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Which Fruit is High In Antioxidants? Food Source

Which Fruit Is High In Antioxidants?/Antioxidants are compounds that inhibit oxidation. Oxidation is a chemical reaction that can produce free radicals, thereby leading to chain reactions that may damage the cells of organisms. Antioxidants such as thiols or ascorbic acid (vitamin C) terminate these chain reactions. To balance the oxidative state, plants and animals maintain complex systems of overlapping antioxidants, such as glutathione and enzymes (e.g., catalase and superoxide dismutase), produced internally, or the dietary antioxidants vitamin A, vitamin C, and vitamin E.

An antioxidant is a molecule stable enough to donate an electron to a rampaging free radical and neutralize it, thus reducing its capacity to damage. These antioxidants delay or inhibit cellular damage mainly through their free radical scavenging property.[rx] These low-molecular-weight antioxidants can safely interact with free radicals and terminate the chain reaction before vital molecules are damaged. Some of such antioxidants, including glutathione, ubiquinol, and uric acid, are produced during normal metabolism in the body.[rx] Other lighter antioxidants are found in the diet. Although there are several enzymes system within the body that scavenge free radicals, the principle micronutrient (vitamins) antioxidants are vitamin E (α-tocopherol), vitamin C (ascorbic acid), and B-carotene.[rx]

Antioxidants are the key to healthy eating. Which foods pack the most nutrients?

Researchers at the University of Oslo wanted to know which foods have the highest concentration of antioxidants, the natural chemicals in food that make it healthy and prevent disease, so they tested 1,113 common foods and drinks, from apples to waffles. Their findings: Ounce for ounce, spices, herbs, nuts, and seeds pack the most nutrients. But if we’re talking typical serving size, berries (five different kinds) also dominate the top ranks. The most surprising find? Chocolate ice cream rated higher than fruits like honeydew and green grapes! Here, the best 10 foods to eat to “anti” up.

Types of Antioxidants

Some compounds contribute to antioxidant defense by chelating transition metals and preventing them from catalyzing the production of free radicals in the cell. Particularly important is the ability to sequester iron, which is the function of iron-binding proteins such as transferrin and ferritin. Selenium and zinc are commonly referred to as antioxidant nutrients, but these chemical elements have no antioxidant action themselves and are instead required for the activity of some antioxidant enzymes, as is discussed below.

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Antioxidant	Solubility	Concentration in human serum (μM)	Concentration in liver tissue (μmol/kg)
Ascorbic acid (vitamin C)	Water	50–60	260 (human)
Glutathione	Water	4	6,400 (human)
Lipoic acid	Water	0.1–0.7	4–5 (rat)
Uric acid	Water	200–400	1,600 (human)
Carotenes	Lipid	β-carotene: 0.5–1retinol (vitamin A): 1–3	5 (human, total carotenoids)
α-Tocopherol (vitamin E)	Lipid	10–40	50 (human)
Ubiquinol (coenzyme Q)	Lipid	5	200 (human)

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Uric acid

Uric acid has the highest concentration of any blood antioxidant and provides over half of the total antioxidant capacity of human serum. Uric acid’s antioxidant activities are also complex, given that it does not react with some oxidants, such as superoxide, but does act against peroxynitrite, peroxides, and hypochlorous acid. Concerns over elevated UA’s contribution to gout must be considered as one of many risk factors. By itself, UA-related risk of gout at high levels (415–530 μmol/L) is only 0.5% per year with an increase to 4.5% per year at UA supersaturation levels (535+ μmol/L). Many of these aforementioned studies determined UA’s antioxidant actions within normal physiological levels, and some found antioxidant activity at levels as high as 285 μmol/L.

Vitamin C

Ascorbic acid or “vitamin C” is a monosaccharide oxidation-reduction (redox) catalyst found in both animals and plants. As one of the enzymes needed to make ascorbic acid has been lost by mutation during primate evolution, humans must obtain it from the diet; it is, therefore, a vitamin. Most other animals are able to produce this compound in their bodies and do not require it in their diets.
Ascorbic acid is required for the conversion of the procollagen to collagen by oxidizing proline residues to hydroxyproline. In other cells, it is maintained in its reduced form by reaction with glutathione, which can be catalyzed by protein disulfide isomerase and glutaredoxins.

Glutathione

The free radical mechanism of lipid peroxidation. Glutathione is a cysteine-containing peptide found in most forms of aerobic life. It is not required in the diet and is instead synthesized in cells from its constituent amino acids. Glutathione has antioxidant properties since the thiol group in its cysteine moiety is a reducing agent and can be reversibly oxidized and reduced.
In cells, glutathione is maintained in the reduced form by the enzyme glutathione reductase and in turn reduces other metabolites and enzyme systems, such as ascorbate in the glutathione-ascorbate cycle, glutathione peroxidases, and glutaredoxins, as well as reacting directly with oxidants.
Due to its high concentration and its central role in maintaining the cell’s redox state, glutathione is one of the most important cellular antioxidants. In some organisms, glutathione is replaced by other thiols, such as by mycothiol in the Actinomycetes, bacillithiol in some Gram-positive bacteria, or by trypanothione in the Kinetoplastids.

Vitamin E

Vitamin E is the collective name for a set of eight related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant properties. Of these, α-tocopherol has been most studied as it has the highest bioavailability, with the body preferentially absorbing and metabolizing this form.
It has been claimed that the α-tocopherol form is the most important lipid-soluble antioxidant and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. This removes the free radical intermediates and prevents the propagation reaction from continuing. This reaction produces oxidized α-tocopherol radicals that can be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol. This is in line with findings showing that α-tocopherol, but not water-soluble antioxidants, efficiently protects glutathione peroxidase 4 (GPX4)-deficient cells from cell death. GPx4 is the only known enzyme that efficiently reduces lipid-hydroperoxides within biological membranes.
Enzymatic antioxidants – benefit you by breaking down and removing free radicals. They can flush out dangerous oxidative products by converting them into hydrogen peroxide, then into the water. This is done through a multi-step process that requires a number of trace metal cofactors, such as zinc, copper, manganese, and iron. Enzymatic antioxidants cannot be found in supplements, but instead, are produced in your body.
Superoxide dismutase (SOD) – can break down superoxide into hydrogen peroxide and oxygen, with the help of copper, zinc, manganese, and iron. It is found in almost all aerobic cells and extracellular fluids.
Catalase (CAT) – works by converting hydrogen peroxide into water and oxygen, using iron and manganese cofactors. It finishes up the detoxification process started by SOD.
Glutathione peroxidase (GSHpx) and glutathione reductase – are selenium-containing enzymes that help break down hydrogen peroxide and organic peroxides into alcohols. They are most abundant in your liver.
Non-enzymatic antioxidants – benefit you by interrupting free radical chain reactions. Some examples are carotenoids, vitamin C, vitamin E, plant polyphenols, and glutathione (GSH). Most antioxidants found in supplements and foods are non-enzymatic, and they provide support to enzymatic antioxidants by doing a “first sweep” and disarming the free radicals. This helps prevent your enzymatic antioxidants from being depleted.
Small-molecule antioxidants – work by mopping up or “scavenging” the reactive oxygen species and carrying them away through chemical neutralization. The main players in this category are vitamins C and E, glutathione, lipoic acid, carotenoids, and CoQ10.
Large-protein antioxidants– tend to be the enzymatic enzymes outlined above, as well as “sacrificial proteins,” that absorb ROS and stop them from attacking your essential proteins. One example of these sacrificial proteins is albumin, which “take the bullet” for crucial enzymes and DNA.
Quercetin –Derived naturally from foods like berries and leafy greens, quercetin seems to be safe for almost everyone and poses little risks. Most studies have found little to no side effects in people eating nutrient-dense diets high in quercetin or taking supplements by mouth short term.
Lutein –Lutein has benefits for the eyes, skin, arteries, heart and immune system, although food sources seem to be generally more effective and safer than supplements. Some evidence shows that people who obtain more lutein from their diets experience lower rates of breast, colon, cervical and lung cancers.
Resveratrol – Resveratrol is an active ingredient found in cocoa, red grapes, and dark berries, such as lingonberries, blueberries, mulberries, and bilberries. It’s a polyphonic bioflavonoid antioxidant that’s produced by these plants as a response to stress, injury and fungal infection, helping protect the heart, arteries and more.
Astaxanthin –Astaxanthin is found in wild-caught salmon and krill and has benefits like reducing age spots, boosting energy levels, supporting joint health and preventing symptoms of ADHD.
Selenium – Selenium is a trace mineral found naturally in the soil that also appears in certain foods, and there are even small amounts in water. It supports the adrenal and thyroid glands and helps protect cognition. It may also fight off viruses, defend against heart disease and slow down symptoms correlated with other serious conditions like asthma.
Lavender Essential Oil –Lavender oil reduces inflammation and helps the body in many ways, such as producing important antioxidant enzymes – especially glutathione, catalase, and superoxide dismutase.
Chlorophyll – Chlorophyll is very helpful for detoxification and linked to natural cancer prevention, blocking carcinogenic effects within the body, and protecting DNA from damage caused by toxins or stress. It’s found in things like spirulina, leafy green veggies, certain powdered green juices, and blue-green algae.
Frankincense Essential Oil – Frankincense oil has been clinically shown to be a vital treatment for various forms of cancer, including breast, brain, colon and prostate cancers. Frankincense has the ability to help regulate cellular epigenetic function, which positively influences genes to promote healing. Rub frankincense essential oil on your body (neck area) three times daily, and take three drops internally in eight ounces of water three times daily as part of a natural prevention plan.

Important Benefits of Antioxidants Include

Repairing damaged molecules – Some unique types of antioxidants can repair damaged molecules by donating a hydrogen atom. This is very important when the molecule is a critical one, like your DNA.
Blocking metal radical production – Some antioxidants have a chelating effect – they can grab toxic metals like mercury and arsenic, which can cause free radical formation, and “hug” them so strongly to prevent any chemical reaction from taking place. Water-soluble chelating agents can also escort toxic metals out of your body through your urine.
Stimulating gene expression and endogenous antioxidant production – Some antioxidants can stimulate your body’s genes and increase your natural defenses.
Providing a “shield effect” – Antioxidants, such as flavonoids, can act as a virtual shield by attaching to your DNA to protect it from free radicals attacks.
Promoting cancer cells to “commit suicide” – Some antioxidants can provide anti-cancer chemicals that halt cancer growth and force some cancer cells to self-destruct (apoptosis).

Antioxidants Foods

Allium sulfur compounds – Leeks, onions, garlic
Anthocyanins – Eggplant, grapes, berries
Beta carotene – Pumpkin, mangoes, apricots, carrots, spinach, parsley
Catechins – Red wine, tea
Copper – Seafood, lean meat, milk, nuts, legumes
Cryptoxanthins – Red peppers, pumpkin, mangoes
Flavonoids – Tea, green tea, red wine, citrus fruits, onion, apples
Indoles – Cruciferous vegetables such as broccoli, cabbage, cauliflower
Lignans – Sesame seeds, bran, whole grains, vegetables
Lutein – Corn, leafy greens (such as spinach)
Lycopene – Tomatoes, pink grapefruit, watermelon
Manganese – Seafood, lean meat, milk, nuts
Polyphenols – Thyme, oregano
Selenium – Seafood, offal, lean meat, whole grains
Vitamin C – Oranges, berries, kiwi fruit, mangoes, broccoli, spinach, peppers
Vitamin E – Vegetable oils, nuts, avocados, seeds, whole grains
Zinc – Seafood, lean meat, milk, nuts
Zoochemical – Red meat, offal, fish

Nutrient antioxidants

Antioxidants from our diet play an important role in helping endogenous antioxidants for the neutralization of oxidative stress. Nutrient antioxidant deficiency is one of the causes of numerous chronic and degenerative pathologies. Each nutrient is unique in terms of its structure and antioxidant function (rx, rx).

Vitamin E

Vitamin E is a fat-soluble vitamin with high antioxidant potency. Vitamin E is a chiral compound with eight stereoisomers: α, β, γ, δ tocopherol and α, β, γ, δ tocotrienol. Only α-tocopherol is the most bioactive form in humans. Studies in both animals and humans indicate that natural dextrorotary d-α-tocopherol is nearly twice as effective as synthetic racemic dl-α-tocopherol (rx).
Because it is fat-soluble, α-tocopherol safeguards cell membranes from damage by free radicals. Its antioxidant function mainly resides in the protection against lipid peroxidation. Vitamin E has been proposed for the prevention against colon, prostate and breast cancers, some cardiovascular diseases, ischemia, cataract, arthritis, and certain neurological disorders. (rx).
However, a recent trial revealed that daily α-tocopherol doses of 400 IU or more can increase the risk of death and should be avoided. In contrast, there is no increased risk of death with a dose of 200 IU per day or less, and there may even be some benefit (rx). Although controversial, the use of long-term vitamin E supplementation in high dose should be approached cautiously until further evidence for its safety is available. The dietary sources of vitamin E are vegetable oils, wheat germ oil, whole grains, nuts, cereals, fruits, eggs, poultry, meat (rx, rx). Cooking and storage may destroy natural d-α-tocopherol in foods (rx).

Vitamin C

Vitamin C also known as ascorbic acid, is a water-soluble vitamin. It is essential for collagen, carnitine and neurotransmitters biosynthesis (rx). Health benefits of vitamin C are antioxidant, anti-atherogenic, anti-carcinogenic, immunomodulator.
The positive effect of vitamin C resides in reducing the incidence of stomach cancer, and in preventing lung and colorectal cancer. Vitamin C works synergistically with vitamin E to quench free radicals and also regenerates the reduced form of vitamin E.
However, the intake of high doses of vitamin C (2000mg or more/day) has been the subject of debate for its eventual pro-oxidant or carcinogen property (rx–rx). Natural sources of vitamin C are acid fruits, green vegetables, tomatoes. Ascorbic acid is a labile molecule, therefore it may be lost from during cooking (rx).

Beta-carotene

Beta-carotene is a fat-soluble member of the carotenoids which are considered provitamins because they can be converted to active vitamin A. Beta-carotene is converted to retinol, which is essential for vision. It is a strong antioxidant and is the best quencher of singlet oxygen.
However, beta-carotene supplement in doses of 20mg daily for 5-8 years has been associated with an increased risk of lung and prostate cancer and increased total mortality in cigarette smokers (rx). Beta-carotene 20-30mg daily in smokers may also increase cardiovascular mortality by 12% to 26% (rx). These adverse effects do not appear to occur in people who eat foods high in beta-carotene content. Beta-carotene is present in many fruits, grains, oil and vegetables (carrots, green plants, squash, spinach) (rx).

Lycopene

Lycopene, a carotenoid, possesses antioxidant and antiproliferative properties in animal and in vitro studies on breast, prostate and lung cell lines, although anticancer activity in humans remains controversial (rx, rx, rx). Lycopene has been found to be very protective, particularly for prostate cancer (rx).
Several prospective cohort studies have found associations between high intake of lycopene and reduced incidence of prostate cancer, though not all studies have produced consistent results (rx). The major dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes, tomato juice and tomato sauce included, being more bioavailable than that in raw tomatoes (rx).

Selenium (Se)

Se is a trace mineral found in soil, water, vegetables (garlic, onion, grains, nuts, soybean), seafood, meat, liver, yeast (rx). It forms the active site of several antioxidant enzymes including glutathione peroxidase. At low dose, health benefits of Se are antioxidant, anti-carcinogenic and immunomodulator (rx). Selenium is also necessary for the thyroid function (rx).
Exceeding the Tolerable Upper Intake Level of 400 μg Se/day can lead to selenosis which is a selenium poisoning characterized by gastrointestinal disorders, hair and nail loss, cirrhosis, pulmonary edema and death (rx).
Selenium deficiency can occur in patients on total parenteral nutrition (TPN) and in patients with gastrointestinal disorders. In certain China areas with Se poor soil, people have developed a fatal cardiomyopathy called Keshan disease which was cured with Se supplement (rx). The role of Se in cancer prevention has been the subject of recent study and debate. Results from clinical and cohort studies about cancer prevention, especially lung, colorectal, and prostate cancers are mixed (rx, rx).

Flavonoids

Flavonoids are polyphenolic compounds which are present in most plants. According to chemical structure, over 4000 flavonoids have been identified and classified into flavonols, flavanones, flavones, isoflavones, catechins, anthocyanins, proanthocyanidins. Beneficial effects of flavonoids on human health mainly reside in their potent antioxidant activity (rx).
They have been reported to prevent or delay a number of chronic and degenerative ailments such as cancer, cardiovascular diseases, arthritis, aging, cataract, memory loss, stroke, Alzheimer’s disease, inflammation, infection. Every plant contains a unique combination of flavonoids, which is why different herbs, all rich in these substances, have very different effects on the body (rx). The main natural sources of flavonoids include green tea, grapes (red wine), apple, cocoa (chocolate), ginkgo Biloba, soybean, Curcuma, berries, onion, broccoli, etc.
For example, green tea is a rich source of flavonoids, especially flavonols (catechins) and quercetin. Catechin levels are 4-6 times greater in green tea than in black tea. Many health benefits of green tea reside in its antioxidant, anticarcinogenic, antihypercholesterolemic, antibacterial (dental caries), anti-inflammatory activities (rx).

Omega-3 and omega-6 fatty acids

They are essential long-chain polyunsaturated fatty acids because the human body cannot synthesize them. Therefore, they are only derived from food. Omega-3 fatty acids can be found in fat fish (salmon, tuna, halibut, sardines, pollock), krill, algae, walnut, nut oils and flaxseed. However, certain big fishes like tilefish, shark, swordfish are to be avoided because of their high mercury levels (rx).
There are three major dietary types of omega-3 fatty acids: eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and alpha-linolenic acid (ALA). EPA and DHA are abundant in fish and are directly used by the body; while ALA is found in nuts and has to be converted to DHA and EPA by the body. Dietary sources of omega-6 fatty acids (linoleic acid) include vegetable oils, nuts, cereals, eggs, poultry.
It is important to maintain an appropriate balance of omega-3s and omega-6s in the diet, as these two substances work together to promote health (rx, rx). Omega-3 fatty acids help reduce inflammation, and most omega-6 fatty acids tend to promote inflammation. An inappropriate balance of these essential fatty acids contributes to the development of disease while a proper balance helps maintain and even improve health. A healthy diet should consist of about 2-4 times more omega-6s than omega-3s. In the American diet, omega-6s are 14-25 times more abundant than omega-3s, that explains the rising rate of inflammatory disorders in the USA (rx). Omega-3s reduce inflammation and prevent chronic ailments such as heart disease, stroke, memory loss, depression, arthritis, cataract, cancer. Omega-6s improve diabetic neuropathy, eczema, psoriasis, osteoporosis, and aid in cancer treatment (rx, rx, rx).

Antioxidants Home Treatments

BLACKBERRIES

One cup of blackberries contains the most antioxidants of all the berries tested, beating out blueberries, strawberries, cranberries, and raspberries. Plus, one cupful provides half your daily recommended intake of vitamin C.
Nutrition facts (1 cup): 62 calories, less than 1g fat, 14g carbohydrates, 7.6g fiber, 2g protein

WALNUTS

Just an ounce of walnuts, or 15 to 20 halves, is loaded with antioxidants. They’re also cholesterol-free and low in sodium and sugar. Nuts are laden with calories, though, so be mindful of your intake.
Nutrition facts (1 ounce): 185 calories, 18.5g fat (1.7g saturated fat), 4g carbohydrates, 8g fiber, 4g protein

STRAWBERRIES

Bursting with fiber and vitamin C (149 percent of your daily recommended intake!), a cup of sliced strawberries is a cup full of healthy benefits.
Nutrition facts (1 cup): 49 calories, 0.5g fat, 11.7g carbohydrates, 3g fiber, 1g protein

ARTICHOKE HEARTS

Add a cup of antioxidant-rich artichoke hearts to your diet.
Nutrition facts (1 cup): 70 calories, 0g fat, 11.5g carbohydrates, 4.5g fiber, 2.5g protein

CRANBERRIES

One cup of whole cranberries is full of disease-fighting and health-boosting antioxidants.
Nutrition facts (1 cup): 51 calories, 0.2g fat, 13.5g carbohydrates, 5g fiber, 1g protein

BREWED COFFEE

Your morning cup of joe does more than perk you up — it also boosts your health.
Nutrition facts (8 fluid ounces): 18 calories, 2mg sodium

RASPBERRIES

Another super-healthy berry to add to your diet. One cup is loaded with vitamin C (54 percent of your daily recommended intake) and antioxidants.
Nutrition facts (1 cup): 64 calories, 1g fat, 15g carbohydrates, 8g fiber, 1.5g protein

PECANS

As if you needed any more reason to take a bite out of that pecan pie. One ounce, or 20 jumbo kernels, of pecans is rich in antioxidants.
Nutrition facts (1 ounce): 196 calories, 20.5g fat (1.7g saturated), 3.9g carbohydrates, 2.7g fiber, 2.6g protein

BLUEBERRIES

This superfood is good for your health and can help protect your skin from premature aging.
Nutrition facts (1 cup): 83 calories, 0.5g fat, 21g carbohydrates, 3.5g fiber, 1.1g protein

GROUND CLOVES

Just a teaspoon of ground cloves can do wonders for your body. Spice up your meals and boost your health at the same time.
Nutrition facts (1 tablespoon): 21 calories, 1.3g fat (0.4g saturated), 4g carbohydrates, 2.3g fiber, 0.4g protein

Kale

Rich in cancer-fighting antioxidants and vitamins, kale is also a good source of beta-carotene and is the top combo of both lutein and zeaxanthin.

Spinach

Spinach is packed with carotenoids—antioxidants that promote healthy eyes and help prevent macular degeneration, the leading cause of blindness in older people.

Brussels Sprouts

These broccoli cousins have plenty of bitter sulforaphane as well as compounds called isothiocyanates, which detoxify cancer-causing substances in the body before they can do their dirty work. In one Dutch study, guys who ate Brussels sprouts daily for three weeks had 28 percent less genetic damage (gene damage is a root cause of cancer) than those who didn’t eat sprouts.

Alfafa Sprouts

This tiny powerhouse is rich in beta-carotene, an antioxidant that protects against lung cancer and helps maintain healthy skin, hair, nails, gums, glands, bones, and teeth. It’s also a good source of vitamin E, which may help prevent heart attacks, strokes, and lower the risk of death from bladder cancer.

Broccoli Flowers

Broccoli is full of cancer-fighting antioxidants. One study found men who ate 5 servings or more per week of cruciferous veggies like broccoli were half as likely to develop bladder cancers over a 10-year period as men who rarely ate them.

Beets

Beets are packed with healthy nutrients, like five essential vitamins, calcium, iron, potassium, and protein.

Red Bell Peppers

One medium pepper is light on calories (only 32!) but heavy on vitamin C, providing 150 percent of your recommended daily value and warding off atherosclerosis, which can lead to heart disease.

Onions

You’ll get the most out of this veggie’s cancer-fighting antioxidants by eating it raw; cooking onions at a high heat significantly reduces the benefits of phytochemicals that protect against lung and prostate cancer.

Corn

A study in the Journal of Agricultural Food and Chemistry found that the longer corn was cooked, the higher the level of antioxidants like lutein, which combats blindness in older adults.

Eggplant

All types of eggplant are rich in bitter chlorogenic acid, which protects against the buildup of heart-threatening plaque in artery walls (and fights cancer, too!), say USDA scientists in Beltsville, Maryland. In lab studies, eggplant lowered cholesterol and helped artery walls relax, which can cut your risk of high blood pressure.

Lifestyle Changes to Maximize Your Antioxidant Intake.

Reduce and eventually eliminate sugar (especially fructose) and grains from your diet – According to Dr. Robert Lustig, professor of pediatrics in the Division of Endocrinology at the University of California, San Francisco, fructose undergoes the Maillard reaction with proteins, which leads to superoxide free radicals to form in your body. These damaging free radicals can cause liver inflammation similar to that caused by alcohol. Less sugar and grains (which convert into sugar in your body) in your diet can help decrease your antioxidant stress, meaning you will need to get fewer amounts. Plus, the antioxidants you have will work better and last longer. I also advise against consuming any type of processed foods, especially soda, as these usually contain high amounts of fructose.
Exercise – Exercise can boost your body’s antioxidant production but in a paradoxical way, as it actually creates potent oxidative stress. However, if you do it properly and in moderation, it can help improve your body’s capacity to produce antioxidants. This is why I recommend doing short bursts of high-intensity exercises like Peak Fitness, instead of prolonged cardio like marathon running, which puts excessive stress on your heart.
Manage your stress – Stress can exacerbate the inflammation and poor immune function caused by free radical formation. Studies have found significant links between acute and/or chronic emotional and psychological stress and numerous health issues. Even the Centers for Disease Control (CDC) acknowledges this link and says that 85 percent of all disease has an emotional element.
Avoid smoking – Smoking forms free radicals in your body, which accelerates the aging process. Even being around people who smoke can affect your health by damaging the microcapillaries in your skin, which limits its ability to absorb nutrients, leading to accelerated wrinkling and aging. Smoking also contributes to the pathobiology of various diseases, the most well-known of which is lung cancer.
Get enough sleep – High-quality sleep is one of the cornerstones of good health, and science has now established that a sleep deficit can have severe far-reaching effects on your health. Six to eight hours of sleep per night seems to be the optimal amount for most adults, and too much or too little can have adverse effects on your wellbeing.
Try grounding – Also called “earthing,” grounding has a potent antioxidant effect that helps alleviate inflammation in your body. There is a constant flow of energy between our bodies and the earth, which has a greater negative charge. Walking barefoot on the earth helps you absorb large amounts of negative electrons through the soles of your feet.

References

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Low Heart Beat; Causes, Symptoms, Treatment

Low Heart Beat/Bradycardia is defined as a resting heart rate below 60 beats per minute (b.p.m.). A slow heart rate can occur naturally under various circumstances and is not necessarily associated with a medical condition. For example, some highly trained athletes have bradycardia. However, there is also pathological bradycardia, which is caused by conditions that affect the electrical conduction system of the heart, including sick sinus syndrome (SSS) and/or atrioventricular (AV) block.^[rx] Bradycardia does not necessarily require treatment unless it causes symptoms. People suffering from symptomatic bradycardia can present with dizziness, confusion, palpitations, breathlessness, exercise intolerance and syncope (blackout or fainting). However, bradycardia and symptoms related to it may be intermittent or may be non-specific, particularly in the elderly.

Bradycardia is a condition typically defined wherein an individual has a resting heart rate of under 60 beats per minute (BPM) in adults.^[rx] Bradycardia typically does not cause symptoms until the rate drops below 50 BPM. When symptomatic, it may cause fatigue, weakness, dizziness, sweating, and at very low rates, fainting.^[rx]During sleep, a slow heartbeat with rates around 40–50 BPM is common and is considered normal. Highly trained athletes may also have athletic heart syndrome, a very slow resting heart rate that occurs as a sport adaptation and helps prevent tachycardia during training.

Pathophysiology

A heart has numerous pacemaker sites within its conduction system which are independently able to keep the heart beating. And the rate of a heartbeat depends upon the pacemaker site, and as we go down its conduction system, the rate of spontaneous depolarization at pacemaker sites decrease. [rx][rx][rx]

Pacemaker sites and their depolarization rates are listed below

Sinoatrial node – 60 to 100 beats per minute
Atria – Less than 60 beats per minute
Atrioventricular node – 40 to 60 beats per minute
Ventricles – 20 to 40 beats per minute

Types of Bradycardia

Sinus – Atrial bradycardias are divided into three types. The first, respiratory sinus arrhythmia, is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation. This is thought to be caused by changes in the vagal tone during respiration.^[rx] If the decrease during exhalation drops the heart rate below 60 bpm on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone.
Atrioventricular nodal – Atrioventricular nodal bradycardia or AV junction rhythm is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an EKG with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.^[rx]An AV junctional escape is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node.^[rx] This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block.^[rx]
Ventricular – Ventricular bradycardia, also known as ventricular escape rhythm or idioventricular rhythm, is a heart rate of less than 50 BPM. This is a safety mechanism when a lack of electrical impulse or stimuli from the atrium occurs.^[rx] Impulses originating within or below the bundle of His in the atrioventricular node will produce a wide QRS complex with heart rates between 20 and 40 BPM. Those above the bundle of His, also known as junctional, will typically range between 40 and 60 BPM with a narrow QRS complex.^[rx]^[rx] In a third-degree heart block, about 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His.^[rx] AV block may be ruled out with an EKG indicating “a 1:1 relationship between P waves and QRS complexes.
Infantile – For infants, bradycardia is defined as a heart rate less than 100 BPM (normal is around 120–160). Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. The spells may be related to centers inside the brain that regulate breathing which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary.

Causes of Bradycardia

Common causes of sinus bradycardia in children include increased vagal tone, hypothyroidism, hypothermia, adrenal insufficiency, and increased intracranial pressure. Inherited arrhythmias and cardiomyopathies may also cause bradycardia. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited disorder.

Pathological causes of sinus bradycardia

A congenital defect –or problem you’re born with
Thyroid disease –an imbalance of hormones in the body
Obstructive sleep apnea – when your breathing pauses many times throughout the night
Drugs—for example, β blockers, digoxin, amiodarone
Problems with the sinoatrial (SA) node – sometimes called the heart’s natural pacemaker
Problems in the conduction pathways of the heart that don’t allow electrical impulses to pass properly from the atria to the ventricles
Metabolic problems such as hypothyroidism (low thyroid hormone)
Damage to the heart from heart disease or heart attack
Certain heart medications that can cause bradycardia as a side effect
Acute myocardial infarction
Obstructive jaundice
Raised intracranial pressure
Sick sinus syndrome
Hypothermia
Hypothyroidism

Sinus bradycardia has many intrinsic and extrinsic etiologies[rx]][rx][rx][rx][rx][rx].

Inherent Etiologies

Chest trauma
Ischemic heart disease
Acute myocardial infarction
Acute and chronic coronary artery disease
Repair of congenital heart disease
Sick sinus syndrome
Radiation therapy
Amyloidosis
Pericarditis
Lyme disease
Rheumatic fever
Collagen vascular disease
Myocarditis
Neuromuscular disorder
X-linked muscular dystrophy
Familial disorder
Inherited channelopathy

Extrinsic Etiologies

Vasovagal simulation (endotracheal suctioning)
Carotid sinus hypersensitivity
Beta-blockers
Calcium channel blockers
Digoxin
Ivabradine
Clonidine
Reserpine
Adenosine
Cimetidine
Antiarrhythmic Class I to IV
Lithium
Amitriptyline
Narcotics
Cannabinoids
Hypothyroidism
Sleep apnea
Hypoxia
Intracranial hypertension
Hyperkalemia
Anorexia nervosa

Syndrome

Heart tissue damage related to aging
Damage to heart tissues from heart disease or heart attack
Heart disorder present at birth (congenital heart defect)
Infection of heart tissue (myocarditis)
A complication of heart surgery
Underactive thyroid gland (hypothyroidism)
Imbalance of chemicals in the blood, such as potassium or calcium
Repeated disruption of breathing during sleep (obstructive sleep apnea)
Inflammatory diseases, such as rheumatic fever or lupus
Medications, including some drugs for other heart rhythm disorders, high blood pressure and psychosis
Common in sick sinus syndrome
Characterized by bursts of atrial tachycardia interspersed with periods of bradycardia
Paroxysmal atrial flutter or fibrillation may also occur, and cardioversion may be followed by a severe bradycardia

Symptoms of Bradycardia

Fatigue or feeling weak
Chest pain, which may signal reduced blood flow to the heart
Dizziness or lightheadedness
Confusion
Fainting (or near-fainting) spells
Shortness of breath
Difficulty when exercising
Cardiac arrest (in extreme cases)
Confusion or memory problems
Easily tiring during physical activity
Heart palpitations or flutters
Limited ability to exercise

Diagnosis of Bradycardia

Electrocardiogram (ECG or EKG) – An electrocardiogram also called an ECG or EKG, is a primary tool for evaluating bradycardia. Using small sensors (electrodes) attached to your chest and arms, it records electrical signals as they travel through your heart. Because an ECG can’t record bradycardia unless it happens during the test, your doctor might have you use a portable ECG device at home. These devices include:
Holter monitor – Carried in your pocket or worn on a belt or shoulder strap, this device records your heart’s activity for 24 to 48 hours. Your doctor will likely ask you to keep a diary during the same 24 hours. You’ll describe any symptoms you experience and record the time they occur.
Event recorder – This device monitors your heart activity over a few weeks. You push a button to activate it when you feel symptoms so that it records your heart’s activity during that time.
LINQ insertable cardiac monitor: This wireless, powerful, small insertable cardiac monitor is ideal for patients experiencing infrequent symptoms that require long-term monitoring or ongoing management.

Your doctor might use an ECG monitor while performing other tests to understand the impact of bradycardia. These tests include

Tilt table test – This test helps your doctor better understand how your bradycardia contributes to fainting spells. You lie flat on a special table, and then the table is tilted as if you were standing up to see if the change in position causes you to faint.
Exercise test – Your doctor might monitor your heart rate while you walk on a treadmill or ride a stationary bike to see whether your heart rate increases appropriately in response to physical activity.
A stress test – can be helpful in bringing out either sinus node disease or heart block that becomes apparent only during exertion.

Treatment of Bradycardia

The treatment of bradycardia is dependent on whether or not the person is stable or unstable.^[rx] If oxygen saturations are low, supplemental oxygen should be provided.

Stable – Emergency treatment is not needed if the person is asymptomatic or minimally symptomatic.^[rx]
Unstable – If a person is unstable, the initial recommended treatment is intravenous atropine.^[rx] Doses less than 0.5 mg should not be used, as this may further decrease the rate.^[rx] If this is not effective, intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used.^[rx] Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.^[rx]
In children – giving oxygen, supporting their breathing, and chest compressions are recommended.^[rx]^[rx]

Antisialagogue

While atropine can be used independently for anti-salivation effects, it most commonly is secondary to anticholinergic or antimuscarinic poisoning which is discussed below. It is not formally recommended for routine use in controlled airways, though can be used off-label for minimizing secretions in the intubated patient.

Anticholinergic Poisoning

Acetylcholine works on three different receptors that must be addressed in nerve agent poisonings. Atropine is only useful to counter muscarinic effects (pralidoxime and benzodiazepines address the others). If there are local symptoms to the eyes or respiratory tract, atropine is not indicated.
Intravenous (IV) atropine is indicated for patients with hypersalivation, bronchial secretions, or bradycardia. Large doses and repeat doses may be required. Ingestions especially require higher doses (up to 20 mg). Titrate to effect by monitoring the patient’s ability to clear excess secretions. Pupils and heart rate are poor indications of appropriate dosing in these patients.

Rapid Sequence Intubation (RSI) Pretreatment

Although not recommended as a routine agent – atropine may be used 3-5min prior to initiation of RSI to prevent bradycardia. In the setting of post-intubation related bradycardia, atropine is indicated. Post induction bradycardia is seen more commonly in the pediatric population due to the predominance of vagal response, even without the use of succinylcholine.
Atropine/Diphenoxylate (Lomotil) – is an antimotility agent that can be used in the treatment of diarrhea as second-line therapy. This allows the central acting opioid effect of diphenoxylate and capitalization on its anticholinergic side effect of constipation to slow motility. Subtherapeutic amounts of atropine are included in the dosage form to discourage diphenoxylate abuse. It may potentiate barbiturates, alcohol, or tranquilizers and therefore must be used with caution.
Under current ACLS protocols – atropine is indicated for symptomatic bradycardia and not in a pulseless patient. All indications for atropine in the pulseless patient have been removed by the AHA.
Atropine is not indicated in beta-blocker-induced bradycardias or hypotension – though its use is unlikely to be harmful. Glucagon is first-line to treat beta-blockade-induced symptoms. Pregnancy Class B: It does cross the placenta and may lead to fetal tachycardia; however, it does not cause fetal abnormalities. [rx]

Administration

Atropine can be administered by intravenous (IV), subcutaneous, intramuscular, or endotracheal (ET) method; IV is preferred. For ET administration dilute 1 mg to 2 mg in 10 mL of sterile water or normal saline prior to administration. For pediatric ET, double the usual IV dose and dilute in 3 to 5 mL.

Antisialagogue/antiviral – 0.5 mg to 1 mg every 1 to 2 hours
Organophosphate or muscarinic poisoning – 2 mg to 3 mg every 20 to 30 minutes (may require doses up to 20 mg, titrate to the effect of secretion control, not VS)
Bradycardia – 1 mg every 3 to 5 minutes (3 mg max), repeat until desired heart rate is obtained, most effective for sinus and AV nodal disease.
Pediatric – 0.01 mg/kg to 0.03 mg/kg every 3 to 5 minutes. Pediatric minimum dose 0.1 mg, maximum dose 0.5 mg (child) and 1.0 mg (adolescent); maximum cumulative dose 1 mg (child) and 2 mg (adolescent).
Rapid Sequence Intubation Pretreatment – 0.01 mg/kg IV for adults with bradycardia secondary to repeat dosing of succinylcholine. Pediatric 0.02 mg/kg IV, minimum dose 0.1 mg. Not recommended as a routine.

In general, dosing of atropine can be repeated every 5 minutes until a maximum of 0.04 mg/kg is reached. Dosing in adults to greater than 0.5 mg and slow IV pushes have been associated with paradoxical bradycardia (though likely transient) and ventricular fibrillation (VF).

If damage to the heart’s electrical system causes your heart to beat too slowly, you will probably need to have a pacemaker. A pacemaker is an implanted device that helps correct the slow heart rate.
If another medical problem, such as hypothyroidism or an electrolyte imbalance, is causing a slow heart rate, treating that problem may cure the bradycardia.
If a medicine is causing your heart to beat too slowly, your doctor may adjust the dose or prescribe a different medicine.

Prevention

The most effective way to prevent bradycardia is to reduce your risk of developing heart disease. If you already have heart disease, monitor it and follow your treatment plan to lower your risk of bradycardia.

Prevent heart disease

Treat or eliminate risk factors that may lead to heart disease. Take the following steps

Exercise and eat a healthy diet – Live a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat, low-salt, low-sugar diet that’s rich in fruits, vegetables, and whole grains. Having a heart-healthy eating plan that includes vegetables, fruits, nuts, beans, lean meat, fish, and whole grains. Limit alcohol, sodium, and sugar.
Maintain a healthy weight –Being overweight increases your risk of developing heart disease.
Keep blood pressure and cholesterol under control – Make lifestyle changes and take medications as prescribed to correct high blood pressure (hypertension) or high cholesterol.
Don’t smoke – If you smoke and can’t quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit.
If you drink, do so in moderation – For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. Ask your doctor if your condition means you should avoid alcohol. If you can’t control your alcohol use, talk to your doctor about a program to quit drinking and manage other behaviors related to alcohol abuse.
Don’t use recreational drugs – If you’re using drugs, talk to your physician about treatment programs.
Exercise and eat healthy – Get regular physical activity and eat a low-fat diet rich in fruits, vegetables and whole grains.
Get regular checkups – Have regular physicals and, if you experience new or changing symptoms, see your physician.
Keep blood pressure and cholesterol under control – Make the lifestyle changes listed above and take medications as prescribed.
Monitor and treat existing heart disease – Understand your treatment plan. Take medications as directed. And report new or worsening symptoms immediately.
Manage stress – Avoid unnecessary stress and learn coping techniques to handle normal stress in a healthy way.
Being active on most – if not all, days of the week. Your doctor can tell you what level of exercise is safe for you.
Losing weight if you need to – and staying at a healthy weight.
Managing other health problems – such as high blood pressure, high cholesterol, and diabetes.
Go to scheduled checkups – Have regular physical exams and report signs or symptoms to your doctor.

Monitor and treat existing heart disease

If you already have heart disease, there are steps you can take to lower your risk of developing bradycardia or another heart rhythm disorder:

Follow the plan – Be sure you understand your treatment plan and take all medications as prescribed.
Report changes immediately – If your symptoms change or worsen or you develop new symptoms, tell your doctor immediately.

Risk Factors

Risk factors that could contribute to bradycardia include:

Age – Men and women age 65 and older are most likely to develop a slow heart rate that needs treatment.
Congenital heart defect – Problems with the structure or function of the heart present at birth can cause a slow heart rate.
Electrolyte imbalance – Any abnormality in the body’s mineral balance – including calcium, chloride, magnesium, phosphate, potassium, and sodium can lead to a slow or irregular heart rate.
Infection of the heart – Certain bacteria, viruses, and parasites can infect the heart muscle, causing inflammation and damage leading to an irregular heart rate.
Previous heart attacks – Heart attacks can weaken the heart muscle or cause problems with its electrical system.
Low thyroid – An abnormally low level of thyroid hormones can cause a slow heart rate.
Medications for other heart problems – Some medications for treating high blood pressure or other heart conditions like beta-blockers, antiarrhythmics and digoxin (for heart failure) can cause bradycardia.

References

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Water Retention Symptoms, Diagnosis, Treatment

Water Retention Symptoms/Water retention (also known as fluid retention) or hydrops, hydropsy, edema, signifies an abnormal accumulation of clear, watery fluid in the tissues or cavities of the body. Water is found both inside and outside the body’s cells. It forms part of the blood, helping to carry the blood cells around the body and keeping oxygen and important nutrients in solution so that they can be taken up by tissues such as glands, bone, and muscle. Even the organs and muscles are mostly water.

The body uses a complex system of hormones and hormone-like substances called prostaglandins to keep its volume of fluid at a constant level. If one were to intake an excessive amount of fluid in one day, the amount of fluid would not be affected in the long term. This is because the kidneys quickly excrete the excess in the form of urine. Likewise, if one did not get enough to drink, the body would hold on to its fluids and urinate less than usual. Imbalances in this system can lead to water retention, which can range from mild and unnoticeable to symptomatic with swelling.

Causes of Water Retention

Where water retention occurs

Fluid rich with oxygen, vitamins and other nutrients passes all the time from the capillaries (the smallest blood vessels) into the surrounding tissues, where it is known as tissue fluid or interstitial fluid. This fluid nourishes the cells and eventually should return to the capillaries.
Water retention is said to occur as a result of changes in the pressure inside the capillaries, or changes that make the capillary walls too leaky (see edema and vascular permeability). If the pressure is wrong, or the capillaries are too leaky, then too much fluid will be released into the tissue spaces between the cells. Sometimes so much fluid is released that it cannot all return to the capillaries and remains in the tissues, where it causes the swelling and waterlogging which is experienced as water retention.
Another set of vessels known as the lymphatic system acts like an “overflow” and can return a lot of excess fluid back to the bloodstream. But even the lymphatic system can be overwhelmed, and if there is simply too much fluid, or if the lymphatic system is congested, then the fluid will remain in the tissues, causing swellings in legs, ankles, feet, abdomen or any other part of the body.

The Heart

The pumping force of the heart should help to keep normal pressure within the blood vessels. But if the heart begins to fail (a condition is known as congestive heart failure) the pressure changes can cause very severe water retention. In this condition, water retention is mostly visible in the legs, feet, and ankles, but also collects in the lungs, where it causes a chronic cough. This condition is usually treated with diuretics, otherwise, the water retention may cause breathing problems and additional stress on the heart.

The Kidneys

Another cause of severe water retention is kidney failure, where the kidneys are no longer able to filter fluid out of the blood and turn it into the urine. Kidney disease often starts with inflammation, for instance in the case of diseases such as nephrotic syndrome or lupus. Once again, this type of water retention is usually visible in the form of swollen legs and ankles.

Other Causes of Swollen legs

Swollen legs, feet, and ankles are common in late pregnancy. The problem is partly caused by the weight of the uterus on the major veins of the pelvis. It usually clears up after delivery of the baby, and is mostly not a cause for concern, though it should always be reported to a doctor.
Lack of exercise is another common cause of water retention in the legs. Exercise helps the leg veins work against gravity to return blood to the heart. If blood travels too slowly and starts to pool in the leg veins, the pressure can force too much fluid out of the leg capillaries into the tissue spaces. The capillaries may break, leaving small blood marks under the skin. The veins themselves can become swollen, painful and distorted – a condition known as varicose veins.
Lack of exercise is a common cause of water retention because muscle action is needed not only to keep blood flowing through the veins but also to stimulate the lymphatic system to fulfill its “overflow” function. Long-haul flights, lengthy bed-rest, immobility caused by disability and so on, are all potential causes of water retention. Even very small exercises such as rotating ankles and wiggling toes can help to reduce it.

Protein

Protein attracts water and plays an important role in water balance. In cases of severe protein deficiency, the blood may not contain enough protein to attract water from the tissue spaces back into the capillaries. This is why starvation often shows an enlarged abdomen. The abdomen is swollen with edema or water retention caused by the lack of protein in their diet.
When the capillary walls are too permeable, protein can leak out of the blood and settle in the tissue spaces. It will then act like a magnet for water, continuously attracting more water from the blood to accumulate in the tissue spaces.

Other factors

Certain medications are prone to causing water retention. These include estrogens, thereby including drugs for hormone replacement therapy or the combined oral contraceptive pill, as well as non-steroidal anti-inflammatory drugs and beta-blockers. Premenstrual water retention, causing bloating and breast tenderness, is common and may be related to hormone imbalances promoted by a lack of nutrients such as B vitamins or magnesium.

Medication-caused water retention

Some medications can cause water retention, including

Drugs that contain estrogen – These can reduce water retention. Examples include birth control pills or hormone replacement therapy (HRT).
Non-steroidal anti-inflammatory drugs (NSAIDs) – These are medications with pain-reducing, fever-reducing effects. In high doses, they are actually effective in reducing inflammation. Examples include aspirin, ibuprofen, and naproxen.
Beta-blockers – These are used to treat abnormal heart rhythms and prevent tachycardias.

Premenstrual water retention

This can cause bloating and breast tenderness. Experts say this is due to hormone imbalances and some nutritional factors, including:

Malnutrition and bad diet – A poor diet low in protein result in low levels of albumin, which may also play a part in developing water retention.
Salt, or sodium – sodium-rich foods may cause water retention.
Allergies – Some foods and insect bites may cause edema in susceptible people.
Thyroid disease – People with a disorder of the thyroid gland commonly experience water retention.

Symptoms of Water Retention

Feet and lower legs get larger when you sit or walk.
Take a look at your feet, ankles and hands. Are they swollen? When you press on the skin with your finger, is there an indentation that stays for a few seconds? If so, you may have “pitting edema.”
Hands feel tight when you make a fist
Rings are too tight
Abdomen appears to be swelling or distended
Shortness of breath (especially when lying down)
Weight gain
Aching limbs
Stiff joints
Discolouration of skin
Hypertension (high blood pressure)

Diagnosis of Water Retention

Testing

For most people with widespread water retention, blood tests are done to evaluate the function of the heart, kidneys, and liver. Urinalysis is usually also done to check for large amounts of protein, which can indicate nephrotic syndrome or, in pregnant women, preeclampsia. Other tests are done based on the suspected cause. For example, in people with isolated leg swelling, doctors may do ultrasonography to look for blockage of a vein in the leg.

[stextbox id=’info’]

Causes water retention	Common Features	Tests^†
Angioedema (allergic, idiopathic, or hereditary)	Painless swelling, most often affecting the face, lips, and sometimes tongue Some times itching or tight sensation water retention that does not remain indented after being pressed	Only a doctor’s examination
A blood clot in a deep-lying vein in a leg (typically), an arm, or the pelvis (deep vein thrombosis)	Sudden swelling Usually pain, redness, warmth, and/or tenderness in the affected area If the clot travels and blocks an artery to the lung (pulmonary embolism), usually shortness of breath and sometimes coughing up blood Sometimes in people who have risk factors for blood clots, such as recent surgery, an injury, bed rest, a cast on a leg, hormone therapy, cancer, or a period of immobility such as a long airplane flight	Ultrasonography
Chronic venous insufficiency (causing blood to pool in the legs)	Swelling in one or both ankles or legs Chronic mild discomfort, aching, or cramps in the legs but no pain Sometimes reddish brown, leathery areas on the skin and shallow sores on the lower legs Often varicose veins	Only a doctor’s examination
Drugs (such as minoxidil, nonsteroidal anti-inflammatory drugs, estrogens, fludrocortisone, and some calcium channel blockers)	Painless swelling in both legs and feet	Only a doctor’s examination
Heart failure	Painless swelling in both legs and feet Often shortness of breath during exertion or while lying down and during sleep Often in people known to have heart disease and/or high blood pressure	Chest x-ray ECG Usually echocardiography
Infection of the skin (cellulitis)	An irregular area of redness, warmth, and tenderness on part of one limb Water retention Sometimes fever	Only a doctor’s examination
Infection deep under the skin or in the muscles (rare)	Deep, constant pain in one limb Redness, warmth, tenderness and swelling that feels tight Signs of severe illness (such as fever, confusion, and a rapid heart rate) Sometimes a foul discharge, blisters, or areas of blackened, dead skin	Blood and tissue cultures X-rays Sometimes MRI
Kidney disease (mainly nephrotic syndrome)	Widespread, painless swelling Often fluid within the abdomen (ascites) Sometimes puffiness around the eyes or frothy urine	Measurement of protein in a urine specimen
Liver disease if chronic	Widespread, painless swelling Often fluid within the abdomen (ascites) Causes that are often apparent based on history (such as alcohol abuse or hepatitis) Sometimes small spiderlike blood vessels that are visible in the skin (spider angiomas), reddening of the palms and, in men, breast enlargement and a decrease in the size of the testes	Measurement of albumin in the blood Other blood tests to evaluate liver function
Lymphatic vessel obstruction due to surgery or radiation therapy for cancer	Painless swelling of one limb A cause (surgery or radiation therapy) that is apparent based on history	Only a doctor’s examination
Lymphatic filariasis (a lymph vessel infection due to certain parasitic worms)	Painless swelling of one limb and sometimes the genitals In people who have been in a developing country where filariasis is common	Examination of a blood sample under a microscope
Normal swelling	A small amount of swelling of both feet and/or ankles that occurs at the end of the day and resolves by morning No pain, redness, or other symptoms	Only a doctor’s examination
Pregnancy or a normal premenstrual symptom	Painless swelling in both legs and feet Usually relieved to some extent by rest and leg elevation In women known to be pregnant or about to have a menstrual period	Only a doctor’s examination
Pregnancy, with preeclampsia	Painless swelling in both legs and feet and sometimes hands High blood pressure (often new) Usually occurring during the 3rd trimester of pregnancy	Measurement of protein in urine
Pressure on a vein (for example, by a tumor, pregnancy, or extreme abdominal obesity)	Painless swelling that develops slowly	Ultrasonography or CT if a tumor is suspected
*Features include symptoms and the results of the doctor’s examination. Features mentioned are typical but not always present.
^†In most people with water retention, doctors do a complete blood count, other blood tests, and urinalysis (to check for protein in the urine).

[/stextbox]

Treatment of Water Retention

Non-medicine

In the acute, or early phase, remember PRICE

P = Protection from further damage
R = Rest to avoid prolonging irritation
I = Ice (cold) for controlling pain, bleeding, and edema
C = Compression for support and controlling swelling
E = Elevation for decreasing bleeding and edema
Protection can mean immobilization with a brace, or a wrap, or even just staying off the body part.
Rest means not moving the body part in a painful way. Movement is good and can increase healing, but it should be pain-free at this stage.
Ice for the first 72 hours – 20 minutes out of every hour. Leaving ice on longer actually reverses the effect it has, and may increase swelling. Chemical icepacks should never be applied directly to the skin, or frostbite can occur. Do not use heat for the first 72 hours; heat will increase the swelling.
Compression – with an ace wrap. Your athletic trainer or doctor can show you how to wrap the body part to minimize swelling.
Elevation – or resting with the injury above heart level, to encourage swelling to return towards the body, instead of collecting in the extremities where it is difficult to get rid of.

Medicine of Water Retention

Acetaminophen,
Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Ibuprofen,
- Naproxen, or Naprosyn
Aspirin (also a nonsteroidal anti-inflammatory drug), such as Bayer or Bufferin

Talk to your child’s doctor before switching back and forth between doses of acetaminophen and ibuprofen. When you switch between two medicines, there is a chance your child will get too much medicine

Elevate your feet as often as possible. (Either sitting in a chair with your feet on a stool with a pillow or in the bed or couch with feet up on two pillows)
Do not stand for long periods of time.
Avoid tight clothing (shoes, girdles, etc).
Do not cross your legs.
Reduce your salt intake if swelling is present. Avoid foods such as bouillon, potato chips, tomato juice, bacon, ham, canned soups, soy sauce, and table salt, for example.
Try to eat a balanced diet (see eating well section).
If your swelling is severe, consider wearing Jobst stockings or TED hose.
Weigh yourself daily. Notify your doctor or health care provider if you have gained 5 pounds or more in a week.
Take your medications exactly as prescribed.

Home Remedies of Water Retention

Dandelion

Dandelions are very high in potassium that can act as a natural diuretic. A big reason why many of us suffer from water retention is that we eat a diet that is too high in sodium and too low in potassium. While sodium makes your body hold on to water, potassium encourages it to release excess fluids. Drinking dandelion tea can make you pee more often and reduce water retention. But the most effective way to use dandelion as a diuretic is to take concentrated dandelion supplements.

Asparagus

Asparagus has been used as a natural diuretic for centuries. This plant contains an amino acid called asparagine which is especially effective in treating water retention due to menstrual cycles and rheumatism. After eating asparagus, you might notice that your pee smells funny. This is because after you eat asparagus, it gets broken down into sulfur compounds that cleanse your body of toxins and makes you pee more frequently.

Parsley

Parsley is a popular medicinal herb and had extensive uses in traditional medicine. A herbal tea made by steeping fresh parsley leaves in boiling water was often used as a natural remedy to treat water retention. Studies on the diuretic effects of parsley conducted on rats did find that rats urinated more frequently after ingesting parsley. While studies on humans haven’t been conducted yet, there’s plenty of anecdotal evidence to support parsley’s diuretic powers.

Caraway

Caraway seeds are small, brown seeds that look very much like cumin. In Eastern traditional medicine, caraway seeds were often used to soothe digestive issues and reduce water retention. Studies conducted on rats found that after being fed caraway extracts, rats urinated a lot more frequently than usual. The lack of studies on humans, however, means that we don’t know just how much caraway is required to reduce water retention. You can start using caraway seeds by adding it as a spice to your meals or boiling it with water and drinking the tea along with the seeds.

Tea

Both green and black tea have strong diuretic properties that can help reduce water retention. However, it’s important that you drink it black and with no sugar as dairy and white sugar can aggravate water retention. Interestingly, studies have shown that tea is most effective as a diuretic when a person doesn’t drink it on a regular basis. Drinking tea everyday can make you develop a tolerance for it which can affect its diuretic properties. So if you’re a coffee drinker, it’s best you switch to tea on days when you feel extra puffy.

Horsetail

Horsetail is one of the most powerful natural diuretics known to us and is available in the form of a tea and as a supplement. One study found that taking horsetail supplements were as effective as certain commercial diuretics. But while horsetail can dramatically reduce water retention in the short run, it can cause harmful side effects if you use it for too long. Horsetail can also be dangerous if you already have kidney disease or diabetes.

Cucumber/Tomato

Cucumbers are almost entirely water themselves, so it isn’t surprising that eating them will make you pee more. Cucumbers contain sulfur and silicon which can help your kidneys function better and remove excess uric acid from them. They are also very high in potassium which helps your body release water. You can even use cucumbers topically to reduce symptoms of water retention. If your eyes get puffy when you have water retention, placing cool slices of cucumber over them can reduce the swelling.

References

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Child Rheumatic Fever, Symptoms, Diagnosis, Treatment

Child Rheumatic Fever/Rheumatic fever (RF) is an autoimmune, multiorgan inflammatory disease that occurs as a result of group A β-hemolytic streptococcal infection in genetically syusceptible individuals [rx].

Rheumatic fever is an immunologically mediated inflammatory disease, that occurs as a delayed sequel to group A streptococcal throat infection, in genetically susceptible individuals. Chronic rheumatic heart disease remains an important public health problem in developing countries. Aetiopathogenesis and guidelines for the diagnosis, prevention and treatment of acute rheumatic fever are reviewed.

Pathophysiology

Although epidemiological and immunological studies have clearly identified group A β-hemolytic streptococcus (GAS) as the etiologic agent triggering ARF in a susceptible host, the molecular pathways linking GAS to ARF are still poorly understood. Molecular mimicry and autoimmunity probably play a pivotal role in the pathogenesis of ARF and carditis [rx] since it was shown that the streptococcal M protein shares an α-helical coiled structure with cardiac proteins such as myosin and that antibodies isolated from ARF patients cross-react with both M protein and heart tissue. Elevated in patients with valvular involvement, these antibodies are significantly reduced after surgical removal of inflamed valves and they correlate with poor prognosis [rx]. Moreover, heart-M protein cross-reactive T cells have been isolated from the myocardium and the valves of RHD patients suggesting their involvement in the pathophysiology of the disease [rx, rx]. However, the role of collagen should not be underestimated, as shown by recent studies demonstrating pathological findings in subendothelial and perivascular connective tissue in ARF [rx].

Causes of Rheumatic Fever

Rheumatic fever – may develop after strep throat or scarlet fever infections that are not treated properly. Bacteria called group A Streptococcus or group A strep cause strep throat and scarlet fever. It usually takes about 1 to 5 weeks after strep throat or scarlet fever for rheumatic fever to develop. Rheumatic fever is thought to be caused by a response of the body’s defense system — the immune system. The immune system responds to the earlier strep throat or scarlet fever infection and causes a generalized inflammatory response.
Rheumatic fever – is an inflammatory condition that may develop approximately 14-28 days after infection with group A Streptococcus bacteria, such as strep throat or scarlet fever. About 5% of those with untreated strep infection will develop rheumatic fever. Although group A Streptococcus bacterial infections are highly contagious, rheumatic fever is not spread from person to person.
Bacteria called group – A Streptococcus (group A strep) can cause many different infections. These infections range from minor illnesses to very serious and deadly diseases. Learn more below about some of these infections, including symptoms, risk factors, treatment options, and how to prevent them.
Strep Throat – When is a sore throat “strep throat”? Your doctor can do a quick test to see if you or your child has strep throat.
Scarlet Fever – Have a sore throat and rash? It could be scarlet fever. Your doctor can do a quick test to find out…
Necrotizing Fasciitis – Sometimes called “flesh-eating” disease, this infection is not common. Good hygiene, proper wound care, and quick recognition and treatment are important.
Rheumatic Fever – This disease affects the heart and other organs. It is not common but can happen if strep throat or scarlet fever aren’t treated properly
Post-Streptococcal Glomerulonephritis – This disease affects the kidneys and is not common but can happen after strep throat or impetigo

Symptoms of Rheumatic Fever

Symptoms of rheumatic fever include

Joint swelling and pain – This may include redness and warmth, mainly of the larger joints like the knees, ankles, wrists and elbows
Fever – Hot and cold fevers which may feel like symptoms of a cold or flu
Sydenham’s Chorea – Jerky, uncontrollable movements called chorea
Erythema marginatum – A rare skin rash, mainly found on the trunk of the body (this is a very a rare symptom)
Subcutaneous nodules – Round, painless nodules over the elbows, wrists, knees, ankles and areas near the spine (also very rare)
Heart problems – Swelling of the heart may cause chest pain, and if severe there may be signs of heart failure (breathlessness, swollen legs and face).
Painful – tender joints (arthritis), most commonly in the knees, ankles, elbows, and wrists
Symptoms of congestive heart failure – including chest pain, shortness of breath, fast heartbeat
Jerky uncontrollable body movements (called chorea)
Painless lumps (nodules) under the skin near joints.
Rash that appears as pink rings with a clear center.
Red raised, lattice-like rash, usually on the chest, back, and abdomen.
Uncontrolled movements of arms, legs, or facial muscles
Swollen, tender, red and extremely painful joints
Weakness and shortness of breath
Nodules over swollen joints
Stomach pains
Weight loss
Fatigue
Fever

Diagnosis of Rheumatic Fever

The diagnostic tests can be considered as those meant for (i) diagnosis of RF, (ii) presence of active vs. inactive RF in recurrences, and (iii) identification of carditis and valve damage in RHD.

Diagnosis of RF

The diagnosis of RF is dependent on some laboratory tests included as minor criteria and consist of the following:

(i)Acute phase reactants (leukocytosis, elevated sedimentation rate and presence of C reactive protein CRP).
(ii)Prolonged PR interval in the electrocardiogram.

The diagnosis requires presence of essential criteria in the form of evidence for recent GAS infection and consists of:

(i) elevated antistreptococcal antibodies,
(ii) positive throat culture for GAS, and
(iii) evidence for recent scarlet fever- rare in India.

Diagnostic criteria for rheumatic fever – modified 1992 Jones criteria [rx]

Major criteria	Minor criteria
Carditis Arthritis Chorea Erythema marginatum Subcutaneous nodules	Hyperpyrexia Arthralgia, without other signs of inflammation Laboratory indicators of acute phase: ESR, CRP Prolonged PR interval in ECG
And evidence of antecedent streptococcal infection – Throat swab culture or rapid antigen test – Elevated/increasing anti-streptococcal antibody titer in serum

ESR – erythrocyte sedimentation rate; CRP – C-reactive protein; ECG – electrocardiography

Major criteria

Polyarthritis – ^[rx] A temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
Carditis – Inflammation of the heart muscle (myocarditis) which can manifest as congestive heart failure with shortness of breath, pericarditiswith a rub, or a new heart murmur.
Subcutaneous nodules – Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
Erythema marginatum – A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance. This rash typically spares the face and is made worse with heat.
Sydenham’s chorea (St. Vitus’ dance) – A characteristic series of involuntary rapid movements of the face and arms. This can occur very late in the disease for at least three months from onset of infection.

Minor criteria

Fever of 38.2–38.9 °C (100.8–102.0 °F)
Arthralgia – Joint pain without swelling (Cannot be included if polyarthritis is present as a major symptom)
Raised erythrocyte sedimentation rate or C reactive protein
Leukocytosis
ECG showing features of heart block, such as a prolonged PR interval^[rx]^[rx] (Cannot be included if carditis is present as a major symptom)
Previous episode of rheumatic fever or inactive heart disease

Diagnostic criteria for rheumatic fever – modified 2015 Jones criteria [rx]

Major criteria
Low risk population	High risk population
Carditis (clinical or subclinical) Arthritis – only polyarthritis Chorea Erythema marginatum Subcutaneous nodules	Carditis (clinical or subclinical) Arthritis – monoarthritis or polyarthritis Polyarthralgia Chorea Erythema marginatum Subcutaneous nodules
Minor criteria
Low risk population	High risk population
Polyarthralgia Hyperpyrexia (≥ 38.5ºC) ESR ≥ 60 mm/h and/or CRP ≥ 3.0 mg/dl Prolonged PR interval (after taking into account the differences related to age; if there is no carditis as a major criterion)	Monoarthralgia Hyperpyrexia (≥ 38.0ºC) ESR ≥ 30 mm/h and/or CRP ≥ 3.0 mg/dl Prolonged PR interval (after taking into account the differences related to age; if there is no carditis as a major criterion)

ESR – erythrocyte sedimentation rate; CRP – C-reactive protein

The modifications introduced in 2015 in the Jones criteria are as follows

In the major criteria

Low risk population – clinical and/or subclinical carditis. AHA recommends that all the patients with suspected RF undergo Doppler echocardiographic examination, even if no clinical signs of carditis are present [rx]. In doubtful cases it is recommended that echocardiography is repeated.
Medium and high risk population – also clinical and/or subclinical carditis and arthritis – monoarthritis or polyarthritis, possibly also with polyarthralgia [rx, rx].

In the minor criteria

Low risk population – the parameters of inflammation and the level of fever were defined precisely.
Medium and high risk population – monoarthralgia, also with defined parameters of inflammation and the level of fever.

The diagnosis of RF in the whole population with evidence of antecedent group A β-hemolytic streptococcal infection requires a confirmation of two major criteria or one major and two minor criteria – the first episode of the disease. The echocardiographic criteria developed by AHA in 2012 are as follows [rx, rx]

Echocardiographic (Doppler) criteria: Pathological mitral regurgitation – 4 criteria (all must be met)

Visible at least in 2 projections.
Regurgitation jet length ≥ 2 cm at least in 1 projection.
Regurgitation peak velocity > 3 m/s.
Regurgitation pansystolic.

Pathological aortic regurgitation – 4 criteria (all must be met)

Visible at least in 2 projections.
Regurgitation jet length ≥ 1 cm at least in 1 projection.
Regurgitation peak velocity > 3 m/s.
Regurgitation pandiastolic.

Echocardiographic (morphological) criteria: In acute mitral valve involvement

Dilatation of mitral annulus.
Elongation of chordae tendineae.
Rupture of chorda tendinea with acute mitral regurgitation.
Prolapse of anterior (less often posterior) leaflet.
Nodular lesions on leaflets.

In chronic mitral valve involvement (invisible in acute involvement)

Thickening of leaflets.
Thickening of chordae tendinea, with their fusion.
Limited mobility of leaflets.
Calcifications.

Lesions in acute and chronic aortic valve involvement

Symmetrical or focal thickening of leaflets.
Disturbed leaflet coaptation (leaflet closing during systole).
Limited mobility of leaflets.
Prolapse of leaflets.

Presence of GAS in throat culture with low values of ASLO suggests a carrier state. As such a positive throat culture for GAS cannot be taken as recent infection unless the antibody titres are elevated.

Echocardiogram (echo) – This test uses sound waves to check the heart’s chambers and valves. The echo sound waves create a picture on a screen as an ultrasound transducer is passed over the skin overlying the heart. Echo can show damage to the valve flaps, backflow of blood through a leaky valve, fluid around the heart, and heart enlargement. It’s the most useful test for diagnosing heart valve problems.
Electrocardiogram (ECG) – This test records the strength and timing of the electrical activity of the heart. It shows abnormal rhythms (arrhythmias or dysrhythmias) and can sometimes detect heart muscle damage. Small sensors are taped to your skin to pick up the electrical activity.
Chest X-ray – An X-ray may be done to check your lungs and see if your heart is enlarged.
Cardiac MRI – This is an imaging test that takes detailed pictures of the heart. It may be used to get a more precise look at the heart valves and heart muscle.
Blood tests – Certain blood tests may be used to look for infection and inflammation.

Presence of active vs. inactive RF in recurrences – Two investigations have been tried to assess the presence or absence of active RF in patients with recurrences besides ESR, CRP and evidence for recent GAS infection.

Induced subcutaneous nodules (SCN) – Massell et al^[rx] tried inducing SCN by injecting five dl autologous blood drawn from a vein and injecting over the olecranon process of one elbow and saline in the other elbow. Frictional pressure was applied to the injected sites. Appearance of a SCN in 5 to 10 days was accepted as indicating active RF. Vasan modified this test and used concentrated leukocyte injection instead of whole blood with 86 per cent sensitivity and 94 per cent specifically to identify active RF. The test offers the advantage of being cheap and easily available everywhere. The potential utility of the test lies in identifying active RF. However, additional validation studies are perhaps needed.
Myocardial biopsy – A study of myocardial histology to identify active vs. inactive RF was utilized in patients of RF^[rx]. Myocardial biopsies were performed in 89 patients of active RF and chronic RHD to identify active carditis Myocardial biopsies failed to improve on clinically assessed presence of active RF. Myocardial biopsy was felt to be insensitive for identifying presence of active carditis^[rx].

Treatment of Rheumatic Fever

Antibiotics used in primary prevention and treatment of group A streptococcal throat infection (World Health Organization guidelines)

Antibiotic	Route of administration and dosage	Dose
Benzathine benzylpenicillin	Intramuscular injection; childen should be kept under observation for 30 minutes	Single dose 1.2 million U; <27 kg, 600 000 U
Phenoxymethylpenicillin (penicillin V)	Oral, 2-4 times daily for 10 days	Children 250 mg twice or three times daily, adolescents or adults 250 mg three or four times daily or 500 mg twice daily
Amoxicillin	Oral, 2-3 times daily for 10 days	25-50 mg/kg/d in three doses; total adult dose 750-1500 mg/d
First generation cephalosporins	Oral, 2-3 times daily for 10 days	Varies with formulation
Erythromycin if allergic to penicillin	Oral, 4 times daily for 10 days	Varies with formulation

Antibiotic	Dose	Duration
Penicillin V	250 mg by mouth 2 to 3 times daily (≤27 kg) or 500 mg by mouth 2 to 3 times daily (>27 kg)	10 days
Benzathine penicillin G	600,000 units intramuscular (≤27 kg) or 1,200,000 units intramuscular (>27 kg)	Once
Amoxicillin	50 mg/kg by mouth daily	10 days
Cephalosporin (first generation)	Drug-dependent	10 days
Clindamycin	20 mg/kg/day divided in 3 doses by mouth	10 days
Clarithromycin	15 mg/kg/day divided in 2 doses by mouth	10 days
Azithromycin	12 mg/kg by mouth daily	5 days

Rheumatic fever treatment has not changed for many years. It covers:

anti-streptococcal treatment (primary and secondary prevention),
anti-inflammatory treatment.

Anti-Streptococcal Treatment

Primary prevention relies on the proper treatment of streptococcal pharyngitis, that is, prevention of the first RF episode.

The drug of choice is still phenoxymethylpenicillin orally at the following doses – adults and children with a body weight > 40 kg – 2–3 MIU/day in 2 divided doses every 12 hours for 10 days, children with a body weight < 40 kg – 100,000 to 200,000 IU/kg/day in 2 divided doses every 12 hours for 10 days.
Benzylpenicillin – administered intramuscularly at a single dose (only in hospital settings), is acceptable, for adults and children with a body weight > 40 kg – 1.2 MIU, children with a body weight < 40 kg – 600,000 IU. In patients with hypersensitivity to penicillin (except for immediate-type reactions), first-generation cephalosporins (cefadroxil or cefalexin) are used.
Cefadroxil – adults and children with a body weight > 40 kg – 1 g, children with a body weight < 40 kg – 30 mg/kg, in a single dose for 10 days.
Cefalexin – adults 500 mg twice per day, children 25–50 mg/kg/day in 2 doses for 10 days. Macrolides should only be administered in patients with immediate-type hypersensitivity to beta-lactam antibiotics. The following can be used: erythromycin, clarithromycin and azithromycin.
Erythromycin – adults and children with a body weight > 40 kg – 0.2–0.4 γ every 6–8 hours, children with a body weight < 40 kg – 30–50 mg/kg/day in 3–4 doses, for 10 days.
Clarithromycin – adults and children with a body weight > 40 kg – 250–500 mg every 12 hours, children with a body weight < 40 kg – 15 mg/kg/day in 2 doses, for 10 days.
Azithromycin – adults and children with a body weight > 40 kg – 500 mg on the first day, then 250 mg for three consecutive days, children with a body weight < 40 kg – a single daily dose of 12 mg/kg/day for 5 days or 20 mg/kg/day for 3 days [rx].
Secondary prevention is the prevention of subsequent rheumatic fever relapses through the chronic anti-streptococcal treatment – phenoxymethylpenicillin or benzathine benzylpenicillin or possibly macrolides. The duration of secondary prevention must be determined individually, depending on whether the patient has developed carditis and complications in the form of chronic valvular heart disease. Secondary prevention should be administered from 5 to 10 years from the last RF relapse, or up to 21 years of age (whichever is longer) [rx, rx]. In RF cases with carditis leading to chronic valvular heart disease, the prevention should be administered for 10 years or until 40 years of age (whichever is longer) [rx]. Secondary prevention makes use of benzathine benzylpenicillin, intramuscularly in adults and children with a body weight > 20 kg – 1.2 MIU, in children with a body weight < 20 kg – 600,000 IU every 4 weeks [rx]. Phenoxymethylpenicillin is administered orally at a dose of 2 × 250 mg (i.e. 2 × 400,000 IU).
Anti-inflammatory drugs – Naproxen, for example, may help to reduce pain, inflammation, and fever.
Corticosteroids – Prednisone may be given if the patient does not respond to first-line anti-inflammatory medications, or if there is inflammation of the heart.
Aspirin – This is not usually recommended for children aged under 16 years because of the risk of developing Reye’s syndrome, which can cause liver and brain damage, and even death, but an exception is usually made in cases of RA because the benefits are greater than the risks.
Anticonvulsant medications – These can treat severe chorea symptoms. Examples include valproic acid, carbamazepine, haloperidol and risperidone.

References

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Avulsions Wound, Causes, Diagnosis, Treatment

Avulsions Wound/Wounds are defined as a disruption of the normal structure and function of skin and underlying soft tissue that is caused by trauma or chronic mechanical stress (e.g., decubitus ulcers). Wounds can be broken down into acute or chronic, and open or closed. Wound treatment is performed according to pathology, the extent, and circumstances of the lesions. To heal, the wound needs to have a vascular supply, be free of necrotic tissue, clear of infection, and moist. General wound treatment includes surgical wound closure, open wound treatment, and plastic reconstruction of skin defects. In addition, infectious or concomitant disease prevention should be considered (e.g., antibiotic therapy, vaccines for tetanus and rabies, diabetes control).

A wound is damaged or disruption to the skin and, before treatment, the exact cause, location, and type of wound must be assessed to provide appropriate treatment.[rx][rx][rx] Each clinician will have widely differing and distinct opinions and understanding of wound care depending on their prior experience. The reason for this because of the widely differing and distinct types of wounds, each with their etiology. An ostomy nurse will have a completely different approach to wound care that will require an orthopedic surgeon who deals with trauma and both will be far different from a dermatologist who treats burn victims. Nevertheless, each of these healthcare providers is performing wound care. How do professionals then approach wound assessment when the causes are so diverse? Below are some basic questions to ask during a wound assessment to best classify and treat a wound presenting in a clinical setting.

Normal Healthy Skin of Wounds

As the interface between the environment and body, the skin has several distinct functions. It protects the underlying tissues from abrasions, the entry of microbes, unwanted water loss, and ultraviolet light damage. Tactile sensations of touch, pressure, and vibration, thermal sensations of heat and cold, and pain sensations all originate in the skin’s nervous system. The body’s thermoregulation relies on the skin’s ability to sweat and to control the flow of blood to the skin to increase or decrease heat loss. The skin’s functions are performed by three distinct tissue layers: a thin outer layer of cells called the epidermis, a thicker middle layer of connective tissue called the dermis, and an inner, subcutaneous layer. The outer layers of the epidermis are composed of flattened, cornified dead keratinocytes that form a barrier to water loss and microbe entry. These cells are derived from a basal layer of constantly dividing keratinocytes that lies next to the dermis. The epidermis does not contain nerves or blood vessels and obtains water and nutrients through diffusion from the dermis. The dermis is composed mostly of collagen fibers and some elastic fibers both produced by fibroblasts and, along with water and large proteoglycan molecules, makes up the extracellular matrix. This layer of the skin provides mechanical strength and a substrate for water and nutrient diffusion; it contains blood vessels, nerves, and cells involved in immune function, growth, and repair. The dermis also contains sweat glands, oil glands, and hair follicles. The subcutaneous layer is composed of adipocytes that form a thick layer of adipose tissue.^[rx]

Types of Wounds

Each of the potential underlying causes must be addressed for the wound to heal. Before determining the underlying cause, it is important to determine what type of wound the patient has. These subclassifications can be acute or chronic.[rx][rx][rx]

1. According to the severity, a wound can be classified as

Acute

Clinicians assess acute wounds by the method of injury and damage to the soft tissues and bony structures. In crush or high impact injuries, there is an area of demarcation which is not fully recognized until sometimes as much as a week or 2 later. For this reason, it is important to determine the method of injury and to keep in mind that the wound seen is not necessarily the entirety of the wound which will be present in a week. In these cases, the patient and their family should be educated on this progression to prevent frustration and misunderstanding.

For all acute types of wounds, it is important to determine the length of time since injury (days or hours), the involvement of neurovascular supply, muscle, tendon, ligament, and bony involvement, and the likelihood of contaminants in the wound. Also of importance is when the patient had their last tetanus shot. CLinicians should start antibiotics if the wound is severely contaminated or if it is longer than 3 hours since the injury. All underlying tissue should be repaired if possible, and the wound should be irrigated to remove contaminants and bacteria.

In cases of open fracture the most used classification is Gustillo-Anderson

Type 1 – Clean wound, less than one cm with minimal soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 2 – Wound with moderate contamination, greater than one cm with moderate soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 3A – Wound with significant contamination, with significant soft tissue damage, adequate soft tissue coverage of bone, and periosteal stripping is present
Type 3B – Wound with significant contamination, with significant soft tissue damage, unable to cover bone with soft tissue (requiring graft), and periosteal stripping
Type 3C – Similar to type A or B, however with Arterial damage requiring repair

Chronic

If a wound becomes arrested in progression through the normal stages of inflammation and wound healing and remains open, then this becomes a chronic wound. While there is no consensus as to when a wound becomes chronic, a study by Sheehan et. al determined that in diabetic wounds, the degree of healing at 4 weeks is a strong predictor of 12 week healing, suggesting that those wounds which have not healed approximately 50% in 4 weeks are likely to have an arrested healing process, and therefore are chronic.[rx][rx]

In the chronic setting, the main goal is to identify why the wound is not healing and to fix this obstacle or obstacles.

There are a limited number of reasons a wound becomes chronic; however, once these reasons are rectified, the wound resumes its natural course of healing.

Arterial – Is there enough blood flow? Generally speaking, an ABI of less than 50 mm Hg, or an absolute toe pressure less than 30 mm Hg (or less than 50 mm Hg for persons with diabetes) indicates critical limb ischemia and predicts failure of wounds to heal.
Venous – Pressure-induced changes in blood vessel wall permeability then lead to leakage of fibrin and other plasma components into the perivascular space. Accumulation of fibrin has direct and negative effects on wound healing as it down-regulates collagen synthesis.
Infection – Underlying infectious processes including cellulitic and osteomyelitis processes will inhibit wound healing. Culturing for aerobic, anaerobic, and fungal pathogens is recommended.
Pressure – Increased pressure to the area of concern will destroy new tissue growth and prevent proper perfusion of blood to the wound site. These areas need to be offloaded to avoid pressure in the area.
Oncologic – Always biopsy areas of concern in nonhealing wounds, as this can be an atypical presentation of some types of malignancies.
Systemic – There are multiple systemic diseases which inhibit wound healing, with diabetes being the most common culprit. It has been determined that uncontrolled blood glucose levels suppresses the body’s normal inflammatory response, as well as causing microvascular disease which limits healing.
Nutrition – While serum albumin has not been found to be a good predictor of wound healing, there is some evidence that protein malnutrition, as well as insufficient levels of certain vitamins and minerals, will limit the body’s ability to heal chronic wounds.
Pharmacological – Hydroxyurea has been reported in multiple instances to cause nonhealing ulcerations.
Self-inflicted/psychosocial – There are instances where a patient is causing the ulceration, either on purpose or as a result of noncompliance. This is often the hardest factor to spot and overcome, but must always be a consideration.

2. According to level of contamination, a wound can be classified as

Clean wound – made under sterile conditions where there are no organisms present, and the skin is likely to heal without complications.
Contaminated wound – usually resulting from accidental injury; there are pathogenic organisms and foreign bodies in the wound.
Infected wound – the wound has pathogenic organisms present and multiplying, exhibiting clinical signs of infection (yellow appearance, soreness, redness, oozing pus).
Colonized wound – a chronic situation, containing pathogenic organisms, difficult to heal (i.e. bedsore).

Open

Open wounds can be classified according to the object that caused the wound

Incisions or incised wounds – caused by a clean, sharp-edged object such as a knife, razor, or glass splinter.
Lacerations – irregular tear-like wounds caused by some blunt trauma. Lacerations and incisions may appear linear (regular) or stellate (irregular). The term laceration is commonly misused in reference to incisions.^[rx]
Abrasions (grazes) – superficial wounds in which the topmost layer of the skin (the epidermis) is scraped off. Abrasions are often caused by a sliding fall onto a rough surface such as asphalt, tree bark or concrete.
Avulsions – injuries in which a body structure is forcibly detached from its normal point of insertion. A type of amputation where the extremity is pulled off rather than cut off. When used in reference to skin avulsions, the term ‘degloving’ is also sometimes used as a synonym.
Puncture wounds – caused by an object puncturing the skin, such as a splinter, nail or needle.
Penetration wounds – caused by an object such as a knife entering and coming out from the skin.
Gunshot wounds – caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a “through-and-through.”

Closed

Closed wounds have fewer categories, but are just as dangerous as open wounds:

Hematomas (or blood tumor) – caused by damage to a blood vessel that in turn causes blood to collect under the skin.
- Hematomas that originate from internal blood vessel pathology are petechiae, purpura, and ecchymosis. The different classifications are based on size.
- Hematomas that originate from an external source of trauma are contusions, also commonly called bruises.
Crush injury – caused by a great or extreme amount of force applied over a long period of time.

3. According to the Visuality, a wound can be classified as

Internal Wounds

Disturbance of the different regulating systems of the human body can lead to wound formation, and may include the following:

Impaired circulation – This can be from either ischemia or stasis. Ischemia is the result of reduced blood supply caused by the narrowing or blockage of blood vessels, which leads to poor circulation. Stasis is caused by immobilization (or difficulty moving) for long periods or failure of the regulating valves in the veins, which leads to blood pooling and failing to flow normally to the heart.

Neuropathy – This is seen mostly in cases of prolonged uncontrolled diabetes mellitus, where high blood sugars, derivative proteins and metabolites accumulate and damage the nervous system. The patients are usually unaware of any trauma or wounds, mainly due to loss of sensation in the affected area.

Medical illness – When chronic and uncontrolled for long periods (such as hypertension, hyperlipidemia, arthrosclerosis, diabetes mellitus, AIDS, malignancy, morbid obesity, hepatitis C virus, etc.), medical illnesses can lead to impairment of the immune system functions, diminishing the circulation and damaging other organs and systems.

External Wounds

External wounds can either be open or closed. In cases of closed wounds, the skin is intact and the underlying tissue is affected but not directly exposed to the outside environment. The following are the most common types of closed wounds:

Contusions – These are a common type of sports injury, where a direct blunt trauma can damage the small blood vessels and capillaries, muscles and underlying tissue, as well the internal organs or bone. Contusions present as a painful bruise with reddish to bluish discoloration that spreads over the injured area of skin.

Hematomas – These include any injury that damages the small blood vessels and capillaries resulting in blood collecting and pooling in a limited space. Hematomas typically present as a painful, spongy rubbery lump-like lesion. Depending on the severity and site of the trauama, hematomas can be small or large, deep inside the body or just under the skin.

Crush injuries – These are usually caused by an external high-pressure force that squeezes part of the body between two surfaces. The degree of injury can range from a minor bruise to a complete destruction of the crushed area of the body, depending on the site, size, duration and power of the trauma.

Causes of Wound

Sudden forceful fall down
Road traffic accident
Burn and injured suddenly
Falls – Falling onto an outstretched hand is one of the most common causes of wound.
Sports injuries – Many sports injury occur during contact sports or sports in which you might fall onto an outstretched hand — such as in-line skating or snowboarding.
Motor vehicle crashes – Motor vehicle crashes can cause wound. Sometimes into many pieces, and often require surgical repair.
Have osteoporosis – a disease that weakens your bones.
Eave low muscle mass or poor muscle strength – or lack agility and have poor balance (these conditions make you more likely to fall)
Walk or do other activities in snow or on the ice – or do activities that require a lot of forwarding momenta, such as in-line skating and skiing
Wave an inadequate intake of calcium or vitamin D
Football or soccer, especially on artificial turf
Rugby
Horseback riding
Hockey
Skiing
Snowboarding
In-line skating
Jumping on a trampoline

Symptoms of Wound

General signs and symptoms of a wound infection include

Redness or discoloration
Swelling
Warmth
Pain, tenderness
Scaling, itching
Pustules, pus drainage
Increased pain around the wound bed
Redness or warmth
Fever /chills or other flu-like symptoms
Pus draining from the wound bed
Increasing odor from the wound
Increased firmness of skin or swelling around the wound bed
Increasing drainage from the wound bed
Delayed wound healing
Discoloration of the wound bed with it turning darker in color
Foul odor
Increased fragility of the wound bed
Wound breakdown /enlargement

The skin may harden or tighten in the area and red streaks may radiate from the wound. Wound infections may also cause fevers, especially when they spread to the blood.

Diagnosis of Wound

Clinicians perform wound assessment as a means for determining the appropriate treatment for an extremely diverse grouping of disease processes. Just as hypertension is not treated the same as diabetes, each of the underlying etiologies of the given wound must be identified and treated as if it were its own disease, not a blanket classification of “wound.”[rx][rx]

The initial assessment should begin with the following:

How – How was the wound created and, if chronic, why is it still open? (underlying etiology)
Where – Where on the body is it located? Is it in an area which is difficult to offload, or to keep clean? Is it in an area of high skin tension? Is it near any vital structures such as a major artery?
When – How long has this wound been present? (eg., chronic or acute)
What – What anatomy does it extend? (e.g., epidermis, dermis, subcutaneous tissue, fascia, muscle, tendon, bone, arteries, nerves)
What – What co-morbidities or social factors does the patient have which might affect which might affect their ability to heal the wound?
Is it life threatening?

All of these factors significantly affect the treatment plan moving forward. While there are many excellent biologics, skin grafts, and other options available, without the appropriate understanding of the nature of the wound the chances of healing decline significantly.

Issues of Concern

While some wounds are simple, the majority of wounds many clinicians encounter are caused by or complicated by some other issue.[rx][rx][rx][rx] These are a few of the possible complications from different wound types:

A chronic wound will have a different makeup than that of an acute wound, requiring conversion for healing.
An underlying infection will prevent wound healing even if the infection is subacute.
A damaged or constricted arterial supply will prevent appropriate blood flow to the wound.
A damaged venous supply will cause venous stasis.
Physical pressure on chronic ulceration will cause repeated damage, preventing healing.

Tests

Many minor and superficial skin and wound infections are diagnosed by a healthcare practitioner based on a physical examination, sign and symptoms, and experience. A clinical evaluation cannot, however, definitively tell the healthcare practitioner which microbe is causing a wound infection or what treatment is likely to be effective. For that, laboratory testing is required.

Laboratory Tests
Examples of common tests include

Bacterial culture – This is the primary test used to diagnose a bacterial infection. Results are usually available within 24-48 hours.
Gram stain – This is usually performed in conjunction with the wound culture. It is a special staining procedure that allows bacteria to be evaluated under the microscope. The results are usually available the same day and provide preliminary information about the microbe that may be causing the infection.
Antimicrobial susceptibility – A follow-up test to a positive wound culture, this is used to determine the bacteria’s likely susceptibility to certain drugs and helps the healthcare practitioner select appropriate antibiotics for treatment. Results are typically available in about 24 hours. This testing can identify resistant bacteria such as MRSA.

Other tests may include

KOH prep – This is a rapid test performed to detect fungi in a sample. The sample is treated with a special solution, placed on a slide, and examined under a microscope.
Fungal culture – This is ordered when a fungal infection is suspected. Many fungi are slow-growing and may take several weeks to identify.
AFB testing – This is ordered when a mycobacterial infection is suspected. Most AFB are slow-growing and may take several weeks to identify.
Blood culture – This is ordered when infection from a wound may have spread to the blood.
Molecular testing – to detect genetic material of a specific microbe
Basic metabolic panel (BMP) or Comprehensive metabolic panel (CMP) – This may be ordered to detect underlying conditions that can affect wound healing, such as a glucose test to detect diabetes.
Complete blood count (CBC) – An elevated white blood cell (WBC) count may be a sign of infection.

Treatment of Wound

Emergency Management

Pain control

Intravenous opiates are often used as patients typically in severe pain
- Highly effective for management of pain
- Lower side effect profile than systemic analgesia
- Always calculate your toxic dose of local anesthetic to avoid local anesthetic systemic toxicity

Closed the wounds should be placed in long leg splint and can also be placed in traction
If open Fractures should receive antibiotics and should proceed to OR for irrigation/debridement.
Cleaning to remove dirt and debris from a fresh wound. This is done very gently and often in the shower.
Vaccinating for tetanus may be recommended in some cases of traumatic injury.
Exploring a deep wound surgically may be necessary. Local anaesthetic will be given before the examination.
Removing dead skin surgically. Local anaesthetic will be given.
Closing large wounds with stitches or staples.
Dressing the wound – The dressing chosen by your doctor depends on the type and severity of the wound. In most cases of chronic wounds, the doctor will recommend a moist dressing.
Relieving pain with medications – Pain can cause the blood vessels to constrict, which slows healing. If your wound is causing discomfort, tell your doctor. The doctor may suggest that you take over-the-counter drugs such as paracetamol or may prescribe stronger pain-killing medication.
Treating signs of infection including pain – pus and fever. The doctor will prescribe antibiotics and antimicrobial dressings if necessary. Take as directed.
Skin Traction (Hare or Thomas) if needed
- May improve wound alignment, blood flow, and pain
- Skin traction splint can cause complications if a patient with a significant injury (i.e. multi ligamentous knee injury)
- Hare Splint Video(link)
- Thomas Splint Video (link)

Medication

Here we review only the commonly used medications that have a significant impact on healing, including glucocorticoid steroids, non-steroidal anti-inflammatory drugs, and chemotherapeutic drugs.

Antibiotic – Cefuroxime or Azithromycin, or Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema. Antibiotics and tetanus vaccination may be used if the bone breaks through the skin creating an open fracture.
NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and Ketorolac, Aceclofenac, Naproxen, Etoricoxib.
Glucocorticoid Steroids – Systemic glucocorticoids (GC), which are frequently used as anti-inflammatory agents, are well-known to inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses, including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction [rx]. Glucocorticoids also inhibit production of hypoxia-inducible factor-1 (HIF-1), a key transcriptional factor in healing wounds [rx].
Non-steroidal Anti-inflammatory Drugs – Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are widely used for the treatment of inflammation and rheumatoid arthritis and for pain management. Low-dosage aspirin, due to its anti-platelet function, is commonly used as a preventive therapeutic for cardiovascular disease, but not as an anti-inflammatory drug [rx]. There are few data to suggest that short-term NSAIDs have a negative impact on healing.
Muscle Relaxants – These medications provide relief from associated muscle spasms or injury
Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
Calcium & vitamin D3 – To improve bones health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
Glucosamine & Diacerein, Chondroitin sulfate – can be used to tightening the loose tendon, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament.
Dietary supplement -to remove general weakness & improved health.
Vitamin C – It help to cure the wounds
Chemotherapeutic Drugs – Most chemotherapeutic drugs are designed to inhibit cellular metabolism, rapid cell division, and angiogenesis and thus inhibit many of the pathways that are critical to appropriate wound repair. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased fibroplasia and neovascularization of wounds [rx].
Nutrition – For more than 100 years, nutrition has been recognized as a very important factor that affects wound healing. Most obvious is that malnutrition or specific nutrient deficiencies can have a profound impact on wound healing after trauma and surgery. Patients with chronic or non-healing wounds and experiencing nutrition deficiency often require special nutrients. Energy, carbohydrate, protein, fat, vitamin, and mineral metabolism all can affect the healing process [rx].
Carbohydrates, Protein, and Amino Acids – Together with fats, carbohydrates are the primary source of energy in the wound-healing process. Glucose is the major source of fuel used to create the cellular ATP that provides energy for angiogenesis and deposition of the new tissues [rx]. The use of glucose as a source for ATP synthesis is essential in preventing the depletion of other amino acid and protein substrates [rx].
Protein – is one of the most important nutrient factors affecting wound healing. A deficiency of protein can impair capillary formation, fibroblast proliferation, proteoglycan synthesis, collagen synthesis, and wound remodeling. A deficiency of protein also affects the immune system, with resultant decreased leukocyte phagocytosis and increased susceptibility to infection [rx]. Collagen is the major protein component of connective tissue and is composed primarily of glycine, proline, and hydroxyproline. Collagen synthesis requires hydroxylation of lysine and proline, and co-factors such as ferrous iron and vitamin C. Impaired wound healing results from deficiencies in any of these co-factors [rx].
Arginine – is a semi-essential amino acid that is required during periods of maximal growth, severe stress, and injury. Arginine has many effects in the body, including modulation of immune function, wound healing, hormone secretion, vascular tone, and endothelial function. Arginine is also a precursor to proline, and, as such, sufficient arginine levels are needed to support collagen deposition, angiogenesis, and wound contraction [rx][rx]. Arginine improves immune function, and stimulates wound healing in healthy and ill individuals [rx]. Under psychological stress situations, the metabolic demand of arginine increases, and its supplementation has been shown to be an effective adjuvant therapy in wound healing [rx].
Glutamine – is the most abundant amino acid in plasma and is a major source of metabolic energy for rapidly proliferating cells such as fibroblasts, lymphocytes, epithelial cells, and macrophages [rx]. The serum concentration of glutamine is reduced after major surgery, trauma, and sepsis, and supplementation of this amino acid improves nitrogen balance and diminishes immunosuppression [rx]. Glutamine has a crucial role in stimulating the inflammatory immune response occurring early in wound healing [rx]. Oral glutamine supplementation has been shown to improve wound breaking strength and to increase levels of mature collagen [rx].
Fatty Acids – Lipids are used as nutritional support for surgical or critically ill patients to help meet energy demands and provide essential building blocks for wound healing and tissue repair. Polyunsaturated fatty acids (PUFAs), which cannot be synthesized de novo by mammals, consist mainly of two families, n-6 (omega-6, found in soybean oil) and n-3 (omega-3, found in fish oil). Fish oil has been widely touted for the health benefits of omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The effects of omega-3 fatty acids on wound healing are not conclusive. They have been reported to affect pro-inflammatory cytokine production, cell metabolism, gene expression, and angiogenesis in wound sites [rx] . The true benefit of omega-3 fatty acids may be in their ability to improve the systemic immune function of the host, thus reducing infectious complications and improving survival [rx].
Vitamins, Micronutrients, and Trace Elements – Vitamins C (L-ascorbic acid), A (retinol), and E (tocopherol) show potent anti-oxidant and anti-inflammatory effects. Vitamin C has many roles in wound healing, and a deficiency in this vitamin has multiple effects on tissue repair. Vitamin C deficiencies result in impaired healing, and have been linked to decreased collagen synthesis and fibroblast proliferation, decreased angiogenesis, and increased capillary fragility. Also, vitamin C deficiency leads to an impaired immune response and increased susceptibility to wound infection [rx;rx]. Similarly, vitamin A deficiency leads to impaired wound healing. The biological properties of vitamin A include anti-oxidant activity, increased fibroblast proliferation, modulation of cellular differentiation and proliferation, increased collagen and hyaluronate synthesis, and decreased MMP-mediated extracellular matrix degradation [rx].
Vitamin E, an anti-oxidant – maintains and stabilizes cellular membrane integrity by providing protection against destruction by oxidation. Vitamin E also has anti-inflammatory properties and has been suggested to have a role in decreasing excess scar formation in chronic wounds. Animal experiments have indicated that vitamin E supplementation is beneficial to wound healing [rx, rx; rx] and topical vitamin E has been widely promoted as an anti-scarring agent. However, clinical studies have not yet proved a role for topical vitamin E treatment in improving healing outcomes [rx,rx].
Several micronutrients – have been shown to be important for optimal repair. Magnesium functions as a co-factor for many enzymes involved in protein and collagen synthesis, while copper is a required co-factor for cytochrome oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the optimal cross-linking of collagen. Zinc is a co-factor for both RNA and DNA polymerase, and a zinc deficiency causes a significant impairment in wound healing. Iron is required for the hydroxylation of proline and lysine, and, as a result, severe iron deficiency can result in impaired collagen production [rx,rx;rx, rx; rx].

Normal Wound-healing Process

Phase	Cellular and Bio-physiologic Events
Hemostasis	vascular constriction platelet aggregation, degranulation, and fibrin formation (thrombus)
Inflammation	neutrophil infiltration monocyte infiltration and differentiation to macrophage lymphocyte infiltration
Proliferation	re-epithelialization angiogenesis collagen synthesis ECM formation
Remodeling	collagen remodeling vascular maturation and regression

Dressing

Some of the unique features of each are described below.

The following dressings may be used on chronic or acute wounds depending on the nature of the wound.

Low or nonadherent dressings – are inexpensive and allow wound exudate to pass through into a secondary dressing while helping to maintain a moist wound environment. These dressings are specially designed to reduce adherence to the wound bed. Non adherent dressings are made from open weave cloth soaked in paraffin, textiles, or multilayered or perforated plastic films. This type of dressing is suitable for flat, shallow wounds with low exudate such as a venous leg ulcer.
Hydrocolloid dressings – are composed of adhesive, absorbent, and elastomeric components. Carboxymethylcellulose is the most common absorptive ingredient. They are permeable to moisture vapor, but not to water. Additionally, they facilitate autolytic débridement, are self-adhesive, mold well, provide light-to-moderate exudate absorption, and can be left in place for several days, minimizing skin trauma and disruption of the healing process. They are intended for use on light-to-moderate exuding, acute or chronic partial- or full-thickness wounds but are not intended for use on infected wounds. Upon sustained contact with wound fluid, the hydrocolloid forms a gel.
Foam dressings – vary widely in composition and construction. They consist of a polymer, often polyurethane, with small, open cells that are able to hold fluids. Some varieties of foam dressings have a waterproof film covering the top surface and may or may not have an adhesive coating on the wound contact side or border. Foams are permeable to water and gas, and are able to absorb light to heavy exudate. This type of dressing is frequently used under compression stockings in patients with venous leg ulcers.
Film dressings consist of a single – thin transparent sheet of polyurethane coated on one side with an adhesive. The sheet is permeable to gases and water vapor but impermeable to wound fluids. Film dressings retain moisture, are impermeable to bacteria and other contaminants, allow wound observation, and do not require a secondary dressing. Excessive fluid buildup may break the adhesive seal and allow leakage. Film dressings are intended for superficial wounds with little exudate and are commonly used as a secondary dressing to attach a primary absorbent dressing. The dressing may remain in place for up to seven days if excessive fluid does not accumulate. Film dressings have been used extensively to treat split-thickness graft donor sites.
Alginate dressings – are made from calcium or calcium-sodium salts of natural polysaccharides derived from brown seaweed. When the alginate material comes into contact with sodium-rich wound exudates, an ion exchange takes place and produces a hydrophilic gel. This hydrophilic gel is capable of absorbing up to 20 times its weight and does not adhere to the wound. This dressing can remain in place for about seven days if enough exudate is present to prevent drying. This category of dressing is best suited for moist, moderate-to-heavy exuding wounds. Alginate dressings require a secondary dressing, such as a film dressing, to hold them in place and to prevent the alginate from drying out.
Hydrofiber dressing – is composed of sodium carboxymethylcellulose fibers.^[rx] The fibers maintain a moist wound environment by absorbing large amounts of exudate and forming a gel. This dressing is not intended for lightly exuding wounds. A secondary dressing is required.
Hydrogel sheets – are three-dimensional networks of cross-linked hydrophilic polymers. Their high water content provides moisture to the wound, but these dressings can absorb small-to-large amounts of fluid, depending on their composition. Depending on wound exudate levels, hydrogels may require more frequent dressing changes, every 1–3 days, compared with other synthetic dressings. Hydrogel sheets can be used on most wound types but may not be effective on heavily exuding wounds. The gel may also contain additional ingredients such as collagens, alginate, or complex carbohydrates. Amorphous hydrogels can donate moisture to a dry wound with eschar and facilitate autolytic débridement in necrotic wounds. A second dressing may be used to retain the gel in shallow wounds.
Polymer-based dressing – Transforming methacrylate (TMD) was compared to carboxymethylcellulose (CMC-Ag) in one study of 34 patients. The study showed that TMD, compared to CMC-Ag, was associated with lower pain scores and better patient satisfaction, but the two dressings did not differ in terms of number of dressing changes and the time to complete healing.^[rx]Suprathel (a polymer-based dressing) was evaluated in a study of 72 patients, and it was compared to a polyurethane dressings (Biatain-Ibu) and a silicone dressing (Mepitel). The three dressings had similar time to re-epithelialization, but Suprathel had a significantly lower number of dressing changes compared to the two other dressings.^[rx]
Crystalline cellulose dressings – Results for the comparison between CMC-Ag and TMD are presented above.^[rx]Veloderm was compared to Vaseline gauze in 96 patients.^[rx] The study showed that Veloderm was associated with lower time to complete healing and number of dressing changes. The two dressings did not differ in terms of incidence of exudate, peri-lesional erythema or pain intensity.^[rx]Rayon dressing was compared to Veloderm in a study of 14 patients and 28 skin graft donor sites.^[rx] Rayon dressing showed lower dressing adherence to wound and lower 1st day pain score; the two dressings did not differ in terms of pain beyond day 14, hyperemia, edema and pruritus.^[rx]
Alginate dressings – The study evaluated the dressing materials in terms of time to healing, pain scores, clinical infections and hypergranulation. Results showed that the six types of dressings did not differ with statistical significance except in the following cases: first, the semi-permeable films (Tegaderm or Opsite) were associated with lower pain scores than any other dressing type; second, the hydrocolloid dressing (DuoDerm E) required lower time (seven days difference) to healing than all other dressings; finally, the gauze dressings (Adaptic or Jelonet) were associated with the highest incidence of clinical infections.^[rx]

Alginate-based dressings – were also evaluated in three other trials; the first one compared Algisite to a keratin dressing (Keramatrix).^[rx]The trial showed that Algisite was associated with higher rate of epithelialization seven days after the operation than Keramatrix in patients older than 50 years; for younger patients, the rate of epithelialization did not significantly differ.^[rx] Ding et al. compared time to healing and pain scores between alginate-silver dressing and hydrofiber dressing (Aquacel-A) in 10 patients and 20 donor sites; the results showed that the alginate dressing was associated with shorter time to healing and lower pain scores.^[rx]The third trial compared Algisite covered by a polyurethane dressing (Opsite) to paraffin gauze dressing; the results showed that the two dressings did not differ in terms of pain scores, time to epithelialization and the assessment of general comfort. Algisite dressings required more dressing changes (34 times) than the paraffin gauze (4 times).^[rx]
Polyurethane dressings – Opsite and Tegaderm films were evaluated in Brolemann’s study, and the results were presented above. Another trial compared the Opsite dressing to a hydrofiber dressing (Aquacel-A); the results showed that Opsite was associated with lower scores of pain.^[rx]The Biatain-Ibu dressing was compared to Suprathel (polymer dressing) and Mepitel (silicone dressing); the results were presented above with polymer-based dressings.^[rx] Another study compared Biatain-Ibu to a gauze dressing (Jelonet), and it was reported that Biatain-Ibu was associated with lower pain and itching than Jelonet; however, the study did not report any statistical testing for the differences between interventions.^[rx]
Gauze dressings – Gauze dressings were evaluated in seven trials; the results of four trials were reported earlier in this section,^[rx^,^rx^,^rx^,^rx]and the remaining three trials were as follows one trial compared Xeroform (gauze dressing) to a multilayer dressing and showed that Xeroform was associated with longer healing time and higher pain scores than Oxyband.^[rx]The second trial compared paraffin gauze to a hydrofiber dressing (Aquacel) and reported that the paraffin gauze was associated with longer re-epithelialization time and higher pain score during dressing.^[rx]The last trial compared Jelonet to a multilayer dressing as a dressing over a skin graft (receiver site); the results showed that the two dressings did not affect the time to graft take, number of nursing interventions, or post-operative infections; however, they showed that Jelonet was associated with higher pain score at the time of dressing removal.^[rx]
Hydrocolloid dressings – The efficacy of DuoDerm E was compared to six other dressing materials in Brolmann’s trial; the results of this trial were presented earlier in this section.^[rx]In another trial, DuoDerm was compared to a silicone-based dressing (AWBAT-D); the trial showed that the two dressings did not differ in terms of pain scores, wound size or time to discharge, but the DuoDerm was associated with shorter time to re-epithelialization.^[rx]
Hydrofiber dressings – The efficacy of Aquacel was studied in six trials; the results of four trials were presented earlier in the section.^[rx^,^rx^,^rx^,^rx]One of the remaining trials compared Aquacel to carbohydrate wound dressing (Glucan II), and it showed that the two interventions did not differ in terms of time to re-epithelialization, pain scores, or donor site infection.^[rx]The second trial compared two different protocols of using Aquacel; in the first protocol, Aquacel dressing was covered with gauze, while in the second one, it was covered with polyurethane film (OpSite).^[rx] The trial reported that the second protocol was associated with a larger number of donor sites healing at day 14 after surgery (88% versus 67%), and it was associated with lower pain during mobility the first day after operation; the two dressings did not differ in pain scores during rest at all time-point evaluations.^[rx]
Silicone dressings – Four trials evaluated the efficacy of silicone-based dressings; the result three of trials were presented earlier in this section.^[rx^,^rx^,^rx] The fourth trial compared Mepitel dressing to a nylon dressing (Bridal veil) when used over a skin graft (receiver site).^[rx] The results of this trial showed that Mepitel dressing was associated with less pain, easier use, and better overall experience for patients.^[rx]
Keratin dressings – The efficacy of Keranatrix was evaluated in one study the results of which were presented earlier in this section.^[rx]
Self-adhesive fabric dressing (Mefix) with or without fibrin sealant – One trial evaluated the difference between using Mefix alone or with a fibrin sealant; the trial showed that the use of fibrin sealant was associated with lower daily pain and incapacity scores, but it did not affect the time to dressing removal or the time to discharge for the hospital.^[rx]
Multilayer (combination) dressings – The efficacy of Oxyband and Allyven was evaluated in two studies the results of which were presented earlier in this section.^[rx^,^rx]
Nylon dressings – The efficacy of Bridal veil was evaluated in one study the results of which were presented earlier in this section.^[rx]
Carbohydrate wound dressings – The efficacy of Glucan dressing was evaluated in one study the results of which were presented earlier in this section.^[rx]
Negative pressure dressings – One trial compared negative pressure dressings with a conventional dressing with gauze; both dressings were used over skin grafts (receiver sites).^[rx]The trial reported that the negative pressure dressing was associated with a higher percentage of graft take and shorter duration of dressing.^[rx]

Complication of Wound Healing

Factors that can slow the wound healing process include

Dead skin (necrosis) – dead skin and foreign materials interfere with the healing process.
Infection – an open wound may develop a bacterial infection. The body fights the infection rather than healing the wound.
Haemorrhage – persistent bleeding will keep the wound margins apart.
Mechanical damage – for example, a person who is immobile is at risk of bedsores because of constant pressure and friction.
Diet – poor food choices may deprive the body of the nutrients it needs to heal the wound, such as vitamin C, zinc and protein.
Medical conditions – such as diabetes, anaemia and some vascular diseases that restrict blood flow to the area, or any disorder that hinders the immune system.
Age – wounds tend to take longer to heal in elderly people.
Medicines – certain drugs or treatments used in the management of some medical conditions may interfere with the body’s healing process.
Smoking – cigarette smoking impairs healing and increases the risk of complications.
Varicose veins – restricted blood flow and swelling can lead to skin break down and persistent ulceration.
Dryness – wounds (such as leg ulcers) that are exposed to the air are less likely to heal. The various cells involved in healing, such as skin cells and immune cells, need a moist environment.

References

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What Can Cause Magnesium Deficiency, Treatment

What Can Cause Magnesium Deficiency/Magnesium deficiency or hypomagnesia (not to be confused with hypomagnesemia) refers to inadequate intake of dietary magnesium or impaired absorption of magnesium, which can result in numerous symptoms and diseases. It is generally corrected by an increase of magnesium in diet, oral supplements, and in severe cases, intravenous supplementation.

‘Normal’ serum magnesium levels

0.75–0.95 mmol/L^[rx]

A serum magnesium <0.82 mmol/L (2.0 mg/dL) with a 24-hour urinary magnesium excretion of 40–80 mg/day is highly suggestive of magnesium deficiency.^[rx]
One group of experts has recommended magnesium supplementation in subjects experiencing symptoms that reflect magnesium deficiency if the serum level is below 0.9 mmol/L,^[rx] with levels less than 0.8 mmol/L necessitating magnesium.
Serum magnesium levels above 0.95 mmol/L may indicate hypermagnesaemia.

Magnesium requirements based on older balance studies^[rx]

Age	Requirement
Infants	150–200 mg/day
Children	200–250 mg/day
Adults	250–300 mg/day
Lactating women	400 mg/day

Causes of magnesium deficiency

Magnesium: Deficiency signs and symptoms [rx].

General – Anxiety, lethargy, weakness, agitation, depression, dysmenorrhea, hyperactivity, headache, irritability, dysacusis, low stress tolerance, loss of appetite, nausea, sleep disorders, impaired athletic performance.

Musculature – Muscle spasm, cramps in the soles of the feet, leg cramps, facial muscles, masticatory muscles, and calves, carpopedal spasm, back aches, neck pain, urinary spasms, magnesium deficiency tetany.

Nerves/CN – Nervousness, increased sensitivity of NMDA receptors to excitatory neurotransmitters, migraine, depression, nystagmus, paraesthesia, poor memory, seizures, tremor, vertigo.

Gastrointestinal tract – Constipation.

Cardiovascular syste – Risk of arrhythmias, supraventricular or ventricular arrhythmias, hypertension, coronary spasm, decreased myocardial pump function, digitalis sensitivity, Torsade de pointes, death from heart disease.

Electrolytes – Hypokalaemia, hypocalcaemia, retention of sodium.

Metabolism – Dyslipoproteinemia (increased blood triglycerides and cholesterol), decreased glucose tolerance, insulin resistance, increased risk of metabolic syndrome, disturbances of bone and vitamin D metabolism, resistance to PTH, low circulating levels of PTH, resistance to vitamin D, low circulating levels of 25(OH)D, recurrence of calcium oxalate calculi.

Miscellaneous – Asthma, chronic fatigue syndrome, osteoporosis, hypertension, altered glucose homeostasis.

Pregnancy -m Pregnancy complications (e.g., miscarriage, premature labor, eclampsia).

Acetaminophen toxicity.^[rx]
Alcoholism.
Aluminium (environmental and dietary).
Aldosteronism.
Alcohol.^[rx]
Ageing (hypochlorhydria, ie, decreased acid in the stomach).
Antacid (including ranitidine and famotidine).
Bariatric surgery (small intestinal bypass surgery).
Calcium supplements (or a high calcium to magnesium diet).
Caffeine.
Cancer.^[rx]
Coeliac disease.
Colon removal
Chronic stress
Cisplatin
Crohn’s disease.^[rx]
Ciclosporin.
Type 1 and type 2 diabetes (uncontrolled glucose levels).
Diarrhoea.
Diet high in fat or sugar.
Digoxin
Diuretics non-potassium-sparing diuretics (thiazide and loop diuretics).
Excessive ingestion of poorly absorbable magnesium^[rx] (such as magnesium oxide), leading to diarrhoea and magnesium loss.
Emotional and/or psychological stress^[rx] (overactivation of the sympathetic nervous system).
Enzymatic dysfunction (impaired magnesium distribution).
Oestrogen therapy^[rx] (shifts magnesium to soft and hard tissues lowering serum levels).
Excessive or prolonged lactation
Excessive menstruation.
Fasting (or low magnesium intake).
Foscarnet
Gentamicin^[rx] and tobramycin.
Hyperparathyroidism and hypoparathyroidism.
Hyperthyroidism.
Kidney diseases^[rx] (glomerulonephritis, pyelonephritis, hydronephrosis, nephrosclerosis and renal tubular acidosis).
Heart failure.
Haemodialysis.
High phosphorus in the diet^[rx] (soda, inorganic phosphates contained in many inactive ingredients in processed foods).
Hyperinsulinaemia (and insulin therapy).^[rx]
Insulin resistance (intracellular magnesium depletion).
Laxatives.^[rx]
Low salt intake.
Low selenium intake.
Gastrointestinal disorders^[rx]—malabsorption syndromes (coeliac disease, non-tropical sprue, bowel resection, Crohn’s disease, ulcerative colitis, steatorrhoea), prolonged diarrhoea or vomiting.
Liver disease^[rx] (acute or chronic liver disease, including cirrhosis).
Metabolic acidosis^[rx] (latent or clinical).
Pancreatitis(acute and chronic).
Parathyroidectomy.
Pentamidine.
Peritoneal dialysis.^[rx]
Porphyria with inappropriate secretion of antidiuretic hormone.
Pregnancy.
Proton pump inhibitors.
Strenuous exercise.
Tacrolimus.^[rx]
Vitamin B₆ (pyridoxine) deficiency.^[rx]
Vitamin D excess or deficienc (chronic kidney disease and liver disease can prevent the activation of vitamin D).

Potential clinical signs of magnesium deficiency^[rx]

Less severe signs

Aggression.^[rx]
Anxiety.
Ataxia.
Chvostek sign^[rx] (twitching of the facial muscles in response to tapping over the area of the facial nerve).
Confusion.
Cramps (spontaneous carpopedal spasm or painful cramps of the muscles in your hands and feet).
Disorientation.
Fasciculations (‘a brief, spontaneous contraction affecting a small number of muscle fibres, often causing a flicker of movement under the skin. It can be a symptom of disease of the motor neurons)’.^[rx]
Hyper-reflexia.
Irritability.
Muscular weakness.
Neuromuscular irritability.
Pain or hyperalgesia^[rx] (decreases the nociceptive threshold).
Photosensitivity.^[rx]
Spasticity.
Tetany (involuntary muscle spasms).
Tinnitus^[rx] (ringing in the ears).
Tremors.
Trousseau sign.
Vertigo.
Vitamin D resistance.

Severe signs

Arrhythmias (caused by over-excitation of the heart due to enhanced depolarisation susceptibility, especially torsades de pointes or ventricular tachycardia with a prolonged QT interval).
Calcifications (soft tissue).
Cataracts.^[rx]
Convulsions.
Coronary artery disease.
Depressed immune response.^[rx]
Depression.
Hearing loss.^[rx]
Heart failure.
Hypertension.
Migraines/headaches.
Mitral valve prolapse.^[rx]
Osteoporosis.
Parathyroid hormone resistance and impaired parathyroid hormone release/function.^[rx]
Psychotic behavior.
Seizures^[rx] (overexcitation of the nervous system (nerve cells), which are more likely to fire due to a reduced electric potential difference between the outer and inner surfaces of the membrane).²
Sudden cardiac death.
Tachycardia.

Lab and ECG signs of magnesium deficiency^[rx]

Hypomagnesaemia.
Hypocalcemia.
Hypokalaemia.
Prolonged QTc.
ST segment depression^[rx] (in animals).

Measurements to diagnose magnesium deficiency (best to worst)

Reliable methods

Retention of magnesium load (intravenous or oral) after its administration^[rx] is likely the best indicator of magnesium deficiency. However, the retention test assumes normal kidney function for intravenous magnesium loads and normal gastrointestinal and renal function for oral load tests and is cumbersome and invasive.
Mononuclear cell magnesium^[rx] and muscle magnesium content^[rx] (muscle biopsy).

Less reliable methods

Hair magnesium content^[rx] (one study concluded: ‘magnesium hair concentration may be an easier, cheaper and less invasive indicator of body magnesium depletion’).^[rx]
Bone magnesium (magnesium depletion in the coccyx may indicate magnesium deficiency).^[rx]
The ratio of ionized magnesium to total magnesium^[rx] (serum or plasma).
Ionized magnesium levels^[rx] (serum or erythrocytes, ionized magnesium is the physiologically active magnesium not bound to proteins). However, this biomarker is controversial and not always available in clinical labs and hard to measure reliably.
Lymphocyte magnesium.^[rx]
Urinary or fecal magnesium excretion^[rx] (low or high levels may indicate deficiency).
Urinary fractional magnesium excretion >4%^[rx] (some authors have suggested >2% in those with normal kidney function).^[rx]
Total erythrocyte magnesium levels^[rx] (magnesium deficiency has been suggested when erythrocyte magnesium levels are <1.65 mmol/L).^[rx]
Total serum magnesium levels.
It is important to note that choosing only one of the aforementioned methods of measuring magnesium deficiency is not appropriate for diagnosing magnesium deficiency. In general, either symptom of magnesium deficiency must accompany the more reliable methods to diagnose magnesium deficiency (eg, intravenous/oral magnesium load, mononuclear cell or muscle), or two or more of the reliable measurements (eg, intravenous/oral magnesium load, mononuclear cell or muscle) should be used in supporting a diagnosis of magnesium deficiency.

Causes of hypermagnesaemia

Oversupplementation (mainly from magnesium-containing antacids).^[rx]
Kidney damage.^[rx]
Inflammation and cellular injury^[rz] (significant increases in total and ionized magnesium in animals during endotoxin challenge).

Magnesium Deficiency & it Basic Role in Human Body

It is an antidote to stress, the most powerful relaxation mineral available, and it can help improve your sleep.

I find it very funny that more doctors aren’t clued in to the benefits of magnesium, because we use it all the time in conventional medicine. But we never stop to think about why or how important it is to our general health or why it helps our bodies function better.

I remember using magnesium when I worked in the emergency room. It was a critical “medication” on the crash cart. If someone was dying of a life-threatening arrhythmia (or irregular heart beat), we used intravenous magnesium. If someone was constipated or needed to prepare for colonoscopy, we gave them milk of magnesia or a green bottle of liquid magnesium citrate, which emptied their bowels.

www.rxharun.com

If pregnant women came in with pre-term labor, or high blood pressure of pregnancy (pre-eclampsia) or seizures, we gave them continuous high doses of intravenous magnesium.

But you don’t have to be in the hospital to benefit from getting more magnesium. You can start taking regular magnesium supplementation today and see results.

The Relaxation Mineral

Think of magnesium as the relaxation mineral. Anything that is tight, irritable, crampy, and stiff — whether it is a body part or an even a mood — is a sign of magnesium deficiency.

This critical mineral is actually responsible for over 300 enzyme reactions and is found in all of your tissues — but mainly in your bones, muscles, and brain. You must have it for your cells to make energy, for many different chemical pumps to work, to stabilize membranes, and to help muscles relax.

When was the last time you had a good dose of seaweed, nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter.

That is why the list of conditions that are found related to magnesium deficiency is so long. In fact, there are over 3,500 medical references on magnesium deficiency!

Even so, this mineral is mostly ignored because it is not a drug, even though it is MORE powerful than drugs in many cases. That’s why we use it in the hospital for life-threatening and emergency situations like seizures and heart failure.

Magnesium Deficiency Symptoms

Muscle cramps or twitches
Insomnia
Irritability
Sensitivity to loud noises
Anxiety
Autism
ADD
Palpitations
Angina
Constipation
Anal spasms
Headaches
Migraines
Fibromyalgia
Chronic fatigue
Asthma
Kidney stones
Diabetes
Obesity
Osteoporosis
High blood pressure
PMS
Menstrual cramps
Irritable bladder
Irritable bowel syndrome
Reflux
Trouble swallowing

Magnesium deficiency has even has been linked to inflammation in the body and higher CRP levels.

In our society, magnesium deficiency is a huge problem. By conservative standards of measurement (blood, or serum, magnesium levels), 65 percent of people admitted to the intensive care unit — and about 15 percent of the general population — have a magnesium deficiency.
But this seriously underestimates the problem, because a serum magnesium level is the LEAST sensitive way to detect a drop in your total body magnesium level. So rates of magnesium deficiency could be even higher!
The reason we are so deficient is simple: Many of us eat a diet that contains practically no magnesium — a highly-processed, refined diet that is based mostly on white flour, meat, and dairy (all of which have no magnesium).
When was the last time you had a good dose of sea vegetables (seaweed), nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter, and mostly in chocolate peanut butter cups.
Much of modern life conspires to help us lose what little magnesium we do get in our diet. Magnesium levels are decreased by excess alcohol, salt, coffee, phosphoric acid in colas, profuse sweating, prolonged or intense stress, chronic diarrhea, excessive menstruation, diuretics (water pills), antibiotics and other drugs, and some intestinal parasites. In fact, in one study in Kosovo, people under chronic war stress lost large amounts of magnesium in their urine.
This is all further complicated by the fact that magnesium is often poorly absorbed and easily lost from our bodies. To properly absorb magnesium we need a lot of it in our diet, plus enough vitamin B6, vitamin D, and selenium to get the job done.
A recent scientific review of magnesium concluded, “It is highly regrettable that the deficiency of such inexpensive, low-toxicity nutrient results in diseases that cause incalculable suffering and expense throughout the world.” (ii) I couldn’t’ have said it better myself.
It is difficult to measure and hard to study, but magnesium deficiency accounts for untold suffering — and is simple to correct. So if you suffer from any of the symptoms I mentioned or have any of the diseases I noted, don’t worry — it is an easy fix!! Here’s how.
Magnesium deficiency can be harmful! Low magnesium levels can cause fatigue, seizures, high blood pressure, blood clots, muscle cramps and so on.
It’s estimated that 80 percent of Americans have a magnesium deficiency. And this is not a good thing since this mineral affects every organ in the body.
According to the Institute of medicine, adult men should consume 400 –
420 mg of magnesium while women should aim for 310 – 360 mg per day. Now, the foods below can help get the recommended amount of magnesium without supplementation.

Magnesium Rich Food to Improve Your Overall Health

Functions of magnesium (selection) [rx,rx,rx,rx,rx].

Magnesium is involved in more than 300 essential metabolic reactions (e.g., all Adenosine Triphosphate (ATP)-dependent reactions).

Energy production (→ ATP production)

Breakdown and energetic utilization of carbohydrates, proteins and fats in intermediate metabolism (e.g., glycolysis, respiratory chain phosphorylation). ATP exists primarily as a complex with magnesium (MgATP).

Enzyme activation (examples)

Mitochondrial ATP synthase, Na⁺/K⁺-ATPase, Hexokinase, Creatine kinase, Adenylate cyclase, Phosphofructokinase, tyrosine kinase activity of the insulin receptor.

Calcium antagonist/NMDA-receptor antagonist

Control of calcium influx at the cell membrane (course of contractions, regulation of vascular muscle tone): muscle contraction/relaxation, neurotransmitter release, action potential conduction in nodal tissue, neuromuscular impulse conduction (inhibition of calcium-dependent acetylcholine release at the motor end plate), maintenance and stabilization of membrane physiology, muscle contraction.

Cardiovascular system

Economization of cardiac pump function, regulation of potassium movement in myocardial cells, protection against stress, vasodilation of the coronary and peripheral arteries, reduction of platelet aggregation.

Membrane function

Transmembrane electrolyte flux, active transport of potassium and calcium across cell membranes, regulation of cell adhesion and cell migration.

Structural roles

Component of mineralized bone (structure, microarchitecture), multiple enzyme complexes, mitochondria, proteins, polyribosomes, and nucleic acids.

Nutrient metabolism

Metabolic activation and the utilisation of vitamin D, B-vitamins (e.g., thiamine) and glutathione.

Okra – One cup of okra has 70 mg of magnesium – approx. 15 percent of the recommended daily intake. Avoid fried okra, boil or roast it.
Dark chocolate – A bar of chocolate has more than half of the daily recommended magnesium.
Pumpkin – A cup of chopped pumpkin has 60 mg of magnesium. This food also other numerous benefits so eat it as often as possible.
Brown rice – A cup of brown rice supplies about 20 percent of recommended magnesium.
Avocado – This alkaline food is a great magnesium source. One medium-size avocado has about 15 percent of the magnesium you need in a day.
Almonds – One ounce of this healthy nut has approx. 20 percent of magnesium you need.
Beet greens – Beet greens may not be popular, but they have lots of magnesium. One cup has 100 mg of magnesium.
Spinach – A cup of spinach has 150 mg of magnesium. This is definitely one of the best sources of this mineral.
Squash – This pumpkin-like will give lots of magnesium. One cup has about 40 mg.
Broccoli – If you’ve never liked broccoli, its magnesium content might change your mind. A cup has 33 mg.
Figs – 4 cups of dried figs can give you all the magnesium you need in a day.
Cashew nuts – An ounce of cashew nuts has about 20 percent of the magnesium you need.
Bananas – Bananas may be known for being potassium-rich, but they also contain some magnesium.
Pumpkin seeds – Pumpkin and squash seeds contain about 19 percent of recommended magnesium per ounce.
Lentils – A cup of lentils will give you 18 percent of recommended magnesium.
Cucumbers – A cup of cucumbers has about 40 mg of magnesium.
Peas – You can get 70 mg of magnesium from a cup of peas.

Magnesium and drug interactions.

Medications that reduce magnesium levels:

(i) H2 blockers: for example, cimetidine and nizatidine

(ii) Proton pump inhibitors: for example, esomeprazole, omeprazole, and pantoprazole (FDA WARNING: supplementing magnesium will not correct deficiency; you must stop the drug)

(iii) Antacids: aluminum and magnesium hydroxide and sodium bicarbonate

(iv) Antibiotics: for example, amoxicillin, azithromycin, doxycycline, minocycline, levofloxacin, ciprofloxacin, cephalexin,

sulfamethoxazole and trimethoprim, and tetracycline

(v) Antihistamines: for example, astemizole and terfenadine

(vi) Antivirals: for example, delavirdine, lamivudine, and zidovudine

(vii) Antiepileptic medications: phenytoin and phenobarbital

(viii) Blood pressure drugs: hydralazine and combination of ACE inhibitors with HCTZ (enalapril and HCTZ)

(ix) Diuretics: for example, furosemide, ethacrynic acid, chlorothiazide, chlorthalidone, metolazone, and indapamide

(x) Cardiac glycoside: digoxin

(xi) Cardiac drugs: sotalol, amiodarone, bretylium, and quinidine

(xii) CNS stimulants: methylphenidate

(xiii) Cholesterol agents: cholestyramine and colestipol

(xiv) Corticosteroids: betamethasone, dexamethasone, hydrocortisone, prednisone, and triamcinolone

(xv) Inhaled corticosteroids: fluticasone, flunisolide, and triamcinolone

(xvi) Estrogens: DES, estradiol, estring, and estrogen-containing drugs: HRT and BCP

(xvii) Immunosuppressants: cyclosporine and tacrolimus

(xviii) Nonsteroidal aromatase inhibitors for breast cancer: anastrozole

(xix) Osteoporosis: raloxifene

(a) On the other hand, magnesium decreases bisphosphonate absorption

(xx) SERMs (selective estrogen receptor modulators): raloxifene, tamoxifen, and toremifene

(xxi) Sulfonamides: antibiotics and some diabetic medications

(xxii) Nutraceuticals: for example, high-dose calcium, high-dose vitamin D, and caffeine

Medications that may increase serum magnesium:

(i) Lithium carbonate

(ii) Antidepressants: for example, sertraline and amitriptyline

(iii) Potassium sparing diuretics: amiloride and spironolactone reduce magnesium excretion

References

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Treatment of Burns, Complications, Prevention

Treatment of Burns/Burns injury also known as combustion injury is an impairment of the tissue, which is caused by extreme heat, electricity, chemicals, friction or radiation. Concerning children, in Hungary and worldwide the most affected age group is below the age of 5 years.^[rx] The most common cause of burn injury in children is scald from hot water.

A burn is a type of injury to skin, or other tissues, caused by heat, cold, electricity, chemicals, friction, or radiation.^[rx] Most burns are due to heat from hot liquids, solids, or fire.^[rx] While rates are similar for males and females the underlying causes often differ.^[rx] Among women in some areas, risk is related to use of open cooking fires or unsafe cook stoves.^[rx] Among men, risk is related to the work environments.^[rx] Alcoholism and smoking are other risk factors.^[rx]Burns can also occur as a result of self harm or violence between people.^[rx]

Types of Burns

Thermal Burns

Thermal burns occur when you come in contact with something hot. Typically, you will suffer a thermal burn when you touch:

Flames or fire
Hot, molten liquid or steam (referred to as a scald)
Hot objects, such as cooking pans, irons, or heated appliances.
Put out any fire or flames and stop contact with the hot or heated source.
Use cold water to cool the burned area. Do not use ice, as it may further damage the skin.
For mild burns, you can find pain relief by applying a cool, wet compress and/or taking acetaminophen or ibuprofen as directed on the bottle. Later, burn creams and ointments can help these burns heal.
For more severe burns, loosely apply a sterile bandage or clean cloth to the burned area. Do not remove parts of your skin or pop blisters. Seek medical attention for further treatment.

Chemical Burns

You may receive a chemical burn if your skin and/or eyes come in contact with a harsh irritant, such as acid. Substances that cause chemical burns include:

Chlorine
Ammonia
Bleach
Battery acid
Strong or harsh cleaners

Take these steps if you have been burned by a chemical: Rinse the burned area under running water for at least 10 minutes. If the chemical has entered your eye, rinse your eye for about 20 minutes to remove traces of the chemical. Then, call 911 or go to the hospital if the burn is:

Larger than three inches
On your face, hands, feet, groin, or buttocks
Still very painful after taking over-the-counter pain medication
On a major joint, like the knee

Medical treatment for both thermal burns and chemical burns is similar and may include:

Wound cleaning and removing dead skin or tissue
IV fluids to regulate body temperature and speed healing
Antibiotics to prevent or fight infection
Skin grafting (covering the wound with healthy skin from another area of the body to close the wound)

Electrical Burns

Electrical burns happen when the body comes in contact with an electric current. Our internal systems are not resistant to electricity, so you may be injured if a strong jolt enters your body.
The most common cause of electrical burn is coming in contact with an extension cord where the insulation material has worn away. Low-voltage electrical burns can also occur in the mouth, most commonly when young children place noninsulated cords in their mouth.
A burn may appear on your skin if an electric current runs through your body. These burns can be treated like a thermal or chemical burn. However, if you come in contact with an electric current, you should seek emergency medical attention immediately. Electricity can affect internal tissues and muscles and have long-term, negative effects on your health.

Friction Burns

A friction burn can occur when skin repeatedly rubs against another surface or is scraped against a hard surface. Like other burns, friction burns are categorized into degrees.
Many friction burns are first degree and often heal on their own within three to six days. You can use moisturizing cream at home to care for it. For more serious friction burns, you should seek medical care immediately.

Radiation Burns

Cancer patients undergoing radiation therapy may suffer from an injury known as radiation burn. High-energy radiation is used to shrink or kill cancerous cells, and when it passes through the body, skin cells may be damaged. If you’re frequently receiving radiation treatments, your skin cells may not have enough time to regenerate, and sores or ulcers may develop. The term burn is a misnomer for these wounds, because skin has not actually been burned. However, the wounds can look and feel like burns. Skin must regenerate for the wounds to heal, which can take two to four weeks for mild skin reactions or a few months for more serious reactions.

Care for radiation burns includes

Cleaning and moisturizing wounds
Avoiding sunlight
Wearing loose clothing or bandages over the wound

If you have an injury from radiation, you may also have internal complications and should seek medical treatment immediately.

The major factors to consider when evaluating the burned skin are the extent of the burns (usually calculated by the percentage of total body surface area (% TBSA) burned) and the estimated depth of the burns (superficial, partial thickness or full thickness).[rx][rx][rx][rx][rx]

Extent of the Burn

Several methods are available to estimate the percentage of total body surface area burned.

Rule of Nines – The head represents 9%, each arm is 9%, the anterior chest and abdomen are 18%, the posterior chest and back are 18%, each leg is 18%, and the perineum is 1%. For children, the head is 18%, and the legs are 13.5% each.
Lund and Browder Chart – This is a more accurate method, especially in children, where each arm is 10%, anterior trunk and posterior trunk are each 13% and the percentage calculated for the head and legs varies based on the patient’s age.
Palmar Surface – For small burns, the patient’s palm surface (excluding the fingers) represents approximately 0.5% of their body surface area, and the hand surface (including the palm and fingers) represents about 1% of their body surface area.

Depth of the Burn

Burn depth is classified into one of three types based on how deeply into the epidermis or dermis the injury might extend.

Superficial burns – (First Degree) involve only the epidermis and are warm, painful, red, soft and blanch when touched. Usually, there is no blistering. A typical example is a sunburn.
Partial thickness burns – (Second Degree) extend through the epidermis and into the dermis. The depth into the dermis can vary (superficial or deep dermis). These burns are typically very painful, red, blistered, moist, soft and blanch when touched. Examples include burns from hot surfaces, hot liquids or flame.
Full-thickness burns – (Third Degree) extend through both the epidermis and dermis and into the subcutaneous fat or deeper. These burns have little or no pain, can be white, brown, or charred and feel firm and leathery to palpation with no blanching. These occur from a flame, hot liquids, or superheated gasses.

When calculating the extent of burn, only partial thickness and full thickness burns are considered, and superficial burns are excluded.

Burns may also produce emotional and psychological distress.

Type^[rx]	Layers involved	Appearance	Texture	Sensation	Healing Time	Prognosis
Superficial (1st-degree)	Epidermis^[rx]	Red without blisters^[rx]	Dry	Painful^[rx]	5–10 days^[rx]^[rx]	Heals well.^[rx] Repeated sunburns increase the risk of skin cancer later in life.^[19]
Superficial partial thickness (2nd-degree)	Extends into superficial (papillary) dermis^[rx]	Redness with clear blister.^[rx]Blanches with pressure.^[rx]	Moist^[rx]	Very painful^[rx]	2–3 weeks^[rx]^[rx]	Local infection (cellulitis) but no scarring typically^[rx]
Deep partial thickness (2nd-degree)	Extends into deep (reticular) dermis^[rx]	Yellow or white. Less blanching. May be blistering.^[rx]	Fairly dry^[rx]	Pressure and discomfort^[rx]	3–8 weeks^[xx]	Scarring, contractures (may require excision and skin grafting)^[rx]
Full thickness (3rd-degree)	Extends through entire dermis^[rx]	Stiff and white/brown.^[rx] No blanching.^[rx]	Leathery^[rx]	Painless^[rx]	Prolonged (months) and incomplete^[rx]	Scarring, contractures, amputation (early excision recommended)^[rx]
4th-degree	Extends through entire skin, and into underlying fat, muscle and bone^[1]	Black; charred with eschar	Dry	Painless	Requires excision^[rx]	Amputation, significant functional impairment and in some cases, death.^[rx]

Cause of Burns

Burns may be caused by

Abuse
Chemicals such as strong acids, lye, paint thinner or gasoline
Electric currents
Fire
Hot liquid
Hot metal, glass or other objects
Steam
Radiation from x-rays
Sunlight or ultraviolet light

Symptoms of Burns

Blisters
Pain – The degree of pain is not related to the severity of the burn as the most serious burns can be painless
Peeling skin
Red skin
Shock – Symptoms of shock include pale and clammy skin, weakness, bluish lips and fingernails, and a drop in alertness
Swelling
White or charred skin
Heart rhythm disturbances following electrical injury

Diagnosis of Burns

Burn injury patients who should be referred to a burn unit include the following:

all burn patients less than 1 year of age
all burn patients from 1 to 2 years of age with burns >5% total body surface area (TBSA)
patients in any age group with third-degree burns of any size
patients older than 2 years with partial-thickness burns greater than 10% TBSA
patients with burns of special areas—face, hands, feet, genitalia, perineum or major joints
patients with electrical burns, including lightning burns
chemical burn patients
patients with inhalation injury resulting from fire or scald burns;
patients with circumferential burns of the limbs or chest;
burn injury patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality;
any patient with burns and concomitant trauma;
paediatric burn cases where child abuse is suspected;
burn patients with treatment requirements exceeding the capabilities of the referring centre;
septic burn wound cases.

Treatment of Burns

Basic guidance on first aid for burns is provided below.

What to do

Stop the burning process by removing clothing and irrigating the burns.
Extinguish flames by allowing the patient to roll on the ground, or by applying a blanket, or by using water or other fire-extinguishing liquids.
Use cool running water to reduce the temperature of the burn.
In chemical burns, remove or dilute the chemical agent by irrigating with large volumes of water.
Wrap the patient in a clean cloth or sheet and transport to the nearest appropriate facility for medical care.

What not to do

Do not start first aid before ensuring your own safety (switch off electrical current, wear gloves for chemicals etc.)
Do not apply paste, oil, haldi (turmeric) or raw cotton to the burn.
Do not apply ice because it deepens the injury.
Avoid prolonged cooling with water because it will lead to hypothermia.
Do not open blisters until topical antimicrobials can be applied, such as by a health-care provider.
Do not apply any material directly to the wound as it might become infected.
Avoid application of topical medication until the patient has been placed under appropriate medical care.

The aims of first aid should be to stop the burning process, cool the burn, provide pain relief, and cover the burn.burn.[rx]

A superficial scald suitable for management in primary care

Stop the burning process—The heat source should be removed. Flames should be doused with water or smothered with a blanket or by rolling the victim on the ground. Rescuers should take care to avoid burn injury to themselves. Clothing can retain heat, even in a scald burn, and should be removed as soon as possible. Adherent material, such as nylon clothing, should be left on. Tar burns should be cooled with water, but the tar itself should not be removed. In the case of electrical burns the victim should be disconnected from the source of electricity before first aid is attempted.
Cooling the burn—Active cooling removes heat and prevents progression of the burn. This is effective if performed within 20 minutes of the injury. Immersion or irrigation with running tepid water (15°C) should be continued for up to 20 minutes. This also removes noxious agents and reduces pain, and may reduce oedema by stabilising mast cells and histamine release. Iced water should not be used as intense vasoconstriction can cause burn progression. Cooling large areas of skin can lead to hypothermia, especially in children. Chemical burns should be irrigated with copious amounts of water.water.[rx]
Analgesia – Exposed nerve endings will cause pain. Cooling and simply covering the exposed burn will reduce the pain. Opioids may be required initially to control pain, but once first aid measures have been effective non-steroidal anti-inflammatory drugs such as ibuprofen or co-dydramol taken orally will suffice.
Covering the burn – Dressings should cover the burn area and keep the patient warm. Polyvinyl chloride film (cling film) is an ideal first aid cover. The commercially available roll is essentially sterile as long as the first few centimetres are discarded. This dressing is pliable, non-adherent, impermeable, acts as a barrier, and is transparent for inspection. It is important to lay this on the wound rather than wrapping the burn. This is especially important on limbs, as later swelling may lead to constriction. A blanket laid over the top will keep the patient warm. If cling film is not available then any clean cotton sheet (preferably sterile) can be used. Hand burns can be covered with a clear plastic bag so as not to restrict mobility. Avoid using wet dressings, as heat loss during transfer to hospital can be considerable.
Water-based treatments – Your care team may use techniques such as ultrasound mist therapy to clean and stimulate the wound tissue.
Fluids to prevent dehydration – You may need intravenous (IV) fluids to prevent dehydration and organ failure.
Pain and anxiety medications – Healing burns can be incredibly painful. You may need morphine and anti-anxiety medications — particularly for dressing changes.
Burn creams and ointments – If you are not being transferred to a burn center, your care team may select from a variety of topical products for wound healing, such as bacitracin and silver sulfadiazine (Silvadene). These help prevent infection and prepare the wound to close.
Dressings – Your care team may also use various specialty wound dressings to prepare the wound to heal. If you are being transferred to a burn center, your wound will likely be covered in dry gauze only.
Drugs that fight infection – If you develop an infection, you may need IV antibiotics.
Tetanus shot – Your doctor might recommend a tetanus shot after a burn injury.
Cleaning – Mild soap and water or mild antibacterial wash. Debate continues over the best treatment for blisters. However, large blisters are debrided while small blisters and blisters involving the palms or soles are left intact.
Covering – Topical antibiotic ointments or cream with absorbent dressing or specialized burn dressing materials are commonly used.
Comfort – Over-the-counter pain medications or prescription pain medications when needed. Splints can also provide support and comfort for certain burned areas.

Use of topical creams should be avoided at this stage as these may interfere with subsequent assessment of the burn. Cooling gels such as Burnshield are often used by paramedics. These are useful in cooling the burn and relieving pain in the initial stages.stages.[rx]

The American Burn Association recommends burn center referrals for patients with

partial thickness burns greater than 10% total body surface area
full thickness burns
burns of the face, hands, feet, genitalia, or major joints
chemical burns, electrical, or lighting strike injuries
significant inhalation injuries
burns in patients with multiple medical disorders
burns in patients with associated traumatic injuries

Patients being transferred to burn centers do not need extensive debridement or topical antibiotics before transfer. Whether transferring or referring to a burn center, you should contact them before beginning extensive local burn care treatments.[rx][rx]

Remove any Sources of Heat

Remove any clothing that may be burned, covered with chemicals, or that is constricting.
Cool any burns less than 3 hours old with cold tap water (18 degrees centigrade is adequate) for at least 30 minutes and then dry the patient.
Cover the patient with a clean dry sheet or blanket to prevent hypothermia.
Use of Burnshield [rx] is a very effective means of cooling and dressing the injury for the first 24 hours.
Rings and constricting garments must be removed.

Assess Airway/Breathing

Careful airway assessment must be done where there are flame or scald burns of the face and neck. Intubation is generally only necessary in the case of unconscious patients, hypoxic patients with severe smoke inhalation, or patients with flame or flash burns involving the face and neck. Indications for airway assessment include the presence of pharyngeal burns, air hunger, stridor, carbonaceous sputum, and hoarseness.
All patients with major burns must receive high-flow oxygen for 24 hours.
Always consider carbon monoxide poisoning in burn patients. They may have the following symptoms: restlessness, headache, nausea, poor co-ordination, memory impairment, disorientation, or coma. Administer 100% oxygen via a non-rebreathing face mask; if possible, measure blood gases including carboxy haemoglobin level.
If breathing seems to be compromised because of tight circumferential trunk burns, consult with the burn centre surgeons immediately regarding the need for escharotomy.

Circulation

Stop any external bleeding.
Identify potential sources of internal bleeding.
Establish large-bore intravenous (IV) lines and provide resuscitation bolus fluid as required in all compromised patients, using standard ATLS protocols [rx]. Perfusion of potentially viable burn wounds is critical.

Estimate the Percentage Total Body Surface Area (%TBSA) Burned

Initially, use the Rule of Nines. In the case of all paediatric patients and for a more accurate assessment, use the Berkow diagram; alternatively, the patient’s unstretched open hand represents 1% of TBSA.

Accurate estimation of burn size is critical to ongoing fluid replacement and management.

Ongoing Losses (Once the Patient Has Been Stabilised)

Patients with <10% TBSA burns can be resuscitated orally (unless the patient has an electrical injury or associated trauma). This needs ongoing evaluation and the patient may still require an IV line.
In the case of patients with burns 10–40% TBSA, secure a large-bore IV line; add a second line if transportation will take longer than 45 minutes.
Burns >40% TBSA require 2 large-bore IV lines.
If the transfer will take less than 30 minutes from the time of call, do not delay transfer for an IV line.

Reminder

IV lines may be placed through the burned area if necessary (suture to secure). Avoid the saphenous vein if at all possible, and avoid cut-downs through unburned skin if possible. An intraosseous line is an excellent alternative in children.

Initiate fluids for ongoing resuscitation and fluid losses using the Parkland formula 4 mL crystalloid×(kg of body weight) ×(%burn)=mL in first 24 hours, with half of this total given in the first 8 hours after injury (note that this is the time from burn, not from presentation to healthcare services). Children must have their daily maintenance fluids added to these replacement fluids (including dextrose).

Example

In the case of a patient weighing 70 kg with a 50% TBSA burn, (4 × 70 × 50) = 14 000 mL needed in the first 24 hours. Half is needed in the first 8 hours after injury.

Example

The fluid requirements of a child weighing 15 kg with a TBSA burn of 40% (4 × 15 × 40) = 2400 mL in the first 24 hours plus maintenance requirements of 1250 mL (1000 mL + 250 mL) = 3650 mL in the first 24 hours. Half is needed in the first 8 hours after injury.

Reminder

Do not give dextrose solutions (except for maintenance fluids in children)—they may cause an osmotic diuresis and confuse adequacy of resuscitation assessment. Ideally, use Ringer’s lactate or normal saline for replacement fluid and a 5% dextrose-balanced salt solution for the child’s maintenance.

This is only a guide, and ongoing evaluation is essential as patients may need more fluids than calculated. Use the patient’s vital signs and, most importantly, urine output to guide ongoing requirements.

Assess Urine Output (This Is the Best Guide to Resuscitation)

Insert a Foley catheter in patients with burns >15% TBSA. Adequate urine output is 0.5 mL/kg/h in adults and 1.5 mL/kg/h in children. Lasix and other diuretics must not be given to improve urine output; increase IV fluid rates to increase urine output. Observe urine for burgundy colour (seen with massive injuries or electrical burns). There is a high incidence of renal failure associated with these injuries, requiring prompt and aggressive intervention.

If the urine is red or brown consult a burn centre.

Insert a Nasogastric Tube

Insert a nasogastric tube in any patient with burns >30% TBSA, or any patient who is unresponsive, shocked, or with burns >20% if preparing for air or long-distance transportation.

Decompression Incisions (Escharotomy)

Assess for circumferential full-thickness burns of the extremities or trunk. Elevate the burned extremities on pillows above the level of the heart. If transfer will be delayed, discuss indications and methods for decompression incisions (escharotomies) with a burn surgeon.

Medication

Give tetanus immunisation.
After fluid resuscitation has been started, pain medication may be titrated in small intravenous doses (not intramuscular). Blood pressure, pulse, respiratory rate, and state of consciousness should be assessed after each increment of IV morphine.

Wound Care

Debridement and application of topical antimicrobials are usually unnecessary. Initial wound care needs to ensure that the burn is kept covered and the patient is kept warm. Plastic food wrap (such as Gladwrap) is ideal.
Apply a thin layer of silver sulfadiazine to open areas if transportation will be delayed for more than 12 hours.
Use of Burnshield is a very effective means of cooling and dressing the injury in the first 24 hours.

General Items

A history, including details of the accident and preexisting diseases/allergies, should be recorded and sent with the patient.
Copies of all medical records, including all fluids (calculation of fluids administered) and medications given, urine outputs, and vital signs must accompany the patient. These specific details may be recorded on the back of the burn size assessment sheet.
The burn centre will arrange transport if appropriate.
In the case of paediatric patients not accompanied by a parent, obtain consent in consultation with your burn centre.

Special Considerations with Chemical Burns (Consult Burn Centre)

Remove all clothing, Brush powdered chemicals off the wound, then flush chemical burns for a minimum of 30 minutes using copious volumes of running water. Be careful to protect yourself.

Never neutralise an acid with a base or vice versa; the heat generated can worsen the burn.

Irrigate burned eyes using a gentle stream of saline. Follow with an ophthalmology consultation if transportation is not imminent. Determine what chemical (and what concentration) caused the injury.

Special Considerations with Electrical Injuries (Consult Burn Centre)

Differentiate between low-voltage (<1000 v) and high-voltage (>1000 v) injuries.
Attach a cardiac monitor; treat life-threatening dysrhythmias as needed.
Assess for associated trauma; assess central and peripheral neurological function.
Administer Ringer’s lactate; titrate fluids to maintain adequate urine output or to flush pigments through the urinary tract (see urine output above). Useful laboratory test: arterial blood gas levels with acid/base balance.
Using pillows, elevate burned extremities above the level of the heart. Monitor distal pulses.

For burns classified as severe (> 20% TBSA), fluid resuscitation should be initiated to maintain urine output > 0.5 mL/kg/hour. One commonly used fluid resuscitation formula is the Parkland formula. The total amount of fluid to be given during the initial 24 hours = 4 ml of LR × patient’s weight (kg) × % TBSA. Half of the calculated amount is administered during the first eight hours beginning when the patient was initially burned. For example, if a 70 kg patient has a 30% TBSA partial thickness burn they will need 8400 mL Lactated Ringer solution in the first 24 hours with 4200 mL of that total in the first 8 hours [(4 mL) × (70 kg) × (30% TBSA) = 8,400 mL LR]. Remember that the fluid resuscitation formula for burns is only an estimate and the patient may need more or less fluid based on vital signs, urine output, other injuries or other medical conditions (see Burns, Resuscitation, and Management for discussion of the management of severely burned patients).

Dressing changes

The practice of subsequent dressing changes is varied. Ideally the dressing should be checked at 24 hours. The burn wound itself should be reassessed at 48 hours and the dressings changed, as they are likely to be soaked through. At this stage the depth of burn should be apparent, and topical agents such as Flamazine can be used.

Depending on how healing is progressing, dressing changes thereafter should be every three to five days. If the Jelonet dressing has become adherent, it should be left in place to avoid damage to delicate healing epithelium. If Flamazine is used it should be changed on alternate days. The dressing should be changed immediately if the wound becomes painful or smelly or the dressing becomes soaked (“strike through”).

Any burn that has not healed within two weeks should be seen by a burn surgeon.

Specialist dressings

Many specialist dressings are available, some developed for specific cases, but most designed for their ease of use. The following are among the more widely used.

Flamazine – is silver sulfadiazine cream and is applied topically on the burn wound. It is effective against gram negative bacteria including Pseudomonas. Infection with the latter will cause the dressing to turn green with a distinctive smell. Apply the cream in a 3-5 mm thick layer and cover with gauze. It should be removed and reapplied every two days. There is a reported 3-5% incidence of reversible leucopenia.

Granulflex – is a hydrocolloid dressing with a thin polyurethane foam sheet bonded onto a semipermeable film. The dressing is adhesive and waterproof and is therefore useful in awkward areas or where normal dressings are not suitable. It should be applied with a 2 cm border. By maintaining a moist atmosphere over the wound, it creates an environment suitable for healing. It usually needs to be changed every three or four days, but it can be left for seven days. A thinner version (Duoderm) is also available.

Mepitel – is a flexible polyamide net coated with soft silicone to give a Jelonet-type of dressing that is non adhesive. It is a useful but expensive alternative to Jelonet when easy removal is desirable, such as with children.

Facial burns

Facial burns should be referred to a specialist unit. However, simple sunburn should be left exposed as dressings can be awkward to retain on the face. The wound should be cleansed twice daily with mild diluted chlorohexidine solution. The burn should be covered with a bland ointment such as liquid paraffin. This should be applied every 1-4 hours as necessary to minimise crust formation. Men should shave daily to reduce risk of infection. All patients should be advised to sleep propped up on two pillows for the first 48 hours to minimise facial oedema.

Follow up

Burns that fail to heal within three weeks should be referred to a plastic surgery unit for review. Healed burns will be sensitive and have dry scaly skin, which may develop pigmental changes. Daily application of moisturiser cream should be encouraged. Healed areas should be protected from the sun with sun block for 6-12 months. Pruritis is a common problem.

Physiotherapy—Patients with minor burns of limbs may need physiotherapy. It is important to identify these patients early and start therapy. Hypertrophic scars may benefit from scar therapy such as pressure garments or silicone. For these reasons, all healed burns should be reviewed at two months for referral to an occupational therapist if necessary.

Support and reassurance – Patients with burn injuries often worry about disfigurement and ugliness, at least in the short term, and parents of burnt children often have feelings of guilt. It is important to address these issues with reassurance.[rx]

Surgical and other procedures

You may need one or more of the following procedures:

Breathing assistance. If you’ve been burned on the face or neck, your throat may swell shut. If that appears likely, your doctor may insert a tube down your windpipe (trachea) to keep oxygen supplied to your lungs.
Feeding tube. People with extensive burns or who are undernourished may need nutritional support. Your doctor may thread a feeding tube through your nose to your stomach.
Easing blood flow around the wound. If a burn scab (eschar) goes completely around a limb, it can tighten and cut off the blood circulation. An eschar that goes completely around the chest can make it difficult to breathe. Your doctor may cut the eschar to relieve this pressure.
Skin grafts. A skin graft is a surgical procedure in which sections of your own healthy skin are used to replace the scar tissue caused by deep burns. Donor skin from deceased donors or pigs can be used as a temporary solution.
Plastic surgery. Plastic surgery (reconstruction) can improve the appearance of burn scars and increase the flexibility of joints affected by scarring.

Complications of Burns

Deep or extensive burns can lead to many complications, including:

Breathing problems
Bone and joint problems
Dangerously low body temperature
Infection and sepsis
Low blood volume
Scarring
Tetanus

Infection is the most common complication. In order of frequency, potential complications include: pneumonia, cellulitis, urinary tract infections and respiratory failure. Pneumonia commonly occurs in those with inhalation injuries.

Other complications may include

Anemia secondary to full thickness burns of greater than 10% TBSA is common.
Electrical burns may result in compartment syndrome or rhabdomyolysis.
Blood clotting in the veins of the legs occurs in 6-25% of patients with extensive burns.
The hypermetabolic state that may persist for years after a major burn may result in a decreased bone density and muscle mass.
Keloids may form subsequent to a burn.
Following a burn, psychological trauma and post-traumatic stress disorder my develop.
Scarring may aresult in a disturbance in body image.
In the developing world, significant burns may result in social isolation, poverty, and child abandonment.

Other Risk Factors

There are a number of other risk factors for burns, including

occupations that increase exposure to fire;
poverty, overcrowding and lack of proper safety measures;
placement of young girls in household roles such as cooking and care of small children;
underlying medical conditions, including epilepsy, peripheral neuropathy, and physical and cognitive disabilities;
alcohol abuse and smoking;
easy access to chemicals used for assault (such as in acid violence attacks);
use of kerosene (paraffin) as a fuel source for non-electric domestic appliances;
inadequate safety measures for liquefied petroleum gas and electricity.

Prevention

Burns are preventable. High-income countries have made considerable progress in lowering rates of burn deaths, through a combination of prevention strategies and improvements in the care of people affected by burns. Most of these advances in prevention and care have been incompletely applied in low- and middle-income countries. Increased efforts to do so would likely lead to significant reductions in rates of burn-related death and disability.

Prevention strategies should address the hazards for specific burn injuries, education for vulnerable populations and training of communities in first aid. An effective burn prevention plan should be multisectoral and include broad efforts to

improve awareness
develop and enforce effective policy
describe burden and identify risk factors
set research priorities with promotion of promising interventions
provide burn prevention programmes
strengthen burn care
strengthen capacities to carry out all of the above.

The document A WHO plan for burn prevention and care discusses these 7 components in detail.

In addition, there are a number of specific recommendations for individuals, communities and public health officials to reduce burn risk.

Enclose fires and limit the height of open flames in domestic environments.
Promote safer cookstoves and less hazardous fuels, and educate regarding loose clothing.
Apply safety regulations to housing designs and materials, and encourage home inspections.
Improve the design of cookstoves, particularly with regard to stability and prevention of access by children.
Lower the temperature in hot water taps.
Promote fire safety education and the use of smoke detectors, fire sprinklers, and fire-escape systems in homes.
Promote the introduction of and compliance with industrial safety regulations, and the use of fire-retardant fabrics for children’s sleepwear.
Avoid smoking in bed and encourage the use of child-resistant lighters.
Promote legislation mandating the production of fire-safe cigarettes.
Improve treatment of epilepsy, particularly in developing countries.
Encourage further development of burn-care systems, including the training of health-care providers in the appropriate triage and management of people with burns.
Support the development and distribution of fire-retardant aprons to be used while cooking around an open flame or kerosene stove.

To reduce the risk of common household burns

Never leave items cooking on the stove unattended.
Turn pot handles toward the rear of the stove.
Don’t carry or hold a child while cooking at the stove.
Keep hot liquids out of the reach of children and pets.
Keep electrical appliances away from water.
Check the temperature of food before serving it to a child. Don’t heat a baby’s bottle in the microwave.
Never cook while wearing loose fitting clothes that could catch fire over the stove.
If a small child is present, block his or her access to heat sources such as stoves, outdoor grills, fireplaces and space heaters.
Before placing a child in a car seat, check for hot straps or buckles.
Unplug irons and similar devices when not in use. Store them out of reach of small children.
Cover unused electrical outlets with safety caps. Keep electrical cords and wires out of the way so that children can’t chew on them.
If you smoke, never smoke in bed.
Be sure you have working smoke detectors on each floor of your home. Check them and change their batteries at least once a year.
Keep a fire extinguisher on every floor of your house.
When using chemicals, always wear protective eyewear and clothing.
Keep chemicals, lighters and matches out of the reach of children. Use safety latches. And don’t use lighters that look like toys.
Set your water heater’s thermostat to below 120 F (48.9 C) to prevent scalding. Test bath water before placing a child in it.

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Acute Motor Sensory Axonal Neuropathy, Treatment

Acute Motor Sensory Axonal Neuropathy/Guillain–Barré syndrome (GBS) is a rapid-onset disorder in which the body’s immune system attacks part of the peripheral nervous system & muscle weakness caused by the immune system damaging the peripheral nervous system. The initial symptoms are typically changes in sensation or pain along with muscle weakness, beginning in the feet and hands. This often spreads to the arms and upper body, with both sides being involved. The symptoms develop over hours to a few weeks. During the acute phase, the disorder can be life-threatening, with about 15% developing weakness of the breathing muscles requiring mechanical ventilation. Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure. Guillain-Barre syndrome is also known as polyneuropathy, which is a disease that involves several nerves.

Another name of Guillain–Barré syndrome

acute inflammatory demyelinating polyradiculoneuropathy
acute motor axonal neuropathy
acute motor neuropathy with conduction block
acute motor-sensory axonal neuropathy

Types of Guillain–Barré syndrome

Once thought to be a single disorder, Guillain-Barre syndrome is now known to occur in several forms. The main types are:

Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most common form in the U.S. The most common sign of AIDP is muscle weakness that starts in the lower part of your body and spreads upward.
Miller Fisher syndrome (MFS), in which paralysis starts in the eyes. MFS is also associated with unsteady gait. MFS occurs in about 5 percent of people with Guillain-Barre syndrome in the U.S. but is more common in Asia.
Acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) are less common in the U.S. But AMAN and AMSAN are more frequent in China, Japan and Mexico.
Acute Motor Sensory Axonal Neuropathy: This is similar to motor axonal neuropathy but in this form also affected are the sensory nerves.
Acute Panautonomic Neuropathy: This is rarest form of GBS. It sometimes occurs with associated encephalopathy. Since there is cardiovascular involvement with this form of GBS, it has a high mortality rate. Some symptoms of this form of GBS are dysphagia, constipation alternating with diarrhea, dry itchy skin, etc.
Bickerstaff’s Brainstem Encephalitis: In this form of GBS, symptoms involve acute onset of ophthalmoplegia, ataxia, altered consciousness, and increased reflexes. It can also be relapsing-remitting.

Clinical subtypes of Guillain–Barré syndrome

A number of subtypes of Guillain–Barré syndrome are recognized.Despite this, many people have overlapping symptoms that can make the classification difficult in individual cases.All types have partial forms. For instance, some people experience only isolated eye-movement or coordination problems; these are thought to be a subtype of Miller Fisher syndrome and have similar antiganglioside antibody patterns.

Type	Symptoms	Population affected	Nerve conduction studies	Antiganglioside antibodies
Acute inflammatory demyelinating polyneuropathy (AIDP)	Sensory symptoms and muscle weakness, often with cranial nerve weakness and autonomic involvement	Most common in Europe and North America	Demyelinating polyneuropathy	No clear association
Acute motor axonal neuropathy (AMAN)	Isolated muscle weakness without sensory symptoms in less than 10%; cranial nerve involvement uncommon	Rare in Europe and North America, substantial proportion (30-65%) in Asia and Central and South America; sometimes called “Chinese paralytic syndrome”	Axonal polyneuropathy, normal sensory action potential	GM1a/b, GD1a & GalNac-GD1a
Acute motor and sensory axonal neuropathy (AMSAN)	Severe muscle weakness similar to AMAN but with sensory loss	–	Axonal polyneuropathy, reduced or absent sensory action potential	GM1, GD1a
Pharyngeal-cervical-brachial variant	Weakness particularly of the throat muscles, and face, neck, and shoulder muscles	–	Generally normal, sometimes axonal neuropathy in arms	Mostly GT1a, occasionally GQ1b, rarely GD1a
Miller Fisher syndrome	Ataxia, eye muscle weakness, areflexia but usually no limb weakness	This variant occurs more commonly in men than in women (2:1 ratio). Cases typically occur in the spring and the average age of occurrence is 43 years old.	Generally normal, sometimes discrete changes in sensory conduction or H-reflex detected	GQ1b, GT1a

Causes of Guillain–Barré syndrome

A viral infection, such as herpes, cytomegalovirus, or Epstein-Barr virus is the cause of over two-thirds of the new cases each year.
It’s uncommon – Guillain-Barre Syndrome is pretty rare, affecting only 1 or 2 people per 100,000.
It’s a serious autoimmune disorder. According to the National Library of Medicine, Guillain-Barre Syndrome is a serious disorder that occurs when the body’s immune system mistakenly attacks part of the nervous system.
It results in muscle weakness – The disorder causes inflammation in the body that creates weakness and sometimes even paralysis.
Much is unknown – The causes of Guillain-Barre Syndrome are widely unknown. Many times Guillain-Barre Syndrome symptoms will follow a minor infection, such as a lung or gastrointestinal infection.
There is no cure – So far, scientists have not found a cure for Guillain-Barre Syndrome, although many treatment options are available to handle complications and speed up recovery.
The cause of the disease is unknown – Many speculate that this is an immune-system disorder. Symptoms often begin 5 days to 3 weeks after a viral infection, immunization, or surgery. The disease affects peripheral nerves, nerve roots, and cranial nerves. Evaluation of the peripheral nerves reveals sections of the nerve with demyelination. Under microscopic exam, the nerve tissue is infiltrated with certain types of white blood cells.
Fluoroquinolones -The Fluoroquinolones have been responsible for triggering many different disease states, including Neuropathies from other causes, and be sure to read our page on how Fluoroquinolones Contribute to Autoimmune Disease to see how other diseases are often triggered by these antibiotics. These dangerous drugs accomplish their damage through multiple methods of action, including causing Mitochondrial Damage, DNA Damage to cells, the binding of and excretion of certain nutrients,
GBS, unlike multiple sclerosis or amyotrophic lateral sclerosis, is a peripheral nerve ailment and does not cause injury to the brain or the spinal cord.
This syndrome causes the destruction, removal, or loss of the myelin sheath of a nerve. Myelin is the substance of the cell membrane that coils to form the myelin sheath. The myelin sheath serves as an electrical insulator to nerve fibers
In 1977, there were over 500 cases of Guillain-Barre syndrome associated with a United States flu vaccination program. The cause of this outbreak was never discovered.
5-10% of new cases will occur up to 4 weeks after surgery.

Symptoms of Guillain–Barré syndrome

Symptoms of GBS, including weakness, instability, and pain, typically start in the lower body and move upwards.

Symptoms and other complications include

weakness in the lower body, moving upward
Prickling, pins and needles sensations in your fingers, toes, ankles or wrists
Weakness in your legs that spreads to your upper body
Unsteady walking or inability to walk or climb stairs
The difficulty with eye or facial movements, including speaking, chewing or swallowing
Severe pain that may feel achy or cramp-like and may be worse at night
The difficulty with bladder control or bowel function
Rapid heart rate
Low or high blood pressure
Difficulty breathing
General instability when walking
Less control over facial muscles during activities such as chewing or talking
Cramp-like pain that gets worse at night
Lack of control over the bowel or bladder
Pain, with around 50 percent of people with GBS experiencing severe nerve pain that may need drug management
A faster heart rate than normal
High or low blood pressure
Blood clots
Pressure sores if a person is immobile for a considerable length of time
Difficulty breathing
A future relapse of the condition in 3 percent of people with GBS
Psychological and cognitive difficulties.

Diagnosis of Guillain–Barré syndrome

After a physical exam, a physician may recommend the following tests:

Blood tests and urine tests – These are done to check for infections and other problems.
Nerve conduction exam – Electrodes are taped to the skin, and the speed of nerve signal conduction is tested by passing small shocks along the nerves through the skin. In GBS, the signals travel more slowly along the nerves.
Electromyography (EMG) – Thin, needle-like electrodes are used to test the nerve function within muscle fibers.
Spinal tap, also known as a lumbar puncture – A sample of cerebrospinal fluid (CSF) is removed from the spinal canal and tested in a laboratory for specific signs of the disease. More protein is present in the CSF of people with GBS. Your cerebrospinal fluid is then tested to detect protein levels. People with Guillain-Barré typically have higher-than-normal levels of protein in their cerebrospinal fluid. This test is also referred to as a lumbar puncture.
Electromyogram (EMG) – This test measures the electrical activity of a muscle or a group of muscles. An EMG can find abnormal electrical muscle activity caused by diseases and conditions that affect the nerves and muscles.
Pulmonary function test –This is a breathing test done by a respiratory therapist. It shows your child’s lung capacity and how strong his or her respiratory muscles are. This test is often used to decide if a child needs breathing support with a ventilator.
Electrolyte levels
Liver function tests (LFTs)
Creatine phosphokinase (CPK) level
Erythrocyte sedimentation rate (ESR)

Biochemical screening can also be conducted and would include the following studies:

Needle EMG and nerve conduction studies

Nerve conduction slowing
Prolongation of the distal latencies
Prolongation of the F-waves
Conduction block or dispersion of responses – Evidence frequently demonstrated at sites of natural nerve compressionWeak muscles showing reduced recruitment: Demonstrated with needle examination.

Associate disease tests

Myasthenia gravis is intermittent and worsened by exertion.
Botulism may cause fixed dilated pupils (in 50%) and prominent cranial nerve dysfunction with normal sensation.
Tick paralysis causes ascending paralysis but spares sensation.
West Nile virus causes headache, fever, and asymmetric flaccid paralysis but spares sensation.
Metabolic neuropathies occur with a chronic metabolic disorder.
Poliomyelitis usually occurs in epidemics.

Treatment of Guillain–Barré syndrome

Plasma exchange (plasmapheresis). The liquid portion of part of your blood (plasma) is removed and separated from your blood cells. The blood cells are then put back into your body, which manufactures more plasma to make up for what was removed. Plasmapheresis may work by ridding plasma of certain antibodies that contribute to the immune system’s attack on the peripheral nerves.
Immunoglobulin therapy. Immunoglobulin containing healthy antibodies from blood donors is given through a vein (intravenously). High doses of immunoglobulin can block the damaging antibodies that may contribute to Guillain-Barre syndrome.
Intensive care unit – Admission to the intensive care unit (ICU) should be considered for all patients with labile dysautonomia, a forced vital capacity of less than 20 mL/kg, or severe bulbar palsy.Any patients exhibiting clinical signs of respiratory compromise to any degree also should be admitted to an ICU.

Competent intensive care includes the following features

Respiratory therapy
Cardiac monitoring
Safe nutritional supplementation
Monitoring for infectious complications (eg, pneumonia, urinary tract infections, septicemia)Subcutaneous unfractionated or low ̶ molecular-weight heparin (LMWH) and thromboguards are often used in the treatment of immobile patients to prevent lower-extremity deep venous thrombosis (DVT) and consequent pulmonary embolism (PE).
Immunomodulation – Immunomodulatory treatment in GBS has been used to hasten recovery. Intravenous immunoglobulin (IVIG) and plasma exchange have proved equally effective.

Physical, occupational & speech therapy of Guillain–Barré syndrome

In I.V.I.G, immunoglobulins are given intravenously which shows a positive impact on the speed of recovery. But it has been shown to be less effective than plasmapheresis.

Further medical management can be done according to the symptoms and the complications :
a. Supportive Care

ICU monitoring
Basic medical management often determines mortality and morbidity.

b. Ventilatory Support

Atelectasis leads to hypoxia.
Hyper-carbia later finding; arterial blood cases may be misleading.
Vidal capacity, tidal volume and negative inspiratory force are best indicators of diaphragmatic function.
Progressive decline of these functionsindicatese an impending need or ventilatory assistance.
Mechanical ventilation usually required if VC drops below about 14 ml/kg; ultimate risk depending on age, presence of accompanying lung disease, aspiration risk, and assessment of respiratory muscle fatigue
Atelectasis treated initially by incentive spirometry, frequent suctioning, and chest physiotherapy to mobilize secretions.
Intubation may be necessary in patients with substantial oro-pharyngeal dysfunction to prevent aspiration.
Tracheostomy may be needed in patients intubated for 2 weeks who do not show improvement.

c. Autonomic dysfunction

Autonomic dysfunction may be self-limited; do not over-treat.
Sustained hypertension managed by angiotensin-converting enzyme inhibitor or beta blocking agent. Use short acting intravenous medication for labile hypertension requiring immediate therapy.
Postural hypotension treated with fluid bolus or positioning.
Urinary difficulties may require intermittent catheterization.

d. Nosocomial infections usually involve pulmonary and urinary tracts.

Occasionally central venous catheters become infected.
Antibiotic therapy should be reserved for those patients showing clinical infection rather than colonization of fluid or sputum specimens.

e. Venous thrombosis due to immobilization poses great risk of thromboembolism.

Physiotherapy of Guillain–Barré syndrome

Aims of the treatment are to

Respiratory therapy
Maintain clear airways
Prevent lung infection
Maintain anatomical joint range
Support joint in functional position to minimize damage or deformit
Prevention of pressure sores
Maintain peripheral circulatio
Provide psychological support for the patient and relatives. 1. Maintenance of clear airway & prevention of lung infection

Respiratory therapy

Respiratory therapy
The patients breathing will be assisted by intermittent positive pressure ventilation (IPPV) via a cuffed tracheostomy tube.
Posturally drain areas of lung tissues, 2-hourly turning into supine or side lying positions.
A suction catheter is used to remove secretions from respective passage until the cough reflex re-appears.
Manual techniques like vibration with/ without over pressure.
2-4 litre anesthetic bag can be used to enhance chest expansion. Therefore , 2 people are necessary for this technique, one to squeeze the bag and another to apply chest manipulation.
Rib springing to stimulate cough.
After the removal of ventilator and adequate expansion, effective coughing must be taught to the patient
As neurons recover, active assisted or active breathing exercises may commence with good amount of relaxing time.

2. To maintain normal joint movement

Gentle passive movements through full ROM at least three times a day especially at hip , shoulder, wrist, ankle, feet.

3.Support joints

Use of light splints(eg. using PLASTAZOTE) may be required for the following purpose listed below

Support the peripheral joints in comfortable and functional position during flaccid paralysis.
To prevent abnormal movements.
To stabilize patients using sandbags, pillows. 4. Prevention of pressure sores :

2- hourly change in patients position from supine to side lying. If the sores have developed then UVR or ice cube massage to enhance healing. 5. Maintenance of circulation

Passive movements
Effleurage massage to lower limbs.

Relief of pain

Transcutaneous electrical nerve stimulation
Massage with passive ROM
Patient can demonstrate increased sensitivity to light touch, a cradle can be used to keep the bed sheet away from the skin.
Low pressure wrapping or snug fitting garments can provide a way to avoid light touch.
Reassurance and explanation of what to expect can help in alleviation of anxiety that could compound the pain.

Exercises to be prescribed to the patient should be started with low repetitions and short, frequent bouts of exercises matched to the patients muscular strength. According to Bensman (1970), the following four guidelines are to be followed for prescription of exercises

Use short periods of non-fatiguing exercises matched to the patients strength.
Progression of the exercise should be done only if the patient improves or if there is no deterioration in status after a week.
Return the patient to bed rest if a decrease in muscle strength or function occurs
The objective should be directed towards not only at improving function but also in improving strength.

Complications of Guillain–Barré syndrome

Guillain-Barre syndrome affects your nerves. Because nerves control your movements and body functions, people with Guillain-Barre may experience

Breathing difficulties – The weakness or paralysis can spread to the muscles that control your breathing, a potentially fatal complication. Up to 30 percent of people with Guillain-Barre syndrome need temporary help from a machine to breathe when they’re hospitalized for treatment.
Residual numbness or other sensations – Most people with Guillain-Barre syndrome recover completely or have only minor, residual weakness, numbness or tingling.
Heart and blood pressure problems – Blood pressure fluctuations and irregular heart rhythms (cardiac arrhythmias) are common side effects of Guillain-Barre syndrome.
Pain – Up to half of people with Guillain-Barre syndrome experience severe nerve pain, which may be eased with medication.
Blood clots – People who are immobile due to Guillain-Barre syndrome are at risk of developing blood clots. Until you’re able to walk independently, taking blood thinners and wearing support stockings may be recommended.
Residual numbness or other sensations – Most people recover completely or have only minor, residual weakness, numbness or tingling.
Heart and blood pressure problems – Blood pressure fluctuations and irregular heart rhythms (cardiac arrhythmias) are common side effects of Guillain-Barre syndrome.
Bowel and bladder function problems – Sluggish bowel function and urine retention may result from Guillain-Barre syndrome.
Blood clotsn – People who are immobile due to this illness are at risk of developing blood clots. Wear support stockings and take blood thinners.
Pressure sores – Being immobile also puts you at risk of developing bedsores (pressure sores). Frequent repositioning may help avoid this problem.
Relapse – Around 3 percent of people with Guillain-Barre syndrome experience a relapse.

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Which Lack of Food Causes Rickets, Prevention

Which Lack of Food Causes Rickets is a condition associated with bone-deformity due to inadequate mineralization in growing bones [rx]. While some cases relate to hereditary syndromes, renal disease, or use of medication, rickets in the world mostly stems from nutritional insufficiency [rx]. Nutritional rickets is prevalent throughout much of the developing world and is again being increasingly seen in more affluent countries [rx].

Rickets is a condition that results in weak or soft bones in children.^[rx] Symptoms include bowed legs, stunted growth, bone pain, large forehead, and trouble sleeping.^[rx]^[rx] Complications may include bone fractures, muscle spasms, an abnormally curved spine, or intellectual disability.^[rx]^[rx]

Types of Rickets

Calcipenic Rickets

Calcipenic (hypocalcemic) rickets is characterized by a deficiency of calcium or more commonly vitamin D. In Indian children living in the UK, diets are typically low in calcium and high in phytate. The calcium content of common foodstuffs is given in [rx]. Rickets can occur despite adequate vitamin D levels if the calcium intake is very low. This problem generally does not occur unless calcium intake is very low because vitamin D increases intestinal calcium absorption. Most children with calcium deficiency rickets have normal serum 25-hydroxyVitamin D [25(OH)D] and high serum 1,25-dihydroxy vitamin D [1,25(OH)₂] concentrations, indicating adequate intake of vitamin D.

Phosphopenic Rickets

Phosphopenic rickets is commonly caused by renal phosphate wasting. This may be isolated or part of a generalized renal tubular disorder such as Fanconi syndrome or Dent disease.[rx] Isolated phosphate loss is seen in X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets, tumor-induced osteomalacia, and hypophosphatemic rickets with hypercalciuria (autosomal recessive) disease. Nutritional deficiency is uncommon. These causes can be distinguished by measuring urinary amino acids, bicarbonate, glucose, calcium, and vitamin D concentrations.[rx]

Renal (kidney) rickets

Similar to hypophosphatemic rickets, renal rickets is caused by a number of kidney disorders. Individuals suffering from kidney disease often have decreased the ability to regulate the amounts of electrolytes lost in the urine. This includes calcium and phosphate, and therefore the affected individuals develop symptoms almost identical to severe nutritional rickets. Treatment of the underlying kidney problem and nutritional supplementation are recommended for these patients.

Vitamin D-related rickets

Vitamin D deficiency
Vitamin D-dependent rickets^[rx]
- - Type 1 (25-Hydroxyvitamin D3 1-alpha-hydroxylase deficiency)
  - Type 2 (calcitriol receptor mutation)

Hypocalcemia-related rickets

Hypocalcemia
Chronic renal failure (CKD-BMD)

Hypophosphatemia-related rickets

Congenital
- - Vitamin D-resistant rickets^[rx]
  - Autosomal dominant hypophosphatemic rickets (ADHR)
  - Autosomal recessive hypophosphatemic rickets (ARHR)^[rx]
Hypophosphatemia (typically secondary to malabsorption)
Fanconi’s syndrome

Secondary to other diseases

Tumor-induced osteomalacia
McCune-Albright syndrome
Epidermal nevus syndrome
Dent’s disease

Causes of Rickets

Sun exposure –Dietary vitamin D deficiency can also occur in children, with differences among ethnic groups depending on skin pigmentation and varied ingestion of supplements.[rx] A Caucasian infant’s vitamin D requirements are met by exposure to sunlight for 30 minutes per week, clothed only in a diaper, or for 2 hours per week fully clothed with no hat. Asians require approximately threefold longer periods of sunlight exposure because of the protective pigmentation in their skin and Africans need six times the same exposure.[rx]
Cold Climates – Vitamin D deficiency is also common at the end of the winter due to less sun exposure.[rx] Vitamin D deficiency has been reported in dark-skinned immigrants from warm climates to cold climates. Asian Indian immigrants to the United States may have vitamin D deficiency, even with adequate sun exposure.[rx]
Extensive burns – In patients with a history of extensive burn injuries, vitamin D synthesis in the skin is below normal, even with sun exposure.[rx]
Nutritional deficiency – Vitamin D deficiency can occur even with adequate sun exposure.[rx] It can occur in people who consume foods that are not fortified with vitamin D or if there is intestinal malabsorption of vitamin D. There are few foods that naturally contain vitamin D and because most of these are meat or fish based, they may not be acceptable to cultures that favor a vegetarian diet. Currently, few foods are fortified with vitamin D. Routine vitamin D fortification should be considered for milk and other food products.
Elderly people – Cutaneous vitamin D production and vitamin D stores decline with age. vitamin D intake is often low in older subjects. Achlorhydria, which is common in the elderly, limits calcium absorption. Older persons, in addition, may also be confined indoors.[rx]
Maternal vitamin D deficiency -Vitamin D is transferred from the mother to the fetus across the placenta, and reduced vitamin D stores in the mother are associated with lower vitamin D levels in the infant.[rx] Low vitamin D levels during pregnancy have been associated with intrauterine growth retardation, premature labor, and hypertension, all of which increase the risk of low birth weight.
Prematurity – Vitamin D levels are low in premature infants, who have less time to accumulate vitamin D from the mother through transplacental transfer. The third trimester is a critical time for vitamin D transfer because this is when the fetal skeleton becomes calcified, requiring increased activation of 25(OH)D to 1,25(OH)₂D in the maternal kidneys and placenta. vitamin D deficiency in the mother during this period can cause fetal vitamin D deficiency, and in severe cases, fetal rickets.[rx,rx] Premature infants are more likely to have enamel defects in both primary and permanent teeth because vitamin D sufficiency is necessary for normal fetal tooth development.
Exclusive breastfeeding -The vitamin D content of breast milk is low (15–50 IU/L) even in a vitamin D replete mother.[rx] Exclusively breastfed infants consuming an average of 750 mL of breast milk daily thus ingest only 10–40 IU/day of vitamin D. Most breastfed infants need to be exposed to sunlight for at least 30 minutes/ week while wearing only a diaper in order to maintain 25(OH)D levels at >20 ng/mL. vitamin D deficiency is uncommon in formula-fed infants because of the fortification of infant formulas (400 IU/L). However, it can still occur if the infant had low vitamin D stores at birth because of maternal vitamin D deficiency and if the vitamin D content of the formula is insufficient.[rx]
Obesity – 25(OH)D levels are low in obese individuals as vitamin D is sequestrated in fat. vitamin D requirements are thus higher in obese individuals.[rx]
Hospitalized patients – Inadequate intake and lack of sun exposure cause vitamin D deficiency in this group of patients.[rx]
Women treated for osteoporosis – Subclinical vitamin D deficiency is common in postmenopausal women on therapy for osteoporosis (bisphosphonates, raloxifene, calcitonin, or PTH).[rx]
Chronic renal disease – In patients with chronic kidney disease, calcitriol [1,25(OH)₂D] production is low due to diminished glomerular filtration, loss of the 1-α-hydroxylase enzyme secondary to structural renal damage, and suppression of enzyme activity secondary to hyperphosphatemia. This results in hypocalcemia, hyperparathyroidism, and bone disease.[rx] In addition to the deficiency of 1,25(OH)₂D, recent studies have shown co-existence of 25(OH)D deficiency in pre-dialysis and dialysis patients, especially in female diabetics and patients on peritoneal dialysis.[rx] Whether improving 25(OH) D concentrations benefit these patients is controversial, but Kidney Dialysis Outcome Initiative (KDOQI) guidelines have recommended supplementation.
Nephrotic syndrome – Most of the calcidiol in serum is bound to DBP. Patients with nephrotic syndrome lose DBP and may develop vitamin D deficiency.[rx,rx]
Distal renal tubular acidosis -Hypocalcemia can occur in dRTA, along with acidosis, which causes rickets. The presence of dRTA is suspected in conditions of hypokalemia, hyperchloremia, and normal anion gap metabolic acidosis.[rx]
Gastrointestinal disease – Malabsorption associated with diseases of the small intestine, a hepatobiliary tree with cholestatic liver disease, extrahepatic biliary obstruction, and diseases of the pancreas may result in decreased absorption of vitamin D and/or depletion of endogenous 25(OH)D stores due to abnormal enterohepatic circulation. Malabsorption of vitamin D occurs as a consequence of steatorrhea, which disturbs fat emulsification and chylomicron-mediated absorption. Patients may have rickets or osteomalacia or only low bone density. Common examples are celiac disease, inflammatory bowel disease, food allergies, cholestasis, and exocrine pancreatic insufficiency (as in cystic fibrosis).[rx]
Gastric bypass – Patients with short-limb bypass have secondary hyperparathyroidism (SHPT) in spite of normal 25(OH)D concentrations, due to calcium malabsorption. vitamin D deficiency also occurs in patients with partial or total gastrectomy for peptic ulcer disease or bariatric surgery due to the loss of gastrointestinal acidity, malfunction of the proximal small bowel which leads to vitamin D malabsorption, the absence of adequate absorbing surface, or failure of intestinal mucosal cells to respond to vitamin D.[rx,rx]
Liver disease – Vitamin D is hydroxylated in the liver to produce calcidiol [25(OH)D]. Hence, patients with significant parenchymal or obstructive liver disease have reduced 25(OH)D. These patients manifest biochemical or histological evidence of osteomalacia only in the presence of concomitant nutritional deficiency or interruption of the enterohepatic circulation.[rx,rx]
Medications – Certain anticonvulsants and antiretroviral drugs used to treat HIV infection can precipitate vitamin D deficiency by enhancing catabolism of 25(OH)D and 1,25(OH)₂D.[rx] decreased circulating levels of calcidiol occur in patients on phenytoin, phenobarbitone, carbamazepine, isoniazid, rifampicin, and theophylline due to induction of P-450 enzyme activity, which metabolizes calcidiol to inactive vitamin D metabolites. Tenofovir can cause rickets. Abnormalities in calcium concentration are seen with medications used in the treatment of the complications of HIV, such as foscarnet, pentamidine, and recombinant growth hormone. vitamin D requirements are higher in patients on glucocorticoids because they inhibit intestinal vitamin D dependent calcium absorption. Ketoconazole and some other antifungal agents increase vitamin D requirements because they block 1-hydroxylation. Supplementation with vitamin D (400–4000 IU/day) may be needed for these patients.[rx]
Insufficient nutritional quantities or faulty metabolism of vitamin D or phosphorus
Renal tubular acidosis
Malnutrition during pregnancy
Malabsorption syndrome
Hypophosphatemia^[rx]
Chronic kidney failure
Tumor-induced osteomalacia (Oncogenic osteomalacia)
Long-term anticonvulsant therapy^[rx]
Celiac disease^[rx]
Cadmium poisoning, iliac disease
Breastfed infants whose mothers are not exposed to sunlight
Breastfed babies who are exposed to little sunlight
Adolescents, in particular when undergoing the pubertal growth spurt^[rx]
Any child whose diet does not contain enough vitamin D or calcium
Diseases causing soft bones in infants, like hypophosphatasia or hypophosphatemia, can also lead to rickets.^[rx]

Rickets Symptoms

Pain or tenderness in the bones of the arms, legs, pelvis, or spine.
Stunted growth and short stature.
Bone fractures.
Muscle cramps.
Teeth deformities, such as delayed tooth formation. holes in the enamel.
Skeletal deformities, including an oddly shaped skull. bowlegs, or legs that bow out.
Delayed growth
Pain in the spine, pelvis, and legs
Muscle weakness
Diffuse joint and bone pain (especially of spine, pelvis, and legs)
Difficulty walking, often with a waddling gait
Hypocalcemia (positive Chvostek sign)
Compressed vertebrae and diminished stature
Pelvic flattening
Weak, soft bones
Easy fracturing
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result as the thickening caused by nodules forming on the costochondral joints.
This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest^[rx] may result in the presence of Harrison’s groove.

Diagnosis of Rickets

Rickets may be diagnosed with the help of

Blood tests – Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones. This can show enlarged limbs and joints.
A bone density scan – may be undertaken.^[rx]
Radiography typically – shows widening of the zones of provisional calcification of the metaphyses secondary to unmineralized osteoid. Cupping, fraying, and splaying of metaphyses typically appears with growth and continued weight bearing.^[rx] These changes are seen predominantly at sites of rapid growth, including the proximal humerus, distal radius, distal femur and both the proximal and the distal tibia. Therefore, a skeletal survey for rickets can be accomplished with anteroposterior radiographs of the knees, wrists, and ankles.^[rx]

Biochemical findings

Biochemical features are similar to those of rickets. The major factor is an abnormally low vitamin D concentration in blood serum. Major typical biochemical findings include:^[rx]

Low serum and urinary calcium
Low serum phosphate, except in cases of renal osteodystrophy
Elevated serum alkaline phosphatase (due to an increase in compensatory osteoblast activity)
Elevated parathyroid hormone (due to low calcium)

Skeletal findings

The skeletal changes are similar in calcipenic and phosphonic rickets.[rx] The anterior fontanelle closes by 18 months and posterior by 3 months normally. However, in rickets, there is a delay in the closure of the fontanelles.
There is parietal and frontal bossing, craniotabes (soft skull bones) with ping pong bones in infants, enlargement of the costochondral junction of ribs (the “rachitic rosary”), Harrison sulcus due to the muscular pull of the diaphragm on the lower ribs, widening of the wrist and bowing of the distal radius and ulna, and progressive lateral bowing of the femur and tibia.

Extraskeletal findings

The child may be asymptomatic or may present with pain, irritability, delay in motor milestones, and poor growth.[rx] Visceroptosis leads to a pot belly. Children may have waddling gait (antalgic gait). Presentation with hypocalcemic seizures is frequent in the first year of life.[rx]
Children with calcipenic rickets are prone to acquiring infectious diseases.[rx] There is hypoplasia of dental enamel. Increased sweating is a common finding in young infants with calcipenic rickets and may be caused by bone pain.

Radiographic findings

In children, the changes of rickets can be seen at the growth plate of rapidly growing bones. Thus, in the upper limbs, the changes are most prominent at the distal ulna, while in lower limbs the changes are most prominent at the metaphyses above and below the knees.
There is widening of the epiphyseal plate due to unmineralized osteoid and loss of definition of the zone of provisional calcification at the epiphyseal/metaphyseal junction.
There is cupping and splaying of the epiphyseal end of metaphysics with the formation of cortical spurs and stippling. The appearance of the epiphyseal bone centers may be delayed, and these are small and osteopenic.[rx]

Bone mineral density

Several studies have demonstrated markedly reduced spine, hip, and forearm bone density [as measured by dual-energy X-ray absorptiometry (DXA)] in patients with osteomalacia related to vitamin D deficiency.
However, bone mineral density (BMD) is not required for the diagnosis of osteomalacia, and reduced BMD does not distinguish osteoporosis from osteomalacia. In contrast, BMD tends to be normal or increased (especially lumbar spine) in adults with XLH.

Bone biopsy

Bone biopsy with tetracycline labeling is the most accurate way to diagnose osteomalacia/rickets. However, it is infrequently performed because it is invasive and the diagnosis can usually be made from a combination of clinical and laboratory findings.
Prolonged mineralization lag time, widened osteoid seams, and increased osteoid volume. All of these features are necessary for the diagnosis because other disorders may show one of these findings. Wide osteoid seams reflecting high turnover can be seen with hyperthyroidism, Paget’s disease, and hyperparathyroidism. However, the mineral apposition rate is elevated in these disorders in contrast to osteomalacia.

https://www.youtube.com/watch?v=5ClZOC6-pSc

Treatment of Rickets

American Academy of Pediatrics (AAP) introduced the protocol of 400 IU/day of vitamin D starting from the 2nd month of life for rickets prophylaxis [rx]. The latest recommendations by AAP about vitamin D supplementation was reported in 2008 [rx] as follows:

A minimum of 400 IU/day vitamin D supplementation is recommended to prevent VDD and rickets in healthy infants, children, and adolescents.
400 IU/day vitamin D should be introduced to the diet of infants fed completely or partially by mother’s milk until they start receiving at least 1 liter of formula per day.
400 IU/day vitamin D should be provided to all infants fed with less than 1-liter formula per day and not receiving mother’s milk. Other sources of nutrition should be calculated individually for infants receiving this type of nutrition.
400 IU vitamin D should be provided to all adolescents not receiving 400 IU vitamin D from milk or other foods fortified with vitamin D.
According to recent evidence, the level of serum 25(OH)D should be above 20 ng/mL, particularly in infants and children.
400 IU/day vitamin D should be continued in cases with chronic fat malabsorption, chronic anticonvulsant intake or similar conditions increasing the risk of VDD. Higher vitamin D supplementation may be necessary in these cases to maintain the normal serum level of vitamin D.

Low dosage and long−term vitamin D therapy

There are different views about the dose and duration of vitamin D therapy. In this treatment model, depending on the age of the c h I l d, vitamin D is usually administered at a dose of 1000− 10 000 IU/day for 2−3 months. In this regimen, vitamin D can be given according to the infant’s age as follows: 1000 IU/day for infants under 1 month of age, 1000 to 5000 IU/ day for children 1 to 12 months old, and 5000 IU/day for children older than 12 months. Afterward, it is recommended to give maintenance therapy of 400 IU/ day.
Levels of Ca and P are normalized in 6−10 days by this therapy, while it takes 1−2 months for PTH to reach normal levels. Depending on the severity of the disease, it may take 3 months for the normal serum ALP levels to be restored and the radiological findings of rickets to disappear. In this treatment model, lack of compliance is an important cause of lack of response [rx, rx, rx, rx, rx, rx].

Stoss therapy

For patients who are suspected to have poor compliance, a high dose of vitamin D can be given orally or intramuscularly as a single dose of 100 000−600 000 IU after the first month of life [rx, rx, rx, rx]. Administration of 600 000 units of vitamin D in infantile rickets has been reported to cause hypercalcemia [rx]. Cesur et al [rx] reported that 150 000−300 000 units of vitamin D is an effective and safe method of treatment.
A recent study also demonstrated that intramuscular administration of a single dose of 300 000 IU of vitamin D is effective in cases of malnutrition with rickets [rx]. Shah and Feinberg have successfully administrated 100 000 IU of vitamin D every two hours over a twelve−hour period [rx, rx]. This treatment evokes a rapid clinical response, resulting in a biochemical recovery in a few days and radiological recovery in 10−15 days.

Monitored Supplementation of Pregnant Women

Low socioeconomic status, covered clothing and lack of supplementation contribute to the high prevalence of vitamin D deficiency in pregnancy [rx]. Congenital rickets and postnatal hypocalcaemic seizures are reported in risk groups in both developed and developing countries [rx , rx, rx]. Poor maternal vitamin D status affects the fetus and of the newborn. In a large Italian study, 76% of newborns of dark-skinned migrant women had 25OHD levels below 25 nmol/L (10 μg/L), compared to 38% of newborns of native Italian women [rx].

Universal Supplementation of Infants Regardless of Mode of Feeding

The amount of vitamin D available in breast milk but also infant formula milk is insufficient to prevent NR; even formula-fed infants can present with the asymptomatic deficiency in the first few months of life [rx, rx, rx] if born to deficient mothers.
In a recent survey of vitamin D supplementation policies across Europe, we found that universal supplementation, currently practiced by 79% (23/29) of countries was significantly (p = 0.007) associated with good adherence to supplements [rx]. The recommended dose of 400 IU/day (10 μg) is safe also in formula-fed infants. Toxicity is usually related to errors in manufacturing, formulation or prescription [rx, rx].

Supplementation Beyond the First Year of Life

The duration of childhood supplementation varies widely across Europe [rx]. Assessment of daily intakes at 18 months and 3.5 years of age in 755 children in the UK showed low daily intakes of vitamin D and calcium [rx].
The incidence of NR rises beyond the recommended age of infant supplementation [rx, rx, rx], especially in dark-skinned (immigrant or resident) individuals. Hence, national policies should ensure that the daily requirement of vitamin D beyond the first year of life is met through supplementation or fortification [rx].

Identifying Successful and Sustainable Implementation Strategies

Although most developed countries have vitamin D supplementation policies in place, some countries lack successful implementation strategies. Recent studies from Canada and New Zealand reported that none of the individuals with NR had received vitamin D supplements for rickets prevention despite the presence of national recommendations [rx, rx].
Similarly, 85% of British parents are unaware of the need for infant vitamin D supplementation for their baby despite existing policy [rx]. There is overwhelming evidence that infant vitamin D supplementation improves 25OHD concentrations [rx] and prevents NR [rx].

Food Fortification with Vitamin D or Calcium

Health benefits of food fortification with micronutrients, including vitamin D, are well established [rx]. Currently, most European countries follow voluntary fortification [rx]; however, evidence from Canada and the USA suggests that mandatory fortification improves vitamin D uptake at the population level [rx].
Fortification should not be restricted to dairy products due to its limited consumption in certain risk groups [rx]; fortification of a variety of food sources is more beneficial [rx]

References

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Rickets Treatment, Causes, Symptoms

Rickets Treatment, Causes, Symptoms/Rickets is a condition associated with bone-deformity due to inadequate mineralization in growing bones [rx]. While some cases relate to hereditary syndromes, renal disease, or use of medication, rickets in the world mostly stems from nutritional insufficiency [rx]. Nutritional rickets is prevalent throughout much of the developing world and is again being increasingly seen in more affluent countries [rx].

Types of Rickets

Calcipenic Rickets

Calcipenic (hypocalcemic) rickets is characterized by a deficiency of calcium or more commonly vitamin D. In Indian children living in the UK, diets are typically low in calcium and high in phytate. The calcium content of common foodstuffs is given in [rx]. Rickets can occur despite adequate vitamin D levels if the calcium intake is very low. This problem generally does not occur unless calcium intake is very low because vitamin D increases intestinal calcium absorption. Most children with calcium deficiency rickets have normal serum 25-hydroxyVitamin D [25(OH)D] and high serum 1,25-dihydroxy vitamin D [1,25(OH)₂] concentrations, indicating adequate intake of vitamin D.

Phosphopenic Rickets

Phosphopenic rickets is commonly caused by renal phosphate wasting. This may be isolated or part of a generalized renal tubular disorder such as Fanconi syndrome or Dent disease.[rx] Isolated phosphate loss is seen in X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets, tumor-induced osteomalacia, and hypophosphatemic rickets with hypercalciuria (autosomal recessive) disease. Nutritional deficiency is uncommon. These causes can be distinguished by measuring urinary amino acids, bicarbonate, glucose, calcium, and vitamin D concentrations.[rx]

Renal (kidney) rickets

Similar to hypophosphatemic rickets, renal rickets is caused by a number of kidney disorders. Individuals suffering from kidney disease often have decreased the ability to regulate the amounts of electrolytes lost in the urine. This includes calcium and phosphate, and therefore the affected individuals develop symptoms almost identical to severe nutritional rickets. Treatment of the underlying kidney problem and nutritional supplementation are recommended for these patients.

Vitamin D-related rickets

Vitamin D deficiency
Vitamin D-dependent rickets^[rx]
- - Type 1 (25-Hydroxyvitamin D3 1-alpha-hydroxylase deficiency)
  - Type 2 (calcitriol receptor mutation)

Hypocalcemia-related rickets

Hypocalcemia
Chronic renal failure (CKD-BMD)

Hypophosphatemia-related rickets

Congenital
- - Vitamin D-resistant rickets^[rx]
  - Autosomal dominant hypophosphatemic rickets (ADHR)
  - Autosomal recessive hypophosphatemic rickets (ARHR)^[rx]
Hypophosphatemia (typically secondary to malabsorption)
Fanconi’s syndrome

Secondary to other diseases

Tumor-induced osteomalacia
McCune-Albright syndrome
Epidermal nevus syndrome
Dent’s disease

Causes of Rickets

Sun exposure –Dietary vitamin D deficiency can also occur in children, with differences among ethnic groups depending on skin pigmentation and varied ingestion of supplements.[rx] A Caucasian infant’s vitamin D requirements are met by exposure to sunlight for 30 minutes per week, clothed only in a diaper, or for 2 hours per week fully clothed with no hat. Asians require approximately threefold longer periods of sunlight exposure because of the protective pigmentation in their skin and Africans need six times the same exposure.[rx]
Cold Climates – Vitamin D deficiency is also common at the end of the winter due to less sun exposure.[rx] Vitamin D deficiency has been reported in dark-skinned immigrants from warm climates to cold climates. Asian Indian immigrants to the United States may have vitamin D deficiency, even with adequate sun exposure.[rx]
Extensive burns – In patients with a history of extensive burn injuries, vitamin D synthesis in the skin is below normal, even with sun exposure.[rx]
Nutritional deficiency – Vitamin D deficiency can occur even with adequate sun exposure.[rx] It can occur in people who consume foods that are not fortified with vitamin D or if there is intestinal malabsorption of vitamin D. There are few foods that naturally contain vitamin D and because most of these are meat or fish based, they may not be acceptable to cultures that favor a vegetarian diet. Currently, few foods are fortified with vitamin D. Routine vitamin D fortification should be considered for milk and other food products.
Elderly people – Cutaneous vitamin D production and vitamin D stores decline with age. vitamin D intake is often low in older subjects. Achlorhydria, which is common in the elderly, limits calcium absorption. Older persons, in addition, may also be confined indoors.[rx]
Maternal vitamin D deficiency -Vitamin D is transferred from the mother to the fetus across the placenta, and reduced vitamin D stores in the mother are associated with lower vitamin D levels in the infant.[rx] Low vitamin D levels during pregnancy have been associated with intrauterine growth retardation, premature labor, and hypertension, all of which increase the risk of low birth weight.
Prematurity – Vitamin D levels are low in premature infants, who have less time to accumulate vitamin D from the mother through transplacental transfer. The third trimester is a critical time for vitamin D transfer because this is when the fetal skeleton becomes calcified, requiring increased activation of 25(OH)D to 1,25(OH)₂D in the maternal kidneys and placenta. vitamin D deficiency in the mother during this period can cause fetal vitamin D deficiency, and in severe cases, fetal rickets.[rx,rx] Premature infants are more likely to have enamel defects in both primary and permanent teeth because vitamin D sufficiency is necessary for normal fetal tooth development.
Exclusive breastfeeding -The vitamin D content of breast milk is low (15–50 IU/L) even in a vitamin D replete mother.[rx] Exclusively breastfed infants consuming an average of 750 mL of breast milk daily thus ingest only 10–40 IU/day of vitamin D. Most breastfed infants need to be exposed to sunlight for at least 30 minutes/ week while wearing only a diaper in order to maintain 25(OH)D levels at >20 ng/mL. vitamin D deficiency is uncommon in formula-fed infants because of the fortification of infant formulas (400 IU/L). However, it can still occur if the infant had low vitamin D stores at birth because of maternal vitamin D deficiency and if the vitamin D content of the formula is insufficient.[rx]
Obesity – 25(OH)D levels are low in obese individuals as vitamin D is sequestrated in fat. vitamin D requirements are thus higher in obese individuals.[rx]
Hospitalized patients – Inadequate intake and lack of sun exposure cause vitamin D deficiency in this group of patients.[rx]
Women treated for osteoporosis – Subclinical vitamin D deficiency is common in postmenopausal women on therapy for osteoporosis (bisphosphonates, raloxifene, calcitonin, or PTH).[rx]
Chronic renal disease – In patients with chronic kidney disease, calcitriol [1,25(OH)₂D] production is low due to diminished glomerular filtration, loss of the 1-α-hydroxylase enzyme secondary to structural renal damage, and suppression of enzyme activity secondary to hyperphosphatemia. This results in hypocalcemia, hyperparathyroidism, and bone disease.[rx] In addition to the deficiency of 1,25(OH)₂D, recent studies have shown co-existence of 25(OH)D deficiency in pre-dialysis and dialysis patients, especially in female diabetics and patients on peritoneal dialysis.[rx] Whether improving 25(OH) D concentrations benefit these patients is controversial, but Kidney Dialysis Outcome Initiative (KDOQI) guidelines have recommended supplementation.
Nephrotic syndrome – Most of the calcidiol in serum is bound to DBP. Patients with nephrotic syndrome lose DBP and may develop vitamin D deficiency.[rx,rx]
Distal renal tubular acidosis -Hypocalcemia can occur in dRTA, along with acidosis, which causes rickets. The presence of dRTA is suspected in conditions of hypokalemia, hyperchloremia, and normal anion gap metabolic acidosis.[rx]
Gastrointestinal disease – Malabsorption associated with diseases of the small intestine, a hepatobiliary tree with cholestatic liver disease, extrahepatic biliary obstruction, and diseases of the pancreas may result in decreased absorption of vitamin D and/or depletion of endogenous 25(OH)D stores due to abnormal enterohepatic circulation. Malabsorption of vitamin D occurs as a consequence of steatorrhea, which disturbs fat emulsification and chylomicron-mediated absorption. Patients may have rickets or osteomalacia or only low bone density. Common examples are celiac disease, inflammatory bowel disease, food allergies, cholestasis, and exocrine pancreatic insufficiency (as in cystic fibrosis).[rx]
Gastric bypass – Patients with short-limb bypass have secondary hyperparathyroidism (SHPT) in spite of normal 25(OH)D concentrations, due to calcium malabsorption. vitamin D deficiency also occurs in patients with partial or total gastrectomy for peptic ulcer disease or bariatric surgery due to the loss of gastrointestinal acidity, malfunction of the proximal small bowel which leads to vitamin D malabsorption, the absence of adequate absorbing surface, or failure of intestinal mucosal cells to respond to vitamin D.[rx,rx]
Liver disease – Vitamin D is hydroxylated in the liver to produce calcidiol [25(OH)D]. Hence, patients with significant parenchymal or obstructive liver disease have reduced 25(OH)D. These patients manifest biochemical or histological evidence of osteomalacia only in the presence of concomitant nutritional deficiency or interruption of the enterohepatic circulation.[rx,rx]
Medications – Certain anticonvulsants and antiretroviral drugs used to treat HIV infection can precipitate vitamin D deficiency by enhancing catabolism of 25(OH)D and 1,25(OH)₂D.[rx] decreased circulating levels of calcidiol occur in patients on phenytoin, phenobarbitone, carbamazepine, isoniazid, rifampicin, and theophylline due to induction of P-450 enzyme activity, which metabolizes calcidiol to inactive vitamin D metabolites. Tenofovir can cause rickets. Abnormalities in calcium concentration are seen with medications used in the treatment of the complications of HIV, such as foscarnet, pentamidine, and recombinant growth hormone. vitamin D requirements are higher in patients on glucocorticoids because they inhibit intestinal vitamin D dependent calcium absorption. Ketoconazole and some other antifungal agents increase vitamin D requirements because they block 1-hydroxylation. Supplementation with vitamin D (400–4000 IU/day) may be needed for these patients.[rx]
Insufficient nutritional quantities or faulty metabolism of vitamin D or phosphorus
Renal tubular acidosis
Malnutrition during pregnancy
Malabsorption syndrome
Hypophosphatemia^[rx]
Chronic kidney failure
Tumor-induced osteomalacia (Oncogenic osteomalacia)
Long-term anticonvulsant therapy^[rx]
Celiac disease^[rx]
Cadmium poisoning, iliac disease
Breastfed infants whose mothers are not exposed to sunlight
Breastfed babies who are exposed to little sunlight
Adolescents, in particular when undergoing the pubertal growth spurt^[rx]
Any child whose diet does not contain enough vitamin D or calcium
Diseases causing soft bones in infants, like hypophosphatasia or hypophosphatemia, can also lead to rickets.^[rx]

Rickets Symptoms

Pain or tenderness in the bones of the arms, legs, pelvis, or spine.
Stunted growth and short stature.
Bone fractures.
Muscle cramps.
Teeth deformities, such as delayed tooth formation. holes in the enamel.
Skeletal deformities, including an oddly shaped skull. bowlegs, or legs that bow out.
Delayed growth
Pain in the spine, pelvis, and legs
Muscle weakness
Diffuse joint and bone pain (especially of spine, pelvis, and legs)
Difficulty walking, often with a waddling gait
Hypocalcemia (positive Chvostek sign)
Compressed vertebrae and diminished stature
Pelvic flattening
Weak, soft bones
Easy fracturing
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result as the thickening caused by nodules forming on the costochondral joints.
This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest^[rx] may result in the presence of Harrison’s groove.

Diagnosis of Rickets

Rickets may be diagnosed with the help of

Blood tests – Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones. This can show enlarged limbs and joints.
A bone density scan – may be undertaken.^[rx]
Radiography typically – shows widening of the zones of provisional calcification of the metaphyses secondary to unmineralized osteoid. Cupping, fraying, and splaying of metaphyses typically appears with growth and continued weight bearing.^[rx] These changes are seen predominantly at sites of rapid growth, including the proximal humerus, distal radius, distal femur and both the proximal and the distal tibia. Therefore, a skeletal survey for rickets can be accomplished with anteroposterior radiographs of the knees, wrists, and ankles.^[rx]

Biochemical findings

Biochemical features are similar to those of rickets. The major factor is an abnormally low vitamin D concentration in blood serum. Major typical biochemical findings include:^[rx]

Low serum and urinary calcium
Low serum phosphate, except in cases of renal osteodystrophy
Elevated serum alkaline phosphatase (due to an increase in compensatory osteoblast activity)
Elevated parathyroid hormone (due to low calcium)

Skeletal findings

The skeletal changes are similar in calcipenic and phosphonic rickets.[rx] The anterior fontanelle closes by 18 months and posterior by 3 months normally. However, in rickets, there is a delay in the closure of the fontanelles.
There is parietal and frontal bossing, craniotabes (soft skull bones) with ping pong bones in infants, enlargement of the costochondral junction of ribs (the “rachitic rosary”), Harrison sulcus due to the muscular pull of the diaphragm on the lower ribs, widening of the wrist and bowing of the distal radius and ulna, and progressive lateral bowing of the femur and tibia.

Extraskeletal findings

The child may be asymptomatic or may present with pain, irritability, delay in motor milestones, and poor growth.[rx] Visceroptosis leads to a pot belly. Children may have waddling gait (antalgic gait). Presentation with hypocalcemic seizures is frequent in the first year of life.[rx]
Children with calcipenic rickets are prone to acquiring infectious diseases.[rx] There is hypoplasia of dental enamel. Increased sweating is a common finding in young infants with calcipenic rickets and may be caused by bone pain.

Radiographic findings

In children, the changes of rickets can be seen at the growth plate of rapidly growing bones. Thus, in the upper limbs, the changes are most prominent at the distal ulna, while in lower limbs the changes are most prominent at the metaphyses above and below the knees.
There is widening of the epiphyseal plate due to unmineralized osteoid and loss of definition of the zone of provisional calcification at the epiphyseal/metaphyseal junction.
There is cupping and splaying of the epiphyseal end of metaphysics with the formation of cortical spurs and stippling. The appearance of the epiphyseal bone centers may be delayed, and these are small and osteopenic.[rx]

Bone mineral density

Several studies have demonstrated markedly reduced spine, hip, and forearm bone density [as measured by dual-energy X-ray absorptiometry (DXA)] in patients with osteomalacia related to vitamin D deficiency.
However, bone mineral density (BMD) is not required for the diagnosis of osteomalacia, and reduced BMD does not distinguish osteoporosis from osteomalacia. In contrast, BMD tends to be normal or increased (especially lumbar spine) in adults with XLH.

Bone biopsy

Bone biopsy with tetracycline labeling is the most accurate way to diagnose osteomalacia/rickets. However, it is infrequently performed because it is invasive and the diagnosis can usually be made from a combination of clinical and laboratory findings.
Prolonged mineralization lag time, widened osteoid seams, and increased osteoid volume. All of these features are necessary for the diagnosis because other disorders may show one of these findings. Wide osteoid seams reflecting high turnover can be seen with hyperthyroidism, Paget’s disease, and hyperparathyroidism. However, the mineral apposition rate is elevated in these disorders in contrast to osteomalacia.

https://www.youtube.com/watch?v=5ClZOC6-pSc

Treatment of Rickets

A minimum of 400 IU/day vitamin D supplementation is recommended to prevent VDD and rickets in healthy infants, children, and adolescents.
400 IU/day vitamin D should be introduced to the diet of infants fed completely or partially by mother’s milk until they start receiving at least 1 liter of formula per day.
400 IU/day vitamin D should be provided to all infants fed with less than 1-liter formula per day and not receiving mother’s milk. Other sources of nutrition should be calculated individually for infants receiving this type of nutrition.
400 IU vitamin D should be provided to all adolescents not receiving 400 IU vitamin D from milk or other foods fortified with vitamin D.
According to recent evidence, the level of serum 25(OH)D should be above 20 ng/mL, particularly in infants and children.
400 IU/day vitamin D should be continued in cases with chronic fat malabsorption, chronic anticonvulsant intake or similar conditions increasing the risk of VDD. Higher vitamin D supplementation may be necessary in these cases to maintain the normal serum level of vitamin D.

Low dosage and long−term vitamin D therapy

There are different views about the dose and duration of vitamin D therapy. In this treatment model, depending on the age of the c h I l d, vitamin D is usually administered at a dose of 1000− 10 000 IU/day for 2−3 months. In this regimen, vitamin D can be given according to the infant’s age as follows: 1000 IU/day for infants under 1 month of age, 1000 to 5000 IU/ day for children 1 to 12 months old, and 5000 IU/day for children older than 12 months. Afterward, it is recommended to give maintenance therapy of 400 IU/ day.
Levels of Ca and P are normalized in 6−10 days by this therapy, while it takes 1−2 months for PTH to reach normal levels. Depending on the severity of the disease, it may take 3 months for the normal serum ALP levels to be restored and the radiological findings of rickets to disappear. In this treatment model, lack of compliance is an important cause of lack of response [rx, rx, rx, rx, rx, rx].

Stoss therapy

For patients who are suspected to have poor compliance, a high dose of vitamin D can be given orally or intramuscularly as a single dose of 100 000−600 000 IU after the first month of life [rx, rx, rx, rx]. Administration of 600 000 units of vitamin D in infantile rickets has been reported to cause hypercalcemia [rx]. Cesur et al [rx] reported that 150 000−300 000 units of vitamin D is an effective and safe method of treatment.
A recent study also demonstrated that intramuscular administration of a single dose of 300 000 IU of vitamin D is effective in cases of malnutrition with rickets [rx]. Shah and Feinberg have successfully administrated 100 000 IU of vitamin D every two hours over a twelve−hour period [rx, rx]. This treatment evokes a rapid clinical response, resulting in a biochemical recovery in a few days and radiological recovery in 10−15 days.

Monitored Supplementation of Pregnant Women

Low socioeconomic status, covered clothing and lack of supplementation contribute to the high prevalence of vitamin D deficiency in pregnancy [rx]. Congenital rickets and postnatal hypocalcaemic seizures are reported in risk groups in both developed and developing countries [rx , rx, rx]. Poor maternal vitamin D status affects the fetus and of the newborn. In a large Italian study, 76% of newborns of dark-skinned migrant women had 25OHD levels below 25 nmol/L (10 μg/L), compared to 38% of newborns of native Italian women [rx].

Universal Supplementation of Infants Regardless of Mode of Feeding

The amount of vitamin D available in breast milk but also infant formula milk is insufficient to prevent NR; even formula-fed infants can present with the asymptomatic deficiency in the first few months of life [rx, rx, rx] if born to deficient mothers.
In a recent survey of vitamin D supplementation policies across Europe, we found that universal supplementation, currently practiced by 79% (23/29) of countries was significantly (p = 0.007) associated with good adherence to supplements [rx]. The recommended dose of 400 IU/day (10 μg) is safe also in formula-fed infants. Toxicity is usually related to errors in manufacturing, formulation or prescription [rx, rx].

Supplementation Beyond the First Year of Life

The duration of childhood supplementation varies widely across Europe [rx]. Assessment of daily intakes at 18 months and 3.5 years of age in 755 children in the UK showed low daily intakes of vitamin D and calcium [rx].
The incidence of NR rises beyond the recommended age of infant supplementation [rx, rx, rx], especially in dark-skinned (immigrant or resident) individuals. Hence, national policies should ensure that the daily requirement of vitamin D beyond the first year of life is met through supplementation or fortification [rx].

Identifying Successful and Sustainable Implementation Strategies

Although most developed countries have vitamin D supplementation policies in place, some countries lack successful implementation strategies. Recent studies from Canada and New Zealand reported that none of the individuals with NR had received vitamin D supplements for rickets prevention despite the presence of national recommendations [rx, rx].
Similarly, 85% of British parents are unaware of the need for infant vitamin D supplementation for their baby despite existing policy [rx]. There is overwhelming evidence that infant vitamin D supplementation improves 25OHD concentrations [rx] and prevents NR [rx].

Food Fortification with Vitamin D or Calcium

Health benefits of food fortification with micronutrients, including vitamin D, are well established [rx]. Currently, most European countries follow voluntary fortification [rx]; however, evidence from Canada and the USA suggests that mandatory fortification improves vitamin D uptake at the population level [rx].
Fortification should not be restricted to dairy products due to its limited consumption in certain risk groups [rx]; fortification of a variety of food sources is more beneficial [rx]

References

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What Does the Pain of Pancreatitis Feel Like

What Does the Pain of Pancreatitis Feel Like/ Pancreatitis is a condition characterized by inflammation of the pancreas?^[rx] The pancreas is a large organ behind the stomach that produces digestive enzymes and a number of hormones.^[rx] There are two main types, acute pancreatitis, and chronic pancreatitis.^[rx] Signs and symptoms of pancreatitis include pain in the upper abdomen, nausea, and vomiting.^[rx] The pain often goes into the back and is usually severe.^[rx] In acute pancreatitis, a fever may occur and symptoms typically resolve in a few days.^[rx] In chronic pancreatitis weight loss, fatty stool, and diarrhea may occur.^[rx] Complications may include infection, bleeding, diabetes mellitus, or problems with other organs.^[rx]

Acute pancreatitis is common and is the leading cause of hospitalization amongst gastrointestinal disorders in the United States. The severity of the disease varies widely, from mild disease needing conservative treatment to severe and complicated disease with high morbidity and mortality. The diagnosis of acute presentation is easy, but the major challenge is predicting the progression of disease course and outcome. This is important to determine the level of care. [rx][rx][rx]

Causes of Pancreatitis

In the majority of cases, alcohol use, gallstones, and hypertriglyceridemia cause acute pancreatitis. The rate of occurrence of each etiology of acute pancreatitis varies across geographic regions and socio-economic strata. Common etiologies of acute pancreatitis are listed below.[rx][rx][rx]

Alcohol use
Gallstones
Hypertriglyceridemia
Idiopathic
Drug-induced pancreatitis
Post-procedural (ERCP or abdominal surgery)
Ampullary stenosis is formerly known as sphincter of Oddi dysfunction type I
Autoimmune pancreatitis, type I (systemic IgG4 disease-related) and type II
Viral infection (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, Varicella)
Bacterial infection (Campylobacter jejuni, Legionella, Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, Mycoplasma)
Trauma
Smoking
Congenital anomalies (annular pancreas)
Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency)
Hypercalcemia
Parasitic infections (Ascaris lumbricoides, Cryptosporidium, Clonorchis sinensis, Microsporidia)
Renal disease (Hemodialysis)
Toxins (Scorpion bites, organophosphate poisoning)
Vasculitis (Polyarteritis nodosa, Systemic lupus erythematosus)

Acute pancreatitis

There are many potential causes of acute pancreatitis, the two major ones being gallstones and alcohol. The majority of recent studies, detailed in the following section, have employed experimental models of acute pancreatitis to explore the molecular basis of subsequent cellular responses.

Causes of Pancreatitis

Recent studies have identified potential mechanisms for several of the common causes of acute pancreatitis.

Bile Acids

Exposure of pancreatic acinar cells to bile during biliary acute pancreatitis may contribute to the disease. Many past studies have shown that pathologic increases in acinar cell cytosolic calcium ([Ca²⁺]_i) are linked to the early events in acute pancreatitis.
Fischer et al. [rx] found that bile acids induced pathologic increases in the acinar cell [Ca²⁺]_i through a phosphatidylinositol-3 kinase (PI3K)-dependent mechanism by preventing reuptake of Ca²⁺ into the endoplasmic reticulum. It was also shown by Barrow et al. [rx] that bile-mediated Ca²⁺ responses are enhanced by cellular ATP depletion, suggesting that elevations in bile acids and ischemia may synergize to cause pancreatic injury.

Alcohol

Disordered secretion, including inhibition of apical secretion and enhanced basolateral exocytosis, are early features of acute pancreatitis and may be central to disease pathogenesis.
Lam et al. [rx] and Cosen-Binker et al. [rx,rx] have now shown that acute ethanol exposure sensitizes the acinar cell to the effects of physiologic concentrations of cholecystokinin (CCK) by causing both inhibitions of apical inhibition and basolateral exocytosis through the same mechanism.

Hypertriglyceridemia

The mechanism of hypertriglyceridemic pancreatitis may involve the release of free fatty acids (FFA) through the hydrolysis of triglycerides by pancreatic lipase. Pancreatitis-associated ascitic fluid plays a critical role in acute pancreatitis. Gutierrez et al. [rx] have now shown ascites to contain high concentrations of oxidized FFA, which interferes with the endogenous regulation of inflammation and may promote macrophage activation in acute pancreatitis.

Hemolysis

Clinical evidence suggests that acute pancreatitis can arise as a complication of massive hemolysis; a recent study by Saruc et al. [rx] supports this hypothesis using an experimental model.
Hemolysis induced in rats by intraperitoneal (i.p.) injection of acetylphenylhydrazine (APH) caused increased pancreatic cytokine levels and histological signs of acute pancreatitis. Furthermore, free vascular heme seems to act as the signaling molecule for triggering inflammation, though the mechanism remains undetermined.

Experimental Models of Pancreatitis

A limiting feature of the commonly used caerulein-hyperstimulation model of acute pancreatitis is that it causes only mild disease. Several new in-vivo mouse models now generate severe acute pancreatitis.
This includes mouse models of acute pancreatitis that use retrograde pancreatic duct infusion of the bile salt, sodium taurocholate by Laukkarinen et al. [rx], and i.p. injection of L-arginine by Dawra et al. [rx]. These models may prove useful for studying therapeutic interventions and examining disease mechanisms in transgenic mice.

Cellular Responses

A series of the acinar cell and inflammatory cell responses underlie the pathogenesis of acute pancreatitis. Some of these have been explored in publications during the last year.

Membrane Permeability

One of the earliest events in acute pancreatitis may be the disruption of the acinar cell plasma membrane. Muller et al. [rx] used both caerulein and taurocholate-induced models of acute pancreatitis in rats to demonstrate that endogenous albumin and immunoglobulin G (IgG) entered acinar cell cytosol.
Such defects could contribute to pathologic increases in [Ca²⁺] and allow cytoplasmic proteins to leak from the cell. It will be of interest to determine how these defects occur, whether they might be related to the plasma membrane blebbing that has been observed in acute pancreatitis or to defects in the complex process of membrane resealing and if such defects are found in human acute pancreatitis.

Zymogen Activation

Premature intracellular activation of trypsinogen by the lysosomal hydrolase cathepsin B has generally been considered a pivotal event in the initiation of acute pancreatitis. However, using a cathepsin B inhibitor, CA074Me, Van Acker et al. [rx] showed that enzyme colocalization and other acute pancreatitis events, such as actin redistribution and inflammation, were cathepsin B independent.
Other mechanisms, such as those mediated by [Ca²⁺]and its protein targets, might mediate these responses. The Ca²⁺-dependent protein phosphatase calcineurin (PP2B) might serve this role. Husain et al. [rx] showed that the calcineurin inhibitor FK506 or a cell-permeable calcineurin inhibitory peptide reduced zymogen activation without affecting initial elevations in [Ca²⁺]or enzyme secretion. Thus, PP2B may be down-stream to the pathologic [Ca²⁺] that typifies acute pancreatitis. The effects of elevating cAMP on acute pancreatitis are complex, but the most important response might be to enhance the secretion of active enzymes.

Inflammation

Two recent studies have focused on the neuropeptide, substance P and its role in pancreatic inflammation. Ramnath et al. [rx] reported that expression of the substance P gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for substance P, were increased in caerulein-treated mouse pancreatic acinar cells. Furthermore, the messenger hydrogen sulphide was shown to provoke inflammation through a substance P, NK-1R related pathway by Tamizhselvi et al. [rx].

Endoplasmic reticulum stress

Endoplasmic reticulum stress can lead to accumulation of unfolded proteins, initiation of the unfolded protein response (UPR), inflammation and cell death. Kubisch and Logsdon [rx] reported that stimulation of rat pancreatic acini with three secretagogues, CCK8, CCK-JVM-180 or bombesin, resulted in distinct UPR responses that included increased chaperone BiP levels, PKR-like endoplasmic reticulum kinase (PERK) phosphorylation, X box-binding protein 1 (XBP1) splicing, and CCAAT/enhancer binding protein homologous protein (CHOP) expression.
Treatment with caerulein and lipopolysaccharide (LPS), a more severe model of acute pancreatitis, resulted in less expression of inflammation-associated caspases (caspase-11 and caspase-1) in CHOP^−/− mice. These studies indicate a pivotal role for the endoplasmic reticulum stress-CHOP pathway in accelerating pancreatitis through induction of inflammation-linked caspases.

Apoptosis

The severity of pancreatitis may depend on the mechanism of cell death; greater levels of apoptosis over necrosis favor milder disease. To examine the mechanisms of apoptosis, Baumgartner et al. [rx] used the oxidative stressor menadione and identified two independent apoptotic pathways in pancreatic acinar cells.
The first is the classical caspase-9-mediated pathway that is Ca²⁺-dependent, mediated by mitochondria and is rapidly initiated. The second is much slower, mediated by caspase-8, depends on the lysosomal activities of cathepsins and is used when the caspase-9 pathway is disabled.
This information might be used to develop strategies for shifting cell death pathways to favor apoptosis during acute pancreatitis.

Protective Mechanisms

A number of protective and restorative mechanisms in acute pancreatitis have been characterized over the past year. Singh et al. [rx] used protease-activated receptor-2 (PAR-2) deficient mice in a caerulein acute pancreatitis model to demonstrate that PAR-2 stimulation caused exocrine secretion, thus protecting acinar cells from the damaging effects of activated enzymes. The study by Bhagat et al. [rx] explored the protective role played by heat shock proteins (HSPs), particularly HSP 70, using both caerulein and L-arginine models of acute pancreatitis. Sodium arsenite pretreatment was used to upregulate HSP 70 expression and significantly reduced the severity of pancreatitis in both models.
The pancreas is a rich source of the polyamine spermidine, and a study by Hyvonen et al. [rx] showed that depletion of these polyamines led to acute necrotizing pancreatitis. Replacement of depleted polyamines using methylated polyamine analogs prior to induction of acute pancreatitis prevented the development of the disease, strongly supporting an endogenous protective role for these compounds.

Genetic Factors

Two studies from the last year have highlighted the importance of genetic factors in predisposing patients to acute pancreatitis [rx]. Gao et al. [rx] investigated why some patients are more prone to pancreatic infection during acute pancreatitis. LPS or endotoxin may cross leaky paracellular barriers in the colon or be released into the bloodstream by circulating Gram-negative bacteria during acute pancreatitis.
LPS can then bind to Toll-like receptors (TLRs) on the surface of the acinar cell, producing a host defense response. However, in some patients, a polymorphism in TLR-4 led to impaired signaling and lack of a defensive response, rendering them more prone to infection.
In another genetic study, Chang et al. [rx] found that mutations on the cystic fibrosis transmembrane conductance regulator (CFTR) predisposed patients with elevated lipids to developing hypertriglyceridemic pancreatitis. Further studies that use newer genome-wide analysis will likely reveal additional genetic factors that affect the risk of developing acute pancreatitis or its severity.

Miscellaneous Mechanisms

Ghrelin is a ligand of the growth hormone secretagogue receptor (GHSR) and has been shown to affect exocrine pancreatic secretion. Previous studies have suggested that ghrelin may modulate the severity of acute pancreatitis and that serum ghrelin levels predict severity in acute pancreatitis.
Lai et al. [rx] reported that both ghrelin and its receptor are present in pancreatic acinar cells and that the receptor was downregulated in acute pancreatitis. The data indicate that a ghrelin-dependent system is present in the exocrine pancreas. However, its function in normal pancreatic physiology and pancreatitis requires further study.

Chronic Pancreatitis

Chronic pancreatitis is characterized by chronic inflammation, progressive fibrosis, pain and loss of exocrine and endocrine function. The molecular basis of these responses is addressed by many of the studies detailed in the following section.

Inflammation and Fibrosis

Pancreatic stellate cells (PSCs) play a key role in pancreatic fibrosis. Masamune et al. [rx] reported that the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in PSCs generated reactive oxygen species that modulate their activation and the subsequent deposition of extracellular matrix (ECM), leading to pancreatic fibrosis.
Coculture experiments with PSCs and peripheral blood mononuclear cells (PBMCs) reported by Michalski et al. [rx] demonstrated increased fibronectin secretion from the PBMCs as well as increased levels of IL-6, MCP-1, transforming growth factor (TGF)-β, and ECM from the PSCs. Thus, increased infiltration of mononuclear cells, as seen in chronic pancreatitis, might be a trigger for PSCs to initiate fibrosis and inflammation.

Inflammation and Pain

They reported that pain levels in patients with chronic pancreatitis correlated with neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) levels. PBMCs from patients with chronic pancreatitis were more responsive to the effects of PACAP. Xu et al. [rx] reported that pancreatic hyperalgesia is mediated by upregulation of the transient receptor potential vanilloid 1 (TRPV1) in a model of chronic pancreatitis. As pharmacologic TRPV1 inhibition reduced visceral pain responses in this model, this might be a target for pain treatment in chronic pancreatitis.

Alcohol Use and Chronic Pancreatitis

Fortunato et al. [rx] reported that chronic alcohol exposure in rats increased the pancreatic activity of an anti-inflammatory nuclear receptor, peroxisome proliferator-activated receptor gamma (PPARγ). Although PPARγ activity was associated with the reduced immune cell and inflammatory responses, damage to acinar cell mitochondria and lysosomes and pericellular fibrosis and protease activation occurred. These results could explain how chronic alcohol use might predispose the pancreas to chronic pancreatitis without causing intense inflammation.

Medications

There are seven classes of medications associated with acute pancreatitis

Statins,
ACE inhibitors
Oral contraceptives/hormone replacement therapy (HRT)
Diuretics
Antiretroviral therapy
Valproic acid, and
Oral hypoglycemic agents
ACE inhibitors cause angioedema of the pancreas through the accumulation of bradykinin.
Oral contraceptives/HRT cause arterial thrombosis of the pancreas through the accumulation of fat (hypertriglyceridemia). Diuretics such as furosemide have a direct toxic effect on the pancreas. Meanwhile, thiazide diuretics cause hypertriglyceridemia and hypercalcemia, where the latter is the risk factor for pancreatic stones.
HIV infection itself can cause a person to be more likely to get pancreatitis. Meanwhile, antiretroviral drugs may cause metabolic disturbances such as hyperglycemia and hypercholesterolemia, which predisposes to pancreatitis.
Valproic acid may have a direct toxic effect on the pancreas.^[rx] There are various oral hypoglycemic agents that contribute to pancreatitis including metformin. But, glucagon-like peptide-1 (GLP-1) is more strongly associated with pancreatitis by promoting inflammation.^[rx]
Atypical antipsychotics such as clozapine, risperidone, and olanzapine can also cause pancreatitis.^[rx]

Infection

A number of infectious agents have been recognized as causes of pancreatitis including:^[rx]^[rx]

Viruses

Coxsackievirus
Cytomegalovirus
Hepatitis B
Herpes simplex virus
Mumps
Varicella-zoster virus

Bacteria

Legionella
Leptospira
Mycoplasma
Salmonella

Fungi

Aspergillus

Parasites

Ascaris
Cryptosporidium
Toxoplasma

Other

Other common causes include trauma, autoimmune disease, high blood calcium, hypothermia, and endoscopic retrograde cholangiopancreatography (ERCP). Pancreas divisum is a common congenital malformation of the pancreas that may underlie some recurrent cases. Diabetes mellitus type 2 is associated with a 2.8-fold higher risk.^[rx]
Less common causes include pancreatic cancer, pancreatic duct stones,^[rx] vasculitis (inflammation of the small blood vessels in the pancreas), and porphyria—particularly acute intermittent porphyria and erythropoietic protoporphyria.
There is an inherited form that results in the activation of trypsinogen within the pancreas, leading to autodigestion. Involved genes may include trypsin 1, which codes for trypsinogen, SPINK1, which codes for a trypsin inhibitor, or cystic fibrosis transmembrane conductance regulator.^[rx]
The mnemonic GETSMASHED is often used to remember the common causes of pancreatitis: G—gallstones, E—ethanol, T—trauma, S—steroids, M—mumps, A—autoimmune pancreatitis, S—scorpion sting, H—hyperlipidemia, hypothermia, hyperparathyroidism, E—endoscopic retrograde cholangiopancreatography, D—drugs (commonly azathioprine, valproic acid, liraglutide)

Symptoms of Pancreatitis

Signs and symptoms of pancreatitis may vary, depending on which type you experience.

Acute pancreatitis signs and symptoms include:

Upper abdominal pain
Abdominal pain that radiates to your back
Abdominal pain that feels worse after eating
Upper abdominal pain that radiates into the back; it may be aggravated by eating, especially foods high in fat.
Swollen and tender abdomen
Nausea and vomiting
Fever
Increased heart rate
Rapid pulse
Tenderness when touching the abdomen

Chronic pancreatitis signs and symptoms include

Upper abdominal pain
Losing weight without trying
Oily, smelly stools (steatorrhea)

Diagnosis of Pancreatitis

The differentials for acute pancreatitis include the overall differential for abdominal pain and can often be greatly narrowed with a good history and physical as described above. Differential diagnoses include but is not limited to the following:

Peptic ulcer disease
Cholangitis
Cholecystitis
Bowel perforation
Bowel obstruction
Mesenteric ischemia
Acute hepatitis
Diabetic ketoacidosis
Basilar pneumonia
Myocardial infarction
Renal colic
Aortic dissection

Blood Tests

In AP, amylase and lipase are typically elevated, whereas in CP, the serum concentrations of these enzymes are usually normal to mildly elevated due to loss of functional exocrine pancreatic tissue from pancreatic fibrosis [rx].
The white cell count and electrolytes are usually unremarkable, unless diminished intake, vomiting, or digestive insufficiency has occurred. Elevations of serum bilirubin and alkaline phosphatase can occur, which suggests compression of the intrapancreatic portion of the bile duct by edema, fibrosis, or pancreatic cancer [rx].
Transabdominal ultrasound and CT imaging – can be used to detect advanced disease. While ultrasound is relatively inexpensive and free of radiation, its ability to visualize the pancreas is poor compared to other imaging modalities. Multiple echogenic foci representing calcifications are the classic findings seen on ultrasound. These are seen in only up to 40% of patients [rx]. CT imaging has been shown to have sensitivity ranging from 74 to 90% and a specificity of 80–90% in diagnosing advanced CP [rx].
Common findings on CT imaging – include pancreatic ductal dilatation, parenchymal atrophy, and pancreatic calcifications [rx]. CT imaging is considered to be the best initial imaging test for CP because of its high sensitivity and specificity, and its ability to potentially identify other causes of abdominal pain [rx].
Magnetic resonance cholangiopancreatography (MRCP) and MRI – have also been used to diagnose CP and have the advantage of no radiation exposure. Moreover, MRI has the advantage of detecting both parenchymal and ductal changes [rx]. MRI/MRCP can be combined with hormonal stimulation using intravenous secretin to aid in the diagnosis of early CP with a sensitivity of 77% and specificity of 83% [rx, rx].
EUS – has emerged as an important imaging modality to detect early morphologic changes in CP. It can detect mild parenchymal and ductal changes not seen on CT scan and can be used when CT and MR imaging are non-diagnostic [rx, rx].
There are nine criteria used in diagnosing CP with EUS – four parenchymal features including hyperechoic foci, hyperechoic strands, lobular contour, and cysts, and five ductal features including main duct dilatation, duct irregularity, hyperechoic margins, visible side branches, and stones [rx].
Endoscopic retrograde cholangiopancreatography (ERCP) – was considered to be the gold standard to detect early changes. However, this procedure is invasive, expensive, and time-consuming. In addition, ERCP can only evaluate for ductal changes. Moreover, given the advent of MRCP and EUS, ERCP has less of a role in diagnosing CP. The most recent guidelines by the American Society for Gastrointestinal Endoscopy (ASGE) in 2006 recommended reserving the use of ERCP for patients in whom the diagnosis is inconclusive despite pancreatic function testing CT/MRI or EUS [rx].
Pancreatic Function Testing – The role of pancreatic function testing is limited based on practicality in comparison with the ease of imaging modalities as previously discussed. However, functional testing can be considered in cases with equivocal morphological imaging [rx]. End-stage CP occurs when more than 90% of exocrine pancreatic function is lost and ultimately leads to pancreatic exocrine insufficiency (PEI) and steatorrhea [rx]. A 72-h quantitative fecal fat determination can be used to diagnose steatorrhea, though it is not specific for CP and can be seen in small bowel mucosal diseases such as celiac disease, Crohn’s disease, and bacterial overgrowth [rx].
Endoscopic transgastric pancreatic necrosectomy – is another alternative that is being increasingly used in select patients with IPN. It involves endoscopic access to the necrotic area through the posterior wall of the stomach. The TENSION trial comparing endoscopic to minimally invasive surgical necrosectomy is currently underway.[rx] The results of this RCT will determine the role of endoscopic necrosectomy in IPN.

Treatment of Pancreatitis

Analgesics – are a mainstay of treatment. The WHO method can be used as a guide for pain relief starting with NSAIDs and progressing to strong opioids [rx]. Tricyclic antidepressants such as amitriptyline and nortriptyline can be used with modest efficacy to reduce neuropathic pain [rx]. Pregabalin has been shown to alleviate pain in CP [rx, rx].
Pancreatic enzyme replacement therapy (PERT) – can also be used to relieve pain, though the data remain controversial. Those with positive studies used uncoated pancreatic enzymes, which are not readily available [rx, rx] and benefits may be related to the placebo effect. A metaanalysis performed in 1997 showed no significant benefit of PERT to relieve pain [rx]. However, PERT has relatively no side effects and is indicated in patients with exocrine pancreatic insufficiency (EPI) and steatorrhea [rx].
Antioxidant therapy – is another option for the medical management of pain. Braganza et al. proposed that one of the mechanisms of CP is through increased oxidative stress leading to damage of pancreatic and acinar cells [rx]. Current evidence suggests the decreased levels of antioxidants in patients with CP may be due to decrease intake and absorption secondary to pain and malabsorption, respectively [rx]. A recent meta-analysis has shown a reduction in pain symptoms with antioxidants consisting of organic selenium, ascorbic acid, beta-carotene, alpha-tocopherol, and methionine [rx].
Simvastatin and atorvastatin – were associated with an overall decrease risk in AP. Further subset analysis found a decrease in risk in patients with chronic alcohol abuse, suggesting the possibility of using simvastatin to prevent recurrent pancreatitis and subsequently, CP. A clinical trial is underway to test this possibility entitled “Simvastatin in reducing pancreatitis in patients with recurrent acute or CP” (ClinicalTrials.gov).

Antibiotic Therapy in Acute Pancreatitis

Secondary infective complications of acute pancreatitis are associated with increased mortality.[rx]
The spectrum of microorganisms responsible for infected necrosis is changing.[rx] Although Gram-negative aerobic bacteria are commonly yielded in cultures of infected pancreatic necrosis, Gram-positive bacteria, anaerobes, and fungi have also been isolated.[rx]
Penicillins, first-generation cephalosporins, aminoglycosides, and tetracyclines are ineffective in acute pancreatitis. Antibiotics that are active against Gram-negative bacteria such as imipenem, clindamycin, piperacillin, fluoroquinolones, and metronidazole have adequate tissue penetration and bactericidal properties in infected pancreatic necrosis.[rx]
Compared with other intravenous antibiotics, carbapenems are associated with a significant reduction in mortality, while the use of imipenem significantly reduced the incidence of infected pancreatic necrosis.[rx],[rx] Caution should be exercised when interpreting the results of the meta-analyses as the patient numbers are relatively small.[rx],[rx]

Fluid Therapy in Acute Pancreatitis

The initial management of acute pancreatitis is largely supportive, with fluid replacement and optimization of electrolyte balance, providing adequate caloric support, and preventing or identifying and treating local and systemic complications.
The local and systemic inflammatory response in acute pancreatitis results in fluid depletion in the form of vomiting, reduced oral fluid intake, third-space fluid loss, and increased insensible losses in sweat and respiration.
Fluid replacement in acute pancreatitis can be undertaken using crystalloid, colloid, or a combination of both. Ringer’s lactate is the preferred crystalloid fluid,[rx] but caution should be exercised in hypercalcemic patients. The literary evidence for recommendations for fluid resuscitation has been summarized previously.[rx] However, to date, there is no clear agreed consensus regarding the ideal fluid type and regimen for fluid resuscitation.[rx],[rx]

Fluid Resuscitation

The disease process leads to acinar cell injury and the consequent proinflammatory cytokine cascade leads to microvascular permeability, interstitial edema, vasoconstriction, and eventually decreased capillary perfusion in animal models. Pancreatitis also causes hypovolemia by inducing poor oral intake, insensible losses, third-spacing of fluids, and emesis. Therefore, fluid resuscitation has become the cornerstone of conservative treatment [rx].
In the absence of cardiac, pulmonary, or renal contraindications, various recommendations on the initial fluid resuscitation regimen have varied from 250–500 cc/hr with or without bolus to achieve hemodynamic stability, targeting a mean arterial pressure > 60 or simply targeting a urine output > 0.5 cc/kg/hr [rx–rx].
While no specific targets are currently recommended, hemodilution (decreased hematocrit), reduced uremia (indicating adequate kidney perfusion), and normalization or maintenance of normal creatinine have been proposed. A practical, evidence-based approach to fluid resuscitation is needed [rx–rx].

Nutrition

Current data support the early resumption of a low-fat solid diet with mild acute pancreatitis. While it does not lead to a shorter length of hospital stay or decreased 30-day readmission rate, a randomized trial evaluating the tolerance of a low fat solid meal versus a liquid diet showed no increased adverse events (pain/nausea necessitating cessation) and led to increased caloric intake [rx].

Role of Endoscopic Retrograde Cholangiopancreatography (ERCP)

The role of ERCP in patients with AP is generally reserved for acute biliary pancreatitis secondary to choledocholithiasis. While many scoring systems and algorithms have been developed, the proposed strategy to assign the risk of choledocholithiasis proposed by the American Society for Gastrointestinal Endoscopy is the most widely used.
It stratifies predictors of choledocholithiasis into very strong (observed on US, cholangitis or total bilirubin > 4 mg/dL), strong (CBD > 6 mm with gallbladder in situ or total bilirubin between 1.8 and 4 mg/dL), and moderate (abnormal AST/ALT or alkaline phosphatase, clinical gallstone pancreatitis, or age > 55). When a patient has one very strong predictor or two strong predictors, the risk of choledocholithiasis is high. All other predictors are considered intermediate and no qualifying predictors is considered low risk [rx, rx].
In patients with mild biliary pancreatitis with improving signs and symptoms, ERCP preceding cholecystectomy has limited value and may be harmful. In these cases, magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS) can be used for diagnostic purposes [rx].

Cholecystectomy

Cholecystectomy should be performed on initial hospitalization in patients with acute biliary pancreatitis. A systematic review of 9 studies involving 998 patients with mild biliary pancreatitis showed that early cholecystectomy in the setting of gallstone pancreatitis (i.e., during the index admission) reduced the incidence of recurrent admissions for repeat biliary-related events including pancreatitis, cholecystitis, and biliary colic. Early cholecystectomy was not associated with increased adverse events including mortality nor conversion from a laparoscopic procedure to an open procedure [rx].

Management of Persistent Fluid Collections or Infected Necrosis

We intervene upon pancreatic fluid collection or infected necrosis only when there are significant symptoms present, including persistent abdominal pain, gastric outlet obstruction, fluid leakage due to disconnected pancreatic duct, and infection [rx].
It is crucial to classify fluid collections as either pseudocyst or walled-off pancreatic necrosis because of the differences in prognosis and treatment. CT imaging can underestimate the existence of necrotic debris; therefore, MRI and endoscopic ultrasound (EUS) are better for assessment [rx].

Open Surgical Drainage

Open necrosectomy is performed via laparotomy through a subcostal incision, where blunt removal of all necrotic tissue is done [rx]. Early conservative management with late surgical intervention is superior to early necrosectomy [rx]. Surgery is delayed preferably four weeks after onset of disease, as this is thought to allow for time for the acute necrotic collection to mature and demarcate, hereby facilitating necrosectomy [rx].
In a recent randomized control trial, open necrosectomy had a high rate of complications or death (69%) [rx]. Those undergoing open necrosectomy also had a higher rate of long-term complications, including incisional hernias (24%), new onset diabetes (38%), and use of pancreatic enzymes (33%).
Therefore, therapy has shifted toward a minimally invasive “step-up” approach. This approach starts with more conservative techniques (percutaneous, laparoscopic, and endoscopic) first and then reserving surgery for cases of salvage therapy [rx].

Minimally Invasive Techniques

There are several different types of noninvasive techniques to drain and debride persistent fluid collections or infected pancreatic necrosis, including image-guided percutaneous drainage, laparoscopy, and retroperitoneoscopy [rx].
Using ultrasound or CT guidance – percutaneous drain placement allows for external access to the area of necrosis to be obtained [rx]. A considerable number of patients can be treated with percutaneous drain (PCD) alone without the need for surgical necrosectomy [rx]. The PANTER trial found that 35% of their patient population undergoing drainage did not need further surgery [rx].
A systematic review by van Baal et al. showed that percutaneous drainage alone was successful in 56% of cases [rx]. In the patients who did need surgery, drain placement delayed operative management for several weeks, by allowing for sepsis control [rx].
Complications of percutaneous drain placement are pancreatic cutaneous and pancreaticoenteric fistulas (most common), as well as procedure-related complications (i.e., bleeding, colonic perforation, abdominal pain, pneumothorax, or catheter dislodgment) [rx].
Transperitoneal laparoscopy is generally not supported because of the technical difficulty and risk of contamination of the peritoneal cavity [45].

Endoscopic Techniques in the Management of Persistent Fluid Collections or Infected Necrosis

Over the last two decades, endoscopic ultrasound- (EUS-) guided intervention of PFCs and infected necrosis has significantly evolved. There are multiple techniques for the drainage of PFCs including lumen-apposing metal stents (LAMS), direct endoscopic necrosectomy (DEN), and a double-pigtail plastic stent [rx]. The TENSION trial is currently underway and will compare the surgical step-up approach versus an endoscopic step-up approach [rx].
While there are no absolute size guidelines as to when to intervene, encapsulated areas less than 3 cm do not allow placement of a stent for drainage [rx].

Surgical treatment modalities in necrotizing pancreatitis[rx]

Surgical treatment modalities
Open necrosectomy with open packing – after necrosectomy, the abdomen maybe left open and repeatedly debrided until there is no residual necrosis, and is allowed to close by secondary intention
Open necrosectomy with closed packing – after the removal of necrotic tissue, the abdomen is closed, packing with external drains left in place. The drains are removed singly every other day, starting 5-7 d postoperatively
Open necrosectomy with continous postoperative lavage – the procedure is based on the insertion of 2 or more double lumen catheters. Repeated open necrosectomy is performed and the packing is removed when there is no residual necrosis. The smaller lumen of the drains is used for the inflow of the lavage, and the larger lumen is used for the outflow. The drains can be removed after 2-3 wk
Programmed open necrosectomy – necrosectomy of necrotic tissue is performed using multiple procedures. After necrosectomy, the pancreatic bed is packed with sponges and soft drains are placed on the top of the packs. The abdomen is closed using a zipper

References

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Respiratory Tract Infections; Causes, Symptoms, Treatment

Respiratory tract infections (RTI) are illnesses caused by an acute infection which involves the upper respiratory tract including the nose, sinuses, pharynx or larynx. This commonly includes nasal obstruction, sore throat, tonsillitis, pharyngitis, laryngitis, sinusitis, otitis media, and the common cold.^[3]Most infections are viral in nature and in other instances the cause is bacterial.^[rx] Upper respiratory tract infections can also be fungal or helminth in origin, but these are far less common.^[rx]

Upper respiratory tract infection (URTI) or the common cold is a symptom complex usually caused by several families of the virus; these are the rhinovirus, coronavirus, parainfluenza, respiratory syncytial virus (RSV), adenovirus, human metapneumovirus, and influenza. Occasionally the enterovirus is implicated in summer. Recently, the newly discovered bocavirus (related to the parvovirus) has also been linked to URTI.^[rx] The term “URTI” is probably a misnomer as it incorrectly implies an absence of lower respiratory tract symptoms. URTI occurs commonly in both children and adults and is a major cause of mild morbidity. URTIs have a high cost to society, being responsible for missed work and unnecessary medical care. Occasionally they have serious sequelae. Often regarded as trivial, URTIs do not receive serious attention in medical school curricula.

Types of RTIs

Upper respiratory tract infections: Symptoms occur mainly in the nose and throat. Viral upper respiratory tract infections may occur at any age and include the common cold and influenza.
Lower respiratory tract infections: Symptoms occur in the windpipe, airways, and lungs. Viral lower respiratory tract infections are more common among children and include croup, bronchiolitis, and pneumonia.

There are several different types. They’re usually grouped into upper and lower RTIs.

Upper RTIs (sinuses and throat)	Lower RTIs (airways and lungs)
Common cold	Bronchitis
Sinusitis (sinus infection)	Bronchiolitis
Tonsillitis	Chest infection
Laryngitis	Pneumonia (lung infection)

A URI may be classified by the area inflamed. Rhinitis affects the nasal mucosa, while rhinosinusitis or sinusitis affects the nose and paranasal sinuses, including frontal, ethmoid, maxillary, and sphenoid sinuses.
Nasopharyngitis (rhinopharyngitis or the common cold) affects the nares, pharynx, hypopharynx, uvula, and tonsils generally.
Without involving the nose, pharyngitis inflames the pharynx, hypopharynx, uvula, and tonsils. Similarly, epiglottitis (supraglottitis) inflames the superior portion of the larynx and supraglottic area; laryngitis is in the larynx; laryngotracheitis is in the larynx, trachea, and subglottic area; and tracheitis is in the trachea and subglottic area.

Causes of Respiratory Tract Infection

Acute pharyngitis
Acute ear infection
Common cold
Bronchitis
Pneumonia
Bronchiolitis

Flu can be an upper or lower RTI

Common cold
Sinusitis – Inflammation of the sinuses
Epiglottitis – Inflammation of the epiglottis, the upper part of the trachea that helps protect the airways from foreign particles – Swelling here is dangerous because it can block air flow
Laryngitis – Inflammation of the larynx (voice box)
Bronchitis – Inflammation of the bronchial tubes

Causes and Risk Factors

Lower Respiratory Tract Infections in Children and Important Etiologic Agents

Syndrome	Etiologic agents
Bronchiolitis	RSV, hMPV, PIV, adenovirus, coronaviruses, influenza viruses, Chlamydophila pneumoniae, Mycoplasma pneumoniae, rhinovirus, bocavirus,
Exacerbations of Wheezing/Asthma	RSV, hMPV, rhinovirus, adenovirus, PIV, coronaviruses, influenza viruses, Chlamydophila pneumoniae, Mycoplasma pneumoniae, bocavirus
Croup	PIV, Influenza, adenovirus,
Pneumonia	Influenza, Streptococcus pneumoniae, Mycoplasma pneumoniae, PIV, adenovirus, RSV,hMPV, Streptococcus pyogenes, Staphylococcus aureus
Pneumonitis in Transplant Recipients	RSV, PIV, influenza, hMPV, adenovirus, rhinovirus

NOTE. Pathogens in bold are thought to be the most common etiologies. hMPV, human metapneumovirus; PIV, parainfluenza virus 1, 2, 3; RSV, respiratory syncytial virus.

URIs can be caused by both viruses and bacteria. There are several sub-types within each of these categories. For viruses, these include:

Rhinovirus
Adenovirus
Coxsackie virus
Parainfluenza virus
Respiratory syncytial virus
Hyman metapneumovirus

For bacteria, these include

Group A beta-hemolytic streptococci (GABHS)
Corynebacterium diphtheriae (diphtheria)
Neisseria gonorrhoeae (gonorrhea)
Chlamydia pneumoniae (chlamydia)
Group C beta-hemolytic streptococci

Other Causes

Typical Bacterial Infections

Haemophilus influenzae
Staphylococcus aureus
Klebsiella pneumonia

Atypical Bacterial Infections

Legionella pneumophila
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Chlamydia psittaci

Parasitic infections

Respiratory cryptosporidiosis

Viral infections

Adenovirus
Influenza A virus
Influenza B virus
Human parainfluenza viruses
Human respiratory syncytial virus
SARS coronavirus
Middle East respiratory syndrome coronavirus
Aspiration pneumonia

Several actions, events or conditions can increase the risk of a URI, including

When someone sick sneezes or coughs without covering their nose and mouth. This causes droplets containing viruses to be sprayed into the air.
Closed areas or crowded conditions, such as hospitals, institutions, schools and daycare centers.
When you touch your nose or your eyes—infection occurs when secretion touches the nose or eyes.
During fall and winter (September to March) while people are more likely to be inside.
When humidity is low—indoor heating promotes the survival of many viruses that lead to URIs.
If you have a weakened immune system.
Chronic respiratory disease
Chronic renal disease
Chronic liver disease
Diabetes
Serious central nervous system diseases (cerebral vascular accident, transient ischaemic attack, Parkinson’s disease, dementia, and multiple sclerosis)
Rheumatoid arthritis
Cancer
Osteoporosis

Increased age (>60 years), especially in the presence of:^[rx]

use of benzodiazepines or antidepressants
heart failure
male sex

Risk factors for poor prognosis

Diabetes, especially in the presence of

Exacerbation of COPD
Antibiotics within the previous month
Pneumonia
Heart failure
Hospitalisation
Current use of glucocorticoids or diabetic medication

Age >80 years, and

Diabetes (especially insulin dependent diabetes)^[rx]
Exacerbation of COPD^[rx]^,^[rx]
≥2 courses oral steroids in previous year^[rx]
Recent antibiotic use^[rx]
Housebound^[rx] (Socioeconomic factors had little additive influence on outcomes)^[rx]
Smoking
Male sex
Aged 21–40 years

Modified CRB-65 score^[rx]

1 point for each of the following

Age >65 years
Presence of new onset pneumonia-associated mental confusion
Hypotension with systolic blood pressure <90 mmHg
Respiratory rate >30/minute

Symptoms

Symptoms of a URI may include

Runny nose, nasal congestion, sneezing, cough and sputum production (these are considered the most common symptoms)
Fever
Fatigue
A headache
Pain during swallowing
Wheezing
congestion, either in the nasal sinuses or lungs
a runny nose
a cough
a sore throat
body aches
fatigue
a fever over 103˚ F (39˚ C) and chills
difficulty breathing
dizziness
loss of consciousness

Acute upper respiratory tract infections include rhinitis, pharyngitis, tonsillitis, and laryngitis. Symptoms of URTIs commonly include

Cough
Sore throat
Runny nose
Nasal congestion
Headache
Low-grade fever
Facial pressure
Sneezing
Malaise
Myalgias

The onset of symptoms usually begins one to three days after exposure and lasts 7–10 days, and can persist up to 3 weeks.

Diagnosis

If your child has a complicated respiratory infection, the doctor may perform one or more of these tests:

Blood tests. These tests are performed to see if bacteria are in the blood.
Imaging tests. A chest X-ray or computed tomography (CT) scan may be performed to check for infections in the chest, lungs, orbits or sinuses.
Throat or nasal swab. This test takes a sample of cells and mucus from the nose, throat or tonsils to find the cause of the infection.

Differential Diagnosis

Common Cold
Allergic rhinitis
Sinusitis
Tracheobronchitis
Pneumonia
Influenza
Atypical Pneumonia
Pertussis
Epiglottitis
Streptococcal Pharyngitis/Tonsillitis
Infectious Mononucleosis

Treatment

In most cases, people with URIs know what they have and are visiting the doctor to find symptom relief. Most diagnoses can be made using medical history and a physical exam. If needed, tests like throat swabs, X-rays or CT scans might be used for a diagnosis.

URI treatments include:

Cough suppressants
Expectorants
Vitamin C or zinc
Nasal decongestants
Steam inhalation and gargling with salt water
Analgesics like acetaminophen and NSAIDs can help with fever, aches and pains
Treatment of the symptoms of upper respiratory infection is usually continued until the infection has resolved.

The 2008 National Institute for Clinical Excellence (NICE) guidelines recommend no antibiotics or delayed antibiotics for most patients with RTI .^[rx]

NICE guidance on antibiotic prescribing for self-limiting respiratory tract infections in primary care^[rx]

Prescribe antibiotics for immediate use and/or arrange further appropriate investigation and management for the following patients:

Those who are systemically very unwell
Those with symptoms and signs suggesting serious illness and/or complications (particularly pneumonia, mastoiditis, peritonsillar abscess, peritonsillar cellulitis, intraorbital and intracranial complications)
Those at high risk of serious complications because of pre-existing comorbidity (including patients with heart, lung, renal, liver, or neuromuscular disease, immunosuppression, or cystic fibrosis, and young children who were born prematurely)

Those who are

>65 years with acute cough and two or more of the following criteria, or
>80 years with one or more of the following criteria
- Admission to hospital in previous year
- Diabetes (type 1 or type 2)
- History of congestive heart failure
- Current use of glucocorticoids

Consider prescribing antibiotics for immediate use in the following situations

Bilateral acute otitis media in children under 2 years
Acute otitis media in children with otorrhoea
Acute sore throat or acute tonsillitis when ≥3 Centor criteria are present
For all others adults and children (over 3 months) with acute otitis media, acute sore throat (or tonsillitis), common cold, acute rhinosinusitis, acute cough, or acute bronchitis, a non-prescribing or delayed-prescribing approach should be adopted.
Explore the patient’s concerns and expectations, and consider these when discussing management options.
Advise on the usual course of the illness and the average total illness duration.
Advise patients how to manage symptoms, including fever.
Provide advice and when to re-consult and /or use a delayed prescription.

Treatment

Amoxicillin 500 mg (children: 15mg/kg; maximum 500mg) orally every 8 hours for 5 days

doxycycline 100 mg (children >8 years: 2mg/kg; maximum 100 mg) orally every 12 hours for 5 days (contraindicated during pregnancy)

sulfamethoxazole 800mg + trimethoprim 160mg (children: 20mg/kg + 4mg/kg; maximum 800mg + 160 mg) orally every 12 hours for 5 days.

Cefalosporins and fluoroquinolones are not recommended for bronchitis.

Acute exacerbations of chronic bronchitis

Acute exacerbations of chronic bronchitis are often due to viral infection and do not require treatment with antimicrobials. Antimicrobial treatment should, however, be considered in patients with increasing cough, dyspnoea and increased production and purulence of sputum. The most common causative organisms are H. influenzae, Moraxella catarrhalis and S. pneumoniae.

Doses refer to adults, as this condition is rarely found in children.

Amoxicillin 500 mg orally every 8 hours for 5 days

amoxicillin 500mg + clavulanic acid orally every 8 hours for 5 days

sulfamethoxazole 800mg + trimethoprim 160 mg orally every 12 – 24 hours for 5 days.

Chronic purulent bronchial infection and chronic airway disease are predominantly diseases of adults. Chronic suppurative lung disease in children (e.g. bronchiectasis) may occasionally require treatment with amoxicillin (30mg/kg (maximum 1g) orally every 8 hours for 5 days) or chloramphenicol (25mg/kg (maximum 1g) i.v. or i.m. every 6 hours for 5 days). Cystic fibrosis infections require specialist clinical management and laboratory services.

Acetaminophen – Read all cold medicine package labels. Do not take more than one drug that contains acetaminophen. Taking too much acetaminophen can damage your liver. Acetaminophen doses should not exceed 4 grams per day. Individuals with liver damage or liver problems should not exceed 2 grams of acetaminophen per day.
Antibiotics – are sometimes used to treat upper respiratory infections if a bacterial infection is suspected or diagnosed. These conditions may include strep throat, bacterial sinusitis, or epiglottitis. Antivirals may occasionally be recommended by doctors in patients who are immunocompromised (poor immune system). The treating doctor can determine which antibiotic would be the best option for a particular infection.
Nonsteroidal anti-inflammatory drugs – such as ibuprofen (Motrin, Advil) can be used for body aches and fever.
Antihistamines – such as diphenhydramine (Benadryl) are helpful in decreasing nasal secretions and congestions.
Nasal ipratropium – (topical) can be used to diminish nasal secretions.
Cough medications – (antitussives) can be used to reduce a cough. Many cough medications are commercially available such as dextromethorphan, guaifenesin (Robitussin), and codeine all have shown benefits in reducing cough in upper respiratory infections.
Target likely organisms with first-line drugs – Amoxicillin, Amoxicillin/Clavulanate
Use shortest effective course – Should see improvement in 2–3 days. Continue treatment for 7 days after symptoms improve or resolve (usually a 10–14-day course).
Honey – can be used in reducing cough.
Steroids – such as dexamethasone and prednisone orally are sometimes used to reduce inflammation of the airway passage and decrease swelling and congestion.
Decongestants – such as pseudoephedrine oral, phenylephrine can be used to reduce nasal congestion (generally not recommended in children less than 2 years of age and not recommended for individuals with high blood pressure).
Oxymetazoline – nasal solution is a decongestant, but should only be used for short-term.
Combination medications containing many of these components are also widely available over the counter.

To ease the discomfort from specific cold and flu symptoms, consider using the following types of OTC medicines

To reduce fever and pain — analgesics- Acetaminophen is generally preferred. Ibuprofen or naproxen is also commonly used. Aspirin should be avoided due to its risk of developing Reye’s syndrome. (Reye’s syndrome is a condition that affects all body organs and is most harmful to the brain and liver.)
To dry out the nose — antihistamines – Try an antihistamine, such as diphenhydramine. Because these products can make you sleepy, avoid driving and other complex tasks while taking these medicines. Loratadine available is a non-drowsy alternative, but may not be as effective as other antihistamines for reducing cold and flu symptoms.
To relieve a stuffy, clogged nose — decongestants – Try an oral decongestant, such as pseudoephedrine. However, insomnia, nervousness, and irritability can occur when taking these drugs. Those who are pregnant or have uncontrolled high blood pressure should avoid pseudoephedrine products. Often decongestants are combined with other drugs (especially antihistamines) in OTC medicines. A “-D” at the end of a medicine’s name means it includes an oral decongestant.
To relieve a runny nose or sinus pressure — nasal steroids- Medications like fluticasone available without a prescription) or mometasone; prescription needed) can relieve symptoms. These medicines are also used for seasonal allergies. These are not the same as or other OTC nasal preparations. Antihistamines will also help.
To make blowing your nose easier or loosening cough/mucus production — expectorants: Try guaifenesin . These products help thin the thick, discolored drainage coming out of the nose and mouth.
To reduce coughing — antitussives – Dextromethorphan can help suppress cough.
To relieve a sore throat – Try throat lozenges or gargle with warm salt water a few times a day. Analgesics are also helpful.
Oral zinc supplementation – has been used in recent years to shorten the duration and reduce the severity of symptoms of upper respiratory infection and common cold. This therapy has been studied in children with upper respiratory infection and the results are mixed. The FDA has not approved the use of oral zinc to treat the common cold or upper respiratory infections. There are reports of nausea and unpleasant taste caused by oral zinc.
Topical nasal zinc products – has been also used to attenuate the symptoms of upper respiratory infection. Some studies suggest loss of the sense of smell associated with the use of this over the counter product.
The use of oral vitamin C – is thought to shorten the duration of upper respiratory infection symptoms, but research data are inconclusive regarding the benefits of vitamin C.

Complications of a Respiratory Infection may include

Empyema – Empyema is a collection of pus beside the lungs, caused by a bacterial infection that can lead to life-threatening problems such as sepsis (bacteria in the blood) and shock. Symptoms include fever, cough, shortness of breath and chest pain.
Lung abscess – A lung abscess is a pus-filled cavity in the lung surrounded by inflamed tissue. It is usually caused by a severe infection such as pneumonia or tuberculosis or from inhaling material into the lungs from the mouth.
Potts puffy tumor – This is an uncommon complication of sinusitis (a type of upper respiratory tract infection that causes inflammation of the sinus cavities in the skull). It is an abscess of the forehead area with frontal swelling. Potts puffy tumor is usually seen in late childhood or adolescence. Symptoms include red, tender swelling in the mid-forehead, headache and fever.
Orbital cellulitis – Orbital cellulitis is another possible complication of sinusitis. This is an infection of the tissue within the eye socket and around the eye. Symptoms include pain, swelling, red eye, fever, a bulging eye, impaired vision and impaired eye movements.
Orbital abscess = Also a further complication of sinusitis causing orbital cellulitis, orbital abscess is a collection of bacteria and pus behind the eye. Symptoms include eye pain, bulging of the eye, redness of the eye, changes in vision and fever.
Mastoiditis – Mastoiditis is a complication of otitis (a type of upper respiratory tract infection that causes inflammation and possible infection of the middle ear). This is a serious bacterial infection that affects the mastoid bone behind the ear. Symptoms may include ear pain, fever, headache, drainage from the infected ear, redness, swelling and tenderness in the affected ear.dentifying patients at risk of poor prognosis for developing pneumonia^[rx]

Non-antibiotic management of RTIs

Beta-2 agonists for acute bronchitis (mainly oral agents): little evidence for routine use in acute bronchitis in primary care, but if there is evidence of airflow obstruction with the symptoms, some adults may derive some symptomatic benefit. Only two included studies were in children, and there was no evidence of benefit.^[rx]
Over-the-counter (OTC) medications for acute cough: review of antitussives, expectorants, mucloytics, antihistamine/decongestant combinations, other drug combinations and antihistamines concluded there was no good evidence for or against the effectiveness of OTC medications in children or adults, but that the few studies were mostly of poor design, with small sample sizes and that interventions and outcomes were so diverse that is was difficult to generalise the findings.^[rx] In 2008, the Commission on Human Medicines (CHM) advised about the unfavourable risk/benefit ratio of these medicines in children. The Medicines and Healthcare Regulatory Authority (MHRA) subsequently amended the product licence for cough medications for children due to safety concerns.^[rx] They should not be used by children under 6 years of age, and can only be purchased for children aged 6–12 years in a pharmacy. The MHRA have also recommended that certain combinations should be phased out (the combination of cough suppressant and expectorant).
Corticosteroids for sore throats: a systematic review and meta-analysis of eight trials involving 369 children and 374 adults found that despite heterogeneity, corticosteroids significantly reduced sore throat pain in addition to antibiotic therapy mainly in patients with severe or exudative sore throat.^[rx]
Vitamin C for preventing and treating pneumonia: review of five trials carried out in extraordinary conditions suggested there may be a benefit at both preventing and treating pneumonia, but possibly only in those with low plasma vitamin C levels.^[rx]
Vitamin C for preventing and treating the common cold: no benefit in the general population, but six trials which showed some evidence may reduce the risk of catching the common cold by half in individuals undergoing short periods of acute physical or cold stress or both (for example, marathon runners and soldiers training at sub-arctic conditions); poor study designs showed inconsistent results on effect of duration or severity of a cold.^[rx]
Vitamin A for preventing acute LRTIs in children up to 7 years of age: some evidence for benefit if poor nutritional status, but some studies actually found increased chances of infection or worsened symptoms.^[rx]
Echinacea for preventing and treating the common cold: some preparations based on Echinacea purpura might be effective, but no clear evidence of other preparation effectiveness or effectiveness in children.^[rx]
Garlic for the common cold: only one study was eligible for inclusion and showed that people taking garlic every day for 3 months had fewer colds than those taking placebo, but the duration of a cold was similar in both groups; there have been no trials examining whether taking garlic at the time of a cold reduces severity or duration.^[rx]
Chinese medicines for bronchitis, influenza, sore throats, and the common cold: no conclusion due to study design limitations and concerns over lack of safety data.^[rx]^–^[rx]
Increased fluids: no evidence for or against, although some evidence from some observational studies that may be harmful.^[rx]
Heated or humidified air for the common cold: in some studies this helped, in others it did not; no studies included children.^[rx]
Humidified air inhalation for treating croup: three small studies in emergency settings in a total of 135 patients with moderate to severe croup showed there did not appear to be any benefit, but there have been no studies in primary care.^[rx]
Non-steroidal anti-inflammatory drugs for the common cold: nine studies with 1064 patients showed improvement in most analgesia-related symptoms, but no clear evidence of improvement in runny noses or cough.^[rx]
Reviews of zinc and the homeopathic remedy, Oscillococcinum, have been withdrawn from the Cochrane database.

Modifying Antibiotic Prescribing

Antibiotics are more likely to be prescribed when patients expect them.^[rx]However, patients frequently consult when antibiotics are not their main expectation,^[rx] and clinicians are not able to discriminate well between those patients who expect and those who do not expect antibiotics.^[rx] Perception of patient pressure is a strong independent predictor of antibiotic prescribing.^,^[rx]^–^[rx] It is a major driver in prescribing antibiotics when faced with normal chest auscultation.
Consultations about RTIs are sometimes seen as an opportunity ‘catch-up’ and information-sharing can be inadequate.^[rx] Sharing information about the likely natural history of RTIs helps set realistic expectations about illness duration, which may reduce expectations (or perceived expectations) for antibiotics and reduce future consulting.^[rx]
RCTs of interventions incorporating shared decision making during consultations, including the use of an interactive booklet in the consultation,^[rx] demonstrated reductions in antibiotic prescribing without adversely effecting recovery or satisfaction with care.^[rx]

Delayed Prescriptions

A Cochrane review that included nine trials found that delayed prescribing can reduce antibiotic use for acute respiratory infections without harming patients. Delayed prescribing compared to immediate antibiotics was associated with reduced patient satisfaction in three trials, and no difference in two.
However, delayed antibiotics may have little advantage over not prescribing them at all where it appears safe to do so.^[rx] Nevertheless some clinicians find delayed antibiotics are easier to implement than refusing antibiotics altogether, and a time trend analysis of UK data suggested that delayed prescribing was responsible for a 10–15% reduction in antibiotic use by children between 1998 and 2003.^[rx]

Prevention and Treatment of Seasonal Influenza

Vaccination

Systematic reviews of the efficacy (ability of the vaccine to prevent confirmed influenza cases), effectiveness (ability of the vaccine to prevent influenza–like illness) and safety of vaccines are limited by lack of current, well-designed RCTs.^[rx]
A systematic review on the use of influenza vaccination for healthy children found evidence of efficacy in children older than 2 years but little evidence for children under 2, no comparisons of safety, and a marked difference between vaccine efficacy and effectiveness.^[rx]
If immunisation in children is to be recommended as a public health policy, large-scale studies assessing important outcomes and directly comparing vaccine types are urgently required. A similar review on the use of influenza vaccination for healthy adults found little support for use as a routine public health measure.^[rx] Even in older people, the effectiveness of influenza vaccination is modest in long-term care settings and less so in community- residing residents.^[rx]
Wash your hands regularly with soap and water to reduce exposure to secretions.
Avoid being in close contact with sick people.
Sanitize commonly-touched objects like remote controls, phones and doorknobs when anyone in the house may have a URI.
Cover your mouth and nose if you are sick.
Stay home if you are sick.

Anti-Virals Neuraminidase Inhibitors

The recent H1N1 influenza pandemic increased interest in neuraminadase inhibitors in preventing and treating influenza. It is unclear whether data from use in seasonal influenza is applicable to pandemic situations. Two recent systematic reviews, based on evidence from prophylaxis (four trials), treatment (12 trials), and post-exposure prophylaxis (four trials), both concluded that these drugs did not result in meaningful symptomatic improvement in seasonal influenza.^[rx]^,^[rx]
Whether oseltamivir reduces influenza-related LRTI complications remains unclear. The 2005 Cochrane systematic review concluded that it did.^[rx] However, the most recent Cochrane review withdrew this conclusion on the basis that none of the original studies had been powered to detect differences in severe adverse events, and the authors had been unable to obtain trial data on complications from eight of 10 trials from an originally included meta-analysis

References

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Category Archive Investments

Antioxidants are the key to healthy eating. Which foods pack the most nutrients?

Types of Antioxidants

Uric acid

Vitamin C

Glutathione

Important Benefits of Antioxidants Include

Antioxidants Foods

Nutrient antioxidants

Vitamin E

Vitamin C

Beta-carotene

Lycopene

Selenium (Se)

Flavonoids

Omega-3 and omega-6 fatty acids

Antioxidants Home Treatments

BLACKBERRIES

WALNUTS

STRAWBERRIES

ARTICHOKE HEARTS

CRANBERRIES

BREWED COFFEE

RASPBERRIES

PECANS

BLUEBERRIES

GROUND CLOVES

Kale

Spinach

Brussels Sprouts

Alfafa Sprouts

Broccoli Flowers

Beets

Red Bell Peppers

Onions

Corn

Eggplant

Lifestyle Changes to Maximize Your Antioxidant Intake.

References

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Pathophysiology

Types of Bradycardia

Causes of Bradycardia

Pathological causes of sinus bradycardia

Inherent Etiologies

Extrinsic Etiologies

Syndrome

Symptoms of Bradycardia

Diagnosis of Bradycardia

Treatment of Bradycardia

Antisialagogue

Anticholinergic Poisoning

Rapid Sequence Intubation (RSI) Pretreatment

Administration

Prevention

Prevent heart disease

Monitor and treat existing heart disease

Risk Factors

References

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Causes of Water Retention

Where water retention occurs

The Heart

The Kidneys

Other Causes of Swollen legs

Protein

Other factors

Medication-caused water retention

Premenstrual water retention

Symptoms of Water Retention

Diagnosis of Water Retention

Treatment of Water Retention

Non-medicine

Medicine of Water Retention

Home Remedies of Water Retention

Dandelion

Asparagus

Parsley

Caraway

Tea

Laboratory Tests
Examples of common tests include

0.75–0.95 mmol/L^[rx]

Potential clinical signs of magnesium deficiency^[rx]

Lab and ECG signs of magnesium deficiency^[rx]