A case of persistent pulmonary hypertension of the newborn (PPHN) is presented. The infant was born via emergency cesarean section at 37 weeks gestation to a mother with uncontrolled hypertension during pregnancy. At birth, the infant had meconium staining of the amniotic fluid and required respiratory support. On day 6, the infant began to develop desaturations down to 84% oxygen saturation while on routine care. The infant is diagnosed with PPHN based on clinical presentation and laboratory findings. PPHN requires aggressive respiratory and pharmacological management to reduce pulmonary vascular resistance and improve oxygenation.
This document discusses persistent pulmonary hypertension of the newborn (PPHN) with a focus on management in resource-limited settings. It provides background on PPHN, including associated conditions, signs and symptoms, diagnostic testing, and supportive care strategies. Key interventions discussed include inhaled nitric oxide (iNO), high frequency ventilation (HFV), and sildenafil. While iNO and HFV are standard treatments, their high costs limit use in many resource-poor areas. The document explores using less expensive options like sildenafil and discusses how HFV could potentially be utilized more in Nepal with appropriate equipment, training, and support.
Persistent pulmonary hypertension of newborn PPHNChandan Gowda
Persistent pulmonary hypertension of the newborn (PPHN) results from failure of the normal decrease in pulmonary vascular resistance after birth, causing right-to-left shunting of blood and hypoxemia. It can be caused by underdevelopment, maldevelopment, or maladaptation of the pulmonary vasculature. Clinical features include cyanosis and respiratory distress within the first 24 hours of life. Diagnosis involves echocardiography demonstrating elevated pulmonary pressures and responding poorly to oxygen challenges. Treatment aims to reduce PVR through ventilation strategies, medications, and potentially extracorporeal membrane oxygenation.
Persistent pulmonary hypertension of the newborn (PPHN) is a major problem in neonatal intensive care units that can lead to death or neurological injury in newborns. It occurs when the pulmonary circulation fails to transition from the high resistance fetal state. Causes include meconium aspiration syndrome, idiopathic PPHN, and pulmonary hypoplasia from conditions like congenital diaphragmatic hernia. Treatment involves optimizing oxygenation and cardiac function along with pulmonary vasodilators like inhaled nitric oxide. Future therapies may include phosphodiesterase inhibitors and prostacyclin analogs to further reduce pulmonary hypertension in newborns.
Pulmonary Hypertension of the Newborn - all you need to knowSid Kaithakkoden
Persistent pulmonary hypertension of the newborn (PPHN) is the failure of the pulmonary vascular resistance to decrease after birth, resulting in right-to-left shunting of blood and hypoxemia. It can be primary or secondary to conditions like meconium aspiration syndrome, asphyxia, or lung hypoplasia. Diagnosis involves signs of cyanosis and hypoxemia unresponsive to oxygen. Treatment aims to maintain oxygenation through supportive care, vasodilator drugs like inhaled nitric oxide, high frequency ventilation, and in severe cases, extracorporeal membrane oxygenation.
This document discusses shock in neonates. It defines shock and describes the unique pathophysiology of shock in newborns, including their immature cardiovascular systems. It outlines various types of shock seen in neonates such as cardiogenic, hypovolumic, obstructive, and distributive shock. Clinical scenarios that can cause neonatal shock are described. The use of echocardiography to evaluate shock is discussed. Parameters to assess shock are provided. Treatment approaches for different shock types are summarized, including fluid resuscitation, inotropic support, and other interventions.
1) Neonatal shock is characterized by an imbalance between oxygen delivery and demand, leading to tissue hypoxia. Myocardial dysfunction, abnormal vasoregulation, and hypovolemia are common causes.
2) Pathophysiology includes an immature myocardium with fewer contractile elements and higher basal contractility, as well as complex vascular smooth muscle tone regulation. Relative adrenal insufficiency also contributes.
3) Clinical assessment of shock includes vital signs, perfusion markers like capillary refill time and lactate, and echocardiography to evaluate cardiac function and filling. Goal-directed management targets normalization of these parameters.
NON INVASIVE VENTILATION IN NEONATES-PART 1Adhi Arya
Non-invasive ventilation techniques like nasal continuous positive airway pressure (nCPAP) are increasingly used for preterm neonates with respiratory distress to avoid intubation and invasive ventilation. nCPAP uses nasal prongs or a mask to deliver continuous distending pressure throughout the respiratory cycle. Evidence shows nCPAP reduces the need for mechanical ventilation and postnatal steroids compared to prophylactic surfactant without increasing adverse outcomes. Proper patient interface selection, initial pressure settings, and troubleshooting are important for safe and effective nCPAP use in neonates.
Pulmonary hypertension of the newborn (PPHN) is defined as failure of the normal decrease in pulmonary vascular resistance after birth, resulting in right-to-left shunting of blood and hypoxemia. It can occur due to underdevelopment, maldevelopment, or maladaptation of the pulmonary vasculature. Clinically, infants present with respiratory distress and hypoxemia unresponsive to oxygen therapy alone. Diagnosis involves echocardiography demonstrating elevated pulmonary pressures and right-to-left shunting. Management consists of supportive care including ventilation and targeting appropriate oxygen saturations, with vasodilating agents like inhaled nitric oxide or ECMO for severe cases.
This document discusses persistent pulmonary hypertension of the newborn (PPHN) with a focus on management in resource-limited settings. It provides background on PPHN, including associated conditions, signs and symptoms, diagnostic testing, and supportive care strategies. Key interventions discussed include inhaled nitric oxide (iNO), high frequency ventilation (HFV), and sildenafil. While iNO and HFV are standard treatments, their high costs limit use in many resource-poor areas. The document explores using less expensive options like sildenafil and discusses how HFV could potentially be utilized more in Nepal with appropriate equipment, training, and support.
Persistent pulmonary hypertension of newborn PPHNChandan Gowda
Persistent pulmonary hypertension of the newborn (PPHN) results from failure of the normal decrease in pulmonary vascular resistance after birth, causing right-to-left shunting of blood and hypoxemia. It can be caused by underdevelopment, maldevelopment, or maladaptation of the pulmonary vasculature. Clinical features include cyanosis and respiratory distress within the first 24 hours of life. Diagnosis involves echocardiography demonstrating elevated pulmonary pressures and responding poorly to oxygen challenges. Treatment aims to reduce PVR through ventilation strategies, medications, and potentially extracorporeal membrane oxygenation.
Persistent pulmonary hypertension of the newborn (PPHN) is a major problem in neonatal intensive care units that can lead to death or neurological injury in newborns. It occurs when the pulmonary circulation fails to transition from the high resistance fetal state. Causes include meconium aspiration syndrome, idiopathic PPHN, and pulmonary hypoplasia from conditions like congenital diaphragmatic hernia. Treatment involves optimizing oxygenation and cardiac function along with pulmonary vasodilators like inhaled nitric oxide. Future therapies may include phosphodiesterase inhibitors and prostacyclin analogs to further reduce pulmonary hypertension in newborns.
Pulmonary Hypertension of the Newborn - all you need to knowSid Kaithakkoden
Persistent pulmonary hypertension of the newborn (PPHN) is the failure of the pulmonary vascular resistance to decrease after birth, resulting in right-to-left shunting of blood and hypoxemia. It can be primary or secondary to conditions like meconium aspiration syndrome, asphyxia, or lung hypoplasia. Diagnosis involves signs of cyanosis and hypoxemia unresponsive to oxygen. Treatment aims to maintain oxygenation through supportive care, vasodilator drugs like inhaled nitric oxide, high frequency ventilation, and in severe cases, extracorporeal membrane oxygenation.
This document discusses shock in neonates. It defines shock and describes the unique pathophysiology of shock in newborns, including their immature cardiovascular systems. It outlines various types of shock seen in neonates such as cardiogenic, hypovolumic, obstructive, and distributive shock. Clinical scenarios that can cause neonatal shock are described. The use of echocardiography to evaluate shock is discussed. Parameters to assess shock are provided. Treatment approaches for different shock types are summarized, including fluid resuscitation, inotropic support, and other interventions.
1) Neonatal shock is characterized by an imbalance between oxygen delivery and demand, leading to tissue hypoxia. Myocardial dysfunction, abnormal vasoregulation, and hypovolemia are common causes.
2) Pathophysiology includes an immature myocardium with fewer contractile elements and higher basal contractility, as well as complex vascular smooth muscle tone regulation. Relative adrenal insufficiency also contributes.
3) Clinical assessment of shock includes vital signs, perfusion markers like capillary refill time and lactate, and echocardiography to evaluate cardiac function and filling. Goal-directed management targets normalization of these parameters.
NON INVASIVE VENTILATION IN NEONATES-PART 1Adhi Arya
Non-invasive ventilation techniques like nasal continuous positive airway pressure (nCPAP) are increasingly used for preterm neonates with respiratory distress to avoid intubation and invasive ventilation. nCPAP uses nasal prongs or a mask to deliver continuous distending pressure throughout the respiratory cycle. Evidence shows nCPAP reduces the need for mechanical ventilation and postnatal steroids compared to prophylactic surfactant without increasing adverse outcomes. Proper patient interface selection, initial pressure settings, and troubleshooting are important for safe and effective nCPAP use in neonates.
Pulmonary hypertension of the newborn (PPHN) is defined as failure of the normal decrease in pulmonary vascular resistance after birth, resulting in right-to-left shunting of blood and hypoxemia. It can occur due to underdevelopment, maldevelopment, or maladaptation of the pulmonary vasculature. Clinically, infants present with respiratory distress and hypoxemia unresponsive to oxygen therapy alone. Diagnosis involves echocardiography demonstrating elevated pulmonary pressures and right-to-left shunting. Management consists of supportive care including ventilation and targeting appropriate oxygen saturations, with vasodilating agents like inhaled nitric oxide or ECMO for severe cases.
This document discusses shock in neonates and neonatal vasoregulation. It begins by defining blood pressure and its components. It then discusses factors that affect blood pressure and the unique features of the neonatal myocardium. It describes the roles of catecholamines and their receptors in relation to blood pressure. The document clarifies terminology around hypotension and shock. It concludes by discussing clinical methods for monitoring systemic hemodynamics in critically ill newborns such as capillary refill time, central-peripheral temperature difference, and blood pressure measurements.
This document discusses various types of arrhythmias that can occur in children. It begins by describing the normal electrical conduction system of the heart and then discusses different types of tachyarrhythmias and bradyarrhythmias. Common pediatric tachyarrhythmias mentioned include supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation. Long QT syndrome is also summarized. Treatment options for unstable and stable rhythms are provided.
Human milk fortifiers are products that can be added to expressed breast milk to increase its nutritional content for premature infants. There are three main approaches to fortification - standard fixed dosage, adjustable based on blood urea nitrogen levels, and targeted fortification using human milk analysis. Fortifiers provide additional protein, calories, and minerals to help premature infants achieve adequate growth. While fortification benefits growth, high osmolality from fortifiers can cause feed intolerance and risks like necrotizing enterocolitis. Careful monitoring of infants on fortified breast milk is needed to optimize nutrition and growth.
Minimally invasive surfactant therapy in pretermdrsadhana86
This study evaluated a technique called minimal invasive surfactant therapy (MIST) which involves administering surfactant through a narrow bore catheter inserted into the trachea of preterm infants on continuous positive airway pressure (CPAP). The study found MIST was successfully applied in two hospitals with no significant complications. Infants receiving MIST at 25-28 weeks gestation had sustained reductions in oxygen requirements and decreased need for intubation compared to historical controls. The study concluded MIST is a promising technique for improving outcomes for preterm infants on CPAP but that a large randomized controlled trial is still needed.
Persistent pulmonary hypertension of the newborn (PPHN) results from failure of normal decrease in pulmonary vascular resistance after birth, leading to right-to-left shunting of blood and hypoxemia. PPHN has a prevalence of 1.9 per 1000 live births and can be caused by underdevelopment, maldevelopment or maladaptation of the pulmonary vasculature. Diagnosis involves assessment of oxygen saturation gradient, blood gases, chest x-ray and echocardiogram. Management includes supportive care, ventilation, circulatory support, sedation and treatments to reduce pulmonary pressures like inhaled nitric oxide, sildenafil or prostaglandins. For severe cases, extracorporeal membrane oxygenation may
Cardiac rhythm disorders in neonates can include sinus arrhythmias, tachyarrhythmias like atrial tachycardia and supraventricular tachycardia, and ventricular arrhythmias like premature ventricular contractions and ventricular tachycardia. The document discusses how to read an ECG, defines various normal and abnormal rhythms like sinus bradycardia, and outlines their evaluation and treatment approaches. Genetic arrhythmia syndromes are also mentioned.
1) Hypoxic-ischemic encephalopathy (HIE) is brain injury caused by lack of oxygen and blood flow before, during, or after birth. It remains a serious condition that can cause death or long-term disabilities like cerebral palsy or intellectual impairment.
2) The document discusses the definition, risk factors, pathophysiology, clinical features based on the Sarnat staging system, diagnosis using imaging and EEG, and treatment approaches for HIE including supportive care, perfusion management, anti-seizure medications, and therapeutic hypothermia.
3) The goal of treatment is to prevent further brain injury by maintaining appropriate oxygenation, blood pressure, glucose levels, and treating seizures
This document discusses bronchopulmonary dysplasia (BPD), a chronic lung disease that occurs in premature infants requiring respiratory support. It covers the definition, risk factors, pathogenesis, clinical features, prevention, and treatment of BPD. The definition has evolved over time from relying solely on oxygen need at 28 days to incorporating factors like oxygen need, pressure support, and gestational age. BPD results from lung injury and disrupted lung development due to prematurity and respiratory support. Management aims to protect the lung from injury through gentle ventilation, optimal oxygen levels, and other strategies.
Apnea of prematurity is common in preterm infants, especially those born before 28 weeks gestation or weighing less than 1800g. It is caused by immature development of the respiratory control centers in the brain. Treatment includes caffeine which reduces apnea by blocking adenosine receptors. Other supportive measures like positioning and CPAP may help as well. Apnea spells usually resolve by 36-37 weeks corrected gestational age. Before discharge, infants should have a period of at least 5-7 days without any recorded apnea events while off caffeine therapy.
The document discusses the approach to evaluating and diagnosing bleeding in neonates. It notes that while the neonatal coagulation system is immature compared to adults, healthy term infants do not typically have bleeding issues. A bleeding neonate should first be assessed for general health and vitamin K administration history. Screening tests include a complete blood count, coagulation tests, and peripheral smear. Abnormal results can indicate disorders like disseminated intravascular coagulation, infection, liver disease, immune thrombocytopenia, or inherited coagulation factor deficiencies. The causes, patterns, and management of various bleeding disorders seen in neonates are described.
Sodium and Potassium Homeostasis in NeonatesKing_maged
This document discusses sodium and potassium homeostasis and management in infants. It covers sodium requirements, causes and treatment of hyponatremia and hypernatremia. It also discusses potassium requirements and causes and treatment of hypokalemia and hyperkalemia. Key points include maintaining serum sodium between 135-145 mEq/L, restricting free water intake to treat dilutional hyponatremia, and slowly correcting chronic hypernatremia to avoid brain edema. The document also outlines serum potassium goals and risks of rapid changes in potassium levels.
This document discusses portal hypertension (PH), including its definition, classification, pathophysiology, etiology, clinical features, complications, and diagnosis. Some key points:
1. PH is defined as a portal venous pressure gradient above 10 mmHg. It can be pre-sinusoidal, sinusoidal, or post-sinusoidal based on location of blockage.
2. Common causes are cirrhosis, portal or hepatic vein thrombosis, and Budd-Chiari syndrome. Cirrhosis results from fibrosis narrowing hepatic sinusoids.
3. Clinical features include splenomegaly, abdominal collaterals, ascites, gastrointestinal bleeding from varices, and hepatic encephalopathy.
A preterm newborn developed respiratory distress soon after birth, with signs including grunting and cyanosis. Evaluation found respiratory distress syndrome (RDS). The baby was treated with nasal CPAP, surfactant, and mechanical ventilation. RDS is caused by surfactant deficiency in premature infants, resulting in alveolar collapse and impaired gas exchange. Management includes respiratory support, surfactant replacement therapy, and care to prevent complications.
Surfactant replacement therapy : RDS & beyondDr-Hasen Mia
This presentation is about Surfactant, its use in Respiratory Distress Syndrome & some other conditions of surfactant deficiency due to inactivation like meconium aspiration syndrome & others
Hypothermia therapy is the standard treatment for hypoxic ischemic encephalopathy (HIE). Mild hypothermia between 34-35°C is initiated within 6 hours and continued for at least 72 hours. This decreases cerebral metabolic rate, excitatory neurotransmitter release, apoptosis, and vascular permeability. Hypothermia reduces mortality and neurodevelopmental disability in HIE. Other promising therapies target oxidative stress, calcium channels, excitatory amino acids, nitric oxide, and apoptosis, but require further study. Stem cell transplantation may also have potential as a future regenerative therapy for HIE.
This document presents treatment threshold graphs from the National Institute for Health and Clinical Excellence (NICE) clinical guideline 98 on neonatal jaundice. The graphs show bilirubin thresholds for phototherapy and exchange transfusion in babies with hyperbilirubinemia. The guideline was developed by the National Collaborating Centre for Women's and Children's Health and thanks two researchers who allowed their Excel spreadsheet to be adapted in developing the treatment threshold graphs.
Apnea of prematurity is common in neonates born before 32 weeks gestation or weighing less than 1000g, with rates as high as 54% in infants born at 30-31 weeks and nearly 100% in infants born below 29 weeks or weighing less than 1000g. Apnea can be classified as central, obstructive, or mixed based on whether there is absence of respiratory effort or upper airway obstruction. Common causes include infection, neurological or cardiovascular issues, pulmonary problems, inborn errors of metabolism, metabolic or hematological conditions, gastrointestinal issues, problems with temperature regulation, and drugs. Evaluation may include investigations and treatment involves general measures as well as specific measures and emergency treatment if needed. Methylxanthines are commonly
1. Perinatal asphyxia refers to impaired gas exchange and oxygen deficiency in a fetus or newborn infant, occurring during labor, delivery, or immediately after birth.
2. It can cause hypoxic-ischemic encephalopathy (HIE), a type of brain injury, in severe or prolonged cases. Clinical features of HIE include seizures, abnormal neurological exam, and multi-organ dysfunction.
3. Diagnosis involves assessing risk factors, signs of asphyxia at birth, abnormal blood gas values, and neurological exam over time. Imaging and EEG can further evaluate brain injury. Prognosis depends on severity of encephalopathy and extent of brain injury.
Seminar on shock in newborn by dr. Sajjad and Dr. OliviaDr. Habibur Rahim
This document summarizes shock in newborns. It discusses definition, pathophysiology, types including hypovolemic, cardiogenic, septic, and distributive shock. Signs and symptoms are tachycardia, decreased blood pressure, prolonged capillary refill time, and decreased urine output. Management involves supportive care, fluid resuscitation, and inotropic drugs like dopamine, dobutamine, and epinephrine to increase cardiac output depending on the cause of shock. Close monitoring is needed to guide therapy and prevent complications.
Approach to Respiratory distress in neonates pptamar naik
This document discusses several cases of respiratory distress in newborns. The key information provided includes potential causes of respiratory distress like respiratory distress syndrome (RDS), meconium aspiration syndrome (MAS), transient tachypnea of newborn (TTN), and persistent pulmonary hypertension of the newborn (PPHN). It also outlines the approach to evaluating a newborn with respiratory distress, including assessing risk factors, clinical examination findings, and initial investigations like chest x-ray and blood gas analysis. Management strategies like oxygen therapy, respiratory support, and surfactant administration are also summarized.
Respiratory distress in neonates can be identified by tachypnea, chest indrawing, and other signs. It can be caused by pulmonary issues like respiratory distress syndrome, meconium aspiration syndrome, or transient tachypnea of the newborn. Non-pulmonary causes include perinatal asphyxia, hypothermia, and congenital heart disease. Transient tachypnea of the newborn involves defective sodium transport leading to retained lung fluid and is often seen in babies delivered by c-section. It typically resolves within a few days with supportive care like oxygen and feeding assistance. Persistent pulmonary hypertension of the newborn results when normal postnatal pulmonary pressure reduction fails and presents a serious
This document discusses shock in neonates and neonatal vasoregulation. It begins by defining blood pressure and its components. It then discusses factors that affect blood pressure and the unique features of the neonatal myocardium. It describes the roles of catecholamines and their receptors in relation to blood pressure. The document clarifies terminology around hypotension and shock. It concludes by discussing clinical methods for monitoring systemic hemodynamics in critically ill newborns such as capillary refill time, central-peripheral temperature difference, and blood pressure measurements.
This document discusses various types of arrhythmias that can occur in children. It begins by describing the normal electrical conduction system of the heart and then discusses different types of tachyarrhythmias and bradyarrhythmias. Common pediatric tachyarrhythmias mentioned include supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation. Long QT syndrome is also summarized. Treatment options for unstable and stable rhythms are provided.
Human milk fortifiers are products that can be added to expressed breast milk to increase its nutritional content for premature infants. There are three main approaches to fortification - standard fixed dosage, adjustable based on blood urea nitrogen levels, and targeted fortification using human milk analysis. Fortifiers provide additional protein, calories, and minerals to help premature infants achieve adequate growth. While fortification benefits growth, high osmolality from fortifiers can cause feed intolerance and risks like necrotizing enterocolitis. Careful monitoring of infants on fortified breast milk is needed to optimize nutrition and growth.
Minimally invasive surfactant therapy in pretermdrsadhana86
This study evaluated a technique called minimal invasive surfactant therapy (MIST) which involves administering surfactant through a narrow bore catheter inserted into the trachea of preterm infants on continuous positive airway pressure (CPAP). The study found MIST was successfully applied in two hospitals with no significant complications. Infants receiving MIST at 25-28 weeks gestation had sustained reductions in oxygen requirements and decreased need for intubation compared to historical controls. The study concluded MIST is a promising technique for improving outcomes for preterm infants on CPAP but that a large randomized controlled trial is still needed.
Persistent pulmonary hypertension of the newborn (PPHN) results from failure of normal decrease in pulmonary vascular resistance after birth, leading to right-to-left shunting of blood and hypoxemia. PPHN has a prevalence of 1.9 per 1000 live births and can be caused by underdevelopment, maldevelopment or maladaptation of the pulmonary vasculature. Diagnosis involves assessment of oxygen saturation gradient, blood gases, chest x-ray and echocardiogram. Management includes supportive care, ventilation, circulatory support, sedation and treatments to reduce pulmonary pressures like inhaled nitric oxide, sildenafil or prostaglandins. For severe cases, extracorporeal membrane oxygenation may
Cardiac rhythm disorders in neonates can include sinus arrhythmias, tachyarrhythmias like atrial tachycardia and supraventricular tachycardia, and ventricular arrhythmias like premature ventricular contractions and ventricular tachycardia. The document discusses how to read an ECG, defines various normal and abnormal rhythms like sinus bradycardia, and outlines their evaluation and treatment approaches. Genetic arrhythmia syndromes are also mentioned.
1) Hypoxic-ischemic encephalopathy (HIE) is brain injury caused by lack of oxygen and blood flow before, during, or after birth. It remains a serious condition that can cause death or long-term disabilities like cerebral palsy or intellectual impairment.
2) The document discusses the definition, risk factors, pathophysiology, clinical features based on the Sarnat staging system, diagnosis using imaging and EEG, and treatment approaches for HIE including supportive care, perfusion management, anti-seizure medications, and therapeutic hypothermia.
3) The goal of treatment is to prevent further brain injury by maintaining appropriate oxygenation, blood pressure, glucose levels, and treating seizures
This document discusses bronchopulmonary dysplasia (BPD), a chronic lung disease that occurs in premature infants requiring respiratory support. It covers the definition, risk factors, pathogenesis, clinical features, prevention, and treatment of BPD. The definition has evolved over time from relying solely on oxygen need at 28 days to incorporating factors like oxygen need, pressure support, and gestational age. BPD results from lung injury and disrupted lung development due to prematurity and respiratory support. Management aims to protect the lung from injury through gentle ventilation, optimal oxygen levels, and other strategies.
Apnea of prematurity is common in preterm infants, especially those born before 28 weeks gestation or weighing less than 1800g. It is caused by immature development of the respiratory control centers in the brain. Treatment includes caffeine which reduces apnea by blocking adenosine receptors. Other supportive measures like positioning and CPAP may help as well. Apnea spells usually resolve by 36-37 weeks corrected gestational age. Before discharge, infants should have a period of at least 5-7 days without any recorded apnea events while off caffeine therapy.
The document discusses the approach to evaluating and diagnosing bleeding in neonates. It notes that while the neonatal coagulation system is immature compared to adults, healthy term infants do not typically have bleeding issues. A bleeding neonate should first be assessed for general health and vitamin K administration history. Screening tests include a complete blood count, coagulation tests, and peripheral smear. Abnormal results can indicate disorders like disseminated intravascular coagulation, infection, liver disease, immune thrombocytopenia, or inherited coagulation factor deficiencies. The causes, patterns, and management of various bleeding disorders seen in neonates are described.
Sodium and Potassium Homeostasis in NeonatesKing_maged
This document discusses sodium and potassium homeostasis and management in infants. It covers sodium requirements, causes and treatment of hyponatremia and hypernatremia. It also discusses potassium requirements and causes and treatment of hypokalemia and hyperkalemia. Key points include maintaining serum sodium between 135-145 mEq/L, restricting free water intake to treat dilutional hyponatremia, and slowly correcting chronic hypernatremia to avoid brain edema. The document also outlines serum potassium goals and risks of rapid changes in potassium levels.
This document discusses portal hypertension (PH), including its definition, classification, pathophysiology, etiology, clinical features, complications, and diagnosis. Some key points:
1. PH is defined as a portal venous pressure gradient above 10 mmHg. It can be pre-sinusoidal, sinusoidal, or post-sinusoidal based on location of blockage.
2. Common causes are cirrhosis, portal or hepatic vein thrombosis, and Budd-Chiari syndrome. Cirrhosis results from fibrosis narrowing hepatic sinusoids.
3. Clinical features include splenomegaly, abdominal collaterals, ascites, gastrointestinal bleeding from varices, and hepatic encephalopathy.
A preterm newborn developed respiratory distress soon after birth, with signs including grunting and cyanosis. Evaluation found respiratory distress syndrome (RDS). The baby was treated with nasal CPAP, surfactant, and mechanical ventilation. RDS is caused by surfactant deficiency in premature infants, resulting in alveolar collapse and impaired gas exchange. Management includes respiratory support, surfactant replacement therapy, and care to prevent complications.
Surfactant replacement therapy : RDS & beyondDr-Hasen Mia
This presentation is about Surfactant, its use in Respiratory Distress Syndrome & some other conditions of surfactant deficiency due to inactivation like meconium aspiration syndrome & others
Hypothermia therapy is the standard treatment for hypoxic ischemic encephalopathy (HIE). Mild hypothermia between 34-35°C is initiated within 6 hours and continued for at least 72 hours. This decreases cerebral metabolic rate, excitatory neurotransmitter release, apoptosis, and vascular permeability. Hypothermia reduces mortality and neurodevelopmental disability in HIE. Other promising therapies target oxidative stress, calcium channels, excitatory amino acids, nitric oxide, and apoptosis, but require further study. Stem cell transplantation may also have potential as a future regenerative therapy for HIE.
This document presents treatment threshold graphs from the National Institute for Health and Clinical Excellence (NICE) clinical guideline 98 on neonatal jaundice. The graphs show bilirubin thresholds for phototherapy and exchange transfusion in babies with hyperbilirubinemia. The guideline was developed by the National Collaborating Centre for Women's and Children's Health and thanks two researchers who allowed their Excel spreadsheet to be adapted in developing the treatment threshold graphs.
Apnea of prematurity is common in neonates born before 32 weeks gestation or weighing less than 1000g, with rates as high as 54% in infants born at 30-31 weeks and nearly 100% in infants born below 29 weeks or weighing less than 1000g. Apnea can be classified as central, obstructive, or mixed based on whether there is absence of respiratory effort or upper airway obstruction. Common causes include infection, neurological or cardiovascular issues, pulmonary problems, inborn errors of metabolism, metabolic or hematological conditions, gastrointestinal issues, problems with temperature regulation, and drugs. Evaluation may include investigations and treatment involves general measures as well as specific measures and emergency treatment if needed. Methylxanthines are commonly
1. Perinatal asphyxia refers to impaired gas exchange and oxygen deficiency in a fetus or newborn infant, occurring during labor, delivery, or immediately after birth.
2. It can cause hypoxic-ischemic encephalopathy (HIE), a type of brain injury, in severe or prolonged cases. Clinical features of HIE include seizures, abnormal neurological exam, and multi-organ dysfunction.
3. Diagnosis involves assessing risk factors, signs of asphyxia at birth, abnormal blood gas values, and neurological exam over time. Imaging and EEG can further evaluate brain injury. Prognosis depends on severity of encephalopathy and extent of brain injury.
Seminar on shock in newborn by dr. Sajjad and Dr. OliviaDr. Habibur Rahim
This document summarizes shock in newborns. It discusses definition, pathophysiology, types including hypovolemic, cardiogenic, septic, and distributive shock. Signs and symptoms are tachycardia, decreased blood pressure, prolonged capillary refill time, and decreased urine output. Management involves supportive care, fluid resuscitation, and inotropic drugs like dopamine, dobutamine, and epinephrine to increase cardiac output depending on the cause of shock. Close monitoring is needed to guide therapy and prevent complications.
Approach to Respiratory distress in neonates pptamar naik
This document discusses several cases of respiratory distress in newborns. The key information provided includes potential causes of respiratory distress like respiratory distress syndrome (RDS), meconium aspiration syndrome (MAS), transient tachypnea of newborn (TTN), and persistent pulmonary hypertension of the newborn (PPHN). It also outlines the approach to evaluating a newborn with respiratory distress, including assessing risk factors, clinical examination findings, and initial investigations like chest x-ray and blood gas analysis. Management strategies like oxygen therapy, respiratory support, and surfactant administration are also summarized.
Respiratory distress in neonates can be identified by tachypnea, chest indrawing, and other signs. It can be caused by pulmonary issues like respiratory distress syndrome, meconium aspiration syndrome, or transient tachypnea of the newborn. Non-pulmonary causes include perinatal asphyxia, hypothermia, and congenital heart disease. Transient tachypnea of the newborn involves defective sodium transport leading to retained lung fluid and is often seen in babies delivered by c-section. It typically resolves within a few days with supportive care like oxygen and feeding assistance. Persistent pulmonary hypertension of the newborn results when normal postnatal pulmonary pressure reduction fails and presents a serious
Critical Congenital Heart Disease (CCHD) refers to several heart defects present at birth that require intervention. Some key points:
- CCHD includes defects where blood flow depends on an open ductus arteriosus after birth, such as Tetralogy of Fallot.
- Clinical presentation varies but may include cyanosis, heart murmur, respiratory distress. Diagnosis involves tests like echocardiogram, EKG, chest x-ray.
- Management depends on the specific defect but may include prostaglandin E1 to keep the ductus arteriosus open, then surgery to repair the anatomical issues. Early detection through newborn pulse oximetry screening can help identify cases
1) Pulmonary arterial hypertension (PAH) is defined as elevated pulmonary artery pressures leading to right heart failure and death. PAH can occur due to various causes in children including congenital heart defects.
2) A pulmonary hypertensive crisis is a life-threatening acute worsening of PAH where pulmonary vascular resistance exceeds systemic pressures, overwhelming the right ventricle. Prompt treatment is needed to prevent right heart failure.
3) Anesthesia for patients with PAH aims to minimize stress and hemodynamic changes through adequate anesthesia while preventing triggers for crisis like hypoxia. Different vasodilators can help treat acute or chronic PAH.
This document provides an outline on pulmonary hypertension (PH) in children. It begins with an introduction to PH and differences from adults. The anatomy of the pulmonary circulation is described along with classifications of PH. Pathophysiology involves abnormalities in pulmonary artery endothelial and smooth muscle cells. Survival rates have improved with newer treatments but are still worse than adults for some groups. Clinical presentation is often subtle in children. Evaluation includes echocardiography, chest imaging and right heart catheterization. Pharmacological therapies are discussed along with other treatment methods.
Hypertensive crisis in children copy copy.pptxAltaf Bhat
The document discusses hypertensive pediatric patients presenting to the emergency department. It describes 5 cases including seizures, altered mental status, behavioral changes, rash and abdominal pain, and tachypnea/cyanosis. It then defines hypertensive crisis, reviews screening and measurement, etiologies like renal and cardiac issues, clinical features, evaluation, and management including intravenous drugs, oral medications, and addressing underlying conditions like aortic coarctation, renovascular hypertension, and endocrine tumors.
This document discusses persistent pulmonary hypertension of the newborn (PPHN). It defines PPHN as failure of the normal circulatory transition at birth, causing elevated pulmonary vascular resistance and decreased pulmonary blood flow. The document covers the incidence, etiology, pathophysiology, diagnosis and management of PPHN. Key aspects of management include supportive care, gentle mechanical ventilation, use of inhaled nitric oxide and high-frequency oscillatory ventilation in severe cases.
Congenital diaphragmatic hernia (CDH) is a birth defect that affects about 1 in 2,000-5,000 live births. It occurs when the diaphragm fails to fully form, allowing abdominal organs to migrate into the chest cavity and compress lung development. Untreated CDH has a high mortality rate of nearly 70%. Prenatal diagnosis by ultrasound is possible as early as the second trimester. Postnatal treatment may involve mechanical ventilation, nitric oxide, surfactant therapy, and in severe cases, extracorporeal membrane oxygenation (ECMO) or surgery to repair the diaphragmatic defect. Long-term outcomes include risks of chronic lung disease, feeding difficulties, growth
This document discusses birth asphyxia, which accounts for approximately 19% of annual newborn deaths worldwide. It defines birth asphyxia as the inability to initiate breathing requiring resuscitation and a cord arterial pH <7.0. The document outlines the approach to newborns not breathing in the delivery room, including steps to take if they do not respond to initial resuscitation measures. It also discusses managing newborns at risk for hypoxic-ischemic cerebral injury in the delivery room and beyond through measures like ventilation, fluid status, glucose levels, and seizures. Phenobarbital is mentioned as a potential treatment to reduce long-term neurodevelopmental effects in some asphyxiated infants.
This document summarizes a seminar on persistent pulmonary hypertension of the newborn (PPHN). It begins with introductions and a case study. It then discusses the fetal circulation, the normal transition at birth, and the pathophysiology of PPHN when this transition is impaired. The definition, epidemiology, risk factors, clinical features, investigations including echocardiography, differential diagnosis, and management including respiratory support, vasodilators like inhaled nitric oxide are described. The objectives of management are outlined as maintaining oxygen delivery while decreasing pulmonary vascular resistance through various supportive, respiratory and pharmacological approaches.
This document provides an overview of shock in neonates. It discusses the pathophysiology of various types of shock seen in newborns, including cardiogenic shock, pulmonary hypertension, right heart hypoplasia/single ventricle lesions, left heart obstructive lesions, and distributive shock. It describes the role of echocardiography in evaluating neonatal shock and outlines the management principles, including aggressive fluid resuscitation, antibiotics for suspected sepsis, respiratory support, metabolic support with glucose and calcium monitoring, nutrition, and inotropic support when needed. The document emphasizes the importance of early recognition and intervention in shock for improved outcomes in neonates.
Recent advances in the management of pulmonary arterial hypertensionDr Siva subramaniyan
This document summarizes recent advances in the management of pulmonary arterial hypertension (PAH). It discusses the pathophysiology and classification of PAH and outlines treatment approaches including nonspecific supportive therapies, prostacyclin pathway drugs, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and combination therapy regimens. Non-medical therapies like atrial septostomy and lung transplantation are also reviewed. Recent research focuses on restoring BMPR-II signaling, targeting inflammation, and cell-based therapies for PAH.
Dr Varsha Atul Shah presented on congenital diaphragmatic hernia. Key points include: CDH occurs when abdominal organs herniate into the chest cavity due to a defect in the diaphragm, causing pulmonary hypoplasia. Presentation is usually respiratory distress after birth. Treatment involves medical stabilization, surgical repair of the defect, and management of long term complications like chronic lung disease and feeding difficulties. Close monitoring is needed due to risks of developmental delays, hearing loss, and other issues.
Congenital diaphragmatic hernia by Dr. Varsha Atul ShahVarsha Shah
Dr. Varsha Atul Shah presented on congenital diaphragmatic hernia (CDH). CDH occurs when abdominal organs protrude into the chest cavity through a hole in the diaphragm. It has an incidence of 1 in 2000-3000 live births. Clinically, CDH presents with respiratory distress in newborns. Treatment involves medical management in the NICU with ventilator support, medications to manage blood pressure and oxygen levels, and surgery to repair the diaphragmatic defect. Outcomes have improved but mortality remains high depending on the severity of lung hypoplasia and pulmonary hypertension.
1) The document discusses the approach to cyanosis in term neonates through case scenarios and discussions of common and uncommon presentations.
2) It covers the fetal circulation, changes at birth, pathologies that can interfere with transition including persistent pulmonary hypertension of the newborn (PPHN), and the diagnostic approach including tests to differentiate PPHN from congenital heart disease.
3) Three case scenarios are presented and discussed to demonstrate different causes of cyanosis including PPHN, total anomalous pulmonary venous connection, and methemoglobinemia. The importance of a thorough evaluation and involvement of specialists is emphasized.
A 31-year-old pregnant woman presented with sudden onset of tachycardia, tachypnea, dyspnea and chest pain. Her medical history included childhood asthma. On examination, she had tachycardia, tachypnea and lower extremity edema. Chest X-ray was normal. The leading differential diagnoses included dyspnea of normal pregnancy, asthma, respiratory infection, pre-eclampsia, pulmonary embolism and other cardiac/vascular conditions. The document discusses the evaluation and distinguishing features of these potential diagnoses.
C. CDH is more commonly found on the left side (around 85% of cases are left-sided).
Capillary alveolar dysplasia, bronchopulmonary sequestration, and chylothorax do not have a strong side predominance. Around half of bronchopulmonary sequestrations are left-sided, but they can occur on either side. Capillary alveolar dysplasia and chylothorax also occur bilaterally or on either side without a clear predominance.
So the developmental lung condition that is most strongly left-sided is congenital diaphragmatic hernia.
This document provides an overview of the approach to evaluating and managing cyanosis in neonatal patients. It begins by defining different types of cyanosis and their causes, including central cyanosis resulting from low oxygen saturation and peripheral cyanosis from poor circulation. The summary then outlines the initial steps in approaching a cyanotic neonate, which include identifying the type of cyanosis, evaluating possible causes, taking a medical history, and performing a physical exam with focus on pulmonary, cardiac, and neurological systems. Specific tests like hyperoxia tests and echocardiography are also discussed. The document concludes by reviewing treatments for common respiratory and cardiac conditions that can cause neonatal cyanosis.
Dr. Nannika Pradhan presented on pulmonary hypertension (PH). The key points discussed include:
1. PH is defined as a mean pulmonary arterial pressure ≥25 mmHg at rest as assessed by right heart catheterization.
2. PH is classified clinically into 5 groups based on etiology.
3. Clinical features include dyspnea, chest pain, syncope, signs of right heart failure. Diagnosis involves echocardiogram, CT scan, ventilation-perfusion scan and right heart catheterization.
4. Treatment depends on disease severity and involves diuretics, oxygen supplementation, calcium channel blockers, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, prostano
Pulmonary hypertension is defined as a mean pulmonary arterial pressure of at least 25 mm Hg. It can be caused by various conditions and is classified accordingly. Idiopathic pulmonary hypertension has no known cause. It presents with dyspnea and right heart failure. Diagnosis involves right heart catheterization showing elevated pulmonary pressures. Treatment includes diuretics, vasodilators like calcium channel blockers, endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and sometimes atrial septostomy or lung transplantation for severe cases refractory to medical therapy. Prognosis depends on factors like functional status, hemodynamics, and response to treatment.
neuromonitoring of a newborn from common nervous system disease perspectives ...Dr. Habibur Rahim
This document summarizes key points about monitoring the nervous system in newborns. It discusses common neurological conditions seen in newborns such as perinatal asphyxia, intraventricular hemorrhage, neonatal stroke, meningitis, and TORCHS infections. For each condition, it outlines the location of injury, pathophysiology, clinical features, monitoring in the NICU, diagnostic testing, potential improvements or deteriorations, and complications. Imaging findings and grading scales for conditions like IVH are also presented.
basics of mechanical ventilator Dr Asaduzzaman.pptxDr. Habibur Rahim
Mechanical ventilation is an important life-saving intervention for extremely premature and sick newborns. While it supports oxygenation and carbon dioxide removal, it can also cause lung injury if not optimized. The document discusses the physiology of ventilation, components of mechanical ventilators like pressures and volumes, basic ventilation modes, and pulmonary graphics. Modes like volume guarantee aim to balance supporting gas exchange while limiting volumes and pressures. Understanding ventilation principles, ventilator operations, and individualizing strategies are important for achieving optimal outcomes for mechanically ventilated newborns.
approach to Rh Isoimmunization Maternal and neonatal aspects | Dr Habibur RahimDr. Habibur Rahim
This document summarizes the approach and management of a baby born to a Rh-negative mother. The baby presented with respiratory distress and signs of Rh isoimmunization. Key points include:
1) The mother's anti-D titer was 1:64 and Doppler ultrasound revealed increased blood flow, indicating Rh isoimmunization.
2) The baby received an exchange transfusion due to signs of hemolysis and hyperbilirubinemia.
3) With oxygen support and treatment, the baby's respiratory distress resolved within 6 hours and the baby improved after exchange transfusion.
Short bowel syndrome (SBS) occurs when extensive segments of the small intestine are resected, severely compromising absorptive capacity. It is a leading cause of intestinal failure in infants, with an incidence of 0.1-0.5% among live births and ICU admissions. The minimal length of small intestine needed to survive is 15-38 cm, though adaptation allows survival with even shorter lengths. Management involves total parenteral nutrition, optimizing enteral nutrition, and treating complications until the remnant intestine sufficiently adapts through processes like increased blood flow and growth. With current treatment, 80% of infants with SBS achieve full enteral nutrition within a year.
Approach to Baby of perinatal asphyxia | Dr Sonia Akter | Dr Habibur RahimDr. Habibur Rahim
This document discusses the management of a baby with perinatal asphyxia who also has issues of infant of diabetic mother, hypocalcemia, hypomagnesemia, and acute kidney injury. It provides background on the prevalence and risks of perinatal asphyxia. It also outlines the principles of management, which include restoration of blood flow, identification and treatment of multiorgan dysfunction, and seizure management. Therapeutic hypothermia and magnesium sulfate for fetal neuroprotection are discussed as standard or emerging treatments.
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria YasminDr. Habibur Rahim
This document discusses the management of critical congenital heart disease in newborns. It describes how prostaglandin E1 (PGE1) is used to maintain ductal patency until definitive treatment. PGE1 is started as a continuous IV infusion at a low dose and titrated to safely establish an open ductus arteriosus. This improves oxygen saturation while definitive diagnosis and treatment are determined. Potential side effects include apnea, hypotension, and hyperthermia, requiring close monitoring during PGE1 infusion. PGE1 therapy is currently standard care for ductal-dependent congenital heart defects until palliative or corrective surgery can be performed.
Seminar on pulmonary hemorrhage in newborn by Dr. Habib, Dr. AshfaqDr. Habibur Rahim
Pulmonary hemorrhage is bleeding into the lungs that commonly affects premature infants. It presents with bloody secretions from the endotracheal tube and causes rapid clinical deterioration. Risk factors include prematurity, respiratory problems, sepsis, and mechanical ventilation. The pathophysiology involves stress on capillaries from transmural pressure, alveolar surface tension, and lung inflation. Management focuses on supportive care like ventilation, volume expansion, and transfusions to improve oxygenation and stop the bleeding. Prognosis depends on the severity and underlying causes, with mortality up to 50% in very premature infants.
- The patient is a 21-day-old male born prematurely at 30 weeks gestation with a birth weight of 1230g.
- He has a history of respiratory distress at birth and was treated for late-onset neonatal sepsis on days 5 and 16 of life.
- He is now presenting with signs of respiratory distress and sepsis including decreased activity, tachypnea, and desaturation. Laboratory results show thrombocytopenia and elevated inflammatory markers.
This document presents two case scenarios for discussion at a seminar on acute kidney injury in newborns. The first case involves a preterm, low birth weight baby with late onset sepsis who develops increased serum creatinine and decreased urine output after being treated with antibiotics. The second case involves a preterm baby with bilateral hydroureteronephrosis who develops oliguria, rising serum creatinine, and hypertension despite treatment. The document asks how each baby would be diagnosed and managed.
(1) Atypical genitalia in a genetic female with clitoromegaly and labial fusion, indicating virilization;
(2) Hyperpigmentation around the nipple and genitalia;
(3) Biochemical findings of elevated 17-OHP, ACTH and DHEA with low cortisol, consistent with 21-hydroxylase deficiency;
(4) Hyponatremia and hyperkalemia, suggestive of salt wasting form of CAH.
The child
This document provides an overview of a seminar on CPAP in neonatal practice. It includes two case scenarios of premature infants with respiratory distress and then outlines what CPAP is, the history of its use, types of CPAP devices, how CPAP works, indications and contraindications for its use, essentials of providing CPAP including monitoring infants on CPAP and managing complications. Studies are summarized that show benefits of CPAP for preventing morbidity and mortality in premature infants as well as its use after extubation. Guidelines are provided on initiating, maintaining and weaning infants from CPAP support.
This document provides information about evaluating a neonate presenting with cholestatic jaundice. It discusses performing a history and physical exam to identify potential etiologies. Key lab investigations are outlined to establish cholestasis and severity of liver injury. Imaging studies like ultrasound and hepatobiliary scintigraphy can help differentiate between extrahepatic and intrahepatic causes. The document reviews various etiologies of neonatal cholestasis including biliary atresia, idiopathic neonatal hepatitis, choledochal cyst, galactosemia, and TPN-related cholestasis. Timely evaluation is important to diagnose treatable conditions and identify those requiring surgical intervention.
- COVID-19 generally causes mild disease in children, but a small proportion can develop severe disease requiring ICU care.
- Symptoms in children are usually fever, cough, sore throat and some may experience diarrhea or vomiting.
- Investigations show lymphopenia and elevated inflammatory markers. Chest imaging may show patchy infiltrates or ground glass opacities.
- Management involves isolation and supportive care. Severe cases are treated in hospitals. Most children recover well but underlying conditions increase risk of severe disease.
The document summarizes the types, causes, pathophysiology, stages, and management of shock in children. It discusses the five major types of shock - hypovolemic, cardiogenic, obstructive, distributive, and septic shock - and their specific causes, pathophysiology, and treatment approaches. General management of shock includes fluid resuscitation, monitoring, laboratory studies, and medication therapy tailored to the underlying shock type. The document provides detailed guidelines on the evaluation and treatment of each shock type.
Management of shock involves positioning, airway support, vascular access, fluid resuscitation, monitoring, and medication therapy. The type of shock determines specific treatment, which may include fluid boluses, vasoactive drugs, and treating the underlying cause. Septic shock, the most common distributive shock, results from infection and involves a complex inflammatory response. Treatment focuses on antibiotics, fluids, and vasopressors like dopamine or norepinephrine to support blood pressure. The goal is to identify and treat shock early before organ dysfunction occurs.
This document provides information about macrophage activation syndrome (MAS) and hemophagocytic lymphohistiocytosis (HLH). MAS is a severe inflammatory condition caused by excessive activation of macrophages and T cells. It can occur secondary to conditions like systemic juvenile idiopathic arthritis. The document discusses the pathogenesis, clinical features, diagnostic criteria, investigations and treatment of MAS. It emphasizes the importance of promptly recognizing and treating MAS as it can be life-threatening.
This document provides an overview of tetralogy of Fallot (TOF), one of the most common cyanotic congenital heart diseases. It discusses the history, epidemiology, pathophysiology, clinical presentation, investigations, management, and prognosis of TOF. Key points include: TOF is characterized by pulmonary stenosis, ventricular septal defect, overriding aorta, and right ventricular hypertrophy. Clinical features include cyanosis, clubbing, and systolic murmur. Investigations include CXR, ECG, echocardiogram and cardiac catheterization. Management involves medical treatment of spells, palliative shunt procedures, and complete repair surgery. Long-term prognosis depends on severity of pulmonary stenosis and associated anomalies,
This document provides information about atrial septal defects (ASD). It discusses the different types of ASDs including ostium secundum, ostium primum, sinus venosus, and coronary sinus defects. It covers the pathophysiology, clinical presentation, investigations including echocardiography and ECG findings, and management including device closure or surgery. Long term outcomes are also summarized such as the potential for spontaneous closure in small defects or complications in adults if left untreated, including congestive heart failure, pulmonary hypertension, and atrial arrhythmias.
A 9 month old girl presented with fever and vomiting for 3 days. She experienced a seizure before arriving at the hospital. On examination, she was febrile, drowsy, irritable, and had a bulging fontanel. Her throat was slightly inflamed. A lumbar puncture showed turbid CSF with a high white blood cell count, indicating bacterial meningitis. Further tests are needed to identify the specific bacteria causing the infection.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
2. Mrs. Nasrin had developed PIH at her 30 weeks of gestration. Αlpha methyl
dopa , nifedipin, labetalol was subsequently added to her in their highest
dose but her BP remained uncontrolled.
At 37 weeks an emergency LUCS was done due to her uncontrolled HTN &
less fetal movement and a male baby weighing 2760g was delivered.
At birth, liquour was found meconium stained & he was non vigorous. After
ensuring endotracheal suction, he needed bag & mask ventilation to cry. He
was admitted immediately & respiratory support was started with CPAP.
Distress was gradually improving & he could be weaned to O2 1L/m through
nasal catheter.
On day 6, the baby was found developing desaturation upto ~ 84% while on
routine follow up.
7. Definition:
PPHN is a condition resulting from a disruption of the normal ‘fetal to neonatal
circulatory transition’ characterized by sustained elevation in pulmonary vascular
resistance (PVR), rather than the decrease which normally occurs at birth.
In 1969, Gersony et al. defined PPHN as a condition having disproportionately severe
hypoxia (a PaO2 < 45mmHg in an FiO2 of 1.0) with mild lung disease & evidence of R-L
shunts in a structurally normal heart on echo.
8. Incidence
• 1.2 to 4.6 per 1000 live births.
(Ref: Narongsak N, Suksham J, Kishore K, Shigeharu H, Majeda
H, Yasser YE, et al. An Asian multicenter retrospective study on persistent pulmonary hypertension of the newborn:
incidence, etiology, diagnosis, treatment and outcome, The Journal of Maternal-Fetal & Neonatal Medicine, 2018)
• 13.59 per 1000 live births.
(Ref: Fatema NN. Persistent Pulmonary Hypertension of the Newborn:
Analysis of 181 cases over one Year. Cardiovasc. j. 2018 )
11. Mohsen AH, Amin AS. Risk factors and outcomes of persistent pulmonary hypertension of the
newborn in NICU of al-minya university hospital in Egypt. J Clin Neonatol 2013;2:78-82.
• Materials and Methods: Prospective study was performed enrolling the term & post term
newborn admitted to the NICU of Al-Minya University Hospital, Egypt from January 2009 to
April 2012.
• Results: Out of the studied 640 infants, 32 infants (5%) developed PPHN. MAS, PNA, RDS,
neonatal septicemia, post-term birth, LGA, LUCS, maternal overweight, and GDM were
associated with an elevated risk for PPHN.
• Conclusion: PPHN was found in 5% of the studied population. Meconium aspiration, birth
asphyxia, neonatal septicemia, post-term were associated with an elevated risk for PPHN.
12. Razzaq A, Quddusi AI, Nizami N. Risk factors and mortality among newborns with persistent
pulmonary hypertension. Pak J Med Sci 2013;29(5):1099-1104.
• Methods: This was an observational study conducted at The Children’s Hospital & the
Institute of Child Health, Multan, Pakistan, from July 2011 to June 2012.
• Results: There were 79 patients, including 61 males and 18 females. The most common risk
factors observed in our study were male gender(72.1%), LUCS (54.2%), PPV while
resuscitation (44.2%), birth asphyxia (40.4%) and MAS (35.4%)
In premature infants, male sex (88.8%), LUCS (77.7%), RDS 44.8% and sepsis
(44.4%) were more associated with PPHN.
• Conclusion: Male gender, LUCS, MAS and RDS are the major risk factors for PPHN in any age
group.
13. Asphyxia & hypoxia
• Acute birth asphyxia (PNA)
hypoxia & acidemia release of
Endothelin 1 (a potent
vasoconstrictor) pulmonary
arterial spasm prevents
normal postnatal change in
circulation.
14. Asphyxia
• Prolonged fetal stress & hypoxemia
↓ in pulmonary VEGF expression
structural remodeling of pul
vasculature increased muscularity
in PA muscle extends to the vessels
surrounding the alveoli (normally,
muscular pulmonary arteries rarely
extends beyond the terminal
bronchiole) increased PAP PPHN.
(Ref: Lessus et al. 2001, Grover et al. 2003)
15. Ahmed T, Abqari S, Shahab T, Ali SM, Firdaus U, Khan IA. Prevalence and outcome of PPHN in
perinatal asphyxia. J Clin Neonatol 2018;7:63-6
• Results: A total number of neonates screened were 41, of which 18 (43.9%) cases had PAH.
Out of 18 cases, 8 (44.4%) had a reversal of shunt at the level of patent ductus
arteriosus/patent foramen ovale.
Eleven neonates expired before 6 weeks of age and rest seven cases were screened at 6
weeks. Only one case showed the persistence of PAH at 6 weeks.
• Conclusion: PNA have a significant association with the development of PAH, and the
mortality is high in neonates with PNA once it is complicated by the development of PAH.
16. Sepsis
obacterial endotoxins
- suppresses endogenous NO production,
- direct myocardial depression,
- recruitment of leucocytes in the lungs release of constrictor
leukotriens (LTC4, LTD4), Thromboxane A2, TNF pulmonary arterial
constriction.
(Ref: Gibson et al. 1988, Navarreta et al. 2003)
17. Pulmonary pathologies
oPulmonary parenchymal diseases (RDS, Pneumonia, MAS) Pumonary
vasospasm raised PAP.
oCDH pruning of the vascular tree, causing reduction of number of
interlobar arteries abnormal development & reduced cross sectional
area of pulmonary vasculature (Ref:Geggel et al. 1985)
• pulmonary parenchymal hypoplasia malalignment of pulmonary vessels
increased PAP PPHN
18. Drug effects
• Adminstration of PGSI (PG synthatase inhibitors,e.g.Aspirin) in pregnant
women PGSI crosses placenta prolonged t ½ of PGSI in fetus
direct pulmonary vasoconstriction & constriction of ductus arteriosus in
utero fetal pulmonary hypertension in utero Smooth muscle
hypertrophy in pulmonary arterioles, extension of muscles into arterioles
---after birth PPHN
Ref: Turner & Levin 1984
19. Genetic predisposition: Infants with PPHN have -
• mutation in the ABCA3 gene & polymorphisms of the CPS (carbamoyl-
phosphate synthetase) gene resulting in diminished expression of
endothelial NO synthase (eNOs) low plasma levels of NO metabolites.
20. Clinical features
• Usual presentation is a neonate having risk factor/s found developing
significant desaturation while on routine care.
21. Clinical presentation
- Respiratory distress despite adequate respiratory support
- significant decreases saturation with routine nursing care or minor stress
- A preductal and postductal SpO2 difference of >5% and PaO2 difference
>10–15 mmHg (indicative of a R-L shunt).
• A +ve Hyperoxia test
• Hyperventilation test: differentiates PPHN vs Cyanotic CHD.
22. Hyperoxia test. Because of intracardiac R-L shunting,
the infant with cyanotic CHD in contrast to the infant
with pulmonary disease is unable to raise the arterial
saturation.
• Measure PaO2 on room air. Then place the infant on
100% oxygen for 10–20 minutes. Then remeasure
arterial oxygen.
• A value of >150 mm Hg does not always rule out
cyanotic CHD.
Hyperventilation test may differentiate PPHN from
cyanotic CHD. It has been suggested that infants
subjected to this test should be hyperventilated for
10 minutes. In case of PPHN, PCO2 will ↓, pH ↑
PVR decreases, there is less right-to-left shunting,
and PaO2 will ↑ (>30 mm Hg). In cyanotic CHD, there
will be no change.
23. B. Cardiac signs:
- prominent right ventricular impulse, a single, accentuated S2, and a murmur of TR.
- In extreme cases, there may be hepatomegaly and signs of heart failure.
C. Imaging: The CXR may show
- cardiomegaly or a normal-sized heart,
- normal or diminished pulmonary vascularity.
- Disease specific findings.
D. The ECG most commonly shows RV predominance.
24.
25. Echocardiography remains the gold standard
diagnostic tool in PPHN. A R-L shunting of blood
at the foramen ovale and/or the ductus
arteriosus , TR or a bowing of ventricular
septum to the left, to evaluate ventricular
function and to exclude CHD (e.g. infra
diaphragmatic TAPVR, HLHS). Ref: Jayasree Nair
et al. 2015
30. Differential diagnosis
Cyanotic CHD
• The newborn developed cyanosis
• O/E: weak pulses, dynamic
precordium, cardiomegaly, Grade 3 +
murmur
• In response to 100% O2, PaO2 will not
rise above 100 mmHg
• Disease specific changes in CXR,ECG &
Ecocardiography
PPHN
• Having risk factors (PNA, MAS, Sepsis
ect.)
• Desaturation on minor stimulus.
• A pre & postductal SpO2 diff of >5%
• Suggestive hyperoxia & hypervent
test.
• RV heave with single S2
• CXR-Normal/oligemic lung field
• Echo: R-L shunt, normal cardiac
anatomy.
34. Minimal handling: Because catecholamine release activates pulmonary
adrenergic receptors, thereby potentially raise PVR, infants with PPHN are
extremely labile with significant deterioration after seemingly “minor”
stimuli.
Noise level and physical manipulation should be kept to a minimum. a
narcotic analgesic that blocks the stress response, such as fentanyl, morphine
sulfate, midazolam (0.06mg/kg/h) infusion are often used.
35. Temperature control is also crucial. Significant acidosis should be avoided.
Correction of metabolic abnormalities: Correction of hypoglycemia and
hypocalcemia is important in treating infants with PPHN in order to provide adequate
substrates for myocardial function and appropriate responses to inotropic agents.
Hemodynamic support : Adequate SBP should be maintained to combat R-L
shunt & optimal CO to maximize tissue oxygenation either by volume
expansion, or by using inotropes (dobutamine, dopamine, epinephrine),
milrinone when cardiac function is poor.
Hb level should be kept >13gm/dl (PCV 40%) to maximize O2 transport to the
tissue.
Broad spectrum antibiotic cover should be given to all babies with PPHN.
36. Respiratory support
Supplemental oxygen: Hypoxia is a powerful pulmonary vasoconstrictor.
Therefore, adequate supplemental oxygen is used to maintain saturation,
to reduce abnormally elevated PVR.
However, as there is also chance of O2 free radical induced injury, therefore,
the aim is to maintain postductal SaO2 >90% to ensure adequate tissue
oxygenation and preductal <98% to avoid hyperoxemia.
37. Mechanical ventilation (MV): When hypoxemia persists despite maximal O2
supplementation, evidenced by marked hypercapnia and acidemia, MV is
needed to ensure adequate oxygenation.
The strategy is to maintain adequate and stable oxygenation, using the
lowest possible MAP, PEEP to minimize barotrauma.
Hyperventilation is also avoided.
38. Those who cannot be adequately oxygenated with conventional ventilation,
HFOV is considered early. HFJV is used in meconium aspiration pneumonitis
and air leak.
When PPHN complicates pulmonary parenchymal disease, ventilator
strategies changed accordingly.
In the presence of parenchymal lung disease, infants treated with HFOV
combined with iNO.
39. Additional pharmacologic agents are directed to optimize CO, systemic BP and
reducing PVR.
iNO: an smooth muscle relaxant.
Sildenafil, a PDEi, (1-2 mg/kg/dose 6 hourly) is an option as a treatment for
PPHN which increases endogenous NO by inhibiting its metabolism.
Other promising agents are:
- Endothelin receptor antagonist: bosentan (Nakwan et al. 2009),
- adenosine,
- MgSO4 (Ho & Rasa, 2007),
- Ca+2 channel blocker: diltiazem (Islam et al. 1999),
- inhaled prostacyclin (de Luca et al. 2007),
- inhaled ethyl nitrite (Moya et al. 2002).
40. ECMO: ECMO is lifesaving therapy for PPHN who fail on conventional management.
Among term or near-term infants meeting ECMO criteria (alveolar-arterial oxygen
difference (AaDO:z)>600 or oxygenation index (OI) >30 on two ABGs >30 minutes apart).
(OI = MAP x FiO2/ PaO2 x 100.)
41. Fatema NN. Persistent Pulmonary Hypertension of the Newborn: Analysis of 181 cases
over one Year. Cardiovasc. j. 2018; 11(1): 17-22
o Results: Most of the patient (69.06%) was diagnosed at first week of life. Associated
congenital lesions like ASD in 52 (28.72%) cases, PDA was found in 14 (7.73%) cases and VSD
was found in 2 (1.10%) cases. Combination of ASD & PDA was found in 75 (44.33%) cases.
Systolic PAP was > 60 mmHg in 103 (56.91%) cases, >50 mmHg in 53 (29.28%) cases and >30
mmHg in 25 (13.81%) cases.
100% patients received high flow O2 along with anti failure (66.30%) and sildenafil 98
(54.14%) therapy as per requirement of the patient.
Complete cure was achieved in 95.58% cases and mortality was only 1.10%.
42. Mamun AAM, Hussain M,Jabbar A. MgSO4 vs Sildenafil in the Treatment of PPHN: A
Randomized Clinical Trial. J of Sci and Tech Res, 2018.
• Abstract: It was a RCT to evaluate the effect of inj. MgSO4 and oral Sildenafil in the
Treatment of PPHN. , conducted from August 2015 to July 2017 among 50 neonates
having moderate to severe PPHN in the Pediatric Cardiac ICU of Dhaka Shishu (Children)
Hospital.
There was significant improvement of oxygenation and decrease in PVR at 72 hours after
treatment in both study groups (p<0.05).
Significant improvement of oxygenation was found in Sildenafil study group than MgSO4
group after 72th hour of treatment (p=0.01).
There was no significant difference in time taken to improve and hospital stay between
two groups (p>0.05).
Sildenafil was more effective than MgSO4 in the treatment of PPHN with regard to
improvement of oxygenation.
43. Agha, H., Tantawy, A., Iskander, I., Samad A. Impact of Management Strategies on the
Outcome of PPHN. Cardiology and Cardiovascular Medicine,2017: 01(02), pp.74-84.
• Study Design: Prospective descriptive study in tertiary center included 40 neonates
having PPHN. All patients received the conventional therapy for PPHN, sildenafil as
adjuvant therapy was added in cases of failure.
• Results: … Sildenafil was effective in the reduction of the duration of NICU stay and SPAP
below 40 mmHg and (p = 0.001, p =0.0001, respectively).
44. Immediate outcome :
Immediate outcome varies with etiology. Outcome becomes guarded
when PPHN complicating RDS, MAS, sepsis, needs ECMO for with primary
PPHN.
Many neonates responds promptly to treatment & the mortality rate is
10-20%.
45. Agha, H., Tantawy, A., Iskander, I., Samad A. Impact of Management Strategies on
the Outcome of PPHN. Cardiology and Cardiovascular Medicine,2017: 01(02),
pp.74-84.
Results: Male patients had significantly higher systolic pulmonary artery pressure
(SPAP) and higher mortality rate compared to females [7/23 (30.4%) versus 1/17
(5.9%), p = 0.04].
Infants of diabetic mothers had significantly higher mortality rate (p = 0.003).
The overall mortality rate was 8/40 neonates (20%), however, the mortality among
the patients who received sildenafil in addition to conventional therapy was 1/14
neonates (7.14%) of those group with p = 0.001).
46. Nakwan, N., Jain, S., Kumar, K., Hosono, S. An Asian multicenter retrospective study on
PPHN: incidence, etiology, diagnosis, treatment and outcome. The Journal of Maternal-
Fetal & Neonatal Medicine,2018.
• Methods: A retrospective chart review of patients with documented PPHN from 7 centers
in 6 Asian countries (Japan, Kuwait, India, Pakistan, Singapore, and Thailand) between
January 2014, and December 2016, was performed.
• Results: A total of 369 PPHN infants were identified. The all-cause mortality rate was
20.6%. Multivariate multiple regression analysis indicated GA < 34 weeks, CDH/lung
hypoplasia, treatment with HFOV with or without inhaled nitric oxide (iNO), and inotropic
agents were independently associated with increased risk of death.
47. Razzaq A, Quddusi AI, Nizami N. Risk factors and mortality among newborns with persistent
pulmonary hypertension. Pak J Med Sci 2013;29(5):1099-1104.
• Methods: This study was conducted at The Children’s Hospital & the Institute of Child
Health, Multan, Pakistan, from July 2011 to June 2012.
• Results: There were 79 patients, including 61 males and 18 females.
Out of the total 79 patients, death occurred among 7 preterm and 14 terms and post term
infants. As a whole, cesarean section mode of delivery (71.4%), birth asphyxia (57.1%) and
female sex (52.4%) were found major risk factors associated with mortality.
However, RDS, PNA and male sex were found to be associated with increased risk of mortality
in preterm than term and post term infants.
• Conclusion: RDS, Birth asphyxia and male sex are associated with increased risk of mortality
in pre term than term and post term infants.
48. The long-term outcome
• The long-term outcome of infants with PPHN may depend on:
- the underlying conditions/ risk factor for the PPHN &
- the therapeutic interventions that they had received at birth.
• The rate of neurodevelopmental disabilities including cognitive delays and
hearing deficit (SNHL) and long term bronchodilator therapy can be seen in
6.4% of PPHN survivors.
(Ref: Eriksen V, et al,. 2009 & Rosenberg AA et al,. 2010)
49. Mohsen AH, Amin AS. Risk factors and outcomes of persistent pulmonary hypertension of the
newborn in NICU of al-minya university hospital in Egypt. J Clin Neonatol 2013;2:78-82.
• Results: Out of the studied 640 infants, 32 infants (5%) developed PPHN. After 6 months
follow-up, 12 (37.54%) improved and followed-up without sequelae, 4 (12.5%) developed
some neurodevelopmental impairment, 8 (25%) died, 3 (9.3%) developed BPD, 2 (6.2%)
developed SNHL and another 3 (9.3%) missed follow-up.
• Conclusion: PPHN was found in 5% of the studied population. Meconium aspiration, birth
asphyxia, neonatal septicemia, post-term were associated with an elevated risk for PPHN.
50. Why such adverse outcome among the survivors:
• Depends of underlying risk factors (PNA, MAS, CDH) for the PPHN and
mode & duration of different treatment modalities used .
• The high incidence of SNHL has been reported to correlate with
duration of hyperventilation.
• Hyperventilation hypocapnea reduce cerebral blood flow, (in
premature babies causes PVL).
• Hyperventilation barotrauma air leakes & BPD.
51. • Thus, after discharge from the NICU, infants with PPHN warrant long-
term follow up.
52. Prevention
• Ensuring ANC.
• Identifying high risk pregnancy
• Prompt & adequate resuscitation and support since in such
preexisting conditions, e.g., adequate and timely ventilation of an
asphyxiated infant with appropriate attention to temperature control.