Pediatrics

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An insulin pen is used to inject insulin for the treatment of diabetes. Insulin is a hormone produced by the pancreas. It is composed of an insulin cartridge (integrated or bought separately) and a dial to measure the dose, and is used with disposable pen needles to deliver the dose. It was introduced and marketed as Novopen by the Danish company Novo Nordisk in 1985.

Types of pens
A number of companies make insulin pens including Novo Nordisk, Aventis and Eli Lilly. These companies produce pens for most of their insulins, includingNovoLog/NovoRapid, Humalog, Levemir and Lantus. There are two pen systems: durable and prefilled:


A durable pen uses a replaceable insulin cartridge. When the insulin cartridge is empty, the empty cartridge is disposed of and a new one is inserted in the pen.



A prefilled pen is entirely disposable. The pen comes pre-filled with insulin, and when the insulin cartridge or reservoir is empty, the entire unit is discarded.

Most brands of insulin are now available for use in pens, these include:
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NovoLog, NovoRapid and Levemir by Novo Nordisk Lantus and Apidra by Sanofi-Aventis Humulin and Humalog by Eli Lilly and Company

Global Patient Uptake
Insulin pens are used by 95% of insulin-treated patients in Europe, Asia, and Scandinavia with excellent results.[1] They are currently underutilized but growing in use in the United States. Insulin pens offer several significant advantages over insulin syringes: ease of handling, accuracy, and they are more discreet to use. [edit]To
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use an insulin pen

Screw or click on a new pen needle If necessary, prime the pen to remove any air from the needle Turn the knob on the end of the pen (or "dial") to the number of units needed Insert the needle into the skin Press the button on the end of the pen to deliver the dose Count to five Remove

[edit]Advantages Insulin pens have a number of advantages:
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More convenient and easier to transport than traditional vial and syringe Repeatedly more accurate dosages Easier to use for those with visual or fine motor skills impairments Less injection pain (as polished and coated needles are not dulled by insertion into a vial of insulin before a second insertion into the skin)

It is important that proper injection sites on the body are used. A healthcare provider helps determine the best injection site for a patient. In general, recommended injection sites include the abdomen, parts of the buttocks and thigh areas.[2]

Disadvantages

Unlike with the traditional syringe, two different insulins cannot be mixed by the user in an insulin pen.[3] On the other hand, some of the newest types of insulin cannot be mixed at all. In addition, using pens and pen needles is usually more expensive than using the traditional vial and syringe method;insurance coverage for insulin pens in the United States may vary widely.

Accessories
Technology has not changed much since the launch of the first insulin pen over 25 years ago by Novo Nordisk.[4] A number of independent companies have created accessories to help people using insulin pens better manage their insulin intake. - Frio UK [5] offers a wallet to help keep insulin pens cool in warm temperatures. - Timesulin [6] is a 'smart cap' that works with all major insulin pen types to show users how long it's been since their insulin pen injection to help avoid missed or accidental double doses.

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a

severe accumulation of keto acids that the pHof the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need forrespiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct byproduct of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also smell, but the odor is usually more subtle due to lower concentrations of acetone.
Contents [hide]
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1 Pathophysiology 2 Etiology 3 See also 4 References 5 External links

[edit]Pathophysiology Ketoacidosis occurs when the body is producing large quantities of ketone bodies via the metabolism of fatty acids (ketosis) and the body is producing insufficient insulin to slow this production. The excess ketone bodies can significantly acidify the blood. The presence of a high concentration of glucose in the blood (hyperglycemia) caused by the lack of insulin can lead to further acidity. In healthy individuals this normally does not occur because the pancreasproduces insulin in response to rising ketone/blood glucose concentration. Acidity results from the dissociation of the H+ ion at physiological pH of metabolic ketone bodies such as acetoacetate, and β-hydroxybutyrate. Acetone has no easily liberated proton, and is thus non-acidic in human biochemical environments. [edit]Etiology Two common types are diabetic and alcoholic ketoacidosis. In diabetic patients, ketoacidosis is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Particularly in type 1 diabetics the

lack of insulin in the bloodstream prevents glucose absorption and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood. Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine (Osmotic diuresis), exacerbating the acidosis. In alcoholic ketoacidosis, alcohol causes dehydration and blocks the first step of gluconeogenesis[citation needed]. The body is unable to synthesize enough glucose to meet its needs, thus creating an energy crisis resulting in fatty acid metabolism, and ketone body formation. A mild acidosis may result from prolonged fasting or when following a ketogenic diet or a very low calorie diet.[3] [4] [edit]See

also

Insulin glargine, marketed by Sanofi-Aventis under the name Lantus, is a long-acting basal insulin analogue, given once daily to help control the blood sugar level of those with diabetes.

An insulin analog is an altered form of insulin, different from any occurring in nature, but still available to the human body for performing the same action as human insulin in terms of glycemic control. Through genetic engineering of the underlying DNA, the amino acid sequence of insulin can be changed to alter its ADME (absorption, distribution, metabolism, and excretion) characteristics. Officially, the U.S. Food and Drug Administration (FDA) refers to these as "insulin receptor ligands", although they are more commonly referred to as insulin analogs.

club foot, also called congenital talipes equinovarus (CTEV), is a congenital deformity involving one foot or both.[1] The affected foot looks like it has been rotated internally at the ankle. Without treatment, people with club feet often appear to walk on their ankles or on the sides of their feet. It is a relatively common birth defect, occurring in about one in every 1,000 live births. Approximately half of people with clubfoot have it affect both feet, which is called bilateral club foot. In most cases it is an isolateddysmelia (disorder of the limbs). It occurs in males twice as frequently as in females.

A condition of the same name appears in some animals, particularly horses.
Contents [hide]
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1 Classification 2 Causes 3 Etymology 4 Prenatal Screening 5 Treatment
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5.1 Non-surgical treatment and the Ponseti Method 5.2 Surgical treatment

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6 History 7 Famous people 8 In literature 9 In animals 10 References 11 External links

[edit]Classification TEV is classified into two groups, postural TEV and structural TEV. The deformities affecting joints of the foot occur at three joints of the foot to varying degrees. They are[1]
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inversion at subtalar joint, adduction at talonavicular joint, and equinus and varus at ankle joint, that is, a plantar flexed position, making the foot tend towards toe walking.[2]

[edit]Causes There are different causes for clubfoot depending on what classification it is given. Structural cTEV is caused by genetic factors such as Edwards syndrome, a genetic defect with three copies of chromosome 18. Growth arrests at roughly 9 weeks and compartment syndrome of the affected limb are also causes of structural cTEV. Genetic influences increase dramatically with family history. cTEV occurs with some frequency in Ehlers–

Danlos syndrome and some other connective tissue disorders, such as Loeys-Dietz syndrome. It was previously assumed that postural cTEV could be caused by external influences in the final trimester such as intrauterine compression fromoligohydramnios or from amniotic band syndrome. However, this is countered by findings that cTEV does not occur more frequently than usual when the intrauterine space is restricted.[3] Breech presentation is also another known cause.[citation needed] It may be associated with other birth defects, such as spina bifida cystica. [edit]Etymology The term talipes is from Latin talus, ankle + pes, foot. Equino-, of or resembling a horse and -varus, turned inward. A horse's hoof is a large toenail, and the horse's joint that points backwards resembles a human heel. Varus means that the part distal segment of a bone or joint slants toward the body mid-line.[4] [edit]Prenatal

Screening

Screening for club foot prenatally is a debatable topic. However, this is commonly done as it is easily identified using an ultrasound scan. Most fetuses undergo a 20 weeks gestation fetal abnormality scan[5] in which club foot is one of the abnormalities that can be picked up. Some doctors have argued that club foot may occasionally be associated with a syndromic disease and should therefore be screened. If no syndromic association is found prenatally, most fetuses with club foot are born and can live a normal life with medical treatment. [edit]Treatment

A Denis Browne brace. Various types of foot-abduction braces are used to hold the child's feet in the desired position.

As medicine evolved, club feet were treated with a complex surgical release, which had many complications. Then a novel idea of serial casting, different from that introduced in the past (such as the Kite method) was introduced by Ponseti with dramatic results. His results were from recognizing how the forefoot and hindfoot interact and lock into position relative to each other. This type of treatment is generally used today for idiopathic cases of clubfoot, while treatment of neuromuscular causes (such as cerebral palsy) differ. Clubfoot is treated with manipulation by podiatrists, physiotherapists, orthopedic surgeons, specialist Ponseti nurses, ororthotists by serial casting and then providing braces to hold the feet in a plantigrade position. After serial casting, bracing using a Denis Browne bar with straight last boots, ankle foot orthoses and/or custom foot orthoses (CFO) may be used. In North America, manipulation is followed by serial casting, most often by the Ponseti Method. Foot manipulations usually begin within two weeks of birth. Even with successful treatment, when only one side is affected, that foot may be smaller than the other, and often that calf, as well. Extensive surgery of the soft tissue or bone is not usually necessary to treat clubfoot; however, there are two minimal surgeries that may be required: 1. Tenotomy (needed in 80% of cases) is a release (clipping) of the Achilles tendon – minor surgery – local anesthesia 2. Anterior Tibial Tendon Transfer (needed in 20% of cases) – where the tendon is moved from the first ray (toe) to the third ray in order to release the inward traction on the foot. Each case is different, but in most cases extensive surgery is not needed to treat clubfoot. Extensive surgery may lead to scar tissue developing inside the child's foot. The scarring may result in functional, growth and aesthetic problems in the foot because the scarred tissue will interfere with the normal development of the appendage. A child who has extensive surgery may require on average two additional surgeries to correct the issues presented above. In stretching and casting therapy the doctor changes the cast multiple times over a few weeks, gradually stretching tendons until the foot is in the correct position of external rotation. The heel cord is released (percutaneous tenotomy) and another cast is put on, which is removed after three weeks. To avoid relapse a corrective brace is worn for a gradually reducing time until it is only at night up to four years of age. [edit]Non-surgical

treatment and the Ponseti Method

Main article: Ponseti Method

Treatment for clubfoot should begin almost immediately to have the best chance for a successful outcome without the need for surgery. Over the past 10 to 15 years, more and more success has been achieved in correcting clubfeet without the need for surgery. The clubfoot treatment method that is becoming the standard in the U.S. and worldwide is known as the Ponseti Method.[6] Foot manipulations differ subtly from the Kite casting method which prevailed during the late 20th century. Although described by Dr. Ignacio Ponseti in the 1950s, it did not reach a wider audience until it was re-popularized around 2000 by Dr. John Herzenberg in the USA and in Europe and Africa by NHS surgeon Steve Mannion while working in Africa. Parents of children with clubfeet using the Internet also helped the Ponseti gain wider attention. The Ponseti method, if correctly done, is successful in >95% of cases[7] in correcting clubfeet using non- or minimal-surgical techniques. Typical clubfoot cases usually require 5 casts over 4 weeks. Atypical clubfeet and complex clubfeet may require a larger number of casts. Approximately 80% of infants require an Achilles tenotomy (microscopic incision in the tendon requiring only local anesthetic and no stitches) performed in a clinic toward the end of the serial casting. Throughout the past decade, physicians at Texas Scottish Rite Hospital for Children have been studying the effectiveness of both the Ponseti casting method and the French functional (physical therapy) method of stretching, massaging and taping and comparing the results with patients who have undergone surgery. Results of these studies have been presented at national and international conferences, such as the Pediatric Orthopaedic Society of North America annual meeting, the International Clubfoot Symposium, Brandon Carrell Visiting Professorship and the American Academy of Orthopaedic Surgeons annual meeting, and have been published in the Journal of Pediatric Orthopaedics. [8] After correction has been achieved, maintenance of correction may require the full-time (23 hours per day) use of a splint—also known as a foot abduction brace (FAB)—on both feet, regardless of whether the TEV is on one side or both, for several weeks after treatment. Part-time use of a brace (generally at night, usually 12 hours per day) is frequently prescribed for up to 4 years. Without the parents' participation, the clubfoot will almost certainly recur, because the muscles around the foot can pull it back into the abnormal position. Approximately 20% of infants successfully treated with the Ponseti casting method may require a surgical tendon transfer after two years of age. While this requires a general anesthetic, it is a relatively minor surgery that corrects a persistent muscle imbalance while avoiding disturbance to the joints of the foot. The developer of the Ponseti Method, Dr Ignacio Ponseti, was still treating children with clubfeet (including complex/atypical clubfeet and failed treatment clubfeet) at the University of Iowa Hospitals and Clinics well into his 90s. He was assisted by Dr Jose Morcuende, president of the Ponseti International Association.

The long-term outlook[9] for children who experienced the Ponseti Method treatment is comparable to that of non-affected children.[10] Botox is also being used as an alternative to surgery. Botox is the trade name for Botulinum Toxin type A. a chemical that acts on the nerves that control the muscle. It causes some paralysis(weakening) of the muscle by preventing muscle contractions (tightening). As part of the treatment for clubfoot, Botox is injected into the child’s calf muscle. In about 1 week the Botox weakens the Achilles tendon. This allows the foot to be turned into a normal position, over a period of 4–6 weeks, without surgery. The weakness from a Botox injection usually lasts from 3–6 months. (Unlike surgery it has no lasting effect). Most club feet can be corrected with just one Botox injection. It is possible to do another if it is needed. There is no scar or lasting damage. [11] [edit]Surgical

treatment
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December
2009)

On occasion, stretching, casting and bracing are not enough to correct a baby's clubfoot. Surgery may be needed to adjust the tendons, ligaments and joints in the foot/ankle. Usually done at 9 to 12 months of age; surgery usually corrects all clubfoot deformities at the same time. After surgery, a cast holds the clubfoot still while it heals. It is still possible for the muscles in the child's foot to try to return to the clubfoot position, and special shoes or braces will likely be used for up to a year or more after surgery. Surgery will likely result in a stiffer foot than nonsurgical treatment, particularly over time. Without any treatment, a child's clubfoot will result in severe functional disability, however with treatment, the child should have a nearly normal foot. He or she can run and play without pain and wear normal shoes. The corrected clubfoot will still not be perfect, however; a clubfoot usually stays 1 to 1½ sizes smaller and somewhat less mobile than a normal foot. The calf muscles in a leg with a clubfoot will also stay smaller. Long-term studies of adults with post-club feet, especially those with substantial numbers of surgeries, may not fare as well in the long term, according to Dobbs, et al., [12] A percentage of adults may require additional surgeries as they age, though there is some dispute as to the effectiveness of such surgeries, in light of the prevalence of scar tissue present from earlier surgeries.

In some cases the leg stops developing earlier than the healthy leg and a substantial length difference may occour. In come cases a leg lengthening will be necessary, most commonly by use of the Ilizarov method. [edit]History Treatment of clubfoot is evident as early as Egyptian paintings. In early days, the foot was manipulated with a Thomas wrench and casting which caused fracture of several bones in the foot. [edit]Famous

people

The club-foot, by José de Ribera, in fact, ahemiplegia[13]

Many notable people have been born with one or both feet in "clubbed" condition, including Roman emperor Claudius, statesman Prince Talleyrand, 19th century American politician Thaddeus Stevens, comedian Damon Wayans, actor Gary Burghoff, and Eric The Midget from The Howard Stern Show, football players Steven Gerrard and Miguel Riffo, sledge hockey player Matt Lloyd, a Paralympian, mathematician Ben Greenberg, and filmmaker Jennifer Lynch. The British Romantic poet George Gordon, Lord Byron had a clubfoot, which caused him much humiliation.

Comedian, musician, and actor Dudley Moore was born with a club foot. This was mostly unknown to the public as he wore one shoe with a slightly bigger sole to compensate when walking. NFL Cornerback Charles Woodson was born with severely clubbed feet and went on to win the Heisman Award at the University of Michigan, played in Super Bowl XXXVII with theOakland Raiders and won Super Bowl XLV with the Green Bay Packers. The figure-skater Kristi Yamaguchi was born with a clubfoot, and went on to win gold medals at both the 1992 Winter Olympics and World Championships. The soccer star Mia Hamm was born with the condition and won Gold twice with team USA in the 1996 Olympics and in the 2004 Olympics. Baseball pitcher Larry Sherry, the 1959 World Series MVP, was born with club feet,[14] as was pitcher Jim Mecir, and both enjoyed long and successful careers. In fact, it was suggested in the book Moneyball that Mecir's club foot contributed to his success on the mound; it caused him to adopt a strange delivery that "put an especially violent spin" on his screwball, his specialty pitch. The San Francisco Giants held the record as the team with the all-time highest number of players with clubbed feet as of July 2010, and Freddy Sanchez, one of its infielders, cites his ability to overcome the defect as a reason for his success.[15] Tom Dempsey of the New Orleans Saints, born with a right club foot and no toes (this was his kicking foot), kicked an NFL record 63-yard (58 m) field goal. This kick became famous as the longest NFL field goal in history. Former NFL quarterback Troy Aikman beat being born with a clubfoot to enjoy a productive Hall of Fame career with 3 Super Bowl Rings in Super Bowl XXVII, Super Bowl XXVIII, and Super Bowl XXX.[16] Despite a club foot, Michael Houser, goaltender for the London Knights of the Ontario Hockey League, won the Red Tilson Trophy as the most oustanding player in the OHL in 2011-2012. He was signed by the National Hockey League's Florida Panthers in July, 2012.[17] The Nazi Propaganda Minister Joseph Goebbels had a deformity caused by a botched operation for the bacterial infection osteomyelitis, which some mistook for clubfoot.[18] De Witt Clinton Fort, who served in the Confederate Army as a captain, was born with a clubfoot, and he was known during the American Civil War as Captain "Clubfoot" Fort, C.S.A. Egyptian pharaoh Tutankhamun had a club foot and a cleft palate, and it is likely that he needed a cane to walk.[1
If your child has been diagnosed with a club foot, you’ll have concerns and questions about his health, treatment, recovery and other issues. It may comfort you to know that Children’s Hospital Boston is a world leader in pediatric orthopedics, and we have a wealth of experience treating children with this fairly common and highly treatable condition.

What to know about club foot Club foot (also known as talipes equinovarus) is a congenital (present at birth) foot deformity. It affects the bones, muscles, tendons and blood vessels and can be present in one or both feet. In club foot, the heel points downward, while the front half of the foot turns inward. The calf muscles on the affected side are smaller than on the normal side; the leg on the affected side is slightly shorter than on the other side. The foot itself is usually short and wide, and the heel cord (Achilles
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tendon) is tight. The condition is fairly common, occurring in about one of every 1,000 newborns. It affects boys twice as often as girls. Fifty percent of club foot cases affect both feet (bilateral). A club foot is visible at birth, and is often detected by fetal ultrasound before birth. The “Ponseti”method—manipulating the foot into correct position without joint surgery—is the standard treatment, and usually begins shortly a baby is born. The method involves: a two to three-month regimen of stretching and casting surgery (tenotomy) to release and lengthen the Achilles tendon several years of bracing Twenty to 30 percent of kids need additional interventions later on in childhood for tendon tightness or to prevent recurrence of the condition. Most instances of club foot are idiopathic (no apparent cause). A club foot that occurs with some genetic syndromes and birth defects—such as Edwards syndrome (trisomy 18) or spina bifida (myelodysplasia)—can be more fixed, rigid and difficult to treat. Most children who are properly treated for club foot can run, play and live active lives, even though technically their foot and leg remain mildly abnormal. How Boston Children's Hospital approaches club foot The goal of treatment for club foot is to correct the position of the foot, so that the bones grow normally. Children's doctors take conservative, non-surgical approaches whenever possible, and we have excellent success rates. If a newborn needs surgery, we try to avoid using general anesthesia, which does pose some risk to infants. Compared with many other institutions, we offer an especially strong and supportive bracing program. We also have an exceptional prenatal counseling program to help parents anticipate and plan for their baby’s care after birth. At Children’s, we recognize the burden of a bracing regimen, which is absolutely necessary to successfully treat club foot, but which places stress on both the child and the family, particularly after a child reaches 2 years old. That’s why we’re initiating a research study to try to predict which children are less likely to have problems with their feet after they’re 2, so that they could reduce or discontinue their bracing programs. One of the first programs.Our Orthopedic Center is one of the world’s first comprehensive pediatric orthopedic programs, and today is the largest pediatric orthopedic surgery center in the United States, performing more than 5,000 procedures each year. Our program, consistently ranked among the top three in the country by U.S.News & World Report, is the nation’s preeminent care center for children and young adults with developmental, congenital, post-traumatic and neuromuscular problems of the musculoskeletal system.

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