Celluitis

Cellulitis is an inflammation of the connective tissue underlying the skin, that can be caused by a bacterial infection. Cellulitis can be caused by normal skin flora or by exogenous bacteria, and often occurs where the skin has previously been broken: cracks in the skin, cuts, burns, insect bites, surgical wounds, or sites of intravenous catheter insertion. The mainstay of therapy remains treatment with appropriate antibiotics. Skin on the face or lower legs is most commonly affected by this infection, though cellulitis can occur on any part of the body. Cellulitis may be superficial — affecting only the surface of the skin — but cellulitis may also affect the tissues underlying the skin and can spread to the lymph nodes and bloodstream.

It is unrelated to cellulite, a cosmetic condition featuring dimpling of the skin.

Forms of cellulitis
A few of the forms of cellulitis are as follows: periorbital cellulitis (an infection of the eye socket), erysipelas, clostridial cellulitis, nonclostridial cellulitis, and synergistic necrotizing cellulitis (Pankey, 1992). A few forms of cellulitis do not have some of the symptoms most commonly listed (for example, clostridial and nonclostridial cellulitis do not cause the skin to turn red [Pankey, 1992]), but the majority do. Necrotizing fasciitis can be mistaken for cellulitis but is notable for involvement of the deeper tissue structures, the fascia, and can be limb and life threatening.


Infected lower leg
Symptoms
Early symptoms may include fever, headache, nausea, and early signs on redness on the leg

Cellulitis is characterized by redness, swelling, warmth, and pain or tenderness. Cellulitis frequently occurs on exposed areas of the body such as the arms, legs, and face. Other symptoms can include fever or chills and headaches. In advanced cases of cellulitis, red streaks (sometimes described as 'fingers') may be seen traveling up the affected area. The swelling can spread rapidly.


Cellulitis in a Limb showing typical red streaks and swelling
Causes
Cellulitis is caused by a type of bacteria entering by way of a break in the skin. This break need not be visible. Group A streptococcus and staphylococcus are the most common of these bacteria, which are part of the normal flora of the skin but cause no actual infection until the skin is broken. Predisposing conditions for cellulitis include insect bite, animal bite, pruritic skin rash, recent surgery, athlete's foot, dry skin, eczema, burns and boils, though there is debate as to whether minor foot lesions contribute.

The appearance of the skin will help a doctor make a diagnosis. The doctor may also suggest blood tests, a wound culture or other tests to help rule out a blood clot deep in the veins of the legs. Cellulitis in the lower leg is characterized by signs and symptoms that may be similar to those of a clot occurring deep in the veins, such as warmth, pain and swelling.

This reddened skin or rash may signal a deeper, more serious infection of the inner layers of skin. Once below the skin, the bacteria can spread rapidly, entering the lymph nodes and the bloodstream and spreading throughout the body.

In rare cases, the infection can spread to the deep layer of tissue called the fascial lining. Necrotizing fasciitis, also called by the media "flesh-eating bacteria", is an example of a deep-layer infection. It represents an extreme medical emergency.


Infected left shin in comparison to shin with no sign of symptoms
Risk factors
The elderly and those with weakened immune systems are especially vulnerable to contracting cellulitis. Diabetics are more prone to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet because their disease causes impairment of blood circulation in their legs leading to their having foot ulcers that commonly become infected. Cellulitis is also a common complication of obesity.

Immunosuppressive drugs, HIV, and other illnesses or infections that weaken the immune system are also factors that make infection more likely. In addition, chickenpox and shingles often result in blisters which break, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.

Diseases that affect blood circulation in the legs and feet, such as chronic venous insufficiency and varicose veins, are also risk factors for cellulitis.

Cellulitis is also extremely prevalent amongst dense populations sharing hygiene facilities and common living quarters. Military installations which require communal showers provide such an environment, as it is prevalent among many recruits going through boot camp.

Diagnosis
Cellulitis is most often a clinical diagnosis, and local cultures do not always identify the causative organism. Blood cultures usually are positive only if the patient develops generalised sepsis. Conditions that may resemble cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow.

Incubation
Cellulitis can develop in as little as twenty-four hours or can take days to develop.

Duration
In many cases, cellulitis takes less than a week to disappear with antibiotic therapy. However, it can take months to resolve completely in more serious cases, and can result in severe debility or even death if untreated. If it is not properly cured it may appear to improve but can resurface again even after months and years.

Treatment
Antibiotics - typically a combination of intravenous and oral antibiotics are administered. Bed rest and elevation of affected limbs is also recommended.

Prevention
Good hygiene and good wound care lower the risk of cellulitis. Any wounds should be cleaned and dressed appropriately. Changing bandages daily or when they become wet or dirty will reduce the risk of contracting cellulitis. Medical advice should be sought for any wounds which are deep, dirty or if there is concern about retained foreign bodies.

Celluitis

Amitriptylin

Amitriptyline (or Amitryptyline) hydrochloride (sold as Elavil, Tryptanol, Endep, Elatrol, Tryptizol, Trepiline, Laroxyl) is a tricyclic antidepressant drug. It is a white, odorless (but tastes like licorice), crystalline compound which is freely soluble in water; it is usually dispensed in tablet form. In terms of its mechanism of action, amitriptyline inhibits serotonin and noradrenaline reuptake almost equally.

Uses

Approved
Amitriptyline is approved for the treatment of endogenous depression and involutional melancholia (depression of late life, which is no longer seen as a disease in its own right.) Adult typical dosages are 25 to 150 mg daily, with half this initially for elderly or adolescents.

It may also be used to treat nocturnal enuresis (bed wetting). Children between the ages of 7 to 10 years having a dose of 10 to 20 mg, older children 25 to 50 mg at night. It should be gradually withdrawn at the end of the course, which overall should be of no more than 3 months.

In some European countries it is also approved as prophylaxis for patients with frequent migraines (usually 25 to 75 mg).


Unapproved/Off-Label/Investigational
Amitriptyline may be prescribed for other conditions such as insomnia, migraine, rebound headache, chronic pain, postherpetic neuralgia (persistent pain following a shingles attack), fibromyalgia, vulvodynia, interstitial cystitis, irritable bowel syndrome, diabetic peripheral neuropathy, neurological pain, and painful paresthesias related to multiple sclerosis and as a preventative (prophylaxis) for patients with frequent migraines. It is also used in small (10 mg) doses to act as a painkiller and ease the effects of Carpal Tunnel Syndrome. Typically lower dosages are required for pain modification of 10 to 50 mg daily.

Amitriptyline in very small doses (5 mg a day) is also sometimes prescribed to help ease the symptoms of chronic fatigue syndrome. It is thought to help combat symptoms of insomnia primarily, in addition to other selected symptoms of the affliction.

A randomized controlled trial published in June 2005 found that amitriptyline was effective in functional dyspepsia refractory to famotidine and mosapride combination therapy.

Side effects
Common side effects of using amitriptyline are weight loss or gain, drowsiness, nervousness, and dizziness insomnia. Some rare side effects include tinnitus, hypotension, mania, psychosis, anticholinergic effects, heart block, arrhythmias, extrapyramidal symptoms, depression, and hepatic toxicity.

Overdose: The symptoms and the treatment of an overdose are largely the same as for the other tricyclic antidepressants.

Amitriptylin

Addisins Disease

Addison's disease (also known as chronic adrenal insufficiency, hypocortisolism or hypocorticism) is a rare endocrine disorder in which the adrenal gland produces insufficient amounts of steroid hormones (glucocorticoids and often mineralocorticoids). It may develop in children as well as adults, and may occur as the result of a large number of underlying causes.

The condition is named after Dr Thomas Addison, the British physician who first described the condition in his 1855 On the Constitutional and Local Effects of Disease of the Suprarenal Capsules. The adjective "Addisonian" is used for features of the condition, as well as patients with Addison's disease.

The condition is generally diagnosed with blood tests, medical imaging and additional investigations. Treatment is with replacement of the hormones (oral hydrocortisone and fludrocortisone). If the disease is caused by an underlying problem, this is addressed. Regular follow-up and monitoring for other health problems is necessary.

Signs and symptoms

Symptoms

The symptoms of Addison's disease develop insidiously, and it may take some time to be recognised. The most common symptoms are fatigue, muscle weakness, weight loss, vomiting, diarrhea, headache, sweating, changes in mood and personality and joint and muscle pains. Some have marked cravings for salty foods due to the urinary losses of sodium.


Clinical signs
On examination, the following may be noticed:

Low blood pressure that falls further when standing (orthostatic hypotension)
Darkening (hyperpigmentation) of the skin, including areas not exposed to the sun; characteristic sites are skin creases (e.g. of the hands), nipples, and the inside of the cheek (buccal mucosa), also old scars may darken.
Signs of conditions that often occur together with Addison's: goiter and vitiligo

Addisonian crisis
An "Addisonian crisis" is a constellation of symptoms that indicate severe adrenal insufficiency. This may be the result of either previously undiagnosed Addison's disease, a disease process suddenly affecting adrenal function (such as adrenal hemorrhage, or in a patient with known Addison's disease who has suffered an intercurrent problem (e.g. infection, trauma). Additionally, this situation may develop in those on long-term oral glucocorticoids who have suddenly ceased taking their medication.

Untreated, an Addisonian crisis can be fatal. It is a medical emergency, usually requiring hospitalization. Characteristic symptoms are:

Sudden penetrating pain in the legs, lower back or abdomen
Severe vomiting and diarrhea, resulting in dehydration
Low blood pressure
Loss of consciousness/Syncope
Hypoglycemia
Confusion, psychosis
Convulsions

Diagnosis

Suggestive features
Routine investigations may show:

Hypoglycemia, low blood sugar (worse in children)
Hyponatraemia (low blood sodium levels)
Hyperkalemia (raised blood potassium levels), due to loss of production of the hormone aldosterone
Eosinophilia and lymphocytosis (increased number of eosinophils or lymphocytes, two types of white blood cells)

Testing

Cortisol
AldosteroneIn suspected cases of Addison's disease, one needs to demonstrate that adrenal hormone levels are low even after appropriate stimulation with synthetic pituitary hormone tetracosactide. Two tests are performed, the short and the long test.

The short test compares blood cortisol levels before and after 250 micrograms of tetracosactide (IM/IV) is given. If, one hour later, plasma cortisol exceeds 170 nmol/L and has risen by at least 330 nmol/L to at least 690 nmol/L, adrenal failure is excluded. If the short test is abnormal, the long test is used to differentiate between primary adrenal failure and secondary adrenocortical failure.

The long test uses 1 mg tetracosactide (IM). Blood is taken 1, 4, 8, and 24 hours later. Normal plasma cortisol level should reach 1000 nmol/L by 4 hours. In primary Addison's disease, the cortisol level is reduced at all stages whereas in secondary corticoadrenal insufficiency, a delayed but normal response is seen.

Other tests that may be performed to distinguish between various causes of hypoadrenalism are renin and adrenocorticotropic hormone levels, as well as medical imaging - usually in the form of ultrasound, computed tomography or magnetic resonance imaging (MRI).


Causes
Causes of adrenal insufficiency can be grouped by the way in which they cause the adrenals to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to the gland being damaged).

Adrenal dysgenesis
All causes in this category are genetic, and generally very rare. These include mutations to the SF1 transcription factor, congenital adrenal hypoplasia (AHC) due to DAX-1 gene mutations and mutations to the ACTH receptor gene (or related genes, such as in the Triple A or Allgrove syndrome). DAX-1 mutations may cluster in a syndrome with glycerol kinase deficiency with a number of other symptoms when DAX-1 is deleted together with a number of other genes.

Impaired steroidogenesis
To form cortisol, the adrenal gland requires cholesterol, which is then converted biochemically into steroid hormones. Interruptions in the delivery of cholesterol include Smith-Lemli-Opitz syndrome and abetalipoproteinemia. Of the synthesis problems, congenital adrenal hyperplasia is the most common (in various forms: 21-hydroxylase, 17α-hydroxylase, 11β-hydroxylase and 3β-hydroxysteroid dehydrogenase), lipod CAH due to deficiency of StAR and mitochondrial DNA mutations.

Adrenal destruction
Autoimmune destruction of the adrenal cortex (often due to antibodies against the enzyme 21-Hydroxylase) is a common cause of Addison's in teenagers and adults. This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2). Adrenal destruction is also a feature of adrenoleukodystrophy (ALD), and when the adrenal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body), hemorrhage (e.g. in Waterhouse-Friderichsen syndrome or antiphospholipid syndrome), particular infections (tuberculosis, histoplasmosis, coccidioidomycosis), deposition of abnormal protein in amyloidosis. Some medications interfere with steroid synthesis enzymes (e.g. ketoconazole), while others accelerate the normal breakdown of hormones by the liver (e.g. rifampicin, phenytoin).


Treatment

Maintenance treatment

Treatment for Addison's disease involves replacing the missing cortisol (usually in the form of hydrocortisone tablets) in a dosing regimen that mimics the physiological concentrations of cortisol. Treatment must usually be continued for life. In addition, many patients require fludrocortisone as replacement for the missing aldosterone. Caution must be exercised when the person with Addison's disease becomes unwell, has surgery or becomes pregnant. Medication may need to be increased during times of stress, infection, or injury.

Addisonian crisis

Treatment for an acute attack, an Addisonian crisis, usually involves intravenous (into blood veins) injections of:

Cortisone (cortisol)
Saline solution (basically a salt water, same clear IV bag as used to treat dehydration)
Glucose

Surgery
Surgeries may require significant adjustments to medication regimens prior to, during, and following any surgical procedure. The best preparation for any surgery, regardless of how minor or routine it may normally be, is to speak to one's primary physician about the procedure and medication implications well in advance of the surgery.


Pregnancy
Many women with Addison's have given birth successfully and without complication, both through natural labor and through cesarean delivery. Both of these methods will require different preventative measures relating to Addison's medications and dosages. As is always the case, thorough communication with one's primary physician is the best course of action. Occasionally, oral intake of medications will cause debilitating nausea and vomiting, and thus the woman may be switched to injected medications until delivery. Addison's treatment courses by the mother are generally considered safe for baby during pregnancy.


Epidemiology
The frequency rate of Addison's disease in the human population is sometimes estimated at roughly 1 in 100,000.[4] Some research and information sites put the number closer to 40-60 cases per 1 million population. (1/25,000-1/16,600) (Determining accurate numbers for Addison's is problematic at best and some incidence figures are thought to be underestimates.[6]) Addison's can afflict persons of any age, gender, or ethnicity, but typically presents in adults between 30 and 50 years of age. Women are slightly more likely to develop Addison's according to some studies. Research has shown no significant predispositions based on ethnicity.


Prognosis
While treatment solutions for Addison's disease are far from precise, overall long-term prognosis is typically good. Because of individual physiological differences, each person with Addison's must work closely with their physician to adjust their medication dosage and schedule to find the most effective routine. Once this is accomplished (and occasional adjustments must be made from time to time, especially during periods of travel, stress, or other medical conditions), symptomology is usually greatly reduced or occasionally eliminated so long as the person continues their dosage schedule.


Canine hypoadrenocorticism
The condition is relatively rare, but has been diagnosed in all breeds of dogs. In general, it is underdiagnosed, and one has to have a clinical suspicion of it as an underlying disorder for many presenting complaints. Females are overrepresented, and the disease often appears in middle age (4-7 years), although any age or gender may be affected.

Hypoadrenocorticism is treated with prednisolone and/or fludrocortisone (Florinef (r)) or a monthly injection called Percorten V (desoxycorticosterone pivlate (DOCP)). Routine blood work is necessary periodically to assess therapy.

Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for the canine sufferer.

If the owner knows about an upcoming stressful situation (shows, traveling etc.), patients generally need an increased dose of prednisone to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism.

Addisins Disease