Pulmonary Infarction

Article Author:
Alec Emerling
Article Editor:
Jeffrey Cook
Updated:
12/19/2018 12:05:44 PM
PubMed Link:
Pulmonary Infarction

Introduction

Pulmonary infarction (PI) is usually a complication of another primary disease state, most commonly pulmonary embolism (PE). Understanding the broad differential diagnosis associated with PI is important, as associated signs and symptoms have limited specificity and PI may be the first indication of significant underlying pathology.

Etiology

During several prospective and retrospective studies, researchers have investigated the prevalence of PI in association with PE, which is the most common etiology for the development of an infarction.[1][2][3][4] Other disease states which can lead to pulmonary infarction include infection,[5] malignancy,[6] surgical iatrogenesis,[4][7] amyloidosis, sickle cell disease,[8] vasculitis,[9] among others.

Smoking is a risk factor for all causes of PI including those associated with PE.[4][10] Young age is associated with an increased likelihood while obesity is associated with a reduced likelihood of developing a PI in patients with PE.[1][2]

Early literature suggested that patients with underlying cardiac disease are at greatest risk for developing a pulmonary infarction.[11][12] Healthcare professionals hypothesize this to be due to poor collateral circulation, which in combination with pulmonary thromboembolism resulted in infarction. However, recent literature suggests the opposite is true. Specifically, younger patients without cardiopulmonary disease were found to be more likely to suffer a PI secondary to a PE.[2] The authors of this study hypothesized longstanding local tissue hypoxia from chronic cardiopulmonary disease states led to the development of more robust vascular collateralization which protected parenchyma from infarction.

Epidemiology

The incidence of pulmonary embolism is approximately 1 in 1000.[13] In one study, the 30-day mortality for patients found to have a PE was 31% and the mortality ratio in the first decade after developing a PE was 41%.[14] Pulmonary emboli are complicated by pulmonary infarction at a rate of 16% to 31%.[1][2] Studies evaluating hospital length-of-stay and mortality suggest similar prognosis for both pulmonary embolism with infarction and PE without radiographic evidence of infarction.[2][3]

Pathophysiology

Lung parenchyma receives its oxygen supply from three non-redundant sources: deoxygenated blood from pulmonary arteries, oxygenated blood from the bronchial circulation, and direct oxygen diffusion from alveoli.[12] Sufficient impedance of these sources can cause infarction and subsequent tissue necrosis. Inflammatory mediators from ischemic parenchyma limit gas exchange following vasoconstriction and bronchoconstriction.[15] When ischemia of lung tissue is not reversed infarction ensues. A unilateral infarct occurs in 77% to 87% of PI, with the strongest predilection for the right lower lobe. Multiple studies show a stark predominance of PI in the lower lobes relative to the upper lobes.[1][2][16] This has been hypothesized to be due to the gravity’s influence on the unique relationship between alveolar pressure, pulmonary arterial pressure, and bronchial arterial pressure.[2]

In patients with sickle cell disease, acute chest syndrome was found to be caused by vascular infarction by direct occlusion of sickle-type hemoglobin (HbS) in 16% of cases.[17] Vasculitides may result in a PI through antibody deposition, the formation of microaneurysms, or macrophage activation leading to vessel wall inflammation.[18] Regardless of the primary etiology, the common end pathway is ischemic lung tissue.

Histopathology

Infarction of a thromboembolic etiology is characterized by organized thrombi and hemorrhage surrounding a core of necrotic alveoli with adjacent structures.[6] The combination of a neutrophilic reaction with a microbiological culture growing a specific organism indicates an infectious etiology.[4]

History and Physical

Given pulmonary embolism serves as the etiology of pulmonary infarction in most cases, it is important to understand the clinical picture representing both conditions. The presenting features of a pulmonary infarction overlap those of pulmonary embolism with a few important distinctions.

In patients with concurrent pulmonary embolism and pulmonary infarction, the following features were present: dyspnea (69% to 78%), chest pain (49% to 70%), swelling or pain in unilateral lower extremity (27% to 31%), fever (5% to 11%), and hemoptysis (4% to 19%).[1][3][11] Presenting features in all patients with the diagnosis of pulmonary embolism, regardless of the presence of PI, included dyspnea (72% to 75%), chest pain (36% to 38%), signs of DVT (22% to 33%), hemoptysis (4% to 8%).[1][19] Thus, pleuritic chest pain and hemoptysis were both more common in patients with PE and PI versus those with PE and no PI. Symptoms noted to have no statistical difference between the 2 groups include cough, syncope, sudden onset dyspnea, signs of DVT, fever, and right ventricular overload.

Among patients incidentally found to have a pulmonary infarction after biopsy of a radiographically discovered lung nodule, 65% of patients had no respiratory complaints, 26% had dyspnea, 7% had chest pain, and 5% had hemoptysis.[4] This data highlights the difficulty of diagnosing a PI and emphasizes the importance of considering a broad differential diagnosis for patients who present with symptoms which could be secondary to a PI.

Evaluation

Computed tomography (CT) is the most likely imaging technique which will diagnose PI in combination with the clinical picture. CT findings associated with pulmonary infarction include a feeding vessel or "vessel sign," central lucency, and a semicircular shape. The finding of air bronchograms made the presence of a PI less likely.[2] If a vessel sign with a central lucency and no air bronchogram is present on CT, the specificity for detecting PI is 99%.[20]

An x-ray image may be the first clue toward a diagnosis of pulmonary infarction. Hampton’s hump (wedge-shaped consolidation at the lung periphery), Westermark’s sign (radiographic oligemia or increased lucency), and Fleischer sign (prominent pulmonary artery) are specific findings but lack sensitivity to be diagnostically sufficient. Other features such as atelectasis or focal consolidation may be present but are neither sensitive nor specific.[21]

In patients suspected of having infective endocarditis, consider that pulmonary infarct is a minor criterion in Dukes Criteria for Infective Carditis. Abnormalities that are seen on diagnostic studies like an electrocardiogram, D-dimer, ventilation/perfusion scan, and echocardiogram play a role in predicting PI and also predict pulmonary embolism (PE).

Treatment / Management

As with any patient, signs of respiratory distress or hemodynamic collapse should be addressed immediately with supportive care measures. Patients with pulmonary infarction may develop obstructive shock associated with a PE or cardiorespiratory collapse secondary to persistent hypoxia.

In addition to supportive management, treatment is guided by the underlying condition that has led to the PI. PE initially requires anticoagulation. In patients requiring admission, heparin or low-molecular-weight heparin are started with the goal of transitioning to warfarin or other oral-anticoagulants for continued outpatient management.[22] In patients with hemodynamic instability due to a sub-massive or massive PE, catheter-based fibrinolytics, systemic fibrinolytics, or surgical interventions exist.[23] Additionally, there is a growing body of evidence that the lowest risk patients may be discharged directly from the emergency department on new or direct oral anticoagulants.[24] Treatment for PI not caused by PE is varied and based upon the etiology. The differential diagnoses are listed below.

The average time of resolution of pulmonary infarction has not been well studied.  However, one retrospective review found that of 32 patients evaluated by CT scanning after pulmonary infarctions with intervals varying from 1 to 69 weeks after initial diagnosis, 10 were found to have continued evidence of PI at an average interval of 10 weeks after the initial diagnosis.[3] Additionally, the presence of PI in patients with PE did not alter long-term perfusion deficits determined by lung scintigraphy.[1]  Thus, there is no standardized recommendation for repeat CT scan to evaluate for resolution of PI and such decisions should be based on the particular clinical status of the patient being evaluated.

Current radiographic technology in the setting of the appropriate clinical picture makes it such that biopsy is rarely used to diagnose PI. A lung biopsy is typically reserved for investigating a pulmonary nodule, suspected mass, interstitial lung disease, or to collect a sample for culture.[4][9][25][26]

Differential Diagnosis

The differential diagnosis is broad and includes the following:

  • Pulmonary embolism
  • Acute chest syndrome (sickle cell anemia)
  • Infective endocarditis
  • Malignancy
  • Heatstroke
  • AV malformation
  • Cocaine toxicity
  • Diffuse intravascular coagulation
  • Diffuse alveolar hemorrhage
  • Iatrogenic instrumentation, for example, bronchial artery embolization, IV catheter ablation
  • Amyloidosis,
  • Pulmonary infection like pneumonia or  aspergillosis
  • Viral pleuritis

Enhancing Healthcare Team Outcomes

While PE is the most likely cause of PI, there is a myriad of other diagnoses that must be considered. Consider the variability in clinical presentations and similarities in radiographic results of disease states which mimic PI such as solitary lung nodules. Evidence of a pulmonary infarction on x-ray or CT imaging may be the first indicator the patient has a pulmonary embolism. Patients require education on tobacco cessation as this further increases the risk of PI.[4] Anticipate an interprofessional approach for patients found to have a pulmonary infarction: internal medicine versus critical care for initial management; surgical specialties or pathology for further diagnostics or resection; and sub-specialists such as hematology or cardiology depending on the etiology of the PI.



  • (Move Mouse on Image to Enlarge)
    • Image 7204 Not availableImage 7204 Not available
      Image courtesy S Bhimji MD

References

[1] Miniati M,Bottai M,Ciccotosto C,Roberto L,Monti S, Predictors of Pulmonary Infarction. Medicine. 2015 Oct     [PubMed PMID: 26469892]
[2] Islam M,Filopei J,Frank M,Ramesh N,Verzosa S,Ehrlich M,Bondarsky E,Miller A,Steiger D, Pulmonary infarction secondary to pulmonary embolism: An evolving paradigm. Respirology (Carlton, Vic.). 2018 Mar 25     [PubMed PMID: 29577524]
[3] Chengsupanimit T,Sundaram B,Lau WB,Keith SW,Kane GC, Clinical characteristics of patients with pulmonary infarction - A retrospective review. Respiratory medicine. 2018 Jun     [PubMed PMID: 29857996]
[4] Parambil JG,Savci CD,Tazelaar HD,Ryu JH, Causes and presenting features of pulmonary infarctions in 43 cases identified by surgical lung biopsy. Chest. 2005 Apr     [PubMed PMID: 15821192]
[5] Morgenthaler TI,Ryu JH,Utz JP, Cavitary pulmonary infarct in immunocompromised hosts. Mayo Clinic proceedings. 1995 Jan     [PubMed PMID: 7808055]
[6] George CJ,Tazelaar HD,Swensen SJ,Ryu JH, Clinicoradiological features of pulmonary infarctions mimicking lung cancer. Mayo Clinic proceedings. 2004 Jul     [PubMed PMID: 15244386]
[7] Terry PB,Buescher PC, Pulmonary Infarction: In the Beginning: The Natural History of Pulmonary Infarction. Chest. 2017 Dec     [PubMed PMID: 28716646]
[8] Knight J,Murphy TM,Browning I, The lung in sickle cell disease. Pediatric pulmonology. 1999 Sep     [PubMed PMID: 10495338]
[9] Yousem SA, The surgical pathology of pulmonary infarcts: diagnostic confusion with granulomatous disease, vasculitis, and neoplasia. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc. 2009 May     [PubMed PMID: 19287460]
[10] Miniati M, Pulmonary Infarction: An Often Unrecognized Clinical Entity. Seminars in thrombosis and hemostasis. 2016 Nov     [PubMed PMID: 27743556]
[11] Dalen JE,Haffajee CI,Alpert JS 3rd,Howe JP,Ockene IS,Paraskos JA, Pulmonary embolism, pulmonary hemorrhage and pulmonary infarction. The New England journal of medicine. 1977 Jun 23     [PubMed PMID: 865513]
[12] Tsao MS,Schraufnagel D,Wang NS, Pathogenesis of pulmonary infarction. The American journal of medicine. 1982 Apr     [PubMed PMID: 6462058]
[13] Wiener RS,Schwartz LM,Woloshin S, Time trends in pulmonary embolism in the United States: evidence of overdiagnosis. Archives of internal medicine. 2011 May 9     [PubMed PMID: 21555660]
[14] Søgaard KK,Schmidt M,Pedersen L,Horváth-Puhó E,Sørensen HT, 30-year mortality after venous thromboembolism: a population-based cohort study. Circulation. 2014 Sep 2     [PubMed PMID: 24970783]
[15] Kroegel C,Reissig A, Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. Respiration; international review of thoracic diseases. 2003 Jan-Feb     [PubMed PMID: 12584387]
[16] Choi SH,Cha SI,Shin KM,Lim JK,Yoo SS,Lee SY,Lee J,Kim CH,Park JY,Lee DH, Clinical Relevance of Pleural Effusion in Patients with Pulmonary Embolism. Respiration; international review of thoracic diseases. 2017     [PubMed PMID: 28196360]
[17] Vichinsky EP,Neumayr LD,Earles AN,Williams R,Lennette ET,Dean D,Nickerson B,Orringer E,McKie V,Bellevue R,Daeschner C,Manci EA, Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. The New England journal of medicine. 2000 Jun 22     [PubMed PMID: 10861320]
[18] Emmi G,Silvestri E,Squatrito D,Amedei A,Niccolai E,D'Elios MM,Della Bella C,Grassi A,Becatti M,Fiorillo C,Emmi L,Vaglio A,Prisco D, Thrombosis in vasculitis: from pathogenesis to treatment. Thrombosis journal. 2015     [PubMed PMID: 25883536]
[19] Bajaj N,Bozarth AL,Guillot J,Kojokittah J,Appalaneni SR,Cestero C,Amankona RK,Pippim JA, Clinical features in patients with pulmonary embolism at a community hospital: analysis of 4 years of data. Journal of thrombosis and thrombolysis. 2014 Apr     [PubMed PMID: 23681675]
[20] Revel MP,Triki R,Chatellier G,Couchon S,Haddad N,Hernigou A,Danel C,Frija G, Is It possible to recognize pulmonary infarction on multisection CT images? Radiology. 2007 Sep     [PubMed PMID: 17709834]
[21] Worsley DF,Alavi A,Aronchick JM,Chen JT,Greenspan RH,Ravin CE, Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study. Radiology. 1993 Oct     [PubMed PMID: 8372182]
[22] Kearon C,Akl EA,Ornelas J,Blaivas A,Jimenez D,Bounameaux H,Huisman M,King CS,Morris TA,Sood N,Stevens SM,Vintch JRE,Wells P,Woller SC,Moores L, Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. Chest. 2016 Feb     [PubMed PMID: 26867832]
[23] Jaff MR,McMurtry MS,Archer SL,Cushman M,Goldenberg N,Goldhaber SZ,Jenkins JS,Kline JA,Michaels AD,Thistlethwaite P,Vedantham S,White RJ,Zierler BK, Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011 Apr 26     [PubMed PMID: 21422387]
[24] Frank Peacock W,Coleman CI,Diercks DB,Francis S,Kabrhel C,Keay C,Kline JA,Manteuffel J,Wildgoose P,Xiang J,Singer AJ, Emergency Department Discharge of Pulmonary Embolus Patients. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2018 Sep     [PubMed PMID: 29757489]
[25] Raj R,Raparia K,Lynch DA,Brown KK, Surgical Lung Biopsy for Interstitial Lung Diseases. Chest. 2017 May     [PubMed PMID: 27471113]
[26] Winokur RS,Pua BB,Sullivan BW,Madoff DC, Percutaneous lung biopsy: technique, efficacy, and complications. Seminars in interventional radiology. 2013 Jun     [PubMed PMID: 24436527]