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BERIBERI DISEASE: SYMPTONS, DIAGNOSIS, TREATMENT

What is a Beriberi Disease?

Thiamine deficiency, or beriberi, refers to the lack of thiamine pyrophosphate, the active form of the vitamin known as thiamine (also spelled thiamin), or vitamin B-1. Thiamine pyrophosphate, the biologically active form of thiamine, acts as a coenzyme in carbohydrate metabolism through the decarboxylation of alpha ketoacids; it also takes part in the formation of glucose by acting as a coenzyme for the transketolase in the pentose monophosphate pathway. Persons may become deficient in thiamine either by not ingesting enough vitamin B-1 through the diet or by excess use, which may occur in hyperthyroidism, pregnancy, lactation, or fever. Prolonged diarrhea may impair the body's ability to absorb vitamin B-1, and severe liver disease impairs its use.


Thiamine is a water-soluble vitamin that is absorbed in the jejunum by 2 processes. When the thiamine level in the small intestines is low, an active transport portal is responsible for absorption. When the thiamine concentration is high, a passive mucosal process takes place. Up to 5 mg of thiamine is absorbed through the small intestines. The small intestine is where phosphorylation of thiamine takes place.



The body cannot produce thiamine and can only store up to 30 mg of thiamine in its tissues. Thiamine is mostly concentrated in the skeletal muscles. Other organs that it is found in are the brain, heart, liver, and kidneys. The half-life of thiamine is 9-18 days. It is excreted by the kidney.



Causes
There are two major types of beriberi:


Wet beriberi affects the cardiovascular system.


Dry beriberi and Wernicke-Korsakoff syndrome affect the nervous system.


Beriberi is rare in the United States because most foods are now vitamin-enriched. If you eat a normal, healthy diet you should get enough thiamine. Today, beriberi occurs mostly in patients who abuse alcohol. 


Drinking heavily can lead to poor nutrition, and excess alcohol makes it harder for the body to absorb and store thiamine.


A rare condition known as genetic beriberi is inherited (passed down through families). People with genetic beriberi lose the ability to absorb thiamine from foods. This can happen slowly over time and symptoms occur when the person is an adult. However, because doctors may not consider beriberi in non-alcoholics, this diagnosis is often missed.


Beriberi can occur in breast-fed infants when the mother's body is lacking in thiamine. The condition can also affect infants who are fed unusual formulas that don't have enough thiamine.
Getting dialysis and taking high doses of diuretics raise your risk of beriberi.




Symptoms

Symptoms of dry beriberi include:
  • Difficulty walking
  • Loss of feeling (sensation) in hands and feet
  • Loss of muscle function or paralysis of the lower legs
  • Mental confusion/speech difficulties
  • Pain
  • Strange eye movements (nystagmus)
  • Tingling
  • Vomiting
Symptoms of wet beriberi include:
  • Awakening at night short of breath
  • Increased heart rate
  • Shortness of breath with activity
  • Swelling of the lower legs


Exams and Tests

A physical examination may show signs of congestive heart failure, including:
  • Difficulty breathing with neck veins that stick out
  • Enlarged heart
  • Fluid in the lungs
  • Rapid heartbeat
  • Swelling in both lower legs
A person with late-stage beriberi may be confused or have memory loss and delusions. The person may be less able to sense vibrations.
A neurological exam may show signs of:
  • Changes in the walk
  • Coordination problems
  • Decreased reflexes
  • Drooping of the eyelids
The following tests may be done:
  • Blood tests to measure the amount of thiamine in the blood
  • Urine tests to see if thiamine is passing through the urine


Treatment

The goal of treatment is to replace the thiamine your body is lacking. This is done with thiamine supplements. Thiamine supplements are given through a shot (injection) or taken by mouth.
Other types of vitamins may also be recommended.
Blood tests may be done after you are given thiamine supplements to see how well you are responding to the medicine.

Outlook (Prognosis)

Untreated, beriberi is often deadly. With treatment, symptoms usually improve quickly.
Heart damage is usually reversible, and a full recovery is expected. However, if acute heart failure has already occurred, the outlook is poor.
Nervous system damage is also reversible, if caught early. If it is not caught early, some symptoms (such as memory loss) may remain even with treatment.
If a patient with Wernicke's encephalopathy receives thiamine replacement, language problems, unusual eye movements, and walking difficulties may go away. However, Korsakoff syndrome (or Korsakoff psychosis) tends to develop as Wernicke's symptoms go away.

Possible Complications

  • Coma
  • Congestive heart failure
  • Death
  • Psychosis

When to Contact a Medical Professional

Beriberi is extremely rare in the United States. However, if you feel your family's diet is inadequate or poorly balanced, and you or your children have any symptoms of beriberi, call your health care provider.

Prevention

Eating a proper diet that is rich in thiamine and other vitamins will prevent beriberi. Nursing mothers should make sure that their diet contains all vitamins and be sure that infant formulas contain thiamine.
People who drink heavily should try to cut down or quit, and take B vitamins to make sure their body is properly absorbing and storing thiamine.

STEVENS JOHNSON SYNDROME SYMPTOMS AND TREATMENT


What is Stevens Johnson Syndrome?

Stevens-Johnson Syndrome is a potentially deadly skin disease that usually results from a drug reaction. Another form of the disease is called Toxic Epidermal Necrolysis, and again this usually results from a drug-related reaction. Both forms of the disease can be deadly as well as very painful and distressing. In most cases, these disorders are caused by a reaction to a drug, and one drug that has come under fire lately is the cox-2 inhibitor Bextra, which is already linked to these disorders.

There are other drugs that have been linked to Stevens-Johnson Syndrome, and these include some other NSAIDS (non-steroid anti-inflammatory drugs), Allopurinol, Phenytoin, Carbamazepine, barbiturates, anticonvulsants, and sulfa antibiotics. The condition can sometimes – although not very often – be attributed to a bacterial infection, and in some cases there is no known cause for the onset of Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. However, the most common cause is through drug related reaction.

Stevens-Johnson Syndrome can affect any age group. However, it occurs most commonly in older people, and this could be because older people tend to use more of the drugs associated with the disease and are therefore collectively more at risk from the disease. People that have AIDS are also at an increased risk of contracting Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. Those in the higher risk groups are urged to remain vigilant for any signs of these skin diseases, and are also advised to remain well informed about the symptoms that could indicate the presence or onset of Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis.

The symptoms :

Both Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis can start with non-specific symptoms such as cough, aching, headaches, and feverishness. This may be followed by a red rash across the face and the trunk of the body, which can continue to spread to other parts of the body. The rash can form into blisters, and these blisters can form in areas such as the eyes, mouth and vaginal area. The mucous membranes can become inflamed, and with Toxic Epidermal Necrolysis layers of the skin can also come away with ease and often the skin peels away in sheets. The hair and nails can also come away in some cases, and sufferers can become cold and feverish.

With Toxic Epidermal Necrolysis the most common cause of death is infection, which can enter through the exposed areas. This disease can leave the skin looking as though it has been burned, and areas where skin has flayed away can seep copiously and quickly become infected.

Treating these diseases:

Those suffering from SJS or TEN are treated in hospital, and if the cause of the problem is drug related then the drugs are stopped with immediate effect. Surviving patients are treated intravenously to replace any lost fluids, and the skin is left to re-grow on its own. However, the chances of survival can be hit and miss depending on the level of damage and the degree of infection incurred by the patient.

It is vital that those taking drugs that could result in these skin diseases are vigilant and can identify the danger signs associated with these problems. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis can be deadly, and the earlier the symptoms are recognised the faster treatment can be initiated.

Of course, those affected by drugs in this way – or the families of those that have passed away from these skin problems – have every right to file for compensation against the manufacturer of the drug in question. Lawyers now specialize in this type of litigation, and those that feel as though they have grounds for compensation are advised to go through an experienced drugs litigation lawyer.

Stevens-Johnson syndrome is an immune-complex–mediated hypersensitivity disorder that may be caused by many drugs, viral infections, and malignancies. Cocaine recently has been added to the list of drugs capable of producing the syndrome. Additionally, the antidepressant mirtazapine and tumor necrosis factor (TNF) – alpha antagonists infliximab, etanercept, and adalimumab have been reported as causes. In up to half of cases, no specific etiology has been identified.

Although not currently relevant to the practice of emergency medicine, research into the pathophysiology of SJS/TEN may soon allow for the development of tests to aid in the diagnosis as well as to identify those at risk.

Pathologically, cell death results causing separation of the epidermis from the dermis. The death receptor, Fas, and its ligand, FasL, have been linked to the process, as has TNF-alpha. Researchers have found increased soluble FasL levels in the sera of patients with SJS/TEN before skin detachment or inset of mucosal lesions.

Others have also linked inflammatory cytokines to the pathogenesis.

A "killer effector molecule" has been identified that may play a role in the activation of cytotoxic lymphocytes.

There is also strong evidence for a genetic predisposition to severe cutaneous adverse drug reactions such as SJS. The US FDA and Health Canada advise screening for a human leukocyte antigen, HLA-B*1502, in patients of southeastern Asian ethnicity before starting treatment with carbamazepine. (The risk is much lower in other ethnic populations, making screening impractical in them). Another HLA antigen, HLA-B*5801, confers a risk of allopurinol-related reactions. Pretreatment screening is not readily available.

NOSEBLEEDING FIRST AID TREATMENT

What is the first aid treatment of nosebleed?

Self-Care at Home

A small amount of bleeding from a nosebleed requires little intervention. A common scenario is when a person with a cold or asinus infection blows his or her nose vigorously and notices some blood in the tissue. Avoiding any more vigorous nose blowing, sneezing, or nose picking is usually enough to keep the bleeding from getting worse.

How to stop a nosebleed

  • Remain calm.
  • Sit up straight.
  • Lean your head forward. Tilting your head back will only cause you to swallow the blood.
  • Pinch the nostrils together with your thumb and index finger for 10 minutes. Have someone time you to make sure you do not release the nostrils any earlier.
  • Spit out any blood in your mouth. Swallowing it may make you vomit.

What to do after the bleeding has stopped

  • Once the bleeding has stopped, try to prevent any irritation to the nose, such as sneezing or nose blowing, for 24 hours.
  • Ice packs do not help.
  • Exposure to dry air, such as in a heated home in the winter, can contribute to the problem. Adding moisture to the air with a humidifier or vaporizer will help keep the nose from drying out and triggering more bleeding. Another option is to place a pan filled with water near a heat source, such as a radiator, which allows the water to evaporate and adds moisture to the air.

Medical Treatment

Anterior nosebleed
A minor nosebleed that has stopped may require no treatment at all. Frequently, the body will form a clot at the site of the bleeding that stops any further bleeding.

If the source of the bleeding is a blood vessel that is easily seen, a doctor may cauterize it (seal the blood vessel) with a chemical called silver nitrate. Cauterization is most effective when the bleeding is coming from the very front part of the nose.

In more complicated cases, a nasal packing may be required to stop the bleeding. The idea behind this is to put pressure from inside the nostril to halt the bleeding. Many different types of packings are available, ranging from petroleum (Vaseline) gauze to balloon packs to synthetic sponge packs that expand when moistened. The decision as to which one to use is usually made by the doctor.

Most people who receive an anterior nasal packing go home with it in place. Because these packings block the drainage pathways of the sinuses, antibiotics may be started to prevent a sinus infection. The packing is usually left in for 24-72 hours.

Posterior nosebleed
A posterior nosebleed that does not stop bleeding on its own requires admission to the hospital. A posterior nasal packing is required. Different types of packings are available, though a balloon pack is most commonly used.

Unlike the anterior nasal packings, posterior nasal packings are very uncomfortable and frequently require sedatives and pain medications. Complications can be associated with these packs, including infection and blockage of the breathing passages. Patients with other medical conditions, such as heart disease, must be monitored closely. Admission to the hospital and close monitoring are required.
Posterior packings are usually left in place for 48-72 hours. If this does not stop the bleeding, surgical procedures can be performed by an ear, nose, and throat specialist to stop the bleeding. Surgery is rarely required.

URINARY TRACT INFECTIONS: UTI SYMPTOMS AND TREATMENT

What is a UTI - Urinary Tract Infection?

Urinary Tract Infections

A urinary tract infection (UTI) is an infection involving the kidneys, ureters, bladder, or urethra. These are the structures that urine passes through before being eliminated from the body.
  • The kidneys are a pair of small organs that lie on either side of the spine at about waist level. They have several important functions in the body, including removing waste and excess water from the blood and eliminating them as urine. These functions make them important in the regulation of blood pressure. Kidneys are also very sensitive to changes in blood sugar levels and blood pressure. Both diabetes and hypertension can cause damage to these organs.
  • Two ureters, narrow tubes about 10 inches long, drain urine from each kidney into the bladder.
  • The bladder is a small saclike organ that collects and stores urine. When the urine reaches a certain level in the bladder, you experience the sensation that you have to void, then the muscle lining the bladder can be voluntarily contracted to expel the urine.
  • The urethra is a small tube connecting the bladder with the outside of the body. A muscle called the urinary sphincter, located at the junction of the bladder and the urethra, must relax at the same time the bladder contracts to expel urine.
Any part of this system can become infected. As a rule, the farther up in the urinary tract the infection is located, the more serious it is.
  • The upper urinary tract is composed of the kidneys and ureters. Infection in the upper urinary tract generally affects the kidneys (pyelonephritis), which can cause fever, chills, nausea, vomiting, and other severe symptoms.
  • The lower urinary tract consists of the bladder and the urethra. Infection in the lower urinary tract can affect the urethra (urethritis) or the bladder (cystitis).
Urinary tract infections are usually referred to as simple or complicated.
  • Simple infections occur in healthy urinary tracts and do not spread to other parts of the body. They usually go away readily with treatment.
  • Complicated infections are caused by anatomic abnormalities, spread to other parts of the body, are worsened by underlying medical conditions, or are resistant to many antibiotics. They are more difficult to cure.
In the United States, urinary tract infections account for more than 7 million visits to medical offices and hospitals each year.
  • Urinary tract infections are much more common in adults than in children, but about 1%-2% of children do get urinary tract infections. Urinary tract infections in children are more likely to be serious than those in adults and should not be ignored (especially in younger children).
  • Urinary tract infection is the most common urinary tract problem in children besides bedwetting.
  • Urinary tract infection is second only to respiratory infection as the most common type of infection.
  • These infections are much more common in girls and women than in boys and men younger than 50 years of age. The reason for this is not well understood, but anatomic differences between the genders (a shorter urethra in women) might be partially responsible.
  • About 40% of women and 12% of men have a urinary tract infection at some time in their life.

Medical Guidebook