Poor prenatal care and nutrition led to early-onset sepsis in a baby girl. The mother had cough and cold during delivery and poor prenatal visits. The baby experienced fever, cyanosis, and breathing difficulties and died of sepsis within 27 hours of birth. Factors like malnutrition, infection, and lack of prenatal care can cause sepsis by allowing bacteria to pass from the mother to the baby during or shortly after delivery.

1. Maternal Infection:
Early-Onset Sepsis due to
Poor Prenatal Care and
Poor Maternal Nutrition

2. INTRODUCTION
Maternal infection is any type of
disease pass from a mother to her
baby before or during childbirth. One
of the maternal infections is the
neonatal sepsis; it is categorized into
two; the early-onset sepsis and late-
onset sepsis.

3. Early-onset neonatal sepsis most often appears within
24 to 48 hours of birth. The baby gets the infection
from the mother before or during delivery. Early-
onset sepsis common risk factors are:
•Maternal GBS Colonization
•Premature Rupture of Membranes Prom
•Preterm Rupture of Membranes
•Prolong Rupture of Membrane
•Premature Birth
•Maternal Urinary Tract Infection
•Maternal fever greater than 38°C or 100 °F
•Chorioamnionitis

4. Other factors are:
•Low APGAR score (<6 @ 1 or 5 mins.)
•Poor Prenatal care
•Poor Maternal Nutrition
•Low Socioeconomic Status
•Black Mother
•History of Recurrent Abortion
•Maternal Substance Abuse
•Low Birth Weight
•Difficult delivery
•Birth Asphyxia
•Meconium Staining
•Congenital Anomalies

5. In this case we will elaborate how does
having poor prenatal care and poor
maternal care caused early-onset sepsis.
This case will also help gain knowledge
about this kind of pregnancy
complication. And to be able to know
the risk factors, to raise awareness for
us midwifery students, future
researchers, mother’s, and to the future
mothers and the community.

6. STATEMENT OF THE PROBLEM
This case study sought to determine the following:
• How does being poor in prenatal care and poor in
maternal nutrition caused early-onset sepsis
• Does the mothers past pregnancy have anything to
do with the present pregnancy
• What are the sign and symptoms for the baby and
mother

7. OBJECTIVES
After the completion of this case we should be
able to;
1. Discuss the Early-Onset Sepsis
2. Discuss the effect of poor prenatal care and
poor maternal care to caused Neonate Sepsis
3. Discuss the anatomy and physiology
4. Elaborate pathophysiology
5. Discuss the complications, signs and symptoms
of the mother and the baby
6. Discuss the nursing care plan and the drug
study

8. SIGNIFICANCE OF THE STUDY
The significance of this study is to give knowledge to any mother or soon to be mothers so that
they will be aware on how to avoid pregnancy complications such as early onset neonatal sepsis.
Patient
The importance of the study to the patient is to be aware about the proper care during their
pregnancy.
Like having a proper checkup also taking vitamins or medicine needed prescribed by the doctor.
Midwife
Midwife should monitor their patient before and after delivery or give postpartum care to a
woman.
Student Midwife
This will guide the midwifery students to gain knowledge or how to lessen the complication of
onset early neonatal sepsis.
Community
It is important to raise awareness or having good prenatal care.
Future Researchers
To give advance knowledge to those who will be soon dealing with their future research.

9. OBSTETRIC HISTORY:
PAST PREGNANCY
Mrs. X’s fist pregnancy G1P1 (1001) was
delivered on May 7, 2017 and the second
pregnancy G2P2 (2002) was delivered on
October 10, 2018 the third pregnancy
G3P3 (3003) was delivered last December
3, 2020. All that Mrs. X gave birth were
through normal delivery after she
delivered the baby, she notes that she
doesn’t experience any signs or unusual
discomfort though-out her pregnancy.

10. OBSTETRIC HISTORY:
PRESENT PREGNANCY
Mrs. X was born January 25, 1996 raised in
Caramoan, Camarines Sur, she is the third child of
Mr. and Mrs. Y. Mrs. X is currently with her
husband considered herself as a housewife. The
AOG of Mrs. X is 38weeks, LMP: February 18,
2022, EDC: November 25, 2022, FH: 29cm and
FHT: 136bpm. Mrs. X delivered her fourth baby,
G4P4 (4004) while she was giving birth to the
baby she had of cough and cold, the temperature
of Mrs. X is 36˚C, Pulse: 88bpm, Respiration:
20bpm and BP: 110/70mmHg. Pregnancy Uterine,
The Cephalic in labor, delivered NSD to a live
baby girl in San Jose lying in Clinic.

11. The anthropometric measurements of the
baby;
• Head Circumference: 29cm
• Chest Circumference: 30cm
• Abdominal Circumference: 29cm
• Length: 49cm
• Weight: 2325grams

12. And the baby was also received Hepa B and
Vitamin K. After giving birth of Mrs. X the vital
sign is Pulse: 140bmp, Respiration: 45bpm
Temperature: 38.3˚C.
November 11, 2022 9:28pm the baby was
admitted at San Jose Medicare Community
Hospital. The baby has a fever experienced
episode of cyanosis and difficulty of breathing.
November 12, 2022 5:55am the baby died.
Immediate cause: Cardio-pulmonary arrest
Underlying cause: Neonatal Sepsis

13. ANATOMY AND PHYSIOLOGY

14. During pregnancy, the fetal circulatory
system works differently than after birth
The fetus is connected by the umbilical cord
to the placenta, the organ that develops and
implants in the mother's uterus during
pregnancy.
Through the blood vessels in the umbilical
cord, the fetus receives all the necessary
nutrition, oxygen, and life support from the
mother through the placenta.

15. Waste products and carbon dioxide from
the fetus are sent back through the
umbilical cord and placenta to the
mother's circulation to be eliminated.
Blood from the mother enters the fetus
through the vein in the umbilical cord. It
goes to the liver and splits into three
branches. The blood then reaches the
inferior vena cava, a major vein connected
to the heart.

16. Inside the fetal heart:
⚫ Blood enters the right atrium, the
chamber on the upper right side of the
heart. Most of the blood flows to the left
side through a special fetal opening between
the left and right atria, called the foramen
ovale.
⚫ Blood then passes into the left ventricle
(lower chamber of the heart) and then to
the aorta, (the large artery coming from the
heart).

17. From the aorta, blood is sent to the head
and upper extremities. After circulating
there, the blood returns to the right
atrium of the heart through the superior
vena cava.
About one-third of the blood entering the
right atrium does not flow through the
foramen ovale, but, instead, stays in the
right side of the heart, eventually flowing
into the pulmonary artery.

18. Because the placenta does the work of
exchanging oxygen (O2) and carbon
dioxide (CO2) through the mother's
circulation, the fetal lungs are not used for
breathing. Instead of blood flowing to the
lungs to pick up oxygen and then flowing
to the rest of the body, the fetal
circulation shunts (bypasses) most of the
blood away from the lungs. In the fetus,
blood is shunted from the pulmonary
artery to the aorta through a connecting
blood vessel called the ductus arteriosus.

19. Blood circulation after birth:
With the first breaths of air the baby takes at
birth, the fetal circulation changes. A larger
amount of blood is sent to the lungs to pick up
oxygen.
Because the ductus arteriosus (the normal
connection between the aorta and the pulmonary
valve) is no longer needed, it begins to wither
and close off.
The circulation in the lungs increases and more
blood flows into the left atrium of the heart. This
increased pressure causes the foramen ovale to
close and blood circulates normally.

20. IMMUNE SYSTEM DEVELOPMENT
The immune system begins very early in
fetal development with the origin of blood
formation in the third week of gestation. In
the fourth week of gestation the thymus
forms. The thymus helps to mature and
develop white blood cells so that they can
play a key role in fighting infections. By the
eighth week of gestation, T cells, B cells,
and natural killer cells can all be found in the
thymus.

21. T cells, which make an important component in
cell-mediated immunity, are formed solely in the
thymus. B cells, which are the precursors of
antibody producing cells, are first produced in the
liver but by 12 weeks gestation move into the
bone marrow where it remains. Natural killer
cells, which are cytotoxic cells that have the
ability to attack viruses, mature in the thymus.
Interestingly, greater concentrations of natural
killer cells are found in the peripheral blood of
newborns and the newborn usually has adult
levels of these cells at birth, but they diminish
rapidly. (Orlando Regional Healthcare, Education
& Development © Copyright 2004 Page 4)

22. Neutrophils are relatively numerous in both the term
and pre-term infant. A neutrophil is a type of white
blood cell that defends the body from organisms that
cause infection. The stages of neutrophil
development, from immature to mature, are
myeloblast, promyelocyte, myelocyte, metamyelocte,
band, and segmented neutrophil. When an infection is
present, the neutrophils migrate out of the capillaries
and into the infected site, where they ingest and
destroy the pathogens causing the infection. The
amount of circulating neutrophils in the newborn
peaks around 12 hours after birth and then starts to
decline to normal levels. Even though a large number
of circulating neutrophils can be found in the
newborn, the bone marrow storage pool of
neutrophils at birth is only 20% to 30% of the
circulating pool in adults.

23. Pregnancy is a critical period of physiological change for both the mother and the
fetus. As gestational age increases, so too does the need for energy to meet the
nutritional demands of fetal development. Although in humans, only a modest
increase of 340 and 450 kcal/day is required for the mother in the second and third
trimester of pregnancy, respectively [1], maternal consumption must support her
own basal metabolic function and continuously supply nutrients to the fetus.
Pregnancy represents a natural state of maternal insulin resistance and the
difference in maternal–fetal glucose concentration that increases with advancing
gestation facilitates increased fetal macronutrient uptake [2]. Consequently, the
metabolic needs of the growing fetus are met in part by the glucose concentration
gradient across the maternal–fetal interface [3]. With advancing gestation,
increases in fetal body weight are accompanied by changes in body composition
such that there is a reduction in total body water concentration and large gains in
white adipose tissue from the second trimester onwards [4,5]. The energy
demands of fetal growth are substantial given the large caloric requirement
associated with fat deposition, which accounts for 90% of energy deposited near
term; the total estimated caloric requirement of a human fetus at term is 90–100
kcal/kg/day [6,7]. Energy intakes that diverge from the appropriate energy
requirement may alter the fetal phenotype through epigenetic processes that alter
expression of the genotype, such that insufficient or excess energy intake may
cause growth restriction and overgrowth, respectively. Placental dysfunction can
also restrict fetal growth by limiting nutrient supply to the fetus [8,9]. Intrauterine
growth restricted (IUGR) fetuses are often born with depleted fat and glycogen
stores [10,11]. In contrast, those born large-for-gestational-age (LGA), from
mothers with obesity or to mothers who gain excessive weight during pregnancy,
have increased adiposity [12,13,14] compared to average birth size newborns and
mothers who gain the appropriate amount of weight, respectively.

24. In order to sustain appropriate fetal development
the mother must provide glucose, amino acids
and fatty acids, which are transported to the
fetus across the placenta. There is increasing
evidence that maternal factors, including body
mass index, gestational weight gain, lifestyle
behaviors (e.g., physical activity, smoking), as
well as placenta-mediated diseases, can affect
fetal growth and pregnancy outcomes. Although
the precise mechanisms through which these
factors affect fetal growth have yet to be fully
elucidated, changes in placental nutrient
transport to the fetus are implicated. (Maternal–Fetal
Nutrient Transport in Pregnancy Pathologies-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200776/)

25. BASELINE DATA
Name: Baby Girl
Address: Zone 4 Calalahan, San Jose Camarines Sur
Age: 27hrs.
Educational Level: N/A
Marital Status: Infant
Religion: N/A
Birthdate: November 11, 2022
No. of Dependents: none
Birthplace: San Jose, Camarines Sur
Gender: Female
Occupation: N/A
Nationality: Filipino
Person next to Kin: Mother
Source of history/reliability: Significant other (mother) and patient's charts
Date of Admission: November 11, 2022 (9:28 pm)
Attending Physician: Jose Carlo L. Formalejo MD
Chief Complaints: Fever, Episode of Cyanosis, Difficulty of Breathing
Admission Diagnosis: Neonatal Sepsis
Temperature: 38.3 C

26. GORDON’S 11 FUNCTIONAL HEALTH
PATTERN
During Pregnancy
Health Perception During the mother’s pregnancy, she doesn’t even take any vitamins, especially ferrous
sulfate.( simula sa unang panganganak hindi sya umiinom ng Ferrous Sulfate)
Nutritional-Metabolic Pattern Doesn’t eat nutritious food due financial
Doesn’t take any Vitamins
Activity and Exercise Pattern The mother usually do household chores
Sleep-Rest Pattern During the mother’s labor she doesn’t consume the right sleep hours because of her 2yrs.
Old daughter, and because of the environment.
Elimination Pattern The Mother usually voids 4-5 times a day, she defecates once a day, and she doesn’t
experience any problem in voiding and defecating.
Cognitive-Perceptual Pattern The patient knows that she is pregnant but not properly oriented.
Self-perception– Self-concept
Pattern
The mother doesn’t express his feelings about her pregnancy. Because she is ashamed “na
pasunod sunod ang kanyang pagbubuntis/pangaganak”
Role-Relationship Pattern The patient plays the role of being a mother to her children and a wife to her husband. And
sometimes having little conflict with her husband because of the finances.
Sexuality-Reproductive Pattern The patient is sexually active. They have 3 children, 5yrs old, 4yrs old and 2yrs old.
Coping-Stress Tolerance Pattern The mother doesn’t copes up with stress during her pregnancy.
Value-Belief Pattern The patient’s religious affiliation is roman catholic.

27. PATHOPHYSIOLOGY

28. SIGN AND SYMPTOMS
Body temperature changes, Breathing problems or breathing
difficulty, Persistent crying, unusual irritability or feeding
Mother
• Poor feeding
• Cough
• Colds
• Pale
• Low body weight
• Vital signs
• Temperature 36C
• Pulse rate: 88bpm
• Respiratory rate: 20cpm
• Blood pressure: 110/70

29. Baby
• Fever
• Difficulty of breathing
• Episode of cyanosis
• Unusual irritability
• Persistent crying
The anthropometric measurements of the baby:
• Head circumference:29cm
• Chest circumference 30cm
• Length 49cm
• Weight: 2325g
• Temperature: 38-40˚C

30. MIDWIFERY/NURSING CARE
PLAN
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION EVALUATION
 Vital Signs
Temp: 38.3-40.1
C
 Difficulty of
Breathing
 (+) Cyanosis
Ineffective Breathing
Pattern
 Observe breathing
pattern
 Assess and record
respiratory rate and
depth at least every
4 hours.
 Provide respiratory
medications and
oxygen, per doctor’s
order.
 Stay with the
patient during acute
episodes of
respiratory distress.
 Still with DOB
 Vital Sign
Temp: 38.3-40.1
C
Ineffective
Thermoregulation
 Provide TSB
 Monitor the baby’s
body temperature
 Evaluate the
patient’s nutrition
and weight.
 The patient’s
temperature is still
high.
Baby

31.  Cyanotic
 Vital Sign
Temp: 38.3-40.1 C
Impaired Gas Exchange  Assess respiratory rate,
depth, and effort
including the use nasal
flaring and abnormal
breathing patterns.
 Observe cyanosis in the
skin and note the color
of the tongue.
 Monitor oxygen
saturation.
 Maintain an oxygen
administration device
as ordered, attempting
to maintain saturation
at 90% or greater.
 The baby’s skin is still
bluish/purplish.
 Fever
 Vital Sign
Temp: 38.3-40.1 C
Risk for Infection  Assess for the presence,
existence, and history of
the common causes of
infection.
 Monitor and report any
signs and symptoms.
 Assess immunization
status and history of
infection.
 Maintain strict asepsis
for dressing changes,
and medical
equipment’s.
 The baby is still
infected.

32. MOTHER
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION EVALUATION
S: “Mayo akong gana
magkakan” as
verbalized by patient.
Objective:
 Vital Sign
Blood
Pressure:110/70mmhg
Temperature:36.5˚C
Pulse: 71bpm
Respiration:20cpm
 Loss of Appetite
 Low body weight
Imbalanced Nutrition
Less than Body
Requirements
 Determine the
patient’s body
mass index (BMI).
 Assess the
patient’s nutrition
risk using
nutrition risk
screening tools.
 Assess the
patient’s nutrition
status.
 Ascertain healthy
body weight for
age and height.
 Educate the
patient about
adequate
nutritional intake.
 Patient has a
normal BMI.
 Patient has a poor
nutrition status.

33. S: “Tigluluya ako
permi”
Objective:
 Vital Sign
Blood
Pressure:110/70mmhg
Temperature:36.5˚C
Pulse: 71bpm
Respiration:20cpm
Body Weakness
Activity Intolerance
 Look for physical
signs of poor
nutritional
intake.
 Assess input and
output records
and nutritional
patterns.
 Monitor
nutritional needs
as they relate to
immobility.
 Encourage
physical activity
with the patient’s
energy levels.
 Promote proper
nutrition and
hydration.
 Lack of nutrition
food intake
 Not taking any
vitamins

34. S: “Dae ko aram”
Objective:
 Lack of
information
about prenatal
care
 Unpreparedness
for changes
during and after
pregnancy
Deficit Knowledge  Determine the
patient’s
knowledge
level.
 Establish the
patient’s
capacity,
readiness, and
learning
obstacles.
 Develop a birth
plan.
 Provide
information at
their
educational
level.
 Patient will
participate in
the learning
process.

35. DRUG STUDY
MEDICINE DOSAGE ACTION CONTRAINCIDATION SIDE EFFECT INDICATION
Ferrous Sulfate Once a day 325 mg
for 2 weeks
Elevates the iron
serum
concentration
Hypersensitivity
Severe hypotension
Dizziness
Nasal congestion
Dyspnea
Hypertension
Muscle cramps
Flushing
Prevention and treatment of iron
deficiency anemia’s
Dietary supplement for iron
Oxytocin Pitocin IM: 3-10 units after
delivery of the
placenta
IV: Mix 5-20 units in
500ml of D5LR;
infuse at 20-40
milliunits
To contract uterus
to stop bleeding
Presence of a second fetus Hypertension or Hypotension
Tachycardia
Dysrhythmias
Angina
Pectoris
Anxiety
Nausea and vomiting
Allergic reaction
Uterine rupture
Excessive administration
Other Vasopressors may potentiate
hypertension
Mother

36. Mefenamic
Acid
500mg Tab For the relief
of pain
following an
episiotomy.
Should not be taken
for more than seven
days after giving
birth.
Premature closure of
the fetal Ductus
arteriosus
Pulmonary
hypertension fetal Renal
impairment
Oligohydramnios
Inhibition of platelet
aggregation
Treatment of primary
dysmenorrhea, headache,
toothache, and
postoperative pain
Cephalexin 500mg Cap Killing the
bacteria that
causes the
infection
This medication poses
minimal risk to the
infant when used
during breastfeeding.
Severe diarrhea that
lasts for more than 4
days or contains blood or
mucus. pale poo and
dark pee, yellowing of
your skin or whites of
your eye.
The treatment of respiratory
tract infections (RTI's),
urinary tract infections
(UTI's), skin and soft tissue
infections, otitis media and
other infections due to
sensitive organisms.

37. BABY
MEDICINE DOSAGE ACTION CONTRAINDICATION SIDE EFFECT INDICATION
PARACETAMOL 0.1ml (IV) every 6
hours
For its analgesic and
antipyretic effects
A good safety profile in
neonates when
administered for a limited
time (48–72 hours).
nausea, vomiting,
constipation
To control mild-to-
moderate pain or to
reduce opioid
exposure as part of
multimodal analgesia
AMPICILLIN 120mg (IV) every 12
hours
Effective against all the
bacterial agents causing
community-acquired
sepsis in neonates.
History of hypersensitivity to
any penicillin.
diarrhea, stomach
pains and may feel
sick or be sick (vomit).
Treatment of
bacterial infections
including sepsis and
meningitis.
GENTAMICIN 8mg (IV) every 24
hours
To treat serious aerobic
bacterial infections.
Hypersensitivity vomiting, stomach
upset, loss of
appetite, and.
injection site
reactions (pain,
irritation, and
redness).
Killing bacteria or
preventing their
growth.

38. D5 IMB 500c x 1.5 To treat low blood sugar
(hypoglycemia), insulin
shock, or dehydration (fluid
loss).
Should not be given to new born
babies whose body weight is
low; patients who have damaged
blood vessels and weakened
kidneys, and heart problems.
Contains Sodium
Metabisulfite, a sulfite
that may cause allergic-
type reactions including
anaphylactoid symptoms
and life-threatening or
less severe asthmatic
episodes in certain
susceptible persons.
For maintenance of fluid
and electrolytes
especially to patients
who need calories and
hydration.
VITAMIN K 1. ml (IM) at birth To protects your baby from
developing dangerous
bleeding which can lead to
brain damage and even
death.
Excessive doses of vitamin K
analogs during the first few days
of life may cause
hyperbilirubinemia
Pain or even bruising or
swelling at the place
where the shot is given
Provides protection
against bleeding that
could occur because of
low levels of this essential
vitamin.
HEPATITIS B 0.5 ml (IM) at birth Stimulates the immune
system to produce anti-HBs
without exposing the patient
to the risks of active
infection.
Severe allergic reaction after a
previous dose or to a vaccine
component
Localized pain, redness
and swelling at the
injection site, low grade
temperature (fever).
Preventing long-term
illness in infants and the
spread of hepatitis B

39. EVALUATION
Last December 4, 2022 at 4:30pm, 3 weeks and 3 days after the
delivery we visited Mrs. X at Calalahan, San Jose Camarines Sur for
follow up interview and verify her condition.
Vital signs were the following:
• Temperature: 36.5˚C
• Pulse rate: 80bpm
• Respiration rate: 17bpm
• Blood pressure: 110/80mmHg
• According to her she is still in trauma stage.
We midwifery student encourage the mother for a proper nutrition.
“Inumin mga dapat inumin na gamut o vitamins”
And as her if she wanted to learn about Birth control and apply
family planning.

40. CONCLUSION
• The ability of mother to provide nutrients and oxygen for her
baby is a critical factor for fetal health and its survival. Failure in
supplying the adequate amount of nutrients to meet fetal
demand can lead to complications.
• The prevalence of Early-Onset Sepsis is high among newborns
of mothers with infection or risk factors for infection Nutritional
problems are severe among pregnant mothers and 60 to 70
percent of pregnant women in developing countries are
estimated to be anemic. Women with poor nutritional status are
more likely to deliver a low-birth -weight infant.
• Majority of prenatal deaths are associated with maternal
complications, poor management techniques during labor and
delivery, and maternal health and nutritional status before and
during pregnancy. The large majority of pregnancies that end in
a maternal death also result in fetal or prenatal death. Among
infants who survive the death of the mother, fewer than 10
percent live beyond their first birthday.

41. RECOMMENDATION
• Ensure a normal pregnancy educate the
mother to have a healthy prenatal care
and healthy maternal care.
• Motivate about the need of the family
planning
• Facilitate health education
• Detect early and treat properly the
compilation
• Prepare the woman for labor, lactation
and care of her infant
• More thorough study about this case

42. TERMINOLOGY
• Early-Onset Sepsis
A category of sepsis in neonates before 72 hours of life.
• GBS
A severe bacterial infection that affect the new infants.
• Premature Birth
When a baby is born too early, before 37 weeks of pregnancy have been
completed
• Prenatal care
A health care provided to a woman during pregnancy. It consists of a
series of clinical visits and ancillary services designed to promote the
health and wellbeing of the mother, fetus and family.
• APGAR score
Describes the condition of the new born infant immediately after birth
• Chorionniomitis
Infection of the placenta and the amniotic fluid. It happens more often
when the amniotic sac is broken for a long time before birth.

43. BIBLIOGRAPHY
Amaral, T. F., Matos, L. C., Tavares, M. M., Subtil, A., Martins, R., Nazare, M., & Pereira, N. S. (2007). The economic impact of disease-related
malnutrition at hospital admission. Clinical nutrition, 26(6), 778-784. https://doi.org/10.1016/j.clnu.2007.08.002
Casadei, K., & Kiel, J. (2020). Anthropometric measurement. StatPearls [Internet]. Centers for Disease Control and Prevention (2000).
https://www.cdc.gov/growthcharts/cdc_charts.htm
Hark, L., & Deen, D. (1999). Taking a nutrition history: a practical approach for family physicians. American Family Physician, 59(6), 1521.
https://www.aafp.org/afp/1999/0315/p1521.html
Jensen, G. L.; Binkley, J. (2002). Clinical Manifestations of Nutrient Deficiency. Journal of Parenteral and Enteral Nutrition, 26(5 Suppl), S29–S33.
https://doi.org/10.1177/014860710202600509
McDowell, M. A., Fryar, C. D., Ogden, C. L., & Flegal, K. M. (2008). Anthropometric reference data for children and adults: United States, 2003–2006.
National health statistics reports, 10(1-45), 5. http://ghk.h-cdn.co/assets/cm/15/11/550017f045e74_-_nhsr010.pdf
Reber E, Gomes F, Vasiloglou MF, Schuetz P, Stanga Z. Nutritional Risk Screening and Assessment. J Clin Med. 2019;8(7):1065. Published 2019 Jul
20.
https://doi.org/10.3390/jcm8071065
Stratton, R. J., King, C. L., Stroud, M. A., Jackson, A. A., & Elia, M. (2006). ‘Malnutrition Universal Screening Tool’predicts mortality and length of
hospital stay in acutely ill elderly. British journal of nutrition, 95(2), 325-330. https://doi.org/10.1079/BJN20051622
https://l.facebook.com/l.php?u=https%3A%2F%2Fmedlineplus.gov%2Fency%2Farticle%2F007303.htm%3Ffbclid%3DIwAR3HAG81DLU5icpRIpTuK7
0v3_hw4dw8TTQ4aQb0TnP0YmWoVJxTTZ3LFeA&h=AT0LYfzpziG7oYXrmQNlgst7QFSUq_F9SAhczHbqcH7Aw5mqxvu6sotdgG2zfMMm_i2-
HGei6D7uuBa2q5s1gCYOyNw6axlIp7BXa0eSGYhWBi5qeeZUQ_JplGKmwKeKL7nipa8Od0L7UIo
Otten J., Pitzi Hellig J., Meyers L. Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. National Academic Press; Washington,
DC, USA: 2006. [Google Scholar]
Marconi A.M., Paolini C., Buscaglia M., Zerbe G., Battaglia F.C., Pardi G. The impact of gestational age and fetal growth on the maternal–fetal
glucose concentration difference. Obstet. Gynecol. 1996;87:937–942. doi: 10.1016/0029-7844(96)00048-8. [PubMed] [CrossRef] [Google Scholar]
Baumann M.U., Deborde S., Illsley N.P. Placental glucose transfer and fetal growth. Endocrine. 2002;19:13–22.
doi: 10.1385/ENDO:19:1:13. [PubMed] [CrossRef] [Google Scholar]
Freinkel N. Banting Lecture 1980. Of pregnancy and progeny. Diabetes. 1980;29:1023–1035. [PubMed] [Google Scholar]
•