Whole lung lavage

Last updated
Whole lung lavage
Other namesLung washing
ICD-9-CM 33.99

Whole lung lavage (WLL), also called lung washing, is a medical procedure in which the patient's lungs are washed with saline (salt water) by filling and draining repeatedly. It is used to treat pulmonary alveolar proteinosis, in which excess lung surfactant proteins prevent the patient from breathing. [1] [2] Some sources consider it a variation of bronchoalveolar lavage. [3]

Contents

WLL has been experimentally used for silicosis, [4] other forms of mineral inhalation, and accidental inhalation of radioactive dust. [5] It appears to effectively remove these foreign particles. [4] [6] WLL treatments may slow down the lung function decline of miners with pneumoconiosis. [7]

Medical uses

High magnification micrograph of pulmonary alveolar proteinosis.The images show the characteristic airspace filling with focally dense hyaline globs. Pulmonary alveolar proteinosis -3- high mag.jpg
High magnification micrograph of pulmonary alveolar proteinosis .The images show the characteristic airspace filling with focally dense hyaline globs.

Whole lung lavage (WLL) is primarily used for treating conditions like pulmonary alveolar proteinosis (PAP), where it helps remove accumulated surfactant proteins from the lungs. [8] However, its application extends to other respiratory conditions, including Acute Respiratory Distress Syndrome (ARDS).In the context of ARDS, whole lung lavage has been explored as a treatment method, especially in experimental models. Studies have shown that WLL can be used to deplete surfactant, followed by the administration of surfactant replacement therapies. This approach helps improve lung function and oxygenation in conditions like neonatal ARDS.WLL is not a standard treatment for ARDS but is used in research settings to model and study ARDS treatment strategies. The primary goal in these scenarios is to understand how surfactant therapy and mechanical ventilation strategies can be optimized to treat ARDS more effectively. [9]

Procedure and technique

WLL is not a standardized procedure. Patients are usually first put under general anesthesia. A double lumen endotracheal tube is used to keep one lung breathing while the other is being washed. The lung to be washed is filled with fluid by gravity, then drained. Drainage can be done by suction [2] or gravity. [10] Some versions add a shaking step between the filling and draining to help with the washing. [2] The procedure typically uses 1020 liters of fluid per patient, but severe cases require up to 50. [2]

Variations on the WLL include a "mini-WLL" with reduced infusion volume. [11] Reducing the suction power seems to reduce lung injury. [12]

Solutions

Saline solution NaCl 0,9%25 500ml white background.jpg
Saline solution

The primary solution used in WLL is a sterile, isotonic saline solution. This solution closely matches the osmolarity of body fluids, making it gentle on the lung tissues. The saline serves several purposes. It helps dissolve the surfactant and proteinaceous material deposited in the alveoli, facilitating its removal from the lungs.Saline instillation helps maintain lung expansion during the lavage process, preventing atelectasis (collapse of lung tissue). The total volume of saline used can vary but typically ranges from 15 to 20 liters per lung, administered in aliquots of 500 to 1000 ml. Exogenous surfactant may be administered to help restore normal lung function after lavage. [13]

Devices

A double-lumen endotracheal tube (DLT) is used to isolate each lung. This allows one lung to be ventilated while the other lung is lavaged. The DLT has two separate lumens for independent lung ventilation and lavage.It ensures that the patient maintains adequate oxygenation during the procedure, as one lung remains functional while the other is being washed [8]

Double-lumen endobronchial tube Carlens.jpg
Double-lumen endobronchial tube

Adverse effects

Whole lung lavage (WLL) is a relatively safe procedure when performed by experienced medical teams, but it carries some risks and potential adverse effects. Here are the main complications and adverse effects associated with WLL. During the procedure, one lung is ventilated while the other is being lavaged, which can temporarily reduce oxygenation. Hypoxemia and dypsnea is a common but usually manageable complication, and oxygen levels are closely monitored throughout the procedure [8]

Mechanism of action

Removal of Accumulated Surfactant

In PAP, surfactant proteins and lipids accumulate in the alveoli, impairing gas exchange and leading to respiratory insufficiency. WLL works by instilling large volumes of saline into the lung, which helps to dissolve and mobilize these accumulated materials. The saline, along with the dissolved surfactant, is then drained from the lung, effectively clearing the alveolar spaces. [13]

Restoration of Alveolar Function

By physically washing out the debris and excess surfactant, WLL restores the normal architecture of the alveoli. This improves their ability to facilitate gas exchange, leading to better oxygenation of the blood and overall respiratory function [14]

Reduction of Inflammatory Mediators

In addition to surfactant removal, WLL can help reduce the concentration of inflammatory mediators within the alveoli. This can be particularly beneficial in conditions involving lung inflammation, as it helps to alleviate the inflammatory response and promote healing of the lung tissue. [13]

Improvement of Lung Compliance and Oxygenation

The removal of excess material from the alveoli improves lung compliance (the ability of the lungs to expand and contract). This leads to more effective ventilation and better oxygenation of the blood. Patients often experience a significant improvement in symptoms such as shortness of breath following WLL [15]

History

In 1963, Dr. Jose Ramirez-Rivera at the Veterans’ Administration Hospital in Baltimore tried repeated instillation of normal saline by a transtracheal plastic catheter positioned in one lung at a time in a series of two patients. Aliquots of 100 mL of warmed saline were instilled at a rate of 50–60 drops per minute. This process was repeated four times a day for 2–3 weeks. This technique showed improvement in chest-X-ray, diffusion capacity and histo-pathological findings. It was a prolonged and distressing procedure. The technique was thought to be imperfect and therefore denounced by many physicians at that time. In 1964, Ramirez-Rivera used a double lumen endotracheal tube (DLT) to isolate each lung, instilling up to 3 L saline containing heparin or acetylcysteine. This trial provided evidence that such a procedure was safe and feasible. Over the next four decades, the procedure has been further refined using general anesthesia, increased lavage volumes use of saline alone and by performing bilateral sequential WLL in the same treatment session [8]

See also

Related Research Articles

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<span class="mw-page-title-main">Pulmonary alveolus</span> Hollow cavity found in the lungs

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<span class="mw-page-title-main">Acute respiratory distress syndrome</span> Respiratory failure due to widespread inflammation in the lungs

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common.

<span class="mw-page-title-main">Pulmonary alveolar proteinosis</span> Medical condition

Pulmonary alveolar proteinosis (PAP) is a rare lung disorder characterized by an abnormal accumulation of surfactant-derived lipoprotein compounds within the alveoli of the lung. The accumulated substances interfere with the normal gas exchange and expansion of the lungs, ultimately leading to difficulty breathing and a predisposition to developing lung infections. The causes of PAP may be grouped into primary, secondary, and congenital causes, although the most common cause is a primary autoimmune condition in an individual.

<span class="mw-page-title-main">Interstitial lung disease</span> Diseases of the space or tissue between the alveoli of the lungs

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<span class="mw-page-title-main">Pulmonary surfactant</span> Complex of phospholipids and proteins

Pulmonary surfactant is a surface-active complex of phospholipids and proteins formed by type II alveolar cells. The proteins and lipids that make up the surfactant have both hydrophilic and hydrophobic regions. By adsorbing to the air-water interface of alveoli, with hydrophilic head groups in the water and the hydrophobic tails facing towards the air, the main lipid component of surfactant, dipalmitoylphosphatidylcholine (DPPC), reduces surface tension.

<span class="mw-page-title-main">Pulmonary hemorrhage</span> Medical condition

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<span class="mw-page-title-main">Acute interstitial pneumonitis</span> Medical condition

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High-frequency ventilation is a type of mechanical ventilation which utilizes a respiratory rate greater than four times the normal value and very small tidal volumes. High frequency ventilation is thought to reduce ventilator-associated lung injury (VALI), especially in the context of ARDS and acute lung injury. This is commonly referred to as lung protective ventilation. There are different types of high-frequency ventilation. Each type has its own unique advantages and disadvantages. The types of HFV are characterized by the delivery system and the type of exhalation phase.

<span class="mw-page-title-main">Surfactant protein B</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">Diffuse alveolar damage</span> Non-fatal disease of the lungs

Diffuse alveolar damage (DAD) is a histologic term used to describe specific changes that occur to the structure of the lungs during injury or disease. Most often DAD is described in association with the early stages of acute respiratory distress syndrome (ARDS). It is important to note that DAD can be seen in situations other than ARDS and that ARDS can occur without DAD.

Surfactant metabolism dysfunction is a condition where pulmonary surfactant is insufficient for adequate respiration. Surface tension at the liquid-air interphase in the alveoli makes the air sacs prone to collapsing post expiration. This is due to the fact that water molecules in the liquid-air surface of alveoli are more attracted to one another than they are to molecules in the air. For sphere-like structures like alveoli, water molecules line the inner walls of the air sacs and stick tightly together through hydrogen bonds. These intermolecular forces put great restraint on the inner walls of the air sac, tighten the surface all together, and unyielding to stretch for inhalation. Thus, without something to alleviate this surface tension, alveoli can collapse and cannot be filled up again. Surfactant is essential mixture that is released into the air-facing surface of inner walls of air sacs to lessen the strength of surface tension. This mixture inserts itself among water molecules and breaks up hydrogen bonds that hold the tension. Multiple lung diseases, like ISD or RDS, in newborns and late-onsets cases have been linked to dysfunction of surfactant metabolism.

<span class="mw-page-title-main">Emphysema</span> Air-filled enlargement in the bodys tissues

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<span class="mw-page-title-main">Pathophysiology of acute respiratory distress syndrome</span>

The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure. It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.

<span class="mw-page-title-main">Lipid-laden alveolar macrophage</span> Pathological cells in lung

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<span class="mw-page-title-main">Collateral ventilation</span>

Collateral ventilation is a back-up system of alveolar ventilation that can bypass the normal route of airflow when airways are restricted or obstructed. The pathways involved include those between adjacent alveoli, between bronchioles and alveoli, and those between bronchioles . Collateral ventilation also serves to modulate imbalances in ventilation and perfusion a feature of many diseases. The pathways are altered in lung diseases particularly asthma, and emphysema. A similar functional pattern of collateralisation is seen in the circulatory system of the heart.

References

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