ACYANOTIC CONGENITAL HEART DISEASE

Acyanotic heart defects are congenital cardiac malformations that affect the atrial or ventricular walls, heart valves, or large blood vessels. Common causes include genetic defects (e.g., trisomies), maternal infections (e.g., rubella), or maternal consumption of drugs or alcohol during pregnancy. Acyanotic heart defects are characterized pathophysiologically by a left-to-right shunt, which causes pulmonary hypertension and right heart hypertrophy.

The symptoms depend on the extent of the malformation and the resulting impairment of cardiac function. Infants may be asymptomatic or present with exercise intolerance, failure to thrive, and symptoms of heart failure. Characteristic heart murmurs are important clues for establishing the diagnosis, which is typically confirmed by visualizing the defect on echocardiography.

A chest x-ray, MRI, or cardiac catheterization may also be required to determine the indications for surgery and plan the procedure. Acyanotic heart defects requiring treatment are repaired via catheter procedures or surgery. Supportive medical therapy is needed in cases of heart failure (e.g., diuretics, inotropic agents) or if surgery cannot be performed (e.g., prostaglandin). Common complications include arrhythmias, embolisms, and infective endocarditis, especially if treatment is delayed.

Overview of acyanotic congenital heart defects

  • General clinical features
  • Normal skin tone
  • Exercise intolerance
  • Fatigue
  • Exertional tachycardia, pallor, and diaphoresis (sweating)
  • Exertional dyspnea, tachypnea
  • Recurrent bronchopulmonary infections
  • Failure to thrive
  • Heart failure in larger defects
  • Tachycardia
  • Right-sided heart failure
  • Hepatic venous congestion with hepatomegaly
  • Peripheral edema is rarely seen in infants.
  • Left-sided heart failure
  • Tachypnea, pulmonary edema
  • Low cardiac output: BP, pallor, sweating, cool extremities, poor growth, syncope
    Differential cyanosis: cyanosis in the lower extremities when the Eisenmenger reaction occurs

ATRIAL SEPTAL DEFECT (ASD)

atrial septal defect
                  atrial septal defect

EPIDEMIOLOGY
Prevalence: ~ 2/1000 live births

ETIOLOGY
Down syndrome
Fetal alchohol syndrome
Holt-Oram syndrome

PATHOPHYSIOLOGY
Impaired growth or excessive resorption of the atrial septa in utero leads to atrial septal defects.
Ostium primum atrial septal defect (ASD I): (~ 15–20%)
Ostium secundum atrial septal defect (ASD II): (~ 70%)
Typically a low-pressure, low-volume, minor left-to-right shunt ? patients are asymptomatic
In larger defects, the shunt may lead to: right heart failure, supraventricular arrhythmias, pulmonary hypertension, cor pulmonale, and/or the Eisenmenger reaction

  • CLINICAL FINDINGS
    Depend on defect size and shunt volume
    Small defects: usually asymptomatic
    Large defects
  • Palpitations
  • ASDs typically manifest with advancing age.
  • Auscultation
  • Systolic ejection murmur over the left second ICS sternal border
  • Widely split second heart sound (S2) over the left second ICS, which is fixed (does not change with respiration ), normal S1
  • Soft mid-diastolic murmur over the lower left sternal border

DIAGNOSTICS
Echocardiography (confirmatory test): to visualize the defect, its extent, and shunt volume
ECG: vertical or right axis, P pulmonale, right bundle branch block (complete or incomplete), signs of right heart hypertrophy, PR prolongation
Chest x-ray: enlarged right atrium, ventricle, and pulmonary arch; increased pulmonary vasculature

TREATMENT
In childhood, spontaneous closure may occur.
Patch repair
Indicated in symptomatic children with significant left-to-right shunt
Surgical or via percutaneous transcatheter procedure

COMPLICATION
Paradoxical embolism risk of stroke

VENTRICULAR SEPTAL DEFECT (VSD)

ventricular septal defect
ventricular septal defect

EPIDEMIOLOGY
The most common congenital heart defect (4/1000 live births)
Occurs as an isolated heart defect or in combination with others

ETIOLOGY
Genetic syndromes: Down syndrome, Edward syndrome, Patau syndrome
Fetal alcohol syndrome
Intrauterine infection (e.g., TORCH)

PATHOPHYSIOLOGY
Localization: most commonly in the membranous part of the ventricular septum (pars membranacea)
Defect in ventricular septum  left-to-right shunt with the following consequences:
LV volume overload  left ventricular hypertrophy
Excessive pulmonary blood flow  increased pulmonary artery pressures  pulmonary hypertension and right-sided heart hypertrophy
Decreased cardiac output
Possibly an Eisenmenger reaction in late stage of disease due to irreversible pulmonary hypertension

CLINICAL FINDING
Small defects: usually asymptomatic
Medium-sized or large defects
Lead to cardiac failure in the first 2–3 months of life

Palpation: Hyperdynamic precordium may be detected in hemodynamically relevant defects.
Auscultatory findings
Harsh holosystolic murmur over the left lower sternal border; typically louder in small defects
Mid-diastolic murmur over cardiac apex
Systolic thrill
Loud pulmonic S2 (if pulmonary hypertension develops)

DIAGNOSIS
Doppler echocardiography: confirms diagnosis; evaluation of defect size and shunt volume; exclusion of other anomalies
ECG: signs of right heart hypertrophy
Chest x-ray
Enhanced pulmonary vascular markings
Left atrial and ventricular enlargement
In later stages, enlarged right ventricle and pulmonary artery (due to elevated PVR)

TREATMENT
Small VSDs: rarely require surgical interventions small to moderate defects often heal spontaneously; follow-up echocardiography recommended
Symptomatic and large VSDs
Surgical (patch) repair in children < 1 year of age with signs of pulmonary hypertension and older children who did not improve with medical therapy
Closure of a VSD results in a decrease in right ventricular and left atrial pressures and an increase in left ventricular pressure when compared to pre-treatment values
Heart-lung transplant or lung transplant with concurrent VSD repair if Eisenmenger’s reaction has occurred

  • COMPLICATIONS
  • Arrhythmias
  • Right heart failure
  • Eisenmenger’s reaction
  • Infective endocarditis
  • Aortic regurgitation

CONGENITAL PATENT DUCTUS ARTERIOSUS (PDA)

patent ductus arteriosus
  patent ductus arteriosus

GLOSSARY
While still in the mother’s womb, a baby does not need their lungs to supply oxygen because they receive oxygen from their mother. Since a baby’s lungs do not provide oxygen, there is no need for the heart to pump blood to the lungs. The ductus arteriosus is a blood vessel that is present in all babies while still in the womb, and it allows blood to bypass the lungs.

When the baby is born and the umbilical cord is cut, their lungs need to supply oxygen to their body. Their lungs expand, their blood vessels relax to accept more blood flow, and the ductus arteriosus usually closes within the first hours of life. Sometimes, the ductus arteriosus does not close on its own. This is known as a patent (“open”) ductus arteriosus. While this condition is seen more often in premature babies, it may also appear in full-term infants.

SYMPTOMS OF PATENT DUCTUS ARTERIOSUS
The symptoms of a patent ductus arteriosus depend on the size of the ductus and how much blood flow it carries. After birth, if a ductus arteriosus is present, blood will flow from the aorta (the main artery in the body) into the pulmonary artery. This extra blood flow into the lungs can overload the lungs and put more burden on the heart to pump this extra blood. Some babies may need more support from a ventilator and have symptoms of congestive heart failure.

A newborn with a patent ductus arteriosus may have:

  • Fast breathing
  • A hard time breathing
  • More respiratory infections
  • Tire more easily
  • Poor growth
    However, if the patent ductus arteriosus is not large, it may cause no symptoms and your doctor may not find it until they do further evaluation of a heart murmur.
    Even if there are no symptoms, the turbulent flow of blood through the patent ductus arteriosus puts a person at a higher risk for a serious infection, known as endocarditis.

DIAGNOSIS
Because of turbulent blood flow, a patent ductus arteriosus causes a distinct sounding heart murmur that is heard on physical exam.

The murmur, along with symptoms of heart failure in a premature infant, most often lead to the diagnosis of patent ductus arteriosus. A chest X-ray will show an enlarged heart and evidence of a large amount of blood flow to the lungs. An echocardiogram is done to confirm the diagnosis. doctor can see the size of the ductus arteriosus and also find out if the heart chambers have become enlarged due to the extra blood flow.

In older children, though, their chest X-ray is typically normal. An echocardiogram will show the flow of blood through the patent ductus arteriosus and is typically done to confirm the diagnosis.

In a newborn, the patent ductus arteriosus still has the chance to close on its own. Doctor may allow more time for the patent ductus arteriosus to close on its own if their heart failure is under control. If a newborn’s symptoms are severe or it is unlikely to close on its own, medical or surgical treatment is needed.

Medicines work best for newborns. They may receive medicine, such as indomethacin or ibuprofen, to constrict the muscle in the wall of the patent ductus arteriosus and help it close. These drugs do have side effects, so not all babies can receive them.

SURGERY
A small incision is made between the ribs on the left side.
The ductus arteriosus is tied and cut.
The risk of complications with any of these treatments is low, determined mostly by how ill the child is prior to treatment.

PDA IS GOOD OR NOT
Yes. Some babies have heart defects that require the patent ductus arteriosus to remain open for them to survive.

In some heart defects, such as pulmonary atresia (an underdeveloped or blocked pulmonary valve), the patent ductus arteriosus supplies the only adequate source of blood flow to the lungs so that oxygen can be delivered to the blood. In these patients, the ductus arteriosus supplies blood to the lungs from the aorta.

COARCTACTION OF AORTA

coarctation of the aorta11
coarctation of the aorta

Coarctation (ko-ahrk-TAY-shun) of the aorta — or aortic coarctation — is a narrowing of the aorta, the large blood vessel that branches off your heart and delivers oxygen-rich blood to body. When this occurs, your heart must pump harder to force blood through the narrowed part of your aorta.
Coarctation of the aorta is generally present at birth (congenital). The condition can range from mild to severe, and might not be detected until adulthood, depending on how much the aorta is narrowed.
Coarctation of the aorta often occurs along with other heart defects. While treatment is usually successful, the condition requires careful lifelong follow-up.

SYMPTOMS
Coarctation of the aorta symptoms depend on the severity of the condition. Most people don’t have symptoms. Children with serious aortic narrowing may show signs and symptoms earlier in life, but mild cases with no symptoms might not be diagnosed until adulthood. People may also have signs or symptoms of other heart defects that they have along with coarctation of the aorta.

  • Babies with severe coarctation of the aorta may begin having signs and symptoms shortly after birth. These include:
  • Pale skin
  • Irritability
  • Heavy sweating
  • Difficulty breathing
  • Difficulty feeding
  • Left untreated, aortic coarctation in babies might lead to heart failure or death.

Older children and adults with coarctation of the aorta often don’t have symptoms because their narrowing may be less severe. If you have signs or symptoms that appear after infancy, you most commonly will have high blood pressure (hypertension) measured in your arms. However, your blood pressure is likely to be lower in your legs.

  • SIGNS AND SYMPTOMS
  • High blood pressure
  • Headache
  • Muscle weakness
  • Leg cramps or cold feet
  • Nosebleeds
  • Chest pain

Seek medical help if child has the following signs or symptoms:

  • Severe chest pain
  • Fainting
  • Sudden shortness of breath
  • Unexplained high blood pressure
  • While experiencing these signs or symptoms doesn’t necessarily mean that you have a serious problem, it’s best to get checked out quickly. Early detection and treatment might help save your life.

CAUSES

Rarely, coarctation of the aorta develops later in life. Traumatic injury might lead to coarctation of the aorta. Rarely, severe hardening of the arteries (atherosclerosis) or a condition causing inflamed arteries (Takayasu’s arteritis) can narrow the aorta, leading to aortic coarctation.

Coarctation of the aorta usually occurs beyond the blood vessels that branch off to your upper body and before the blood vessels that lead to your lower body. This can often lead to high blood pressure in your arms but low blood pressure in your legs and ankles.

With coarctation of the aorta, the lower left heart chamber (left ventricle) of your heart works harder to pump blood through the narrowed aorta, and blood pressure increases in the left ventricle. This may cause the wall of the left ventricle to thicken (hypertrophy).

Prevention

Coarctation of the aorta can’t be prevented, because it’s usually present at birth (congenital). However, if you or your child has a condition that increases the risk of aortic coarctation, such as Turner syndrome, bicuspid aortic valve or another heart defect, or a family history of congenital heart disease, early detection can help. Discuss the risk of aortic coarctation with your doctor.

Advertisements

CYANOTIC CONGENITAL HEART DISEASE

CYANOTIC CONGENITAL 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:

CLASSIFICATION OF CHD
Classification of CHD. 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
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 DISEASETRETMENT 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.

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. Your doctor often will use them together to help decide your most appropriate treatment options. Ask your doctor about your score if you’re interested in determining the severity of your heart failure. Your doctor can help you interpret your score and plan your treatment based on your condition.

CAUSES OF CHF

RISK FACTORS
                                                    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
                                                     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

X- RAYS
X- RAYS

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 (ICDs)-

 

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

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-arrest
difference-between-Heart-attack-and-Cardiac-arrest

During 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
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
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-injury
medial-collateral-ligament-grading-injury

Grade 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.

PHYSIOTHERAPYPHYSIOTHERAPY 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.

PRVENTION 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.

POSTURAL DRAINAGE

INTRODUCTION-
Postural Drainage removes mucus from certain parts of the lungs by using gravity and proper positioning to bring the secretions into the throat where it is easier to remove them. The lungs are divided into segments called lobes, the right lung is divided into three lobes (right upper lobe, right middle lobe and right lower lobe) while the left lung has only two lobes (left upper lobe and lower lobe).

SCHEDULING TREATMENT
The treatment often works best in the morning. This allows the mucus to be removed that has built up during the night. Sometimes a treatment can be done at night to reduce the need for coughing during sleep. Make sure you wait at least 1-2 hours after eating before starting you treatment. This helps to prevent nausea and or vomiting. CPT just before meals may cause you to become tired and may decrease appetite.

ANATOMY OF LUNGS

 

lung-anatomy-illustration
LUNG ANATOMY ILLUSTRATION

STEPS
1. Use specific positions so the force of gravity can assist in the removal of bronchial secretions from affected lung segments to central airways by means of coughing and suctioning.
2. The patient is positioned so that the diseased area is in a near vertical position, and gravity is used to assist the drainage of specific segment.
3. The positions assumed are determined by the location, severity, and duration of mucous obstruction.
4. The exercises are performed two to three times a day, before meals and bedtime. Each position is done for 3-15 minutes.
5. The procedure should be discontinued if tachycardia, palpitations, dyspnea, or chest occurs. These symptoms may indicate hypoxemia. Discontinue if hemoptysis occurs.
6. Bronchodilators, mucolytics agents, water, or saline may be nebulised and inhaled before postural drainage and chest percussion to reduce bronchospasm, decrease thickness of mucus and sputum, and combat edema of the bronchial walls, there by enhancing secretion removal.
7. Perform secretion removal procedures before eating.
8. Make sure patient is comfortable before the procedure starts and as comfortable as possible he or she assumes each position.
9. Auscultate the chest to determine the areas of needed drainage.
10. Encourage the patient to deep breathe and cough after spending the allotted time in each position.
11. Encourage diaphragmatic breathing through out postural drainage: this helps widen airways so secretions can be drained.

POSITION

POSTURAL DRAINAGE POSITIONS
POSTURAL DRAINAGE POSITIONS

To drain the middle and lower portions of your lungs, you should be positioned with your chest above your head. Possible techniques to achieve this position are:

If a hospital bed is available, put in Trendelenburg position (head lower than feet).
Place 3-5 wood blocks, that are 2 inches by 4 inches, in a stack that is 5 inches high, under the foot of a regular bed. Blocks should have indentations or a 1 inch rim on top so that the bed does not slip.
Stack 18-20 inches of pillow under hips.
Place on a tilt table, with head lower than feet.
Lower head and chest over the side of the bed.
To drain the upper portions of your lungs, you should be in a sitting position at about a 45 degree angle.

Postural drainage therapy is designed to improve the mobilization of bronchial secretions and the matching of ventilation and perfusion, and to normalize functional residual capacity (FRC) based on the effects of gravity and external manipulation of the thorax. This includes turning, postural drainage, percussion, vibration, and cough.

TURNING
Turning is the rotation of the body around the longitudinal axis to promote unilateral or bilateral lung expansion and improve arterial oxygenation. Regular turning can be to either side or the prone position, with the bed at any degree of inclination (as indicated and tolerated). Patients may turn themselves or they may turned by the caregiver or by a special bed or device.

POSTURAL DRAINAGE
Postural drainage is the drainage of secretions, by the effect of gravity, from one or more lung segments to the central airways (where they can be removed by cough or mechanical aspiration). Each position consists of placing the target lung segment(s) superior to the carina. Positions should generally be held for 3 to 15 minutes (longer in special situations). Standard positions are modified as the patient’s condition and tolerance warrant.

EXTERNAL MANIPULATION OF THE THORAX
A-PERCUSSION
Percussion is also referred to as cupping, clapping, and tapotement. The purpose of percussion is to intermittently apply kinetic energy to the chest wall and lung. This is accomplished by rhythmically striking the thorax with cupped hand or mechanical device directly over the lung segment(s) being drained. No convincing evidence demonstrates the superiority of one method over the other.

B-VIBRATION
Vibration involves the application of a fine tremorous action (manually performed by pressing in the direction that the ribs and soft tissue of the chest move during expiration) over the draining area. No conclusive evidence supports the efficacy of vibration, the superiority of either manual or mechanical methods, or an optimum frequency.

INDICATIONS
Turning
Inability or reluctance of patient to change body position. (eg, mechanical ventilation, neuromuscular disease, drug-induced paralysis)
Poor oxygenation associated with position(eg, unilateral lung disease)
Potential for or presence of atelectasis
Presence of artificial airway
Postural Drainage

Evidence or suggestion of difficulty with secretion clearance
(a)Difficulty clearing secretions with expectorated sputum production greater than 25-30 mL/day (adult)

(b)Evidence or suggestion of retained secretions in the presence of an artificial airway

-Presence of atelectasis caused by or suspected of being caused by mucus plugging.
-Diagnosis of diseases such as cystic fibrosis,bronchiectasis, or cavitating lung disease
-Presence of foreign body in airway.
-External Manipulation of the Thorax

(a)Sputum volume or consistency suggesting a need for additional manipulation (eg, percussion and/or vibration) to assist movement of secretions by gravity, in a patient receiving postural drainage

CONTRAINDICATIONS
The decision to use postural drainage therapy requires assessment of potential benefits versus potential risks. Therapy should be provided for no longer than necessary to obtain the desired therapeutic results. Listed contraindications are relative unless marked as absolute .

1 Positioning

All positions are contraindicated for

Intracranial pressure (ICP) > 20 mm Hg(59,60)
Head and neck injury until stabilized
Active hemorrhage with hemodynamic instability
Recent spinal surgery (eg, laminectomy) or acute spinal injury
Acute spinal injury or active hemoptysis
Empyema
Bronchopleural fistula
Pulmonary edema associated with congestive heart failure
Large pleural effusions
Pulmonary embolism
Aged, confused, or anxious patients who do not tolerate position changes
Rib fracture, with or without flail chest surgical wound or healing tissue

Trendelenburg position is contraindicated for

Intracranial pressure (ICP) > 20 mm Hg(59,60) patients in whom increased intracranial pressure is to be avoided (eg, neurosurgery, aneurysms, eye surgery)
Uncontrolled hypertension
Distended abdomen
Esophageal surgery
Recent gross hemoptysis related to recent lung carcinoma treated surgically or with radiation therapy
Uncontrolled airway at risk for aspiration (tube feeding or recent meal)

Reverse Trendelenburg is contraindicated in the presence of hypotension or vasoactive medication

2 External Manipulation of the Thorax
In addition to contraindications previously listed

subcutaneous emphysema
Recent epidural spinal infusion or spinal anesthesia
Recent skin grafts, or flaps, on the thorax
Burns, open wounds, and skin infections of the thorax
Recently placed transvenous pacemaker or subcutaneous pacemaker (particularly if mechanical devices are to be used)
Suspected pulmonary tuberculosis lung contusion
Bronchospasm
Osteomyelitis of the ribs
Osteoporosis
Coagulopathy
Complaint of chest-wall pain

COMPLICATIONS
Hypoxemia
Increased Intracranial Pressure
Acute Hypotension during Procedure
Pulmonary Hemorrhage
Pain or Injury to Muscles, Ribs, or Spine
Vomiting and Aspiration
Bronchospasm
Dysrhythmias

LIMITATIONS OF METHOD
1-Presumed effectiveness of PDT and its application may be based more on tradition and anecdotal report than on scientific evidence. The procedure has been used excessively and in patients in whom it is not indicated.

2-Airway clearance may be less than optimal in patients with ineffective cough.
3-Optimal positioning is difficult in critically ill patients.

ASSESSMENT OF OUTCOME

These represent individual criteria that indicate a positive response to therapy (and support continuation of therapy). Not all criteria are required to justify continuation of therapy (eg, a ventilated patient may not have sputum production > 30 mL/day, but have improvement in breath sounds, chest x-ray, or increased compliance or decreased resistance).

1.CHANGE IN SPUTUM PRODUCTION
If sputum production in an optimally hydrated patient is less than 25 mL/day with PDT the procedure is not justified. Some patients have productive coughs with sputum production from 15 to 30 mL/day (occasionally as high as 70 or 100 mL/day) without postural drainage. If postural drainage does not increase sputum in a patient who produces > 30 mL/day of sputum without postural drainage, the continuation of the therapy is not indicated. Because sputum production is affected by systemic hydration, apparently ineffective PDT probably should be continued for at least 24 hours after optimal hydration has been judged to be present.

2. CHANGE IN BREATH SOUNDS AND LUNG FIELDS ARE DRAINED
With effective therapy, breath sounds may ‘worsen’ following the therapy as secretions move into the larger airways and increase rhonchi. An increase in adventitious breath sounds can be a marked improvement over absent or diminished breath sounds. Note any effect that coughing may have on breath sounds. One of the favorable effects of coughing is clearing of adventitious breath sounds.

3 PATIENT SUBJECTIVE RESPONSE TO THERAPY
The caregiver should ask patient how he or she feels before, during, and after therapy. Feelings of pain, discomfort, shortness of breath, dizziness, and nausea should be considered in decisions to modify or stop therapy. Easier clearance of secretions and increased volume of secretions during and after treatments support continuation.

4. CHANGES IN VITAL SIGNS
Moderate changes in respiratory rate and/or pulse rate are expected. Bradycardia, tachycardia, or an increase in irregularity of pulse, or fall or dramatic increase in blood pressure are indications for stopping therapy.

5. CHANGES IN X-RAYS
Resolution or improvement of atelectasis may be slow or dramatic.

6. CHANGES IN ARERIAL BLOOD GAS VALUE AND OXYGN SATURATION
Oxygenation should improve as atelectasis resolves.

7. CHANGE IN VENTILATOE VARIABLE
Resolution of atelectasis and plugging reduces resistance and increases compliance.

LUNG VOLUMES AND CAPACITIES

RESPIRATORY PHYSIOLOGY
The respiratory physiology is on the process of incorporation of oxygen in the environment for the utilization of energy from the organic compounds and for the elimination of carbon dioxide.

 

LUNG VOLUMES AND CAPACITIES
                              LUNG VOLUMES AND CAPACITIES

TIDAL VOLUME(500 ml)
The volume of air breathed in and out at rest is known as the tidal volume (TV). This is found to be about 500 ml in an averagely built (70 kg), healthy, young adult. The tidal volume tends to decrease in restrictive lung diseases. In restrictive lung diseases, the lungs fail to expand properly as a result of restrictive forces exerted from within the lungs (e.g. – fibrosing alveolitis) or from the thoracic wall (e.g. – severe scoliosis, ankylosing spondylitis). Weakness of the respiratory muscles (e.g. – myasthenia gravis, Guillain Barre syndrome and phrenic nerve palsy) can also give rise to restricted movements of the chest wall resulting in the reduction of the tidal volume.

INSPIRATORY RESERVE VOLUME (IRV)(3100 ml) AND
EXPIRATORY RESERVE VOLUME(ERV)(1200 ml)
In addition to the amount of air that could be inspired at rest, the lungs are capable of accommodating an additional amount of air during a deep inspiration. This amount of air that can be inhaled in addition to the tidal volume is known as the inspiratory reserve volume (IRV). Similarly, in a deep and forceful expiration, the lungs are capable of exhaling a volume which is in excess to the tidal volume and the inspiratory reserve volume. This is known as the expiratory reserve volume (ERV). In a healthy young adult, IRV measures about 3100 ml and the ERV is approximately 1200 ml.

RESIDUAL VOLUME(1200 ml)
The lungs do not collapse completely following a deep, forceful expiration. A certain volume of air remains within the lungs, maintaining the alveoli expanded and the airways patent. This volume, which cannot be expelled even after a maximally forceful expiration, is known as the residual volume (RV).

MEASURMENT OF LUNG VOLUMES – (SPIROMETRY)

The tidal volume,tidal volume, IRV and ERV can be measured using a device known as a spirometer. Here, the volume changes that occur in a closed circuit are measured while an individual is breathing through a mouthpiece into a measuring device. The volume change that occurs while the individual is engaged in quite breathing is the tidal volume. The volume that the individual inhales in excess of the tidal volume during a deep inspiration is the IRV and the volume that is exhaled in excess to the tidal volume during a deep expiration is the ERV.

MEASURMENT OF RESIDUAL VOLUME – (HELIUM DILUTION)

 

helium dilution method
                         HELIUM DILUTION METHOD

The residual volume cannot be measured with a conventional spirometer. Therefore, to measure the residual volume, several techniques have been described. In one such technique, an individual breaths into a closed circuit, which contains a known amount of Helium. Helium does not cross the blood-gas barrier and is not excreted by the lungs. Thus, decrease in the concentration of Helium is brought about by the increase in the volume of the circuit by connecting the circuit to the respiratory system. When, the concentration of Helium is measured following a deep expiration, the total volume is the volume of the breathing circuit + the residual volume. Since concentration = amount of a substance / volume of distribution, the residual volume can be calculated.

LUNG CAPACITIES-

Four capacities have been described based on the four lung volumes:

1.Inspiratory Capacity (IC) is the maximum volume of air that can be inhaled following a resting state. This can be calculated by the addition of tidal volume and the IRV-3600 ml

2.Vital Capacity (VC) is the maximum volume of air that can be exhaled following a deep inspiration. This is the total of IRV + TV + ERV- 4800ml

3.Functional Residual Capacity (FRC) is the volume of air that remains in the lungs during quite breathing. FRC = ERV + RV 2400 ml

4.Total Lung Capacity (TLC) is the volume the whole respiratory system can accommodate. Therefore, TLC= IRV + TV + ERV + RV 6000ml.

Lung capacities and lung volumes are affected in different types of physiological processes as well as in lung diseases. The specific changes that occur in different types of diseases will be described in a separate hub along with examples for different patterns of abnormalities seen in the lung volumes.

NEBULISER

DEFINITION
Nebulization is the process of medication administration via inhalation. It utilizes a nebulizer which transports medications to the lungs by means of mist inhalation.

TYPES OF NEBULISER-
There is a huge market for different types of nebulizers and each of them have some unique features although they all function in a similar way. Here are the two basic types of nebulizers available in the market:

STATIONARY NEBULISER – these are the nebulizers that are sturdy, rest on top of the table and they can provide durability as most of them come with a longer warranty period. They are cheaper than the mobile nebulizers and serve as a good aid for usage for children or elderly patients. Stationery nebulizers are mostly for indoor use only and are seldom used outdoors.

MOBILE NEBULISER – these nebulizers provide most mobility as they can be hand held and carried with the patient wherever they go. They have alternative power sources like batteries or auto adapters which enable them with usage at areas where there is no or limited access to AC power. Since they are mobile in nature, these nebulizers are lighter than the stationery ones and also smaller in size.

ULTRASONIC NEBULISER – Ultrasonic nebulizers deliver the medicine through high frequency vibrations in order to change the liquid medication into a mist to inhale and feel relaxed.

The fine mist is inhaled through an attached mask or the mouthpiece as the ultrasonic nebulizers doesn’t condense air, they function quietly and are small in size to fit into any container to begin the function. Being portable, compact and battery operated, they work fast when compared to other nebulizers and utilize the ultrasonic waves to aerosolize the liquid medication.

JET NEBULISER – A jet nebulizer is a machine which changes the prescribed liquid medicine into a fine mist to let the child or the patient breathes in through the mouthpiece or the face mask. It delivers the medicine directly to the inhaler’s lungs, making it easy to use.

These are less expensive and are usually in the form of a plastic cup which holds the medication and allows the air pass through the tube with the help of the compressor. Basically, jet nebulizers require electricity, frequently to function which is not advised safe to carry or depend on during travel. It produces loud sound and offers a range of particle sizes to change a liquid into a mist.

MESH NEBULISER – A Mesh Nebulizer is considered as the fastest working device and is more expensive when compared to the other nebulizers. It operates on a battery power supply and is quiet, efficient and well suits to the aerosolize solutions. It generates the mono-disperse aerosol particles of 4.5 to 5µm. It utilizes a vibrating membrane to generate the aerosol mist from the medication.

Available in a compact and portable body, it is perfect to carry while travelling and use in case of need. Besides this, Mesh nebulizer requires proper care, careful handling and intense cleaning as the membrane is more prone to get blocked and requires replacement many times in a year for proper function of inhalation process.

INDICATION
Nebulization therapy is used to deliver medications along the respiratory tract and is indicated to various respiratory problems and diseases such as:
•Broncho-spasms
•chest tightness
•Excessive and thick mucus secretions
•Respiratory congestions
•Pneumonia

CONTRAINDICATIONS
In some cases, nebulization is restricted or avoided due to possible untoward results or rather decreased effectiveness such as:
•Patients with unstable and increased blood pressure
•Individuals with cardiac irritability (may result to dysrhythmias)
•Persons with increased pulses
•Unconscious patients (inhalation may be done via mask but the therapeutic effect may be significantly low

EQUIPMENTS
•Nebulizer and nebulizer connecting tubes
•Compressor oxygen tank
•Mouthpies, Respiratory medication to be administered
•Normal saline solution

PROCEDURE

1.Position the patient appropriately, allowing optimal ventilation.

2.Assess and record breath sounds, respiratory status, pulse rate and other significant respiratory functions.

3.Teach patient the proper way of inhalation:

Slow inhalation through the mouth via the mouthpiece
Short pause after the inspiration
Slow and complete exhalation
Some resting breaths before another deep inhalation.

4.Prepare equipments at hand

5.Check doctor’s orders for the medication, prepare thereafter
6.Place the medication in the nebulizer while adding the amount of saline solution ordered
7.Attach the nebulizer to the compressed gas source
8.Attach the connecting tubes and mouthpiece to the nebulizer
9.Turn the machine on (notice the mist produced by the nebulizer)
10.Offer the nebulizer to the patient, offer assistance until he is able to perform proper inhalation (if unable to hold the nebulizer [pediatric/geriatric/special cases], replace the mouthpiece with mask.

COMPLICATIONS
Possible effects and reactions after nebulization therapy are as follows:
•Palpitations
•Tremors
•Tachycardia
•Headache
•Nausea
•Broncho-spasms (too mu

NEBULISERch ventilation may result or exacerbate Broncho-spasms)

•TEACHINGS
As nurses, it is important that we teach the patients the proper way of doing the therapy to facilitate effective results and prevent complications (demonstration is very useful). Emphasize compliance to therapy and to report untoward symptoms immediately for apposite intervention.

Auscultatory gap is the temporary disappearance of sounds normally heard over the brachial artery when the cuff pressure is high and the reappearance of the sounds at a lower level.

Provide excellent clues to the physiological functioning of the body.
•Alterations in body flexion are reflected in the body temp, pulse, respirations and blood pressure.
•These data provide part of the baseline info from which plan of care is developed.
•Any change from normal is considered to be an indication of the person’s state of health.

PNEUMOTHORAX AND PHYSIOTHERAPY MANAGEMENT

DEFINATION-
”A pneumothorax is an abnormal collection of air in the pleural space between the lung and the chest wall”. Symptoms typically include sudden onset of sharp, one-sided chest pain and shortness of breath. In a minority of cases the amount of air in the chest increases when a one-way valve is formed by an area of damaged tissue, leading to a tension pneumothorax.
This condition can cause a steadily worsening oxygen shortage and low blood pressure. Unless reversed by effective treatment, it can result in death.Very rarely both lungs may be affected by a pneumothorax.It is often called a collapsed lung, although that term may also refer to atelectasis.

TYPES OF PNEUMOTHORAX

TYPES OF PNEUMOTHORAX
TYPES OF PNEUMOTHORAX

The two basic types of pneumothorax are traumatic pneumothorax and nontraumatic pneumothorax. Either type can lead to a tension pneumothorax if the air surrounding the lung increases in pressure. A tension pneumothorax is common in cases of trauma and requires emergency medical treatment.

TENSION PNEUMOTHORAX
    TENSION PNEUMOTHORAX

TRAUMATIC PNEUMOTHORAX
Traumatic pneumothorax occurs after some type of trauma or injury has happened to the chest or lung wall. It can be a minor or significant injury. The trauma can damage chest structures and cause air to leak into the pleural space.

Examples of injuries that can cause a traumatic pneumothorax include:

Trauma to the chest from a motor vehicle accident
Broken ribs
A hard hit to the chest from a contact sport, such as from a football tackle
A stab wound or bullet wound to the chest
Medical procedures that can damage the lung, such as a central line placement, ventilator use, lung biopsies, or CPR
Changes in air pressure from scuba diving or mountain climbing can also cause a traumatic pneumothorax.
The change in altitude can result in air blisters developing on your lungs and then rupturing, leading to the lung collapsing.

Quick treatment of a pneumothorax due to significant chest trauma is critical. The symptoms are often severe, and they could contribute to potentially fatal complications such as cardiac arrest, respiratory failure, shock, and death.

NON-TRAUMATIC PNEUMOTHORAX-
This type of pneumothorax doesn’t occur after injury. Instead, it happens spontaneously, which is why it’s also referred to as spontaneous pneumothorax.

There are two major types of spontaneous pneumothorax:
1.primary and 2. secondary.
1.Primary spontaneous pneumothorax (PSP) occurs in people who have no known lung disease, often affecting young males who are tall and thin.
2.Secondary spontaneous pneumothorax (SSP) tends to occur in older people with known lung problems.

Some conditions that increase your risk of SSP include:

  • Chronic obstructive pulmonary disease (COPD), such as emphysema or chronic bronchitis
  • Acute or chronic infection, such as tuberculosis or pneumonia
  • Lung cancer
  • Cystic fibrosis, a genetic lung disease that causes mucus to build up in the lungs
  • Asthma, a chronic obstructive airway disease that causes inflammation
  • Spontaneous hemopneumothorax (SHP) is a rare subtype of spontaneous pneumothorax. It occurs when both blood and air fill the pleural cavity Without any recent trauma or history of lung disease.

SYMPTOMS OF PNEUMOTHORAX
The symptoms of a traumatic pneumothorax often appear at the time of chest trauma or injury, or shortly afterward. The onset of symptoms for a spontaneous pneumothorax normally occurs at rest. A sudden attack of chest pain is often the first symptom.

Other symptoms may include:

  • A steady ache in the chest
  • Shortness of breath, or dyspnea
  • Breaking out in a cold sweat
  • Tightness in the chest
  • Turning blue, or cyanosis
  • Severe tachycardia, or a fast heart rate

RISK FACTOR FOR TRAUMATIC PNEUMOTHORAX
The risk factors are different for a traumatic and spontaneous pneumothorax.

Risk factors for a traumatic pneumothorax include:

  • Playing hard contact sports, such as football or hockey
  • Performing stunts that may cause damage to the chest
  • Having a history of violent fighting
  • Having a recent car accident or fall from a height
  • Recent medical procedure or ongoing assisted respiratory care

The people at highest risk for a PSP are those who are:

  • Young
  • Thin
  • Male
  • Between the ages of 10 and 30
  • Affected by congenital disorders like Marfan’s syndrome
  • Smokers
  • Exposed to environmental or occupational factors, such as silicosis
  • Exposed to changes in atmospheric pressure and severe weather changes
  • The main risk factor for SSP is having previously been diagnosed with a lung disease. It’s more common in people over 40.

DIAGNOSIS
Diagnosis is based on the presence of air in the space around the lungs. A stethoscope may pick up changes in lungs sounds, but detecting a small pneumothorax can be difficult. Some imaging tests may be hard to interpret due to the air’s position between the chest wall and lung.

Imaging tests commonly used to diagnose pneumothorax include:

An upright posteroanterior chest radiograph

CHEST RADIOGRAPH
CHEST RADIOGRAPH

A CT scan
A thoracic ultrasound

TREATMENT

Treatment will depend on the severity of condition. It will also depend on whether you’ve experienced pneumothorax before and what symptoms you are experiencing. Both surgical and nonsurgical treatments are available.Treatment options can include close observation combined with the insertion of chest tubes, or more invasive surgical procedures to resolve and prevent further collapse of the lung. Oxygen may be administered.

OBSERVATION-
Observation or “watchful waiting” is typically recommended for those with a small PSP and who aren’t short of breath. In this case, your doctor will monitor your condition on a regular basis as the air absorbs from the pleural space. Frequent X-rays will be taken to check if your lung has fully expanded again. doctor will likely instruct you to avoid air travel until the pneumothorax as completely resolved.

Routine physical activity hasn’t been shown to worsen or delay healing of a pneumothorax. However, it’s often advised that intense physical activity or high-contact sports be delayed until the lung is fully healed and the pneumothorax is gone.

A pneumothorax can cause oxygen levels to drop in some people. This condition is called HYPOXEMIA . If this is the case, doctor will order oxygen supplementation along with activity limitations.

DRAINING EXCESS AIR
Needle aspiration and chest tube insertion are two procedures designed to remove excess air from the pleural space in the chest. These can be done at the bedside without requiring general anesthesia.Needle aspiration may be less uncomfortable than placement of a chest tube, but it’s also more likely to need to be repeated.For a chest tube insertion, doctor will insert a hollowed tube between your ribs. This allows air to drain and the lung to reinflate. The chest tube may remain in place for several days if a large pneumothorax exists.

PLEURODESIS
Pleurodesis is a more invasive form of treatment for a pneumothorax. This procedure is commonly recommended for individuals who’ve had repeated episodes of pneumothorax.During pleurodesis, doctor irritates the pleural space so that air and fluid can no longer accumulate. The term “PLEURA” refers to the membrane surrounding each lung. Pleurodesis is performed to make your lungs’ membranes stick to the chest cavity. Once the pleura adheres to the chest wall, the pleural space no longer expands, and this prevents formation of a future pneumothorax.

Mechanical pleurodesis is performed manually. During surgery, your surgeon brushes the pleura to cause inflammation. Chemical pleurodesis is another form of treatment. doctor will deliver chemical irritants to the pleura through a chest tube. The irritation and inflammation cause the lung pleura and chest wall lining to stick together.

SURGERY
Surgical treatment for pneumothorax is required in certain situations. You may need surgery if you’ve had a repeated spontaneous pneumothorax. A large amount of air trapped in chest cavity or other lung conditions may also warrant surgical repair.There are several types of surgery for pneumothorax. One option is a THORACOTOMY. During this surgery, surgeon will create an incision in the pleural space to help them see the problem. Once your surgeon has performed a thoracotomy, they’ll decide what must be done to help you heal.

Another option is THORACOSCOPY, also known as video-assisted thoracoscopic surgery (VATS). surgeon inserts a tiny camera through chest wall to help them see inside your chest. A thoracoscopy can help surgeon decide on the treatment for pneumothorax. The possibilities include sewing blisters closed, closing air leaks, or removing the collapsed portion of lung, which is called a LOBECTOMY.

PHYSIOTHERAPY MANAGEMENT

Indications for Physiotherapy

Lung collapse
Increased work of breathing
Thick sputum plugs predisposing to ventilation difficulty
Blood gas abnormalities
Sputum retention

Goals for Physiotherapy

To reinflate atelectatic lung areas
To improve distribution of ventilation
To increase oxygenation
Maintain airway clearance
Improve exercise tolerance

Physiotherapy Management
       To reduce work of breathing

  • Body positioning
  • Breathing control
  • Relaxation technique
    To improve ventilation
  • Localised thoracic expansion exercise
  • Sputum mobilisation techniques
  • Postural drainage
  • Deep breathing exercise
  • Percussion, shaking and vibrations
  • Sputum removal techniques
  • Coughing and huffing
  • Airway suctioning

Physiotherapy outcome evaluation includes

Respiratory rate
Breathing pattern
Sputum quantity
Ausculatation
Cough sound
Oxygen requirement
SpO2
Arterial blood gases
Chest x-ray changes
Muscle strength
Functional performance

LEPROSY

DEFINATION OF LEPROSY :

1 : A chronic infectious disease caused by a mycobacterium (Mycobacterium leprae) affecting especially the skin and peripheral nerves and characterized by the formation of nodules or macules that enlarge and spread accompanied by loss of sensation with eventual paralysis, wasting of muscle, and production of deformities — called also Hansen’s disease
2 : A morally or spiritually harmful influenceThe first system recognizes two types of leprosy: tuberculoid and lepromatous. A person’s immune response to the disease determines their type of leprosy.

The immune response is good and the disease only exhibits a few lesions (sores on the skin) in tuberculoid leprosy. The disease is mild and only mildly contagious.

The immune response is poor in lepromatous leprosy and affects the skin, nerves, and other organs. There are widespread lesions and nodules (large lumps and bumps). This disease is more contagious.

WHO categorizes the disease based on the type and number of affected skin areas. The first category is paucibacillary, in which five or fewer lesions with no bacteria are detected in the skin sample. The second category is multibacillary, in which there are more than five lesions, bacteria is detected in the skin smear, or both.

CLASSIFICATION OF LEPROSY :

Clinical studies use the Ridley-Jopling system. It has six classifications based on severity of symptoms. They are:

1. Intermediate leprosy: a few flat lesions that sometimes heal by themselves and can progress to a more severe type

2. Tuberculoid leprosy: a few flat lesions, some large and numb; some nerve involvement; can heal on its own, persist, or may progress to a more severe form.

3. Borderline tuberculoid leprosy: lesions similar to tuberculoid but smaller and more numerous; less nerve enlargement; may persist, revert to tuberculoid, or advance to another form.

4. Mid-borderline leprosy: reddish plaques, moderate numbness, swollen lymph glands; may regress, persist, or progress to other forms.

5. Borderline lepromatous leprosy: many lesions including flat lesions, raised bumps, plaques, and nodules, sometimes numb; may persist, regress, or progress.

6. Lepromatous leprosy: many lesions with bacteria; hair loss; nerve involvement; limb weakness; disfigurement; doesn’t regress.

TRANSMISSION OF LEPROSY :

Leprosy spreads through contact with the mucus of an infected person. This usually occurs when the infected person sneezes or coughs. The disease isn’t highly contagious. Close, repeated contact with an untreated person can lead to contracting leprosy.

The bacteria responsible for leprosy multiply very slowly. The disease has an incubation period (the time between infection and the appearance of the first symptoms) of up to five years. Symptoms may not appear for as long as 20 years.

According to the New England Journal of Medicine, an armadillo native to the southern United States can also carry and transmit the disease to humans.

SYMPTOMS :

 

BLISTER FORMATION IN LEPROSY

Symptoms mainly affect the skin, nerves, and mucous membranes (the soft, moist areas just inside the body’s openings).

The disease can cause skin symptoms such as:

A large, discolored lesion on the chest of a person with Hansen’s disease.
A large, discolored lesion on the chest of a person with Hansen’s disease.

Discolored patches of skin, usually flat, that may be numb and look faded (lighter than the skin around)
Growths (nodules) on the skin
Thick, stiff or dry skin
Painless ulcers on the soles of feet
Painless swelling or lumps on the face or earlobes
Loss of eyebrows or eyelashes
Symptoms caused by damage to the nerves are:

Numbness of affected areas of the skin
Muscle weakness or paralysis (especially in the hands and feet)
Enlarged nerves (especially those around the elbow and knee and in the sides of the neck)
Eye problems that may lead to blindness (when facial nerves are affected)
Enlarged nerves below the skin and dark reddish skin patch overlying the nerves affected by the bacteria on the chest of a patient with Hansen’s disease. This skin patch was numb when touched.
Enlarged nerves below the skin and dark reddish skin patch overlying the nerves affected by the bacteria on the chest of a patient with Hansen’s disease. This skin patch was numb when touched.

Symptoms caused by the disease in the mucous membranes are:

A stuffy nose
Nosebleeds
Since Hansen’s disease affects the nerves, loss of feeling or sensation can occur. When loss of sensation occurs, injuries such as burns may go unnoticed. Because you may not feel the pain that can warn you of harm to your body, take extra caution to ensure the affected parts of your body are not injured.

If left untreated, the signs of advanced leprosy can include:

Paralysis and crippling of hands and feet
Shortening of toes and fingers due to reabsorption
Chronic non-healing ulcers on the bottoms of the feet
Blindness
Loss of eyebrows
Nose disfigurement
Other complications that may sometimes occur are:

Painful or tender nerves
Redness and pain around the affected area
Burning sensation in the skin

LEPROSY DIAGNOSIS :

The diagnosis of leprosy is often established from the patient’s clinical signs and symptoms. A careful skin exam and neurologic exam will be undertaken by a health-care professional. If a laboratory is available, skin smears or skin biopsies may be obtained for a more definitive diagnosis. Skin smears or biopsy material that show acid-fast bacilli with the Ziel-Neelsen stain or the Fite stain can diagnose multibacillary leprosy. If bacteria are absent, paucibacillary leprosy can be diagnosed. Other less commonly used tests include blood exams, nasal smears, and nerve biopsies. Specialized tests can be done to place the patient in the more detailed Ridley-Jopling classification.

PREVENTION:

Early detection of the disease is important, since physical and neurological damage may be irreversible even if cured. Medications can decrease the risk of those living with people with leprosy from acquiring the disease and likely those with whom people with leprosy come into contact outside the home.However, concerns are known of resistance, cost, and disclosure of a person’s infection status when doing follow-up of contacts. Therefore, the WHO recommends that people who live in the same household be examined for leprosy and be treated only if symptoms are present.

The Bacillus Calmette–Guérin (BCG) vaccine offers a variable amount of protection against leprosy in addition to its target of tuberculosis. It appears to be 26 to 41% effective (based on controlled trials) and about 60% effective based on observational studies with two doses possibly working better than one. Development of a more effective vaccine is ongoing.

SELF-CARE AT HOME FOR LEPROSY

Prescribed antibiotics medications are the primary treatment for leprosy. Compliance with the full course of antibiotics is crucial to successful treatment.

Patients should also be educated to closely inspect their hands and feet for possible injuries sustained which may go unnoticed because of the loss of sensation.

1. Ulcers or tissue damage can result, leading to skin infections and disability.
2. Proper footwear and injury prevention should be encouraged.

LEPROSY TREATMENT:

Leprosy is a curable disease using the highly effective MDT (multidrug therapy).

In 1981, a World Health Organization Study Group recommended multidrug treatment with three medications: dapsone, rifampicin (Rifadin), and clofazimine (Lamprene).

This long-term treatment regimen cures the disease and prevents the complications associated with leprosy if started in its early stages.

The National Hansen’s Disease Programs (NHDP) currently recommends different treatment regimens for patients with tuberculoid and lepromatous leprosy.

NHDP recommendations:

1.Tuberculoid leprosy:

Twelve months of treatment using rifampin and Dapsone daily

2. Lepromatous leprosy
Twenty-four months of treatment using rifampin, dapsone, and clofazimine daily
The WHO recommended therapy for leprosy is given significantly shorter and less often, as this treatment policy is based upon practical considerations in countries with fewer medical resources. However, the relapses with treatment according to the WHO recommendations are significantly greater than those with the NHDP recommended therapy.

Individuals who develop type 1 or type 2 reactions may require other medications.

Type 1 reaction (reversal reaction):
Treatment may include the use of corticosteroids, salicylates, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Type 2 reaction (ENL):
Treatment may include the use of corticosteroids, salicylates, NSAIDs, clofazimine, and thalidomide (Thalomid).

SYRGICAL TREATMENT FOR LEPROSY:

There are various surgical procedures available for certain patients with leprosy. These surgical procedures are aimed at restoring function of affected body parts (for example, correcting clawed hand deformities) and to cosmetically improving areas damaged by the disease. Amputation of affected body parts is sometimes necessary. Surgery may also be necessary to drain a nerve abscess (pus collection) or to relieve the compression of nerves.

Some patients with leprosy may require psychological counseling, physical therapy, and occupational therapy.

DEFORMITIES IN LEPROSY:

Deformities occurring in leprosy:

1 .nose deformities
2. Face Deformities
3. Mask face, faces leonina, sagging face, lagophthaimos, loss of eye brows (supercilliary madorosis and eyelashes (ciliary madarosis),
4. ulcers and opacities, perforated nose, depressed nose, ear deformities, e.g. nodules on the ear and elongated lobules.

5. Hands deformities Hands deformitiesHands Deformities:

 

CLAW HAND DEFORMITY

Claw hand, wrist drop, ulcers, absorption of digits, thumb – web contracture, hollowing of the interossecus spaces and swollen hand.

6. Feet Deformities
Planter ulcer, foot drop, inversion of the foot, clawing of the toes, absorption of the toes, collapsed foot, swollen foot and callosities.

7. Other Deformities
Gynecomastia and perforation of the palate. All along it has commonly been believed that it is highly contagious and incurable. Even today, in spite of scientific information available about leprosy, it is deeply rooted in the minds of most people at all levels of society, with the result that social ostracism is apparent everywhere. This has led patients to hide their early lesions, and thereby delay treatment just at the period when they could be most speedily cured. Failure to appreciate the importance of the social and psychological factors has resulted in the failure of otherwise well conceived programs.

GOALS OF PHYSICAL THERAPY FOR NON-SURGICAL PATIENT’S OF LEPROSY DISEASE :

The major aim is to prevent or reduce complication, deformity and disability in body through Physical Therapy.

Means

The ways of reaching these Goals are-

By teaching the patient.
By treating and helping the patient.
Teachings

What the disease of leprosy is?
The possible complications and deformities resulting from leprosy.
prevention of complication, deformities and disabilities.
Treating and Helping

To respect themselves enough to take medication regularly and to take care of complications.
To protect their own anaesthetic hands, feets and eyes.
To keep their skin soft and supple.
To keep their joint flexible.
To preserve all posible movements of hands and feet.
To keep their muscles strong.
To use their hands, feet and eyes safely, in daily work

GOALS OF PHYSICAL THERAPY FOR SURGICAL PATIENTS OF LEPROSY:

To protect and prevent further damage and deformity.
To improve and restore function.
To improve appearance of hands, feet, face and eyLEPROSY AND SPLINT FOR HAND

Surgical Techniques used in Leprosy Disease

Tendon Transfer: Moving the distal end of the tendon to a new place so that contraction of muscle belly will produce a needed movements used to replace paralysed muscles. Example- Transfer of fore-arm muscle to make finger movements.
Tendon Lengthening: Lengthening the tendon of a muscle to permit more movement and reduce contracture. Example- Tendo Calcaneus lengthening.
Capsulotomy: To loosen tight joint capsule often done with tendon lengthening and tendon transfer to improve range of motions. Tighten the loose joint capsule using suture.
Arthrodesis: Elimination of unstable and deformed joints.
Tenodesis: Attach a piece of tendon across the joint to reduce the movement. The tendon then act as ligament. Example- Tenodesis of MCP joint to prevent hyperextension.
Physical Therapy Goals:

To increase and regain range of motion.
Improve muscle strength perticularly in muscles to be transferred.
Clean supple skin in areas of surgery.
Teach home self care.
Protect tissue during wearing.
Prevent/reduce swelling.
Muscle re-education after tendon transfer.
Safe use of any new restored skill in work.

PHYSICAL THERAPY TREATMENT::

For increasing/regaining ROM: ROM can be increased by soaking the skin or part in warm water and then performing passive movement to the part affected.
To improve strength specially in tendon transfer: Active exercise in all part in which surgery is performed.
Clean supple skin: It is provided by soaking the part in soap water, rubbing off thick skin, oiling, self massage and protecting the part from infection.
Home care: teaching skin, hand, foot and eye care to groups and individuals and teaching the patients actual home care.
Protect tissue during healing: Rest, body position and POP cast.
Prevent/Reduce swelling: Elevation, active and passive exercise.
Muscle Re-education after tendon transfer: Teaching new restored skills in movements provided by tendon transfer.
Self restored skills in daily work: Teaching patient ot use any new skill safely in specific task. Providing hand, eye and foot protection.

SPLINT FOR LEG