When to correct coagulopathy in acute kidney injury?

Incidence of acute kidney injury (AKI) in adult trauma patients is 18% with 70% requiring renal replacement therapy. It is a challenge to treat AKI with coagulopathy since there are no defined transfusion triggers for these patients. We report a case wherein a polytrauma patient developed AKI for which he/she was dialysed and subsequently had an intracerebral bleed. There is a need to develop guidelines to transfusion triggers in AKI patients keeping vigilance on fluid overload, hyperkalemia and uraemia-induced platelet dysfunction.

INTRODUCTION

Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid reduction in the renal excretory function and is associated with increased morbidity and mortality in intensive care trauma units. Incidence of AKI in adult trauma patients is 18%[1] of which 70% of patients require some form of renal replacement therapy.[2] In the trauma setting, transfusion of blood and blood products in AKI patients pose a challenge. When to start transfusion and how much to transfuse in a patient with oliguria with concerns of fluid overload, hyperkalemia and uraemia-induced coagulopathy is a dilemma.

CASE REPORT

A 40-year-old male was referred to our centre 2 days after he sustained polytrauma in a road traffic accident. He had blunt trauma to the chest (with right hemothorax) and abdomen (with right lower lobe liver laceration) with fractured right tibia.

On admission patient had Injury severity scoring (ISS)[3] of 26, Sequential Organ Failure Assessment (SOFA) score of 12 and Acute Physiology and Chronic Health Evaluation (APACHE II) score of 18 which indicated that patient would need intensive critical care. A CECT of the chest and abdomen revealed right hemothorax and right lower lobe liver laceration. His renal parameters were deranged on admission with coagulopathy. During his stay in ICU, the patient progressively became oliguric and was anuric by third ICU day. He developed sepsis with multiorgan failure (respiratory failure, renal failure, and metabolic disturbance). He required intubation and ventilator support on sixth day of his ICU stay in view of respiratory distress. Trend of laboratory parameters is shown in Table 1. He received heparin-free dialysis on third, fourth, and sixth days in view of coagulopathy. However, no blood products were transfused as there was no active bleeding. On the sixth day, patients GCS decreased from 15 to 6. A noncontrast computed tomography head [Figure 1] revealed massive hemorrhage in parieto-occipital region with intraventricular extension. Surgical intervention was planned once coagulation profile was corrected. Patient expired within 6 h.

Table 1

Trend of laboratory parameters

Figure 1

Axial noncontrast CT image at the level of lateral ventricle shows large parenchymal hemorrhage in the left parietooccipital region with extension into the left lateral and third ventricle causing midline shift

DISCUSSION

Renal failure is multifactorial in most of the critically ill patients. Our patient developed AKI possibly attributable to the hypovolemia (prior to shifting to ICU depicted by high lactate), contrast induced nephropathy (CECT chest and abdomen done by referring hospital), inadequate hydration, abdominal compartment syndrome and myoglobinuria due to the injuries sustained Coagulopathy is frequently seen in patients with the multiorgan failure. However, blood products (FFP and platelets) are withheld until any clinically active bleeding occurs.[4] In patients with AKI, transfusing plasma and platelets increases the overall fluid overload and subjects the patient to hyperkalemia. To prevent fluid overload, blood products have to be usually deferred predialysis and administered during dialysis. As per conventional practice, correction of coagulopathy was not attempted as there was no active bleeding. Our patient developed a massive intracerebral bleed as depicted in CT scan [Figure 1] head. An attempt to correct the coagulopathy at an earlier stage may have averted this outcome.

FFP transfusions are recommended for coagulation factor deficiencies, microvascular bleeding in the presence of elevated (>1.5 times normal) prothrombin time (PT) or partial thromboplastin time (PTT) and microvascular bleeding. Platelet transfusions are recommended prior to major operations in patients with platelet counts <50000/μL, intraoperatively with microvascular bleeding at platelet counts <50000/μL.[5] In patients with AKI, uraemia further contributes to platelet dysfunction and coagulopathy. Awaiting active bleeding to initiate correction of coagulopathy may adversely affect the outcome in such situation.

There are medications that have been tested and studied for treatment of bleeding in subset of patients with severe uraemia associated with prolonged bleeding times. These therapies include conjugated estrogens, desmopressin, and the blood product cryoprecipitate. The exact mechanism of action of these medications has not been elucidated though they have shown to shorten the prolonged bleeding time. The duration of action of cryoprecipitate and desmopressin are usually less than 24 h while that of conjugated estrogens may be two weeks in patients receiving large doses for 5 days.[6] These do not have a proven role in the acute setting.

The current transfusion guidelines[5] do not specifically consider coagulopathy in patients with AKI. Waiting for active clinical bleeding to transfuse blood and blood products may in turn increase morbidity and thus add to the high incidence of mortality in AKI patients. We require studies in this specific setting of AKI to identify whether early correction of coagulopathy with various products would significantly reduce incidence of bleeding and provide guidelines specific to the setting of AKI. The thromboelastography (TEG) allows for judicious and protocol assisted utilization of blood components in a trauma setting;[7] hence, we suggest use of TEG to guide transfusion especially in such patients.