GLASGOW COMA SCALE (GCS) :

Glasgow Coma Scale ( GCS)

There are a few different systems that medical practioners use to diagnose the symptoms of Traumatic Brain Injury. This section discusses the Glasgow Coma Scale.
The Glasgow Coma Scale is based on a 15 point scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others.

The test measures the motor response, verbal response and eye opening response with these values:

I. Motor Response(M)

6 - Obeys commands fully
5 - Localizes to noxious stimuli
4 - Withdraws from noxious stimuli
3 - Abnormal flexion, i.e. decorticate posturing
2 - Extensor response, i.e. decerebrate posturing
1 - No response

II. Verbal Response(V) 
5 - Alert and Oriented
4 - Confused, yet coherent, speech
3 - Inappropriate words and jumbled phrases consisting of words
2 - Incomprehensible sounds
1 - No sounds

III. Eye Opening(E)
4 - Spontaneous eye opening
3 - Eyes open to speech
2 - Eyes open to pain
1 - No eye opening

The final score is determined by adding the values of (E+V+M = ? score).

This number helps medical practioners categorize the four possible levels for survival, with a lower number indicating a more severe injury and a poorer prognosis:

Mild (13-15):
More in-depth discussion on the Mild TBI Symptoms page.

Moderate Disability (9-12):
Loss of consciousness greater than 30 minutes
Physical or cognitive impairments which may or may resolve
Benefit from Rehabilitation

Severe Disability (3-8):
Coma: unconscious state. No meaningful response, no voluntary activities
Vegetative State (Less Than 3):

Sleep wake cycles
Aruosal, but no interaction with environment
No localized response to pain

Persistent Vegetative State:
Vegetative state lasting longer than one month

Brain Death:
No brain function
Specific criteria needed for making this diagnosis

CONGESTIVE HEART FAILURE (CHF) : A BRIEF REVIEW

Congestive Heart Failure - Diastolic

Introduction

Congestive heart failure (CHF) occurs when the cardiac output is not adequate enough to meet the demands of the body. This can occur for several reasons as congestive heart failure is the predominant clinical presentation in multiple disease states. Heart failure can be due to:

Systolic dysfunction (reduced ejection fraction)Diastolic dysfunction (relaxation or filling abnormality)Valvular heart diseaseRight heart failureArrhythmiaHigh output CHF (i.e. severe anemia, arteriovenous malformations)

Review of diastolic congestive heart failure will be presented here. Review of systolic congestive heart failure, valvular heart disease, right heart failure and high output heart failure are presented elsewhere.

Pathophysiology

Diastolic dysfunction occurs when the left ventricular myocardium is non-compliant and not able to accept blood return in a normal fashion from the left atrium. This can be a normal physiologic change with aging of the heart or result in elevated left atrial pressures leading to the clinical manifestations of diastolic congestive heart failure.

While there is some degree of activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) in states of diastolic heart failure, it is not as dramatic as seen with systolic heart failure. Also, these neurohormonal systems do not exert the negative remodeling effect on the heart during diastolic heart failure as much as occurs with systolic congestive heart failure. Below is a schematic of the neurohormal mechanisms present in congestive heart failure:

Etiology

There are a number of causes of diastolic congestive heart failure:

Hypertensive heart diseaseAging of the heartRestrictive cardiomyopathyValvular heart diseaseTachyarrhythmiasConstrictive pericarditis

Hypertension causes left ventricular hypertrophy and impaired relaxation. Over time, this progressing resulting in higher degrees of diastolic dysfunction, low cardiac output and symptoms of congestive heart failure.

The aging process of the heart is not well understood, however fibrotic changes are seen within the myocardium. This results in a relaxation abnormality that is almost universally present by the age of 60. In the elderly, this can progress causing significant diastolic impairment and congestive heart failure.

Restrictive cardiomyopathies frequently cause deposition of substances (i.e. amyloid protein) within the myocardium causing diastolic relaxation abnormalities and when severe, diastolic congestive heart failure.

Valvular heart disease such as mitral stenosis, technically causes heart failure due to diastolic dysfunction of the left ventricle. Severe aortic stenosis causes left ventricular hypertrophy and when left ventricular pressures increase a significant amount, diastolic heart failure can occur.

When a tachyarrhythmia occurs such as atrial fibrillation with an uncontrolled ventricular response, congestive heart failure can occur in the setting of normal systolic function from a shortened diastolic filling time. This is technically a form of diastolic heart failure, however once ventricular rates are controlled, the cardiac hemodynamics should dramatically improve.

Symptoms

The general symptoms of congestive heart failure are the same regardless of the etiology (systolic or diastolic) and are attributed to either fluid retention (related to the activated RAAS) or low cardiac output. They can also be categorized as from left heart failure versus right heart failure.

Left heart failure will result in low cardiac output symptoms and transmission of the increased left-sided cardiac pressures into the lungs causing pulmonary edema and a sense of dyspnea. With physical exertion the heart demands increased cardiac output which is not able to be satisfied in states of heart failure and thus left heart pressures increase significantly causing this transient pulmonary edema.

As those increased pressures from the left heart affect the right ventricle, right heart failure can ensue. The most common cause of right heart failure is left heart failure.
Right heart failure symptoms include lower extremity dependant edema. When the legs are elevated at night, the fluid redistributes centrally causing pulmonary edema resulting in orthopnea (dyspnea while laying flat) or paroxysmal nocturnal dyspnea (PND). Hepatic congestion can occur causing right upper quadrant abdominal pain.

Symptoms related to low cardiac output include fatigue, weakness and in extreme cases, cardiac cachexia can occur.

The New york Heart Association (NYHA) functional class helps to classify patients based on their symptoms of heart failure.

Class I: No symptoms of heart failure
Class II: Symptoms of heart failure with moderate exertion such as ambulating 2 blocks or 2 flights of stairs
Class III: Symptoms of heart failure with minimal exertion such as ambulating 1 block or 1 flight of stairs, but no symptoms at rest
Class IV:  Symptoms of heart failure at rest

Note that the NYHA functional class differs from the ACC/AHA heart failure classification system in that the former allows movement from one class to the other while the ACC/AHA classification does not (see below).

Diagnosis

Echocardiography is the gold standard to diagnose diastolic dysfunction. There are four grades of diastolic dysfunction as described below. Clinical manifestations of congestive heart failure may start to occur once grade II diastolic dysfunction is present, however not in the presence of grade I diastolic dysfunction (impaired relaxation).

Grade I (impaired relaxation): This is a normal finding and occurs in nearly 100% of individuals by the age of 60. The E wave velocity is reduced resulting in E/A reversal (ratio < 1.0). The left atrial pressures are normal. The deceleration time of the E wave is prolonged measuring > 200 ms. The e/e’ ratio measured by tissue Doppler is normal.

Grade II (pseudonormal): This is pathological and results in elevated left atrial pressures. The E/A ratio is normal (0.8 +- 1.5), the deceleration time is normal (160-200 ms), however the e/e’ ratio is elevated. The E/A ratio will be < 1 with Valsalva. A major clue to the presence of grade II diastolic dysfunction as compared to normal diastolic function is the presence of structural heart disease such as left atrial enlargement, left ventricular hypertrophy or systolic dysfunction. If significant structural heart disease is present and the E/A ratio as well as the deceleration time appear normal, suspect a pseudonormal pattern. Valsalva distinguishes pseudonormal from normal as well as the e/e’ ratio. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.

Grade III (reversible restrictive): This results in significantly elevated left atrial pressures. Also known as a “restrictive filling pattern”, the E/A ratio is > 2.0, the deceleration time is < 160 ms, and the e/e’ ratio is elevated. The E/A ratio changes to  < 1.0 with Valsalva. Diuresis can frequently reduce the left atrial pressure relieving symptoms of heart failure and returning the hemodynamics to those of grade I diastolic dysfunction.

Grade IV (fixed restrictive): This indicates a poor prognosis and very elevated left atrial pressures. The E/A ratio is > 2.0, the deceleration time is low and the e/e’ ratio is elevated. The major difference distinguishing grade III from grade IV diastolic dysfunction is the lack of E/A reversal with the Valsalva maneuver (no effect will be seen with Valsalva). Diuresis will not have a major effect on the left atrial pressures and clinic heart failure is likely permanent. Grade IV diastolic dysfunction is present only in very advanced heart failure and frequently seen in end-stage restrictive cardiomyopathies such as amyloid cardiomyopathy.

Treatment

There is a relative lack of data to guide medical therapy in patients with diastolic congestive heart failure, especially when compared to systolic congestive heart failure.

The ACC/AHA guidelines give three class I recommendations to medically treat chronic diastolic congestive heart failure.

The first is to control the heart rate in patients with atrial fibrillation in order to improve diastolic filling. Tachycardia shortens diastolic filling time and so keeping heart rates < 100 beats per minute and preferably between 60-80 beats per minute will improve cardiac output when significant diastolic heart failure is present. Rate control can be achieved using beta-blockers, non-dihydropyridine calcium channel blockers, or digoxin.

The second recommendation is to control systolic and diastolic blood pressure using the standard treatment for hypertension.

The third is to use diuretics to control pulmonary congestion and peripheral edema.

BASIC ANATOMY OF EYEBALL :

Cornea

The cornea is the clear window to the eye.  It is at the front of the eye just in front of the coloured part of the eye, the iris.  It has no blood vessels in it, and normally is completely transparent.  When it is scarred or infected, it may appear white in some areas.  When a person gets a "scratch" to the eye or a corneal abrasion, the superficial layer of the cornea is torn off.  This can be very painful but heals quickly with the proper treatment.  People who have permanent corneal scarring may be candidates for a corneal transplant.  When people wear contact lenses, these lenses sit on top of the cornea.  The cornea is the structure that is lasered during procedures like LASIK or PRK, which help people see without glasses (Refractive Laser).

Anterior Chamber

The anterior chamber is the area just in front of the iris inside the eye.  It is filled with watery fluid calledaqueous.  Aqueous is produced in the cilary body muscle (in the posterior chamber) and flows through the pupil, into the anterior chamber angle or drainage canal, to exit the eye.  This is a very important pathway of study in glaucoma research.

Posterior Chamber

The posterior chamber is behind the iris and includes the ciliary body muscle and the lens complex.  The aqueous is produced in this chamber and flows to the front of the eye to be drained in the anterior chamber angle.

 

Iris

The iris is the part of the eye that gives us the colour of the eye, whether it be blue, brown, green or hazel.  It acts like the diaphragm of a camera and expands (dilates) and contracts to allow more or less light into the eye.

 

Sclera

This is the white hard shell around the eye which is connected to the cornea.

 

Conjunctiva

The conjunctiva is a thin membranous layer of tissue on top of the sclera.  It covers the eyeball up to the lids and then folds under the lids and covers the underside of the upper and lower lids.  You can never lose a contact lens behind the eye, since the conjunctiva creates a natural barrier.  The conjunctiva is what gets inflamed and red when we have any infection or allergic reaction of the eyes giving the appearance of "pink eyes". Sometimes, people get a red spot under the conjunctiva, which can be a bit of blood, that can arise spontaneously or with minor trauma, and usually clears up within a few days.

 

Pupil

The pupil is the hole in the iris.  The pupil gets larger when it is dark letting more light into the eye, and smaller when it is bright letting less light into the eye.  When you eye doctor dilates your eyes with eye drops, the pupil becomes large for a few hours and it becomes blurry up close.  This allows more visibility inside your eyes to do a more thorough examination of the inside of your eyes.

 

Lens

This is the natural lens of the eye.  Just as a camera has a lens, so does the eye.  This lens is clear for most of our lives, and changes shape as we try to focus on things up close and things in the distance.  With some medications or diseases, the ability of our lenses to change shape becomes temporarily (or permanently)impaired.  For example, pregnant women may notice that their glasses prescription changes during pregnancy, and then stabilizes after giving birth.  This is due to hormonal changes that affect the shape of the lens during pregnancy.  Overtime, and earlier with some medications (like steroids) and diseases (like diabetes), or lifestyle issues (such as smoking or excessive exposure to UV radiation), clouding of our lenses develops which we call "cataract".  Cataracts blur our vision and can be treated with cataract surgery.

 

Ciliary Body and Ciliary Muscle

This is the muscle that enables the iris to move back and forth to change the shape of the pupil.  It also produces the fluid of the eye called "aqueous".  Diode laser is a treatment for glaucoma that targets the ciliary body to decrease the production of aqueous thereby decreasing the build-up of fluid and pressure in the eye.

 

Vitreous

The vitreous is a clear gel that fills the bulk of the eyeball.  It is solid when we are born and is attached to the inside of the eye.  As we get older, the vitreous becomes loose, and "floaters" are created.  These are just pieces of more solid vitreous, floating in the more liquid vitreous, and creating shadows on the retina.  Sometimes the vitreous falls off the back of the eye abruptly (posterior vitreous detachment), and creates sudden floaters and flashing light sensation.  The flashing is from the vitreous pulling on the retina.  Sometimes, the retina is torn during this spontaneous event (happens with aging).  This is called a retinal tearand can be a risk factor for a retinal detachment.  This can be lasered close to avoid further problems.

 

Retina

The retina is the "film" of the eye, if you think if the eye as a camera.  It is a very thin layer of nerve tissue.  If a person has a retinal detachment, this means that this layer has come loose and is not attached to the circulation.  This is an eye emergency that needs to be surgically treated to prevent permanent vision loss.

 

Macula

The macula is the centre of the retina that is responsible for our central, reading vision. The retina outside the macula provides us with our peripheral or side vision.  Macular degeneration is degeneration of this central, very important part of the retina.  Although people with macular degeneration may lose their central, reading vision, they will still have their peripheral vision, if the rest of the retina is okay.

 

Retinal vessels

The retina is provided with oxygen and nutrients by vessels both within it and underneath it (in the choroid).  The retinal layers need both sets of circulation to function properly.  Sometimes, people may have a "stroke" in the eye.  This means that the circulation an artery of the eye has been blocked.  This is often due to "atherosclerosis".  Veins can also become blocked, especially from uncontrolled high blood pressure.

 

Choroid

This is the layer of mostly blood vessels between the retina and the sclera.

 

Optic Nerve

The optic nerve is like a large fibreoptic cable, bringing together all the nerve endings from the retina and connecting them to the brain for interpretation of the pictures that have been taken by the eye.  The brain is our "super computer " that translates these photo messages for us.  In glaucoma, the optic nerve degenerates over time, and we lose this vital connection to the brain.  The result is weakening and loss of vision, without proper treatment.  HRT and OCT imaging is used to track changes in the optic nerve over time that may be too subtle for the naked eye to detect.

ANAPHYLAXIS / HYPERSENSITIVITY / ALLERGY - OVERVIEW

What are allergies? What is an allergy?

                         Allergies are hypersensitive immune responses to substances that either enter or come in contact with the body, such as pet dander, pollen or bee venom. A substance that causes an allergic reaction is called an "allergen". Allergens can be found in food, drinks or the environment.

Most allergens are harmless, i.e. the majority of people are not affected by them.

If you are allergic to a substance, such as pollen, your immune system reacts to it as if it were a pathogen (a foreign harmful substance), and tries to destroy it.

Allergies are very common. Public health authorities estimate that about 20% of people in North America and Western Europe suffer from some degree of hay fever (allergic rhinitis, allergy to pollen).

A study published in JAMA Pediatrics (September 2013 issue) reported that kids' food allergies cost both families and the US as a whole nearly $25 billion annually.

The number of people worldwide with allergies is increasing. According to Allergy UK, about 30% to 40% of people have an allergy at some stage in their lives. Some years ago, this increase was only apparent in industrialized nations. However, middle-income nations are now reporting higher rates of allergies across their populations.

The steepest increase in allergies has been observed in children, particularly food allergies.

A team of researchers from Northwestern University Feinberg School of Medicine reported in Pediatrics that about 8% of American children have some kind of food allergy. 38.7% of those with food allergies have a history of anaphylaxis (severe allergic reactions), and 30.4% are allergic to more than one food.

Researchers from St. Luke's Roosevelt Hospital Center, New York, found that foreign-born children who live in the USA have a lower risk of allergies. This risk grows the longer they remain in America.

What are the signs and symptoms of allergies?

A symptom is something the patient feels and describes, while a sign can be detected by others too. Pain is a symptom and a rash is a sign.

When a person with an allergy comes into contact with an allergen, the allergic reaction is not immediate. The immune system gradually builds up sensitivity to the substance before overreacting to it.

The immune system needs time to recognize and remember the allergen. As it becomes sensitive to it, it starts making antibodies to attack it - this process is called sensitization.

Sensitization can take from a few days to several years. In many cases the sensitization process is not completed and the patient experiences some symptoms but never a full allergy.

When the immune system reacts to an allergen, there is inflammation and irritation. Signs and symptoms depend on the type of allergen. Allergic reactions may occur in the gut (digestive system), skin, sinuses, airways, eyes, and nasal passages.

Allergies from dust and pollen may have the following symptoms:

Blocked noseItchy eyesItchy noseRunny noseSwollen eyesWatery eyesCough.

Skin reactions, as in eczema (atopic dermatitis) may include:

Flaking skinItchy skinPeeling skinRed skin, rashes.

Food allergies may include several types of reactions:

VomitingTongue swellingTingling in the mouthSwelling of the lipsSwelling of the faceSwelling in the throatStomach crampsShortness of breathRectal bleeding (in children, rare in adults)Itchiness in the mouthDiarrheaAnaphylaxis - a very severe, often life-threatening allergic reaction.

The following allergic reactions are possible after an insect sting:

WheezingSwelling where the sting occurredSudden drop in blood pressureSkin itchingShortness of breathRestlessnessHives - a red and very itchy rash that spreadsDizzinessCoughChest tightnessAnxietyAnaphylaxis.

The following may be signs of an allergic reaction to medication:

WheezingSwollen tongueSwollen lipsSwelling of the faceSkin rashItchinessAnaphylaxis.

Signs and symptoms of anaphylaxis

Anaphylaxis is a serious allergic reaction of rapid onset. Anaphylaxis can be life-threatening and must be treated as a medical emergency.

This type of allergic reaction presents several different symptoms which can appear minutes or hours after exposure to the allergen. If the exposure is intravenous, onset is usually between 5 to 30 minutes. A food allergen will take longer.Anaphylaxis is a medical emergency

Researchers from the University of Manitoba, Canada, reported in The Journal of Allergy & Clinical Immunology that the most commonly affected areas in anaphylaxis are the skin (80-90%), respiratory (70%), gastrointestinal (30-45%), cardiovascular 10-45%) and the central nervous system (10-15%). In most cases two areas are affected simultaneously.

Anaphylaxis - skin symptoms

Hives all over the body, flushing and itchiness. The affected tissues may also become swollen (angioedema). Some patients may experience a burning sensation on the skin.

In about 20% of cases, there is swelling of the tongue and throat.

If the skin has a strange bluish color, it could be a sign of hypoxia (lack of oxygen).

Some patients may experience a runny nose. The membrane that covers the front of the eye and the inside of the eyelid (conjunctiva) may become inflamed.

Anaphylaxis - respiratory symptoms:

Shortness of breathWheezing - caused by bronchial muscle spasmsStridor - a high-pitched vibrating wheezing sound when breathing. Caused by upper airway obstruction due to swellingHoarsenessOdynophagia - pain when swallowingCough.

Anaphylaxis - cardiovascular symptoms

Coronary artery spasm - sudden tightening of the muscle in the artery wall (temporary) due to cells in the heart that release histamine. This can lead to myocardial infarction (heart attack), dysrhythmia (abnormal heart rhythm), or cardiac arrest (heart stops).

Low blood pressure can cause the heart rate to accelerate. In some cases a slow heart rate can occur as a result of low blood pressure (Bezold-Jarisch reflex).

Patients whose blood pressure suddenly drops can feel lightheaded and dizzy. Some may lose consciousness. In some rare cases, the only sign of anaphylaxis might be low blood pressure.

Anaphylaxis - gastrointestinal symptoms

Abdominal crampsDiarrheaVomitingLoss of bladder controlPelvic pain (like uterine cramps).

Patients may also have a sense of impending doom.

What are the causes of allergies?

The immune system of a person with an allergy reacts to the allergen as though it were a harmful pathogen - such as an undesirable bacterium, virus, fungus or toxin. However, the allergen is not harmful. The immune system has simply become oversensitive to that substance.

When the immune system reacts to an allergen, it releases immunoglobulin E (IgE), a type of antibody. IgE is released to destroy the allergen. IgE causes chemicals in the body to be produced. These chemicals cause the allergic reaction.

One of these chemicals is called histamine. Histamine causes tightening of the muscles, including those in the airways and the walls of blood vessels. It also makes the lining of the nose produce more mucus.

People with allergies blame the allergen for their symptoms - a friend's pet, pollen or dust mites. However, the allergens are not harmful. The problem is not the allergen but the allergic person's immune system which mistakes harmless substances for harmful ones.

What are the risk factors for allergies?

In medicine, a risk factor is something that raises the risk of developing a disease or condition. This risk can come from something a person does. For example, smoking is a risk factor for lung disease. It can also be something you are born with. For example, if your mother had breast cancer, her daughter has a higher risk of developing breast cancer too. A family history of breast cancer is a risk factor.

Below are some risk factors associated with allergies:

A family history of asthma - if your parents, grandparents or siblings have/had asthma, your risk of having an allergy is higher.

A family history of allergies - if a close relative has/had an allergy, your risk of having an allergy yourself is greater.
Being a child - a child is much more likely to have an allergy than an adult. On a positive note, this means that many children outgrow their allergies.
Having asthma - people with asthma are significantly more likely to develop allergies.
Not enough sunlight exposure - scientists from the European Centre for Environment & Human Health, together with researchers from various Australian centers found that children living in areas with less sunlight had higher rates of allergies.
Having an allergy - if you already have an allergy, there is a greater risk that you will develop an allergy to something else.
C-section babies - a team from the Henry Ford Hospital reported that C-section babies have a considerably higher risk of developing allergies compared to those born naturally.
Chemicals used in water purification - Elina Jerschow, M.D., M.Sc., a fellow of the American College of Allergy, Asthma and Immunology, said that pesticides in tap water could be partly to blame for the increased food allergy rates in the USA.

What are the most common allergens?

An allergen is a substance which causes an allergic reaction in some susceptible people.

Below are the most common allergens, apart from foreign proteins found in blood transfusions and vaccines:

Allergens from animals

Dust mites - their excrementCockroaches calyxWoolFurDander - skin flakes (dandruff)Fel d 1 - a protein found in cat saliva and sebaceous glands. Proteins from the urine, saliva or hair of household pets can cause allergic reactions in some people.

Medications

PenicillinSalicylates - a salt of salicylic acid commonly found in many medications, including aspirinSulfonamides

Foods - theoretically, any food can cause an allergy. The eight foods most likely to cause allergies are eggs (especially egg-white, albumen), fish, milk, nuts from trees, peanuts (groundnuts), wheat, soy, and shellfish.

Scott H. Sicherer, MD, Professor of Pediatrics, Jaffe Food Allergy Institute at Mount Sinai School of Medicine, and colleagues reported in the Journal of Allergy and Clinical Immunology that the number of kids with peanut allergies more than tripled between 1997 and 2008.

The following foods can also cause allergies:

Corn (maize)CeleryPumpkinBeansSesame.

Insect stings

wasp sting venommosquito stingsbee sting venomfire ants.

Insect bites

kissing bugshorsefliesfleasblackflies.

Insects that cause respiratory allergies

cockroachescaddis flieslake fliesmidgesmoths.

Mold spores

AlternariaAspergillusAureobasidium (Pullularia)Cladosporium (Hormodendrum)EpicoccumFusariumHelmin thosporiumMucorPenicilliumRhizopus.

Plant pollens - cause hay fever.

grass - the most common cause of hay fevertrees - including oak, ash, cedar, willow, and hazelweeds - such as mugwort and ragweed.

Other allergens

household chemicalsmetal - nickel, cobalt, chromium, and zinclatex.

Diagnosing allergies

The doctor will ask the patient questions regarding the allergy symptoms, when they occur, how often and what seems to cause them.

The patient will also be asked whether there is a family history of allergies, and whether other household members (who might not be relatives) have allergies.

The doctor, probably a primary care physician initially, may either recommend some tests to find out which allergen is causing the symptoms, or refer the patient to a specialist.

In the American College of Allergy, Asthma and Immunology's website there is a page called "Find an Allergist", where you can find a specialist who has been certified by the College.

On The British Society for Allergy & Clinical Immunology: BSACI homepage you can find an allergy clinic near you (UK only).

Even if the patient knows what causes his/her allergy, the doctor will wish to carry out tests to determine whether a particular substance within the food, drink, or something else is the culprit.

Below are some examples of allergy tests

Blood test - to measures levels of IgE antibodies released by the immune system. This test is sometimes called the radioallergosorbent test (RAST).
Skin prick test - also known as puncture testing or prick testing. The skin is pricked with a small amount of a possible allergen. If there is a skin reaction - itchy, red and swollen skin - it may mean there is an allergy.
Patch test - for patients with contact dermatitis (eczema). Special metal discs with trace amounts of a suspect allergen are taped onto the back. The doctor checks for a skin reaction 48 hours later, and then again after a couple of days.

The National Health Service says that commercial allergy-testing kits are not recommended and that patients should have these tests done by specialized health care professionals.

The National Institute for Health and Clinical Excellence (NICE), in the UK, found that the IgE antibody test and the skin prick test were cost effective compared with no test.

What are the treatment options for allergies?

The most effective treatment and management of an allergy is to avoid exposure to the allergen.

However, sometimes it is not possible to completely avoid an allergy. A person with hay fever cannot avoid exposure to pollens, unless he/she closes all the windows in the house and never goes out. Even then, there is a risk of other people bringing pollen into the house.

It is also important to educate patients so that they know how to identify their allergenic foods properly. Many people with peanut or tree nut allergy could not correctly identify which items they were allergic to in a study carried out at Ohio State University.

Study leader, Professor Todd Hostetler, said "When we ask patients to avoid peanuts and tree nuts, we shouldn't assume patients know what they're looking for, because they may not. It's worthwhile to do some education about what a tree nut is, what a peanut is, and what they all look like."

Medications for allergies

Drugs can help treat the symptoms of allergy, but do not cure it. The majority of allergy medications are OTC (over-the-counter, no prescription required). Before considering a medication, speak to a pharmacist or your doctor.

Antihistamines (histamine antagonists) - they block the action of histamine, a chemical released in the body as part of an allergic reaction. Some antihistamines are not suitable for children.
Decongestants - some patients say they help with a blocked nose in cases of hay fever, pet allergy or dust allergy. Decongestants are short-term medications.
Leukotriene receptor antagonists (anti-leukotrienes) - for asthma when other treatments have not worked. Anti-leukotrienes block the effects of leukotrienes, chemicals that cause swelling. Leukotrienes are released in the body when there is an allergic reaction.
Steroid sprays - applied to the inside lining of the nose. Corticosteroid sprays help reduce nasal congestion.

Immunotherapy

Also known as hyponsesitization. This type of therapy rehabilitates the immune system. The doctor administers gradually increasing doses of allergens over a period of years. The aim is to induce long-term tolerance by reducing the allergen's tendency to trigger IgE production.

Immunotherapy is only used in cases of severe allergies.

ANATOMY OF THE LIVER

 

Anatomy

The liver is the largest organ in the abdominal cavity and the most complex. It consists of a myriad of individual microscopic functional units call lobules. The liver performs a variety of functions including the removal of endogenous and exogenous materials from the blood, complex metabolic processes including bile production, carbohydrate homeostasis , lipid metabolism, urea formation, and immune functions. 

The liver arises from the ventral mesogastrium and only the upper posterior surface is outside of that structure. The ligamentum teres and falciform ligament connect the liver to the anterior body wall. The lesser omentum connects it to the stomach and the coronary and triangular ligaments to the diaphragm. The liver is smooth and featureless on the diaphragmatic surface and presents with a series of indentations on the visceral surface where it meets the right kidney, adrenal gland, inferior vena cava, hepatoduodenal ligament and stomach (Figure 4).

Figure . A, Normal gross anatomy of a liver; B, histological slide; B’, histological view.

The liver can be considered in terms of blood supply hepatocytes, Kupffer cells and biliary passages. The liver receives its blood supply from the portal vein and hepatic artery, the former providing about 75% of the total 1500 ml/min flow. Small branches from each vessel—the terminal portal venule and the terminal hepatic arteriole—enter each acinus at the portal triad. Pooled blood then flows through sinusoids between plates and hepatocytes in order to exchange nutrients. The hepatic vein carries efferent blood into the inferior vena cava and a supply of lymphatic vessels drains the liver. 

Parenchymal cells or hepatocytes comprise the bulk of the organ and carry out complex metabolic processes. Hepatocytes are responsible for the liver’s central role in metabolism (Figure 4B'). These cells are responsible for the formation and excretion of bile ; regulation of carbohydrate homeostasis ; lipid synthesis and secretion of plasma lipoproteins; control of cholesterol metabolism; and formation of urea, serum albumin, clotting factors, enzymes, and numerous proteins. The liver also aids in the metabolism and detoxification of drugs and other foreign substances. 

Kupffer cells line the hepatic sinusoids and are part of the reticuloendothelial system, filtering out minute foreign particles, bacteria, and gut-derived toxins. They also play a role in immune processes that involve the liver. 

Biliary passages begin as tiny bile canaliculi formed by hepatocytes. These microvilli -lined structures progress into ductules, interlobular bile ducts, and larger hepatic ducts. Outside the porta hepatis, the main hepatic duct joins the cystic duct from the gallbladder to form the common bile duct, which drains into the duodenum. 

RHEUMATIC HEART DISEASE :

Rheumatic heart disease

Introduction

Rheumatic heart disease is a chronic condition that results years after acute rheumatic fever which is caused by group A beta-hemolytic Streptococcus (Streptococcus pyogenes). This organism produces a pharyngitis that can be followed by rheumatic fever in about 0.3-3% of cases and occurs several weeks after the pharyngitis resolves.

Rheumatic heart disease chronically manifests as congestive heart failure form valvular involvement. Most commonly the mitral valve is affected resulting in mitral stenosis or mitral regurgitation. Less commonly the aortic valve can be involved and tricuspid valve involvement is rare, but reported. In approximately 50% of cases of rheumatic heart disease, the patient does not give a history of having rheumatic fever as a child.

Symptoms

Rheumatic fever acutely causes symptoms of pericarditis and congestive heart failure depending on the degree of valvulitis and myocarditis present. Migratory polyarthritis is the most common symptom in acute rheumatic fever. Subcutaneous nodules arise over the bones and tendons. A rash that starts on the trunk and extends to the limbs. The rash has a characteristic erythematous ring with a pale center and is referred to as erythema marginatum. Sydenham's chorea (St. Vitus’ dance) occurs and is described as uncontrollable rapid movements of the arms and facial muscles.

Rheumatic heart disease chronically manifests as congestive heart failure from valvular heart disease including mitral stenosis, mitral regurgitation and aortic stenosis.

Diagnosis

Rheumatic fever is diagnosed with the Jones criteria:
 

Rheumatic valvular disease is diagnosed predominantly via echocardiography. The mitral valve will give a classic “hockey stick” appearance.

Physical Examination

Physical examination findings include inflamed joints, subcutaneous nodules, a pericardial friction rub, findings of congestive heart failure (edema, pulmonary rales, elevated jugular venous pressure), and the rash of erythema marginatum

The Carey Coombs Murmur occurs during acute rheumatic fever. Mitral valvulitis can occur causing thickening of the leaflets. A murmur is created by increased blood flow across the thickened mitral valve. This can be distinguished from rheumatic mitral valve stenosis by the absence of an opening snap. The murmur is described as a mid diastolic murmur heard at the mitral listening post with the bell of the stethoscope with the patient in the left lateral decubitus position at end expiration. As the rheumatic valvulitis resolves, the murmur disappears.

Rheumatic heart disease chronically will most commonly reveal the murmur of mitral valve stenosis:

 

Treatment

Reducing the inflammatory response with corticosteroids is the mainstay of therapy during acute rheumatic fever when there is significant cardiac involvement. Aspirin historically had been used however the risk of Reye’s syndrome causing fulminant hepatic failure and death in children has decreased its use.

Long-term therapy with penicillin is recommended as re-infection with group A beta-hemolytic Streptococcus can cause a serious recurrence.

See the review on mitral valve stenosis for treatment strategies for rheumatic mitral stenosis, the most common manifestation of rheumatic valvular disease.

KETOGENIC DIET GUIDE :

What to Eat and What to Avoid

In short, you should eat REAL food (meat, eggs, nuts, yogurt, vegetables and occasionally some fruits). Apart from the obvious limitation of net carbs content in food, it is also recommended to avoid processed food and any food that may contain preservatives and colourings.

KetoDiet is not just about losing weight at any cost; it's about adopting a healthier lifestyle.

Below is a list of the most common low-carb foods recommended for the ketogenic diet.

EAT Freely

Grass-fed and wild animal sources

grass-fed meat (beef, lamb, goat, venison), wild-caught fish & seafood (avoid farmed fish), pastured pork and poultry, pastured eggs, gelatin, ghee, butter - these are high in healthy omega 3 fatty acids (avoid sausages and meat covered in breadcrumbs, hot dogs, meat that comes with sugary or starchy sauces)offal, grass-fed (liver, heart, kidneys and other organ meats)

Healthy fats

saturated (lard, tallow, chicken fat, duck fat, goose fat, clarified butter / ghee, butter, coconut oil)monounsaturated (avocado, macadamia and olive oil)polyunsaturated omega 3s, especially from animal sources (fatty fish and seafood)You can find a complete guide to fats & oils in my post here. (which to use for cold use, which for high-heat cooking and which to avoid)

Non-starchy vegetables

leafy greens (Swiss chard, bok choy, spinach, lettuce, chard, chives, endive, radicchio, etc.)some cruciferous vegetables like kale (dark leaf), kohlrabi, radishescelery stalk, asparagus, cucumber, summer squash (zucchini, spaghetti squash), bamboo shoots

Fruits, Nuts and Seeds

avocado, coconut, macadamia nuts

Beverages and Condiments

water (still), coffee (black or with cream or coconut milk), tea (black, herbal)pork rinds (cracklings) for "breading"mayonnaise, mustard, pesto, bone broth (make your own), pickles, fermented foods (kimchi, kombucha and sauerkraut (make your own) - best home-made with no additives (my recipes for home-made condiments are here)all spices and herbs, lemon or lime juice and zestwhey protein (beware of additives, artificial sweeteners, hormones and soy lecithin), egg white protein and gelatin (grass-fed, hormone free)

Eat Occasionally

Vegetables, Mushrooms and Fruits

some cruciferous vegetables (white and green cabbage, red cabbage, cauliflower, broccoli, Brussels sprouts, fennel, turnips, rutabaga / swede)nightshades (eggplant, tomatoes, peppers)some root vegetables (parsley root), spring onion, leek, onion, garlic, mushrooms, winter squash (pumpkin)sea vegetables (nori, kombu), okra, bean sprouts, sugar snap peas, wax beans, globe or French artichokes, water chestnutsberries (blackberries, blueberries, strawberries, raspberries, cranberries, mulberries, etc.), rhubarb, olives

Grain-fed animal sources and Dairy

beef, poultry, eggs and ghee (avoid farmed pork, it's too high in omega 6s!)dairy products (plain full-fat yogurt, cottage cheese, cream, sour cream, cheese) - avoid products labeled "low-fat", most of them are packed with sugar and starch and have little sating effectbacon - beware of preservatives and added starches (nitrates are acceptable if you eat enough antioxidants)

Nuts and seeds

pecans, almonds, walnuts, hazelnuts, pine nuts, flaxseed, pumpkin seeds, sesame seeds, sunflower seeds, hemp seedsbrazil nuts (beware of very high level of selenium - don't eat too many of them!)

Fermented soy products

if eaten, only non GMO and fermented soy products (Natto, Tempeh, soy sauce or paleo-friendly coconut aminos)Edamame (green soy beans), black soybeans - unprocessed

Condiments

healthy "zero-carb" sweeteners (Stevia, Swerve, Erythritol, etc.)thickeners: arrowroot powder, xanthan gum (keep in mind xanthan gum is not paleo-friendly - some people following the paleo diet use it, as you only need a very little amount)sugar-free tomato products (puree, passata, ketchup)cocoa and carob powder, extra dark chocolate (more than 70%, better 90% and beware of soy lecithin), cocoa powderbeware of sugar-free chewing gums and mints - some of them have carbs

Some Vegetables, Fruits, Nuts and Seeds with Average Carbohydrates

root vegetables (celery root, carrot, beetroot, parsnip and sweet potato)apricot, watermelon, Cantaloupe / Galia / Honeydew melons, dragon fruit (Pitaya), peach, nectarine, apple, grapefruit, kiwifruit, kiwi berries, orange, plums, cherries, ears, figs (fresh)dried fruit (dates, berries, raisins, figs, etc.) – only in very small quantities (if any)pistachio and cashew nuts, chestnuts

Alcohol

dry red wine, dry white wine, spirits (unsweetened) - avoid for weight loss, only for weight maintenance

AVOID Completely: Food rich in carbohydrates, factory-farmed meat and processed foods

1) All grains, even whole meal (wheat, rye, oats, corn, barley, millet, bulgur, sorghum, rice, amaranth, buckwheat, sprouted grains), quinoa and white potatoes. this includes all products made from grains (pasta, bread, pizza, cookies, crackers, etc.) sugar and sweets (table sugar, HFCS, agave syrup, ice creams, cakes, sweet puddings and sugary soft-drinks)

2) Factory-farmed pork and fish are high ininflammatory omega 6 fatty acids and farmed fish may contain PCBs, avoid fish high in mercury.

3) Processed foods containing carrageenan (e.g. almond milk products), MSG (e.g. in some whey protein products), sulphites (e.g. in dried fruits, gelatin), BPAs (they don't have to be labeled!), wheat gluten

4) Artificial sweeteners (Splenda, Equal, sweeteners containing Aspartame, Acesulfame, Sucralose, Saccharin, etc.)

5) Refined fats / oils (e.g. sunflower, safflower, cottonseed, canola, soybean, grapeseed, corn oil), trans fats such as margarine.

6) "Low-fat", "low-carb" and "zero-carb" products (Atkins products, diet soda and drinks, chewing gums and mints may be high in carbs or contain artificial additives, gluten, etc.)

7) Milk (only small amounts of raw, full-fat milk is allowed). Milk is not recommended for several reasons. Firstly, from all the diary products, milk is difficult to digest, as it lacks the "good" bacteria (eliminated through pasteurization) and may even contain hormones. Secondly, it is quite high in carbs (4-5 grams of carbs per 100 ml). For coffee and tea, replace milk with cream in reasonable amounts. You may have a small amount of raw milk but be aware of the extra carbs.

8) Alcoholic, sweet drinks (beer, sweet wine, cocktails, etc.) - you can try my healthier versions of popular cocktails and drinks.

9) Tropical fruit (pineapple, mango, banana, papaya, etc.) and some high-carb fruit(tangerine, grapes, etc.) Also avoid fruit juices (yes, even 100% fresh juices!) - better to drink smoothies if any, but either way very limited. Juices are just like sugary water, but smoothies have fiber, which is at least more sating. This also includes dried fruit (dates, raisins, etc.) if eaten in large quantities.

10) Mainly for health reasons, avoid soy products apart from a few non-GMO fermented products which are known for their health benefits. Also avoid wheat gluten which may be used in low-carb foods. When you give up bread, you shouldn't eat any part of it. Beware ofBPA-lined cans. If possible, use naturally BPA-free packaging like glass jars or make my own ingredients such as ghee, ketchup, coconut milk or mayonnaise. BPA has been linked to many negative health effects such as impaired thyroid function and cancer. Other additives to avoid:carrageenan (e.g. almond milk products), MSG (e.g. in some whey protein products) andsulfites (e.g. in dried fruits, gelatin)

And here is everything in a nutshell...

POSITION OF THE CHILD WHILE TAKING RECTAL TEMPERATURE :

ECTOPIC PREGNANCY :

What Is An Ectopic Pregnancy?

An ectopic pregnancy is a pregnancy that, for some reason, is located outside of the uterus. The vast majority of ectopic pregnancies (98 percent) occur when the egg implants inside the fallopian tube, and are sometimes known as tubal pregnancies.

Other places in the body that ectopic pregnancies occur include the ovary, cervix, and abdominal cavities. Ectopic pregnancies are also pretty common, occurring in about one in every fifty pregnancies.

What Happens If I Have An Ectopic Pregnancy?

Before the 19th century, ectopic pregnancies ended in death of the mother in more than 50 percent of cases. However, with all of the medical technological advancements that we have today, now the mortality rate of ectopic pregnancy is somewhere around five in 10,000.

Unfortunately, there is no way for an embryo to survive outside of the womb, and there is no way for a baby to survive an ectopic pregnancy. For some women, the ectopic pregnancy resolves on it’s own with no need for medical intervention. However, some women need to have a surgical procedure done to remove the ectopic pregnancy with only a small amount of risk to the mother.

Signs and Symptoms of Ectopic Pregnancy

Keep in mind that an ectopic pregnancy usually starts out feeling like a normal pregnancy, with symptoms like bloating, nausea, breast tenderness, and a missed period. However, as time progresses, more signs and symptoms show up to indicate that something is not right with the pregnancy.

Light bleeding or spotting is usually one of the very first symptoms, along with stomach pain or pelvic pain. These symptoms usually start showing up around 6-8 weeks after a missed period. As time goes on, a woman might notice severe vaginal bleeding or stomach/pelvic pain that is worse on one side, and gets worse with movement or straining.

 There will also be pain during sexual intercourse, and there might also be dizziness, lightheadedness, or even fainting caused by internal bleeding. For the most part, the signs of miscarriage are also indicative of the signs of an ectopic pregnancy.

What to Know

If you are experiencing any of these symptoms and think that you might be experiencing an ectopic pregnancy or a miscarriage, get to a doctor or hospital right away. Keep in mind that there are great risks associated with an ectopic pregnancy.

If the fallopian tube ruptures, a woman can experience severe internal bleeding, and that can lead to shock or even death in severe cases. This is why it is so very important to seek medical attention if you think that you might possibly be experiencing an ectopic pregnancy.

ANATOMY OF THE ABDOMEN

INTERCOSTAL DRAINAGE :

Fluid or air that accumulates in the pleural space will reduce lung expansion and lead to respiratory compromise and hypoxia.

Insertion of an intercostal catheter (ICC) enables drainage of air or fluid from the pleural space, allowing negative intra-thoracic pressures to be re-established leading to lung re-expansion.

Indications:

Pneumothorax

Haemothorax

Pleural effusion

Contraindications:

Need for immediate thoracotomy  

Complications:

Pain

Thoracic or abdominal visceral trauma

Tension pneumothorax

Equipment

Special procedures tray

Under water sealed drain system (UWSD)

use cell saver UWSD for massive haemothorax

Intercostal Catheter (guide sizes only)

use smaller size for draining air

larger size for draining blood/fluid

Newborn 8-12 FG

Infant   12-16 FG 

Child  16-24 FG 

Adolescent 20-32 FG

Spigot connector / tube adaptor - 2 sizes

Suction must be available and working

Sterile gloves & gown

Mask

Sterile towels x 2

500ml bottle of sterile water

Antiseptic solution

1% lignocaine + 1:100,000 adrenaline 5mL ampoule 

5ml/10ml syringe and needle

Scalpel blade

Suture material - black silk or nylon with needle size 3.0 x 2

Sleek and Tegaderm x 2

Analgesia, Anaesthesia, Sedation

Local anaesthetic and intravenous analgesia are mandatory, as ICC placement is a painful procedure. The use of sedation should always be discussed with a senior emergency doctor, as it can potentially worsen the patient's clinical condition.

Procedure

Establish patient on continuous cardiac monitoring and pulse oximetry

Place conscious patient in a sitting position at 45 degrees with arm of same side placed above head

Palpate the fourth or fifth intercostal space just anterior to the mid-axillary line

Surgically prepare the area

Ensure local anaesthetic is infiltrated from subcutaneous tissue down to pleura. 

Select the appropriate size I.C.C. and remove stylet.

Incise the skin parallel to the upper border of the rib below the chosen intercostal space. Incise down to the fascia.

"Blunt dissect" (using an artery forcep) down to the pleura, enter the pleural space, and then widen the hole by opening the forceps.

Sweep the pleural space with a gloved finger to widen the hole and push the lung away from the hole (only possible in older children, beware of rib fractures in injured child).

Hold the tip of the catheter with a curved artery clamp and advance it into the pleural space, directing the catheter posteriorly and superiorly.

Advance so that all apertures of the tube are in the chest and not visible

Attach the tube to UWSD below the patient's chest level

Anchor the drain and suture the wound. Tape in place with tegaderm sandwich and anchor the tube to the patient's side.

Connect to the UWSD.

Watch for "swinging" of water in tube connection.

Post-Procedure Care

Reassess ABCs and ensure ICC is functioning

Reassess need for analgesia.

In children following the removal of the tube coverage with a large tegaderm is sufficient for closure rather than a formal purse string suture.

Mantoux test for Tuberculosis & its interpretation :

INTRODUCTION

Tuberculosis (TB) remains a leading cause of morbidity and mortality in the world, especially in developing countries. A combination of factors including high costs, limited resources and the poor performance of various diagnostic tests make the diagnosis of TB difficult in developing countries. Short of demonstrating viable organisms in body tissues and fluids the tuberculin skin test (TST) is the only method of detecting M. tuberculosis infection in an individual and is used in the diagnosis of TB in individual patients, as well as in epidemiological settings, to measure the prevalence of tuberculous infection in populations.

It was developed by Koch in 1890 but the intradermal technique currently in use was described in 1912 by Charles Mantoux, a French physician who developed on the work of Koch and Clemens von Pirquetto to create his test in 1907. After such a long history it is surprising that the interpretation of the test remains controversial.

However, various factors both in the host and inherent in the test lower both its specificity and sensitivity. Consequently, its application in any group of patients will usually yield a wide range of results, from the presence of a reaction in uninfected children to the complete absence of a reaction in some children with confirmed TB disease. The distribution of results generally falls into one of two patterns depending on the rate of false-positive (cross-reactions from other mycobacterial infections) in the population.

The tuberculin most widely used is purified protein derivative (PPD), which is derived from cultures of M. tuberculosis. The “old tuberculin” is no longer used for this purpose; instead, a more standardized product called PPD-S (purified protein derivative, prepared according to the method described by Siebert, from M. tuberculosis is used. PPD of non-tuberculous (i.e. atypical) mycobacterium are identified by a letter other than S. PPD-A is from M. avium; PPD-G from the Gause strain of schotochromogen; PPD-B from the nonphotochromogen Battey bacilli; PPD-F from the rapid grower M. fortuitum and PPD-Y from the yellow photochromogen M. kanasasii. It is PPD-RT (Research Tuberculin) 23 that is commonly used Indian clinician, are not easily available and may have different interpretation parameters.

IMMUNOLOGIC BASIS FOR THE TUBERCULIN REACTION

The reaction to intracutaneously injected tuberculin is the classic example of a delayed (cellular) hypersensitivity reaction. T-cells sensitized by prior infection are recruited to the skin site where they release lymphokines. These lymphokines induce induration through local vasodilatation, edema, fibrin deposition, and recruitment of other inflammatory cells to the area. Features of the reaction include (1) its delayed course, reaching a peak more than 24 h after injection of the antigen; (2) its indurated character; and (3) its occasional vesiculation and necrosis.

ADMINISTRATION

A standard dose of five tuberculin units (TU) (0.1ml) is injected intradermally (into the skin) and read 48 to 72 h later. PPD-RT 23 with Tween 80 of strength 1 TU and 2 TU are standardized tuberculins available in India supplied by the Bacillus Calmette-Guérin (BCG) vaccine Laboratory, Guindy, Chennai. Other tuberculins available in the market are not standardized. Tween 80 is a detergent added to tuberculin to prevent its adsorption on glass or plastic surface. Presently, all tuberculins are manufactured and standardized with Tween 80.

A person who has been exposed to the bacteria is expected to mount an immune response in the skin containing the bacterial proteins. For the sake of standardization of reading and interpretation of results, 5 TU of tuberculin PPD RT23 is used almost universally. It is to be injected strictly intradermally, using 28 or 26-gauge needle and tuberculin syringe from which 0.1 ml can be delivered accurately. A discrete, pale elevation of the skin (a wheal) 6 to 10 mm in diameter should be produced when the injection is given correctly. If it is recognized that the first test was improperly administered, another test dose can be given at once, selecting a site several centimeters away from the original injection. A note in the record should indicate the site chosen for the second test.

Conventionally, the test is given on the left forearm to avoid errors in reading. However, right arm may be used in case of any contraindication to use the left arm. The volar aspect of the forearm is the preferred site of test. After having a TB skin test, it is extremely important to make sure that the patient keeps the appointment to have the test reaction read. The patient is instructed to keep the test site clean, uncovered, and to not scratch or rub the area. The Mantoux skin test should be read between 48 and 72 h after administration. Reading should be performed in a good light, with the forearm slightly flexed at the elbow. The basis of reading is the presence or absence of induration, which may be determined by inspection (from a side view against the light as well as by direct light) and by palpation. For standardization, the diameter of induration should be measured transversely to the long axis of the forearm and recorded in millimeters. Reliable reading of the Mantoux skin test requires standardization of procedures, training, supervision, and practice. This may also include periodic standardized reliability testing. The exact measurement of the induration in millimeters (mm) should be recorded. Erythema (redness) should not be measured.

ADVERSE EFFECTS

Though rare there have been reports of anaphylactic reaction and foreign body reaction involving a Mantoux test site. There is a very slight risk of having a severe reaction to the test, including swelling and redness of the arm, particularly in people who have had TB or been infected previously and in those who have previously had the BCG vaccine. Allergic reactions are also rare complications. Live bacteria are not used in the test so there is no chance of developing TB from the test. Local reactions such as regional lymphangitis and adenitis may also occur on rare occasions.

INTERPRETATION OF TUBERCULIN REACTION

The Mantoux test does not measure immunity to TB but the degree of hypersensitivity to tuberculin. There is no correlation between the size of induration and likelihood of current active TB disease but the reaction size is correlated with the future risk of developing TB disease. The test has a poor positive predictive value for current active disease.There is no correlation between the size of post-vaccination Mantoux reactions and protection against TB disease and routine post-BCG Mantoux testing serves no purpose.

The results of this test must be interpreted carefully. The person's medical risk factors determine the size of induration the result is positive (5 mm, 10 mm, or 15 mm).

A record should also be made of formation of vesicles, bullae, lymphangitis, ulceration and necrosis at the test site. The formation of vesicles, bullae or necrosis at the test site indicates high degree of tuberculin sensitivity and thus presence of infection with tubercle bacilli.

Five mm or more is positive in

HIV-positive person

Recent contacts of active tuberculosis cases

Persons with nodular or fibrotic changes on Chest X-ray consistent with old healed TB

Organ transplant recipients and other immunosuppressed patients who are on cytotoxic immune-suppressive agents such as cyclophosphamide or methotrexate.

Patients on long term systemic corticosteroid therapy (> than six weeks) and those on a dose of prednisone ≥ 15 mg/day or equivalent.

End stage renal disease

Ten mm or more is positive in

Recent arrivals (less than five years) from high-prevalence countries

Injectable drug users

Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.)

Mycobacteriology lab personnel

Persons with clinical conditions that place them at high risk (e.g., diabetes, prolonged corticosteroid therapy, leukemia, end-stage renal disease, chronic malabsorption syndromes, low body weight, etc.)

Children less than four years of age, or children and adolescents exposed to adults in high-risk categories

Infants, children, and adolescents exposed to adults in high-risk categories

Fifteen mm or more is positive in

Persons with no known risk factors for TB. Reactions larger than 15 mm are unlikely to be due to previous BCG vaccination or exposure to environmental mycobacteria.

False-positive result

Some persons may react to the TST even though they are not infected with M. tuberculosis. The causes of these false-positive reactions may include, but are not limited to, the following:

Infection with non tuberculous mycobacteria

Previous BCG vaccination

Incorrect method of TST administration

Incorrect interpretation of reaction

Incorrect bottle of antigen used

Due to the test's low specificity, most positive reactions in low-risk individuals are false-positives. A false-positive result may be caused by nontuberculous mycobacteria or previous administration of BCG vaccine. Prior vaccination with BCG may result in a false-positive result for many years later.

False-negative result

A negative Mantoux result usually signifies that the individual has never been exposed toM. tuberculosis. However, there are factors that may cause a false-negative result or diminished ability to respond to tuberculin.

Cutaneous anergy (anergy is the inability to react to skin tests because of a weakened immune system)

Recent TB infection (within 8-10 weeks of exposure)

Very old TB infection (many years)

Very young age (less than six months old)

Recent live-virus vaccination (e.g., measles and smallpox)

Overwhelming TB disease

Some viral illnesses (e.g., measles and chicken pox)

Incorrect method of TST administration

Incorrect interpretation of reaction, insufficient dose and inadvertent subcutaneous injection.

The absence of cell mediated immunity to tuberculin may be due to the lack of previous sensitization or due to a false-negative result for various reasons or due to anergy because of immune suppression. Most children with negative result have not been infected withM. tuberculosis. A small proportion of otherwise normal children with M. tuberculosis infection remain PPD-negative for unknown reasons. From the time of infection to the development of CMI there is a window period of some two to six weeks, when the Mantoux test would be negative. Those that are immunologically compromised, especially those with HIV and low CD4 T-cell counts, frequently show negative results from the PPD test. This is because the immune system needs to be functional to mount a response to the protein derivative injected under the skin.

Negative tests can be interpreted to mean that the person has not been infected with the TB bacteria or that the person has been infected recently and not enough time has elapsed for the body to react to the skin test. A repeat test is not advocated before one week as the tuberculin injected for the first test has a booster effect on the subsequent dose. TST may convert to positive ≤eight weeks after Mycobacterium tuberculosisinfection, an interval that is usually referred to as the “window period”. A negative TST obtained < eight weeks before does not exclude infection, and a second test is recommended after eight weeks.Also, because it may take longer than 72 h for an elderly individual to develop a reaction, it may be useful to repeat the TB skin test after 96 h and again at one week to adequately screen these individuals. Immunocompromised persons may be unable to react sufficiently to the Mantoux test, and either a chest X-ray or sputum sample may be required.

Interpretation in children: A correctly applied Mantoux test can be invaluable in the assessment of a child with suspected TB. The interpretation of the result, however, is often difficult, with different workers using different induration sizes to indicate a positive reaction. Although the test itself is neither 100% sensitive nor 100% specific, the predictive value of a positive reaction is very high in such a group. Malnutrition has previously been shown to affect the results of tuberculin testing. As in other studies, underweight children in this study were significantly more likely to have a negative Mantoux result.

Cutoff size of reaction for a positive Mantoux test in children

As in many other studies, the majority of children did not have any reaction to tuberculin despite having received BCG immunization soon after birth. The reasons for this are not always clear but clearly whatever tuberculin sensitivity BCG might have caused could not have been significant or persistent. This agrees with the current recommendation that for patients with a high risk for TB the history of BCG vaccination should not be a consideration in the interpretation of the tuberculin test.

THE BOOSTER EFFECT

In some persons who are infected with M. tuberculosis, the ability to react to tuberculin may wane over time. When given TST years after infection, these persons may have a false-negative reaction. However, the TST may stimulate the immune system, causing a positive or boosted reaction to subsequent tests. Giving a second TST after an initial negative TST reaction is called two-step testing. When sensitization to mycobacteria has occurred many years earlier, an initial intradermal injection of tuberculin may produce a negative or weakly positive response due to there being too few sensitized lymphocytes in circulation to produce a significant local response. If the test is repeated, a larger reading may be obtained due to the immune response being ‘recalled‘ or ‘boosted’ by the first test. The second boosted reading is the correct one – that is, the result that should be used for decision-making or future comparison. Boosting is maximal if the second test is placed between one and five weeks after the initial test, and it may continue to be observed for up to two years.

MANTOUX REVERSION

Reversion is defined as the change to a negative Mantoux result following a previous positive result. Generally this phenomenon is uncommon in healthy individuals, occurring in less than 10% of such people with a previously positive Mantoux.

Reversion is more common

in older adults (estimated at 8% per year)

when the initial Mantoux is < 14 mm

in those where the initial positive reaction was a boosted result (identified by two-step testing).

MANTOUX CONVERSION

Whereas boosting is a recall of the hypersensitivity response in the absence of new Infection, conversion is the development of new or enhanced hypersensitivity due to infection with tuberculous or non-tuberculous mycobacteria, including BCG vaccination.

Mantoux conversion is defined as a change (within a two-year period) of Mantoux reactivity which meets either of the following criteria:

a change from a negative to a positive reaction

an increase of ≥ 10 mm.

Conversion has been associated with an annual incidence of TB disease of 4% in adolescents or 6% in contacts of smear-positive cases.

There is debate about the time required for the immunological changes that produce Mantoux conversion following infection. After inadvertent vaccination with M. tuberculosis (the Lubeck disaster), children developed positive reactions in three to seven weeks. Other studies have shown clinical illness, with a positive tuberculin test, from 19 to 57 days after exposure, with a mean of 37 days.

Therefore, when testing TB contacts for conversion, the second tuberculin test is done eight weeks after the date of last contact with the source case. (In the past, the traditional window period, or interval, of 12 weeks was used.)

BACILLUS CALMETTE-GUÉRIN VACCINE AND THE MANTOUX TEST

There is disagreement about the role of Mantoux testing in people who have been vaccinated. The US recommendation is that TST is not contraindicated for BCG-vaccinated persons and that prior BCG vaccination should not influence the interpretation of the test.

According to the US guidelines latent TB infection (LTBI) diagnosis and treatment for LTBI is considered for any BCG-vaccinated person whose skin test is 10 mm or greater, if any of these circumstances are present:

Was in contact with another person with infectious TB

Was born or has lived in a high TB prevalence country

Is continually exposed to populations where TB prevalence is high.

SITUATIONS WHERE MANTOUX TESTING IS NOT RECOMMENDED

Mantoux testing is not recommended in the following situations:

Past Mantoux reactions ≥ 15 mm: repeating the test will provide no new diagnostic information and will create discomfort

Previous TB disease: no useful diagnostic information will be gained and significant discomfort is likely

Infants under 12 weeks old: a positive reaction is very important, but a negative reaction may indicate that the child is too young to mount a response, and the test will need to be repeated if exposure has occurred. Pre-vaccination Mantoux testing before 12 weeks of age is not necessary unless the baby has been exposed to TB.

INTRAUTERINE INSEMINATION :

Intrauterine Insemination (IUI): Uses Risks Success Rate

Intrauterine insemination (IUI) is a fertility treatment that involves placing sperm inside a woman’s uterus to facilitate fertilization. The goal of IUI is to increase the number of sperm that reach the fallopian tubes and subsequently increase the chance of fertilization.

IUI provides the sperm an advantage by giving it a head start, but still requires a sperm to reach and fertilize the egg on its own. It is a less invasive and less expensive option compared toin vitro fertilization.

When is IUI used?

The most common reasons for IUI are a low sperm count or decreased sperm mobility.

However, IUI may be selected as a fertility treatment for any of the following conditions as well:

Unexplained infertilityA hostile cervical condition, including cervical mucusproblemsCervical scar tissue from past procedures which may hinder the sperms’ ability to enter the uterusEjaculation dysfunction

IUI is not recommended for the following patients:

Women who have severe disease of the fallopian tubesWomen with a history of pelvic infectionsWomen with moderate to severe endometriosis

How does IUI work?

Before intrauterine insemination,ovulation stimulating medications may be used, in which case careful monitoring will be necessary to determine when the eggs are mature. The IUI procedure will then be performed around the time of ovulation, typically about 24-36 hours after the surge in LH hormone that indicates ovulation will occur soon.

A semen sample will be washed by the lab to separate the semen from the seminal fluid. A catheter will then be used to insert the sperm directly into the uterus. This process maximizes the number of sperm cells that are placed in the uterus, thus increasing the possibility of conception.

The IUI procedure takes only a few minutes and involves minimal discomfort. The next step is to watch for signs and symptoms of pregnancy.

What are the risks of IUI?

The chances of becoming pregnant with multiples is increased if you take fertility medication when having IUI. There is also a small risk of infection after IUI.

How successful is IUI?

The success of IUI depends on several factors. If a couple has the IUI procedure performed each month, success rates may reach as high as 20% per cycle depending on variables such as female age, the reason for infertility, and whether fertility drugs were used, among other variables.

While IUI is a less invasive and less expensive option, pregnancy rates from IUI are lower than those from IVF. If you think you may be interested in IUI, talk with your doctor to discuss your options.