Comprehensive Review of Chest Tube ManagementA Review


Abstract

Importance  Thoracostomy, or chest tube placement, is used in a variety of clinical indications and can be lifesaving in certain circumstances. There have been developments and modifications to thoracostomy tubes, or chest tubes, over time, but they continue to be a staple in the thoracic surgeon’s toolbox as well as adjacent specialties in medicine. This review will provide the nonexpert clinician a comprehensive understanding of the types of chest tubes, indications for their effective use, and key management details for ideal patient outcomes.

Observations  This review describes the types of chest tubes, indications for use, techniques for placement, common anatomical landmarks that are encountered with placement and management, and an overview of complications that may arise with tube thoracostomy. In addition, the future direction of chest tubes is explored, as well as the management of chest tubes during the COVID-19 pandemic.

Conclusions and Relevance  Chest tube management is subjective, but the compilation of data can inform best practices and safe application to successfully manage the pleural space and ameliorate acquired pleural space disease.

Introduction

Thoracostomy tube, otherwise known as chest tube, insertion can be traced back to the fifth century bce when Hippocrates described using a hollow tin tube to drain what was likely an empyema.1 In 1889, valved tubes with air-tight seals were first reported to prevent outside atmospheric pressure from collapsing the lung on inspiration.2 In 1922, chest tubes were first documented in the postoperative care of patients undergoing modern thoracic surgery.3 They were used throughout World War II to restore lung function after traumatic thoracotomies, were used during the Korean War, and later became the standard of care for drainage of the pleural space for trauma during the Vietnam War.4 Chest tubes and their management continue to evolve and are modified to fit modern needs, including clinical conditions associated with the COVID-19 pandemic.

Indications

The potential space between the visceral pleura that envelops the lungs and the parietal pleura covering the chest wall, diaphragm, and mediastinum is the pleural cavity, which contains lubricating pleural fluid secreted by the parietal pleural capillaries. Air and abnormal fluid can accumulate in this space, causing mass effect and disruptions in the normal negative intrathoracic pressure.

When air fills the pleural cavity, it is called a pneumothorax, which is further categorized according to its etiology as primary spontaneous, secondary spontaneous, or traumatic.57 Chest tubes are used to evacuate air in the pleural cavity and reestablish the negative intrathoracic pressure, allowing the lung to reexpand and restore physiologic ventilation and cardiac function.69 A tension pneumothorax develops when air enters on inspiration and is unable to escape on expiration. This leads to effective mass effect on intrathoracic structures, such as the lung itself; mediastinal structures, such as the venae cavae; and cardiac chambers, resulting in hemodynamic compromise from restricted venous return and cardiac output. This is a medical emergency and should initially be managed with immediate needle thoracentesis to decompress trapped and expanding pleural air before the placement of a formal chest tube.

Chest tubes are also used to evacuate excessive fluid from the pleural cavity, which is known as a pleural effusion. When there is pus in the pleural cavity, then it is considered an empyema. There are several ways to evacuate fluid from the pleural cavity and chest tubes are only one of the many options. A Cochrane review from 201710 compared the surgical option of video-assisted thoracic surgery (VATS) with chest tube drainage of pleural empyema and found no difference in mortality or complications between the groups, but early VATS reduced the hospital length of stay. VATS has been considered the first-line treatment for retained hemothorax and empyemas with other modalities, such as intrapleural lytic therapy, reserved for poor operative candidates or as a second line treatment.11 However, a meta-analysis by Hendriksen et al11 found that treating retained hemothorax with lytic therapy rather than VATS allowed for an overall operative avoidance rate of 87% (95% CI, 81%-92%), with no heterogeneity in the pooled studies (Q = 10.2; df = 9; P = .33; I2 = 15.07%). The type of intrapleural lytic treatment is also important as Hendriksen et al11 found that using tissue plasminogen activator (t-PA) as the lytic agent allowed for a favorable number of patients to avoid surgical intervention compared with other lytic agents. The combination of t-PA and dornase (DNase) was associated with a 60% reduction in pleural fluid collection as seen on imaging and with a significant reduction in pleural opacity, compared with placebo in the randomized clinical trial by Rahman et al.12 When t-PA and DNase were used on their own as opposed to in combination, this study did not find a significant reduction in the pleural fluid collection compared with placebo.12 The evidence supports combining t-PA and DNase for intrapleural lytic therapy. Given the effectiveness of treating early-phase empyema with a chest tube and intrapleural use of t-PA and DNase, as well as the use of VATS to reduce length of hospital stay, the authors developed a multidisciplinary protocol with general thoracic surgery and interventional pulmonary medicine for the algorithmic care of patients presenting with empyema, starting with a small-bore chest tube placement followed by intrapleural use of t-PA and DNase. If this initial step is unsuccessful, the next stage of the pathway is thoracic surgical consultation for VATS decortication (Figure 1).

Types of Chest Tubes

Chest tubes come in a variety of sizes and materials to best suit the clinical needs of the patient. In the US, they are generally measured by the internal diameter of the tube in units of French. One increment of the French scale is equal to a one-third–millimeter diameter, (eg, 24F is equal to an 8-mm caliber). By most prevalent convention, a tube of 20F or larger is considered a large-bore chest tube and a tube less than 20F tube is considered a small-bore chest tube, although there are some studies that define a large-bore chest tube as larger than 14F.5,13,14 A common type of small-bore chest tube is a pigtail catheter, named because the tip coils at the end like a pig’s tail to prevent dislodgement.13

Small-bore chest tubes are used as the first-line treatment for pneumothorax, transudative pleural effusions, and simple empyemas, whereas large-bore chest tubes are often necessary for more viscous disease processes, such as a hemothorax and complex exudative effusions and empyemas.13,15 A meta-analysis by Chang et al5 demonstrated that small-bore chest tubes are associated with lower complications rates and shorter drainage duration and hospital stay compared with large-bore chest tubes. A randomized clinical trial by Hussain et al16 identified similar findings of a reduction in drainage duration and hospital stay with small-bore pigtail catheters compared with large-bore chest tubes in patients with secondary spontaneous pneumothorax. The most prominent advantage of a small-bore chest tube is its size, which allows for a smaller incision and decreased pain experienced by the patient.16,17 The randomized clinical trial by Kulvatunyou et al17 demonstrated a lower pain score in individuals with a pigtail catheter compared with a large-bore chest tube for traumatic pneumothorax. However, the small diameter of small-bore chest tubes may come at the cost of inefficient flow, as per Poiseuille’s law (ΔP = 8μLQ/πR4, where Δp is change in pressure, μ is viscosity, Q is flow and R is radius) the decreasing radius of small-bore chest tubes can lend to a lower flow rate, which is the reason large-bore chest tubes are necessary in conditions that would otherwise clog a smaller tube, such as high-viscosity (μ) fluid.5,13,15

Insertion

The placement of a chest tube is important and is performed by many different specialties in various settings. The ideal point of insertion is through an external landmark space known as the triangle of safety (Figure 2), which is bordered by the edge of the latissimus dorsi muscle, pectoralis major muscle, the base of the axilla, and transverse to the nipple line or inframammary fold, at or above the fifth intercostal space.13,14,1820 However, placement of chest tubes is also influenced by the indication. For an apical pneumothorax, a chest tube can be placed in the second intercostal space in the midclavicular line, although less comfortable for the patient, and adequate drainage of an unloculated pneumothorax can be performed via lateral insertion at the fifth intercostal space.14,18 If the tube is placed in the triangle of safety, it is important to place it in a line anterior to the anterior superior iliac spine. Placing in the tube in a line behind this surface landmark may cause the patient to lie on the tube when in the supine position and mechanically occlude the tube. For a pleural effusion, a lower intercostal space may be used for insertion but special care must be taken to avoid penetrating the diaphragm, and subsequently the liver on the right and spleen and bowel on the left.13

The 3 ways to insert a chest tube are dissective, Seldinger (often ultrasonography guided), and the trocar technique, again often ultrasonography guided.13,14,19,20 Ultrasonography can be an invaluable tool to safely identify internal landmarks for chest tube placement. Figure 3 presents a representative sonographic image demonstrating the target abnormal collection of pleural fluid, in the right chest, for chest tube drainage, and adjacent structures of atelectatic lung, diaphragm and liver. Figure 4A highlights an important step for chest tube placement, which is using a finder needle (often a syringe with local anesthetic) just above the target rib to avoid the intercostal neurovascular bundle and aspirating the pleural space to confirm the location of the pleural pathology. For dissective insertion, a 1- to 2-cm incision is made overlying the rib of choice (the authors do not tunnel to a rib above), a Schnidt tonsil clamp is used to bluntly dissect through the subcutaneous tissue, the 3 muscular layers of the intercostal space (ie, the external intercostal muscle, the internal intercostal muscle, and innermost intercostal muscle), transthoracic fascia, and the parietal pleural until the clamp enters the pleural cavity. When attempting to enter the fifth intercostal space, it is important to dissect not perpendicular to the chest wall, but generally posterior and apical, the direction that most tubes should be placed (Figure 4B). Dissecting perpendicular to the chest wall and into the fifth intercostal space can lead to the tube heading directly into the oblique fissure, and then be entrapped by the subsequent expanded lung, rendering the tube ineffective after lung expansion. After successful spreading into the pleura space, a finger is used to confirm entry into the pleural space and the presence of adhesions. Adhesions are not bluntly broken with the finger, as pleural adhesions are often vascular and blunt dissection can lead to small vessel disruption and subsequently hemothorax.13,14 The Seldinger technique uses guidewires and tract dilators to assist the tube into the pleural cavity, all under ultrasonography guidance.19,21 Lastly, the trocar method may be used; however, it is associated with more complications owing to the rigid tip of the trocar causing intrathoracic injuries and has subsequently fallen out of favor for chest tube insertion.19,20,22 Regardless of the insertion technique, the chest tube needs to be advanced on the superior edge of the rib to avoid the neurovascular bundle bordering the rib above.13,14 It should also be positioned posteriorly and advanced until the tip is in a posteroapical location. The tube should also be fully inserted to ensure that the most proximal (sentinel) hole is within the pleural space to allow the chest tube to function properly.14 Lastly, it is important to secure the chest tube with a suture to prevent it from falling out. Most tubes can be removed without suture skin closure, but in children and adults with very low body mass index (calculated as weight in kilograms divided by height in meters squared), placement of an untied adjunctive chest tube suture at the time of insertion allows for closure of skin defects at the time of tube removal, especially large-bore tubes, to prevent entraining atmospheric air with tube removal.

Management

Once a chest tube is placed, it is connected to a drainage device, which, like the chest tube itself, has evolved over the years. The first rendition was a 1-compartment system reported by Playfair23 in 1875, which used a 1-way valve to allow air to egress from the pleural cavity during expiration without returning on inspiration. In 1926, Lilienthal24 developed a 2-compartment system, which allowed the accumulation of fluid in the first collection bottle without compromising the efficiency of the system and its ability to drain, as would have been observed in the first model. Then, the 3-compartment system emerged in 1952 with Howe, which allowed collection, water sealing, and suction and manometer capabilities that are combined into a single pleural drainage unit (PDU).19,25 This forms the foundation of the modern PDU devices today, some of which are digitally operated.

Once placed, chest tubes may be attached to a PDU and set to active suction or to water seal, which is simple dependent drainage. The phrase “place a chest tube on water seal” is a misnomer, as modern PDUs have a constitutive water seal chamber that serves as a 1-way valve, preventing air from returning into the pleural space; placing a chest tube on water seal simply means taking the tube off active suction. The randomized clinical trial by Cerfolio et al26 found that water sealing the chest tube on postoperative day 2 after thoracic surgery resulted in a significant resolution of small air leak the following day, with the authors noting that large air leaks do not benefit from water sealing. Another randomized clinical trial27 demonstrated similar results of a shorter duration of air leak with early water sealing for postthoracic surgery chest tubes, which subsequently decreased the duration the chest tube was needed. Both of these studies, albeit randomized clinical trials, are limited by their small sample sizes. Brunelli et al28 performed a randomized clinical trial with a larger sample size, did not find an advantage with water seal over suction for postthoracic surgery patients and the authors favor a hybrid approach of moderate suction overnight and water sealing during the day to allow for mobilization of the patient. The systematic review and meta-analysis by Coughlin et al29 determined that there was no advantage of suction over water seal after thoracic surgery, with the exception of suction being superior to water seal in preventing a radiographic identification of pneumothoraces.

For patients with a traumatic chest injury, the systemic review and meta-analysis by Feenstra et al9 demonstrated evidence that favors low-pressure suction over water seal. This meta-analysis is limited in the number of studies, and therefore patient sample size, included. In addition, there are few patients with chest tubes in the setting of mechanical ventilation included in this study, which is an important subset of trauma patients. Patients who have an occult pneumothorax and are receiving positive pressure mechanical ventilation are at risk of developing a tension pneumothorax, therefore it may be necessary for a chest tube to be placed on suction in this subset of patients.30 Overall, the management of a chest tube depends on the indication for insertion with evidence favoring suction over water seal for both postthoracic surgery patients and traumatic chest injury patients, until resolution of air leak.

Removal

There are many factors that come into play when determining the correct time to remove a chest tube. The quality of the fluid should be free of chyle, or blood suggestive of active bleeding, and be nonpurulent.31,32 However, the quantity of fluid that is acceptable before the removal of a chest tube is without consensus, with varying recommended volume thresholds ranging from 200 mL per day to 500 mL per day.3133 Cerfolio et al32 performed a retrospective cohort analysis that demonstrated that chest tube removal up to 450 mL per day was acceptable in patients who underwent elective pulmonary resection. They reported that 364 of 1988 patients (18%) were able to go home sooner owing to surgeons changing to the higher threshold (450 mL per day) and only 11 patients (0.55%) were readmitted as a result of a recurrent symptomatic effusion. Grodzki et al34 tested this conclusion a year later and removed chest tubes at the higher threshold of 450 mL per day and found that 6 of 40 patients (15%) were readmitted with pleural effusions, thus leading the authors to revert to their original practice of following a threshold of 200 mL per day for chest tube removal. The limitation in the former study is the lack of reliable follow-up, which could account for the low readmission rate, and the limitation in the latter study is the small sample size. Larger randomized clinical trials would be helpful in clarifying this gap in our understanding.

Whether to remove the chest tube at the end of expiration or inspiration is another question that has been widely debated. Novoa et al31 recommended removing the chest tube at the end of expiration during a Valsalva maneuver, which corresponds to the time when the difference between the atmospheric pressure and pleural pressure is at its lowest.31 Other studies, such as French et al,35 emphasized the importance of a Valsalva maneuver during chest tube removal regardless of the respiratory phase in which it is removed. The chest tube should be removed swiftly and the defect in the chest wall should be closed with either a suture that was placed at the time of chest tube placement or with a properly occlusive dressing.

Complications

The retrospective review by Platnick et al36 found that certain risk factors, such as chest tube placement in the emergency department, placement by emergency medicine clinicians, and placement in patients with a body mass index greater than 30 were all associated with chest tube complications. However, the exact complication rate associated with chest tubes is variable and has been quoted as high as 40%.3638 The variability in the reported complication rate can be attributed to a lack of a universally accepted way to categorize the many different complications. Aho et al20 proposed a way to standardize the reporting of complications surrounding chest tubes to allow for easier recording and collection of data. The 5 complication categories proposed were insertional, positional, removal, infectious, and malfunction. Insertional complications include injury to intrathoracic or extrathoracic organs within 24 hours of insertion, which is a complication most common with chest tubes being inserted via the trocar technique.19,20 Positional complications are defined as occurring 24 hours after insertion, including erosions into adjacent organs or any tube kinking, obstruction, or being entrapped in the fissure after lung expansion.19,20 Removal complications encompass failure to seal the chest defect after the chest tube is removed, resulting in entraining atmospheric air, or the retention of any foreign objects after removal.20 Infectious complications involve any infection, either external from improper sterilizing techniques or internal with the development of an empyema.20 Malfunction complications include problems that may arise from the health care clinician managing the chest tube or equipment issues.20 Defining complications in these distinct categories allows clinicians to create a foundation to compare data collected in future studies and protocols to reduce the risk of complication associated with chest tubes.

COVID-19

Chest tube management during the COVID-19 pandemic, or any future coronavirus or H1N1 pandemic, is challenging owing to the risk of aerosolizing dangerous virions. Proper personal protective equipment, minimizing water seal, and using filters to decrease the number of aerosolized particles escaping into the air are modifications that have been implemented in many intensive care units around the world.37,39 A small observational cohort study40 found that connecting 2 closed underwater drainage systems in series with an air filter attached to the second system was associated with a decrease in the dissemination of coronavirus particles, as evidenced by a lack of COVID-19 infection reported in their health care workers during the study. However, this study was limited with its small power.

Future Directions

More recent studies are leaning toward conservative management in some specific pleural disease processes. The randomized clinical trial by Hallifax et al41 demonstrated that the use of ambulatory devices for the treatment of primary spontaneous pneumothorax compared with usual care, which included aspiration or chest tube insertion, was associated with a significantly shorter hospital length of stay. These findings suggest that this subset of patients can be treated in an outpatient setting and that ambulatory devices should be considered as an effective treatment strategy for this disease process. However, there was an increase in the number of adverse events associated with the treatment with ambulatory devices, including enlarging pneumothorax and problems associated with the device, such as kinking or dislodgement, which will require more research if this approach is going to replace the current standard of care.

In a study by Brown et al,42 conservative treatments, such as observation of moderate- to large-sized primary spontaneous pneumothorax, were found to be noninferior to the placement of a small-bore chest tube regarding resolution of the pneumothorax within 8 weeks. The study reports that 118 of 125 patients (94%) of patients undergoing conservative management did not require an invasive procedure, thus challenging the paradigm that all patients with a hemodynamic and respiratory stable primary pneumothorax should routinely undergo decompression with a chest tube as the first treatment option.

The routine placement of a chest tube after thoracic surgery is another area with emerging research. The randomized clinical trial by Zhang et al43 showed that the placement of a novel air-extraction double-lumen catheter was noninferior to the placement of a traditional chest tube in the incidence of a pneumothorax on postoperative day 1. The use of this air-extraction catheter was also associated with a significantly lower patient-reported pain score, which supports the argument that more conservative techniques can be used to optimize patient comfort without compromising clinical outcomes.

Conclusions

With the advancement of technology and the push toward less invasive approaches, the treatment of pleural conditions that were once managed solely by chest tubes continues to evolve. However, chest tubes are likely to continue to be a vital part of a clinician’s repertoire as they are still considered the standard of care for certain pleural disease processes and life-saving devices in others. It is imperative that trainees have a solid foundation on the management of chest tubes, as their use is a dynamic process that will continue to change as time progresses. This review highlights the studies that have shaped the way chest tubes are managed today and allows the reader to develop and cultivate their understanding.

FDA grants RET inhibitor breakthrough therapy designation for lung, thyroid cancers


The FDA granted breakthrough therapy designation to LOXO-292, a selective RET inhibitor, for the treatment certain patients with RET-altered non-small cell lung cancer or medullary thyroid cancer, according to the agent’s manufacturer.

The designation includes patients with RET-fusion positive NSCLC who have progressed on platinum-based chemotherapy and a PD-1 or PD-L1 inhibitor, and patients with RET-mutant thyroid cancer who have progressed following prior treatment and have no alternative treatment options.

The FDA based the breakthrough designation of LOXO-292 (Loxo Oncology) on the ongoing phase 1/phase 2 LIBRETTO-001 clinical trial of patients with RET-altered advanced solid tumors.

“We look forward to working with FDA to streamline the development of LOXO-292 in the two patient populations that have comprised the bulk of our initial clinical trial enrollment,” Josh Bilenker, MD, CEO of Loxo Oncology, said in a company-issued press release. “Given the many available therapies for non-small cell lung cancer and medullary thyroid cancer, we are pleased that LOXO-292 has shown encouraging data in refractory patients and hope to demonstrate the full potential of this treatment in additional populations over time.”

Nerve cells actively repress alternative cell fates, researchers find


A neural cell maintains its identity by actively suppressing the expression of genes associated with non-neuronal cell types, including skin, heart, lung, cartilage and liver, according to a study by researchers at the Stanford University School of Medicine.

 It does so with a powerful . “When this protein is missing, neural cells get a little confused,” said Marius Wernig, MD, associate professor of pathology. “They become less efficient at transmitting nerve signals and begin to express genes associated with other cell fates.”

The study marks the first identification of a near-global repressor that works to block many cell fates but one. It also suggests the possibility of a network of as-yet-unidentified master regulators specific to each cell type in the body.

“The concept of an inverse master regulator, one that represses many different developmental programs rather than activating a single program, is a unique way to control neuronal cell identity, and a completely new paradigm as to how cells maintain their throughout an organism’s lifetime,” Wernig said.

Because the protein, Myt1l, has been found to be mutated in people with autism, schizophrenia and major depression, the discovered mode of action may provide new opportunities for therapeutic intervention for these conditions, the researchers said.

Wernig is the senior author of the study, which will be published online April 5 in Nature. Postdoctoral scholars Moritz Mall, PhD, and Michael Kareta, PhD, are the lead authors.

Repressors

Myt1l is not the only protein known to repress certain cell fates. But most other known repressors specifically block only one type of developmental program, rather than many. For example, a well-known repressor called REST is known to block the neuronal pathway, but no others.

“Until now, researchers have focused only on identifying these types of single-lineage repressors,” said Wernig. “The concept of an ‘everything but’ repressor is entirely new.”

In 2010, Wernig showed that it is possible to convert skin into functional neurons over the course of three weeks by exposing them to a combination of just three proteins that are typically expressed in neurons. This “direct reprogramming” bypassed a step called induced pluripotency that many scientists had thought was necessary to transform one cell type into another.

 One of the proteins necessary to accomplish the transformation of skin to neurons was Myt1l. But until this study the researchers were unaware precisely how it functioned.

“Usually we think in terms about what regulatory programs need to be activated to direct a cell to a specific developmental state,” said Wernig. “So we were surprised when we took a closer look and saw that Myt1l was actually suppressing the expression of many genes.”

These genes, the researchers found, encoded proteins important for the development of lung, heart, liver, cartilage and other types of non-neuronal tissue. Furthermore, two of the proteins, Notch and Wnt, are known to actively block neurogenesis in the developing brain.

Blocking Myt1l expression in the brains of embryonic mice reduced the number of mature neurons that developed in the animals. Furthermore, knocking down Myt1l expression in mature neurons caused them to express lower-than-normal levels of neural-specific genes and to fire less readily in response to an electrical pulse.

‘A perfect team’

Wernig and his colleagues contrasted the effect of Myt1l with that of another protein called Ascl1, which is required to directly reprogram skin fibroblasts into neurons. Ascl1 is known to specifically induce the expression of neuronal genes in the fibroblasts.

“Together, these proteins work as a perfect team to funnel a developing cell, or a cell that is being reprogrammed, into the desired cell fate,” said Wernig. “It’s a beautiful scenario that both blocks the fibroblast program and promotes the neuronal program. My gut feeling would be that there are many more master repressors like Myt1l to be found for specific cell types, each of which would block all but one cell fate.”

Source:medicalxpress.com

Stem Cells Converted Into Lung Tissue.


Lung transplant recipients have a relatively low 10 year survival rate of about 28%. Cellular rejection of the donor organ occurs about 90% of the time, which brings additional obstacles for the patient and doctors. This might be about to change, as functional lung tissue has been created from human stem cells. The research comes from Hans-Willem Snoeck from the Columbia Center for Translational Immunology and was published in the current edition of Nature Biotechnology.

A couple of years ago, Dr. Snoeck was able to convert stem cells into the precursor endoderm cells that can eventually differentiate into lung cells. This was done with human embryonic stem cells as well as human induced pluripotent stem cells, which involve a bit more work but are easier to come by. Those precursor cells were shown to actually differentiate into six different respiratory tissues, including the coveted type II alveolar cells. which facilitate gas exchange and produce surfactant.

Type 2 alveolar cells, also called pneumocytes, are responsible for producing surfactant, the compound that allows the lungs to remain inflated with air. These type II cells also aid in gas exchange and lung repair.

The lung tissue produced by stem cells could give researchers a unique perspective to study the tissue and learn more about how lung diseases originate. This could lead to better treatment options for lung diseases.

If treatments do not work and transplant becomes inevitable, physicians can use the patient’s own cells to provide a new disease-free organ. This eliminates both the potential for cellular rejection as well as the stress of waiting on the transplant list. To make a replacement lung, researchers would first remove the patient’s lung and decellularize it, leaving only a cartilaginous scaffold. The stem cells would then be used to coat the scaffold and regrow functional tissue to be put back into the patient.

Though it is a long way from getting implanted into a human body, these results are exciting. A patent has been filed by Columbia University for their technique of converting induced pluripotent stem cells into the functional tissue.

Stop smoking, stay good-looking.


If bad lungs don't scare you then this should. Screenshot: tobaccobody.fi
If bad lungs don’t scare you then this should.
A public health agency in Finland is using an interesting approach to shock teens into not smoking

The Tobacco Body website features an interactive image of a man and a woman. Users zoom in and out of their body parts to observe the effects smoking has on a male and female body.

This is a new campaign by the Cancer Society of Finland, whose objective, according to the website of their ad agency, is to use this as a tool to show teenagers “to think critically about smoking.” The idea is to move beyond the black lungs, gooey tar and damaged livers, and use technology to “make the shock effect more shocking.”

And pretty shocking it is. Before-lady and Before-man are indeed much better-looking than After-lady and the After-man.

The strategy employed is clear: teens today don’t care about lungs, livers and cancer, or if they do, the constant exposure to such warnings has rendered them ineffective. What they do care about is appearances. So let’s show them how ugly smoking makes them.

On one hand you can’t argue with facts: smoking does give you spots, increase your testosterone levels, give you bad breath and unhealthy hair, yellow your teeth and nails, etc. Fact-wise there’s not much to dispute in the Tobacco Body website. But how advisable is it to resort to telling teenagers what is beautiful/popular/acceptable and what is not, even if it is towards the noble cause of telling them to not smoke?

Sample these snippets taken from the website:

[Man & Woman] “Dear Smoker, we’re sorry to inform you that according to nail fashion experts, nicotine yellow is not this season’s colour.”

[Woman] “Hey non-smoking girl, you are on a wonder-diet and you don’t even know it! Your body shape is closer to the average, whereas research shows that smokers weigh more and are rounder around the abdominal area.”

[Woman] “The non-smoking woman is less-likely to have as much hair growing on her arms as a smoker.”

[Woman] “The non-smoking woman usually has no additional hairs growing under her nose… No need for a five-bladed special razor.”

[Man & Woman] “Smokers have bad breath. As many as 20 per cent of people have ended relationships because of smoking. In Burn Magazine’s interviews several celebrities reveal they prefer kissing non-smokers.”

[Man & Woman] “A weary face is not a popular one: out of the 100 most popular profile pictures in a dating service only 2 were pictures of smokers.”

Basically, the Cancer Society of Finland is telling youngsters that smoking makes you hairy, fat, yellow-toothed and gives you bad breath. I found it slightly bothersome how features that are quite normal in several healthy teenagers, like rounded abdomens and hair on arms (for women), was being grouped with those which are blatantly undesirable and unhealthy, like yellowing teeth, bad breath and damaged lungs.

I wondered if this ad could be sending negative body image messages to kids who are naturally fat or hairy – are they implying that these kids are not as desirable?

But the more I thought about it the harder I realised it was to completely buy into that line of reasoning. Because, as a friend pointed out, this may be a case where the end could perhaps justify the means.

It was different in the case of the Dove ‘You’re more beautiful than you think you are’ campaign which also used a similar strategy to sell their product. They too inadvertently (?) went about setting definitions for beauty. The glaring difference of course was that Dove, at the end of the day, was trying to sell us soap under the guise of the noble motive of wanting women to feel good about themselves.

In the case of Tobacco Body, there’s no such deception. As questionable as their strategy might be, we can probably be sure that all this campaign wants is for teenagers to say no to smoking. They are, after all, the Cancer Society of Finland.

A Small RNA That Promotes Lung Cancer.


Gene expression in both healthy and cancerous tissues is controlled by a wide array of regulatory molecules including a group of small RNA molecules known as microRNAs. New research, performed by Ethan Dmitrovsky and colleagues, at Dartmouth Medical School, Hanover, now provides evidence that the microRNA miR-31 promotes lung cancer by repressing the expression of a number of tumor suppressor genes (i.e., genes that generate proteins that suppress the development of cancer).

The initial series of experiments conducted in the study indicated that miR-136, miR-376a, and miR-31 were all overexpressed in mouse and human malignant lung tissue compared with paired normal tissue. Importantly, knockdown of miR-31 expression repressed the in vitro growth of mouse and human lung cancer cell lines and reduced the in vivo tumorigenicity of mouse lung cancer cell lines.

Further analysis provided a potential mechanism by which modulation of miR-31 expression levels could affect lung cancer cell growth: miR-31 repressed expression of the tumor-suppressor genes LATS2 and PPP2R2A. As miR-31 and these target genes were inversely expressed in human lung cancers, the authors conclude that their data has clinical relevance and that miR-31 promotes lung cancer by repressing expression of specific tumor suppressors.

Source: http://www.sciencedaily.com

 

 

TIP30 Inhibits Lung Cancer Metastasis, Study Suggests. Researchers in Shanghai, China suggest that TIP30 prevents metastatic progression of lung cancer.


Researchers in Shanghai, China suggest that TIP30 prevents metastatic progression of lung cancer.

They report these findings in the May 2009 issue of The American Journal of Pathology.

TIP30 is a putative tumor suppressor with decreased expression in numerous cancers including melanoma, breast cancer, and colon cancer. Lung cancer is the most common cancer worldwide, both in terms of incidence and of mortality.

To determine if TIP30 plays a role in lung cancer progression and metastasis, Tong et al examined TIP30 expression in paired cancerous and non-cancerous lung tissue. TIP30 expression was decreased in a third of non-small cell lung cancers compared with normal controls, and reduced TIP30 expression correlated with lymph node metastasis. In addition, inhibition of TIP30 expression promoted lung cancer metastasis and angiogenesis in mice,

Tong et al conclude that “TIP30 may function as a tumor suppressor gene and play important roles in suppressing the progression and metastasis of lung cancer.” These findings highlight TIP30 as a potential new therapeutic for metastatic lung cancer.

They report these findings in the May 2009 issue of The American Journal of Pathology.

TIP30 is a putative tumor suppressor with decreased expression in numerous cancers including melanoma, breast cancer, and colon cancer. Lung cancer is the most common cancer worldwide, both in terms of incidence and of mortality.

To determine if TIP30 plays a role in lung cancer progression and metastasis, Tong et al examined TIP30 expression in paired cancerous and non-cancerous lung tissue. TIP30 expression was decreased in a third of non-small cell lung cancers compared with normal controls, and reduced TIP30 expression correlated with lymph node metastasis. In addition, inhibition of TIP30 expression promoted lung cancer metastasis and angiogenesis in mice,

Tong et al conclude that “TIP30 may function as a tumor suppressor gene and play important roles in suppressing the progression and metastasis of lung cancer.” These findings highlight TIP30 as a potential new therapeutic for metastatic lung cancer.

Source: http://www.sciencedaily.com

 

Pulmonary drug delivery: from generating aerosols to overcoming biological barriers—therapeutic possibilities and technological challenges.


Summary

Research in pulmonary drug delivery has focused mainly on new particle or device technologies to improve the aerosol generation and pulmonary deposition of inhaled drugs. Although substantial progress has been made in this respect, no significant advances have been made that would lead pulmonary drug delivery beyond the treatment of some respiratory diseases. One main reason for this stagnation is the still very scarce knowledge about the fate of inhaled drug or carrier particles after deposition in the lungs. Improvement of the aerosol component alone is no longer sufficient for therapeutic success of inhalation drugs; a paradigm shift is needed, with an increased focus on the pulmonary barriers to drug delivery. In this Review, we discuss some pathophysiological disorders that could benefit from better control of the processes after aerosol deposition, and pharmaceutical approaches to achieve improved absorption across the alveolar epithelium, prolonged pulmonary clearance, and targeted delivery to specific cells or tissues.

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Conclusions

Since the introduction of the first metered dose inhalers to the market in 1956,88 pulmonary drug delivery has made substantial progress, even leading to the first introduction of an inhalation form of insulin (Exubera) to the market. However, since the withdrawal of Exubera from the market in 2007, the field of advanced pulmonary drug delivery, other than delivery of anti-asthma and bronchodilating drugs, has stagnated. Until now the main focus of research and development efforts has been on generation of better aerosols by engineering more sophisticated particles or devices. However, optimised aerosol deposition is a necessary, but not sufficient component of pulmonary drug delivery. To overcome the biopharmaceutical challenges associated with absorption across the alveolar epithelium, control of particle clearance and targeting of specific regions or cells within the lungs requires a thorough understanding of the processes occurring at the cellular and non-cellular elements of the air—blood—barrier after aerosol drug deposition.

To achieve these goals, advanced in-vitro models, preferentially based on human cells and tissues, will be important. Furthermore, nanotechnology might contribute to the development of aerosol drug carriers, and might be necessary for the success of pulmonary drug delivery in the future.

Source: Lancet

 

 

 

 

Gastrobronchial fistula.


A 67-year-old man presented with left anterior chest pain of sudden onset. On admission, chest radiography showed left lower lobe infiltrates.

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8 days later, chest radiography showed a cavitating lesion, consistent with a pulmonary abscess. CT of the chest revealed a pulmonary abscess in the left lower lobe. Suspecting an oesophagobronchial fistula, we did a barium contrast study, which showed a passage from the gastric fundus to the pulmonary abscess (figure). Oesophagogastroduodenoscopy confirmed the presence of a fistula in the gastric fundus; gastric contents were seen to enter the fistula. The fistula, and the left lower lobe to which it was adherent, were surgically resected, and the diaphragm was repaired. The patient’s recovery was uneventful.

Source: Lancet

Targeting of Low-Dose CT Screening According to the Risk of Lung-Cancer Death.


BACKGROUND

In the National Lung Screening Trial (NLST), screening with low-dose computed tomography (CT) resulted in a 20% reduction in lung-cancer mortality among participants between the ages of 55 and 74 years with a minimum of 30 pack-years of smoking and no more than 15 years since quitting. It is not known whether the benefits and potential harms of such screening vary according to lung-cancer risk.

METHODS

We assessed the variation in efficacy, the number of false positive results, and the number of lung-cancer deaths prevented among 26,604 participants in the NLST who underwent low-dose CT screening, as compared with the 26,554 participants who underwent chest radiography, according to the quintile of 5-year risk of lung-cancer death (ranging from 0.15 to 0.55% in the lowest-risk group [quintile 1] to more than 2.00% in the highest-risk group [quintile 5]).

RESULTS

The number of lung-cancer deaths per 10,000 person-years that were prevented in the CT-screening group, as compared with the radiography group, increased according to risk quintile (0.2 in quintile 1, 3.5 in quintile 2, 5.1 in quintile 3, 11.0 in quintile 4, and 12.0 in quintile 5; P=0.01 for trend). Across risk quintiles, there were significant decreasing trends in the number of participants with false positive results per screening-prevented lung-cancer death (1648 in quintile 1, 181 in quintile 2, 147 in quintile 3, 64 in quintile 4, and 65 in quintile 5). The 60% of participants at highest risk for lung-cancer death (quintiles 3 through 5) accounted for 88% of the screening-prevented lung-cancer deaths and for 64% of participants with false positive results. The 20% of participants at lowest risk (quintile 1) accounted for only 1% of prevented lung-cancer deaths.

CONCLUSIONS

Screening with low-dose CT prevented the greatest number of deaths from lung cancer among participants who were at highest risk and prevented very few deaths among those at lowest risk. These findings provide empirical support for risk-based targeting of smokers for such screening.

Source: NEJM