Loschner first described pediatric pulmonary embolism (PE) in the 1860s. Deep venous thromboses (DVT) and pulmonary emboli are relatively rare phenomena in pediatric practice; however, when they do occur, they are associated with significant morbidity and mortality. Because of the rarity of pulmonary emboli in children, they are probably underdiagnosed. For the same reason, much of the information pertaining to diagnosis and management of pulmonary embolism has been derived from adult practice.
A specific diagnosis that should be mentioned because of its prevalence is sickle cell disease. Prompt recognition and management of pulmonary problems may lead to a decreased rate of pulmonary complications.
Most pulmonary emboli derive from a free-floating thrombus. In rare situations, extension of an existing pulmonary thrombus may result in pulmonary infarction. Many materials and substances may form emboli and move to the pulmonary circulation; these include fat, tumor, septic emboli, air, amniotic fluid, and injected foreign material.
The size of a pulmonary embolism determines at which points in the pulmonary vasculature it lodges. After the embolus lodges, it occludes the vessel, reducing distal blood flow to the area directly supplied by the vessel. The degree of obstruction of the pulmonary circulation directly affects the resulting pathophysiology.
In all cases of pulmonary embolism, ventilation/perfusion (V/Q) mismatch occurs to some degree, in which continued ventilation of lung units without circulation is present. Oxygenation is usually not affected by the V/Q mismatch, in contrast with V/Q mismatch that arises from obstruction of airways and lung parenchyma. Impaired oxygenation in the context of suspected pulmonary embolism implies a massive obstruction.
An increase in effective alveolar dead space is a direct result of the V/Q mismatch. Ventilation (carbon dioxide removal) is usually compensated for by tachypnea.
In cases in which the pulmonary embolus is large, a sudden increase in pulmonary artery pressure may lead to right ventricular strain and right heart failure. A sudden rise in the right ventricular pressure may cause a leftward shift of the intraventricular septum, which may impair left ventricular filling and output (classic obstructive shock).
Reflex bronchoconstriction is often associated with pulmonary embolism. This increases the work of breathing and decreases pulmonary compliance. Pulmonary infarction is also associated with diminished surfactant levels, which may contribute to the increased work of breathing and diminished oxygenation.
Children with pulmonary emboli often have a serious underlying condition that predisposes them to embolus development and may worsen their clinical outcome. Some of the more common underlying conditions include the following:
Sickle cell disease
Inherited hypercoagulable state
In sickle cell disease, an initial trigger (often infection) exacerbated by dehydration (eg, due to fever, tachypnea, or decreased intake) leads to sickling of RBCs within small blood vessels of the lung and other organs. This precipitates a cycle of relative deoxygenation that further exacerbates the sickling tendency, leading to small vessel occlusion and, ultimately, infarction of areas of the pulmonary parenchyma. Allied to this sequence is the tendency of many patients with sickle cell disease to have a component of reactive airways disease, which further decreases oxygenation.
Pulmonary embolism is a rare disorder in pediatric practice. In 1993, David et al identified 308 children reported in the medical literature from 1975-1993 with DVT of an extremity, pulmonary embolism, or both.  In 1986, Bernstein reported 78 episodes of pulmonary embolism per 100,000 hospitalized adolescents.  Unselected autopsy studies in children estimate the incidence of pulmonary embolism from 0.05-3.7%.
Canadian data derived from 15 tertiary care centers show a frequency of 0.86 events per 10,000 pediatric hospital admissions for patients aged 1 month to 1 year.  Frequency of pulmonary embolism in developed countries has been increasing when compared with historical data. This increase in frequency is linked with the increased use of central venous lines in the pediatric population.  The overall frequency is still considerably less than that seen in adults.
Separating mortality attributable to pulmonary embolism from that due to conditions that may be associated with pulmonary embolism, such as trauma and surgery, is difficult.
The data regarding death from pulmonary embolism in children are conflicting. Various authors suggest that pulmonary embolism contributes to the death of affected children in approximately 30% of cases.  Others, however, have reported pulmonary embolism as a cause of death in fewer than 5% of affected children.  As in adults, the mortality rate is highest in the period immediately following embolization. If no major cardiovascular sequelae are present, a full recovery may be anticipated without complications.
Morbidity may include pulmonary hypertension, right ventricular failure and cor pulmonale, paradoxical embolization to the systemic circulation in patients with intracardiac defects, and side effects of medications used to treat pulmonary embolism. [2, 7, 8]
In a case series and literature review of massive pediatric pulmonary embolism, children with massive PE had higher rates of mortality and were more likely to have the PE diagnosed postmortem. 
No data are available regarding the risk of recurrence of pulmonary embolism in children.
Complications of pulmonary embolism include the following:
No data outlining variations in pulmonary embolism prevalence by race are available.
Some authors have reported a female-to-male ratio of 2:1. Others have found that this ratio is reversed.
Given the rarity of pulmonary embolism in childhood, no definitive data identify age as an independent risk factor for pulmonary embolism. The frequency of pulmonary embolism has a bimodal distribution, with peaks in the neonatal period and adolescence.
David M, Andrew M. Venous thromboembolic complications in children. J Pediatr. 1993 Sep. 123(3):337-46. [Medline].
Bernstein D, Coupey S, Schonberg SK. Pulmonary embolism in adolescents. Am J Dis Child. 1986 Jul. 140(7):667-71. [Medline].
Kotsakis A, Cook D, Griffith L, et al. Clinically important venous thromboembolism in pediatric critical care: a Canadian survey. J Crit Care. 2005 Dec. 20(4):373-80. [Medline].
Van Ommen CH, Peters M. Acute pulmonary embolism in childhood. Thromb Res. 2006. 118(1):13-25. [Medline].
Evans DA, Wilmott RW. Pulmonary embolism in children. Pediatr Clin North Am. 1994 Jun. 41(3):569-84. [Medline].
Rajpurkar M, Warrier I, Chitlur M, et al. Pulmonary embolism-experience at a single children’s hospital. Thromb Res. 2007. 119(6):699-703. [Medline].
Babyn PS, Gahunia HK, Massicotte P. Pulmonary thromboembolism in children. Pediatr Radiol. 2005 Mar. 35(3):258-74. [Medline].
Cook A, Shackford S, Osler T, et al. Use of vena cava filters in pediatric trauma patients: data from the National Trauma Data Bank. J Trauma. 2005 Nov. 59(5):1114-20. [Medline].
Baird JS, Killinger JS, Kalkbrenner KJ, Bye MR, Schleien CL. Massive pulmonary embolism in children. J Pediatr. 2010 Jan. 156(1):148-51. [Medline].
Biss TT, Brandao LR, Kahr WH, Chan AK, Williams S. Clinical features and outcome of pulmonary embolism in children. Br J Haematol. 2008 Jun 17. [Medline].
Vichinsky EP, Neumayr LD, Earles AN, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. N Engl J Med. 2000 Jun 22. 342(25):1855-65. [Medline].
van den Heuvel-Eibrink MM, Lankhorst B, Egeler RM, Corel LJ, Kollen WJ. Sudden death due to pulmonary embolism as presenting symptom of renal tumors. Pediatr Blood Cancer. 2008 May. 50(5):1062-4. [Medline].
Dollery CM. Pulmonary embolism in parenteral nutrition. Arch Dis Child. 1996 Feb. 74(2):95-8. [Medline].
Nuss R, Hays T, Chudgar U, Manco-Johnson M. Antiphospholipid antibodies and coagulation regulatory protein abnormalities in children with pulmonary emboli. J Pediatr Hematol Oncol. 1997 May-Jun. 19(3):202-7. [Medline].
Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct. 132(4):663-7. [Medline].
Lee EY, Tse SK, Zurakowski D, et al. Children suspected of having pulmonary embolism: multidetector CT pulmonary angiography–thromboembolic risk factors and implications for appropriate use. Radiology. 2012 Jan. 262(1):242-51. [Medline].
Lee EY, Zurakowski D, Boiselle PM. Pulmonary embolism in pediatric patients survey of CT pulmonary angiography practices and policies. Acad Radiol. 2010 Dec. 17(12):1543-9. [Medline].
The PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA. 1990 May 23-30. 263(20):2753-9. [Medline].
Revel MP, Sanchez O, Couchon S, et al. Diagnostic accuracy of magnetic resonance imaging for an acute pulmonary embolism: results of the ‘IRM-EP’ study. J Thromb Haemost. 2012 May. 10(5):743-50. [Medline].
Goldenberg NA, Durham JD, Knapp-Clevenger R, Manco-Johnson MJ. A thrombolytic regimen for high-risk deep venous thrombosis may substantially reduce the risk of postthrombotic syndrome in children. Blood. 2007 Jul 1. 110(1):45-53. [Medline].
Raffini L, Cahill AM, Hellinger J, Manno C. A prospective observational study of IVC filters in pediatric patients. Pediatr Blood Cancer. 2008 Jun 16. [Medline].
Hull RD, Raskob GE, Brant RF, et al. Low-molecular-weight heparin vs heparin in the treatment of patients with pulmonary embolism. American-Canadian Thrombosis Study Group. Arch Intern Med. 2000 Jan 24. 160(2):229-36. [Medline].
Faustino EV, Patel S, Thiagarajan RR, Cook DJ, Northrup V, Randolph AG. Survey of pharmacologic thromboprophylaxis in critically ill children. Crit Care Med. 2011 Jul. 39(7):1773-8. [Medline]. [Full Text].
Baird JS, Greene A, Schleien CL. Massive pulmonary embolus without hypoxemia. Pediatr Crit Care Med. 2005 Sep. 6(5):602-3. [Medline].
Beitzke A, Zobel G, Zenz W, et al. Catheter-directed thrombolysis with recombinant tissue plasminogen activator for acute pulmonary embolism after fontan operation. Pediatr Cardiol. 1996 Nov-Dec. 17(6):410-2. [Medline].
Brandao LR, Labarque V, Diab Y, Williams S, Manson DE. Pulmonary embolism in children. Semin Thromb Hemost. 2011 Oct. 37(7):772-85. [Medline].
Kossel H, Bartsch H, Philippi W, et al. Pulmonary embolism and myocardial hypoxia during extracorporeal membrane oxygenation. J Pediatr Surg. 1999 Mar. 34(3):485-7. [Medline].
Kossoff EH, Poirier MP. Peripherally inserted central venous catheter fracture and embolization to the lung. Pediatr Emerg Care. 1998 Dec. 14(6):403-5. [Medline].
Macartney CA, Chan AK. Thrombosis in children. Semin Thromb Hemost. 2011 Oct. 37(7):763-1. [Medline].
McCrory MC, Brady KM, Takemoto C, Tobias JD, Easley RB. Thrombotic disease in critically ill children. Pediatr Crit Care Med. 2010 Feb 11. [Medline].
Monagle P, Chan A, DeVeber G. Andrew’s Pediatric Thromboembolism and Stroke. 3rd ed. Ontario, Canada; BC Decker: 2006.
Sandoval JA, Sheehan MP, Stonerock CE, Shafique S, Rescorla FJ, Dalsing MC. Incidence, risk factors, and treatment patterns for deep venous thrombosis in hospitalized children: an increasing population at risk. J Vasc Surg. 2008 Apr. 47(4):837-43. [Medline].
Tay ET, Stone MB, Tsung JW. Emergency ultrasound diagnosis of deep venous thrombosis in the pediatric emergency department: a case series. Pediatr Emerg Care. 2012 Jan. 28(1):90-5. [Medline].
Truitt AK, Sorrells DL, Halvorson E, et al. Pulmonary embolism: which pediatric trauma patients are at risk?. J Pediatr Surg. 2005 Jan. 40(1):124-7. [Medline].
Lennox H Huang, MD, FAAP Chief Medical Officer, The Hospital for Sick Children; Associate Professor of Pediatrics, University of Toronto Faculty of Medicine; Associate Clinical Professor of Pediatrics, McMaster University School of Medicine, Canada
Lennox H Huang, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children’s Medical Center
Disclosure: Nothing to disclose.
Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women’s and Children’s Hospital of Buffalo
Disclosure: Nothing to disclose.
G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children’s Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children’s Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2
G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society
Disclosure: Nothing to disclose.
Research & References of Pulmonary Infarction|A&C Accounting And Tax Services