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IVH (intraventricular hemorrhage): ?????

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(1) IVH (intraventricular hemorrhage): PVL (periventricular leukomalacia): ROP (retinopathy of prematurity ... – PowerPoint PPT presentation

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Title: 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) ???????

3
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

4
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

5
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)

6
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

7
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)

8
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.

9
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.

10
(No Transcript)
11
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

12
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

13
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.

14
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).

15
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

16
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

17
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

18
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

19
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

20
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

21
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

22
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

23
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

24
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

25
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

26
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

27
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

28
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.)

29
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.

30
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
31
Contraindications for indomethacin
  • 1.serum creatine gt1.7 mg/dl
  • 2.Frank renal or gastrointestinal bleeding or
    generalized coagulopathy
  • 3.NEC
  • 4.sepsis

32
Necrotizing enterocolitis (NEC)
33
Necrotizing enterocolitis
  • 1.Definition 2.Incidence 3.Pathology
    Pathogenesis 4.Clinical manifestations 5.Diagnosis
    6.Management 7.Complication

34
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.

35
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.

36
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)

37
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

38
  • 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

39
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.

40
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

41
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

42
  • KUB demonstrating abdominal distention, hepatic
    portal venous gas (arrow),and bubbly appearance
    of pneumatosis intestinalis (arrowhead). The
    latter two signs are pathognomonic for NEC.

43
  • 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.

44
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

45
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

46
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

47
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

48
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,.

49
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

50
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.

51
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.

52
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.

53
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.

54
?????!
55
  • 1.????????? (Intraventricular hemorrhage)
    ????????
  • A.???????????(posthemorrhagic hydrocephalus)
  • B.?????
  • C.??????????
  • D.1015 ???????

56
  • 2.??????????????
  • ?????
  • ???????????????
  • ???????
  • ???????

57
  • 3.????????????,?????
  • ?????
  • ????
  • ????
  • ??????

58
  • 4. ??PDA???,??????
  • ????????12
  • Indomethacin ????PDA
  • ???????PDA
  • Prostaglandin E ????PDA

59
  • 5. ??PDA???,?????
  • PDA???????pansystolic murmur
  • ?????????
  • ????PDA??indomethacin????
  • ????????indomethacin???????PDA

60
  • 6.??????????????????
  • (A)???????????
  • (B)???????,????????
  • (C)X?????????? (pneumomatosis intestinalis)
  • (D)???????????

61
  • 7. ?????????????????
  • (A)????????distal ileum and proximal colon
  • (B)????????????????
  • (C)??X???pneumomatosis intestinalis
  • (D)?????40??

62
  • 8.??????????,???????
  • (A)?????????,???????
  • (B)?????,???????
  • (C)??????????????
  • (D)???????????

63
  • 9.???????????????,
  • ????????
  • (A)????
  • (B)?????
  • (C)????
  • (D)??????
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