Blockage of extracorporeal circulation during emergency surgery for fulminant infective endocarditis

Introduction

Clinical presentation of severe infective endocarditis (IE) may include acute heart failure (HF) with dyspnoea, pulmonary oedema and cardiogenic shock.^1,2 HF is observed in 42%–60% of cases of native valve endocarditis and is more often present when IE affects the aortic valve.^1,3,4 Aortic valve endocarditis with severe acute regurgitation causing refractory pulmonary oedema or cardiogenic shock is an indication for immediate surgery. ⁵ We present a case of fulminant endocarditis successfully managed emergency surgery complicated by an extremely rare intraoperative event.

Case history

A 37-years-old man was admitted to the emergency department because of severe dyspnoea increasing from about a week and fever up to 39°C. The patient had a history of alcohol abuse and chronic pancreatitis. The patient’s condition at admission was very severe, shortness of breath caused the forced sitting position. Physical examination revealed skin paleness and advanced tooth decay. Heart rate was regular, 120/min, blood pressure100/40 mmHg, arterial blood saturation 77%. Heart sounds were loud, with diastolic murmur at Erb’s point. Diffuse rales were found over the entire lung fields.

ECG revealed sinus tachycardia 120/min and ST-segment depressions in I, aVL, II, aVF, V4–V6 leads. Chest radiograph demonstrated bilateral parenchymal densities of the lungs (Figure 1(a)). Transthoracic echocardiography (TTE) revealed bicuspid aortic valve with additional mobile structure with dimensions 5 mm × 10 mm flowing into the left ventricular outflow tract and asymmetrically thickened valve annulus with a cavity including heterogeneous echostructure – suspected abscess. Additionally, a perforation of aortic valve leaflet with significant regurgitation with short pressure half time (PHT-150 ms) was demonstrated. Moreover, TTE showed significant left ventricular dilatation (64/52 mm) with generalized hypokinesis – LVEF-40% (Figure 1(b)–(d)).

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Figure 1.

A. Chest X-ray: parenchymal densitis of the lungs. B and C. TTE: bicuspid aortic valve with vegetation. D. TTE: acute aortic regurgitation. E. blocked filter. F. replaced oxygenator

Laboratory tests demonstrated: leukocytosis: 18.2 K/ul ( n. 4.0–10.0 K/ul), C-reactive protein: 131 mg/dl (n. 0–5 mg/dl), troponin T hs: 335.4 ng/l (n. 0–14.1 ng/l), platelet count: 443 K/ul (n. 150–300 K/ul), dimer D: 1366 ug/l (n.m 0.0–500.0 ug/l), prothrombin time: 15.7 sek (n. 9.4–12.5 sek), INR: 1,4 (n. 0.8–1.2), creatinine clearance: 63 ml/min (n. 75–110 ml/min), triglyceride level: 368 mg/dl (n. 40–150 mg/dl), uric acid level: 17.5 mg/dl (n. 3.4–7.0 mg/dl). Other laboratory parameters were normal.

The patient’s condition rapidly deteriorated with increasing shortness of breath and a fall in blood pressure to 70/40, despite the use of catecholamines. Due to the diagnosis of severe endocarditis with acute heart failure, an emergency surgery decision was made. In the operating room, after cutting the skin, cardiac arrest in the asystole mechanism occurred. Extracorporeal circulation was turned on during direct heart massage. After clumping and opening of the aorta, the circulation was blocked by total clogging of the filter on the arterial line – by organic particles (Figure 1(e)). First the revolution pump was exchanged, when it didn’t help the oxygenator was replaced (Figure 1(f)) which resulted in the need to replace the entire perfusion set with a break in extracorporeal circulation lasting about 10 min. After opening the aorta, bicuspid aortic valve with vegetations on both leaflets and perforation of the leaflet in the area of the commissure between the left and right leaflets were revealed. In this area, an abscess in the annulus of the valve was found (about 1/3 of the valve circumference) with detachment of the intima from the annulus. The leaflets were removed and the abscess was emptied and cultured. Afterwards, St Jude Medical 27A artificial aortic valve was implanted. Due to hemodynamic instability (lack of return of haemodynamically efficient heart function, despite prolonged reperfusion on the roller pump) prolonged reperfusion and extracorporeal membrane oxygenation were necessary. Moreover, in the postoperative course massive bleeding was observed and patient required retoracotomy and repeated blood transfusions. Due to the presence of Streptococcus Pneumoniae in the blood and tissue culture, the patient received targeted, prolonged antibiotic therapy (consistent with results of antibiogram): Vancomycin with Levofloxacin. During further hospitalization, the patient’s condition improved systematically and after a 6-week therapy he was discharged.

Discussion

The case report illustrates a very rare event of perioperative cardiac arrest caused by blockage of the extracorporeal circulation filter by organic particles released during a fulminant systemic inflammatory reaction. Previous reports have found a description of the only one case of venous cannula obstruction due to infective endocarditis in patient with cardiac implantable electronic device and septic pulmonary embolism. In this case, the cannula in the inferior vena cava was completely clogged by moving large vegetation. ⁶ Our patient probably experienced the phenomenon of massive intravascular tissue breakdown with coagulation during the fulminant infection process. The confirmation of this theory is the presence of high levels of uric acid, troponins and d-dimers.

Conclusion

The probable cause of the blockage of the extracorporeal circulation was tissue disintegration in the course of a massive inflammatory process with coagulation disorders in a patient with a history of alcohol abuse and pancreatitis.