Management of common preterm

problems
Outline
Introduction
Hypothermia
Hypoglycemia
Respiratory distress syndrome
Necrotizing enterocolitis
Preterm Infants
 Infants born before 37 week
◦ before 28 week gestation are extremely preterm
◦ between 28 and 31(6/7) are very preterm
◦ between 32 and 33(6/7) are Moderate preterm
◦ between 34 and 36(6/7) are late preterm
• other classification is based on birth weight:-
1500 - < 2500 are low birth weight
1000 - <1500 very low birth weight
< 1000 are extremely low birth weight
Identifiable Risk Factors for Preterm Birth
Fetal
Placental
Uterine
Maternal
 Common preterm problems
 RESPIRATORY

◦ Respiratory distress syndrome (hyaline HEMATOLOGIC

membrane disease) -Anemia (early or late onset)
◦ Bronchopulmonary dysplasia
GASTROINTESTINAL
◦ Apnea of prematurity
 CARDIOVASCULAR Necrotizing enterocolitis

◦ Patent ductus arteriosus Hyperbilirubinemia—direct and indirect

◦ Hypotension Spontaneous gastrointestinal isolated perforation

◦ Bradycardia (with apnea)

CENTRAL NERVOUS METABOLIC-ENDOCRINE
SYSTEM • Hypocalcaemia
◦ Intraventricular hemorrhage • Hypoglycemia or hyperglycemia
◦ Periventricular leukomalacia • Metabolic acidosis
◦ Retinopathy of prematurity • Hypothermia
◦ Hypotonia OTHER
RENAL Infection
• Electrolyte imbalance
• Renal tubular acidosis
• Edema of prematurity
 1.Hypothermia

Core body temperature below 36.5°c

Classification
◦ Cold stress : 36 - 36.5°c
◦ Mild hypothermia : 34 - 36°c
◦ Moderate hypothermia : 30 - 34°c
◦ Severe hypothermia : <30°c
Mechanism of heat loss
1. Convection- when heat is lost from skin to moving air
2. Radiation- when heat is dissipated from the baby to a colder
object in the surrounding like to the floor, wall or window
3. Conduction- where the baby loses heat to the surface on which
he or she lies
4. Evaporation- major cause of heat loss immediately after birth
where water is evaporated from wet infant skin like evaporation
from boiling water.
 Cause of Hypothermia in preterm infants
Large surface area to their small body mass
Highly permeable skin
Defficient subcutaneous fat with less insulation
Defficient stores of brown fat and glycogen
Immature cenral thermoregulation & poor muscle mass
Poor calorie intake
Hypoglycemia
Poor oxygen consumption because of associated pulmonary problems
Sepsis
Clinical manifestation
◦ Mild hypothermia
 acrocyanosis, cold body, delayed capillary refill time
◦ Moderate hypothermia
 confusion, agitation, lethargy, decreased pulse and ventilation ,
unsatisfactory weight gain and slow increase in head size
◦ Severe hypothermia
 Failure to suck , hypoglycemia , coma, dilated and fixed pupils,
hypotension, bradycardia , arrythmia, irregular and slow
breathing, dilated vascular leak leading to shock, bleeding and
fixed rigid body , DIC
 Prevention
 Before delivery
◦ Warm the delivery room
◦ Organize newborn corner with adequate heat source
 At delivery

◦ Deliver the baby on mother's abdomen

◦ Dry the baby thoroughly immediately after birth
◦ Remove wet clothes
◦ Use cap to prevent significant heat loss through the scalp
◦ Keep the newborn in skin to skin contact with the mother
◦ Keep the newborn under pre heated radiant warmer if needed for resuscitation
◦ Cover weighing scales with warm towel
◦ Initiate early breast feeding
Subsequent care
 Arrange appropriate transportation if needed
including KMC
Postpone bathing (after 24 hours)
Warm hands and stethoscope before touching the baby
Do examination/resuscitation of the infant under the
radiant warmer
Practice rooming in wards/post natal rooms
Keep the newborn away from windows and drafts
 Continue breast feeding
 General principles
Warm the new born slowly
Put hypothermic infants on KMC, in incubators or under radiant
warmer
Identify and treat cause of hypothermia
Monitor for complications
Monitor axillary temperature every 30 minutes till newborn
temperature becomes stable
Management of hypothermia
 Warm the baby using a pre-warmed radiant warmer.
 Remove cold or wet cloths.
 Cover the baby with warm clothes and hat.
 Treat for sepsis ,if present
 Measure blood glucose and treat if hypoglycemic.
 Keep IV line under the radiant warmer to warm the fluid.
 Measure the baby’s temperature every 30 min
 If the baby’s temperature is increasing at least 0.5 °C per hour in the
1st three hours, re-warming is successful.
 Then measure the baby’s temperature every two hours
Monitor for complications and manage accordingly
◦ Look for respiratory problems
◦ Monitor vital signs
◦ Monitor urine output
◦ Monitor blood sugars
◦ Look for signs multi organ failure
◦ Dangers of warmers
◦ Hyperthermia
◦ Dehydration
◦ Mask serious infections
KMC(Kangaroo Mother Care)

“Let nature do the nurturing”

skin-to-skin care of babies
Cornerstones of KMC
◦ Kangaroo Position
◦ Kangaroo Nutrition
◦ Kangaroo Support
Kangaroo positions
◦ Steps in positioning the baby for KMC
1. Dress the baby in socks, a nappy, and a cap
2. Place the baby between the mother’s breasts
3. Secure the baby on to the mother’s chest with a cloth
4. Put a blanket or a shawl on top for additional warmth
5. Instruct the mother to put on a front-opened top
When do we start KMC
◦ Intermittent KMC
 can be practiced while the baby is still in NICU.
 It is possible even with babies on oxygen and IV therapy
◦ Continuous KMC
 can be instituted once the baby is stable, suckling well and
needs no additional care.
 The baby can then be transferred to an adjoining KMC
ward
• Daily routine of a KMC Ward
◦ Monitoring Babies should be weighed daily, and feeds adjusted according to weight
gain.
◦ If not yet breastfeeding on demand, they should receive 175ml/kg/day, in 8 feeds 3
hourly.
◦ Babies on oxygen should have their oxygen saturation monitored 3 hourly
Discharge:
◦ when the baby has a sustained weight gain of at least 15 grams /kg /day for three
consecutive days
◦ when the baby can maintain temperature in a normal range for three days
◦ when the baby is able to suck breast adequately
◦ if the mother is confident and able to give KMC at home
◦ Bring the baby back for follow up in the next few days to ensure that baby is well
and growing
2. Hypoglycemia
any value of blood glucose <55 mg/dL in neonates be viewed
with suspicion( 40-45mg/dL )
severe, prolonged hypoglycemia are :

◦ cognitive impairment,
◦ recurrent seizure activity,
◦ cerebral palsy, and
◦ autonomic dysregulation
 Thesymptoms of hypoglycemia in newborns are non specific and
may confuse with other disorders of the newborn but the
presentation includes:-
Abnormal crying (weak or high-pitched cry)
Tremors , jitteriness, irritability, hypotonia
Grunting , tachypnea , tachycardia
cyanosis, apnea, hypothermia
poor feeding, vomiting lethargy, and seizures ,coma
Classification of hypoglycemia in infants and children
◦ Neonatal transitional hypoglycemia
◦ Neonatal, infantile or childhood persistent hypoglycemia
 Cause
Transient hypoglycemia could be: -
Related with changes in maternal metabolism
 Intrapartum glucose administration
 Diabetes in pregnancy-infant of diabetic mother
 Maternal drug

Related with neonatal problems

 Intrauterine growth retardation(IGUR)
 Prematurity
 Delayed onset of feedings ( tocolytics , propranolol ,thiazide diuretics)
 Birth asphyxia
 Infection
 Post exchange transfusion
 Hypothermia , erythroblastosis fetalis
 Inadequate feeding ,polycythemia
 Cont…
 Newborns at risk for hypoglycemia include:-
 Preterm infants
 Small for gestational age(SGA)
 Large for gestational age(LGA)
 Infants of diabetic mothers(IDM)
 Sick infants who require intensive care
 Post exchange blood transfusion
 Infants on intravenous fluids or parenteral fluids
 Infants whose mothers were treated with beta adrenergic or oral hypoglucemic agents
 Intrapartum dextrose infusion
 Infants with polycythemia
 Hypothermic newborns
 Diagnosis
 Diagnosis is based on :-
 Supportive perinatal history (risk factors).
 Signs and symptoms of hypoglycemia.
 Whole blood glucose level.

NB Glucometers measure whole blood glucose, which is 15% lower

than plasma glucose levels.
 Persistent or recurrent hypoglycemia need additional testing
including:
hormone analysis: Insulin, glucagon, GH, cortison
imaging studies.
 Treatment
 Treatmentof acute symptomatic neonatal or infant
hypoglycemia
- secure IV line then
◦ IV administration(bolus) of 2 mL/kg of 10% dextrose in water (D10W)
◦ followed by a continuous infusion of glucose at 6-8 mg/kg/min
◦ If hypoglycemic seizures are present, some recommend a 4 mL/kg bolus
of D10W
◦ Recheck blood glucose after 30 mins and if it’s above 55mg/dl the 1
hrly till 3 consecutive normal values then 2hrly, 3hrly,6hrly each for 2-3
normal values .
◦ Then if neonate requires Glucose infusion rate (GIR)> 12mg/kg/min
persistent hypoglycemia should be considered.
Treatment of asymptomatic hypoglycemia in at-risk infants
◦ Enteral feedings rather than parenteral glucose is the initial treatment
◦ Check blood glucose 30 mins after feeding to insure normal glucose
level before the next feeding
◦ If symptoms develop or the hypoglycemia persists despite enteral
feedings, IV glucose is indicated
◦ Dextrose gel (40% at 400 mg/kg) administered into the mouth if
breast milk or if formula is not available
Management of persistent neonatal or infantile
hypoglycemia
◦ increasing the rate of IV glucose infusion to 10-15
mg/kg/min or more
◦ If hyperinsulinism is present
 medically managed initially with diazoxide and then
somatostatin analogs
◦ If hypoglycemia is unresponsive to IV glucose plus
diazoxide (maximal doses up to 15 mg/kg/day) and
somatostatin analogs
 partial or near-total pancreatectomy should be considered
Practical points

 Do not use > 12 % dextrose infusion through a peripheral vein due to the
risk of thrombophlebitis.
 In addition to glucose infusion and monitoring, reduce energy needs by
correcting acidosis, maintaining a thermo neutral environment and
treatment of other underlying conditions like sepsis.
 Do not stop an IV infusion of glucose abruptly, severe rebound
hypoglycemia may occur.
 If the patient needs repeated boluses, this may be an indication for
increasing the rate of continuous glucose infusion, and for considering
other causes
 3.Anemia of Prematurity

 Three basic mechanisms for the development of anemia prematurity (AOP)

include
 Inadequate RBC production
 Shortened RBC life span
 Blood loss.
BLOOD LOSS ↑ RBC
DESTRUCTION
Iatrogenic blood loss (phlebotomy) Immune- Mediated Hemolytic
Placental hemorrhage Rh incompatibility
Placental previa
Injury of umbilical or placental vessels ABO incompatibility
Fetomaternal transfusion
Fetoplacental transfusion Minor antigen incompatibility
Twin-twin transfusion RBC Membrane Disorders
Acute perinatal hemorrhage (e.g.,
cesarean birth, other obstetric trauma) Hereditary spherocytosis
Chronic in utero blood loss
Hereditary elliptocytosis
Hereditary pyropoikilocytosis
Hereditary stomatocytosis
RBC Enzyme Disorders
G6PD deficiency
Pyruvate kinase
↓ RBC PRODUCTION
Physiologic anemia and anemia of
prematurity
Infection (rubella, CMV, parvovirus
B19)
Bone marrow suppression (acute stress
in perinatal period)
Hemoglobinopathy (γ-globin mutation,
unstable
β-hemoglobinopathy, α-thalassemia
major)
Bone marrow suppression (CMV, EBV)
Diamond Blackfan anemia
Schwachman-Diamond syndrome
Congenital dyserythropoietic anemia
Fanconi anemia
Pearson syndrome
Congenital leukemia
 Presentation
Many clinical findings have been atributed to AOP but they are
neither specific nor diagnostic.
These symptoms include:

- poor weight gain despite adequate calorie intake

- cardiorespiratory symptoms - tachycardia , tachypnea , flow
murmurs
- decreased activity, lethargy and difficulty with oral feeding
- pallor
- increase in apenic amd bradycardic episodes and worsened periodic
breathing
- metabolic acidemia
 Treatment
1.Blood transfusion(s)
Treatment of neonatal anemia by blood transfusion depends on
 The severity of symptoms,
 The hemoglobin concentration, and
 The presence of comorbidities
 The benefits of blood transfusion should be balanced against its risks
Suggested Transfusion Thresholds
POSTNATAL PRESENCE OF ABSENCE OF RESPIRATORY
AGE RESPIRATORY SUPPORT
SUPPORT
Hgb and hct
week1 11.5(35%) 10(30%)

Week 2 10.0(30%) 8.5(25%)

Week 3 8.5(25%) 7.5(23%)

Appropriate blood product and a safe volume of blood should be
transfused at a safe rate.
 It is important to transfuse packed erythrocytes (PRBCs)
 Transfusion volume ranging from 10-20 mL/kg
 At a rate of 3-5ml/kg/hr
 Transfusion should be completed with in 4 hr
 2.Recombinant erythropoietin (EPO)
 Because of low physiologic level of erythropoietin in neonates,
rhEPO is used in treatment of anemia
 It decreases the number of transfussion per infant
 But increases the risk of ROP
 Respiratory tract disorders
Respiratory disorders are the most frequent cause of admission
for neonatal intensive care in both term and preterm infants.
Signs and symptoms of respiratory distress include
cyanosis, expiratory grunting, nasal flaring,
retractions, tachypnea, decreased breath sounds with or without
rales and/or rhonchi, and pallor.
 4.Apnea of prematurity
Apnea is usually defined as cessation of breathing for a period of
≥20 sec, or a period <20 sec that is associated with a change in
tone, hypoxia, pallor, cyanosis, or bradycardia (<80-100 beats/min)
Based on the absence of respiratory effort and/or airflow, apnea
can be obstructive, central, or mixed.
Apnea of prematurity results from immature respiratory control,
most frequently occurs in infants <34 wk of gestational age (GA),
and occurs in the absence of identifiable predisposing diseases.
 Cont….
The onset of apnea of prematurity can be during the initial days to
weeks of age but is often delayed if there is RDS or other causes
of respiratory distress.
In premature infants without respiratory disease, apneic episodes
can occur throughout the 1st 7 postnatal days with equal
frequency.
Preterm infants born at <35 wk GA are at risk for apnea of
prematurity and therefore should receive cardiorespiratory
monitoring
 Cont…
Apnea that occurs in the absence of other clinical signs of illness
in the 1st 2 wk in a preterm infant is likely apnea of prematurity,
and therefore additional evaluation for other etiologies is often
unwarranted.
However, the onset of apnea in a previously well preterm neonate
after the 2nd wk of life (or, as previously, in a term infant at any
time) is a critical event that may be associated with serious
underlying pathology.
CNS Intraventricular hemorrhage, drugs, seizures, hypoxic injury, herniation,
neuromuscular
disorders, Leigh syndrome, brainstem infarction or anomalies (e.g.,
olivopontocerebellar atrophy), spinal cord injury after general anesthesia

RESPIRATORY Pneumonia, obstructive airway lesions, upper airway collapse, atelectasis,

extreme prematurity, laryngeal reflex, phrenic nerve paralysis, pneumothorax,
hypoxia

INFECTION Sepsis, meningitis (bacterial, fungal, viral), respiratory syncytial virus, pertussis

GASTROINTESTINAL Oral feeding, bowel movement, necrotizing enterocolitis, intestinal perforation

METABOLIC ↓ Glucose, ↓ calcium, ↓/↑ sodium, ↑ ammonia, ↑ organic acids, ↑ ambient

temperature, hypothermia

CVS Hypotension, hypertension, heart failure, anemia, hypovolemia, vagal tone

OTHER Immaturity of respiratory center, sleep state

Sudden unexpected postnatal collapse
Laboratory studies
CBC , blood gas analysis , serum glucose , and electrolyte and
calcium levels
Radiological stidies
Chest X - ray , abdominal X ray , cranial sonar , and CT for infants with
definite signs of neurological involvement.
Prevention
- Maintain normal hct , electrolytes and PaO2
- Avoid neck flexion and abdominal distension
- KMC
 Treatment
Gentle tactile stimulation or provision of flow and/or
supplemental oxygen by nasal cannula is often adequate therapy
for mild and intermittent episodes.
Nasal continuous positive airway pressure (nCPAP, 3-5 cm
H2O) and Heated Humidified High-Flow nasal Cannula
(HHHFNC, 1-4 L/min) are appropriate therapies for mixed or
obstructive apnea.
Recurrent or persistent apnea of prematurity is effectively treated
with methylxanthines .
 Cont…
Caffeine and theophylline are similarly effective methylxanthines,
Caffeine therapy can be safely administered orally (PO) or
intravenously (IV) with an initial loading dose of 20 to 25mg/kg of
caffeine citrate followed 24 hr later by once-daily maintenance
doses of 5 mg/kg (increased to 10 mg/kg daily as needed for
persistent apnea).
Caffeine therapy is usually continued until an infant is free of
clinically significant apnea or bradycardia for 5-7 days without
positive pressure respiratory support .
Treat underlying etiology.
Prognosis
In92% of infants by 37 wk PMA and in 98% of infants by 40 wk
PMA, apnea of prematurity resolves spontaneously
5.Neonatal Respiratory Distress Syndrome
(HMD)
 Introduction
 RDS is caused by Surfactant deficiency (decreased production and
secretion ) is the primary cause of RDS

 Ittakes up important part of neonatal mortality and mortality

 30% of all neonatal mortality
 50-70% of premature death

 Incidenceis inversely proportional to GA and birth weight

 60-80% in GA <28 weeks,
 15-30 % in GA 32-36 weeks
 O.3% at GA 38 weeks
 Cont…
RDS risk increases
Maternal DM ,
Multiple pregnancy ,
Precipitous delivery ,
Cesarean delivery ,
Asphyxia ,
Maternal history of previous affected infants ,
Male
 Pathophysiology
Surfactant is present in fetal lung homogenates by 20 weeks of
gestation
But it doesn’t reach the surface of the lungs until later
It appears in amniotic fluid by 28-32 weeks
Mature level of pulmonary surfactant are present usually after 35
weeks of gestation
With advancing GA increasing amount of phospholipids are
synthesized and stored in alveoli
 Cont…
 As pulmonary surfactant is absent there is a significant increase in alveolar
surface tension
 If surface tension is high and the radius small, the end of expiratory
pressure required to open alveoli is high
 If this pressure is not generated >collapse>atelectasis
 Surfactant decreases surface tension ,thus decreases opening pressure
 cont…
Alveolar atelectasis ,hyaline membrane formation and interstitial
edema makes the lung less compliant in RDS so greater pressure
may be required to expand the alveoli and small airways
Chest wall of preterm infants is also highly compliant thus doesn’t
provide resistance to collapse.
Due to this at end of expiration ,volume of the lungs and thorax
tends to approach residual volume and atelectasis may develop
Pathology
 Clinical manifestation
Signs of RDS appear within minutes of birth with rapid shallow
respiration
Some neonate with borderline surfactant may be well first but
develop symptoms within few hrs because it is consumed or
inactivated
Later onset of tachypnea should suggest other etiology
Tachypnea ,grunting, nasal flaring, intercostal subcostal retractions
and cyanosis
Breath sound may be decreased or normal
On deep inspiration fine crackles may be noted
Untreated RDS worsens with cyanosis, and dyspnea, hypotension ,
pallor, grunting decreases or disappear
Apnea and irregular respiration are obvious signs requiring
intervention
In most cases signs reach peak within 3 days due to endogenous
production of surfactant after which improvement is gradual
Improvement is often heralded/sign of thing to come / with
spontaneous diuresis and improved gas values at low support
Respiratory distress usually resolve within 1week
Causes of death : impairment of gas exchange, air leak ,pulmonary
hemorrhage ,IVH
DIAGNOSIS
 Cont…
CXR: characteristic but not pathognomonic
 Low lung volume
 Fine reticular granularity of parenchyma
 Ground glass appearance and
 Air bronchogram

ABG:
 hypoxemia,
 hypercapnea,
 metabolic acidosis
 Chest X grades
Grade I:fine granularity with some air bronchograms visible
Grade II :more apparent ,distinct , and coarse
granularity to the lung field ,more extensive air
bronchogram
Grade III: increasing opacity ,with decreasing air
bronchogram and granularity ;heart border still visible
Grade 4:diffuse bilateral opacification is present ,with
lack of apparent heart borders and loss of air
bronchograms-a ;whiteout; on chest X-ray
 Shake test
Gastricaspirate 0.5ml
Add 0.5ml of NS
Add 1cc of 95% ethyl alcohol
 Shake for 15 second and leave on rack for 15min

Negative (decreased surfactant )

Positve (adequate surfactant )
 Treatment
The basic defect requiring treatment in RDS is inadequate
pulmonary O2 -CO2 exchange.
Basic supportive care (thermoregulatory, circulatory, fluid,
electrolyte, and respiratory) is essential while FRC is established
and maintained.
Careful and frequent monitoring of heart and respiratory rates,
SaO2 , PaO2 , PaCO2 , PH, electrolytes, glucose, blood pressure,
and temperature are essential.
Supportive care
Put in incubator and keep Temperature between 36.5-37 c
10% Dextrose solution for first 24 hour
Electrolytes added on 2nd day
Fluid shouldn’t exceed 140ml/kg because this may contribute to
development of PDA and BPD
 Oxygen delivery
 Nasal Continuous Positive Airway Pressure
 Warm, humidified oxygen should be provided at a concentration sufficient
to keep PaO2 between 50 and 70 mm Hg(91–95% SaO2 ) to maintain
normal tissue oxygenation while minimizing the risk of O2 toxicity.

 Ifthere is significant respiratory distress (severe retractions and expiratory

grunting) or if SaO2 cannot be kept >90%, applying nCPAP at 5-10 cm
H2O is indicated and usually produces a rapid improvement in
oxygenation.
 cont..
CPAP reduces collapse of alveoli and improves both FRC and
Ventilation perfusion (V/Q) matching

Early use of nCPAP for stabilization of at risk preterm infants

beginning early (in the delivery room) reduces the need for mechanical
ventilation.

CPAP requirement is usually decreases in 72 hrs and patients can be

weaned /cease shortly
 Cont…
Assisted
ventilation and surfactant are indicated for infants with
RDS who cannot keep oxygen saturation >90% while breathing
40–70% oxygen and receiving nCPAP

Infants at the extremes of GA (<28 wk) and those that were not
exposed to antenatal corticosteroids may still benefit from
intubation and surfactant prophylaxis
 Mechanical ventilation
Infants with respiratory failure or persistent apnea require assisted
mechanical Ventilation
Definitions for respiratory failure in extremely preterm infants
with RDS are
(1) arterial blood pH <7.20,
(2) PaCO2 ≥60 mm Hg,
(3) SaO2 <90% at O2 concentration of 40–70% and nCPAP of 5-
10 cm H2 O, and
(4) persistent or severe apnea.
 Cont….

The goal of mechanical ventilation is to improve oxygenation and

ventilation without causing pulmonary injury or oxygen toxicity

Acceptable ranges of ABG values generally range from

PaO2 50-70 mm Hg,
PaCO2 45-65 mm Hg (and higher after the 1st few days when
risk of IVH interaventricular hemorrhage is less), and
PH 7.20-7.35.
Surfactant replacement therapy
Immediate effects of surfactant replacement therapy include
improved alveolar-arterial oxygen gradients, reduced ventilatory
support, increased pulmonary compliance, and improved chest
radiograph appearance.
In neonates with RDS who fail nCPAP and require intubation and
mechanical ventilation, treatment with endotracheal surfactant
should be initiated immediately to avoid lung injury.
Repeated dosing is given every 6-12 hr for a total of 2-4 doses,
depending on the preparation
 complications of Surfactant Rx
pulmonary air leaks
Oxygen toxicity
Patent ductus arteriosus
NEC
Pulmonary hemorrhage or IVH
Death
 Cont….
 ulceration of the nares caused by pressure from the tube,
 permanent narrowing of the nostril as a result of tissue damage
and scarring from irritation or infection around the tube,
erosion of the palate,
avulsion of a vocal cord,
6.Necrotizing Enterocolitis
 Definition
Acute inflammatory injury of the distal small and often proximal large
intestine
It is characterized by various degrees of mucosal and transmural
necrosis of the intestine.
Incidence is 5-10% among infants <1500g with mortality rate 20-30%
Pathology=segmental coagulative necrosis of the mucosa with focal
hemorrhage as evidence of Ischemia
Pneumatosis intestinalis(gas accumulation in submucosa) , sloughing
of mucosa, submucosa and muscularis mucosa
 Risk factors
The three main riskfactor to develop NEC is prematurity, bactrial
colonization of gut and formula feeding
Prematurity is the single greatest risk factor =90% of cases
Decreasing gestational age is associated with an increased risk of
NEC
The postnatal age at onset is inversely related to birth weight and
gestational age, with a mean age at onset of 12 days(2nd or 3rd
week) can be as late as 3 months in VLBW infants.
 Incidence in term babies is that it occurred in 10% of cases.
Antenatal steroids improve the maturity of the GI tract and have
been shown to reduce the incidence of NEC
 Pathology
The triad
Intestinal ischemia (injury),
Enteral nutrition (metabolic substrate), and
Bacterial translocation
 Escherichia coli, Klebsiella, Clostridium perfringens,
Staphylococcus epidermidis , Bacteroides astrovirus, norovirus,
and rotavirus, have been recovered from cultures.
 Pathogenesis
 NEC develops primarily in premature infants with exposure to
metabolic substrate in the context of immature intestinal immunity,
microbial dysbiosis, and mucosal ischemia.
An underlying genetic predisposition is being recognized with
variants in genes regulating immunomodulation and inflammation
(e.g., Toll-like receptor-4, IL-6), apoptosis and cellular repair (e.g.,
platelet-activating factor), and oxidant stress (e.g. vascular
endothelial growth factor, arginine, nitric oxide
Although nearly 90% of all cases of NEC occur in preterm infants,
the disease can occur in full-term neonates
 Clinical manifestations
The course of the disease varies among infants
(I ) Fulminant, rapidly progressive presentation of signs
consistent with intestinal necrosis and sepsis (common)
(ii) Slow, paroxysmal presentation of abdominal
distension, ileus, and possible infection
 Diagnosis
This is accomplished by a high index of suspicion
and careful clinical observation for nonspecific
signs in infants at risk
 Imaging
Pneumatosis intestinalis the radiologic hallmark used to
confirm the diagnosis 50-75%
Portal or hepatic venous air(in severe cases),pneumoperitoneum
(indicates perforation) with the appearance of gas under the
diaphragm, gasless abdomen indicating ascites
Abdominal ultrasound can be a more sensitive method to detect
intramural air and portal venous gas. With the help of Doppler it
evaluates free fluid, abscess, and bowel wall thickness,
peristalsis and perforation.
Portal venous gas vs perforation
 Blood and serum studies
CBC =Thrombocytopenia, anemia, leucopenia
Serum Electrolytes severe refractory hyponatremia
Blood cultures are positive in 20-30% of cases
CRP for diagnosis and follow up
Grossly bloody stools may be an indication of NEC…but
Approximately 60% of infants will have Hemoccult-positive stools
at any given time during hospitalization without NEC
Bell staging Diagnosis management (usual attention to respiratory,
cardiovascular and hematologic resuscitation
criteria Presumed)

Stage I Clinical signs and symptoms

Non-diagnostic
NPO with IV fluids
• Nasogastric drainage
(suspect) radiograph • CBC, electrolytes, Serial Abdominal x-ray
• Blood culture
• Stool heme test and Clinitest
• Ampicillin and gentamicin × 48 hours

Stage II Clinical signs and symptoms

Pneumatosis intestinalis on
NPO with parenteral nutrition (by CVL once
sepsis ruled out)
(definite) radiograph • Nasogastric drainage
• CBC, electrolytes, Abdominal x-ray, Blood culture
• Stool heme test and Clinitest
• Ampicillin, gentamicin and clindamycin × 14 days
• Surgical consultation

Stage III Clinical signs and symptoms NPO with parenteral nutrition (by CVL once sepsis ruled out)
(Advanced) Critically ill • Nasogastric drainage
Pneumatosis intestinalis or • CBC, electrolytes, Abdominal x-ray Stool heme test and Clinitest
• Ampicillin, gentamicin, and clindamycin × 14 days
pneumoperitoneum
• Surgical consultation with intervention, if indicated:
on radiograph • Resection with enterostomy or primary anastomosis
Surgical management
GI perforation is probably the only absolute indication for
surgical intervention
Perforation occurs in 20% to 30% of patients, usually 12 to 48
hours after the onset of NEC, although it can occur later
 Complications
GI strictures,
Enteric fistulas
Short bowel syndrome, malabsorption and
Chronic diarrhea
 Fluid and electrolyte losses with rapid dehydration
Cholestasis related to long-term Paraenteral nutrition
 prognosis

The incidence of recurrent NEC is 4% and appears to be

independent of type of management
uncomplicated NEC, the long-term prognosis may be comparable
with that of other low birth weight infants
Stage III NEC have a higher incidence of mortality (of over
50%),& growth delay
 Prevention
Preventing premature birth
Induction of GI maturation
Exclusive feeding of human milk based diet Donor breast milk
reduces the risk of NEC compared to formula
Strict adherence to a particular standardized feeding regimen
reduces the risk of NEC
PREBIOTICS are a special form of dietary fiber that acts as a
fertilizer for the good bacteria in your gut
 PROBIOTICS are live bacteria that can be found in yogurt and
other fermented foods
 Reference
Nelson textbook of pediatrics 21st edition