Four fibrinolytic agents were used in these cases: streptokinase, urokinase and actilyse (Alteplase-rtPA), tenecteplase ®. Most of these patients received streptokinase,

Tothe best of our knowledge, only one case associated with Tenecteplase (Metalysis) has been previously reported in the literature [3].

Through the analysis of these cases, we find that HA usually occurs from a few hours to 5 days after thrombolysis.[ [3]

The literature review identified 23 cases [3,22]. Surprisingly, all 23 patients (including ours) were male, ranging in age from 24 to 75 years, making male a predisposing factor [3]. Streptokinase was the thrombolytic agent in 16 of 23 patients (69.5%) [3,21]. Streptokinase immune reactions that range from simple allergy to anaphylactic shock may be a contributing factor. It has been suggested that immune-mediated capillaritis maybe a possible etiology of HA following streptokinase administration [3,21,23]

The pathogenesis of HA attributable to thrombolytic therapy remains uncertain and may be explained by pre-existing fibrinolytic states, the presence of parenchymal abnormalities, or an immune response to streptokinase causing pulmonary capillaritis as proposed [20].

It was mentioned that some potential cofactors may predispose to this complication, such as underlying lung diseases (chronic obstructive pulmonary disease, anterior emphysema), recent pneumonia, cardiac catheterization, arrhythmias requiring defibrillation shock or cardiopulmonary resuscitation, heart failure, and substance abuse such as cocaine and tobacco [24]. Green et al [25] described that some patients with alveolar hemorrhage had capillaritis, suggesting an immune reaction since streptokinase is associated with a wide range of allergic reactions, such as anaphylaxis, bronchospasm, and type III immune reactions. Tio et al [8] described the discovery of antibodies to streptokinase in HA patients treated with thrombolytics, which would support this theory. However, in some cases, no predisposing factors have been identified.

For our patient, pneumonia and defibrillation after thrombolytic administration could be the cause of the worsening HA.

Typically, the diagnosis of HA is evoked in the clinical triad of haemoptysis, anemia and radiological pulmonary infiltrates, with a variable mode of onset (insidious to abrupt). Hemoptysis is rarely abundant due to its distal nature. It may be associated with coughing or chest pain. Frequent anaemia, possibly of rapid onset with a sudden loss of 10 to 20 g/L, given thealveolar surface during active H A [1].

Chest X-rays may be normal (about 5%). Anemia may also be missing [1]. It varies depending on when it is done in relation to the beginning of the bleeding, and its intensity. In the initial phase, bilateral micronodular images are observed, which will often converge and give predominantly perihilar and peribasal alveolar opacities, sparing the apexes and costophrenic angles [21]. These opacities over time will give way to interstitial opacities (indicating the resorption of the hemorrhagic alveolitis in the interstitium) in principle transient (10 days to 2 weeks) [1].

Chest computed tomography (CT) scans are of little interest in the acute phase and can only be considered in stable patients. It may show areas of bilateral alveolar condensation and/or frosted glass, diffuse, sometimes associated with cross-linking giving a crazy paving appearance [1].

Diagnostic confirmation is based on bronchial endoscopy and AML, the appearance of which varies according to the length of the intraalveolar hemorrhage. A lung biopsy is not necessary [1].

When the diagnosis is suggested, bronchial endoscopy with Bronchoalveolar Lavage (BAL) is the gold standard to confirm the diagnosis.  However, this is usually not possible. In cases of post-thrombolysis H A reported in the literature, these examinations have not been performed [3].

The prognosis can sometimes be life-threatening. In some all-cause H series, between 20 and 70% of patients are ventilated and 50 to 90% are on dialysis. Mortality ranges from 20% to 100% with early mortality (first 15 days) attributable to HA of about 10% [1].

To identify patients at risk of hospital death, the following parameters are available in the first 24 hours: resuscitation severity scores (IGS II, APACHE II), an LDH level greater than twice normal, the presence of shock or severe kidney damage [1].

Regarding the cases of post-thrombolysis H A described in the literature, the clinical course was good in about 80% of cases with complete recovery within one to two weeks. The prognosis depends on the extent of the myocardial infarction, the volume of the hemorrhage and the degree of cardiorespiratory involvement.

Prior to our publication, only 23 cases were reported in theliterature with five deaths; therefore, the mortality rate was 21%[3].

Symptomatic treatment of acute respiratory failure has no specificity. If mechanical ventilation becomes necessary, it should limit barotrauma. The volume of blood glucose levels should be assessed regularly, as any overload is deleterious, especially in the case of associated renal failure. Any abnormality in haemostasis can aggravate the disease: non-essential antiaggregation or anticoagulant treatments should be discontinued.

In severe cases, some people use desmopressin or corticosteroid therapy, the effectiveness of which is controversial [1].

Antifibrinolytic agents, such as tranexamic acid, were used in one case.