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Determining the cause of recurrent pneumonia requires that you run through an extensive differential, then order the diagnostic tests that narrow the field.
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Determining the cause of recurrent pneumonia requires that you run through an extensive differential, then order the diagnostic tests that narrow the field of possibilities.
Pneumonia is a common problem among children around the world. Mortality has declined over the years in the United States but, worldwide, more than 2 million children die of pneumonia annually. The incidence of pneumonia in the US is 35 to 40 for every 1,000 children younger than 5 years of age, and 16 to 22 for every 1,000 children older than 5 years.13
Although the incidence of recurrent pneumonia in children is unknown, it is often a common diagnostic challenge for the primary care physician because the differential is extensive. For purposes of this article, recurrent pneumonia is defined as at least two episodes in one year or a lifelong total of three or more episodes.4,5 Any child who meets the criterion warrants thorough investigation by the practitioner, with referral to a specialist as appropriate.
Normal airways have built-in defense mechanisms from the nares to the alveoli that protect the lungs from infection and injury. These defenses start with the nares, which, in addition to warming and humidifying air, filter particles. The epiglottal reflex directs food and secretions to the esophagus and prevents aspiration. The cough reflex quickly removes any substances inadvertently headed down the wrong pathway. The mucociliary system produces mucus that traps foreign and infectious particles, which are then cleared by the upsweep motion of the ciliary epithelium lining the airways. The alveolar macrophages, which engulf and kill bacteria; the immune system, which neutralizes bacteria; and the lymphatic system, which removes particles from the lungs, are also important lung defense mechanisms. The absence or impairment of any these natural defenses or a compromised immune system leads to increased susceptibility to recurrent infections.6,7
A thorough history is imperative in tracing the origin of recurrent pneumonia. This includes determining how old the child was when symptoms first occurred, since different disorders have their onset at different ages. Certain immunodeficiency syndromes, for example, may present early in infancy.
Obtain details of perinatal and early infancy events such as feeding difficulties and choking episodes. These events may be caused by an impaired swallowing mechanism secondary to a neurologic defect, by gastroesophageal reflux (GER), or by aspiration of a foreign body.
Inquire, too, about environmental exposure to toxins, allergens, and irritants such as smoke. Over time, second-hand smoking compromises natural host defenses and predisposes to respiratory infections. The daily environment, such as a school or day-care center, also provides clues to infectious exposure. As always, family history should be an integral part of the evaluation.7
The definition of pneumonia varies widely. In this review, pneumonia is defined as the presence of fever or acute respiratory symptoms plus evidence of parenchymal infiltrates on a chest radiograph. Cough, tachypnea, or dyspnea, which may be either abrupt or insidious in onset; fever; and decreased appetite are common presenting symptoms. Physical findings may include use of accessory muscles, retractions, decreased breath sounds, crackles, wheezes, and dullness to percussion. Careful examination may reveal clues such as failure to thrive, pallor, eczema, nasal polyps, chronic otitis media, digital clubbing, or lymphadenopathy that may suggest a particular underlying disease.
In diagnosing recurrent pneumonia, chest radiographs are essential not only to confirm the diagnosis but also to determine if the pneumonia is localized or diffuse, recurrent or persistent. A review of all films with an experienced radiologist may be necessary for accurate diagnosis.
Recurrent pneumonia in a single anatomic region (localized pneumonia) is usually caused by intraluminal bronchial obstruction or extraluminal compression (Table 1). It may also be caused by an anatomic abnormality of the airway or lung parenchyma, or by both.
Infection (tuberculosis, histoplasmosis, coccidioidomycosis)
Malignancy (lymphadenopathy or direct compression,
e.g., Hodgkin's disease)
Intraluminal obstruction. Foreign body is the most frequent intraluminal obstruction in children age 6 months to 3 years. Most foreign bodies impact in the right bronchus because it takes off at a less acute angle from the trachea than the left bronchus does. Commonly aspirated items include food such as nuts, corn, and carrots. Less commonly, but still often aspirated, are plastic toys, pills, and metal objects, which may sit in the airway for weeks or months.8 Initial signs of foreign body aspiration include localized wheezing and asymmetry of breath sounds, which are decreased on the side of aspiration.9
Although it is important to obtain a detailed history of any choking and coughing episodes, the physician should maintain a high index of suspicion for foreign body aspiration even in the absence of such history. Most episodes are not observed when they occur, and respiratory symptoms may not manifest immediately afterward. As a result, some children are treated for pneumonia and "recover," only to present later with recurring symptoms.
Other causes of intraluminal obstruction are less common in children. Some patients with active disease caused by Mycobacterium tuberculosis may present with persistent focal infiltrates or atelectasis caused by endobronchial granulomas. Tumors are a rare cause of intraluminal obstruction in children but should not be overlooked as a reason for recurrent localized pneumonia. Of all the tumors that may arise in the bronchus, hemangiomas are the most common in children.8 Other, less common tumors that cause intraluminal obstruction in children include bronchial adenomas, endobronchial lipomas, and papillomas.
Extraluminal compression. Infectious lymphadenopathy is the most common cause of extraluminal compression. Local airway narrowing leads to retained secretions in the area distal to the obstruction. Mucociliary clearance is impaired and infection supervenes. Infectious lymph nodes causing airway compression are most commonly caused by infection with M tuberculosis. In active pulmonary tuberculosis, enlarged lymph nodes occur in the perihilar, carinal, and peribronchial regions. In certain geographic areas, enlarged lymph nodes may be caused by infection with the agents of histoplasmosis or coccidioidomycosis, producing manifestations similar to those produced by tuberculosis, including airway compression. Although rare in children, sarcoidosis may also cause lymph node enlargement that may produce extraluminal airway compression.
Tumors such as lymphoma can also cause extraluminal airway compression. Inflammatory pseudotumors are the most common benign primary pulmonary growths in children. These lesions, also called plasma cell granulomas and histiocytomas, are generally regarded as reactive in origin. Most patients have no symptoms; in those who do, clinical manifestations include fever, cough, chest pain, and recurrent pneumonia. On radiographic studies, inflammatory pseudotumors appear as solitary, well-circumscribed, round nodules of soft-tissue density, 0.5 to 3.6 cm in diameter.
Congenital anomalies of the heart and great vessels can also cause extrinsic obstruction of the large airways. Vascular rings and slings and esophageal foreign bodies are other causes of extraluminal compression.
Structural abnormalities, either congenital or acquired, can lead to recurrent lower respiratory tract infection. These abnormalities include tracheal bronchus, bronchiectasis, bronchial stenosis, and bronchomalacia. Tracheal bronchus is an ectopic bronchus that originates directly from the right wall of the trachea and connects to the right upper lobe. It impairs drainage of this lobe, often leading to recurrent infection and, in turn, bronchiectasis.4,10
Bronchiectasis is a term that describes bronchi abnormally dilated to an ectatic condition; the lesions may be focal or generalized, congenital or acquired. Bronchiectasis is seen most often with cystic fibrosis (CF) and primary ciliary dyskinesia (PCD). It may occur after severe bacterial or viral lower respiratory tract infection, which causes bronchial wall damage. It can also be secondary to so-called right middle-lobe syndrome. The right middle lobe is often described as being predisposed to atelectasis and infiltrates, a susceptibility attributed to anatomic and physiologic causes. Its bronchus, which is narrow and short and takes off at a very acute angle from the bronchus intermedius, is surrounded by lymph nodes, which may enlarge and cause compression. In addition, in infants and young children, the right middle lobe has limited collateral ventilation. Right middle-lobe syndrome is seen most often in children with asthma.4,10
Congenital bronchial stenosis may occur in the main stem or lobar bronchi. In bronchomalacia, the affected bronchi are of normal caliber but collapse easily during expiration because of deficient cartilaginous support.
Other congenital anomalies of foregut development, such as congenital cystic adenomatoid malformation (CCAM), congenital lobar emphysema (CLE), bronchogenic cyst, and pulmonary sequestration, can also lead to recurrent pneumonia.8 CCAMs represent about 25% of congenital lung abnormalities. Most are diagnosed by prenatal ultrasonography or present shortly after birth as respiratory distress. A small number present later accompanied by recurrent pneumonia caused by bronchial compression.
CLE, marked hyperinflation of an anatomical lobe (particularly the left upper lobe) or lobes, is a relatively common cause of respiratory distress in the newborn. Some cases, however, present later with recurrent pneumonia caused by extraluminal compression. Although CLE commonly presents as a hyperlucent thoracic lesion, some cases have initially presented as a solid, homogenous pattern associated with retained fetal fluid.
Bronchogenic cysts are anomalies that interrupt the continuity of the airway during embryologic development. They usually present as a discrete mass of nonfunctional pulmonary tissue in the paratracheal or subcarinal areas. Infection may rarely occur in the cyst itself or in the surrounding lung compressed by the cystic lesion.
Pulmonary sequestration is also nonfunctional pulmonary tissue; it is separate from the tracheobronchial tree and receives systemic blood supply from the aorta or its branches. Pulmonary sequestration can be intralobar (most cases) or extralobar. Most often, the left lower lobe is involved. Recurrent pneumonia usually occurs in children with intralobar sequestration. Although some children with extralobar sequestration may be asymptomatic, for those presenting with recurrent infection, surgical excision may be the only cure.5
Once chest radiographs have confirmed recurrent localized pneumonia, bronchoscopy is usually the next diagnostic approach (Figure 2); when a foreign body can be removed, it is both diagnostic and a therapeutic intervention. In addition, bronchoscopy can identify other intraluminal lesions such as tumors, which can be biopsied and removed, and help diagnose structural abnormalities such as tracheal bronchus and bronchial stenosis.
In evaluating a child with possible foreign body aspiration, rigid bronchoscopy is the procedure of choice because it is easier to remove any foreign body by passing a forceps through an open tube. This avoids subjecting the child to a second procedure after fiberoptic bronchoscopy (solid tube).
If bronchoscopy is normal, a multislice computed tomography (CT) scan of the chest should be obtained. The speed of multislice CT allows dynamic imaging of the airway during the respiratory cycle. In a single study of tracheobronchomalacia with multislice CT, the degree of dynamic collapse correlated well with bronchoscopic results.11 Indications for airway evaluation by CT include detection or characterization of congenital airway anomalies, evaluation of the extent of tracheobronchial stenosis, and detection of airway fistula and bronchiectasis. Also, many foreign objects that are not radiopaque on plain film radiography are apparent on CT, allowing CT to be used in the evaluation of possible aspirated foreign body.
Magnetic resonance imaging (MRI) is the standard means of imaging airway compression due to vascular anomaly. However, multislice CT scan of the chest is a viable alternative in the evaluation of vascular anomalies of the mediastinum. Multislice CT has similar capabilities to an MRI, with the advantages that sedation may not be required and associated or unsuspected airway or parenchymal abnormalities can be detected.12 Multislice CT angiography can be used in the evaluation of suspected mediastinal vascular anomalies such as rings and slings and those involving the great vessels.
A purified protein derivative (PPD) 5 tuberculin unit test should be part of the initial evaluation of the child with recurrent pneumonia. Consider the possibility of CF and order a sweat chloride test for a child with recurrent unilobar infection, especially in the right upper lobe, who has other clinical manifestations, such as chronic sinusitis, steatorrhea, and failure to thrive.
Additional evaluations in the child with recurrent unilobar infection include acute and convalescent titers for antibodies to histoplasmosis and coccidioidomycosis if the child has been in an endemic area. In cases of suspected heart disease, electrocardiography and echocardiography are appropriate.
It is also recommended that all children 6 years of age or older who have chronic cough with or without wheezing and recurrent pneumonia be evaluated with spirometry. If the study shows airway obstruction, it should be repeated after administration of inhaled bronchodilators to assess reversibility. If the initial study is normal, spirometry post-exercise challenge should be obtained to try to uncover latent airway hyperreactivity.
Whereas recurrent unilobar pneumonia is usually the result of an obstruction, recurrent infection in multiple lobes (diffuse) is usually caused by an underlying disorder (Table 2).
Aspiration is the most common cause of recurrent multifocal pneumonia in children.3 The location of radiographic infiltrates depends on the position the child was in when aspiration occurred. The severity of pulmonary involvement depends, in part, on the pH of the aspirated material and on the amount and type of material aspirated.3 Aspiration is most often caused by impaired swallowing due to central nervous system (CNS) disorders, neuromuscular diseases, structural abnormalities of the oropharynx, or forceful feeding.13
Esophageal obstruction, whether extrinsic (vascular rings or mediastinal masses) or intrinsic (foreign bodies or strictures), can lead to difficulty swallowing. Another esophageal cause of recurrent diffuse pneumonia is dysmotility caused by achalasia. Tracheoesophageal fistula (TEF) can also be associated with esophageal dysmotility. Most forms of TEF are diagnosed in the neonatal period, but small, H-type fistulae may not present until later in childhood, when chronic aspiration through the persistent abnormal communication leads to recurrent lower respiratory tract infection. Some children continue to aspirate even after repair of a TEF because of persistent esophageal stricture, GER, and tracheomalacia.5
There is a clear association among gastroesophageal reflux disease (GERD), aspiration, and recurrent pneumonia. However, the lack of reliable diagnostic tests for both GERD and aspiration confounds attempts to establish the contribution of GERD to recurrent pneumonia.
Asthma. In children without an apparent predisposing cause of pneumonia, asthma is the most common cause of recurrent/persistent infiltrates.14 These children typically present with wheezing. Initial manifestation may, however, be shortness of breath on exertion or nocturnal cough with or without wheezing. The pathophysiology of this condition includes mucous plugging and edema of peripheral airways and, as a result, atelectasis. Infiltrates often appear, usually in the right middle lobe. Consequently, a simple viral upper respiratory infection with atelectasis secondary to asthma is often misdiagnosed as pneumonia.15
Allergic bronchopulmonary aspergillosis (ABPA) occurs if there is endobronchial colonization with Aspergillus fumigatus and hypersensitivity to the organism. Suspect ABPA in children with asthma of any severity or CF who have recurrent pulmonary infiltrates, peripheral eosinophilia, and an elevated total serum IgE. A negative immediate-type skin test excludes ABPA, but the diagnosis can be established only by careful serologic studies showing positive precipitin reactions against A fumigatus and elevated immunoglobulin E (IgE) and immunoglobulin G (IgG) antibodies against A fumigatus antigen.
Immunodeficiency. The primary immunodeficiency diseases were originally viewed as rare disorders, characterized by severe clinical expression early in life. However, these diseases are not as rare as originally suspected, their clinical expression can sometimes be relatively mild, and they are seen nearly as often in adolescents as they are in infants and children. The list of primary or secondary immune disorders that can lead to recurrent multilobar pneumonia is long; these infections are sometimes the first manifestation of such disorders.14
Primary immunodeficiencies include disorders of antibody, cell-mediated immunity, complement, and phagocytosis. Children with an antibody deficiency present with recurrent sinopulmonary infections due to encapsulated bacteria and enteroviruses. Individuals with defects in cell-mediated immunity, such as severe combined immunodeficiency (SCID), DiGeorge syndrome, and Wiskott-Aldrich syndrome (WAS), may have difficulty with recurrent pneumonia due to pyogenic bacteria, Pneumocystis carinii, and viruses. Patients with complement deficiencies most often present with bacteremia, septic arthritis, and meningitis caused by encapsulated bacteria. Phagocytic disorders such as chronic granulomatous disease (CGD), are characterized by infections of the skin, reticuloendothelial system, and respiratory tract caused by catalase-positive bacteria or fungus.14
Recurrent diffuse pneumonia may also be caused by secondary immunodeficiency from chemotherapy, steroid therapy, sickle cell disease, diabetes, or human immunodeficiency virus. Risk factors for HIV must be assessed in a child with other recurrent infections, because respiratory infections such as Pneumocystis carinii pneumonia are common in acquired immunodeficiency syndrome.4
Mucociliary dysfunction. Because natural clearance of the airway can be compromised by a disorder of the mucociliary system, the physician must not overlook disorders such as CF and PCD as causes of recurrent lower respiratory infection.
CF is an inherited autosomal recessive disorder recognized by a classic triad of chronic pulmonary disease, pancreatic insufficiency, and elevated sweat chloride concentration. The cause of CF is a defect in a single gene on chromosome 7 that encodes a protein called the CF transmembrane regulator (CFTR). The defect results in abnormalities in the electrolytes and fluid transport in the airways and other organs containing exocrine glands. It predisposes to a paucity of water in mucous secretions, leading to thick secretions in the airway that impair mucociliary clearance, cause obstruction, and lead to secondary infection with organisms, such as Staphylococcus aureus and Pseudomonas aeruginosa.5,16
The inflammatory response initially manifests as chronic bronchiolitis and bronchitis but, ultimately, causes structural changes in the airways and produces bronchiolectasis and bronchiectasis. Recurrent pneumonia with chronic sinusitis, steatorrhea, or failure to thrive should lead you to order a sweat chloride test. Because CF can present across a wide spectrum, however, do not overlook the possibility of CF when a child presents solely with recurrent lower respiratory infections.5
PCD, another autosomal recessive disorder, is caused by ultrastructural defects in the cilia or abnormal organization of microtubules within each cilium. These defects cause abnormal beating of the cilia and, consequently, impaired mucociliary clearance, leading to retention of secretions and, in turn, to recurring respiratory tract infection. A child with recurrent pneumonia, chronic otitis media, or sinusitis must be evaluated for PCD once other diagnoses, such as CF and immunodeficiency, have been excluded.17 As with CF, however, the spectrum of presentation for PCD is wide. Kartagener syndrome is the most severe clinical expression of PCD. Patients with this syndrome have situs inversus, chronic sinusitis, nasal polyposis, and bronchiectasis.17
Congenital heart disease. Children with congenital heart disease are predisposed to recurrent multilobar pneumonia, especially those with an anomaly or chamber enlargement that causes obstruction. As noted, obstruction is a predisposing factor for pulmonary infection. An enlarged cardiac chamber and pulmonary arteries can cause extrinsic compression of the airway, impairing its drainage.
Also at risk of recurrent multilobar pneumonia are children with a large volume, left-to-right shunt such as ventricular septal defect, patent ductus arteriosus, and atrial septal defect. The shunt increases pulmonary blood flow, leading to pulmonary edema and congestion. Impaired drainage due to pulmonary edema and congestion may predispose to secondary infection, although the exact mechanism by which a large volume, left-to-right shunt increases the occurrence of pulmonary infection is unclear.18
Structural abnormalities. Although rare, structural abnormalities such as tracheobronchomegaly, cartilage deficiency, and segmental bronchomalacia can lead to bronchiectasis and, consequently, recurrent multilobar pneumonia.
Bronchopulmonary dysplasia. Children with BPD have risk factors that predispose them to recurrent pneumonia. These include feeding difficulties that make them susceptible to aspiration, an increased incidence of bronchomalacia, impaired airway clearance mechanisms, focal airway strictures, and a high incidence of GERD.5
Other conditions. Last, conditions such as pulmonary hemosiderosis (PH), hypersensitivity pneumonitis (HP), alpha1-antitrypsin (A1AT) deficiency, pulmonary alveolar proteinosis (PAP), and pulmonary-renal syndromes must be considered as the cause of recurrent multilobar pneumonia.
PH, a combination of pulmonary infiltrates and iron-deficiency anemia, is characterized by accumulation of iron as hemosiderin within the macrophages in the interstitium and alveolar spaces. It can occur either as a primary disease of the lungs or secondary complication of cardiac or systemic disease. In children, the primary form is more common. PH is sometimes associated with allergy to cow's milk.19
HP, another rare cause of recurrent pneumonia in children, is an inflammatory lung disease that is usually the result of repeated inhalation of organic dusts. Most cases are related to having pet birds or raising pigeons; other causes include indoor mold exposures. The primary immunologic test is the detection of relevant precipitating antibodies. The condition improves with removal of the antigen.20
Alpha1-antitrypsin, a glycoprotein produced in the liver, inhibits neutrophil elastase, a protease capable of cleaving elastin, the macromolecule that provides elastic recoil to connective tissue. A1AT deficiency is a rare genetic cause of recurrent pulmonary infection in children, characterized by a serum A1AT level less than 35% of normal, emphysema that commonly develops by age 30 to 40, and, to a lesser extent, liver disease, usually manifesting in the neonatal period. Liver involvement is its most common presentation in childhood. The destruction of pulmonary tissue and subsequent development of emphysema in the fourth decade of life provides an environment for recurrent lung infections.
PAP is a rare disorder characterized by abnormal accumulation of intra-alveolar surfactant. Acquired PAP, the more common type, usually presents as progressive dyspnea of gradual onset, at times associated with minimally productive cough, weight loss, and low-grade fever. Most cases require open lung biopsy for diagnosis.21
After the initial history, physical examination, and chest radiographs, the physician must take a systematic approach to narrowing the possible diagnosis (Figures 2 and 3).
Evaluation of suspected aspiration should begin with a barium swallow, which can show structural defects and abnormalities of swallowing. It is not, however, sensitive for chronic aspiration of small quantities of secretions or food. A pH probe may confirm GER but does not provide specific information about aspiration. If bronchoscopy is done to rule out any other cause, bronchoalveolar lavage (BAL) should be performed to look for lipid-laden macrophages.
For the child who is wheezing, do not assume that infiltrates seen on a chest film have an infectious basis. If there is a family history of asthma and atopy, the answer may come from pulmonary function testing with exercise challengeif the child's age allows it. If the child is too young to undergo such testing, a trial of a bronchodilator may be diagnostic and therapeutic. If there is any possibility the child has CF, obtain a sweat test. Keep in mind that manifestations of pancreatic insufficiency are absent in 10% to 15% of patients with CF. Never believe, therefore, that a child "looks too good" to have CF.
Once the diagnoses of CF and immunodeficiency have been excluded in a child with recurrent pneumonia, otitis media, and sinusitis, mucociliary function should be evaluated by assessing ciliary function and morphology. A bronchial biopsy, or scrapings or a brushing of nasal mucosa, can also be examined on light microscopy for ciliary waveform and beat pattern, and on electron microscopy for ultrastructure. Evaluation for PCD should be done a few weeks after the patient has recovered from a respiratory tract infection, to avoid confusion with temporarily acquired ciliary defects that are a consequence of recent injury. Mucociliary clearance can be assessed in older children by time-to-taste perception of a saccharin particle placed on the inferior nasal turbinate.
Immunodeficiency evaluation is necessary in a child with recurrent or prolonged pneumonia. Begin with a complete blood count with differential and peripheral smear. This readily available test provides important diagnostic information about a number of immunodeficiencies, discussed in ("What the CBC can show").
The initial screening test for humoral immune function is the quantitative measurement of serum immunoglobulins (G, A, M). A clue to immunodeficiency may be a normal IgG level that is at the low end in a child with recurrent pneumonia. In such a case, it is essential to assess antibody function; antibody levels generated in response to childhood immunization with tetanus toxoid or Haemophilus influenzae protein conjugate vaccine are convenient numbers to check. In children older than 2 years, it is also important to assess antibody response to 23-valent pneumococcal capsular polysaccharide vaccine. The role of IgG subclass levels is controversial; their significance in the presence of a normal antibody response to protein and polysaccharide antigens is unknown.
Evaluation of cell-mediated immunity should include a lymphocyte count, T lymphocyte enumeration (CD4, CD8), HIV serologic analysis, and delayed hypersensitivity skin tests.
Most genetically determined deficiencies of complement can be detected with the total serum hemolytic complement (CH50) assay. Evaluation of phagocytic cells usually entails assessment of both their number and function. The most common phagocytic disorder, chronic granulomatous disease, can be identified by the nitroblue tetrazolium (NBT) dye test.
Congenital heart disease may be diagnosed on electrocardiogram and echocardiogram. If you suspect a structural defect, consider bronchoscopy or a multislice CT scan of the chest. Last, if clinical suspicion of other causes of recurrent multilobar pneumoniaPH, HP, A1AT, PAPis strong, consider an appropriate work-up. For PH, this would include BAL, gastric washings, or lung biopsy for Prussian blue staining; for HP, relevant precipitating antibodies by immunoelectrophoresis or Ouchterlony double gel diffusion; for A1AT, the serum alpha1-antitrypsin level; and for PAP, BAL or lung biopsy for periodic acid-Schiff (PAS) staining.
1. Dowell SF: Mortality from pneumonia in children in the United States, 1939 through 1996. N Engl J Med 2000;342:1399
2. Gaston B: Pneumonia. Pediatr Rev 2002;23:132
3. Owayed AF, Campbell DM, Wang EE: Underlying causes of recurrent pneumonia in children. Arch Pediatr Adolesc Med 2000;54:190
4. Wald ER: Recurrent and nonresolving pneumonia in children. Semin Respir Infect 1993;8:46
5. Vaughan D, Katkin J: Chronic and recurrent pneumonias in children. Semin Respir Infect 2002;17:1
6. Schidlow DV, Callahan W: Pneumonia. Pediatr Rev 1996;17:30
7. Shears BJ: Recurrent pneumonia in children. Pediatr Ann 2002;31:1098
8. Sawin R: Pediatric chest lesions. Pediatr Clin North Am 1998;4:861
9. Muniz AE, Joeffe MD: Foreign bodies, ingested and inhaled. Contemporary Pediatrics 1997;78(12):78
10. McDowell KM, Kercsmar CM: Evaluating the child with recurrent unilobar pneumonia. J Respir Dis 1994; 15:633
11. Gilkeson RC, Ciancibello LM, Hejal RB, et al: Tracheobronchomalacia: Dynamic airway evaluation with multidetector CT. AJR Am J Roentgenol 2001;176:205
12. Altes TA: Multislice computed tomographic scanning: Technological innovations bring new indications in pediatric chest CT. Pediatr Ann 2002;31:671
13. Avital A, Godfrey S, Bortz R, et al: Gavaging the infant lung. Pediatr Pulmonol 2002;34:388
14. Lederman H: The clinical presentation of primary immune deficiencies. Clinical Focus on Primary Immune Deficiencies, 2002;1(10):1
15. Eigen H, Laughlin JJ, Homnighausen J: Recurrent pneumonia in children and its relationship to bronchial hyperreactivity. Pediatrics 1982;70:698
16. McDowell KM, Kercsmar CM: When a child has recurrent multilobar pneumonia. J Respir Dis 1994; 15:66
17. Turcios NL: Does your patient have primary ciliary dyskinesia? The Journal of Respiratory Diseases for Pediatricians 2001;3(2):96
18. Lister G, Fontan T: Congenital Heart Disease, in Respiratory Disease in Children, Loughlin G, Eigen H (eds). Philadelphia, J P Lippincott, 1999; pp 601619
19. Turcios NL, Cintas M: Case report: A child with lung infiltrates and anemia. Resident and Staff Physician 1992;38:77
20. Zacharisen M, Fink J: Pediatric hypersensitivity pneumonitis: The keys to early detection. The Journal of Respiratory Diseases for Pediatricians 2002;4:3
21. Seymour JF, Presneill JJ: Pulmonary alveolar proteinosis. Am J Respir Crit Care Med 2002;166:215
22. Case Records of Massachusetts General Hospital, N Engl J Med, 2002;347:13
Information obtained from a complete blood count with differential and peripheral smear can point you in the direction of a number of immunodeficiencies:
Neutropenia most often occurs secondary to immunosuppressive therapy, infection, malnutrition, and autoimmunity, but it may be a primary problem (congenital or cyclic neutropenia).
Persistent neutrophilia is characteristic of leukocyte adhesion molecule deficiency, and abnormal cytoplasmic granules may be seen in the peripheral smear of patients with Chediak-Higashi syndrome.
Lymphopenia is often a presenting feature of T-cell immunodeficiency or combined immunodeficiency, such as severe combined immunodeficiency and DiGeorge syndrome.
Thrombocytopenia may occur as a secondary manifestation of immunodeficiency, but is often a presenting manifestation of Wiskott-Aldrich syndrome.
Splenic dysfunction may be revealed by examining red blood cell morphology. Howell-Jolly bodies may be visible in the peripheral blood of patients with splenic dysfunction or asplenia.
Nelson Turcios, Parul Patel. Pneumonia that recurs: Your diagnostic challenge. Contemporary Pediatrics 2003;3:82.