PED2 LE1 01 Sick Newborn (2026-07-09)

Hi Algin. How many students do we need to do we expect to join us for this lecture?

>> 400 plus po.

>> 400. So I cannot wait for them because this going to be a long lecture. So do they have to open their ano videos to document the attendance?

>> Yes po ma'am.

Okay. Good morning everyone. So uh it's 8:05. uh we have to start our lecture for today. So I am uh Dr. Duke uh one of the assistant professor the department of pediatrics. So to document your attendance for this lecture kindly open your video and um Algin we take note of the uh of your attendance.

So for this morning we're going to discuss the first part of the uh sick newborn. So okay teka net okay so the nital period is a a very highly vulnerable period for newborns as they undergo many physiologic adjustments required for exer life so most infant transition well however certain few uh would need additional support and close monitoring so this is what these are what we call the sick newborn so Newborn may be described as someone with or a baby who is not feeding well or detergic or with decreased activity or has a systemic um illness and th and those would poor weight gain. So these are infants who would require additional support such as oxygen, IV, antibiotics etc. So it is imperative to obtain a good history to determine the nature of the illness and as well as determining the presence or absence of risk factors uh both maternal and the fit and fetal factors as well as during the entire course of pregnancy and delivery. So likewise meticulous um examination of the sick newborns can provide useful clues of to the theology of the of the sickness and also provides a basis for management plan later on.

A variety of conditions that affect the newborn can either start ino or during delivery or during birth or in the immediate postal period. So we call this the perle period. So this disorder can be due to prematurity or congental um anomalies or acquired diseases or injuries sustained um during the livery process. So it is therefore essential to recognize different disease manifestations in the newborn and a good clinical knowledge of the pathophysiology and evaluation of this um non-specific signs and symptoms is crucial. So this would be the objective of our lecture for today. So at the end you should be able of the two part lecture you should be able to have a good clinical knowledge of the most common diseases disease manifestations during thisatal period. It will be um this will be our lecture outline.

So uh why do we choose medicine? It can uh because I can think of no other professional avenue, more challenging, rewarding, evolving and novel. Now the first 28 days of life after birth are described as newborn period. So proper care of newborn babies form the foundation of the subsequent life not only in terms of longevity or survival but also in terms of qualitative um outcomes without any mental or physical disabilities. So the first 28 days of life remained the most vulnerable period for uh child survival. So in 2021 approximately 2.3 million children died during the first month of life which translates to 6,400 babies every day. So this date deaths constituted nearly 47% of the under 5 um debts that uh took place that same year. So this prematurity and low birth weight um responsible for 1/3d of the neatal debts followed by perinatal asphicia which is about 10% and is known to cause in the survival such um a long-term sequel um which include impaired attention span or hyperactivity or epilepsy mental retardation or any um sensory neur neural deficit and third would be seriously natal infections which includes starch infections and clearly a tri of prematurity low birth weight and Ir plus serious infections and birth aspictia accounts for as high as 85 to 90% of the neither mortality so samming it up congental malformations are responsible for nearly 10% of the deaths so these are the top for um causes of death so the risk of mortality and uh major morbidity is particularly high around the time of birth so during the inchapital period so therefore within the spectrum of infant mortality certain subcategories are used in maternal and child health practice to focus on specific period of high risk so the perinatal period is typically defined as a time from 28 weeks of pregnancy through the seventh um postpartum day while neonital period spans 28 days of life and can [sumisingasing] be further um subdivid into early ninital which is the first 7 days or the late needle which is days 8 to 28 uh days of life so the primary causes of mortality ships as infancy progresses so during the the perin and the neital periods preterm birth sepsis and asfic predominate. Moreover, in developing countries with limited resources wherein the ninetal mortality rate is high. Prettym birds remain a concern but other causes such as infection, uh asphictia and complication of labor and delivery add in in the in this burden.

Most infants complete the transition to exterior time life without difficulty. However, a small proportion will require resusitation after birth. So as you see in this uh figure so for a uh for a newborn uh infant the need for rescitation is often caused by a problem with respiratory respiration leading to inadequate ventilation. So this is inconscious to an adult cardiac arrest which is usually caused by inadequate circulation. Now the objective of or the goals of nito resuscitation are to establish adequate spins respirations, obtain adequate cardiac output and prevent morbidity and mortality associated with hypox um schemic tissue injury and high risk situation should be anticipated from pregnancy uh ah from history pregnancy history and labor. So improve prenatal um care and prenatal diagnosis of fetal anomalies allow for appropriate and maternal transports for high risk um deliveries. Okay. All babies must be assessed for need of rescitation at birth. So infants who are both more limpotic or apnic or pulse um require immedius before assignments of the first minute upcar score. So main goal is to establish ventilation within the first minute of life and rapid in appropriate resuscitative efforts improve the likelihood of preventing brain injury and achieving a successful outcome. So we call this the first minute of life.

Now we go to CNS um disorders. This is um one of the most important causes of morbidity and mortality both short and long-term um short and longterm. So CNS can be damaged as a result of asphy or hemorage or trauma or could be metabolic like hypoglycemia or direct cytotoxicity. Causes are often multifactorial and include peral or complications such as in um hypoxchemic encephalopathy or postnatal hemodynamic instability in presence of developmental abnormalities that may either genetic or environmental. So among the predisposing factors for brain injury included acute and chronic maternal illnesses resulting in uteroplacental insufficiency infections or IGR intern growth restrictions are having premature birds. So also unavidable emergencies during delivery process may sometime result in hypoxemic brain injury.

Okay, let's go to cranial hemorages. Uh, these are birth injuries that are uh that range from minor to extremely severe. um cases this can be due to birth aspixure or birth trauma uh using excessive mechanical forces uh forest to the head of uh the baby uh likely with the use of a vars or vacuum they can be classified into exraasial or intracranial so the most common extracial injury of the and the most benine is the caps ofxodanium so the presenting part which is often The parital bone is the usual site. Edema is um soft and superficial in fitting and crosses the midline. So the lion steadily resolves over the first few days of life and there is no intervention needed. While cap while um sefal hematoma on the other hand is usually seen over the parital and parital area and has a distinct margin. So since this bleeding is confined in the supperal area that's why it does not cross the midlight. So there can be associated linear fracture in 10 to 20% of cases. Hence a cranial um x-ray is warranted. Spontaneous resolution is expected in 2 to 3 weeks uh which really has a significant um neurologic standpoint neurological point of view. However complicated if there is an underlying cerebral deed. Subcal hemorage ah naman and is bleeding in the galea poneuretica. Hence it is sometimes called subaponeurotic hemorage. Uh blood may spread beneath the entire sculp and may even dissect into the subcutaneous tissues of the neck. So it is strongly associated with vacuum delivery. So the lesions generally present 1 hour of age and manifest as a fair fractuant mass increasing in size postnatally. So this infants have high a relatively uh have a relatively high incidence of mortality if left untreated uh due to um hypovelemic shock. So others would require uh excessive or volume expansionic support and um extensive or um massive transfusions for anemia. So after the upgate phase ion usually resolve in 2 to 3 weeks if baby would um uh intervention is timely.

Okay. What about hemorage? Can either be a result of birth trauma caused by mechanical application of instrument to the baby said or by aspia. So it is correct um hence a correct prompt and accurate diagnosis important for proper and timely management to prevent complication. So nital traumatic heads are estimated to affect approximately 3% of pregnancies and represents about 2% of the natal death. So subural hemorage is uncommon inates but more common in term than preterm. Symptoms depend on the severity and location of the bleed and surgical evacuation is needed if with severe um hemorage. Child abuse must be suspected in all infants with subtural hemorage after the immediateal period. While subarachnoid hemorage on the other hand is the most frequent type of bleed and is often asymptomatic but may cause refractor seizures. So IVH and perventricular hemorage are commonly seen in preterm infants um probably due to prematurity perer or due to hypoxic ischemic um injury or infection.

Let's go to this case. So this is a 3day old infant born 26 weeks with the weight of 800 grams. Patient was placed on IPPV and blood pressure dropped accurately and developed seizures after. Uh PE demonstrated um actual bets with no heart murmur with hypotonia and a bulching anterior fontanel in. So once you have a patient with bulching anterior fontanel you have to think of what? So you have to think of an IVH. So a patient with IVH would typically reveal anemia in laboratory metabolic acidosis and hyperglycemia as because of a stress hypergly it's a more of a stress hyperglycemia rather than a hypoglycemia. So you see an ecosenicity in the intravoventricular um space. uh uh confirming diagnosis of um IVH. So IVH is the most common CNS complication of preterm birth. It is usually it usually develop spontaneously and less frequently uh maybe due to trauma or asphicure and rarely from a hemorragic disturbances or cerebrovascular anomaly. So overall incidence is 30% for all very lowbth weight infants and the risk is inversely related to gestational age and birthweight with the smallest and most immature infants being at the highest risk. site of bleeding is in the terminal matrix or subependal germinal matrix. So the germinal matrix begins to involvet at around 34 weeks post conception. So as um vulnerability of this pterm decpeces after this but it is not totally eliminated. So by 36 weeks the terminal matrix has involuted in most infants. Hence IVH is really seen in term infants. Why is prterm uh most acceptable to um uh IVH? So cerebrovascular author regulation is the ability to maintain constant cerebral blood flow over a range of systemic profusion state. So in prms they have a very limited ability to autoregulate cerebral blood flow hence the passive pressure exists. Sovascular regulation is most sensitive to changes in the arterial PO2 with hypercarbia or increase in CO2 and acidosis causing increased blood flow to the brain. Hence any pathologic fluctuations in the cereal blood flow velocity may cause IVH. Also the terminal matrix has a rich blood supply because it producesendes which is a type ofal cells which produce the myin sheet which covers the the ano ba the neurons. So between 23 and 32 weeks uh there is a reach a high inigodenocytes in this area. However, the blood vessels on this germinal matrix have a poor basement membrane support. Any changes in the cerebal blood flow make this region susceptible to bleeding. So IVH premature infance primary occurs in the gelatin subependal germinal metric. So this periventricular area is the site of origin for embryonal neurons and fetal cells which migrates outwardly as you see in here um to the cortex. So the cortical neuronal and leal cell precursors developed from the germinal matrix and the ventricular germinal zone during the late second and third trimester. So the ependimal germinal matrix is highly vascularized region with arterial supply from the anterior and the middle cerebral arteries and the anterior corodal vessels. However, the immature blood vessels in this highly vascularized region of the developing brain combined with poor tissue vascular support produce post premature infas to hemorage. So thas bleed may be confined uh to the terminal matrix or it may rapture into the either lateral ventricles and may thereby become a unilateral or a bilateral germinal uh matrix or inventricular hemorage. So IBH may be um as may be asymptomatic if bleeding is small or sometimes it can present as a gradual clinical deterioration. We call the saltatory progression with altered levels of consciousness or hypotonia in abnormal eye movements. It can also be catastrophic leading to sudden deterioration during the second to third day of life in the form of neurologic science like um sudden ons set of seizures posturing decreasing in activity and super are decreasing in sensorum. So full fontanel with sudden power support the diagnosis of um of IVH your clinical this is your clinical parameter. It can be accompanied by hemodynamic instability such as hypotension, blood cardiaper profusion with hyperglycemia, acidemia and hypercademia in your laboratories. So the majority of cases of IVH and preterm infants occur within the first 3 days of life. So this is the catastrophic event or of those approximately 50% occur within the first 5 hours and 70% occur within the first day of uh first uh day of life or the first 24 hours and by the 7 days of life 95% of IVH will have occurred. That's why it is important that we do uh cranials um ultrasound during the this crucial time. So a percent a small percentage of infants have late um herage between day 14 and 30 and um IVH as I've mentioned is rare after the first month of life.

Now how do we diagnose nga? As I've mentioned we have to do cranial ultrasound serial cranial ultrasound. This is the procedure of choice for screening and diagnosis of IPH. So the severity of ivage is defined by the location the degree of bleeding and ventricular dilutation as you see in this um imaging studies. So in grade one so this picture is the normal the one on the left is the normal um picture of a sagital view of your queen o sound. So in grade one this one um bleeding is isolated as you see in the subependal area or to less than 10% of the ventricle is actually affected while in grade two this is grade 2. Okay. So in grade two, so there is leading within the ventricle without evidence of ventricular dilitation. As you see in this um uh picture while in grade 3, there is about more than 50% um cervical intraventricular dilutation. As you see ah dito saital portion ano lang stet like pa rin iyung ano iyung ah ventricle lateral ventricle but you see in this uh third picture letter C there is more than 50% dilatation while in grade 4 which is the most severe grade 3 and grade 4 are actually severe but uh grade 4 is the most severe. There is actually intrapar criminal hemorage as well. So one of the major complication resulting from IVH is the development of postymoretic ventricular dilutation and it develops in 30 to 50% of patient with severe IVH and it is initially asymptomatic in most infants. So therefore sequential canalisonography facilitates early detection. So the term ventricular megali is occasionally used for both invants with ventricular enment following IVH as well as those without hemorage. So infants without IVH ventricular endgement is most more likely due to a white matter loss rather than accumulation CSF. So therefore it is preferable to use the term uh posthemagic ventricle dilation when ventricular hemorage uh follows an IVH.

Okay. What about periventricular Malaysia? Uh it is characterized by focal necrotic lions in the periventricular white matter that may be cystic or diffuse. As you see in this picture no risk of PBL increases in infants with severe IVH or in the presence of ventriculare. So the corticospinal tract through the periventricular um white matter. Hence the association between cerebral uh white matter injury or what we call the PVL and development of CP kasi ' ba that's the watershed area. So pred factor predisposing factors include prematurity or any disregulation in the cerebral blood flow if there is maternal infections or any disturbances in the alleodendcite precursors as we seal in IVH uh and factors contributing to the development of um hypoxchemic and um encephalopathy uh or anything that will decrease cerebral perfusion leading to intern to uh periventricular hemorage and necrosis. So the watershed areas I mention the area around the ped ventricular white water is the most vulnerable um area when a hypoxic chemic condition um arises. So diminished blood flow in this area and fluctuation the blood pressure lead to a state of schemia in this area with a consequently causing salted due to um inadequate blood flow. Ultimately the schemy results in white matter that is decrease in volume due to the um decrease in white matter. So uh PVL may initially uh may be observed during the first week of life in the very low birthweight infants uh or increase ecogenicity of the periventricular white matter sometimes described as um ecogenetic ecogenic blush or flare. So this area of white matter abnormalities may become cystic or on ultra stonography within the first three weeks of life which could lead to ventriculomegally from white matter volume loss and which can be visible on repeat oonography at serm equivalent of age so meaning a 37 week gestation or corrected age so pvl is usually clinically asymptomatic until the neurologic sequally of white matter damage become apparent in later infancy as spastic we or without motor deficit. So they would usually present uh with uh poor sock lang or difficult feeding and then later on they would develop CP.

Co management is largely symptomatic. So seizure should be treated with anticonvolsant drugs and anemia and coagalopathy require transfusion with pack RBCs and fresh frozen plasma. Shock and acidosis are treated with um fluid restrictions. Insertions of a ventricular peritoneal chance are BPS is the preferred method to treat progressive and symptomatic post hemoragic hydrocephaluse. So some infants require temporary CSF diversion before a permanent shan can be safely inserted. So diuretics and acetasolamid or uh these are actually uh diuretics no uh based on studies are not effective uh ventricular access devices or reserva and externalized ventricular genes are potential temporizing interventions although there is an associated risk of infections and puncture forignence from injury to the surrounding paranema so a ventriculous uh ventriculous subgal sh inserted from the ventricle into a surgically created subgall pocket provides a close system for constant ventricular decompression without additional um ris factors. So the compression is regulated by the presence of a gradient between the ventricle and the subgallal pocket. So one approach to therapeutic intervention is based on the severity of the ultra ultrasographic dimensions of the ventricular size as seen in this table. So it depends on the size of the ventricular. So in they have to cat restratify first and then the management will be dependent on the restratification. Okay.

So in terms of prognosis several studies show that the degree of IVH and the presence of PVL are strongly linked to survival and neurodevelopmental impairments for infants uh with a birth weight of less than 1,000 grams the incidence of severe neurologic impairment um as defined by baily scales of infant developmental for or mental developmental index of less than 70 or psychomotor development index of less than 70 or presence of CP or presence of sensorineural deficit like deafness and blindness after an IVH is highest with grade for hemorage and low birth weight so PVL cystic PVL and progressive um hydrogencephalose requiring shunt insertions are each independently associated with the prognosis so there is a poor um neurodevelopmental outcome is significantly higher when severe IVASH is complicated by postsic ventricular dilutation and seen in 40 to 60% of cases and more so in infants who are who eventually develop postsoratchic hydrocephalose in 75 to 80% of of infants so in the presurfactant area era uh this is before early 1990s up to 82% of infants with posthoragic um hydrocephalus who survived develop significant neurologic impairment with CP being the most um clinical a common clinical sequel. So the trial what we call the genage irrigation fibronalytic therapy trial perform neurocognitive assessment in at both 2 years and 10 years after birth and demonstrated improved cognitive ability when considering birthweight um intraventical hemorage grade and sex and based on this uh infants to receive the drift were almost choices as likely to survive without severe cognitive disability than those who receive standard treatment alone. So with regard the early versus late ventricular intervention study naman, the demonstrated the effectiveness of intervention at a low threshold of ventricular dilation and the outcomes of death and severe neurodevelopmental disability in pretterm infants with postragic ventricularitation. Post talk analysis of this study demonstrated that infants who went on to having a shunt had better neurodevelopmental outcome scores if interventions were done at a low threshold.

So are there ways to prevent development of intraventrical hemorage? So the most important protective factors against development of IVH is actually antinatal administration of corticosides. So a single course of antinetal corticosid is recommended for pregnant people. uh women between 24 0 over 7 weeks and 36 over 7 week station meaning less than all in pretterm labors who are at risk of pretterm delivery within the 7 days of life within the 7 days so antinatal administration of magnesium sulfate was not associated with reduction in the incidence of ivh although it has been associated with the reduction in the development or the risk of developing cp later on or cerebral policy. So prophylactic in the metacine showed a significant reduction in the incidence of sever IVH. However, this reduction in sever IVH was not associated with the reduction in severe neurosensory impairment later on. So the most protective actually is giving antinetal particles to yourid.

Okay, now we go to this case. Uh, a mother rushed in for ST CS due to abrups placenta um up scores at birthd are 2 3 and 8 improving after intermin positive pressure ventilation chest compression and fluid resuscitation. So baby was admitted to Niku and mother had an eventful antinatal course. Baby develop seizure um tonic clonic se generalized tonic clonic seizures with bradicardia at the 12 hour of life and given um phenobarbetal. So the most likely cost ofure in this case is what? So what are the uh causes of ninetal seizures? So nineal seizures are have a distinct form and features compared to older infants. Soures can be classified based on their most prominent component. So they can range from satle seizures or automatism. We call this automatism to focal multifocal tonic or myoclonic seizures. Settle seizures involve only one uh like mga phase actually facial um features their deviation eye deviation or blinking or mouth movements or apnia or any fluctuations in the vital signs. They're common both in pretterm and term in fund. So this is the most common. Next would be multifocal clonic seizures which involve shaking of one limb that migrates to another without apne or eye movement. So they are primarily seen in term infants. While focal clonic seizures naman involve one only one limp in or area. This is may may indicate a focal disease. Uh while tone exasures involve changes in posture such as posturing or stiphany or rigidity and and more common in preterm than interm infants. You have to think of the ano iyung ah ano iyung commonly affected in area in the brain of a preterm infants. Kaya siya tonic is more common in preterm than in term. While myoclonicures naman there it is a rapid sudden jerky movements of the reflections of both arm and legs and you see it is typically in either preterm and term infants. Soizures can be caused by various factors including post ashia or post hem posthemoragic or metabolic also it could be from a neonal necrotic uh neonal narcotic withdrawal or any with bilary encephalopathy or cicterus it could be secondary to infection genetic or structural causes as well treatment involves the underlying cause of seizure.

So going back to this case what is the most likely cause ofure is the aspect event as you see in the poor upgar course. So see uh what is pernatal asphy it is a pathologic condition referred to nenate who have no spontaneous breeding or represent represented irregular breeding movement after bird. Usually it is caused by perinatal hypoxia meaning decrease in oxygen during it is an emergency condition will need a resuscitation so incidence is between 1 to 1.5% 5% um overall with 9% uh in newborns than 36 weeks gestation and3% in news more than 36 um gestation it accounts for 23% of the perinital death as you see in the it's the number two cost of mortality and about 33 to 50% of the survivors would have permanent brain injury leading to cerebral policy and factor which interfers with circulation between matern and the fetal blood um exchange could result in peratal aspixia so this factors can be maternal needital or even during the birth of the baby so this definition using upgr as you see in this on the right side of ano of the slide so the moderate depress are considered to be asfixiated so however uh we have to use this upar scoring as a as um as an as a cause or as a reliable index for asficia with caution because for prerm infants you cannot actually use this okay in terms of timing of the injury is very critical so insults can either happen nga as I've mentioned at um inpart antinatal or antipartum or inchapum or even post postnatal period so during the antipartum There is abnormal maternal oxygenation, acine in severe anemia or cardiopulmonary disease if there is inadicate perfusion causing maternal um severe hypertension or maternal vascular disease while intrapartum um causes include interruption of the umbilical circulation when there is presence of corn prolaps or trunat or there is inadequateal perfusion as in abra placenta or uterine rapture or if there is abnormal maternal oxygenation or presence of vasapevia. So in postnatally naman there is persistent pulmonary hypertension or civircitary insufficiency uh in the presence of blood loss during the livery or shock. So of this tree the most asfixia uh most aspixia event um happens during the inpartal stage.

So the initial um circ of the fetus is increasing the shan through the ductus venosus or the shans ' ba the ductus venosisus the ductus arteriosis and the pharamen avaldi with trancient maintenance of perfusion of the brain heart and adrenal. So these are your critical or your uh important organs or vital organs. So in in preference the lung, kidnees, liver and non and intestines which are your non vital organs. So this is what we call the diving reflex. So the pathology of hypoxia schemia depends on the affected organs and the severity of the injury as you see in this um slide. So among the most targeted organs are the following. So uh first is uh kidney. So renal dysfunction which is accompanies perital asphicia. Renal damage ranges from reversible cloud swelling of the tubules uh to infction of the internon. So this leads to a decrease in the urine output of about5 ml per kilo which may be which may last for 2 days to several weeks. So protein and gas may be seen in urine and gross hematery may be present. So there will be derangements in the renal function uh that's why it's important to uh monitor your bua and polyurea will follow the allergic phase. What needs to be done is to prevent anoria during this crucial stage. Next is CVC or the cardiovascular dysfunction. So this may cause uh maricardial inf infarction or MI which is usually transent. So takardia takip and hepatomegali which are consistent with congestive heart failure may be seen and this would s lead to cardiogenic shock or death if severe. So pulmonary dysfunction is the initial findings uh you see is pulmonary edema to the marcaral dysfunction and can manifest with respiratory distress. So acute respiratory distress syndrome sets in which is secondary to the increased plasma protein that will lead to inactivation of surfactan and um the most severe or most um yes the most severe or uh damage organ is actually the CNS and this is uh the most serious complications as well of perital asphicia the neurologic sequil often persist uh even after the onset. So hypoxia impairs the cerebral oxidative mechanism and leads to uh marartal infection that will lead to failure in the cerebral blood flow which will result to schemia of the brain tissues. So persistence of the hypox leads to an increase in anaerobic glycolysis ending up with lactic acidosis. So if not corrected on time uh on a timely manner you will loss it will cause loss of cerebral vascular regulation.

Now this is the what this is what happens after an asfixial event. So primary energy failure occurs due to the initial reduction as you see in this corner of the cerebral blood flow. This impairs oxygen and glucose delivery leading to less um energy and um increased lactate reduction. So low A level low ATP levels cause of the mechanism maintaining cellular integrity or especially the sodium potassium pumps and intercellular calcium levels. When the sodium potassium pumps failed, excessive sodium influx causes massive neuron depolarization releasing glutamate and which is an excitatory neurotransmitter. Glutamate by um receptor um increasing cellular calcium and sodium influx. So the increase in calcium causes cerebral edema, ischemia or microvascular damage or necrosis and aptoptosis. So both the primary and the secondary energy failure cause um salance. So more uh most primary energy failure affects uh affects uh lead to uh cellular necrosis due to impaired integrity and cytoskeleton disruption and cell membrane damage. So severe hypoxemia causes uh cause necrosis and less sever insults may lead to cell um recover or apoptosis. So apoptosis causes cell shrink or membrane preservation and no inflammation. It can occurs days after the injury. So both necrosis and apoptosis can reduce brain function. So once blood flow is restored there is a brief recovery period we call this the latent period which is characterized by normal cerebral metabolism. So the latent period varies based on the severity of the hypoxic chemic insult. So the more severe the shorter it is. So it is considered the optimal timing for therapeutic interventions. Secondary energy failure occurs for 6 to 48 hours after the initial um injury. So the exact mechanisms are unclear but they involve oxidative stress excitator and inflammation. Oxidative um stress occurs when free radicals damage in rinal cell membranes leading to necrosis or apoptosis. It's particularly harmful to the neuronal brain uh due to the low oxidant um levels and high oxygen consumption during the fetal and the neatal transition. So the decrease ability to eliminate three radicals and increase susceptibility lead to neuronal tissue damage. Excitatory occurs when excessive extracellular neurotransmitter especially the glutamate overstimulate exitory receptors causing additional sodium and calcium influx into the neuronal cells. So glutamate is involved in various neuronal patteries including hearing, vision, somatosensory functions as well as learning in memory which can disrupt subsequent development of this crucial areas. So infl in inflammation is also thought to be important in the HI related pain injury but the exact mechanism is unknown. So animals um models such as that neutrophil infiltration into the cerebral tissue in the early stage lead to cerebral uh cerebral edema. So complicating more the or worsening the cerebral edema. So after an acute insult blood supply to the injuries inured state is restablished leading to a 30 to 60 period of minute uh period of cellular energy pathway recovery. So this is what we call the reperfusion phase. So depending on the insults severity the intracellular apoptotic cascades may trigger a laten face starting about 6 hours after injury lasting up to up to 15 hours. Discuscate cause neuronal cell death and simulates an inflammatory sequence that can further trigger a secondary phase of cell death.

So as you see uh based on this path of physiology uh this is how we manage this um condition. So it is crucial to maintain a good um oxygen level na to oversaturate um or not uh not parang not to give high O2 um oxygen uh high O2 tension avoiding high O2 to2 delivery and as well as uh managing the latent period uh with therapeutic hemothermely.

Encephalopathy severity depends on the injury injury duration in the timing. So hypoxemic encephalopathy due to perinatal ashfishia can cause various neurologic finding. So this is what we call the umut saging system which is uh a useful um system where you uh the where you ano parang ah assess the level of sensorium, the reflexes and the autonomic response uh after an artificial event. So stage one is the least severe uh which shows generous sympathetic tone with hyper alertness and prolong weightfulness as well asis increased deep tenton reflexes while stage two there could be a lether gr tundation with decreased tone and strong distal flections with a generous parasympathetic tone myosis and predicardia in increase secretions seizures are common in this stage while stage 3 naman on the other hand which is the most civic Beir shows profound decrease in consciousness with the flacid tone decrease deep tendon reflexes and abnormal eg. So clinical seizure are less common stage due to the severe brain injury preventing seizure propagation. So the topography of cerebral injury correlates with decreased cerebral blood flow and a higher metabolic demand. So but um especially in regional vulnerabilities depend on the gestational age and the insult severity. So term infant show neuronal necrosis corticaly and par paraurgicalital um schemic injury while prerm infant exhibit prevl of periventrical lucomalasia or spastic typedia uh with basal gangly status marmeratus and intravoventricular hemerage so term infants more often have focal to to multifocal um critical infarcts causing seizures and hemiplatia so diagnosis of hi varies is by um infant age. So pretm infants uh we use CTT CTT cranial sound as the preferred modality of choice while for term infants um CT scan is helpful for hemorage and cartical injuries but not sensitive early in life or after an asfixia. Therefore, it is important that we use diffusion weighted MRI uh for better lesion um delineation and and you know that CT scan is high in radiation that's why uh MRI is the preferred modality of choice.

Treatment is supportive. So therapeutic hypothermia whether head cooling or systematic or systemic cooling meaning whole body cooling maintaining the temperature of the core temperature uh between 33.5 and 35 uh so within the first 6 hours after birth and should be maintained within 72 hours or uh within from 6 hours after birth to 72 hours after birth. So reducing mortality and mature neurodevelopmental impairment at 18 months. So systemic uh hypothermia has a lower incidence of cortical neuronal injury on MRI such asing more uniforming and deeper CNS cooling than selective head cooling. So therapeutic hypothermiaal likely reduce a secondary neuronal injury by decreasing apoptosis and neurotoxic med production. As you see in the path of fish it is also it also reduces seizures. The outcome of HI varies from complete recovery to death depending on the insults timing and severity. So infants with the initial cord or blood pH of 6.7 or low have a high have a 90% race of death or severe neurodevelopmental impairment at 18 months if they do the recover. So infants with upper scores of 0 to3 at 5 minutes of life with a high base deficit which is more than 20 mimore per liter or at the cereelbrate posturing with severe basal gang ganglialamicions and persistent of um abtundation or severe ivage uh for more than 72 hours and lack of spontaneous activity thereafter are also a trist uh of dying or having a severe neur impment later on. So this predictor variables can be combined to determine of prognosis score. So infance with the highest risk likely to die or have severe disability despite aggressive treatment including hypothermia. So this patients have the poorest um prognosis.

Now we go to spinal cord injury. This typically occur when the cord stretches due to longitudinal attraction on the trunk while the head remain engaged. So this leads to vertebral um fracture or dislication resulting in court section. There are four clinical patterns of affected infants as described. So the first group are the stillborns. They have the severe respiratory depression, shock and hypothermia. There is rapid uh deterioration and death often with high cervical or brain stems. Uh for the second group naman, the appear normal at birth uh with the same signs as the first group. So they die after several uh days withions in the upper uh or mid cervical region and undetected for several days. So negative um findings for naman on C the third group which is on the C7 to T1 they may be reversible though may have some permanent but they have the longer period of survival uh ah based on the three and the fourth group fourth group uh these are the spastic with satal neurologic signs okay risk factors include beach delivery requiring version and extraction and those with brow our face presentation are presence of dystosia prematurity or premaparity and precipitus delivery.

Treatment is most disappo we have is very important. Uh what about facial nerve policy? It results from birth trauma of or facial nerve nucleuseis. It can present at birth or within the first two days of life. It may be central affecting one side of the eyelid and forehead movement. And if it's central uh the eyelid is uh affected, one side of the eyelid is affected with the forehead um uh the forehead is paired or peripheral affecting the entire phase most of cases undergo spontaneous or complete resolution. You just have to be patient. What about plexus policy? It is caused by mechanical trauma from C5 to T1 spinal nerve rules resulting in paralysis of the muscle of the upper extremity. So there are three types based on location. The herb the shen or the upper arm paralysis involved the C5 to C6 which is the most common. Ah ito iyung waiter stip sign. The clamky of the lower arm paralysis involve the C8 to T1 and which is the rarest because of T1 involvement it could have lateral hornor syndrome um when there is paralysis of the entire arm and the third would be paralysis of the third of the entire arm. So treatment plan includes initial conservative management, closer followups and vigilant decision making for surgical intervention. So 93 to 95% attain function of the affected extremity with conservative management.

Okay. How about phenic nerve policy or C3 to C5 nerve involvement? So it is really isolated and causes deragmatic paralysis. It is usually unilateral and accompanied by epsilateral bacal plexus paralysis. Symptoms include ineffective breathing on the affected side with no abn abdominal elevation on inspiration and there is recurrent cenosis. Uh physical exam reveal dellness uh with diminished breath sounds on the affected area with chest rakes show serial films of elevated diaphragm in heart and which isal shift to the opposite side andctis of the affected side. So supported medical treatment is given for a month if no improvement. uh within the month then surgery is indicated.

Now let's go to respiratory distress or the respiratory diseases. So the successful transition from placental oxygen to pulmonary respiration requires timely fetal long fluid clearance, creation of a functional residual capacity, increase pulmonary blood flow and normal breathing patterns. So in any of this task leads to um respiratory disorders in the neons. the most common cause of ncoadmissions for both term and preterm infonds so early recognition timely referral and appropriate treatment are crucial for the survival of this newborns. So what are signs and symptoms of respiratory distress in the newborn? So these are the commonly seen signs and symptoms and the clinical correlation of this uh clinical symptoms. So these are the following diagnostic tests procedures to determine the ethyology of the respiratory distress.

Okay. Based on this figure various pathologic lesions can cause respiratory distress including pulmonary and non-pulmonary causes. So clinicians may struggle to distinguish respiratory from non-respiratory etologies based holy on clinical science. Hence chest radiographs are crucial for accurate diagnosis. So timely intervention is essential for a favorable outcome as I've mentioned. So these are common pulmonary causes of uh respiratory distress in the neital period and these are naman the extramonary causes. This is actually in your book.

Okay. So how do we approach a newborn with respiratory distress syndrome or respiratory distress? First is a crucial um a very thorough history where you get the onset of the distress you get the gestational age whether it is an series were given if this is a prterm um patient the predisposing factors such as maternal infections or presence of prom if there is miconium steining in during the delivery and there is aspixia as well for physical examination you check the severative to respiratory distress the neurological status of the patient the hemodynamics parameters presence of cyanosis or hepatomegally or features of sepsis and look for animal formations. So if there is what do you see you typically see a a patient with respiratory rate of more than 60 and with significant lower chest retractions or presence of granting or even with or without cyanosis. So on physic so on physical examination you observe the vital signs the capillary field time and saturations. This is actually your hemodynamic parameters. So no foronium staining as you see it in the ano sa ilical stump as well is as well on the nails nail beds of the patient and also the uh ear. So if there is chest hyperinflation um if there is vowel sounds or cyenosis or presence of tachicardia or murmur so check for scaffoid abdomen kasi baka pala siya ay may congental anomal. So on chest examination observe air entry the magestinal shift adventicious sounds if there is hyperinflation as seen in increase ap diameter and presence of heart and the heart sounds you check the uh quality of the heart sounds and check for presence of murmur so then you assess the severity of respiratory distress and determine the underlying factors to initiate appropriate management so there we have this two sparing systems uh the down uh scoring system and the silverman sun scoring system. For the D scoring system we use this primarily in term patients and you see this is the scoring system for downs for for term patients. Ah important to note is the may five parameters para siyang upcar scoring no so respiratory rate the sinusis central central sinusis presence of retractions granting and air entry. So then you know the score if this is less than 4 or 0 to 4 then oxygen requirements less than 40% then if it's 5 to 7 you have to place this patient on CP kasi it's moderate distress and if it's more than 8 that is severe. Uh it would warrant assisted ventilation in view of an impending respiratory arrest or respiratory failure. This is the silver man scoring for premature patients. As you see it um assess five parameters as well. The chest movement, intercostal retractions, cipid retractions, masal flaring and expiratory grant. So based on this scoring also you score 0 to 4 pag 0 to 4 ah ano lang siya meld siya would require less than 40% oxygen if 5 to 7 would require pap or continuous positive pressure and if it's more than 8 it would require um NIPP or non-invasive positive pressure ventilation in due of uh intubating this patient.

Okay, now we go to uh this case. So this is a 1.5 male delivered viac uh with a pretterm labor of 33 33 weeks gestation. UPGAR scores are 7 and 8 and infant isutic and requires pop immediately after delivery. There is subcostal retractions, granting and nasal flaring. So nga based nga on the ano silverman scoring, anong silverman scoring nitong patient na ito? So meron siyang sinosis, um subcostal retractions, granting and nasal flaring and grant. So ano yung based on this score? Can you type it in the chat box kung ano yung score ng patient? Okay. Notaded. So what do you think is this uh there is um sifage retractions there is flaring intercostal retraction and grant based on this ano scoring system guys are still awake can you answer it in the type in the chat box please so I know I would know that you are awake. You're still awake. Okay. Yeah. At least at 8: right? No. Kasi wala naman siyang chest ano eh movement. Wala naman siyang wala naman sinabingo respiration siya. It's more of um intercust retractions probably 1 to two or kung may cid nasal flaring. So two granting audible granting na yon ibig sabihin kung naririnig na niya yung granting. So 2 yeah I agree with um at least so audible granting so to ah nail na nisan fliring kasi hindi sinabi kung marketly mark siya so sasabihin na lang nating evident siya. So let's give it a two. So cidd retraction siguro probably ah two rin. So six with intercostal siguro or 1 to two. So between 7 and 8 siguro no 7 to 8. So correct for this patient to receive CPAP um right away. That's why CPAP was patient was placed on CPAP immediately. So what is RDS naman? So premature infants are most susceptible to this condition which is inversely related to gestational age and birthweight. So ganun yon. So ah the smaller the infant, the lesser the gestational age, the higher the incidence of this patient developing RDS. So important ris factors include yan nga prematurity uh maternal DM meal sex twin births and CS delivery as well as pernatal asficia so surfactant deficiency leads toelectis or decrease functional residual capacity as well as arterial hypo hypoxemia and respiratory distress so the alvili are perfused but not ventilated so causing a pulmonary shunt and hypoxy emia. So asidectasis increases um lung compliance decreases and the chest of the premature infants attempt to overcome this with increased inspiratory pressures resulting in chestful retractions. That's

Why nagre-retract sila? Because of the, uh, highly compliant chest wall but poorly compliant lung. Okay.

So this sequence relates to poor air exchange, increasing dead space, um, alveolar hypoventilation, and hypercapnia. So, cyclical hypoxia, hypercapnia, and acidosis reduce surfactant synthesis in the type 2 cells, further aggravating the surfactant deficiency. So, uh, and in turn, this would cause, um, pulmonary hypertension. So, RDS may develop immediately in extremely immature infants, uh, meaning that 26 to 30 weeks gestation, or 3 to 4 weeks after birth in more premature infants at around 34 weeks. Kasi meron na silang surfactant pool. Kasi it's more of naman iyung maturation of the surfactant, um, pool ang pinag-uusapan dito. So the less, uh, the more premature the baby, the less the surfactant pool, then the higher the incidence of RDS or the earlier the onset of symptoms of RDS. Okay.

So, manifestations include cyanosis, takip nial, laying intercostal with intercostal, sternal retractions, and grunting. So, grunting maintains lung volume and gas exchange during, um, exhalation by closing the glottis. Kaya nga siya nagga-grunting because the baby is trying to expire through a closed glottis. So, radiographic examination shows a ground glass hazy opacity, as you see in this x-ray, uh, with, um, air bronchogram. Ito yung air bronchogram na sinasabi, or lung is airfield, um, surrounded by airfield bronchi with an atelectasis, uh, at the background. So, severe RDS may have airless lung fields, as you see in this, yung white out lang, totally obliterated na ang distinction between the heart and the liver, as well as, well as the, the lung.

So, what are predisposing factors? So, predisposing factors include prematurity, as I've mentioned, CS delivery, asphyxia, and maternal DM. Kasi maternal DM decreases or impairs, um, surfactant maturation. While protective factors naman, meaning it actually decreases incidence of RDS, include PROM, IUGR, or giving steroids. Why PROM and IUGR? Kasi pag IUGR baby, it means baby is chronically under stressed. That's why it hastens lung maturation. While for PROM naman, based on studies, if the PROM is beyond 48 hours, it hastens lung maturation as well. However, you would have a patient who is septic naman because of pneumonia.

Okay. How do we prevent, um, um, RDS? So, by preventing, um, preterm delivery. So, paano natin ipi-prevent yan? Usually, ano yung cause ng preterm delivery? So, we can, if there is cervical insufficiency, you can put a cervical cerclage, bed rest, and infection control, and tocolytic medications. If birth, if delivery is warranted, then antenatal corticosteroids in the form of betamethasone and dexamethasone, as you see in this slide, should be given. And surfactant should be administered, uh, when there is onset of respiratory distress postnatally or at birth. So, for, ano naman, um, for steroids, multidose steroid daw is not beneficial, sabi sa study.

Okay. Now, we go to complications naman of, um, severe RDS. So, BPD, or what we call the chronic lung disease, also, um, is a clinical pulmonary syndrome that develops in most extremely preterm patients. So, it is characterized by prolonged need for respiratory support and supplemental oxygen. So, nearly 60% of, um, of infants born less than 28 weeks gestation develop BPD, with an incidence decreasing as gestational age increases. So, for infants born at 22 to 24 weeks, almost all develop BPD, mostly with moderate to severe disease. Improved neonatal care and standard use of antenatal corticosteroids have increased the survival of infants born at extreme, uh, viability, leading to a higher prevalence of BPD naman. So, yun yung ano niya eh, yung parang yung, um, ah, anong tawag doon? In exchange of a, a lower threshold of survival, you have a higher incidence naman of, um, BPD.

So, the pathogenesis of BPD is likely multifactorial, but, uh, pulmonary inflammation and lung injury in immature lungs are consistently observed. So, alveolar collapse, what we call atelectrauma due to surfactant deficiency, combined ventilator-induced, uh, overdistension disease, volutrauma, promotes inflammation and injury. Supplemental oxygen produces free radicals that immature antioxidant systems of the very low birth weight infants cannot metabolize, further contributing to injury. So, you see, iyung high, giving supplemental oxygen is actually detrimental to the developing brain of the baby, as well as to the developing lung. So, pulmonary hyperinflation, pulmonary inflammation evidenced by neutrophil and macrophage infiltration in the alveolar fluid and proinflammatory cytokines contribute to the injury progression. So, pre- and postnatal infection, excessive pulmonary blood flow via the patent ductus arteriosus, or the PDA, with excessive, um, intravenous fluid administration, and, um, prenatal and postnatal growth failure are also significantly associated with development of BPD. So, pulmonary arterial hypertension may complicate BPD, although the mechanism is unclear. All likely promote lung injury by, um, necessitating increased or prolonged respiratory support or interfering with lung repair.

Okay. So, BPD is diagnosed when a preterm infant needs supplemental oxygen, um, beyond 28 days of life. So, it is classified at 36 weeks PMA, or postmenstrual age, based on oxygen supplementation. So, severe BPD if the, uh, positive pressure support, or if the patient would still require positive pressure support, or still incubated, or would require more than 30% of supplemental O2 at 36 weeks PMA or at discharge. So, moderate if less than 30%, iyung mga naka-regular oxygen lang. And mild if previously requiring oxygen for at least 28 days but now breathing room air. So, infants needing oxygen for less than 28 days, uh, have no BPD. So, oxygen should be gradually reduced, uh, to room air at 36 weeks, while under continuous observation with pulse oximetry monitoring to determine if they can be weaned off oxygen. And, uh, this is what we call the physiologic, um, definition of BPD. So, this is reliable and correlates with discharge home, um, oxygen or hospital stay, and, uh, during the first year, hospital readmissions. Neurodevelopmental impairment, pulmonary morbidity, and BPD severity are directly correlated.

So, the treatment of, uh, established BPD is actually supportive. So, key aspects include appropriate ventilation management, or aggressive nutritional support to optimize growth and encourage lung repair and development.

Okay. Now, the clinical manifestations of BPD include oxygen dependence, hypercapnia with compensatory metabolic alkalosis, with pulmonary hypertension, or with poor growth, or presence of right-sided heart failure if severe or if longstanding, with increased airway resistance with reactive airway bronchoconstriction, uh, which should be treated with bronchodilators. Ah, pag severe, if there is severe chest retractions causing negative intra-abdominal pressure, or fluid retention and necessitates fluid restrictions and diuretics.

So, radiographically, BPD initially shows, um, pacification, as you see in this first, uh, x-ray, followed by cystic or overdistensions, as you see in this, um, x-ray, also with areas of disease. This resembles actually the Wilson-Mikity syndrome. So, the third, uh, x-ray showed a 7-month-old infant with irregular, um, dense chances in both lungs with hyperinflation and cardiomegaly, as you see with the RV actually, um, enlargement and cardiomegaly, which is suggestive of a chronic lung disease. In this picture, the last one on the right is a large right ventricle and a cobblestone, irregular, aerated lung of an infant who died at 11 months of age.

Okay. Now, we go to this one, which is a 3.2 kg delivered CS at 38 weeks without a trial of labor. The patient's Apgar scores are 9. Develops dyspnea and subcostal retractions with nasal flaring at the first hour of life. Temperature is 36.6, with a heart rate of, respiratory rate of 74. Aside from increased work of breathing on physical examination, findings are normal. Sige nga, tingnan niyo nga yung down scoring naman nito. So, takip niya, so 74 with subcostal retraction and nasal flaring. Okay.

So, let's go to the slide, ah, to this, uh, go back. Let's go back. So, this is the down scoring for preterm patients naman. So, ano yung scoring niya sa kanya? Itakip niya lang siya with mild retractions. There is no mention of grunting nor, ah, decreased air entry nor cyanosis. So, what is your score? Okay, correct. Two to, ah, oo, kung one is respiratory, then minimal retraction. So, mga two lang siya, no? Is three. So, based on the scoring, our management lang is, kasi you, you get the score. So, your score is, uh, just 2 to 3. So, paano mo siya ima-manage? Based on the scoring system, agag less than 4, minimal, minimal O2 requirement lang siya, less than 40%. So, you can give low flow oxygen in the form of nasal cannula.

So, this is an x-ray of a patient with TTN. So, based on our scenario, that is a patient with tachypnea of the newborn. It is self-limiting, largely seen in patients, in premature patients or term patients born via CS. It is caused by retained fluid or decreased, uh, lung clearance, ah, lung fluid clearance. So, you expect this to improve, um, by 48 to 72 hours.

So, management is purely supportive. So, only requirements just less than 40%. Okay. Compared to this patient naman. So, I hope you still remember the down scoring at 2.9 kg delivered due to PROM with 8 and 8 Apgar scores, requiring 40% oxygen, still tachypneic and has cyanosis. Uh, there are scores, rales bilaterally with 37, and a heart rate of 144 with an RR of 65. Despite being given CPAP, still with grunting and takip niya. Grunting and takip niya would require intubation, ventilation for progressive increased work of breathing and respiratory acidosis and oxygen requirement during the next 6 hours. So, two na siya for, ano ba, two na siya for respiratory rate. Then there is grunting, audible grunting, that's two. Worsening respiratory distress. So, that's two with, ah, for sure there is, uh, anong tawag dito? The air entry is also poor, kasi nga nag-ano na siya eh, ah, intubated na siya. So, this is at least 8, that's why patient, or 7 to, that's why patient was intubated.

So, this is a patient presenting with neonatal pneumonia. How do we acquire pneumonia? It could be transplacental or perinatal. It is the most common manifestation of early onset sepsis in the newborn. It is diagnosed clinically and treated with antimicrobials with a generally good prognosis when treated promptly. So, what do we give? We have to think of the common etiologic agents for early onset sepsis, which is GBS, E. coli, as well as Listeria. So, pag ganon, ampicillin and gentamicin, yung inyong antibiotic of choice.

Okay. Another case or another scenario. 4.4 kg, so that's large for gestational age, 41 weeks, almost, ano na siya, post-term, with, as you see in the picture, 'di ba, sickly stained na siya, yellow na yung baby, with a poor Apgar scores 2 and 7, ah, poor score at the first minute of life, with tachycardia and tachypnea, with markedly increased work of breathing, with nasal flaring, subcostal, suprasternal retractions, and with, uh, barrel-shaped chest and coarse rales on bilateral lung fields. So, this is a patient, typically presenting with meconium aspiration syndrome. So, MAS is a condition in which a newborn infant born through meconium-stained amniotic fluid. It affects 10 to 15% of, um, births, and 5% would develop MAS or meconium aspiration syndrome, and 30% of this would require mechanical ventilation, with a 3 to 5% of dying.

So, meconium aspiration syndrome, uh, symptomatology include respiratory distress shortly after birth, with chest hyperinflation and skin and core discoloration and dark urine. So, kailangan before you diagnose MAS, dapat talaga thickly stained yung baby na meconium. So, meconium aspiration syndrome is characterized by tachypnea, hypoxia, and hypercapnia with small airway obstruction leading to air trapping, overdistension, and extra-alveolar air leak. You see this in this x-ray. So, if there is complete obstruction, there would be complete atelectasis of the affected area, as you see in this, um, pathophysiology. But if there is partial airway obstruction, there would be a ball valve effect causing air trapping, um, causing air leak eventually.

Okay. So, within 24 to 48 hours, chemical pneumonitis develops in addition to mechanical effects, and abnormal pulmonary function may be due to surfactant inactivation. So, if there is, um, if there is chemical pneumonitis, it actually interferes with surfactant production, that's why there is surfactant inactivation. So, primary pulmonary hypertension of the newborn, or PPHN, often accompanies MAS, caused by increased pulmonary vascular resistance and right-to-left shunting, as you see in this pathophysiology.

So, the, ano yan, syndrome kaya yung tinawag na meconium aspiration syndrome. There is clinical features of, um, tachypnea, hypoxia, or hypoxemia with unequal oxygen saturations, meaning there is discrepancy of at least 3 to, uh, 3% between their preductal and their postductal saturations, and then the presence of, um, respiratory and metabolic acidosis on, on, uh, ABG, with radiographic findings of MAS. So, ano ba nakita sa x-ray na MAS? There is patchy infiltrate, as you see in this side, with overdistension. There is, pag overdistension, you see there's flattening of the diaphragm, increased AP diameter, as you see in this, kita mo, inflated yung lungs with, um, presence of, um, air trapping. Yung air trapping actually, iyun yung mga area of lucas with area of disease, as you see in this x-ray. So, um, air trapping complicates or could predispose to, uh, formation of, um, air leaks such as pneumomediastinum and pneumothorax. And comorbidities include, um, asphyxia in utero.

So, how do we treat this patients? Generally, it's supportive, um, with assisted ventilation. And if there is PPHN-like symptoms, so it should be treated as such. So, if severe hypoxia persists despite conventional, uh, modality, then we give, um, surfactant therapy, inhaled nitric oxide, as well as placing the patient on ECMO. So, this is a patient with a delivery term to a DM mother. So, there is, as you see, there is baby is large for gestational age with a saturation of 70 on the right hand and 45 on the left leg. So, that's your preductal. Preductal is the right hand, meaning the autosats is actually preductal sites, kasi kaya siya preductal before the ductus arteriosus. The postductal naman is from your left hand down. So, that's your postductal. So, chest x-ray revealed, uh, pulmonary decreasing pulmonary blood flow. So, the most likely, uh, cause of the respiratory distress of this infant is what we call the persistent pulmonary hypertension of the newborn.

So, what is PPHN? So, as you see, PPHN is there is persistence of the fetal circulatory pattern of right-to-left shunting through the PDA or the foramen ovale after birth, and this is due to excessively high pulmonary vascular resistance. So, fetal, you know that fetal PVR is usually higher than fetal systemic or postnatal pulmonary pressure. So, in this fetal state, it allows oxygenated, um, umbilical venous blood to bypass the lungs through the ductus arteriosus and the, uh, descending aorta. So, after birth, PVR declines rapidly due to vasodilation from lung inflation and increased postnatal O2 saturations, thereby decreasing carbon dioxide saturation and increasing the pH, and as well as the release of vasoactive substances causing further relaxation of your pulmonary vessels. So, increased postnatal PVR may be due to: first, maladaptive from an acute injury not responding to increased oxygen and other changes after birth. Sorry, I could be due to increased pulmonary arterial medial muscle thickness. Iyung first, maladaptive ito yung mga usually nakikita mo for in patients with meconium aspiration syndrome or in patients with severe pneumonia like in GBS pneumonia. Second would be if there is increased pulmonary arterial medial muscle thickness and smooth muscle extension into the peripheral pulmonary arterioles in response to chronic fetal hypoxia. So, ano yung mga ganitong condition? So, if there is actually maternal, uh, intake of SSRIs and ibuprofen can actually cause, um, ano siya, malformed. This is maldeveloped naman. Maladaptive. Normal yung lung, ah, lung mo, yung parenchyma mo, yung vasculature mo, but, uh, because of the severe pneumonia and, um, presence of meconium aspiration, then maladapted siya. While maldeveloped naman, there is thickening of the tunica media muscle. Third would be a consequence of pulmonary hypoplasia. So, it is parang, in a parang, in essence, is maldeveloped, kasi nga ba, there's underdevelopment of the lung parenchyma because of extrinsic causes like presence of oligohydramnios or if there is severe oligohydramnios, anong tawag doon? Severe, ah, unhydramnios in the presence of Potter syndrome, wherein there is failure of the lung to develop. And the fourth naman is obstructive, due to polycythemia or total, in patients with, uh, alveolar capillary dysplasia. So, ang problem dito ay there is, yung blood flow to the lungs is actually impaired, kaya ano siya, um, ano siya, ah, because obstructive siya in nature. So, walang problem yung lung or there is, ah, um, anong tawag dito, because of the increased, um, hematocrit concentration like in polycythemia. So, there is obstructive. So, more of, ano rin siya, para siyang pumapasok under maladapted. Okay.

So, regardless of the cause, profound hypoxemia from right-to-left shunting and normal or elevated PaCO2 is actually present. Okay. How do we, uh, uh, what are the clinical features? Most, uh, most term or post-term infants with severe cyanosis or severe respiratory distress within the first 24 hours of life with severe hypoxemia or unequal oxygenation. When you say unequal oxygenation, there is discrepancy between the pre-ductal and postductal saturations. You could appreciate a single or narrowly split S2, or a loud S2, kasi 'ba, loud ang S2 is the closure of your, ah, semilunar valves, your aortic and the pulmonary valve. So, if the pulmonary side is actually mataas yung pressure, then there is delayed or there's splitting of your S2 sound with increase in the component of the pulmonary or the P sound. So, if the ductus arteriosus is present, there is, uh, no atrial or ventricular shunting, then the preductal oxygen saturation will be greater than the postductal oxygen saturation, indicating differential cyanosis. However, if atrial or ventricular mixing occur at the level of PDA, the ductus arteriosus, the foramen ovale, then the your preductal postductal saturation may be equal.

Okay. How do we manage PPHN? It involves, um, importantly, first is you get an echo to rule out critical cyanotic heart diseases. So, echo findings typically suggesting of PPHN involves, um, there is, uh, the PVR, the pressure is exceedingly high than the systemic pressure, with tricuspid regurgitation, VSD, the ventricular septum bowing into the left ventricle, and the right-to-left shunting across the PDA or the foramen ovale. Antibiotics and treatment of underlying lung disease are essential. Supportive measures including sedation of the baby, maximizing oxygen delivery, ah, oxygen carrying capacity with packed red cell transfusion, kasi we have to maintain a, at least a hematocrit level of 40. Maintaining cardiac output with a slightly higher systemic blood pressure than the PA pressure to decrease or to increase the left-to-right shunting compared to right-to-left shunting. So, gusto mo kung ang systemic blood pressure, kung ang kanyang pulmonary pressure is 70, then the systemic blood pressure should be 80, and then we could as well, uh, maximize ventilatory support, consider high-frequency ventilation if the, ah, if the required, if you were able to maximize, uh, ventilate the conventional, uh, ventilation, then giving inhaled nitric oxide, sildenafil may be of use, and ECMO is actually considered if all these therapies, uh, fail. Survival in PPHN patients varies with underlying diagnosis, but is generally 90% if timely intervention, uh, if there is timely intervention. So, long-term survivors face risk of neurodevelopmental impairment and, since the neural, uh, hearing loss occurring in 25% of patients, especially those placed on high-frequency ventilation. ECMO treatment has a favorable outcome of more than 80%, with 60 to 75% of these survivors appearing normal at 1 to 3, uh, years of age. However, limited lang ang nag-e-ECMO. Actually, ah, yung mga meron lang, uh, newborn, uh, newborn, uh, medicine fellowship training program.

Okay. Okay. What is this? This is, um, high peak inspiratory pressure and positive expiratory pressure in assisted ventilation can cause alveolar rupture leading to this pneumothorax. So, this is pneumothorax on the left. So, diagnosis is confirmed by chest radiograph, and treatment involves chest tube insertion. So, you have to change this, kasi if pneumothorax is on the left, so this is tension, and patient would deteriorate, uh, fast if not treated or evacuated properly.

Okay. So, let's proceed to congenital diaphragmatic hernia. I think we're almost done. So, CDH is a communication between the abdominal and thoracic cavity, sometimes with abdominal contents in the thorax. So, it is usually congenital but rarely traumatic. So, the symptoms and prognosis depend on the defect, location, and associated anomalies. So, there are four types: the hiatal hernia, or the esophageal hiatus, at the esophageal hiatus, or the paraesophageal, which is adjacent to the hiatus, or retrosternal, meaning in the foramen of Morgagni, and Bochdalek hernia, which is posterolateral to the diaphragm. So, in CDH, Bochdalek remains accounts up to 70 to up to 90% of cases, so mostly on the left. So, Morgagni naman is rare, 2 to 6%, and the defect size varies from small to complete diaphragmatic, um, agenesis. So, these lesions cause significant respiratory distress at birth and can be associated with other congenital anomalies and have a high mortality and long-term morbidity. So, CDH is characterized by structural diaphragmatic defect, but other anomalies or syndromes and primarily pulmonary hypoplasia limit survival. Survival. So, pulmonary hypoplasia reduces pulmonary mass and the number of bronchial divisions, with respiratory bronchioles and the alveoli. That's why ba, iyung isang type ng PPHN is because of failure to develop or they're underdeveloped because of, uh, CDH. So, the pathology of pulmonary hypoplasia in CDH includes abnormal septa in the terminal saccules with thick alveoli and thickened pulmonary arterioles. So, biochemical abnormalities include relative surfactant deficiency with increased glycogen in the alveoli and decreased levels of phosphatidylcholine, with the total, total DNA and total lung, lung protein, all contributing to the limited gas exchange and respiratory failure of this patient.

Okay. So, how do we manage patients with CDH? So, during your clerkship, you will be rotating to NCH. So, you will have, actually, most of our, we do get patients with CDH in NCH, and this is one of the common causes of admission in our, in that institution. So, delivery in a tertiary hospital with experience in CDH management is crucial for early appropriate respiratory support. So, in the delivery room, infants with respiratory distress should be rapidly stabilized with intubation. So, hindi mo na siya iaambubag, kasi you don't want the stomach to, ano, to be inflated. So, prolonged bag-mask ventilation should be avoided, as it enlarges the stomach and the small bowels, making oxygenation difficult. So, NGT or gastric tube should be placed immediately for decompression. So, once in the NICU, you, we have to put central lines, and then we have to monitor the pre- and postductal saturations, and as well as gastric content should be decompressed to prevent enlargement, kasi this is will actually complicate your pulmonary function. So, the preductal arterial oxygen saturation of at least 85% is the minimum goal, and an initial arterial PaCO2 of greater than 80 mmHg predicts mortality. So, pag alam mo mataas ang PCO2, then you know that this patient has a concurrent pulmonary hypoplasia, then you can predict this patient would have a higher mortality. So, conventional mechanical ventilation, high-frequency oscillatory ventilation, and ECMO are the main strategies to support respiratory failure in newborns with CDH. So, the goal is to maintain oxygenation and carbon dioxide elimination without inducing volutrauma. So, conventional ventilation using a gentle, um, lung protective strategy, meaning, uh, limiting the PIP for at 25 lang yung maximum, with positive pressure of 3 to 5, ah, PEEP, I mean, of 3 to 5, allows permissive hypercapnia of, dapat less than 65 is actually recommended. So, dapat gentle ventilation, permissive hypercapnia reduces lung injury and improves lung survival. Um, high-frequency oscillatory ventilation is indicated if the PIP is greater than 25 to, uh, maintain appropriate ventilation or if hypoxemia persists. So, inhaled nitric oxide is a selective pulmonary vasodilator that reduces, um, ductal shunting and pulmonary pressures, improving oxygenation also. So, while, um, helpful in PPHN, randomized trials have not demonstrated improvement, improved survival, or reduced need for ECMO when nitric oxide is used in newborns with CDH. So, however, nitric oxide is used as a bridge to ECMO. But, yun nga, sa studies, they did not improve survival. But if you have, if you have nitric oxide, then it might as well use it. Experts, um, plan surgery at least 48 hours after stabilizing and resolving pulmonary hypertension. So, indicators of stability include conventional ventilation only, or a low PIP, or a FiO2 requirement of less than 50%. ECMO weaning should be considered before surgery if the newborn is receiving ECMO. Post-surgery naman, monitor the infant for worsening of pulmonary hypertension, kasi expected yun, 'ba, na may pulmonary hypertension siya. ECMO, uh, may be needed in some patients. Complications include bleeding or chylothorax, bowel obstructions, and CDH recurrence in 10% of cases. So, overall survival, uh, of liveborn infants with CDH is 75% in the first world, in the developed countries. So, poor prognosis is associated with major anomalies or with syndromes, or in patients with severe pulmonary hypoplasia, or with the contralateral lung herniation, or in with use of ECMO. So, defect size is the strongest predictor of morbidity, kasi the larger the defect, the more the herniated content, then the all the more the higher the pulmonary pressure is expected. So, GERD is common in more than 50% of cases, especially in those with diaphragmatic defect involving the esophageal hiatus. Intestinal obstructions of up to 20% may result from midgut volvulus or adhesions or incarcerated hernias. Uh, delayed growth in the first two years is common due to poor intake or presence of GERD or due to high caloric requirements. So, many children normalize and catch up by age of 2 and beyond. Neurocognitive defects naman, common, often resulting from the disease or from the interventions. So, infants requiring ECMO have a higher incidence of having, uh, abnormalities or moderate, uh, neurodevelopmental, uh, abnormalities. Hearing loss may occur in up to 28% of patients who received ECMO.

Okay. Now, let's go to apnea. What is apnea? It is defined as cessation of breathing or cessation of pulmonary blood flow for a specific time interval, usually 20 seconds and more, or a period of less than 20 seconds if associated with bradycardia. So, there are three types: central, obstructive, and the mixed. Central apnea if there is complete cessation of airflow and respiratory efforts with no chest wall movement. So, talagang yung baby hindi siya humihinga. While obstructive apnea naman, there is absence of noticeable airflow but with chest wall movement. So, paano mo sasabihin yun? So, halimbawa, nag-humihinga siya but wala, on auscultation, wala kang naririnig na airflow. While the mixed type naman is a combination of the two, the central and the obstructive. So, what is the most common? Actually, it's the mixed type. So, a careful evaluation should be performed immediately in any infant with apnea. Incidence of apnea increases as gestational age decreases. Kasi nga ba, immature ang respiratory center nila. That's why, ah, they're prone to develop apnea, especially ito yung mga central apnea, no? Kaya sila nag-o-obstructive apnea naman because of their large head, yung mga premature patients. So, idiopathic apnea is a disease of premature infants, or we call this the apnea of prematurity. It appears in the absence of other identifiable disease states during the first week of life, and it resolves by 36 to 40 weeks postconceptional age. So, before you diagnose patient with idiopathic apnea or apnea of prematurity, then you have to rule out any other causes or organic causes of apnea, like infection, metabolic, no, so dapat, you have to rule those out first. So, preterm infants paradoxically develop apnea rather than increasing respirations in response to hypoxia. So, the poor tone of the laryngeal muscles may cause upper airway collapse leading to obstruction. So, isolated obstructive apnea may occur due to flexion or extreme lateral positioning of the head obstructing the soft palate. Yeah. That's why important na you play, you manage, the nurse, the NICU nurse should be able to manage, uh, the head properly, the position of the head. So, treatment of apnea of prematurity involves oxygen administration to hypoxic infants, with, uh, transfusion of anemic infants. So, may threshold tayo for transfusion in premature infants, as well as physical cutaneous stimulation for mild apnea. So, methylxanthines or caffeine or theophylline are the mainstays of pharmacologic treatment, increasing, um, minute ventilation, improving carbon dioxide sensitivity, decreasing hypoxic depression of breathing, as well as enhancing their diaphragmatic activity and decreasing periodic breathing. That's why we give caffeine up to at least 34 weeks, just, uh, postconceptional age. High flow nasal cannula therapy, or the, uh, giving providing and possibly safe methods of treating obstructive or mixed apneas, possibly by stimulating the infant and splinting the airway, the upper airway. So, CPAP also likely increases functional residual capacity, improving oxygenation.

Okay. So, this is the last, uh, of our topic for today, cardiovascular. I hope we're familiar with the fetal and neonatal circulation. So, hemodynamically, several things happen as the baby adapts to extrauterine environment. So, uh, fetal circulation is unique because gas exchange occurs in the placenta. You know this. Oxygenated blood returning via the umbilical vein, um, mixes with the deoxygenated blood from the superior vena cava and the inferior vena cava and is distributed throughout the body. So, the most oxygenated blood is directed to the brain, while the most deoxygenated blood is directed to the placenta. So, the umbilical vein carries the highest oxygenated blood, while the umbilical arteries carry the lowest oxygenated blood. So, blood returning from the right atrium is preferentially streamed, uh, via foramen ovale to the left atrium and ventricles, then to the ascending aorta, providing the brain with the most oxygenated blood. So, this is, uh, primarily from the umbilical vein. So, yung kasi yun yung higher, highest concentration of oxygen, 'ba. So, it is preferentially shunted to the foramen ovale, then siya yung pupunta ngayon sa ascending aorta to the brain. So, fetal shunts include ductus arteriosus and foramen ovale, allow blood flow to bypass the lungs with their higher vascular, um, resistance, which receives only about 80% of the fetal cardiac output. So, with the onset naman of ventilation, fetal circulatory system assumes the adult pattern, requiring lungs to receive 100% of the cardiac output. So, nadodoble na siya, 'ba. So, after birth, um, the low resistance and placental circulation is removed through the cutting of the cord, increasing systemic vascular resistance, while pulmonary vascular resistance decreases due to pulmonary expansion, increased postnatal O2 saturations, and local vasodilators.

So, what could go wrong? So, why is, um, CHD or congenital heart disease not present in utero, or they don't manifest in utero? Uh, partly because of three reasons. Fetal oxygen is not dependent on pulmonary blood flow. Next, both the RV and the left V, and left V, the left ventricle are important for systemic blood flow. So, 'ba, pareho sila nagwo-work. And then, communications between the left and the right sides of the heart because of mixing at the atrial and the ductal level because of the presence of the foramen ovale and the PDA. That's why these conditions don't manifest in utero.

So, this is just an overview of the common, uh, cyanotic heart diseases. So, VSD is the most common, most common cyanotic disease beyond the neonatal period. Kasi, in the new, within the neonatal period, TGA is the most common, or the congenital, uh, DTGA actually. And hypoplastic left heart syndrome, uh, most common in the first week, but it has the highest mortality, uh, during this period.

Okay. So, a severely ill neonate with cardiorespiratory distress and cyanosis presents a diagnostic dilemma or challenge. So, clinicians must quickly assess for congenital heart disease to institute potentially life-saving measures. Central cyanosis observed when deoxygenated hemoglobin reaches 5 grams per dcl, such as cyanotic heart disease, isis without obvious respiratory difficulty. How you differentiate actually the two, kung pulmonary siya or cardiac in nature. Kasi, a patient with pulmonary origin will have a severe respiratory distress with cyanosis. Then, a patient with central cyanosis, na very comfortable siya, but you see that the patient is cyanotic or saturating. So, causes, uh, cyanosis due to obstruction to the right ventricular inflow or outflow leading to increased right-to-left shunting, or a complex anatomic defect causing pulmonary and systemic, systemic venous return at mixture. So, pulmonary edema also causes cyanosis in heart failure due to left-to-right shunt, though the degree is less severe, uh, iyung cyanosis niya. So, cyanosis may persist from fetal pathways like the foramen ovale and the ductus arteriosus in the presence of pulmonary outflow tract obstruction, or in the presence of pulmonary persistent pulmonary hypertension. That's why it's important that you do, you do an echo prior to intervening, kasi nga iba yung management ng patient with severe PPHN, you have to give rich oxygen, while in patient with critical cyanotic heart disease, you have to limit oxygen. Okay. So, critical cyanotic heart disease requiring surgery or catheter intervention in the first year, in the first year of life, accounts for 25% of this CHD or congenital heart disease. So, many newborns with critical cyanotic heart disease are diagnosed prenatally or soon after birth, but some are not diagnosed until after discharge. So, delays in diagnosis and timely referrals to a tertiary center with expertise increase the risk of morbidity and mortality in infants with critical cyanotic heart disease.

So, how do you, um, prevent this from happening? So, screening. So, we have this screening tool, the CCHD screening tool. The screen is usually done when the baby is 24 to 48 hours, uh, hours old, or shortly before discharge if the discharge is less than 24 hours of age. So, it screens for seven main, um, diseases, namely hypoplastic left heart syndrome, pulmonary artery, uh, pulmonary atresia, tetralogy of Fallot, the TAPVR, or transposition of great arteries, tricuspid atresia, and the truncus arteriosus. So, the, ang positive pulse, uh, oximetry screen indicates a measured oxygen saturation of less than 90%. Yun yung red is, ano ba, sa warning or alert ba? Ag sa traffic light, red stop, or it is, ano, red is, basta red means, ah, parang alert. Then orange is equivocal, green is good, parang ganon, para madaliin niyo lang siyang ma-memorize. So, for pag 90% on either right hand or left or right hand and foot, that is a positive screen. So, repeat testing is unnecessary if the saturation is less than 95% or if there is more than 3% difference between the right hand and the foot, uh, O2 saturation. So, any infant with a positive screen should have a diagnostic echocardiograph. So, newborns with a CCHD can receive special carement to prevent death or disability. So, pulse oximetry screening doesn't detect all CCHDs, though. So, a complete medical and pregnancy history, as well as physical examination, is needed to detect CCHD before hypoxemia develops. So, early detection allows for appropriate delivery and management of the heart defects. So, ag more than 90%, it's discrepancy. It's positive. Ag less than 95% and more than 3% ang kanyang saturation, it's still positive, then you, uh, you don't have to repeat the screening. Okay? And then, we go to the last of our slide.

So, this is PDA, which is a physiologic event in the life of a newborn. 'Di ba? Kasi, you know that PDA or ductus arteriosus is needed in utero to sustain life in utero. However, there is physiologic closure within 12 to 15 hours and anatomic closure several months after. It depends on the gestational age of the baby, actually. No, for term patients, they're expected to close within the first month of life. So, for 4% of these patients would have failure to close. And, uh, for the, ano naman, extremely preterm, 50% would not close beyond 72 hours and would require PDA management. So, what are the common signs and symptoms for term patients? They are usually asymptomatic, or, if they become symptomatic early on, then you would know that this is a large PDA. So, there would be presence of a murmur, a systolic or machinery murmur, bounding pulses, and CHF if not treated properly. And for preterm patients naman, there would be decreased, uh, blood flow, kasi may still phenomena ng, tawag doon? So, there will be decreased blood flow into the other areas, especially the intestines. Ah, kaya what you see is actually, um, abdominal distension or intolerance of feeding, as well as hemodynamic instability. So, kaya pwede siyang mag-NEC. You would appreciate bounding pulses, you would appreciate, um, congestions and pulmonary hemorrhage. And this actually complicates BPD. How do we treat, um, PDA? It depends, kasi kung, if it's asymptomatic for term patients, we can actually, um, manage it conservatively, kasi you have to wait for anatomic closure, 'di ba? Especially if the lesion is small. But you have to get an echo to measure the LA-aorta ratio. If the LA-aorta ratio is less than 1.5, then spontaneous closure is high. But if the LA-aorta reaches more than, ah, sabi nila pala, if it's one, it's likely of spontaneous closure is high. If it's 1 to 1.5, then medical closure, uh, is recommended. More than five, you can attempt medical closure with ibuprofen or indomethacin, but if 3 to 4 times ka mag-fail, then surgery is warranted, or percutaneous closure via device is actually warranted. I think that's the end of our lecture. Uh, it's almost 10:00. I will stop sharing. Do you have any questions for this lecture? I hope it's clear. I'm sorry if I was, uh, if I was too fast sa umpisa, but I hope you were able to understand the lecture. So, if you do have questions, you can message.