Tranexamic acid is a synthetic derivative of lysine and acts as an antifibrinolytic by competitively inhibiting the activation of plasminogen to plasmin. It is used to treat menorrhagia and its efficacy in treating trauma victims has also been demonstrated. It is widely used in an attempt to reduce major hemoptysis, particularly whilst other measures are being organized. However, although this has been common practice for years, there is surprisingly little formal evidence of benefit. The only formal trial of which I am aware randomized 46 patients with hemoptysis of variable cause to either tranexamic acid or placebo and failed to demonstrate any benefit in terms of reducing blood loss or shortening the duration of hemoptysis [32]. However, this trial can be criticized in a number of ways, and in particular the patient group were atypical of those in whom tranexamic acid would usually be employed in that the degree of hemoptysis was modest in many of them. Moreover, in a significant ­proportion of those studied no underlying lung disease was identified (although investigation was not extensive).

Anecdotally most physicians who deal frequently with hemoptysis believe that tranexamic acid has a role and will remember patients whose hemoptysis has recurred and improved in timing with the cessation and reintroduction of tranexamic acid. One such case has been described in a patient with cystic fibrosis recurring after bronchial artery embolization [33]. Despite the lack of firm evidence the use of tranexamic acid can be recommended as a holding procedure in cases of major hemoptysis. The usual dose used is 1 g three times daily orally or 500 mg – 1 g by slow intravenous injection (over 5–10 min) three time daily or 25–50 mg/kg by intravenous infusion over 24 h. Etamsylate, 500 mg four times daily orally, is an alternative agent with an unknown mechanism of action, although it is believed to work by altering the permeability of the capillary wall and possibly by promoting platelet aggregation. There is even less evidence for its benefit in hemoptysis than there is for tranexamic acid.

Occasionally hemoptysis is caused or significantly exacerbated by abnormalities of the coagulation system. In the palliative care context this is not common, but will be seen in a proportion of patients who require treatment with warfarin for some other condition. In patients with persistent low or modest volume hemoptysis, the question of whether anticoagulation should be stopped will depend on an individual risk assessment which must take into account the reason for starting anticoagulation. When hemoptysis is more substantial, and certainly when life-threatening, it is undoubtedly appropriate to stop anticoagulation and even to consider the use of prothrombin complex concentrates. The use of fresh frozen plasma may also be appropriate.

Patients receiving chemotherapy may present with significant hemoptysis and low platelet counts. If bleeding cannot be controlled and platelet count is below 50 × 10⁹/l, it may be necessary to offer platelet transfusion. Among the commonest pharmaceutical agents used by patients with hemoptysis is some form of antiplatelet therapy, such as aspirin or clopidogrel, since these are in widespread use for primary and secondary prevention of atherosclerotic diseases. Again, decisions about stopping these drugs are based on an individual assessment of risk. There are no clinical trials to guide the decision in patients with hemoptysis, although one interesting study in patients with upper gastrointestinal bleeding showed an increase in mortality if antiplatelet agents were stopped beyond the immediate period in which treatment to the bleeding source was carried out [34]. These patients were taking aspirin for secondary prevention of known cardiovascular disease. This is clearly indirect evidence, but it would be reasonable to stop antiplatelet agents briefly in cases of major hemoptysis and to restart them once the bleeding is controlled, where there is a good indication for their use.