American Academy of Pediatrics

A 5-week-old, ex-38-week boy with a history of neonatal abstinence syndrome is brought to the pediatric emergency department (ED) by his biological mother for labored breathing and change in cry. His symptoms began the evening before presentation with nasal congestion and decreased oral intake. The patient's mother brought him to the ED when she could “feel the congestion” on touching the baby's chest. She noted that he is crying more frequently than usual and that his cry sounds different. She denies associated cyanosis and changes in color. There is no associated fever, cough, apnea, rash, vomiting, diarrhea, decreased urine output, or sick contacts.

Return to play (RTP) is the process of safely returning an injured athlete back to sport or activity. RTP protocols for surgical procedures such as anterior cruciate ligament repair have been researched and documented extensively. Other than concussion, detailed RTP guidelines for common, nonoperative sport injuries are less available. For this brief, we will concentrate on sports injuries frequently encountered by primary care providers (PCPs). Given their pivotal role as initial evaluators, we aim to present a holistic and comprehensive clinical perspective on RTP decisions for the general pediatrician.

A 14-year-old girl with a 6-month history of recurrent epigastric and right upper quadrant abdominal pain, nausea, and nonbilious emesis presents to the emergency department (ED) with symptom recurrence for 48 hours. Her pain is a 7/10 stabbing sensation radiating to her back. Her pain improves after intravenous pain medication and vomiting; eating and drinking worsen her symptoms. Episodes have lasted a few days, with symptom resolution between episodes. She has had no weight loss, stool changes, or fevers. Her periods are irregular, and she is not sexually active. She has no relevant family history, and her past medical history is significant only for these episodes. She has no prior hospitalizations or surgeries.

Congenital tuberculosis (TB) is a rare condition, and diagnosis is challenging due to its nonspecific clinical presentation and rarity. It has a very high case-fatality rate (estimated at 30%–50%).We report the case of a 2-week-old male neonate, born from an uncomplicated diamniotic, dichorionic twin pregnancy at 36 weeks 1 day’s gestation, who presented with poor feeding and low-grade fever. Blood, urine, and cerebrospinal fluid (CSF) cultures, as well as nasopharyngeal and CSF viral polymerase chain reactions were negative. However, persistent poor feeding and rising inflammatory markers prompted continued hospitalization. On the fourth day of admission, he developed acute hypoxemic, hypercarbic respiratory failure with apneas and progressive lung parenchymal disease requiring intubation. The diagnosis of congenital TB was confirmed through endotracheal aspirates. He was initiated on TB treatment but ultimately developed a paradoxical reaction, requiring readmission and initiation of corticosteroids.His mother, father, and twin brother were initially asymptomatic. His twin was subsequently admitted to the hospital and was diagnosed with congenital TB as well. His mother was ultimately diagnosed with genitourinary TB based on an endometrial biopsy.This case contributes to the limited literature on congenital TB, highlighting the broad clinical spectrum and complications in managing the disease. Additionally, the unique presentation of disseminated congenital TB in an infant with an asymptomatic mother and a fraternal twin who initially did not require hospitalization underscores the importance of heightened awareness of tuberculosis during pregnancy, particularly in populations at risk, to facilitate early diagnosis and prevent perinatal transmission.

An 18-year-old male patient with a history of autism spectrum disorder and attention-deficit/hyperactivity disorder (ADHD) presents to the emergency department (ED) with progressive bruising and myalgia. He first experienced intermittent myalgia on the left leg 3 months prior to the ED visit. At that time, he had not participated in strenuous physical activities, and there had been no trauma to the bruised areas. He was brought to his primary care pediatrician because of swelling in the left ankle and thigh. A basic laboratory evaluation, including a complete metabolic panel, complete blood cell count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), creatinine kinase (CK), and thyroid panel, had results within normal limits.

Interfacility transport of pediatric patients represents a critical and multifaceted process that entails significant transitions in care, each of which can influence clinical outcomes. Although this is a critical part of caring for children, most graduating pediatrics residents have limited or no exposure to pediatric transport medicine because it is typically offered only as an elective rotation during their pediatric training. This lack of formal training can leave pediatricians unfamiliar with the foundational understanding of pediatric transport medicine, including best practices, principles, regulatory considerations, team composition and dynamics, mode selection, and decision-making processes essential for safe and efficient interfacility transfer of critically ill children.

Approximately 80% of the more than 192 medical schools that confer either allopathic (MD) or osteopathic (DO) degrees have integrated some form of Narrative Medicine (NM) training into their educational curricula.

A 34-year-old G4P3003 pregnant woman with a history of moderate-to-severe aortic stenosis (AS) and aortic regurgitation with a bicuspid aortic valve presented at 15 weeks’ gestation with an unplanned pregnancy to establish prenatal care. At the time of presentation, she was symptomatic with mild dyspnea on moderate exertion but was able to ambulate and complete activities of daily living without difficulty. She reported palpitations with activity but was without clinical signs of heart failure on examination. An echocardiogram revealed normal left ventricular size, an ejection fraction of 57%, and moderate-to-severe AS (modified World Health Organization Classification III).Her history was notable for 1 prior cesarean section for breech malpresentation followed by 2 subsequent term vaginal births after cesarean, with her most recent delivery 12 years prior, before progression of her aortic valvular disease. She tolerated those deliveries and postpartum courses well without any cardiac implications for her or her infants. She developed worsening dyspnea on exertion 5 years prior, with serial echocardiograms demonstrating stable ejection fraction and mild progression of AS. She was briefly managed on metoprolol, which was discontinued due to low blood pressures.During this pregnancy, she was seen by a multidisciplinary care team including maternal-fetal medicine, cardiology, and anesthesia. At her initial prenatal visit, she was counseled on maternal risks including arrhythmias, myocardial infarction, and death, as well as neonatal risks including congenital anomalies and growth restriction, and was offered termination. She was followed with monthly serum assessments of brain natriuretic peptide, frequent physical examination assessments, and serial echocardiograms. She was counseled on signs and symptoms of pulmonary edema and heart failure. Fetal assessment included a detailed anatomic survey and a fetal echocardiogram and serial fetal biometry. A multidisciplinary care plan was developed in anticipation of delivery.She had an unremarkable detailed fetal anatomic survey and an unremarkable fetal echocardiogram at 22 weeks’ gestation. Estimated fetal growth ultrasonographies were normal at 24, 28, and 32 weeks’ gestation. At her 36-week ultrasonography, the estimated fetal weight was noted to be 2300 g (7th percentile). Doppler interrogation of the umbilical artery was normal at 36 and 37 weeks’ gestation; delivery was advised between 38 and 39 weeks’ gestation.In terms of her cardiac status, she underwent testing for serum brain natriuretic protein levels, and echocardiograms remained stable. However, she developed worsening dyspnea in the third trimester, which limited her exertion. But she was still able to ambulate for short distances, climb 1 to 2 flights of stairs, and complete all activities of daily living throughout gestation.Her delivery plan involved a trial of labor after cesarean and consideration of forceps-assisted vaginal delivery to avoid prolonged Valsalva with pushing efforts, which can increase afterload and further limit the volume of blood able to exit left ventricle. Additionally, the multidisciplinary team recommended placement of an arterial line for continuous blood pressure monitoring, early epidural placement with slow titration of neuraxial analgesia to minimize hypotension and impact on cardiac perfusion during labor, and strict intake and output monitoring to maintain euvolemia. The patient was crossmatched for 2 units of packed red blood cells in case of postpartum hemorrhage as an additional precautionary measure to maintain euvolemia.She was admitted for scheduled induction of labor at 38 weeks and 4 days’ gestation. Anesthesia placed an arterial line and a slowly titrated epidural. Her cervix was noted to be favorable on arrival, so she was induced with oxytocin and amniotomy. She remained asymptomatic from a cardiac perspective throughout her labor course. Upon progression to full cervical dilation, she began pushing with notable fetal descent. Given asymptomatic status, normal vitals, and appropriate labor progress, operative vaginal delivery was deferred.She had a vaginal birth after cesarean with normal blood loss. Active management of the third stage of labor was performed to minimize the risk of postpartum hemorrhage. She was monitored on continuous telemetry for 24 hours postpartum without cardiac events or symptoms, and the arterial line was removed 24 hours after delivery. Strict measurement of maternal intake and output were collected to ensure the patient remained euvolemic. She was discharged 2 days postpartum with follow-up with maternal-fetal medicine and cardiology 2 weeks later. Her symptoms of fatigue and dyspnea transiently worsened in the first week postpartum but had improved by her postpartum visits. Echocardiogram was performed at 1 and 3 months postpartum, which demonstrated stable findings.The infant was born without complications and had an Apgar score of 8 and 9 at 1 and 5 minutes of age, respectively, and a birth weight of 2750 g (8th percentile). The infant was transferred to the newborn nursery without issues, and routine neonatal cardiac screening was normal.AS is the second-most common form of valvular heart disease, representing 3% to 6% of congenital heart disease.1 Although AS can be acquired with increasing age, congenital AS can be found in the setting of underlying structural variants such as a bicuspid aortic value. AS is diagnosed by the peak velocity of blood flow and mean pressure gradient across the aortic valve as measured on echocardiogram, as well as valve surface area. Severity, from mild to severe, is graded on these parameters.2 When valve leaflets are not well approximated due to scarring or a congenital variant, the valve opening is narrowed and the left ventricular muscle fibers hypertrophy as they work harder to propel blood forward across the abnormal valve (Figure 1). Over time, those muscle fibers become weaker as the heart remains under strain, ultimately leading to reduced cardiac output and, in some cases, heart failure.Cardiac output and intravascular volume are increased from baseline during pregnancy to facilitate perfusion of the placenta for the growing fetus (Figure 1). Pregnant patients with AS are therefore at increased risk for cardiac strain in pregnancy as their heart may not be able to compensate for the increased demand.3 Greater preload due to intravascular volume shifts in pregnancy with high afterload pressures due to a stenotic valve creates increased pressures in the left atrium with back up into the pulmonary vasculature and right heart. Ultimately, this can predispose patients to congestive heart failure, myocardial ischemia, and arrhythmias due to decreased perfusion of coronary vasculature. Maternal cardiac disease has direct implications not only for the circulatory system for the pregnant person but also on placental perfusion, which may result in fetal or neonatal complications. Progressive maternal disease affects timing of delivery, risk of preterm birth, and implications from placental malperfusion including fetal growth restriction and stillbirth. In a multinational cohort of individuals in the Registry on Pregnancy and Cardiac Disease, increasing severity of AS was associated with delivery at earlier gestational ages, increased risk of cesarean delivery, and lower birthweight.4 Additionally, pregnant people with congenital causes for AS are at increased risk for congenital heart defects in their offspring.Multiple risk stratification tools have been established in the setting of maternal cardiac disease to stratify risks of adverse maternal and neonatal outcomes and provide guidance on the resources needed to optimize outcomes. The most commonly used of these tools is the modified World Health Organization Pregnancy Risk Classification, which stratifies patients with preexisting cardiovascular disease into classes I through IV, with more significant pregnancy-associated morbidity with higher class level (Table 1).5 Class I disorders do not have associated increased risks of maternal morbidity, whereas class IV conditions are considered to be a contraindication to pregnancy due to the high risk of maternal morbidity and mortality. Moderate AS is considered class II-III, indicative of a moderate-to-significant increase in morbidity with an estimated 15% risk of cardiac events during pregnancy.Guidance from the American College of Obstetricians and Gynecologists recognizes the complex nature of caring for pregnant people with cardiac conditions such as AS with the potential for significant maternal and fetal morbidity and mortality, particularly with advanced valvular or other congenital heart disease.6 Therefore, they advise coordinated care from a “pregnancy heart team” involving multidisciplinary representation from maternal-fetal medicine, cardiology, anesthesiology, and neonatology to prioritize maternal and fetal safety during the antepartum, intrapartum, and immediate postpartum periods in patients with advanced cardiac conditions.Management of AS in pregnancy is guided by symptomatology and the severity of the disorder. For symptomatic disease, serial echocardiograms are recommended to evaluate for disease progression. The patient in this vignette presented with dyspnea with moderate exertion and intermittent palpitations but otherwise had stable findings on her echocardiograms. An exercise stress test can be considered to evaluate for the ability to tolerate the physiologic changes of pregnancy, particularly when weighing the potential risks and benefits to surgical repair prior to conception. Ongoing multidisciplinary care with cardiology and maternal-fetal medicine is essential to monitor for development of symptoms concerning for arrhythmia, pulmonary edema, or development of heart failure.A detailed anatomic survey is recommended at 18 to 20 weeks’ gestation, and in the case of congenital AS in the pregnant person, a fetal echocardiogram is recommended to evaluate for congenital heart disease in their offspring. Acquired causes of AS do not necessitate fetal echocardiogram as this does not confer an elevated risk of congenital heart disease in the offspring. Serial growth scans are recommended given the association with fetal growth restriction. Antenatal testing in the third trimester can be considered particularly in the setting of fetal growth restriction, evidence of heart failure, or other obstetric indication.With advancing gestation, patients are at particular risk for development of arrhythmias, heart failure, and myocardial infarction due to physiologic changes of pregnancy including increased intravascular volume, increased heart rate, and decreased blood pressure due to peripheral vasoconstriction. The intrapartum period poses particular risks of maternal decompensation secondary to rapid fluid shifts, including an up to 75% increase in cardiac output in the immediate postpartum period due to relieved compression of the uterus on the inferior vena cava and blood no longer being preferentially shunted to the uterus following delivery.3 Neuraxial anesthesia is recommended for patients with symptomatic AS to reduce cardiac strain (deformation, stretching, or stress placed on the heart muscle) during labor and must be carefully titrated to an appropriate level to avoid hypotension and the resulting decrease in cardiac perfusion. The majority of patients with AS can attempt vaginal delivery; however, operative vaginal delivery may be recommended to minimize or eliminate decreased preload and increased afterload associated with Valsalva during pushing efforts in the second stage of labor.Ongoing surveillance in the postpartum period is essential to prevent severe morbidity. Large intravascular fluid shifts following delivery can lead to complications like pulmonary edema and acute heart failure, particularly for patients with moderate-to-severe cardiac valve conditions. Acute coronary syndrome is most common in the early postpartum period. Given these increased risks, close cardiac monitoring in the first 24 to 48 hours postpartum is warranted with close postpartum follow-up after hospital discharge. By 3 to 6 months postpartum, cardiac parameters generally return to baseline, and by 1 year postpartum, cardiac structure generally returns to its prepregnancy form.If heart failure develops during pregnancy, maternal cardiovascular stability is paramount to optimize both maternal and fetal/neonatal outcomes. Medication management to control blood pressure and decrease the risk of left ventricular hypertrophy can be used along with exercise limitations to optimize function and symptom control.7 For severe cases, valve replacement or balloon valvuloplasty can be performed if risks of hemodynamic compromise or symptoms outweigh perioperative risks to the fetus, especially when occurring at previable or periviable gestational ages.8 Expert consultation with a multidisciplinary pregnancy heart team at a tertiary care center is warranted in these select cases.In summary, AS in pregnancy is a risk factor for maternal heart failure and arrythmias as well as preterm birth, fetal growth restriction, and low birthweight neonates. For patients with moderate-to-severe AS, multidisciplinary team collaboration to optimize the pregnant individual’s cardiovascular status, discuss maternal and fetal surveillance antepartum, coordinate mode and timing of delivery, and ensure appropriate postpartum and neonatal care is warranted.American Board of Pediatrics Neonatal-Perinatal Content SpecificationUnderstand cardiovascular physiology.Know maternal medical disorders and medications affecting the fetus and newborn infant.Understand pregnancy physiology.

A previously healthy, immunized, 5-year-old boy presents to the pediatric emergency department (ED) with tachycardia, tachypnea, hypoxemia, and irritability. His family describes 2 weeks of upper respiratory (URI) symptoms, including fever, rhinorrhea, cough, fatigue, poor oral intake, and resolving conjunctivitis. He was taken to a primary care provider 9 days prior for presumed viral conjunctivitis, returning 6 days later because of a cough. He was diagnosed with pneumonia and prescribed azithromycin. His family also describes 2 episodes of hematemesis and 1 episode of blood in his stool during the week before the current presentation to the ED. Due to worsening lethargy requiring the normally ambulatory patient to be carried by his parents, the family sought further evaluation. His history includes living on a farm in rural Colorado and recent travel to Wyoming. Multiple family members also had upper respiratory symptoms 3 weeks ago but have since recovered. There is no family history of hematologic, immunologic, or metabolic disorders.His initial vital signs are temperature of 36 °C, heart rate of 158 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 89% in room air. On examination, he appears tired and responds agitatedly to voice and light touch. He has dry mucous membranes but no cracked lips or strawberry tongue. His prior conjunctivitis has resolved. Breath sounds are clear bilaterally, and he has no retractions. He is pale with a 4-second capillary refill time. His abdomen is soft with mild generalized tenderness and distension. He has no rash or petechiae. Laboratory findings (Table 1) show hemoconcentration, leukemoid reaction, thrombocytopenia, coagulopathy, and evidence of multiorgan failure (elevated transaminase levels, acute kidney injury, metabolic acidosis with elevated lactate level). Blood bacterial and fungal cultures and polymerase chain reaction (PCR) testing for common respiratory pathogens are sent (testing included adenovirus, cytomegalovirus, Epstein-Barr virus, SARS-CoV-2, human metapneumovirus, rhinovirus, enterovirus, parainfluenza, Bordetella pertussis, Mycoplasma pneumoniae, and Chlamydia pneumoniae). His C-reactive protein (CRP) level and erythrocyte sedimentation rate are normal, and procalcitonin level is mildly elevated. Flow cytometry studies are performed, and the negative results make leukemia and lymphoma unlikely. His chest radiograph demonstrates moderate diffuse interstitial coarsening (Figure 1).The patient is admitted to the pediatric intensive care unit (PICU) with 4 L of 21% FiO2 nasal cannula following 60 ml/kg of crystalloid fluid resuscitation. An additional 20 ml/kg of crystalloid fluid is given in the PICU for downward-trending blood pressure values. He starts receiving cefepime, linezolid, metronidazole, and doxycycline. His respiratory support is escalated to noninvasive pressure ventilation, but due to increasing somnolence, he is intubated 6 hours after PICU admission.The differential diagnosis for a child with significant leukocytosis, respiratory distress, and signs of multiorgan failure includes infection (viral, bacterial, or atypical sepsis), an oncologic process (leukemia or lymphoma), or inflammatory (hemophagocytic lymphohistiocytosis [HLH], Kawasaki disease [KD], and multisystem inflammatory syndrome in children [MIS-C]). Given the acuity of symptoms, infectious causes such as community-acquired pneumonia, toxic shock syndrome, atypical respiratory infections (legionella, chlamydia, mycoplasma, and Q fever), or zoonotic diseases (plague, tularemia, leptospirosis, hantavirus) were considered most likely. His continued decline despite broad antibiotic coverage suggested an infection with an atypical pathogen. Bacterial and fungal cultures from blood, trachea, and the pleural space remained negative during PICU admission. Viral testing results were negative. Peripheral smear results were negative for dysplasia or blasts, making leukemia unlikely,1 but the smear was notable for thrombocytopenia and marked leukocytosis with lymphocytosis, monocytosis, and neutrophilia with a left shift. Although ferritin was elevated, and the patient had fever prior to presentation, he did not have splenomegaly or hypertriglyceridemia, and his thrombocytopenia was not accompanied by any other cytopenia; thus, he did not meet the diagnostic criteria for HLH.2 KD was considered given his fevers and history of conjunctivitis; however, he did not meet diagnostic criteria for classic or incomplete KD. In addition, his CRP level was low, and an echocardiogram did not demonstrate coronary artery changes.3 Although he developed a significant systemic illness following a respiratory infection, his low CRP level and the presence of a more likely diagnosis made MIS-C less likely.4Based on the severity and rapidity of his illness progression, as well as his exposures, hantavirus was considered, and serologic samples were sent. Fifteen days after the patient’s admission, hantavirus testing by the Colorado Department of Public Health and Environment laboratory indicated serologic evidence of recent or current infection with the Sin Nombre virus (SNV), with negative immunoglobulin G (IgG) and positive immunoglobulin M (IgM; 1:6400) findings. Our patient’s final diagnosis was hantavirus cardiopulmonary syndrome (HCPS).Hantavirus is an enveloped RNA virus transmitted to humans primarily via inhalation of aerosolized rodent excrement. The risk of contracting hantavirus is associated with the likelihood of exposure to rodents. The clinical syndromes associated with the infection are HCPS and hemorrhagic fever with renal syndrome, although the latter is almost exclusively outside of the United States. Hantavirus infection is most prevalent in Asia, although approximately 200 cases occur annually in the Americas.5 In the Americas, hantavirus infection is postulated to have a seroprevalence of 3.77% in rural settings compared with 2.43% in regions overall.6SNV, the hantavirus species responsible in this case, has one of the highest rates of fatality at 35%, is responsible for most hantavirus infections in the United States, and is associated with HCPS. The main mechanisms of hantavirus pathology are thought to be a strong inflammatory response with an effect on endothelial cells, leading to increased permeability of capillaries.5 HCPS has fatality rates between 30% and 50%,7 and a retrospective review of hantavirus cases in children in the United States between 1993 and 2018 showed that the median time from symptom onset to death was 2 days. Degree of capillary leak and resulting hemoconcentration and elevated creatinine has been associated with higher fatality rates.8HCPS demonstrates a clinical progression through sequential clinical stages, summarized in Table 2. HCPS is a challenging diagnosis due to clinical features that are shared with other severe infections and inflammatory syndromes. Hantavirus diagnosis relies on antibody analysis, which can cause delayed diagnosis due to testing capabilities and possible false negatives early in the clinical course prior to antibody formation. Reverse transcription quantitative PCR shows promise as a more rapid and reliable test for suspected hantavirus.9 Unlike patients with classic septic shock, patients with hantavirus often present with normal or elevated blood pressure.10 A complete blood cell count and peripheral blood smear can assist in diagnosis. Previous literature has demonstrated that the following characteristic pentad is associated with HCPS: thrombocytopenia, myelocytosis, absence of toxic granulation in neutrophils, hemoconcentration, and an immunoblast population greater than 10% of the total leukocyte population.1,5 One study found that meeting 4 out of 5 of these criteria has a sensitivity of 96% and specificity of 99% for HCPS.8 If hantavirus is suspected, the Centers for Disease Control and Prevention (CDC) recommends contacting the appropriate health department, which can help with diagnosis and testing using IgM and IgG antibody levels, enzyme-linked immunosorbent assay, or PCR.11There are currently no Federal Drug Administration (FDA)–approved medications for hantavirus infection, although there are ongoing studies of novel agents.12,13 The treatment for hantavirus infection is supportive care. Management of fluid status, respiratory compromise, and cardiac output are imperative.9 Given the clinical uncertainty often present in these cases because of delayed definitive diagnostic results, decisions about early invasive intervention can be difficult. Children with concern for HCPS should be transferred to an institution with a PICU for monitoring, initiation of mechanical ventilation, and veno-arterial extracorporeal membrane oxygenation (VA ECMO) as needed. Fluid resuscitation plays a critical role in addressing the hypotension that often occurs in the HCPS cardiopulmonary phase. Fluid administration should be judicious, when possible, as significant capillary leak associated with the disease process causes pulmonary edema and third-spacing of fluids.10 VA ECMO has been used successfully in several cases, especially in those patients with a compromised cardiac output despite administration of pressors and inotropic agents.14Our patient’s family reported 2 weeks of URI and flu-like symptoms with rhinorrhea and conjunctival injection prior to presentation, which is atypical for the prodromal phase of hantavirus and likely was a respiratory viral illness that was shared with his family members. However, our patient’s rapid decline in the cardiopulmonary phase progressed in the expected time frame. Overnight, on hospital day (HD) 1, the patient rapidly developed hemodynamic instability and profound biventricular dysfunction that progressed despite initiation of multiple vasoactive and inotropic medications. Approximately 13 hours after admission, he had a hypoxemic cardiac arrest with pulseless electrical activity. At 35 minutes of cardiopulmonary resuscitation, he was cannulated to VA ECMO. Given worsening hyperleukocytosis, apheresis was performed after cannulation. Despite these measures, he had multiorgan failure with acute kidney injury, acute liver injury, and worsening cardiorespiratory failure. Computed tomography (CT) of the chest, abdomen, and pelvis demonstrated small bilateral pleural effusions with complete consolidation of the lungs, large ascites in the peritoneal cavity, and free fluid in the perinephric spaces. This timeline for rapid progression of disease is consistent with prior literature.8 Neurologic evaluation the next day demonstrated lack of brainstem responses on examination, electroencephalogram without cortical activity, and head CT showing severe cerebral edema with tonsillar herniation. In discussing goals of care, his family decided to redirect care, and life-sustaining therapies were stopped on HD 3.Following serologic diagnosis on postmortem day 12, the public health department was informed and provided surveillance and care instructions to those who potentially shared a common exposure. His mother, who also lived on the farm, developed respiratory symptoms near the end of his hospitalization and was ultimately hospitalized, requiring ICU care. She survived and was discharged home but is still recovering.Hantavirus is an RNA virus transmitted primarily through aerosolized rodent excrement and is most prevalent in rural areas in North and South America.Hantavirus infection is a rare but potentially devastating disease, particularly due to the lack of rapid diagnostic tools and lack of targeted treatments.Recognition of early hematologic clues is important when clinicians suspect hantavirus infection. The presence of diagnostic characteristics on peripheral blood smear: thrombocytopenia, extreme myelocytosis, absent toxic granulation in neutrophils, hemoconcentration, and greater than 10% immunoblasts can be suggestive of infection.HCPS is a clinical syndrome associated with hantavirus and is a result of the inflammatory response elicited by the virus. HCPS is characterized by rapid respiratory failure secondary to pulmonary edema and subsequent cardiac failure often within 24 hours of the onset of shock.HCPS should be suspected in a patient with a prodrome of flu-like illness, possible exposure to wild rodents, and radiographic evidence of pulmonary edema. Clinicians should consider early consultation with infectious disease and critical care colleagues in patients with these characteristics.If HCPS is suspected, appropriate supportive care should be initiated and escalated appropriately. Cardiopulmonary collapse can occur within 24 hours, and ECMO and mechanical ventilation should be available to maximize the possibility of survival as the syndrome progresses.

The AAP continues to recommend RSV antibody for all infants under 8 months born during or entering their first RSV season who are not protected by vaccination of their pregnant parent.