitoring is mandatory, given the risk of fatal evolution. Fortunately, for our patient, the evolution was favorable.
