Pulmonary Infarction

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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

Nephrotic syndrome

Cancer

Chemotherapy

Inherited hypercoagulable state

Vasculitis

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.

United States

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. [1] In 1986, Bernstein reported 78 episodes of pulmonary embolism per 100,000 hospitalized adolescents. [2] Unselected autopsy studies in children estimate the incidence of pulmonary embolism from 0.05-3.7%.

International

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. [3] 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. [4] 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. [5] Others, however, have reported pulmonary embolism as a cause of death in fewer than 5% of affected children. [6] 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. [9]

Recurrence

No data are available regarding the risk of recurrence of pulmonary embolism in children.

Complications

Complications of pulmonary embolism include the following:

Death

Hemorrhage

Heparin-induced thrombocytopenia

Thrombophlebitis

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.

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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].

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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].

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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].

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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

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

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

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society

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.

Pulmonary Infarction

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