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Ailmemts & Remedies

Hemolytic Uremic Syndrome (HUS)

Alternative names:  Haemolytic-uraemic syndrome, HUS

Definition:
Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys‘ filtering system. Red blood cells contain hemoglobin—an iron-rich protein that gives blood its red color and carries oxygen from the lungs to all parts of the body.

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When the kidneys and glomeruli—the tiny units within the kidneys where blood is filtered—become clogged with the damaged red blood cells, they are unable to do their jobs. If the kidneys stop functioning, a child can develop acute kidney injury—the sudden and temporary loss of kidney function. Hemolytic uremic syndrome is the most common cause of acute kidney injury in children.

It is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from a contaminated water supply and caused by E. coli O157:H7, although Shigella, Campylobacter and a variety of viruses have also been implicated. It is now the most common cause of acquired acute renal failure in childhood. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.

The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Symptoms:
STEC-HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.

A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis—an inflammation of the lining of the stomach, small intestine, and large intestine—such as

*vomiting
*bloody diarrhea
*abdominal pain
*fever and chills
*headache

As the infection progresses, the toxins released in the intestine begin to destroy red blood cells. When the red blood cells are destroyed, the child may experience the signs and symptoms of anemia—a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen.

Signs and symptoms of anemia may include:-

*fatigue, or feeling tired
*weakness
*fainting
*paleness

As the damaged red blood cells clog the glomeruli, the kidneys may become damaged and make less urine. When damaged, the kidneys work harder to remove wastes and extra fluid from the blood, sometimes leading to acute kidney injury.

Other signs and symptoms of hemolytic uremic syndrome may include bruising and seizures.

When hemolytic uremic syndrome causes acute kidney injury, a child may have the following signs and symptoms:

*edema—swelling, most often in the legs, feet, or ankles and less often in the hands or face
*albuminuria—when a child’s urine has high levels of albumin, the main protein in the blood
*decreased urine output
*hypoalbuminemia—when a child’s blood has low levels of albumin
*blood in the urine

Causes:
A number of things can cause hemolytic uremic syndrome, but the most common cause — particularly in children — is an infection with a specific strain of E. coli, usually the strain known as O157:H7. However, other strains of E. coli have been linked to hemolytic uremic syndrome, too.

Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream. The toxins travel through the bloodstream and can destroy the red blood cells. E. coli O157:H7 can be found in:

*Contaminated meat or produce
*Swimming pools or lakes contaminated with feces
*undercooked meat, most often ground beef
*unpasteurized, or raw, milk
*unwashed, contaminated raw fruits and vegetables
*contaminated juice

Less common causes, sometimes called atypical hemolytic uremic syndrome, can include:-

*taking certain medications, such as chemotherapy
*having other viral or bacterial infections
*inheriting a certain type of hemolytic uremicsyndrome that runs in families

Children who are more likely to develop hemolytic uremic syndrome include those who
are younger than age 5 and have been diagnosedwith an E. coli O157:H7 infection

*have a weakened immune system
*have a family history of inherited hemolyticuremic syndrome
*Hemolytic uremic syndrome occurs in about two out of every 100,000 children.

Most people who are infected with E. coli, even the more dangerous strains, won’t develop hemolytic uremic syndrome. It’s also possible for hemolytic uremic syndrome to follow infection with other types of bacteria.

In adults, hemolytic uremic syndrome is more commonly caused by other factors, including:

*The use of certain medications, such as quinine (an over-the-counter muscle cramp remedy), some chemotherapy drugs, the immunosuppressant medication cyclosporine (Neoral, Sandimmune) and anti-platelet medications

*Pregnancy

*Certain infections, such as HIV/AIDS or an infection with the pneumococcal bacteria

*Genes, which can be a factor because a certain type of HUS — atypical hemolytic uremic syndrome — may be passed down from your parents

The cause of hemolytic uremic syndrome in adults is often unknown

Diagnosis:
The Doctor diagnoses hemolytic uremic syndrome with

*a medical and family history
*a physical exam
*urine tests
*a blood test
*a stool test
*kidney biopsy

The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e.g., confusion, cerebral convulsions, seizures); renal impairment (e.g., elevated creatinine, decreased estimated glomerular filtration rate [eGFR], abnormal urinalysis ); and gastrointestinal (GI) symptoms (e.g., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis).The presence of diarrhea does not exclude aHUS as the etiology of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the etiology of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.

Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms an etiological cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e., ?5% of normal ADAMTS13 levels) confirms a diagnosis of TTP

Complications:
Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.1
However, children with hemolytic uremic syndrome may have serious and sometimes life-threatening complications, including

*acute kidney injury
*high blood pressure
*blood-clotting problems that can lead to bleeding
*seizures
*heart problems
*chronic, or long lasting, kidney disease
*stroke
*coma

Treatment:
The Doctor will treat a child’s urgent symptoms and try to prevent complications by

*observing the child closely in the hospital
*replacing minerals, such as potassium and salt, and fluids through an intravenous (IV) tube
*giving the child red blood cells and platelets—cells in the blood that help with clotting—through an IV
*giving the child IV nutrition
*treating high blood pressure with medications

Treating Acute Kidney Injury:
If necessary,the Doctor will treat acute kidney injury with dialysis—the process of filtering wastes and extra fluid from the body with an artificial kidney. The two forms of dialysis are hemodialysis and peritoneal dialysis. Most children with acute kidney injury need dialysis for a short time only.

Treating Chronic Kidney Disease:
Some children may sustain significant kidney damage that slowly develops into CKD. Children who develop CKD must receive treatment to replace the work the kidneys do. The two types of treatment are dialysis and transplantation.

In most cases, The Doctor treat CKD with a kidney transplant. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a person’s body to take over the job of the failing kidney. Though some children receive a kidney transplant before their kidneys fail completely, many children begin with dialysis to stay healthy until they can have a transplant. click to know more

Prevention:

Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys’ filtering system.
The most common cause of hemolytic uremic syndrome in children is an Escherichia coli (E. coli) infection of the digestive system.
Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream.
A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis, an inflammation of the lining of the stomach, small intestine, and large intestine.

Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.
Some children may sustain significant kidney damage that slowly develops into chronic kidney disease (CKD).

Parents and caregivers can help prevent childhood hemolytic uremic syndrome due to E. coli O157:H7 by

*avoiding unclean swimming areas
*avoiding unpasteurized milk, juice, and cider
*cleaning utensils and food surfaces often
*cooking meat to an internal temperature of at least 160° F
*defrosting meat in the microwave or refrigerator
*keeping children out of pools if they have had diarrhea
*keeping raw foods separate
*washing hands before eating
*washing hands well after using the restroom and after changing diapers

When a child is taking medications that may cause hemolytic uremic syndrome, it is important that the parent or caretaker watch for symptoms and report any changes in the child’s condition to the Doctor as soon as possible.

Prognosis:
Acute renal failure occurs in 55-70% of patients with STEC-HUS, although up to 70-85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5-15%. Children and the elderly have a worse prognosis.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://kidney.niddk.nih.gov/KUDiseases/pubs/childkidneydiseases/hemolytic_uremic_syndrome/
http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome
http://www.mayoclinic.org/diseases-conditions/hemolytic-uremic-syndrome/basics/causes/con-20029487

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Categories
Ailmemts & Remedies

Progeria

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Other names :Hutchinson–Gilford progeria syndrome, Hutchinson–Gilford syndrome

Definition:-

Progeria is a disease that produces rapid aging, beginning in childhood. It  is an extremely rare, severe, genetic condition wherein symptoms resembling aspects of aging are manifested at an early age. The disorder has a very low incidence and occurs in one per eight million live births. Those born with progeria typically live about thirteen years, although many have been known to live into their late teens and early twenties and rare individuals may even reach their forties. It is a genetic condition that occurs as a new mutation and is not usually inherited, although there is a uniquely inheritable form. This is in contrast to another rare but similar premature aging syndrome, dyskeratosis congenita (DKC), which is inheritable and will often be expressed multiple times in a family line.

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Scientists are particularly interested in progeria because it might reveal clues about the normal process of aging. Progeria was first described in 1886 by Jonathan Hutchinson and also described independently in 1897 by Hastings Gilford. The condition was later named Hutchinson-Gilford Progeria syndrome (HGPS).

Heart problems or stroke is the eventual cause of death in most children with progeria. There’s no cure for this condition, but ongoing research shows some promise for treatment.

Symptoms:-

Usually within the first year of life, growth of a child with progeria slows markedly so that height and weight fall below average for his or her age, and weight falls low for height. Motor development and mental development remain normal.

The symptoms of this progressive disorder include:

*Slowed growth, with below-average height and weight
*A narrowed face and beaked nose, which makes the child look old
*Hair loss (alopecia), including eyelashes and eyebrows
*Hardening and tightening of skin on trunk and extremities (scleroderma)
*Loose, aged-looking skin
*Head too large for face
*Prominent scalp veins
*Prominent eyes
*Small lower jaw (micrognathia)
*High-pitched voice
*Delayed and abnormal tooth formation
*Loss of body fat and muscle
*Stiff joints
*Hip dislocation
*Growth failure during the first year of life
*Narrow, shrunken or wrinkled face
*Baldness
*Loss of eyebrows and eyelashes
*Short stature
*Large head for size of face (macrocephaly)
*Open soft spot (fontanelle)
*Small jaw (micrognathia)
*Dry, scaly, thin skin
*Limited range of motion
*Teeth – delayed or absent formation

The earliest symptoms include failure to thrive and a localized scleroderma-like skin condition. As a child ages past infancy, additional conditions become apparent. Limited growth, alopecia, and a distinctive appearance (small face and jaw, pinched nose) are all characteristic of progeria. People diagnosed with this disorder usually have small, fragile bodies, like those of elderly people. Later, the condition causes wrinkled skin, atherosclerosis, and cardiovascular problems.

Causes:-
Hutchinson-Gilford progeria syndrome (HGPS) is a childhood disorder caused by a point mutation in position 1824 of the LMNA gene, replacing cytosine with thymine, creating an unusable form of the protein Lamin A. Lamin A is part of the building blocks of the nuclear envelope.

Unlike most other “accelerated aging diseases” (such as Werner’s syndrome, Cockayne’s syndrome, or xeroderma pigmentosum), progeria is not caused by defective DNA repair. Because these “accelerated aging” diseases display different aspects of aging but never every aspect, they are often called “segmental progerias.

Diagnosis:-
Diagnosis is suspected according to signs and symptoms, such as skin changes, abnormal growth, and loss of hair. It can be confirmed through a genetic test.

Exams and Tests:-
The signs include:

*Insulin-resistant diabetes (diabetes that does not respond readily to insulin injections)
*Skin changes similar to that seen in scleroderma (the connective tissue becomes tough and hardened)

Cardiac stress testing may reveal signs of early atherosclerosis of blood vessels.

Genetic testing can detect mutations in lamin A that cause progeria.

Treatment:-
No treatments have been proven effective. Most treatment focuses on reducing complications (such as cardiovascular disease) with heart bypass surgery or low-dose aspirin. Children may also benefit from a high-calorie diet.

Growth hormone treatment has been attempted.

A type of anticancer drug, the farnesyltransferase inhibitors (FTIs), has been proposed, but their use has been mostly limited to animal models. A Phase II clinical trial using the FTI Lonafarnib began in May 2007.

Prognosis:-
There is no known cure. Few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis, such as heart attack or stroke.

Mental development is not affected. The development of symptoms is comparable to aging at a rate eight to ten times faster than normal, although certain age-related conditions do not occur. Specifically, patients show no neurodegeneration or cancer predisposition. They do not develop physically mediated “wear and tear” conditions commonly associated with aging, like cataracts (caused by UV exposure) and osteoarthritis (caused by mechanical wear).

Although there may not be any successful treatments for Progeria itself, there are treatments for the problems it causes, such as arthritic, respiratory, and cardiovascular problems.

Epidemiology:-
A study from the Netherlands has shown an incidence of 1 in 4 million births. Currently, there are between 35 and 45 known cases in the world.Approximately 100 cases have been formally identified in medical history.

Classical Hutchinson-Gilford Progeria Syndrome is almost never passed on from parent to child. It is usually caused by a new (sporadic) mutation during the early division of the cells in the child. It is usually genetically dominant; therefore, parents who are healthy will normally not pass it on to their children. Affected children rarely live long enough to have children themselves.

There have been only two known cases in which it became evident that a healthy parent can carry the LMNA mutation that causes progeria. A family from India has five children with progeria; they were the subject of a 2005 Bodyshock documentary entitled The 80 Year Old Children. In the other case, a family from Belgium has two children with progeria.

Research:-
Several discoveries have been made that have led to greater understanding and perhaps eventual treatment.

A 2003 report in Nature said that progeria may be a de novo dominant trait. It develops during cell division in a newly conceived zygote or in the gametes of one of the parents. It is caused by mutations in the LMNA (lamin A protein) gene on chromosome 1; the mutated form of lamin A is commonly known as progerin. One of the authors, Leslie Gordon, was a physician who didn’t know anything about progeria until her own son, Sam, was diagnosed at 21 months. Gordon and her husband, pediatrician Scott Berns, founded the Progeria Research Foundation.

Support Groups:  ->Progeria Research Foundation, Inc.

Lamin A:-
Nuclear lamin A is a protein scaffold on the inner edge of the nucleus that helps organize nuclear processes such as RNA and DNA synthesis.

Prelamin A contains a CAAX box at the C-terminus of the protein (where C is a cysteine and A is any aliphatic amino acids). This ensures that the cysteine is farnesylated and allows prelamin A to bind membranes, specifically the nuclear membrane. After prelamin A has been localized to the cell nuclear membrane, the C-terminal amino acids, including the farnesylated cysteine, are cleaved off by a specific protease. The resulting protein is now lamin A, is no longer membrane-bound, and carries out functions inside the nucleus.

In HGPS, the recognition site that the enzyme requires for cleavage of prelamin A to lamin A is mutated. Lamin A cannot be produced, and prelamin A builds up on the nuclear membrane, causing a characteristic nuclear blebbing. This results in the premature aging symptoms of progeria, although the mechanism connecting the misshapen nucleus to the symptoms is not known.

A study that compared HGPS patient cells with the skin cells from LMNA young and elderly human subjects found similar defects in the HGPS and elderly cells, including down-regulation of certain nuclear proteins, increased DNA damage, and demethylation of histone, leading to reduced heterochromatin. Nematodes over their lifespan show progressive lamin changes comparable to HGPS in all cells but neurons and gametes. These studies suggest that lamin A defects contribute to normal aging.

Mouse model of progeria:-
A mouse model of progeria exists, though in the mouse, the LMNA prelamin A is not mutated. Instead, ZMPSTE24, the specific protease that is required to remove the C-terminus of prelamin A, is missing. Both cases result in the buildup of farnesylated prelamin A on the nuclear membrane and in the characteristic nuclear LMNA blebbing. Fong et al. use a farnesyl transferase inhibitor (FTI) in this mouse model to inhibit protein farnesylation of prelamin A. Treated mice had greater grip strength and lower likelihood of rib fracture and may live longer than untreated mice.

This method does not directly “cure” the underlying cause of progeria. This method prevents prelamin A from going to the nucleus in the first place so that no prelamin A can build up on the nuclear membrane, but equally, there is no production of normal lamin A in the nucleus. Luckily, lamin A does not appear to be essential; indeed, mouse models in which the genes for prelamin A and C are knocked out show no symptoms. This also shows that it is the buildup of prelamin A in the wrong place, rather than the loss of the normal function of lamin A, that causes the disease.

Confocal microscopy photographs of the descending aortas of two 15-month-old progeria mice, one untreated (left picture) and the other treated with the farnsyltransferase inhibitor drug tipifarnib (right picture). The microphotographs show prevention of the vascular smooth muscle cell loss that is otherwise rampant by this age. Staining was smooth muscle alpha-actin (green), lamins A/C (red) and DAPI (blue). (Original magnification, x 40)It was hypothesized that part of the reason that treatment with an FFI such as alendronate is inefficient is due to prenylation by geranylgeranyltransferase. Since statins inhibit geranylgeranyltransferase, the combination of an FFI and statins was tried, and markedly improved “the aging-like phenotypes of mice in the metalloproteinase ZMPSTE24, including growth retardation, loss of weight, lipodystrophy, hair loss, and bone defects”.

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Untreated cells from children with the genetic disease progeria (left) compared to similar cells treated with farnesyltransferase inhibitors (FTIs). In the test tube, FTIs reverse the nuclear damage caused by the disease.

Popular culture:-
The 1922 short story “The Curious Case of Benjamin Button” by F. Scott Fitzgerald (and later released as a feature film in 2008) may have been inspired by progeria. The main character, Benjamin Button, is born as a seventy-year-old man and rapidly ages backwards.

The Indian film Paa, released in December 2009, has its story line around progeria (starring Amitabh Bachchan playing a twelve year old boy Auro).

Progeria is also a central theme in the animated film Renaisance in which one of the characters finds the much sought cure.

You may click & see:-
*Biogerontology
*Degenerative disease
*Laminopathies
*Hayley Okines, (an English girl with progeria who is known for spreading progeria awareness)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Progeria
http://www.nlm.nih.gov/medlineplus/ency/article/001657.htm
http://www.mayoclinic.com/health/progeria/DS00936

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Diagnonistic Test

Echocardiogram

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Definition
An echocardiogram uses sound waves to produce images of your heart. This common test allows your doctor to see how your heart is beating and pumping blood. Your doctor can use the images from an echocardiogram to identify various abnormalities in the heart muscle and valves.

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It determines the size of your heart, and assess how well it is functioning. The test can estimate how forcefully your heart is pumping blood, and can spot areas of the heart wall that have been injured by a previous heart attack or some other cause.

Depending on what information your doctor needs, you may have one of several types of echocardiograms. Each type of echocardiogram has very few risks involved.

Why it’s done
Your doctor may suggest an echocardiogram if he or she suspects problems with the valves or chambers of your heart or your heart’s ability to pump. An echocardiogram can also be used to detect congenital heart defects in unborn babies.

Depending on what information your doctor needs, you may have one of the following kinds of echocardiograms:

*Transthoracic echocardiogram. This is a standard, noninvasive echocardiogram. A technician (sonographer) spreads gel on your chest and then presses a device known as a transducer firmly against your skin, aiming an ultrasound beam through your chest to your heart. The transducer records the sound wave echoes your heart produces. A computer converts the echoes into moving images on a monitor. If your lungs or ribs obscure the view, a small amount of intravenous dye may be used to improve the images.

*Transesophageal echocardiogram. If it’s difficult to get a clear picture of your heart with a standard echocardiogram, your doctor may recommend a transesophageal echocardiogram. In this procedure, a flexible tube containing a transducer is guided down your throat and into your esophagus, which connects your mouth to your stomach. From there, the transducer can obtain more detailed images of your heart.

*Doppler echocardiogram. When sound waves bounce off blood cells moving through your heart and blood vessels, they change pitch. These changes (Doppler signals) can help your doctor measure the speed and direction of the blood flow in your heart. Doppler techniques are used in most transthoracic and transesophageal echocardiograms.

*Stress echocardiogram. Some heart problems — particularly those involving the coronary arteries that feed your heart muscle — occur only during physical activity. For a stress echocardiogram, ultrasound images of your heart are taken before and immediately after walking on a treadmill or riding a stationary bike. If you’re unable to exercise, you may get an injection of a medication to make your heart work as hard as if you were exercising.

Risk Factors:
There are minimal risks associated with a standard transthoracic echocardiogram. You may feel some discomfort similar to pulling off an adhesive bandage when the technician removes the electrodes placed on your chest during the procedure.

If you have a transesophageal echocardiogram, your throat may be sore for a few hours afterward. Rarely, the tube may scrape the inside of your throat. Your oxygen level will be monitored during the exam to check for any breathing problems caused by the sedation medication.

During a stress echocardiogram, exercise or medication — not the echocardiogram itself — may temporarily cause an irregular heartbeat. Serious complications, such as a heart attack, are rare.

How do you prepare for the test?
No special preparations are necessary for a standard transthoracic echocardiogram. Your doctor will ask you not to eat for a few hours beforehand if you’re having a transesophageal or stress echocardiogram. If you’ll be walking on a treadmill during a stress echocardiogram, wear comfortable shoes. If you’re having a transesophageal echocardiogram, you won’t be able to drive afterward because of the sedating medication you’ll receive. Be sure to make arrangements to get home before you have your test.

What happens when the test is performed?

During the procedure
An echocardiogram can be done in the doctor’s office or a hospital. After undressing from the waist up, you’ll lie on an examining table or bed. The technician will attach sticky patches (electrodes) to your body to help detect and conduct the electrical currents of your heart.

If you’ll have a transesophageal echocardiogram, your throat will be numbed with a numbing spray or gel. You’ll likely be given a sedative to help you relax.

During the echocardiogram, the technician will dim the lights to better view the image on the monitor. You may hear a pulsing “whoosh” sound, which is the machine recording the blood flowing through your heart.

Most echocardiograms take less than an hour, but the timing may vary depending on your condition. During a transthoracic echocardiogram, you may be asked to breathe in a certain way or to roll onto your left side. Sometimes the transducer must be held very firmly against your chest. This can be uncomfortable – but it helps the technician produce the best images of your heart.

After the procedure
If your echocardiogram is normal, no further testing may be needed. If the results are concerning, you may be referred to a heart specialist (cardiologist) for further assessment. Treatment depends on what’s found during the exam and your specific signs and symptoms. You may need a repeat echocardiogram in several months or other diagnostic tests, such as a cardiac computerized tomography (CT) scan or coronary angiogram.

How long is it before the result of the test is known?
If a doctor does the test, you might get some results immediately. If a technician performs the test, he or she records the echocardiogram on a videotape for a cardiologist to review later on. In this case, you’ll probably receive results in several days.

Results:
Your doctor will look for healthy heart valves and chambers, as well as normal heartbeats. Information from the echocardiogram can reveal many aspects of your heart health, including:

*Heart size. Weakened or damaged heart valves, high blood pressure or other diseases can cause the chambers of your heart to enlarge. Your doctor can use an echocardiogram to evaluate the need for treatment or monitor treatment effectiveness.

*Pumping strength. An echocardiogram can help your doctor determine your heart’s pumping strength. Specific measurements may include the percentage of blood that’s pumped out of a filled ventricle with each heartbeat (ejection fraction) or the volume of blood pumped by the heart in one minute (cardiac output). If your heart isn’t pumping enough blood to meet your body’s needs, heart failure may be a concern.

*Damage to the heart muscle. During an echocardiogram, your doctor can determine whether all parts of the heart wall are contributing equally to your heart’s pumping activity. Parts that move weakly may have been damaged during a heart attack or be receiving too little oxygen. This may indicate coronary artery disease or various other conditions.

*Valve problems. An echocardiogram shows how your heart valves move as your heart beats. Your doctor can determine if the valves open wide enough for adequate blood flow or close fully to prevent blood leakage. Abnormal blood flow patterns and conditions such as aortic valve stenosis — when the heart’s aortic valve is narrowed — can be detected as well.

*Heart defects. Many heart defects can be detected with an echocardiogram, including problems with the heart chambers, abnormal connections between the heart and major blood vessels, and complex heart defects that are present at birth. Echocardiograms can even be used to monitor a baby’s heart development before birth.

Resources:
https://www.health.harvard.edu/fhg/diagnostics/echocardiogram.shtml
http://www.mayoclinic.com/health/echocardiogram/MY00095

http://www.sads.org.uk/cardiac_tests.htm

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News on Health & Science

Now, Bypass Without Cutting a Single Bone

In what is claimed to be the first of its kind procedure in the country, doctors at Indraprastha Apollo hospital have used a minimally  invasive technique to perform a multiple graft heart bypass surgery on a 53-year-old woman without cutting through a single bone.
..
The new procedure, doctors claim, is less painful than conventional bypass surgery and leads to much faster healing. “This is the first time in India multiple grafts have been put, especially at the backside of the heart, through minimally invasive coronary surgery. In conventional bypass, the sternum is cut open and that takes at least 6-8 weeks to heal. In the new method no bone is cut,” said Dr Naresh Trehan, senior cardiovascular and thoracic surgeon, Indraprastha Apollo hospital.

The new procedure can be performed on any patient needing a coronory bypass and would be especially helpful for diabetics, who take longer to recover from conventional surgery, Dr Trehan said.

The surgery was performed on Suman Singhal, who was rushed to Apollo after she had radiating pain in her left arm and was diagnosed with multiple blockages last week. Suman was informed about the new technique and was quick to give her consent. “The cosmetic damage is very less. In women, one can’t even see the scar as it is below the breast. We procured specialized instruments on Friday and operated on her the next day,” said Dr Trehan.

Three incisions were made, two of which were used to insert the equipment that stabilized the heart and from the third the surgeon manually performed the bypass. “The equipment is designed such that the two instruments stabilize the heart. One instrument, called an octopus stabiliser, is inserted from the right side and has a suction pump attached to it. This instrument sucks the heart and stabilizes it. The other instrument, inserted from the left, also helps in stabilizing the beating heart. An 8cm-long incision is made underneath the breast through which we manually put the grafts taken from the internal mammary artery and radial artery,” explained Dr Trehan.

The new technique helps put grafts at the backside of the heart. “Accessing the backside of the heart is difficult through minimally invasive surgery. Even in robotic surgery, we can’t put grafts at the backside of the heart, but we are developing it further. But here, the instrument that holds the heart is able to rotate it such that the backside is clearly visible to the surgeon,” he added.

The advantages over conventional bypass are many, say doctors. “We don’t require many blood transfusions. In Suman’s case, we didn’t require any blood transfusion. The hospital stay is also short as compared to conventional surgery in which the patient stays in hospital for 7-8 days and takes 6-8 weeks for complete recovery,” said Dr Yatin Mehta, senior consultant, anaesthesia, Indraprastha Apollo Hospital. This surgery costs less than a conventional surgery “as the number of consumables used are less and hospital stay is just for 3-4 days,” said Dr Mehta.

Sources: The Times Of India

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Now, a Bandage for Bypass Surgery

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Scientists have designed what they claim is a bandage which could be used for wrapping around a transplanted blood vessel for the first few hours or days after surgery.

Heart bypass surgery involves transplanting arteries or veins from elsewhere in the body to route blood around the partially blocked areas of the coronary vessels which actually supply heart muscle.

However, a significant number of bypasses fail as the walls of the transplanted arteries get thickened, restricting blood flow, which surgeons believe happens due to the stress of being transplanted and suddenly having to handle altogether a different blood pressure and flow rate.

Now, a team at biopharmaceutical giant Geron has developed the biodegradable polymer bandage which they claim could take the strain for the first few days after surgery, according to a report in the ‘New Scientist‘.

And, the good news is that tests on pigs have revealed that the bandage works and can very well prevent the dangerous stress response after a bypass.

“The US scientists tested the bandage on animals. But we need to see whether it works on humans. And, if successful, it could be a boon for bypass surgery patients not only in the US but also in India and across the globe,” India-based doctor SK Dasgupta said.

The pharma company has filed a patent application for the polymer bandage.

Sources: The Times Of India

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