Non-Surgical Cure for Sinusitis Available

Left Maxillary Sinusitis

Balloon sinuplasty, a technique in which a balloon is inflated in the affected nasal area to clear blockage, is likely to help many patients of  acute or chronic sinusitis.

“The usual treatment was to open the nasal tract in order to reach the blockage and then remove the mucus.

Sinusitis is the inflammation of the sinuses. Sinuses are air filled cavities around nasal passage which makes skull lighter and help in conditioning of the air.  When inflammation occurs collection of secretions make head heavier and patient finds it difficult to breathe.

In this condition one is prone to catching viral or bacterial infections.

With balloon sinuplasty, the blockage can be cleared without open surgery and the patient can go home the same day.

Procedure

A wire catheter is introduced through the nostril and guided to the blockage. The catheter has a balloon in the front. Once the balloon reaches the site of blockage, it is inflated and the blockage is cleared. Then the catheter is pulled out.

Symptoms of Sinusitis

1. Reduced sense of smell, taste
2. Difficulty in breathing
3. Pain and swelling around eyes, cheeks, nose or forehead
4. Pain in upper jaw and teeth
5. Discharge of thick mucus
6. Nasal congestion
7. Cough

Making A Diagnosis In Patient of Edema

Congestive Cardiac Failure

• The edema is found on the most dependent parts of the body as gravity plays an important part.
• In an ambulatory patient edema is in the feet, ankles and legs
• In the recumbent patient it is mainly over the sacrum, lumbar region and genitalia.
• Edema is most marked in the evening.

Left ventricular failure

Here accumulation of fluid in the lung comes much earlier than edema of the feet, resulting in

• Dyspnea
• Cough
• Basal rales.

Pericardial effusion

Here since there is obstruction to the flow of blood into the right atrium, edema of feet may occur, but no edema of lungs occurs because the heart is able to pump the little blood it receives into the lungs and general circulation. It is associated with raised JVP, hepatomegaly and ascites.

Acute nephritis

• Edema is generalized and not restricted to the dependent parts of the body.
• It is more noticeable in the early morning.
• The fluid accumulates initially in the loose connective tissues, hence it is most marked around the eyelids and face.
• The cause of edema is damage to the endothelial lining of the capillaries, disturbance of fluid and sodium excretion and later also due to hypoproteinemia.

Nephrosis

The swelling is generalized and massive due to hypoproteinemia following massive albuminuria.

Hepatic (Portal hypertension):

Here ascites occurs before edema of feet. This occurs due to hypoproteinemia and compression of the hepatic branches of the portal vein. Ascites leads to pressure on the venous circulation in the lower limbs leading to edema of the legs.

Inferior vena cava obstruction

This is characterized by bilateral nondependent painless pitting edema. Collateral dilated veins are usually present in the flanks with flow of blood from below upwards.

Myxedema

Here edema is non-pitting, associated with puffy face, weight gain, weakness, alopecia, hoarse voice, rough dry skin, constipation, anemia and menstrual disturbances.

6. Allergic (Angioneurotic edema):

This often resembles myxedema with swelling over the face and limbs. There is usually intense itching and bronchospasm.

7. Nutritional:

This is characterized by dependent edema with puffiness of face, pallor and cachexia.

8. Filariasis:

In filariasis, edema occurs due to destruction of the lymphatic filter action of the lymph glands with consequent blocking and dilation of the lymph vessels. Subsequently there is transudation of lymph, rich in proteins, into the tissues. Later connective tissues proliferate leading to elephantiasis. This is characterized by unilateral non-pitting edema with rough skin. There may be history of fever with rigors especially at night and initially pitting edema. Blood smear may show microfilaria.

9. Gout:

This commonly affects the big toe with marked pain, edema and deformity of the part involved. Tophi may be present. There may be history of renal colic or renal stones.

10. Venous Thrombosis:

This is characterized by unilateral painful pitting edema.

Digital Clubbing and Its Causes

Clubbing

Clubbing is bulbous enlargement of soft parts of the terminal phalanges with both transverse and longitudinal curving of the nails. The swelling of the terminal phalanges in clubbing occurs due to interstitial edema and dilation of the arterioles and capillaries.
Clubbing develops in five steps:[1]

The red line shows the outline of a clubbed nail.

1. Fluctuation and softening of the nail bed (increased ballotability)
2. Loss of the normal <165° angle (”Lovibond angle”) between the nailbed and the fold (cuticula)
3. Increased convexity of the nail fold
4. Thickening of the whole distal (end part of the) finger (resembling a drumstick)
5. Shiny aspect and striation of the nail and skin

Causes of Clubbing

Pulmonary

• Bronchogenic carcinoma
• Lung abscess
• Bronchiectasis
• Tuberculois with secondary infection
• Diffuse fibrosing alveolitis

Cardiac

• Infective endocarditis
• Cyanotic heart disease
• Congenital heart disease

Alimentary

• Ulcerative colitis
• Crohn’s disease
• Cholangiolitic cirrhosis

Endocrine

• Iatrogenic myxedema
• Exophthalmic ophthalmoplegia
• Acromegaly

Miscellaneous

• Hereditary
• Idiopathic
• Unilateral: Pancoast tumor, subclavian and innominate artery aneurysm
• Unidigital- traumatic or tophi deposit in gout
• Only in the upper limbs in heroin addicts due to chronic obstructive phlebitis

Grades of Clubbing

Grade I: Softening of nail bed
Grade II: Obliteration of the angle of the nail bed
Grade III: Swelling of the subcutaneous tissues over the base of the nail causing the overlying skin to become tense, shiny and wet and increasing the curvature of the nail, resulting in parrot beak or drumstick appearance.
Grade IV: Swelling of the fingers in all dimensions associated with hypertrophic pulmonary osteoarthropathy causing pain and swelling of the hand, wrist etc, and radiographic evidence of subperiosteal new bone formation.

Mechanism

The exact mechanism is not known. It is believed that the stimulus for clubbing is hypoxia. Hypoxia leads to opening up of deep arteriovenous fistulas which increase the blood supply of the fingers and toes causing it to hypertrophy.

Another hypothesis is that when reduced ferritin in venous blood escapes oxidation in the lungs and enters the systemic circulation., it causes dilation of arterio-venous anastomosis and hypertrophy of the terminal phalanx resulting in clubbing.

Pseudoclubbing

In hyperparathyroidism excessive bone resorption may result in disappearance of the terminal phalanges with telescoping of soft tissues and a drumstick appearance of the finger resembling clubbing. However, the curvature of the nail is not present.

Schamroth’s test or Schamroth’s window test

This test was originally demonstrated by South African cardiologist Dr Leo Schamroth on himself and  is a popular test for clubbing.

When the distal phalanges (bones nearest the fingertips) of corresponding fingers of opposite hands are directly apposed (placed against each other back to back), a small diamond-shaped “window” is normally apparent between the nailbeds.

If this window is obliterated, the test is positive and clubbing is present.