prematurity_and_low_birth_weight,_asphxia_neonatorum new.pptx

abd12medy 33 views 85 slides Jul 19, 2024
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About This Presentation

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PREMATURITY AND LOW BIRTH WEIGHT, ASPHYXIA NEONATORUM Presentors LUGHANO O MWAMBENE AUGUSTIN EMMANUEL Supervisor; Dr. …………..

Presentation outline for prematurity Introduction Epidemiology Complications of prematurity Short term complications Long term complications Conditions for discharge Monitoring after discharge

Introduction Prematurity is a term for the broad category of neonates born at less than 37 completed weeks of gestation. Preterm birth is the leading cause of neonatal mortality and the most common reason for antenatal hospitalization

Classification of prematurity by birth weight or gestational age Birth weight Low birth weight (LBW) <2500 g Very low birth weight (VLBW) <1500 g Extremely low birth weight (ELBW) <1000 g Gestational age Late preterm 34 weeks to <37 weeks Moderate preterm 32 weeks to <34 weeks Very preterm <32 weeks Extremely preterm <28 weeks In using these definitions, the definition of VLBW infants includes ELBW infants, and the category of very preterm infants also includes those who are extremely preterm. This is an important consideration when one is reviewing published data of VLBW and very preterm infants. Graphic 119362 Version 2.0

Epidemiology Every year, an estimated 15 million babies are born preterm world wide(before 37 completed weeks of gestation), and this number is rising. Preterm birth complications are the leading cause of death among children under 5 years of age, responsible for approximately 1 million deaths in (WHO, 2015). In Tanzania, 236,000 babies are born too soon each year and 11,500 children under five die due to direct preterm complications (Tanzania profile of preterm and low birth weight prevention and care, 2017) In Tanzania, pre-term birth account for18.5% of all perinatal deaths( Mpembeni et al.,2015)

Maternal risk factors Maternal illness like gestational HTN, pre eclampsia or eclampsia Infection (e.g. untreated urinary tract infections, bacterial vaginosis) Cervical incompetence Age: common in the under age (<20 years) mothers and > 40 years mothers

Cont.. Abnormalities of the uterus eg bicornuate uterus PROM (Premature rapture of membranes) Trauma Excessive smoking during pregnancy Maternal malnutrition Anemia Prior preterm labor

Fetal factors Multiple pregnancy Congenital infection like with TORCH group polyhydramnion

PATHOPHYSIOLOGY Placenta serves three major roles for the fetus: provision of all the nutrients for growth (electrolytes, blood glucose, elimination of fetal waste products (heat, urea, bilirubin, CO2- excreted through mothers liver, lung, kidney and skin), and synthesis of hormones that promote fetal growth (+barrier to infection, through mucosal macrophages and maternal transfer of IgG to fetus from 32 to 34wks GA.

ASSESMENT OF GESTATIONAL AGE Gestational age can be assessed appropriately in weeks by simple visual assessment of certain physical signs and more accurately by using Ballard scoring system

New ballad score PHYSICAL MATURITY Skin Lanugo Plantar surface Breast Eye/Ear Male genitals Female genitals

Complications of prematurity . Short Term Complications Long Term Complications Hypoglycemia Bronchopulmonary dysplasia Hypothermia Poor growth Respiratory Distress Syndrome Retinopathy of prematurity Apnea of prematurity Late anemia of prematurity NEC CNS dysfunction Infections Intra-ventricular hemorrhage (IVH) PDA Periventricular leukomalacia

Short term complications 1. Hypoglycemia (RBG <2.6 mmol/l as per STG Causes a. Decreased production of glucose Inadequate gluconeogenesis Inadequate glycogen / fat stores i.e. in prematurity, intrauterine growth restriction. b. Increased glucose consumption Hyperinsulinemia as seen in infants of a diabetic mother (IDM).

Signs & symptoms of hypoglycemia Feeding difficulties / poor sucking Weak or high-pitched cry Irritability Lethargy / stupor Hypothermia Diaphoresis Hypotonia Convulsions Apnea / grunting / tachypnea Tachycardia Cyanosis

Short term complications cont.. Management of Hypoglycaemia Give a bolus of D 10%, 2 ml/kg IV stat. Re-check RBG after 30 minutes while the newborn is on maintenance fluids appropriate for age.

Short term complications cont.. 2. Hypothermia (Temp< 36.5C) It occurs in preterm babies due to: Little subcutaneous fat, Muscular inactivity, Inadequate sweating mechanism, Decreased brown fat (metabolic heat production) , Immature heat regulation mechanism. Signs and symptoms CNS-Decreased reflexes, lethargy, hypotonia. RS - Tachypnea, apnea GIT- Poor feeding / feeding intolerance, vomiting CVS-Peripheral cyanosis, bradycardia / tachycardia, hypotension.

Short term complications cont.. Management of hypothermia Keep the baby dry (dry nappies and sheets) Cover the baby adequately with dry and warm sheets, as well nesting. KMC care (skin to skin contact) Radiant warmers and incubators Warm room Rub coconut oil to the body to prevent heat loss.

Hypothermia .

Short term complications cont.. 3 . Respiratory distress syndrome It is a disease of immature lungs, characterized by impaired surfactant synthesis and secretion which results into increased surface tension in the lungs leading into alveolar collapse and decreased lung compliance. More common in premature infants especially born six weeks or more before their due date.

Short term complications cont.. Surfactant production starts around 20wks of life and peaks at 35wks. Therefore any neonate less than 35wks is prone to develop RDS, without surfactant infants are unable to keep their lungs inflated Signs and symptoms Tachypnea , expiratory grunting, subcostal / intercostal recession / retraction, sternal retraction, nasal dilatation, cyanosis

Short term complications cont.. Management a. Respiratory support therapy: Put the baby on nasal continuous positive pressure ventilation (CPAP). CPAP offers both ventilation(Pressure support) and oxygenation for neonates with RDS. If the baby does not respond to CPAP i.e. has intractable apnea or respiratory failure then put the baby on a mechanical ventilator if not responding to CPAP.

Short term complications cont.. b. Surfactant replacement therapy: Give early pulmonary surfactant (survanta) 4ml/kg through ETT within 6h of life A repeated dose may be given at 6hrs to 12hrs interval followed by nasal CPAP if no improvement. If the baby is not responding to CPAP then will need mechanical ventilation

Short term complications cont.. c. Keep warm d. IV fluids (Dextrose 10%) e. Encourage feeding f. Treat with antibiotics until sepsis is ruled out Prevention: Prenatal administration of corticosteroids Decreases incidence and severity of RDS Given to women with high-risk of preterm birth at 24 – 34 weeks gestation Dose: IM Betamethasone 12mg od / 48 hours or IM Dexamethasone 6mg 12 hourly / 48 hours

Short term complications cont.. 4. Apnoea of prematurity Definition: cessation of breathing for more than 20 seconds, with bradycardia (<100bpm) or cyanosis Signs and symptoms : Periodic cessation of breathing for >20 seconds, periodic cessation of breathing >10 seconds with cyanosis or bradycardia

Short term complications cont.. Treatment : physical stimulation, Aminophylline IV (Loading dose: 5mg/kg, maintenance dose: 1-3mg/kg BD) PO caffeine citrate (20mg/kg loading dose, then2.5mg/kg BD) High flow oxygen (CPAP) for those with spontaneous breathing

Short term complications cont.. 5. Necrotizing Enterocolitis (NEC) Ischemic and inflammatory necrosis of the bowel after initiation of enteral feeding. Signs and symptoms : Abdominal distension, vomiting brownish materials, feeding intolerance, increasing gastric residual, occult or gross blood in stool, abdominal tenderness, apnoea, bradycardia, temperature instability

Short term complications cont.. Treatment : NPO, NGT for decompression, IV fluids , TPN, antibiotics, monitor fluid input and output, vitamine K, surgical consultation,

Short term complications cont.. 6. Infections Results from lack of maternal immunoglobulins (IgG), which are transferred across the placenta during the last trimester. In addition to this, delicate surfaces of skin and mucous membranes also predispose to infections. Insertion of IV cannula, endotracheal tubes, nasogastric tubes also increase the risk of infections.

Short term complications cont.. Signs and symptoms Temperature irregularity : hypo- / hyperthermia Change in behavior: lethargy, irritability, or change in tone, bulging fontanel, convulsions Feeding problems : Feeding intolerance, vomiting, diarrhea (watery loose stool), abdominal distention, passage of blood stained stool . Skin : Poor peripheral perfusion, Cyanosis, mottling, pallor, petechiae, rashes, sclerema, jaundice Cardiopulmonary: Tachypnea, respiratory distress(grunting, flaring, and retractions), apnea within the first 24 h of birth or of new onset (especially after 1 week of age), tachycardia, hypotension which tends to be a late sign. Metabolic: Hypo- or hyperglycemia or metabolic acidosis.

Short term complications cont.. Management Empirical antibiotics to premature below 32 weeks (1500 g) recommended for at least 48 hours A full course of antibiotics if there are signs of sepsis or mother with risk factors of infection: ( fever >38°C, membrane ruptured >18 hours before birth , foul smelling or purulent amniotic fluid ). Hygienic practices when handling premature infants.

Short term complications cont.. .

Short term complications cont.. 7 . Intra-ventricular hemorrhage (IVH) It is common in preterm infants due to; Immature vasculature Disturbed cerebral auto-regulation of blood flow Clotting factor deficiency.

Short term complications cont..

Short term complications cont.. Signs and symptoms coma, hypoventilation, decerebrate posturing, fixed pupils, bulging anterior fontanelle, hypotension, acidosis, or acute drop in hematocrit) Management Supportive; incubator care, oxygen therapy, IV fluids. Symptomatic treatment; convulsions ( IV phenobarbitone) Anemia (fresh , packed RBCs transfusion) Raise intracranial tension (mannitol IV, mechanical hyperventilation).

Short term complications cont.. 8. Periventricular leukomalacia Periventricular leukomalacia (PVL) is a type of brain injury that affects premature infants. The condition involves the death of small areas of brain tissue around fluid-filled areas called ventricles. The damage creates "holes" in the brain. " Leuko " refers to the brain's white matter. "Periventricular" refers to the area around the ventricles. Causes A major cause is thought to be changes in blood flow to the area around the ventricles of the brain. This area is fragile and prone to injury, especially before 32 weeks of gestation.

Short term complications cont.. Infection around the time of delivery may also play a role in causing PVL. The risk for PVL is higher for babies who are more premature and more unstable at birth. Premature babies who have intraventricular hemorrhage (IVH) are also at increased risk for developing this condition. Treatment There is no specific treatment for PVL. Supportive; incubator care, oxygen therapy, IV fluids.

Long term complications 1. Chronic lung disease (bronchopulmonary dysplasia) BPD is defined as an ongoing need for supplemental oxygen and/or respiratory support at either 28 days postnatal age or 36 weeks postmenstrual age (PMA) in a preterm neonate with radiographic evidence of parenchymal lung disease Prolonged ventilation and oxygen toxicity results in chronic oxygen dependency. Management Supportive Growth and nutrition — Nutrition is provided to meet the increased total energy needs of infants with BPD and to support lung growth and healing. Caloric demands are generally high to meet the metabolic requirements for growth and healing.

Long term complications Fluid restriction — For most infants with BPD, we suggest modest fluid restriction (140 to 150 mL/kg per day). In severely affected infants, fluid restriction to 110 to 120 mL/kg per day may be necessary. Based upon our clinical experience, modest fluid restriction appears to improve pulmonary function and reduces the risk of pulmonary edema Respiratory support — Respiratory care is supportive. The goal is to maintain adequate gas exchange while minimizing further lung injury supplemental oxygen therapy in neonates with BPD is to meet the metabolic needs of the neonate while avoiding high concentrations of oxygen, hyperoxia, and hypoxia. The initial target range for oxygen therapy is a peripheral oxygen saturation (SpO2) of 90 to 95 percent.

Long term complications Pharmacological Bronchodilators — Bronchodilator therapy is usually reserved for infant s who have episodes of acute pulmonary decompensation with evidence of airway reactivity. Glucocorticoids — F or extremely preterm (EPT) infants ( ie , GA <28 weeks) who remain ventilator-dependent and/or require oxygen supplementation >50 percent at two to four weeks postnatal age. In this high-risk population, we use systemic glucocorticoids to prevent development of severe BPD and other pulmonary morbidity. Diuretics - For patients with acute pulmonary exercerbation attributed to pulmonary edema

Long term complications 2. Poor growth Growth is restricted due to feeding problems, vitamin and iron deficiency which may lead to developmental delay Before 35 weeks of gestation sucking and swallowing not yet well coordinated leading to significant feeding difficulties, with risk of regurgitation(GERD) and aspiration . Stomach emptying and gut motility is slower. Abdominal distension due to a relatively atonic bowel aggravates feeding difficulties. Immaturity of digestive enzymes affects feed tolerance in some babies

Long term complications 3.Retinopathy of prematurity This is an abnormal vascularization due to immaturity and prolonged oxygen therapy leading to partial or complete blindness. After the initial injury, normal vessel development may follow abnormal vascularization which occur due to excessive vascular endothelial growth factor (VEGF) The process can regress at this point or may continue, with growth of fibrovascular tissue into the vitreous associated with inflammation, scarring, and retinal folds or detachment

Long term complications Signs and symptoms Gradually occurring astigmatism, retinal detachment, amblyopia. Management Mainly prophylactic Optimal oxygen therapy is essential for the least duration. Any premature exposed to prolonged oxygen therapy should be examined by ophthalmoscope at the age of 1 to 3 months.

Long term complications 4. CNS dysfunction Cerebral palsy Post hemorrhagic hydrocephalus Learning problems Deafness Mental sub normality

Rickets Preterm babies got poor vitamin D stores and rapid growth So it is better to put them on vitamin D supplements from 6th week of life of 400 iu / day

Anemia of prematurity The primary factor is renal immaturity which leads to decreased level of EPO hence anemia but contributing factors are like lack of stored iron , hypofunction of bone marrow and excessive hemolysis. It occurs in preterm infants after 6 weeks This anemia is purely iron deficiency anemia, so put patients on prophylactic iron 3-6mg/kg/day of elemental iron that started from 6th week of life or once full enteral feeding is achieved (around 2 weeks)

Discharge From 1.5kg Feeding Many have significant ongoing medical needs after discharge

monitoring Growth Vaccinations Hearing Vision Development Respiratory Parental/social concerns

BIRTH ASPHYXIA

Presentation outline introduction Epidemiology Risk factors Hypoxic ischemic encephalopathy

Introduction Hypoxemia ; decreased arterial concentration of oxygen Hypoxia ; decreased oxygenation to cells or organs Ischemia; reduction or complete cessation of blood flow to an organ, which compromises both oxygen delivery (hypoxia) and substrate delivery to an organ

Cont … Birth asphyxia ; defined as failure of the baby to establish spontaneous breathing after delivery and/or 5 minute APGAR score of <7 Caused by a lack of oxygen to organ systems due to a hypoxic/ischemic insult that occurs during labor and delivery The lack of oxygen may lead to multi-organ failure with brain involvement as the major organ of concern – HIE It is marked by acidosis, hypoxemia and multi-organ involvement

Epidemiology 2.4 million newborns died in 2020 Nearly half (47%) of all under-5 deaths occurred in the ne onatal period (first 28 days of life), an increase from 1990 (40%), because the global level of under-5 mortality is declining faster than that of neonatal mortality Sub-Saharan Africa has the highest neonatal mortality rate in the world (27 deaths per 1000 live births) with 43% of global newborn deaths

causes of neonatal deaths in tanzania

Etiology high risk Maternal: hypoxia, anemia, diabetes, hypertension, smoking, renal diseases, heart disease, teenage mother and advanced maternal age Intrapartum: Abruptio placenta, placenta previa, cord prolapse, premature rupture of membranes, cord around the neck, instrumental delivery, prolonged labor and obstructed labor etc.

Cont … Fetal factor: Multiple birth, congenital or malformed fetus, meconium aspiration, post term etc.

Common risk factors/predictors of BA in Africa Herbal medicine use Prolonged labour Prolonged rupture of membranes Referred mothers APH Caesarian delivery Prime parity Prolonged pregnancy Non use of partograph Fetal distress Cord prolapsed PIH Meconium-stained amniotic fluid Maternal age Maternal illiteracy

Pathophysiology

Cont … After the early compensatory adjustments fail, the CBF can become pressure-passive , at which time brain perfusion depends on systemic BP Brain injury secondary to diminished blood supply and a lack of sufficient oxygen occurs This leads to intracellular energy failure

Cont … At the cellular level; neuronal injury in HIE is an evolving process The magnitude of the final neuronal damage depends on the duration and severity of the initial insult, combined with the effects of reperfusion injury, and apoptosis Hypoxia  Anaerobic metabolism  increased lactate Excitatory and toxic amino acids (glutamate) accumulate  Increased intracellular Na and Ca  tissue swelling and cerebral edema

Cont … Accumulation of Na +  plus the failure of energy dependent enzymes (Na +/ K +  -ATPase)  rapid cytotoxic edema and necrotic cell death Intracellular Ca ++  accumulation and further cascades pathologic activation and apoptosis There is also increased production of free radicals

Cont... The hypoxic cellular damage can be reversible (time) or irreversible (complications)

Cont … Progressive Hypoxia leads to: Primary apnea -Impaired breathing with normal muscular tone or hypertonia tachycardia and hypertension Happens early and shortly, auto regulatory mechanism to maintain vital organs perfusion

Cont … b. Secondary apnea Features of severe hypoxemia due to lack or unsuccessful resuscitation, usually leads to organ dysfunction .

Diagnosis of birth asphyxia APGAR score Signs of fetal distress Fetal metabolic acidosis (Ph <7) Abnormal neurological state Multi-organ involvement

Apgar score

Cont … 7 – 10 ; reassuring 4 – 6 ; moderately abnormal 3 and below ; critically low

Systemic Effects/complications SYSTEM EFFECTS CNS CVS Pulmonary Renal Adrenal Gastrointestinal Integument Hematology HIE, infarction, intracranial hemorrhage Myocardial ischemia, poor contractility, hypotension PHTN, pulmonary hemorrhage, RDS Acute tubular or cortical necrosis Adrenal hemorrhage Perforation, ulceration with hemorrhage, necrosis Subcutaneous fat necrosis DIC

Management-Resuscitation 1 st minute – Golden minute ABCDE resuscitation A (air way) B (breathing) C (circulation) D (drug) E (evaluation)

Cont … Airway Open airway Check for any obstruction If meconium stained – deep tracheal suctioning Breathing Bag and mask Establish respiration of 30-40/min with chest wall movement If response consider advanced airway management-intubation & mechanic ventilation

Circulation 1/ if heart rate <60/bpm, start external cardiac compression with fingers 2/ ratio 3:1

Helping babies breathe action plan Divided into three zones Routine care (Green zone) The Golden Minute (Yellow zone) Continued ventilation with normal or slow heart rate (Red zone)

Cont...

Hypoxic–ischemic encephalopathy (HIE) The brain damage after perinatal asphyxia and the most severe condition showed high mortality or remain cerebral complications such as mental retardation & cerebral palsy Clinical manifestations CNS – seizures, apnoea , abnormal posture, decreased tone, impaired primitive reflexes, bulging fontanelle, irritability or loss of consciousness CVS – shock/hypotension, myocardial dysfunction

Cont … Respiration – Respiratory distress, pulmonary haemorrhage , pulmonary edema Renal – oliguria/anuria, renal failure GI – paralytic ileus, bloody stools, necrotizing enterocolitis Hepatic – Liver enzymes elevation, impaired coagulation of blood Haematology – thrombocytopenia, DIC Metabolic – acidosis, hypoglycaemia , hypocalcaemia

assessment Use the HIE score (Thompson score, annex) to assess daily for the first 7 days.

Tompson score

Diagnosis of HIE Guidelines from the (AAP) and (ACOG) for HIE indicate that all of the following must be present for the designation of perinatal asphyxia severe enough to result in acute neurologic injury; Profound metabolic or mixed acidemia (pH < 7) in an umbilical artery blood sample, if obtained Persistence of an Apgar score of 0-3 for longer than 5 minutes Neonatal neurologic sequelae ( eg , seizures, coma, hypotonia) Multiple organ involvements ( eg , kidney, lungs, liver, heart, intestines)

Investigation Baseline : FBP, RBG Laboratory studies Serum electrolyte levels, Renal function studies Cardiac and liver enzymes - These values are an adjunct to assess the degree of hypoxic-ischemic injury to the heart and liver  Coagulation system - Includes prothrombin time, partial thromboplastin time, and fibrinogen levels  Arterial blood gas - Blood gas monitoring is used to assess acid-base status and to avoid hyperoxia and hypoxia, as well as hypercapnia and hypocapnia 

Cont … Imaging studies  Magnetic resonance imaging (MRI) of the brain Cranial ultrasonography, brain CT scan Echocardiography Others Retinal and ophthalmological evaluation, EEG

Management Following resuscitation and stabilization, HIE treatment is supportive: Oxygen therapy Intubation and Mechanical ventilation Feeding and fluid therapy Anticonvulsants (for seizures) empirical antibiotics Check for glucose levels and urine output

Feeding and fluids o Mild HIE: Assess ability to feed and only give oral feeds if there is suckling reflex. Amount of oral feeds should be adjusted according to the Condition and ability to tolerate, and the deficit should be Given as IV fluids (to a total of 60 ml/kg on day 1) If the newborn cannot be breastfed, give expressed breast milk using an alternative feeding method (cup feeding, NGT) If having significant emesis or high residual amounts, consider nil per oral (NPO) for 24 hours, evaluate for NEC. If stable 24 hours later, resume feeds at 50% the amount was previously being given, and advance gradually

Cont … o Moderate and severe HIE: Do not feed orally on day 1, but Swab the mouth with breast milk (colostrum swabs) Start Dextrose 10 % IV. Restrict the volume of fluid to 60-ml/kg body weights for the first three days, and monitor urine output.is applies for preterm and term babies.

Cont … Check glucose levels Give oxygen to maintain SpO2 target range o Term newborns: 90 % - 95% o Preterm infants: 88 % - 95% Give antibiotics o Antibiotics should be given for; Severe HIE or, Evidence of existing sepsis or, Concern for maternal chorioamnionitis. Use recommended combination of ampicillin and gentamicin for 7 days.

References Mpembeni ,R ., Jonathan, R. & Mughamba , J.(2015) Perinatalmortality and associated factorsamong deliveries in three municipal hospitals of Dar es Salaam, Tanzania.Journal ofPediatrics and Neonatal Care WHO pocket book of hospital care for children, 2013 edition national guideline for neonatal care and establishment of neonatal care unit, first edition 2019 Nelson textbook of pediatrics, 21th edition

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