CONGENITAL CYANOTIC HEART DISEASE

CYANOTIC CONGENITAL HEART DISEASE

                                     CYANOTIC CONGENITAL HEART DISEASE
                                 

Cyanotic congenital heart disease (CCHD) is a condition present at birth. CYANOTIC CONGENITAL HEART DISEASE causes low levels of oxygen in the blood. A common symptom is a bluish tint to the skin, called cyanosis.
Several birth defects can cause this type of heart disease, including:
issues with the heart valves, which are the flaps in the heart that make sure the blood flows through in the right direction
an interruption in the aorta, which is the largest artery in the body
abnormalities in the large blood vessels leading to or from the heart
In many cases, if only one defect is present, there’s no cyanosis. Often more than one defect is present in CCHD.
Doctors use imaging tests to confirm the presence of defects that lead to CCHD. These include chest X-rays and echocardiograms. Medication can help relieve symptoms of cyanosis. Ultimately, most infants need to have surgery to correct the defects causing the disease. The success of the surgery depends on the severity of the defects.
RISK FACTOR FOR CONGENITAL CYANOTIC HEART DISEASE
In many cases, an infant will be born with this disease in association with a genetic factor. An infant is more at risk for CCHD when there’s a family history of congenital heart diseases. Certain genetic syndromes can be accompanied by defects that cause CCHD. These include:
Down syndrome
Turner syndrome
Marfan’s syndrome
Noonan syndrome
In some instances, outside factors can cause this disease. If a pregnant woman is exposed to toxic chemicals or certain drugs, her infant may have a higher risk of developing heart defects. Infections during pregnancy are also a factor. Poorly controlled gestational diabetes can also lead to a higher risk of the infant developing CCHD.
Defects that cause cyanotic congenital heart disease
Many physical defects in the heart can cause CCHD. Some infants may be born with several defects. Common causes can include:

 Cyanotic Heart Disease. Acyanotic Heart Disease. Decreased pulmonary flow: Tetralogy of Fallot. Tricuspid atresia. Other univentricular heart with pulmonary stenosis. Increased pulmonary flow: Transposition of great arteries. Total anomalous pulmonary venous return. Left – Right shunt lesions: Ventricular septal defect. Atrial Septal Defect. Atrio-ventricular Septal Defect. Patent Ductus Arteriosus. Obstructive lesions: Aortic stenosis. Pulmonary valve stenosis. Coarctation of Aorta.
TETRALOGY OF FALLOT (TOF) TETRALOGY OF FALLOT

TOF is the most common cause of CCHD. It’s a combination of four different defects. TOF includes:
A hole between the right and left ventricles of the heart
A narrow pulmonary valve
A thickening of the right ventricle muscles
A misplaced aortic valve
The defects lead to blood with and without oxygen getting mixed together and pumped throughout the body.
TRANSPOSITION OF GRAET ARTERIES (TGA)
In infants with TGA, the pulmonary and aortic valves have switched positions with their arteries. This results in low-oxygen blood getting pumped out to the rest of the body through the aorta. This blood should actually go to the lungs through the pulmonary artery.
TRICUSPID ATRESIA
In this type of defect, the tricuspid heart valve has developed abnormally or is missing entirely. This causes disruption to the normal flow of blood. Low-oxygen blood is pumped out to the body as a result.
TOTAL ANOMOLUS PULMONARY VENOUS CONNECTION (TAPVC)
TAPVC occurs when veins that bring high-oxygen blood from the lungs to the heart are connected to the right atrium. The veins should be connected to the left atrium. This defect may also be accompanied by a blockage in these veins between the lungs and the heart.
SYMPTOMS
The classic symptom of CCHD is cyanosis, or the blue coloring of the skin. This often occurs in the lips, toes, or fingers. Another common symptom is difficulty breathing, especially after physical activity.
Some children also experience spells during which their oxygen levels are very low. As a result, they get anxious, exhibit blue skin, and may hyperventilate.
Other symptoms of CCHD depend on the exact physical defect:
SYMPTOMS OF TOF
Low birth weight
Cyanosis
Poor feeding
Clubbed, or rounded, large fingers
Delayed growth
Rapid breathing
SYMPTOMS OF TGA
Rapid heartbeat
Rapid breathing
Slow weight gain
Heavy sweating
SYMPTOMS OF TRICUSPID ATRESIA
Cyanosis
Tiredness
Shortness of breath
Difficulty feeding
Heavy sweating
Slow growth
Chronic respiratory infections
SYMPTOMS TAPVC WITHOUT A BLOCKAGE
Shortness of breath
Chronic respiratory infections
Slow growth
TAPVC WITH BLOCKAGE
Cyanosis
Rapid heartbeat
Rapid breathing
Breathing difficulty, becoming very severe with time
DIAGNOSIS
Symptoms such as cyanosis, rapid heartbeat, and abnormal heart sounds can lead your child’s doctor to suspect heart defects are present. The observation of symptoms isn’t enough to make a diagnosis, though. To understand which defects are present, your child’s doctor will use tests to confirm a diagnosis.
A chest X-ray can show the outline of the heart and the location of several of the arteries and veins. To get another image of the heart, your child’s doctor may order an echocardiogram. This is an ultrasound of the heart. This test gives more details than an X-ray image.
A cardiac catheterization is a more invasive test that’s often needed to investigate the interior of the heart. This test involves moving a small tube, or a catheter, into the heart from the groin or the arm
.
TRETMENT OF CYANOTIC CONGENITAL HEART DISEASE
Treatment for CCHD may or may not be necessary depending on the severity of symptoms. In many cases, surgery to correct the physical defects in the heart is eventually necessary.
When the defect is very dangerous, the surgery may need to be performed soon after birth. In other instances, the surgery can be delayed until the child is older. Sometimes, more than one surgery is needed.
If surgery is delayed, a child may be given medications to treat the disease. Medications can help:
Eliminate extra fluids from the body
Get the heart pumping better
Keep blood vessels open
Regulate abnormal heart rhythms
OUTLOOK FOR CYANOTIC CONGENITAL HEART DISEASE
The outlook for children with CCHD varies based on the severity of the underlying defects. In mild cases, the child may be able to live a normal lifestyle with minimal medications or other treatments.
More severe cases will need surgery. Your child’s doctor will work with you toward the best treatment for your child. They can discuss your child’s particular outlook with you and if any further procedures are needed.

CONGENITAL HEART DISEASE

DEFINATION
Congenital heart disease, or a congenital heart defect, is a heart abnormality present at birth. The problem can affect:

• The heart walls
• The heart valves
• The blood vessels
  There are numerous types of congenital heart defects. They can range from simple conditions that don’t cause symptoms to complex problems that cause severe, life-threatening symptoms.

According to the Centers for Disease Control and Prevention, there are currently 1 million adults and 1 million children in the United States living with congenital heart defects. Treatments and follow-up care for defects have improved drastically over the past few decades, so nearly all children with heart defects survive into adulthood. Some need continuous care for their heart defect throughout their lives. However, many go on to have active and productive lives despite their condition.

TYPES OF CONGENOITAL HEART DISEASE
Though there are many different types of congenital heart defects, they can be divided into three main categories:
In heart valve defects, the valves inside the heart that direct blood flow may close up or leak. This interferes with the heart’s ability to pump blood correctly.
In heart wall defects, the natural walls that exist between the left and right sides and the upper and lower chambers of the heart may not develop correctly, causing blood to back up into the heart or to build up in places where it doesn’t belong. The defect puts pressure on the heart to work harder, which may result in high blood pressure.
In blood vessel defects, the arteries and veins that carry blood to the heart and back out to the body may not function correctly. This can reduce or block blood flow, leading to various health complications.
Cyanotic and Acyanotic Congenital Heart Disease
Many doctors classify congenital heart disease as either cyanotic congenital heart disease or acyanotic congenital heart disease. In both types, the heart isn’t pumping blood as efficiently as it should. The main difference is that cyanotic congenital heart disease causes low levels of oxygen in the blood, and acyanotic congenital heart disease doesn’t. Babies with reduced oxygen levels may experience breathlessness and a bluish tint to their skin. Babies who have enough oxygen in their blood don’t display these symptoms, but they may still develop complications later in life, such as high blood pressure.
SYMPTOMS OF CONGENITAL HEART DISEASE

 
A congenital heart defect is often detected during a pregnancy ultrasound. If your doctor hears an abnormal heartbeat, for instance, they may further investigate the issue by performing certain tests. These may include an echocardiogram, a chest X-ray, or an MRI scan. If a diagnosis is made, your doctor will make sure the appropriate specialists are available during delivery.
In some cases, the symptoms of a congenital heart defect may not appear until shortly after birth. Newborns with heart defects may experience:

• Bluish lips, skin, fingers, and toes
• Breathlessness or trouble breathing
• Feeding difficulties
• Low birth weight
• Chest pain
• Delayed growth
• In other cases, the symptoms of a congenital heart defect may not appear until many years after birth. Once symptoms do develop, they may include:
• Abnormal heart rhythms
• Dizziness
• Trouble breathing
• Fainting
• Swelling
• Fatigue

CAUSES OF CONGENITALL HEART DISEASE
Congenital heart disease occurs as a result of an early developmental problem in the heart’s structure. The defect typically interferes with the normal flow of blood through the heart, which may affect breathing. Although researchers aren’t exactly sure why the heart fails to develop correctly, suspected causes include the following:

• The heart defect may run in families.
• Taking certain prescription drugs during pregnancy puts a child at a higher risk for a heart defect.
• Using alcohol or illegal drugs during pregnancy can increase a child’s risk of having a heart defect.
• Mothers who had a viral infection during the first trimester of pregnancy are more likely to give birth to a child with a heart defect.
• Increased blood sugar levels, such as occurs with diabetes, may affect childhood development.

TREATMENT
The treatment for a congenital heart defect depends on the type and severity of the defect. Some babies have mild heart defects that heal on their own with time. Others may have severe defects that require extensive treatment. In these cases, treatment may include the following:
MEDICATION
There are various medications that can help the heart work more efficiently. Some can also be used to prevent blood clots from forming or to control an irregular heartbeat.
IMPLANTABLE HEART DEVICE
Some of the complications associated with congenital heart defects can be prevented with the use of certain devices, including pacemakers and implantable cardioverter defibrillators (ICDs). A pacemaker can help regulate an abnormal heart rate, and an ICD may correct life-threatening irregular heartbeats.
CATHETER PROCEDURE
Catheterization techniques allow doctors to repair certain congenital heart defects without surgically opening the chest and heart. During these procedures, the doctor will insert a thin tube into a vein in the leg and guide it up to the heart. Once the catheter is in the correct position, the doctor will use small tools threaded through the catheter to correct the defect.
OPEN-HEART SURGERY
This type of surgery may be needed if catheter procedures aren't enough to repair a congenital heart defect. A surgeon may perform open-heart surgery to close holes in the heart, repair heart valves, or widen blood vessels.
HEART TRANSPLANT
In the rare cases in which a congenital heart defect is too complex to fix, a heart transplant may be needed. During this procedure, the child's heart is replaced with a healthy heart from a donor.
CONGENITAL HEART DISEASE IN ADULTS
Depending on the defect, diagnosis and treatment may begin shortly after birth, during childhood, or in adulthood. Some defects don’t cause any symptoms until the child becomes an adult, so diagnosis and treatment may be delayed. In these cases, the symptoms of a newly discovered congenital heart defect may include:

• Shortness of breath
• Chest pain
• A reduced ability to exercise
• Being easily fatigued
• The treatment for congenital heart disease in adults can also vary depending on the severity of the heart defect. Some people may only need to monitor their condition closely, and others may require medications and surgeries.

In some cases, defects that may have been treated in childhood can present problems again in adulthood. The original repair may no longer be effective or the initial defect may have become worse over time. Scar tissue that developed around the original repair may also end up causing problems, such as heart arrhythmias.
Regardless of your situation, it’s important to continue seeing your doctor for follow-up care. Treatment may not cure your condition, but it can help you maintain an active, productive life. It will also reduce your risk for serious complications, such as heart infections, heart failure, and stroke.
PREVENTION OF CONGENITAL HEART DISEASE
Women who are pregnant or plan on becoming pregnant can take certain precautions to lower their risk of giving birth to a baby with a congenital heart defect:

• If you’re planning on becoming pregnant, talk to your doctor about any prescription or over-the-counter medications you’re taking.
• If you have diabetes, make sure your blood sugar levels are under control before becoming pregnant. It’s also important to work with your doctor to manage the disease while pregnant.
• If you weren’t vaccinated against rubella, or German measles, avoid exposure to the disease and speak with your doctor about prevention options.
• If you have a family history of congenital heart defects, ask your doctor about genetic screening. Certain genes may contribute to abnormal heart development.
• Avoid drinking alcohol and using illegal drugs during pregnancy.

CONGESTIVE HEART FAILURE

DEFINATION

Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently.
Heart failure does not mean the heart has stopped working. Rather, it means that the heart's pumping power is weaker than normal. With heart failure, blood moves through the heart and body at a slower rate, and pressure in the heart increases. As a result, the heart cannot pump enough oxygen and nutrients to meet the body's needs. The chambers of the heart may respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened. This helps to keep the blood moving, but the heart muscle walls may eventually weaken and become unable to pump as efficiently. As a result, the kidneys may respond by causing the body to retain fluid (water) and salt. If fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart failure is the term used to describe the condition.
ANATOMY
You have four heart chambers. The upper half of your heart has two atria, and the lower half of your heart has two ventricles. The ventricles pump blood to your body’s organs and tissues, and the atria receive blood from your body as it circulates back from the rest of your body.
CHF develops when your ventricles can’t pump enough blood volume to the body. Eventually, blood and other fluids can back up inside your:
Lungs
Abdomen
Liver
Lower body
CHF can be life-threatening. If you suspect you or someone near you has CHF, seek immediate medical treatment.
TYPES OF CHF
Results of these tests help doctors determine the cause of your signs and symptoms and develop a program to treat your heart. To determine the most appropriate treatment for your condition, doctors may classify heart failure using two systems:
New York Heart Association classification. This symptom-based scale classifies heart failure in four categories. In Class I heart failure, you don't have any symptoms. In Class II heart failure, you can perform everyday activities without difficulty but become winded or fatigued when you exert yourself. With Class III, you'll have trouble completing everyday activities, and Class IV is the most severe, and you're short of breath even at rest.
American College of Cardiology/American Heart Association guidelines. This stage-based classification system uses letters A to D. The system includes a category for people who are at risk of developing heart failure.
For example, a person who has several risk factors for heart failure but no signs or symptoms of heart failure is Stage A. A person who has heart disease but no signs or symptoms of heart failure is Stage B. Someone who has heart disease and is experiencing or has experienced signs or symptoms of heart failure is Stage C. A person with advanced heart failure requiring specialized treatments is Stage D.
Doctors use this classification system to identify your risk factors and begin early, more aggressive treatment to help prevent or delay heart failure.
These scoring systems are not independent of each other.



CAUSES OF CHF

                                                                RISK FACTORS
      CHF may result from other health conditions that directly affect your cardiovascular system. This is why it’s important to get annual checkups to lower your risk for heart health problems, including high blood pressure (hypertension), coronary artery disease, and valve conditions

• HYPERTENSION
  When your blood pressure is higher than normal, it may lead to CHF. Hypertension has many different causes. Among them is the narrowing of your arteries, which makes it harder for your blood to flow through them.
• CORONARY ARTERY DISEASE
  Cholesterol and other types of fatty substances can block the coronary arteries, which are the small arteries that supply blood to the heart. This causes the arteries to become narrow. Narrower coronary arteries restrict your blood flow and can lead to damage in your arteries.
• VALVE CONDITIONS
  Heart valves regulate blood flow through your heart by opening and closing to let blood in and out of the chambers. Valves that don’t open and close correctly may force your ventricles to work harder to pump blood. This can be a result of a heart infection or defect.

• OTHER CONDITIONS
  While heart-related diseases can lead to CHF, there are other seemingly unrelated conditions that may increase your risk, too. These include diabetes, thyroid disease, and obesity. Severe infections and allergic reactions may also contribute to CHF.

SYMPTOMS OF CHF   

                                                        symptoms of CHD

                                       
In the early stages of CHF, you most likely won’t notice any changes in your health. If your condition progresses, you’ll experience gradual changes in your body.

• Symptoms you may notice first Symptoms that indicate your condition has worsened
• Symptoms that indicate a severe heart condition
• fatigue
• irregular heartbeat
• chest pain that radiates through the upper body
• swelling in your ankles, feet, and legs
• a cough that develops from congested lungs
• rapid breathing
• weight gain
• wheezing skin that appears blue, which is due to lack of oxygen in your lungs
• increased need to urinate, especially at night
• shortness of breath, which may indicate pulmonary edema
• fainting
• Chest pain that radiates through the upper body can also be a sign of a heart attack. If you experience this or any other symptoms that may point to a severe heart condition, seek immediate medical attention.

SYMPTOMS OF HEART FAILURE IN CHILDREEN 
It can be difficult to recognize heart failure in infants and young children. Symptoms may include:

• Poor feeding
• Excessive sweating
• Difficulty breathing
• These symptoms can easily be misunderstood as colic or a respiratory infection. Poor growth and low blood pressure can also be signs of heart failure in children. In some cases, you may be able to feel a resting baby’s rapid heart rate through the chest wall.

DIAGNOSIS OF CHD

After reporting symptoms to doctor, they may refer you to a heart specialist, or cardiologist.
Cardiologist will perform a physical exam, which will involve listening to your heart with a stethoscope to detect abnormal heart rhythms. To confirm an initial diagnosis, cardiologist might order certain diagnostic tests to examine your heart’s valves, blood vessels, and chambers.
There are a variety of tests used to diagnose heart conditions. Because these tests measure different things, doctor may recommend a few to get a full picture of your current condition.

• ELECTROCARDIOGRAM
  An electrocardiogram (EKG or ECG) records heart’s rhythm. Abnormalities in your heart’s rhythm, such as a rapid heartbeat or irregular rhythm, could suggest that the walls of your heart’s chamber are thicker than normal. That could be a warning sign for a heart attack.
• ECHOCARDIOGRAM
  An echocardiogram uses sound waves to record the heart’s structure and motion. The test can determine if you already have poor blood flow, muscle damage, or a heart muscle that doesn’t contract normally.
• MRI
  An MRI takes pictures of your heart. With both still and moving pictures, this allows doctor to see if there’s damage to you heart.
• STRESS TEST
  Stress tests show how well your heart performs under different levels of stress. Making your heart work harder makes it easier for doctor to diagnose problems.
• BLOOD TEST
  Blood tests can check for abnormal blood cells and infections. They can also check the level of BNP, a hormone that rises with heart failure.
• CARDIAC CATHETERISATION
  Cardiac catheterization can show blockages of the coronary arteries. Doctor will insert a small tube into blood vessel and thread it from your upper thigh (groin area), arm, or wrist.
•  
• CORONARY ANGIOGRAM. In this test, a thin, flexible tube (catheter) is inserted into a blood vessel at your groin or in your arm and guided through the aorta into your coronary arteries. A dye injected through the catheter makes the arteries supplying your heart visible on an X-ray, helping doctors spot blockages.

Myocardial biopsy. In this test, your doctor inserts a small, flexible biopsy cord into a vein in your neck or groin, and small pieces of the heart muscle are taken. This test may be performed to diagnose certain types of heart muscle diseases that cause heart failure.
MEDICATIONS
Doctors usually treat heart failure with a combination of medications. Depending on your symptoms, you might take one or more medications, including:
ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITOR- These drugs help people with systolic heart failure live longer and feel better. ACE inhibitors are a type of vasodilator, a drug that widens blood vessels to lower blood pressure, improve blood flow and decrease the workload on the heart. Examples include enalapril (Vasotec), lisinopril (Zestril) and captopril (Capoten).
ANGIOTENSIN 2 RECEPTOR BLOCKER -These drugs, which include losartan (Cozaar) and valsartan (Diovan), have many of the same benefits as ACE inhibitors. They may be an alternative for people who can't tolerate ACE inhibitors.
BETA BLOCKERS- This class of drugs not only slows your heart rate and reduces blood pressure but also limits or reverses some of the damage to your heart if you have systolic heart failure. Examples include carvedilol (Coreg), metoprolol (Lopressor) and bisoprolol (Zebeta).
These medicines reduce the risk of some abnormal heart rhythms and lessen your chance of dying unexpectedly. Beta blockers may reduce signs and symptoms of heart failure, improve heart function, and help you live longer.

DIURETICS- Often called water pills, diuretics make you urinate more frequently and keep fluid from collecting in your body. Diuretics, such as furosemide (Lasix), also decrease fluid in your lungs so you can breathe more easily.
Because diuretics make your body lose potassium and magnesium, Doctor may also prescribe supplements of these minerals. If you're taking a diuretic, Doctor will likely monitor levels of potassium and magnesium in your blood through regular blood tests.

ALDOSTERON ANTAGONIST- These drugs include spironolactone (Aldactone) and eplerenone (Inspra). These are potassium-sparing diuretics, which also have additional properties that may help people with severe systolic heart failure live longer.
Unlike some other diuretics, spironolactone and eplerenone can raise the level of potassium in your blood to dangerous levels, so talk to your doctor if increased potassium is a concern, and learn if you need to modify your intake of food that's high in potassium.

INOTROPES- These are intravenous medications used in people with severe heart failure in the hospital to improve heart pumping function and maintain blood pressure.

DIGOXIN (Lanoxin) - This drug, also referred to as digitalis, increases the strength of your heart muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure symptoms in systolic heart failure. It may be more likely to be given to someone with a heart rhythm problem, such as atrial fibrillation.
You may need to take two or more medications to treat heart failure. Your doctor may prescribe other heart medications as well — such as nitrates for chest pain, a statin to lower cholesterol or blood-thinning medications to help prevent blood clots — along with heart failure medications. Your doctor may need to adjust your doses frequently, especially when you've just started a new medication or when your condition is worsening.
You may be hospitalized if you have a flare-up of heart failure symptoms. While in the hospital, you may receive additional medications to help your heart pump better and relieve your symptoms. You may also receive supplemental oxygen through a mask or small tubes placed in your nose. If you have severe heart failure, you may need to use supplemental oxygen long term.

SURGERY AND MEDICAL DEVICE
In some cases, doctors recommend surgery to treat the underlying problem that led to heart failure. Some treatments being studied and used in certain people include:
CORONARY BYPASS SURGERY- If severely blocked arteries are contributing to your heart failure, doctor may recommend coronary artery bypass surgery. In this procedure, blood vessels from your leg, arm or chest bypass a blocked artery in your heart to allow blood to flow through your heart more freely.
HEART VALVE REPAIR OR REPLACEMENT. If a faulty heart valve causes your heart failure, your doctor may recommend repairing or replacing the valve. The surgeon can modify the original valve to eliminate backward blood flow. Surgeons can also repair the valve by reconnecting valve leaflets or by removing excess valve tissue so that the leaflets can close tightly. Sometimes repairing the valve includes tightening or replacing the ring around the valve (annuloplasty).
Valve replacement is done when valve repair isn't possible. In valve replacement surgery, the damaged valve is replaced by an artificial (prosthetic) valve.
Certain types of heart valve repair or replacement can now be done without open heart surgery, using either minimally invasive surgery or cardiac catheterization techniques.
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICD)

                                                                           ICD

An ICD is a device similar to a pacemaker. It's implanted under the skin in your chest with wires leading through your veins and into your heart.
The ICD monitors the heart rhythm. If the heart starts beating at a dangerous rhythm, or if your heart stops, the ICD tries to pace your heart or shock it back into normal rhythm. An ICD can also function as a pacemaker and speed your heart up if it is going too slow.
SYNCHRONISATION
CARDIAC RESYNCRHRONISATION THERAPY(CRT)- or biventricular pacing. A biventricular pacemaker sends timed electrical impulses to both of the heart's lower chambers (the left and right ventricles) so that they pump in a more efficient, coordinated manner.
Many people with heart failure have problems with their heart's electrical system that cause their already-weak heart muscle to beat in an uncoordinated fashion. This inefficient muscle contraction may cause heart failure to worsen. Often a biventricular pacemaker is combined with an ICD for people with heart failure.
VENTRICULAR ASSIST DEVICE (VADs)- A VAD, also known as a mechanical circulatory support device, is an implantable mechanical pump that helps pump blood from the lower chambers of your heart (the ventricles) to the rest of your body. A VAD is implanted into the abdomen or chest and attached to a weakened heart to help it pump blood to the rest of your body.
Doctors first used heart pumps to help keep heart transplant candidates alive while they waited for a donor heart. VADs may also be used as an alternative to transplantation. Implanted heart pumps can enhance the quality of life of some people with severe heart failure who aren't eligible for or able to undergo heart transplantation or are waiting for a new heart.
HEART TRANSPLANT. Some people have such severe heart failure that surgery or medications don't help. They may need to have their diseased heart replaced with a healthy donor heart.
Heart transplants can improve the survival and quality of life of some people with severe heart failure. However, candidates for transplantation often have to wait a long time before a suitable donor heart is found. Some transplant candidates improve during this waiting period through drug treatment or device therapy and can be removed from the transplant waiting list.A heart transplant isn't the right treatment for everyone.
PALLIATIVE CARE AND END OF-LIFE CARE
Doctor may recommend including palliative care in your treatment plan. Palliative care is specialized medical care that focuses on easing your symptoms and improving your quality of life. Anyone who has a serious or life-threatening illness can benefit from palliative care, either to treat symptoms of the disease, such as pain or shortness of breath, or to ease the side effects of treatment, such as fatigue or nausea.
It's possible that your heart failure may worsen to the point where medications are no longer working and a heart transplant or device isn't an option. If this occurs, you may need to enter hospice care. Hospice care provides a special course of treatment to terminally ill people.
HOSPICE CARE ows family and friends — with the aid of nurses, social workers and trained volunteers — to care for and comfort a loved one at home or in hospice residences. Hospice care provides emotional, psychological, social and spiritual support for people who are ill and those closest to them.
Although most people under hospice care remain in their own homes, the program is available anywhere — including nursing homes and assisted living centers. For people who stay in a hospital, specialists in end-of-life care can provide comfort, compassionate care and dignity.
If you have an implantable cardioverter-defibrillator (ICD), one important consideration to discuss with your family and doctors is turning off the defibrillator so that it can't deliver shocks to make your heart continue beating.
LIFE STYLE AND HOME REMEDIES
Making lifestyle changes can often help relieve signs and symptoms of heart failure and prevent the disease from worsening. These changes may be among the most important and beneficial you can make. Lifestyle changes your doctor may recommend include:
Stop smoking. Smoking damages your blood vessels, raises blood pressure, reduces the amount of oxygen in your blood and makes your heart beat faster.If you smoke, ask your doctor to recommend a program to help you quit. You can't be considered for a heart transplant if you continue to smoke. Avoid secondhand smoke, too.
Discuss weight monitoring with your doctor. Discuss with doctor how often you should weigh yourself. Ask doctor how much weight gain you should notify him or her about. Weight gain may mean that you're retaining fluids and need a change in your treatment plan.
Check your legs, ankles and feet for swelling daily. Check for any changes in swelling in your legs, ankles or feet daily. Check with your doctor if the swelling worsens.
Eat a healthy diet. Aim to eat a diet that includes fruits and vegetables, whole grains, fat-free or low-fat dairy products, and lean proteins.
Restrict sodium in diet. Too much sodium contributes to water retention, which makes your heart work harder and causes shortness of breath and swollen legs, ankles and feet.
Check with doctor for the sodium restriction recommended for you. Keep in mind that salt is already added to prepared foods, and be careful when using salt substitutes.
Maintain a healthy weight. If you're overweight, your dietitian will help you work toward your ideal weight. Even losing a small amount of weight can help.
Consider getting vaccinations. If you have heart failure, you may want to get influenza and pneumonia vaccinations.
Limit saturated or 'trans' fats in your diet. In addition to avoiding high-sodium foods, limit the amount of saturated fat and trans fat — also called trans-fatty acids — in your diet. These potentially harmful dietary fats increase your risk of heart disease.
Limit alcohol and fluids. Doctor may recommend that you don't drink alcohol if you have heart failure, since it can interact with your medication, weaken your heart muscle and increase your risk of abnormal heart rhythms.
If you have severe heart failure, doctor may also suggest you limit the amount of fluids you drink.
Reduce stress. When you're anxious or upset, your heart beats faster, you breathe more heavily and your blood pressure often goes up. This can make heart failure worse, since your heart is already having trouble meeting the body's demands.
Find ways to reduce stress in your life. To give your heart a rest, try napping or putting your feet up when possible. Spend time with friends and family to be social and help keep stress at bay.
Sleep easy. If you're having shortness of breath, especially at night, sleep with your head propped up using a pillow or a wedge. If you snore or have had other sleep problems, make sure you get tested for sleep apnea.

CARDIAC ARREST

CARDIAC ARREST

Cardiac arrest is a serious heart condition. The word arrest means to stop or bring to a halt. In cardiac arrest, the heart ceases to beat. It’s also known as sudden cardiac death.
Your heartbeat is controlled by electrical impulses. When these impulses change pattern, the heartbeat becomes irregular. This is also known as an arrhythmia. Some arrhythmias are slow, others are rapid. Cardiac arrest occurs when the rhythm of the heart stops.
Cardiac arrest is an extremely serious health issue. The Institute of Medicine reports that every year, more than half a million people experience cardiac arrest in the United States. The condition can cause death or disability. If someone is experiencing symptoms of cardiac arrest, seek emergency health assistance immediately. It can be fatal. Immediate response and treatment can save a life.
CLASSIFICATION
Clinicians classify cardiac arrest into "shockable" versus "non–shockable", as determined by the ECG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using defibrillation. The two "shockable" rhythms are ventricular fibrillation and pulseless ventricular tachycardia while the two "non–shockable" rhythms are asystole and pulseless electrical activity.
CAUSES OF CARDIAC ARREST
A number of factors can cause sudden cardiac arrest. Two of the most common are ventricular and atrial fibrillation.
VENTRICULAR FIBRILLATION
Your heart has four chambers. The two lower chambers are the ventricles. In ventricular fibrillation, these chambers quiver out of control. This causes the heart’s rhythm to change dramatically. The ventricles begin to pump inefficiently, which severely decreases the amount of blood pumped through the body. In some cases, the circulation of blood stops completely. This may lead to sudden cardiac death.
The most frequent cause of cardiac arrest is ventricular fibrillation.
ATRIAL FIBRILATION
The heart can also stop beating efficiently after an arrhythmia in the upper chambers. These chambers are known as the atria.
Atrial fibrillation begins when the sinoatrial (SA) node doesn’t send out the correct electrical impulses. Your SA node is located in the right atrium. It regulates how quickly the heart pumps blood. When the electrical impulse goes into atrial fibrillation, the ventricles can’t pump blood out to the body efficiently.
RISK FOR CARDIAC ARREST
Certain heart conditions and health factors can increase your risk of cardiac arrest.
CORONARY ARTERY DISEASE
This type of heart disease begins in the coronary arteries. These arteries supply the heart muscle itself. When they become blocked, your heart does not receive blood. It may stop working properly.
LARGE HEART
Having an abnormally large heart places you at increased risk for cardiac arrest. A large heart may not beat correctly. The muscle may also be more prone to damage.
IRREGULAR HEART BEAT
Valve disease can make heart valves leaky or narrower. This means blood circulating through the heart either overloads the chambers with blood or does not fill them to capacity. The chambers may become weakened or enlarged.
CONGENITAL HEART DISEASE
Some people are born with heart damage. This is known as a congenital heart problem. Sudden cardiac arrest may occur in children who were born with a serious heart problem.
ELECTRICAL IMPULSE PROBLEMS
Problems with your heart’s electrical system can increase your risk of sudden cardiac death. These problems are known as primary heart rhythm abnormalities.
Other risk factors for cardiac arrest include:

• Smoking
• Sedentary lifestyle
• High blood pressure
• Obesity
• Family history of heart disease
• History of a previous heart attack
• Age over 45 for men, or over 55 for women
• Male gender
• Substance abuse
• Low potassium or magnesium

SIGNS AND SYMPTOMS
Early symptoms of cardiac arrest are often warning signs. Getting treatment before your heart stops could save your life.
If you are in cardiac arrest, you may:

• Become dizzy
• Be short of breath
• Feel fatigued or weak
• Vomit
• Experience heart palpitations                                                                                                                                          Immediate EMERGENCY care is needed if someone are with experiences these symptoms
• Chest pain
• No pulse
• Not breathing or difficulty breathing
• Loss of consciousness
• Collapse
• Cardiac arrest may not have symptoms before it occurs. If you do have symptoms that persist, seek prompt medical care.

DIAGNOSIS
difference-between-Heart-attack-and-Cardiac-arresDuring a cardiac event that causes your heart to stop beating efficiently, it’s vital to seek medical attention immediately. Medical treatment will focus on getting blood flowing back to your body. Doctor will most likely perform a test called an electrocardiogram to identify the type of abnormal rhythm your heart is experiencing. To treat the condition, doctor will likely use a defibrillator to shock your heart. An electric shock can often return the heart to a normal rhythm.
Other tests can also be used after you have experienced a cardiac event:
Blood tests can be used to look for signs of a heart attack. They can also measure potassium and magnesium levels.
Chest X-ray can look for other signs of disease in the heart.

TREATING THE CARDIAC ARREST

Defibrillator

 
 Cardiopulmonary resuscitation (CPR) is one form of emergency treatment for cardiac arrest. Defibrillation is another. These treatments get your heart beating again once it has stopped.
Medication can lower high blood pressure and cholesterol.
Surgery can repair damaged blood vessels or heart valves. It can also bypass or remove blockages in the arteries.
Exercise may improve cardiovascular fitness.
Dietary changes can help you lower cholesterol.
LONG TERM OUTLOOK OF CARDIAC ARREST
Cardiac arrest can be fatal. However, prompt treatment increases your odds of survival. Treatment is most effective within a few minutes of the arrest.
If you have experienced cardiac arrest, it’s important to understand the cause. Your long-term outlook will depend on the reason you experienced cardiac arrest. Your doctor can talk to you about treatment options to help protect your heart and prevent cardiac arrest from happening again.

PHYSICAL REHABILITATION OF CARDIOVASCULAR DISEASE

INDICATIONS
Cardiac rehabilitation should be offered to all cardiac patients who would benefit. CR is mainly prescribed to patients with ischemic heart disease, with myocardial infarction, after coronary angioplasty, after coronaro-aortic by-pass graft surgery and to patients with chronic heart failure. CR begins as soon as possible in intensive care units, only if the patient is in stable medical condition. Intensity of rehabilitation depends on patient´s condition and complications in acute phase of disease.
Cardiac rehabilitation typically comprises of four phases. The term phase is used to describe the varying time frames following a cardiac event. The secondary prevention component of CR requires delivery of exercise training, education and counseling, risk factor intervention and follow up.
Appropriate referral pathways should be set up so appropriate patients can be identified and invited to attend. Referrals should be invited by cardiologist/physician, cardiothoracic surgeon, cardiac team, cardic rehab co-ordinator, G.P., CCU nurses or members of the MDT. All referrals should include the following;
Patients name, age, address and contact number
Type of cardiac event and date of event
Cardiac history, complications and meds
Reason for referral
Referring persons name and contact number, date of request
Clinically relevant information – results of exercise stress test, echo, fasting lipid profile and fasting glucose profile
PHASES OF CARDIAC REHABILATION
PHASE 1 : IN HOSPITAL PATIENT PERIOD
2-5 days
Member of Cardiac Rehab team (CRT) should visit the patient to;
Give support and information to them and their families re: heart disease
Assist the patient to identify personal CV risk factors
Discuss lifestyle modifications of personal risk factors and help provide an individual plan to support these lifestyle changes
Gain support from family members to assist the patient in maintaining the necessary progress
Plan a personal discharge activity programme and encourage the patient to adhere to this and commence daily walks
Inform patients regarding phase II and phase III programs if available and encourage their attendance
At this stage emphasis is on counteracting the negative effects of a cardiac event not promoting training adaptations . Activity levels should be progressed using a staged approach which should be based on the patient’s medical condition. Patient should be closely monitored for any signs of cardiac decompensation.
Educational sessions should be commenced providing information re:

• The cardiac event
• Psychological reactions to the event
• Cardiac pain/symptom management
• Correction of cardiac misconceptions
• The use of educational materials such as the heart manual and leaflets from the Irish Heart Foundation should be considered.

PHASE II: POST DISCHARGE PERIOD
GOALS :
Reinforce cardiac risk factor modification
Provide education and support to patient and family
Promote continuing adherence to lifestyle recommendations.
PHASE III: CARDIAC REHABILITATION AND SECONDARY PREVENTION
Structured exercise training with continual educational and psychological support and advice on risk factors
Should take a menu based approach and be individually tailored.
Exercise class will consist of warm up, exercise class, cool down – may also include resistance training with active recovery stations where appropriate.
Patient shouldn’t exercise if they are generally unwell, symptomatic or clinically unstable on arrival;

• Fever/acute systemic illness
• Unresolved/unstable angina
• Resting BP systolic >200mmHg and diastolic > 110mmHg
• Significant drop in BP
• Symptomatic hypotension
• Resting/uncontrolled tachycardia (>100bpm)
• Uncontrolled atrial or ventricular arrhythmias
• New/recurrent symptoms of breathlessness, lethargy, palpitations, dizziness
• Unstable heart failure
• Unstable/uncontrolled diabetes

NEED TO CONSIDER THE FOLLOWING ;
Local written policy clearly displayed for the management of emergency situations
Rapid access to emergency team in hospital or via ambulance
Regular checking and maintenance of all equipment
Drinking water and glucose supplements available as required
Access to and from venue, emergency exits, toilets and changing areas, lighting, surface and room space checked to ensure they’re appropriate
Enough space for patient traffic and safe placement of equipment
Adequate temperature and ventilation

MEDIAL COLLATERAL LIGAMENT INJURY

INTRODUCTION-
Your medial collateral ligament (MCL) is the knee ligament on the medial (inner) side of your knee connecting the medial femoral condyle and the medial tibial condyle. It is one of four major knee ligaments that help to stabilise the knee joint. It is a flat band of tough fibrous connective tissue composed of long, stringy collagen molecules.
The main function of the MCL is to resist valgus force, which occurs if the tibia/foot is forced outwards in relation to the knee.

                                                         ANATOMY OF MCL
CAUSES OF MCL INJURY
The MCL is injured when the (valgus) force is too great for the ligament to resist and the ligament is overstretched. This can occur through a sharp change in direction, twisting the knee whilst the foot is fixed, landing wrong from a jump, or the most common a blunt force hit to the knee, such as in football tackle. The incident usually needs to happen at speed. Muscle weakness or incoordination predispose you to a ligament sprain or tear.
SEVERITY OF MCL INJURY
The severity and symptoms of a knee ligament sprain depend on the degree of stretching or tearing of the knee ligament. You may notice an audible snap or tearing sound at the time of your ligment injury.
In a mild Grade I MCL sprain, the knee ligament has a slight stretch, but they don't actually tear. Although the knee joint may not hurt or swell very much, a mild ligament sprain can increase the risk of a repeat injury.
With a moderate Grade II MCL sprain, the knee ligament tears partially. Knee swelling and bruising are common, and use of the knee joint is usually painful and difficult. You may have some complaints of instability or a feeling of the knee giving way.
With a severe Grade III MCL sprain, the ligament tears completely, causing swelling and sometimes bleeding under the skin. As a result, the joint is unstable and can be difficult to bear weight. You may have a feeling of the knee giving way. Often there will be no pain or severe pain that subsides quickly following a grade 3 tear as all of the pain fibres are torn at the time of injury. With these more severe tears, other structures are at risk of injury including the meniscus and/or ACL.
DIAGNOSIS
On examination, your physiotherapist will look for signs of ligament injury. There will be tenderness over the ligament site, possible swelling and pain with stress tests. MRI may also be used to diagnose a knee ligament injury and look at other surrounding structures for combination injuries.
RECOVERY TIME
Treatment of an MCL injury varies depending on its severity and whether there are other combination injuries.

 medial-collateral-ligament-grading-injuryGrade I sprains usually heal within a few weeks. Maximal ligament strength will occur after six weeks when the collagen fibres have matured. Resting from painful activity, icing the injury, and some anti-inflammatory medications are useful. Physiotherapy will help to hasten the healing process via electrical modalities, massage, strengthening and joint exercises to guide the direction that the ligament fibres heal. This helps to prevent a future tear.

When a Grade II sprain occurs, use of a weight-bearing brace or some supportive taping is common in early treatment. This helps to ease the pain and avoid stretching of the healing ligament. After a grade II injury, you can usually return to activity once the joint is stable and you are no longer having pain. This may take up to six weeks. Physiotherapy helps to hasten the healing process via electrical modalities, massage, strengthening and joint exercises to guide the direction that the ligament fibres heal. This helps to prevent a future tear and quickly return you to your pre-injury status.

When a Grade III injury occurs, you usually wear a hinged knee brace, locked into extension, and use crutches for 1-2 weeks to protect the injury from weight-bearing stresses. As pain resolves the brace can be unlocked to allow movement as tolerated. The aim is to allow for ligament healing and gradually return to normal activities. These injuries are most successfully treated via physiotherapy and may not return to their full level of activity for 3 to 4 months. All Grade III injuries should be rehabilitated under the guidance of your physiotherapist and knee specialist.

PHYSIOTHERAPY TREATMENT
Depending on the grade of injury you can start to feel better within days to just a few weeks of the injury. Your physiotherapy treatment will aim to:
1.Reduce pain and inflammation.
2.Normalise joint range of motion.
3.Strengthen your knee: esp quadriceps (esp VMO) and hamstrings.
4.Strengthen your lower limb: calves, hip and pelvis muscles.
5.Improve patellofemoral (knee cap) alignment
6.Normalise your muscle lengths
7.Improve your proprioception, agility and balance
8.Improve your technique and function eg walking, running, squatting, hopping and landing.
9.Guide return to sport activities and exercises
10.Minimise your chance of re-injury.

AIMS OF REHABILITATION-
The following examples are for information purposes only. We recommend seeking professional advice before attempting any rehabilitation. The aim of rehabilitation is to reduce pain and swelling, restore full mobility, improve strength and stability before a gradual return to full training.

GRADE 1 MCL INJURY
For a grade 1 MCL injury there may be mild tenderness on the inside of the knee over the ligament and usually no swelling. The rehabilitation guidelines for a mild medial ligament sprain can be split into 4 phases:

Phase 1: immediately following injury
Duration 1 week. Aims to reduce swelling if there is any, ensure the knee can be straightened fully and bent to more than 90 degrees and begin pain free strengthening exercises.
Rest from activities that cause pain. As pain allows, aim to walk normally without support or pain. Apply cold therapy and a compression support to limit any swelling. Apply ice for 15 minutes every 2 hours for the first day. The frequency can be gradually reduced to 3 times a day over the next few days. Do not apply ice directly to the skin as it may burn.
Sports massage techniques can usually be applied from day 2, specifically to the ligament. Ultrasound can also be applied to the ligament area. Maintain aerobic fitness with cycling. Apply cold therapy after each strengthening and stretching session.
Pain free stretching exercises for quadriceps and hamstring muscles as well as flexion and extension mobility exercises. Static strengthening exercises can begin as soon as pain allows. Isometric quadriceps exercises, calf raises with both legs and resistance band exercises for the hamstrings, hip abductors and hip extension but not for adduction as this will stress the medial ligament.

Phase 2: after 1 week
Duration 1 week. Aims - Eliminate any swelling completely, regain full range of movement, continue with strengthening exercises and return to slow jogging.
Rest from painful activities, however the athlete may be able to jog slowly as long as it is not painful. Apply cold therapy following exercise or rehabilitation exercises. Continue with stretching and strengthening exercises from phase 1.
Introduce dynamic strengthening exercises such as knee extension, knee flexion, half squats, step ups, single leg calf raise, bridging and leg press are suitable exercises if pain allows.
Cross friction massage to the ligament can be performed on alternate days. Maintain aerobic fitness with cycling, stepping machine and gentle jogging but no sudden changes of direction.

Phase 3: after 2 weeks
Duration 2 weeks. Aims to maintain full range of motion, equal strength of both legs, return to running and some sports specific training.
Continue to apply cold therapy after training sessions. Continue with sports massage techniques every 3 days. Continue with stretching exercises.
Build on dynamic strengthening exercises such as leg extension and leg curls exercises as well as squats to horizontal and lunges. Increase the intensity, weight lifted and number of repetitions. Aim for between 10 and 20 reps. Increase until the strength is equal in both legs.
In addition to straight running, start to include sideways and backwards running, agility drills and plyometric exercises. Increase speed to sprinting and changing direction drills.


Phase 4: after 4 weeks
Duration 3 to 6 weeks. Aims to return to full sports specific training and competition.
Sports massage for surrounding muscles on as weekly basis. Continue with strength training as above but start to include hopping and bounding exercises. The athlete should now be ready to gradually return to full sports specific training and then competition.
A knee support or a strapping / taping techniques may provide extra support on return to full training, however do not become reliant on this. It will weaken the joint. Use initially for confidence building.

GRADE 2 OR 3 SPRAIN-
For a grade 2+ and particularly 3 sprain it is important that the ends of the ligament are protected and left to heal without continually being disrupted. The rehabilitation guidelines for a grade 2+ or 3 medial ligament sprain (more severe) can be split into 4 phases:

Phase 1: immediately following injury
Duration 4 weeks. Aims to control swelling, maintain ability to straighten the leg bend the knee to more than 90 degrees, begin strengthening exercises.
Rest from all painful activities. Use crutches if necessary, non weight bearing to start with, then partial weight bearing from week 2 and by end of week 4 aim to be walking normally.
Wear a hinged or stabilised knee brace to protect the medial ligament. Apply cold therapy and compression. Apply ice / cold therapy for 15 minutes every 2 hours for the first 2 days and gradually reduce the frequency to 3 times a day over the next week. Pain free stretches for the hamstrings, quads, groin and calf muscles in particular. Mobility exercises should be done in the knee brace.
Sports massage (gentle cross frictions) may be possible from day 2 but allow a week for more severe injuries. As pain allows, static quads and hamstring exercises, double leg calf raises, hip abduction and extension. Knee extension mobility should only be to 30 degrees though. Maintain aerobic fitness on stationary cycle as soon as pain allows.

Phase 2: Following week 4
Duration 2 weeks. Aims to eliminate swelling, full weight bearing on the injured knee, full range of motion, injured leg almost as strong as the good one.
Continue with cold therapy and compression to eliminate swelling following exercises. Remove the knee brace at this stage. A simple stablized knee support is more suitable at this stage to apply compression to the knee. A therapist will continue with ultrasound and massage.
Range of motion exercises should continue along with isometric quadriceps exercises. Mini squats, lunges, double leg press, hamstring curls, step ups, bridges, hip abduction, hip extension and single leg calf raises can begin or be continued. It may be possible to begin to swim (not breaststroke!) or use stepper for aerobic fitness.

Phase 3: after week 6
Duration 4 weeks. Aims to regain full range of motion, strength, return to light jogging and by week 10 from injury, return to sports specific exercises.
Continue with cold therapy following training sessions. Wear a brace or support as required. Sports massage techniques to the ligament 2 to 3 times a weeks. Strengthening exercises as above increasing intensity and moving double leg exercises to single.
After week 6, no sooner, begin to run if comfortable, no sudden changes of direction though.
After week 8 begin to run sideways and backwards so by week 10 the athlete is able to begin to change direction at speed. For footballers, kicking may now be possible.
When confident enough plyometric drills, hopping, box jumps and agility drills can begin.
Phase 4: after week 10
Duration 2 to 4 weeks. Aims to return to full sports specific training and competition without a brace for support, full strength and mobility.
Gradually bring into training more and more sports specific drills, changing direction and plyometric, hopping and bounding exercises. Normal sports specific training can begin.

KNEE LIGAMENT SURGERY
Most MCL injuries resolve well with conservative management, however, surgery may be considered if there is significant ligament disruption eg Grade III. Surgery may also be required if the are significant combination injuries involving the ACL and/or meniscus. In these cases a knee specialist will guide the need for surgery.
Risks of surgery include infection, persistent instability and pain, stiffness, and difficulty returning to your previous level of activity. The good news is that better than 90% of patients have no complications post-surgery.

POST SURGICAL REHABILITATION
Post-operative knee rehabilitation is one of the most important aspects of knee surgery. The most successful and quickest outcomes result from the guidance and supervision of an experienced sports physiotherapist.
Your physiotherapy rehabilitation following knee surgery focuses on restoring full knee motion, strength, power and endurance. You'll also require balance, proprioception and agility retraining that is individualised towards your specific sporting or functional needs.
As mentioned earlier your sports physiotherapist is an expert in this field. We suggest you contact them for the best advice in your circumstances.
Your physiotherapist will guide your return to sport. It is highly variable and depends upon on your specific knee ligament injury and the demands of your demands of your sports.

PREVENTION OF RECURRENCE
A knee strengthening, agility and proprioceptive training program is the best way to reduce your chance of a knee ligament sprain. Premature return to high-risk activities such as sport are best discussed with your physiotherapist or surgeon.

 

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FACIAL NERVE PALSY

 INTRODUCTION

ANATOMY:

 
The facial nerve is the seventh cranial nerve, or simply cranial nerve VII. It emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue. The nerves typically travels from the pons through the facial canal in the temporal bone and exits the skull at the stylomastoid foramen. It arises from the brainstem from an area posterior to the cranial nerve VI (abducens nerve) and anterior to cranial nerve VIII (vestibulocochlear nerve).
The facial nerve also supplies preganglionic parasympathetic fibers to several head and neck ganglia.
The facial and intermediate nerves can be collectively referred to as the nervus intermediofacialis.

STRUCTURE:

 
The path of the facial nerve can be divided into six segments.
1. Iintracranial (cisternal) segment
2. Meatal segment (brainstem to internal auditory canal)
3. Labyrinthine segment (internal auditory canal to geniculate ganglion)
4. Tympanic segment (from geniculate ganglion to pyramidal eminence)
5. Mastoid segment (from pyramidal eminence to stylomastoid foramen)
6. Extratemporal segment (from stylomastoid foramen to post parotid branches)
1.The motor part of the facial nerve arises from the facial nerve nucleus in the pons while the sensory and parasympathetic parts of the facial nerve arise from the intermediate nerve.
2.From the brain stem, the motor and sensory parts of the facial nerve join together and traverse the posterior cranial fossa before entering the petrous temporal bone via the internal auditory meatus. Upon exiting the internal auditory meatus, the nerve then runs a tortuous course through the facial canal, which is divided into the labyrinthine, tympanic, and mastoid segments.
3.The labyrinthine segment is very short, and ends where the facial nerve forms a bend known as the geniculum of the facial nerve ("genu" meaning knee), which contains the geniculate ganglion for sensory nerve bodies. The first branch of the facial nerve, the greater superficial petrosal nerve, arises here from the geniculate ganglion. The greater petrosal nerve runs through the pterygoid canal and synapses at the pterygopalatine ganglion. Post synaptic fibers of the greater petrosal nerve innervate the lacrimal gland.
4.In the tympanic segment, the facial nerve runs through the tympanic cavity, medial to the incus.
5The pyramidal eminence is the second bend in the facial nerve, where the nerve runs downward as the mastoid segment. In the temporal part of the facial canal, the nerve gives rise to the stapedius and chorda tympani. The chorda tympani supplies taste fibers to the anterior two thirds of the tongue, and also synapses with the submandibular ganglion. Postsynaptic fibers from the submandibular ganglion supply the sublingual and submandibular glands.
6.Upon emerging from the stylomastoid foramen, the facial nerve gives rise to the posterior auricular branch. The facial nerve then passes through the parotid gland, which it does not innervate, to form the parotid plexus, which splits into five branches innervating the muscles of facial expression (temporal, zygomatic, buccal, marginal mandibular, cervical).

INTRACRANIAL BRANCH :

 
1.Greater petrosal nerve – It arises at the geniculate ganglion and provides parasympathetic innervation to several glands, including the nasal glands, the palatine glands, the lacrimal gland, and the pharyngeal gland. It also provides parasympathetic innervation to the sphenoid sinus, frontal sinus, maxillary sinus, ethmoid sinus and nasal cavity. This nerve also includes taste fibers for palate via lesser palatine nerve and greater palatine nerve.

2.Communicating branch to the otic ganglion – It arises at the geniculate ganglion and joins the lesser petrosal nerve to reach the otic ganglion.

3..Nerve to stapedius – provides motor innervation for stapedius muscle in middle ear

4.Chorda tympani
Parasympathetic innervation to submandibular gland
Parasympathetic innervation to sublingual gland
Special sensory taste fibers for the anterior 2/3 of the tongue.

EXTRACRANIAL BRANCHES
Distal to stylomastoid foramen, the following nerves branch off the facial nerve:
Posterior auricular nerve – controls movements of some of the scalp muscles around the ear
Branch to Posterior belly of Digastric muscle as well as the Stylohyoid muscle
Five major facial branches (in parotid gland) – from top to bottom:

                                                       
EXRACRANIAL BRANCH
1.Temporal branch
2.Zygomatic branch
3.Buccal branch
4.Marginal mandibular branch
5.Cervical branch
Intra operatively the facial nerve is recognized at 3 constant landmarks:
1.At the tip of tragal cartilage where the nerve is 1cm deep and inferior
2.At the posterior belly of digastric by tracing this backwards to the tympanic plate the nerve can be found between these two structures
3.By locating the posterior facial vein at the inferior aspect of the gland where the marginal branch would be seen crossing it.
4.lateral semicircular canal
5.Foot of incus

NUCLEUS
The cell bodies for the facial nerve are grouped in anatomical areas called nuclei or ganglia. The cell bodies for the afferent nerves are found in
the geniculate ganglion for taste sensation. The cell bodies for muscular efferent nerves are found in the facial motor nucleus whereas the cell
bodies for the parasympathetic efferent nerves are found in the superior salivatory nucleus.

DEVELOPMENT
The facial nerve is developmentally derived from the second pharyngeal arch, or branchial arch. The second arch is called the hyoid arch because it contributes to the formation of the lesser horn and upper body of the hyoid bone (the rest of the hyoid is formed by the third arch). The facial nerve supplies motor and sensory innervation to the muscles formed by the second pharyngeal arch, including the muscles of facial expression, the posterior belly of the digastric, stylohyoid and stapedius. The motor division of the facial nerve is derived from the basal plate of the embryonic pons, while the sensory division originates from the cranial neural crest.
Although the anterior two thirds of the tongue are derived from the first pharyngeal arch, which gives rise to cranial nerve V, not all innervation of the tongue is supplied by CN V. The lingual branch of the mandibular division (V3) of CN V supplies non-taste sensation (pressure, heat, texture) from the anterior part of the tongue via general visceral afferent fibers. Nerve fibers for taste are supplied by the chorda tympani branch of cranial nerve VII via special visceral afferent fibers.

FUNCTIONS
Facial expression
The main function of the facial nerve is motor control of all of the muscles of facial expression. It also innervates the posterior belly of the digastric muscle, the stylohyoid muscle, and the stapedius muscle of the middle ear. All of these muscles are striated muscles of branchiomeric origin developing from the 2nd pharyngeal arch.

FACIAL SENSATION
In addition, the facial nerve receives taste sensations from the anterior two-thirds of the tongue via the chorda tympani. Taste sensation is sent to the gustatory portion (superior part) of the solitary nucleus. General sensation from the anterior two-thirds of tongue are supplied by afferent fibers of the third division of the fifth cranial nerve (V-3). These sensory (V-3) and taste (VII) fibers travel together as the lingual nerve briefly before the chorda tympani leaves the lingual nerve to enter the tympanic cavity (middle ear) via the petrotympanic fissure.

It joins the rest of the facial nerve via the canaliculus for chorda tympani. The facial nerve then forms the geniculate ganglion, which contains the cell bodies of the tastefibers of chorda tympani and other taste and sensory pathways. From the geniculate ganglion, the taste fibers continue as the intermediate nervewhich goes to the upper anterior quadrant of the fundus of the internal acoustic meatus along with the motor root of the facial nerve. The intermediate nerve reaches the posterior cranial fossa via the internal acoustic meatus before synapsing in the solitary nucleus.
The facial nerve also supplies a small amount of afferent innervation to the oropharynx below the palatine tonsil. There is also a small amount of cutaneous sensation carried by the nervus intermedius from the skin in and around the auricle (outer ear).

OTHERS-
The facial nerve also supplies parasympathetic fibers to the submandibular gland and sublingual glands via chorda tympani. Parasympathetic innervation serves to increase the flow of saliva from these glands. It also supplies parasympathetic innervation to the nasal mucosa and the lacrimal gland via the pterygopalatine ganglion. The parasympathetic fibers that travel in the facial nerve originate in the superior salivatory nucleus.

The facial nerve also functions as the efferent limb of the corneal reflex.

FUNCTIONAL COMPONNENT-
The facial nerve carries axons of type GSA, general somatic afferent, to skin of the posterior ear.
The facial nerve also carries axons of type GVE, general visceral efferent, which innervate the sublingual, submandibular, and lacrimal glands, also mucosa of nasal cavity.
Axons of type SVE, special visceral efferent, innervate muscles of facial expression, stapedius, the posterior belly of digastric, and the stylohyoid.
The axons of type SVA, special visceral afferent, provide taste to the anterior two-thirds of tongue via chorda tympani.
Finally, the facial nerve also carries axons of type GVA, general visceral afferent, which provide sensation to the soft palate and parts of the nasal
cavity.

CLINICAL SIGNIFICANCE-

PALSY
People may suffer from acute facial nerve paralysis, which is usually manifested by facial paralysis. Bell's palsy is one type of idiopathic acute facial nerve paralysis, which is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most likely results from viral infection and also sometimes as a result of Lyme disease. Iatrogenic Bell's Palsy may also be as a result of an incorrectly placed dental local-anesthetic (Inferior alveolar nerve block). Although giving the appearance of a hemi-plegic stroke, effects dissipate with the drug.
When the facial nerve is permanently damaged due to a birth defect, trauma, or other disorder, surgery including a cross facial nerve graft or masseteric facial nerve transfer may be performed to help regain facial movement.Facial nerve decompression surgery is also sometimes carried out in certain cases of facial nerve compression.

EXAMINATION-
Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called lagophthalmos) , pursing the lips and puffing out the cheeks, all test the facial nerve. There should be no noticeable asymmetry.

In an UMN lesion, called central seven, only the lower part of the face on the contralateral side will be affected, due to the bilateral control to the upper facial muscles (frontalis and orbicularis oculi).
LMN lesions can result in a CNVII palsy (Bell's palsy is the idiopathic form of facial nerve palsy), manifested as both upper and lower facial weakness on the same side of the lesion.
Taste can be tested on the anterior 2/3 of the tongue. This can be tested with a swab dipped in a flavoured solution, or with electronic stimulation (similar to putting your tongue on a battery).
Corneal reflex. The afferent arc is mediated by the General Sensory afferents of the Trigeminal Nerve. The efferent arc occurs via the Facial Nerve.
The reflex involves consensual blinking of both eyes in response to stimulation of one eye. This is due to the Facial Nerve's innervation of the muscles of facial expression, namely Orbicularis oculi, responsible for blinking. Thus, the corneal reflex effectively tests the proper functioning of both Cranial Nerves V and VII.

FACIAL NERVE PALSY-
A facial palsy is weakness or paralysis of the muscles of the face.
Whilst the majority of cases are idiopathic, termed Bell’s Palsy, there are a wide range of potential causes of a facial palsy .
Bell’s palsy is a diagnosis of exclusion and hence all possible causes have to be excluded first prior to diagnosing Bell’s palsy. The majority of this article will discuss Bell’s Palsy and its associated clinical features and management.

RISK FACTORS-
Bell’s palsy remains a poorly understood condition. Many causative associations have been proposed, the most universally accepted theory suggests a viral origin, yet no conclusive evidence is available at present.
The main risk factor for developing Bell’s palsy is known concurrent viral infection, such as HSV-1(HERPES SIMPLEX  VIRUS 1), CMV (CYTOMEGALOVIRUS), and EBV (EBSTEIN VIRUS), whilst less common risk factors.
include diabetes mellitus and pregnancy.

CLINICAL FEATURE-
Patients with a Bell’s Palsy will present with varying severity of painless unilateral lower motor neuron weakness of the facial muscles .
Depending on the severity and the ximity of the nerve affected, it can also result in:
Inability to close their eye (temporal and zygomatic branches)
Hyperacusis (nerve to stapedius)
Metallic taste (chorda tympani)
Reduced lacrimation (greater petrosal nerve)

DIFFERENCE BETWEEN THE UMN AND LMN LESION-
To distinguish clinically between a LMN cause and UMN cause of the facial palsy, a patient with forehead sparing (i.e. no involvement to the occipitofrontalis muscle) will have a UMN origin to the palsy, due to the bilateral innervation of the forehead muscle).

DIFFERENTIAL DIAGNOSIS-

LMN AND UMN LESIONImportant differential diagnosis for a facial palsy, other than Bell’s Palsy, include:

      UMN causes, such as a stroke, SDH, or tumour
Will present with forehead sparing

• LMN CAUSES
• Infective such as acute otitis media, cholesteatoma, viral infection (including HSV-1, CMV, and EBV)
• Neoplasm (parotid malignancy)
• Trauma or iatrogenic
• Neurological (Multiple sclerosis or Guillain-Barré syndrome)

SYMPTOMS OF BELLS PALSY :

 

                                                  SYMPTOMS OF BELLS PALSY

                                                    

The onset of facial paralysis is sudden with Bell’s palsy, and can worsen during the early stages. Symptoms will usually manifest and peak within 2-3 days, although it can take as long as 2 weeks. Common symptoms include, but are not limited to:
Muscle weakness or paralysis
Facial droop
Impossible or difficult to blink
Difficulty speaking
Difficulty eating and drinking
Nose runs
Nose is constantly stuffed
Difficulty breathing out of nostril on affected side
Nostril collapse on affected side
Forehead wrinkles disappear
Sensitivity to sound
Excess or reduced salivation
Facial swelling
Drooling
Diminished or distorted taste
Pain behind ear
There are also some eye related symptoms, which may include but are not limited to:
Difficulty closing the eye
Sensitivity to light
Lower eyelid droop
Tears fail to coat cornea
Brow droop
Excessive tearing
Lack of tears

INVESTIGATION
Most cases of Bell’s Palsy can be diagnosed clinically and no further investigations are required, unless any other clinical features are present that suggest another pathology.
Serology for HSV-1 and VZV can be performed, yet will unlikely alter future management if detected.

MANAGEMENT-
Patient reassurance is essential, as most cases return spontaneously to full function. Eye care is one of the most important aspect of the management, ensuring the patient uses lubricating drops hourly and potential for eye ointment at night and / or an eye patch.

MEDICAL MANAGEMENT
All patients presenting within 72 hours of symptoms onset should be started oral steroids. Current NICE guidance recommends either:
Giving 25 mg twice daily for 10 days
Giving 60 mg daily for five days followed by a daily reduction in dose of 10 mg
Use of anti-viral agents is controversial.
A Cochrane Review found low level evidence that the combination of anti-virals and corticosteroids are more effective in Bell’s palsy treatment; many centers currently treat Bell’s palsy with both.

SURGICAL REFFERAL
Referral to an ENT surgeon should be considered if there is any doubt over the diagnosis, recurrent or bilateral Bell’s palsy, or no sign of improvement after 1 month. There are surgical options available for patients who have persistent weakness or synkinesis. Synkinesis could be treated with botox injections whilst persistent weakness can be treated with anterior belly of diagastric transfer, fascia lata sling, or cross-facial nerve grafting.
A referral to ophthalmology should be made if the cornea remains exposed after attempting to close the eyelid (House Brackmann grade of IV or more).

COMPLICATIONS
85% of cases will recover from Bell’s palsy, the majority of which make a fully recovery with no evidence of residual symptoms. The factors that suggest a poor prognosis from a facial palsy include:
Complete palsy
No signs of recovery within 3 weeks
Age >60yrs
Associated pain
Ramsey Hunt syndrome
Associated HTN, DM, or pregnancy

PHYSICAL THERAPY TREATMENT FOR FACIAL PARALYSIS :

 
In the first couple of days to a week after symptoms start,  physical therapist will evaluate your condition, including:
Review your medical history, and discuss any previous surgery or health conditions
Review when your current symptoms started and what makes them worse or better
Conduct a physical examination, focusing on identifying the patterns of weakness that are caused by Bell palsy

• Facial movements of the eyebrow
•  Eye closure
• Ability to use the cheek in smiling
• Ability to use the lips in a pucker
• Ability to suck the cheeks between the teeth
• Raising the upper lip
• Raising or lowering the lower lip

Your physical therapist will immediately:

• Educate you about how to protect your face and your eye
• Show you how to manage your daily life functions while you have facial paralysis
• Explain the expected path to recovery, so that you will know the signs and symptoms of recovery
• Evaluate your progress, and determine whether you need to be referred to a specialist if progress is not being made The first priority is to protect your eye. The inability to completely and quickly
• close your eye makes the eye vulnerable to injury from dryness and debris. Debris can scratch the cornea—the transparent front part of the eye that covers the iris, pupil, and front chamber of the eye—and could permanently harm your vision. physical therapist will immediately show you how to protect your eye, such as:
• Using self-made and commercial patches
• Setting a regular schedule for refreshing eye fluids
• Carefully closing the eye with your fingers
• If you have partial facial movement, your therapist will teach you a few general facial exercises to do at home. These exercises will help you learn to move the weak side of your face and help you use both sides of your face together. One of the exercises is a gentle blowing action through your lips.

DURING RECOVERY :

 
Physical therapist will help you regain the healthy pattern of movements that you need for facial expressions and function. Recovery can be challenging because:
Normally, the ability to make facial expressions and many facial movements is "automatic";—that is, you're born with this ability and never had to think about it before Unlike other muscles in your body, the facial muscles do not have sensors that tell your brain all of the necessary "details" about how to move Physical therapist will be your coach throughout this challenging time, guiding you through special exercises that are designed to help you relearn facial movements based on your particular movement problems. Your exercises may change over the course of recovery:
"Initiation" exercises. In the early stages, when you might have difficulty producing any facial movement at all, your therapist will teach you exercises that cause ("initiate") facial movement. Your therapist will show you how to position your face to make it easier to move (called "assisted range of motion") or how to "trigger" the facial muscles to do what you want them to do.
"Facilitation" exercises. Once you're able to initiate movement of the facial muscles, your therapist will design exercises to increase the activity of the muscles, strengthen the muscles, and improve your ability to use the muscles for longer periods of time ("facilitate" muscle activity).

Movement control exercises. therapist will design exercises to:

• Improve the coordination of your facial muscles
• Refine your facial movements for specific functions, such as speaking or closing your eye
• Refine movements for facial expressions, such as smiling
• Correct abnormal patterns of facial movement that can occur during recovery
• To work on coordinating your facial muscles, you'll need to have a sufficient level of activation of facial muscles first.

RELAXATION- During recovery, you might have facial spasms or twitches. Your physical therapist will design exercises to reduce this unwanted muscle activity. The therapist will teach you how to recognize when you are activating the facial muscle and when the muscle is at rest. By learning to contract the facial muscle forcefully and then stop, you will be able to relax your facial muscles at will and decrease twitches and spasms.
AFTER RECOVERY-
Some people might have greater difficulty moving their face after a period of improvement in facial movement, which can make them worry that the facial paralysis is returning. However, actual recurrence of facial paralysis of the Bell Palsy type is uncommon.
New difficulty in moving the face is more likely the result of increasing the strength of the facial muscles without improving the ability to coordinate and control the movement. To keep this from happening, physical therapist will show you what facial movements you should avoid during recovery. For instance, the following might lead to abnormal patterns of facial muscle use:
Trying to make the biggest facial movement or muscle contraction that you can, such as smiling as much as you can

• Chewing gum with great force
• Blowing up a balloon with all of your effort to work the facial muscles
  Therapist will coach you to use your face as naturally as possible, without trying to restrict facial expressions because they look "different."

NEUROMUSCULAR RETRAINING (NMR)
NMR involves the use of subtle but critically important exercises to teach and retrain the brain to coordinate the facial muscles more effectively and efficiently.

BENEFITS OF NMR
NMR re-teaches facial paralysis patients which muscles are required to move different parts of the face. This type of physical therapy enables a patient’s brain to reconnect facial muscles and corresponding facial movements. It teaches patients how to isolate facial muscles, use only the correct muscles to make their desired facial movements and suppress muscles that otherwise cause unwanted facial movements.
VIABLE CANDIDATE FOR NMR
Patients dealing with Bell’s palsy or other viral infections of the facial nerve often recover on their own completely and spontaneously within about three months of an initial diagnosis. For those who do not fully recover, it is possible that the facial nerve will heal improperly, which causes spontaneous, unwanted facial movements (or synkinesis). For example, when a Bell’s palsy patient tries to smile, his or her eye may twitch at the same time. In this scenario, the patient does not require additional strength in the facial muscles. Instead, he or she needs to improve facial muscle coordination to prevent facial muscles from flexing out of sequence – something that causes distorted facial movements.

MANUAL MASSAGE
Manual massage involves a series of different massage techniques. The goal of manual massage is to decrease facial muscle tightness and improve flexibility and range of motion. Initially, manual massage techniques may be performed by physical therapists, but the therapist ultimately will teach a patient the techniques so he or she can perform them regularly at home.

 

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