HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
The patient in our clinical case is a 40-year-old woman from León, with no contact with the rural environment or animals. She has no drug allergies and her relevant history includes epidemiological contact with tuberculosis that required chemoprophylactic treatment in childhood, with no evidence of subsequent development of the disease, and a benign ovarian tumour being followed up by gynaecology.

She attended her referral hospital with a clinical picture of one week's evolution consisting of general malaise, dyspnoea and suprasternal pain with palpitations. She also reported an episode of generalised urticaria that resolved after taking antihistamines at home. Suspecting thyroid pathology, she was discharged under beta-blocker treatment, pending analytical results.


Due to persistent symptoms, she requested a second opinion at another centre, where she underwent a transthoracic echocardiogram that showed dilatation of the right chambers and pulmonary hypertension, together with cystic images in the liver. She was referred to the emergency department of her referral hospital to rule out acute pulmonary thromboembolism.

Physical examination on arrival:
BP: 102/55 mm Hg. HR: 100 bpm. Ta: 36.2oC. SpO2: 93% basal.
Regular general condition. Conscious, oriented in the 3 spheres and cooperative. Normal colour, normohydrated and normoperfused. Discreetly tachypnoeic at rest, with good respiratory dynamics.
Head and neck: absence of jugular ingurgitation. No palpable goitres or adenopathies.
Cardiac auscultation: rhythmic, tachycardic heart sounds. No murmurs or extratonos are heard.
Pulmonary auscultation: preserved vesicular murmur in both hemithoraxes, no extra sounds.
Abdomen: hydro-aerial sounds present and of normal characteristics. Soft, depressible, not painful on superficial or deep palpation, with no signs of peritoneal irritation.
Lower extremities: pedial pulses present and symmetrical. No oedema or signs of deep vein thrombosis.

COMPLEMENTARY TESTS
Laboratory tests at the referral hospital: elevated NT proBNP (5981 pg/ml), D-dimers (20887 ng/ml). Other parameters in normal range.
Angio-CT scan at the referral hospital: hypodense mass was observed occupying the left pulmonary artery and extending obstructing all ipsilateral lobar and segmental arteries, as well as a second mass of similar characteristics in the right interlobar artery, in addition to an area in the right lower lobe suggestive of pneumonitis or pulmonary infarction and a cavity with a mass inside it in the meniscus sign in the left lower lobe. There was also dilatation of the pulmonary artery trunk and evidence of right ventricular overload, findings suggestive of pulmonary hypertension.
Magnetic resonance imaging (MRI) of the liver at his referral hospital: a large cystic lesion with calcified wall in the right hepatic lobe corresponding to a hydatid cyst with daughter vesicles, with rupture of the capsule with focal extension and invasion of the inferior vena cava.
Transthoracic echocardiogram in our centre: mild right ventricular dysfunction, with severe pulmonary hypertension (estimated PSAP: 60-65 mmHg), showing intraluminal masses in the pulmonary artery and extrinsic compression of the vena cava. Normal left ventricular function and absence of significant valvular heart disease.

CLINICAL EVOLUTION
In view of these findings, serology for hydatidosis was performed, which was positive, so antiparasitic treatment was started with albendazole 400 mg/12 h and oral praziquantel 600 mg/8 h. Initial evolution was favourable, although he persisted with hypoxaemia dependent on oxygen therapy. The patient was transferred to our centre for assessment by the multidisciplinary pulmonary hypertension unit.

On arrival at our centre, the patient was haemodynamically stable. Laboratory tests showed discrete elevation of NT-proBNP (2612 pg/ml) and acute phase reactants (leukocyte count at the upper limit of normal with significant neutrophilia, C-reactive protein 24.5 mg/dl, fibrinogen 1320 mg/dl). Positive serology for hydatidosis was confirmed by ELISA test. A new transthoracic echocardiogram was repeated (images 7-9), showing mild right ventricular dysfunction, with severe pulmonary hypertension (estimated PSP 60-65 mmHg), intraluminal masses in the pulmonary artery and extrinsic compression of the vena cava, as well as normal left ventricular function and no significant valvular heart disease. After reviewing the tests performed at his referral centre, the case was presented at a multidisciplinary session involving the cardiology, radiology, infectious diseases unit, cardiac surgery, thoracic surgery and general surgery departments. At this session, a two-stage approach was decided: initially cyst extraction and scheduled hepatectomy and subsequently pulmonary endarterectomy of hydatid cysts.
While awaiting this intervention, admitted to the cardiology ward, the patient presented symptoms compatible with anaphylactic shock requiring administration of intramuscular adrenaline and steroid boluses and the start of intensive fluid therapy, despite which she remained unstable both respiratory (SpO2 < 70%) and haemodynamic (BP 50/40 mmHg), so she was transferred to the coronary unit, where a central line was started and adrenaline and noradrenaline perfusion was started. She was also connected to non-invasive mechanical ventilation (EPAP 2, IPAP 9, FiO2 100%).
Given the persistence of haemodynamic deterioration despite adequate support measures, a new transthoracic echocardiogram was performed, showing severe left ventricular dysfunction.
The electrocardiogram showed no evidence of ischaemia and no significant elevation of myocardial damage markers (troponin T hs 84 ng/l, CK 152 U/l).
With the suspicion of stress cardiomyopathy in relation to the episode of anaphylactic shock requiring high doses of catecholamines (which at this time included the administration of dobutamine), the possibility of implantation of veno-arterial ECMO was assessed. However, the implantation of the device was rejected for various reasons: the presence of left ventricular dysfunction that made the risk of the surgical intervention that the patient needed to cure her unacceptable at that time; the risk of new dissemination or rupture of cysts with the manipulation of lines and cannulas in the venous territory, and the complexity of the management of assistance in a patient with severe pulmonary circulation alteration. In this context, expectant management was decided, awaiting spontaneous recovery to reactivate the initial plan.
During the hours immediately after the episode, the patient showed discrete haemodynamic improvement that allowed suspension of adrenaline perfusion and a decrease in noradrenaline to 0.2 μg/kg/min with progressive improvement of the distal hypoperfusion data. Under low doses of dobutamine, a new echocardiogram was performed where severe left ventricular dysfunction persisted. Respiratory stability was such that ventilatory support could be reduced with acceptable clinical tolerance.
However, 24 hours after the anaphylactic shock episode, she presented a sudden episode of desaturation, with associated hypotension and spontaneous recovery after starting support with high-flow glasses with FiO2 of 1, with data compatible with pulmonary congestion on chest X-ray.
Hours later, he presented with frank haemodynamic deterioration, with associated episodes of desaturation and urticaria suggesting a new case of anaphylaxis, probably due to the release of hydatid vesicles. Initially, doses of vasoactive drugs were increased, intramuscular adrenaline and bolus corticotherapy were started, despite which she presented with new haemodynamic deterioration, with moderate-severe dilatation of the right ventricle on urgent echocardiography, maintaining severe left ventricular dysfunction. The patient presented with a new episode of desaturation, associated urticaria and loss of consciousness that required orotracheal intubation, after which electromechanical dissociation was observed, which could not be reversed after 25 minutes of advanced CPR manoeuvres. When these manoeuvres were stopped, asystole and thrombosis of both ventricles were observed on transthoracic echocardiography. Relatives were informed and the possibility of performing an autopsy was explained, which they rejected.

DIAGNOSIS
Severe pulmonary hypertension secondary to compromise of the pulmonary arterial tree by hydatid vesicles, probably secondary to migration from a giant hepatic hydatid cyst.
Right ventricular dysfunction in the context of the above.
Anaphylactic shock in relation to disseminated hepatic hydatid disease, with stress cardiomyopathy with development of secondary severe left ventricular dysfunction.
Cardiorespiratory arrest in electromechanical dissociation.
