The Clinical Significance of Collateral Ventilation.

Oxygen delivery and carbon dioxide removal being critical to cell survival, mammals have developed collateral vascular and ventilation systems to ensure tissue viability. Collateral ventilation, defined as ventilation of alveoli via pathways that bypass normal airways, is present in humans and many other species. The presence of collateral ventilation can be beneficial in certain disease states, whereas its relative absence can predispose to other diseases. These well defined anatomical pathways contribute little to ventilation in normal humans, but modulate ventilation perfusion imbalance in a variety of diseases, including obstructive diseases, such as asthma and emphysema. These pathways can be affected by pharmaceuticals and inhaled gas compositions. The middle lobe and lingula, constrained by their isolated, segmental anatomy, have reduced collateral ventilation, which predisposes them to disease. Recently, attempts to improve the quality of life of patients with emphysema, by performing nonsurgical lung volume reduction via use of endobronchial valves, have led to mixed results, because the role of collateral ventilation in the success or failure of the procedure was not initially appreciated. This review describes the anatomical pathways of collateral ventilation, their physiology and relationship to disease states, their modulatory effects on gas exchange, treatment considerations, and their effect on diagnostic procedures.

Middle lobe syndrome: a rare presentation of allergic bronchopulmonary aspergillosis.

Allergic bronchopulmonary aspergillosis (ABPA) is a disease predominantly seen in susceptible asthmatic subjects, due to a hypersensitivity phenomenon caused by colonisation of the airways by Aspergillus species. Although collapse, both lobar and segmental due to mucoid impaction, is not uncommon in ABPA, a middle lobe syndrome (MLS) secondary to ABPA is rather an uncommon association. We report this rare and unusual clinical presentation in a 36-year-old male, who presented for evaluation of a "non resolving pneumonia". Imaging suggested the presence of a MLS and central bronchiectasis. Further investigations revealed that the patient met 6/8 of the essential diagnostic criteria for ABPA. Appropriate therapy with oral corticosteroids resulted in remarkable symptomatic improvement.

Middle lobe syndrome: a review of clinicopathological features, diagnosis and treatment.

Middle lobe syndrome (MLS) is a rare but important clinical entity that has been poorly defined in the literature. It is characterized by recurrent or chronic collapse of the middle lobe of the right lung but can also involve the lingula of the left lung. Pathophysiologically, there are two forms of MLS, namely obstructive and nonobstructive. Obstructive MLS is usually caused by endobronchial lesions or extrinsic compression of the middle lobe bronchus such as from hilar lymphadenopathy or tumors of neoplastic origin, resulting in postobstructive atelectasis and pneumonitis. In the nonobstructive type, no obstruction of the middle lobe bronchus is evident during bronchoscopy or with computerized tomography of the chest. The etiology of the nonobstructive form is not completely understood. Inefficient collateral ventilation, infection and inflammation in the middle lobe or lingula are thought to play a role, and bronchiectasis is the most common histological finding. Patients with proven endobronchial lesions or malignancy are usually offered surgical resection directly. This contrasts with nonobstructive MLS, where most patients respond to medical treatment consisting of bronchodilators, mucolytics and broad-spectrum antibiotics. However, some patients do not respond to conservative treatment and may suffer irreversible damage of the middle lobe or lingula, in addition to having recurrent symptoms of infection or inflammation. These selected patients can be offered surgical resection of the middle lobe or lingula, which is associated with a low mortality rate and favorable outcome.

[Pulmonary function of children with right lung middle lobe syndrome].

OBJECTIVE: To study the changes of pulmonary function in children with right lung middle lobe syndrome before and after treatment. METHODS: Thirty children with right lung middle lobe syndrome were classified into two age groups: < or =4 years old and >4 years old. Pulmonary function was tested by the 2600-type and the MIR-type pulmonary function spirometry in the < or =4 years and the >4 years age groups, respectively before and after treatment. Terminal flows/peak expiratory flow (25/PF) and the percentage of tidal volume to peak tidal expiratory flow (% V-PF) were measured in the <4 years age group. Forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and peak expiratory flow (PEF) were measured in the >4 years age group. RESULTS: The values of 25/PF and %V-PF in the < or =4 years age group were 0.42+/-0.08 and 0.28+/-0.03, respectively before treatment. The values were improved after treatment (0.58+/-0.12 and 0.39+/-0.06 respectively) (P<0.05). The values of FVC, FEV1 and PEF were 1.75+/-0.32, 1.36+/-0.52 and 2.56+/-0.78, respectively in the >4 years age group before treatment. The values were also improved after treatment (2.37+/-0.78, 2.08+/-0.65 and 3.68+/-0.80 respectively) (P<0.05). CONCLUSIONS: There are significant differences in the pulmonary function before and after treatment in children with right lung middle lobe syndrome. The pulmonary function can return to normal after treatment.

Outcome after right middle lobe syndrome.

The long-term pulmonary consequences of right middle lobe syndrome (RMLS) in childhood are not known. Therefore, outcome was evaluated in 17 children with RMLS diagnosed in early childhood (mean age, 3.3 years; SD, 1.1 year). Mean age at follow-up was 10.1 years (SD, 2.6 years). RMLS was defined as atelectasis of the right middle lobe (RML) of at least 1 month's duration and visible on the lateral view of the chest radiograph as a wedge-shaped density extending from the hilum anteriorly and downward. Seventeen children without personal history of allergy or respiratory tract disease were studied as control group. Five of 17 study group children had ongoing respiratory problems: symptoms of asthma were present in 4 patients, and cylindrical bronchiectasis was present in one patient. Chest radiograph at follow-up was abnormal in six patients. Pulmonary function tests, including mean and SEM for vital capacity (VC) (82% of predicted +/- 7 vs 94% predicted +/- 3), FEV1 (77% of predicted +/- 12 vs 96% of predicted +/- 4) and their ratio (75 +/- 5 vs 85 +/- 3) were significantly lower in patients with ongoing respiratory symptoms than in the control children. The provocative dose causing a 20% decrease in FEV1 (PD20) of methacholine was significantly lower in patients with ongoing symptoms at follow-up than in control children and in patients without symptoms at follow-up (2.8[2.2 to 3.1] vs 4.5[2.2 to 8.8] and 9.2[2.3 to 24] mg/mL; median and P25-75, p < 0.05). Age at initial diagnosis tended to be younger in patients with ongoing symptoms at follow-up (2.3 +/- 0.7 years vs 3.8 +/- 0.4 years; p < 0.08).

[Middle lobe syndrome]. / Síndrome del lóbulo medio.

Middle lobe syndrome (MLS) or atelectasis syndrome can affect any pulmonary lobe but occurs more frequently in the right middle lobe. Only 15 per cent of the reported cases are children. We report two cases of MLS in two boys of 4 and 12 years of age who were referred to our institution because they had suffered from recurrent pneumonies of the right middle lobe for ten months and six years respectively. We performed chest radiographs, computed tomography scanning, ventilation-perfusion scintigraphy and flexible bronchoscopy. The evolution in both cases to an atelectasic middle lobe with pulmonary shrinkage and lack of perfusion was the indication to lobectomy. Histological examination showed a bronchial obstructive process in the young patient and a chronic non specific inflammation of the pulmonary parenchyma in both. The resection brought about a cure. The identification of MLS is usually a late diagnosis. Thus, if atelectasis persists after an adequate medical therapy, resection of the lobe is indicated.

Peripheral middle lobe syndrome.

Classically, the middle lobe syndrome has been described as being caused by a central obstruction. Clinical records and radiologic findings were reviewed in 129 patients examined between 1955-1981 who had chronic disease in the right middle lobe and/or lingula. Fifty-eight patients (45%) had no evidence of a central obstructive lesion. The majority were middle-aged women with histories of chronic cough and chest pain. Bronchoscopic and radiologic evaluation served to exclude central lesions. Surgical confirmation was available in 38 patients. Pathologic study showed varying degrees of chronic inflammation, pneumonia, and bronchiectasis. Surgical results were excellent in isolated disease. Chronic atelectasis and pneumonitis of the right middle lobe and/or lingula do not always imply central obstruction. A lack of collateral ventilation is a plausible theory to explain the pathophysiology in such patients.

Middle lobe syndrome.

A review of the major literature dealing with the middle lobe syndrome shows that benign inflammatory disease is the most common etiological factor (62%), with bronchiectasis responsible for at least a quarter of the patients in these series. Early workers indicated that carcinoma rarely originates in the right middle lobe; however, 22% of patients reviewed had malignant tumors as a cause of the syndrome. The original view that bronchial compression was the pathophysiological abnormality leading to development of the syndrome has been rejected by more recent authors. The focus has now turned to the relative isolation of the middle lobe, especially when a complete minor fissure is present. This isolation prevents the aerating effects of collateral ventilation of the upper lobe from reaching the middle lobe and thus impairs the clearing of secretions from the middle lobe bronchus. Bronchoscopy and bronchography are vital in the rational approach to this syndrome. Severe stenosis of the bronchus or tumor can be seen endoscopically in about 40% of patients, and bronchography will demonstrate an anatomical abnormality more than 70% of the time. Both the surgical and the medical approaches to therapy have been endorsed strongly by various authors in the 30 years since the syndrome was described. It now appears that bronchoscopy and, if need be, bronchography should be undertaken to rule out an endobronchial lesion. Timing of these studies will depend on the patient's age, with early examination advocated for the older patient at high risk for lung cancer. If there is reasonable evidence that the process is benign, medical management should be attempted. Lobectomy is performed if malignancy is suspected or if medical therapy fails.

Collateral ventilation and the middle lobe syndrome.

The mechanics of collateral ventilation in the right middle lobe of 5 young, normal volunteers were studied using a bronchoscopic wedge technique, and the results were compared with those from an upper lobe of the same subjects. At functional residual capacity, the resistance to collateral ventilation in the right middle lobe was 4,042 +/- 559 cm H2O per liter per sec (mean +/- SE), whereas that of the upper lobes was 799 +/- 168 cm H2O per liter per sec. The time constant for collateral ventilation could not be measured in the right middle lobe of any of the subjects because it exceeded their breath-holding times of 6 to 16 sec. The time constant for collateral ventilation in the upper lobes was 4.5 +/- 1.0 sec. We concluded that collateral ventilation in the right middle lobe of young normal subjects is characterized by a high resistance and a long-time constant relative to the upper lobes. This is probably explained by a greater ratio of pleural surface to nonpleural surface in the right middle lobe as compared to the upper lobes. We suggest that ineffective collateral ventilation is a major factor in the pathophysiology of the Middle Lobe Syndrome.