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MBBS, MD, DM (Nephrology), FASN
Professor of Medicine, Mayo Clinic College of Medicine & Science
Consultant, Critical Care Medicine & Nephrology | Mayo Clinic Florida
Dr. Pramod K. Guru is a Professor of Medicine at the Mayo Clinic College of Medicine and serves as a Consultant in the Department of Critical Care Medicine, with a joint appointment in Transplant and Nephrology at Mayo Clinic Florida. He graduated from SCB Medical College and Hospital, Cuttack, and earned his MD in Internal Medicine and DM in Nephrology from PGIMER, Chandigarh, India. Dr. Guru is board-certified in Internal Medicine, Nephrology, and Critical Care Medicine in the USA and completed an additional year of Critical Care training focused on ECMO at Mayo Clinic Rochester.
At Mayo Clinic Florida, he directs the Adult ECMO Practice, serves as Program Director for the Critical Care Medicine Fellowship, and is Chair of the Mortality Review Committee. He previously served as MICU Director (2016–2019). For the past eight years, Dr. Guru has been the Course Director for Mayo Clinic’s flagship program on Current Concepts in the Management of ECMO Patients, leading ECMO education nationally and internationally. His research interests include ECMO, Critical Care Medicine, and Acute Renal Failure.
60-year-old male previously DM,HTN, poorly controlled who presents to the ED with acute chest pain, profuse sweating, and in develops cardiac arrest. He is resuscitated with VA ECMO and ROSC is achieved after 45 min and an ECG reveals an anterior wall myocardial infarction with severe LV dysfunction and mild MR.Â
After initial stabilization, he’s taken for an angiogram. The angiogram shows triple vessel disease without a single clear culprit lesion to stent immediately.Â
Cardiologist advice for CABG. He’s now on ECMO for cardiogenic shock, but his BP is maintained with three Vasopressor support norad, adrenaline and vasopressin and team suspects vasodilatory component to shock —essentially a mixed shock picture.Â
His lactate are >10 and down trending ,liver enzymes are 5000 and repeat after 24 hr showing increasing trend with NH3 >200, platelet droping to 80k, INR elevated to 6.Â
However post arrest post ecmo on clinical exam he is conscious and trying to obey commands. He is macro – responsive to fluid as shown by improving MAP and pulse pressure with decreasing requirement for Vasopressor and reduced chattering.Â
However he is developing capillary leakage as seen by new onset of ascites,pleural effusion and peripheral oedema. He is making 20-30ml/hr with reducing trend. His labs show creat of 2.4mg/dl.
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ANS: ECMO-associated acute kidney injury (E-AKI) incidence varies across studies, with most reporting a higher frequency in VA-ECMO compared to VV-ECMO. The etiopathogenesis is multifactorial and differs between early and late stages of support. The likely increased incidence of AKI in VA-ECMO patients may be attributed to greater illness severity, multiple organ dysfunction, alterations in renal hemodynamics due to loss of pulsatile flow, hemolysis-related renal injury, and an elevated risk of infection. Intra-aortic balloon pump (IABP) does not directly improve renal hemodynamics; rather, it provides indirect benefit by enhancing overall cardiac function.
ANS: ECMO circuits allow for the integration of CRRT without requiring an additional access site. This can primarily be achieved in three ways: placing both the arterial and venous limbs of the CRRT line on the pre-pump (drainage/negative pressure) side of the ECMO circuit; positioning both limbs on the post-pump (return/positive pressure) side; or using a combination—such as connecting the arterial limb pre-pump and the venous limb post-pump, or vice versa. The main challenges for CRRT functioning in this setup include the risk of pressure alarms due to transmission of high pressures from the ECMO circuit to the CRRT lines, maintaining adequate flow, and achieving effective ultrafiltration. Risks associated with the ECMO circuit itself include shunting of oxygenated blood through the CRRT line, circuit disturbances leading to air entrapment and potential air embolism or bleeding, increased likelihood of clotting in the circuit, and the risk of infection.
ANS: Anticoagulation strategies during the combination of two extracorporeal circuits, ECMO and CRRT, represent an evolving area of research. Available options include omitting anticoagulation by maintaining high ECMO flow and employing pre-pump (CRRT) replacement fluid; systemic anticoagulation with agents such as heparin or bivalirudin; and regional anticoagulation using heparin or bivalirudin administered directly into the circuit, or citrate anticoagulation. The literature regarding the role of citrate anticoagulation in combined ECMO and CRRT remains limited, preventing a definitive conclusion that it is superior to other methods described above.
ANS: Post-cardiac arrest syndrome presents a challenging and often underrecognized clinical scenario in the intensive care unit. The development of multiple organ dysfunction syndrome (MODS) following return of spontaneous circulation (ROSC) is a significant risk factor for acute kidney injury (AKI). The use of extracorporeal membrane oxygenation (ECMO) as a therapeutic option in the form of extracorporeal cardiopulmonary resuscitation (ECPR) introduces additional risks for AKI due to loss of pulsatility, hemolysis, and infection.
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ANS:The primary objective in managing post-cardiac arrest syndrome is to prevent further brain injury. Continuous renal replacement therapy (CRRT) offers the distinct advantage of better preserving cerebral autoregulation compared to other modalities of renal replacement therapy. Extrapolating these benefits from non-ECMO supported patients to those who have experienced cardiac arrest may be the most effective strategy available for improving neurological outcomes.
ANS:Post-cardiac arrest syndrome exemplifies the often underrecognized capillary leak syndrome frequently seen in critical care settings. Managing these patients is challenging due to a lack of clear evidence-based guidelines. Although fluids are commonly the first line of intervention for hemodynamic instability—regardless of ECMO status—they may not always be ideal and should be used cautiously. A multimodal assessment strategy, including bedside examination, POCUS, hemodynamic monitoring, and laboratory parameters, is recommended to determine fluid needs. Management goals should be individualized according to both patient and circuit requirements, prioritizing fluid-conservative strategies.
ANS: LV venting during VA-ECMO can be accomplished using several non-pharmacologic approaches, including IABP, Impella, atrial septostomy, and direct ventriculotomy. Each of these methods theoretically carries added risks for acute kidney injury due to secondary procedures, hemodynamic changes, and circuit-related complications.
ANS: Continuous Renal Replacement Therapy (CRRT) offers significant advantages, including controlled and continuous fluid removal that helps prevent sudden shifts in volume and maintain stable hemodynamics. The goal is to customize fluid removal based on each patient’s specific needs, rather than adhering to arbitrary or fixed numbers. Hourly and 24-hour fluid targets should be individualized to achieve a net negative balance when hemodynamic status allows, while minimizing the need for frequent fluid boluses, additional vasopressor or inotropic support, and circuit interruptions.
