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PERINATALTimesVol. 31 | APRIL 2019
in this issue:
Understanding and Managing Maternal Sepsis and
Bubble CPAP A Simple Idea that Changed the World
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St. Mary’s Hospital – St. LouisCardinal Glennon Children’s Hospital
THE PERINATAL OUTREACH PROGRAM
The Perinatal Outreach Program is a collaborative effort between SSM Health Women’s Health at SSM Health St. Mary’s Hospital - St. Louis, SSM Health Cardinal Glennon Children’s Hospital and Saint Louis University School of Medicine.
It is designed to improve outcomes for mothers and babies through educational programs and quality improvement activities for regional perinatal care providers in eastern Missouri and southern Illinois.
SSM Health Cardinal Glennon Children’s Hospital and SSM Health St. Mary’s Hospital - St. Louis are designated by the Illinois Department of Public Health as the Administrative Perinatal Center for Southern Illinois.
PERINATAL TIMES EDITORIAL BOARD
Meredith Meyer, MSN, RNC, Editor
SSM Health Cardinal Glennon Children’s Hospital
SSM Health St. Mary’s Hospital – St. Louis
Glenn Barber, BSN, RNC Shilpa Babbar, MD
Christopher Brownsworth, MD Emily Berghult, MSN, RN
Robyn Gude, MSN, RN Gilad G. Gross, MD
Mary Hope, BSN, RN Kathleen Klug, BSN, RN
Justin Josephsen, MD Laurie Niewoehner, PharmD
William Keenan, MD Pam Randazzo, BSN, RNC
Patricia Oberkirsch Sharon Rector, MSN, RNC
Rebecca Petersen, MD Judy Wilson-Griffin, MSN, PNCNS, RNC
FUNDING
Financial support for The Perinatal Times is provided by SSM Health and the Illinois Department of Public Health.
LETTERS
The Perinatal Times welcomes comments on any of its articles and will consider such letters for publication. Suggestions for future topics of interest or announcements are encouraged.
PLEASE SEND CORRESPONDENCE TO:
The Perinatal Times Meredith Meyer, Editor
SSM Health St. Mary’s Hospital 6420 Clayton Road St. Louis, MO 63117
To receive an electronic version of The Perinatal Times, please email Patricia Oberkirsch at [email protected]
Vol. 31 | April 2019
INSIDE THIS ISSUE:
1 NRP IN THE KNOW Providing Effective Ventilation
4 FORMULARY FACTS Treating Maternal Sepsis
8 MATERNAL TOPIC Understanding and Managing Maternal Sepsis
14 NEONATAL TOPIC Bubble CPAP — A Simple Idea that Changed the World
18 FETAL CARE IN FOCUS Understanding Gastroschisis Sutureless Closure
21 THE MONITOR CORNER Fetal Tachycardia
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NRP in the KNOW
About the Authors
Marya Strand, MD, MS is an associate professor in the Department of Pediatrics, Division of Neonatology, at Saint Louis University School of Medicine and specializes in the care of newborns, with particular interest in neonatal resuscitation, medical education and simulation-based education. She treats premature and extremely premature infants, normal and sick newborns, and patients in a Level II nursery to Level IV neonatal intensive care. She also provides outpatient care in the high-risk nursery clinic and antenatal consultation for expectant mothers. Dr. Strand is involved in clinical and educational research and directs the research program for pediatric residents. Dr. Strand is a member of the Neonatal Taskforce for the International Liaison Committee on Resuscitation, an international group of physicians that determines guidelines for resuscitation of infants. She is also an active member of the Neonatal Resuscitation Program Steering Committee.
Justin Josephsen, MD is an assistant professor in the Department of Pediatrics, Division of Neonatology, at Saint Louis University School of Medicine, Director of the Neonatal Resuscitation Video-Review QI Program at SSM Health St. Mary’s Hospital - St. Louis, and the Neonatal Co-Lead for the Illinois Perinatal Quality Collaborative. He specializes in the care of critically ill newborns and his interests include community outreach, improving the management of frail neonates in the delivery room, and simulation-based medical education research.
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St. Mary’s Hospital – St. LouisCardinal Glennon Children’s Hospital
CARDIOVASCULAR TRANSITION AT DELIVERY
Blood flow during fetal life is focused on perfusion of the brain and major organs with oxygenated blood and avoidance of perfusion of the fluid-filled lungs. The oxygenated blood from the placenta travels through the umbilical vein, up to the right side of the heart, and is preferentially shunted across the patent foramen ovale to the left side of the heart (Figure 1 ). Less than 10% of the cardiac output of the fetus is pumped into the pulmonary arteries prior to delivery.1
Normal cardiopulmonary transition for the newborn at delivery requires a rapid and complex process of fetal lung fluid clearance, expansion of the lungs with air and redirection of cardiac output toward the lungs. All of these events take place independent of intervention in the majority of newborn infants at the time of delivery.2 Failure of any of these events can cause delays in transition or progress to depression in the newborn.
Fetal lung fluid produced by the lung tissue fills the pulmonary spaces during gestation. The pressure of the fluid within the air spaces and resistance to outflow through closed vocal cords facilitates the growth and development of the lungs. Rapid fetal lung fluid clearance at birth likely occurs by several mechanisms, including fetal postural changes, cellular sodium channel pumps, and transpulmonary pressure from inspiration at delivery.3 Apneic infants, who
NRP in the KNOW
Providing Effective By Marya Strand, MD, MS & Justin Josephsen, MD
NRP in the KNOW
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Effective Ventilation (continued)
FIGURE 1 Oxygenated Placental Blood Flow1
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don’t contribute the transpulmonary pressure, can have significantly compromised fluid clearance from the air spaces.
Once the fluid is cleared and air fills the alveoli, the pulmonary arterial pressure drops rapidly to increase blood flow from the heart to the lungs. With this change in cardiac output and transition of gas exchange to the pulmonary bed, the left ventricular volume shifts from the umbilical venous return from the placenta to pulmonary venous return. The peripheral vascular resistance increases simultaneously to result in left-to-right flow through the ductus arteriosus and the beginning of ductal closure.4
Lung expansion and establishment of baseline pulmonary expansion (functional residual capacity,
FRC) is vital to the normal transition of the newborn. When the umbilical cord is clamped and cut at delivery the venous return from the placenta abruptly ceases. If the lungs have not yet expanded and established vascular perfusion before the clamping of the umbilical cord the blood return to the left ventricle is compromised and cardiac output falls. With a low cardiac output, the infant becomes hypoxemic and bradycardia ensues with further respiratory failure and asphyxia.
ESTABLISHING FRC
In a normal delivery of a term infant, FRC is established primarily by the newborn breathing spontaneously as the fetal lung fluid is reabsorbed. Lack of pulmonary inflation, whether from apnea or surfactant deficiency as seen in prematurity, may cause the infant to require assistance to establish FRC at delivery. Being mindful of establishing FRC when delivering PPV is helpful to assist in the transition of the compromised neonate. Positive end expiratory pressure (PEEP) is critical in maintaining lung expansion during PPV.5 PEEP can be provided using the T-piece resuscitator, flow-inflating bag or self-inflating bag with a PEEP valve in place. An appropriate inspiratory time is also important in establishing the FRC. With a PPV rate of 40 to 60 breaths/minute the inspiratory time should be 0.3 to 0.5 seconds for each breath. Very short inspiratory times do not allow for inflation of the air spaces and FRC cannot be effectively established. The ventilator should be mindful of both the PPV rate and the inspiratory time by counting in her or his head
“Breathe-two-three, breathe-two-three, …” during ventilation. This rhythm assures a 1:2 inspiratory: expiratory ratio.
For premature infants with surfactant deficiency, administration of exogenous surfactant can be extremely helpful in both increasing lung compliance and increasing FRC. Further discussion of exogenous surfactant is outside the scope of this article, but Lesson 9 of the NRP Textbook is an excellent resource on this topic.1
ASSESSMENT OF VENTILATION
An increasing heart rate is the most reliable indicator of adequate ventilation.6 When PPV is begun in a neonatal resuscitation, the assessment (within 15
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References
1 Textbook of neonatal resuscitation. Elk Grove Village, IL: American Academy of Pediatrics; 2016.
2 Perlman JM, Risser R. Cardiopulmonary resuscitation in the delivery room. Associated clinical events. Archives of pediatrics & adolescent medicine 1995; 149:20-25.
3 Jain L, Eaton DC. Physiology of fetal lung fluid clearance and the effect of labor. Seminars in perinatology 2006; 30:34-43.
4 Hooper SB, Te Pas AB, Kitchen MJ. Respiratory transition in the newborn: A three-phase process. Archives of disease in childhood Fetal and neonatal edition 2016; 101:F266-271.
5 Hooper SB, Te Pas AB, Lewis RA, Morley CJ. Establishing functional residual capacity at birth. NeoReviews 2010; 11:e474-481.
6 Wyckoff MH, Aziz K, Escobedo MB, Kapadia VS, Kattwinkel J, Perlman JM, Simon WM, Weiner GM, Zaichkin JG. Part 13: Neonatal resuscitation: 2015 american heart association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care (reprint). Pediatrics 2015; 136 Suppl 2: S196-218.
7 Leone TA, Lange A, Rich W, Finer NN. Disposable colorimetric carbon dioxide detector use as an indicator of a patent airway during noninvasive mask ventilation. Pediatrics 2006; 118:e202-204.
8 Blank D, Rich W, Leone T, Garey D, Finer N. Pedi-cap color change precedes a significant increase in heart rate during neonatal resuscitation. Resuscitation 2014; 85:1568-1572.
9 Schmolzer GM, Kamlin OC, O’Donnell CP, Dawson JA, Morley CJ, Davis PG. Assessment of tidal volume and gas leak during mask ventilation of preterm infants in the delivery room. Archives of disease in childhood Fetal and neonatal edition 2010; 95:F393-397.
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seconds) must include an indication of heart rate response. The person assessing ventilation should relay the presence or absence of chest wall rise AND any changes in heart rate found during auscultation.
Colorimetric carbon dioxide monitoring has been studied as a proxy for adequacy of gas exchange during PPV. Placement of the CO2 monitor in line with the PPV device and mask can reflect the inspiratory/expiratory cycle of PPV. A cycling color change during PPV indicates the presence of a patent airway.7 A change in color on the monitor, when used, is also seen prior to the response in heart rate, indicating efficacy of ventilation precedes a heart rate response.8
TROUBLESHOOTING INEFFECTIVE VENTILATION
A lack of heart rate response to PPV requires immediate investigation. The mnemonic MR. SOPA has been introduced through NRP.1 This mnemonic addresses the fact that usually the difficulty with effective PPV results from mask leak or position as well as maintaining an open airway.9 If repositioning the airway and adjustment of the mask to eliminate leak do not result in lung expansion with increase in heart rate there may be a blockage to airway patency. Suctioning with a bulb or catheter may be indicated. Opening the mouth of the newborn decreases resistance to airflow compared to the nares. If PPV remains ineffective, the newborn may require increased pressure to inflate the lungs and establish functional residual capacity. If the newborn does not respond to increased inspiratory pressure an alternative airway, such as a laryngeal mask or endotracheal tube, may be required. This entire process of troubleshooting ventilation should be completed in 15-30 seconds, exclusive of alternative airway placement. A video demonstrating the troubleshooting can be found on the NRP mobile app.
SUMMARY
Normal cardiopulmonary transition in the newborn is dependent upon lung inflation and establishment of FRC. While most newborns will achieve this independently, compromised infants must be supported in this transition. Infants are effectively resuscitated when the newborn providers are knowledgeable about the physiology underlying this transition and are skilled in providing PPV appropriately.
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About the Author
Laurie Niewoehner, PharmD is a clinical pharmacy specialist at SSM Health St. Mary’s Hospital – St. Louis. She attended the University of Minnesota and completed a specialty residency program in pediatrics at Children’s Mercy Hospital and the University of Missouri-Kansas City School of Pharmacy in Kansas City. Laurie is also a preceptor for neonatology and women’s health pharmacy students.
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Formulary FACTS
BY LAURIE NIEWOEHNER, PHARM D
Treating Maternal
R ecent estimates suggest that infection accounts for 12.7% of maternal mortality
in the United States, 6% of this group are characterized as having sepsis. Recent
data suggests that infection is currently the third most common cause of
maternal death, and in contrast to maternal deaths from hypertensive disorders and
hemorrhage, the number of deaths related
to infection are increasing. Undetected
or poorly managed maternal infections
can lead to sepsis, maternal morbidity or
mortality, and increased likelihood of early
neonatal infection or adverse outcome.
Maternal sepsis is a life-threatening organ
dysfunction resulting from infection during
pregnancy, childbirth, post-abortion,
or the postpartum period.
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Early recognition of sepsis allows for achievement of the three primary goals:
➊ Source control
➋ Maintenance of perfusion
➌ Initiation of antibiotic therapy
SEPSIS BUNDLE — FIRST 3 HOURS
During the first three hours of recognition of suspected sepsis, the following are essential components:
➊ Lactate level should be obtained
➋ Pertinent cultures including: blood, urine, surgical, wound, or airway cultures, and MRSA status via nose swab
➌ Initiation of broad spectrum antibiotics
➍ Administering 30 mL/kg LR or NS for hypotension or lactate ≥ 4 mmol/L, which indicates tissue hypo perfusion
This care should be initiated regardless of the patient’s location (antepartum/L&D or post-partum) with anticipation of moving to the ICU. Antibiotics should be initiated within one hour of diagnosis to improve outcomes. With a pregnant mom with sepsis, frequent or continuous fetal monitoring is recommended especially if fetal intervention would be considered. If the septic process can’t be stopped, shunting of blood away from the fetus is likely. If the hypotension is not responding to initial fluid resuscitation to maintain mean arterial pressure (MAP) > 65 mm Hg, then the addition of vasopressors such as dopamine or norepinephrine may be needed. Vasoconstrictive agents, such as norepinephrine, used to improve the MAP, may further reduce uteroplacental perfusion.
This will result in fetal heart rate changes and uterine contractions. In a preterm infant, corticosteroids should be considered to promote lung maturity in case delivery may be necessary.3
COMMON INFECTION AND ORGANISMS
The underlying conditions most likely to be associated with sepsis in pregnant women are: pyelonephritis, pneumonia, chorioamnionitis/endometritis, GI tract perforation/rupture, or retained products of conception. Organisms frequently associated with obstetric sepsis include: Beta hemolytic strep Group A, E. coli, Strep pneumoniae, and influenza A and B. E.coli is the most common sepsis pathogen in pregnancy.
TABLE 1
RISK FACTORS FOR MATERNAL SEPSIS
Birth Condition Factors Maternal Factors Community Factors
C-section Anemia Low socioeconomic status
Multiple vaginal exams (>5) Poor nutrition Lack of health care
PROM Multiple pregnancy
Prolonged labor Obesity
Retained products of conception Primiparity
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Formulary FACTS (continued)
TABLE 2
TYPE OF INFECTION ANTIBIOTIC REGIMEN PENICILLIN ALLERGY PENICILLIN + CEPHALOSPORIN ALLERGY
Zosyn 3.375 gm IV Q6h
PLUS Clindamycin 900 mg IV Q8h
Ceftriaxone 2 gm IV Q24h
PLUS Metronidazole 500 mg IV Q8h PLUS Clindamycin 900 mg IV Q8h
Meropenem 1000 mg IV Q8h PLUS Clindamycin 900 mg IV Q8h
Ceftriaxone 2 gram IV Q24 Ceftriaxone 2 gram IV Q24h Levofloxacin 750 mg IV Q24h PLUS Gent dosing per pharmacy (if post-partum)
( community acquired)
Ceftriaxone 2 g IV Q24h PLUS Azithromycin 500 mg IV Q24h
Ceftriaxone 2 g IV Q24h PLUS Azithromycin 500 mg IV Q24h
Levofloxacin 750 mg IV Q24h PLUS/MINUS *Vancomycin dosing per pharmacy
Zosyn 3.375 gm IV Q6h PLUS/MINUS *Vancomycin per pharmacy
Cefepime 2 gm IV Q8h PLUS/MINUS *Vancomycin per pharmacy
Meropenem 1 gram IV Q8h PLUS/MINUS *Vancomycin dosing per pharmacy
PROPHYLAXIS
<120 kg Cefazolin 2 gram IV X1 >120 kg Cefazolin 3 gram IV X1
<120 kg Cefazolin 2 gram IV X1 >120 kg Cefazolin 3 gram IV X1
Clindamycin 900 mg IV x1 PLUS Gentamicin 5 mg/kg IV x1
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Ampicillin 2 gram IV X1 Cefazolin 2 gram IV X1
*Vancomycin to be considered if patient has MRSA risk factors *Vancomycin to be considered if patient has MRSA risk factors
Pre-op ( give within 30 min of surgical incision)
Laboring to C-section
Manual removal of placenta
Pneumonia
C-section wound infection
Urinary tract infection
Chorioamnionitis
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Data shows rising rates of infection due to Group A Strep, which is a highly virulent pathogen that can lead to increased morbidity and mortality. It is important to recognize infection early and administer broad spectrum antibiotics in addition to clindamycin, which is capable of preventing exotoxin production from Group A strep. Polymicrobial infections are also common in pregnancy and require broad-spectrum antimicrobial coverage. Table 2 includes common dosing regimens for common pregnancy and post-partum infections with options for penicillin allergic patients and penicillin/cephalosporin allergic patients. Coliform infection is particularly associated with urinary sepsis, preterm rupture of membranes and cerclage. Therapy should be narrowed once the causative organism is identified. In many cases the cause of the infection is undetermined. Prevention of
sepsis relies on administering prophylactic antibiotics (pre-op- included in Table 2) prior to cesarean section to prevent endometritis.
SOURCE CONTROL
The source of infection must be actively explored, aiming to remove it. Surgical treatment may be needed for abscesses, retained placental fragments, pus collections, exploration of infected abdominal cavity, debridement of necrotic tissues, or drainage of surgery-related pus collections. Source control may also involve the infections of the uterus (chorio) and thus delivery of the fetus, regardless of gestational age.
PROPHYLAXIS
Because of the state of hypercoagulability induced by both pregnancy and sepsis, thromboembolism prophylaxis should initiated. Prophylaxis includes
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Formulary FACTS
TABLE 2
TYPE OF INFECTION ANTIBIOTIC REGIMEN PENICILLIN ALLERGY PENICILLIN + CEPHALOSPORIN ALLERGY
Zosyn 3.375 gm IV Q6h
PLUS Clindamycin 900 mg IV Q8h
Ceftriaxone 2 gm IV Q24h
PLUS Metronidazole 500 mg IV Q8h PLUS Clindamycin 900 mg IV Q8h
Meropenem 1000 mg IV Q8h PLUS Clindamycin 900 mg IV Q8h
Ceftriaxone 2 gram IV Q24 Ceftriaxone 2 gram IV Q24h Levofloxacin 750 mg IV Q24h PLUS Gent dosing per pharmacy (if post-partum)
( community acquired)
Ceftriaxone 2 g IV Q24h PLUS Azithromycin 500 mg IV Q24h
Ceftriaxone 2 g IV Q24h PLUS Azithromycin 500 mg IV Q24h
Levofloxacin 750 mg IV Q24h PLUS/MINUS *Vancomycin dosing per pharmacy
Zosyn 3.375 gm IV Q6h PLUS/MINUS *Vancomycin per pharmacy
Cefepime 2 gm IV Q8h PLUS/MINUS *Vancomycin per pharmacy
Meropenem 1 gram IV Q8h PLUS/MINUS *Vancomycin dosing per pharmacy
PROPHYLAXIS
<120 kg Cefazolin 2 gram IV X1 >120 kg Cefazolin 3 gram IV X1
<120 kg Cefazolin 2 gram IV X1 >120 kg Cefazolin 3 gram IV X1
Clindamycin 900 mg IV x1 PLUS Gentamicin 5 mg/kg IV x1
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Azithromycin 500 mg IV x1 PLUS Pre-op antibiotic above
Ampicillin 2 gram IV X1 Cefazolin 2 gram IV X1
*Vancomycin to be considered if patient has MRSA risk factors *Vancomycin to be considered if patient has MRSA risk factors
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References
1 Martin, S. & Baird, S.M. Sepsis and Septic Shock in Pregnancy. Infections Ob Gyn June 2018
2 Rochin, Elizabeth (2017) Sepsis Standard Work: Improving Compliance with Early Recognition and Management of Perinatal Sepsis. [Power point Slides] retrieved from: www.cdc.gov/infectioncontrol/pdf/webinarslides/CDC-ANA-AWHONN-SCCM-Maternal-Sepsis-Webinar_1.pdf
3 www.who.int/reproductivehealth Statement on Maternal Sepsis
compression stockings, sequential compression device (SCD’s) low molecular weight heparin or unfractionated heparin, in addition to early ambulation. Gastric or duodenal ulcers can be induced by sepsis so H2 receptor antagonists, such as famotidine 20 mg IV/PO BID are indicated.3
PATIENTS WITH A PCN ALLERGY
The cross reactivity between penicillin and cephalosporin is only 1-3%. The highest risk is when the side chain of the cephalosporin is similar to that of penicillin. If that patient has an unknown penicillin allergy or even anaphylaxis or hives, it is safe to use cefazolin or any 3rd or 4th generation cephalosporin. Note, if the patient has a history of Stevens – Johnson syndrome (SJS), Toxic Epidermal Necrosis (TEN) or Drug Rash with Eosinophilia and Systemic Symptom (DRESS) with a beta-lactam, all antibiotics in that category need to be avoided.
PHARMACOKINETICS IN PREGNANCY AND POST-PARTUM
Pregnant women have a greater volume of distribution and clearance of antibiotics such as vancomycin so increased dosing frequency may be needed. Typically pregnant or post-partum patients with CrCl > 80 mL/min should be initiated on every 8-hour dosing regimen. The vancomycin dose and frequency can be modified based on trough concentrations (goal 15-20 mcg/mL in most patients).
Sepsis in obstetric patients is increasing in the United States and is a leading cause of maternal death. Early recognition is critical to preventing disease progression. Building a sepsis order set with labs, cultures, fluids and antibiotic options may expedite ordering the needed treatment in these emergent cases.
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Understandingand Managing MATERNAL By Alexandra Edwards, MD and Alexandre Lacasse, MD, FACP, MSc
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About the Authors
Alexandra Edwards, MD is a second-year Maternal Fetal Medicine (“High Risk” OB) fellow with Saint Louis University. Dr. Edwards obtained her medical degree from UMKC in 2012. She trained at University of Kentucky for residency in obstetrics and gynecology and a fellowship in surgical critical care. She also practices critical care at SSM Health St. Mary’s Hospital, St. Louis, MO.
Alexandre Lacasse, MD, FACP, MSc is Associate Program Director of the Internal Medicine residency program, Associate Medical Director of the Internal Medicine Outpatient Clinic and the Educational Director of Infectious Diseases at SSM Health St Mary’s Hospital – St. Louis. Dr. Lacasse has served as an Internal Medicine resident clinical educator and instructor since 2009. He obtained his medical degree from the SABA University School of Medicine Netherlands. He completed his Internal Medicine residency and chief-residency at SSM St. Mary’s Hospital - Saint Louis and an Infectious Disease fellowship at the University of Tennessee Health Science Center. Dr. Lacasse is the Chair of the hospital Sepsis Committee and serves on several other committees including IM/ED peer review, citizenship, GME, antimicrobial stewardship, and infection prevention.
Maternal Sepsis
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M aternal sepsis or sepsis in pregnancy is a challenging and
potentially life-threatening clinical entity. Sepsis is a clinical
diagnosis describing a systemic inflammatory response to infection leading
to organ dysfunction, organ failure and possibly death.1 Maternal sepsis is
unique due to its diagnostic challenges,
etiology and complications. Pregnancies
complicated by sepsis are associated
with increased rates of preterm labor,
fetal infection and preterm birth.2
Here we review the definition of
sepsis, its incidence in pregnancy and
management strategies.
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Maternal Sepsis (continued)
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DEFINITION
The definition of sepsis is complex. Originally stated in 1991, the definition of sepsis has refined as our understanding has evolved. Sepsis is now better defined as a life-threatening organ dysfunction caused by dysregulated host responses to infection.3 Septic shock is a subset of sepsis with circulatory, cellular and metabolic dysfunctions associated with higher mortality.3 These definitions are a departure from previous more simplistic or rigid definitions used in the SIRS-sepsis spectrum (Figure 1, p12). The newer definition helps identify the most severely ill patients but may delay potential interventions in patients with sepsis without organ dysfunction. Early identification and intervention in patients with sepsis is beneficial, including the obstetric population. A study assessing the benefit of early identification of obstetric patients showed that the MEWT (Maternal Early Warning Trigger) tool can reduce severe maternal morbidity and increase sepsis identification.4
INCIDENCE AND PREVALENCE
Sepsis is a widespread problem. Within ICUs, sepsis is the leading cause of mortality and critical illness.3
Sepsis in pregnancy is fortunately uncommon, though infections are common. The reported incidence of septic shock in pregnancy is approximately 0.01% of all deliveries. Of septic patients, only 0.3-0.6% are pregnant.5,6 However, maternal morbidity and mortality are increasing within the U.S., sepsis being an important contributor.
ETIOLOGY
Maternal sepsis can result from obstetric or non-obstetric-related infections. Potential causes in pregnancy as well as intrapartum and postpartum periods are listed (Table 1). Pregnancy itself leads to profound alterations in human physiology with most notable changes in cardiovascular, pulmonary and renal function. These changes influence vital signs and laboratory parameters and thus can make the diagnosis of sepsis and septic shock in the peripartum period more challenging by interfering with obstetric specific scoring warning tools (Figure 2, p13).
Perinatal infection can occur in antepartum, intrapartum or postpartum periods. Antepartum infections are common, the most common being urinary tract infections. Due to anatomic and physiologic changes in pregnancy, increased urinary stasis occurs. E. coli is the most common pathogen and has specific virulence factors leading to infection within the urinary tract. Pyelonephritis can result from ascending infection and is characterized by severe flank pain and systemic symptoms i.e. fever, nausea, vomiting. If left untreated, pyelonephritis in pregnancy can lead to sepsis and ARDS in up to 10-15% of patients.7
Intrapartum, chorioamnionitis is a common infection from ascending bacteria infecting the chorion, amnion and ultimately the fetus. Chorioamnionitis is typically a clinical diagnosis when fever, uterine tenderness, purulent vaginal discharge, and maternal and fetal tachycardia are seen. Delivery usually leads to defervescence, however the risk for sepsis continues, especially if cesarean delivery is required (Barton Obstetrics and Gynecology 2013). Prior to the advent of handwashing, beta-hemolytic group A streptococcus (S. pyogenes) was the main microorganism causing peripartum infections and maternal death, in the classically referred “Childbed fever”.8 Nowadays, the main causative bacterial pathogens include facultative aerobic and anaerobic enteric bacterias, and less commonly S. pyogenes.
TABLE 1
POTENTIAL CAUSES OF MATERNAL SEPSIS
Obstetric Specific
Chorioamnionitis
Retained products/placenta
Septic abortion
Endometritis
Post-operative superficial & deep wound infection
Non-Obstetric
Pyelonephritis
Pneumonia
Skin and soft tissue infection
Appendicitis
Cholecystitis
Endocarditis
Meningitis
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MATERNAL AND PERINATAL COMPLICATIONS
Pregnancies complicated by sepsis or septic shock are associated with increased rates of fetal infection, preterm labor and delivery, and operative delivery.9 Generally, pregnant patients can be treated and pregnancy can be maintained. The inflammation that occurs in sepsis may however lead to contractions and labor. Delivery remote from term solely because of sepsis is not typically necessary. However, in the setting of profound shock or maternal death, a resuscitative delivery may be necessary.
MANAGEMENT
Management of sepsis is directed towards eliminating the source (source control) and restoring normal physiology. The Surviving Sepsis Campaign published more recent updated detailed recommendations in 2016. The important tenants of care are firstly to recognize infection, secondly take action surgically or procedurally to reduce or remove the source of sepsis and thirdly, to give appropriate targeted antimicrobial therapy and intravenous isotonic fluids and/or vasopressor support to augment cardiac output and delivery of oxygen to vital organs.
The appropriate amount of fluid resuscitation in patients with sepsis is of current debate. Large fluid volumes can lead to complications such as pulmonary edema, respiratory failure, ARDS, myocardial ischemia and abdominal compartment syndrome.10 Currently, the recommendation for volume resuscitation in sepsis include an initial 30 mL/kg of crystalloid bolus within the first 3 hours of care (SSC). The crystalloid of choice is also up for debate, however recent evidence suggests that lactated ringers may be associated with reduced renal injury (NEJM). After the initial fluid bolus, timely reevaluation and need for ongoing fluid resuscitation or vasopressor treatment should be performed. A multidisciplinary approach may be necessary including consultation with Critical Care or Infectious Diseases physicians.
ANTIMICROBIAL THERAPY
Broad spectrum antimicrobial treatment is indicated in patients with sepsis, targeted to microorganisms associated with the suspected site of infection (source).11 When possible, culture data from the suspected source of infection should be collected. Based on culture data results, antimicrobial therapy should be de-escalated and appropriate antimicrobial drugs with narrowest spectrum of activity should be used.
CONCLUSION
Sepsis is potentially life-threatening and in the context of pregnancy, both mother and fetus can be affected. Specific causes of sepsis in pregnancy and postpartum should be investigated and treated accordingly in a promptly manner. To improve both maternal and fetal outcome, a multidisciplinary approach comprising of nursing teams as well as obstetric, maternal-fetal medicine, critical care and infectious disease physicians should be implemented.
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Maternal Sepsis (continued)
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References
1 Rhodes A, et al, Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Medicine 2017 Mar; 43(3):304-377.
2 Barton JR, Sibai BM. Severe sepsis and septic shock in pregnancy. Obstet Gynecol. 2012 Sep; 120(3):689-706
3 Singer et al, The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23; 315(8):801-10
4 Shields LE. Wiesner S, Klein C, Pelletreau B, Hedriana HL. Use of maternal early warning trigger tool reduces maternal morbidity. AJOG Apr 2016.
5 Fernandez-Perez ER, Salman S, Pendem S, Farmer JC. Sepsis during pregnancy. Crit Care Med 2005 Oct; 33
6 Martin GS. The epidemiology of sepsis in the US, NEJM 2003 Apr 17:328(16):1546-54
7 Williams Obstetrics 24th Edition
8 Noakes TD, Semmelweis and the aetiology of puerperal sepsis 160 years on: an historical review. Epidemiol Infect 2008 Jan; 136(1):1-9
9 Kankuri E, Incidence, treatment and outcome of peripartum sepsis. Acta Obstet Gynecol Scand. 2003 Aug; 82(8):730-5
10 Chang DW et al. Volume of fluids administered during resuscitation for severe sepsis and septic shock and the development of ARDS. J Critical Care 2014 Dec; 29(6):1011-5
11 Levy MM, Evans LE, Rhodes A. The surviving sepsis campaign bundle 2018: update. Crit Care Med 2018 Jun;46 (6)
Figure 1 SIRS, Sepsis, Severe Sepsis, Septic Shock vs Sepsis 3
PREVIOUS Definition NEW Definition
SIRS T >100.4, <96.8
RR >20
HR >90
WBC >12K, <4K, >10% bands
PCOS <32 mmHg
Category removed
Sepsis Suspected infection + SIRS Suspected infection + 2 >qSOFA* or rise in SOFA score by >2
Severe Sepsis Sepsis + hypotension, hypoxia, elevated lactate or other lab markers of end organ dysfunction
Category removed
Septic Shock Sepsis + hypotension after adequate fluid resuscitation
Sepsis + vasopressors + lactate >2
*qSOFA= Altered mental status, Hypotension with SBP <100 mm Hg, Tachypnea with RR >22
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Figure 2 SSM Health Modified Early Obstetric Warning System Scoring
DATA 0 POINTS 1 POINTS 2 POINTS
Temp (°F) 96.8 - 100.2 < 96.8 100.3 - 100.9
> 100.9
Pulse 60 - 110 50 - 59 111 - 129
< 50 ≥ 130
Respiration Rate
10 - 24 25 - 30 < 10 > 30
SpO2 (%) 96 - 100 < 96
Systolic BP 100 - 139 140 - 159 < 100 ≥ 160
Diastolic BP 50 - 89 40 - 49 90 - 99
< 40 > 99
Level of Consciousness (LOC)
Alert
Drowsy
Eyes open to verbal stimuli
Eyes open spontaneously
Sleeping
Agitated
Irritable
Lethargic
Restless
Sedated
Other (comment)
Anesthetized
Comatose
Eyes do not open to any stimulus
Eyes open not tracking
Eyes open to pain
Obtunded
Pharmacologically paralyzed
Stuporous
Orientation Level
Oriented x 4
Unable to obtain
(if LOC = 0 pts)
Disoriented x 1
Other (comment)
Unable to obtain
(if LOC = 1 pt)
Disoriented x 4 = 4 pts
Disoriented x 3 = 3 pts
Disoriented x 2 = 2 pts
Unable to obtain (if LOC = 2 pts)
Urine Output
( unmeasured; no I/O order, no Foley)
Any UO documented in past 8 hrs (including unmeasured)
No UO documented in past 8 hrs (including unmeasured)
Urine Output
( measured; I/O order, Foley)
≥ 240 ml in past 8 hrs < 240 ml in past 8 hrs
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14 | vol. 31 | april 2019
By Noah Hillman, MD
A Simple Idea that Changed the World
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Bubble CPAP
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FIGURE 1 SIMPLE BUBBLE-CPAP SETUP | COMPONENTS | PRESSURE FLUCTUATION
uring his anesthesia residency in the late 1960s, Dr. George Gregory got frustrated by watching preterm babies
die from respiratory distress syndrome (RDS) in the ICU. So one night he went out to his
garage and fashioned a device to provide continuous distending pressure to the lungs. The following day he placed a premature infant on the device, and continuous positive airway pressure (CPAP) for the treatment of RDS was born. The subsequent publication in the New England Journal of Medicine in 1971 changed how people treated RDS across the world, and saved thousands of lives. The device Gregory built in his garage was the first bubble CPAP (BCPAP) device and only small alterations have been made throughout the years (Figure 1A,1B,1C).
As ventilators became better designed for smaller infants and surfactant treatment became commercially available, people used CPAP less for the small babies and bronchopulmonary dysplasia (BPD), the chronic lung disease found in extremely
preterm infants, became more prevalent. It wasn’t until people examined BPD rates between medical school NICUs that people noticed a very low rate at one hospital in New York. That hospital was New York Presbyterian, the exact hospital where Dr. Gregory had invented BCPAP, and where they had continued to use a version of his invention for even the smallest babies. After multiple international trials comparing
About the Author
Noah Hillman, MD is an associate professor in the Department of Pediatrics, Division of Neonatology at Saint Louis University School of Medicine. He specializes in care for newborns, with particular interest in preterm lung injury, mechanical and non-invasive ventilation and bronchopulmonary dysplasia. He treats premature and extremely premature infants, normal and sick newborns and those needing Level II-IV neonatal intensive care. His research interests include ventilator-induced lung injury and the progression of inflammation and injury toward bronchopulmonary dysplasia in preterm infants.
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Bubble CPAP (continued)
16 | vol. 31 | april 2019
CPAP versus intubation and surfactant in thousands of very preterm infants, it is now recognized that initial stabilization with CPAP in the smallest babies decreases the rate of BPD by 10%. Resuscitation guidelines now suggest an attempt of CPAP on all infants with spontaneous breathing. Approximately 50% of infants under 750 grams can be maintained on CPAP and never need intubation. Infants with severe respiratory distress or poor respiratory effort should be intubated to provide adequate ventilation. CPAP can be most consistently given with either T-piece resuscitator or BCPAP device in the delivery room, though a resuscitation bag with a PEEP valve can provide some CPAP to infants.
BCPAP is based on the notion that distending pressure is proportionate to the distance the exhalation tubing is placed below the water level (Figure 1A). The air flows into the oropharynx of the patient until it generates a pressure level (denoted in cmH2O) that is higher than distance under the water, at which point the air more easily flows into the collection chamber. As the air enters the water, it makes bubbles. If you were to listen to the lungs of a baby on BCPAP, you will hear a gentle bubbling sound. The sound, sometimes referred to the ‘noise’ of BCPAP, is the pressure difference that is created when the bubbles are formed and released in the bottle (Figure 1B). If you watch the end of some BCPAP devices, you will see that the bubble distends further into the water (creating more pressure) and when it is released there is a small period of time when the water seems to be inside the tubing (creating less pressure) (Figure 1C). It is this pressure fluctuation that gives BCPAP, in animal models, an advantage over ventilator-derived CPAP for oxygenation and ventilation. When this bubbling is extremely vigorous, the oscillatory pressure can cause similar gas exchange to a ventilator. The higher the flow rate, the more the BCPAP device will bubble and the more frequent the bubble will be formed. We typically use an air flow rate of 8L to generate consistent bubbling within the device. There are subtle differences between the bubble CPAP
devices, and the choice of which system to use is based on institutional preference.
The nasal interface used on the infant can have dramatic impacts on the CPAP level provided to the infant (Figure 2). Initial stabilization of infants in the delivery room is often done with a face mask with either a T-piece resuscitator (Neopuff is a version) or a resuscitation bag. In these situations, it is appropriate to provide 5 or 6 cmH2O of CPAP pressure to help open the lungs and decrease the work of breathing. The CPAP pressure is built up in the oropharynx of the infant and transmitted into the lungs. After initial stabilization on CPAP, the infant is often transferred to either nasal Hudson prong CPAP (Figure 2A), Mask CPAP (Figure 2B) or the RAM cannula (Figure 2C). Different institutions may use different interfaces. If your hospital is using the Hudson prongs or face mask CPAP (multiple companies make both types), then the CPAP is generated in the oropharynx of the infant and the CPAP level correlates moderately well with the level set on the machine or BCPAP bottle (Figure 2D). Unfortunately the RAM cannula has a
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high resistance in the tubing so the CPAP is generated in the RAM cannula cap and only about 65% of the CPAP pressure is transmitted to the infant (Figure 2E). Thus if you use the RAM cannula, like our transport team, then you will likely need to used higher set pressures to achieve the CPAP level of 5 to 6 cmH2O. Our transport team will now begin infants on 6 cmH2O with the RAM cannula and if no improvement increase the pressure to 8 cmH2O. Understanding the nasal interface you are using is important for proper CPAP use, and Neonatology from SSM Health Cardinal Glennon Children’s Hospital can help advise you.
The use of BCPAP through a nasal interface has changed only slightly from the original design published by Gregory in 1971. This simple design can be recreated with a bucket of water, a ruler, an air flow source, and a nasal interface, but has changed how we treat babies in all parts of the world. So the next time you hear the bubbles of CPAP through the back of the premature baby, think about a young physician sitting in his garage late at night with a flashlight and a strange idea.
THE TYPE OF NASAL INTERPHASE USED CAN HAVE DRAMATIC IMPACTS ON THE CPAP LEVEL PROVIDED
FIGURE 2
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18 | vol. 31 | april 2019
Gastroschisis is a birth defect in which a baby’s abdominal wall does not fully form during fetal development causing the bowel and abdominal organs to protrude outside the body. According to the Centers for Disease Control and Prevention (CDC), approximately 1,871 babies with gastroschisis are born in the United States each year.1 The incidence is thought to be rising worldwide.6 Risk factors associated with gastroschisis include a maternal age younger than 20 years, smoking, drug or alcohol use during pregnancy, low body mass index and first trimester genitourinary tract infections.3 In the United States, survival is well over 95%.6
Gastroschisis occurs early in fetal development, around 6-10 weeks gestation. Free floating bowel is often seen on ultrasound in the first trimester. The differential diagnosis includes: ruptured omphalocele, cloacal exstrophy, hernia of the cord and urachal cyst.3
The diagnosis of gastroschisis warrants referral to a specialized fetal care center where level II ultrasound and care coordination can be accomplished as well as prenatal consultations with maternal fetal medicine, pediatric surgery and neonatology. At the SSM Health Cardinal Glennon St. Louis Fetal Care Institute, prenatal consultations include coordination with subspecialty groups as well as a tour of the NICU and meeting with a social worker and nurse coordinator.
Associated congenital malformations, which are more common with omphaloceles, are relatively rare in gastroschisis. Babies with gastroschisis may have fetal growth restriction, polyhydramnios, oligohydramnios, spontaneous preterm delivery and stillbirth.3 As a result, weekly antenatal monitoring typically starts at 32 weeks gestation. Chromosomal abnormalities are rare, and genetic testing is not typically suggested.
Fetal CARE in FOCUS UNDERSTANDING
sutureless closure By Katie Francis, MSN, CPNP
GASTROSCHISIS
About the Author
Katie Francis, MSN, CPNP is a Certified Pediatric Nurse Practitioner and is the program coordinator at SSM Health Cardinal Glennon St. Louis Fetal Care Institiutel.
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Fetal CARE in FOCUS
7 days post bedside reduction
10 days post bedside reduction
20 days post bedside reduction
Sutureless Gastroschisis Repair
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Delivery at a tertiary care center is recommended, where neonatology and pediatric surgery are readily available. Vaginal delivery is acceptable, unless there are obstetrical indications for a cesarean section. Timing of delivery continues to be a topic of debate. Currently, no scientific data exists to show which delivery method (early or closer to term) is better. The Gastroschisis Outcomes of Delivery (GOOD) Study is a new randomized controlled trial endorsed by the North American Fetal Therapy Network (2018) that will look at delivery timing. For more information about this study, visit the GOOD Study website at thegoodstudy.org/GOOD. The SSM Health Cardinal Glennon St. Louis Fetal Care Institute plans to participate in this study when approved as a multicenter trial.
After delivery, parents can expect their newborn to spend several weeks in the Neonatal Intensive Care Unit with co-management by neonatology and pediatric surgery. Immediate postnatal care includes orogastric tube placement and minimizing fluid loss, which can be 2.5 times that of a normal newborn.3
Surgical intervention is a priority for babies with gastroschisis and typically occurs within the first 24 hours of life. There are three main approaches to surgical repair, which have evolved significantly in the last 20 years. The choice of repair is based on surgeon preference and the severity of the defect, including bowel appearance, degree of edema and matting, and patient stability.3
The traditional repair is a primary fascial closure, usually in the operating room, where the eviscerated bowel is reduced back into the abdomen and surgically closed. This approach requires general anesthesia and can lead to increased intraabdominal pressure, inadequate ventilation and prolonged ventilation.5 In the early 2000s, the introduction of the Silastic silo changed surgical care for many of these babies. A sterile spring loaded silo is placed at the bedside and allows for staged reduction of the intestines.5 Silos are still used in conjunction with a delayed surgical fascial closure, or with the newest approach, a sutureless closure technique.
The sutureless closure technique has become standard of care for certain gastroschisis babies at SSM Health Cardinal Glennon Children’s Hospital. This new approach is showing promising results and decreased complications. The sutureless closure uses the baby’s own umbilical cord to close the defect. A large remnant of the umbilical cord is left in place at delivery and draped over the defect. The cord is then held in place by a large
UNDERSTANDING
sutureless closure
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20 | vol. 31 | april 2019
sterile medical dressing. As the umbilical cord dries, epithelialization occurs over the defect.
There are several proposed advantages to the sutureless closure approach. This intervention can be done at the bedside with minimal sedation and, in most cases, no intubation at all.4 In addition, because the fascia is not closed primarily, abdominal compartment syndrome may be less likely.
Dressing changes are performed by the surgery team after the first five to seven days, and then twice
weekly. The orogastric tube will remain in place to decompress the stomach until bowel function is evident. When the infant is passing flatus and has spontaneous bowel movements, enteral feeds may be slowly introduced.
Long-term follow-up for these children includes close monitoring by the
primary physician for growth and development, feeding concerns and nutritional needs. Pediatric surgery will usually follow up one month post discharge and then every three to six months for the first year. Patients with intestinal failure should be referred to a gastroenterologist specialized in intestinal rehabilitation, such as the Glennon Intestinal Rehab and Feeding Team (GIRAF Team) at SSM Health Cardinal Glennon Children’s Hospital. Babies with gastroschisis may have long-term issues with abdominal pain and bowel obstruction. Although usually small for gestational age at birth, these children typically will catch up in growth by the time they are school age.
Although an alarming diagnosis, gastroschisis can be successfully managed with coordinated and collaborative care. The comprehensive teams at Cardinal Glennon Children’s Hospital and SSM Health Cardinal Glennon St. Louis Fetal Care Institute work closely with the patient and primary care physicians to provide the best possible treatment plan from diagnosis through delivery and into childhood.
Gastroschisis (continued)
References
1 Centers for Disease Control and Prevention (2018) Facts about gastroschisis. Retrieved November 12, 2018, from https://www.cdc.gov/ncbddd/birthdefects/gastroschisis.html
2 North American Fetal Therapy Network (2018). Gastroschisis Outcomes of Delivery. Retrieved November 12, 2018, from https://www.thegoodstudy.org/GOOD
3 O’Connell, R. V., Dotters-Katz, S. K., Kuller, J. A., & Strauss, R. A. (2016). Gastroschisis: a review of management and outcomes. Obstetrical & Gynecological Survey, 71(9), 537-544. doi:10.1097/ogx.0000000000000344
4 Pet, G. E., Stark, R. A., Meehan, J. J., & Javid, P. J. (2017). Outcomes of bedside sutureless umbilical closure without endotracheal
intubation for Gastroschisis repair in surgical infants. The American Journal of Surgery, 213, 958-962. doi:10.1016/j.amjsurg.2017.03.017
5 Witt, R. G., Zobel, M., Padilla, B., Lee, H., & MacKenzie, T. C. (2018). Evaluation of Clinical Outcomes of Sutureless vs Sutured Closure Techniques in Gastroschisis Repair. JAMA Surgery. doi:10.1001/jamasurg.2018.3216
6 Zalles-Vidal, C., Peñarrieta-Daher, A., Bracho-Blanchet, E., Ibarra-Rios, D., Dávila-Perez, R., Villegas-Silva, R., & Nieto-Zermeño, J. (2018). A Gastroschisis bundle: Effects of a quality improvement protocol on morbidity and mortality. Journal of Pediatric Surgery, 53(11), 2117-2122. doi:10.1016/j.jpedsurg.2018.06.014
For more information about the GOOD Study, visit their website at thegoodstudy.org/GOOD
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he baseline fetal heart rate (FHR)
is regulated by intrinsic cardiac
pacemakers, cardiac conduction
pathways, autonomic innervation
(sympathetic and parasympathetic
nervous system) and a number of intrinsic and extrinsic factors.1
The intrinsic rate in early gestation is primarily influenced by the
sympathetic nervous system, resulting in a marginally higher baseline
About the Author
Meredith MeyerMSN, RNC-OB, C-EFM is a perinatal outreach educator in the perinatal outreach department at SSM Health St. Mary’s Hospital – St. Louis with clinical nursing experience in high-risk obstetrics. She is an intermediate and advanced instructor of the AWHONN Fetal Heart Rate Monitoring Program.
Fetal TACHYCARDIABy Meredith Meyer, MSN, RNC-OB, C-EFM
The MONITOR Corner
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The MONITOR CornerFetal TACHYCARDIA (continued)
22 | vol. 31 | april 2019
rate in the preterm fetus compared to that of the term fetus. The parasympathetic nervous system has a greater influence as the fetus matures, resulting in a gradual decrease in the intrinsic fetal heart rate.2 A normal baseline fetal heart rate is considered to be 110 to 160 beats per minute (bpm).3 A baseline rate of greater than 160 bpm for 10 minutes or longer is tachycardia. When utilizing electronic fetal monitoring (EFM), the baseline fetal heart rate is determined by evaluating the tracing over at least a 10-minute period of time and approximating the mean rate rounded to the closest 5 bpm interval. Within that 10-minute time period, at least 2 minutes of interpretable tracing is required to determine baseline. The 2 minutes of tracing need not be contiguous, but periods of marked variability and episodic or periodic changes in the fetal heart rate must be excluded.2
While the preterm fetus may be expected to have a higher baseline rate than the term fetus, the difference in rate between 28-30 weeks gestation and term is roughly 10 bpm.2 So in a preterm fetus, it should not be assumed that a FHR baseline of greater than 160 bpm is attributable to prematurity. Furthermore, preterm fetuses have immature compensatory responses resulting in a potentially lower tolerance to stressors.4 A preterm fetus with tachycardia requires physician evaluation to rule out fetal compromise.
Tachycardia results from increased sympathetic or decreased parasympathetic tone.2 (Box 1 provides a list of various conditions that may cause fetal tachycardia.) A number of these conditions are not necessarily indicative of a risk of acidemia, and on its own, tachycardia is poorly predictive for fetal hypoxia or acidemia.2,4 However, it is important to note that tachycardia increases myocardial oxygen demand and may challenge fetal reserve.2 Other components of the fetal heart tracing must be assessed, especially baseline variability as an indicator of fetal acid-base status. Tachycardia in the setting of minimal or absent variability, recurrent decelerations, or both is associated with indeterminate or abnormal fetal acid-base status.4
Appropriate treatment and management of fetal tachycardia is dependent upon identifying the underlying cause. The most common causes during the intrapartum period are maternal fever and medications affecting the heart rate.1,2 Fetal tachycardia related to maternal fever is believed to be the result of the increased fetal metabolic rate in response to the rise in maternal core temperature and not necessarily an indicator of fetal sepsis.2 This highlights the importance of not only treating the maternal infection, but also treatment with antipyretics.5
BOX 1 CONDITIONS POTENTIALLY ASSOCIATED WITH FETAL TACHYCARDIA1,4
MATERNAL Conditions FETAL Conditions
Fever Increased Metabolic Rate
Infection Anemia
Sympathomimetic Medications Metabolic Acidemia
Parasympatholytic Medications Infection or Sepsis
Dehydration Tachyarrhythmia
Hyperthyroidism » Sinus tachycardia
Caffeine » Supraventricular tachycardia
Cocaine » Atrial Fibrillation
Methamphetamine » Atrial Flutter
» Ventricular arrhythmia
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CASE STUDY
27 y/o G3P1011 at 34 1/7 weeks gestation presents to labor and delivery at 1400 with complaint of spontaneous rupture of membranes with clear fluid at approximately 0800.
ADMISSION
VITAL SIGNS BP: 116/64 | P: 113 | R: 18 |Temp: 98.9°F | SpO2: 99%
CERVICAL EXAM 1cm | 50% |-3
EFM TRACING Category II; baseline 165, moderate variability, no contractions per toco or patient report
PLAN OF CARE Treat with PCN for GBS prophylaxis and begin induction of labor with 25mcg misoprostol PV.
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References
1 Miller, D. A. (2017). Intrapartum Fetal Evaluation. In S. G. Gabbe (Ed.), Obstetrics: Normal and Problem Pregnancies (7th ed.). (pp. 308-343). Philadelphia, PA: Elsevier.
2 Lyndon, A., O’Brien-Abel, N., & Rice Simpson, K. (2015). Fetal Heart Rate Interpretation. In A. Lyndon & L. U. Ali (Eds.) Fetal Heart Monitoring: Principles and Practices (5th ed.). (pp. 125-162). Washington, DC: Kendall Hunt.
3 Macones G. A., Hankins G. D. V., Spong C. Y., Hauth J., & Moore T. (2008). The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstetrics & Gynecology, 112(3), 661–666.
4 Freeman, R. K. Garite, T. J., Nageotee, M. P., & Miller, L. A. (2012). Fetal heart rate monitoring (4th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
5 Heine, R. P., Puopolo, K. M., Beigi, R., Silverman, N. S., & El-Sayed, Y. Y. (2017). Committee Opinion No. 712: Intrapartum management of intraamniotic infection. Obstetrics & Gynecology, 130(2), 490–492.
Fetal Tachycardia (continued)
24 | vol. 31 | april 2019
FOUR HOURS LATER
VITAL SIGNS BP: 112/65 | P: 134 | R: 22 | Temp: 99.3°F | SpO2: 100%
CERVICAL EXAM 1-2cm | 75% | -3
EFM TRACING Category II; baseline 185, minimal variability, patient reports occasional contractions, none per toco, toco adjusted
PLAN OF CARE Continue induction with oxytocin IV infusion
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45 MINUTES LATER
VITAL SIGNS BP: 121/77 | P: 132 | R: 22 | Temp: 100.9°F | SpO2: 99%
CERVICAL EXAM Unchanged
EFM TRACING Category III; baseline 185, absent variability, recurrent variable decelerations
PLAN OF CARE Cervix remains unchanged, intrauterine resuscitative measures did not resolve EFM pattern, delivered by emergent cesarean 15 min later
CASE STUDY OUTCOME
✓ Cesarean delivery under general anesthesia of 4250g infant with Apgars 2, 7 at 1 and 5 minutes, respectively
✓ Cord arterial blood gas revealed a respiratory acidosis. Infant blood cultures returned negative
✓ Patient received antibiotics in the immediate postpartum period for suspected intraamniotic infection
✓ Placental pathology revealed acute chorioamnionitis
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St. Mary’s Hospital – St. LouisCardinal Glennon Children’s Hospital
SSM Health Cardinal Glennon Children’s Hospital1465 S. Grand Blvd.St. Louis, MO 63104
ADDRESS SERVICE REQUESTED
Continuing Education OpportunitiesMany continuing education opportunities, including traditional lectures, hands-on skills sessions, as well as online presentations, are available for perinatal professionals in eastern Missouri and southern Illinois. These are offered through SSM Health St. Mary’s Hospital – St. Louis, SSM Health Cardinal Glennon Children’s Hospital, Saint Louis University School of Medicine and the Perinatal Outreach Program. Most programs offer nursing contact hours and/or CMEs.
For course calendars or more specific information on programs, please go to cardinalglennon.com/perinataloutreach or call the Perinatal Outreach Program at 314-577-5317.
©2019 SSM Health. All rights reserved. SM-STL-16-172723-R03 04/19
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