Short Essay on Mesothelioma

Author: admin  //  Category: Homeopathy General, Oncology, Respiratory Diseases

Mesothelioma


It is a rare tumour complicating asbestos exposure.

Clinical Features

The person develops cough, severe progressive exertional dyspoea

Signs:

Finger clubbing on auscultation during the end of inspiration end inspiratory basal crackles
1. Chest X-ray shows linear shadowing of the basal areas of lung like a honey comb appearance
2. Calcified pleural plaques are seen on X-ray giving a shaggy appearance

Prevention:

Only by a detailed occupational history. 
Protective measures during work.
Avoid smocking.

Treatment:

Commonly using medicines are:-

Ars.alb, Ars.iod, Aur, Apis, Carb.an, Carb.veg, Con., Hydr., Kali.ars, Kali. cy, Phyt., Sil, Thuja

ICTHYOSIS AND ITS HOMOEOPATHIC MANAGEMENT

Author: shebees  //  Category: Disease Conditions, Homeopathic Therapeutics, Skin Diseases

ICTHYOSIS AND ITS HOMOEOPATHIC MANAGEMENT

SREEJA L

dr.sreeja.l@gmail.com

Ichthyosis means resemblance to fish skin.  It is a hereditary disorder of keratinisation.  Skin became dry and scaly.

Different types:

Ichthyosis Vulgaris
:

It is inherited as an autosomal dominant gene.  Lesions are usually not present at birth.  Lesions develop between 1-4 years of age.  Lesions present all over the body sparing flexors like cubital and popliteal fossae, axillae and groins, even in the most severe forms.  The lesions consists of dirty brown, angulated scales.  The scales are more prominent on the extensor surface of the back than chest and abdomen.  In children face ad scalp are initially affected but rend to clear later.  In addition, some patients show increased marking of palms and soles.  Follicular hyperkeratotic papules are present on the shoulders, arm, buttocks and thighs.  Usually the lesions are asymptomatic but some times irritation occur especially during winter season.  The lesions improved during summer months and get aggravated during winter.  Some times the lesions persist throughout life there is some spontaneous improvement at puberty.

Treatment

Ars. Iod
:
Skin dry, scaly,, itching
Marked exfoliation of skin in large scales leaving a raw exuding surface beneath
Ichthyosis, enlarged scrofulous glands.
Graphitis:
Rough, hard, persistent dryness of portions of skin unaffected by eczema.
Unhealthy skin
Cracks in nipples, mouth, between toes, anus
Burning and stinging pain
< Warmth, at night, during and after menstruation
> In the dark, from wrapping up.
Petroleum
Itching at night
Skin dry, constricted, very sensitive, cough and cracked leathery
Thick, greenish crusts, burning and itching, redness, raw, cracks bleed easily.
Thyroidinum
Skin dry, impoverished.
Cold hands and feet
Icthyosis lupus.
Itching without eruption, worse night
Sulphur
Dry, scaly, unhealthy
Every little injury suppurates
Itching, burning, worse scratching and washing.
Excoriation, especially in folds.
Skin affection after local medication.
Pruritus especially from warmth, in evening, often recurs in spring-time,damp weather.

X-Linked Ichthyosis

It is transmitted through a recessive gene located on the distal short arm of the x-chromosome.  It is transmitted by females, but seen in the males.  In such patients there is a deficiency of an enzyme called steroid sulphatase.  It appears more or less like icthyosis vulgaris unlike it is more widespread and involves the cubital and popliteal fossae also.  Follicular hyperkeratolic papules on shoulders, buttocks and thighs.  It does not improve at puberty.  Scales may be present on the side of face and even scalp.  Between 20-30 years of age corneal opacity may develop in majority of the patients.  Some times associated with cryptorchidism, hypogenitalia and mental retardation.

Treatment:

Aur, Clc., Nat-m., Thuja, Platina

Lamellar Ichthyosis:

It is inherited through autosomal recessive gene of variable expression.  Clinical features include erythema and hyperkeratosis, erythema with scaling, which is more severe on flexors.  The skin smooth, shiny and shows fine wrinkles when passed between the thumb and the index
finger.  The face and scalp are usually scaly.  The scalp may even be crusted.  It is associated with corneal dystrophes, photo phobia, small stature and mental retardation.

Treatment:

Nat-c, Bell, Aur, Calc-f, Plat.,Sil,Zinc.s, Nat.c

Nat-Carb

  • Inclination to perspire easily, or dry, rough, cracked skin.
  • Eruption on finger-tips, knuckles and toes.
  • Soles of feet raw and sore.

Calc-Flur

  • Marked whiteness of skin.
  • Chaps and cracks.
  • Fissures or cracks in the palms of the hands and hard skin
  • Fissure of the anus

Bell.

  • Dry and hot skin
  • Swollen, sensitive
  • Burns scarlet, smooth
  • Eruptions like scarlatina suddently spreading
  • Erythema, pustules on face
  • Alternate redness and paleness of skin
  • Induration afger inflammation
  • Erysipelas


Epidermolytic Hyperkeratosis

It is also known as bullous vatiety of ichtyoriforn erythioderma and is transmitted by an autosomal dominant gene.  The affected children develop crops of bullae and occasionally erythema and also desquamation within a few hours to a week after birth. Bulllae are followed by hyperkeratotic lesions.  Irregular even linear warty lesions are seen specially on flexors like axillae cubital and popliteal fossae, groins and some time even on neck, dorsum of the hands and feet.  In some cases lesions may offensive due to secondary infection.  In some patients palmo-plantar keratoderma is seen.  Skin is generally dry.

Treatment

Alum., Sal-ac, Calc-f, Thuja

Salicylicum acidium:

  • Itching vesicles and pustules, better by scratching.
  • Sweat without sleep
  • Urticaria
  • Hot and burning skin
  • Purpura
  • Herpes zoster

ECZEMA

Author: admin  //  Category: Disease Conditions, Skin Diseases

ECZEMA

Dr. Mujeeb Rehuman

drmujeebrehuman@rediffmail.com

The term eczema and dermatitis are synonymous. They refer to distinctive reaction pattern in the skin, which can be either acute or chronic.

Acute eczema

  • Ø Redness, swelling, usually with ill defined margins.
  • Ø Papules, vesicles and more rarely large blisters.
  • Ø Exudation and cracking.
  • Ø Scaling.

Chronic eczema

  • Ø Many show all of the above features, though it is usually less vesicular and exudative.
  • Ø Lichenification, a dry leathery thickening with increased skin markings and is secondary to rubbing and scratching.
  • Ø Fissures and scratch marks.
  • Ø Hypo or hyper pigmentary changes.

Clinical Features

1. Atopic eczema: The cardinal feature of atopic eczema is itch and scratching. Widespread dryness of skin is another feature. The eczema is often acute and involves the face and trunk. The napkin areas are frequently spared. The rash settles on the back of the knees, front of the elbow, wrist and ankles in childhood. In adults the face and trunks are more involved. Lichenification is common.
2. Seborrhoeic eczema: This condition is characterized by a red scaly rash classically affecting the scalp, central face, nasolabial folds, eyebrows and central chest. It is due to pityrosparum ovale infection.
3. Discoid eczema: This is a common form of eczema recognized by discrete coin shaped lesion of eczema seen on the limbs of young men, associated with alcohol excess and of elderly men.
4. Irritant eczema: Detergents, alkalies, acids, solvents and abrasive dusts are common causes. There is a wide range of susceptibility to weak irritants. The elderly those with fair and dry skin and atopic background are especially vulnerable. Napkin eczema in babies is the commonest example.
5. Allergic contact eczema: This is due to delayed hypersensitivity reaction following contact with antigens or haptens. Previous exposure to allergen is required for sensitization and the reaction is specific to the allergen or closely related to chemicals.
6. Asteatotic eczema: This is seen in hospitalized elderly, especially when the skin is dry. Low humidity caused by central healing, over washing and diuretics are contributory factors. It occurs most often on the lower legs as a rippled or ‘crazy paving’ pattern of fine fissuring on an erythematous background.
7. Stasis eczema: This occurs on the lower legs and is often associated with signs of venous insufficiency (oedema, red or bluish discolouration, loss of hair, indurations, hemosiderin pigmentation and ulceration).
8. Lichen planus: This describes a plaque of lichenified eczema due to repeated rubbing or scratching as a habit or in response to stress. Common sites include the neck, lower legs, and the ano-genital areas.

Investigation of eczema

Ø Patch test: In suspected case of contact allergic dermatitis.

Ø Specific IgE: These are occasionally performed to support the diagnosis of atopic eczema and to determine specific allergens.

Ø Prick test: The indications are same for specific IgE but are less commonly performed.

Ø Microscopy and culture test: Tests in suspected secondary infection. Skin swabs for bacteriological assessment invariably reveal the presence of bacteria.

MIASMATIC BASIS

Eruptions suppressed by local means have produced the following skin diseases, according to Hahnemann.

All skin eruptions are either secondary or tertiary expressions of miasmatic actions. The skin is the mirror or reflector of the internal stress, the internal dynamis, the internal working of the human machine. It has in the skin its reflections, its kaleidoscope, and its kinetoscopic views of its internal movements and its multiple shading of disease, its lights and its shadows that go to make up a picture thrown upon that human canvas, the skin, showing much of perverted life action in the organism.

Pathologically speaking, we look upon the outer man for signs, for marking or penciling that tell of the kind of life within the organism itself. Sometimes these pencilling are like the shadowgraphs, showing only faint trainings of the presence of a latent miasm and again they may be well defined and well developed even to physiological changes of form, colour and proportions. When we look upon these lesions of skin as local states or changes in itself, we simply ignore that co-operative principle that rules throughout the organism as a whole and we attribute that power to a part and not that which governs the whole. Therefore our therapeutic efforts are themselves misdiverted and instead of directing the perverted forces, we misguide them, bringing about nothing but confusion.

It was upon the skin that Hahnemann first saw the true psoric vesicle. It was there he first became familiar with psora as it came forth or receded under the potent influence of the applied law (similia). It was there that the mysterious veil was sent or lifted and he was permitted to look into the psoric mystery and see the true etiology of disease.

The skin of psora is dry, rough, dirty or unhealthy looking, has an unwashed appearance. Pruritis, very little suppurative in psoric skin disease, apt to be dry with scanty suppuration, seropurulent and occasionally bloody. Eruptions often papular in form accompanied by intense itching. Psora presents with normal colour of skin unless there is an inflammatory process. Itching scales and crusts thin and light, fine and small and usually quite general over the affected part. Vesicles of the itch, voluptuous tickling itching. Patient rubs and scratches, better for a few moments after which there is a long continuous burning of the affected part late in evening and before midnight. This itching is more frequent and more un bearable. Eczema with papular eruption. Eruption formed about the joints, flexors of the body or arranged in circular groupings, rings ,or segments of circles. The copper coloured or raw ham coloured or brownish or very reddened at their base. Scales and crusts thick and heavy patchy and in circumscribed spots.

Eczema with pustular is pseudo-psoric. Eczema exfoliata is sycotic. Condylomata will reveal the presence of both syphilis and sycosis and also verucae accuminata, pointed papillary growths, cox’comb and warts. The malignancies of psora snd syphilis are prone to develop at the age of 40. It is the tubercular diathesis that complaints all over skin diseases and makes them so difficult to remove. Malignancies may develop at any areas. Malignancies of skin are more violent intiactable in proportion as the sycotic taint is increased.

Erythematous eczema comes under sycotic miasm. Psora spends its force when suppressed, upon the venous system largely or upon the nerve centers often producing nervous and mental phenomenon of a serious character, all ameliorated when eruption is thrown upon the skin. There is no itching in syphilitic, very little soreness. Itching is wholly psoric symptom. The vesicle is also a psoric lesion when found in non syphilitic cases. If scalp is affected in psora, the scaly condition is quite universal while in other conditions like syphilis or sycosis, it is patchy or in circumscribed spots. The skin looses all moisture and becomes exceedingly dry and free from oil or sebaceous secretions we recognize it by the touch in psora. It is very oily or greasy; we will find the sycotic element present or the pseudo psoric. Skin affections with glandular involvement will necessarily have the syphilitic or the tubercular element to confirm with the glandular involvement.

All throughout Hahnemann’s experience the suppression of pseudo psoric eruption produces hemorrhages, spasms, convulsions, coma and death. It has also produced reflexes of all kinds, nervous disorder, asthma, paralysis stomach and intestinal disorders, catarrhal conditions and chronic cough. When the tubercular taint is present we have dyspnoea, infiltration of lung, pneumonia, chronic lung affection, tuberculosis and especially chest diseases.

Treatment of eczema can be achieved only by means of anti miasmatic remedy either anti psoric or anti syphilitic or anti sycotic depending on the dominant miasm which the patient has.

Dr. Mujeeb Rehuman

drmujeebrehuman@rediffmail.com

APPENDICITIS

Author: admin  //  Category: Disease Conditions, Inflammatory Diseases

APPENDICITIS

The appendix is a closed-ended, narrow tube up to several inches in length that attaches to the cecum (the first part of the colon) like a worm. (The anatomical name for the appendix, vermiform appendix, means worm-like appendage.) The inner lining of the appendix produces a small amount of mucus that flows through the open center of the appendix and into the cecum. The wall of the appendix contains lymphatic tissue that is part of the immune system for making antibodies. Like the rest of the colon, the wall of the appendix also contains a layer of muscle, but the muscle is poorly developed.

Appendicitis (or epityphlitis) is a condition characterized by inflammation of the appendix. While mild cases may resolve without treatment, most require removal of the inflamed appendix, either by laparotomy or laparoscopy. Untreated, mortality is high, mainly due to peritonitis and shock. Reginald Fitz first described acute appendicitis in 1886, and it has been recognized as one of the most common causes of acute abdomen pain worldwide.

It is thought that appendicitis begins when the opening from the appendix into the cecum becomes blocked. The blockage may be due to a build-up of thick mucus within the appendix or to stool that enters the appendix from the cecum. The mucus or stool hardens, becomes rock-like, and blocks the opening. This rock is called a fecalith (literally, a rock of stool). At other times, the lymphatic tissue in the appendix may swell and block the appendix. After the blockage occurs, bacteria which normally are found within the appendix begin to invade (infect) the wall of the appendix. The body responds to the invasion by mounting an attack on the bacteria, an attack called inflammation. An alternative theory for the cause of appendicitis is an initial rupture of the appendix followed by spread of bacteria outside the appendix.. The cause of such a rupture is unclear, but it may relate to changes that occur in the lymphatic tissue, for example, inflammation, that line the wall of the appendix.)

If the inflammation and infection spread through the wall of the appendix, the appendix can rupture. After rupture, infection can spread throughout the abdomen; however, it usually is confined to a small area surrounding the appendix (forming a peri-appendiceal abscess).

Sometimes, the body is successful in containing (”healing”) the appendicitis without surgical treatment if the infection and accompanying inflammation do not spread throughout the abdomen. The inflammation, pain and symptoms may disappear. This is particularly true in elderly patients and when antibiotics are used. The patients then may come to the doctor long after the episode of appendicitis with a lump or a mass in the right lower abdomen that is due to the scarring that occurs during healing. This lump might raise the suspicion of cancer.

Causes

Obstruction of the appendiceal lumen has been attributed to a number of common sources including from fecaliths (a hard mass of fecal matter), normal stool, viral induced ulcers, or lymphoid hyperplasia. Once this obstruction occurs the appendix subsequently becomes filled with mucus and distends, increasing intraluminal and intramural pressures, resulting in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. As these progress, the appendix becomes ischemic and then necrotic. Rarely, spontaneous recovery can occur at this point. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture causing peritonitis, which may lead to septicemia and eventually death.

A number of environmental factors involving diet and hygiene have been proposed to be alternate causes of appendicitis, none of which has been studied in detail. According to the Medical Journal of Australia, “Dietary theories, notably an inadequate fibre intake, have been advanced to account for the geography of the disease, but it is clear that diet can not fully explain the epidemiology.

Complications of Appendicitis

The most frequent complication of appendicitis is perforation. Perforation of the appendix can lead to a periappendiceal abscess (a collection of infected pus) or diffuse peritonitis (infection of the entire lining of the abdomen and the pelvis). The major reason for appendiceal perforation is delay in diagnosis and treatment. In general, the longer the delay between diagnosis and surgery, the more likely is perforation. The risk of perforation 36 hours after the onset of symptoms is at least 15%. Therefore, once appendicitis is diagnosed, surgery should be done without unnecessary delay.

A less common complication of appendicitis is blockage of the intestine. Blockage occurs when the inflammation surrounding the appendix causes the intestinal muscle to stop working, and this prevents the intestinal contents from passing. If the intestine above the blockage begins to fill with liquid and gas, the abdomen distends and nausea and vomiting may occur. It then may be necessary to drain the contents of the intestine through a tube passed through the nose and esophagus and into the stomach and intestine.

A feared complication of appendicitis is sepsis, a condition in which infecting bacteria enter the blood and travel to other parts of the body. This is a very serious, even life-threatening complication. Fortunately, it occurs infrequently.

Symptoms

Symptoms of acute appendicitis can be classified into two types, typical and atypical (Hobler, K., 1998). The typical history includes pain starting centrally (periumbilical) before localising to the right iliac fossa (the lower right side of the abdomen); this is due to the poor localizing (spatial) property of visceral nerves from the mid-gut, followed by the involvement of somatic nerves (parietal peritoneum) as the inflammation progresses. The pain is usually associated with loss of appetite and fever. Nausea or vomiting may or may not occur. With the typical type, diagnosis is easier to make, surgery occurs earlier and findings are often less severe (Hobler, K., 1998).

Atypical symptoms may include pain beginning in the right lower quadrant, diarrhea and a more prolonged, smoldering course. Being more difficult to diagnose, CT scans and ultrasound tests are more useful. Surgical findings are more apt to be severe (suppuration, abscess, perforation, etc.(Hobler,K., 1998).

In either type of history, physical findings of appendicitis usually include localized findings in the right lower quadrant suggesting peritonitis. The abdominal wall becomes very sensitive to gentle pressure (palpation)and tapping (percussion). Coughing causes point tenderness in this area (McBurney’s Point) and this is the least painful way to localize the inflamed appendix. If the abdomen on palpation is also involuntarily guarded (rigid), there should be a strong suspicion of peritonitis requiring urgent surgical intervention.

The main symptom of appendicitis is abdominal pain. The pain is at first diffuse and poorly localized, that is, not confined to one spot. (Poorly localized pain is typical whenever a problem is confined to the small intestine or colon, including the appendix.) The pain is so difficult to pinpoint that when asked to point to the area of the pain, most people indicate the location of the pain with a circular motion of their hand around the central part of their abdomen. A second, common, early symptom of appendicitis is loss of appetite which may progress to nausea and even vomiting. Nausea and vomiting also may occur later due to intestinal obstruction.

As appendiceal inflammation increases, it extends through the appendix to its outer covering and then to the lining of the abdomen, a thin membrane called the peritoneum. Once the peritoneum becomes inflamed, the pain changes and then can be localized clearly to one small area. Generally, this area is between the front of the right hip bone and the belly button. The exact point is named after Dr. Charles McBurney–McBurney’s point. If the appendix ruptures and infection spreads throughout the abdomen, the pain becomes diffuse again as the entire lining of the abdomen becomes inflamed.

Diagnosis

Diagnosis is based on history and physical examination backed by an elevation of neutrophilic white cells. Atypical histories often requires ultrasound and/or CT scanning (Hobler, K., 1998).

The classical history in appendicitis is diffuse pain in the periumbilical region which then localizes as pain and tenderness at McBurney’s point (associated with an inflamed appendix coming in contact with the surrounding parietal peritoneum). This point is located on the right-hand side of the abdomen one-third of the distance between the anterior superior iliac spine and the navel. Here, on gentle palpation, the abdominal muscles often feel firm to rigid because of involuntary spasm, and a cough also produces a localized soreness.

Other physical findings include right-side tenderness on a digital rectal exam. Since the appendix normally lies on the right, if a finger is inserted into the rectum and there may be tenderness when pressure is applied toward the right indicating an increased likelihood that the patient has a pelvic appendix.

Other signs used in the diagnosis of appendicitis are the psoas sign (useful in retrocecal appendicitis), the obturator sign (specifically the obturator internus muscle), Blumberg’s sign, and Rovsing’s sign.

Ultrasonography and Doppler sonography also provide useful means to detect appendicitis, especially in children. In some cases (15% approximately), however, ultrasonography of the iliac fossa does not reveal any abnormalities despite the presence of appendicitis. This is especially true of early appendicitis before the appendix has become significantly distended and in adults where larger amounts of fat and bowel gas make actually seeing the appendix technically difficult. Despite these limitations, in experienced hands sonographic imaging can often distinguish between appendicitis and other diseases with very similar symptoms such as inflammation of lymph nodes near the appendix or pain originating from other pelvic organs such as the ovaries or fallopian tubes.

In places where it is readily available, CT scan has become the diagnostic test of choice, especially in adults whose diagnosis is not obvious on history and physical. (The use of CT in pregnant women and children is significantly limited, however, by concerns regarding radiation exposure.) A properly performed CT scan with modern equipment has a detection rate (sensitivity) of over 95% and a similar specificity. Signs of appendicitis on CT scan include lack of contrast (oral dye) in the appendix and direct visualization of appendiceal enlargement (greater than 6 mm in diameter on cross section). The inflammation caused by appendicitis in the surrounding peritoneal fat (so called “fat stranding”) can also be observed on CT, providing a mechanism to detect early appendicitis and a clue that appendicitis may be present even when the appendix is not well seen. Thus, diagnosis of appendicitis by CT is made more difficult in very thin patients and in children, both of whom tend to lack significant fat within the abdomen. The utility of CT scanning is made clear, however, by the impact it has had on negative appendectomy rates. For example, use of CT for diagnosis of appendicitis in Boston, MA has decreased the chance of finding a normal appendix at surgery from 20% in the pre-CT era to only 3% according to data from the Massachusetts General Hospital.

The white blood cell count in the blood usually becomes elevated with infection. In early appendicitis, before infection sets in, it can be normal, but most often there is at least a mild elevation even early. Unfortunately, appendicitis is not the only condition that causes elevated white blood cell counts. Almost any infection or inflammation can cause this count to be abnormally high. Therefore, an elevated white blood cell count alone cannot be used as a sign of appendicitis.

Urinalysis is a microscopic examination of the urine that detects red blood cells, white blood cells and bacteria in the urine. Urinalysis usually is abnormal when there is inflammation or stones in the kidneys or bladder. The urinalysis also may be abnormal with appendicitis because the appendix lies near the ureter and bladder. If the inflammation of appendicitis is great enough, it can spread to the ureter and bladder leading to an abnormal urinalysis. Most patients with appendicitis, however, have a normal urinalysis. Therefore, a normal urinalysis suggests appendicitis more than a urinary tract problem.

The surgeon faced with a patient suspected of having appendicitis always must consider and look for other conditions that can mimic appendicitis. Among the conditions that mimic appendicitis are:

  • Meckel’s diverticulitis. A Meckel’s diverticulum is a small outpouching of the small intestine which usually is located in the right lower abdomen near the appendix. The diverticulum may become inflamed or even perforate (break open or rupture). If inflamed and/or perforated, it usually is removed surgically.
  • Pelvic inflammatory disease. The right fallopian tube and ovary lie near the appendix. Sexually active women may contract infectious diseases that involve the tube and ovary. Usually, antibiotic therapy is sufficient treatment, and surgical removal of the tube and ovary are not necessary.
  • Inflammatory diseases of the right upper abdomen. Fluids from the right upper abdomen may drain into the lower abdomen where they stimulate inflammation and mimic appendicitis. Such fluids may come from a perforated duodenal ulcer, gallbladder disease, or inflammatory diseases of the liver, e.g., a liver abscess.
  • Right-sided diverticulitis. Although most diverticuli are located on the left side of the colon, they occasionally occur on the right side. When a right-sided diverticulum ruptures it can provoke inflammation they mimics appendicitis.
  • Kidney diseases. The right kidney is close enough to the appendix that inflammatory problems in the kidney-for example, an abscess-can mimic appendicitis.

Treatment

Once a diagnosis of appendicitis is made, an appendectomy usually is performed. Antibiotics almost always are begun prior to surgery and as soon as appendicitis is suspected.

There is a small group of patients in whom the inflammation and infection of appendicitis remain mild and localized to a small area. The body is able not only to contain the inflammation and infection but to resolve it as well. These patients usually are not very ill and improve during several days of observation. This type of appendicitis is referred to as “confined appendicitis” and may be treated with antibiotics alone. The appendix may or may not be removed at a later time.

On occasion, a person may not see their doctor until appendicitis with rupture has been present for many days or even weeks. In this situation, an abscess usually has formed, and the appendiceal perforation may have closed over. If the abscess is small, it initially can be treated with antibiotics; however, the abscess usually requires drainage. A drain (a small plastic or rubber tube) usually is inserted through the skin and into the abscess with the aid of an ultrasound or CT scan that can determine the exact location of the abscess. The drain allows pus to flow from the abscess out of the body. The appendix may be removed several weeks or months after the abscess has resolved. This is called an interval appendectomy and is done to prevent a second attack of appendicitis.

The treatment begins by keeping the patient from eating or drinking anything, even water, in preparation for surgery. An intravenous drip is used to hydrate the patient. Antibiotics given intravenously such as cefuroxime and metronidazole may be administered early to help kill bacteria and thus reduce the spread of infection in the abdomen and postoperative complications in the abdomen or wound. Equivocal cases may become more difficult to assess with antibiotic treatment and benefit from serieal examinations. If the stomach is empty (no food in the past six hours) general anaesthesia is usually used. Otherwise, spinal anaesthesia may be used.

The surgical procedure for the removal of the appendix is called an appendicectomy (also known as an appendectomy). Often now the operation can be performed via a laparoscopic approach, or via three small incisions with a camera to visualize the area of interest in the abdomen. If the findings reveal suppurative appendicitis with complications such as rupture, abscess, adhesions, etc., conversion to open laparotomy may be necessary. An open laparotomy incision if required most often centers on the area of maximum tenderess, McBurney’s Point, in the right lower quadrant. A transverse or a gridiron diagonal incision is used most commonly.

According to a meta-analysis from the Cochrane Collaboration comparing laparoscopic and open procedures, laparoscopic procedures seem to have various advantages over the open procedure. Wound infections were less likely after laparoscopic appendicectomy than after open appendicectomy (odds ratio 0.45; CI 0.35 to 0.58), but the incidence of intraabdominal abscesses was increased (odds ratio 2.48; CI 1.45 to 4.21). The duration of surgery was 12 minutes (CI 7 to 16) longer for laparoscopic procedures. Pain on day 1 after surgery was reduced after laparoscopic procedures by 9 mm (CI 5 to 13 mm) on a 100 mm visual analogue scale. Hospital stay was shortened by 1.1 day (CI 0.6 to 1.5). Return to normal activity, work, and sport occurred earlier after laparoscopic procedures than after open procedures. While the operation costs of laparoscopic procedures were significantly higher, the costs outside hospital were reduced. Young female, obese, and employed patients seem to benefit from the laparoscopic procedure more than other groups.

Surgery may last from 15 minutes in typical appendicitis in thin patients to several hours in complicated cases. Hospital lengths of stay usually range from overnight to a matter of days (rarely weeks in complicated cases.) The pain is not always constant, in some cases it can stop for a day and then come back.

Prognosis

Most appendicitis patients recover easily with treatment, but complications can occur if treatment is delayed or if peritonitis occurs.

Recovery time depends on age, condition, complications, and other circumstances, including the amount of alcohol consumption, but usually is between 10 and 28 days. For young children (around 10 years old) the recovery takes three weeks.

The real possibility of life-threatening peritonitis is the reason why acute appendicitis warrants speedy evaluation and treatment. The patient may have to undergo a medical evacuation. Appendectomies have occasionally been performed in emergency conditions (i.e. outside of a proper hospital), when a timely medical evaluation was impossible.

Typical acute appendicitis responds quickly to appendectomy and occasionally will resolve spontaneously. If appendicitis resolves spontaneously, it remains controversial whether an elective interval appendectomy should be performed to prevent a recurrent episode of appendicitis. Atypical appendicitis (associated with suppurative appendicitis) is more difficult to diagnose and is more apt to be complicated even when operated early. In either condition prompt diagnosis and appendectomy yield the best results with full recovery in two to four weeks usually. Mortality and severe complications are unusual but do occur, especially if peritonitis persists and is untreated.

An unusual complication of an appendectomy is “stump appendicitis”: inflammation occurs in the remnant appendiceal stump left after a prior, incomplete appendectomy.

What is new about appendicitis?

Recently it has been hypothesized that some episodes of appendicitis-like symptoms, especially recurrent symptoms, may be due to an increased sensitivity of the intestine and appendix from a prior episode of inflammation. That is, the recurrent symptoms are not due to recurrent episodes of inflammation. Rather, prior inflammation has made the nerves of the intestines and appendix or the central nervous system that innervate them more sensitive to normal stimuli, that is, with stimuli other than inflammation. This will be a difficult, if not impossible, hypothesis to confirm.

dr.rahees.k@live.in

HEART ATTACK (MYOCARDIAL INFARCTION)

Author: admin  //  Category: Disease Conditions, Heart Diseases

HEART ATTACK (MYOCARDIAL INFARCTION)

A heart attack (also known as a myocardial infarction) is the death of heart muscle from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle. Injury to the heart muscle causes chest pain and pressure. If blood flow is not restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is “complete.” The dead heart muscle is replaced by scar tissue.

CAUSES OF HEART ATTACK

ha1.jpg

With advancing age, cholesterol and calcium are deposited gradually in the walls of the coronary arteries. These deposits are called plaques. The process is known as atherosclerosis, or “hardening of the arteries.”

  • A diet high in cholesterol combined with smoking and lack of exercise can accelerate this process.
  • As these plaques grow, they begin to impede the flow of blood.
  • The growing plaque is like a firm shell with a soft inner core containing cholesterol.
  • As blood hits a plaque during each heartbeat, the plaque may crack open and expose the inner cholesterol.
  • The cholesterol may cause a blood clot to begin to form.
  • The plaque and the blood clot block the artery partially or completely. The more the artery is blocked, the greater the resulting damage to the heart.

Atherosclerotic coronary artery disease

This most common type of heart disease is associated with several risk factors. The greater the number of risk factors you have, the more likely you are to have atherosclerosis. The most common risk factors are as follows:

  • Hereditary (runs in the family)
  • High cholesterol in blood, especially high levels of “bad cholesterol” (LDL, low-density lipoprotein) and low levels of “good cholesterol” (HDL, high-density lipoprotein)
  • Cigarette smoking or other tobacco use, including cigars and chewing tobacco
  • Obesity or excess weight
  • High blood pressure (hypertension)
  • Diabetes
  • Physical inactivity, lack of regular exercise (sedentary lifestyle)
  • High-fat diet
  • Emotional stress
  • Type-A personality (hard-driving, perfectionist)

Nonatherosclerotic coronary artery disease

Coronary arteries can be blocked by conditions other than atherosclerosis. These include inflammatory diseases of the arteries, trauma such as a cut or stab wound to the heart, and diseases that cause thickening of the coronary arteries.

Coronary embolization may cause a heart attack. Coronary embolization refers to a clot from elsewhere in the body breaking off and traveling to the heart.

Other causes of heart attack are blood or oxygen supply problems or outside influences such as cocaine abuse and complications from bypass or catheterization.

Certain heart problems leading to heart attack may be present from birth.

SYMPTOMS

Although chest pain or pressure is the most common symptom of a heart attack, heart attack victims may experience a diversity of symptoms that include:

  • Pain, fullness, and/or squeezing sensation of the chest
  • Jaw pain, toothache, headache
  • Shortness of breath
  • Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort
  • Sweating
  • Heartburn and/or indigestion
  • Arm pain (more commonly the left arm, but may be either arm)
  • Upper back pain
  • General malaise (vague feeling of illness)
  • No symptoms (Approximately one quarter of all heart attacks are silent, without chest pain or new symptoms. Silent heart attacks are especially common among patients with diabetes mellitus.)

Even though the symptoms of a heart attack at times can be vague and mild, it is important to remember that heart attacks producing no symptoms or only mild symptoms can be just as serious and life–threatening as heart attacks that cause severe chest pain. Too often patients attribute heart attack symptoms to “indigestion,” “fatigue,” or “stress,” and consequently delay seeking prompt medical attention. One cannot overemphasize the importance of seeking prompt medical attention in the presence of symptoms that suggest a heart attack. Early diagnosis and treatment saves lives, and delays in reaching medical assistance can be fatal. A delay in treatment can lead to permanently reduced function of the heart due to more extensive damage to the heart muscle. Death also may occur as a result of the sudden onset of arrhythmias such as ventricular fibrillation.

Chest pressure, discomfort, or a bandlike sensation around the chest with squeezing or heaviness is a common symptom of heart attack.

  • About one fourth of people having a heart attack have no pain (”silent” heart attack).
  • Silent heart attacks are more frequent in people with diabetes.

The following symptoms suggest a heart attack:

  • Chest pain or pressure (heaviness)
  • Jaw pain, or extension of pain into the arms or shoulder, especially the left arm
  • Unexplained shortness of breath
  • Unexplained sweating
  • Heartburn or feeling of indigestion
  • Nausea or vomiting
  • Back pain or upper abdominal pain
  • General lethargy or listlessness (malaise)

COMPLICATIONS

Heart failure

If a large amount of heart muscle dies, the ability of the heart to pump blood to the rest of the body is diminished, and this can result in heart failure. The body retains fluid, and organs, for example, the kidneys, begin to fail

Ventricular fibrillation

Injury to heart muscle also can lead to ventricular fibrillation. Ventricular fibrillation occurs when the normal, regular, electrical activation of heart muscle contraction is replaced by chaotic electrical activity that causes the heart to stop beating and pumping blood to the brain and other parts of the body. Permanent brain damage and death can occur unless the flow of blood to the brain is restored within five minutes.

Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart that occurs before the victim of the heart attack can reach an emergency room. Those who reach the emergency room have an excellent prognosis; survival from a heart attack with modern treatment should exceed 90%. The 1% to 10% of heart attack victims who die later include those victims who suffer major damage to the heart muscle initially or who suffer additional damage at a later time.

Deaths from ventricular fibrillation can be avoided by cardiopulmonary resuscitation (CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires breathing for the victim and applying external compression to the chest to squeeze the heart and force it to pump blood. When paramedics arrive, medications and/or an electrical shock (cardioversion) can be administered to convert ventricular fibrillation back to a normal heart rhythm and allow the heart to pump blood normally. Therefore, prompt CPR and a rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have defibrillators that provide the electrical shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances of survival.

DIAGNOSIS

A heart attack is not a quick event that lasts a few minutes and is over.

  • A heart attack is a process that continues over several hours.
  • Every minute that passes before treatment is begun, your heart sustains more damage.
  • You must seek medical attention as soon as you suspect you are having a heart attack.

If you arrive at the hospital in an ambulance, the staff will be ready for you.

  • They will evaluate your condition rapidly by examining you and, if you can answer, asking you questions about your symptoms.
  • They will obtain an electrocardiogram (ECG) right away to look for signs of heart attack.
  • A quick diagnosis is essential for starting treatment as soon as possible.

If you are thought to be having a heart attack, you may undergo the following tests upon arrival and/or during the next few days of your hospital stay.

Blood tests: Routine blood tests include blood cell counts, chemistry and electrolytes, and coagulation (clotting) function.

  • Cardiac enzymes: When heart muscle is damaged, certain muscle proteins are released into the bloodstream and can be measured. Elevations of the levels of certain of these proteins, known as cardiac enzymes, strongly suggest that a heart attack is in progress or has occurred recently. Repeated testing of blood samples for cardiac enzymes is helpful in making the diagnosis of a heart attack, especially when the ECG is not diagnostic.
  • Other enzymes: Some other enzymes tested include AST (SGOT, aspartate transferase) and LDH (lactate dehydrogenase).
  • The 2 most measured enzymes are creatine kinase (CK) and troponin.
    • Creatine kinase is released from the cardiac muscle cells as they die and as their membranes dissolve. The level of this enzyme takes a number of hours after the beginning of the heart attack to peak. It returns to normal by 24 hours after the beginning of the heart attack. A form of this enzyme called MB subform is quite specific in showing cardiac damage.
    • Troponin-I and troponin-T are very useful enzyme tests. The levels of these enzymes rise by 6-8 hours after the heart attack begins and remain elevated above normal for as long as a week. To some extent, the level of troponin can predict the likelihood of complications for a person with a heart attack. The levels may also helpful in deciding what treatments should be used.

Electrocardiogram: This test detects the electrical activity of the heart and records graphlike tracings of each heartbeat (waves).

  • It is safe and painless, and it takes only a few minutes.
  • An ECG is performed by taping electrodes on your arms, legs, and chest. The electrodes pick up the electrical impulses of your heart from different points of view in your chest.
  • ECG abnormalities diagnostic of heart attack are sometimes seen early in a heart attack, but the ECG may be normal at first and need to be repeated.
  • Sometimes existing ECG abnormalities may make the diagnosis difficult.

Chest x-ray: This is not always done, but it can show abnormalities in the size or shape of the heart and indicate if fluid is collecting in the lungs, a sign or poor circulation.

Echocardiogram (echo): This is an ultrasound examination of the heart. The ultrasound device uses sound waves to create a detailed “picture” of the heart, which are then transmitted to a video monitor.

  • This is a safe, noninvasive, and very helpful test.
  • Echo may show problems in the heart structure, such as abnormalities in the movements of the heart wall. A heart attack is a damaged heart wall.
  • It can show abnormal enlargement or pouching of the heart wall (aneurysm).
  • Echo may also visualize complications of heart attack including valve problems, rupture of the heart muscle, or accumulation of fluid in the cardiac sac (pericardial effusion).
  • The most important information obtained from the echo is the ejection fraction. This is a measurement of the strength of heart muscle. This information may be used to help predict outcome and to decide on treatment.

Coronary angiography: This is the best test for identifying blockages in the coronary arteries.

  • It often is performed for people with persistent pain and those who have not received “clot-busting” drugs to re-open their blocked artery.
  • At some hospitals, people are taken directly into the catheterization, or cath, lab from the emergency department after initial evaluation.
  • In the cath lab, a long, thin plastic tube (catheter) is put into the femoral artery (in the groin) or the brachial or radial artery (in the arm) and guided into the openings of the coronary arteries. Dye is injected into the arteries to make them stand out on x-ray. Pictures are recorded for later review.
  • Coronary angiography is an invasive test with potentially serious complications, but when performed by an experienced doctor, the risk of complications is relatively small.
  • An angiogram is the best test to determine which treatment is most appropriate: medication, angioplasty, stent placement, or bypass surgery.

A stress test may be performed before a person leaves the hospital, after the patient is stable and recovering from the heart attack and/or procedure.

  • Exercise stress testing involves recording an ECG while the heart is stressed and again at rest.
    • The “stress” is usually exercise, namely, walking on a treadmill.
    • Speed and elevation are gradually increased while recording the ECG.
    • Certain changes in the ECG indicate possible coronary artery blockage.
    • The exercise stress test is about 60-70% accurate in predicting increased risk of future heart attacks.
    • If the stress test indicates fairly severe blockage, coronary angiography may be needed to confirm the diagnosis and determine the need for further treatment.
  • Radionuclide stress testing is another type of stress testing.
    • It uses a special camera that sees blood flow after a tiny dose of a radioactive “dye” (isotope) is injected into the blood.
    • It measures the quantities of blood flow that reach the different parts of the heart muscle through the coronary arteries.
    • Like the exercise stress test, pictures are obtained with exercise on the treadmill and then with rest.
    • People who are unable to walk on the treadmill may be given medication to “stress” the heart muscle.
    • If a particular coronary artery is blocked partially or completely, the part of the heart supplied with blood by that artery would appear as a “cold spot” on the pictures because no radioactive isotope reaches that area.
    • This test is quite accurate in diagnosing coronary artery blockage. The small amount of radioactivity is not considered to be harmful.

TREATMENT

Medical treatment may be started immediately, before a definite diagnosis of a heart problem is made.

General treatment measures include the following:

  • Oxygen through a tube in the nose or face mask
  • Nitroglycerin under the tongue
  • Pain medicines (morphine or meperidine)
  • Aspirin: Those with allergy to aspirin may be given clopidogrel (Plavix).

Clot-dissolving medicines: The tissue plasminogen activators (tPAs) can actually dissolve clots.

  • The earlier these drugs are given, the better the chance of dissolving the clot and opening the blocked artery, protecting the heart muscle from further injury.
  • If more than 12 hours has passed since the onset of chest pain, these drugs are less helpful.
  • Potential risks of this therapy include bleeding.
  • The most serious risk is a stroke (bleeding into the brain).

Angioplasty: Emergency coronary angiography and coronary balloon angioplasty (percutaneous transluminal coronary angioplasty, or PTCA) are available in hospitals equipped with a full-service cardiac catheterization laboratory. This is the most direct method of removing blockage in a coronary artery.

  • Coronary balloon angioplasty is an extension of coronary angiography.
  • A long, thin tube (catheter) is inserted in an artery in the groin or arm.
  • At the tip of the catheter is a tiny, elongated balloon, which is threaded over a hair-thin guidewire into the narrowed coronary artery.
  • Once the balloon is positioned at the blockage in the coronary artery, it is inflated.
  • The balloon pushes aside the plaque and clot that are blocking the artery, allowing blood to flow more freely.
  • The balloon is then deflated and removed with the catheter.

Stenting: A stent is a small, metal springlike device that may be inserted into a coronary artery after balloon angioplasty. After the catheter and balloon are removed, the stent stays in place, holding the artery open. A stent is better than angioplasty alone at keeping the artery from narrowing again.

Atherectomy: Sometimes the plaques are too rigid, bulky, or calcified to be treated by balloon angioplasty. In these cases, the plaque often can be removed by cutting it out with a drill-like rotary blade or a laser or other tool.

Medications

If you are having a heart attack, you will almost certainly be given some or all of these medications while you are in the hospital. Some you will continue taking at home.

  • Intravenous (IV) nitroglycerin has been shown to improve blood flow to the heart muscle by relaxing (dilating) the coronary arteries and increasing blood flow. It is usually given for 24-48 hours continuously.
  • Heparin is a “blood thinner,” or anticoagulant, which may be given after a heart attack. Heparin does not remove an existing clot, but it reduces the tendency of blood to clot in the coronary arteries. Some newer forms of heparin have recently been introduced that can be given as a shot instead of through an IV line.
  • Beta-blockers are medications that decrease the heart rate and blood pressure. This reduces the heart’s workload and thus the amount of oxygen it needs. Beta-blockers may help prevent heart irregularities/life threatening rhythm disorders and future heart attacks.
  • Angiotensin-converting enzyme (ACE) inhibitors may prevent repeat heart attacks and other problems when started early during a heart attack. They are especially useful in people with diabetes and those with a weakened heart muscle congestive heart failure).

Surgery

  • Sometimes cardiac catheterization reveals extensive coronary artery disease. In such cases, you will need to undergo coronary bypass surgery.
  • Standard coronary artery bypass grafting (CABG) is performed if many coronary arteries are narrowed or blocked. This is especially recommended when the left main coronary artery shows significant blockage. This is “open heart surgery,” meaning that the chest wall is opened. When performing a bypass, heart surgeons use sections of the mammary artery from the chest, radial arteries from the arms, or veins from the legs to create detours around the blocked arteries. For this surgery, you will be connected to a bypass pump, which does the work of the heart during the operation. Although this sounds dangerous, this surgery is considered very safe and has a very low rate of complications.
  • Off-pump bypass surgery: Sometimes the surgeon can perform open heart surgery without using a bypass pump. The heart continues to beat during surgery. This type of surgery has even fewer complications than the standard procedure but is not always feasible.
  • Minimally invasive coronary bypass: If just the front or the right coronary artery needs bypass, the bypass may be performed via a small keyhole-type incision without a large incision in the chest. The internal mammary artery is used for the bypass.

Follow-up

If you have a heart attack, you will receive detailed instructions for your care after leaving the hospital. You should follow these instructions carefully. The following general guidelines apply to recovery from an uncomplicated heart attack.

You may return to work or prior activity levels after about 2 weeks, resume sexual activity in 7-10 days, drive a week after leaving the hospital, and continue commercial air travel after 2 weeks, if you are feeling fine and totally asymptomatic. Those with complicated heart attacks or who still have symptoms should wait at least 2-3 weeks after symptoms go away before driving.

After a heart attack, you will need close follow-up with your health care provider.

  • Coronary heart disease is a chronic (ongoing, long-term), progressive condition.
  • Changing your risk factors only slows its pace.
  • Angioplasty or bypass surgery only alleviates the symptoms and is not a cure. The disease may recur and progress.

Your health care provider will watch you carefully for the following developments:

  • Any new symptoms or signs of disease progression through clinical evaluation, physical examination, and periodic ECGs or stress tests
  • Silent ischemia by periodic treadmill or radionuclide stress tests or stress echocardiography

He or she will also manage the following aspects of your treatment and recovery:

  • Risk factor management by checking blood pressure and cholesterol levels periodically
  • Adjustment of medicines and management of their side effects
  • Prescription for an exercise program (cardiac rehabilitation)

What is new in heart attack?

Greater public awareness about heart attacks and changes in lifestyle have contributed to a dramatic reduction in the incidence of heart attacks during the last four decades. Improved anticoagulant drugs such as hirudin and hirulog, are being tested and may complement current therapies. The role of the “super aspirins” (Reopro and Integrilin) is currently being investigated as well. More effective versions of TPA are being developed. Increasingly, paramedics can do ECGs in the field, diagnose a heart attack, and take patients directly to hospitals that have the ability to do PTCA and stenting. This can save time and reduce damage to the heart. Recent data has shown that lowering blood LDL levels even further than previously suggested may further decrease the risk of heart attacks. Research also has shown that inflammation may play a role in the development of atherosclerosis, and this is an active area of current investigation. There also is early evidence that with genetic engineering it may be possible to develop a drug that can be administered to clear plaques from arteries (a “scavenger molecule”).

CHIKUNGUNYA FEVER

Author: admin  //  Category: Disease Conditions, Viral Diseases

CHIKUNGUNYA FEVER

aedes_aegypti_biting_human.jpg

Chikungunya fever is a viral disease acquired by humans through the bite of infected mosquitoes. Chikungunya virus (CHIKV) was first identified in Tanzania in 1953, and has since been found in west, central and southern Africa and many areas of Asia. Chikungunya virus has caused many human epidemics in those areas since that time. CHIKV infection can cause a severe illness, that most often includes symptoms such as fever, headache, fatigue, nausea, vomiting, muscle pain, rash, and joint pain. There is no vaccine or specific antiviral treatment for chikungunya fever available. The best way to avoid CHIKV infection is to prevent mosquito bites.

Chikungunya is a relatively rare form of viral fever caused by an alphavirus that is spread by mosquito bites from Aedes aegypti mosquitoes, though recent research by the Pasteur Institute in Paris claims the virus has suffered a mutation that enables it to be transmitted by Aedes albopictus (Tiger mosquito). This was the cause of the plague in the Indian Ocean and a threat to the Mediterranean coast at present, requiring urgent meetings of health officials in the region.

The name is derived from the Makonde word meaning “that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease.

Chikungunya is generally not fatal. However, in 2005-2006, 200 deaths were associated with chikungunya on Réunion island and a widespread outbreak in India, primarily in Tamil Nadu, Karnataka, Kerala, and Andhra Pradesh. After flood and heavy rains in Rajasthan, India in August 2006, thousands of cases were detected in Rajsamand, Bhilwara, Udaipur, and Chittorgarh districts and also in adjoining regions of Gujarat and Madhya Pradesh, and in the neighbouring country of Sri Lanka. In the southern Indian state of Kerala, 125 deaths were attributed to Chikungunya with the majority of the casualties reported in the district of Alapuzha, primarily in Cherthala. In December 2006, an outbreak of 3,500 confirmed cases occurred in Maldives, and over 60,000 cases in Sri Lanka, with over 80 deaths. [1]. In October 2006 more than a dozen cases of Chikungunya were reported in Pakistan. A recent outbreak of the disease during June 2007 in Pathanamthitta, Kottayam and Alappuzha districts of South Kerala, India claimed more than 50 lives. It is confirmed officially that there are 7000 confirmed Chikungunya patients in these areas. Unofficial reports suggest that more than one hundred thousand are suffering from symptoms of chikungunya. Rumors float around of radio active waste from Tamil Nadu being dumped at the outskirts of this region, which mutated the mosquitos and spread the disease. The European Network for Diagnostics of “Imported” Viral Diseases claims new phylogenetic variants of virus which are fatal have been identified on Réunion. In August/September 2007 some 160 people were infected in Italies northern Ravenna region, resulting in one fatality.

Acute chikungunya fever typically lasts a few days to a couple of weeks, but as with dengue, West Nile fever, o’nyong-nyong fever and other arboviral fevers, some patients have prolonged fatigue lasting several weeks. Additionally, some patients have reported
incapacitating joint pain, or arthritis which may last for weeks or months. The prolonged joint pain associated with CHIKV is not typical of dengue. Co-circulation of dengue fever in many areas may mean that chikungunya fever cases are sometimes clinically misdiagnosed as dengue infections, therefore the incidence of chikungunya fever could be much higher than what has been previously reported.

No deaths, neuroinvasive cases, or hemorrhagic cases related to CHIKV infection have been conclusively documented in the scientific literature.

CHIKV infection (whether clinical or silent) is thought to confer life-long immunity.

chiqun-map_map.jpg

Cases of chikungunya fever (between 1952-2006) have been reported in the countries depicted in red on this map.
In Africa, these include Burundi; Central African Republic; Comoros; Democratic Republic of Congo; Guinea; Kenya; Nigeria; Madagascar; Malawi; Mauritius; Mayotte; Reunion; Senegal; Seychelles, South Africa; Tanzania; Uganda; Zimbabwe.In Asia, these include Australia; Burma; Cambodia; India; Indonesia; Malaysia; Pakistan; Philippines; Taiwan; Thailand; Timor; Vietnam.

Symptoms

The symptoms of Chikungunya include fever which can reach 39°C, (102.2°F) a petechial or maculopapular rash usually involving the limbs and trunk, and arthralgia or arthritis affecting multiple joints which can be debilitating. The symptoms could also include headache, conjunctival injection, and slight photophobia. In the present epidemic in the states of Andhra Pradesh and Tamil Nadu, India, high fever and crippling joint pain are the prevalent complaint. The fever typically lasts for two days and abruptly comes down. However, other symptoms, namely joint pain, intense headache, insomnia and an extreme degree of prostration last for a variable period, usually for about 5 to 7 days. But, patients have complained joint pains for much longer time periods depending on age of the patient. With younger patients recovering within 5 to 15 days and middle aged recovering in 1 to 2.5 months and more for old people. It has been observed that the severity of the disease as well as its duration is less in younger patients and pregnant women. No untoward effects of pregnancy is noticed following the infection.

Dermatological manifestations observed in a recent outbreak of Chikungunya fever in Southern India and Eastern Indiaincludes the following:

  • Maculopapular rash
  • Nasal blotchy erythema
  • Freckle-like pigmentation over centro-facial area
  • Flagellate pigmentation on face and extremities
  • Lichenoid eruption and hyperpigmentation in photodistributed areas
  • Multiple aphthous-like ulcers over scrotum, crural areas and axilla.
  • Lympoedema in acral distribution (bilateral/unilateral)
  • Multiple ecchymotic spots (Children)
  • Vesiculobullous lesions (infants)
  • Subungual hemorrhage
  • Photo Urticaria
  • Acral Urticaria
  • Cephalgia
  • Lumbago
  • Vomiting
  • Epistaxis and haemetemesis

Histopathologically, pigmentary changes, maculopapular rash, lichenoid rash, aphthous-like ulcers show lymphocytic infiltration around dermal blood vessels (Inamadar et al). Pedal oedema (swelling of legs) is observed in many patients, the cause of which remains obscure as it is not related to any cardiovascular, renal or hepatic abnormalities.

Prevention of CHIKV Infection

The best way to avoid CHIKV infection is to prevent mosquito bites. There is no vaccine or preventive drug. Prevention tips are similar to those for dengue or West Nile virus:

  • Use insect repellent containing an DEET or another EPA-registered active ingredient on exposed skin. Always follow the directions on the package.
  • Wear long sleeves and pants (ideally treat clothes with permethrin or another repellent).
  • Have secure screens on windows and doors to keep mosquitoes out.
  • Get rid of mosquito breeding sites by emptying standing water from flower pots, buckets and barrels. Change the water in pet dishes and replace the water in bird baths weekly. Drill holes in tire swings so water drains out. Keep children’s wading pools empty and on their sides when they aren’t being used.
  • Additionally, a person with chikungunya fever or dengue should limit their exposure to mosquito bites in order to avoid further spreading the infection. The person should stay indoors or under a mosquito net.
  • Homoeopathic medicines are found to be very effective in preventing the disease.

dr.rahees.k@live.in

CHICKENPOX

Author: admin  //  Category: Disease Conditions, Viral Diseases

CKICKENPOX (VARICELLA)

Chickenpox, also spelled chicken pox, is the common name for Varicella zoster, classically one of the childhood infectious diseases caught by and survived by almost every child.

Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus 3 (HHV-3), one of the eight herpes viruses known to affect humans. It starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head rather than the hands and becoming itchy raw pox (pocks), small open sores which heal mostly without scarring.

Most people contract chickenpox by age 15, the majority between age 5 and 9, but all ages can contract it. Chickenpox is usually more severe in adults than children. Winter and spring are the most common times of the year for chickenpox to occur.

Chickenpox has a 10-14 day incubation period and is highly contagious through physical contact two days before symptoms appear. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox. Recurrent chickenpox, commonly known as shingles, is fairly rare but more likely in people with compromised immune systems.

Chickenpox is very highly contagious. It is easily passed between members of families and school classmates through airborne particles, droplets in exhaled air and fluid from the blisters or sores. It also can be transmitted indirectly by contact with articles of clothing and other items exposed to fresh drainage from open sores. Patients are contagious up to five days (more commonly, one to two days) before and five days after the date that their rash appears. When the sores have crusted over, the person is usually no longer contagious.

Chickenpox is rarely fatal (usually from varicella pneumonia), with pregnant women and those with a suppressed immune systems being more at risk. Pregnant women not known to be immune and who come into contact with chickenpox may need urgent treatment as the virus can cause serious problems for the baby. This is less of an issue after 20 weeks.

Later in life, viruses remaining dormant in the nerves can reactivate causing localised eruptions of shingles. This occurs particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Unlike chickenpox which normally fully settles, shingles may result in persisting post-herpetic neuralgia pain.

Signs and Symptoms

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Chickenpox is a highly contagious disease that spreads from person to person by direct contact or through the air from an infected person’s coughing or sneezing. Touching the fluid from a chickenpox blister can also spread the disease. A person with chickenpox is contagious from 1-2 days before the rash appears until all blisters have formed scabs. This may take 5-10 days. It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.

Symptoms tend to appear 14 to 16 days after initial exposure but can occur any time from 10 days up to 21 days after contact with the virus. Chickenpox is characterized by one to two days of mild fever up to 102 degrees F, general weakness, and a rash, often the first sign of the disease. Rarely, a person may have the disease without the rash. The rash of chickenpox develops in crops with raised red spots arriving first, progressing to blisters that burst, creating open sores, before crusting over. This process usually starts on the scalp, then the trunk (its area of greatest concentration), and finally the arms and legs. Any area of skin that is irritated (by diaper rash, poison ivy, eczema, sunburn, etc.) is likely to be hard hit by the rash. The rash is typically very itchy (pruritic).

The chickenpox lesions (blisters) start as a 2–4 mm red papule which develops an irregular outline (rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This “dew drop on a rose petal” lesion is very characteristic for chickenpox. After about 8–12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust. The fluid is highly contagious, but once the lesion crusts over, it is not considered contagious. The crust usually falls off after 7 days sometimes leaving a crater-like scar. Although one lesion goes through this complete cycle in about 7 days, another hallmark of chickenpox is the fact that new lesions crop up every day for several days. Therefore, it may take about a week until new lesions stop appearing and existing lesions crust over. Children are not to be sent back to school until all lesions have crusted over.

Second infections with chickenpox occur in immunocompetent individuals, but are uncommon. Such second infections are rarely severe. A soundly-based conjecture being carefully assessed in countries with low prevalence of chickenpox due to immunisation, low birth rates, and increased separation is that immunity has been reinforced by subclinical challenges and this is now less common.(Meaning is unclear please FIXME) This is more dangerous with shingles. There have been reported cases of repeat infections. Chickenpox is highly contagious and is spread through the air when infected people cough or sneeze, or through physical contact with fluid from lesions on the skin. Zoster, also known as shingles, is a reactivation of chickenpox and may also be a source of the virus for susceptible children and adults. It is not necessary to have physical contact with the infected person for the disease to spread. Those infected can spread chickenpox before they know they have the disease - even before any rash develops. In fact, people with chickenpox can infect others from about 2 days before the rash develops until all the sores have crusted over, usually 4-5 days after the rash starts.

Complications

Complications can and do occur from chickenpox. Infection of the open pox sore by bacteria can injure the skin, sometimes causing scarring, especially if the patient scratches the inflamed area. Bacterial skin infection is, in fact, the most common complication of chickenpox in children. The next most common complications in children affect the central nervous system and include a disorder of the cerebellar portion of the brain (cerebellar ataxia with wobbliness, dizziness, tremor, and altered speech), encephalitis (inflammation of the brain with headaches, seizures, and decreased consciousness), damaged nerves (nerve palsies) and Reye’s syndrome (a potentially fatal combination of liver and brain disease that can be associated with aspirin. Children with fever should not take aspirin.). Especially serious complications can occur in patients with AIDS, lupus, leukemia, and cancer. Complications also occur in people taking immune-suppressing drugs, such as cortisone-related medications. Newborn infants whose mothers have chickenpox in the last trimester of pregnancy are at increased risk from the disease. If the mother develops the disease from five days before to two days after delivery, the fatality rate for the baby is up to 30%.

Congenital defects in Babies

These may occur if the child’s mother was exposed to VZV during pregnancy. Effects on the foetus may be minimal in nature but physical deformities range in severity from under developed toes and fingers, to severe anal and bladder malformation. Possible problems include:

  • Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
  • Damage to the eye (optic stalk, optic cap, and lens vesicles), microphthalmia, cataracts, chorioretinitis, optic atrophy.
  • Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner’s syndrome
  • Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
  • Skin disorders: (cicatricial) skin lesions, hypopigmentation

Most people develop lifetime immunity to chickenpox after the first occurrence and never experience it again. But the virus can sometimes resurface later in life as shingles (zoster). The current aim in the U.S. and many other countries is to achieve universal (or nearly universal) immunization of children with the chickenpox vaccine. The vaccination requires only one shot given at about one year of age. If an older person has not had chickenpox, the shot may be given at any time. There have been few significant adverse reactions to the chickenpox vaccine. All children, except those with a compromised immune system, should have the vaccination.

dr.rahees.k@live.in