ECMO Flashcards

1
Q

What is ECMO and how did it come about?

A

Extracorporeal membrane oxygenation (ECMO; sometimes called extracorporeal life support, or ECLS) is a lifesaving technology that employs partial heart/lung bypass for extended periods. It provides gas exchange and perfusion for patients with acute, reversible cardiac or respiratory failure.

This allows the patient’s cardiopulmonary system to rest, during which the patient is spared the deleterious effects of high airway pressure, high FiO2 , traumatic mechanical ventilation, and impaired perfusion.

As of 2017, the Extracorporeal Life Support Organization (ELSO) has registered nearly 60,000 neonates and children treated with ECMO for a variety of cardiopulmonary disorders.

The number of centers providing extracorporeal support and reporting to ELSO has increased every year up to 2016, and the total number of cases continues to rise.

The initial effort to develop extracorporeal bypass came from cardiac surgeons. Their goal was to correct intracardiac lesions and, therefore, they needed to arrest the heart, divert and oxygenate the blood, and perfuse the patient so that the intracardiac repair could be performed.

The first cardiopulmonary bypass circuits involved cross circulation between the patient and another subject (usually the patient’s mother or father) acting as both the pump and the oxygenator.

The first devices used for establishing cardiopulmonary bypass and oxygenation by complete artificial circuitry were constructed with disk-and-bubble oxygenators, and were limited because of hemolysis encountered by direct mixing of oxygen and blood.

The discovery of heparin and the development of semipermeable membranes (silicone rubber) capable of supporting gas exchange by diffusion were major advancements during the development of ECMO.
During the 1960s and early 1970s, these silicone membranes were configured into a number of oxygenator models.4–7

In 1972, the first successful use of prolonged cardiopulmonary bypass was reported.

The patient had sustained a ruptured aorta following a motorcycle accident. Venoarterial extracorporeal bypass support was maintained for 3 days.

Soon thereafter, a multicenter prospective randomized trial sponsored by the National Heart, Lung, and Blood Institute (a branch of the National Institutes of Health) studied the efficacy of ECMO for adult respiratory distress syndrome.

In 1979, the researchers concluded that the use of ECMO had no advantage over conventional mechanical ventilation, and the trial was stopped before completion.

However, Bartlett and colleagues noted that all of the patients in the study had irreversible pulmonary fibrosis before the initiation of ECMO.

In 1976, they reported the first series of infants with ECMO. Six (43%) of 14 babies with respiratory distress syndrome survived. Many of these infants were premature and weighed <2 kg. In addition, 22 patients with meconium aspiration syndrome had a 70% survival rate, although these neonates tended to be larger.

Since then, despite study design issues, three randomized controlled trials and a number of retrospective published reports have confirmed the efficacy of ECMO over conventional mechanical ventilation. By 1996, 113 centers had ECMO programs registered with ELSO.

Over the next two decades, improvements in technology, a better understanding of the pathophysiology of pulmonary failure, and a greater experience using ECMO have contributed to improved outcomes for infants with respiratory failure.

In 2003, the University of Michigan reported an association between ECMO volume and an observed reduction in neonatal mortality seen in that state between 1980 and 1999.

ELSO, formed in 1989, is a collaboration of health care professionals and scientists with an interest in ECMO. The organization provides the medical community with guidelines, training manuals and courses, and a forum in which interested individuals can meet and discuss the future of ECLS. The group also provides a registry for the collection of data from most centers with an ECMO program throughout the world. This database provides valuable information for analysis of this lifesaving biotechnology.

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2
Q

What are the clinical applications of ECMO?

A

Neonates benefit substantially from ECMO.

Cardiopulmonary failure in this population secondary to meconium aspiration syndrome (MAS), congenital diaphragmatic hernia (CDH), persistent pulmonary hypertension of the newborn (PPHN), and congenital cardiac disease are the most common pathophysiologic processes requiring ECMO.

In children, the most common disorders treated with ECMO are viral and bacterial pneumonia, acute respiratory distress syndrome (ARDS), acute respiratory failure (non-ARDS), sepsis, and cardiac disease.

Treatment of patients who cannot be weaned from bypass after cardiac surgery and patients with end-stage ventricular failure needing a bridge to heart transplantation are areas where ECMO use is increasing.

Some less frequently used indications for ECMO include respiratory failure secondary to smoke inhalation, severe asthma, rewarming of hypercoagulopathic/hypothermic trauma patients, and maintenance of an organ donor pending liver allograft harvest and transplantation.

It should be noted that, while neonates have historically had the highest survival with ECMO, ECMO use and survival in adult patients is increasing. This is especially true in adults with acute respiratory failure.

The CESAR (Conventional ventilation or ECMO for Severe Adult Respiratory failure) trial established that adult patients with acute lung failure have significantly greater survival with referral to an ECMO center than by treatment with conventional ventilation.

This finding was corroborated in patients severely affected by the 2009 H1N1 influenza epidemic when the vast majority of patients referred to ECMO centers were supported with ECMO.

For the purposes of this chapter, we will focus on the use of ECMO in neonates and children.

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3
Q

How are patients selected as candidates for ECMO?

A

The selection of patients as potential ECMO candidates can be challenging.

The selection criteria are based on data from multiple institutions, patient safety, and mechanical limitations related to the equipment.

The risk of performing an invasive procedure that requires heparinization in a critically ill infant or child must be weighed against the predicted mortality of the patient with conventional therapy alone.

Currently accepted treatment modalities of cardiopulmonary failure, particularly in neonates, include low-volume protective ventilation, inhaled nitric oxide, surfactant therapy, and high-frequency oscillatory ventilation.

If the cardiac or pulmonary failure is refractory to maximal medical therapy, then ECMO should be considered.

Historically, a predictive mortality of >80% after exhausting all conventional therapies was the criterion most institutions used to select patients for ECMO.

However, the subjectivity of these criteria and variance between facilities requires that ECMO centers develop their own criteria and continually evaluate their patient selection based on ongoing outcomes data.

Overall, there appears to be a trend toward earlier initiation of ECMO to avoid ongoing iatrogenic lung injury.

Recommended pre-ECMO studies are as follows:

Head ultrasonography
Cardiac echocardiography
Chest radiography
Complete blood cell count, with platelets
Type and cross-match of blood
Electrolytes, calcium
Coagulation studies (prothrombin time, partial thromboplastin time, fibrinogen, fibrin degradation products)
Serial arterial blood gas analysis

The definition of “conventional therapy” is not consistent for each indication.

Nevertheless, ECMO is indicated when
(1) there is a reversible disease process,
(2) the ventilator treatment is causing more harm than good, and
(3) tissue oxygenation requirements are not being met.

A discussion of generally accepted selection criteria for using neonatal ECMO follows.

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4
Q

What are indications for ECMO?

A

REVERSIBLE CARDIOPULMONARY DISORDERS

The underlying principle of ECMO relies on the premise that the patient has a reversible disease process that can be corrected with either therapy (including the possibility of organ transplantation) or rest.

Prolonged exposure to high-pressure mechanical ventilation with high concentrations of oxygen can have a traumatic effect on the newborn’s lungs and frequently leads to the development of bronchopulmonary dysplasia (BPD).

It has been suggested that BPD can result from high levels of ventilatory support for as little as 4 days or less.

The pulmonary dysfunction that follows barotrauma and oxygen toxicity associated with mechanical ventilation typically requires weeks to months to resolve.

Therefore, patients who have been ventilated for a long time and in whom lung injury has developed require multidisciplinary decision-making.

Echocardiography should be performed on every patient being considered for ECMO to determine cardiac anatomy and function.

Treatable conditions such as total anomalous pulmonary venous return and transposition of the great vessels, which may masquerade initially as pulmonary failure, can be surgically corrected but may require ECMO resuscitation initially.

Infants with correctable cardiac disease should be considered on an individual basis.

Indications for ECMO support in infants with cardiac pathology are based on clinical signs such as hypotension despite the administration of inotropes or volume resuscitation, oliguria (urine output < 0.5 mL/kg/h), and decreased peripheral perfusion.

Also, ECMO is an excellent bridge to cardiac and lung transplantation.

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5
Q

What clinical measurement systems have been developed to help identify patients who will benefit from
ECMO support?

A

CLINICAL MEASUREMENT SYSTEMS

Because of the invasive nature of ECMO, and the potentially life-threatening complications, investigators have worked to develop an objective set of criteria to predict which infants will have an 80% mortality without ECMO.

Three clinical measurement systems have been developed and tested to assist in identifying patients who will benefit from ECMO support.

  1. Oxygenation Index (OI) = (MAP × FiO 2 × 100)/PaO2 where MAP = mean airway pressure.

This index has been evaluated and found that an OI >40 in 3–5 postductal gases is predictive of a mortality risk ≥80%.

Currently, most centers begin considering application of ECMO with an OI of 25 to reduce the barotrauma associated with high pressure mechanical ventilation.

  1. Postductal Alveolar-Arterial Oxygen Gradient [(A-a)DO2 ] An (A-a)DO 2 of 610 Torr or greater despite 8 hours of maximal medical therapy predicted a mortality of 79%.
  2. Ventilation Index = (Respiratory Rate × PaCO 2 × Peak Inspiratory Pressure)/1000

Rivera et al. found that a ventilation index >40 and OI >40 were associated with a 77% mortality risk.

They also found that the combination of peak inspiratory pressure ≥40 cmH2O and an (A-a)DO 2 >580 mmHg was associated with a mortality of 81%.

These clinical measurement systems are useful to quantitate the degree of cardiopulmonary derangement and subsequently categorize patients into candidates for ECMO or continued maximal medical therapy.

However, the decision to initiate ECMO is often a clinical decision based on clinical judgment and the patient’s individual response to maximal medical therapy.

Patients are commonly started on ECMO when they have failed maximal medical support, significant barotrauma is imminent, and are believed to have good potential for survivable organ recovery.

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6
Q

What are the classic contraindications to ECMO?

A

The classic contraindications to ECMO are listed below. As ECMO treatment evolves and technology advances, many of these traditional contraindications to ECMO are being challenged.

  1. Estimated gestational age <34 weeks:
    The higher incidence of intracranial bleeding in premature infants has historically precluded the use of ECMO in neonates <34 weeks estimated gestational age (EGA).

However, recent data indicate that ECMO can potentially be used in infants with an EGA as low as 29 weeks with acceptable survival and rates of intracranial hemorrhage (ICH).

Ideally, the development of nonthrombogenic coating of circuit components would obviate the need for systemic heparinization and decrease the risk of using ECMO in premature infants.

  1. Birth weight <2 kg:
    Technical considerations and limitation of cannula size restrict ECMO candidates to infants weighing at least 2 kg.

The smallest single-lumen ECMO cannula is 8 French, and flow through a tube is proportional to the fourth power of the radius.

Small veins permit only small cannulas, resulting in flow that will be reduced by a power of four.

Neonates who weigh <2 kg present technical challenges in cannulation and in maintaining adequate blood flow through the small catheters.

However, as with EGA, this weight cut-off has been challenged, as survival of up to 40% can be achieved at birth weights as low as 1.6kg.

  1. ICH greater than grade II:
    Patients with small intraventricular hemorrhages (grade I) or small intraparenchymal hemorrhage can be successfully treated on ECMO by maintaining a lower than optimal activated clotting time in the range of 180–200 seconds.

These patients should be closely observed for extension of the intracranial bleeding.

Patients posing a particularly high risk for ICH are those with a previous ICH, a cerebral infarct, prematurity, coagulopathy, ischemic central nervous system injury, or sepsis.

Consideration of these patients for ECMO should be individualized.

Neonates with ICH of higher grades are at increased risk of extension of their hemorrhage with systemic heparinization. This remains true today, but the development of technologies that obviate the need for heparinization may allow the use of ECMO in neonates with preexisting ICH in the future. In addition, our experience has suggested that ECMO can be applied when expected mortality is higher in neonates with grade II ICH. In that setting, lower levels of anticoagulation are cautiously applied.

  1. Bleeding complications:
    Infants with ongoing, uncontrollable bleeding or an uncorrectable bleeding diathesis pose a relative contraindication to ECMO.

Any coagulopathy should be corrected before initiating ECMO because the need for continuous systemic heparinization adds an unacceptable risk of bleeding.

  1. Mechanical ventilation for longer than 7–10 days:
    Classically, mechanical ventilation has been associated with a higher incidence of BPD and irreversible fibroproliferative lung disease.
    The duration of pre-ECMO mechanical ventilation is being challenged, as data from the ELSO registry demonstrate survival of 50–60% after preECMO mechanical ventilation of up to 14 days.
  2. Cardiac arrest that requires cardiopulmonary resuscitation (CPR):
    Many centers now consider patients who experience pre-ECMO cardiac arrest candidates for support.

Survival rates up to 60% have been demonstrated in neonates who experience cardiac arrest prior to or during cannulation. Predictably, good outcomes are associated with effective CPR during the resuscitation.

  1. Conditions incompatible with meaningful life after therapy—profound neurologic impairment, congenital anomalies, or other conditions:
    Every effort should be made to establish a clear diagnosis before the initiation of ECMO.

Infants with anomalies incompatible with life do not benefit from ECMO (i.e., trisomy 13 or 18).

ECMO is not a resource that is intended to delay an inevitable death.

Many lethal pulmonary conditions, such as overwhelming pulmonary hypoplasia, congenital alveolar proteinosis, and alveolar capillary dysplasia, may present as reversible conditions but are considered lethal.

However, with improvement in medical and surgical care, conditions once thought to be nonsurvivable require constant reassessment.

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7
Q

What are indications for ECMO in patients with PPHN?

A

PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN

Pulmonary vascular resistance (PVR) is the hallmark and driving force of fetal circulation.

Normal fetal circulation is characterized by PVR that exceeds systemic pressures, resulting in higher right-sided heart pressures and, therefore, preferential right-to-left blood flow through fetal shunts.

The fetal umbilical vein carries oxygenated blood from the placenta to the inferior vena cava (IVC) via the ductus venosus.

Because of the high PVR, the major portion of the blood that reaches the right atrium (RA) from the IVC is directed to the left atrium through the foramen ovale.

The superior vena cava delivers deoxygenated blood to the RA that is preferentially directed to the right ventricle and pulmonary artery.

This blood then takes the path of least resistance and shunts from the main pulmonary artery directly to the descending aorta via the ductus arteriosus, bypassing the pulmonary vascular bed and the left side of the heart.

The lungs are therefore almost completely bypassed during fetal circulation.

At birth, with the infant’s initial breath, the alveoli distend and begin to fill with air.

This is paralleled by relaxation of the muscular arterioles of the pulmonary circulation and the expansion of the pulmonary vascular bed.

These effects lead to a rapid drop in PVR to below systemic levels that causes the left atrial pressure to become higher than the RA pressure.

The result is closure of the foramen ovale, and all venous blood flows from the RA to the right ventricle and into the pulmonary artery.

The ductus arteriosus also begins to close at this time.

Therefore, all fetal right-to-left circulation ceases, completing separation of the pulmonary and systemic circulations.

Anatomic closure of these structures takes several days to weeks. Thus, maintaining systemic pressure greater than the pulmonary circulation is vital to sustaining normal circulation.

Failure of the transition from fetal circulation to newborn circulation is described as PPHN or persistent fetal circulation (PFC). Clinically, PPHN is characterized by hypoxemia out of proportion to pulmonary parenchymal or anatomic disease.

In hypoxic fetuses and infants, the proliferation of smooth muscle in the arterioles may extend far beyond the terminal bronchioles, resulting in thickened and more reactive vessels. In response to hypoxia, these vessels undergo significant self-perpetuating vasoconstriction.

Although sometimes idiopathic, PPHN can occur secondary to a number of disease processes such as MAS, CDH, polycythemia, and sepsis.

Treatment for PPHN is directed at decreasing right-to-left shunting and increasing pulmonary blood flow.

Previously, most newborns were treated with hyperventilation, induction of alkalosis, neuromuscular blockade, and sedation. Unfortunately, these therapies did not reduce morbidity, mortality, or the need for ECMO.

ECMO allows for the interruption of the vicious cycle of pulmonary vasoconstriction and hypoxia. By providing richly oxygenated blood, ECMO promotes relaxation of the vasoreactive pulmonary vascular bed, allowing the pulmonary blood pressure to return to subsystemic values without the iatrogenic complications encumbered by overly aggressive conventional therapy.

Data recommending permissive hypercapnia and spontaneous respirations as principles of treatment for these children have been reported.

Hyperventilation and neuromuscular blockade are not part of the treatment strategy.

This strategy has decreased morbidity, mortality, and the need for ECMO in several centers.

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8
Q

What are indications for ECMO in patients with CDH?

A

Of particular interest to pediatric surgeons are neonates with CDH. These patients are plagued with pulmonary hypertension and have pulmonary hypoplasia of both lungs.

Often, pulmonary insufficiency ensues with a vicious cycle of hypoxia, hypercarbia, and acidosis. This process must be interrupted by medical management, which has vastly improved over the past two decades with the use of permissive hypercapnia/spontaneous respiration, pharmacologic therapy, and delayed elective repair.

Various other strategies have been tried to manage critically ill newborns with CDH.

High-frequency oscillation may have its major role in forestalling respiratory failure when used as a front-line strategy rather than as a “rescue therapy.”

Surfactant plays no more than an anecdotal role.

Nitric oxide is frequently used as a vasodilator in the treatment of pulmonary hypertension in these patients, though evidence backing this practice is lacking.

Other pulmonary vasodilators such as epoprostenol, sildenafil, and iloprost are starting to demonstrate some efficacy in babies with CDH.

The primary indicator for ECMO in the CDH infant occurs when tissue oxygen requirements are not being met, as evidenced by progressive metabolic acidosis, mixed venous oxygen desaturation, and multiple organ failure.

The other major indicator is increasing iatrogenic pulmonary injury.

The goal is to maintain preductal oxygen saturations >85%.

Spontaneous breathing is preserved by avoiding muscle relaxants.

Sedation is used as needed.

Meticulous attention to maintaining a clear airway is obvious but critical.

Permissive hypercapnia with spontaneous respiration is initiated with intermittent mandatory ventilation (IMV), 30–40 breaths per minute, equal I/E time, inspiratory gas flow of 5–7 L/min, peak inspiratory pressure (PIP) of 20–22 cmH2O, and positive end-expiratory pressure (PEEP) of 5 cmH2O.

The FiO2 is selected to maintain preductal SaO2 >85%.

If this method of ventilation is not effective, as demonstrated by severe paradoxical chest movement, severe retractions, tachypnea, inadequate or labile oxygenation (preductal O2 saturations <85%), or PaCO2 >60 mmHg, then a new mode of ventilation is needed.

High-frequency ventilation would be the next option. It is delivered by setting the ventilator to IMV mode with a rate of 100, inspiratory time of 0.3 second, an inspiratory gas flow of 10–12 L, a PIP of 20, and a PEEP of 0 (due to auto-PEEP).

The PIP is adjusted as needed based on chest excursion, trying to maintain the PIP at <25 mmHg.

If high-frequency ventilation at the aforementioned parameters is unable to improve the hypoxia and hypercarbia, high-frequency jet ventilation (HFJV) or high-frequency oscillatory ventilation (HFOV) can be instituted.

HFJV provide smaller volumes (1–3 mL/kg) more often at a much higher rate (240–660 breaths per minute), and expiration is passive. Oxygenation is proportional to mean airway pressure, and ventilation is proportional to amplitude (PIP vs PEEP). Jet pulsations produce high-velocity laminar flow that has the ability to bypass airway disruptions.

HFOV differs in that it delivers smaller tidal volumes (1–2 mL/kg) at an even faster rate (8–15 Hz). The lung is inflated to a static volume and then oscillated around the mean airway pressure.

Of all the indications for ECMO in neonates, CDH has the worst prognosis, with survival of 50%.

Therefore, patient selection for ECMO in neonates with CDH is of particular importance.

There are several prenatal markers that can help risk stratify CDH severity and predict the need for ECMO postnatally.

The lung-to-head ratio (LHR) is measured by prenatal ultrasonography (US). It is defined as the product of the orthogonal diameters of the contralateral lung divided by the head circumference.

Severe pulmonary hypoplasia is considered when the LHR is <1.0 with liver herniation.

The LHR is operator dependent and can be obtained only in a narrow gestational window. Therefore, O/E (observed/expected) LHR was developed that is accurate at any gestational age.

Many centers are also relying on fetal magnetic resonance imaging (MRI) to measure total lung volume to predict mortality in fetuses with CDH.

The total lung volume can be compared with the predicted lung volume based on gestational age.

This O/E total fetal lung volume (TFLV) has been reported as a better predictor of mortality and the subsequent need for ECMO.

Whether a baby should first demonstrate some evidence of adequate lung parenchyma remains controversial.

Some physicians believe the best method to evaluate pulmonary hypoplasia and predict outcome is to evaluate the patient clinically.

This is assessed by having a recorded best PaCO2 <50 mmHg and a preductal oxygen saturation >90% for at least 1 hour at any time in the clinical course.

With these criteria, successful ECMO should yield an overall survival rate of 75% or better.

If patients with lethal anomalies, overwhelming pulmonary hypoplasia, or neurologic complications are not included, survival approaches 85%.

At the other extreme, Kays et al. have demonstrated 55% survival in infants who had a best pCO2 >100 and pH <7.0 during the initial resuscitation.

He therefore suggests offering ECMO to all patients regardless of physiologic parameters.

At the University of Michigan, we choose an intermediate approach.

Infants with potentially lethal pulmonary hypoplasia are identified prenatally based on an LHR <0.8 with liver herniation, and a fetal MRI with O/E TFLV of <25%.

These infants are resuscitated, and if the baby cannot demonstrate a pH >7, pCO 2 <100, preductal SaO 2 >80%, and PaO 2 >40 (least important, as it will likely be potductl) on ventilatory support utilizing a PIP <25 on CMV or MAP <20 on HFOV, with appropriate sedation and optimization of blood pressure over the first 2 hours of life, we would not proceed to ECMO, but would move to comfort care.

If the baby meets these criteria at any point prior to 2 hours, we proceed directly to ECMO.

It should be noted that the most severe CDH patients who are offered ECMO will likely have significant long-term morbidity if they survive.

The proper ECMO modality in infants with CDH is also debatable. Most centers use venoarterial (VA) ECMO in CDH patients.

However, 10- and 15-year reviews of the ELSO database have concluded that mortality is no different between venovenous (VV) and VA ECMO.

Renal complications and inotrope use were more common with VV, but neurologic complications were more common with VA.

Cannula size is the main limitation to VV ECMO use in infants with CDH, but our institutional practice is to use VV ECMO whenever double-lumen internal jugular vein (IJV) cannulation is possible. However, the choice between VA and VV should largely be based on the comfort of the surgeon and institution with each modality.

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9
Q

When is extracorporeal cardiopulmonary resuscitation indicated?

A

EXTRACORPOREAL CARDIOPULMONARY RESUSCITATION

Studies demonstrate that 1–4% of pediatric intensive care unit (PICU) admissions suffer a cardiac arrest.

Survival to discharge for a patient who has an arrest in the PICU ranges from 14–42%.

The ELSO data demonstrate that approximately 73% of extracorporeal cardiopulmonary resuscitation (ECPR) has been used for patients with primary cardiac disease.

Overall survival to discharge in this population has more recently been reported as high as 49%.

The American Heart Association recommends ECPR for in-hospital cardiac arrest refractory to initial resuscitation, secondary to a process that is reversible or amenable to heart transplantation.

Conventional CPR must have failed, no more than several minutes should have elapsed, and ECMO must be readily available.

Future research needs to analyze long-term neurologic status among survivors and which patients will benefit the most with as little morbidity as possible.

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10
Q

Which patients will benefit from a second course of ECMO?

A

Approximately 3% of patients who are treated with ECMO will require a second course.

Survival after a second course of ECMO appear lower than after a single course in neonates, but in pediatric patients, the survival rates are comparable to those associated with the first course.

Negative prognostic indicators for second-course ECMO patients include patients with renal impairment, higher number of first-course complications, age >3 years old, or a prolonged second course.

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11
Q

What configurations are used for ECMO?

A

The goal of ECMO support is to provide an alternate means for oxygen delivery.

Four different extracorporeal configurations are used clinically: VA, two-cannula VV, double-lumen single-cannula venovenous (DLVV), and veno-veno-arterial (VVA) bypass.

The inception of ECMO and its early days were characterized by VA ECMO because it offered the ability to augment both cardiac and pulmonary function.

Venous blood is drained from the RA through the right IJV, and oxygenated blood is returned via the right common carotid artery to the aorta.

VV and DLVV bypass provide pulmonary support but do not provide cardiac support.

VV bypass is dependent on drainage from the RA via the right IJV with reinfusion into a femoral vein.

DLVV is accomplished by means of a double-lumen catheter inserted into the RA via the right IJV.

A major limitation of VV or DLVV ECMO is that a fraction of the infused oxygenated blood reenters the pump and, at high flows, may limit oxygen delivery due to recirculation.

A limitation specific to DLVV is catheter size, which confines use of this method of support to larger neonates, infants, and smaller children.

VV and DLVV bypass have become the preferred method of extracorporeal support for all appropriate patients who do not require cardiac support.

Oxygen delivery to the head and upper extremities during femoral VA ECMO is often poor, (so-called north–south syndrome).

In these cases, a hybrid modality, VVA, can be used, which utilizes additional venous reinfusion via the IJV, thereby increasing the mixed venous oxygen content and the oxygen delivery to the upper body.

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12
Q

How is cannulation done for ECMO?

A

Cannulation can be performed with proper monitoring in the neonatal ICU or PICU under adequate sedation and intravenous anesthesia.

The infant is positioned supine with the patient’s head at the foot of the bed. The head and neck are hyperextended over a shoulder roll and turned to the left.

Local anesthesia is administered in the incision site.

A transverse cervical incision is made along the anterior border of the sternocleidomastoid muscle (SCM), one fingerbreadth above the right clavicle.

The platysma muscle is divided, and dissection is carried down through the SCM, which is split and retracted to expose the carotid sheath.

The sheath is opened, and the IJV, common carotid artery, and vagus nerve are identified.

The vein is exposed first and encircled with proximal and distal silk ligatures. Occasionally it is necessary to ligate the inferior thyroid vein.

The common carotid artery lies medial and posterior, contains no branches, and is mobilized in a similar fashion. The vagus nerve should be identified and protected.

The arterial cannula (usually 10 French for newborns) is measured so that the tip will lie in the ascending aorta. This is approximately one-third the distance between the sternal notch and the xiphoid.

The venous cannula (usually 12–14 French for neonates) is measured so that its tip lies in the distal right atrium, which is approximately half the distance between the suprasternal notch and the xiphoid process.

The patient is then systemically heparinized with 100 units/kg of heparin, which is allowed to circulate for 3 minutes, which should result in an ACT of >300 seconds.

With VA ECMO, the venous cannula is usually inserted first.

The proximal IJV is ligated cephalad to the site selected for the venotomy.

Gentle cephalad traction on this ligature helps during insertion of the venous catheter.

A venotomy is made close to the ligature.

To aid in cannulation, 5-0 Prolene sutures can be placed around the venotomy for retraction when introducing the venous cannula.

The saline-filled venous catheter is inserted and advanced into the RA and secured with two silk ligatures (0 or 2-0) over a vessel loop placed under the ligatures on the anterior aspect of the vein to protect the vessel from injury during decannulation.

In preparation for arterial cannulation, the carotid artery is ligated cephalad. Proximal control is obtained, and a transverse arteriotomy is made near the cephalad ligature.

To help prevent intimal dissection, 5-0 Prolene sutures can be placed around the arteriotomy and used for retraction when introducing the arterial cannula.

The saline-filled cannula is inserted to its premeasured position and secured in a fashion similar to the venous cannula.

A small piece of vessel loop (bumper) can be placed under the ligatures on the anterior aspect of the carotid to protect the vessel from injury during decannulation.

Any air bubbles are removed from the cannulas as they are connected to the ECMO circuit, and circuit flow is initiated.

The cannulas are then secured to the skin above the incision.

The incision is closed in layers, ensuring that hemostasis is intact.

The cannula positions are confirmed by chest radiograph (Fig. 6.2) and/or transthoracic echocardiogram.

The tip of the venous catheter should be positioned in the inferior aspect of the RA, and the arterial catheter in the ascending aorta about 1–2 cm above the aortic valve.

For cutdown two-cannula VV and DLVV ECMO, the procedure begins similarly to that with VA ECMO.

Venous cannulation is performed with the venous catheter tip in the mid-RA (5 cm in the neonate).

Venous reinfusion in VV ECMO is via a femoral venous cannula, which can be inserted either by cutdown or percutaneously with US guidance.

Two-cannula VV-ECMO is not used in neonates and has been almost entirely supplanted by the DLVV approach in most patients due to the small size of the femoral vein.

For the DLVV approach, two DLVV cannulas are available.

With a double-lumen OriGen (OriGen Biomedical Inc., Austin, TX) venous catheter, the tip should be in the mid-RA with oxygenated blood flow directed toward the tricuspid valve.

Special consideration is required when using an Avalon double-lumen cannula (Avalon Elite, Avalon Laboratories, Rancho Dominguez, CA).

This cannula has both proximal and distal drainage side holes that must be positioned in the superior and inferior vena cavae, respectively, while the reinfusion port, which is located between them, must lie in the RA and direct the oxygenated blood flow toward the tricuspid valve.

Although this allows for efficient circulation, it also makes accurate positioning of the cannula essential.

Directing the cannula tip into the IVC can be challenging, and echocardiography and fluoroscopy should be used during placement to maximize safety and minimize episodes of malposition.

A challenging situation may arise when one attempts to cannulate a newborn with a right-sided CDH.

Anatomic distortion of the mediastinum can lead to cannulation of the azygos vein or to impaired preload, which will then fail to provide adequate ECMO support.

This is usually detected by poor pump function and echocardiography. In these patients, attempted manipulation of a malpositioned cannula is often wrought with failure.

Solutions include emergent CDH repair or central cannulation.

The pediatric population (2–18 years of age) presents a difficult and controversial scenario with regard to VA cannulation.

Due to concern about carotid ligation, some centers will cannulate these patients via femoral access.

One potential problem with this approach is the “northsouth” syndrome, which necessitates conversion to VVA ECMO with an additional right IJV reinfusion cannula to oxygenate the upper body.

In addition, the arterial cannula is large and can either partially or completely obstruct antegrade arterial flow.

This can result in distal limb ischemia, which can lead to sensory or motor deficits, tissue loss, or even limb loss.

One potential way to avoid this problem is to provide antegrade flow via a percutaneously placed distal perfusion catheter.

On the other hand, some centers continue to perform arterial cannulation via the carotid artery.

A recent study supporting carotid cannulation in the pediatric age group found that carotid ligation is associated with a 5.1% rate of stroke, which was only a 1.4% increase when compared with non–carotid ligation approaches. Furthermore, the data suggested that the rate of stroke may actually decrease with age when other factors are adjusted.

H&A

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13
Q

How is the circuit flow for ECMO?

A

Venous blood is drained from the RA via the IJV cannula.

Sensors can be placed into the circuit to measure arterial oxygen saturation, mixed venous saturation, hematocrit, and pump flow.

Hypovolemia is one of the most common causes of decreased venous inflow into the circuit, but kinking and occlusion of the venous line should be suspected first.

Two types of ECMO pumps, centrifugal and roller head, are used to pump blood through the membrane oxygenator.

Centrifugal pumps are dependent on adequate preload and afterload, and have continuous flow.

The revolutions per minute (RPM) are adjusted to maintain the desired flow rate.

A low preload or high afterload will lead to lower flow despite a fixed RPM. Alternatively, roller pumps operate by displacing a fixed volume of blood per revolution and are afterload independent.

The roller pumps are designed with microprocessors that allow for calculation of the blood flow based on the roller-head speed and tubing diameter of the circuit.

The pumps are connected to continuous pressure monitoring throughout the circuit and are servoregulated if pressures within the circuit exceed preset parameters.

Another safety device, the bubble detector (not depicted in Fig. 6.6), is interposed between the pump and the membrane oxygenator that halts perfusion to the patient if air is detected in the circuit.

The oxygenator consists of a hollow-fiber membrane made of polymethylpentene. This provides an interface for blood and gas exchange. These oxygenators have built-in heat exchangers to maintain patient normothermia. Oxygen diffuses through the membrane into the circuit, and carbon dioxide and water vapor diffuse from the blood into the sweep gas. The size (surface area) of the oxygenator is based on the patient’s size, with smaller infants utilizing a pediatric oxygenator and larger patients using an adultsized oxygenator.

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14
Q

How do you manage inadequate venous return during ECMO?

A
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15
Q

How do you manage a patient on ECMO?

A

Once the cannulas are connected to the circuit, bypass is initiated, and the flow is slowly increased to 100–150 mL/ kg/min.

Continuous in-line monitoring of the (pre-pump) SvO2 and arterial (post-pump) PaO2 as well as pulse oximetry is vital.

The goal of VA ECMO is to maintain an SvO2 of 37–40 mmHg and saturation of 65–70%.

VV ECMO is more difficult to monitor because of recirculation, which may produce a falsely elevated SvO2 .

Inadequate oxygenation and perfusion are indicated by metabolic acidosis, oliguria, hypotension, elevated liver function studies, and seizures.

Arterial blood gases should be monitored closely with PaO2 and PaCO 2 maintained as close to normal levels as possible.

The oxygen level of the blood returning to the patient should be fully saturated.

To increase a patient’s oxygen delivery on ECMO, one can either increase the ECMO flow rate (analogous to cardiac output) or the hemoglobin can be increased to maintain hemoglobin at 15 g/dL (increased oxygen carrying capacity and therefore increased oxygen content).

CO2 elimination is extremely efficient, and it is important to adjust the sweep (gas mixing) to maintain a PaCO2 in the range of 40–45 mmHg.

This is important, especially during weaning, because a low PaCO2 inhibits the infant’s spontaneous respiratory drive.

Serial monitoring allows timely adjustments. The arterial blood gas is measured hourly. As soon as these parameters are met, all vasoactive drugs are weaned and ventilator levels are adjusted to minimal settings.

Gastrointestinal prophylaxis (H2 antagonists or proton pump inhibitors) is initiated, and mild sedation and analgesia are provided, usually with fentanyl and midazolam.

Paralyzing agents are avoided.

Though antimicrobial prophylaxis with cefazolin is routinely used immediately prior to cannulation, there is no evidence for continuing prophylaxis during support, nor is there evidence for routine surveillance blood cultures.

A daily chest radiograph, on the other hand, should be performed.

Opacification or “white out” is often noted during the early ECMO course. The reasons for this are multifactorial and include decreased ventilatory pressures (both PIP and PEEP), reperfusion of the injured lung, and exposure of the blood to a foreign surface, causing an inflammatory response with the release of cytokines.

Heparin is administered (30–60 units/kg/h) throughout the ECMO course to preserve a thrombus-free circuit.

ACTs should be monitored hourly and maintained at 180–220 seconds.

A complete blood cell count should be obtained every 6 hours and coagulation profiles obtained daily.

To prevent thrombocytopenia, platelets are transfused to maintain a platelet count >100,000/mm3 .

The use of fibrinogen and other clotting factors is controversial.

Fresh frozen plasma should be considered in infants with international normalized ratio (INR) levels >1.5 in order to replete coagulation cascade factors and allow for adequate anticoagulation.

In cases of heparin resistance, antithrombin 3 levels should be checked and repleted as necessary.

The hematocrit should remain above 40% by using red blood cell transfusions so that oxygen delivery is maximized.

Management of volume status in patients on ECMO is very important and difficult.

It is imperative that all inputs and outputs be diligently recorded and electrolytes monitored every 6 hours.

Fluid losses should be repleted and electrolyte abnormalities corrected.

Patients should receive maintenance fluids as well as adequate parenteral nutrition.

Patients on ECMO have energy requirements similar to healthy neonates, but elevated protein requirements, up to 3 g/kg/day.

The first 48–72 hours on ECMO typically involve fluid extravasation into the soft tissues.

The patient becomes edematous and often requires volume replacement (crystalloid, colloid, or blood products) to maintain adequate intravascular and bypass flows, appropriate hemodynamics, and urine output >1 mL/ kg/h.

By the third day of bypass, diuresis of the excess extracellular fluid begins and can be facilitated with the use of diuretics and, if necessary, an in-line hemofilter.

Selective hypothermia for cerebral ischemia/hypoxia may improve neurologic outcome.

It is not yet clear if whole body or cap cooling provides significant improvement in ECMO outcomes.

It is possible to maintain temperature of 34°C for 45 hours on ECMO without increasing morbidity.

The largest study to date was performed in the United Kingdom. The Neonatal ECMO Study of Temperature (NEST) was a multicenter prospective randomized control trial of mild hypothermia (34°C for the first 48–72 hours) versus normothermia in neonates on ECMO, and showed no advantage of either strategy on 2-year neurodevelopmental outcomes.

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16
Q

Can operative procedures be performed on a patient while on ECMO?

A

Operations, such as CDH repair, can be performed while the child remains on ECMO, but one must account for the challenges associated with operations on an anticoagulated patient.

Hemorrhagic complications are a frequent morbidity associated with an operation on ECMO, and these complications increase mortality.

Strategies to avoid these problems include the following:

the platelet count should be >150,000/mm3,

the ACT should be reduced to 170–200 seconds, and

the cautery should be used liberally, along with meticulous operative technique and hemostasis.

The fibrinolysis inhibitor aminocaproic acid (100 mg/kg) is administered 6 hours prior to incision, and is infused continuously (30 mg/kg/h) for 24 hours.

For larger operations such as thoracotomy, consideration should be given to use of the argon beam coagulator for large raw surfaces and application of topical hemostatic agents.

H&A

17
Q

How is weaning done in ECMO?

A

As the patient improves, less blood flow is required to pass through the ECMO circuit and the flow can be weaned at a rate of 10–20 mL/h as long as the patient maintains good oxygenation and perfusion.

The most important guide to VA ECMO weaning is the SvO2.

For VV ECMO, it is the SaO2.

Regardless of the cannulation format, successful weaning is marked by stable acid–base balance and good urine output.

Other criteria for successful weaning include a body weight close to the patient’s dry weight, a clear chest film, and adequate lung volumes as measured by the ventilator.

When weaning, flows should be decreased to 30–50 mL/ kg/min, and the ACT should be at a higher level (200–240 seconds) to prevent thrombosis.

Newer oxygenators have higher limits of allowable flow, which may limit full weaning.

Adjustable shunts placed across the oxygenator allow higher overall flow to the oxygenator with a lower flow being delivered to the patient.

Also, flow probes placed on the arterial cannula can be used to accurately guide weaning.

Twenty-four hours prior to a trial, the ventilator settings are increased and lung recruitment strategies are employed.

At the time of the weaning trial, if the child tolerates the reduced flow, all medications and fluids should be switched to the vascular access on the patient instead of the circuit.

In VA ECMO, the patient can be trialed off ECMO by flushing and clamping the cannulas, with the circuit bypassing the patient via the bridge.

If it is possible that the child may need to be returned to bypass, then the cannulas should be briefly unclamped every 10 minutes to “flash” them and prevent thrombosis.

In VV ECMO, flow can continue, but sweep gas is stopped to trial the patient off support.

In either case, the patient is then observed for 2–4 hours.

If this is tolerated, decannulation can be accomplished.

In select high-risk patients, it may be wise to leave the cannulas in place with a continuous low-dose heparin infusion for 24 hours prior to decannulation.

Decannulation is performed under sterile conditions with the patient in the Trendelenburg position.

With the use of a short acting muscle relaxant to prevent air aspiration into the vein, ventilator settings should be increased.

The venous catheter is typically removed first, and the jugular vein is ligated.

Repair of the carotid artery is controversial.

Short-term results demonstrate acceptable patency rates and equivalent short-term neurodevelopmental outcomes when compared with children undergoing carotid artery ligation.

Another study of neonates who underwent arterial repair found a 72% incidence of an occluded or highly stenotic right common carotid artery at 2 years of age.

Similar to other studies, there was no significant difference in neurologic development when compared with controls.

H&A

18
Q

What are mechanical complications of ECMO?

A

Given its invasive nature and reliance on anticoagulation, complications are common during ECMO and range from minor to catastrophic.

Management of patients on ECMO requires knowledge of these complications and how to treat them.

Complications can be broken into the following categories.

MECHANICAL COMPLICATIONS

1) Membrane Failure
Failure of the membrane oxygenator is seen with a decreasing oxygenation or increasing CO2 levels in the postoxygenator blood.

The causes of this complication include thrombosis or water condensation, both of which diminish the oxygenator’s ability to transfer oxygen and CO2 .

Oxygenator failure has been reported in 6.7% of respiratory ECMO runs in the neonatal and pediatric population.

The oxygenator should not be subject to high pressures, which should be continuously monitored.

Pressure limits are specific for different manufacturers and for the size of the membrane.

Thrombi in the oxygenator can be seen, but their extent is difficult to determine.

The progressive consumption of coagulation factors, such as platelets and fibrinogen, also indicates that the membrane may be progressively clotting, and changing the oxygenator should be considered.

2) Accidental Decannulation
Securing the cannulas properly will help prevent accidental decannulation.

Unexpected decannulation is an emergency, and immediate pressure should be applied to the cannula site along with discontinuation of circuit flow.

Conventional ventilator settings should be increased simultaneously.

The cervical incision must be immediately reexplored to prevent further hemorrhage and the cannulas replaced if continued ECMO is needed.

3) Air Embolism
The ECMO circuit has several potential sources for entry of air, the first of which occurs at initial cannulation.

Thus, all visible air bubbles should be removed by filling the cannulas with heparinized saline.

Other entry points in the circuit include connectors and stopcocks as well as the membrane oxygenator.

Therefore, the circuit must be continually inspected.

Air on the arterial side requires stopping ECMO.

Next, the air should be aspirated from a port until all air has been removed. Air on the venous side is not as urgent a problem, and the air can often be “walked” to an access point and aspirated without coming off bypass.

In the event that an air embolism reaches the patient, the patient should be immediately taken off ECMO and conventional ventilator settings adjusted to best meet the patient’s needs.

The patient should be placed in the Trendelenburg position to prevent air from entering the cerebral circulation.

Next, an attempt should be made to aspirate any accessible air out of the arterial cannula.

If air enters the coronary circulation, inotropic support may be necessary.

Before reinstituting ECMO, identifying and correcting the cause of the air embolus is essential.

H&A

19
Q

What are the neurological complications of ECMO?

A

Neurologic complications, including ICH, cerebral infarct, and seizures, have developed in 26% of infants and children on ECMO over 40 years of clinical use.

These complications carry significant mortality when encountered in ECMO patients.

Frequent neurologic examinations should be performed and the use of paralytic agents avoided.

The neurologic examination should include evaluation of alertness and interaction, spontaneous movements, eye exams, the presence of seizures, fullness of the fontanelles, tone, and reflexes.

Electroencephalography (EEG) may also be helpful.

Cranial US should be performed on all neonates before initiating ECMO to identify those patients in whom significant ICH already exists.

A retrospective analysis revealed that birth weight and gestational age were the most significant correlating factors with ICH in neonates on ECMO, though in premature neonates the use of inotropes and the incidence of mechanical complications appear more significant risk factors for ICH than gestational age.

Once the patient is placed on ECMO, US is repeated during the first 3 days when indicated by the clinical condition.

If the examination reveals a new, moderate (grade II) hemorrhage or an expanding ICH, ECMO is usually discontinued.

If ICH is suspected or detected on cranial US and deemed to be small in size, it is reasonable to maintain a low ACT (180–200 seconds) with a platelet count >125,000150,000/mm3.

Serial head US should be performed to monitor the progression of the hemorrhage.

H&A

20
Q

What hemorrhagic complications can arise from ECMO?

A

The ECMO registry reports an 11.6% incidence of cannulation site bleeding and a 13% incidence of other surgical site bleeding.

Contact of blood with the foreign surface of the circuit activates the coagulation cascade.

Platelet count and function are also affected.

With anticoagulation, bleeding risks associated with operative procedures are increased considerably, and meticulous hemostasis, often aided by topical hemostatic agents, is imperative.

If bleeding from the cervical incision is >10 mL/h for 2 hours despite conservative treatment strategies, exploration may be needed.

Bleeding into previous operative sites occurs frequently and must be handled aggressively.

A decreasing hematocrit, an increasing heart rate, a decline in the blood pressure, or inadequate venous return are signs of ongoing hemorrhage.

Treatment includes blood product resuscitation, including coagulation factors if necessary.

ACT parameters should be decreased to 180–200 seconds and the platelet count maintained above 125,000/mm3 .

Antifibrinolytics, such as aminocaproic acid, also can help prevent bleeding.

The use of recombinant activated factor VII (NovoSeven, Novo Nordisk, Inc., Princeton, NJ) has been described in the management of bleeding unresponsive to conventional methods.

This is an off-label use, and thrombosis is a significant concern. Frequently, one must evacuate the hematoma and explore for the cause, which is often needed in the postcardiac surgery patient with an open chest and central cannulation.

If bleeding is not quickly controlled, decannulation and cessation of anticoagulation may need to be strongly considered.

H&A

21
Q

What other complications can arise from
ECMO?

A

COAGULATION ABNORMALITIES

ECMO patients develop a coagulopathy secondary to consumption of clotting factors by the circuit, and if severe, may mandate a circuit change.

Disseminated intravascular coagulation (DIC) represents a much less common cause of coagulopathy in ECMO patients, occurring in approximately 4% of cases.

DIC is characterized by the consumption of plasma clotting factors and platelets, resulting in deposition of fibrin thrombi in the microvasculature and hemorrhage.

Sepsis, acidosis, hypoxia, and hypotension are the primary risk factors of DIC.

PATENT DUCTUS ARTERIOSUS

A dramatic decrease in pulmonary hypertension is frequently seen after the initiation of ECMO, usually within the first 48 hours.

In the presence of a patent ductus arteriosus (PDA), this change in pressure results in a left-to-right shunt and contributes to decreased oxygenation efficiency, pulmonary edema, and poor peripheral perfusion.

Fortunately, the PDA usually closes spontaneously with fluid restriction and diuresis.

The use of indomethacin should be avoided because of its adverse effects on platelet function. Rarely is PDA ligation required or indicated while on ECMO.

RENAL FAILURE

Oliguria is common in ECMO patients and is often seen during the first 24–48 hours.

The capillary leak that occurs with ECMO initiation can cause decreased renal perfusion, and the nonpulsatile blood flow that occurs with VA ECMO may contribute as well.

Once the patient is adequately volume resuscitated and fluid shifts have stabilized, the use of furosemide (1–2 mg/kg) can improve urine output. If the creatinine continues to rise, then renal US is recommended.

Continuous hemofiltration, which can be added in-line to the ECMO circuit, can also assist in managing the fluid shifts, hyperkalemia, and azotemia.

Hemofiltration removes plasma water and dissolved solutes while retaining proteins and the cellular components of the intravascular space.

HYPERTENSION

The incidence of hypertension during ECMO varies from 28% to as high as 92%.

According to the ELSO registry, 13% of ECMO patients require pharmacologic intervention. One group reported that detectable ICH occurred in 44% of their hypertensive patients and clinically significant ICH developed in 27%.

The patient should be assessed initially for reversible causes of hypertension, such as pain, hypercarbia, and hypoxia.

Embolic renal infarction is another cause of hypertension.

Medical management includes the use of hydralazine, nitroglycerin, and captopril.

INFECTION

The ELSO registry data up to January 2017 describes an 8% culture-proven infection rate in ECMO neonates and pediatric patients. This is remarkably low, considering the large surface area of the circuit, the duration of bypass, and the frequency of access to the circuit.

Risk factors for infection include the duration of ECMO support, the length of hospitalization, and procedures performed before the initiation of ECMO or during the run.

Fungal infections carry a significantly higher hospital mortality rate, and sepsis confers higher morbidity and mortality in neonates.

Access to the circuit should be minimized, and meticulous sterile techniques are important.

H&A

22
Q

What are the outcomes of ECMO?

A

ECMO is a prime example of the evolution from an experimental technique to a commonly used therapeutic approach.

Today, ECMO is a part of routine management in the neonatal and pediatric ICUs.

Overall survival to discharge for neonates and children is 61% for all diagnoses.

Higher survival rates are seen in neonates with respiratory diseases (73%) versus children with respiratory failure (57%), but older patients (50%) fair better than neonates (40%) with cardiac failure as the reason for ECMO.

Newborns with MAS who require ECMO have the best survival rate at 93%, whereas ECMO survival for infants with CDH is only 50%.

Overall survival after ECMO for neonatal respiratory failure has recently declined. There are likely a few reasons for this decrease in survival.

Since its peak in 1992 of 1500 cases, ECMO has been used with less frequency for critically ill neonates.

The fewer number of cases is due to an improvement in other modalities of support such as inhaled nitric oxide (iNO), HFOV, and surfactant therapy.

To some extent, these improvements have been realized as a result of lessons learned from early ECMO experience. As a result, the neonatal patients undergoing ECMO as the initial form of therapy for cardiopulmonary failure are declining, and the patients that ultimately require ECMO are probably more ill and further along the timeline of their illness.

The pediatric population of ECMO patients represents a diverse group with regard to patient age as well as diagnoses. Almost an equal number of respiratory cases (n = 8070) and cardiac cases (n = 9362) have been reported. This is in contrast to the neonatal population in which there is an over 4:1 ratio of primary respiratory to a primary cardiac diagnoses.

A higher complication rate is found in children, reflecting the longer duration of bypass required for reversal of the respiratory failure.

H&A

23
Q

What are long-term sequelae of ECMO?

A

FEEDING AND GROWTH SEQUELAE

Approximately one-third of ECMO-treated infants have feeding problems.

The possible causes for the poor feeding are numerous and include tachypnea, generalized central nervous system depression, poor hunger drive, soreness in the neck from the operation, manipulation or compression of the vagus nerve during the cannulation, sore throat from prolonged intubation, and poor oral motor coordination.

Newborns with CDH have a higher incidence of feeding difficulties when compared with those with MAS.

CDH children often have foregut dysmotility, which leads to significant gastroesophageal reflux, delayed gastric emptying, and feeding difficulties.

Respiratory compromise and chronic lung disease add to the problem.

Although normal growth is commonly reported in ECMOtreated patients, these children are more likely to experience problems with growth when compared with normal controls.

Head circumference below the fifth percentile occurs in 10% of ECMO-treated children.

Growth problems are most commonly associated with ECMO patients who had CDH or have residual lung disease.

RESPIRATORY SEQUELAE

Respiratory morbidity is more likely to be iatrogenic than a consequence of congenital lung disease. Nevertheless, approximately 15% of infants require supplemental oxygen at 4 weeks of age in some series.

At age 5 years, ECMO children are twice as likely to have reported cases of pneumonia as compared with controls (25% vs 13%).

These children with pneumonia are more likely to require hospitalization, and the pneumonia occurs at a younger age (half of the pneumonias are diagnosed before 1 year of life).

CDH infants often have severe lung disease after ECMO and often require supplemental oxygen at the time of discharge.

NEURODEVELOPMENTAL SEQUELAE

Probably the most serious post-ECMO morbidity is neuromotor injury. The total rate of neurologic injury from 540 patients at 12 institutions was 6%, with a range from 2–18%.

ECMO survivors have significant developmental delay, up to 21%.

This is comparable to other critically ill, non-ECMO-treated neonates.

Ventilator time appears to be the most important predictor of motor problems in CDH patients.

Auditory defects are reported in more than one-quarter of ECMO neonates at discharge. These deficits are detected by brain stem auditory evoked response (BAER) testing, are considered mild to moderate, and generally resolve over time.

The auditory defects may be iatrogenic, or caused by induced alkalosis, diuretics, or gentamicin ototoxicity.

As a result, all patients should have a hearing screening at the time of discharge.

Visual deficits are uncommon in ECMO neonates who weigh >2 kg.

Seizures are widely reported among ECMO neonates, ranging from 20–70%. However, by age 5 years, only 2% have a diagnosis of epilepsy.

Seizures in the neonatal population are associated with neurologic disease and worse outcomes, including in-hospital mortality, cerebral palsy, and epilepsy.

Severe nonambulatory cerebral palsy has an incidence of <5% and is usually accompanied by significant developmental delay. Milder cases of cerebral palsy are seen in up to 20% of ECMO survivors.

Overall, ECMO-treated neonates function within the normal range and the rate of handicap appears to be stable across studies with an average of 11%, ranging from 2–18%.

This morbidity may reflect how desperately ill these children are during treatment, and these deleterious complications may not be a direct result of ECLS.

H&A

24
Q

Common complications of extracorporeal membrane oxygenation (ECMO) do not include:

A barotrauma to lungs

B intracranial haemorrhage

C pulmonary haemorrhage

D carotid artery ligation

E need for renal haemofiltration.

A

A

ECMO is used to ‘rest’ the lungs while the underlying pathology recovers.

Patients are placed on a cardiopulmonary bypass circuit to provide oxygenation and CO2 removal.

Pulmonary barotrauma therefore does not occur as minimal pressure is used to ventilate.

Haemorrhage is a complication due to the need for anticoagulation to maintain patency of the ECMO circuit, with 15% of neonates suffering an intracranial haemorrhage and 12% pulmonary haemorrhage in one study.

In the same study, 25% of infants required haemofiltration.

SPSE 1

25
Q

The highest neonatal ECMO survival rate is in infants with:

A persistent pulmonary hypertension

B congenital diaphragmatic hernia

C meconium aspiration syndrome

D sepsis

E pulmonary hypoplasia.

A

C

Ninety-four percent of infants with meconium aspiration syndrome survive to discharge.

This compares with 79% with PPHN, 75% with sepsis and 54% with congenital diaphragmatic hernia.

Pulmonary hypoplasia alone is not an indication for ECMO as it is a non-reversible condition.

SPSE 1

26
Q

Contraindications to ECMO include:

A respiratory distress syndrome (RDS)
B gestational age below term (37 weeks)
C ventilation for less than 7 days
D ventilation more than 14 days
E cardiac abnormality.

A

D ventilation more than 14 days

ECMO can be used for infants with reversible disease, therefore RDS can be an indication if other selection criteria are met.

Pre-term infants below 35 weeks are not considered candidates for ECMO because of the risk of intraventricular haemorrhage, which is increased because of their gestation and need for anticoagulation on ECMO.

Ventilation for over 14 days is considered a contraindication because of the irreversible lung damage that will have occurred, whatever the underlying pathology.

There is no minimum time of ventilation before ECMO is considered, and early referral is considered best practice to minimise barotraumas.

Cardiac abnormality per se is not a contraindication, and ECMO can be used occasionally as a bridge to cardiac transplantation.

SPSE 1

27
Q

Contraindications for continuous positive airway pressure (CPAP) include:

A gastroschisis (postoperative)
B oesophageal atresia (preoperative)
C congenital diaphragmatic hernia (preoperative)
D cardiac malformation
E laryngomalacia

A

C congenital diaphragmatic hernia (preoperative)

CPAP provides a continuous distending pressure to the lungs.

It is most commonly used in infants with RDS to minimise the work of breathing and reduce atelectasis.

For infants with repaired gastroschisis, it may help with the respiratory complications of increased intra-abdominal pressure.

Preoperatively CPAP should be avoided in infants with gastroschisis, exomphalos and congenital diaphragmatic hernia, as it will cause intestinal distension.

It is safe to deliver CPAP to infants with pure oesophageal atresia provided a Replogle tube is in place or frequent aspiration of the upper pouch is performed.

CPAP can be used as supportive therapy for infants with laryngomalacia, because of the airway support provided.

SPSE 1