Introduction
Post-operative bleeding can occur because the primary insult was not adequately addressed, as a complication of surgery or because of a multifactorial systematic coagulopathy. The first consideration after diagnosing post-operative bleeding is whether further surgical or trans-vascular intervention is indicated to arrest the haemorrhage. Deciding on the most appropriate course of action should be done in consultation with an experienced surgeon and/or interventional radiologist. If a systemic coagulopathy is suspected, an attempt should be made to understand the cause of the coagulopathy so that it can be addressed appropriately.
Most of the therapies discussed here have been studied in the context of pre- and intra-operative interventions to reduce the need for peri-operative blood transfusion or as treatment for patients with inherent disorders of coagulation. Recently, a lot of work has been reported on the coagulopathy of trauma, its influence on mortality and how to treat it. It is acknowledged that patients admitted to the ICU with post-operative bleeding may not exactly resemble these scenarios, but a pragmatic approach is advocated. It is necessary to pause briefly and describe the clotting process as we currently understand it.
In its unprovoked in vivo state, blood does not clot due to the prevailing anticoagulant effects of antithrombin on activated factors IX, X and XI; thrombomodulin–protein S–protein C complex on activated factors V and VIII; and tissue factor pathway inhibitor (TFPI) on the crucial haemostasis initiating activation of factor X (FXa) through activated factor VII (FVIIa) and tissue factor (TF).
When an injury occurs, robust haemostasis is dependent on an adequate number of functional platelets and the generation of a sufficient burst of thrombin. Injuring endothelial cells exposes collagen and von Willebrand factor (vWF), which facilitates platelet adhesion. The platelet membrane provides a crucial support structure and many essential molecules for the coagulation process. TF is presented and combines with FVIIa that activates both factor IX and factor X. This TF pathway provides the initial thrombin burst. The addition of activated factor VIII (FVIIIa) and activated factor IX (FIXa) subsequently activates factor X (FXa).
The FXa complexes formed thus are also called tenases and combine with activated factor V (FVa) and activate factor II (prothrombin) to form thrombin. Thrombin further stimulates its own production by activating factor XI, but the ultimate goal is for thrombin to convert fibrinogen to fibrin. Fibrin strands provide a meshwork for platelets to aggregate in and plug the hole in the injured blood vessel. The fibrin mesh is stabilized by factor XIII cross links.
Thrombin also switches off the clotting process by altering the configuration of thrombomodulin, which then interacts with protein S and protein C, while antithrombin and TFPI are stoichiometric inhibitors. Fibrin converts plasminogen to plasmin, which dissolves the clot and hence re-establishes blood flow.
General measures
Hypothermia and acidosis along with coagulopathy have been described as the lethal triad or bloody vicious cycle of haemorrhagic shock. Simple measures such as avoiding excessive exposure and an appropriate ambient temperature are usually enough to maintain normothermia but are easily overlooked. Heated air blankets are also useful in the ICU. Always ensure that the patient has been rewarmed and that the temperature is maintained at 37 °C. Acidosis should be corrected through adequate resuscitation. Hypocalcaemia due to chelation of calcium ions with citrate in packed red cell units is common after blood transfusion and inhibits clotting. Give calcium if the ionized calcium level is less than 0.9 mmol/L [1].
These measures will ensure the optimum haemostatic milieu. The term damage control resuscitation has been coined in the trauma literature, but the approach is equally important in the non-traumatic bleeding patient.
