A 77-year-old man with no drug allergies, hypertension as the only cardiovascular risk factor, on treatment with lisinopril. Other antecedents included nephritic colic, biliary lithiasis and prostatitis.
Previously asymptomatic, the patient consulted the emergency department for diaphoresis and dysthermic sensation of 24 h of evolution, associated with alimentary vomiting, without thermometric fever or abdominal pain. He was asymptomatic from the cardiovascular point of view.
On arrival, temperature 37.8oC, blood pressure 98/56 mmHg, HR 112 bpm and SatO2 94% on room air. Glasgow 14 with a tendency to somnolence. Skin pallor with lividity as a sign of poor peripheral perfusion. Rhythmic heart tones, no audible murmurs. Pulmonary auscultation with preserved vesicular murmur, without rales. The abdomen at this time is depressible, with generalised pain on palpation, without clear signs of peritoneal irritation. No oedema in the lower extremities.
Suspicion of acute abdomen led to a blood test showing acute renal failure with creatinine 3.45 mg/dl and GFR 18 ml/min, metabolic acidosis (pH 7.3, lactate 5 mmol/l) and increased acute phase reactants (CRP > 170 mg/l, procalcitonin > 100 ng/ml, leukocytosis of 14,000/μl). While in the emergency department awaiting further tests, he presented sudden dyspnoea with significant respiratory work and a slight decrease in the level of consciousness (somnolence), pulmonary auscultation compatible with acute pulmonary oedema and electrocardiogram in sinus tachycardia with necrosis and current from an inferoposterior subepicardial lesion. At this point, oxygen therapy was started and the cardiology department was consulted. Bicarbonate perfusion and non-invasive mechanical ventilation were started with improvement of the poor perfusion data and a bedside echocardiogram was performed which showed moderate left ventricular dysfunction due to global hypocontractility with inferior hypokinesia, without pericardial effusion. Given the suspicion of Killip IV inferoposterior STEMI, double platelet antiplatelet therapy was administered and emergent coronary angiography was performed, showing 2-vessel disease with occlusion of the right coronary artery at distal level, on which PCI was performed with implantation of a drug-eluting stent. During the procedure, he presented progressive haemodynamic deterioration, so intravenous perfusion of dobutamine was started. Despite this, the patient continued to deteriorate with frank hypotension and tachycardia, and it was decided to add noradrenaline and implant an intra-aortic balloon counterpulsation device. After this, he was admitted to the cardiac critical care unit.

COMPLEMENTARY TESTS

In the emergency department:

Blood tests:
Glucose 214 mg/dl, urea 84 mg/dl, creatinine 3.45 mg/dl, bilirubin 1.35 mg/dl, GOT 113 U/l, GPT 45 U/l, Na 135.6 mEq/l, K 5'17 mEq/l, Cl 99 mEq/l, CRP 178 mg/l, procalcitonin > 100 mg/l. Haemogram: leucocytes 14,590/μl (77% neutrophils), haemoglobin 18.8 g/dl, haematocrit 55.2%, platelets 311,000/μl. INR 1.19. DD 3,443 ng/ml.
Markers of myocardial necrosis: troponin I US 11,955 pg/ml (normal < 25 pg/ml), CK 1,265 U/l.
Blood gases: pH 7.01, bicarbonate 17.4 mmol/l, lactate 15.5 mmol/l.

Chest X-ray, paucisymptomatic: cardiac silhouette of normal size, free costophrenic sinuses. Normal lung parenchyma.
ECG: sinus tachycardia at 138 bpm. Normal PR. Narrow QRS. QR pattern in DII, DIII and aVF with ST segment elevation of 4-5 mm. ST-segment depression of 1 mm in DI, 2 mm in aVL due to reciprocal changes. Flat ST-segment depression up to 4 mm in V1-V3.
Echocardioscopy: LV systolic function at least moderately depressed by global hypocontractility and severe inferior hypokinesia. Absence of pericardial effusion.

Emergent coronary angiography: 2-vessel coronary artery disease:
Anterior descending: with diffuse atheromatosis, ectatic area at mid level with 40% stenosis, in distal LAD 70% lesion.
Right coronary: ectatic vessel with occlusion in the middle segment. Percutaneous coronary intervention with implantation of 1 drug-eluting stent.
In the cardiology critical care unit:
Abdominal X-ray: levels suggestive of upper intestinal obstruction in the left hypochondrium.
Chest X-ray: increased perihilar density with bilateral vascular redistribution.
Abdominal CT scan: findings compatible with obstructive intestinal ileus of biliary origin.

Microbiology:
Urinary sediment: erythrocytes 51-80/field, leukocytes 3-5/field. Blood cultures: Bacteroides vulgatus.
Urine culture: negative.
Tracheal aspirate: negative.

CLINICAL EVOLUTION
On admission to the critical cardiology unit, haemodynamic instability persisted under perfusion with noradrenaline, dobutamine and intra-aortic balloon counterpulsation. Due to progressive respiratory worsening, orotracheal intubation and mechanical ventilation were decided.
Swan-Ganz catheter was implanted and the following parameters were obtained, compatible with distributive shock: mean arterial pressure 70 mmHg, HR 125 bpm, central venous pressure 6 mmHg, pulmonary artery pressure 32/18 mmHg, pulmonary capillary pressure 12 mmHg, cardiac output 6.8 l/min, cardiac index 3.47 l/min/m, systemic vascular resistances 752 dyn/s/cm .
Following these findings, intensive fluid therapy is started, noradrenaline dose is increased and dobutamine dose is reduced. Intra-aortic balloon counterpulsation support was decreased to 1:2 and withdrawn after a few hours along with dobutamine.
In view of the suspicion of intestinal occlusive symptoms, a nasogastric tube was placed with a 1-litre fecal contents debit. Good haemodynamic evolution with adjustment of vasoactive treatment guided by information from the Swan-Ganz catheter, with a control echocardiography showing preserved ventricular function. A thoracoabdominal CT scan was performed showing findings compatible with obstructive intestinal ileus of biliary origin.
A multidisciplinary team (cardiology, surgery, anaesthesia and intensive care unit) agreed on the indication for surgery and decided to delay it until haemodynamic stabilisation. Fever persisted at the infectious level. Blood cultures were taken and empirical antibiotic therapy with piperacillin-tazobactam was prescribed. Microbiological screening showed Bacteroides vulgatus in blood cultures, compatible with sepsis of abdominal origin.
Finally, after 48 hours, supra-infraumbilical laparotomy was performed, opting to maintain the double antiplatelet therapy with acetylsalicylic acid and clopidogrel during the operation due to the high thrombotic risk following the recent stent implantation in an ectatic vessel that had an abundant amount of thrombotic material. During surgery, seropurulent free fluid and biliary ileus were found, resulting in a punctate perforation of the jejuno-ileum, and resection and anastomosis were performed.
After surgery, the patient was transferred to the intensive care unit, with a slow but correct evolution, and was finally discharged home after 15 days of hospitalisation. The echocardiogram at discharge showed mild LV systolic dysfunction due to inferior hypokinesia (LVEF 49%). Treatment at discharge consisted of double antiplatelet therapy with acetylsalicylic acid 100 mg/24 h and clopidogrel 75 mg/24 h, neurohormonal treatment with bisoprolol 2.5 mg/24 h and ramipril 2.5 mg/24 h and treatment with a high-potency statin atorvastatin 80 mg/24 h.

DIAGNOSIS
Septic shock with multi-organ dysfunction, secondary to peritonitis due to intestinal perforation caused by biliary ileus. Bacteraemia due to Bacteroides vulgatus.
Acute infero-posterior myocardial infarction in the previous context. Urgent percutaneous revascularisation of the middle right coronary artery. Moderate systolic dysfunction in acute phase, mild at discharge.
