PART-2 COMMON NEONATAL PROBLEMS. (2).pptx

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1. Common Neonatal Problems Prepared by: Bedhasa Girma ( C1 student) Moderator : Dr. Bethelhem ( Assistant prof. of pediatrics and child health) July,2024 1

2. Objectives To know common neonatal problems To know basic management principles of common neonatal problems 2

3. Outline Neonatal Sepsis Perinatal Asphyxia Respiratory Problems RDS Meconium Aspiration Syndrome NEC 3

4. NEONATAL SEPSIS 4

5. Introduction Newborn babies are at higher risk of infection because of their weak immune systems related to their age. Neonatal infection is one of the major causes of mortality and morbidity. Most infections in newborn babies are caused by bacteria, and some by viruses. Bacterial Sepsis and Meningitis often are linked closely in neonates; Meningitis is present with Early-onset sepsis (in 30% of cases), late onset sepsis (in 75% of cases). 5

6. Definition & Classification Neonatal Sepsis: Is SIRS in the presence of or as a result of suspected or proven infection in the first 28 days of life. SIRS= two or more of the following Temperature instability : < 35°C /> 38.5°C Respiratory dysfunction: Tachypnea >2 SD above the mean for age Hypoxemia (Pao2 <70 mm Hg on room air) Cardiac dysfunction: Tachycardia >2 SD above the mean for age Delayed capillary refill >3 sec Hypotension >2 SD below the mean for age Perfusion abnormalities: Oliguria (urine output <0.5 mL/kg/ hr ) Lactic acidosis (elevated plasma lactate and/or arterial pH <7.25) Altered mental status It is typically refers to culture-confirmed infection of the blood, cerebrospinal fluid, and/or urine 6

7. 1. EARLY ONSET NEONATAL SEPSIS ( EONS ): (1st 72 hr of life) Is usually due to vertical transmission by Ascending contaminated amniotic fluid or during vaginal delivery from bacteria colonizing mother's lower genital tract . In chorioamnionitis -risk increases from 1 to 4 percent 2.LATE-ONSET NEONATAL SEPSIS (LONS) ( 72hrs to 30 days ) Can be acquired by : a. Maternal vertical transmission : resulting in initial neonatal colonization that evolves into later infection. b . Horizontal transmission: can be exposed in the hospital or in the community (including family and caretakers ). Most common source of postnatal infections in hospitalized new-borns is hand contamination of healthcare personnel Classifications 7

8. Maternal Neonatal Maternal fever (T >38ºC) during labor or within 24 hours after delivery ROM > 18 hours Prolonged labor (>24 hours) Repeated PV Chorioaminitis ( Triple I ) Maternal UTI or bacteriura Muconium stained liquor Prematurity Resuscitation at birth CPAP Home delivery LBW Vaginal delivery … Invasive procedures (ETT , Umblical catheter,IV ) Bottle feeding Catheterization poor cord care Risk factors of Neonatal Sepsis 8

9. Etiology The Commonest : in order of decreasing frequency : EONS Group B Streptococcus ( term ) Escherichia Coli ( PT ) Klebsiella Staphylococcus aureus Hemophilus influenza Listeria monocytogenes Gram negative anaerobes Fungi Chlamydia trachomatis Some viral causes are: - CMV, HSV, enteroviruses , and HIV. LONS Coagulase negative Staphylococcus Staphylococcus aureus Escherichia Coli Klebsiella Enterobacter Pseudomonas Group B streptococcus Enterococcus Candida albicans … 9

10. EPIDEMIOLOGY Up to 10% of infants have infections in the 1st mo. of life. The overall incidence of neonatal sepsis ranges from 1 to 5 cases per 1,000 live births. Neonatal sepsis is one of top three causes of neonatal death and accounts for approximately 15% of all neonatal deaths. 10

11. Pathophysiology Pathways of Ascending or Intrapartum infection(EONS) 11

12. CLINICAL MANIFESTATIONS of NS Fever Failure to suck Change in behaviour Fast breathing Poor feeding and vomiting Diarrhea High pitched cry Yellowish discoloration of eye and skin Staring Abnormal body movement Loss of consciousness…. HISTORY 12

13. Physical Examination General appearance ▪ Respiratory distress ▪ Lethargy Vital signs: - ▪Tachycardia or sometimes Bradycardia ▪ Tachypnea or Apnea ▪ Hypothermia or fever HEENT: - Bulging fontanel Icteric sclera Pale conjunctiva Respiratory system: Irregular breathing Nasal flaring Cyanosis, grunting IC/SC retractions Lower chest indrawing Use of accessory muscles 13

14. P/E.. Abdomen : - Distended abdomen Tender abdomen (if peritonitis ) Hepatosplenomegaly Genitourinary system : Oliguria Nervous system : -Irritability Poor moro reflex Hypotonia Hyporeflexia Seizure Integumentary system : - Cold, clammy skin Pallor Jaundice Petechiae, purpura Bleeding Edema 14

15. Investigations ( Septic workup ) 1 . CBC with differential: Concern for sepsis if: Total WBC is abnormal (<5,000 or > 20,000) Differential with granulocytes >70%. Anemia Thrombocytopenia(<100,000/mm) 2. Micro- ESR (>15mm/ hr ) or CRP 3. Culture (blood, CSF and urine) 4 . U/A and Gram Stain : IF Sx of UTI 5 . LP : -Consider if concern for meningitis: - (lethargy, irritability, convulsions, bulging fontanel ) 6 . CXR : -Consider if Respiratory Distress or oxygen desaturation 7. Serum electrolyte 15

16. Diagnosis Definitive Clinical syndrome of signs associated with sepsis along with growth of bacteria from one of sterile body parts Probable Suggestive C/F with negative culture but positive biochemical , CSF, U/A tests and X-ray findings Possible Only C/F of sepsis but negative lab and culture 16

17. Sepsis with meningitis A Diagnosis of meningitis should be made based on clinical evidence and risk of infection for babies less than 72 hours of age, For babies age greater than 72 hours of age diagnosed with sepsis : CSF analysis should be done to rule out meningitis despite absence of overt signs of meningitis . The most common bacterial causes of neonatal meningitis are: GBS , E. coli, L. monocytogenes, Strep. pneumoniae CSF analysis suggestive of meningitis: Identification of organism on gram stain or culture ( 70-80 ) WBC count greater than or equal to 15 cells/mm3 in term and 30 cell in preterm Low glucose (less than 2/3 rd of serum value-70%) or 30mg/dl Protein greater than 150 mg/dl in term and 175mg/dl in preterm infant 17

18. Management Principles of Neonatal Sepsis Take culture samples Empirical Antibiotics : in absence of specific signs of focal infection; should cover GBS, gram-negative organisms, Listeria, and Entero coccus - Ampicillin ( Listeria & Entero coccus ) and gentamycin Definitive : based on identification and susceptibility of the offending organism Culture-proven sepsis, the usual course of therapy is 10 days Longer treatment : Meningitis, Osteomyelitis, Septic Arthritis Complication and symptomatic management 18

19. Management 1. General Supportive Measures: Assess airway, breathing, saturation and provide oxygen if needed. Provide maintenance iv fluid for the first 12hr Treat convulsion , hypoglycemia & hypothermia if present. 2 . Antibiotic treatment: - EONS : Ampicillin and Gentamycin ▪ Duration: If positive cultures – minimum 7 days If no improvement after 48 hours, or worsens Change to: Ceftriaxone and gentamicin LONS : (Amp & Gent.). If Critically sick or staphylococcal infection is likely- Triple antibiotics ( Clox ., Amp.& Gent.) If condition worsens after 48 hours- Clox , ceftriaxone and gentamicin or vancomycin and gentamicin . 3 . Treatment of Neonatal Sepsis with Meningitis Antibiotics is the same- higher dose and prolonged duration 19

20. Prevention of NS Aggressive management of suspected maternal chorioamnionitis with antibiotic therapy Vertical transmission of GBS(EONS) is significantly reduced by selective intrapartum chemoprophylaxis, but LONS rate not reduced. Prevention of Nosocomial Infection 20

21. Complications of NS Multi -Organ dysfunction CVS- Septic shock, Cardiac failure Hypoglycemia CNS- Meningitis , Encephalitis, Cerebral palsy & edema Bone marrow dysfunction- ( Anemia , Neutropenia, Thrombocytopenia) GIT: NEC to bowel perforation, liver dysfunction Renal- Adrenal hemorrhage and/or insufficiency, AKI to Renal Failure Respiratory: distress to failure, pulmonary HTN Bleeding disorders- DIC Air leak syndrome 21

22. Perinatal Asphyxia 22

23. Introduction Important Terminologies Anoxia : Indicate the consequences of complete lack of oxygen as a result of a number of primary causes. Hypoxemia : Decreased arterial concentration of oxygen . Hypoxia : Decreased oxygenation to cells or organs . Ischemia : Blood flow to cells or organs that is insufficient to maintain their normal function . Encephalopathy –Altered level of consciousness Hypoxic Ischemic Encephalopathy – Etiologic term to describe encephalopathy caused by ischemia / hypoxia . 23

24. Introduction Definition: PNA WHO defines as:- Failure to initiate and sustain breathing at birth AAP and ACOG Criteria for diagnosis of Perinatal Asphyxia An Arterial Cord PH < 7.0 and base deficit more than 1 2mmol/L APGAR score of less than 7 at 5 minutes . Evidence of altered neurological status (altered level of consciousness, seizures, hypotonia , obtundation ). Evidence of multiple organ involvement (such as that of kidneys, lungs, liver, heart and intestine). This definition using APGAR score is not applicable in Preterm babies Babies with birth trauma Congenital neurologic abnormalities . 24

25. Risk Factors of PNA • Asphyxia can occur before, during, or after birth. • Antepartum cause (20%) o Maternal hypotension of any cause usually APH o Severe anemia o Cardiopulmonary diseases o Maternal hypertension o Maternal diabetes 25

26. RISK FACTORS… Intrapartum cause (70%) o Cord compression (E.g., Cord prolapses) o Meconium Aspiration o Prolonged labor • Postpartum cause (10%) Prematurity Cardiovascular abnormalities Pulmonary malformations Neurologic abnormalities Severe infections Bleeding , shock Congenital heart disease 26

27. EPIDEMIOLOGY Perinatal Asphyxia is the second commonest cause of neonatal mortality . Incidence 1.0 – 1.5 % of live births . Inversely related to gestational age and birth weight until term Higher in post terms than in terms Accounts about 20 % of perinatal deaths 27

28. PATHOPHYSIOLOGY of PNA Note : Perinatal Asphyxia results from compromised placental or pulmonary gas exchange . This lead to Hypoxia and hypercarbia Anaerobic glycolysis and lactic acid production Hypoxia and acidosis Depress myocardial function, leading to hypotension and ischemia Further compromise, specifically to CNS and kidney 28

29. Clinical Manifestations • Depends on duration & severity of Asphyxia A. In the fetus: Slow , weak, irregular Heartbeats ▪ Scalp pH less than 7.2 B. After delivery: ▪ Meconium Staining of the newborn, amniotic fluid and vernix caseosa ▪ Decreased consciousness with failure of spontaneous breathing. ▪ Low Apgar score with cyanosis and flaccidity . 29

30. Clinical…. C. Later manifestations: Multi-organ Dysfunction CNS : Hypoxic- Ischemic Encephalopathy ( HIE) Cardiac : - Heart failure, hypotension Respiratory : - Meconium Aspiration, PPHN, RD Renal : - Acute tubular necrosis, hematuria, oliguria GIT : - NEC and Intestinal Perforation Metabolic : -Hypoglycemia, hypocalcemia , hypomagnesemia,hyponatremia , lactic acidosis and syndrome of inappropriate secretion of ADH 30

31. Hypoxic- Ischemic Encephalopathy (HIE) HIE : is a leading cause of neonatal brain injury, morbidity, and mortality globally. Incidence : Developing 26 per 1,000. Modified sarnat scoring for severity of HIE 31

32. Investigations of PNA CBC-(Anemia) RBS Urine analysis Stool for blood Renal function Liver function test Echocardiography as needed Serum electrolytes EEG CXR Brain imaging-MRI 32

33. MANAGEMENT PRINCIPLE Keep NPO for severe PNA - for 48 hrs ( risk of NEC ). Start feeding (with 5 to 10ml) when the neonate is passing meconium, clear gastric content, normoactive bowel sound and then advance as tolerated Fluid Management- 2/3 rd of the maintenance fluid ( avoid both overload and inadequate circulating volume) Oxygenation –maintain Saturation b/n 90-95% Maintain normal temperatures Cooling therapy is the standard treatment for HIE Correction of Metabolic States : Keep Blood glucose in the normal range. Hypoglycemia -has to be treated Hypocalcemia (can cause seizure and decreased cardiac contractility) 33

34. MANAGEMENT PRINCIPLE … Seizure Treatment Management of other organ system dysfunctions CHF – diuretics, dopamine or dobutamine Acute Renal Failure – dopamine Parent counseling has to be the integral part of management Follow up- with Perinatal Asphyxia Follow up chart 34

35. CPX: Multiorgan Systemic Effects of Asphyxia Early Seizure Poor feeding Infections Renal failure Multi-Organ dysfunction CNS : HIE,ICH RS : MAS, RDS, Pulm.h’ge CVS : Heart Failure GIS:NEC OTHERS : Hypoglycaemia ,hypocalcaemia, hyponatremia Late Mental retardation Cerebral palsy Epilepsy … 35

36. Respiratory Problems RDS Meconium Aspiration Syndrome 36

37. Formerly known as Hyaline Membrane Disease (HMD), Neonatal RDS: describes a disease typical of preterm infants that is caused by insufficient pulmonary surfactant in alveoli. Due to impaired synthesis and secretion of surfactant . 37 RESPIRATORY DISTRESS SYNDROME (RDS)

38. Introduction Surfactant is a mixture of phospholipids and proteins Produced by type II alveolar cells. It reduces alveolar surface tension, Preventing the alveoli from collapsing. Surfactant deficiency is most likely to occur in preterm infants, because: Surfactant production begins at approximately 20 weeks gestation; But not reach the surface of the lungs It appears in Amniotic Fluid between 28 and 32 weeks. Mature levels of pulmonary surfactant are present usually after 35 weeks of gestation. 38

39. RISK FACTORS of RDS : Prematurity Low birth weight Birth Asphyxia Multifetal gestation Diaphragmatic hernia of newborn Newborn of Diabetic mother Male predominance C/S 39

40. Epidemiology Incidence is inversely related to gestational age and birth weight. Less than 28 weeks: 60 – 80%, 32-36 weeks: 15-35 % >37 weeks : 5 %. 40

41. Pathophysiology Contributing factors in the pathogenesis of hyaline membrane disease. The potential “ vicious circle ” perpetuates hypoxia and pulmonary insufficiency. 41

42. Clinical Manifestations… RDS Signs usually appear with in minutes of birth , but may not be recognized for several hours in larger premature infants. Characteristically : Tachypnea , Nasal flaring, fine crackles Subcostal and intercostal retractions Cyanosis and Expiratory grunting. Markedly decreased air entry bilaterally The natural course is characterized by: Progressive worsening of cyanosis and dyspnea . In most cases, the symptoms and signs may reach a peak within 3 days , after which improvement is gradual . 42

43. Diagnosis of RDS Shake test is a reliable means of diagnosing RDS in preterm infants less than 34 weeks Performed on the gastric fluid within one hour of age by passing a nasogastric tube into the stomach. 0.5 ml of gastric fluid is obtained then mixed with an equal volume of normal saline for 15 sec; Add 1 ml of 95 to 100% ethanol and agitate the mixture for 15 sec. Let it stand for 15 min, then examine for bubbles 43

44. Shake test Interpretation 44

45. Diagnosis… Chest X-ray - Low volume in poorly inflated lungs is typical finding. Grade-1 : Fine homogeneous reticulogranular pattern Grade-2 : Widespread air bronchograms become visible Grade-3 : Cardio pulmonary differentiation difficult due to alveolar shadowing Grade-4 : Complete white-out of the lung fields 45

46. 46 There is a diffuse ground-glass or finely granular appearance (circle) in a bilateral and symmetric distribution. Hypoaeration is seen in nonventilated lungs (double arrow).

47. INVESTIGATION…RDS CBC Chest X-ray Interstitial pulmonary edema with perihilar streaking Diffuse , fine, reticulogranular (ground-glass) densities with low lung volumes and air bronchograms Atelectasis Arterial Blood Gas Analysis - findings are ; initially hypoxemia and later by progressive hypoxemia , hypercapnia , and variable metabolic acidosis . ECHO : If no response to surfactant replacement (to rule out cyanotic congenital heart disease) Septic work up- Sepsis and RDS may co exist 47

48. Prevention Prenatal screening for markers of fetal lung immaturity Lecithin/ Sphingomyelin ratio (L/S) ratio ( ≥ 2 is considered mature ) Lamellar body count- > 50,000 per microliter of Amniotic Fluid has been correlated with lung maturity Antenatal corticosteroids : is the only preventive strategy to decrease occurrence of RDS. Best if given at least 24-48 hrs before delivery Given to pregnant women < 34 weeks of GA Prevention of preterm delivery 48

49. Management Principles Basic supportive care: ( ( thermoregulatory, circula tory, fluid, electrolyte, and respiratory ) Thermoregulation - Require an optimum thermal environment to minimize oxygen consumption and oxygen requirements. Maintained body temperature between 36.5 and 37. Fluid:- Maintenance of fluid requirements Antibiotics- EONS may be indistinguishable from RDS Mechanical Ventilation: For Infants with respiratory failure or persistent apnea require assisted mechanical ventilation . Warm humidified oxygen should be provided Nasal CPAP with continuous monitoring Physiologic O2 saturation in neonates is around 90%. A saturation of 100% is considered toxic for neonates ! Surfactant therapy Multi-dose endotracheal instillation of exogenous surfactant has dramatically improved survival and reduced the incidence of pulmonary air leaks 49

50. Complications Mixed Respiratory-Metabolic Acidosis with hypoxia progress to Respiratory Failure with multisystem organ dysfunction due to inadequate oxygen delivery Pulmonary Air Leaks: Pulmonary interstitial emphysema Pneumothorax Pneumomediastinum Intracranial bleeding ( Intraventricular hemorrhage) Pulmonary hemorrhage Bronchopulmonary dysplasia Retinopathy of prematurity 50

51. Meconium Aspiration Syndrome 51

52. Introduction Meconium is the first stool of the baby, which is: Odorless, thick, blackish green material, Consisting of desquamated cells from GI tract, skin, lanugo, fatty material from the vernix , Amniotic Fluid and digestive enzymes. 52

53. Introduction… Definition : MAS is the Neonatal Respiratory Distress that occurs in a newborn in the context of Meconium-stained Amniotic Fluid ( MSAF) where respiratory symptoms cannot be attributed to another etiology . 53

54. Common Risk factors Prolonged labor Post maturity Maternal illness : Infection, Diabetes, Hypertension Umbilical cord complications Intrauterine Growth Retardation Placental Insufficiency Oligohydraminos 54

55. Epidemiology MSAF complicates approximately 10 – 15 % of deliveries And 3 to 4% of neonate born through MSAF develop Meconium Aspiration Syndrome ( MAS ). 30% need mechanical ventilation 3-5% die 55

56. Pathophysiology of MAS MAS occurs when a neonate inhales thick, particulate meconium. Usually occur in term & post term neonates . This is usually secondary to fetal hypoxia, which causes Increased peristalsis , Relaxation of anal sphincters with the release of meconium in to Amniotic Fluid ; And reflex gasping which leads to aspiration of the meconium in to the lungs. 56

57. Pathophysiology … Prompt Significant Aspiration of thick meconium can induce 4 major pulmonary effects: Airway obstruction, Surfactant dysfunction, Chemical pneumonitis and Bacterial pneumonia 57

58. 58

59. Clinical manifestations of MAS Meconium staining , Nails, Skin, Umbilical cord Low APGAR score Increased AP diameter of the chest ( Barrel ) Tachypnea , retractions, grunting, and cyanosis Bradycardia, Nasal flaring, Rhonchi Pneumothorax , or pneumomediastinum 59

60. Downes Score for Grading Respiratory Distress in a term baby 60

61. Investigations of MAS CBC : Hb and Hct levels (perinatal blood loss -> postnatal stress/low oxygen carrying capacity) polycythemia (chronic fetal hypoxia ) Serum electrolyte: CXR: The typical chest radiograph is characterized by: Patchy infiltrates, Coarse streaking of both lung fields Increased anteroposterior diameter, and Flattening of the diaphragm with possible pneumothorax ECHO : Brain MRI & CT : are indicated in stable neonate with abnormal neurological examination 61

62. Management Principle of MAS Oxygen: is critically important, maintain saturation 90-95 % Antibiotics : are indicated, since the clinical picture of MAS and congenital pneumonia are similar. Treat the complications: (pneumothorax, PPHN and pneumonia, respiratory failure ). Surfactant administration: may be beneficial. Inhaled Nitric Oxide: is indicated for associated persistent pulmonary hypertension .( Vasodilator ) Sedation and analgesia . 62

63. Complications of MAS Short Term Complications Persistent Pulmonary Hypertension Air Leak Syndromes— pneumomediastinum , pneumothorax , cystic lung disease Pulmonary haemorrhage Perinatal Asphyxia Long Term Complications Reactive airway disease Neurodevelopmental impairment: related to- prolonged intubation, mechanical ventilation, prolonged oxygen need 63

64. NECROTIZING ENTEROCOLITIS (NEC) 64

65. Introduction DEFINITION : NEC is an acute inflammatory disease in the newborn’s intestine characterized by haemorrhagic necrosis , which may lead to perforation and destruction of the gut. Unknown aetiology . Although mainly a disease of prematurity, it can also occur in full term infants It is a life-threatening illness with a mortality rate as high as 50 percent . 65

66. Risk Factors of NEC Prematurity :is the single greatest risk factor (90% of NEC). A mean onset between 30 and 32 weeks Immature host defence, immature regulation of circulation Formula feeding : 90 to 95% affected neonates had been fed formula, IUGR Sepsis Hypoxia Altered intestinal microbe ( dysbiosis )/ prolonged antibiotic use 66

67. Epidemiology Epidemiologic studies have reported changes in NEC incidence in the past decade. In very low birth weight infants ( VLBW<1,500gm ) overall rate of NEC was 7.6 % s (2006-2017) From 2006–2017, there was a significant reduction in the prevalence of medical but not surgical NEC; Mortality with NEC also decreased from: 20.7 % to16.8% among infants with medical NEC , and 36.6 % to 31.6% for neonates with surgical NEC The most commonly affected part is the terminal ileum and proximal colon parts of intestine. 67

68. Pathophysiology The pathophysiology of NEC is inflammation of the Intestine leading to bacterial invasion causing cellular damage and cellular death and Necrosis of the colon and Small Intestine. 68

69. Clinical Manifestations GASTROINTESTINAL Abdominal distention Abdominal tenderness Feeding intolerance Delayed gastric emptying Emesis Occult/gross blood in stool Change in stool pattern/diarrhea Abdominal mass Erythema of abdominal wall SYSTEMIC Lethargy Apnea/respiratory distress Temperature instability Acidosis (metabolic and/or respiratory) Glucose instability Poor perfusion/shock Thrombocytopenia DIC 69

70. Investigations CBC (Leucopenia, thrombocytopenia) Serum Electrolytes ( Hyponatremia , hypokalemia, metabolic acidosis) Coagulation profile - Disseminated intravascular coagulopathy (DIC) RBS Plain Abdominal X-ray Pneumatosis intestinalis Dilated loops , Ileus Thickened bowel wall, Pneumoperitoneum 70

71. NEC Staging using a combination of clinical and radiographic signs NEC stage Features X-ray findng 1. Suspected (stage I) Occult blood on S/E Overt blood on stool Normal 2. Definite (stage II ) No bowel sound, distended bowel, Bowel wall cellulitis , tenderness & ascitis Pneumatosis intestinalis , Portal venous gas, or ileus 3. Advanced (stage III) signs of stage II plus severe systemic signs of inflammation and acidosis with or without signs of intestinal perforation Multiple air-fluid level Air under the diaphragm 71

72. Summary of risk factors , mechanisms of injury ,associated presentation and management approaches . 72

73. Complication and prognosis of NEC Sepsis Intestinal strictures, Short Bowel Syndrome, Neurodevelopmental delay Mortality 30 to 40% Recurrence (6%) 73

74. Reference Nelson Textbook of Paediatrics 22 nd Edition. Clinical Reference Manual for Advanced Neonatal Care MOH, Ethiopia 2021 74

75. Thank you 75