COPD day 17th November

celebrate COPD day on 17th November by education patient and public.............

Stop smoking and prevent COPD

NEW CPR GUIDELINES AHA 2010

american heart association has published the new CPR guidelines emphasizing more on chest compression. for detail follw the AHA link

http://circ.ahajournals.org/content/vol122/18_suppl_3/


major changes are :

The newest development in the 2010 AHA Guidelines for CPR and ECC is a change in the basic life support (BLS) sequence of steps from “A-B-C” (Airway, Breathing, Chest compressions) to “C-A-B” (Chest compressions, Airway, Breathing) for adults and pediatric patients (children and infants, excluding newly
borns).

The BLS algorithm has been simplified, and “Look, Listen and Feel” has been removed from the algorithm. Performance of these steps is inconsistent and time consuming. For this reason the 2010 AHA Guidelines for CPR and ECC stress immediate activation of the emergency response system and starting chest compressions for any unresponsive adult victim with no breathing or no normal breathing.

Snoring and Sleep Apnea : information for patient

Sleep related breathing disorders are less diagnosed but not negligible in population. Snoring and sleep apneas are commonest type of sleep related breathing disorders. 2-5% of world populations suffer from sleep apnea disorders. Prevalence in India of sleep breathing disorders is around-19.5% and OSAHS (obstructive sleep apnea hypoapnea syndrome) is around 7.5% among urban Indian males. However 80-90% of these patients do not present to physician for their problem mostly due to lack of awareness.

Snoring is a sound made in the upper airway when a person sleeps. It normally occurs as one breathes in air during inspiration. It is a sign of partial obstruction of airways. Snoring disturb bed partner’s sleep and may cause dry mouth or an irritated throat when wake up. Snoring is not always associated with disease however pathological snoring is usually associated with sleep apnea syndrome.

Sleep apnea is a disorder of repeated interruption of breathing during sleep. About one-half of people who snore loudly have obstructive sleep apnea (OSA). OSA happens when the tissue in the back of the throat collapses to block the entire airway. It can happen a few times a night or several hundred times per night. People with severe snoring and OSA suffer from repeated awakening at night and excessive sleepiness during the day. The recurrent episodes of awakenings may lead to personality changes such as irritability or depression, morning headaches, a loss of interest in sex, or a decline in mental functioning. It also is linked to high blood pressure, irregular heartbeats, and an increased risk of heart attacks and stroke. Patients with severe, untreated sleep apnea are two to three times more likely to have automobile accidents than the general population. In some high-risk individuals, sleep apnea may even lead to sudden death from respiratory arrest during sleep.

Patients with the typical features of sleep apnea should be referred to a specialized sleep center or specialist that can perform a test called sleep study also known as polysomnography. This test records the patient's brain waves, heartbeat, and breathing during an entire night. If sleep apnea is diagnosed, several treatments are available. The following are treatment options for snoring and sleep apnea:

Weight loss is the initial treatment of patients with sleep apnea. With significant weight loss some patient may relieve from symptoms. Avoiding alcohol, muscle relaxants, and certain medications is also necessary. Some patient has apnea episodes in particular posture. Avoidance of such posture will lead to decrease apnea episodes.

Oral appliances: It keeps the airway open when patient’s snoring does not improve with weight loss or side sleeping. It may also help in some cases of mild to moderate sleep apnea.

Continuous positive airway pressure (CPAP): CPAP is the standard treatment for moderate to severe cases of OSA. It also may be used for mild sleep apnea, but not for simple snoring. It provides a steady stream of air through a mask to keep airway open during sleep.

Surgery: Surgery may be an option if other treatments fail to improve your snoring or sleep apnea. There are many types of nasal, throat and jaw surgeries. They have very limited role in management of sleep apnea.

WORLD SPIRMOETRY DAY 14TH OCTOBER 2010

14TH OCTOBER IS WORLD SPIROMETRY DAY...........A TIME FOR AWARENESS AND INCREASE KNOWLEGE

WE HERE IN GUWAHATI ORGANIZED A  FREE SPIROMETRY WORKSHOP FOR PG STUDENTS AND DOCTORS .. IT WAS A GREAT SUCESS

WORLD SPIROMETRY DAY

ON 14TH OCTOBER IS WORLD SPIROMETRY DAY. WE HAVE PLANNED A WORKSHOP FOR THIS PURPOSE. WHAT UR DOING ??????



 YEAR OF THE LUNG 2010

PULMONARY COMPLICATION OF SICKLE CELL ANAEMIA

Sickle cell disease (SCD) encompasses a group of hemoglobinopathies characterized by a single amino acid substitution in the beta globin chain. Hemoglobin S results from the substitution of a valine for glutamic acid as the sixth amino acid of the beta globin chain. The resulting hemoglobin tetramer (alpha2/betaS2) is poorly soluble when deoxygenated. This deoxygenated hemoglobin polymerizes into sheets of elongated rope-like fibers, causing a marked decrease in red cell deformability and distortion of the cell into the classic crescent or sickle shape. The most frequently occurring form of SCD is sickle cell anemia (HbSS).


Acute and chronic pulmonary complications occur frequently in patients with SCD, and represent the most common cause of death from SCD in adult.The common pulmonary complications are:

1. Infection
2. Embolic phenomena due to bone marrow infarction and fat emboli
3. Infarction caused by in-situ thrombosis
4. Rib and sternal infarctions
5. Pulmonary edema

Acute chest syndrome — The acute chest syndrome (ACS) is the most common form of acute pulmonary disease in patients with SCD. Signs and symptoms are

• Presence of a new pulmonary infiltrate
• Chest pain
• Temperature >38.5ºC
• Tachypnea, wheezing, or cough

Etiology of ACS is unclear.
Unknown cause — 46 %
Pulmonary infarction — 16 %
Fat embolism, with or without infection — 9 %
Chlamydophila (formerly Chlamydia) pneumoniae infection — 7 %
Mycoplasma pneumoniae infection — 7 %
Viral infection — 6 %
Mixed infections — 4 %
Other pathogens — 1%
Clinicl findings
following symptoms were present at the time of diagnosis of ACS
Fever — 80 %
Cough — 62 %
Tachypnea — 45 %
Chest pain — 44 %
Shortness of breath — 41 %
Arm and leg pain — 37 %
Abdominal pain — 35%
Rib or sternal pain — 21 %
Wheezing — 13 %
Management — The acute treatment of ACS is primarily supportive and is based upon the potential etiology.

Pneumonia — Patients with SCD are predisposed to develop pneumonia due to impaired host defenses, including loss of antibody protection (in the setting of auto-splenectomy), altered phagocytic function, and defective opsonization
Fat and bone marrow embolism — Bone marrow infarction resulting from
microvascular occlusion is the probable pathogenic mechanism common to the initiation of both fat and bone marrow embolism in patients with SCD  . Patients with SCD and pulmonary fat embolism (PFE) frequently have mental status changes, thrombocytopenia, falling hematocrit, and severe hypoxemia, a clinical presentation similar to that in patients in whom PFE develops following the fracture of long bones
Treatment options
Exchange transfusion
Plasma infusions
Glucocorticoids

Venous thromboembolism — Autopsy data of the lungs of patients with SCD reveal fibrin thromboembolism in larger arteries with or without infarction, and extensive thrombosis in smaller arteries

Sickle cell chronic lung disease — SCCLD may begin to develop as early as the second decade of life. Pulmonary dysfunction rapidly progresses, with death occurring within seven years of diagnosis Patients characteristically progress through four clinical stages based upon physiologic and radiographic data and symptoms
Stage 1 - recurrent chest pain and cough, mild reductions in forced vital
capacity (FVC) and total lung capacity (TLC), normal oxygen saturation,
and near normal chest radiographs with slightly increased interstitial
markings.
Stage 2 - greater pain than stage 1, moderate reductions in FVC and
TLC, normal oxygen saturation, and diffuse interstitial fibrosis (all lobes
on chest radiograph).
Stage 3 - severe, crushing chest pain, hypoxemia during stable periods
(PO2 approximately 70 mmHg), severe reductions in FVC and TLC, and
pulmonary fibrosis on chest imaging.
Stage 4 - prolonged chest pain, fixed dyspnea, hypoxemia at rest,
severe pulmonary fibrosis on chest radiograph, and elevated pulmonary
artery pressure at rest

Obstructive sleep apnea — Upper airway obstruction during sleep due to adenoid and tonsillar enlargement has been found in up to one-third of children with SCD

Alterations in baseline pulmonary function —M any different parameters of
pulmonary function are altered in patients with sickle cell lung disease. As examples:
Total lung capacity and vital capacity may be reduced
Even when corrected for anemia, the diffusing capacity for carbonmonoxide (DLCO) is abnormally low
Arterial oxygen saturation (SaO2) is reduced
The alveolar-arterial difference is widened both at rest and with exercise
Mild to moderate airflow obstruction may be present, particularly among patients with recurrent episodes of acute chest syndrome

pulmonary hypertension in patients with SCD is 20 to 40 percent

DNB final for board speciality ---- respiratory diseases

HERE FIND WITH THE LINK FOR DNB FINAL EXAM IN DEC 2010


http://natboard.edu.in/dnbfinal.php


BEST OF LUCK FOR ALL

MONITORING OF PATIENT WITH IDIOPATHIC PULMONARY FIBROSIS

CLICK ON IMAGES FOR ENLARGED VIEW

Impact of Tiotropium on the Course of Moderate-to-very Severe COPD

Impact of Tiotropium on the Course of Moderate-to-very Severe COPD :The UPLIFT® Trial

has shown that tritropium reduced all cause mortality. although there is no effect on lung function decline. for more detail log on to http://www.medscape.com/viewarticle/724139_9

EORTC/MSG Consensus Revised definitions on fungal infection

Proven invasive fungal diseases

Deep tissue disease

Moulds[1]

Histopathologic, cytopathologic, or direct microscopic examination[2] of a needle aspiration or biopsy specimen showing hyphal forms with evidence of associated tissue damage (either microscopically or as an infiltrate or lesion by imaging)[3]

OR

Recovery of a mould by culture from a sample obtained by a sterile procedure from a normally sterile and clinically or radiologically abnormal site consistent with an infectious disease process, excluding BAL, cranial sinus cavity, and urine.

Yeasts

Histopathologic or cytopathologic examination² of a needle aspiration or biopsy specimen from a normally sterile site excluding mucous membranes showing yeast cells (Candida species may also show pseudohyphae or true hyphae)

OR

Recovery of a yeast by culture from a sample obtained by a sterile procedure (including a freshly (<24h) placed drain) from a normally sterile and clinically or radiologically abnormal site consistent with an infectious disease process,

Fungemia

Moulds

Blood culture that yields a mould e.g. Fusarium spp. in the context of a compatible infectious disease process[4].

Yeasts

Blood culture that yields yeast (e.g. Candida species) or yeast-like fungi (e.g. Trichosporon spp.)

Endemic fungal disease[5]

Disseminated and/or pulmonary[6] disease

Must be proven by recovery in culture from a specimen obtained from the affected site, in host with a temporally related illness consistent with a fungal infectious disease process;

OR

if culture is sterile or not obtained, histopathologic or direct microscopic demonstration of appropriate morphological forms is considered adequate for dimorphic fungi having truly distinctive appearance.[7]

OR

Positive blood culture

In the case of histoplasmosis a diagnosis of disseminated disease may be established by a positive Histoplasma antigen test[8] on CSF, urine or serum by EIA, or the presence of characteristic intracellular yeast forms in a peripheral blood smear or in bone marrow.

Or in the case of coccidioidomycosis a diagnosis of disseminated disease may be established by demonstration of coccidioidal antibody⁹ in CSF, or a 2-dilution rise measured in two consecutive blood samples tested concurrently in the setting of a temporally related infectious disease process.

Cryptococcosis

Probable invasive fungal disease

Defined by at least

a) one host criterion

AND

b) one clinical criterion

AND

c) one microbiological criterion

Possible invasive fungal disease[9]

Defined by at least

a) one host criterion

AND

b) one clinical criterion

BUT

c) no microbiological criterion

Host factors

Host factors are not synonymous with risk factors and are characteristics by which individuals predisposed to invasive fungal diseases can be recognized. They are intended primarily to apply to patients treated for malignant disease and to recipients of allogeneic hematopoietic stem cell and solid organ transplant. These host factors are also applicable to those receiving corticosteroids and other T-cell suppressants as well as those with primary immune deficiencies

1)   Recent history of neutropenia (< 0.5 x 10⁹/L {<500 neutrophils/mm³} for >10 days) temporally related to the onset of fungal disease or ongoing neutropenia

2)   Receipt of an allogeneic stem cell transplant

3)   Prolonged use of corticosteroids (excluding patients with ABPA) at an average minimum dose of 0.3 mg/kg/day prednisone equivalent for > 3 weeks

4)   Treatment with other recognized T-cell immune suppressants such as ciclosporin, TNF-a blockers, specific monoclonal antibodies alemtuzumab, nucleoside analogues during the past 90 days

5)   Inherited severe immunodeficiency (e.g., chronic granulomatous disease, severe combined immunodeficiency)

Clinical criteria

Must be consistent with the microbiological findings, if any, temporally related to current episode and other potential causes must have been eliminated

Lower respiratory tract fungal disease

A) the presence of one of the following “specific” imaging signs on CT:-

·         Well defined nodule(s) with or without a halo sign

·         Wedge-shaped infiltrate

·         Air crescent sign

·         Cavity

B) the presence of a new non-specific focal infiltrate

PLUS at least one of the following[10]:-

Pleural rub

Pleural pain

Hemoptysis

Tracheobronchitis

Tracheobronchial ulceration, nodule, pseudomembrane, plaque or eschar seen on bronchoscopy

Sinonasal infection

Imaging showing sinusitis

PLUS

at least one of the following:-

Acute localized Pain (including pain radiating to eye)

Nasal ulcer, black eschar

extension from the paranasal sinus across bony barriers, including into the orbit

Endophthalmitis

as determined by ophthalmologic examination

CNS infection

at least one of the following:-

Focal lesions on imaging

Meningeal enhancement on MRI or CT

Chronic disseminated candidiasis

Small, peripheral, target like abscesses (new nodular filling defects, bull’s-eye lesions) in liver and/or spleen

Microbiological Criteria

Cytology, direct microscopy or culture:

1.      sputum, BAL and bronchial brush samples demonstrating the presence of fungal elements either by recovery by culture of a mould (e.g. Aspergillus spp., Fusarium spp., Zygomycetes, Scedosporium spp.) or detection by cytology or direct microscopy of hyphal forms

2.      sinus aspirate: recovery by culture of moulds from or detection of hyphal forms by cytology or direct microscopy.

3.      Skin ulcers, draining soft tissue lesions or fissure for which both microscopy and culture are required

Detection of antigen, cell wall constituents or nucleic acid

4.    Galactomannan antigen EIA (Platelia).

a)      a single plasma or serum sample positive for galactomannan

b)      a single BAL, pleural fluid or CSF sample positive for galactomannan

6. Glucan Assay is primarily applicable for aspergillosis and candidiasis and does not detect Cryptococcus species nor the Zygomycetes (Rhizopus spp., Mucor spp. Absidia spp.)

a single serum sample positive for beta-D-glucan

7. Polymerase Chain Reaction to detect nucleic acid

Until a PCR system is developed that has been externally validated, a positive PCR result for blood, tissue, or BAL fluid for the specific fungus studied will not be considered microbiological evidence of invasive fungal disease.

---

[1] Append identification at genus or species level from culture, if available.

[2] tissue and cells submitted for histopathology or cytopathology should be stained by Grocott-Gomorri methenamine silver stain or by periodic acid Schiff stains to facilitate inspection of fungal structures. Where possible, wet mounts of specimens from foci related to invasive fungal infectious disease should be stained with a fluorescent marker (e.g., calcofluor or Blancophor)

[3] Individual fungal invasive disease entities e.g. proven aspergillosis require culture and identification. Faiiling this the disease is designated as proven mould invasive fungal disease

[4] Other moulds can cause fungemia. However contamination should be excluded before assigning the diagnosis of proven invasive fungal disease

[5] Histoplasmosis, blastomycosis, coccidioidomycosis, and paracoccidioidomycosis, sporotrichosis and infection due to Penicillium marneffei

[6] the medical history must be established to distinguish between a primary and chronic pulmonary infection. Onset within 3 months defines a primary pulmonary infection.

[7] Histoplasma capsulatum variety capsulatum may resemble Candida glabrata or Leishmania in tissue but can be distinguished from them by the characteristic histologic features of granulomatous inflammation and staining by Grocott-Gomorri methenamine silver stain

[8] Testing should be performed only in laboratories where the assays have been validated; i.e., clinical correlations made with results and titers, and with data available on false positive and false negative rates with the test as performed in that laboratory.

[9] provided other plausible causes have been excluded

[10] symptoms not necessary if there is mycological evidence

diagnostic criteria for FAT EMBOLISM

Gurd’s criteria for the diagnosis of fat embolism syndrome


Major criteria
1 Axillary or subconjuctival petechia. This occurs transiently over 4–6 h in
50%–60% of patients
2 Hypoxemia (PaO2 <60mmHg; FiO2 <0.4)
3 Central nervous system depression disproportionate to hypoxemia, and
pulmonary edema
Minor criteria
1 Tachycardia (>110 beats/min)
2 Pyrexia (>38.5°)
3 Emboli in the retina on fundoscopic examination
4 Fat present in urine
5 Sudden unexplained drop in hematocrit or platelet values
6 Increasing erythrocyte sedimentation rate
7 Fat globules in the sputum
8 Symptoms within 72h of skeletal trauma
9 Shortness of breath
10 Altered mental status
11 Occasional long tract signs and posturing
12 Urinary incontinence

Criteria for the diagnosis of fat embolism syndrome according to Gurd and Wilson

Major criteria
1 Respiratory insufficiency
2 Cerebral involvement
3 Petechial rash
Minor criteria
1 Pyrexia (usually <39°C)
2 Tachycardia (>120 beats/min)
3 Retinal changes (fat or petechiae)
4 Jaundice
5 Renal changes (anuria or oliguria)
6 Anemia (a drop of more than 20% of the admission hemoglobin value)
7 Thrombocytopenia (a drop of >50% of the admission thrombocyte value)
8 High erythrocyte sedimentation rate (ESR >71mm/h)
9 Fat macroglobulinemia

At least two major symptoms
or signs or one major and four minor symptoms or
signs must be present to diagnose the syndrome

current concept in acute embolism ;FLOWCHART FOR DIAGNOSIS

reference new england journal of medicine 2010 june

group for discussion of respiratory medicine in orkut and facebook

please join group/ community for discussion on respiratory, critical care and sleep medicine in orkut and facebook. follow the link

http://www.orkut.co.in/Main#Community?cmm=92421330

http://www.facebook.com/home.php?ref=home#!/group.php?gid=232602082762

sleep apnea screening

Take the sleep test!

NO SMOKING DAY 31ST MAY

LETS MAKE THIS WORLD SMOKE FREE..... LET INITIATE A HEALTHY LIVING

ACR Criteria for the diagnosis of Churg-Strauss Syndrome

Patient is classified as CSS if at least four of six criteria are present

1. History of asthma
2. Eosinophilia: Eosinophilia >10% on differential white blood cell count.
3. Mono- or polyneuropathy
4. Pulmonary infiltrates, migratory or transitory pulmonary infiltrates due to vasculitis.
5. History of acute or chronic paranasal sinus pain or tenderness or radiographic opacification of the paranasal sinuses.
6. Extravascular eosinophils

Preoperative assessment of patients with pulmonary diseases

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world asthma day..................... HOW I CAN ASSESS MY ASTHMA CONTROL

ASTHMA IS A CHRONIC INFLAMMATORY DISORDER OF THA AIRWAY. THE PRESENT AIM OF ASTHMA MANAGEMENT IS TO KEEP IT UNDER CONTROL. THERE ARE SEVERAY WAY TO ASSESS ASTHMA CONTROL. A PATIENT CAN ASSESS ASTHMA CONTROL BY FOLLOWING QUESTION--

1. HOW MANY TIME UR ASTHMA KEEP U AWAY FROM UR DAY TO DAY ACTIVITIES

2. HOW FREQUENTLY U HAVE BREATHING PROBLEM

3. HOW FREQUENT UR NIGHT SYMPTOMS

4. HOW FREQUENTLY U NEED RESQUE INHALER /NEBULIZER

5. WHAT IS UR PEAK FLOW READING

6. DO U THING UR ASTHMA IS IN CONTROL

BY ASKING ABOVE QUESTION AND SUBSEQUENT RESULT WILL GIVE IDEA ABOUT ASTHMA CONTROL. THE BETTER UR ASTHMA CONTROL THE BETTER IS UR QUALITY OF LIFE.

emphysema in non smoker

Emphysema develop mostly in smokers however there is report of emphysema in person who does not smoke. The causes of emphysema in non smokers includes

Nutritional Emphysema
alfa-1 antitrypsin deficiency
HIV
chronic asthma
treated pulmonary tuberculosis
Drugs—injectables
             Methylphenidate
             Methadone
              Heroin
Drugs—inhalation
             Marijuana
             Toluene (glue sniffing)
Connective tissue disease
              Cutis Laxa, Marfan syndrome, Ehlers-Danlos syndrome
Occupational exposures
              Coal mine dust, silica dust, cadmium
Biological dusts
              Farmers, grain workers, wood workers, cotton textile worker
Biomass fuels
Congenital
              Salla’s disease, Menkes disease, Hypocomplimentemic urticarial vasculitis (HUVS)


ref
1 . Emphysema in the Nonsmoker. Delano S. Fabro, Jr, DO,*† and Douglas S. Frenia, MD*. Clinical Pulmonary Medicine • Volume 15, Number 1, January 2008
2 . COPD in non smoker. PJ Barens Lancet aug.2009

ASTHMA ............INFORMATION FOR PATIENTS

                                                                 ASTHMA

Dr Kripesh Ranjan Sarmah                                                                                          

CONSULTANT PULMONOLOGIST 

09864152139

Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by increased airway hyper-reactivity (AHR) and variable airflow obstruction. Its importance is underpinned by the recognition that an estimated 300 million people worldwide suffer from asthma and an estimated additional 100 million persons may be expected to develop the disease by 2025.

Asthma is a chronic lung disease associated with inflammation and narrowing of the airways. Asthma causes recurring episodes of wheezing (a whistling sound when breathe), chest tightness, shortness of breath, and coughing. The coughing often occurs at night or early in the morning. Asthma affects people of all ages and it most often starts in childhood. In the United States, more than 22 million people are known to have asthma. Nearly 6 million of these people are children. In Indian prevalence of asthma varies from 2 to 16% in different areas.

People who have asthma have inflammed airways. This makes the airways swollen and very sensitive. They tend to react strongly to many of substances that are breathed in to which a normal person would not react at all. When the airways react, the muscles around them tighten. This causes the airways to narrow and less air flows to the lungs. The swelling of the airways also makes the airways even narrower. Cells in the airways may make more mucus than normal. Mucus is a sticky, thick liquid that can further narrow your airways. This chain reaction can result in asthma symptoms. Symptoms can happen each time the airways are provoked. Sometimes symptoms are mild and go away on their own or after minimal treatment with an asthma medicine. At other times, symptoms continue to get worse. When symptoms get more intense and/or additional symptoms appear, this is an asthma attack. Asthma attacks also are called flare-ups or exacerbations. It's important to treat symptoms when patient first notice them. This will help prevent the symptoms from worsening and causing a severe asthma attack. Severe asthma attacks may require emergency care, and sometimes it can cause death.

Asthma can't be cured it can be controlled. Even when patient feel fine, he or she still continue to have the disease i.e. inflammation and it can flare up at any time. But with today's knowledge and treatments, most asthmatics can lead a normal life.

Causes Asthma

The exact cause of asthma isn't known. Combination of factors, family genes and certain environmental exposures interact to cause asthma to develop, most often  in early life. These factors include:

• An inherited tendency to develop allergies, called atopy
• Parents who have asthma
• Certain respiratory infections during childhood
• Exposure to some airborne allergens or exposure to some viral infections in infancy or in early childhood when the immune system is developing
• Obesity
• Exposure to fumes, gases at workplaces
• In-door and outdoor pollution
• Tobacco smoke

If asthma or atopy runs in the family then the airways when exposed to airborne allergens (for example, house dust mites, cockroaches, and possibly cat or dog dander) and irritants (for example, tobacco smoke) will react in an exaggerated manner. the effect of different factors varies from patient to patient.

The "Hygiene Hypothesis"

One theory related to causes of asthma is the "hygiene hypothesis”. Some people believe that Western lifestyle—with its emphasis on hygiene and sanitation—has resulted in changes in living conditions and an overall decline in infections in early childhood. Many young children no longer experience the same types of environmental exposures and infections as children did in the past and it may increase their risk for atopy and asthma.

Factors that can trigger asthma attack

There are number of things can bring about or worsen asthma symptoms when an asthmatics can in contact with then. Triggers may include:

• Allergens found in dust, animal fur, cockroaches, mold, and pollens from trees, grasses, and flowers
• Irritants such as cigarette smoke, air pollution, chemicals or dust, fumes in the workplace, compounds in home décor products, and sprays (such as hairspray)
• Certain medicines such as aspirin or other nonsteroidal anti-inflammatory drugs like ibuprofen and nonselective beta-blockers.
• Viral upper respiratory infections such as colds
• Exercise (physical activity) in cold enverionment
• Tobacco smoke
• Some foods
• Food preservative
• Strong emotions
• Perfume
• Spray-on deodorants

Diagnosis

Diagnosis of asthma primarily based on medical history supported by a physical exam, and laboratory tests. Diagnosis and severity of asthma is determined by pulmonary function test.

Medical History

Symptoms of Asthma

Common asthma symptoms include:

• Coughing. Usually worse at night or early in the morning, making it hard to sleep.
• Wheezing. Wheezing is a whistling or squeaky sound that occurs over chest while breathing.
• Chest tightness. This may feel like something is squeezing or sitting on chest.
• Shortness of breath. Patient often feel as if he or she can't get air out of the lungs.

Finding during examination

Some patient may have normal examination while others may have extensive signs of airflow limitation. Usually patient have wheezing on auscultation. During severe attack patient may have hyperinflated chest, cyanosis, drowsiness, difficulty in speaking, tachycardia, use of    accessory muscles, intercostal recession etc

Diagnostic Tests

Pulmonary function test

The function of the lung is measured with an equipment/instrument called spirometer. A series of tests are done with the help of spirometer and these are together called Pulmonary Function Test. As we measure one’s degree of temperature in fever with the help of a clinical thermometer, spirometry helps us to measure degree and extent of airway obstruction. With the help of spirometry the severity of asthma can be detected.

Peak Flow Meter

This device can be used both in clinic and home. This small, hand-held device shows how well air moves out of the lungs. Patient blow into the device and it gives a score, or peak flow number. Score shows how well lungs are working at the time of the test. Measuring peak flow regularly can help whether asthma is getting worse. This device is useful for self monitoring of asthma.

Other Tests

Other tests are required if needed for more information or to exclude other diagnosis. Other tests may include:

• Allergy testing to find out which particular allergens affect patient’s asthma symptoms,
•  Bronchoprovocation test. Using spirometry, this test repeatedly measures lung function during physical activity or after patient receive increasing doses of cold air or a special chemical to breathe in. This test measure airway hyperreactivity.
• A chest x ray or an EKG (electrocardiogram). These tests will help find out whether a foreign object or other disease may be causing asthma like symptoms.

Diagnosing Asthma in Young Children

Most children who have asthma develop their first symptoms before 5 years of age. However, asthma in young children (aged 0 to 5 years) can be hard to diagnose. Sometimes it can be difficult to tell whether a child has asthma or another childhood condition because the symptoms of both conditions can be similar.

Also, many young children who have wheezing episodes when they get colds or respiratory infections don't go on to have asthma after they're 6 years old. These symptoms may be due to the fact that infants have smaller airways that can narrow even further when they get a cold or respiratory infection. The airways grow as a child grows older, so wheezing no longer occurs when the child gets a cold.

A young child who has frequent wheezing with colds or respiratory infections is more likely to have asthma if:

• One or both parents have asthma
• The child has signs of allergies, including the allergic skin condition eczema
• The child has allergic reactions to pollens or other airborne allergens
• The child wheezes even when he or she doesn't have a cold or other infection

Asthma Treatment and Control

Asthma is a long-term disease that can't be cured. The goal of asthma treatment is to control the disease. Good asthma control will:

• Prevent chronic and troublesome symptoms such as coughing and shortness of breath
• Reduce need of quick-relief medicines  
• Maintain good lung function
• Maintain normal activity levels and sleep throughout the night
• Prevent asthma attacks that could result in emergency room visit or being admitted to the hospital for treatment

The steps in asthma management includes

·        Development of Patient/Doctor Partnership

·        Identify and reduce exposure to risk factors

·        Assess, Treat and Monitor Asthma

·        Manage asthma exacerbations

·        Special considerations

Patient doctor partnership/Asthma action plan

Patient doctor partnership help to attain guided self asthma management. The essential component include

• Education

• Joint setting of goals

• Self-monitoring. The person with asthma is taught to combine assessment of asthma control with educated interpretation of key symptoms

• Regular review of asthma control, treatment, and skills by a health care professional

• Written action plan. An asthma action plan gives guidance on taking medicines properly, avoiding factors that worsen asthma, tracking level of asthma control, responding to worsening asthma, and seeking emergency care when needed.

Avoid Things That Can Worsen Your Asthma

A number of things (sometimes called asthma triggers) can  often set off or worsen asthma symptoms. Asthma patients should avoid these triggers as far as possible.

Several health conditions can make asthma more difficult to manage. These conditions include runny nose, sinus infections, reflux disease, psychological stress, and sleep apnea. These conditions also need to be treated along side of asthma.

Medicines

Asthma is treated with two types of medicines: long-term control and quick-relief medicines. Long-term control medicines help reduce airway inflammation and prevent asthma symptoms. Quick-relief, or "rescue," medicines relieve asthma symptoms that may flare up.

Initial asthma treatment will depend on how severe the disease is. Follow-up asthma treatment will depend on how well asthma action plan is working to control ones symptoms and prevent patient from having asthma attacks. The level of asthma control can vary over time and with changes in home, school, or work environments that alter how often patient is exposed to the factors that can make asthma worse. Medicines are prescribed in a stepwise approach. Asthma medicines can be taken by mouth or by inhaled form. An inhaler allows the medicine to go right to the lungs. Medication by inhaler devices act fast, less medication is required hence side effect are less.

Drug delivery devices

Inhalers dispense either a fluid or a powdered mist. It is very important to understand how to take inhalers, because if not taken properly, over 95% of inhaled medication may never reach the lungs. By inhalation small amount of drugs delivered into the lung with no systemic side effect but with desired clinical response. Different types of inhaler devices like metered dose inhaler (MDI), dry powder inhaler (DPI), nebulizer etc. are available.

Basic steps of taking inhaler are:

1.   Remove the cap and hold the inhaler upright.

2.   Shake the canister.

3.   Tilt head back and breathe out.

4.   Put the inhaler in mouth. Or, if patient is using a spacer, put the end of it in mouth and seal your lips around it. (A spacer is a tube that attach to your inhaler. It makes using an inhaler easier.)

5.   Press down on the inhaler to release the medicine as patient slowly breathe in for 3 to 5 seconds. (If patient use inhaled dry powder capsules, close mouth tightly around the mouthpiece of the inhaler and inhale rapidly.)

6.   Hold breath for 10 seconds so as to allow the medicine to get into lungs.

7.   Repeat as many times as doctor suggests. Wait 1 minute between puffs.

Long-Term Control Medicines

Long term control medicines reduces airway inflammation and most asthma patients are required to take long-term control medicines daily to help prevent symptoms.

Inhaled corticosteroids. Inhaled corticosteroids are the preferred medicines for long-term control of asthma. These medicines are the most effective long-term control medicine to relieve airway inflammation and swelling that makes the airways sensitive to certain substances that are breathed in. Reducing inflammation helps prevent the chain reaction that causes asthma symptoms. Most people who take these medicines daily find they greatly reduce how severe symptoms are and how often they occur. Inhaled corticosteroids are generally safe when taken as prescribed. They're very different from the illegal anabolic steroids taken by some athletes. Inhaled corticosteroids aren't habit-forming, even if patient take them every day for many years.

But, like many other medicines, inhaled corticosteroids can have side effects. However benefits of taking inhaled corticosteroids and preventing asthma attacks far outweigh the risks of side effects. One common side effect from inhaled corticosteroids is a mouth infection called thrush. Patient can use a spacer or holding chamber to avoid thrush. A spacer or holding chamber is attached to the inhaler when taking medicine to keep the medicine from landing in mouth or on the back of throat. Rinsing of mouth with water after taking inhaled corticosteroids also can lower the risk of thrush formation.

In case of severe asthma, systemic corticosteroid in the form of injectable or pills for short periods is required to get asthma under control. If taken for long periods, these medicines raise the risk for cataracts and osteoporosis.

Other long-term control medicines. Other long-term control medicines include:

• Systemic corticosteroids
• Inhaled long-acting beta₂-agonists. These medicines open the airways and may be added to low-dose inhaled corticosteroids to improve asthma control. An inhaled long-acting beta₂-agonist shouldn't be used alone.
• Leukotriene modifiers. These medicines are taken by mouth.
• Cromolyn and nedocromil. These inhaled medicines also help prevent inflammation and can be used to treat asthma of mild severity.
• Theophylline. This medicine is taken by mouth and helps open the airways.
• Anti-IgE

Quick-Relief Medicines

Asthmatics need a quick-relief medicine to help relieve asthma symptoms that may flare up. Inhaled short-acting beta₂-agonists are the first choice for quick relief. Other medications are inhaled anticholinergics, short-acting theophylline, and short-acting oral beta2-agonists.

These medicines act quickly to relax small muscles around airways. This allows the airways to open up so air can flow through them.

Patient should take quick-relief medicine when he or she first notice asthma symptoms. If patient need to use this medicine more than 2 days a week, patient may need to visit doctor to get better control of symptoms.

Anti-IgE

Anti-IgE (omalizumab) is a treatment option limited to patients with elevated serum levels of IgE. Its current indication is for patients with severe allergic asthma who are uncontrolled on inhaled glucocorticosteroids.

Allergen-specific immunotherapy.

The role of specific immunotherapy in adult asthma is limited. Appropriate immunotherapy requires the identification and use of a single well-defined clinically relevant allergen. The later is administered in progressively higher doses in order to induce tolerance. Specific immunotherapy should be considered only after strict environmental avoidance and pharmacologic intervention, including inhaled glucocorticosteroids, have failed to control a patient’s asthma.

Control of asthma

patient can record asthma symptoms in a diary to see how well treatments are controlling patient’s asthma.

Asthma is "well controlled" if:

• Patients have symptoms no more than 2 days a week and they don't have night time symptoms
• Patients can carry out all normal activities.
• Patients take quick-relief medicines no more than 2 days a week.
• Patients have no history of asthma attack that requires to take corticosteroids by mouth or emergency visit.
• Patients’ peak flow doesn't drop below 80 percent of personal best number or have normal or near normal lung function.

If asthma isn't well controlled, patient need to contact doctor. He or she may need to change asthma action plan.

Emergency Care

Most people who have asthma, including many children, can safely manage their symptoms by following the steps for worsening asthma provided in the asthma action plan. However, patient may need medical attention. Visit doctor for advice if:

• Medicines don't relieve an asthma attack.
• Peak flow is less than half of your personal best peak flow number.

Pregnant Women with asthma

Pregnant women who have asthma need to control the disease to ensure a good supply of oxygen to their babies. Poor asthma control raises the chance that a baby will be born early and have a low birth weight. Poor asthma control can even risk the baby's life. Studies show that it's safer to take asthma medicines during pregnant than to risk having an asthma attack. Patient need to inform doctor if she have asthma and are pregnant or planning to get pregnant. Level of asthma control may get better or it may get worse while pregnant.

Exercise induced asthma                                                                     (People Whose Asthma Symptoms Occur With Physical Activity)

Physical activity is an important part of a healthy lifestyle. Adults need physical activity to maintain good health. Children need it for growth and development.

In many people, however, physical activity may set off asthma symptoms. If this happens patient need to talk to doctor about the best ways to control asthma so patient can stay active.

The following medicines may help to prevent asthma symptoms due to physical activity:

• Short-acting beta₂-agonists (quick-relief medicine) taken shortly before physical activity can last 2 to 3 hours and prevent exercise-related symptoms in most people who take them.
• Long-acting beta₂-agonists can be protective up to 12 hours. However, with daily use, they will no longer give up to 12 hours of protection. Also, frequent use for physical activity may be a sign that asthma is poorly controlled.
• Leukotriene modifiers. These pills are taken several hours before physical activity. They help relieve asthma symptoms brought on by physical activity in up to half of the people who take them.
• Cromolyn or nedocromil. These medicines are taken shortly before physical activity to help control asthma symptoms.
• Long-term control medicines. Frequent or severe symptoms due to physical activity may indicate poorly controlled asthma and the need to either start or increase long-term control medicines that reduce inflammation. This will help prevent exercise-related symptoms.

Easing into physical activity with a warm-up period may be helpful.

Summery

bronchial asthma is a chronic inflammatory disease of the airways and is characterized by episodic attack of respiratory distress, cough wheezing, chest tightness etc. Patient must have regular asthma checkups with doctor so that he or she can assess level of asthma control and adjust treatment if needed. The main goal of asthma treatment is to achieve the best control of asthma using the least amount of medicine. This may require frequent adjustments to treatments. It is a treatable condition and with proper treatment reasonable control can be achieved.