WATER AND ELECTROLYTES

Water and electrolytes

Electrolytes play a vital role in maintaining homeostasis within the body. They help to regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base balance and much more. Electrolyte imbalances can develop by the following mechanisms: excessive ingestion; diminished elimination of an electrolyte; diminished ingestion or excessive elimination of an electrolyte. The most common cause of electrolyte disturbances is renal failure.

The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium. Other electrolyte imbalances are less common, and often occur in conjunction with major electrolyte changes. Chronic laxative abuse or severe diarrheaor vomiting (Gastroenteritis) can lead to electrolyte disturbances along with dehydration. People suffering from bulimia or anorexia nervosa are at especially high risk for an electrolyte imbalance.

Electrolytes are important because they are what cells (especially nerve, heart, muscle) use to maintain voltages across their cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells. Kidneys work to keep the electrolyte concentrations in blood constant despite changes in your body. For example, during heavy exercise, electrolytes are lost in sweat, particularly sodium and potassium. These electrolytes must be replaced to keep the electrolyte concentrations of the body fluids constant.

Diabetes mellitus

Diabetes mellitus, often simply referred to as diabetes, is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced.This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).

There are three main types of diabetes mellitus (DM). Type 1 DM results from the body's failure to produce insulin, and presently requires the person to inject insulin or wear an insulin pump. This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes". Type 2 DM results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency. This form was Previously referred to as non insulin-dependent diabetes mellitus (NIDDM) or "adult-onset diabetes". The third main form, gestational diabetes occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. It may precede development of type 2 DM.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.

All forms of diabetes have been treatable since insulin became available in 1921, and type 2 diabetes may be controlled with medications. Both types 1 and 2 are chronic conditions that cannot be cured. Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass surgery has been successful in many with morbid obesity and type 2 DM. Gestational diabetes usually resolves after delivery. Diabetes without proper treatments can cause many complications. Acute complications includehypoglycemia, diabetic ketoacidosis, or nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular disease, chronic renal failure, and diabetic retinopathy (retinal damage). Adequate treatment of diabetes is thus important, as well asblood pressure control and lifestyle factors such as smoking cessation and maintaining a healthy body weight.

Globally, as of 2012, an estimated 346 million people have type 2 diabetes.

Gestational diabetes 

Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetesexhibit high blood glucose levels during pregnancy (especially during third trimester). There is some question whether the condition is natural during pregnancy. Gestational diabetes is caused when the insulin receptors do not function properly. This is likely due to pregnancy related factors such as the presence of human placental lactagen that interferes with susceptible insulin receptors. This in turn causes inappropriately elevated blood sugar levels.

Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose in blood samples. Gestational diabetes affects 3-10% of pregnancies, depending on the population studied, so may be a natural phenomenon.

As with diabetes mellitus in pregnancy in general, babies born to mothers with gestational diabetes are typically at increased risk of problems such as being large for gestational age (which may lead to delivery complications), low blood sugar, and jaundice. If untreated, it can also cause seizures or still birth. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks.

Women with gestational diabetes are at increased risk of developing type 2 diabetes mellitus (or, very rarely, latent autoimmune diabetes or Type 1) after pregnancy, as well as having a higher incidence of pre-eclampsia and Caesarean section; their offspring are prone to developing childhood obesity, with type 2 diabetes later in life. Most patients are treated only with diet modification and moderate exercise, but some take antidiabetic drugs, including insulin.

Women treated for gestational diabetes generally have smaller birthweight babies, leading to other problems, such as survival rate of premature and early births, particularly male babies.

Diabetes insipidus

Diabetes insipidus is a condition in which the kidneys are unable to conserve water.

Causes

Diabetes insipidus (DI) is an uncommon condition that occurs when the kidneys are unable to conserve water as they perform their function of filtering blood. The amount of water conserved is controlled by antidiuretic hormone (ADH), also called vasopressin.

ADH is a hormone produced in a region of the brain called the hypothalamus. It is then stored and released from the pituitary gland, a small gland at the base of the brain.

DI caused by a lack of ADH is called central diabetes insipidus. When DI is caused by a failure of the kidneys to respond to ADH, the condition is called nephrogenic diabetes insipidus.

Central diabetes insipidus can be caused by damage to the hypothalamus or pituitary gland as a result of:

• Head injury
• Infection
• Loss of blood supply to the gland
• Surgery
• Tumor

There is also a form of central diabetes insipidus that runs in families.

Nephrogenic DI involves a defect in the parts of the kidneys that reabsorb water back into the bloodstream. It occurs less often than central DI. Nephrogenic DI may occur as an inherited disorder in which male children receive the abnormal gene that causes the disease from their mothers.

Nephrogenic DI may also be caused by:

• Certain drugs (such as lithium, amphotericin B, and demeclocycline)
• High levels of calcium in the body (hypercalcemia)
• Kidney disease (such as polycystic kidney disease)

Symptoms

• Excessive thirst
• May be intense or uncontrollable
• May involve a craving for ice water
• Excessive urine volume

Treatment

The cause of the underlying condition should be treated when possible.

Central diabetes insipidus may be controlled with vasopressin (desmopressin, DDAVP). You take vasopressin as either a nasal spray or tablets.

If nephrogenic DI is caused by medication (for example, lithium), stopping the medication may help restore normal kidney function. However, after many years of lithium use, the nephrogenic DI may be permanent.

Hereditary nephrogenic DI and lithium-induced nephrogenic DI are treated by drinking enough fluids to match urine output and with drugs that lower urine output. Drugs used to treat nephrogenic DI include:

• Anti-inflammatory medication (indomethacin)
• Diuretics [hydrochlorothiazide (HCTZ) and amiloride]

The outcome depends on the underlying disorder. If treated, diabetes insipidus does not cause severe problems or reduce life expectancy.

hypernatremia

Sodium levels are tightly controlled in a healthy individual by regulation of urine concentration and production and regulation of the thirst response. In patients with an intact thirst response, hypernatremia (defined as a serum sodium level >145 mEq/L) is a rare entity. When hypernatremia does occur, it is associated with a high mortality rate (>50% in most studies).

Given this high mortality rate, the emergency physician must be able to recognize and treat this condition. Accordingly, this article discusses the patients in whom hypernatremia should be suspected and a treatment strategy for patients in whom the condition is discovered.

In general, hypernatremia can be caused by derangement of the thirst response or the behavioral response thereto (primarily in infants, psychiatric patients, and elderly patients who are institutionalized), by problems with the renal concentrating mechanism (diabetes insipidus [DI]) secondary to kidney pathology (nephrogenic DI) or difficulty with the neurohormonal control of this concentrating mechanism (central DI), or by losses of free water from other sources.

hyponatremia

Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Clinically significant hyponatremia is relatively uncommon and is nonspecific in its presentation; therefore, the physician must consider the diagnosis in patients presenting with vague constitutional symptoms or with altered level of consciousness. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. The physician must have a thorough understanding of the pathophysiology of hyponatremia to initiate safe and effective corrective therapy. The patient's fluid status must be accurately assessed upon presentation, as it guides the approach to correction.