To relieve reactive hypoglycemia, the NIH recommends taking the following steps:

- Avoiding or limiting sugar intake;

- Exercising regularly; exercise increases sugar uptake which decreases excessive insulin release

- Eating a variety of foods, including meat, poultry, fish, or nonmeat sources of protein, foods such as whole-grains, fruits, nuts, vegetables, and dairy products;

- Choosing high-fiber foods.

Other tips to prevent sugar crashes include:

- Avoiding eating meals or snacks composed entirely of carbohydrates; simultaneously ingest fats and proteins, which have slower rates of absorption.

- Consistently choosing longer lasting, complex carbohydrates to prevent rapid blood-sugar dips in the event that one does consume a disproportionately large amount of carbohydrates with a meal

- Monitoring any effects medication may have on symptoms.

Low-carbohydrate diet and/or frequent small split meals is the first treatment of this condition. The first important point is to add small meals at the middle of the morning and of the afternoon, when glycemia would start to decrease. If adequate composition of the meal is found, the fall in blood glucose is thus prevented. Patients should avoid rapidly absorbable sugars and thus avoid popular soft drinks rich in glucose or sucrose. They should also be cautious with drinks associating sugar and alcohol, mainly in the fasting state.

As it is a short-term ailment, a sugar crash does not usually require medical intervention in most people. The most important factors to consider when addressing this issue are the composition and timing of foods.

Acute low blood sugar symptoms are best treated by consuming small amounts of sweet foods, so as to regain balance in the body’s carbohydrate metabolism. Suggestions include sugary foods that are quickly digested, such as:

- Dried fruit

- Soft drinks

- Juice

- Sugar as sweets, tablets or cubes.

Treatment of some forms of hypoglycemia, such as in diabetes, involves immediately raising the blood sugar to normal through the ingestion of carbohydrates, determining the cause, and taking measures to hopefully prevent future episodes. However, this treatment is not optimal in other forms such as reactive hypoglycemia, where rapid carbohydrate ingestion may lead to a further hypoglycemic episode.

Blood glucose can be raised to normal within minutes by taking (or receiving) 10–20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3–4 ounces (100–120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4–5 ounces (120–150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10–20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards. A mnemonic used by the American Diabetes Association and others is the "rule of 15" – consuming 15 grams of carbohydrate followed by a 15-minute wait, repeated if glucose remains low (variable by individual, sometimes 70 mg/dl).

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel such as paramedics, or in-hospital personnel can establish IV access and give intravenous dextrose, concentrations varying depending on age (infants are given 2 ml/kg dextrose 10%, children are given dextrose 25%, and adults are given dextrose 50%). Care must be taken in giving these solutions because they can cause skin necrosis if the IV is infiltrated, sclerosis of veins, and many other fluid and electrolyte disturbances if administered incorrectly. If IV access cannot be established, the patient can be given 1 to 2 milligrams of glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia. If a person is suffering less severe effects, and is conscious with the ability to swallow, medical personal such as EMT-B's may administer gelatinous oral glucose.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or decreasing alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress. See the following section of this article.

Acute hypoglycemia is reversed by raising the blood glucose. Glucagon should be injected intramuscularly or intravenously, or dextrose can be infused intravenously to raise the blood glucose. Oral administration of glucose can worsen the outcome, as more insulin is eventually produced. Most people recover fully even from severe hypoglycemia after the blood glucose is restored to normal. Recovery time varies from minutes to hours depending on the severity and duration of the hypoglycemia. Death or permanent brain damage resembling stroke can occur rarely as a result of severe hypoglycemia. See hypoglycemia for more on effects, recovery, and risks.

Further therapy and prevention depends upon the specific cause.

Most hypoglycemia due to excessive insulin occurs in people who take insulin for type 1 diabetes. Management of this hypoglycemia is sugar or starch by mouth (or in severe cases, an injection of glucagon or intravenous dextrose). When the glucose has been restored, recovery is usually complete. Prevention of further episodes consists of maintaining balance between insulin, food, and exercise. Management of hypoglycemia due to treatment of type 2 diabetes is similar, and the dose of the oral hypoglycemic agent may need to be reduced. Reversal and prevention of hypoglycemia is a major aspect of the management of type 1 diabetes.

Hypoglycemia due to drug overdose or effect is supported with extra glucose until the drugs have been metabolized. The drug doses or combination often needs to be altered.

Hypoglycemia due to a tumor of the pancreas or elsewhere is usually curable by surgical removal. Most of these tumors are benign. Streptozotocin is a specific beta cell toxin and has been used to treat insulin-producing pancreatic carcinoma.

Hyperinsulinism due to diffuse overactivity of beta cells, such as in many of the forms of congenital hyperinsulinism, and more rarely in adults, can often be treated with diazoxide or a somatostatin analog called octreotide. Diazoxide is given by mouth, octreotide by injection or continuous subcutaneous pump infusion. When congenital hyperinsulinism is due to focal defects of the insulin-secretion mechanism, surgical removal of that part of the pancreas may cure the problem. In more severe cases of persistent congenital hyperinsulinism unresponsive to drugs, a near-total pancreatectomy may be needed to prevent continuing hypoglycemia. Even after pancreatectomy, continuous glucose may be needed in the form of gastric infusion of formula or dextrose.

High dose glucocorticoid is an older treatment used for presumptive transient hyperinsulinism but incurs side effects with prolonged use.

If there is no hypoglycemia at the time of the symptoms, this condition is called "postprandial syndrome." It might be an "adrenergic postprandial syndrome" — blood glucose levels are normal, but the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient. This is often seen in dysautonomic disorders as well. Dietary recommendations for reactive hypoglycemia can help to relieve symptoms of postprandial syndrome.

For treatment of type II, dietary modification is the initial approach, but many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates (peroxisome proliferator-activated receptor-alpha agonists) may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis, so is only done under close supervision. Other agents commonly added to statins are ezetimibe, niacin, and bile acid sequestrants. Dietary supplementation with fish oil is also used to reduce elevated triglycerides, with the greatest effect occurring in patients with the greatest severity. Some evidence exists for benefit of plant sterol-containing products and omega-3 fatty acids.

The primary treatment for insulin resistance is exercise and weight loss. Research shows that a low-carbohydrate diet may help. Both metformin and thiazolidinediones improve insulin resistance, but only are approved therapies for type 2 diabetes, not for insulin resistance. By contrast, growth hormone replacement therapy may be associated with increased insulin resistance.

Metformin has become one of the more commonly prescribed medications for insulin resistance. Unfortunately, Metformin also masks Vitamin B12 deficiency, so accompanying sub-lingual Vitamin B12 tablets are recommended.

Insulin resistance is often associated with abnormalities in lipids particularly high blood triglycerides and low high density lipoprotein.

The "Diabetes Prevention Program" (DPP) showed that exercise and diet were nearly twice as effective as metformin at reducing the risk of progressing to type 2 diabetes. However, the participants in the DPP trial regained about 40% of the weight that they had lost at the end of 2.8 years, resulting in a similar incidence of diabetes development in both the lifestyle intervention and the control arms of the trial. One 2009 study found that carbohydrate deficit after exercise, but not energy deficit, contributed to insulin sensitivity increase.

Resistant starch from high-amylose corn, amylomaize, has been shown to reduce insulin resistance in healthy individuals, in individuals with insulin resistance, and in individuals with type 2 diabetes. Animal studies demonstrate that it cannot reverse damage already done by high glucose levels, but that it reduces insulin resistance and reduces the development of further damage.

Some types of polyunsaturated fatty acids (omega-3) may moderate the progression of insulin resistance into type 2 diabetes, however, omega-3 fatty acids appear to have limited ability to reverse insulin resistance, and they cease to be efficacious once type 2 diabetes is established.

Caffeine intake limits insulin action, but not enough to increase blood-sugar levels in healthy persons. People who already have type 2 diabetes may see a small increase in levels if they take 2 or 2-1/2 cups of coffee per day.

Medium-term (and less well-demonstrated) treatments of hypotension include:

- Blood sugar control (80–150 by one study)

- Early nutrition (by mouth or by tube to prevent ileus)

- Steroid support

Flumazenil is the only GABA receptor antagonist on the market as of Jan 2013, and it is currently manufactured only as an intravenous formulation. It is approved by the FDA for use in anesthesia reversal and benzodiazepine overdose. However, given its pharmacology, researchers consider it to be a promising medication in the treatment of idiopathic hypersomnia. Results of a small, double-blind, randomized, controlled clinical trial were published in November 2012. This research showed that flumazenil provides relief for most patients whose CSF contains the unknown "somnogen" that enhances the function of GABA receptors, making them more susceptible to the sleep-inducing effect of GABA. For one patient, daily administration of flumazenil by sublingual lozenge and topical cream has proven effective for several years. A 2014 case report also showed improvement in idiopathic hypersomnia symptoms after treatment with a continuous subcutaneous flumazenil infusion. The supply of generic flumazenil was initially thought to be too low to meet the potential demand for treatment of idiopathic hypersomnia. However, this scarcity has eased, and dozens of patients are now being treated with flumazenil off-label.

"Based on the role of histamine in keeping people awake (and hence the common side effect of anti-histamines such as diphenhydramine causing sleepiness), medications that act on histamine are under development for the treatment of excessive sleepiness." It remains to be seen whether these H3 antagonists (i.e., compounds such as pitolisant that promote the release of the wake-promoting amine histamine) will be particularly useful as wake-promoting agents in the treatment of idiopathic hypersomnia.

There is some evidence of the existence of a so-called "adrenergic postprandial syndrome": the glycemia is normal, and the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient.

The goal for treatment of GSD type 0 is to avoid hypoglycemia. This is accomplished by avoiding fasting by eating every 3-4 hours during the day. At night, uncooked corn starch can be given because it is a complex glucose polymer. This will be acted on slowly by pancreatic amylase and glucose will be absorbed over a 6 hour period.

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. A morning dose of caffeine can also be effective. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs increases venous return, thus making more blood available to critical organs in the chest and head. The Trendelenburg position, though used historically, is no longer recommended.

Hypotensive shock treatment always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed that hypotension is corrected. Still-debated methods are in parentheses, as are benchmarks for evaluating progress in correcting hypotension. A study on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

When the cause of hypoglycemia is not obvious, the most valuable diagnostic information is obtained from a blood sample (a "critical specimen") drawn during the hypoglycemia. Detectable amounts of insulin are abnormal and indicate that hyperinsulinism is likely to be the cause. Other aspects of the person's metabolic state, especially low levels of free fatty acids, beta-hydroxybutyrate and ketones, and either high or low levels of C-peptide and proinsulin can provide confirmation.

Clinical features and circumstances can provide other indirect evidence of hyperinsulinism. For instance, babies with neonatal hyperinsulinism are often large for gestational age and may have other features such as enlarged heart and liver. Knowing that someone takes insulin or oral hypoglycemic agents for diabetes obviously makes insulin excess the presumptive cause of any hypoglycemia.

Most sulfonylureas and aspirin can be detected on a blood or urine drug screen tests, but insulin cannot. Endogenous and exogenous insulin can be distinguished by the presence or absence of C-peptide, a by-product of endogenous insulin secretion which is not present in pharmaceutical insulin. Some of the newer analog insulins are not measured by the usual insulin level assays.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.

The Greek root "oxy" means "sharp" or "pointy". The OGTT curve in this condition appears sharp and somewhat pointy (at least relative to the other forms of hyperglycemia)- hence this name.

Dorlands dictionary defines oxyhyperglycemia as:

A blood level of approximately 180 mg/dL is the renal glucose threshold below which all glucose is reabsorbed from glomerular filtrate. But at blood concentrations above the renal threshold sugar starts appearing in the urine.

Oxyhyperglycemia, like other forms of Impaired glucose tolerance has also been suggested to be a prediabetic condition

Recent research has been directed towards finding better treatment options. Multi-drug therapy using insulin sensitizers, such as metformin and pioglitazone, has been linked to improving residual insulin action. High doses of insulin-like growth factor 1 has also been effective in patients with Rabson–Mendenhall syndrome. Future studies are also focusing on the relation between genotype and phenotype. Though there is no cure, researchers remain optimistic on finding a cure.

There is no known cure for Rabson–Mendenhall syndrome. However, a series of steps can be directed towards treating the specific symptoms. For example, surgery may be performed to treat dental abnormalities. Furthermore, the goal of the treatment is also to maintain blood glucose levels as constantly as possible. Insulin is not as effective at normal doses, and even large doses show minimal effects. Frequent feeding is the most effective treatment to control blood glucose levels. Well thought out meals with complex combinations of carbohydrates are put together and assigned to the patient in hope of seeing a constant glucose level maintained. Though effective, these treatments tend to show more of an impact initially, and can become ineffective within months.

Treatment of Rabson–Mendenhall syndrome with pharmacologic doses of human leptin may result in improvement of fasting hyperglycemia, hyperinsulinemia, basal glucose, and glucose and insulin tolerance.

Quality of life is impacted severely and the prognosis of patients with Rabson–Mendenhall syndrome remains poor. This is due to the lack of a long term treatment. Life expectancy is 1–2 years.

Idiopathic hypoglycemia is, literally, a medical condition in which the glucose level in the blood (blood glucose) is abnormally low due to an undeterminable cause. This is considered an incomplete and unsatisfactory diagnosis by physicians and is rarely used by endocrinologists, as it implies an unfinished diagnostic evaluation. In general, the more severe the hypoglycemia and the more clearly it is proven, the less likely it is to remain "idiopathic".

"Idiopathic hypoglycemia" can also be a synonym for reactive hypoglycemia or for hypoglycemia that is not diagnosed by a physician and does not fulfill the Whipple triad criteria. A more precise term for that condition is idiopathic postprandial syndrome.

Oxyhyperglycemia is most commonly caused by early dumping syndrome, but it can rarely caused by other conditions like Graves' disease. It was first described by Lawrence et al. in 1936 as often happening after gastroenterostomy. It is seen in most forms of gastrectomy, gastric bypass and gastrostomy procedures, all of which are surgical causes of dumping syndrome.

As of 2017, data on optimal treatment was limited. Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral

corticosteroids such as prednisone. Vigabatrin is also a common consideration, though there is a risk of visual field loss with long term use. The high cost of ACTH leads doctors to avoid it in the US; higher dose prednisone appears to generate equivalent outcomes.

As of 2017 data from clinical trials of the ketogenic diet for treating infantile spams was inconsistent; most trials were as a second-line therapy after failure of drug treatment, and as of 2017 it had not been explored as a first line treatment in an adequately designed clinical trial.

Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.

Treatment is similar to treatment for benign fasciculation syndrome.

Carbamazepine therapy has been found to provide moderate reductions in symptoms.

Where an underlying neoplasm is the cause, treatment of this condition is indicated in order to reduce progression of symptoms. For cases without a known cause, treatment involves suppression of the immune system with corticosteroid treatment, intravenous immunoglobulin, immunosuppressive agents like Rituximab, Cellcept, or Imuran or plasmapheresis.

In general, there are two broad classes of treatment, and the two may be combined: psychological (cognitive-behavioral) and pharmacological. In situations of acute distress such as a grief reaction, pharmacologic measures may be most appropriate. With primary insomnia, however, initial efforts should be psychologically based, including discussion of good sleep hygiene. Other specific treatments are appropriate for some of the disorders, such as ingestion of the hormone melatonin, correctly timed bright light therapy and correctly timed dark therapy or light restriction for the circadian rhythm sleep disorders. Specialists in sleep medicine are trained to diagnose and treat these disorders, though many specialize in just some of them.