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Hypoglycaemia Classification and external resources
Glucose test
ICD-10	E16.0-E16.2
ICD-9	250.8, 251.0, 251.1, 251.2, 270.3, 775.6, 962.3
DiseasesDB	6431
MedlinePlus	000386
eMedicine	emerg/272  med/1123 med/1939 ped/1117
MeSH	D007003

Hypoglycaemia or hypoglycemia is the medical term for a pathologic state produced by a lower than normal level of blood glucose. The term hypoglycemia literally means "under-sweet blood" (Gr. hypo-, glykys, haima).

Hypoglycemia can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose as fuel to the brain, resulting in impairment of function (neuroglycopenia). Derangements of function can range from vaguely "feeling bad" to coma, seizures, and (rarely) permanent brain damage or death. Hypoglycemia can arise from many causes and can occur at any age. It also sometimes occurs at random.

The most common forms of moderate and severe hypoglycemia occur as a complication of treatment of diabetes mellitus treated with insulin or less frequently with certain oral medications. Hypoglycemia is usually treated by the ingestion or administration of dextrose, or foods quickly digestible to glucose.

Endocrinologists (specialists in hormones, including those which regulate glucose metabolism) typically consider the following criteria (referred to as Whipple's triad) as proving that individual's symptoms can be attributed to hypoglycemia:

1. Symptoms known to be caused by hypoglycemia
2. Low glucose at the time the symptoms occur
3. Reversal or improvement of symptoms or problems when the glucose is restored to normal

However, not everyone has accepted these suggested diagnostic criteria, and even the level of glucose low enough to define hypoglycemia has been a source of controversy in several contexts. For many purposes, plasma glucose levels below 70 mg/dl or 3.9 mmol/L are considered hypoglycemic; these issues are detailed below.

Contents 1 Defining hypoglycemia 2 Alternate theory: Rate of decrease in blood sugar rather than depth of decrease affects the nervous system 2.1 Method of measurement 2.2 Age differences 2.3 Presence or absence of effects 2.4 Purpose of definition 3 Pathophysiology 4 Signs and symptoms 4.1 Adrenergic manifestations 4.2 Glucagon manifestations 4.3 Neuroglycopenic manifestations 5 Determining the cause 5.1 The circumstances of hypoglycemia provide most of the clues to diagnosis 5.2 In less obvious cases, a "critical sample" may provide the diagnosis 5.3 Further diagnostic steps 6 Causes 6.1 Hypoglycemia in newborn infants 6.2 Hypoglycemia in young children 6.3 Hypoglycemia in older children and young adults 6.4 Hypoglycemia in older adults 7 Treatment and prevention 7.1 Reversing acute hypoglycemia 7.2 Prevention 8 Hypoglycemia as holistic medicine 9 See also 10 References 11 External links

[edit] Defining hypoglycemia

No single glucose value alone serves to define the medical condition termed hypoglycemia for all people and purposes. Throughout the 24 hour cycles of eating, digestion, and fasting, blood plasma glucose levels are generally maintained within a range of 70-150 mg/dL (3.9-7.8 mmol/L) for healthy humans.^[1] Although 60 or 70 mg/dL (3.3 or 3.9 mmol/L) is commonly cited as the lower limit of normal glucose, different values (typically below 40, 50, 60, or 70 mg/dL) have been defined as low for different populations, clinical purposes, or circumstances.

The precise level of glucose considered low enough to define hypoglycemia is dependent on (1) the measurement method, (2) the age of the person, (3) presence or absence of effects, and (4) the purpose of the definition. While there is no disagreement as to the normal range of blood sugar, debate continues as to what degree of hypoglycemia warrants medical evaluation or treatment, or can cause harm.^[2][3][4]

This article expresses glucose in milligrams per deciliter (mg/dL or mg/100 mL) as is customary in the United States, while millimoles per litre (mmol/L or mM) are the units used in most of the rest of the world. Glucose concentrations expressed as mg/dL can be converted to mmol/L by dividing by 18.0 g/dmol (the molar mass of glucose). For example, a glucose concentration of 90 mg/dL is 5.0 mmol/L or 5.0 mM.

[edit] Alternate theory: Rate of decrease in blood sugar rather than depth of decrease affects the nervous system

An alternate view of the syndrome advanced by researchers at Johns Hopkins University Medical School is that the rate of the decrease in blood sugar rather than its absolute low mark is what triggers the reported symptoms. It is surmised that the nervous system is not given sufficient time to adjust to a rapid rather than a gradual drop in blood sugar, which then triggers the reported symptoms of anxiety, fainting, tinnitus, and so on. Johns Hopkins Family Health Book, page 1183. (Viewable Online)Consuming food that helps maintain a more even level of blood sugar and paying attention to the glycemic index or glycemic load of various foods are also recommended, along with eating several smaller meals a day rather than traditional three larger meals. However, the utility of the glycemic index is disputed within the medical profession, and it may be of little value in managing hypoglycemia-associated autonomic failure (HAAF).

[edit] Method of measurement

Blood glucose levels discussed in this article are venous plasma or serum levels measured by standard, automated glucose oxidase methods used in medical laboratories. For clinical purposes, plasma and serum levels are similar enough to be interchangeable. Arterial plasma or serum levels are slightly higher than venous levels, and capillary levels are typically in between.^[5] This difference between arterial and venous levels is small in the fasting state but is amplified and can be greater than 10% in the postprandial state.^[6] On the other hand, whole blood glucose levels (e.g., by fingerprick meters) are about 10%-15% lower than venous plasma levels.^[5] Furthermore, available fingerstick glucose meters are only warranted to be accurate to within 15% of a simultaneous laboratory value under optimal conditions, and home use in the investigation of hypoglycemia is fraught with misleading low numbers.^[7][8] In other words, a meter glucose reading of 39 mg/dL could be properly obtained from a person whose laboratory serum glucose was 53 mg/dL; even wider variations can occur with "real world" home use. Ironically, most meters sold are routinely tested for accuracy at the high-end of the scale, sometimes up to 800 mg/dL, despite the fact that there is little immediate danger from hyperglycemia, whereas there is very real immediate danger from hypoglycemia, making accuracy at the low-end extremely critical.

Two other factors significantly affect glucose measurement: hematocrit and delay after phletocrit is high,^[6] as in newborn infants, or adults with polycythemia. High neonatal hematocrits are particularly likely to confound glucose measurement by meter. Second, unless the specimen is drawn into a fluoride tube or processed immediately to separate the serum or plasma from the cells, the measurable glucose will be gradually lowered by in vitro metabolism of the glucose at a rate of approximately 7 mg/dL/hr, or even more in the presence of leukocytosis.^[9][10][6]

[edit] Age differences

Surveys of healthy children and adults show that plasma glucoses below 60 mg/dL (3.3 mM) or above 100 mg/dL (5.6 mM) are found in less than 5% of samples after an overnight fast.^[11] As the duration of fasting is extended, plasma glucose levels can fall further, even in healthy people. In other words, many healthy people can occasionally have glucose levels in the hypoglycemic range without symptoms or disease.

The normal range of newborn blood sugars continues to be debated. It has been proposed that newborn brains are able to use alternate fuels when glucose levels are low more readily than adults. Experts continue to debate the significance and risk of such levels, though the trend has been to recommend maintenance of glucose levels above 60-70 mg/dL after the first day after birth.

[edit] Presence or absence of effects

Research in healthy adults shows that mental efficiency declines slightly but measurably as blood glucose falls below 65 mg/dL (3.6 mM) in many people. Hormonal defense mechanisms (adrenaline and glucagon) are normally activated as it drops below a threshold level (about 55 mg/dL (3.0 mM) for most people), producing the typical symptoms of shakiness and dysphoria. However, because type 1 diabetes mellitus is an autoimmune disease resulting from inflammation to the Islets of Langerhans, these counterregulatory responses are severely impaired in this group. On the other hand, obvious impairment does not often occur until the glucose falls below 40 mg/dL, and up to 10% of the population may occasionally have glucose levels below 65 in the morning without apparent effects. Brain effects of hypoglycemia, termed neuroglycopenia, determine whether a given low glucose is a "problem" for that person, and hence some people tend to use the term hypoglycemia only when a moderately low glucose is accompanied by symptoms.

Even this criterion is complicated by the facts that A) hypoglycemic symptoms are vague and can be produced by other conditions; B) people with persistently or recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning; and C) many measurement methods (especially glucose meters) are imprecise at low levels.

Diabetic hypoglycemia represents a special case with respect to the relationship of measured glucose and hypoglycemic symptoms for several reasons. First, it is almost always iatrogenic. Second, although home glucose meter readings are too often misleading, the probability that a low reading which may or may not be accompanied by symptoms represents real hypoglycemia is also significantly higher in a person who takes insulin, and is 25 times higher in patients with type 1 diabetes relative to those with type 2 diabetes^[12][13]. Third, the hypoglycemia has a greater chance of progressing to more serious impairment if not treated, compared to most other forms of hypoglycemia that occur in adults because insulin is dosed in a non-physiological manner. Fourth, because glucose levels are above normal more often than they are in people without diabetes, hypoglycemic symptoms may sometimes occur at higher thresholds than in people who are normoglycemic most of the time. For all of these reasons, people with diabetes are instructed to use higher meter glucose thresholds to determine hypoglycemia, although the absence of symptoms can sometimes impede patients' ability to do so.

[edit] Purpose of definition

For all of the reasons explained in the above paragraphs, deciding whether a blood glucose in the borderline range of 45-75 mg/dL (2.5-4.2 mM) represents clinically problematic hypoglycemia is not always simple. This leads people to use different "cutoff levels" of glucose in different contexts and for different purposes.

[edit] Pathophysiology

Like most animal tissues, brain metabolism depends primarily on glucose for fuel in most circumstances. A limited amount of glucose can be derived from glycogen stored in astrocytes, but it is consumed within minutes. For most practical purposes, the brain is dependent on a continual supply of glucose diffusing from the blood into the interstitial tissue within the central nervous system and into the neurons themselves.

Therefore, if the amount of glucose supplied by the blood falls, the brain is one of the first organs affected. In most people, subtle reduction of mental efficiency can be observed when the glucose falls below 65 mg/dl (3.6 mM). Impairment of action and judgment usually becomes obvious below 40 mg/dl (2.2 mM). Seizures may occur as the glucose falls further. As blood glucose levels fall below 10 mg/dl (0.55 mM), most neurons become electrically silent and nonfunctional, resulting in coma. These brain effects are collectively referred to as neuroglycopenia.

The importance of an adequate supply of glucose to the brain is apparent from the number of nervous, hormonal and metabolic responses to a falling glucose level. Most of these are defensive or adaptive, tending to raise the blood sugar via glycogenolysis and gluconeogenesis or provide alternative fuels. If the blood sugar level falls too low the liver converts a storage of glycogen into glucose and releases it into the bloodstream, to prevent the person going into a diabetic coma, for a short period of time.

Brief or mild hypoglycemia produces no lasting effects on the brain, though it can temporarily alter brain responses to additional hypoglycemia. Prolonged, severe hypoglycemia can produce lasting damage of a wide range. This can include impairment of cognitive function, motor control, or even consciousness. The likelihood of permanent brain damage from any given instance of severe hypoglycemia is difficult to estimate, and depends on a multitude of factors such as age, recent blood and brain glucose experience, concurrent problems such as hypoxia, and availability of alternative fuels. The vast majority of symptomatic hypoglycemic episodes result in no detectable permanent harm.^[14]

[edit] Signs and symptoms

Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

[edit] Adrenergic manifestations

• Shakiness, anxiety, nervousness, tremor
• Palpitations, tachycardia
• Sweating, feeling of warmth
• Pallor, coldness, clamminess
• Dilated pupils (mydriasis)
• Feeling of numbness "pins and needles" (parasthaesia) in the fingers

[edit] Glucagon manifestations

• Hunger, borborygmus
• Nausea, vomiting, abdominal discomfort
• Headache

[edit] Neuroglycopenic manifestations

• Abnormal mentation, impaired judgement
• Nonspecific dysphoria, anxiety, moodiness, depression, crying
• Negativism, irritability, belligerence, combativeness, rage
• Personality change, emotional lability
• Fatigue, weakness, apathy, lethargy, daydreaming, sleep
• Confusion, amnesia, dizziness, delirium
• Staring, "glassy" look, blurred vision, double vision
• Automatic behavior, also known as automatism
• Difficulty speaking, slurred speech
• Ataxia, incoordination, sometimes mistaken for "drunkenness"
• Focal or general motor deficit, paralysis, hemiparesis
• Paresthesia, headache
• Stupor, coma, abnormal breathing
• Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may also vary by age, by severity of the hypoglycemia and the speed of the decline. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, as well as previous incidence.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or "spells". Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Nearly always, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

[edit] Determining the cause

Hundreds of conditions can cause hypoglycemia. Common causes by age are listed below. While many aspects of the medical history and physical examination may be informative, the two best guides to the cause of unexplained hypoglycemia are usually

1. the circumstances
2. a critical sample of blood obtained at the time of hypoglycemia, before it is reversed.

[edit] The circumstances of hypoglycemia provide most of the clues to diagnosis

Circumstances include the age of the patient, time of day, time since last meal, previous episodes, nutritional status, physical and mental development, drugs or toxins (especially insulin or other diabetes drugs), diseases of other organ systems, family history, and response to treatment. When hypoglycemia occurs repeatedly, a record or "diary" of the spells over several months, noting the circumstances of each spell (time of day, relation to last meal, nature of last meal, response to carbohydrate, and so forth) may be useful in recognizing the nature and cause of the hypoglycemia.

An especially important aspect is whether the patient is seriously ill with another problem. Severe disease of nearly all major organ systems can cause hypoglycemia as a secondary problem. Hospitalized patients, especially in intensive care units or those prevented from eating, can suffer hypoglycemia from a variety of circumstances related to the care of their primary disease. Hypoglycemia in these circumstances is often multifactorial or even iatrogenic. Once identified, these types of hypoglycemia are readily reversed and prevented, and the underlying disease becomes the primary problem.

Apart from determining nutritional status and identifying whether there is likely to be an underlying disease more serious than hypoglycemia, the physical examination of the patient is only occasionally helpful. Macrosomia in infancy usually indicates hyperinsulinism. A few syndromes and metabolic diseases may be recognizable by clues such as hepatomegaly or micropenis.

It may take longer to recover from severe hypoglycemia with unconsciousness or seizure even after restoration of normal blood glucose. When a person has not been unconscious, failure of carbohydrate to reverse the symptoms in 10-15 minutes increases the likelihood that hypoglycemia was not the cause of the symptoms. When severe hypoglycemia has persisted in a hospitalized patient, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism. In this context this is referred to as the glucose infusion rate (GIR). Finally, the blood glucose response to glucagon given when the glucose is low can also help distinguish among various types of hypoglycemia. A rise of blood glucose by more than 30 mg/dl (1.70 mmol/l) suggests insulin excess as the probable cause of the hypoglycemia.

[edit] In less obvious cases, a "critical sample" may provide the diagnosis

In the majority of children and adults with recurrent, unexplained hypoglycemia, the diagnosis may be determined by obtaining a sample of blood during hypoglycemia. If this critical sample is obtained at the time of hypoglycemia, before it is reversed, it can provide information that would otherwise require a hospital admission and unpleasant starvation testing. Perhaps the most common inadequacy of emergency department care in cases of unexplained hypoglycemia is the failure to obtain at least a basic sample before giving glucose to reverse it.

Part of the value of the critical sample may simply be the proof that the symptoms are indeed due to hypoglycemia. More often, measurement of certain hormones and metabolites at the time of hypoglycemia indicates which organs and body systems are responding appropriately and which are functioning abnormally. For example, when the blood glucose is low, hormones which raise the glucose should be rising and insulin secretion should be completely suppressed.

The following is a brief list of hormones and metabolites which may be measured in a critical sample. Not all tests are checked on every patient. A "basic version" would include insulin, cortisol, and electrolytes, with C-peptide and drug screen for adults and growth hormone in children. The value of additional specific tests depends on the most likely diagnoses for an individual patient, based on the circumstances described above. Many of these levels change within minutes, especially if glucose is given, and there is no value in measuring them after the hypoglycemia is reversed. Others, especially those lower in the list, remain abnormal even after hypoglycemia is reversed, and can be usefully measured even if a critical specimen is missed. Although interpretation in difficult cases is beyond the scope of this article, for most of the tests, the primary significance is briefly noted.

• Glucose: needed to document actual hypoglycemia
• Insulin: any detectable amount is abnormal during hypoglycemia, but physician must know assay characteristics
• Cortisol: should be high during hypoglycemia if pituitary and adrenals are functioning normally
• Growth hormone: should rise after hypoglycemia if pituitary is functioning normally
• Electrolytes and total carbon dioxide: electrolyte abnormalities may suggest renal or adrenal disease; mild acidosis is normal with starvation hypoglycemia; usually no acidosis with hyperinsulinism
• Liver enzymes: elevation suggests liver disease
• Ketones: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism or fatty acid oxidation disorder
• Beta-hydroxybutyrate: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism or fatty acid oxidation disorder
• Free fatty acids: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism; high with low ketones suggests fatty acid oxidation disorder
• Lactic acid: high levels suggest sepsis or an inborn error of gluconeogenesis such as glycogen storage disease
• Ammonia: if elevated suggests hyperinsulinism due to glutamate dehydrogenase deficiency, Reye syndrome, or certain types of liver failure
• C-peptide: should be low or undetectable; if elevated suggests hyperinsulinism; low c-peptide with high insulin suggests exogenous (injected) insulin
• Proinsulin: detectable levels suggest hyperinsulinism; levels disproportionate to a detectable insulin level suggest insulinoma
• Ethanol: suggests alcohol intoxication
• Toxicology screen: can detect many drugs causing hypoglycemia, especially for sulfonylureas
• Insulin antibodies: if positive suggests repeated insulin injection or antibody-mediated hypoglycemia
• Urine organic acids: elevated in various characteristic patterns in several types of organic aciduria
• Carnitine, free and total: low in certain disorders of fatty acid metabolism and certain types of drug toxicity and pancreatic disease
• Thyroxine and TSH: low T4 without elevated TSH suggests hypopituitarism or malnutrition
• Acylglycine: elevation suggests a disorder of fatty acid oxidation
• Epinephrine: should be elevated during hypoglycemia
• Glucagon: should be elevated during hypoglycemia, except in the case of type 1 diabetes mellitus where irreparable damage is done to the cells which produce this counterregulatory hormone.
• IGF-1: low levels suggest hypopituitarism or chronic malnutrition
• IGF-2: low levels suggest hypopituitarism; high levels suggest non-pancreatic tumor hypoglycemia
• ACTH: should be elevated during hypoglycemia; unusually high ACTH with low cortisol suggests Addison's disease
• Alanine or other plasma amino acids: abnormal patterns may suggest certain inborn errors of amino acid metabolism or gluconeogenesis
• Somatostatin should be elevated during hypoglycemia as it acts to inhibit insulin production and increase blood glucose level

[edit] Further diagnostic steps

When suspected hypoglycemia recurs and a critical specimen has not been obtained, the diagnostic evaluation may take several paths. However good nutrition and prompt intake is essential.

When general health is good, the symptoms are not severe, and the person can fast normally through the night, experimentation with diet (extra snacks with fat or protein, reduced sugar) may be enough to solve the problem. If it is uncertain whether "spells" are indeed due to hypoglycemia, some physicians will recommend use of a home glucose meter to test at the time of the spells to confirm that glucoses are low. This approach may be most useful when spells are fairly frequent or the patient is confident that he or she can provoke a spell. The principal drawback of this approach is the high rate of false positive or equivocal levels due to the imprecision of the currently available meters: both physician and patient need an accurate understanding of what a meter can and cannot do to avoid frustrating and inconclusive results.

In cases of recurrent hypoglycemia with severe symptoms, the best method of excluding dangerous conditions is often a diagnostic fast. This is usually conducted in the hospital, and the duration depends on the age of the patient and response to the fast. A healthy adult can usually maintain a glucose level above 50 mg/dl (2.8 mM) for 72 hours, a child for 36 hours, and an infant for 24 hours. The purpose of the fast is to determine whether the person can maintain his or her blood glucose as long as normal, and can respond to fasting with the appropriate metabolic changes. At the end of the fast the insulin should be nearly undetectable and ketosis should be fully established. The patient's blood glucose levels are monitored and a critical specimen is obtained if the glucose falls. Despite its unpleasantness and expense, a diagnostic fast may be the only effective way to confirm or refute a number of serious forms of hypoglycemia, especially those involving excessive insulin.

A traditional method for investigating suspected hypoglycemia is the oral glucose tolerance test, especially when prolonged to 3, 4, or 5 hours. Although quite popular in the United States in the 1960s, repeated research studies have demonstrated that many healthy people will have glucose levels below 70 or 60 during a prolonged test, and that many types of significant hypoglycemia may go undetected with it. This combination of poor sensitivity and specificity has resulted in its abandonment for this purpose by physicians experienced in disorders of glucose metabolism.

[edit] Causes

There are several ways to classify hypoglycemia. The following is a list of the more common causes and factors which may contribute to hypoglycemia grouped by age, followed by some causes that are relatively age-independent. See causes of hypoglycemia for a more complete list grouped by etiology.

[edit] Hypoglycemia in newborn infants

Hypoglycemia is a common problem in critically ill or extremely low birthweight infants. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant hyperinsulinism, hypopituitarism or an inborn error of metabolism and presents more of a management challenge.

• Transient neonatal hypoglycemia
  • Prematurity, intrauterine growth retardation, perinatal asphyxia
  • Maternal hyperglycemia due to diabetes or iatrogenic glucose administration
  • Sepsis
  • Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)
• Congenital hypopituitarism
• Congenital hyperinsulinism, several types, both transient and persistent
• Inborn errors of carbohydrate metabolism such as glycogen storage disease

[edit] Hypoglycemia in young children

Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:

• Prolonged fasting
  • Diarrheal illness in young children, especially rotavirus gastroenteritis
• Idiopathic ketotic hypoglycemia
• Isolated growth hormone deficiency, hypopituitarism
• Insulin excess
  • Hyperinsulinism due to several congenital disorders of insulin secretion
  • Insulin injected for type 1 diabetes
  • Hyperinsulin Hyperammonia syndrome (HIHA)due toGlutamate dehydrogenase 1gene.Can cause mental retardation and epilepsy in severe cases.^[15]
• Gastric dumping syndrome (after gastrointestinal surgery)
• Other congenital metabolic diseases; some of the common include
  • Maple syrup urine disease and other organic acidurias
  • Type 1 glycogen storage disease
  • Type III glycogen storage disease. Can cause less severe hypoglycemia than type I
  • Phosphoenolpyruvate carboxykinase deficiency Causes metabolic acidosis and severe hypoglycemia.
  • Disorders of fatty acid oxidation
  • Medium chain acylCoA dehydrogenase deficiency (MCAD)
  • Familial Leucine sensitive hypoglycemia ^[16]
• Accidental ingestions
  • Sulfonylureas, propranolol and others
  • Ethanol (mouthwash, "leftover morning-after-the-party drinks")

[edit] Hypoglycemia in older children and young adults

By far, the most common cause of severe hypoglycemia in this age range is insulin injected for type 1 diabetes. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of hyperinsulinism, and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. Body mass is large enough to make starvation hypoglycemia and idiopathic ketotic hypoglycemia quite uncommon. Recurrent mild hypoglycemia may fit a reactive hypoglycemia pattern, but this is also the peak age for idiopathic postprandial syndrome, and recurrent "spells" in this age group can be traced to orthostatic hypotension or hyperventilation as often as demonstrable hypoglycemia.

• Insulin-induced hypoglycemia
  • Insulin injected for type 1 diabetes
  • Factitious insulin injection (Munchausen syndrome)
  • Insulin-secreting pancreatic tumor
  • Reactive hypoglycemia and idiopathic postprandial syndrome
• Addison's disease
• Sepsis

[edit] Hypoglycemia in older adults

The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults.

• Insulin-induced hypoglycemia
  • Insulin injected for diabetes
  • Factitious insulin injection (Munchausen syndrome)
  • Excessive effects of oral diabetes drugs, beta-blockers, or drug interactions
  • Insulin-secreting pancreatic tumor
  • Alcohol induced hypoglycemia often linked with ketoacidosis
  • Alimentary (rapid jejunal emptying with exaggerated insulin response)
    • After gastrectomy dumping syndrome or bowel bypass surgery or resection
  • Reactive hypoglycemia and idiopathic postprandial syndrome
• Tumor hypoglycemia, Doege-Potter syndrome
• Acquired adrenal insufficiency
• Acquired hypopituitarism
• Immunopathologic hypoglycemia ^[17]

[edit] Treatment and prevention

Management of hypoglycemia involves immediately raising the blood sugar to normal, determining the cause, and taking measures to hopefully prevent future episodes.

[edit] Reversing acute hypoglycemia

The 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.

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 EMTs and Paramedics, or in-hospital personnel can establish an IV and give intravenous Dextrose, concentrations varying depending on age (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). Care must be taken in giving these solutions because they can be very necrotic if the IV is infiltrated. If an IV 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.

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.

[edit] Prevention

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 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.

[edit] Hypoglycemia as holistic medicine

Hypoglycemia is also a term of contemporary Alternative medicine which refers to a recurrent state of symptoms of altered mood and subjective cognitive efficiency, sometimes accompanied by adrenergic symptoms, which may or may not be associated with low blood glucose. Symptoms are primarily those of altered mood, behavior, and mental efficiency. This condition is usually treated by dietary changes which range from simple to elaborate, sometimes with good results. Advising people on management of this condition has been the focus of alternative medicine. More information about this form of "hypoglycemia", with far more elaborate dietary recommendations, is available on the internet and in health food stores.

[edit] See also

• Hyperglycemia
• Glucose
• Diabetes
• Diabetic coma
• Diabetic hypoglycemia
• Hyperinsulinemic hypoglycemia
• Congenital hyperinsulinism
• Idiopathic hypoglycemia
• Idiopathic postprandial syndrome
• Reactive hypoglycemia

[edit] References

[edit] External links

• The National Diabetes Information Clearinghouse

v • d • e Endocrine pathology: endocrine diseases (E00-35, 240-259) Pancreas/ glucose metabolism Hypofunction Diabetes mellitus types: (type 1, type 2, MODY) · complications (coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy, cardiomyopathy) insulin receptor (Rabson-Mendenhall syndrome) · Insulin resistance Hyperfunction Hypoglycemia · Hyperinsulinism · Zollinger-Ellison syndrome Hypothalamic/ pituitary axes Pituitary Hyperpituitarism anterior (Acromegaly, Hyperprolactinaemia, Pituitary ACTH hypersecretion) · posterior (SIADH) · general (Nelson's syndrome) Hypopituitarism anterior (Kallmann syndrome, Growth hormone deficiency, ACTH deficiency) · posterior (Neurogenic diabetes insipidus) · general (Empty sella syndrome, Pituitary apoplexy, Sheehan's syndrome, Lymphocytic hypophysitis) Thyroid Hypothyroidism Iodine deficiency · Cretinism (Congenital hypothyroidism) · Myxedema · Euthyroid sick syndrome Hyperthyroidism Hyperthyroxinemia (Thyroid hormone resistance, Familial dysalbuminemic hyperthyroxinemia) · Hashitoxicosis · Thyrotoxicosis factitia · Graves' disease Thyroiditis Acute infectious · Subacute (De Quervain's, Subacute lymphocytic) · Autoimmune/chronic (Hashimoto's, Postpartum, Riedel's) Goitre Endemic goitre · Toxic nodular goitre · Toxic multinodular goitre Thyroid nodule Parathyroid Hypoparathyroidism Pseudohypoparathyroidism Hyperparathyroidism Primary · Secondary · Tertiary · Osteitis fibrosa cystica Adrenal Hyperfunction aldosterone: Hyperaldosteronism/Primary aldosteronism (Conn syndrome, Bartter syndrome, Glucocorticoid remediable aldosteronism) · AME · Liddle's syndrome · 17α CAH cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome) sex hormones: 21α CAH · 11β CAH Hypofunction/ Adrenal insufficiency (Addison's, WF) aldosterone: Hypoaldosteronism (21α CAH, 11β CAH) cortisol: CAH (Lipoid, 3β, 11β, 17α, 21α) sex hormones: 17α CAH Gonads ovarian (Polycystic ovary syndrome, Premature ovarian failure) testicular (5-alpha-reductase deficiency, 17-beta-hydroxysteroid dehydrogenase deficiency) · Androgen receptor (Androgen insensitivity syndrome) general (Hypogonadism, Delayed puberty, Precocious puberty) Height Gigantism · Dwarfism/Short stature (Laron syndrome, Psychogenic dwarfism) Multiple Autoimmune polyendocrine syndrome (APS1, APS2) · Carcinoid syndrome · Multiple endocrine neoplasia (1, 2A, 2B) · Progeria · Woodhouse-Sakati syndrome see also congenital, neoplasia