Short Note: Neonatal Emergencies

Short Note: Neonatal Emergencies Short Note: Neonatal Emergencies India . United Kingdom Author(s) Elsharif Ahmed Bazie a* and Mona Isam El-Din Osman b a Elimam Elmahdi University, Sudan. Sudan International University, Sudan. *Corresponding author: E-mail: elsharifbazie@gmail.com; b FIRST EDITION 2024 ISBN 978-81-970064-0-1 (Print) ISBN 978-81-970064-7-0 (eBook) DOI: 10.9734/bpi/mono/978-81-970064-0-1 __________________________________________________________ © Copyright (2024): Author(s). The licensee is the publisher (B P International). Peer-Review Policy: Advanced Open Peer Review policy has been followed for review. This book was thoroughly checked to prevent plagiarism. As per editorial policy, a minimum of two peer-reviewers reviewed the manuscript. After review and revision of the manuscript, the Book Editor approved the manuscript for final publication. Contents PREFACE i ABSTRACT 1 1. CYANOSIS 1 2. JAUNDICE 2 3. HYDROCEPHALUS 3 4. CEPHALOHEMATOMA 4 5. SCLERAL AND SUBCONJUNCTIVAL HEMORRHAGE 5 6. NEONATAL CONJUNCTIVITIS (OPHTHALMIA NEONATORUM) 5 7. DUCTAL-RELATED STRUCTURAL HEART DISEASE IN THE NEONATE 5 8. LARYNGOTRACHEOMALACIA 7 9. NEONATAL RESPIRATORY DISTRESS 7 10. CHRONIC LUNG DISEASE OR BRONCHOPULMONARY DYSPLASIA (BPD) 8 11. PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN 9 12. MALROTATION AND VOLVULUS 9 13. HYPERTROPHIC PYLORIC STENOSIS 10 14. NECROTIZING ENTEROCOLITIS 11 15. OMPHALITIS 11 16. AMBIGUOUS GENITALIA 12 17. SEIZURES 12 18. COMMON CAUSES OF NEONATAL SEIZURES 13 19. INVESTIGATIONS 14 20. NEONATAL INFECTIONS 14 21. NEONATAL HERPES SIMPLEX VIRUS INFECTION 15 COMPETING INTERESTS 16 REFERENCE 16 BIOGRAPHY OF AUTHOR(S) 17 INDEX 18 Short Note: Neonatal Emergencies Preface PREFACE A neonatal emergency is a common practice. This book concisely details some neonatal emergency management and approaches to emergency conditions. In this book, busy physicians and neonatologists found it easy to approach their patients. Also, it is easy for students to remember essential topics in neonatal diseases. This book did not discuss neonatal emergency disease in detail as it’s a short notebook. Elsharif Bazie, M D. Pediatric Mona Esam, M.D. Pediatric ___________________________________________________________________________________ © Copyright (2024): Author(s). The licensee is the publisher (B P International). i Print ISBN: 978-81-970064-0-1, eBook ISBN: 978-81-970064-7-0 Short Note: Neonatal Emergencies Elsharif Ahmed Bazie a++* and Mona Isam El-Din Osman b# DOI: 10.9734/bpi/mono/978-81-970064-0-1 Peer-Review History: This book was reviewed by following the Advanced Open Peer Review policy. This book was thoroughly checked to prevent plagiarism. As per editorial policy, a minimum of two peer-reviewers reviewed the manuscript. After review and revision of the manuscript, the Book Editor approved the manuscript for final publication. Peer review comments, comments of the editor(s), etc. are available here: https://peerreviewarchive.com/review-history/8471A ABSTRACT Cyanosis refers to a blue tone visible in the skin and mucous membranes, caused by desaturated or abnormal hemoglobin. Jaundice in the first 24 hours of life of a term newborn is pathologic. Cardiac disease presenting in the neonatal period are often congenital but can be acquired. Age at presentation of CHD varies with the underlying lesion, its impact on cardiac performance, and its dependence upon the ductus arteriosus. Neonatal sepsis can be categorized into early onset (occurring in newborns who are less than 72 hours of life) or late onset (occurring between 3 and 7 days of life). Keywords: Neonate; emergency; notes. 1. CYANOSIS Cyanosis refers to a blue tone visible in the skin and mucous membranes, caused by desaturated or abnormal hemoglobin. Central cyanosis: Central cyanosis is caused by deoxygenated blood entering the systemic circulation. This is usually due to congenital heart disease (CHD), specifically cardiac defects allowing systemic venous blood to bypass the lungs (right-to-left shunt), rarely it can be caused by respiratory compromise or pharmacologic agents. Acrocyanosis: Acrocyanosis is the transient blue discoloration of the hands and feet in response to vasomotor instability or a cool environment. It is caused by vasoconstriction of the small arterioles and does not reflect reduced systemic arterial oxygenation. ________________________________________________________________________ a Elimam Elmahdi University, Sudan. Sudan International University, Sudan. Associate Professor; # Assistant Professor; *Corresponding author: E-mail: elsharifbazie@gmail.com; b ++ Short Note: Neonatal Emergencies Mottling: Mottling is the patchy-colored appearance of the body surface, resulting from dilation of the superficial veins showing through the thin neonatal skin. Cyanosis accompanied by mottling in a lethargic neonate with tachycardia indicates shock. Other differential diagnoses for cyanosis are: sepsis, hypovolemia, intraabdominal surgical emergency, and metabolic crisis from inborn errors of metabolism (IEM). Methemoglobinemia: Methemoglobinemia is characterized by cyanosis without underlying cardiac or pulmonary disease. The infant can look cyanotic to gray, with an almost normal-appearing pulse oximetry. Supplemental oxygen will not alter the color. Methemoglobinemia is confirmed by venous or capillary blood gas or the persistence of a chocolate-brown color of a blood drop on filter paper. Initial treatment for methemoglobinemia is first searching and removing the offending agent, which is most often topical anesthetic agents, aniline dyes, and high levels of nitrate in the water supplies. Levels of methemoglobinemia above 20% are associated with clinical symptoms. If methemoglobinemia is greater than 30% of total hemoglobin, consider a dose of methylene blue, 1 to 2 mg/kg, given over 5 minutes. 2. JAUNDICE Jaundice in the first 24 hours of life of a term newborn is pathologic. Full-term, well-appearing neonates over 1 day of age often have physiologic or breast-milk jaundice. Physiologic jaundice is benign. Bilirubin levels spike close to day 3 of life and then decrease. Breast-feeding jaundice may present in the first few days, before sufficient milk production, or may present later, for unknown reasons. Breast-fed infants may have prolonged unconjugated hyperbilirubinemia lasting up to several weeks, thought to be related to compounds in breast-milk. Unconjugated hyperbilirubinemia: Unconjugated hyperbilirubinemia causes include: physiologic jaundice, breast-milk jaundice, breast-feeding jaundice, hemolytic disease, blood group incompatibility, infection, dehydration, polycythemia, abnormalities in the conjugating enzyme (UDPglucuronosyltransferase or UGT) as with Crigler–Najjar syndrome or Lucey– Driscoll syndrome, Gilbert syndrome, or hypothyroidism. CBC, total bilirubin level, and direct bilirubin level should be obtained. A direct Coombs test should be obtained if maternal blood type is unknown, hemoglobin is low, or total bilirubin is at levels requiring intervention. 2 Short Note: Neonatal Emergencies Direct bilirubin: Direct bilirubin or conjugated hyperbilirubinemia, which is always pathologic. Usually due to biliary obstruction, hepatocellular pathology, or metabolic disorder. Hepatitis, and in particular, idiopathic neonatal hepatitis, is a common cause of conjugated hyperbilirubinemia. Prolonged parenteral alimentation is another common cause of conjugated hyperbilirubinemia that can persist several months beyond the cessation of parenteral nutrition. Metabolic disorders of the liver that can also result in conjugated hyperbilirubinemia include alpha 1-antitrypsin deficiency, galactosemia, tyrosinemia, fructosemia, glycogen storage diseases, lipid storage diseases, cerebrohepatorenal syndrome, trisomy 18, cystic fibrosis, hemochromatosis, and idiopathic hypopituitarism. Obtain CBC, blood culture, albumin, LFT’s PT/PTT, hepatitis serologies, urinalysis, urine culture, and urine-reducing substances. Biliary atresia and neonatal hepatitis are the most common etiologies and patients with biliary atresia have better outcomes the earlier they are diagnosed. Management of jaundice: - - Infants with direct (conjugated) hyperbilirubinemia or acholic stools require admission for further diagnostic evaluation. Treatment of neonatal hepatitis is supportive, with supplementation of the fat-soluble vitamins. Prevention of hepatitis B infection requires early administration of HBIG and HBV vaccines to prevent chronic infection in exposed newborns. Septic infants should be treated with broad-spectrum antibiotics. Metabolic disorders (galactosemia, tyrosinemia, fructosemia, and the storage diseases) may be palliated with dietary restrictions; most progress to chronic cirrhosis and liver failure. Infants with physiologic jaundice can be discharged if they do not meet criteria for phototherapy or exchange transfusion. Infants with breast-milk jaundice usually require increased breastfeedings, and close follow-up with pediatrician until adequate milk supply is insured. Infants of diabetic mothers, infants with congenital hypothyroidism, or with resorption from large cephalohematomas may have higher levels of icterus than expected physiologically and may require serial bilirubin level checks. Some may benefit from prophylactic phototherapy. 3. HYDROCEPHALUS The majority of cases result either from obstruction to the CSF circulation, called obstructive or non-communicating hydrocephalus, or from failure to absorb CSF by the arachnoid villi and cisterns, called communicating hydrocephalus. Causes of Hydrocephalus: Both types of hydrocephalus can be caused by a congenital lesion (e.g., aqueductal stenosis, Dandy–Walker malformation, or 3 Short Note: Neonatal Emergencies Arnold–Chiari II malformation), or by acquired disease (e.g., posthemorrhagic, postmeningitic [bacterial, viral, fungal, or parasitic]), tumor-related compression (least common), or ventriculoperitoneal shunt malfunction. Overproduction by a choroid plexus papilloma or villous hypertrophy is rare. Investigations: 1. 2. 3. Head US is the most rapid diagnostic tool for evaluation. MRI gives detailed examination, can show meningeal enhancement in case of meningitis, and can delineate complications (intracranial abscess, venous thrombosis, and empyema). CT scan. Treatment of hydrocephalus: should be directed decompression, or resection of the mass, or both. toward ventricular Shunt complications includes: occlusion of proximal or distal ends, fracture, displacement, migration, and infection. 4. CEPHALOHEMATOMA Cephalohematoma is a subperiosteal hemorrhage occurring commonly over a parietal bone, distinguished from a caput succedaneum by the fact that the swelling never crosses suture lines. It occurs in 0.4% to 2.5% of live births due to rupture of blood vessels traversing the skull to the periosteum. The overlying skin is intact with no petechiae or hemorrhage. Cephalohematomas often feel fluctuant and may be bordered by elevated ridges of surrounding tissue, giving a false sensation of a skull depression. They may be associated with intracranial hemorrhage and 5.4% are also associated with linear skull fractures. Cephalohematomas often become prominent after the immediate newborn period when scalp edema subsides. Most commonly, a cephalohematoma is unilateral, but it can be bilateral. They resolve slowly over 4 to 6 weeks, possibly with calcification and the formation of a hard bump on the scalp that may be a source of great concern to parents. Complications of cephalohematoma are hyperbilirubinemia or anemia. Rare complications of localized infection of cephalohematoma include osteomyelitis, meningitis, and venous sinus thrombosis. No therapy is required for uncomplicated lesions. Routine incision or aspiration of a cephalohematoma is contraindicated due to the high risk of introducing infection. 4 Short Note: Neonatal Emergencies 5. SCLERAL AND SUBCONJUNCTIVAL HEMORRHAGE Scleral and subconjunctival hemorrhage are often noted in the newborn as a result of normal delivery or birth trauma. Spontaneous resolution occurs within 1 to 2 weeks. Retinal hemorrhage can occurs in about 25% of newborns. The presence of retinal hemorrhages should also raise the possibility of intentional trauma. Specifically, the shaken baby syndrome has been associated with flame-shaped retinal hemorrhages and subdural hematomas 6. NEONATAL CONJUNCTIVITIS (OPHTHALMIA NEONATORUM) The major causes of neonatal conjunctivitis, or ophthalmia neonatorum, are chemicals, chlamydia, bacteria, and viruses. Chlamydial conjunctivitis is the most common conjunctivitis in neonates. Neisseria gonorrhoeae conjunctivitis generally appears 2 to 5 days after birth, whereas conjunctivitis caused by Chlamydia trachomatis presents between 5 and 14 days after birth because of its longer incubation period. Gonococcal infection usually manifests as marked inflammation of the eyelids, chemosis, and copious purulent discharge. Gonococcal conjunctivitis is considered a medical emergency because the infection can cause corneal ulceration and perforation. HSV is a less common cause of neonatal conjunctivitis. The presence of skin lesions can help in the diagnosis. Giemsa staining from conjunctival scrapings and direct immunofluorescence antibody test can identify chlamydial disease. Gonococcal conjunctivitis should be treated immediately with intravenous penicillin or a third-generation cephalosporin in addition to topical antibiotics and irrigation. Chlamydial conjunctivitis should be treated with oral azithromycin. Chemical conjunctivitis usually resolves by 48 hours of age. 7. DUCTAL-RELATED STRUCTURAL HEART DISEASE IN THE NEONATE Cardiac disease presenting in the neonatal period are often congenital but can be acquired. Age at presentation of CHD varies with the underlying lesion, its 5 Short Note: Neonatal Emergencies impact on cardiac performance, and its dependence upon the ductus arteriosus (DA). The DA closes functionally within the first day of life and is generally structurally closed by 3 weeks. Symptoms in neonates with ductal-dependent lesions therefore typically present as early as the first few days of life and up to 2 to 3 weeks of age. Ductal-dependent cardiac lesions are divided into two categories: 12- Ductal-dependent pulmonary blood flow lesions, or right-sided obstructive lesions, include pulmonary atresia, tricuspid atresia, and critical pulmonary stenosis. Ductal-dependent systemic blood flow lesions, or left-sided obstructive lesions, include hypo-plastic left heart syndrome (aortic atresia), aortic coarctation, and aortic arch interruption. Baby with CHD and obstruction of the systemic or pulmonary blood flow, closure of the ductus precipitate rapid clinical deterioration. Emergency intervention with prostaglandins is lifesaving and therapy must be initiated even before a precise diagnosis is confirmed. Once supportive care is initiated and the neonate stabilized, immediate consultation with cardiology is warranted, with timely transfer to appropriate pediatric cardiac care center. Chest radiographs should be obtained to rule out pulmonary disease as well as to evaluate for pulmonary vascular markings, cardiomegaly, and characteristic features found with some CHD—as in a “boot-shaped heart” seen with tetralogy of Fallot (TOF). Electrocardiogram (ECG) and echocardiogram should be obtained. CBC, blood culture, urinalysis, and urine culture should be obtained to rule out sepsis. Consider lumbar puncture in light of clinical examination and history and the overall stability of the patient. Management: - Airway management is always of primary concern. Intubation with sedation and paralysis may reduce cardiac demand significantly. Neonates with hypotension require fluid and resuscitation and possibly inotropic support with dopamine or dobutamine. Neonates with strong clinical suspicion for ductal dependent CHD should receive prostaglandin E1 (PGE1) infusion in advance of a definitive diagnosis. The initial intravenous dose of PGE1 is 0.01 mcg/kg/min in neonates with echocardiographic confirmation of a large patent DA to prevent closure and maintain ductal patency. If the size of ductus is unknown or the ductus is restrictive, the starting dose is 0.05 mcg/kg/min. If no improvement, the dose can be increased incrementally to a 6 Short Note: Neonatal Emergencies maximum of 0.1 mcg/kg/min. After the infant’s condition has stabilized, the usual maintenance dose is 0.025 mcg/kg/min. Side effects of PGE1: Apnea, bradycardia, hypotension, fluid–electrolyte imbalances, irritability, fever, and cutaneous flushing. Consult immediately with a cardiovascular specialist and transfer to a facility with pediatric cardiac expertise. 8. LARYNGOTRACHEOMALACIA Laryngotracheomalacia accounts for approximately 60% to 70% of laryngeal problems in neonates and infants. It can be compounded by the presence of gastroesophageal reflux disease (GERD). Neonates present around 2 to 4 weeks of age with noisy breathing or coarse inspiratory stridor that is accentuated by agitation, crying, and being in a supine position. Stridor improves at rest and in the prone position. Severe cases may present with cyanosis, apnea, choking, and feeding difficulties. Laryngomalacia improves over time with complete resolution by approximately 18 months of age. Severe airway obstruction can occur when there are secondary lesions, such as neuromuscular disorders, subglottic stenosis, or vascular rings. In moderate to severe cases, diagnosis can be confirmed by flexible fiberoptic nasolaryngoscopy. Occasionally, the ENT surgeon will request a modified barium swallow or rigid bronchoscopy to rule out secondary comorbidities in cases where stridor is out of proportion to the degree of laryngomalacia seen on flexible laryngoscopy or in the presence of aspiration suspicious for posterior laryngeal cleft or tracheosophageal fistula. Management is mainly conservative (watchful waiting). Surgery (supraglottoplasty) is rarely required and is only indicated for cases with severe obstruction, hypoxic episodes, pulmonary hypertension, and failure to thrive. 9. NEONATAL RESPIRATORY DISTRESS Respiratory distress is one of the most common presenting symptoms for newborns. Most respiratory conditions (pneumonia, intrathoracic tumors, congenital lung disorders, chest wall deformities) produce respiratory distress; other extrapulmonary causes (cardiac disease, neuromuscular disorders, diaphragmatic disorders, anemia, polycythemia, metabolic acidosis, and neonatal sepsis) can present in this manner. 7 Short Note: Neonatal Emergencies Classical neonatal respiratory disorders (respiratory distress syndrome, meconium aspiration syndrome, transient tachypnea of the newborn, persistent pulmonary hypertension, and congenital pneumonia) usually appear in the first few hours to days following birth. A small group of neonates may present after discharge with pneumonia (lateonset GBS, chlamydial, respiratory syncytial virus [RSV], and Haemophilus influenzae) or exacerbation of bronchopulmonary dysplasia (BPD). Neonatal Respiratory Distress can present with nonspecific symptoms of poor feeding, hypothermia, and lethargy. Physical examination will reveal signs of respiratory distress (nasal flaring, grunting, retractions, head bobbing, cyanosis, and tachypnea). Other respiratory signs such as paradoxical motion can be seen in cases with diaphragmatic paralysis. Asymmetry of chest wall motion could signify pneumothorax or a large effusion. Pulse oximetry to measure O2 saturation. Blood gas analysis to detect hypercarbia and can differentiate between respiratory and metabolic acidosis. Chest x-ray is useful for defining etiology and complications. The first priority is, stabilization with supplemental oxygen, nasal cannula, or intubation and mechanical ventilation if needed. 10. CHRONIC LUNG DYSPLASIA (BPD) DISEASE OR BRONCHOPULMONARY BPD, or chronic lung disease, is defined as the presence of an oxygen requirement beyond 28 days of life or >36 weeks corrected gestational age. Respiratory distress syndrome, infection, increased circulation in the lung, and increase in fluid from a patent DA are thought to be contributing factors. Smaller, sicker premature newborns are more prone to the disease. Infants with BPD can present in the ED with acute exacerbations due to respiratory infections, resulting in catastrophic respiratory failure. Coarse breath sounds, crackles, and wheezing may be heard on auscultation. Pulse oximetry reveals desaturations and hypoxemia, often requiring an increase in FiO2 above baseline. Arterial blood gas may show chronic respiratory insufficiency (chronic CO2 retention) with hypoxia if the baby is desaturated. 8 Short Note: Neonatal Emergencies Chest x-ray of a neonate with severe BPD may show extensive scarring and fibrosis of the lung. An echocardiogram to determine the extent of pulmonary hypertension. Management: by giving oxygen, and escalating respiratory support as needed. Bronchodilators (albuterol, ipratropium), and steroids may be helpful. Avoid fluid overload. Correct anemia to maximize oxygen delivery. Admit patients to an intensive care unit for continuous monitoring. Prophylactic: Palivizumab is administered monthly during RSV season. 11. PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN This entity is mainly recognized in the cyanotic neonate with respiratory distress. It is more common in full-term infants in the hours to days after birth. Hypoxia, meconium aspiration, congenital diaphragmatic hernia, and pulmonary hypoplasia are common causes immediately after birth; however, any condition that precipitates hypoxic respiratory failure may cause pulmonary hypertension later (e.g., acute viral infections). Infants may continue to have low oxygen saturations despite 100% inspired oxygen and aggressive mechanical ventilation. Pulse oximetry readings taken separately in each of the four extremities, oxygenation can be 10% higher in the right arm, the preductal extremity. Arterial blood gases will show hypoxemia with or without hypercarbia. CXR will show variable findings according to the underlying etiology. Treatment: aggressive treatment should include fluid resuscitation, minimal stimulation including darkening the room and adequate sedation, and maintaining adequate systemic pressures with pressors if needed. Use of high-frequency oscillatory ventilation, inhaled nitric oxide, and extracorporeal membrane oxygenation are lifesaving. 12. MALROTATION AND VOLVULUS Approximately 1 in 6,000 live births will have clinically evident malrotation, and over half present within the first month of life. The most common presenting sign in the neonate is bilious emesis. The examination may reveal a distended abdomen; however, signs of peritonitis or shock are late findings and may not be present. 9 Short Note: Neonatal Emergencies Abdominal radiograph may reveal obstruction of the stomach with little or no distal air in the bowel. However, plain radiographs can be nonspecific or even normal appearing, particularly with intermittent volvulus, or may show a complete lack of bowel gas. US with Doppler interrogation of the superior mesenteric vessels may reveal abnormal configuration of the superior mesenteric vein in relation to the mesenteric artery. Contrast enema may reveal abnormal position of the cecum, but again, a normal study does not exclude malrotation. The diagnostic test is the upper GI series using fluoroscopy to determine the position of the ligament of Trietz. In volvulus, the site of the obstruction tapers, similar in appearance to a bird’s beak. In a partial or intermittent obstruction, the upper GI may reveal a spiral or corkscrew appearance. Laboratory findings including CBC, BMP, and inflammatory markers may be normal, particularly early in diagnoses. Management: The definitive treatment is emergent surgical repair. 13. HYPERTROPHIC PYLORIC STENOSIS Hypertrophic pyloric stenosis is an acquired disease where the muscle of the pyloric sphincter becomes enlarged and obstructs gastric emptying. It most often presents between 4 and 6 weeks of age, but can present in neonates as young as 2 weeks. Infants will present with progressive, projectile non-bilious emesis, and in advanced cases, severe dehydration, electrolyte imbalances, and hypoglycemia. Some infants may tolerate clear fluids, such as Pedialyte, but will vomit with milk. Early exposure to macrolides has been associated with the development of hypertrophic pyloric stenosis. Diagnosis can be confirmed by clinical examination of a palpable mass in the epigastrium that is roughly the size and shape of an olive. In the absence of a palpable mass, diagnosis can be made by US, which would reveal increased diameter, thickness and length of the pylorus. The infant should be fully stabilized and resuscitated with adequate fluids and any electrolyte disturbances corrected prior to surgical repair. Definitive treatment remains surgical pyloromyotomy. 10 Short Note: Neonatal Emergencies 14. NECROTIZING ENTEROCOLITIS NEC is a gastrointestinal emergency where progressive mucosal injury and inflammation result in bowel necrosis. While the incidence of NEC is inversely proportional to gestational age, up to 10% of cases occur in the term neonate. The etiology remains unknown, elements of ischemic injury, intestinal hypoxia, coagulation necrosis, acute or chronic inflammation, and bacterial overgrowth of the GI tract are all likely contributors. Term infants with a history of intrauterine growth restriction or SGA, congenital heart disease, meningomyelocele, and gastroschisis have increased risk of developing NEC. Term and preterm infants with a history of polycythemia, exchange transfusion, umbilical catheterization or asphyxia, are at increased risk of developing NEC. The most common presenting sign is emesis. The examination may reveal a distended abdomen; however signs of peritonitis or shock are often late findings and may not be present. The diagnosis is made by the identification of pneumatosis intestinalis, portal venous gas, or pneumoperitoneum on abdominal radiograph. In mild cases, plain radiographs may reveal signs of ileus but no evidence of pneumatosis; in these cases, portal venous gas may be appreciated by US. Laboratory: blood cultures, complete blood count, basic metabolic profile, blood gas, and, in severe cases accompanied by disseminated intravascular coagulation, coagulation studies. Management: There is no specific treatment for NEC other than supportive therapy. Bowel rest is indicated, with gastric decompression. Fluid resuscitation is often required, and blood pressure support may be needed. Surgical intervention is warranted if there is evidence of intestinal perforation or if there is worsening of clinical symptoms that suggest a necrotic segment. Bowel necrosis is often accompanied by persistent thrombocytopenia and acidosis, with systemic signs of respiratory failure and shock. 15. OMPHALITIS Omphalitis is an infection of the umbilical cord that presents with purulent or serosanguinous drainage from the umbilical stump. Signs include purulent and/or foul-smelling discharge from the umbilical stump. There may be associated periumbilical edema, erythema, or induration in more extensive disease. 11 Short Note: Neonatal Emergencies Complications: included life-threatening necrotizing fasciitis, ascending infection to the liver and systemic circulation, and staphylococcal scalded skin syndrome. In non-sterile births, there is also the risk of tetanus. Infection may spread through the umbilical artery and contaminate the peritoneum, causing infectious peritonitis, or may spread through the arterial system, causing loculated infections along the iliac or femoral arteries. Parenteral antibiotics are required. Infants with necrotizing fasciitis may also need surgical resection of the affected area. 16. AMBIGUOUS GENITALIA A normal genital examination in newborn girls includes a fully opening vagina (without posterior labial fusion), clitoris width of 2 to 6 mm, and absence of gonads in the labia majora or inguinal region. In boys, the urethral opening should be at the tip of the glans, with a stretched penile length of 2.5 to 5 cm, and bilateral testes in the scrotal sacs. Patients with male-appearing genitalia but micropenis, moderate to severe hypospadias or bilateral cryptorchidism, or patient with female-appearing genitalia but posterior labial fusion, clitoromegaly, or a labial/inguinal mass, require further evaluation for an intersex disorder. Diagnostic evaluation includes peripheral blood karyotype, serum testosterone and 17-OH progesterone levels, and pelvic US. The most immediate concern is when ambiguous genitalia results from CAH. Typically, adrenal insufficiency will present between 3 and 21 days. Early signs of adrenal insufficiency may include lethargy, decrease oral intake, increased emesis, failure to thrive, and weight loss. In severe cases, patients will present with obtundation, hypotension, gray appearance, cardiac arrhythmias (due to hyperkalemia), or seizures (due to hyponatremia or hypoglycemia). For patients with suspected CAH, serum electrolytes and glucose should be checked, and any abnormalities corrected, and cortisol replacement should be instituted. In the salt-wasting form of CAH, patients may also require mineralocorticoid replacement and salt supplementation. 17. SEIZURES The true incidence of neonatal seizures remains unclear, with reported ranges between 0.5% in term infants and 22% in preterm infants. Clinical seizures can be focal clonic, multifocal or migratory clonic, tonic, myoclonic, or subtle. 12 Short Note: Neonatal Emergencies The most common is the subtle seizure, often presenting with repetitive tongue or lip-smacking movements, eye deviations, or unusual bicycling or peddling movements. These movements may be associated with autonomic dysfunction, such as changes in heart rate, blood pressure, or oxygenation. The converse, autonomic disturbances such as apnea or bradycardia without associated movement anomalies rarely reflect seizure activity. 18. COMMON CAUSES OF NEONATAL SEIZURES 1-Asphyxia-related events: Intrapartum stress or infection, postnatal hypoxia due to trauma or systemic illness. 2-Metabolic derangements: Hypoglycemia, Hypocalcemia, Hyponatremia/Hypernatremia. 3-Cerebrovascular lesions: Neonatal stroke, venous thrombosis, subarachnoid hemorrhage, subdural hematoma. 4-Infection: - Congenital infections (e.g., toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus) Viral meningitis or meningoencephalitis (e.g., herpes simplex virus, enterovirus, parvovirus) Bacterial meningitis 5-Central nervous system malformations: Dysgenetic syndromes (e.g., holoprosencephaly, lissencephaly), Chromosomal anomalies (e.g., trisomy 18), Acquired malformations. 6-Inborn errors of metabolism: Nonketotic hyperglycinemia, Branched-chain aminoacidopathies, Urea cycle defects with hyperammonemia, Adrenoleukodystrophies (e.g., Zellweger syndrome), Mitochondrial disorders with elevated lactate and pyruvate, Pyridoxine deficiency. 7-Drug withdrawal or intoxication: Prenatal exposure to barbiturates, alcohol, heroin, cocaine, methadone may seize within 2 days to 6 weeks of age. 13 Short Note: Neonatal Emergencies 19. INVESTIGATIONS - STAT bedside glucose and sodium testing should be performed. Serum evaluation should include glucose and electrolytes (including magnesium, calcium, and phosphorus). Ammonia, lactate, and pyruvate. Serum blood gas evaluation. Cultures and viral testing of the blood, urine, and CSF. CNS imaging may include head US, CT, or MRI. Management: Metabolic derangements should be managed first. Hypoglycemia can be corrected by parenteral administration of a 10% dextrose solution (D10): initial administration should include a bolus of 5 mL/kg followed by continuous dextrose infusion. Hypocalcemia should be treated with parenteral infusion of calcium gluconate; concordant hypomagnesemia should be also corrected (as calcium levels may not normalize until serum magnesium normalizes). Hyper or hyponatremia should generally be correctly slowly to avoid sudden fluid shifts in the brain. Ongoing seizures caused by hyponatremia will often stop with a simple normal saline bolus of 20 mL/kg; continued seizures due to hyponatremia refractory to standard sodium corrections may require administration of hypertonic saline (3%) at a dose of 4 mL/kg. Infants at risk for infection or meningitis should be treated with broad-spectrum antibiotics as soon as cultures are obtained. The use of antiepileptics is controversial, the most common treatment includes phenobarbital and phenytoin/fosphenytoin. Benzodiazepines are the second most common medications, but the associated sedative effects and potential for respiratory depression requires close monitoring of the infant’s cardiorespiratory status. The decision to treat thrombotic cerebrovascular lesions should be made in conjunction with a pediatric hematologist. Severe hyperammonemia and other metabolites due to IEM may require dialysis and should be managed in conjunction with a metabolic geneticist. Pyridoxine deficiency may respond to parenteral administration of pyridoxine, but requires continuous EEG monitoring to assess effectiveness. 20. NEONATAL INFECTIONS Neonatal sepsis can be categorized into early onset (occurring in newborns who are less than 72 hours of life) or late onset (occurring between 3 and 7 days of life). 14 Short Note: Neonatal Emergencies Early-onset disease is caused by microbial flora present in the vaginal tract (GBS, E. coli or other gram-negative bacilli, Staphylococcus aureus, Enterococci, viridans group Streptococci, Group A Streptococci, syphilis, H. influenzae, Listeria monocytogenes). Risk factors for early-onset disease include prolonged rupture of membranes, chorioamnionitis, GBS-colonized mother with inadequate intrapartum antibiotics. Late-onset disease may occur through horizontal transmission from the infant’s environment or caregivers and is caused by environmental flora (Staphylococci, E. coli, GBS, and candidiasis). Risk factors for late-onset disease include prematurity, presence of congenital heart disease, gut pathology, and presence of central catheters. Other pathogens causing sepsis include viral (herpes simplex, enterovirus, cytomegalovirus, adenoviruses), fungal (systemic candidiasis), and atypical bacteria (Toxoplasma) agents. Neonatal sepsis presents within the first 4 weeks of life with symptoms ranging from simply poor feeding to frank respiratory distress and cardiovascular collapse. Hypothermia often occurs in babies with sepsis. Neonates with signs of shock should be presumed to have neonatal sepsis but should also be evaluated for coarctation of the aorta and cardiogenic shock. Investigations: Complete blood count with differential, C-reactive protein (CRP). Other acute phase reactants including procalcitonin and interleukin (IL)-6, IL-8, tumor necrosis factor-alpha. Definitive diagnosis is isolation of a specific pathogen from a normally sterile site, such as blood, urine, or CSF culture. Management: Initial management should include placing the infant on cardiorespiratory monitoring, with vital sign monitoring and clinical reassessments. Antibiotics should be given as soon as possible. 21. NEONATAL HERPES SIMPLEX VIRUS INFECTION Neonatal HSV disease can result from infection with HSV-1 or HSV-2. Infection occurs through vertical transmission in utero (congenital infection) (5%), or while passing through an infected birth canal (intrapartum) (85%), or from contact with infected oral secretions (postpartum) (10%). HSV disease in neonates is usually symptomatic. It can present in two forms: (a) Congenital HSV infection from an in utero transmission (characterized by vesicular skin lesions, or scarring, neurologic lesions [microcephaly, 15 Short Note: Neonatal Emergencies hydranencephaly, intracranial calcifications, hypertonicity, or seizures] and ocular findings [chorioretinitis, microphthalmia, cataracts, or optic atrophy]) or (b) neonatal HSV, which may present 2 to 3 weeks after discharge from the newborn nursery. Neonatal HSV classically produces three presentations (skin, eyes, mouth [SEM] [45%], CNS disease [30%], or disseminated HSV [25%]). Fever occurs in 30% of neonates with HSV, whereas 20% present with hypothermia. Neonates presenting with fever, irritability, and CSF pleocytosis should be worked up for HSV disease, particularly if seizures occur. Neonates with disseminated disease typically present at about 10 to 12 days with septic shock. These infants have the worst prognosis. Neonates suspected of having HSV disease should undergo a full sepsis workup including CBC, urinalysis and urine culture, blood culture, liver functions, lumbar puncture, and HSV cultures. Treatment in the ED should be directed at cardiorespiratory stabilization of the infants, fluid resuscitation, followed by assessment for bacterial and viral causes of sepsis. Intravenous acyclovir therapy (60 mg/kg/day in three divided doses) should be started. Infants with keratitis or ocular disease should also be given topical antiviral ophthalmic drops (1% trifluridine, 0.1% iododeoxyuridine, or 3% vidarabine), in addition to intravenous acyclovir therapy. COMPETING INTERESTS Authors have declared that no competing interests exist. REFERENCE Fleisher, & Ludwig. Textbook of pediatric emergency medicine (8th Ed.). Wolters Kluwer; 2021. 16 Short Note: Neonatal Emergencies Biography of author(s) Elsharif Ahmed Bazie (Associate Professor) Elimam Elmahdi University, Sudan. Research and Academic Experience: Dr. Elsharif Bazie is an M.D. in Paediatrics and Child Health. Research Specialization: Dr. Elsharif Bazie's area of research mainly includes general paediatrics, paediatrics emergency, and medical education. Number of Published papers: Dr. Elsharif Bazie has published more than 30 papers and case reports. Dr. Elsharif Bazie published a book entitled Screening of Children with Symptomatic Renal Diseases. Mona Isam El-Din Osman Sudan International University, Sudan. Research and Academic Experience: Mona Isam El-Din Osman is an M.D. in Pediatrics and Child Health. Research Specialization: Dr. Mona’s research areas include general paediatrics and medical education. Number of Published papers: Dr. Mona has published 5 papers in reputed journals. ___________________________________________________________________________________ © Copyright (2024): Author(s). The licensee is the publisher (B P International). 17 Short Note: Neonatal Emergencies Index INDEX A Acrocyanosis, 1 Airway management, 6 C Cardiac disease, 1, 5, 7 Cephalohematoma, 4 Chronic lung disease, 8 Clinical seizures, 12 Congenital heart disease, 1, 11, 15 Cyanosis, 1–2, 7–8 E Electrolyte imbalances, 7, 10 G Gonococcal infection, 5 H Hydrocephalus, 3–4 Hypoglycemia, 10, 12–14 Hypoxemia, 8–9 I Inborn errors of metabolism, 2, 13 Intracranial calcifications, 16 Intravenous acyclovir therapy, 16 M Metabolic crisis, 2 Metabolic derangements, 13–14 Metabolic disorders, 3 Methemoglobinemia, 2 Mineralocorticoid replacement, 12 Mottling, 2 N Neonatal conjunctivitis, 5 P Parenteral nutrition, 3 Peripheral blood karyotype, 12 Physiologic jaundice, 2–3 Polycythemia, 2, 7, 11 Pulmonary hypoplasia, 9 R Respiratory distress, 7–9, 15 18 Short Note: Neonatal Emergencies Index S Scleral and subconjunctival hemorrhage, 5 Surgical pyloromyotomy, 10 T Tetralogy of fallot, 6 Thrombotic cerebrovascular lesions, 14 ___________________________________________________________________________________ © Copyright (2024): Author(s). The licensee is the publisher (B P International). Peer-Review History: This book was reviewed by following the Advanced Open Peer Review policy. This book was thoroughly checked to prevent plagiarism. As per editorial policy, a minimum of two peer-reviewers reviewed the manuscript. After review and revision of the manuscript, the Book Editor approved the manuscript for final publication. Peer review comments, comments of the editor(s), etc. are available here: https://peerreviewarchive.com/review-history/8471A 19 London Kolkata Tarakeswar India: Guest House Road, Street no - 1/6, Hooghly, West Bengal, India (Reg. Address), Diamond Heritage Building, 16, Strand Road, Kolkata, 700001 West Bengal, India (Corporate Address), Tele: +91 7439016438 | +91 9748770553, Email: director@bookpi.org, (Headquarters) UK: 27 Old Gloucester Street London WC1N 3AX, UK, Fax: +44 20-3031-1429, Email: director@bookpi.org, (Branch office)