Pediatrics

Tuberculous Pleural Effusion

CASE

A 7 year-old girl presents to a hospital in Lilongwe, Malawi with worsening tactile fevers, shortness of breath, and productive cough over the past week. Her mother reports subjective weight loss, but denies night sweats, hemoptysis, or a significant respiratory history.

The patient’s vital signs were significant for a temperature of 100.6 F, pulse of 69, blood pressure of 107/72, tachypnea to 33, and hypoxia to 87% on room air. Her physical exam was notable for diminished breath sounds throughout the right side. An x-ray was performed revealing a large right-sided pleural effusion (Figure 1). A bedside ultrasound was then performed, showing a loculated pleural effusion (Figure 2). The patient underwent a therapeutic and diagnostic thoracentesis, returning straw colored fluid. In addition to standard pleural fluid studies, the patient’s fluid was also sent for Xpert MTB/RIF nucleic acid amplification test given the high prevalence of tuberculosis in the region, eventually returning a confirmatory diagnosis of Mycobacterium tuberculosis

Figure 1. Chest x-ray of a 7 year-old girl presenting with worsening shortness of breath, productive cough, and subjective fevers, found to have a large right-sided pleural effusion.

Figure 1. Chest x-ray of a 7 year-old girl presenting with worsening shortness of breath, productive cough, and subjective fevers, found to have a large right-sided pleural effusion.

Figure 2. Still image of a point-of-care ultrasound performed on a 7 year-old girl with a large right-sided pleural effusion, showing a loculated pleural effusion.

Figure 2. Still image of a point-of-care ultrasound performed on a 7 year-old girl with a large right-sided pleural effusion, showing a loculated pleural effusion.

 FINAL DIAGNOSIS

Tuberculous pleural effusion

 

CLINICAL PRESENTATION

The classic chest x-ray findings of primary pulmonary tuberculosis (TB) are parenchymal consolidation with or without hilar lymphadenopathy. Tuberculous pleural effusion (also known as tuberculous pleurisy) is the second most common form of extrapulmonary TB (after lymphatic involvement) (Figure 3), and is the most common cause of pleural effusions in TB endemic regions.[1] In children, tuberculous pleural effusion most often occur in the setting of primary TB,[2] whereas in adults they occur most frequently due to reactivation disease.[3] Patients typically present with an acute febrile illness with nonproductive cough and pleuritic chest pain, though dyspnea, night sweats, and weight loss can also occur. Most tuberculous pleural effusions are unilateral and, in contrast to our patient, small to moderate in size.[4] On chest x-ray, pleural disease is often appreciated.[5] Loculation of pleural effusions is not uncommon in tuberculous pleural effusion, and is thought to be due to direct pleural infection and the resulting intense intra-pleural inflammation and organization.[6]

Figure 3. Common sites of extrapulmonary TB.

Figure 3. Common sites of extrapulmonary TB.

 

DIAGNOSIS

 Tuberculous pleural effusion should be suspected in patients with pleural effusion and TB risk factors including history of TB infection, TB exposure, or time spent in TB endemic regions. Unfortunately, definitive diagnosis of tuberculous pleural effusion can be challenging. Tuberculin skin test and interferon-gamma release assays do not distinguish between latent tuberculosis infection and active tuberculosis disease, and thus cannot be used for definitive diagnosis. The gold standard of diagnosis remains demonstration of M. tuberculosis in pleural fluid or pleural biopsy specimen.[4] Presumptive diagnosis can reasonably be made in patients with a known history of pulmonary TB and a pleural effusion without any alternative cause.

In the undifferentiated patient, a workup for pulmonary TB should be initiated including sputum smear and culture for acid-fast bacilli (AFB). Next, a diagnostic thoracentesis can be performed. Pleural fluid from tuberculous pleural effusion is typically an exudative, lymphocyte-predominant pleural effusion, and should be sent for smear and culture for AFB, though cultures are positive in less than 30% of HIV-uninfected patients,[4] and only approximately 50% of HIV-infected patients with CD4 counts less than 100 cells/mm3 (a higher sensitivity due to the greater bacterial burden).[7] Pleural fluid should also be sent for analysis, with typical findings shown in Table 1. 

Laboratory test Typical finding
Color Straw colored(14)
Protein concentration >3.0 g/dL(15)
LDH >500 international units/L(15)
pH <7.4
Glucose 60-100 mg/dL(15)
ADA >40 units/L
Cell count 1,000-6,000 cells/mm^3.(16)
Early neutrophil predominance. After the
first few days, lymphocytes predominate.(15)
Table 1. Pleural fluid findings typical for tuberculous pleural effusion.

 A presumptive diagnosis can be made if there is a lymphocytic-to-neutrophil ratio >0.75 and ADA >40 units/L.[8-10] While nucleic acid amplification (NAA) tests for M. tuberculosis that are FDA-approved for use with sputum have not yet been approved for pleural fluid in the United States, some laboratories use NAA testing of pleural fluid as a validated, "off-label" application. If the patient still remains undifferentiated after this testing and there is concern for the medically complex patient or suspected drug resistance, a pleural biopsy can be pursued by thoracoscopy or closed percutaneous needle biopsy with resulting tissue sample sent for AFB smear and culture as well as histopathology for evaluation of granulomas. Additionally, all patients with suspected tuberculous pleural effusions should be tested for HIV infection.

 

TREATMENT

The mainstay of treatment of tuberculous pleural effusion is antituberculosis therapy, the same as active pulmonary tuberculosis. A typical drug regimen consists of isoniazid, rifampin, pyrazinamide, and ethambutol for 8 weeks, followed by isoniazid and rifampin for an additional 18 weeks. Empiric antituberculous therapy is warranted if a presumptive diagnosis is made as described above, and patients typically defervesce within two weeks and pleural fluid is resorbed within six weeks. However, some patients take up to two months to defervesce with fluid resorption taking up to four months. In areas with high rates of antituberculous drug resistance, organism isolation is more critical as it can guide drug selection. Currently, corticosteroids are not recommended as an adjuvant therapy as there is insufficient evidence for benefit.[11] Therapeutic thoracentesis can be considered in patients with larger pleural effusions or significant dyspnea, as it has been shown to more quickly resolve dyspnea, though there is no effect on long-term outcomes.[12,13]

 

DISPOSITION AND CASE CONCLUSION

Empiric antituberculosis therapy was initiated after thoracentesis, with resulting clinical improvement.  The patient was soon thereafter discharged to complete the remainder of her antituberculosis therapy through a directly observed therapy (DOT) program and was doing well at her follow up visit.

 

TEACHING POINTS

  • Tuberculosis is the most common cause of pleural effusions in endemic regions.

  • The gold standard of diagnosis is demonstration of M. tuberculosis in pleural fluid or pleural biopsy specimen.

  • A presumptive diagnosis can be made if pleural fluid shows a lymphocytic-to-neutrophil ratio >0.75 and ADA >40 units/L.

  • Treatment of tuberculous pleural effusions is the same as for pulmonary tuberculosis.


Faculty Reviewer: Dr. Lauren Allister

 


REFERENCES

  1.  Zhai, K, Lu, Y, Shi, HZ. Tuberculous pleural effusion. J Thorac Dis 2016;8:E486-94.

  2. Merino, JM, Carpintero, I, Alvarez, T, Rodrigo, J, Sanchez, J, Coello, JM. Tuberculous pleural effusion in children. Chest 1999;115:26-30.

  3. Torgersen, J, Dorman, SE, Baruch, N, Hooper, N, Cronin, W. Molecular epidemiology of pleural and other extrapulmonary tuberculosis: a Maryland state review. Clin Infect Dis 2006;42:1375-82.

  4. Gopi, A, Madhavan, SM, Sharma, SK, Sahn, SA. Diagnosis and treatment of tuberculous pleural effusion in 2006. Chest 2007;131:880-9.

  5. Seibert, AF, Haynes, J, Jr., Middleton, R, Bass, JB, Jr. Tuberculous pleural effusion. Twenty-year experience. Chest 1991;99:883-6.

  6. Ko, Y, Kim, C, Chang, B, Lee, SY, Park, SY, Mo, EK, et al. Loculated Tuberculous Pleural Effusion: Easily Identifiable and Clinically Useful Predictor of Positive Mycobacterial Culture from Pleural Fluid. Tuberc Respir Dis (Seoul) 2017;80:35-44.

  7. Gil, V, Cordero, PJ, Greses, JV, Soler, JJ. Pleural tuberculosis in HIV-infected patients. Chest 1995;107:1775-6.

  8. Light, RW. Update on tuberculous pleural effusion. Respirology 2010;15:451-8.

  9. Sahn, SA, Huggins, JT, San Jose, ME, Alvarez-Dobano, JM, Valdes, L. Can tuberculous pleural effusions be diagnosed by pleural fluid analysis alone? Int J Tuberc Lung Dis 2013;17:787-93.

  10. Jimenez Castro, D, Diaz Nuevo, G, Perez-Rodriguez, E, Light, RW. Diagnostic value of adenosine deaminase in nontuberculous lymphocytic pleural effusions. Eur Respir J 2003;21:220-4.

  11. Ryan, H, Yoo, J, Darsini, P. Corticosteroids for tuberculous pleurisy. Cochrane Database Syst Rev 2017;3:CD001876.

  12. Bhuniya, S, Arunabha, DC, Choudhury, S, Saha, I, Roy, TS, Saha, M. Role of therapeutic thoracentesis in tuberculous pleural effusion. Ann Thorac Med 2012;7:215-9.

  13. Lai, YF, Chao, TY, Wang, YH, Lin, AS. Pigtail drainage in the treatment of tuberculous pleural effusions: a randomised study. Thorax 2003;58:149-51.

  14. Levine, H, Metzger, W, Lacera, D, Kay, L. Diagnosis of tuberculous pleurisy by culture of pleural biopsy specimen. Arch Intern Med 1970;126:269-71.

  15. Epstein, DM, Kline, LR, Albelda, SM, Miller, WT. Tuberculous pleural effusions. Chest 1987;91:106-9.

  16. Valdes, L, Alvarez, D, San Jose, E, Penela, P, Valle, JM, Garcia-Pazos, JM, et al. Tuberculous pleurisy: a study of 254 patients. Arch Intern Med 1998;158:2017-21.

FPIES: Expanding the Differential for Hypotension in the Pediatric Patient

CASE

An 8-month-old male, full term, infant with no significant past medical history presents to the ED for nausea, vomiting, and non-bloody diarrhea for the past several hours. His family has slowly been introducing new foods into his diet. There are no known sick contacts. He is well-appearing, hemodynamically stable, and tolerating PO in the ED. After some observation, the patient was discharged with the diagnosis of viral gastroenteritis.

Six days later, the same patient presented with profuse vomiting, diarrhea, and profound lethargy. He was found to be tachycardic and hypotensive. He was taken to the critical care area for altered mental status, unstable vital signs, and undifferentiated shock. His exam was notable for lethargy, pallor, and a distended abdomen. Initial labs showed a metabolic acidosis, eosinophilia, and thrombocytosis. Stool studies and UA were unrevealing. Abdominal plain films were normal.

DISCUSSION

FPIES - What is it?

As many ED practitioners are aware, food allergies are common in the first 2 years of life, with a prevalence cited between 1-10% of the population. Most food allergies are IgE-mediated hypersensitivity reactions. Food protein-induced enterocolitis (FPIES) is a syndrome characterized by a severe non-IgE mediated food hypersensitivity reaction. FPIES is important to keep on the differential as the syndrome often goes unrecognized or is misdiagnosed at the initial (or subsequent) presentation. (1)

FPIES is characterized by profound and repetitive vomiting, and occasionally diarrhea, 1-4 hours after exposure to the causal protein. In the acute setting, this can manifest as dehydration and lethargy. More than 15% of FPIES patients will require admission for hemodynamic instability secondary to dehydration. In the chronic setting, pediatric patients can present as failure to thrive and/or unexplained weight loss. The most common food triggers in FPIES are cow milk's and soy. FPIES may be induced by solid food, including grains, meat and poultry, eggs, vegetables and fruit, seafood, and legumes. (1,3)

Though the underlying mechanism of FPIES is not clearly understood, it differs from other allergen mediated reactions as it is not triggered by an (IgE)-mediated hypersensitivity. Preliminary research indicates that there is inflammation within the lamina propria and epithelium in both the small and large intestine secondary to increased tumor necrosis factor-alpha (TNF-α) expression by activated T cells. Downstream, this causes increased intestinal permeability which contributes to pathogenesis of FPIES. (4, 8)

Figure A.

Figure A.

CLINICAL FEATURES

Patients with acute presentations tend to be sicker and may develop pallor, hypotension/shock, and/or hypothermia. Failure to thrive and weight loss are seen in patients with chronic FPIES.

  • Lethargy (70%)

  • Pallor (70%)

  • Dehydration

  • Hypotension (15%)

  • Hypothermia (25%)

  • Abdominal distension

LAB AND IMAGING FINDINGS

Labs often reveal anemia, hypoalbuminemia, and an elevated white blood cell count with a left shift. Eosinophilia is often seen in chronic FPIES. Thrombocytosis was found in 65 percent of acute FPIES. Metabolic acidosis (mean pH 7.03) and methemoglobinemia have been reported in both acute and chronic FPIES. Transient methemoglobinemia was reported in about one-third of acute FPIES infants with some requiring methylene blue treatment. Methemoglobinemia may be caused by severe intestinal inflammation and reduced catalase activity resulting in increased nitrites. (5)

Diagnostic imaging studies are not part of the standard FPIES workup, but some older studies have analyzed trends. Although findings are nonspecific, it is important to be familiar with them as often these infants get imaging as part of their workup.

Findings include:

  • Air fluid levels

  • Nonspecific narrowing and thumb-printing of rectum and sigmoid colon

  • Thickening of plicae circulares in duodenum and jejunum

  • Excess luminal fluid

  • Rarely intramural gas (which can lead to misdiagnosis of NEC)

Resolution of radiographic abnormalities after dietary restriction has been documented. (1, 3, 5)

THE DIFFERENTIAL: HOW DO THEY DIFFER?

Given the clinical picture of FPIES is nonspecific, the ED physician can arrive at the diagnosis more quickly by obtaining a brief dietary history. This especially holds true if the patient has been seen multiple times in the ED prior for similar complaints. In infants, the causes of acute repetitive vomiting and severely altered mental status includes a broad differential diagnosis. Sepsis, infectious gastroenteritis, head injury, toxicologic, gut malrotation, intussusception, NEC, pyloric stenosis, as well as other metabolic and cardiogenic causes can present similarly. In patients with such symptoms, allergy as a cause is sometimes not considered by ED physicians. Diagnosis of FPIES is based on the recognition of clinical manifestations, exclusion of alternative causes, and a physician-supervised oral food challenge (OFC). Diagnosis is often made in the inpatient or primary care setting, and is based on presence of a major criterion as well as three minor criteria as seen below.

Below are some quick and dirty rules to differentiate FPIES from other diagnoses:

Food protein-induced proctocolitis: Infants are well-appearing and thriving, unlike acute FPIES children. Present with blood streaked stools in first months of life.

Anaphylaxis: Time to symptoms is much shorter (usually minutes vs. 2-4 hours). Have constellation of associated symptoms not seen in FPIES: rash, respiratory distress/stridor. Symptoms resolve with IM epinephrine.

Infections/Sepsis: Usually present febrile (or less often hypothermic) and often with a history of sick contacts. Labs showing leukocytosis with a left shift/bandemia (vs eosinophilia in FPIES). There may be a presence of respiratory symptoms if sepsis 2/2 to PNA, viral URI. Septic patients typically do not improve with IVF alone (unlike FPIES patients).

Necrotizing enterocolitis: Systemic and abdominal symptoms seen in NEC that are not typical of FPIES include apnea, respiratory failure, temperature instability, intramural gas on abdominal radiograph. NEC is usually at a much earlier age, and often within the first few days of life.

Intestinal obstruction: There are reports of ex-laps being performed when acute FPIES was mistaken for ileus. Obstruction often presents with more pronounced distention and history of decreased to no stool output (FPIES infants can have normal stool output and/or diarrhea).

Intussusception: While the classic teaching is currant jelly stools, this is rarely present. Vomiting/discomfort waxing and waning over protracted period of time, and pain may be more predominant.

Pyloric Stenosis: Usually between 2 weeks and 2 months of life before the introduction of solid foods. There may be an olive-shaped mass in epigastrium, and ultrasound confirms the diagnosis.

Metabolic disorders: May have other features, such as hypoglycemia, hematologic abnormalities (ex, anemia, neutropenia, thrombocytopenia), liver dysfunction (hepatomegaly, jaundice), renal disease, and developmental delay.

Data shows that of FPIES patients presenting to the ED, 34% of patients undergoing abdominal imaging, 28% undergoing a septic evaluation, and 22% having a surgical consultation. Misdiagnosis and delays in diagnosis for children with food protein-induced enterocolitis syndrome were common, leading many children to undergo unnecessary investigations. (6, 7, 9)

DISPOSITION AND CASE CONCLUSION

The patient mentioned in the case earlier was subsequently admitted to the PICU for further workup and resuscitation. After many diagnoses were ruled out, and in conjunction with thorough dietary review, it was found that the patient had both of these episodes after exposure to sweet potato. The diagnoses of FPIES was made and patient was discharged to home in good health with rheumatology follow up.

For acute presentations, patients often require admission for fluid resuscitation, symptom management, and parent education. For chronic FPIES patients, it is sometimes reasonable to discharge patient to home, but this should always be done in conjunction with primary care doctor as well as expectant management and education. Often times, labs can be drawn in the emergency setting as a conduit to help the patient’s PCP rule out other causes (such as IgE-mediated allergies). (2, 3)

Faculty Reviewer: Dr. Jane Preotle

 

REFERENCES

  1. Nowak-Węgrzyn A, Katz Y, Mehr SS, Koletzko S. Non-IgE-mediated gastrointestinal food allergy. J Allergy Clin Immunol 2015; 135:1114.

  2. Nowak-Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein-induced enterocolitis syndrome: Executive summary-Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol 2017; 139:1111.

  3. Mehr S, Kakakios A, Frith K, Kemp AS. Food protein-induced enterocolitis syndrome: 16-year experience. Pediatrics 2009; 123:e459.

  4. Caubet JC, Nowak-Węgrzyn A. Current understanding of the immune mechanisms of food protein-induced enterocolitis syndrome. Expert Rev Clin Immunol 2011; 7:317.

  5. Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein-induced enterocolitis syndrome. J Pediatr 1998; 133:214.

  6. Ruffner MA, Ruymann K, Barni S, et al. Food protein-induced enterocolitis syndrome: insights from review of a large referral population. J Allergy Clin Immunol Pract 2013; 1:343.

  7. Coates RW, Weaver KR, Lloyd R, et al. Food protein-induced enterocolitis syndrome as a cause for infant hypotension. West J Emerg Med 2011; 12:512.

  8. Sampson HA, Anderson JA. Summary and recommendations: Classification of gastrointestinal manifestations due to immunologic reactions to foods in infants and young children. J Pediatr Gastroenterol Nutr 2000; 30 Suppl:S87.

  9. Jayasooriya S, Fox AT, Murch SH. Do not laparotomize food-protein-induced enterocolitis syndrome. Pediatr Emerg Care 2007; 23:173.

  10. Figure A: Berin, M. Cecilia. Immunopathophysiology of food protein-induced enterocolitis syndrome. Journal of Allergy and Clinical Immunology, Volume 135. Issue5. 1108-1113

Hey Kiddo, Take a Seat…

Case 1:

A 13-month-old boy arrives by EMS after a motor vehicle accident. He was a rear passenger, restrained in a front-facing car seat when the vehicle struck a utility pole at high speed. Initially, he was responsive and crying, but became unresponsive and lost vital signs en-route to the ED. In the trauma bay, ROSC is achieved after a brief period of CPR and airway management. His imaging is notable for significant fractures at C1/C2 as well as complex ligamentous disruption; he requires emergent surgical intervention for his spinal injuries, and suffers a severe anoxic brain injury.

Case 2:

Two boys, a 4-month-old and a 3-year-old, arrive by EMS after a low speed, T-bone motor vehicle accident with airbag deployment. Both patients were restrained rear passengers, the 4-month-old in a rear-facing seat, and the 3-year-old in a front-facing seat. In the ED, exam is significant only for some mild abrasions, and both are discharged after a period of observation. The car seats involved in the accident are brought to the ED, and family attempts to use them to transport the children home.

Case 3:

A 5-year-old girl arrives by EMS unresponsive after a front-end collision. She was restrained in her front-facing car seat, when the vehicle struck a telephone pole. Per EMS providers, the seat was not properly restrained within the vehicle. She is apneic with obvious, severe head injuries and asymmetric pupils, with imaging confirming multiple skull fractures and intracranial hemorrhage. Despite maximal interventions, she succumbs to her injuries.

 

Case 4:

A new mother brings her 31-day-old infant for evaluation of vomiting. An exam is performed and is reassuring, consistent with likely reflux, and she is discharged home with close pediatrician follow up in the coming days. On the way out of the exam room, she asks if her car seat is safe to use, as it was a hand-me-down from another family member, and she is not sure if this seat is “expired.”

The Facts:

Unintentional injuries remain a leading cause of death in children. While the number of fatalities from motor vehicle collisions has declined, it remains the cause of death in 1 out of 4 children ages 1-13 [1]. Car safety seats (CSS) have been demonstrated to reduce the risk of injury and death in children, and are credited with saving the lives of 328 children under age 4 in 2016 [2]. Currently, laws exist in all 50 states and Washington D.C. governing the use of child safety seats. The use of car safety seats has been well studied by multiple agencies, including the National Highway Traffic Safety Administration, the Center for Disease Control and Prevention, the Insurance Institute for Highway Safety, and the American Academy of Pediatrics.

We have a duty to our pediatric patients and their families to be familiar with the current recommendations for car safety seats, and provide education and resources when necessary to help prevent morbidity and mortality. In two of the above cases, provider knowledge about these recommendations is critical, and allows rapid intervention on discharge to prevent possible further injuries. As unfortunately common to practitioners in the emergency department, the remaining two cases help reinforce the need for a high index of suspicion for injuries when children present with a history consistent with improper restraint.

 

Current Recommendations [3,10]:

The American Academy of Pediatrics recently released a policy statement published November 2018, highlighting the current recommendations for child safety seats. A summary of recommendations along with a useful flow chart is shown below*:

  • All infants and toddlers should ride in a rear-facing car seat as long as possible, until they reach the height or weight limit listed by the car seat manufacturer

    • It is important to check which type of seat is used rear-facing: infant-only seats have a much lower height and weight limit than convertible or 3-in-1 car seats

  • All children that have outgrown the height or weight limit on a rear-facing seat should ride in a forward-facing seat with a harness until they reach the height/weight limit listed by the manufacturer

  • When children outgrow the height or weight limit of a forward-facing seat, they should use a booster seat until the vehicle lap and shoulder belt fits appropriately, typically when they reach a height of 4 feet 9 inches, and between the age of 8-12

  • When children are old/tall enough to use the vehicle seat belt alone, they should always use both a lap and shoulder belt

  • All children under age 13 should remain restrained in the back seat for optimal protection

*Modified from Table 1: Summary of Best Practice Recommendations, Durbin and Hoffman, Pediatrics, Vol 145 No 5, November 2018

Algorithm to guide implementation of best practice recommendations for optimal child passenger safety:

From: Durbin and Hoffman,  Pediatrics,  Vol 145 No 5, November 2018

From: Durbin and Hoffman, Pediatrics, Vol 145 No 5, November 2018

For the visual learners, the CDC has a graphical representation of the seats with corresponding ages[9]:

Picture2.png

In Rhode Island, specific laws were enacted in 2017, outlining the proper restraint of passengers in vehicles, including children, with a pertinent summary below [4]:

  • All children under age 8, less than 57 inches in height (4 feet 9 inches), and less than 80 pounds should be restrained in a rear sitting position in an approved child restraint system

  • All infants and toddlers less than 2 years of age, or weighing less than 30 pounds, should be restrained in a rear-facing car seat

  • All children 2 years of age or older who outgrow rear-facing car seats should use a forward-facing car seat with harness, up to the maximum allowed by the car seat manufacturer

Frequently Asked Questions:

I have a car seat and am not sure it is installed properly, or am expecting a new baby and not sure how to install my car seat. Where can I go to make sure this is done correctly?

  • There are several options to ensure a child safety seat is installed correctly. The easiest way to do this is to simply search through the National Child Passenger Safety Certification webpage, listed below for a car seat check station. Several options exist, including locating a local agency that will perform a car seat check/installation teaching (most often a local police or fire department), attending a child safety event, or locating a specific inspection station not included in the above [5]. Many children’s hospitals, such as Hasbro Children’s Hospital, also have staff certified for safe car seat installation.

I received a car seat as a hand-me down from another family member, but heard car seats expire. Is this true, and how can I tell if this seat is okay?

  • This is an important, sometimes overlooked fact of child safety seats. While both vehicle and car seat technology have dramatically improved the safety of children riding in vehicles, there are limitations of the seats. Most car seats carry an expiration date 6 years after the manufacture date (although this may vary slightly based on seat construction) [6]. The primary reason for this is the wear and tear placed on the seats themselves, including temperature variation, spills, and physical wear from use of the seat. It is also important to recognize that new technology is continually being produced, which quickly makes older seats less superior in safety. Find the label on the child’s seat, which will list both the manufacture date and expiration date. An example of a label can be found below, as seen in a blog post about this topic from Cincinnati Children’s Hospital [7]:

Picture3.png
  • An additional checklist is provided in the “Additional Resources” section below that should be reviewed before purchasing, and using a used car seat

My child was involved in a car accident in a car seat. Is this seat safe to use after the accident?

  • The National Highway Traffic Safety Administration has some guidelines for when a car seat should be replaced. In cases of minor accidents, a car seat does not necessarily have to be replaced, but the accident must meet all of the following criteria [8]:

    • Vehicle was driven away from crash site

    • Vehicle door nearest car seat was not damaged

    • No passengers in the vehicle sustained injuries

    • No airbag deployment in the vehicle

    • The car seat has no obvious damage

  • If there is any doubt about the severity of the accident, or of the integrity of the car seat, the safest option is to replace the seat

Is there anything else I should do after purchasing a car seat to help ensure it remains up-to-date?

  • Like all new technology, product failures sometimes happen, requiring replacement parts or adjustments. After purchasing a car seat, it is important to register the seat with the appropriate manufacturer to ensure prompt notification of any recall notices in a timely manner. Most manufacturers provide a card that can be submitted, which can also be done online through the specific manufacturer’s page, or using the finder link on the National Highway Traffic Safety Administration website.

Additional Resources:

 

* A special thank you to the providers, nurses, staff, and most importantly, patients/families at Hasbro Children’s Hospital, and to my faculty reviewer, Dr. Jane Preotle

Faculty Reviewer: Jane Preotle, MD

References:

  1. Insurance Institute for Highway Safety, Highway Loss Data Institute, accessed at: https://www.iihs.org/iihs/topics/t/child-safety/fatalityfacts/child-safety, posted December 2017.

  2. US Department of Transportation, National Highway Traffic Safety Administration, “Quick Facts 2016”, accessed at: https://crashstats.nhtsa.dot.gov/Api/Public/ViewPublication/812451

  3. Durbin, DR, Hoffman, BD; “Child Passenger Safety”, AAP Council on Injury, Violence, and Poison Prevention Policy Statement, Pediatrics, Volume 142, No. 5, November 2018

  4. Rhode Island State Police, Department of Public Safety, “Seat belt laws and car seat recommendations”, accessed at: http://risp.ri.gov/safety/vehiclesafety/seatbelts.php

  5. National Child Passenger Safety Certification webpage, accessed at: https://cert.safekids.org/get-car-seat-checked

  6. National Safety Commission Alert, published October 2011, accessed at: http://alerts.nationalsafetycommission.com/2011/10/child-safety-seats-have-expiration-date.html

  7. Cincinnati Children’s Blog, “Car seat expiration dates: have you checked yours?”, published online June 22, 2015, accessed at: https://blog.cincinnatichildrens.org/safety-and-prevention/car-seat-expiration-dates-have-you-checked-yours/

  8. National Highway Traffic Safety Administration, “Car seat use after a crash”, accessed at: https://www.nhtsa.gov/car-seats-and-booster-seats/car-seat-use-after-crash

  9. Centers for Disease Control and Prevention, Child  Passenger Safety summary page, accessed at: https://www.cdc.gov/features/passengersafety/index.html

  10. Car Seats: Information for Families, accessed at: https://www.healthychildren.org/English/safety-prevention/on-the-go/Pages/Car-Safety-Seats-Information-for-Families.aspx