Clinical Case Scenario
A 59‑year‑old female with acute gallstone pancreatitis develops infected necrotic peripancreatic collection and septic shock requiring noradrenaline. She is oligo‑anuric with pre‑renal AKI and is initiated on CRRT with regional citrate anticoagulation (RCA). After 16 hours, she becomes hypotensive, requires addition of vasopressin infusion, however, the filter clots twice, and ABG shows metabolic acidosis with rising lactate.
Key Lab Findings:
CRRT Settings:
Wrong Answer: Repeating the post filter iCa2+ is crucial in this particular scenario as the vignette curiously mentions that the nurse took the sample for ABG, and spent some time attaching a 2 nd vasopressor and then went on to analyze the sample Post filter blood is citrate rich blood. It has the highest concentration of citrate in the entire circuit and this citrate is actively binding the calcium invitro as well . When analysis of the sample is delayed, citrate continuously keeps binding calcium and the post -filter Ca 2+ levels may be spuriously low. The caregivers may get tricked into thinking the anticoagulation is adequate and not increase the citrate dosing which can in turn precipitating circuit clotting In order to avoid inaccurate Post -filter I Ca2+ measurements: ● Samples have to be analyzed immediately: draw and run – no pause in between ● Use a dedicated heparin free bubble free syringe ● Remove dead space : first 5-10 ml has dilute blood or replacement fluid ● Avoid air bubbles as CO2 get released with bubbles, pH increases and alkalotic pH binds the calcium more to albumin ● Use paired samples when in doubt
Right Answer: This scenario is classical of resistance to citrate based anticoagulation. Although this situation also raises the suspicion of citrate accumulation with the metabolic acidosis rising lactate , increasing noradrenaline requirements with a Total Ca: I Ca 2+ of 2.45 which is borderline for citrate accumulation , here the serum iCa2+ is 0.9 is normal . The most important cue lies in the observation that the post -filter I Ca2+ is high and the filter clotting twice in less than 16hours. If this patient had citrate toxicity, the post filter calcium would have been low or within range with a high total to ionized calcium ratio. The acidosis and worsening shock are probably from the pancreatitis per se or worsening inflammatory response from the blocked filter. Increasing the calcium supplementation addresses low systemic iCa (hypocalcemia). Improves hemodynamic stability and corrects hypocalcemia symptoms. However it does not fix the filter clotting problem, because systemic calcium supplementation doesn’t reduce post‑filter iCa. So while clinically useful, it is supportive, not the definitive anticoagulation fix is not in alignment with the situation and so does continuing with the same rate of citrate infusion. The patient needs up titration of citrate infusion by probably 10ml/hr or more
Wrong Answer: Shifting to a pre-dilution replacement fluid strategy can help by decreasing blood viscosity and lowering filtering fraction , although it can decrease solute clearance.
Wrong Answer: This patient has sepsis induced AKI with liver parameters not amounting to acute liver failure / acute on chronic liver dysfunction. Th elevated liver parameters are probably the systemic response of a multi organ dysfunction. RCA is a reasonable option in such patients and evidence suggests that RCA is better as compared to heparin / no anticoagulation in terms of filter life. However, close titration of citrate and monitoring for resistance is crucial as the hyperdynamic circulation may pose the risk of inadequate anticoagulation from enhanced citrate metabolism If citrate resistance persists despite achieving a high post filter Ca2+ Of <0.25-0.35 then considering alternative strategies to heparin based or no anticoagulation is appropriate
