Dermatophytosis

Nursing care plans for Dermatophytosis

Dermatophytosis (tinea) is a group of superficial fungal infections usually classified according to their anatomic location. Dermatophytosis may affect the scalp (tinea capitis), the bearded skin of the face (tinea barbae), the body (tinea corporis, occurring mainly in children), the groin (tinea cruris, or jock itch), the nails (tinea unguium, also called onychomycosis), and the feet (tinea pedis, or athlete's foot). These disorders vary from mild inflammations to acute vesicular reactions.
Tinea infections are prevalent in the United States and are usually more common in males than in females. Although remissions and exacerbations are common, with effective treatment, the cure rate is very high. About 20% of infected people develop chronic conditions.

Causes

Tinea infections result from dermatophytes (fungi) of the genera Trichophyton, Microsporum, and Epidermophyton. Transmission can occur directly through contact with infected lesions or indirectly through contact with contaminated articles, such as shoes, towels, or shower stalls. Some cases come from contact with contaminated animals or soil. Warm weather, humidity, and tight clothing encourage fungus growth

Complications

Hair or nail loss and secondary bacterial or candidal infections, resulting in inflammation, itching, tenderness, and maceration, are common complications of tinea infections.

Assessment Nursing care plans for Dermatophytosis

Tinea lesions vary in appearance and duration. Inspection of the patient with tinea capitis may expose small, spreading papules on the scalp that may progress to inflamed, pus-filled lesions (kerions). Patchy hair loss with scaling may be visible. Tinea barbae appears as pustular folliculitis in the bearded area.
In patients with tinea corporis, inspection and palpation reveal flat skin lesions at any site except the scalp, bearded skin, or feet. These lesions may be dry and scaly or moist and crusty; as they enlarge, their centers heal, producing the classic ring-shaped appearance. In patients with tinea cruris, inspection and palpation find raised, sharply defined, itchy red lesions in the groin that may extend to the buttocks, inner thighs, and external genitalia. Tinea unguium starts at the tip of one or more toenails (fingernail infection is less common). Inspection reveals gradual thickening, discoloration, and crumbling of the nail, with accumulation of subungual debris. Eventually, the nail may be completely destroyed.

Diagnoses Nursing care plans for Dermatophytosis (tinea)

• Acute pain
• Deficient knowledge (skin care regimen)
• Disturbed body image
• Impaired skin integrity
• Risk for infection

Key outcomes Diagnoses Nursing care plans for Dermatophytosis (tinea)

1. patient will report feelings of increased comfort.
2. patient and his family will demonstrate the appropriate skin care regimen.
3. patient will voice feelings about his changed body image.
4. patient will exhibit improved or healed wounds or lesions.
5. patient will avoid or minimize the risk of secondary infection.

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Bell's palsy Information

Looking at yourself in front of the mirror, you noticed that half of your face is somewhat "sagging", eyelid is drooping such that you cannot fully open your eye. Probably you are eating your favorite food and all of a sudden you cannot enjoy the food because you can't taste anything. These signs might indicate that you are experiencing a condition called Bell's Palsy.

Bell's palsy is a form of temporary facial paralysis resulting from damage or trauma to one of the two facial nerves. It is the most common cause of facial paralysis. Generally, Bell's palsy affects only one of the paired facial nerves and one side of the face, however, in rare cases, it can affect both sides. Symptoms of Bell's palsy usually begin suddenly and reach their peak within 48 hours. Symptoms range in severity from mild weakness to total paralysis and may include twitching, weakness, or paralysis, drooping eyelid or corner of the mouth, drooling, dry eye or mouth, impairment of taste, and excessive tearing in the eye. Bell’s palsy often causes significant facial distortion. Most scientists believe that a viral infection such as viral meningitis or the common cold sore virus -- herpes simplex-- causes the disorder when the facial nerve swells and becomes inflamed in reaction to the infection.



Is there any treatment?



There is no cure or standard course of treatment for Bell's palsy. The most important factor in treatment is to eliminate the source of the nerve damage. Some cases are mild and do not require treatment since the symptoms usually subside on their own within 2 weeks. For others, treatment may include medications such as acyclovir -- used to fight viral infections -- combined with an anti-inflammatory drug such as the steroid prednisone -- used to reduce inflammation and swelling. Analgesics such as aspirin, acetaminophen, or ibuprofen may relieve pain, but because of possible drug interactions, patients should always talk to their doctors before taking any over-the-counter medicines.



Physical therapy to stimulate the facial nerve and help maintain muscle tone may be beneficial to some. Facial massage and exercises may help prevent permanent contractures (shrinkage or shortening of muscles) of the paralyzed muscles before recovery takes place. Moist heat applied to the affected side of the face may help reduce pain.



Other therapies that may be useful for some individuals include relaxation techniques, acupuncture, electrical stimulation, biofeedback training, and vitamin therapy (including vitamin B12, B6, and zinc), which may help nerve growth.



In general, decompression surgery for Bell's palsy -- to relieve pressure on the nerve -- is controversial and is seldom recommended.



Will I recover from Bell's Palsy?



The prognosis for individuals with Bell's palsy is generally very good. The extent of nerve damage determines the extent of recovery. With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and recover completely within 3 to 6 months.

---

Sources:

National Institute of Neurological Disorders and Stroke(NINDS)(December, 2007). Bell's Palsy Information Page. Retrieved January 10, 2007, from NINDS, National Institutes of Health. Web site: http://www.ninds.nih.gov/disorders/bells/bells.htm



National Institute of Neurological Disorders and Stroke(NINDS)(April, 2003). Bell's Palsy Fact Sheet (NIH Publication No. 03-5114). Retrieved January 10, 2007, from NINDS, National Institutes of Health. Web site: http://www.ninds.nih.gov/disorders/bells/detail_bells.htm

Selenium Curbs AIDS Virus, may Fight Cancer

(NaturalNews) After decades of attempting to fight AIDS with experimental vaccines and drugs, scientists have recently discovered how several natural substances could be powerful weapons against the disease. For example, in mid-November, UCLA AIDS researchers published research concluding that the herb astragalus contains a substance with the potential to possibly replace the side-effect plagued HAART (highly active antiretroviral therapy) currently used to treat AIDS patients. http://www.naturalnews.com/024799.html

Now Penn State immunologists say they've documented how a micronutrient could help battle AIDS. Their findings, just published in the Journal of Biological Chemistry, show how selenium could dramatically put the brakes on the replication of HIV, the virus that causes AIDS.

Selenium is needed by the body to maintain normal metabolism. It's also increasingly being studied for its anti-cancer properties. Although other nutrients usually bind to proteins, selenium actually becomes incorporated into proteins, forming what are called selenoproteins. These selenium-containing proteins are believed to slow the spread of infections. However, when HIV infects a person, the virus manages to degrade selenoproteins, probably due to a protein, dubbed Tat, produced by the HIV virus. In particular, Tat seems to target a selenoprotein known as TR1.

But there may be a way to get around this degradation of selenoproteins -- supplementation with selenium. "Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body," K. Sandeep Prabhu, assistant professor of immunology and molecular toxicology at Penn State, said in a statement to the press.
To test their idea, the scientists isolated blood cells from human volunteers who did not have HIV. Then they infected those cells with the virus and added a form of selenium called sodium selenite to the cell culture.

The result? The added selenium inhibited the replication of the HIV virus at least 10-fold, in comparison to cell cultures with no added selenium. The scientists also selectively reduced the production pf the selenoprotein TRI. When there was less selenium-containing protein, the HIV virus replication soared 3.5 times. Bottom line: The research confirms that an increase in selenium in cells zaps replication of HIV while a reduction in the amount of selenium-containing TR1 protein gives the virus a boost.

"We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV. Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs," said Dr. Prabhu in the prepared statement for the media.

Two more new studies offer additional evidence that selenium may impact the immune system. German scientists from St. Josefs-Hospital in Wiesbaden recently published a study in the Swedish medical journal Acta Oncologica that suggests the micronutrient could help prevent prostate cancer and prostate enlargement. The researchers found that whole blood selenium levels were significantly lower in all men tested who had prostate cancer or benign prostate hypertrophy (which can cause difficulty with urination) and concluded, "our findings may support the recommendation of selenium supplementation" to help prostate health. What's more, a study just published in the journal Molecular Nutrition and Food Research suggests enzymes that contain selenium have anti-oxidative and anti-inflammatory effects that could make them important in preventing prostate and colorectal cancers.

Too much selenium in can cause a condition called selenosis, resulting in loss of hair, nail problems, nausea, irritability, fatigue, and mild nerve damage. However, selenium toxicity is extremely rare. A lack of selenium may, in fact, be far more common and potentially more dangerous to health. According to the National Institutes of Health, people age 14 and older should take in about 44 micrograms of selenium a day. Good sources of the micronutrient include Brazil nuts, eggs, brown rice, whole wheat bread and pasta, walnuts and oatmeal.

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SEORANG PASIEN SEMBUH DARI HIV

Bone marrow 'cures HIV patient'

About one in 1,000 Europeans and Americans have a resistance to HIV

Doctors in Germany say a patient appears to have been cured of HIV by a bone marrow transplant from a donor who had a genetic resistance to the virus.

The researchers in Berlin said the man, who suffered from leukaemia and HIV, had shown no sign of either disease since the transplant two years ago.

But they stressed it was an unusual case which needed further investigation.

Experts said the result may boost interest in gene therapy for HIV.

Berlin's Charite clinic said the 42-year-old patient was an American living in Berlin, but the man has not been identified.

Genetic mutation

He had been infected with the human immunodeficiency virus, that causes Aids, for more than a decade and also had leukaemia.

The clinic said since the transplant was carried out 20 months ago, tests on the patient's bone marrow, blood and other organ tissues have all been clear.

In a statement, Professor Rodolf Tauber from the Charite clinic said: "This is an interesting case for research.

"But to promise to millions of people infected with HIV that there is hope of a cure would not be right."

Roughly one in 1,000 Europeans and Americans have an inherited genetic mutation, which prevents HIV from attaching itself to cells.

Two million people die of Aids every year and HIV is estimated to have infected 33 million people worldwide.

Option 'for a few'

Professor Andrew Sewell, from the Department of Medical Biochemistry and Immunology at the University of Cardiff said in theory a bone marrow transplant such as this one "should work" and it was surprising that no one had tried it before.

"The problem is most people with HIV live in sub-Saharan Africa and this is hugely expensive, you have to find a matched donor, and it's a pretty severe and painful operation.

"So it's going to be an option for very few people."

He added that gene therapy to knock out the mutation of the key CCR5 receptor was a possibility for future treatment.

Professor Philip Goulder, an immunologist at the University of Oxford said: "It's a really interesting case which looks at a treatment which really hasn't been thought about before.

"But without having that much information about the specific case you would want to be very cautious about getting too excited and you wouldn't be able to replicate that treatment for a lot of people with HIV."

Paul Ward, deputy chief executive at the Terrence Higgins Trust said: "This case gives us something to explore in future studies but it's certainly not a quick fix as gene therapy is complex and expensive.

"With no cure in sight, prevention should be our number one priority."

source : http://news.bbc.co.uk/

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Carbon Taxes and Health Care User Fees

What do carbon taxes and health care user fees have in common?

The Liberal Party of Canada has announced the Green Shift. A tax shift program where industry is taxed based on the amount of carbon it produces. The increased cost incentivizes' companies to find production solutions with a lower carbon footprint. The additional costs to the citizen are compensated through lower income taxes and tariffs are placed to equalize the playing field for non-Canadian companies.

Not surprisingly, the concept is not sitting well with Canadians. In a time of economic turmoil, it's an inopportune time to suggest a new taxation system.

It raises an interesting contradiction in the Liberal Party platform (as well as the Green Party since the agree with the strategy). The carbon tax is social engineering through taxation. Conceptually, there is little difference between it and health care user fees.

Health care user fees incentivize people not to use the health care system. Where there is abuse and overuse the effect is positive. Where there is poverty and marginalization the effect will be horrific. I wonder whether the same would apply to the carbon tax?

Where companies are operating with willful disregard to the amount of carbon produced, in markets where the margins are thick and the competition weak there is no excuse for not lowering emissions. Where technology is lacking, margins thin and competition fierce the carbon tax will cost jobs.

Without taxation, we cannot be strong as a nation. If we hand over the basis for taxation to whatever elected officials declare the latest cause do we run the larger risk of wild fluctuations in revenue? One could equally argue that taxation should be based on homeland defense, obesity, crime rates or any other key issue.

The larger question is do we, as Canadians, want to leverage our tax system to the vacillating opinions and priorities of elected officials.

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Can Vitamin B3 Reduce Memory Problems (Nicotinamide)

Researchers are reporting that huge doses of Nicotinamide (a form of vitamin B3) appear to eliminate memory problems in mice with the rodent equivalent of Alzheimer's disease. This information is being reported in The Journal of Neuroscience.

This science gets my attention because Nicotinamide is a water-soluble vitamin sold over the counter in health food stores.

While it is impossible for me to know how and why, a combination of exercise, Aricept, vitamin B, multiple vitamins, vitamin supplements, a healthy diet, cocoa flavanols, bright light, and a heavy emphasis on socialization has slowed the progression of Alzheimer's in my mother. We will be adding Nicotinamide to this regimen shortly.

The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve," Frank LaFerla, UC Irvine neurobiology and behavior professor.

The Institute for Brain Aging and Dementia is conducting a clinical trial to show that, nicotinamide (NA), a B3 vitamin, is safe and effective for the treatment of patients with mild to moderate Alzheimer's disease. They are receiving funding from the Alzheimer's Association.


From the Press Release

An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.

Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.

“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”

The study appears online Nov. 5 in the Journal of Neuroscience.

Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.

Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.

In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.

The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.

Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.

Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.

“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”

LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.

The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.

For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.

UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.

source : http://alzheimersreadingroom.blogspot.com

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Diet drug 'doubles weight loss'

The drug helped people lose significant amounts of weight

An anti-obesity drug vastly outperforms currently available rivals, early trials suggest.

Danish tests of tesofensine, reported in The Lancet, found dieting patients on the highest doses lost up to 12.8kg (28.2lbs) in six months.

This is twice the level achieved by drugs such as sibutramine and rimonabant.

But UK experts warned that more trials were needed, and expressed concerned the results may have been hyped.

At the moment there is a definite plateau which limits the effectiveness of current drugs, and if this new drug could break through that, that would be great Dr David Haslam National Obesity Forum

Tesofensine first came to the attention of obesity researchers when it caused unintended weight loss when given to overweight patients with Parkinson's or Alzheimer's disease.

It works by changing the way that three nerve signalling chemicals, noradrenaline, dopamine, and serotonin have their effects on the brain.

This in turn reduces appetite, so that the person will eat smaller meals and have a reduced urge to snack.

The Danish study, led by Professor Arne Astrup, from the University of Copenhagen, split a group of 203 obese patients into two groups.

Both groups were given a once-daily pill to take, and told to go on a moderate diet, but half the pills were tesofensine, in varying doses, and the other half were "dummy" placebo pills.

After six months, all were re-measured, and the researchers found that while the placebo group had lost an average 2.2kg (4.85lbs) those taking tesofensine had lost much more.

On the lowest dose, the average weight loss was 6.7kg (14.8lbs), the medium dose produced 11.3kg weight loss (24.9lbs) and the highest dose 12.8kg (28.2lbs).

This performance is roughly twice that achieved by the best weight-loss drugs already approved for use in Europe.

Blood pressure warning

The drugs did produce side-effects, ranging from dry mouth and insomnia to nausea and diarrhoea, with the highest dose increasing patients' blood pressure, a concern given that many obese patients may have heart problems or diabetes.

The researchers said that the middle dose was more promising because it produced almost as great a weight loss as the highest dose, without the worst side-effect.

They called for bigger trials to confirm their result, and the drug is unlikely to become available across Europe until these are completed over the next couple of years.

Professor Steve O'Rahilly, an obesity expert at the University of Cambridge, said: "If we could treat obesity like we treat high blood pressure, with safe, effective and affordable drugs, this would be an enormous boon to health care.

"However, to date obesity drugs that have been effective have not been safe, and conversely those that are safer are relatively ineffective.

"The results with this new drug demonstrate that, over a six-month period, it is quite effective.

"However, as the drug is likely to have actions on parts of the brain not involved in weight control, the risk of serious side-effects on longer term administration will need to be watched very carefully."

Professor Iain Broom, of Robert Gordon University, said it was premature to claim that tesofensine significantly out-performed other anti-obesity drugs, as it had not been widely tested, unlike its rivals.

And Professor Mike Lean, a human nutrition expert from the University of Glasgow, said the drug seemed similar to sibutramine - which is licenced and has a very good safety record.

"The results are generally interesting but a lot more research is needed before anyone should be given it in routine practice."

SOURCE : http://news.bbc.co.uk

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Drug 'tricks body to lose weight'

The drug is the chemical cousin of an extract in red wine

French scientists say they have found a drug that tricks the body into burning off fat even when on a high-fat diet.

The University of Louis Pasteur team found the drug protected mice against weight gain and insulin resistance.

The drug SRT1720 - a chemical cousin of red wine extract resveratrol - targets the protein SIRT1, which is thought to combat ageing, Cell Metabolism reports.

UK obesity experts said new drug treatments were needed but should be used alongside lifestyle changes.

About a quarter of men and a third of women in the UK are overweight, according to government statistics.

A change in diet and an increase in physical exercise can shift excess weight, but can be hard for many to maintain.

With the removal of the anti-obesity pill rimonabant, also known as Acomplia, from the market amid safety concerns, fewer drug options exist.

Potent drug

The French team from the University Louis Pasteur became interested in the SIRT1 protein after earlier studies showing resveratrol countered some effects of a high-calorie diet via SIRT1.

We do need new treatments for obesity, particularly as there are 1,000 deaths a week in the UK from obesity Professor Stephen Bloom of Imperial College London

But tests in mice suggested gallons of wine would be necessary for humans to stand a chance of getting the same benefits.

The scientists turned their attention to creating a more potent drug that would specifically target SIRT1.

They found that a low dose of SRT1720 partially protected mice from gaining weight on a high-fat diet after 10 weeks of treatment.

The drug worked by shifting the metabolism to a fat-burning mode that normally takes over only when energy levels are low.

At higher doses, the drug completely prevented weight gain. It also improved the rodents' blood sugar tolerance and insulin sensitivity, which are important for warding off diabetes.

The mice showed no sign of side effects. However, the scientists say further studies are needed to test the drug's safety and efficacy before it could be used in humans.

Other scientists are investigating SIRT1 activators similar to SRT1720 developed by Sirtris Pharmaceuticals.

Professor Stephen Bloom, who has been researching obesity at Imperial College London, said: "This sounds interesting but is terribly early.

"We do need new treatments for obesity, particularly as there are 1,000 deaths a week in the UK from obesity."

Prof Ian Broom, of the Centre for Obesity Research and Epidemiology at The Robert Gordon University, said: "Research in this area is to be welcomed as an additional route of combating the obesity epidemic and associated comorbid disease."

He added that any such drug should be used alongside dietary and lifestyle changes to tackle obesity.

source : http://news.bbc.co.uk

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New Method Provides Panoramic View of Protein-RNA Interactions in Living Cells

DNA, it has turned out, isn’t all it was cracked up to be. In recent years we learned that the molecule of life, the discovery of the 20th century, did not — could not — by itself explain the huge differences in complexity between a human and a worm. Forced to look elsewhere, scientists turned to RNA, a direct yet more complex transcript of DNA. But methodological problems have historically plagued the study of RNA regulation in living cells, limiting not only the accuracy of results but also our understanding of RNA’s role in human disease.

But now, in research to appear in the advance online issue of Nature, Robert B. Darnell, head of the Laboratory of Molecular Neuro-oncology at Rockefeller University and a Howard Hughes Medical Institute investigator, and his team have changed all that.

By adapting techniques mastered in the test tube and combining them with high throughput technology, the team has developed a genome-wide platform to study how specialized proteins regulate RNA in living, intact cells. The platform allows researchers to identify, in a single experiment, every sequence within every strand of RNA to which proteins bind. The result is an unbiased and unprecedented look at how differences in RNA can explain how a worm and a human can each have 25,000 genes yet be so different.

“RNA offers a way to make the cell much more complex than what this limited set of genes can offer,” says Darnell, who is Robert and Harriet Heilbrunn Professor at Rockefeller. “But how is RNA being regulated in different conditions and diseases, and in different cell types? With this platform, we now have a way to address all these questions.”

Release date: November 2, 2008

Source: Rockefeller University

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Designer Molecule Tackles Skin Cancer from Two Sides

By playing it safe and using a two-pronged attack, a novel designer molecule fights malignant melanoma. It was created and tested by an international team of researchers led by the University of Bonn. On the one hand, the substance is similar to components of viruses and in this way alerts the immune system. The body's own defences are also strengthened against cancer cells in this process. At the same time, the novel molecule also puts pressure on the tumour in a different way. It switches off a specific gene in the malignant cells, thus driving them to suicide. With mice suffering from cancer, the researchers have thus been able to fight metastases in the lung. In Nature Medicine's November issue they report about this promising strategy.

For their research project, the scientists drew on the latest insights into biology's box of tricks. A close relative of the nuclear DNA, known as RNA, served them as therapy. It has only been known for a few years that small RNA molecules can basically be used to target certain genes and switch them off. This effect is called RNA interference; the Americans Craig Mellow and Andrew Fire were awarded the Nobel Prize in 2006 for its discovery.

'We used this method in order to drive the tumour cells to suicide,' the Bonn dermatology researcher Professor Thomas Tüting explains. Every single body cell is equipped with a corresponding suicide programme. It is activated, for example, if the cell becomes malignant. It dies before it can do any more harm. 'But in tumours a gene is active that suppresses this suicide programme,' Professor Tüting, who is head of the Experimental Dermatology Laboratory, explains. 'We have pinpointed this gene and switched it off by using RNA interference.'

At the same time the researchers also crept up on cancer by another route: 'We basically "disguised" our RNA,? Professor Gunther Hartmann, director of the Institute of Clinical Chemistry and Pharmacology says. 'That is why the immune system took it for the genetic makeup of a virus.' Many viruses actually do use RNA to store information. So if the body discovers RNA fragments which it takes to be the genetic makeup of a virus, it mounts an attack on them. By means of this trick the body?s defences were prompted to tackle the tumour cells far more aggressively than normal.

Release date: November 2, 2008

Source: University of Bonn

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syndactyly

One of the common birth defects is syndactyly, in which two or more fingers are fused together. Surgical correction involves cutting the tissue that connects the fingers, then grafting skin from another part of the body. (The procedure is more complicated if bones are also fused.) Surgery can usually provide a full range of motion and a fairly normal appearance, although the color of the grafted skin may be slightly different from the rest of the hand. Other common congenital defects include short, missing, or deformed fingers, immobile tendons, and abnormal nerves or blood vessels. In most cases, these defects can be treated surgically and significant improvement can be expected.

Medical therapy

Syndactyly requires surgical intervention. Full-term infants can be scheduled for elective surgical procedures as early as 5 or 6 months of age. Surgery before this age can increase anesthetic risks. Prior to that time, there is generally no intervention necessary if there are no problems. If there is an associated paronychia which can occur with complex syndactyly, the parents are given instructions to wash the child's hands thoroughly with soap and water and toa apply a topical antibacterial solution or ointment. Oral antibiotics are given when indicated.

Surgical therapy

The timing of surgery is variable. However, if more fingers are involved and the syndactyly is more complex, release should be performed earlier. Early release can prevent the malrotation and angulation that develops from differential growth rates of the involved fingers.

In persons with complex syndactyly, the author performs the first release of the border digits when the individual is approximately 6 months old. This approach is used because differential growth rates are observed, particularly between the small finger and ring finger or between the thumb and index finger. Prolonged syndactyly between these digits can cause permanent deformities. If more than one syndactyly is present in the same hand, simultaneous surgical release can be performed, provided only one side of the involved fingers is released. For example, in a 4-finger syndactyly involving the index, long, ring, and small fingers, the index finger can be released from the long finger, and the small finger can be released from the ring finger, leaving a central syndactyly involving the long and ring fingers (see Images 27-28). If both hands are involved, bilateral releases can be performed at one operative setting.

Perform bilateral releases whenever feasible to reduce the number of surgeries and the associated risks. Postoperative bilateral immobilization of the upper extremities is well tolerated in the child who is younger than 18 months. The increasingly active child who is older than 18 months has a difficult time with bilateral immobilization. Therefore, in children older than 18 months, any procedures must be staged unilaterally. The remaining syndactyly between the long finger and ring finger can be released approximately 6 months later (see Images 29-30). In an individual with isolated central syndactyly between the long finger and ring finger, the release need not be accomplished until the second year of life because of similar growth rates between the long finger and ring finger. It is preferable to complete all major reconstructions before a child is school age.

However, even if the child is older than the ideal age (which is usually before school age for functional, developmental, and psychological reasons), it is not too late to release the central rays (long and ring fingers) at a later age, as they have similar growth rates. For example, a 5° flexion contracture could eventually improve once the fingers are released. In children, unlike in adults, persistent flexion contractures are rare. The technical details of syndactyly release are similar to the release performed in infants. In older patients, splints are still applied but can be removed earlier, at about 7-10 days, because the patients are more compliant with activity and with dressing changes after the splint is removed

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Bullous Pemphigoid

Major points

• Large, tense blisters arising on normal or erythematous skin
• Mucous membrane involvement in 10–35%
• Sites of predilection: lower abdomen, inner thighs, flexor forearms or generalized
• Bullae may have clear or hemorrhagic fluid
  

(Figures 1 and 2)

Figure 1. Bullous pemphigoid - large bullae on erythematous patches

Figure 2. Pemphigoid gestationis - in a young pregnant woman. Her child was unaffected

• Erosions tend to re-epithelialize quickly
• Nikolsky sign is negative
• New vesicles may form at the edge of old blisters
• Blisters do not tend to scar but may be hyperpigmented
• Mild to moderate pruritus
• Early lesions tend to look urticarial
• Rare in childhood

• 
  

Pathogenesis

Bullous pemphigoid (BP) antigens are proteins in the hemidesmosomes (HDs). Autoantibody binds both inside the cell to plaques of HDs and outside cells to the extracellular section of HDs
BP antibodies are directed against both BPAg-1 (230 kDa) component and also BPAg-2 (180kDa) (also called type XVII collagen)

BP IgG can activate complement by the classical pathway causing leukocyte adherence to the basement membrane, degranulation of polymorphonuclear leukocytes and subsequent dermal–epidermal separation

Diagnosis

Histology: Subepidermal blister without necrosis, and superficial dermal infiltrate with lymphocytes, histiocytes and eosinophils
DIF: linear pattern of C3 and IgG at BMZ

Indirect immunoflourescence: 70–80% of patients will have circulating IgG which binds to stratified squamous epithelium; titers do not correlate with disease extent or activity ~50% have elevated IgE, and sometimes eosinophilia, which correlates with pruritus

Differential diagnosis

1. Bullous insect bite reactions
2. Bullous impetigo
3. Bullous erythema multiforme
4. Chronic bullous disease of childhood

1. 
   

Treatment

• Prednisone 1–2mg/kg per day until activity is suppressed. Once under control, steroids should be tapered to avoid side-effects

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• Steroid-sparing agents can be used as an adjunct: cyclophosphamide, azathioprine, cyclosporine, methotrexate, or gold
• Localized BP can be treated with high-potency topical steroids
• Some patients respond to sulfones, tetracycline, or nicotinamide

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Prognosis
BP may be self-limited and can last several months to many years
Prognosis is good. In adults, half of treated patients go into remission in 2.5–6 years

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Venomous SnakebiteVenomous Snakebite

Epidemiology

Venomous snakes (Fig. 1) of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes, and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are nonvenomous and only a few are dangerously toxic to humans). Bite rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with >125,000 deaths.

Figure 1. Types of highly venomous snakes. (A).The Viperidae, (B). The Elapidae, (C). Hydrophiidae (D). Atractaspididae

Snake Anatomy/Identification

The typical snake-venom apparatus consists of bilateral venom glands located below and behind the eye and connected by ducts to hollow, anterior maxillary teeth. In viperids (vipers and pit vipers), these teeth are long mobile fangs that retract against the roof of the mouth when the animal is at rest. In elapids and sea snakes, the fangs are smaller and are relatively fixed in an erect position. In ~20% of pit viper bites and higher percentages of other snakebites (e.g., up to 75% for sea snakes), no venom is released ("dry" bites). Significant envenomation probably occurs in ~50% of all venomous snakebites.

Differentiation of venomous from nonvenomous snake species can be difficult. Viperids are characterized by somewhat triangular heads (a feature shared with many harmless snakes); elliptical pupils (also seen in some nonvenomous snakes, such as boas and pythons); enlarged maxillary fangs; and, in pit vipers, paired heat-sensing pits (foveal organs) on each side of the head. The New World rattlesnakes generally have a series of interlocking keratin plates (the rattle) on the tip of the tail; the rattle is used to warn potentially threatening intruders. Color pattern is notoriously misleading in identifying most venomous snakes. Many harmless snakes have color patterns that closely mimic venomous snakes found in the same region.

Venoms and Clinical Manifestations

Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding. Proteolytic enzymes cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Myocardial depressant factors reduce cardiac output, and neurotoxins act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms have multisystem effects in their victims.

Envenomations by most viperids and some elapids with necrotizing venoms typically cause progressive local swelling, pain, ecchymosis (Fig. 2), and (over a period of hours or days) hemorrhagic bullae and serum-filled vesicles. In serious bites, tissue loss can be significant (Fig. 3). Systemic findings can include changes in taste, mouth numbness, muscle fasciculations, tachycardia or bradycardia, hypotension, pulmonary edema, hemorrhage (from essentially any anatomic site), and renal dysfunction. Envenomations by neurotoxic elapids such as kraits (Bungarus spp.), many Australian elapids [e.g., death adders (Atractaspis spp.) and tiger snakes (Notechis spp.)], some cobras (Naja spp.), and some viperids [e.g., the South American rattlesnake (Crotalus durissus) and some Indian Russell's vipers (Daboia russelii)] cause neurologic dysfunction. Early findings may consist of cranial nerve weakness (e.g., manifested by ptosis) and altered mental status. Severe poisoning may result in paralysis, including the muscles of respiration, and lead to death due to respiratory failure and aspiration. After elapid bites, the time of onset of venom intoxication varies from minutes to hours depending on the species involved, the anatomic location of the bite, and the amount of venom injected. Sea snake envenomation usually causes local pain (variable), myalgias, rhabdomyolysis, and neurotoxicity; these manifestations are occasionally delayed for hours.

Figure 2. Northern Pacific rattlesnake (Crotalus oreganus oreganus) envenomations. Top: Moderately severe envenomation. Note edema and early ecchymosis 2 h after a bite to the finger. Bottom: Severe envenomation. Note extensive ecchymosis 5 days after a bite to the ankle.

Figure3. Early stages of severe, full-thickness necrosis 5 days after a Russell's viper (Daboia russelii) bite in southwestern India

Treatment

Field Management

The most important aspect of prehospital care of a victim bitten by a venomous snake is rapid delivery to a medical facility equipped to provide supportive care (airway, breathing, and circulation) and antivenom administration. Most first aid recommendations made in the past are of little benefit, and some can actually worsen outcome. It is reasonable to apply a splint to the bitten extremity in order to lessen bleeding and discomfort and, if possible, to keep the extremity at approximately heart level. In developing regions, indigenous people should be encouraged to seek care quickly at health care facilities equipped with antivenoms as opposed to consulting traditional healers.

Although mechanical suction has been recommended in the field management of venomous snakebite for many years, there is now evidence that this intervention is of no benefit and can actually be deleterious in terms of local tissue damage.

Techniques or devices used for centuries in an effort to limit venom spread remain controversial. Lympho-occlusive bandages or tourniquets may limit spread only at the cost of greater local tissue damage, particularly with necrotic venoms. Because tourniquets lead to higher rates of amputation and loss of function, they absolutely should not be used. Elapid venoms that are primarily neurotoxic and have no significant local tissue effects may be localized by pressure-immobilization, in which the entire limb is immediately wrapped with a bandage (e.g., crepe or elastic) and then splinted. The wrap pressure must reach ~40–70 mmHg to be effective. Furthermore, if more than a few minutes from medical care, the victim must be carried out from the scene of the bite. Otherwise, muscular pumping will promote venom dispersal, even in bites to the upper extremities. In short, pressure-immobilization should be used only in cases where the offending snake is reliably identified and has a primarily neurotoxic venom, the rescuer is skilled in pressure-wrap application, and the victim can be carried to medical care—an uncommon combination of conditions. Besides tourniquets, other forbidden measures include incising or cooling the bite site, giving the victim alcoholic beverages, and applying electric shocks. The best first aid advice, as coined by Dr. Ian Simpson of the World Health Organization's Snakebite Treatment Group, is to "do it 'RIGHT'": reassure the victim, immobilize the extremity, get to the hospital, and inform the physician of telltale symptoms and signs.

Hospital Management

In the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, oxygen saturation, urine output) while a history is quickly obtained and a rapid, thorough physical examination is performed. Victims of neurotoxic envenomation should be watched carefully for evidence of difficulty swallowing or respiratory insufficiency, which should prompt definitive securing of the airway by endotracheal intubation. To provide objective evidence of the progression of envenomation, the level of swelling in a bitten extremity should be marked and limb circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore IV access in unaffected extremities should be established. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds. Later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with isotonic saline should be initiated for clinical shock. If the blood pressure response to administration of crystalloid (20–40 mL/kg) is inadequate, a trial of 5% albumin (10–20 mL/kg) is prudent. If tissue perfusion fails to respond to volume resuscitation and antivenom infusion (see below), vasopressors (e.g., dopamine) can be added. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases, although obtaining access is risky if coagulopathy has developed.

Blood should be drawn for typing and cross-matching and for laboratory evaluation as soon as possible. Important studies include a complete blood count (to evaluate degree of hemorrhage or hemolysis and effects on platelet count), studies of renal and hepatic function, coagulation studies (to identify consumptive coagulopathy), and testing of urine for blood or myoglobin. In developing regions, the 20-min whole-blood clotting test (WBCT) can be used to diagnose coagulopathy reliably. A few milliliters of fresh blood are placed in a new, plain glass receptacle (e.g., test tube) and left undisturbed for 20 min. The tube is then tipped once to 45° to determine whether a clot has formed. If not, coagulopathy is diagnosed. In severe envenomations or with significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be helpful. Any arterial puncture in the setting of coagulopathy, however, requires great caution and must be performed at an anatomic site amenable to direct-pressure tamponade. After antivenom therapy (see below), laboratory values should be rechecked every 6 h until clinical stability is achieved.

The key to management of venomous snakebite is the administration of specific antivenom. Circulating venom components bind quickly with heterologous antibodies produced in animals immunized with the venom in question (or a very closely related venom). Antivenoms may be monospecific (for a particular snake species) or polyspecific (covering several medically important species in the region) but rarely offer cross-protection against snake species other than those used in their production unless the species are known to have homologous venoms. In the United States, assistance in finding antivenom can be obtained 24 h a day from regional poison control centers.

Indications for antivenom administration in victims of viperid bites include any evidence of systemic envenomation (systemic symptoms or signs; laboratory abnormalities) and (possibly) significant, progressive local findings (e.g., soft tissue swelling crossing a joint or involving more than half the bitten limb in the absence of a tourniquet). Care must be used in determining the significance of isolated soft-tissue swelling as, in many countries, the saliva of some relatively harmless snakes causes mild edema at the bite site. In such bites, antivenoms are unhelpful and unnecessary.

In the developing world (e.g., much of Asia and Africa), elapid bites are generally treated similarly to viperid bites. Systemic symptoms such as ptosis, other manifestations of cranial nerve impairment, or respiratory compromise constitute grounds for antivenom administration. Decisions about antivenom administration to victims with isolated local signs or symptoms are based on the criteria listed above for viperid bites.

Production of the only antivenom currently available in the United States for coral snake bites has been discontinued, and remaining stocks will be exhausted or will expire shortly. Until a suitable substitute is produced or imported, physicians caring for victims of Micrurus bites may have to rely on sound supportive care, especially airway management and respiratory support.

The package insert for the selected antivenom can be consulted regarding species covered, method of administration, starting dose, and need (if any) for re-dosing. The information in antivenom package inserts, however, is not always accurate and reliable. Whenever possible, it is advisable for treating physicians to seek advice from experts in snakebite management regarding indications for and dosing of antivenom. For viperid bites, antivenom administration should generally be continued as needed until the victim shows definite improvement (e.g., stabilized vital signs, reduced pain, restored coagulation). Neurotoxicity from elapid bites may be harder to reverse with antivenom. Once neurotoxicity is established and endotracheal intubation is required, further doses of antivenom are unlikely to be beneficial. In such cases, the victim must be maintained on mechanical ventilation until recovery occurs, which may take days to weeks.

The newest available antivenom in the United States (CroFab; Fougera, Melville, NY) is an ovine, Fab fragment antivenom that covers systemic venom effects of all North American pit viper species and carries a low risk of allergic sequelae. Table 1 compares the two antivenoms recently available for the treatment of pit viper bites in the United States. The manufacturer of Antivenin (Crotalidae) Polyvalent has recently discontinued its production, leaving CroFab as the current drug of choice for the management of indigenous pit viper envenomations in the United States. Use of any heterologous serum product carries a risk of anaphylactoid reactions and delayed-hypersensitivity reactions (serum sickness). Skin testing for potential allergy is insensitive and nonspecific and should be omitted. Worldwide, the quality and availability of antivenoms are highly variable. In many developing countries, antivenom resources are scarce, contributing to high morbidity and mortality rates in these regions. The rates of acute anaphylactoid reactions to some of these products exceed 50%. If the risk of allergic reaction is significant, pretreatment with appropriate loading doses of IV antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5–10 mg/kg to a maximum of 300 mg) may be considered. In some regions, a prophylactic SC or IM dose of epinephrine is given in an effort to reduce the risk of reaction. Further research is necessary to determine whether any pretreatment measures are truly beneficial. Modest expansion of the patient's intravascular volume with crystalloids could blunt an acute adverse reaction.

Table 1 Comparison of Antivenoms Recently Available for Treatment of Pit Viper Bites in the United States

Antivenin (Crotalidae) Polyvalenta

CroFabb

Available since 1954 2000 Origin Equine Ovine Snakes used in manufacture Crotalus adamanteus C. adamanteus C. atrox C. atrox C. durissus terrificus C. scutulatus Bothrops atrox Agkistrodon piscivorus Snakes covered All North, Central, and South American and some Asian pit vipers All North American pit vipers (and possibly other Latin American pit vipers) Contains IgG, equine albumin Fab fragments Skin testing recommended by manufacturer Yes No Pretreatment with antihistamines recommended Yes No Dosing (for North American pit viper bites only)c

Dry bite None None Mild 0 or 5 vials 4 vials Moderate 10 vials 4–6 vials Severe 15–20 vials 6 vials Repeat dosing As needed Repeat starting dose if patient fails to stabilize. After stabilization, give 2 vials q6h for 3 more doses. (Alternatively, re-dose on an as-needed basis with close observation for recurrence of abnormalities.) Volume of diluent 1000 mLd 250 mL Administer over 2 h 1 h Incidence of anaphylactic/-oid reaction 23–56%e 14%f Incidence of delayed serum sickness 18–86%g 3%

aWyeth-Ayerst Laboratories, Philadelphia, PA. bFougera, Melville, NY. cDegrees of envenomation: mild = progressive local findings (no systemic findings and normal laboratory tests); moderate = local findings plus either mild systemic findings or mild laboratory abnormalities; and severe = local findings plus either severe systemic findings or severe laboratory abnormalities. dReduce for children and for patients with congestive heart failure. eSome reactions have been severe, and some have been fatal. fTo date, all reactions have been relatively mild. gIncidence is higher with larger doses.

Pretreatment is not recommended by the manufacturer of CroFab. Epinephrine should, however, always be immediately available, and the antivenom dose to be administered should be diluted in an appropriate volume of crystalloid according to the package insert. Antivenom should be given only by the IV route, and the infusion should be started slowly, with the physician at the bedside during the initial period to intervene immediately at the first signs of any acute reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered (over a total period of ~1 h). Further antivenom may be necessary if the patient's clinical condition fails to stabilize or worsens. After stabilization, additional doses of CroFab are often recommended as the small-molecular-weight Fab fragments are rapidly cleared from the circulation. Larger, whole IgG or F(ab)2 antivenoms have longer half-lives that eliminate the need for re-dosing after initial stabilization unless definitive symptoms of envenomation reappear.

If the patient develops an acute reaction to antivenom, the infusion should be temporarily stopped and the reaction immediately treated with IM epinephrine and IV antihistamine and steroids (Chap. 311). If the severity of envenomation warrants additional antivenom, the dose should be further diluted in isotonic saline and restarted as soon as possible. Rarely, in recalcitrant cases, a concomitant IV infusion of epinephrine may be required to hold allergic sequelae at bay while further antivenom is administered. The patient must be very closely monitored, preferably in an intensive care setting, during such therapy.

Blood products are rarely necessary in the management of the envenomated patient. The venoms of many snake species can cause a drop in platelet count or hematocrit and depletion of coagulation factors. Nevertheless, these components usually rebound within hours after administration of adequate antivenom. If the need for blood products is thought to be great (e.g., for a dangerously low platelet count in a hemorrhaging patient), these products still should be given only after adequate antivenom administration to avoid adding fuel to ongoing consumptive coagulopathy.

Rhabdomyolysis and hemolysis should be managed in standard fashion. Victims who develop acute renal failure should be evaluated by a nephrologist and referred for dialysis (peritoneal or hemodialysis) as needed. Such renal failure, usually due to acute tubular necrosis, is frequently reversible. If bilateral cortical necrosis occurs, however, the prognosis for renal recovery is more grim, and long-term dialysis with possible renal transplantation may be necessary.

Acetylcholinesterase inhibitors (e.g., edrophonium and neostigmine) may promote neurologic improvement in patients bitten by snakes with postsynaptic neurotoxins. Victims with objective evidence of neurologic dysfunction after snakebite should receive a trial of acetylcholinesterase inhibitors as outlined in Table 2. If they respond, additional doses of long-acting neostigmine can be continued as needed. Special vigilance is required to prevent aspiration if repetitive dosing of neostigmine is used in an attempt to obviate endotracheal intubation.

Table 2 Use of Acetylcholinesterase Inhibitors in Neurotoxic Snake Envenomation

1. Patients with clear, objective evidence of neurotoxicity after snakebite (e.g., ptosis or inability to maintain upward gaze) should receive a trial of edrophonium (if available) or neostigmine. a. Pretreat with atropine: 0.6 mg IV (children, 0.02 mg/kg; minimum of 0.1 mg) b. Follow with: Edrophonium: 10 mg IV (children, 0.25 mg/kg) or Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg) 2. If objective improvement is evident at 5 min, continue neostigmine at a dose of 0.5 mg (children, 0.01 mg/kg) every 30 min as needed, with continued administration of atropine by continuous infusion of 0.6 mg over 8 h (children, 0.02 mg/kg over 8 h). 3. Maintain vigilance regarding aspiration risk, and secure the airway with endotracheal intubation as needed.

Care of the bite wound includes application of a dry sterile dressing and splinting of the extremity with padding between the digits. Once the administration of an indicated antivenom has been initiated, the extremity should be elevated above heart level to relieve edema. Tetanus immunization should be updated as appropriate. Prophylactic antibiotics are generally unnecessary after bites by North American snakes, as the incidence of secondary infection is low. Antibiotics can be considered, however, if misguided first-aid efforts have included incisions or mouth suction. In some regions of the world, secondary bacterial infection is more common and the consequences are dire. In these regions, prophylactic antibiotics (e.g., cephalosporins) are commonly used.

Most snake envenomations involve subcutaneous deposition of venom. On occasion, however, venom can be injected more deeply into muscle compartments. If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures (ICPs) should be checked by any minimally invasive technique—e.g., wick catheter or ICP monitor (Stryker Instruments, Kalamazoo, MI). If any ICP is high (>30–40 mmHg), the extremity should be kept elevated while further antivenom is given. A dose of IV mannitol (1 g/kg) can be given in an effort to reduce muscle edema if the patient's hemodynamic status is stable. If, after 1 h of such therapy, the ICP remains elevated, a surgical consultation for possible fasciotomy should be obtained. While evidence from studies of animals suggests that fasciotomy may actually worsen myonecrosis, compartmental decompression is still required to preserve nerve function. Fortunately, the incidence of muscle-compartment syndrome is very low following snakebite.

Wound care in the days after the bite may require careful aseptic debridement of clearly necrotic tissue once coagulation has been restored. Intact serum-filled vesicles or hemorrhagic blebs should be left undisturbed. If ruptured, they should be debrided with sterile technique.

Physical therapy should be started when pain allows in order to return the victim to a functional state. The incidence of long-term loss of function (e.g., reduced range of motion, impaired sensory function) is unclear but is probably quite high (>30%), particularly after viperid bites.

Any patient with signs of venom poisoning should be observed in the hospital for at least 24 h. In North America, a patient with an apparently "dry" viperid bite should be watched for at least 8 h before discharge, as significant toxicity occasionally develops after a delay of several hours. The onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (including coral snakes), some non–North American viperids [e.g., the hump-nosed pit viper (Hypnale hypnale)], and sea snakes. Patients bitten by these reptiles should be observed in the hospital for at least 24 h. Unstable patients should be admitted to a monitored setting.

At discharge, victims of venomous snakebite should be warned about signs and symptoms of wound infection and serum sickness as well as other potential long-term sequelae, such as pituitary insufficiency in Russell's viper (D. russelii) bites. If the victim had evidence of coagulopathy early on, this abnormality can recur during the first 2–3 weeks after the bite. Such victims should be warned to avoid elective surgery or activities posing a high risk of trauma during this period. Outpatient analgesic treatment and physical therapy should be continued.

In the event of serum sickness (fever, chills, urticaria, myalgias, arthralgias, and possibly renal or neurologic dysfunction developing 1–2 weeks after antivenom administration), the victim should be treated with systemic glucocorticoids (e.g., oral prednisone, 1–2 mg/kg daily) until all findings resolve, at which point the dose is tapered over 1–2 weeks. Oral antihistamines (e.g., diphenhydramine in standard doses) provide additional relief of symptoms.

Morbidity and Mortality

The overall mortality rates for venomous snakebite are low in areas with rapid access to medical care and appropriate antivenoms. In the United States, for example, the mortality rate is <1%>

The incidence of morbidity—defined as permanent functional loss in a bitten extremity—is difficult to estimate but is substantial. Morbidity may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss tends to be more common and severe after rattlesnake bites than after bites by copperheads (Agkistrodon contortrix) or water moccasins (A. piscivorus).

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