Symptoms may be absent or mild for the early onset of EAH and can include impaired exercise performance, nausea, vomiting, headache, bloating, and swelling of hands, legs, and feet. As water retention increases, weight gain may also occur. More severe symptoms include pulmonary edema and hyponatremic encephalopathy. Symptoms of hyponatremic encephalopathy are associated with an altered level of consciousness and can include sullenness, sleepiness, withdrawing from social interaction, photophobia, and seizures. In some reported cases, death has occurred.

Exercise-associated hyponatremia, or EAH, is a fluid-electrolyte disorder caused by a decrease in sodium levels (hyponatremia) during or up to 24 hours after prolonged physical activity. This disorder can develop when marathon runners or endurance event athletes drink more fluid, usually water or sports drinks, than their kidneys can excrete. This excess water can severely dilute the level of sodium in the blood needed for organs, especially the brain, to function properly.

The incidence of EAH in athletes has increased in recent years, especially in the United States, as marathon races and endurance events have become more popular. A recent study showed 13% of the Boston 2002 marathon runners experienced EAH; most cases were mild. Eight deaths from EAH have been documented since 1985.

Signs and symptoms of hyponatremia include nausea and vomiting, headache, short-term memory loss, confusion, lethargy, fatigue, loss of appetite, irritability, muscle weakness, spasms or cramps, seizures, and decreased consciousness or coma. The presence and severity of signs and symptoms are related to the level of salt in the blood, with lower levels of plasma sodium associated with more severe symptoms. However, emerging data suggest that mild hyponatremia (plasma sodium levels at 131–135 mmol/L) is associated with numerous complications or subtle, presently unrecognized symptoms (for example, increased falls, altered posture and gait, reduced attention).

Neurological symptoms typically occur with very low levels of plasma sodium (usually <115 mmol/L). When sodium levels in the blood become very low, water enters the brain cells and causes them to swell. This results in increased pressure in the skull and causes "hyponatremic encephalopathy". As pressure increases in the skull, herniation of the brain can occur, which is a squeezing of the brain across the internal structures of the skull. This can lead to headache, nausea, vomiting, confusion, seizures, brain stem compression and respiratory arrest, and non-cardiogenic accumulation of fluid in the lungs. This is usually fatal if not immediately treated.

Symptom severity depends on how fast and how severe the drop in blood salt level. A gradual drop, even to very low levels, may be tolerated well if it occurs over several days or weeks, because of neuronal adaptation. The presence of underlying neurological disease such as a seizure disorder or non-neurological metabolic abnormalities, also affects the severity of neurologic symptoms.

Chronic hyponatremia can lead to such complications as neurological impairments. These neurological impairments most often affect gait (walking) and attention, and can lead to increased reaction time and falls. Hyponatremia, by interfering with bone metabolism, has been linked with a doubled risk of osteoporosis and an increased risk of bone fracture.

The specific causes of hyponatremia are generally divided into those with low tonicity (lower than normal concentration of solutes), without low tonicity, and falsely low sodiums. Those with low tonicity are then grouped by whether the person has high fluid volume, normal fluid volume, or low fluid volume. Too little sodium in the diet alone is very rarely the cause of hyponatremia.

Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24-hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine, low blood sodium concentration, excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, and dehydration. Patients often self-medicate by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting. Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.

CSWS is usually caused by brain injury/trauma or cerebral lesion, tumor, or hematoma. CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume whereas SIADH is consistent with a normal or high blood volume. If blood-sodium levels increase when fluids are restricted, SIADH is more likely.

Congestive heart failure is the most common result of fluid overload. Also, it may be associated with hyponatremia (hypervolemic hyponatremia).

The excess fluid, primarily salt and water, builds up in various locations in the body and leads to an increase in weight, swelling in the legs and arms (peripheral edema), and/or fluid in the abdomen (ascites). Eventually, the fluid enters the air spaces in the lungs (pulmonary edema) reduces the amount of oxygen that can enter the blood, and causes shortness of breath (dyspnea) or enters pleural space by transudation (pleural effusion which also causes dyspnea), which is the best indicator of estimating central venous pressure is increased. It can also cause swelling of the face. Fluid can also collect in the lungs when lying down at night, possibly making nighttime breathing and sleeping difficult (paroxysmal nocturnal dyspnea).

Potomania, also known as beer potomania, beer drinker's potomania, and beer drinker's hyponatremia, is a specific hypo-osmolality syndrome related to massive consumption of beer, which is poor in solutes and electrolytes. With little food or other sources of electrolytes, consumption of large amounts of beer or other dilute alcoholic drinks leads to electrolyte disturbances, where the body does not have enough of nutrients known as electrolytes, namely sodium, potassium, and magnesium. The symptoms of potomania are similar to other causes of hyponatremia and include dizziness, muscular weakness, neurological impairment and seizures, all related to hyponatremia and hypokalaemia. While the symptoms of potomania are similar to other causes of hyponatremia and acute water intoxication, it should be considered an independent clinical entity because of its often chronic nature of onset, pathophysiology, and presentation of symptoms.

Characteristic symptoms are:

- Sudden penetrating pain in the legs, lower back or abdomen

- Confusion, psychosis, slurred speech

- Severe lethargy

- Convulsions

- Fever

- Hyperkalemia (elevated potassium level in the blood)

- Hypercalcemia (elevated calcium level in the blood): the cause of hypercalcemia is a combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney, this last caused by decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors are secondary to volume depletion and, in fact, improve rapidly during rehydration with saline infusion.

- Hypoglycemia (reduced level of blood glucose)

- Hyponatremia (low sodium level in the blood)

- Hypotension (low blood pressure)

- Hypothyroid (low T4 level)

- Severe vomiting and diarrhea, resulting in dehydration

- Syncope (loss of consciousness and ability to stand)

The normal human kidney, through suppression of anti-diuretic hormone, is normally able to excrete vast amounts of dilute urine. Thus a normal adult can drink up to 20 liters per day of water without becoming hyponatremic. However, the intake of solutes is also necessary to excrete free water. Under normal circumstances, this is clinically irrelevant. In the lack of proper solute intake, the amount of free water excretion can be severely limited. Without adequate solute intake, the normal functioning electrolyte gradient that pulls water into urine will be effectively destroyed.

Briefly, to excrete free water from urine, the urine flow (which is solute clearance + free water clearance) will equal the rate of solute excretion divided by the urine osmolality. With a diet of only solute poor beer, only about 200-300 mOSM (normal 750 mOSM to greater than 900 mOSM) of solute will be excreted per day, capping the amount of free water excretion at four liters. Any intake above 4 liters would lead to a dilution of the serum sodium concentration and thus hyponatremia.

Any vomiting or GI absorptive problems due to alcohol intoxication can also compound the effect of potomania due to additional electrolyte and acid-base disturbances.

Antidiuretic hormone (ADH) is released from the posterior pituitary for a number of physiologic reasons. The majority of people with hyponatremia, other than those with excessive water intake (polydipsia) or renal salt wasting, will have elevated ADH as the cause of their hyponatremia. However, not every person with hyponatremia and elevated ADH has SIADH. One approach to a diagnosis is to divide ADH release into appropriate (not SIADH) or inappropriate (SIADH).

Appropriate ADH release can be a result of hypovolemia, a so-called osmotic trigger of ADH release. This may be true hypovolemia, as a result of dehydration with fluid losses replaced by free water. It can also be perceived hypovolemia, as in the conditions of congestive heart failure (CHF) and cirrhosis in which the kidneys perceive a lack of intravascular volume. The hyponatremia caused by appropriate ADH release (from the kidneys' perspective) in both CHF and cirrhosis have been shown to be an independent poor prognostic indicator of mortality.

Appropriate ADH release can also be a result of non-osmotic triggers. Symptoms such as nausea/vomiting and pain are significant causes of ADH release. The combination of osmotic and non-osmotic triggers of ADH release can adequately explain the hyponatremia in the majority of people who are hospitalized with acute illness and are found to have mild to moderate hyponatremia. SIADH is less common than appropriate release of ADH. While it should be considered in a differential, other causes should be considered as well.

Cerebral salt wasting syndrome (CSWS) also presents with hyponatremia, there are signs of dehydration for which reason the management is diametrically opposed to SIADH. Importantly CSWS can be associated with subarachnoid hemorrhage (SAH) which may require fluid supplementation rather than restriction to prevent brain damage.

Most cases of hyponatremia in children are caused by appropriate secretion of antidiuretic hormone rather than SIADH or another cause.

Clinical presentation of CPM is heterogeneous and depend on the regions of the brain involved. Prior to its onset, patients may present with the neurological signs and symptoms of hyponatraemic encephalopathy such as nausea and vomiting, confusion, headache and seizures. These symptoms may resolve with normalisation of the serum sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function.

The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.

Adrenal crisis is caused by a deficiency of cortisol resulting from Addison's disease, congenital adrenal hyperplasia (CAH), corticosteroid biosynthetic enzyme defects or pituitary disorders (such as Sheehan's syndrome, pituitary adenoma, hypopituitarism (inactive or underactive pituitary) causing failure to activate the adrenal glands.

Abnormal basal metabolic rate refers to a high or low basal metabolic rate (BMR). It has numerous causes, both physiological (part of the body's normal function) and pathological (associated with disease).

If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.

The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.

Symptoms of hypoadrenocorticism can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters. Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning hypoadrenocorticism the nicknames of "the Great Mimic" and "the Great Imitator". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venous circulation.

ADH is derived from a preprohormone precursor that is synthesized in cells in the hypothalamus and stored in vesicles in the posterior pituitary. "Appropriate" ADH secretion is regulated by osmoreceptors on the hypothalamic cells that synthesize and store ADH: plasma hypertonicity activates these receptors, ADH is released into the blood stream, the kidney increases solute-free water return to the circulation, and the hypertonicity is alleviated. "Inappropriate" ADH secretion causes a "unrelenting increase" in solute-free water ("free water") absorption by the kidneys, with two consequences. First, in the extracellular fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration - hyponatremia. Then virtually simultaneously, in the intracellular space, cells swell, i.e. intracellular volume increases. Swelling of brain cells causes various neurological abnormalities which in severe or acute cases can result in convulsions, coma, and death.

The causes of SIADH are grouped into six categories: 1) central nervous system diseases that directly stimulate the hypothalamus, the site of control of ADH secretion; 2) various cancers that synthesize and secrete ectopic ADH; 3) various pulmonary diseases; 4) numerous (at least seventeen) drugs that chemically stimulate the hypothalamus; 5) inherited mutations that cause aquaporins always to be "turned on"; and 6) miscellaneous largely transient conditions.

Potential treatments of SIADH include restriction of fluid intake, correction of an identifiable reversible underlying cause, and/or medication which promotes solute-free water excretion by the kidney. The presence of cerebral edema may necessitate intravenous isotonic or hypertonic saline administration.

SIADH was originally described in 1957 in two people with small-cell carcinoma of the lung.

The most common cause of is overly rapid correction of low blood sodium levels (hyponatremia). Apart from rapid correction of hyponatraemia, there are case reports of central pontine myelinolysis in association with hypokalaemia, anorexia nervosa when feeding is started, patients undergoing dialysis and burns victims. There is a case report of central pontine myelinolysis occurring in the context of re-feeding syndrome, in the absence of hyponatremia.

It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It could affect patients who take some prescription medicines that are able to cross the blood-brain barrier and cause abnormal thirst reception - in this scenario the CPM is caused by polydipsia leading to low blood sodium levels (hyponatremia).

In schizophrenic patients with psychogenic polydipsia, inadequate thirst reception leads to excessive water intake, severely diluting serum sodium. With this excessive thirst combined with psychotic symptoms, brain damage such as CPM may result from hyperosmolarity caused by excess intake of fluids, (primary polydipsia) although this is difficult to determine because such patients are often institutionalised and have a long history of mental health conditions.

It has been observed following hematopoietic stem cell transplantation.

CPM may also occur in patients prone to hyponatraemia affected by

- severe liver disease

- liver transplant

- alcoholism

- severe burns

- malnutrition

- anorexia

- severe electrolyte disorders

- AIDS

- hyperemesis gravidarum

- hyponatremia due to Peritoneal Dialysis

- Wernicke encephalopathy

An abnormal basal metabolic rate is not necessarily indicative of disease; a number of physiological factors can alter the BMR by influencing cellular metabolic activity. For instance, males are more likely than females to have a high BMR, and in women, the BMR may rise to abnormal levels during pregnancy or lactation. An individual's BMR varies greatly with age: infants and children typically have a high BMR, required for growth, while the elderly have a low BMR. Tall, thin people have a higher BMR than their shorter counterparts, even with the same weight, due to the greater surface area of their skin. The metabolic rate also decreases during sleep and increases in exercise, and individuals who exercise regularly have a higher BMR than those who are sedentary. Environmental temperature also has an effect: the BMR is increased in both heat and cold.

There are often no visible symptoms of hyperinsulinemia unless hypoglycaemia (low blood sugar) is present.

Some patients may experience a variety of symptoms when hypoglycaemia is present, including:

- Temporary muscle weakness

- Brain fog

- Fatigue

- Temporary thought disorder, or inability to concentrate

- Visual problems such as blurred vision or double vision

- Headaches

- Shaking/Trembling

- Thirst

If a person experiences any of these symptoms, a visit to a qualified medical practitioner is advised, and diagnostic blood testing may be required.

The onset of this disease is usually noticed in childhood, but often not diagnosed until the third or fourth decade of life. Symptoms include exercise intolerance with muscle pain, early fatigue, painful cramps, and myoglobin in the urine (often provoked by a bout of exercise). Myoglobinuria may result from the breakdown of skeletal muscle known as rhabdomyolysis, a condition in which muscle cells breakdown, sending their contents into the bloodstream.

Patients may exhibit a “second wind” phenomenon. This is characterized by the patient’s better tolerance for aerobic exercise such as walking and cycling after approximately 10 minutes. This is attributed to the combination of increased blood flow and the ability of the body to find alternative sources of energy, like fatty acids and proteins. In the long term, patients may exhibit renal failure due to the myoglobinuria, and with age, patients may exhibit progressively increasing weakness and substantial muscle loss.

Patients may present at emergency rooms with severe fixed contractures of the muscles and often severe pain. These require urgent assessment for rhabdomyolysis as in about 30% of cases this leads to acute renal failure. Left untreated this can be life-threatening. In a small number of cases compartment syndrome has developed, requiring prompt surgical referral.

Sarcopenia is characterized first by a muscle atrophy (a decrease in the size of the muscle), along with a reduction in muscle tissue quality, characterized by such factors as replacement of muscle fibres with fat, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction and leading to progressive loss of muscle function and frailty. Sarcopenia is determined by two factors: initial amount of muscle mass and rate at which aging decreases muscle mass. Due to the loss of independence associated with loss of muscle strength, the threshold at which muscle wasting becomes a disease is different pathologically from person to person.

Simple circumference measurement does not provide enough data to determine whether or not an individual is suffering from severe sarcopenia. Sarcopenia is also marked by a decrease in the circumference of distinct types of muscle fibers. Skeletal muscle has different fiber-types, which are characterized by expression of distinct myosin variants. During sarcopenia, there is a decrease in "type 2" fiber circumference (Type II), with little to no decrease in "type I" fiber circumference (Type I), and deinervated type 2 fibers are often converted to type 1 fibers by reinnervation by slow type 1 fiber motor nerves.

List of types of malnutrition or list of nutritional disorders include diseases that results from excessive or inadequate intake of food and nutrients. They come in two broad categories: undernutrition and overnutrition.

Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.