IVH (intraventricular hemorrhage): ?????

1
????????(1)

• IVH (intraventricular hemorrhage) ?????
• PVL (periventricular leukomalacia) ?????
• ROP (retinopathy of prematurity)????????
• RDS (respiratory distress syndrome) ???????

2
????????(2)

• BPD (bronchopulmonary dysplasia) ????????
• NEC (necrotizing enterocolitis) ?????
• PDA (patent ductus arteriosus) ???????

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Gestational age estimation and birth weight
classification

• Infant are classified by GA as
• Preterm (lt37 weeks)
• Term (37-41 6/7 weeks)
• Postterm (42 weeks or more)
• Birth weight classification
• Normal birth weight (NBW) 2500 gm or more
• Low birth weight (LBW) lt 2500 gm
• Very low birth weight (VLBW) lt 1500 gm
• Extreme low birth weight (ELBW) lt1000gm

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Prematurity

• Incidence 5-10
• Etiology most for unknown reasons

• Low socioeconomic status
• Malnutrition
• Women under age 16 or over 35
• Increased maternal activity
• Smoking
• Ac. or chr. maternal illness

• Multiple-gestation births
• Prior poor birth outcome
• Obstetric factors
• Fetal conditions
• Inadvertent early delivery

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Problem of prematurity (1)

• Respiratory
• Respiratory distress syndrome (RDS)
• Apnea
• Bronchopulmonary dysplasia (BPD)
• Neurologic
• Intraventricular hemorrhage (IVH)
• Periventricular leukomalacia (PVL)
• Cardiovascular
• Hypotension
• Patent ductus arteriosus (PDA)

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Problem of prematurity (2)

• Hematologic
• Anemia
• Hyperbilirubinemia
• Nutritional
• Feeding problems
• Type, amount, and route of feeding
• Gastrointestinal
• Necrotizing enterocolitis (NEC)
• Metabolic
• Acidosis
• Hyper- or hypoglycemia
• hypocalcemia

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Problem of prematurity (3)

• Renal
• Low GFR
• Inability to handle water, solute, and acid loads
• Temperature regulation
• Hypothermia and hyperthermia
• Immunologic
• Greater risk for infection
• Ophthalmologic
• Retinopathy of prematurity (ROP)

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Intraventricular hemorrhage (IVH)

• In premature infant --occurs in the gelatinous
  subependymal germinal matrix
• --highly vascular area with immature blood
  vessels
• In term infant
• --germinal matrix become attenuated and
  tissues vascular support has strengthened.

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Intraventricular hemorrhage (IVH)

• The incidence of IVH ---6070 of 500-750 g
  infants---1020 of 1000-1500 g infants
• 8090 of cases occur between birth and the 3rd
  day of life 50 occur on the 1st day.
• 2040 of cases progress during the 1st week of
  life delayed hemorrhage may occur in 1015 of
  patients after the 1st week of life.
• New-onset IVH is rare after the 1st month of life
  regardless of birth weight.

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Predisposing factors for IVH

• --prematurity--RDS--Hypoxic-ischemic or
  hypotensive injury--reperfusion of damaged
  vessels--increased or decreased cerebral blood
  flow--reduced vascular integrity--increased
  venous pressure--pneumothorax--hypervolemia--hy
  pertension

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Clinical manifestations

• Diminished or absent Mono reflex
• Poor muscle tone
• Lethargy
• Apnea
• Somnolence
• Periods of apnea, pallor, or cyanosis
• Failure to suck well
• Abnormal eye signs
• Decreased muscle tone or paralysis
• Metabolic acidosis
• Shock
• Decreased hematocrit or its failure to increase
  after transfusion

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Periventricular leukomalacia (PVL)

• A common associated cystic finding
• May be due to prenatal or neonatal ischemic or
  reperfusion injury
• The result of necrosis of the periventrucular
  white matter
• Damage to the corticospinal fibers in the
  internal capsule.

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Periventricular leukomalacia (PVL)

• Usually asymptomatic until the neurological
  sequelae of white matter necrosis become apparent
  in later infancy as spastic diplegia.
• May be present at birth but usually occurs later
  as an early echodense phase (3-10 days of life)
  followed by the typical echolucent (cystic) phase
  (14-20 days of life).

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Intraventricular hemorrhage (IVH)

• Grade I - Germinal matrix hemorrhage
  (subependymal region or less than 10 of the
  ventricle 35 of IVH)
• Grade II - IVH with 10-50 filling of the
  ventricle (40 of IVH)
• Grade III more than 50 involvement with
  dilated ventricles
• Grade IV - IVH with extension into the parenchyma

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Patent ductus arteriosus (PDA)

• Connect the main pulmonary trunk (or proximal
  left pulmonary artery) with the descending aorta,
  5-10 mm distal to the origin of the left
  subclavian artery
• Arising from the distal dorsal sixth aortic arch
• Is well developed by the sixth week of
  gestational age
• Is more prevalent in female than male
• Is a frequent complication of HMD in preterm
  infant, in infant born at high altitudes

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Normal postnatal closure

• First stage contraction and cellular migration
  of medial smooth muscle --gtresult functional
  closure commonly occurred within 12 hours in full
  term baby
• Second stage connective tissue formation and
  replacement of muscle fibers with fibrosis--gt
  ligmentum arteriosum
• Both PGE2 and PGI2 relax the ductus arteriosus

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Incidence

• Prematurity inverse with GA, PDA is found in
  about 45 of infant under 1750g and 80 in
  infants weighting lt1000g
• Risk factor
• 1.RDS and surfactant treatment
• 2.Fluid overload
• 3.Asphyxia
• 4.Congenital syndrome,congenital heart disease
• 5.High altitude

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Pathophysiology

• Ductal constriction is caused by multiple factors
  1. oxygen 2. the level of prostaglandin 3.
  available ductus muscle mass
• Within the first hours after birth -gt fall in
  pulmonary vascular resistance and a rise in
  systemic resistance if PDA opened left to right
  shunt() --gt result in increased pulmonary blood
  flow ,left ventricular volume overload, increased
  left ventricular end-diastolic volume and
  pressure -gtCHF

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Pathophysiology

• Renal, mesenteric and cerebral blood flow
  decreased due to ductal steal
• These with moderate and large ducts are prone to
  the development of pulmonary vascular obstructive
  disease by 1 year of age or beyond
• Preterm infant may develop CHF earlier because of
  incomplete development of the medial musculature
  in the small pulmonary arterioles
• Among those with RDS, they may be a initial
  period of improvement as the pulmonary status
  improves

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Clinical findings (Term infants )

• Pulmonary vascular resistance determines the
  clinical manifestations
• A continuous murmur is heard infrequently
• Large PDA has
• 1. bounding peripheral pulse pressure,
• 2. wide pulse pressure(difference between
  systolic and diastolic pressure)
• 3. hyperactive precordium due to elevated
  stroke volume

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Clinical findings (Term infants )

• 4. Hypotension particular in these of ELBW
  
• 5. Heart failure in large PDA doesnt develop
  until 3 to 6 weeks of age
• Associated with pulmonary disease ,left heart
  obstructive lesion and coarctation of aorta ,
  pulmonary resistance may be high --gt right to
  left shunt --gt no murmur

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Clinical findings (preterm infants)

• 1.The same clinical sign as term baby
• 2.However, many preterm baby with large PDA
  have no murmur
• 3.Most will have an increased pressure

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Diagnosis

• Chest x ray cardiac enlargement ,pulmonary
  plethora, a prominent main pulmonary artery and
  left atrial enlargement
• EKG left ventricular hypertrophy, left atrial
  hypertrophy
• Echocardiography
• 1. M-mode normal LA Aa ratio in infants is
  between 0.8-1.0, A ratio gt 1.2 suggests left
  atrial enlargement (in the absence of left
  ventricular failure or volume overload)
• 2. 2-DPDA

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Treatment

• Term infants No evidence of cardiovascular
  embarrassment should be followed and catheter
  closure or thoracoscopic or surgical diversion
• Digoxin and diuretics for PDA with CHF

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Preterm infants

• 1. Ventilator support and fluid restriction
• 2. Indomethacin treatment produces closure in
  85 of patients
• 3. Prophylactic administration of indomethacin
  early after birth in very premature infants
  (lt1250 g) decreased the incidence of PDA, CHF,
  IVH and possibly mortality ----but not routine
  due to the risk of leukomalacia, decreased renal
  function, platelet function and NEC

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Preterm infants

• 4.Ibuprofen(10 mg/kg) may have fewer side effect.
  Archives of Disease in Childhood Fetal
  Neonatal Edition. 76(3)F179-84, 1997 May.
• (ibuprofen did not significantly reduce
  mesenteric and renal blood flow velocity.)
  Journal of Pediatrics. 135(6)733-8, 1999 Dec.
• 5.Blood transfusion in anemic preterm baby
  diminishes the left ventricle volume overload and
  hasten ductus closure by increasing arterial
  oxygen content

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Preterm infants

• Early indomethacin treatment (in premature
  infants with respiratory distress syndrome)
• improves PDA closure but is associated with
  increased renal side effects and more severe
  complications and has no respiratory advantage
  over late indomethacin administration in
  ventilated, surfactant-treated, preterm infants
  lt32 weeks' gestational age.(Journal of
  Pediatrics. 138(2)205-11, 2001 Feb.)

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PDA

• Coil occlusion is a safe and effective method of
  percutaneous closure of small to moderate-size
  (minimum diameter lt or 4 mm) PDAs.
• The largest PDA that can be closed with this
  technique remains to be determined. Journal of
  Pediatrics. 130(3)447-54, 1997 Mar.

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Age of onset of treatment IV dosage(mg/dl) IV dosage(mg/dl) IV dosage(mg/dl)
Age of onset of treatment 1st 2nd 3rd 12-24 hours,4th dose or 2nd course
lt3 days 0.2 0.1 0.1
3-7 days 0.2 0.2 0.2
gt7 days 0.2 0.25 0.25
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Contraindications for indomethacin

• 1.serum creatine gt1.7 mg/dl
• 2.Frank renal or gastrointestinal bleeding or
  generalized coagulopathy
• 3.NEC
• 4.sepsis

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Necrotizing enterocolitis(NEC)
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Necrotizing enterocolitis

• 1.Definition2.Incidence3.Pathology
  Pathogenesis4.Clinical manifestations5.Diagnosis
  6.Management7.Complication

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Definition

• The most common life-threatening emergency of the
  gastrointestinal tract in the newborn stage.
• An acquired neonatal disorder characterized by
  various degrees of mucosal or transmural necrosis
  of the intestine.

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Incidence

• Decreased birth weight gestational age ?
  incidence fatility
• Rare in term infants.
• Overall mortality ? 20 40.
• Neonatal ICU ? 1 5
• No association with or race.
• Occures sporadically or in epidemic clusters.
• Most involved the distal part of the ileum and
  the proximal segment of colon.

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Pathology Pathogenesis (1)

• Cause remains unclear but is multifactorial.
• No proven cause has been estabilished.
• The greatest risk Premature
• Interactions between mucosal injury (ischemia,
  infection, inflammation) and the hosts response
  to the injury (circulatory, immunologic,
  inflammatory)

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Pathology Pathogenesis (2)

• Clustering of the cases infectious agent
• (E. Coli., Klebisella, Enterobacter,
  Salmonella, Coronavirus, Rotavirus, Enterovirus)
• No pathogen is identified.
• Rarely occures before enteral feeding.
• Much less common in infants fed human milk.
• Triad intestinal ischemia, oral feeding,
  pathogenic organisms

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• Initial ischemic or toxic mucosal damage
• Loss of mucosal integrity
• Enteral feedings Bacterial proliferation
• Necrosis of the intestine
• Gas accumulation in the submucosa of bowel wall
  
• (penumatosis intestinalis)
• Transmural necrosis or gangrane
• Perforation, Sepsis, Death

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Clinical manifestations

• A variety of signs and symptoms and may be onset
  insidiously or suddenly.
• Usually occurs in the first 2 weeks.
• Age of onset is inversely relatede to the
  gestational age (VLBW ? 3 month).
• First signs abdominal distension with
• gastric retention.
• 25 ? bloody stool
• Progress maybe be rapid, but unusually to
  progress from mild to severe after 72 hr.

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Signs and symptoms associated with necrotizing
enterocolitis

• Systemic
• Lethargy
• Apnea/ respiratory distress
• Temperature instability
• Acidosis
• Glucose instability
• Poor perfusion/ shock
• DIC
• Positive results of blood culture

• Gastrointestinal
• Abdominal distention
• Abdominal tenderness
• Feeding intolerance
• Delayed gastric emptying
• Vomitting
• Occult/gross blood stool
• Change in stool
• pattern/ diarrhea
• Abdominal mass
• Erythema of abdominal
• wall

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Diagnosis

• A very high index of suspicion in treating
  infants at risk is essential.
• Clinical triad Feeding intolerance, abdominal
  distention, grossly bloody stools.
• Lab studies CBC, electrolytes, blood culture,
  stool screening, stool culture,
• Radiologic studies
• 1.X-ray of abdomen
• Pneumomatosis intestinalis (50-75)
• Portal venous gas
• 2.Hepatic ultrasonography

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• KUB demonstrating abdominal distention, hepatic
  portal venous gas (arrow),and bubbly appearance
  of pneumatosis intestinalis (arrowhead). The
  latter two signs are pathognomonic for NEC.

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• Intestinal perforation. Cross-table abdominal
  roentgenogram in a patient with NEC demonstrating
  marked distention and massive pneumoperitoneum as
  evident by the free air below the anterior
  abdominal wall.

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Management

• Basic NEC protocol
• 1.Nothing by mouth (NPO)
• 2.Use of a nasogastric tube
• 3.Antibiotics
• 4.Monitoring of vital signs abdominal
  circumference
• 5.Removal of the umbilical catheter
• 6.Monitoring of fluid intake and output
• 7.Monitoring for gastrointestinal bleeding
• 8.Laboratory monitoring
• 9.Septic workup
• 10.Radiologic studies

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Management by Stages

• Classified by clinical syndrome
• (1986 Walsh and Kliegman)

• Stage I Suspected NEC
• Systemic Nonspecific, apnea, bradycardia,
  and temperature instability
• Gastrointestinal Increased gastric residuals
  Occult blood stool
• Radiographic Normal or nonspecific
• Treatment NPO with antibiotics for 3 days

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Stage II A Mild NEC

• Systemic Nonspecific, similar to stage 1
• Gastrointestinal Absent bowel sounds and Gross
  blood stools.
• Radiographic Ileus with dilated loops,
• focal areas of pneumatosis intestinalis
• Treatment NPO with antibiotics for 10-14 days

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Stage II B Moderate NEC

• Systemic Mild metabolic acidosis and
• mild thrombocytopenia
• Gastrointestinal Tenderness, abdomianl
• wall edema, palpable mass
• Radiographic Extensive pneumatosis,
• portal venous gas, early ascites
• Treatment Similar to stage II B

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Stage III A Advanced NEC

• Systemic Hypotension, bradycardia,
• respiratory failure,
  coagulopathy
• severe metabolic acidosis
• Gastrointestinal Spreading edema, erythema
• induration of the
  abdomen
• Radiographic Prominent ascites
• Treatment paracentesis, fluid resuscitation
• ,inotropic agent support,
  
• ventilator support,.

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Stage III B Advanced NEC

• Systemic Deteriorating vital signs,
• shock, electrolyte imbalance
• Gastrointestinal Perforation of the bowel
• Radiographic Perforation of the bowel
• Treatment Surgical management

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Surgical management

• Indication for operation
• 1.Evidence of intestinal perforation
• 2.A spersistent, fixed senile loop
• 3.Erythema of the abdominal wall
• 4.A palpable mass
• 5.Brown paracentesis fluid with organisms on Gram
  stain
• 6.Failure to response to medical treatment.

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Prognosis

• Pneumatosis intestinalis 20 fails in medical
  management , 9-25 die.
• About 75 of all patient survival ?
• 50 develop a long-term complication
• The 2 most common complications are intestinal
  stricture and short-gut syndrome.

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Complication (1)

• Intestinal stricture
• 1.Occur in 10 of patirnts.
• 2.Diagnosed by barium enema
• 3.S/S feeding intolerance and bowel
• obstruction occur 2-3 weeks after
• recovery from the initial event
• 4.Tx. Resection of the affected portion.

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Complication (2)

• Short-gut syndrome
• 1.Most in patients lost most of the small
• bowel or portion of the ieocecal valve.
• 2.S/SMalabsorption, growth failure,
• malnutrition
• 3.Take 2 years for the gut to grow and adapt.
• 4.Follow the nutritional condition.

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55

• 1.????????? (Intraventricular hemorrhage)
  ????????
• A.???????????(posthemorrhagic hydrocephalus)
• B.?????
• C.??????????
• D.1015 ???????

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• 2.??????????????
• ?????
• ???????????????
• ???????
• ???????

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• 3.????????????,?????
• ?????
• ????
• ????
• ??????

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• 4. ??PDA???,??????
• ????????12
• Indomethacin ????PDA
• ???????PDA
• Prostaglandin E ????PDA

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• 5. ??PDA???,?????
• PDA???????pansystolic murmur
• ?????????
• ????PDA??indomethacin????
• ????????indomethacin???????PDA

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• 6.??????????????????
• (A)???????????
• (B)???????,????????
• (C)X?????????? (pneumomatosis intestinalis)
• (D)???????????

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• 7. ?????????????????
• (A)????????distal ileum and proximal colon
• (B)????????????????
• (C)??X???pneumomatosis intestinalis
• (D)?????40??

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• 8.??????????,???????
• (A)?????????,???????
• (B)?????,???????
• (C)??????????????
• (D)???????????

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• 9.???????????????,
• ????????
• (A)????
• (B)?????
• (C)????
• (D)??????