Health Promotion

Issues to consider in Part A:

“Hey – maybe we can quit together”

Role of Doctors in helping patient quit smoking:

Treatment depends on patient’s status. 3 different catergories:
- Patients willing to quit
- patients unwilling to quit and
- patients who have recently quit.

patient has to want to quit before you can encourage him/her!! Patient’s own decision.

Motivational
- assistance and support of a doctor in helping a patient quit smoking has been proven to be more successful (most patient’s stuck in pre-contemplation/contemplation phase - don’t know how to go about the next step and carry out action plan – role of GP)
- a little encouragement goes a long way!
- Keep track of where patient is in Prochaska Di Clemete cycle and facilitate the steps (of course don’t facilitate relapse la!)
- Motivational approaches include detrimental effects of smoking and benefits of quiting, not jut health wise but financial wise, encourage patient’s to think about love life, family, social life
- Reinforcement for success (have a buddy, quit together, motivate each other, praise each other on successes no matter how small)


Strategies for behavioral change:
1. pick appropriate behaviour – quit smoking

2. pick appropriate methods
- (SAME)
- set time frame
- Stimulus control (eg stay away from places where people smoke a lot such as clubs and pubs)
- doctors should help patient decide methods (therapeutic? Pharmacological – quit smoking medications?) cold turkey/gradual cessation? Methods depend on tobacco status of patient

3. do not expect too much
about 70% of smokers trying to quit will fail using any particular method

4. give method a chance to work
- observe behavious : Think over Antecedents and address these issues – ie has the patient tried to quit before? What went wrong? What is preventing him quitting now? Ask him to keep a record of his quit campaign so you can see what works and what doesn’t, so you can change these if patient fails on the first attempt.

5. people are not failure, but the methods maybe
- If methods fail, reiterate to patient that it is the method that is a failure, not him.
- lapses are likely to occur with any behaviour change program. Does not mean failure!

“They’ve never been to this clinic before” (suggests that they’ve been GP hopping)

Benefits of continuity of care

The concept of a long-term relationship between a patient and a doctor is a hallmark of primary care and has long been thought to improve health outcomes. Recent research has confirmed that better continuity of care is associated with a higher level of trust between doctor and patient, and contributes to better quality health care. Conversely, discontinuity of care plays a role in many medical adverse events.

Benefit of having a regular family doctor for patients who are chronically ill:
- Doctor is able to accumulate a thorough and continuos knowledge of the progression of the patient’s condition
- Doctor is more in control of the healthcare network surrounding the sick patient, ie specialist referrals, hospital admissions, etc.
- Doctor comes to know the patient, his family, and their psycho-social needs, and thus can better understand and manage the patient’s response to various aspects of the management of his disease
- Can develop a strong, good relationship with patient, thus aiding his compliance to treatment
- Provides continuation to patient in a tumultuous time

~*Shantz*~

Pathophysiology of Asthma & COPD

Pathophysiology of Asthma

1. Broncho-spasm
2. Mucous Secretion
3. Oedema

Airway Inflammation (related to mucous secretion)

Immune system components:

1. Antibodies: specific proteins created by the immune system to identify and bind to foreign and potentially invading substances (IgE for allergens)
2. Inflammatory cells circulate in the bloodstream and can "sense" the body's surroundings or exposures to create immune responses directed against those exposures (mast cells, eosinophils, activated T-lymphocytes)
3. Inflammatory mediators: chemical substances that are secreted by immune cells to induce (or respond to) an ongoing immune response generated against a specific exposure to the body (cytokines)

Infectious agents constantly enter the body via the respiratory system. The bronchi have several protective methods against these invaders. These include:

• recruitment of inflammatory cells from the bloodstream into the bronchial wall, where they directly attack the invading organisms and secrete inflammatory chemicals that are toxic to the organisms
• swelling of the bronchial wall
• mucus secretion
• constriction of the airway

The fundamental defect in asthma is that, for reasons that are unclear, these inflammatory actions occur in the bronchi when no serious infection, toxin, or other inhaled threat to the body exists.

Airway inflammation in asthma is:

• a direct response of the immune system to a trigger
• a cascade of immunologic events that includes inflammatory cells and mediators
• an immune-mediated process that leads to inflammatory changes in the airway, including eosinophil recruitment and airway edema.

Normal airway	Inflamed airway
Epithelial cells lines and protects bronchial wall	Bronchial wall edema (due to plasma leakage from blood vessels) à thickening of wall
Mucous gland – protective layer of mucus	Enlarged mucous glands secrete excess mucus
Lumen free of mucus	Lumen has mucus
Few eosinophils in bronchial wall	Eosinophils migrate from bloodstream into bronchial wall & lumen à release eosinophil cationic protein & leukotrienes

Airway walls thicken --> (smooth muscle in) bronchial walls contract --> greater airway narrowing, coz’ the walls are already thickened --> greater airway resistance.

Bronchial Hyper-reactivity/responsiveness (related to broncho-spasm)

Hyper-reactivity of the airways to several stimuli is a hallmark of clinical asthma, and it appears bronchial hyper-reactivity (BHR) is caused by airway inflammation.

The presence of airway hyper-responsiveness or bronchial hyper-reactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or non-myelinated sensory neurons. The degree of airway hyper-responsiveness generally correlates with the clinical severity of asthma.

Intermittent Airflow Obstruction (related to oedema)

Airflow obstruction can be caused by a variety of changes, including acute broncho-constriction, airway edema, chronic mucous plug formation, and airway remodeling.

Acute broncho-constriction is the consequence of immunoglobulin E–dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response.

Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response.

Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve.

Airway remodeling is associated with structural changes due to long-standing inflammation. Airway remodeling and fibrosis may be the cause of "fixed" airflow obstruction in asthma that is not reversible with steroids, bronchodilators, or both.

Sources:

http://www.emedicine.com/med/topic177.htm
http://www.merckmedicus.com/pp/us/hcp/diseasemodules/asthma/pathophysiology.jsp

Pathophysiology of COPD

The pathophysiology of COPD is not completely understood; it is progressive with time.

1. Airway obstruction
2. Airflow limitation

Airway obstruction

Prominent inflammatory cells: neutrophils, macrophages, CD8+ T-lymphocytes
Inflammatory mediators: Leukotriene B4, Interleukin 8, and Tumor Necrosis Factor

Smoking and, occasionally, other inhaled irritants, perpetuates an ongoing inflammatory response. Oxidative stress caused by free radicals in cigarette smoke activate neutrophils. Activated neutrophils release proteases as part of the inflammatory process. Neutrophil influx also causes the secretion of MMPs (macrophage-derived matrix metalloproteinases) from macrophages.

Protease activity exceeds antiprotease activity, and tissue destruction and mucus hypersecretion result.

Neutrophil and macrophage activation also leads to accumulation of free radicals, superoxide anions, and hydrogen peroxide, which inhibit antiproteases and cause broncho-constriction, mucosal edema, and mucous hypersecretion. Neutrophil-induced oxidative damage, release of profibrotic neuropeptides (eg, bombesin), and reduced levels of vascular endothelial growth factor may also play a role, as does infection (we learnt about acute exacerbations of COPD in Thursday’s lecture, so I will not repeat. Go look at your lecture notes for that). :)

Physically, airways become edematous, excess mucus production occurs and cilia function poorly. With disease progression, patients have increasing difficulty clearing secretions.

Incr. airway resistance --> Incr. work of respiration (breathing) --> Incr. alveolar hypoventilation with hypoxia and hypercapnia --> Incr. pulmonary vascular tone --> pulmonary hypertension and cor pulmonale.

O₂ administration may then worsen hypercapnia in some patients by decreasing hypoxic ventilatory drive, leading to alveolar hypoventilation.

In order to understand the mechanisms, we need to study Chronic Bronchitis and Emphysema:

Chronic bronchitis

Mucous gland enlargement is the histologic hallmark of chronic bronchitis.

The structural changes described in the airways include atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening.

Neutrophilia develops in the airway lumen, and neutrophilic infiltrates accumulate in the submucosa. The respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucous plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis (this is a repeat of inflammatory process as mentioned above).

These changes, combined with loss of supporting alveolar attachments, cause airflow limitation by allowing airway walls to deform and narrow the airway lumen.

Airflow Limitation

Emphysema

1. Centriacinar: limited to the respiratory bronchioles; assoc. with cigarette smoking; severe in upper lobes
2. Panacinar: entire alveolus distal to the terminal bronchiole; alpha1-antitrypsin deficiency; severe in lower lung
3. Distal acinar/paraseptal: distal airway structures, alveolar ducts, sacs; least common

Both emphysematous destruction and small airway inflammation often are found in combination in individual patients.

When emphysema is moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the mechanism of airflow limitation.

By contrast, when emphysema is mild, bronchiolar abnormalities are most responsible for the deficit in lung function. Although airflow obstruction in emphysema is virtually irreversible, broncho-constriction due to inflammation accounts for a limited amount of reversibility.

Sources:

http://www.emedicine.com/med/topic373.htm
http://www.merckmedicus.com/pp/us/hcp/framemm.jsp?pg=www.merck.com/mmpe/sec05/ch049/ch049a.html
http://www.aafp.org/afp/20010815/603.html
http://www.clevelandclinicmeded.com/diseasemanagement/pulmonary/copd/copd.htm
http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page2.htm

Cigarette Smoking

Cigarette Smoking

Light vs Heavy Smokers
Light smokers – < 20 cigarettes / day
Heavy smokers – ≥ 20 cigarettes / day
* 1 packet contains 20 cigarettes

Differences in the Amount of Tar and Nicotine in Cigarettes
High-tar cigarettes – ≥ 22 mg tar
Moderate-tar cigarettes – 15 -21 mg tar
Low-tar cigarettes – 8-14 mg tar
Very low-tar cigarettes – ≤ 7 mg tar
* The amount of nicotine changes with the amount of tar in the cigarettes

Tobacco Smoking
1. Cigarette
- a product manufactured from cured and cut tobacco leaves, combined with other addictives including nicotine, which are rolled and/or stuffed into a paper-wrapped cylinder
- usually less than 120 mm in length and 10 mm in diameter

2. Cigar
- a cylinder of tobacco rolled in tobacco leaves for smoking
- 3 parts: wrappers, fillers and binders
Wrappers: cigar’s outermost leaves; determines the cigar’s character and flavour
Fillers: wrapped-up bunches of leaves in the interior of the cigar
Binders: elastic leaves used to hold together the bunches of fillers
- varies in size and shape
- different flavours: spice, cocoa/chocolate, coffee, nut, wood, berry

3. Smoking Pipe
- a device used for smoking tobacco
- consists of a small chamber for the combustion of the tobacco to be smoked (the bowl), and a thin stem (shank) that ends in a mouthpiece (the bit)
- bowl – briar, corncob, meerschaum, clay
- stems and bits – vulcanite, lucite, Bakelite, soft plastic
- steps involved: packing, lighting, prevent burning, smoking, cleaning, sweetening

Sources:
http://en.wikipedia.org/wiki/Tobacco_smoking
http://www.cigoutlet.net/cigarettes/marlboro_miles.html
http://www.cigarhandbook.com/RingGuide.asp
http://www.cigar.com/info/classify.asp

(Posted by: Vivian)

Psychosocial Aspects

Name: Anna
Age: 18
Netballer
Suffers from exertional asthma

Anna may feel:

Denial (refuse to admit that she is suffering from asthma, makes up excuses for her coughing fits. May refuse to take her asthmatic medications)
Anger (feels frustrated that she cannot perform as well as she used to in netball, why does this have to happen to her? May blame others for her medical condition i.e. her mom)
Bargaining ( partial compliance with treatment)
Depression (gets upset about her condition and how it has decreased her quality of life)
Acceptance (accepts her condition, deals with it, is compliant with her medications )

How the doctor can help

Counsel and educate (purpose of education is to empower patients to undertake self-management more appropriately and effectively) Anna on asthma to help her understand the disease more and hence aid her to cope with asthma.
This can be done by:
􀂄providing resources on asthma. This should include written asthma action plans and information leaflets, etc. Non-promotional material is available from Asthma UK (www.asthma.org.uk).
􀂄Tailor the education and advice to the individual needs of the patient, respecting differing ambitions, wishes for autonomy and age.

When counseling Anna, it may help to tell her these points
􀂄Nature of the disease
􀂄Nature of the treatment
􀂄Identify areas where patient most wants treatment to have effect
􀂄How to use the treatment
􀂄Development of self-monitoring/self-assessment skills
􀂄Negotiation of the asthma action plan in light of identified patient goals
􀂄Recognition and management of acute exacerbations
􀂄Appropriate allergen or trigger avoidance

In addition, create a treatment plan that is preventative so Anna can carry on playing her netball. Thus the treatment plan may be aimed to minimize the effect of asthma on her life.

Anna and her mom could join a self-help asthma group so as to have emotional support from other people suffering the same disease.

Her mom can help in reducing incidences of asthma attacks by stopping smoking. This reduces the amount of passive smoking done by anna. It will be good to advice anna to quit smoking as well.


http://www.sign.ac.uk/guidelines/published/support/guideline63/download.html

Contributed by Christine

Management of Asthma

Specific treatment will be determined by your physicians based on:

1. overall health and medical history

2. extent of the disease

3. tolerance of specific medications, procedures and therapies

4. patient’s opinion and preference

Aim of treatment:

1. to achieve and maintain control of symptoms

2. to reduce or eliminate patient’s asthma episodes if possible

3. to reduce the side effects from medications given

4. to restore normal lung activity level

The four parts of continually managing asthma are:

1.Identify and minimize contact with asthma triggers.

2.Understand and take medications as prescribed.

3.Monitor asthma to recognize signs when it is getting worse.

4.Know what to do when asthma gets worse.

Medications for asthmatic patients:

I) Drugs-divided into 3 classes:

1. relievers –known as rescue medication for eg short-acting b2-agonists (broncodilator);

2. preventers –long acting b2-agonists

3. symptoms controller-long term for eg corticosteroid (anti-inflammatory)

II) Inhalers-divided into 3 groups:

1. metered dose inhaler- require hand-breath inhalation coordination (not easy to use)-in the form of gas

2. dry powder inhaler- no coordination problem (easy to use by children and elderly)-in the form of powder

3. spacer inhaler- commonly use by children- in conjunction with MDI

how it works…

–make sure the drugs enter directly into the lungs (the point where the drugs is needed the most!!!)

Management of COPD

1. Identify the risk factors – for eg occupational hazards

2. use bronchodilators

3. oxygen therapy to reduce mortality

4. antibiotics if there is an evidence of bacterial infection

5. cease smoking

6. use anti-inflammatory (usage of corticosteroid reduces mortality???)

prepared by SRI MURNIATI ROSLI

Reference: Lecture notes, Pulmonary Pharmacology by K.Amudha

Allergy

Allergy is also known as a Type I Hypersensitivity reaction, Immediate Hypersensitivity reaction or Atopy. Allergies occur when the body perceives a relatively harmless substance as a threat and activates the immune system to deal with this perceived threat. These reactions are mediated by IgE antibody and mast cells, and followed by inflammation. Allergies are present in atopic individuals (persons with a genetic tendency towards allergies).

Sequence of events in the development of an allergy:
1) Production of IgE antibodies in response to antigen with the assistance of T helper cells. T helper cells secrete cytokines which stimulates B lymphocytes specific to the antigen to proliferate and produce IgE.
2) IgE antibodies produced are specific to the antigen and bind to Fc receptors of Mast cells in a process called sensitization.
3) When antigen is re-intoduced, there’s cross-linking of IgE antibodies bound on the mast cells by the antigen.
4) When a critical mass of IgE antibodies on a mast cell has been cross-linked, the mast cell gets activated and release mediators like histamines, prostaglandins and leukotrienes (which cause vasodilation, smooth muscles contraction and increases vascular permeability; histamines increase mucus secretion), proteases (which damage local tissues and cause inflammation), and cytokines (which stimulates recruitment of leukocytes and prolongs inflammation).

NB: An allergen is a substance that causes an allergy, i.e. the antigen that leads to the development of an allergy.

Now that we know what an allergy is, we can better understand what hay fever and eczema are all about.

Hay Fever

It is also known as allergic rhinitis or inflammation of the nasal mucosa. It is a misnomer since hay is not the usual cause of the problem and it also does not cause fever. It is an allergic reaction to inhaled allergens, most commonly pollen from weeds, grasses and trees. Other common allergens include animal protein, dust mites and pores from mold. A point to note is that any substance can be an allergen as long as it triggers an allergic response in the individual. The ones listed are the more common ones. Signs and symptoms are a result of the mediators released by mast cells activated by the allergen. They include nasal congestion, clear running nose, swelling and sneezing. Allergic rhinitis can often lead to sinusitis (inflammation of the paranasal sinuses or air cavities within the passages of the nose), allergic conjunctivitis and asthma. Allergens that cause hay fever often travel up the upper respiratory tract and sensitize mast cells present in the bronchial tubes, priming the immune system. A re-exposure to the allergen or to other asthmatic triggers like exercise and irritants can cause an asthma episode.

Eczema

Eczema is a general term for many types of skin inflammation or dermatitis. The most common form is atopic dermatitis which is what we are interested in as it is an allergic disorder and associated with asthmatic patients.

Atopic dermatitis refers to the chronic inflammation of skin and is characterized by dry, itchy, inflamed skin. It often occurs in people with a family history of allergic conditions i.e. asthma and hay fever, and is most commonly found in infants and children. It is not contagious. At present, the exact cause is not known but evidence points towards genetic and environmental factors. It is thought that the sensitivity of the skin is passed down through genes and that exposure of allergens and/or irritants to the super sensitized skin results in the disease. Common allergens include pollen, animal dander (tiny particles from skin or hair) dust mites or pores from mold. Irritants include dust, sand, cigarette smoke, wool or synthetic fibers, soaps, perfumes, cosmetics. A point to note: it is often difficult to tell if the basis of the disease is allergic or irritant as irritants produce the same symptoms as allergens. The differentiation between the two is that allergens are specific to B lymphocytes and causes an increase in IgE antibodies while irritants are non-specific and there is no rise in IgE levels. Signs and symptoms include dry, scaly patches of skin; papules which are small, raised bumps that may open when scratched becoming crusty and infected; hives which are red, raised bumps; Lichenification or thick, leathery skin resulting from constant scratching and rubbing; Hyperlinear palms; Keratosis pilaris: small, rough bumps, generally on the face, upper arms, and thighs.



End-Note
Asthma, hay fever and atopic dermatitis are all atopic disorders i.e. type I hypersensitivity. They are often associated with one another due to their similar etiologies. A patient with asthma would probably have a history of hay fever or atopic dermatitis.

Contributed by John Lee

Complications of smoking

Basically, the major complications of smoking are lung and cardiovascular disease.

Intro

• Cigarettes have literally thousands of chemical components, at least 400 of which are toxic. Its tar component can cause lung cancer, its gas can cause pulmonary disease and its carbon monoxide and nicotine significantly increase your risk of cardiovascular disease.
• incidence of smoking in patients suffering from post traumatic stress disorder, bipolar disorder, major depression and other mental illnesses twofold or fourfold higher than the general population, and smoking incidence among patient with schizophrenia is as high as 90 percents

Heart

• UK studies show that smokers in their 30s and 40s are five times more likely to have a heart attack than non-smokers.

• Tobacco contributes to the hardening of the arteries(Atherosclerosis), which can then become blocked and starve the heart of bloodflow, causing the attack.
• Inflammation of the artery wall and the development of blood clots can obstruct blood flow and cause heart attacks or strokes.
• Often, smokers who develop this will require complex and risky heart bypass surgery.
• Smoking also increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot.
• Smoking decreases HDL (good) cholesterol.
• If you smoke for a lifetime, there is a 50% chance that your eventual death will be smoking-related - half of all these deaths will be in middle age
• Smoking also increases the risk of having a stroke due to high blood pressure and tendency of the blood to clot.
• Smoking-related coronary heart disease may contribute to congestive heart failure.

Cancer

• The primary health risk associated with smoking are lung cancer
• Lung cancer commonly follows or accompanies COPD
• There are three forms of lung cancer that are associated with smoking.
• The most common is squamous-cell carcinoma. In its early stage, basal cells of the bronchial epithelium multiply, and the ciliated pseudostratified columnar epithelium transforms into the stratified squamous type. As the dividing epithelial cells invade the underlying tissues of the bronchial wall, the bronchus develops bleeding lesions. Dense swirled masses of keratin appear in the lung parenchyma and replace functional respiratory tissue.f
• Cancer-causing agents (carcinogens) in tobacco smoke damage important genes that control the growth of cells, causing them to grow abnormally or to reproduce too rapidly.
• For smoking-attributable cancers, the risk generally increases with the number of cigarettes smoked and the number of years of smoking, and generally decreases after quitting completely.
• Smoking cigarettes that have a lower yield of tar does not substantially reduce the risk for lung cancer.
• Smoking also increases the risk of oral, uterine, liver, kidney, bladder, stomach, and cervical cancers, and leukaemia.
• Cigarette smoking is a major cause of esophageal cancer in the United States.

Respiratory

• Smoking damages airways and alveoli of the lung
• Another health problem associated with tobacco is emphysema, which, when combined with chronic bronchitis, produces chronic obstructive pulmonary disease.
• Chronic bronchitis and emphysema can exacerbate asthma symptoms in adults and children.
• In 2001, chronic obstructive pulmonary disease (COPD) was the fourth leading cause of death in the United States, resulting in more than 118,000 deaths. More than 90% of these deaths were attributed to smoking.
• According to the American Cancer Society’s second Cancer Prevention Study, female smokers were nearly 13 times as likely to die from COPD as women who had never smoked. Male smokers were nearly 12 times as likely to die from COPD as men who had never smoked. (p. 500)
• Smokers are more likely than nonsmokers to have upper and lower respiratory tract infections, perhaps because smoking suppresses immune function
• In general, smokers’ lung function declines faster than that of nonsmokers

Pregnancy

• Research has shown that women’s smoking during pregnancy increases the risk of pregnancy complications, premature delivery, low-birth-weight infants, stillbirth, and sudden infant death syndrome (SIDS).
• The nicotine in cigarettes may cause constrictions in the blood vessels of the umbilical cord and uterus, thereby decreasing the amount of oxygen available to the fetus. Nicotine also may reduce the amount of blood in the fetal cardiovascular system. Nicotine is found in breast milk.
• Babies of mothers who smoked during pregnancy have lower birth weights. Low birth weight is a leading cause of infant deaths.
• Mothers’ smoking during pregnancy reduces their babies’ lung function.

Contributed by Lawrence Oh

hypovolemic shock and haemothorax

Hypovolemic shock

-acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia due to loss of circulatory volume.

Complications
Inadequate tissue perfusion:
a) skin- cold, pale, blue, slow capillary refill, clammy (peripheral cyanosis)
b) kidneys- oliguria, anuria (Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL/day in adults. Anuria is defined as absent production of urine)
c) brain- drowsiness, confusion and irritability
d) multi organ failure due to lack of perfusion to organs

Increased sympathetic tone:
a) tachycardia, narrowed pulse pressure, “weak” or “thready” pulse
b) cold and clammy
c) blood pressure- maybe maintained initially but later hypotension will occur

Metabolic acidosis- anaerobic glycolysis occur within tissues to lack of oxygen


Haemothorax

A haemothorax is a condition that results from blood accumulating in the pleural cavity. Its cause is usually traumatic, from a blunt or penetrating injury to the thorax, resulting in a rupture of either of the serous membrane lining the thorax and covering the lungs. This rupture allows blood to spill into the pleural space, equalizing the pressures between it and the lungs. Blood loss may be massive in people with these conditions, as each side of the thorax can hold 30%-40% of a person's blood volume. If left untreated, the condition can progress to a point where the blood accumulation begins to put pressure on the mediastinum and the trachea, effectively limiting the amount of diastolic filling of the ventricles and deviating the trachea to the unaffected side.

Same pressure between pleural cavity and atmosphere means that there is no pressure gradient. Thus air does not enter or leave the lungs. There is no ventilation of the alveoli hence blood flowing through the capillaries do not get adequately oxygenated. This will result in hypoxia and infarct of tissues.
abnormal fast breathing
Dyspnoea.
Cyanosis.
Decreased or absent breath sounds on affected side.
Tracheal deviation.
Dull resonance on percussion.
Unequal chest rise.
Tachycardia.
Hypotension.
Pale, cool, clammy skin.
Possibly subcutaneous air
Narrowing pulse pressure

Asthma

ASTHMA
Resource Sites
· http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Asthma
· http://www.mayoclinic.com/health/asthma/DS00021/DSECTION=4
· http://www.healthinsite.gov.au/topics/Asthma
· http://www.mayoclinic.com/health/asthma/AS00003
Asthma is a common condition which affects the small air passages (bronchi) of the lungs. These passages become swollen and inflamed, and this leads to the production of mucus (fluid). During an asthma attack, these small airways become narrow. This reduces the flow of air in and out of the lungs. This may lead to wheezing, coughing and difficulty with breathing. Not all children who have asthma will wheeze or cough.Asthma attacks can be controlledAn asthma attack can be controlled with medication. Asthma is an illness that comes and goes at different times. Most children with asthma will have an occasional attack, while a few will have symptoms every day.Asthma is triggered by different thingsAsthma tends to run in families. It is also associated with other conditions such as eczema, hayfever and allergies. Asthma is triggered by different things for different children. Some common triggers are:
Colds
Changes in the weather
Cigarette smoke
Dust and dust mites
Pollen
Some animals.
Coughing is a symptomWheezing and coughing are common symptoms of asthma. Coughing is most likely to happen:
At night
During the early hours of the morning
In cool weather
During exercise.
Things to remember
The common signs of asthma are coughing and wheezing.
Different triggers bring on asthma in different people.
Asthma can be controlled with reliever and preventer medication.
See your doctor if your child does not respond to reliever medication.
Find out more about asthma and its treatment to help you feel more confident to look after your child.

People with asthma are sensitive to different triggers in their environment. Triggers, or allergens, cause inflammation or swelling in your airways and make your asthma worse. An allergen is any substance that can bring on an allergic reaction. An allergy is your body’s response to a substance that is normally harmless to most people. If you are allergic to something, then eating it, breathing it or touching it can bring on an allergic reaction. Most people with asthma are atopic; that is, they have a general tendency to develop allergic diseases. More than 80 per cent of people with asthma find their symptoms get worse when they are exposed to allergens. Managing your asthma includes identifying the triggers that make your symptoms worse and doing all you can to avoid exposure to those triggers.Many allergens are carried in dust
Minute particles of dust float around in the air you breathe. Depending on the environment you’re in (such as city or country, home or work) and the time of year (such as spring), these dust particles can contain allergens such as:
House dust mite droppings
Skin, scales, fur particles (called ‘dander’) from animals
Insect debris
Food dust
Pollens
Moulds.
Other types of triggers
It’s not just allergens that can trigger asthma symptoms. Other common triggers include:
Respiratory infections (common cold)
Cold, dry air
Some medications
Exercise
Cigarette smoke
Wood fire smoke
Perfumes
Paint
Chemicals
Gases.
Identifying your triggers
It is important to know which particular triggers bring on your asthma symptoms. This can be easy with triggers you can see, such as cigarette smoke or animals. However, sometimes it can be tricky. Try to keep a diary of the times and situations when your asthma is worse. Some general tips to help you in your investigations include:
If you have asthma all year round, with symptoms worsening a little in autumn, you may be allergic to house dust mite droppings.
If your asthma symptoms are worse in spring and early summer, you may be allergic to pollens. Your symptoms will depend on what type of pollen you are allergic to.
Skin prick testing
Allergy testing can help to pinpoint your allergens. The doctor puts small dabs of different allergen solutions, such as pollen extract, along your arm. Then the doctor slightly pricks the skin underneath with a needle. If the skin swells or develops a welt, you are allergic to that substance. Blood tests are available too. However, these skin and blood tests are not conclusive. Just because your skin and blood reacts to the allergen, doesn’t mean your lungs will too. Think of these tests as a helpful starting point. Other types of allergic reactions
When a person with asthma is exposed to allergens, their asthma gets worse. Depending on the allergen and where it enters your body, you may experience different symptoms.Other allergic reactions may include:
Rhinitis (or hay fever) – sneezing, blocked and runny nose, itchy eyes and throat.
Eczema – dry, red, itchy skin.
Hives – skin rashes.
Investigation (Diagnosis)
Asthma symptoms raise a red flag, but firm diagnosis of asthma is more complicated.
If you have bouts of wheezing, coughing and shortness of breath, your doctor may suspect asthma. But symptoms alone aren't enough for him or her to arrive at a diagnosis of asthma. Your doctor will also need to understand how, when and where your symptoms occur. After gathering that information, your doctor will probably recommend a lung function test, followed by a trial of medication that helps people with asthma breathe more easily. If the medication works, you probably do have asthma.
Diagnosis of asthma: Medical history holds clues
During an assessment for asthma, your doctor may ask a series of questions about your symptoms. It's best if you can provide detailed answers. Here are some questions that explore symptoms of asthma and help with the diagnosis of asthma.
During the past 12 months, have you:
§ Had a sudden, severe episode or recurrent episodes of wheezing, coughing or shortness of breath?
§ Had colds that "go to the chest" or take more than 10 days to get over?
§ Had wheezing, coughing or shortness of breath only when you're in certain places, such as your home or workplace, or outdoors?
§ Had wheezing, coughing or shortness of breath when exposed to certain substances such as pollen, tobacco smoke, cat dander or perfume?
§ Used any medications that help you breathe better? If so, how often did you use them and how well did they work?
In the past four weeks, have you had wheezing, coughing or shortness of breath:
§ At night that has awakened you?
§ In the early morning?
§ After running, moderate exercise or other physical activity?
A "yes" answer to any of these questions may suggest that you have asthma.
Because the tendency to develop asthma may run in families, be prepared to talk about your family's health history. Your childhood illnesses and exposure to certain substances are also of interest. These questions may include:
§ Have your parents, brothers, sisters or children ever been diagnosed with asthma, allergies, sinusitis or nasal growths (polyps)?
§ Have you ever been diagnosed with an allergic condition such as hay fever or eczema?
§ As a young child, did you ever develop pneumonia?
§ As a young child, were you exposed to second-hand smoke from your parents or other family members?
Physical exam: Detecting signs of asthma
A physical examination of your upper respiratory tract, chest and skin generally follows the history. Using a nasal speculum, your doctor may look inside your nose for signs of allergic disease such as increased nasal secretions, swelling or polyps. These signs may suggest that allergies are responsible for triggering your suspected asthma.
Your doctor also may use a stethoscope to listen to the sounds your lungs make as you breathe. Wheezing sounds indicate one of the main signs of asthma: obstructed airways.
Finally, your doctor may examine your skin for signs of allergic conditions such as eczema or hives, which are often associated with asthma
answer to any of these questions may suggest that you have asthma.
Because the tendency to develop asthma may run in families, be prepared to talk about your family's health history. Your childhood illnesses and exposure to certain substances are also of interest. These questions may include:
§ Have your parents, brothers, sisters or children ever been diagnosed with asthma, allergies, sinusitis or nasal growths (polyps)?
§ Have you ever been diagnosed with an allergic condition such as hay fever or eczema?
§ As a young child, did you ever develop pneumonia?
§ As a young child, were you exposed to second-hand smoke from your parents or other family members?
MORE ON THIS TOPIC
§ Asthma
Lung function tests: Measurements of breathing to assess possible asthma
Although your symptoms, medical history and physical examination may suggest that you have asthma, one final step, a lung (pulmonary) function test, is required to confirm an asthma diagnosis. A pulmonary function test may include one or more of the following tests.
SpirometryThis noninvasive test, which takes 10 to 15 minutes and measures how well you breathe, is the preferred test for diagnosing asthma. During spirometry, you take deep breaths and forcefully exhale into a hose connected to a machine called a spirometer.
Spirometry measures three values that are important in diagnosing asthma:
§ Vital capacity, which is the maximum amount of air that you can inhale and exhale
§ Peak expiratory flow rate, also known as the peak flow rate, which is the maximum flow rate you can generate during a forced exhalation
§ Forced expiratory volume, which is the maximum amount of air you can exhale in one second
If certain key measurements are below normal for a person your age, it may be a sign that your airways are obstructed. Your doctor may ask you to inhale a bronchodilator drug used in asthma treatment to open obstructed air passages. Then you retake the spirometry test. If your measurements improve significantly, it's likely that you have asthma.
Spirometry isn't foolproof. Your doctor may still suspect that you have asthma even if your initial spirometry measurements are normal. If so, he or she may recommend the next test — a challenge test.
Challenge testDuring this test, you deliberately trigger airway obstruction and asthma symptoms by inhaling an airway-constricting chemical or taking several breaths of cold air. If you appear to have exercise-induced asthma, you may bring on symptoms by doing vigorous physical activity.
After inhaling the symptom-producing substance or engaging in physical activity, you retake the spirometry test. If your spirometry measurements are still normal, it's likely that you don't have asthma. But if your measurements have fallen significantly, it may be an indication that you have asthma.
Peak expiratory flowThis test, an alternative to spirometry, also measures how well you breathe. What you do is exhale forcefully into a peak flow meter, a small, hand-held device that measures the rate at which you can force air out of your lungs.
Although peak expiratory flow is less accurate than spirometry in measuring airway obstruction, it can still play a role in asthma diagnosis. If your spirometry and challenge tests are normal but your doctor still suspects asthma, he or she may send you home with a peak flow meter and a trial prescription for asthma medications.
Over a six- to eight-week period, you record your peak flow readings before and after taking your medications. If your readings improve significantly, it may be the evidence your doctor needs to make an asthma diagnosis.
Additional tests: Ruling out conditions other than asthma
Your doctor may suspect that you have a condition other than or in addition to asthma. Possibilities include chronic obstructive pulmonary disease (COPD), pneumonia, bronchitis, pulmonary embolism, panic disorder and heart failure, all of which may mimic asthma. Conditions that often accompany asthma include gastroesophageal reflux disease, hay fever and sinusitis.
If your doctor suspects that you have another condition, he or she may conduct other tests or assessments, such as:
§ Complete blood count
§ Chest and sinus X-rays
§ Computerized tomography (CT) scans
§ Gastroesophageal reflux assessment
§ Sputum induction and examination
Your doctor may also perform allergy tests. Although allergy tests aren't used to diagnose asthma, they can help identify substances that may be causing or worsening your asthma.
MORE ON THIS TOPIC
§ Double trouble: The link between allergies and asthma
§ Allergy skin tests: Identify the sources of your sneezing
Diagnosing asthma in children
When assessing children under age 5, doctors seldom conduct lung function tests because young children usually have trouble following the instructions. Instead, when a child's signs and symptoms, medical history and physical examination suggest asthma, the doctor may prescribe a bronchodilator — a drug that opens the airways. If your child's signs and symptoms improve after using the bronchodilator, an asthma diagnosis is likely.
MORE ON THIS TOPIC
§ Childhood asthma
A new diagnostic approach: Exhaled nitric oxide
Because diagnostic tests such as spirometry aren't always accurate, doctors are looking for better ways to diagnose asthma. One newer approach is to measure a chemical marker of asthma — nitric oxide — in exhaled air. In general, higher levels of nitric oxide correspond with higher degrees of asthma severity.

Prepared by Ji Keon
Note: Abridged version is emailed in a PPT form.

Anatomy Task for Week 5

Anatomy Task (Week 5)

􀂾 Describe the bones of the cranial vault & their relations (Christine)
􀂾 Describe the boundaries and contents of the cranial fossae (Chris)
􀂾 Describe the meninges & related spaces (Ji Keon)
􀂾 Discuss intracranial haemorrhages (Ji Keon)
􀂾 Describe the venous sinuses of the skull (John)
􀂾 Describe contents & communications of the cavernous sinus (Madhura)
􀂾 Describe the sensory cutaneous supply to the head (Shanthini)
􀂾 Describe the boundaries & contents of the scalp (Sri)
􀂾 Explain why scalp wounds bleed profusely(Sri)
􀂾 Explain CSF rhinorrhoea & otorrhoea (Vivian)
􀂾 Demonstrate the surface anatomy of the cranial vault; indicate clinical situations when this knowledge may be useful (Lawrence)

Happy researching =)

Resuscitation Procedures

Arrhythmias associated with cardiac arrest are divided into two groups: shockable rhythms (VF/VT) and non-shockable rhythms (asystole and PEA). The principle difference in management is the need for attempted defibrillation in patients with VF/VT. Subsequent actions, including chest compression, airway management and ventilation, venous access, administration of adrenaline, and the identification and correction of reversible factors, are common to both groups.

Non-shockable rhythms (PEA and asystole)
Pulseless electrical activity (PEA) is defined as cardiac electrical activity in the absence of any palpable pulse. These patients often have some mechanical myocardial contractions but they are too weak to produce a detectable pulse or blood pressure. PEA may be caused by reversible conditions that can be treated if they are identified and corrected. Asystole refers to a state of no cardiac activity. Survival following cardiac arrest with asystole or PEA is unlikely unless reversible cause can be found and treated effectively.
In asystole, the heart will not respond to defibrillation because it is already depolarized while in PEA, the heart is very unlikely to be shocked successfully into a perfusing rhythm and delivering repeated shocks will increase myocardial injury, both directly from the electric current and indirectly from the interruptions in coronary blood flow.


Sequence of actions for PEA
• Start CPR.
• Give adrenaline as soon as intravascular access is achieved.
• Continue CPR until the airway is secured, then continue chest compressions without pausing during ventilation.
• Recheck the rhythm after 2 min.
o If there is no change in the ECG appearance:
• Continue CPR.
• Recheck the rhythm after 2 min and proceed accordingly.
• Give further adrenaline every 3-5 min.
o If the ECG changes and organized electrical activity is seen, check for a pulse.
• If a pulse is present, start post-resuscitation care.
• If no pulse is present:
O Continue CPR.
o Recheck the rhythm after 2 min and proceed accordingly.
o Give further adrenaline every 3-5 min

Shockable rhythms (VF/VT)
VF refers to ventricular fibrillation with the presence of a pulse and VT refers to ventricular tachycardia.

Sequence of actions
• Attempt defibrillation
• Immediately resume chest compressions without reassessing the rhythm or feeling for a pulse.
• Continue CPR for 2 min, then pause briefly to check the monitor:
o If VF/VT persists:
• Give a further (2nd) shock
• Resume CPR immediately and continue for 2 min.
• Pause briefly to check the monitor.
• If VF/VT persists give adrenaline IV followed immediately by a (3rd) shock
• Resume CPR immediately and continue for 2 min.
• Pause briefly to check the monitor.
• If VF/VT persists give amiodarone (anti-arrhythmic drug) IV followed immediately by a (4th) shock
• Resume CPR immediately and continue for 2 min.
• Give adrenaline IV immediately before alternate shocks (i.e. approximately every 3-5 min).
• Give a further shock after each 2 min period of CPR and after confirming that VF/VT persists.
o If organised electrical activity is seen during this brief pause in compressions, check for a pulse.
• If a pulse is present, start post-resuscitation care.
• If no pulse is present, continue CPR and switch to the nonshockable algorithm.
o If asystole is seen, continue CPR and switch to the nonshockable algorithm.

Potentially reversible causes
Potential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest. For ease of memory, these are divided into two groups of four, based upon their initial letter, either H or T:
• Hypoxia
• Hypovolaemia
• Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other
metabolic disorders
• Hypothermia
• Tension pneumothorax
• Tamponade (fluid in the pericardial sac)
• Toxic substances
• Thromboembolism (pulmonary embolus/coronary thrombosis)

Signs of life
If signs of life (such as regular respiratory effort or movement) reappear during CPR, or readings from the patient’s monitors (e.g. exhaled carbon dioxide or arterial blood pressure) are compatible with a return of spontaneous circulation, stop CPR and check the monitors briefly. If an organized cardiac rhythm is present, check for a pulse. If a pulse is palpable, continue post-resuscitation care. If no pulse is present, continue CPR.

Contributed by John Lee

Stabilising a Trauma Patient

Trauma patient usually refer to someone who has suffered serious and life-threatening physical injury which has the potential to result in secondary complications such as shock, respiratory failure and death. Trauma patients require specialized care within the so-called golden hour of emergency medicine, the first sixty minutes after trauma occurs.

When a trauma patient is brought to the hospital, a primary survey should have already been conducted by the ambulance officers. Any problems related to the ABCs (Airway, Breathing, and Circulation) that are highlighted by the officers should be dealt with immediately.

Any obstruction in the airway would probably have been removed by the ambulance officers. However, if the trauma patient still has an obstructed airway, the cause of the obstruction should be removed immediately.

In the case of breathing difficulties, the trauma patient may have to be intubated and undergo positive pressure ventilation.

In a trauma patient with falling blood pressure, for example, in someone who is suffering from hypovolaemic shock caused by bleeding, it is necessary to immediately control the bleeding and restore the victim's blood volume by giving infusions of balanced salt solutions. Blood transfusions are necessary for loss of large amounts of blood (e.g. greater than 20% of blood volume). Sodium is essential to keep the fluid infused in the extracellular and intravascular space whilst preventing water intoxication and brain swelling. Metabolic acidosis (mainly due to lactic acid) accumulates as a result of poor delivery of oxygen to the tissues, and mirrors the severity of the shock. It is best treated by rapidly restoring intravascular volume and perfusion. Inotropic and vasoconstrictive drugs should be avoided, as they may prevent us from accurately assessing the blood volume.

Regardless of the cause, the restoration of the circulating volume is priority. As soon as the airway is maintained and oxygen administered the next step is to commence replacement of fluids via the intravenous route.

Once the ABCs have been stabilized, a secondary survey consists of a systematic assessment of the abdominal, pelvic and thoracic viscera, complete inspection of the body surface to find all injuries, and neurological exam. Priority should be given to regions of the body that are suspected to be damaged after considering the history given by the ambulance officers. The purpose of the secondary survey is to identify all injuries so that they may be treated

In this PCL case, a haemothorax was identified and an attempt was made to remove the blood by the insertion of a chest tube.

Contributed by John Lee

Physiology of Pneumothorax and Haemothorax

Pressure Relationships In The Thoracic Cavity
Atmospheric pressure = 760 mmHg = 1 atm
Intrapulmonary pressure – the pressure in the alveoli
– rises and falls with the phases of breathing
Intrapleural pressure – the pressure in the pleural cavity
– always about 4 mmHg less than intrapulmonary pressure
due to the strong adhesive force between the parietal and visceral
pleura
– the amount of pleural fluid in the pleural cavity must remain minimal in
order for the negative intrapleural pressure to be maintained
(active pumping of the pleural fluid into the lymphatics)
Transpulmonary pressure – the difference between the intrapulmonary and intrapleural
pressures
– keeps the air spaces of the lung open and prevent the lungs from

collapsing

Pneumothorax and Haemothorax
1. Pneumothorax
- presence of air in the pleural cavity
- spontaneous pneumothorax
caused by rupture of a small bleb
often occur in tall, thin men who smoke where mechanical stresses at the apex weaken the lung tissue
chronic obstructive pulmonary disease, cystic fibrosis, necrotizing pneumonia and AIDS patients with pneumocytis carinii infection
- traumatic pneumothorax
internal trauma such as rib fracture
external trauma such as stab wound or bullet wound
invasive or therapeutic procedures (iatrogenic pneumothorax)
- tension pneumothorax
air accumulates in the pleural cavity more rapidly than it can be evacuated
lung collapses
can also shift the mediastinum and severely impede venous return and cardiac ouput
2. Haemothorax
- presence of blood in the pleural cavity
- chest trauma where virtually every blood vessel in the chest can bleed into the pleural space


When air or fluid enters the pleural cavity:
visceral and parietal pleura are separated, disrupting the negative pressure that prevents the lungs from collapsing
compresses the lungs
Thus, lungs collapse.

Sources:
mcb.berkeley.edu/courses/mcb136/topic/Respiration/SlideSet1/Resp1.pdf
www.teleflexmedical.com/ucd/normal_anatomy_physiology.pdf

(Posted by: Vivian)

Chest Drainage

Chest Drain/Tube Thoracotomy/Intercostal Chest Drain/Chest Tube Insertion/Chest Catheter Insertion

Definition: A chest tube inserted to drain the contents of the pleural space, be it air, blood or other fluid (e.g. pus).

Rationale behind a chest tube/Why insert it?

Recall Badariah’s Lecture on Mechanics of Breathing: When air/fluid enters pleural cavity, outside (atmospheric) pressure = inside (pleural cavity) pressure --> pleural cavity pressure = lung pressure --> pressure difference destroyed --> lung collapses

By draining the air/fluid out of cavity --> pressure difference restored --> re-expansion of lung

In order to do this, you must prevent entry of air/drained fluid back into the chest, and hence, a chest drain must have three components:

• An unobstructed chest drain
• A collecting container below chest level
• A one-way mechanism such as water seal or Heimlich valve

Indications for Chest Drain
(should wait for confirmation via X-Ray/ultrasound before proceeding)

Pneumothorax (pleural space filled with air) (tension, spontaneous, traumatic)
Haemothorax (pleural space filled with blood)
Empyema (pleural space filled with pus) and other Pleural effusion (pleural space filled with fluid)
Post-operative- thoracotomy, oesophagectomy and cardiac surgery

Emergency Circumstances:
Traumatic Arrest (with no cardiac output)
Patients in shock, or hypoxic due to penetrating trauma
Traumatic haemopneumothorax

Chest drain can be diagnostic and/or therapeutic

Therapeutic (as above)

Diagnostic:
Feel the texture of lung surface (for contusions)
Feel surface of diaphragm (for lacerations)
Feel heart (for presence of tamponade)

Examine material being drained:
Bright red/arterial blood – patient requires a thoracotomy
Intestinal contents – oesophageal injury or stomach/bowel injury
Persistent air leak – lung laceration
Large leaks – bronchial disruption

Contraindications

Infection over insertion site
Bleeding

Pre-procedure Patient Education

Obtain informed consent
Inform the patient of the possibility of major complications and their treatment
Explain the major steps of the procedure, and necessity for repeated chest radiographs

Procedure

1. Get materials ready, determine size of chest tube
2. Confirm site of insertion
3. Maintain sterile environment
4. Position patient
5. Anesthesia/Analgesia
6. Insertion

Materials

Chest tube
Chest tube suction unit
Chest tube tray to include scalpel blade and handle, large clamps of choice, needle driver, scissors
Packet of 0 or 1.0 silk suture on a curved needle
Tape, gauze
Anaesthesia of choice, 20cc syringe, 23-gauge needle for infiltration
Sterile prep solution; mask, gown and gloves

Selection of Chest Tube (measurement is Frenches: Fr/F)

Small, medium, large Chest Tube
Depends on what is being drained (larger for blood)
Depends on age (larger for older people)

Confirm Site of Insertion

Mid- or anterior- axillary line
Behind Pectoralis Major (to avoid having to dissect through this thick muscle)
Line lateral to the nipple (On expiration, the diaphragm rises to the 5th rib at the level of the nipple, and thus chest drains should be placed above this level)
Between 4^th or 5^th rib (highest rib space that can be easily felt in the axilla)

Sterile Environment/Position Patient

Don mask, gown, gloves.
Prep and drape area of insertion.
Position the patient. Have patient place arm over head to “open up” ribs.

Anesthesia/Analgesia

Chest tube insertion is a painful procedure, especially in muscular individuals; usually a combination of anaesthesia and analgesia is used.

Intravenous analgesia:

Opiods e.g. Morphine
Ketamine (alternative to opiods) (20mg)

Widely anesthetize area of insertion with local anaesthesia. Infiltrate skin, muscle tissues, and right down to pleura.

Local anaesthesia:

2% lidocaine (10-20ml)

Insertion

1. Make a 3-4 cm incision through skin and subcutaneous tissues between the 4^th and 5^th ribs, parallel to the rib margins.

2. Continue incision through the intercostal muscles, and right down to the pleura.

3. Insert Kelly clamp (or other curved clamp) through the pleura and open the jaws widely again parallel to the direction of the ribs (blunt dissection).

4. Insert finger through your incision and into the thoracic cavity. Make sure you are feeling lung (or empty space) and not liver or spleen.

5. Grasp end of chest tube with the Kelly forceps (convex angle towards ribs), and insert chest tube through the hole you have made in the pleura. Direct the tube over the top of the lower rib to avoid the intercostal vessels lying below each rib.

6. After tube has entered thoracic cavity, remove Kelly, and manually advance the tube in.

7. Suture/secure the tube in place. Certain closure sutures can be used in anticipation of removal.

8. Connect the tube to the drainage unit.

9. The chest is re-examined to confirm effect.

10. A chest X-ray is taken to confirm placement & position.

Drainage Unit

All chest tubes should be connected to a single flow (one direction of flow) drainage system e.g. underwater seal bottle or flutter valve.

A closed underwater seal bottle is one in which the tube is placed underwater (distilled water) at a depth of approximately 3 cm with a side vent which allows escape of air.

The drainage bottle should always be kept below the level of the patient, otherwise its contents will siphon back into the chest cavity.

The bottle may also be connected to a suction pump (when suction is turned on, air and fluid are pulled out of the pleural space and into the drainage collection bottle).

In basic terms:

Drainage occurs during expiration when pleural pressure is positive
Fluid within pleural cavity drains into water seal
Air bubbles through water seal to outside world

Complications

Tube placed subcutaneously: tube goes along chest wall instead of into chest cavity
Tube inserted too deep (lung laceration), or not deep enough (holes in tube sticking out)
Tube inserted too low: diaphragm and abdominal cavity penetration; puncture liver or spleen
Bleeding (usually ceases)
Pneumothorax after removal

Removal

Remove drain as soon as it has served it purpose
To remove drain ask patient to perform a Valsalva manoeuvre
Remove drain at the height of expiration
Tie pre-inserted closure suture.
Perform a post-procedure chest x-ray.

Documentation

1. Consent if obtained

2. Indications and contraindications for the procedure on this patient

3. Procedure used (trocar vs. non-trocar)

4. Any complications, or “none”

5. Who was notified of any complication (family, attending physician)

6. Patient education materials on chest drainage

Sources:

http://apps.med.buffalo.edu/procedures/chesttube.asp?p=7
http://www.nlm.nih.gov/medlineplus/ency/article/002947.htm
http://www.cssolutions.biz/cts.html
http://thorax.bmjjournals.com/cgi/reprint/58/suppl_2/ii53.pdf (fantastic article for everything one needs to know about chest drains)
http://www.surgical-tutor.org.uk/default-home.htm?specialities/cardiothoracic/chest_drains.htm~right
http://www.trauma.org/index.php/main/article/400/