Utility of MDCT in Hemoptysis. A Clinico-Radiological Study

Table of Contents

Introduction

Review of the literature

Chapter I: Anatomical Overview
The Pulmonary arteries
The pulmonary veins

Chapter II: Pathophysiology of hemoptysis
Clinical Significance
Causes of Hemoptysis
Physical Examination:
Pathophysiology:
Diagnostic modalities in hemoptysis:

Chapter III: Multi-detector row CT & hemoptysis
Multi–Detector Row CT Technique
Data Manipulation and Image Interpretation
Assessment of the Lung Parenchyma
Assessment of Pulmonary and Systemic Vasculature Arteries
Bronchial Arteries
Nonbronchial Systemic Arteries
Bronchial-to-Systemic Artery Communications
Cryptogenic Hemoptysis
Patients and Methods
Patients
Multidetector CT
Results
Case presentations
Case 1
Case 2
Case 3
Case 4
Case 5
Case 6
Case 7
Case 8
Case 9
Case 10
Discussion
Conclusions

References

List of Abbreviations

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Introduction

Hemoptysis is defined as bleeding arising from the lower airways. (Bruzzi, et al, 2006 ) Identifying the etiology of hemoptysis and classifying it in terms of the amount of blood expectorated as well as the rate of bleeding play a fundamental role in defining the timing, way and place of managing a patient with hemoptysis. (Agmy, et al, 2013 )

There are multiple causes of hemoptysis, including airway diseases, parenchymal lung diseases, cardiovascular diseases, and others. (Jeudy, et al, 2010) However, no cause is identified in 15–30% of all cases, and is termed idiopathic or cryptogenic hemoptysis (Pires, et al, 2011 ). In the majority of cases, the source of massive hemoptysis is the bronchial circulation. However, nonbronchial systemic arteries can be also a significant source. (Gupta, et al, 2013 )

Imaging modalities pertinent to the evaluation of hemoptysis include chest radiography, computed tomography (CT), and bronchial arteriography.

Conditions such as bronchiectasis, chronic bronchitis, lung malignancy, tuberculosis, and chronic fungal infection are easily detected with conventional CT. ( Sirajuddin et al, 2008) Even, CT is superior to fiberoptic bronchoscopy in finding a cause of hemoptysis, its main advantage being its ability to show distal airways beyond the reach of the bronchoscope, and the lung parenchyma surrounding these distal airways. (Pires, et al, 2011 )

However, more recently, the development of multidetector row CT (MDCT) has provided a comprehensive, noninvasive method of evaluating the entire thorax (Remy-Jardin, et al, 2004, and Bruzzi, et al, 2006 ). At the same time, the combined use of thin-section axial scans and more complex reformatted images allows clear depiction of the origins and trajectories of abnormally dilated bronchial or non-bronchial systemic arteries that may be the source of hemorrhage requiring

embolization. (Remy-Jardin, et al, 2004 and Gupta, et al, 2013 )

Assiut University Hospital is a tertiary referral center, where many patients, from all over Upper Egypt, are referred for the evaluation and management of hemoptysis.

Aim of the work:

In the current study, we aimed to report our experience with the use of MDCT, especially with its new applications such as reformatted images, high resolution imaging and postprocessing techniques, in the management of patients with hemoptysis. We aimed also to determine the additional benefit of MDCT angiographic technique in identifying the site of bleeding and its vascular origin.

Review of the literature - Chapter I: Anatomical Overview

Two separate but vital vascular networks, often forming rich anastomoses, support the complex anatomy and physiology of the lung parenchyma (Frazier et al., 2000).

The primary pulmonary circulation comprises the entire venous return of the body, flowing forward from the main pulmonary artery, ramifying throughout the pulmonary interstitium and airways, and reconstituting itself into pulmonary veins before entering the left atrium. A second, "bronchial" circulation draws approximately 1% of the systemic cardiac output and transmits blood at six times the pressure of the pulmonary circulation. The pulmonary and bronchial circulations communicate with one another by several microvascular interconnections (Frazier et al., 2000).

Bronchial arteries vary greatly in terms of origin, parent artery, and course through the mediastinum (Yoshiaki M etal 2010).

In over 70% of the general population, the bronchial arteries arise from the descending thoracic aorta, most commonly between the levels of T5 and T6.There are normally one or two bronchial arteries supplying each lung, arising either independently or from a common trunk.

On the right side, an intercosto-bronchial trunk usually exists, arising from the right posteromedial aspect of the aorta and coursing cranially before giving rise to one or more posterior intercostal arteries and a right bronchial arterial component. This component turns sharply in the caudal direction to the level of the right main bronchus, where it ramifies in the lung parenchyma parallel to the bronchus and more distal airways. The left bronchial artery usually arises from the anterior aspect of the descending thoracic aorta, either singly or as a common trunk with a second right bronchial artery before coursing toward the left hilum and perhaps through the aortopulmonary window (john F et al., 2010). (Fig I & 2)

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Figure 1: Volume rendering of segmented anatomic structures. The following structures are simulated: (a) right bronchial artery arising from right intercostal bronchialtrunk (IBT), (b) two left bronchial arteries arising directly from thoracic aorta, (c) major vessels (aorta and its main branches, vena cava, brachiocephalic andsubclavian veins, and pulmonary vessels) and heart, (d) azygos vein, (e) bones, (f) esophagus, (g) trachea and lungs, and (h) swollen lymph nodes, esophagus, and trachea and bronchial tree

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Figure 2 : (a) Diagrammatic cross section of thoracic aorta shows circumferential locations of ostium of bronchial and parent arteries. A = anterior , AL = anterolateral, AM = anteromedial, L = lateral, M = medial, P = posterior, PL = posterolateral, PM = posteromedial. (b) Axial CT image shows ostium(arrow) of right bronchial artery in anteromedial wall of thoracic aorta. (c) Axial CT image shows ostium (arrow) of left bronchial artery in lateral wall of thoracic aorta.

It is reported that there is four classic bronchial artery branching patterns: two on the left and one on the right that presents as an intercostobronchial trunk (ICBT) (40% of cases); one on the left and one ICBT on the right (21%); two on the left and two on the right (one ICBT and one bronchial artery) (20%); and one on the left and two on the right (one ICBT and one bronchial artery) (9.7%) (Fig 3). (Yoon W etal 2002)

Bronchial arteries that arise in the expected location from the descending thoracic aorta between the levels of T5 and T6 are called orthotopic bronchial arteries. Anomalous bronchial arteries, defined as bronchial arteries that originate outside the T5 through T6 (Remy J et al 2004). This anomalous artery arises from the concavity of the aortic arch in most cases, but it may less commonly originate from the lower thoracic aorta, subclavian arteries, thyrocervical trunk, costocervical trunk, brachiocephalic artery, internal mammary artery, pericardiophrenic artery, or inferior phrenic artery (Yoon W et al 2002)

Bronchial arteries can be distinguished from non bronchial systemic arteries in that their trajectory into the pulmonary parenchyma parallels the bronchovascular axis. In contrast, non bronchial systemic collateral vessels do not run parallel to the airways and have a more unpredictable origin from infra diaphragmatic arteries or from the supra aortic great vessels or their branches. These arteries provide systemic collateral vessels that reach the lung parenchyma via the inferior pulmonary ligaments (in the case of the inferior phrenic arteries) or transpleural adhesions (in the case of branches from the intercostal and supraaortic arteries) and that form anastomoses with the pulmonary arterial circulation in regions of inflammation or neoplasia (Do KH etal 2001).

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Fig. 3: Diagrams illustrate the types of bronchial arterial supply: Type I, two bronchial arteries on the left and one on the right that manifests as an ICBT (40% of cases); Type II, one on the left and one ICBT on the right (21%); Type III, two on the left and two on the right (one ICBT and one bronchial artery) (20%); and Type IV, one on the left and two on the right (one ICBT and one bronchial artery) (9.7%) (Yoon et al., 2002).

In adults, normal bronchial arteries measure less than 1.5 mm in diameter at their origin and 0.5 mm at their point of entry into a broncho-pulmonary segment. A bronchial artery larger than 2 mm at CT is most likely abnormal (Yoon et al., 2002).

The bronchial arteries supply the trachea, extra- and intra- pulmonary airways, broncho-vascular bundles, nerves, supporting structures, regional lymph nodes, visceral pleura, and esophagus as well as the vasa vasorum of the aorta, pulmonary artery, and pulmonary vein. (Deffenbach et al., 1987).

Each lung is typically supplied by two bronchial vessels that impart several branches to the extrapulmonary mediastinal structures en route to the pulmonary hila, where they enter the peribronchial sheath of each main stem airway. The bronchial arteries then form a dual-layered adventitial and submucosal plexus along the airways that communicates freely across airway muscular walls and nourishes the bronchial tree down to the terminal bronchioles (Burke and Virmani, 1996)..

Normally, the bronchial circulation only supplies nutrients and is not involved in gas exchange. However, in certain pathologic conditions (eg, occlusion of a main pulmonary artery), the bronchial vessels do participate in blood oxygenation. The bronchial circulation responds with enlargement and hypertrophy to decreased pulmonary flow and ischemia ; transpleural systemic collateral vessels (eg, intercostal arteries, internal mammary arteries) also may develop (Yoon et al., 2002).

The pulmonary and bronchial vascular networks communicate via several microvascular interconnections. There are also transpleural systemic–pulmonary artery anastomoses (Deffenbach et al., 1987).

Unlike the pulmonary arteries, bronchial arteries are notably smaller than their adjacent airways and follow more tortuous paths (Burke and Virmani, 1996).

The Pulmonary arteries

The main pulmonary artery arises from the right ventricular outflow tract. It passes to the left of and posterior to the aorta and divides into the right and left pulmonary arteries (Fig. 4). The main, the right, and the proximal portion of the left pulmonary arteries are intrapericardial structures (Goo et al., 2003).

The pulmonary artery branches to both lungs usually following the corresponding bronchial course with the right and left pulmonary arteries dividing into ascending and descending branches, however, variations may occur in the upper lobes (Goo et al., 2003).

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Fig. 4: Axial CT scan showing the main pulmonary artery branching

into right and left branches (Goo et al., 2003).

The left pulmonary artery is shorter and higher than the right pulmonary artery and courses in a more posterior direction. It courses over the left upper lobe bronchus (hypoarterial bronchus) (Fig. 5) (Goo et al., 2003).

It penetrates the root of the left lung, where it divides into two lobar branches. The upper division supplies the apico-posterior and anterior segments of the left upper lobe. The interlobar artery curves sharply over the top of the left upper lobe and descends along the lateral aspect of the left lower lobe bronchus. It enters the oblique fissure. Its lingular branch arises from the anterior aspect and the superior segmental artery from the posterior aspect. It supplies branches to the left lower lobe basal segments (Remy-Jardin et al., 2001).

The right pulmonary artery passes behind the ascending aorta, superior vena cava (SVC), and right upper pulmonary vein. It courses anterior and lateral to the right bronchus. It divides into two lobar branches at the root of the right lung (Fig. 6a) (Fig. 7b). The right upper lobe bronchus is superior to the descending branch of the right pulmonary artery (epiarterial bronchus) (Goo et al., 2003).

The right pulmonary artery divides into truncus anterior and interlobar artery. The truncus anterior artery supplies the right upper lobe. It curves anteriorly and superiorly over the upper lobe bronchus, then, divides into three branches corresponding to the bronchial segments (Goo et al., 2003).

The interlobar artery is larger and passes in front of and along the lateral side of the intermediate bronchus. Its transverse diameter measures 15-16 mm during inspiration. It enters into the oblique fissure supplying the right middle lobe and segments of the lower lobe (Goo et al., 2003).

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Fig. 5 Axial CT showing normal right and left pulmonary arteries

In the normal adult anatomy, the pulmonary trunk, or main pulmonary artery, may have a diameter as great as 28 mm (Castaner et al., 2006).

Pulmonary arteries (main, lobar, segmental, and subsegmental) with a diameter greater than 0.5 mm are referred to as elastic pulmonary arteries (Castaner et al., 2006).

The right and left pulmonary arteries should be of approximately equal size, although the left pulmonary artery appears slightly larger in most subjects. The segmental arteries are always seen near the accompanying branches of the bronchial tree, and the subsegmental arteries are easily recognized as dichotomous divisions of the corresponding segmental artery. They course downward along the bronchi to the subsegmental level, and their diameters are similar to those of the adjacent airways (Castaner et al., 2006).

The function of the elastic arteries is similar to that of the aorta: to provide a distensible reservoir for ventricular ejection. The normal pulmonary circulation is a low-pressure system that has approximately one-tenth the flow resistance of the systemic circulation, as well as a high capacitance (Frazier et al., 2000).

Beyond the subsegmental bronchi, these vessels transition to muscular arteries which accompany the peripheral airways downward to the level of the terminal bronchioles. As the smooth-muscle layer progressively thins, these arteries become arterioles (0.15–0.015 mm in diameter), which proceed along the respiratory bronchioles and alveolar ducts to eventually form a capillary network in the alveolar walls (Frazier et al., 2000).

Their walls comprise multiple parallel elastic lamellae, smooth muscle cells, and collagen fibrils. Medial smooth muscle fibers in the muscular arteries provide active vasodilatation and constriction (Frazier et al., 2000).

The venules accept flow from these capillary beds and unite to form pulmonary veins, which course within interlobular fibrous septa, apart from the airways. Two veins from each hilum drain into the left atrium. (Frazier et al., 2000).

The pulmonary veins

The pulmonary veins normally drain into the left atrium (Fig. 6). The right middle and upper lobe veins join to form the right superior pulmonary vein. The left superior pulmonary vein receives blood from the left upper lobe. The right and left inferior pulmonary veins receive blood from the right and left lower lobes respectively (Goo et al., 2003).

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Fig. 6: Normal pulmonary veins. CT scan shows all the pulmonary veins, including the right superior (RS), right inferior (RI), left superior (LS), and left inferior (LI) pulmonary veins, with a normal veno-atrial connection with the left atrium (Goo et al., 2003).

Chapter II: Pathophysiology of hemoptysis

Hemoptysis is defined as the spitting of blood derived from the lungs or bronchial tubes as a result of pulmonary or bronchial hemorrhage (Bidwell, et al., 2005).

Hemoptysis is classified as non-massive or massive based on the volume of blood loss; however, there are no uniform definitions for these categories., hemoptysis is considered non-massive if blood loss is less than 200 mL per day. The lungs receive blood from the pulmonary and bronchial arterial systems (Stedman, et al., 2004).

The low-pressure pulmonary system tends to produce small volume hemoptysis, whereas bleeding from the bronchial system, which is at systemic pressure, tends to be profuse. Blood loss volume is more useful in directing management than in reaching a diagnosis (Godfrey, 2004).

After confirming the presence of blood, an initial task is differentiating between hemoptysis, pseudo-hemoptysis (i.e., the spitting of blood that does not come from the lungs or bronchial tubes), and hematemesis (i.e., the vomiting of blood) (Corder, et al., 2003).

Hemoptysis is an important symptom that elicits fear in both the patient and physician. Work-up for this symptom should be undertaken immediately unless the problem is both mild and recurrent, in which case a conservative approach may sometimes be preferable (Rita Larici, et al., 2014).

The history may help define not only the site but also the cause of bleeding. When evaluating hemoptysis, the first step is to convince your-self that the lower respiratory tract is the source of the bleeding. Coughing is important because non-pulmonary sources of bleeding are not usually associated with cough. Questions regarding epistaxis and spitting blood without coughing help rule out the upper respiratory tract as the source of bleeding, but do not replace a nose and throat examination ( Jeudy, et al., 2010).

Further, the physician must be convinced that `the bleeding is not of gastrointestinal origin. A history of nausea, vomiting, heartburn, and abdominal pain may be helpful, but occasionally the differential diagnosis is difficult and requires either direct observation of the patient's hemoptysis or endoscopic evaluation of the upper gastrointestinal tract ( Lordan, et al., 2003).

The physician should quantify the amount of bleeding that has taken place, being as specific as possible (e.g., a teaspoon, a cupful) . Patients and physicians usually overestimate the amount of bleeding, so nothing can replace direct observation. The approximate rate of bleeding requires careful quantification. Because the rapidity and the extent of the work-up depend to a large degree on the above quantification, the importance of this aspect of the history cannot be overemphasized (Ibrahim, 2008).

Note if this is the first episode of hemoptysis or whether it is a chronic and/or recurrent problem. The quantity of past bleeding and the extent of previous evaluations are quite helpful. Despite the fact that repeated evaluations for recurrent hemoptysis are often advocated by experts, such evaluations can be both expensive and unrewarding in many patients (Yoon, et al., 2002).

One should next investigate thoroughly the material being produced. Is the patient coughing up bright red blood or blood clots (as in carcinoma of the lung, tuberculosis, pulmonary embolism); blood-streaked, purulent sputum (as in bronchitis, bronchiectasis, or pneumonia); blood-tinged, white, frothy sputum (as in congestive heart failure); or foul smelling, bloody sputum (as in an anaerobic lung abscess) (Jean-Baptiste, 2000).

Red sputum that contains no blood is seen in a rare case of Serratia marcescens pneumonia with its red pigmentation, in glass sanders with sputum discolored by iron oxide, and in ruptured hepatic amebic liver abscess with its "anchovy paste" sputum. Rarely, a patient will present with pseudohemoptysis created artificially by various means ( Chun, et al., 2010).

Associated pulmonary symptoms such as chronic cough with sputum production, change in cough, shortness of breath on exertion, chest pain (especially of a pleuritic nature), and wheezing are also important in the evaluation of hemoptysis. The relation between these symptoms and the onset of hemoptysis can be quite helpful. For example, hemoptysis in lung cancer or tuberculosis usually is a late symptom preceded by weight loss, change in cough, fatigue, and other chronic symptoms (Andersen, 2006).

Other points of the history that must be addressed include previous pulmonary infections, recent blunt chest trauma, seizures, and lower extremity pain or swelling ; exposure to such agents as cigarette smoke, alcohol, asbestos, and tuberculosis ; use of medications (e .g ., anticoagulants) ; and finally, systemic symptoms such as fever, weight loss, and other bleeding problems, especially hematuria (Bruzzi, et al., 2006) .

The age of the patient is also useful in narrowing the differential diagnosis. Cystic fibrosis is a disease of children and young adults; mitral stenosis, bronchial adenomas, Goodpasture's syndrome, and primary pulmonary hypertension occur in the middle aged; and carcinoma of the lung is usually seen in patients over 50 years of age (Pump,2003).

Depending on the underlying disease, hemoptysis is a result of several different pathologic mechanisms. Remember that the lung contains two separate vascular systems: the pulmonary and the bronchial vessels. Hemoptysis can occur with involvement of either. (Sirajuddin, et al., 2008).

Infarction of lung tissue with hemoptysis can occur in numerous diseases. Pulmonary emboli often present with hemoptysis as a result of ischemic pulmonary parenchymal necrosis. A similar ischemic necrosis can be seen in all idiopathic vacuities involving the pulmonary vessels, including: Wegener's granulomatosis. Infections causing blood vessel invasion with infarction include primarily Staphylococcus aureus, Pseudomonas aeruginosa, Aspergillus fumigatus, and the phycomycetes (McDonald, et al., 2001).

Clinical Significance

Hemoptysis must always be considered a serious and potentially lethal complication of the underlying process. When an aggressive approach is taken in the evaluation of hemoptysis, a cause can be determined in approximately 90% of cases.

Marked variation is seen from center to center depending on whether inpatients or outpatients are categorized, whether tuberculosis is prevalent, and whether one is evaluating surgical or medical patients (Cauldwell, et al., 2008).

The amount of bleeding is useful in the differential diagnosis of hemoptysis. More benign processes such as bronchitis and pneumonia cause the majority of all cases of hemoptysis, but they are less common as the severity of the bleeding increases. Massive hemoptysis is most commonly associated with lung cancer, bleeding diathesis (e .g., leukemia during chemotherapy, anticoagulation), cystic fibrosis, and tuberculosis (Jaitovich, et al., 2012).

Causes of Hemoptysis

In the primary care setting, the most common causes of hemoptysis are acute and chronic bronchitis, pneumonia, tuberculosis, and lung cancer. (Table 1)

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Table 1: Causes of hemoptysis, Numbers in parentheses are reference numbers, within Bruzzi, et al, 2006

Infections:

Infection is the most common cause of hemoptysis, accounting for 60 to 70 percent of cases. Infection causes superficial mucosal inflammation and edema that can lead to the rupture of the superficial blood vessels.

In a retrospective study of inpatient and outpatient hemoptysis in the United States, bronchitis caused 26 percent of cases, pneumonia caused 10 percent, and tuberculosis accounted for 8 percent. Invasive bacteria (e.g., Staphylococcus aureus, Pseudomonas aeruginosa) or fungi (e.g., Aspergillus species) are the most common infectious causes of hemoptysis. Viruses such as influenza also may cause severe hemoptysis (Harrison, et al., 2001).

Human immunodeficiency virus (HIV) infection predisposes patients to several conditions that may produce hemoptysis, including pulmonary Kaposi’s sarcoma (Nelson, 2006).

Cancer

Primary lung cancers account for 23 percent of cases of hemoptysis in the United States. Bronchogenic carcinoma is a common lung cancer responsible for hemoptysis in 5 to 44 percent of all cases.

In a recent study by Mohamed et al, 2016(a) ; the usefulness of MDCTA, as well as its generated virtual bronchoscopy (VB) in the evaluation of patients with hemoptysis due to lung cancer, was carried out. A prospective study was carried out on 24 patients diagnosed as primary lung cancer and presented with hemoptysis. They underwent MDCT using a 16-detector row scanner with bronchial and pulmonary angiographic techniques. MDCT-generated VB was carried out and compared to findings obtained by fiberoptic bronchoscopy (FOB). MDCT identified the cause of hemoptysis and its angiography detected the site and vascular source of bleeding in 96% of patients. Virtual bronchoscopy had sensitivity, specificity, and accuracy of 91%, 50%, and 87.5%, respectively. While FOB detected 11, 19, 3 and 2 endoluminal lesions, obstructive lesions, external compressions, and mucosal abnormalities; VB detected 7, 25, 11, and 0 lesions, respectively. (Mohamed et al, 2016, a)

Bleeding from malignant or benign tumors can be secondary to superficial mucosal invasion, erosion into blood vessels, or highly vascular lesions. In a prospective study, by Mohamed et al, 2013(a) ; the diagnostic utility of transbronchial needle aspiration (TBNA) in patients with malignant endobronchial lesions detected during routine bronchoscopy was evaluated. Ninety-four patients were enrolled. TBNA and conventional diagnostic techniques (CDTs: forceps biopsy, brushing, and washing) were performed in all patients. Endobronchial lesions were classified into exophytic mass lesions (EMLs), submucosal disease (SD), and peribronchial disease (PD).The diagnostic yields of TBNA and CDT alone and together were compared according to the lesions’ types, histopathology, and locations. During 3-year period, the addition of TBNA to CDT improved bronchoscopic sensitivity from 70.2% to 94.7% in all lesion types. Addition of TBNA to CDT increased the diagnostic success from 74% to 95% and from 50% to 94% in NSCLC and SCLC, respectively. The diagnostic success was increased in all localizations by the addition of TBNA to CDT, particularly for lesions located at the trachea, main bronchi, and upper lobes. We conclude that the addition of TBNA to CDT increases the diagnostic yield in patients with visible malignant endobronchial lesions, particularly in peribronchial disease, and improves the diagnostic yield of bronchoscopy, in both NSCLC and SCLC and in all bronchoscopic locations, particularly in central and upper lobar lesions. (Mohamed, et al, 2013, a )

Breast, renal, and colon cancers have a predilection for lung metastasis; however metastatic lung carcinoma rarely results in bleeding. Obstructive lesions may cause a secondary infection, resulting in hemoptysis (Corder, 2003).

Pulmonary venous hypertension

Cardiovascular conditions that result in pulmonary venous hypertension can cause cardiac hemoptysis. The most common of these is left ventricular systolic heart failure (Humphrey, et al., 2004).

Other cardiovascular causes include severe mitral stenosis and pulmonary embolism. Although hemoptysis is a recognized pulmonary embolism symptom, pulmonary embolism is an uncommon cause of hemoptysis (Weber, 2001).

For example, in a patient without underlying cardiopulmonary disease, the positive and negative likelihood ratios for hemoptysis in pulmonary embolism are 1.6 and 0.95, respectively. Therefore, the presence or absence of hemoptysis alone has no significant effect on the likelihood of pulmonary embolism (Weber, et al.,2001).

Idiopathic.

Idiopathic hemoptysis is a diagnosis of exclusion. In 7 to 34 percent of patients with hemoptysis, no identifiable cause can be found after careful evaluation. Prognosis for idiopathic hemoptysis usually is good, and the majority of patients have resolution of bleeding within six months of evaluation (Procop, et al., 2000).

However, results from one study found an increasing incidence of lung cancer in smokers older than 40 years with idiopathic hemoptysis, and suggested that these patients may warrant close monitoring (Kaygusuz, et al., 2001).

Hemoptysis in children

The major cause of hemoptysis in children is lower respiratory tract infection. The second most common cause is foreign body aspiration, with most cases occurring in children younger than four years (Inglesby, et al., 2000).

Another important cause is bronchiectasis, which often is secondary to cystic fibrosis. Primary pulmonary tuberculosis is a rare cause estimated to occur in less than 1 percent of cases. Although uncommon, trauma is another possible cause. Blunt-force trauma may result in hemoptysis secondary to pulmonary contusion and hemorrhage. Bleeding caused by suffocation, deliberate or accidental, also should be considered (Jean-Baptiste, 2000).

Patient History:

Historic clues are useful for differentiating hemoptysis from hematemesis . Patient history also can help identify the anatomic site of bleeding, differentiate between hemoptysis and pseudohemoptysis, and narrow the differential diagnosis . Factors such as age, nutrition status, and comorbid conditions can assist in the diagnosis and management of hemoptysis (Tasker, et al., 2008).

Once true hemoptysis is suspected, the investigation should focus on the respiratory system. Blood from the lower bronchial tree typically induces cough, whereas a history of epistaxis or expectorating without cough would be consistent with an upper respiratory source but does not exclude a lower tract site (O’Neil KM & Lazarus, 2001).

Bleeding is difficult to quantify clinically. Patients may find it difficult to discern whether they are throwing up, coughing, or spitting out bloody material. The amount of blood loss usually is overestimated by patients and physicians, but an attempt to determine the volume and rate of blood loss should be made. Methods of determination include observing as the patient coughs and the use of a graduated container (Gregory, et al., 2006).

Blood-streaked sputum deserves the same diagnostic consideration as blood alone. The amount or frequency of bleeding does not correlate with the diagnosis or incidence of cancer (Inglesby, et al., 2000).

It is helpful to determine whether there have been previous episodes of hemoptysis and what diagnostic assessments have been done. Mild hemoptysis recurring sporadically over a few years is common in smokers who have chronic bronchitis punctuated with superimposed acute bronchitis (Inglesby, et al., 2000).

Because smoking is an important risk factor, these patients are at higher risk for lung cancer. Chronic obstructive pulmonary disease also is an independent risk factor for hemoptysis.

Environmental exposure to asbestos, arsenic, chromium, nickel, and certain ethers increases risk for hemoptysis. Bronchial adenomas, although malignant, are slow growing and may present with occasional bleeding over many years. Malignancy in general, especially adenocarcinomas, can induce a hypercoagulable state, thereby increasing the risk for a pulmonary embolism (Corder, 2003).

A history of chronic, purulent sputum production and frequent pneumonias, including tuberculosis, may represent bronchiectasis. Association of hemoptysis with menses (i.e., catamenial hemoptysis) may represent intrathoracic endometriosis (Weber, 2001).

A travel history may be helpful. Tuberculosis is endemic in many parts of the world, and parasitic etiologies should be considered (Tasker, et al., 2008).

In regions where drinking from springs is common, there are case reports of hemoptysis caused by leeches attaching to the upper respiratory tract mucosa. Also, biologic weapons such as plague may cause hemoptysis (Khalil, et al., 2007).

Physical Examination:

Historic clues often will narrow the differential diagnosis and help focus the physical examination . Examining the expectoration may help localize the source of bleeding (Corder , et al., 2003).

The physician should record vital signs, including pulse oximetry levels, to document fever, tachycardia, tachypnea, weight changes, and hypoxia. Constitutional signs such as cachexia and level of patient distress also should be noted. The skin and mucous membranes should be inspected for cyanosis, pallor, ecchymoses, telangiectasia, gingivitis, or evidence of bleeding from the oral or nasal mucosa (Humphrey, et al., 2004).

The examination for lymph node enlargement should include the neck, supraclavicular region, and axillae. The cardiovascular examination includes an evaluation for jugular venous distention, abnormal heart sounds, and edema. The physician should check the chest and lungs for signs of consolidation, wheezing, rales, and trauma (Godfrey, 2004).

The abdominal examination should focus on signs of hepatic congestion or masses, with an inspection of the extremities for signs of edema, cyanosis, or clubbing (Bond & Vyas, 2001).

Pathophysiology:

Hemoptysis has multiple causes usually categorized under parenchymal diseases, airway diseases, and vascular diseases.

Bleeding may originate from small or large lung vessels. Bleeding from the small vessels usually causes a focal or diffuse alveolar hemorrhage and is mainly due to immunologic, vasculitic, cardiovascular, and coagulatory causes. Causes of bleeding from the large vessels include infectious, cardiovascular, congenital, neoplastic, and vasculitic diseases . However, the most frequent diseases causing hemoptysis are bronchiectasis, tuberculosis, fungal infections, and cancer . (Menchini, et al., 2009).

Two arterial vascular systems supply blood to the lungs: the pulmonary arteries and the bronchial arteries. The pulmonary arteries provide 99% of the arterial blood to the lungs and are involved in the gas exchange. The bronchial arteries supply nourishment to the extra- and intrapulmonary airways and to the pulmonary arteries (vasa vasorum), without being involved in the gas exchange . Mediastinal lymph nodes and nerves, visceral pleura, esophagus, vasa vasorum of the aorta, and pulmonary veins are also provided by the bronchial arteries ( Hartmann , et al., 2007).

Complex capillary anastomoses exist between the pulmonary arteries and the systemic bronchial arteries When pulmonary circulation is compromised (e.g., in thromboembolic disease, vasculitic disorders, or in hypoxic vasoconstriction), the bronchial supply gradually increases causing a hyper flow in the anastomotic vessels, which become hypertrophic with thin walls and tend to break into the alveoli and bronchi, giving rise to hemoptysis. Likewise, in chronic inflammatory disorders, such as bronchiectasis, chronic bronchitis, tuberculosis, mycotic lung diseases, and lung abscess, as well as in neoplastic diseases, the release of angiogenic growth factors promote neovascularization and pulmonary vessel remodeling, with engagement of collateral systemic vessels . These new and collateral vessels are fragile and prone to rupture into the airways ( McDonald, 2001).

In cases of severe hemoptysis requiring treatment, the source of bleeding originates from bronchial and pulmonary arteries in 90% and 5% of cases, respectively. In the remaining 5% of cases, hemoptysis may derive from nonbronchial systemic arteries. Very rarely, hemoptysis has been reported originating from pulmonary and bronchial veins and capillaries . A recent study by Noë et al. (2011) shows that bleeding from bronchial arteries can coexist with bleeding from nonbronchial and pulmonary arteries in the same patient.

According to different authors, etiology of hemoptysis cannot be determined in 3% to 42% of cases and it is defined as cryptogenic . Nevertheless, it has been demonstrated that a proportion of patients presenting with hemoptysis without any morbidity are smokers, and bleeding in smokers should be defined as smoke-related (occurring as a result of tobacco-induced bronchial wall inflammation), rather than cryptogenic . Moreover, with a more systematic use of chest computed tomography (CT), particularly multidetector CT (MDCT), a decrease in the prevalence of hemoptysis without known cause might be expected ( Menchini, et al., 2009 ).

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