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DISEASES OF THE NEWBORN

DISEASES OF THE NEWBORN. Belen Amparo E. Velasco, M.D. BIRTH INJURIES. INTRACRANIAL INJURIES SPINAL CORD INJURIES NERVE INJURIES. INTRACRANIAL INJURIES. Most common site of fatal and disabling injury – intracranial cavity

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DISEASES OF THE NEWBORN

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  1. DISEASES OF THE NEWBORN Belen Amparo E. Velasco, M.D.

  2. BIRTH INJURIES INTRACRANIAL INJURIES SPINAL CORD INJURIES NERVE INJURIES

  3. INTRACRANIAL INJURIES Most common site of fatal and disabling injury – intracranial cavity Preterm – more prone to hypoxic cerebral injury – spontaneous intraventricular hemorrhage Term infants – more prone to subdural hemorrhages which are traumatic in origin

  4. INTRACRANIAL INJURIES CLINICAL MANIFESTATIONS: Nonspecific Most common: Respiratory distress Pallor Lethargy/somnolence with poor response to stimuli Hypo- or hyperreflexia Convulsions Signs of ICP Unequal pupils Tachy- or bradycardia

  5. INTRACRANIAL INJURIES DIAGNOSIS: Clinical history/course Spinal taps (done in extreme caution) Cranial ultrasount vs CT scan of the head TREATMENT: Minimal handling Management of ICP – fluid restriction Furosemide paCO2 25-30 torr Thermoregulation Oxygen and ventilatory support, as warranted Anticonvulsant for siezure Vitamin K for coagulation defect

  6. SPINAL CORD INJURIES Associated with difficult delivery Types of injury Complete transection – permanent paralysis Partial transection Cord compression – transient paralysis

  7. NERVE INJURIES BRACHIAL PALSY FACIAL PARALYSIS DIAPHRAGMATIC PARALYSIS SCIATIC NERVE INJURY

  8. BRACHIAL PALSY ERB-DUCHENNE PARALYSIS Injury to the 5th-6th crevical root Absent Moro on the affected side KLUMPKE’S PARALYSIS Injury to the 7th cervical and 8th thoracic root Loss of sensory and motor fxn of hand and wrist

  9. BRACHIAL PALSY DIAPHRAGMATIC PARALYSIS Injury to 4th cervical root HORNER’S SYNDROME Injury to the sympathetic ganglion Characterized by ptosis, enophthalmos, miosis, and anhydrosis of the face on the affected side

  10. OTHER NERVE INJURIES FACIAL PALSY Injury to the 7th nerve SCIATIC NERVE INJURY

  11. CLAVICULAR FRACTURE Associated with difficult delivery esp shoulder dystocia

  12. INTRAABDOMINAL INJURIES More common in breech deliveries Commonly ass with liver laceration and intraabdominal bleed

  13. INFECTIONS OF THE NEWBORN INCIDENCE: 1-5 per 1000 livebirths PREDISPOSING FACTORS Prematurity Male gender Maternal infection Difficult delivery Congenital anomalies

  14. INFECTIONS OF THE NEWBORN ROUTES OF ENTRY Hematogenous spread Ascending infection Direct contact along birth canal Breaks in the skin

  15. INFECTIONS OF THE NEWBORN CHANGING SPECTRUM OF PREDOMINANT PATHOGENS EARLY ONSET SEPSIS 1930’s Grp A Strep Others:E.coli,Staph 1940’s E.coli Others:Streptococci 1950’s S. aureus Others:E.coli/Pseudo 1960’s E.coli Others:Pseudo/Kleb 1970’s Grp B Strep Others:E.coli/ Listeria 1980’s Grp B Strep up to E.coli present

  16. LATE-ONSET SEPSIS 1970’s S. aureus Others:Grp D Strep 1980’s Coagulase(-) Others: G(-) enteric Staph & Streptococci up to S. aureus Untypable H.influenzae Present LATE LATE-ONSET SEPSIS 1990’s Candida sp. Coagulase (-)Staph

  17. INFECTIONS OF THE NEWBORN EARLY-ONSET VS LATE-ONSET VS LATE LATE-ONSET EARLY LATE LATE-LATE Onset <4 days >4 days > 30 days Incidence 0.1-0.4% 5-25% - Transmission vertical vertical/ postnatal env. postnatal env. Clinical fulminant insiduous insiduous Sxs pneumonia meningitis multisystem Morbidity neurologic prolonged prolonged handicap hospitalization hospitalization Mortality 15-50% 10-15%

  18. INFECTIONS OF THE NEWBORN DIAGNOSIS OF SEPSIS • Clinical judgment • Recovery of the organism from a meaningful site: Blood culture • UA vs UV specimens - The best alternative is still blood culture from a peripheral vein • Volume of blood – 0.5 ml should be adequate. Larger specimens will often grow faster • Single vs multiple blood cultures- With early onset sepsis, a single culture would suffice. With late-onset sepsis esp with possible CONS, at least two cultures should be obtained.

  19. INFECTIONS OF THE NEWBORN TREATMENT MODALITIES AGAINST SEPSIS METHODS GENERALLY USED: • Early Detection • Fluids, nutrition, antibiotics, ventilatory support • Catecholamines AGENTS POSTULATED TO IMPROVE OUTCOME OF SEPSIS: • Antiserum to endotoxin • Monoclonal antibodies to endotoxin

  20. SPECIFIC INFECTIONS MENINGITIS PNEUMONIA DIARRHEA/NEC URINARY TRACT INFECTION ARTHRITIS CONJUNCTIVITIS

  21. OTHER BACTERIAL INFECTIONS TETANUS NEONATORUM History of unhygienic cord practices Clinical diagnosis characterized by TRISMUS Prevention with tetanus immunization of the mother

  22. OTHER BACTERIAL INFECTIONS CONGENITAL TUBERCULOSIS Ghons complex in the liver Diagnostics include: AFB smear of gastric aspirate Tuberculin test Placental pathologic exam

  23. OTHER BACTERIAL INFECTIONS CONGENITAL SYPHILIS May occur with other STDs Characterized by jaundice, hepatosplenomegaly, macular rashes with wet desquamating skin teeming with spirochetes VDRL for screening. Confirmatory test FTA-ABS

  24. NON-BACTERIAL INFECTIONS TORCHS TOXOPLASMOSIS CONGENITAL RUBELLA CYTOMEGALOVIRUS INFECTION HERPES SIMPLEX INFECTION

  25. NON-BACTERIAL INFECTIONS OTHER VIRAL INFECTIONS: MUMPS HEPATITIS B AIDS

  26. TREATMENT OF INFECTION SPECIFIC THERAPY: Ampicillin Gentamicin 3rd generation Cephalosporin: SUPPORTIVE THERAPY Fluid resuscitation (crystalloids/colloids) Inotropes Nutritional support Immunotherapy

  27. TREATMENT OF INFECTION SPECIFIC THERAPY: TETANUS: Penicillin, TIG, Anticonvulsant TUBERCULOSIS: INH, Rifampicin, PZA SYPHILIS: Penicillin TOXOPLASMOSIS: Spiramycin CYTOMEGALOVIRUS INFECTION: Ganciclovir HERPES SIMPLEX INFECTION/VARICELLA: Acyclovir HIV: Zimovudine

  28. JAUNDICE IN THE NEWBORN BILIRUBIN METABOLISM Heme oxygenase biliverdin Hemoglobin biliverdin bilirubin reductase C0 Iron 1 mole of Hgb = 1 mole each of C0 & bilirubin Transport = bilirubin is transported to liver bound to serum albumin Uptake = nonpolar bilirubin (dissociated from albumin) crosses the hepatocyte plasma membrane, binds to cytoplasmic ligandin (Y protein) for transport to SER Note: Phenobarbital increases concentration of ligandin

  29. BILIRUBIN METABOLISM CONJUGATION SER Bil. Mono glucuronide (CB) Bil. Diglu- curonide Bile canaliculi UCB UDPG-T (Pb) EXCRETION CB biliary tree GIT B-glucuronidase UCB (liver) stool Enterohepatic circ.

  30. JAUNDICE • Color is due to accumulation in the skin of unconjugated, nonpolar, lipid-soluble bilirubin (indirect) formed from Hgb by heme oxygenase, biliverdin reductase, and nonenzymatic reducing agents in the RES

  31. RISK FACTORS FOR HYPERBILIRUBINEMIA • History of previous sibling with hyperbilirubinemia • Decreasing gestational age • Breastfeeding • Large weight loss after birth

  32. CAUSES OF HYPERBILIRUBINEMIA • Enhanced enterohepatic circulation due to: • High levels of intestinal B-glucuronidase •  bilirubin monoglucuronide •  intestinal bacteria •  gut motility with poor evacuation of meconium

  33. CAUSES OF HYPERBILIRUBINEMIA • Defective uptake of bilirubin from plasma •  ligandin • Binding of ligandin by other anions • Defective conjugation due to  UDPG-T activity • Decreased hepatic excretion of bilirubin

  34. PHYSIOLOGIC HYPERBILIRUBINEMIA • Onset of jaundice beyond 24 hours of age • Rise in TSB less then 0.5 mg/dL/hour or 5mg/dl/day • Peaks at 3-5 days • Resolves in a week • Levels not rising above 12mg/dl • No associated illness

  35. NONPHYSIOLOGIC HYPERBILIRUBINEMIA • Onset of jaundice before 24 hours of age • Any elevation of TSB that requires phototherapy • Rise in TSB over 0.5 mg/dL/hour • Signs of underlying illness eg. vomiting, lethargy, poor feeding, excessive weight loss, apnea, tachypnea, To instability • Jaundice persisting after 8 days in FT, 14 days in PT

  36. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • PRODUCTION • Isoimmunizatioin: Rh, ABO, minor blood grps • Erythrocyte biochem. Defect: G6PD, pyruvate kinase, hexokinase, porphyria • Structural abnormalities of RBCs: hereditary spherocytosis, eliptocytosis

  37. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • PRODUCTION • Infection: bacterial, viral, protozoal (mixed jaundice) • Sequestered blood: subdural hematoma, cephalhematoma, ecchymoses, hemangiomas • Others: IDM, obstructive jaundice, galactosemia, hemolysis (DIC, vit K deficiency)

  38. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • UPTAKE • Gilbert’s syndrome • hypothyroidism • galactosemia

  39. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • CONJUGATION • Crigler-Najjar syndromes (types I, II) • Transient familial neonatal hyperbilirubinemia • Galactosemia, hypothyroidism

  40. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • EXCRETION • Idiopathic neonatal hepatitis • Biliary atresia

  41. PATHOLOGIC CAUSES OF HYPERBILIRUBINEMIA • ENTEROHEPATIC CIRCULATION • Breastmilk jaundice (early, late onset) • Starvation • Pyloric stenosis • Intestinal obstruction

  42. WORK-UP FOR JAUNDICE • Total serum bilirubin, B1, B2 • Blood type, Rh, direct Coombs test of the infant • Blood type, Rh, antibody screen of the mother • Peripheral smear and reticulocyte count • Hct

  43. WORK-UP FOR JAUNDICE • If direct Coombs + - antibody on infant’s RBC • G6PD screen, congenital hypothyroidism, metabolic defects (urine metabolic screen) • For neonatal cholestasis: Liver function test, TORCH assay, UTZ, liver biopsy

  44. TREATMENT OF HYPERBILIRUBINEMIA • Phototherapy • Exchange Transfusion • Phenobarbital ? • Tin (Sn) protoporyhyrin or tin mesoporphyrin: inhibits conversion of biliverdin to bilirubin by heme oxgenase • Dose: single IM on D1 of life • Complications:transient erythema

  45. TREATMENT OF CHOLESTASIS • Ursodeoxycholic acid 10mg/k/day • Kasai Procedure for biliary atresia

  46. MANAGEMENT OF HYPERBILIRUBINEMIA IN THE HEALTHY TERM NEWBORN Serum bilirubin = mg/dL

  47. JAUNDICE IN PREMATURE INFANTS

  48. CLINICAL MANIFESTATIONS OF KERNICTERUS • Onset of symptoms: 2-5 d (FT), 7 d (PT) • Early phase: lethargy, poor feeding, loss of Moro reflex • Second phase: prostration, dec. DTRs, respiratory distress • Late phase: opisthotonus, bulging fontanel. Twitching of face & limbs, high-pitched cry • Advanced cases: convulsions, spasm, stiff extension of arms inward rotation with fists clenched

  49. COMPLICATIONS OF KERNICTERUS • Cerebral palsy • Mental retardation • Seizure disorder • Behavioral problem • Dental dysplasia

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