Download Maternal Renal Insufficiency

Running head: MATERNAL RENAL INSUFFICIENCY/FAILURE
Maternal Renal Insufficiency/Failure
Presented to:
Debra Armentrout, APRN, MSoN, NNP-BC, PhD
and
Sandra Priest, RN, MSN, NNP-BC
In Partial Fulfillment
Of the Requirements for the Course
GNRS 5631 Neonatal Nurse Practitioner I
By:
Alaana Garris, RNC, BSN
On:
March 22, 2016
THE UNIVERSITY OF TEXAS MEDICAL BRANCH
AT GALVESTON
SCHOOL OF NURSING
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With advancements in medical technology and a newer staging systems for identifying
chronic kidney disease (CKD), more women are being diagnosed with renal insufficiency or
renal failure at an earlier age (Hussain, Karovitch, & Carson, 2015). Women are also waiting
longer to have children and with advancing maternal age, the likelihood of renal disease prior to
pregnancy is higher. Although information about pregnancy in the woman with renal disease is
limited, available treatment options are advancing and so is the information. Although maternal
morbidity is improving, maternal renal insufficiency poses risk the fetus even with advancing
knowledge of renal disease and treatment options
Pathophysiology of Renal Failure
Kidneys are the organs responsible for regulating water and electrolytes as well as
eliminating waste from the blood. The renal system serves a vital function in regulating vitamin
D activity, production of erythrocytes, glycogenesis, and control of arterial blood pressure
(Blackburn, 2013). Chronic kidney disease is identified by structural or functional abnormalities
for more than 3 months along with having accumulation of waste products in the blood (Ferri,
2016). Causes of CKD are diabetes, hypertension, chronic glomerulonephritis, polycystic kidney
disease, tubular interstitial nephritis, obstructive nephropathies, vascular disease, and
autoimmune disease with diabetes and hypertension being the most prevalent (Ferri, 2016).
According to Whittier and Lewis, (2014) because each of the causes of CKD have a different
pathophysiology mechanisms for which it causes damage to the kidneys, the treatment must be
aimed at correcting the underlying disease process in an effort to slow or stop its progression.
Specific alterations occur to many parts of the renal system during pregnancy. Normal
physiologic changes include an increase in renal blood flow by up to eighty percent. Renal
tubular function has an increase in reabsorption of solutes. Glomerular filtration rate increases
forty to sixty percent and the renin-angiotensin-aldosterone system has an increase in all
components. Normal structural changes occur as well, including dilatation of the renal calyces
MATERNAL RENAL INSUFFICIENCY/FAILURE
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and pelvis. Size alterations in the ureters are caused by decreased motility and hypertonicity of
the ureter and the kidney itself enlarges due to the increased renal blood flow (Blackburn, 2013).
Pregnancy is difficult to achieve for the woman with renal failure because of the
accompanying endocrine changes that lead to a decline in fertility (Nadeau-Fredette,
Hladunewich, Hui, Keunen, & Chan, 2013). Normal renal changes that occur during pregnancy
are not well tolerated by women with already compromised renal function and may actually
accelerate the progression of the underlying renal disease. The mechanism of why pregnancy
tends to increase the progression of renal failure is unknown, however Vellanki (2013) discusses
how the non-pregnant patient when experiencing prolonged periods of renal vasodilation has an
“increase in intraglomerular pressure contributing to further progression of renal disease” (p.
224). With normal changes in pregnancy, intraglomerular pressure is increased and there is
significant renal vasodilation. This could indicate the same mechanism could be true for the
progression of renal disease in pregnancy.
Physiological Impact of Maternal Renal Failure on the Fetus
Fetal and placental nutrition is completely dependent upon placental metabolism and is
vitally important in the early gestational period (Blackburn, 2013). Mother’s with renal disease
have decreased perfusion to the developing placenta an is directly related to the mother’s
compromised ability to adapt to the increase in maternal intravascular blood volume and
reduction in vascular tone. Diminished perfusion to the placenta during its development and
throughout pregnancy causes an equal decrease in the transportation of nutrients and oxygen
which deprives the developing fetus of sustenance (Redline, 2015). A poorly functioning
placenta, termed uteroplacental vascular deficiency, is considered insufficient to meet the needs
of the fetus.
An insufficient placenta is notably smaller and has less surface area for vital
transportation of nutrition and oxygen to the fetus. When microscopically examined, an
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insufficient placenta “has a decreased number of glucose and amino acid transporters… resulting
in fetal hypoglycemia and hypoxemia” (Calkins & Devaskar, 2015, p. 232). Neonates with
placental insufficiency are at a higher risk for complications such as polycythemia due to chronic
in utero hypoxia, meconium aspiration syndrome due to intrauterine stress, and perinatal
asphyxia due to insufficient placental perfusion and intolerance to labor (Gooding & McClead,
2015). Other associated factors of placental insufficiency is poor organ growth and less than
ideal fetal structure. The fetus adapts to its suboptimal environment by concentrating available
nutrition to brain preservation resulting in an asymmetric fetal growth pattern (Brand & Boyd,
2015).
Intrauterine growth restriction (IUGR) occurs when an infant is not able to reach its
genetic growth potential due to maternal, fetal, or environmental factors. In the case of maternal
renal insufficiency the factor causing growth restriction is maternal in nature. According to
Chonchol, et al., (2015), infants born to mothers with kidney disease are two times more likely to
have low birth weight. Prenatally, IUGR is determined by “diminished growth velocity” in more
than one documented ultrasound evaluation (Smith, 2012, p. 86). Ideally, the best time to deliver
a neonate once IUGR is diagnosed is before the fetus is severely compromised (Calkins &
Devaskar, 2015), therefore timing of delivery is crucial. There is a narrow margin for timing of
delivery to maximize gestation while minimizing fetal compromise.
IUGR infants have a higher morbidity and mortality than their appropriate for gestational
age counterparts. These infants are more likely to be delivered by cesarean section and to be
admitted into the neonatal intensive care unit. Outcomes for infants with growth restriction are
hypoglycemia due to decreased glycogen stores, hypothermia due to decreased brown fat,
polycythemia secondary to in utero hypoxia, and poor feeding related to decreased muscle tone
and stamina (Calkins & Devaskar, 2015).
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Preterm birth is a physiological impact of maternal renal insufficiency. When fetal
development is halted before the end of 37 weeks gestation, a myriad of pathophysiologic events
take place in each body system. The premature neonate’s ability to adapt to extrauterine life is at
best difficult and is completely dependent on their degree of immaturity. Lawn, et al., (2013)
describes how infants born prematurely, even those that are late preterm (delivery between 35
and 37 weeks gestation) suffer significant adverse effects even into adulthood.
Respiratory complications are related to pulmonary immaturity, lack of surfactant, and
chronic lung damage related directly to the immaturity and surfactant deficiency (Smith, 2012).
Another aspect of respiratory complications of prematurity is apnea of prematurity and is related
to the immature mechanisms that control the neonate’s respiratory drive. Cardiovascular issues
such as hypotension related to hypovolemia, septic shock, and cardiac dysfunction are often
accompanied and exacerbated by a delay in the closure of the patent ductus arteriosus.
Neurologic complications such as increased risk for intracranial hemorrhage is a
significant concern for the infant’s mortality and overall cognitive function. Ophthalmologic
problems are associated with infants born before 32 weeks gestation. These groups of preemies
are at a higher risk for developing retinopathy of prematurity which can lead to retinal
detachment and blindness. Hematologic and immunologic concerns include anemia,
hyperbilirubinemia, diminished humoral responses as well as cellular responses to infection
(Diehl-Jones & Fraser, 2015).
Renal difficulties are caused by a decrease in glomerular filtration rate which make fluid
and electrolyte balance difficult for the neonate. Metabolic complications are triggered by a
diminished ability for metabolism of such elements as glucose and calcium (Smith, 2012).
Nutritional concerns are of upmost importance due to the premature infant’s specialized need for
caloric intake, which is often impaired by their intolerance to enteral nutrition. Premature
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neonates are at a high risk for developing necrotizing enterocolitis which is a complication with a
high mortality rate.
Therapeutic Treatment Options of Maternal Renal Failure and their Effect on the Neonate
As mentioned earlier, close monitoring is key in determining whether the fetus is in
distress and if delivery is necessary. Monitoring is done with nonstress and oxytocin challenge
tests, a biophysical profile, fetal “kick” counts, and frequent evaluation of growth and amniotic
fluid volumes by ultrasound (Smith, 2012). If any indication of poor fetal well-being is
discovered, bedrest and management of underlying complication is recommended if imminent
delivery is not required.
Outpatient management can be accomplished with women who have ready access to
medical facilities, can demonstrate compliance to bedrest, and who have an understanding of the
symptoms of worsening renal disease as well as signs of preeclampsia. For women who do not
display responsible outpatient management with compliance and close follow up care,
hospitalization may need to be considered until delivery occurs (Jeyabalan, 2015). If early
delivery is suspected or anticipated, administration of corticosteroids should be considered.
Jeyabalan (2015) states “As per the National Institutes of Health consensus guidelines, antenatal
glucocorticoids should be administered to women less than 34 weeks gestation who are at risk
for preterm delivery to decrease neonatal morbidity and mortality” (p. 256).
Women with CKD are at best mildly hypertensive thus creating a prime foundation for
the development of preeclampsia during pregnancy (Vellanki, 2013). It is widely known that
hypertension in pregnant women is associated with maternal and fetal morbidity. This morbidity
is related to the development of preeclampsia (Hussain, Karovitch, & Carson, 2015). Blood
pressures in the pregnant population actually decrease during the first trimester and reaches their
lowest values around the 20th week of gestation. After this time frame blood pressures will
return to normal values and anything higher than pre-pregnancy values could indicate the
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beginnings of preeclampsia (Hussain, Karovitch, & Carson, 2015). According to Vellanki
(2013), administration of low-dose aspirin (50-150 mg) starting at 12 weeks gestation and
continuing until delivery can reduce the risk of preeclampsia in the pregnant patient with CKD.
Clinical presentation of preeclampsia varies widely from patient to patient. Frequent
antenatal visits should be routine management for the patient with renal insufficiency to closely
monitor for changes in maternal blood pressure and proteinuria. Clinical manifestations of
preeclampsia include headaches, visual changes, epigastric pain, unusual nausea or vomiting,
swelling of the hands and face, as well as decreased urine output (Jeyabalan, 2015). All patients
should be questioned upon each prenatal visit about such symptoms and those with renal
insufficiency should be more acutely aware of these symptoms and instructed to seek medical
attention if they should develop.
Often the use of antihypertensives are initiated prior to conception because of the already
established chronic hypertension that goes along with renal disease. Angiotensin-converting
enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) are a popular medication
used to manage hypertension for patients with CKD. These however should be stopped when
pregnancy is diagnosed due to the possibility of teratogenic effects on the fetus (Hussain,
Karovitch, & Carson, 2015). Hussain, Karovitch, and Carson (2015) also claim that
pharmacologic management of hypertension “should mirror that of the non-pregnant patient” (p.
168). Methyldopa is considered one of the first-line medications for treatment of hypertension in
the pregnant woman and has been used as such since the 1960’s (Hussain, Karovitch, & Carson,
2015). Other pharmaceuticals that are used to control hypertension during pregnancy include, in
order of preference, Labetalol, Nifedipine, Hydrochlorothizide and Hydralazine.
It is suggested that attempting to keep too tight of control on maternal blood pressure
could actually be harmful by increasing the risk for hypotension and further decreasing perfusion
to the fetus (Nadeau-Fredette, Hladunewich, Hui, Keunen, & Chan, 2013). Hypertension in the
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pregnant patient with CKD according to Hussain, Karovitch, & Carson (2015) should be treated
to prevent more severe damage to the kidneys, but should be tailored specifically to each
individual taking into consideration their comorbidities, symptoms, and compliance with
treatment.
It is recommended that women with advanced kidney disease to delay pregnancy until
after successful renal transplantation due to the high rate of pregnancy induced complications to
both the mother and her fetus (Nadeau-Fredette, Hladunewich, Hui, Keunen, & Chan, 2013).
However, delay in conception is not always achieved and women who choose to carry out a
pregnancy must have intensive prenatal and renal care to have a successful pregnancy. When it
comes to pregnancy and renal replacement therapy, “dialysis remains the most readily available
method” (Alkhhunaizi, Melamed, & Hladunewich, 2015, p. 253). This method is however not
without its concerns. Fetal polyhydramnios and severe maternal anemia appear to be the most
prominent concern directly related to the maternal-fetal dyad receiving dialysis.
When conception takes place for a woman when she is already receiving dialysis, the
prognosis is poorer than those who conceive prior to beginning treatment. Alkhhunaizi,
Melamed, and Hladunewich (2015) explain that this may be due to the existing residual kidney
function and the clearance of urea as well as other solutes. For those with end-stage renal
disease and with no residual kidney function, adequate dialysis is vital to a successful pregnancy.
When a young woman with advanced kidney disease becomes pregnant, the amount of dialysis
treatment should be increased to a minimum of 20 hours per week (Nadeau-Fredette, et al.,
2013).
Intensive hemodialysis is described as greater than 24 hours per week of treatment. In a
study review by Nadeau-Fredette, et al (2013), it was shown that increasing dialysis time to a
minimum of 24 hours per week and up to 48 hours per week of treatment provided the best
pregnancy outcomes. Fetal polyhydramnios is best controlled with intensive dialysis and is
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directly related to the improved maternal urea concentration. Intensive dialysis appears to have
better maternal volume control but requires very specific and close management of the
components of the dialysate (Nadeau-Fredette, Hladunewich, Hui, Keunen, & Chan, 2013). The
components of the dialysate must account for normal changes that occur in pregnancy. For
example, decreasing the bicarbonate accounts for the natural respiratory alkalosis that
accompanies pregnancy and increasing the calcium in the dialysate assists in fetal skeletal
growth. Nadeau-Fredette, et al., (2013) also confirms that “intensive hemodialysis is a
promising therapy to improve conception rate and outcomes of pregnancies in women on
dialysis” (p. 247).
Neonatal Clinical Manifestations at Birth and Within the First 36 Hours of Life
The majority of the clinical manifestations for the neonate born to a mother with renal
disease will be determined by the extent of the neonate’s prematurity. As discussed earlier
prematurity affects all of the body systems and will all need to be supported to provide the best
quality of life and the best chance at reducing morbidity and mortality for the neonate.
Prematurity is classically manifested with respiratory insufficiency, cardiovascular compromise,
hypoglycemia, and hypothermia (Smith, 2012). At birth immediate resuscitation and
stabilization of all systems are to be initiated and continued until the infant is stable or care is
redirected.
Identification of infants that are IUGR is important as they have special considerations
for their transition to extrauterine life. Suspicion of IUGR starts with close review of maternal
history and is confirmed with the use of gestational age scoring and growth charts to determine
where the infant plots on an appropriate growth curve. IUGR can be estimated when an infant
plots 2 standard deviations below the mean weight and length for gestation on a standardized
growth chart (Gooding & McClead, 2015). Another option for determination of IUGR is the use
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of the ponderal index. This index helps to identify infants whose soft tissue mass is below the
stage of their skeletal development. The formula for determining ponderal index is;
𝐵𝑖𝑟𝑡ℎ𝑤𝑒𝑖𝑔ℎ𝑡 𝑥 100
𝑐𝑟𝑜𝑤𝑛 𝑡𝑜 ℎ𝑒𝑒𝑙 𝑙𝑒𝑛𝑔𝑡ℎ
= Ponderal Index
A ponderal index of less than 10 percent identifies infants that are IUGR (Gomella, Cunningham,
& Eyal, 2013).
Chronic intrauterine hypoxia and preeclampsia are the most common causes for
thrombocytopenia in preterm infants. A neonate with a platelet count of less than 150,000/mm3
is considered thrombocytopenic (Gomella, Cunningham, & Eyal, 2013) and is at risk for
hemmorhage. Thrombocytopenia in neonates can be caused by a number of factors that should
not be overlooked, but knowledge that an infant’s response to a suboptimal environment when its
mother has CKD is a diagnostic benefit. Clinical manifestations of thrombocytopenia include
platelet-type bleeding such as petechiae, purpura, ecchymosis cephalhematoma, bleeding from
GI tract, mucous membranes and superficial abrasions (Diehl-Jones & Fraser, 2015). Signs of
thrombocytopenia can be seen immediately after birth and until the platelet levels return to
normal.
Maternal hypertension, placental insufficiency, and growth restriction, all of which are
linked to maternal renal disease, can directly stimulate erythropoietin production in the fetus.
Over stimulation of erythropoietin production in the fetus is typically related to fetal hypoxia
exposure (Gomella, Cunningham, & Eyal, 2013) and causes an overproduction of erythrocytes to
be released into to blood stream. Polycythemia is diagnosed when a central venous hematocrit is
greater than 65 percent. Clinical manifestations of polycythemia include plethora, cyanosis,
lethargy, jitteriness, respiratory distress, tachycardia, hypoglycemia, and poor feeding (DiehlJones & Fraser, 2015). Signs and symptoms of polycythemia can be seen immediately following
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birth and persist until the hematocrit returns to normal.
Evidence Based Management Guidelines in Caring for the Mother with Renal Insufficiency
Women with risk factors for IUGR or whom IUGR is diagnosed should receive intensive
monitoring to ensure fetal well-being. As discussed earlier, the timing of delivery relies heavily
on the health of the fetus. Timing of delivery can be difficult and must be done prior to
compromise while making all efforts to reach maximal gestational age. According to Lausman
and Kingdom (2013) guidelines for clinical monitoring of IUGR include, counseling on smoking
cessation, first and second trimester screening for aneuploidy, and maternal-fetal medicine
consult. Placenta and uterine artery Doppler imaging via ultrasound is recommended at 19 to 23
weeks’ gestation. Low dose aspirin therapy can be initiated as well as administration of
corticosteroids to enhance fetal lung maturity. Perhaps most importantly though is frequent
prenatal visits to facilitate early recognition of complications with the use of serial ultrasounds.
In a series titled Born Too Soon, Lawn, et al., (2013) focuses on the care of the preterm
infant and explains how “Detailed quality of care protocols for almost every aspect of care have
improved quality” (p. 3). Three “care packages” are described within this article and are broken
down according to specific categories of infants. Package one: Essential Newborn Care is
intended for all newborns and focuses on warmth, feeding support, and cleanliness. Package
two: Extra Care for Small Babies focuses on package one in addition to extra support for feeding
and provision of kangaroo care for infants weighing less than 2,000 grams. Package three: Care
for Preterm Babies with Complications focuses on both package one and two and integrates extra
focus on complications of the very low birth weight infant (Lawn, et al., 2013). These guidelines
although relatively vague create a good foundation for evidence based practice for preterm
babies and other newborns with special needs.
Impact of Emotional and Economic Implications on the Family Unit
MATERNAL RENAL INSUFFICIENCY/FAILURE
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Infants born to mothers with chronic kidney disease have a 71 percent increase in
likelihood to be admitted to the neonatal intensive care unit (Chonchol, et al., 2015). Living
through a high risk pregnancy is difficult in itself but with the addition of a preterm birth or an ill
newborn, this is a stressor that most families are not emotionally prepared to deal with.
Emotional stress of this magnitude on the family unit is enough to put them into crisis (Kenner &
Boykova, 2015). Kenner and Boykova (2015) describe crisis as being a period of time when
“people face an important problem or transitional phase so stressful that they are unable to cope
by their customary problem-solving resources” (p. 331). During a time of crisis, families will
often display signs of anxiety, nervousness, fear, and depression, all of which can inhibit their
ability to clearly communicate and comprehend what is happening with their infant.
In a study published in 2015, the cost of the hospital stay for the late preterm infant and
the preterm infant was significantly higher than that of a healthy full term newborn (Khan, et al.,
2015). Resource use was shown to be higher in this population as well as the amount of care
required post discharge. Follow up healthcare management for up to 2 years also showed to be
more than that of the healthy newborn further increasing the burden of medical costs to the
family even after discharge (Khan, et al., 2015).
According to a policy statement from the American Academy of Pediatrics, the
recommended length of stay for newborns is 48 to 72 hours to ensure a safe discharge for the
health of both the mother and her baby (Benitz, 2015). Infants who are born to mothers with
chronic conditions and who are at a higher risk of complications tend to have an increased length
of stay in the hospital at birth and higher readmission rates. A prolonged hospital stay is very
cumbersome for parents. There is often other children involved that have to be tended to while
parents are trying to visit the baby. A delay in returning to work due to the need to be available
for the infant is very hindering to a family unit both financially and emotionally. However, in a
study reviewing shortened length of hospital stay for very premature infants, Gonya, Martin,
MATERNAL RENAL INSUFFICIENCY/FAILURE
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McClead, Nelin, and Shepherd, (2014) noted that the intense involvement of families with their
infants in the neonatal intensive care units reduced the overall length of stay for their newborns.
This theory would also be applicable for the high-risk babies born to mothers with renal disease
since their babies are likely to be ill and have longer length of hospitalization.
Conclusion
Although maternal morbidity is improving with advancing knowledge of renal disease
treatment options during pregnancy, it still poses a significant risk the fetus. Even with the
continued high rate of fetal loss for pregnant women with renal disease, there is an increase in
the number of surviving pregnancies. This is directly related to good maternal care, early
diagnosis of renal disease and better knowledge of the available treatment options. However,
neonatal morbidity is still prevalent due to the complications of maternal renal disease. Infants
born early, infants born small, and infants born chronically exposed to hypoxemia in utero have
life-long sequelae. Beyond the initial hurdles of birth with these odds, there is also cognitive,
functional and learning impairments that may persist through adulthood. Survival of pregnancy
with the best possible outcomes for women with renal impairment is completely dependent on
the mother’s compliance with care, knowledge of her risks and close monitoring by her
physicians.
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