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The annual incidence of blocked mechanical valvular prosthesis (BMVP) is 0.3–5.7%. 78% of cases are due to thrombosis and development of pannus is the second more frequent etiology. The risk of thrombosis is higher for mitral prosthesis, during the 1st year after valve replacement, and for poor INR trend. TEE is the gold standard for diagnoses, but it is seldom required if adequate TTE and cine–fluoroscopy are performed. As therapy, redo surgery is recommended in case of NYHA III–IV patients or in presence of big thrombi: if surgery is contraindicated or too high–risk, systemic thrombolysis is a reasonable option. In less compromised patients, upgrading of the anti–thrombotic therapy can be considered. In our Centre (around 600 valve replacement surgeries/year, mainly high risk patients) we use thrombolysis for BMVP in decompensated patients, choosing between two different protocols: the so called “fast” protocol (alteplase 15 mg iv bolus, then 0.75 mg/kg over 30’ and 0.5 mg/kg over 1h) is provided for NYHA IV patients, while the “slow” protocol (25 mg over 6 h) is the treatment of choice for the NYHA III ones. Many complications, mainly bleeding, are associated to thrombolysis. A 30 years old lady who underwent MVR in 08/2021, already successfully treated with thrombolysis in 11/2021 due to BMVP, presented in 01/2023 due to NYHA IV heart failure. TTE and cine–fluoroscopy showed BMVP (grad. 29/21 mmHg, area 0.7 cm2). The LV was hypekynetic (EF 81%), and severe pulmonary hypertension (calcSPAP 82 mmHg) was present. Fast thrombolysis was performed, with decrease of gradients (11/6 mmHg) and of pulmonary pressure (45 mmHg), and preserved LV function (EF 55%), without acute complications. On the 2nd day, the patient developed generalized seizures and pulsless VT, with ROSC after DC shock (7’ low–flow time). The neurological recovery was complete, but haemodynamic instability developed; new onset LBBB, and progressive worsening of the LV function (EF 40%, then 25%, medioapical hypokinesia) were documented. The coronary angiography showed a thrombus in the proximal LAD, not occluding the vessel, and TIMI 3 downstream flow. Heparin continuous infusion was provided for 48 h with a 1.8–2.3 aPTT ratio target. The patient was eventually discharged home with normal gradients (12/7 mmHg), EF (67%), ECG and pulmonary pressure. Coronary embolism is a possible complication of BMVP, and can follow systemic thrombolysis. Close multimodal clinical monitoring is mandatory.

Status asthmaticus is an acute exacerbation of asthma that is unresponsive to initial treatment with bronchodilators and can rapidly escalate into acute ventilatory failure. The clinical picture of severe asthma include agitation, drowsiness or confusion, breathlessness at rest, tachypnea, use of accessory respiratory muscles, tachycardia, and pulsus paradoxus. Pharmacological treatments include but are not limited to beta–2–mimetics, anticholinergic agents, magnesium sulphate, steroids and aminophylline. Asthma exacerbations can be triggered by interrupting chronic treatment: in war torn areas as Sudan it is mainly due to the abrupt lack of availability of drugs. A 58 years old 80 kg man with history of severe asthma presented to our triage complaining of severe dyspnea in the last 3 days, unresponsive to treatment with bronchodilators and systemic corticosteroids. He stopped his chronic therapy with budesonide/formeterol due to the unavailability of the drug. At the arrival he showed orthopnea, severe tachypnoea (60 breaths/min) and sinus tachicardia (130 bpm), silent chest and SpO2 86% on reservoir mask 15 l O2/min. The ABG showed pH7.27, pO2 47, pCO2 60. The chest Xray and the transthoracic echo were unremarkable. After receiving repeated nebulizers (salbutamol 5 mg + adrenaline 1 mg every 20’ for 2 h), iv hydrocortisone high dose (1 g), iv aminophylline 240 mg, iv magnesium sulphate 2 g, iv ketamine 100 mg there were neither clinical nor ABG improvement. Given the unavailability of drugs as ipratropium and sevofluorane and of treatments like V–V ECMO, a rescue trial with iv enoximone was performed, administrating 0.3 mg/kg iv bolus followed by 3 mg/kg/min continuous infusion, conbined with NIV to decrease the respiratory workload and salbutamol nebulizers. Improvement of the respiratory mechanics and of the gas exhange were immediate, leading to normal ABG, mild tachypnoea and mild chest wheezes after the administration of 200 mg of enoximone, with no cardiovascular side effects. The patient was discharged home on the 6th day, without respiratory symptoms. Enoximone acts as an inotrope by inhibiting PDE–3 activity and increasing intracellular cAMP levels in cardiac myocytes. Increasing intracellular cAMP is also the main mechanism of β2–agonists bronchodilators, and both experimental models and clinical experience suggest that enoximone can overcome the asthma–related β–receptors downregulation, providing a therapeutic role in status asthmaticus.

Superior vena cava (SVC) syndrome (SVCS) is due to the obstruction of the SVC leading to swelling of the upper body and to low cardiac output. Non tumoral causes, mainly thrombosis of endovascular devices, account for 30% of cases. We report a case of acute iatrogenic SVCS. A 7 years old 16 kg boy underwent mitral valve surgery in severe rheumatic mitral regurgitation. After induction a 15 cm 5.5 Fr 3 lumens central venous catheter (CVC) was inserted in the right internal jugular vein (IJV) under ultrasound guidance without issues. After achieving proper anticoagulation ascending aorta (18 Fr) and bicaval cannulation were performed (20 Fr single stage cannula with right–angled metal tip in the SVC and 26 Fr single stage cannula in the inferior vena cava). Cardiopulmonary bypass (CPB) was performed with pediatric circuit and the mitral valve was repaired. Despite apparently good result of the repair and uneventful weaning from CPB a more accurate transesophageal echo (TEE) showed moderate iatrogenic mitral stenosis. Cannulation was re–performed with same size cannulas and mitral valve replacement (St.Jude 25 mm) was provided. After weaning from CPB with mild cardiovascular support (adrenaline 0.03 mcg/kg/min and noradrenaline 0.05 mcg/kg/min) the TEE showed no abnormalities and the patient was transferred to the ICU in stable conditions. The central venous pressure (CVP) never raised over 10 mmHg. In the ICU the patient developed sinus tachicardia and hypotension, unresponsive to fluids and vasopressors, and swelling of the face with no increase in CVP. The chest Xray showed enlargement of the right upper mediastinum with TEE evidence of accellerated flow in the SVC around the CVC (fig.1). The patient was taken to the operating room and a too tigh pursue string suture was found on the SVC. After optimization of the suture the flow through the SVC was restored with immediate clinical improvement and de–escalation of the cardiovascular support. The face oedema quickly decreased allowing extubation on the day after surgery. The following course was uneventful. SVCS is a life threatening complication of cardiac surgery. A too tight pledgetted pursue–string suture is an uncommon cause compared to clot compression. The CVP measured by a IJV CVC is generally elevated in SVCS, but in our case the tip of the CVC was downstream to the stenosis so showing normal values. Multimodal monitoring is mandatory to lead to emergency surgical treatment in case of need.