Cardiogenic Shock from Fulminant Constrictive Pericarditis due to Campylobacter jejuni
Patrick McBride, DO, Henry Ford Health, Macomb, MI
Patrick McBride, DO1, Allison Zimmerman, MD2, Mustafa Mohammed, DO2, Khaled Nour, MD2, Mohammad Alqarqaz, M.D.3, Herb D. Aronow, MD, MPH, MSCAI4, Kyle Miletic, MD2 and Babar B Basir, DO, FSCAI2, (1)Henry Ford Health, Macomb, MI, (2)Henry Ford Health System, Detroit, MI, (3)Henry Ford Health System, West Bloomfield, MI, (4)Henry Ford Health, Detroit, MI
Keywords: Cardiogenic Shock
Title: Cardiogenic Shock from Fulminant Constrictive Pericarditis due to Campylobacter jejuni
Introduction: Campylobacter jejuni infection can range from self-limited infection to fulminant constrictive pericarditis with cardiogenic shock. Only a few cases involving immunocompetent patients have been described. We present a case in which VA-ECMO was successfully used as a bridge to definitive therapy.
Clinical Case: 54-year-old male with no comorbidities presented with progressive dyspnea. Several weeks previously, he was hospitalized for a symptomatic pericardial effusion after returning from a trip to Southeast Asia. Pericardial fluid cultures grew Campylobacter jejuni. He underwent pericardial window with debridement of thick, necrotic myocardium. Cardiac MRI prior to representation revealed significant pericardial inflammation of both the parietal and visceral layers and atypical septal motion. Upon the index presentation he was hypotensive, and tachycardic. JVP was estimated to be 14cm water, and extremities were cool to touch. Labs were notable for creatinine 1.99 mg/dL, ALT 2059 IU/dL, and AST 6730 IU/dL. Blood gas revealed a pH 6.94. Lactic acid was 17 mmol/L. Troponin was 4 ng/L and BNP was 575 pg/mL. Echocardiogram revealed an ejection fraction of 10-15% with thickening and calcification of the pericardium and septal bounce. Right heart catheterization (RHC) showed (mmHg): CVP 26, RV 42/23/26, PA pressure 46/25/32, pulmonary capillary wedge pressure of 30, and a cardiac index 1.25. He was initiated on high dose vasopressors and ultimately placed on VA-ECMO as a bridge to pericardiectomy. He stabilized and was decannulated after 12 days of VA-ECMO support with placement of IABP. He was taken for surgery a week later for definitive management. Intra-operatively, there was a thick fibrinous rind covering the entire surface of the heart and anterior pericardiectomy was performed with improvement of echocardiographic parameters and hemodynamics. A small portion of pericardium was left behind the left ventricle to avoid further blood loss and avoid cardiopulmonary bypass. He initially did well post-operatively and was able to be weaned off vasopressor support. Unfortunately, he deteriorated a few weeks later due to GI bleeding and elected for comfort care.
Discussion: To date, seven cases have described C. Jejuni related pericarditis, typically involving immunocompetent hosts. To our knowledge, our case is the first to describe the development of acute constriction with cardiogenic shock and the second case of hemodynamically significant constrictive pericarditis managed with VA-ECMO. The diagnosis of constrictive pericarditis in the ECMO population can be challenging due to the alteration in underlying hemodynamics. The use of VA-ECMO in patients with constrictive pericarditis is not well described, and the mortality after radical pericardiectomy is high, particularly in those with pre-existing LV dysfunction or advanced disease (40-60% estimated perioperative mortality rate). Constrictive pericarditis as a complication from purulent pericarditis occurs in at least 3.5% of cases. Factors influencing progression from purulent pericarditis to constrictive pericarditis are not well described, and thus close surveillance of these patients is essential. ESC guidelines recommend medical therapy when feasible in cases of transient constrictive pericarditis. Radical pericardiectomy is the only definitive treatment and is recommended once the diagnosis is confirmed.