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needed. A Cochrane review found no randomized controlled trials on ephedrine

in the treatment of neonatal MG.
D. Other. Exchange transfusion and IV immunoglobulin have been used with some
benefit in the few infants who are resistant to anticholinesterase therapy. Adults
with MG (including pregnant women) are currently being managed with a variety
of other treatments including steroids, immunosuppressants, immunomodulators,
chemotherapeutics, thymectomy, and plasmapheresis, and their potential effects on
the fetus and neonate should be considered.
E. Caution with medications. Many medications interfere with the neuromuscular
junction and may worsen MG or be associated with an exacerbation. Medications
that should be avoided include antibiotics (aminoglycosides, tobramycin, macrolides,
clindamycin, ampicillin [safe but some cases of respiratory depression reported]),
high-dose steroids, β-blockers, neuromuscular blocking agents, antiarrhythmic med-
ications, some anticonvulsants, and ophthalmologic medications (Timolol).
VIII. Prognosis. TNMG can be life-threatening if not identified and treated promptly, but
for the majority of infants, it is a transient illness with no lasting effects. Symptoms
last for an average of 18 days (5 days to 4 weeks), and full recovery is seen in 90% of
patients by 2 months of age. The remaining 10% of patients recover by 4 months. In
rare cases, symptoms persist and can lead to permanent disability including persistent
myopathy, multiple joint contractures, dysarthria, velopharyngeal incompetence, mild
learning disabilities, and hearing impairment. Rarely, persistent myopathic sequelae
(usually facial and bulbar myopathy) have been reported following TNMG and can be
caused by maternal antibodies against the AChR-γ subunit. Fetal AChR inactivation
syndrome (FARIS) should be considered in this group of infants, especially those with
marked dysarthria and velopharyngeal incompetence. Treatment with albuterol was
beneficial in 1 child with this disorder. Infants with TNMG should be followed up for
subtle myopathic signs and potential complications.

109 Necrotizing Enterocolitis

I. Definition. Necrotizing enterocolitis (NEC) is an ischemic and inflammatory necrosis
of the bowel primarily affecting premature neonates after the initiation of enteral feeding.
II. Incidence. NEC develops in 4% to 10% of infants weighing <1500 g, with the high-
est incidence in the most premature infants. About 10% of NEC cases occur in term
infants, many of whom have preexisting medical conditions.
III. Pathophysiology. Multifactorial theory has been suggested in which several risk fac-
tors, including prematurity, formula feeds, ischemia, and altered intestinal microbiota,
interact to initiate mucosal damage via a final common pathway involving activation
of the inflammatory cascade. A recently proposed unifying hypothesis suggests that
the premature intestine exists in a hyperreactive state with higher expression of toll-
like receptor-4 (TLR-4). Activation of TLR-4 by lipopolysaccharide from colonizing
gram-negative bacteria leads to inflammation, impaired healing (impaired crypt stem
cell function), and apoptosis of enterocytes. Translocation of bacteria leads to TLR-4
activation on the endothelium of the bowel mesentery, leading to intestinal ischemia
via decreased production of endothelial nitric oxide. This and other described pathways
(eg, those involving platelet-activating factor [PAF]) may lead to intestinal necrosis.
The process can be exacerbated by an upregulation of proinflammatory T-helper cells
and activation of intestinal macrophages.

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IV. Risk factors

A. Prematurity. There is an inverse relationship between gestational age (GA), birth
weight, and risk for developing NEC. Although most preterm infants develop NEC
at postmenstrual age (PMA) of 30 to 32 weeks, various factors resulting from pre-
mature birth places them at increased risk for NEC. These may involve immature
mucosal (mucin) barrier, mucosal enzymes, and various gastrointestinal (GI) hor-
mones, as well as immature bowel motility and function. Premature infants have
immature local host defenses and may have an imbalance between pro- and anti-
inflammatory factors, and thus have increased activation of inflammatory media-
tors and decreased inactivation of specific mediators such as PAF, which have been
linked to NEC. Abnormal TLR-4 signaling in the premature intestine and increased
activation of nuclear factor-κB (NFKB) may play a role in the pathogenesis of NEC.
An inability to effectively regulate the intestinal microcirculation and differences
in bacterial colonization may also make preterm infants more susceptible to NEC.
B. Abnormal intestinal microbiome. Microbial colonization of the intestine starts in
utero and is dependent on the mode of delivery, level of maturity, and exposure to
antibiotics. During the first week of life in healthy infants, the intestinal microbi-
ome changes to a preponderance of organisms (eg, Bifidobacterium longum subspe-
cies infantis and lactobacilli) capable of consuming human milk oligosaccharides
(HMO). These normal microbiota play a symbiotic role with the intestine through
toll-like receptors by regulating the expression of genes involved in intestinal physi-
ology, postnatal maturation and function (eg, barrier, digestion, angiogenesis, and
production of immunoglobulin A [IgA]), and protection against more pathologic
organisms. Exposure to prolonged antibiotic courses (>5 days) or increased use of
H2 blockers can lead to colonization with gram-negative bacteria (intestinal dys-
biosis), which promotes inflammation and apoptosis by signaling pathways such
as NFKB. Abundance of proteobacteria (gram-negative facultative bacteria such
as Escherichia coli and Klebsiella) and underrepresentation of obligate anaerobic
bacteria such as Firmicutes and Bacteroidetes in infants’ intestines has been noted
before NEC develops. Although several bacteria and viruses have been implicated
in NEC, blood cultures are positive in only 20% to 30% of cases.
C. Enteral feedings. NEC is rare in unfed infants, and 90% to 95% infants with NEC
have received at least 1 enteral feed. Enteral feeding provides necessary substrate for
proliferation of enteric pathogens. Hyperosmolar formulas/medications may alter
mucosal permeability and cause mucosal damage. Short-chain fatty acids, produced
as a result of colonic fermentation, may add to the damage.
Breast milk significantly lowers risk of NEC. Mammalian breast milk is a bio-
logic fluid that has been highly conserved for millions of years to provide survival
advantage to the newborn. It contains immune cells, growth factors (eg, epidermal
growth factor), anti-inflammatory factors (eg, interleukin [IL]-10), secretory IgA,
lactoferrin, and live bacteria. It also contains HMOs that have no nutritive value
for the infant but can be consumed by bacteria such as B infantis and help protect
and develop the neonatal GI tract. Additionally, breast milk inactivates PAF as well
as inhibits TLR-4 signaling. In 1 study, receiving a diet of >50% breast milk in the
first 14 days of life resulted in an 83% reduction in the incidence of NEC.
D. Intestinal ischemia. During periods of hypoxia/ischemia, blood is diverted away
from the splanchnic circulation (diving reflex). This is usually followed by reper-
fusion, which may lead to oxidant damage and bowel injury. Imbalance between
vascular dilator (eg, endothelial nitric oxide) and constrictor (eg, endothelin-1)
molecules leads to defective splanchnic blood flow autoregulation and may contrib-
ute to injury. Infants who subsequently develop NEC have been shown (by Doppler
flow) to have higher flow resistance in the superior mesenteric artery on the first
day of life. Infants with a symptomatic patent ductus arteriosus are at higher risk
for NEC possibly due to intestinal ischemia associated with aortopulmonary shunt
and diastolic steal. A diminished blood supply to the gut in infants exposed to

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maternal cocaine (and other vasoconstrictive drugs) may also increase the risk for
NEC. Most term infants who develop NEC have predisposing conditions associated
with hypoxia/ischemia including congenital heart disease (eg, hypoplastic left heart
syndrome), polycythemia/hyperviscosity, and birth asphyxia.
E. Other factors. A recent study has found an association between maternal cigarette
smoking during pregnancy and development of NEC in the newborn infant. The
underlying mechanism may be the effect of nicotine on blood vessel development
in the fetal GI tract. A significant association between red blood cell transfusion
and NEC has been reported in some retrospective studies, with about 25% to 35%
of NEC cases occurring within 48 hours of packed red blood cell (PRBC) trans-
fusions. However, 3 randomized controlled trials performed to date comparing
liberal versus restrictive blood transfusion parameters have not shown a causative
relationship. A recent prospective, multicenter observational cohort study found
that, among very low birthweight infants, severe anemia, but not PRBC transfu-
sion, was associated with an increased risk of NEC. It is possible that anemia may
place significant stress on the intestine, leading to reperfusion-type injury follow-
ing transfusion. H2-receptor antagonists, which are inhibitors of gastric acid pro-
duction, increase the gastric pH, which may enhance pathogenic bacterial growth
and increase the risk of NEC. Finally, a genetic predisposition, through variation
in pattern recognition receptors such as TLR-4 and NFKB, can lead to unregu-
lated inflammation and NEC. In addition, immune-modulating single nucleotide
polymorphisms involving certain cytokines (eg, IL-6) and growth factors (eg,
transforming growth factor-β1) have been associated with severe NEC. Similarly,
alterations in antioxidants, vascular endothelial growth factor, arginine, and nitric
oxide may also increase the risk for developing NEC.
V. Clinical presentation. Although term infants who develop NEC are often diagnosed
in the first week of life, most premature infants who develop NEC are older than
14 days or at 30 to 32 weeks’ PMA. Most of them are healthy, feeding well, and grow-
ing. The early clinical presentation may include feeding intolerance, increased gastric
residuals, and blood in stools. Specific abdominal signs include abdominal distension,
tenderness, abdominal skin discoloration, and bilious drainage from nasogastric tube.
Systemic symptoms are nonspecific (similar to those of neonatal sepsis) and include
increased apnea/bradycardia episodes, temperature instability, hypotension, and circu-
latory shock. The clinical course of NEC is variable. Although about 30% may have a
mild presentation that responds to medical treatment, about 7% may have a fulminant
course with rapid progression to NEC totalis, septic shock, severe metabolic acidosis,
and death. The modified Bell’s staging criteria are often used to classify NEC accord-
ing to clinical and radiographic presentations and are broken down into 3 stages.
A. Stage I: Suspected necrotizing enterocolitis. Characterized by nonspecific sys-
temic signs, such as temperature instability, apnea, and lethargy. Abdominal signs
include increased gastric residuals, abdominal distention, emesis, and heme-pos-
itive stool. Abdominal radiographs may be normal or show dilation of the bowel
loops consistent with mild ileus. There is disagreement among experts in the field
regarding whether or not the entity described as Bell stage I is actually NEC.
B. Stage II: Proven necrotizing enterocolitis. Includes symptoms and signs of stage
I plus absent bowel sounds with abdominal tenderness. Some infants have cel-
lulitis of the abdominal wall or a mass in the right lower quadrant. Other findings
include mild metabolic acidosis and thrombocytopenia (stage IIb). Radiographic
signs include pneumatosis intestinalis with or without portal venous gas (PVG).
(See Figures 12–27 and 12–28.)
C. Stage III: Advanced necrotizing enterocolitis. Findings include severe respiratory
and metabolic acidosis, respiratory failure, hypotension, oliguria, shock, neutrope-
nia, and disseminated intravascular coagulation (DIC). The abdomen is tense and
discolored with spreading erythema, edema, and induration (signs of peritonitis).
The hallmark radiographic sign is pneumoperitoneum (free air; see Figure 12–26).

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VI. Diagnosis. NEC is a tentative diagnosis in any infant presenting with the triad of feed-
ing intolerance, abdominal distension, and grossly bloody stools.
A. Laboratory studies. These tests should be performed and repeated as necessary:
1. Complete blood count with differential. The white blood cell count is fre-
quently either elevated with increased left shift or depressed with low neutrophil
count (neutropenia). Thrombocytopenia is often seen.
2. C-reactive protein (CRP) correlates with the inflammatory response. Because
initial CRP may be normal, serial CRP levels done at 12- to 24-hour intervals
are more useful. Markers of inflammation, such as tumor necrosis factor-α, Il-6,
IL-8, fecal calprotectin levels, and urine intestinal fatty acid-binding proteins,
have been suggested as screening tools but have not gained widespread use.
3. Blood culture for aerobes, anaerobes, and fungi (Candida species) is indicated.
4. Stool cultures for rotavirus and enteroviruses may be useful when there is clus-
tering of cases within a single unit.
5. Electrolyte panel may show hyponatremia and hyperkalemia.
6. Arterial blood gas measurements often show metabolic or combined acidosis.
7. Coagulation studies include prothrombin time (PT), partial thromboplastin
time (PTT), fibrinogen, and fibrin degradation products (FDP and d-dimer). An
elevated PT, PTT, and FDP indicate DIC, a frequent complication of severe NEC.
B. Imaging and other studies
1. Radiographs of the abdomen (supine with left lateral decubitus or cross-
table views)
a. Suspicious for necrotizing enterocolitis. Abnormal bowel gas pattern, ileus,
dilated or thickened bowel loops.
b. Confirmatory for necrotizing enterocolitis. Pneumatosis intestinalis, PVG
(in the absence of umbilical venous catheter (see Figures 12–27 and 12–28),
and free air (pneumoperitoneum). Left lateral decubitus or cross-table views
are very helpful in confirming free peritoneal air. Serial radiographic stud-
ies of the abdomen should be obtained every 6 to 8 hours in the presence
of pneumatosis intestinalis or PVG to look for pneumoperitoneum because
these infants are at risk for bowel perforation within 48 to 72 hours of dis-
ease onset.
2. Abdominal ultrasound. May be useful in the presence of nonspecific clinical
and radiologic findings (gasless abdomen) or in infants with NEC not respond-
ing to medical management. Ultrasound (US) can detect intramural intestinal
gas (pneumatosis) and intermittent gas bubbles in the liver parenchyma and
the portal venous system. In addition, focal fluid collections, bowel wall thick-
ness, and bowel motility can be viewed in real time. Color Doppler US is useful
in detecting bowel necrosis and mesenteric flow. Point-of-care US is currently
being evaluated and offers some promise for the future. See Chapter 44.
3. Mesenteric oxygen saturation. Recent studies have shown the possibility of
using near-infrared spectroscopy to detect mesenteric oxygen saturations. This
provides hope of early detection and real-time noninvasive monitoring for
mesenteric bowel perfusion in infants at risk for NEC. This technique is still
experimental.
VII. Differential diagnosis. The differential diagnosis of NEC includes other conditions
that cause rectal bleeding, abdominal distension, gastric retention, or intestinal perforation.
These include infectious enteritis, spontaneous intestinal perforation (see Chapter 121),
anal fissure, neonatal appendicitis, neonatal sepsis (presents similar to stage I NEC),
and cow’s milk protein allergy.
VIII. Management. The goal is to provide bowel rest and prevent progression of disease to
intestinal perforation, septic peritonitis, and shock.
A. Medical management
1. Nil per os (NPO) to allow GI rest for 7 to 14 days (shorter course for stage I
NEC). Total parenteral nutrition (TPN) to provide basic nutritional needs.

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2. Gastric decompression with large-bore orogastric tube (Replogle) at low inter-

mittent or continuous suctioning.
3. Close monitoring of vital signs and abdominal circumference. Check all gastric
aspirates and stools for blood.
4. Respiratory support. Provide optimal respiratory support to maintain accept-
able blood gas parameters. Progressive abdominal distension causing loss of lung
volume may increase need for positive-pressure ventilation.
5. Circulatory support. There may be excessive third spacing of fluid, which
requires effective volume replacement. Inotropic support may be needed to
maintain normal blood pressure. Maintain urine output of 1 to 3 mL/kg/h.
Remove potassium from intravenous fluids in the presence of hyperkalemia
or anuria.
6. Laboratory monitoring. Check complete blood count and electrolyte panel
every 12 to 24 hours until stable. Obtain blood and urine culture prior to start-
ing antibiotics.
7. Antibiotic therapy. Treat with parenteral antibiotics for 10 to 14 days. Antibi-
otic regimen should cover pathogens that cause late-onset sepsis in premature
infants. Add anaerobic coverage if bowel necrosis or perforation is suspected.
Reasonable antibiotic regimens include the following:
a. Ampicillin (or vancomycin, in the presence of central line), gentamicin,
and clindamycin (or metronidazole).
b. Vancomycin (in the presence of central line) and piperacillin/tazobactam.
8. Monitoring for bleeding and disseminated intravascular coagulation. Infants
in stage II and III may develop DIC and require fresh frozen plasma and cryo-
precipitate. PRBC and platelet transfusions may also be needed.
9. Surgical consultation is needed for confirmed stage II and III NEC, especially
when the condition is rapidly progressing or there is evidence of GI perforation.
B. Surgical management. Goal is to prevent enteric spillage and resect necrotic intes-
tine while preserving as much of viable intestine as possible. A pneumoperitoneum
is the only absolute indication for surgical intervention but is present in only half
of the infants with intestinal perforation and necrosis at time of surgery. Relative
indications for surgery include PVG, abdominal wall edema and cellulitis (indicat-
ing peritonitis), fixed dilated intestinal segment by x-ray (sentinel loop), tender
abdominal mass, and clinical deterioration refractory to medical management.
Biochemical markers such as thrombocytopenia, elevated CRP, fecal calprotectin,
intestinal fatty acid binding protein, and elevated IL-6 and IL-8 levels have been
suggested as markers to predict surgical NEC, but their practical clinical application
remains questionable.
1. Exploratory laparotomy. This involves examining the bowel and resecting the
necrotic segments. A portion of viable bowel is used to create an enterostomy
and mucous fistula. Reanastomosis takes place after 8 to 12 weeks. If NEC only
involves a short segment of bowel with limited resection, primary anastomosis
is used by some surgeons; this avoids complications associated with ileostomy
and need for second reanastomosis surgery. In situations of widespread intestinal
necrosis, the abdomen may be closed after placement of a drain and reexplored
later. A poor prognosis is associated with severe short bowel syndrome, and
foregoing further treatment may be considered.
2. Peritoneal drain placement. A small transverse incision is made at McBurney’s
point. Abdominal layers are bluntly dissected, and a Penrose drain is threaded
into the abdomen and secured.
Two multicenter trials have shown that use of a peritoneal drain (PD) and
laparotomy in infants with bowel perforation have similar mortality, need for
TPN, and length of hospital stay. Secondary laparotomy after PD has varied from
38% in the study by Moss et al to 74% in that by Rees et al, without affecting sur-
vival. PD is a relatively simple procedure and can be done with local anesthesia

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at the bedside. Hence, it is often used as a temporizing procedure in critically

sick infants. However, PD has been questioned by Rees et al because they have
shown lack of improvement in physiologic measurements following PD and the
majority of infants required definitive laparotomy later. Currently, the optimal
surgical management for infants with bowel perforation remains controversial.
The Necrotizing Enterocolitis Surgery Trial (NEST), which is evaluating survival
without neurodevelopmental impairment at 18 to 22 months for infants under-
going laparotomy or PD for NEC or intestinal perforation, is currently underway
(ClinicalTrials.gov identifier: NCT01029353).
IX. Prevention
A. Human milk has been shown to prevent NEC. Although a mother’s own milk is
ideal, a meta-analysis of 9 randomized clinical trials of donor human milk versus
formula suggests that human milk was beneficial; infants randomized to formula
had a 2.8 times increased risk of NEC. The rate of NEC was also shown to be
lower in infants receiving human milk fortifier compared to those receiving bovine
milk–based fortifier.
B. Use of standardized feeding regimens with initial period of trophic feeds has
been shown to decrease the incidence of NEC. A cautious approach to feeding in
high-risk infants with circulatory compromise or congenital heart disease or those
receiving PRBC transfusions is recommended.
C. Probiotics. Probiotics are live nonpathogenic microbial preparations that colonize
the healthy intestine. They have the potential to prevent NEC by promoting coloni-
zation of the gut with beneficial organisms, preventing colonization by pathogens
and improving the maturity and function of gut mucosal barrier and modulation of
the immune system. Probiotics have been studied extensively to prevent NEC; the
largest clinical trial to date of 1315 preterm infants (GA 23–30 weeks) demonstrated
no difference in the incidence of Bell stage II or III NEC between patients randomly
assigned to receive the probiotic Bifidobacterium breve BBG-001 compared with
the placebo group (9% vs 10%). A recent meta-analysis, which included 38 trials
(total of 10,520 preterm infants), showed a significant reduction of NEC (relative
risk [RR], 0.43; confidence interval [CI], 33–0.56) and mortality (RR, 0.79; CI,
0.68–0.93) with no significant change in incidence of culture-proven sepsis (RR,
0.88; CI, 0.77–1). However, this benefit was not seen in the most premature infants
with birthweight <1 kg. Because probiotics are considered nutritional supplements
and not “drugs,” they are not controlled by the US Food and Drug Administra-
tion. As such, there are no established regimens of optimal strain and dosing and
no quality control regulations to ensure consistency and safety of these products;
therefore, they cannot be recommended at this time. In addition, there have been
some case reports of bacteremia from the probiotic strain used and 1 case of fatal
mucormycosis in a preterm infant exposed to probiotics.
D. Prebiotics, or nutrients that enhance the growth of beneficial microbes, have
been proposed as a preventive strategy. These include oligosaccharides, inulin,
galactose, fructose, lactose, and others. Although prebiotics enhance the prolifera-
tion of endogenous flora, their efficacy in prevention of NEC is unclear.
E. Avoidance of prolonged empiric antibiotic use. Antibiotics alter the gut flora,
promoting growth of pathogens, and should be avoided in premature infants. This
is supported by a retrospective study that showed that extremely low birthweight
infants receiving an initial antibiotic course of >5 days had an increased risk of
NEC or death. The association was confirmed in a recent systematic review and
meta-analysis.
F. Avoidance of H2 blockers. Innate GI immunity provided by gastric acid may be
important in preventing the cascade of infectious and inflammatory events leading
to NEC. A large retrospective study from the National Institute of Child Health and
Human Development (NICHD) Neonatal Research Network showed that infants
with NEC were more likely to have received H2 blockers compared to matched

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controls (odds ratio, 1.71; CI, 1.34–2.19). Therefore, routine use of H2 blockers in
premature infants should be avoided.
X. Complications
A. Recurrence of NEC may occur in about 5% to 10% of cases.
B. Colonic strictures may occur in 10% to 20% cases and present with recurrent
abdominal distension and persisting feeding intolerance. Contrast radiographic
studies are usually diagnostic. The most common site for stricture formation is the
colonic splenic flexure.
C. Short bowel syndrome may develop in infants undergoing extensive resection of
bowel (occurs in 9% of surgical NEC cases). The traditional limits of intestinal
length for successful survival (at least 20 cm of viable small bowel remaining with an
intact ileocecal valve, or 40 cm viable remaining small bowel with loss of ileocecal
valve) are now being challenged with improvements in short bowel management by
multidisciplinary teams. Fewer infants are now being referred for intestinal trans-
plant after the use of intestinal lengthening procedures such as serial transverse
enteroplasty and improved TPN and infection prevention strategies. Intestinal
(with or without liver) transplant remains an option for some of these infants.
D. Total parenteral nutrition–associated liver disease occurs more frequently in
infants with surgical therapy for NEC.
XI. Prognosis. Risk of mortality is 20% to 30%; the mortality is higher with lower GA
and surgical interventions. Infants with surgical NEC have been shown to have sig-
nificant growth and neurodevelopmental impairment. They are at risk for developing
periventricular leukomalacia, cerebral palsy, deafness, and blindness. In a report from
NICHD, only half the infants with surgical NEC survived. Among the survivors, 56.7%
had neurodevelopmental impairment (cerebral palsy, mental development index <70,
physical development index <70, blindness, or deafness). Overall, mortality or neu-
rodevelopmental impairment was present in 82.3% of infants in this high-risk group.

110 Neonatal Encephalopathy

I. Definition
A. Neonatal encephalopathy (NE) is a clinically defined syndrome of disturbed neu-
rologic function in the earliest days of life in infants born ≥35 weeks’ gestation,
demonstrated by an altered level of consciousness or seizures and frequently associ-
ated with depressed respiratory drive, hypotonia, and depressed or absent reflexes.
NE may result from a metabolic disorder, infection, drug exposure, hypoxic isch-
emic encephalopathy (HIE), or neonatal stroke. NE is the preferred terminology
to describe a depressed newborn from any cause at the time of birth.
B. Perinatal asphyxia is a condition of impaired blood gas exchange that, if it per-
sistent, leads to progressive hypoxemia and hypercapnia. HIE, which is a subset of
NE, can result from perinatal asphyxia whereby inadequate oxygen delivery to the
brain leads to compromised brain metabolism
C. The likelihood that acute intrapartum or peripartum hypoxia-ischemia
(HI) may have contributed to NE is based on the following factors identified by the
American College of Obstetricians and Gynecologists (ACOG) task force on NE:
1. Neonatal signs
a. Apgar score <5 at 5 minutes and 10 minutes.
b. Fetal umbilical artery acidemia pH <7 and base deficit >12 mmol/L or both.

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