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9 Extracorporeal Membrane Oxygenation
Table 9.7 Physiochemical properties of select diuretics used in ECMO
Diuretic Protein binding LogP
Bumetanide 96% 2.6
Chlorothiazide 40% −0.24
Furosemide 99% 2.09
Metolazone 95% 2.5
Torsemide >99% 3.36
LogP log of partition coefcient
Information adapted from Lexicomp and DrugBank Online
251
(e.g., thiazide diuretics) for uid removal. A paucity of data exists on appropriate
dosing of diuretics in ECMO. The suitable dose required to achieve the desired
urine output is often determined through a process of trial and error by clinicians.
Limited data in pediatric patients suggest that there may be a need to administer
higher initial bolus doses of bumetanide and furosemide [122, 142].
Bumetanide and furosemide have high lipophilicity and are highly protein bound
(Table9.7), which may make them susceptible to circuit sequestration. An invitro
analysis of furosemide disposition within four neonatal ECMO circuits demonstrated 63–87% reduction in serum concentrations over a 4-hour observation period
when doses of 5 mg and 10 mg were administered [23]. While intermittent and
continuous infusion dosing of loop diuretics is a common practice in many institutions, limited data exists to guide practice in patients on ECMO.Some institutions
prefer the use of continuous infusions over intermittent doses to prevent uctuations
in diuretic serum concentrations and to potentially overcome drug sequestration.
Nevertheless, there is no available comparative data to endorse one dosing strategy
over the other in ECMO patients. Thiazide diuretics display widely variable physiochemical properties, with chlorothiazide being the least protein bound and lipophilic. There are no studies evaluating the effect of ECMO on thiazide diuretics.
Standard doses can be initiated and titrated for clinical response. For cases of refractory diuresis or overt renal failure, renal replacement therapy (RRT) can be initiated.
9.8.1 Acute Kidney Injury andRenal Replacement Therapies
Acute kidney injury (AKI) is a frequent complication in patients receiving ECMO
treatment, resulting in increased morbidity and mortality [108]. The incidence of
AKI in ECMO-supported patients is widely variable and ranges from 26% to 85%
due to differences in AKI denition, patient characteristics, ECMO modes, and
clinical setting [121]. The combined estimated incidence of severe AKI necessitating RRT is approximately 45%. The prevalence of AKI is greater with VA-ECMO
compared to VV-ECMO at 61% and 46%, respectively, and is most often observed
on the day of ECMO cannulation [108]. Patient-specic factors prior to ECMO
initiation that contribute to AKI include hemodynamic instability, reduced cardiac
output, elevated intrathoracic and intra-abdominal pressures, exposure to nephrotoxic agents, sepsis, bleeding, coagulopathy, severe hypoxemia, and hypercapnia.
252
S. Davis et al.
Following cannulation, ECMO-related factors that contribute to AKI include ischemia–reperfusion injury, continuous ow during VA-ECMO, hemolysis, malposition of cannulas, higher pump speeds, and release of inammatory cytokines
induced by blood exposure to articial surfaces. Several standardized denitions
including the Risk, Injury, Failure, Loss, End-stage (RIFLE) criteria, the Acute
Kidney Injury Network (AKIN) criteria, and the Kidney Disease Improving Global
Outcomes (KDIGO) guidelines have been validated in non-ECMO-supported
patients and allow for the classication of AKI by both serum creatinine and urine
output. Fluid overload is another manifestation of kidney dysfunction and, as previously mentioned, is associated with negative clinical outcomes. Since AKI and uid
overload are both linked to higher mortality rates, treatment of these comorbidities
is recommended to improve ECMO outcomes.
Fluid overload and AKI are the most common indications for RRT on
ECMO. According to an international survey, the primary reasons for initiating
RRT during ECMO were the management of uid overload (43%) and prevention
(16%) of uid overload (16%). This was followed by AKI (35%) and electrolyte
disturbances (4%) [52]. Early initiation of continuous renal replacement therapy
(CRRT) while on ECMO has demonstrated benecial outcomes in neonates [108];
however, similar data in adult patients receiving ECMO are lacking, and optimal
timing to initiate CRRT is not well dened. Several randomized controlled trials
conducted in critically ill adult patients with AKI have failed to demonstrate a survival benet of the early (<12 hours) strategy for RRT initiation compared to
delayed (>48–72 hours) strategy. Instead, earlier initiation increased the risk of
dialysis dependence at 90days and adverse events [9, 11, 55]. A retrospective study
using propensity score matching of 94 adult patients on ECMO compared early
initiation of CRRT to delayed initiation (median time to CRRT initiation, 1.1 vs.
14.6days) and found no benet on hospital length of stay (LOS) or mortality benet
with early initiation [109]. Given that serum creatinine, urine output, and staging of
AKI have been proven to be unreliable markers for guiding initiation of RRT, a
concept known as “demand-capacity” has been suggested to assist in the decisionmaking process.
This concept proposes that RRT should be considered if the extent
of AKI-related metabolic disturbances and uid overload are going to surpass the
kidney’s ability to compensate and when conventional pharmacological interventions like diuretics and sodium bicarbonate are going to be ineffective. Therefore,
RRT should be initiated in adult ECMO patients in situations where uid overload
is refractory to diuretic therapies and when AKI-related metabolic derangements
impede chances of cardiopulmonary failure recovery.
While on ECMO, various modalities of RRT can be administered including
intermittent hemodialysis (IHD), sustained low-efciency dialysis (SLED), peritoneal dialysis, and any CRRT modality such as hemoltration (CVVH), hemodialysis (CVVHD), and hemodialtration (CVVHDF). Each RRT modality has
advantages and disadvantages. Three main techniques exist for delivering RRT with
ECMO: (1) RRT device connected using independent access from ECMO circuit
(parallel system), (2) in-line hemolter, and (3) RRT device connected within the
ECMO circuit (integrated system) (Fig. 9.5). For parallel systems, a separate
9 Extracorporeal Membrane Oxygenation
253
vascular access point ensures that the RRT machine does not interfere with ECMO
ows. While this technique is a simple approach in patients who have vascular
access prior to ECMO cannulation, a potential disadvantage is an increased risk of
bleeding when introducing a new dialysis catheter since ECMO patients commonly
receive anticoagulation to minimize clot formation in the ECMO circuit. With this
conguration, CRRT is managed similarly to patients not on ECMO, with the
exception that additional anticoagulation for the CRRT circuit may not be necessary. In-line hemolters are inserted by creating a shunt post-pump and preoxygenator within the ECMO circuit. In-line hemolters are mainly used for
ultraltration using SCUF mode; however, CVVH or CVVHD can be delivered
through standard infusion pumps (Fig.9.5). In-line hemolters were the rst method
to provide CRRT during ECMO, with the advantages of being inexpensive, less
resource intensive, and simple to set up. However, multiple disadvantages include
inaccurate uid removal, ECMO recirculation, and absence of a pressure monitor to
detect hemolysis, lter rupture, or thrombus formation. Integrating a commercially
available CRRT machine in-line with the ECMO circuit provides superior control of
uid balance and clearance of solutes compared to an in-line hemolter. This technique requires a thorough understanding of circuit pressures since pre-ECMO pump
pressures are negative (−20 to −100mmHg) and post-ECMO pump pressures are
positive (+150 to +350mmHg), and these pressure differences might interfere with
the CRRT circuit [108]. There are many ways to integrate the CRRT device into the
ECMO circuit, and the optimal connection depends on multiple factors, including
ECMO circuit design, type of ECMO pump, and CRRT device. Risks associated
with introducing additional catheters to the ECMO circuit for RRT delivery include
hemolysis and thrombosis because of ECMO circuit manipulation. The effectiveness of any specic RRT technique is not well supported by existing evidence, and
therefore, clinical practices rely on expert opinion, local expertise, and availability
of machines and resources. A 2012 international survey of 65 ECMO centers
revealed that most centers (50.8%) use independent CRRT circuits within the
ECMO circuit, compared to in-line hemolters (21.5%) [52]. In general, many centers prefer to perform CRRT through venous access independent of the ECMO
circuit.
As with ECMO support, the addition of RRT does not resolve the underlying
cause of organ failure, and providing effective pharmacotherapy is imperative to
treat these causes. The presence of extracorporeal therapies (e.g., ECMO and RRT),
especially when combined, can further exacerbate existing pathophysiological
changes from critical illness. Consequently, the interplay between critical illness,
ECMO, and RRT signicantly alters the pharmacokinetics (i.e., volume of distribution and drug clearance) of important medications such as antibiotics, opioids, and
sedatives. Conventional dosing strategies seldom consider the impact of altered
pharmacokinetics and thus may lead to variations in drug concentrations resulting
in therapeutic failure or drug toxicity in a considerable portion of critically ill
patients receiving ECMO and RRT. Literature supporting optimal dosing strategies
in patients receiving both ECMO and RRT is lacking, which can be explained by
difculties in estimating pharmacokinetic parameters in the presence of two
a
b
c
Fig. 9.5 Continuous renal replacement therapy with ECMO. Various options of combining
ECMO and CRRT: (1) An in-line hemolter is integrated into the ECMO circuit. Replacement
uid is directly administered into the ECMO circuit. Alternatively, dialysis uid can be supplied in
a countercurrent position. Replacement/dialysis uid rates and ultraltration rates can be controlled via infusion pumps. (2) The CRRT device is connected to the patient through a separate
catheter independent of the ECMO circuit. The access (inlet) and the return (outlet) lines of the
CRRT device are connected before the centrifugal blood pump (low-pressure part) of the ECMO
circuit [108]. CRRT, continuous renal replacement therapy, ECMO extracorporeal membrane
oxygenation
9 Extracorporeal Membrane Oxygenation
extracorporeal circuits. To make informed decisions in the absence of robust data,
an in-depth understanding of physicochemical properties of medications must be
considered when assessing the impact both ECMO and RRT have on pharmacokinetic changes (see “Properties of the Drug Affecting Pharmacokinetics” section).
For RRT, serum concentrations and half-life of medications depend on blood/dialysate ow and sieving coefcient of the hemodialyzer. In general, modifying conventional RRT dosing strategies based on pharmacokinetic changes from ECMO and
patient-specic factors can be employed until more data becomes available.
255
9.9 Other Complications
9.9.1 Bleeding
Bleeding is the most common medical complication of ECMO, with an incidence
ranging between 30% and 60% [103]. Data shows that the risk of major bleeding is
similar between VA- and VV-ECMO and can be contributed to the use of anticoagulation, platelet dysfunction, underlying comorbidities, critical condition of the
patient during ECMO, or supratherapeutic aPTT [103]. Bleeding can happen at any
site, including surgical, cannulation, intrathoracic, abdominal, intracerebral, retroperitoneal, or pulmonary [88]. Bleeding is associated with worse outcomes; studies
have shown that major bleeding on the rst day of ECMO is associated with a twoto three-fold increase in the risk of in-hospital or 90-day mortality as well as longer
ECMO durations [103].
Management of bleeding may vary slightly depending on the site of the bleeding;
however, there is consensus that anticoagulation should be temporarily held until
bleeding is controlled [88, 92]. While anticoagulation is held, serial monitoring for
circuit thrombosis is essential [92]. If bleeding occurs at the surgical or cannulation
site, topical hemostatics may sufce, with consideration for systemic aminocaproic
acid or tranexamic acid [92]. Internal bleeding or more severe surgical or cannulation site bleeding may require transfusions; however, studies are lacking in regard to
best practices. Table9.8 outlines recommended goals per the ELSO guidelines.
Reversal agents for severe hemorrhage, such as prothrombin complex concentrates or activated recombinant factor VII (rFVIIa), have limited use and data in the
ECMO population. One small case series in pediatric patients on ECMO showed
successful hemostasis with no thromboembolic events following the use of rFVIIa;
however, a larger case series showed success in bleeding cessation but a major
stroke, circuit thrombosis, and a high mortality rate [118, 144]. The use of these
agents should only be considered at this time for intractable bleeding where the
benets outweigh the risks.
Steps have been taken to prevent bleeding complications including improvements in surgical techniques and changes in the coatings of ECMO cannulas and
tubing [103]. A small, retrospective study showed that the use of prophylactic anticoagulation with subcutaneous enoxaparin 40 mg daily resulted in no fatal or
256
Table 9.8 Blood product and goals for bleeding and non-bleeding patients [49]
Blood product Goal
Platelets >100,000×10
50,000−100,000×10
Fibrinogen >150mg/L (bleeding)
>100g/L (non-bleeding)
Hemoglobin >7–9g/dL
9
/L (bleeding)
9
/L (non-bleeding)
S. Davis et al.
intracranial hemorrhage, 18% incidence of clinically relevant bleeding, and 6.5%
incidence of thrombosis resulting in pump exchange [75]. Other studies demonstrated that the use of no anticoagulation resulted in a similar prevalence of bleeding
events as those who were anticoagulated and meeting ACT or aPTT targets, with
either a signicantly higher or a similar prevalence of thromboembolic events
[104, 133].
9.9.2 Thrombosis
Thrombotic complications typically occur within the circuit and are less likely to
occur compared to bleeding complications, with an incidence of 10–20% [88, 104].
The pathogenesis of thrombotic complications stems paradoxically from many of
the same factors that cause bleeding, including critical illness, underlying comorbidities, and aspects of the ECMO circuit itself such as its nonpulsatile blood ow
and exposure of blood to the circuit tubing [104]. Thrombosis is more likely to
occur in VV- versus VA-ECMO at 22.1% and 15.6%, respectively, potentially due
to lower ow states with VV-ECMO [104].
Thrombosis most commonly occurs within the circuit itself, and particularly
within the oxygenator of the circuit [88, 104]. Circuit thrombosis only becomes
clinically relevant when it requires circuit/oxygenator exchange, or when high levels of hemolysis are present, as measured by plasma free hemoglobin [92].
Hemolysis leading to high plasma free hemoglobin levels can cause hemoglobinuria nephropathy, endothelial dysfunction, and vasoconstriction and increases the
risk of death [92]. Circuit thrombosis can cause malfunction or reduced efciency
of the device [104]. Thrombosis is prevented and treated with the use of anticoagulation and serial visual inspections of the circuit and oxygenator [88]. One small
case report shows success with the use of low-dose tissue plasminogen activator
(5–20mg) to treat life-threatening oxygenator thrombosis [134]. Of note, HIT is a
possible underlying cause of thrombosis in the ECMO population treated with heparin and should be considered as part of the thrombotic workup [88].
Outside of circuit thrombosis, leg ischemia is also a possible thrombotic complication with an incidence of 10% and has primarily been reported in VA-ECMO due
to cannulation of the femoral artery, although it is still possible in VV-ECMO [104].
The use of distal perfusion catheters helps to ensure perfusion and potentially prevent limb ischemia [17, 104]. Conservative strategies, including removal and
9 Extracorporeal Membrane Oxygenation
257
repositioning of the cannula, maintaining anticoagulation on the high end of the
therapeutic range, optimizing peripheral temperature, and limiting the use of vasoconstrictors, are often enough to reverse limb ischemia; however, fasciotomy or
amputation may be necessary in severe or irreversible cases [17].
9.9.3 Neurologic
The indications and cannulation techniques of ECMO are commonly associated
with alterations in perfusion, which can frequently result in neurologic injury.
Neurologic injury increases mortality in hospitalized patients, and this trend continues in ECMO patients with neurologic complications [148]. Neurologic injury has
been reported more frequently in patients on VA-ECMO compared to VV-ECMO;
however, when excluding eCPR, the incidence is similar between VA- and
VV-ECMO [97, 148].
Patients undergoing VA-ECMO may experience reduced blood ow to the left
heart and thrombosis in the circuit or cannula, resulting in a neurologic event, most
typically acute ischemic stroke (AIS). A meta-analysis of 878 VA-ECMO patients
found a 7.4% overall rate of brain injury with 5.3% acute ischemic stroke and 2.8%
intracranial bleeding [80]. Risk factors for AIS identied in this study were central
cannulation and platelets >350K/cu mm at the time of cannulation. AIS was not
associated with anticoagulant use, brinogen level, or platelet counts during
ECMO.Risk factors for intracranial bleeding were female sex, central cannulation,
and platelets <100K/cu mm at the time of cannulation. Platelet count <100K/cu
mm at the time of cannulation was also associated with mortality in this study [80].
North VV-ECMO is most often associated with intracranial hemorrhage, including
subarachnoid and petechial intraparenchymal hemorrhage [148]. A retrospective
analysis of the ELSO database found that 7.1% of VV-ECMO patients experienced
a neurologic injury, most often intracranial hemorrhage (42.5%). Neurologic injury
was associated with a 75.8% in-hospital mortality compared to 37.8% in VV-ECMO
patients without neurologic injury [86]. Despite advances in ECMO and medical
therapy over the study time period (1992–2015), the prevalence of neurologic injury
did not change. Risk factors associated with neurologic injury included pre-ECMO
cardiac arrest, hyperbilirubinemia during ECMO, and use of CVVH [86].
Routine neurologic exams should be performed on all patients receiving ECMO
therapy. Exams should include at minimum Glasgow coma scale assessment, pupil
examinations, and brainstem, tendon, and pathologic reex testing [148]. Other
high-sensitivity methods, such as neurological pupil index, near-infrared spectroscopy (NIRS), transcranial Doppler (TCD), and EEG, may be considered; however,
data is conicting on their routine use in ECMO patients [148]. The ELSO guidelines recommend holding sedation and analgesia daily to assess neurological status
and note that eCPR is associated with the highest rate of neurologic injury, but do
not make a recommendation on any specic neuroprognostication tools [119].
258
S. Davis et al.
9.10 Conclusion
VV- and VA-ECMO are important strategies in the management of ARDS, cardiogenic shock, and post-cardiac arrest. Use of these strategies improves mortality outcomes compared to conventional management, but overall mortality is high for
these patient populations. The use of this potentially lifesaving intervention requires
constant monitoring, as both VV- and VA-ECMO remain associated with many
complications, including, but not limited to, coagulopathy (bleeding and thrombosis), hypervolemia, infection, limb ischemia, renal failure, intracerebral hemorrhage, and stroke. Medication dosing in ECMO is complicated by the increased
volume of distribution, renal failure, and potential sequestration of drug in the circuit. Clinicians should carefully consider the effects that ECMO may have on various medications to guide optimal choice and dosing. Use of therapeutic drug
monitoring should be used when possible to ensure that appropriate drug concentrations are achieved. Despite the signicant advances made in the use of ECMO, there
are still many areas of uncertainty and limited data that require further research to
ensure continued improved outcomes with its use.
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