What causes ankle disorders?

What are the symptoms of ankle disorders?

Endometriosis is a medical condition that occurs when the lining of the uterus, called the endometrium, grows in other places, such as the fallopian tubes, ovaries or along the pelvis. When that lining breaks down, like the regular lining in the uterus that produces the menstruation, it has nowhere to go. This causes cysts, heavy periods, severe cramps and even infertility.

The endometrial tissue may also grow in the vagina, cervix, bowel or bladder, and in rare cases it may spread to other parts of the body, such as the lungs.

What is an atrial septal defect?

An atrial septal defect or ASD is an opening between the upper two chambers of the heart, known as the right atrium and the left atrium. A congenital heart defect, an ASD permits mixing of deoxygenated blood returning to the heart from the body (right atrium) and freshly oxygenated blood coming from the lungs (left atrium). The degree of mixing is largely related to the size of the defect and the relative pressures in each atrium. Early in life, blood from the left atrium preferentially moves into the right atrium, causing excessive blood to flow through the lungs. If this flow, otherwise known as “shunting” is significant enough, resistance to flow develops in the lung resulting in a gradual reversal of shunting of deoxygenated blood from the right atrium into the left atrium and subsequently through the body. This latter condition can lead to a condition called “cyanosis” whereby inadequately oxygenated blood is delivered to the body causing early fatigue and congestive heart failure.

How is an atrial septal defect treated?

Small atrial septal defects can often be followed conservatively without surgery, due to minimal shunting. Larger ASDs should be closed to prevent the late irreversible consequences of excessive left-to-right shunting. ASDs can be closed surgically by simply sewing them closed or, in the case of larger ASDs, placing a patch of the patient’s own tissue or synthetic material (e.g., Dacron) over it.

How is an atrial septal defect repaired?

ASD repairs require the use of cardiopulmonary bypass, otherwise known as “the heart-lung machine.” This permits the surgeon to safely open the right atrium and access the ASD in a relatively bloodless field. In some cases, the heart is also stopped for 1 to 2 hours to facilitate the repair. Repairs range from relatively simple operations to more complex procedures depending on the location, size, and characteristics of the ASD. The total duration of the operation ranges from 2 to 3 hours.

What are minimally invasive approaches to an atrial septal defect?

The most common surgical approach requires the surgeon to saw open the breastbone and spread the edges apart to gain direct access to the heart. Although this approach provides excellent access to the heart, the resulting wound requires several months to heal completely, an extended recovery period with substantial activity restrictions, and can be subject to serious complications including infection, breakdown, and even death.

Mini-ASD Repair

Currently at The Johns Hopkins Hospital, the most commonly employed minimally invasive approach to ASDs is a “mini-thoracotomy” which consists of a 3 inch incision made through the right side of the chest between the ribs. Heart-lung bypass is instituted with small tubes placed in the main artery and vein of the right leg through a 1 to 2 inch incision placed in the right groin crease. The heart is then stopped and the right atrium is opened to expose the ASD. At this point, specialized hand-held “chopstick” like instruments are inserted through this small incision by the surgeon to repair the defect. After the defect is repaired, the heart is then closed and restarted. Finally, heart-lung bypass is discontinued and the incisions are closed.

 

 

 

Systemic sclerosis (SSc) is a multisystem autoimmune disease in which there is increased fibroblast activity resulting in abnormal growth of connective tissue. This causes vascular damage and fibrosis. Fibrosis occurs in skin, the gastrointestinal (GI) tract and other internal organs.

The name scleroderma is derived from the Greek for ‘hard skin’ and emphasises the dermatological component of the disease. It was described by Hippocrates. There is a localised form of scleroderma, also known as morphoea

General features

• Fatigue.
• Weight loss.

Skin features

• Signs in the hand:
  • Swelling (non-pitting oedema) of fingers and toes – a common early sign; digits may look sausage-like; hand movement may be limited.
  • Skin becomes hard and thickened – this may limit joint movement or cause joint contractures; in the fingers, this is known as sclerodactyly.
  • Swelling and sclerosis reduce hand movements, so patients may be unable to make a fist, or to place the palmar surfaces together – the ‘prayer sign’.
  • Fingertips may have pitting, ulcers or loss of bulk from finger pads.
  • Raynaud’s phenomenon. This is the most common symptom and is present at some point in 90% of cases. Raynaud’s phenomenon with puffy fingers is thought to be a cardinal sign of likely SSc.
• Calcinosis – nodules or lumps of chalky material which may break through the skin.
• Face and mouth:
  • Tightening of facial skin.
  • Tight lips (microstomia) – can make dental hygiene difficult.
• Telangiectasia.
• ‘Salt and pepper’ appearance of skin, due to areas of hypopigmentation and hyperpigmentation.
• Dry or itchy skin; reduced hair over affected skin areas.

Musculoskeletal features

• Joint pain and swelling.
• Myalgia (due to inflammatory myopathy).
• Restriction of joint movement, contractures and muscle atrophy due to skin sclerosis.
• Tendon friction rubs – palpable/audible over the flexor/extensor tendons of the hands, knees and ankles.

GI features

• Heartburn and reflux oesophagitis.
• Oesophageal scarring and dysphagia.
• Delayed gastric emptying – eg, fullness after meals.
• Reduced small bowel motility – can cause bacterial overgrowth, with bloating, malabsorption, diarrhoea and malnutrition.
• Constipation due to reduced colonic motility.

Pulmonary features

• Pulmonary fibrosis (interstitial lung disease):
  • Occurs in as many as 75% of scleroderma patients, but only a few develop end-stage disease.
  • Causes restrictive lung disease.
  • Symptoms and signs: exertional dyspnoea, cough, coarse basal crackles.
• Pulmonary arterial hypertension (PAH):
  • Occurs in about 10-15% of patients with scleroderma.
  • A leading cause of death in SSc. The presence of PAH drastically reduces survival rate.
  • Symptoms and signs: exertional dyspnoea, syncope, right ventricular strain features.
  • Recent research has attempted to define predictive screening tools. These include monitoring lung function, ECG, urate levels, and N-terminal prohormone of brain natriuretic peptide (NT-proBNP); and by taking into account anti-centromere antibody (ACA) presence and history or presence of telangiectasia.

Management of GI symptoms

For upper GI symptoms:

• Maintain upright posture after meals; raise the head of the bed; limit alcohol.
• Proton pump inhibitors.
• May also need H2-receptor antagonists and pro-motility agents (metoclopramide or domperidone).
• Dilatation of oesophageal strictures if required.

For intestinal bacterial overgrowth and malabsorption:

• Cyclical antibiotics.
• Nutritional advice and nutritional supplements; rarely, parenteral nutrition is required.

For constipation:

• Dietary fibre and good fluid intake.
• Softening laxatives (such as lactulose) and/or soluble fibre (such as ispaghula).

Management of pulmonary disease

Pulmonary fibrosis (interstitial lung disease)

• Benefits of cyclophosphamide seem clear, but must be weighed against side-effects.
• Supportive treatment: prompt treatment of chest infections – oxygen if needed.

Pulmonary arterial hypertension (PAH)

• Drug treatment of PAH has improved recently and includes:
  • Endothelin receptor antagonists – eg, bosentan or sitaxsentan.
  • Vasodilators – eg, sildenafil.
  • Prostaglandin derivatives – eg, iloprost (nebulised or intravenous) or epoprostenol (infusion).
• Supportive treatment – eg, oxygen.

Complications

GI complications

See also specific GI sections under ‘Clinical features’ and ‘Management’ headings.

• Malnutrition due to swallowing problems and other digestive issues.
• ‘Watermelon stomach’ (gastric antral vascular ectasia):
  • May cause anaemia and GI bleeding.
  • May need endoscopic laser coagulation to prevent bleeding.
• Obstruction and pseudo-obstruction:
  • Can occur due to reduced motility and bacterial overgrowth.
  • Can be complicated by perforation and peritonitis.
  • Pseudo-obstruction is treated initially by bowel rest and antibiotics.
  • Laparotomy may be needed.
• Anorectal dysfunction:
  • In some cases, the rectum and anus are involved, causing faecal incontinence.
  • This may require surgery.

Scleroderma renal crisis

• A serious complication with features of accelerated hypertension.
• Can lead to renal failure if not treated promptly.
• Occurs in 5-10% of patients with scleroderma and is more common in those with diffuse or rapidly progressive disease.
• Presentation:
  • Usually presents as accelerated hypertension with oliguria, headache, fatigue, oedema, rapidly rising serum creatinine levels, proteinuria and microscopic haematuria.
  • Scleroderma renal crises can occur with apparently normal blood pressure, but the blood pressure is higher than baseline values – hence the importance of regular blood pressure monitoring.
• Treatment is with angiotensin-converting enzyme (ACE) inhibitors, plus dialysis if necessary.
• Testing patients with scleroderma for anti-RNA polymerase III antibodies may help identify at-risk patients.

Pulmonary complications

• Aspiration pneumonia from severe reflux.
• Respiratory muscle weakness if there is severe myositis or extensive skin disease involving the chest.
• Pneumothorax

Cardiac complications

• Many different cardiac abnormalities can be associated with SSc. These include:
  • Microvascular coronary artery disease (with resultant myocardial ischemia).
  • Myocardial fibrosis.
  • Left ventricular (LV) systolic dysfunction, LV diastolic dysfunction.
  • Pericarditis or pericardial effusion; these may cause cardiac impairment or congestive cardiac failure.
  • Arrhythmias and conduction defects (including bradyarrhythmias and tachyarrhythmias).
• The wide variety of abnormalities makes it difficult to assess prevalence. It is likely that the subclinical cardiac involvement rates are very high.
• Treatment is according to the clinical features.

Other complications

• Erectile dysfunction.
• Depression.
• Osteoporosis – due to reduced blood flow.
• Hypothyroidism may be associated.

 

Treatments:

Management: general

There is no cure for SSc, and management consists of controlling symptoms and preventing complications.

Monitoring

Regular monitoring and reviews are aimed at early detection and treatment of complications. Monitoring includes:

• Regular review of symptoms.
• Blood pressure monitoring.
• Renal function monitoring.
• Lung function tests and chest CT scan.
• ECG and echocardiography.

Non-drug treatments

• Patient involvement and education:
  • ‘Expert patient’ programmes and the Scleroderma Society.
  • Awareness of urgent problems such as renal crisis or intestinal obstruction symptoms.
• Physiotherapy to promote joint mobility and muscle strength.
• Home exercises to maintain range of motion (such as gentle mouth, face and hand stretches).
• Avoid tobacco and maintain healthy weight.
• Nutritional advice, and supplements if needed.
• For Raynaud’s phenomenon:
  • Prevention – avoid cold and trauma; use warm clothing or heated clothing.
  • For an attack – warm the body, hands and feet gently (the skin may be numb and unable to feel if the heat source is too hot); use gentle arm movements or gentle massage to help restore circulation.
• Occupational therapists – for adaptations to assist in daily living.
• Camouflage products – for cosmetic help with skin changes.

 

 

What is Idiopathic Thrombocytopenic Purpura (ITP)?

Idiopathic thrombocytopenic purpura (ITP) is a platelet disorder that occurs in people who have an abnormally low number of platelets in the blood. Platelets are essential in forming blood clots, which consist of a mass of fibers and blood cells. Platelets travel to a damaged or cut area of the body and stick together to form a clot. Having fewer platelets can result in easy bruising, bleeding gums and internal bleeding.

Idiopathic means the cause is unknown.
Thrombocytopenia means a decreased number of platelets in the blood.
Purpura refers to the purple discoloring of the skin, as with a bruise.

Acute thrombocytopenic purpura is most commonly seen in young children (2 to 6 years old). The symptoms may follow a viral illness, such as chicken pox. Acute ITP usually has a very sudden onset, and the symptoms usually disappear in less than six months (often within a few weeks). The disorder usually does not recur. Acute ITP is the most common form of the disorder.
Chronic thrombocytopenic purpura can happen at any age, and the symptoms can last a minimum of six months or several years. It is more common in adults than in children, but it does affect adolescents. Two to three times more females have ITP than males. Chronic ITP can recur often and requires continual follow-up care with a hematologist.
What are the causes of ITP?

In most cases, the cause of ITP is unknown. It is not contagious, meaning a child cannot “catch it” from playing with another child with ITP. It also is important to know that nothing the parents or the child did caused the disorder.

Often, the child may have had a virus or viral infection approximately three weeks before developing ITP. It is believed that the body’s immune system, when making antibodies to fight against a virus, “accidentally” also made an antibody that can stick to the platelet cells. The body recognizes any cells with antibodies as foreign cells and destroys them. Doctors think that in people who have ITP, platelets are being destroyed because they have antibodies. That is why ITP is also referred to as immune thrombocytopenic purpura.

Although there has been research looking at whether certain medications can cause ITP, no direct link has been made with any specific medication that may cause ITP.

What are the symptoms of ITP?

A normal platelet count is 150,000 to 450,000. With ITP, the platelet count is less than 100,000. By the time significant bleeding occurs, the child may have a platelet count of less than 10,000. The lower the platelet count, the greater the risk of bleeding.

Because platelets help stop bleeding, the symptoms of ITP are related to increased bleeding. However, each child may experience symptoms differently. Symptoms can include:

1. Purpura, which is the purple color of the skin after blood has “leaked” under it.
2. A bruise is blood under the skin.
3. Children with ITP can have large bruises from no known trauma. Bruises can appear at the joints of elbows Petechia, which are tiny red dots under the skin caused by very small bleeds.
4. Nosebleeds.
5. Bleeding in the mouth and/or in and around the gums.
6. Blood in the vomit, urine or stool.
7. Bleeding in the head, which is the most dangerous symptom of ITP.

Any head trauma that occurs when there are not enough platelets to stop the bleeding can be life-threatening.
The symptoms of ITP can resemble other blood disorders or medical problems. Always consult your child’s physician for a diagnosis.

How is ITP diagnosed?

In addition to a complete medical history and physical examination, diagnostic procedures for ITP can include:

Complete blood count (CBC), which is a measurement of size, number, and maturity of different blood cells in a specific volume of blood.
Additional blood and urine tests to measure bleeding time and detect possible infections.
Careful review of the child’s medications.
A bone marrow aspiration, which involves taking a small amount of bone marrow fluid, to look at the production of platelets and to rule out that any abnormal cells the marrow may be producing could lower platelet counts.
Treatment

A child’s specific treatment plan, including the frequency of visits, the length of treatment, side effects and long-term effects are determined by the:

Child’s age, overall health, and medical history
Extent of the disease
Child’s tolerance for specific medications, procedures, or therapies
Expectations for the course of the disease
The patient and family’s opinion or preference
Not all children with ITP require treatment. Close monitoring of a child’s platelets and prevention of serious bleeding complications may be the course of action chosen until the body is able to correct the disorder on its own.

When treatment is necessary, the two most common forms of treatment are:

Steroids, which can help prevent bleeding by decreasing the rate of platelet destruction. Steroids, if effective, will increase platelet counts within two to three weeks.
Intravenous gamma globulin (IVGG), a protein that contains many antibodies and also slows the destruction of platelets. It works more quickly than steroids (within 24 to 48 hours).
Other treatments for ITP can include:

Immune globulin, which is a medication that temporarily stops the spleen from destroying platelets. A child must be Rh positive and have a spleen for this medication to be effective.
Medication changes, because when a medication is the suspected cause, stopping the use of or changing the medication may be necessary.
Infection treatment to increase platelet counts, if infection is the cause for ITP.
Splenectomy to remove a child’s spleen if the spleen is the site of platelet destruction. This is considered more often in older children with chronic ITP.
Hormone therapy in teenage girls to stop their menstrual cycle when their platelets are low if excessive bleeding occurs.
Preventing bleeding

Parents of a child with ITP need to be aware of how to prevent injuries and bleeding. Consider the following:

Making the environment as safe as possible for young children by padding a crib, having the child wear a helmet, and providing protective clothing when platelet counts are low.
Restricting contact sports, riding bicycles, and rough play may be necessary.
Avoiding medications that contain aspirin, ibuprofen, naprosen, or other non-steroidal anti-inflammatory drugs because they may interfere with the body’s ability to control bleeding.
Discuss prevention measures with the child’s physician.

“Heart Attack”, technically termed Myocardial Infarction, is a result of total blockage of the blood vessel (coronary artery) which supplies blood to the heart. The blockage is due to the formation of plug composed of cholesterol, blood cells, fibrin and calcium. The heart attack may manifest with a sudden onset of severe central chest pain described as heavy, compressing pain, which can radiate to the left hand, jaw or to the back. It is often associated with profuse sweating and weakness. The presentation can be so sudden that the patient suddenly collapses and becomes unresponsive with profuse sweating and cold peripheries.

A patient with the above mentioned symptoms has to be rushed to the nearest hospital equipped with ECG facilities and a physician / cardiologists on call. Emergency measures include supplemental oxygen through a face mask, pain relief with strong analgesics, intravenous access and initial dose of aspirin and statins (lipid lowering drug). Once the diagnosis of heart attack is confirmed, the treatment is initiated. The important aim of early institution of treatment is to save the heart muscle from damage following lack of blood supply. Blood thinning medications, drugs that improve demand-supply imbalance (beta blockers), drugs that reduce blood cholesterol (statins) and drugs that improve the remodeling of the heart after the attack (ACE inhibitors) form the mainstay of management of heart attacks.

However, the most important component of the treatment consists of Conventional Thrombolytic Therapy -Using clot dissolving medications like Streptokinase, Urokinase or Recombinant TPA to improve blood flow.

Primary Percutaneous Coronary Intervention or Primary Angioplasty (PCI)-An emergency coronary angiogram (to visualize the blockade) followed by balloon Angioplasty with stenting thereby improving the blood flow.

Both methods have got their own merits and demerits. Advantages of primary PCI are that the blockage is visualized, opened and stented, ensuring normal blood flow. The chances of recurrent heart attack, recurrent block and death are less when compared to the clot dissolving medications. Disadvantages include inadequate availability of cathlabs with trained professionals who could perform PCI, and the high cost of the procedure.

Thrombolysis with clot dissolving medications is a time-tested method of treatment. The chief advantage is its universal availability at affordable cost. The disadvantages are the lesser degree of blood flow improvement (54% success rate when compared to 93-98% success with primary PCI), bleeding complications and allergic reactions.

Whatever may be the modality of treatment, the earlier it is instituted the better will be the outcome for the patient. The first one hour is called “The Golden hour” and if treatment as described above is given, the complications and mortality are significantly reduced.

Leg veins come in many shapes and sizes. Spider veins are generally characterized as smaller blue, red, and purple veins. Varicose veins are characterized as large, ropy, bulging, and sometimes painful veins.

Where did these visible leg veins come from?

There are many different factors that contribute to spider veins and varicose veins including age, occupations that involve long periods of sitting and standing, childbirth, hormones, obesity, history of blood clots, and heredity.

How do I know if I have Varicose Veins?

Visible bulging or ropy veins are usually an indication of varicose veins. Other indications are pain in the legs, ulcers, swelling, leg cramps or pinching sensations, as well as no response to cosmetic vein treatments. An ultrasound is used to determine if varicose veins are present.

What exactly are varicose veins and how are they treated?

The legs are made up of a series of one way valves that carry blood to the heart. If there is reflux present the blood is coming back down instead of going one way. The good news is that varicose veins are treatable and with minimal downtime. Endovenous Laser Therapy is a minimally invasive surgical procedure that allows patients to return to their normal activities directly post treatment. If you don’t have varicose veins and are unhappy with leg vein appearance there is a treatment called sclerotherapy that diminishes the appearance of the veins with just a few injections.

Causes:

There is no one single factor that causes breast cancer. Breast cancer is multi-factorial disease caused by a combination of stress, abdominal obesity, smoking, lack of exercise, alcohol, pollution, birth control pills, delayed breast feeding, large breasts, advancing age and genetic factors. You do not have to have all these factors get breast cancer but the more factors you have the more likely that you get breast cancer.

Symptoms: