Hypoglycemia is a medical term referring to a pathologic state produced and usually defined by a lower than normal amount of sugar (glucose) in the blood. The term hypoglycemia literally means "low blood sugar". 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 and (rarely) death. Hypoglycemia can arise from many conditions, and can occur at any age.
Endocrinologists (specialists in disorders of blood glucose metabolism) typically consider the following criteria (referred to as Whipple's triad) as confirming a diagnosis of hypoglycemia:
- Measurably low level of blood glucose
- Presence of symptoms or problems at the time of the low glucose
- Reversal or improvement of symptoms or problems when the glucose is restored to normal
Hypoglycemia as American folk medicine
Hypoglycemia is also a term of contemporary American folk medicine which refers to a recurrent state of symptoms of altered mood and cognitive efficiency, sometimes accompanied by adrenergic symptoms, but not necessarily by measured low blood glucose. The 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.
This condition therefore overlaps with the condition of hypoglycemia described in the remainder of this article but is not entirely congruent. When low glucose levels can be measured, this condition is what is usually described by physicians as idiopathic reactive hypoglycemia. When glucose levels are not low enough to distinguish the patient's glucose from normal levels, this type of hypoglycemia does not carry the same risks of coma or brain damage as measurable hypoglycemia that meets the Whipple criteria. A variety of terms have been used in the medical literature: idiopathic postprandial syndrome, functional hypoglycemia, pseudohypoglycemia, nonhypoglycemia, and "hypoglycemia". The terms range from neutral to pejorative and reflect the range of attitudes of physicians as much as the nature of the condition. Most hypoglycemia websites describe a conflated mixture of reactive hypoglycemia and idiopathic postprandial syndrome but do not recognize a distinction.
Defining hypoglycemia: what's normal and what's low?
Varying values of blood glucose are defined as low depending on whether the definition is based on metabolic responses, population norms, or likelihood of clinical consequences. This article expresses glucose in milligrams per deciliter (mg/dl or mg/100 ml) as is customary in North America, while millimoles per liter (mmol/l or mM) are often the units used in the rest of the world. Values in mg/dl can be converted to mmol/l by dividing by 18 (e.g., 90 mg/dl = 5 mmol/l or 5 mM).
Research in healthy adults shows that mental efficiency declines measurably as blood glucose falls below 65 mg/dl. Hormonal defense mechanisms (adrenaline and glucagon) are activated as it drops below 55 mg/dl. Surveys of children and young adults show that fasting blood glucoses below 60 mg/dl or above 100 mg/dl are uncommon in the healthy population. On the other hand, individuals vary and not everyone with a blood sugar below 60 mg/dl will have symptoms, let alone a disease.
Fasting blood sugars in infancy and early childhood are lower, though still above 60 mg/dl after the newborn period except in illness or other unusual circumstances.
The normal range of newborn blood sugars is more problematic. Surveys and experience have revealed blood sugars often below 40 mg/dl and occasionally below 30 mg/dl in apparently healthy full-term infants on day one. Newborn brains seem to be able to use alternate fuels when glucose levels are low. Experts continue to debate the significance and risk of such levels, though the trend has been to recommend maintenance of glucose levels above 60 mg/dl. In ill, undersized, or premature newborns, low blood sugars are even more common, but there is a consensus that sugars should be maintained at least above 40 mg/dl in such circumstances. Some experts advocate 70 mg/dl as a therapeutic target, especially in circumstances such as hyperinsulinism where alternate fuels may be less available.
Glucose levels discussed above are venous serum levels. For clinical purposes, plasma and capillary serum levels are similar, and arterial levels slightly higher. On the other hand, whole blood glucose levels (e.g., by fingerprick meters) are about 15% lower than venous serum levels. Furthermore, available fingerstick glucose meters are warranted to be accurate to within 15% of a simultaneous laboratory value. In other words, a meter glucose of 39 mg/dl could be properly obtained from a person whose serum glucose was 55 mg/dl.
Two other factors affect reported glucose values. The disparity between venous and whole blood concentrations is greater when the hematocrit is high, as in newborns. High neonatal hematocrits are particularly likely to confound meter glucose measurement. Second, unless the specimen is drawn into a fluoride tube or processed immediately to separate the serum from the cells, the measurable glucose will be gradually lowered by in vitro processes.
Pathophysiology: why low blood sugar primarily affects the brain
Like most animal tissues, brain metabolism depends primarily on glucose for fuel in most circumstances. Some tissues, like muscle, liver, kidneys, intestines, and even white blood cells, can store varying amounts of glycogen, which serves as a rapid glucose source if blood levels are inadequate. However, 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. As blood glucose levels fall below 10 mg/dl, most neurons become electrically silent and nonfunctional.
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. Most of these are defensive or adaptive, tending to raise the blood sugar via glycogenolysis and gluconeogenesis or provide alternative fuels.
Signs and symptoms of hypoglycemia
Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.
- Shakiness, anxiety, nervousness, tremor
- Palpitations, tachycardia
- Sweating, feeling of warmth
- Pallor, coldness, clamminess
- Dilated pupils
- Abnormal mentation, impaired judgement
- Nonspecific dysphoria, anxiety, moodiness, depression, crying, fear of dying
- 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
- Difficulty speaking, slurred speech
- Ataxia, incoordination, sometimes mistaken for "drunkenness"
- Focal or general motor deficit, paralysis, hemiparesis
- Paresthesias, 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. Specific manifestations vary by age and by the severity of the hypoglycemia. In young children vomiting often accompanies 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 do tend to be similar from episode to episode.
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.
In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurologic 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.
Determining the cause
Hundreds of conditions can cause hypoglycemia (Table 1, below) The two best guides to the cause of acute, unexplained hypoglycemia are (1) the clinical circumstances and (2) a critical specimen of blood obtained before the hypoglycemia is reversed.
The clinical 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, physical abnormalities, maternal glucose status, and response to treatment.
- AGE: Factors contributing to hypoglycemia in the first day of life differ from common causes in older children. Even beyond the newborn period, causes vary by age. Young adults have a different range of probable causes than older adults.
- TIME OF DAY & TIME SINCE LAST MEAL: Fasting hypoglycemia has different causes than postprandial. E.g., ketotic hypoglycemia is the most common hypoglycemia occurring before breakfast in young children past the first year of life.
- PREVIOUS EPISODES: If a truly low blood sugar has been discovered, a history of similar episodes increases the likelihood of significant organic disease and gives clues to the nature. E.g., ingestion or drug effect is less likely.
- NUTRITIONAL STATUS: Obesity or large size suggests hyperinsulinism. E.g., a large-for-gestational-age newborn suggests maternal diabetes. Children with ketotic hypoglycemia are nearly always underweight for height. Adults with chronic hyperinsulinism due to a pancreatic tumor will usually have gained weight.
- PHYSICAL & MENTAL DEVELOPMENT: Growth failure with onset in second 6 months of life suggests hypopituitarism or a significant inborn error of metabolism, such as glycogen storage disease. Developmental delay also points toward congenital metabolic diseases.
- DRUGS OR TOXINS: See Table of Causes, below, for drugs causing hypoglycemia. A toddler with a sudden onset of hypoglycemia is at highest risk of this cause; alcohol and grandparent's diabetes pills are notorious. An older adult on multiple medications may well be suffering a drug interaction amplifying the hypoglycemic effect of one of the drugs.
- DISEASES OF OTHER ORGAN SYSTEMS: Advanced dysfunction of any major organ system may cause hypoglycemia.
- PHYSICAL ABNORMALITIES: Individual anomalies may indicate specific causes. E.g., omphalocele (Beckwith-Wiedemann syndrome), hepatomegaly (glycogen storage disease), micropenis (hypopituitarism).
- MATERNAL GLUCOSE STATUS: Maternal hyperglycemia (even unsuspected) is a common cause of hypoglycemia due to hyperinsulinism in the first two days of life.
- RESPONSE TO TREATMENT: Once hypoglycemia has been recognized, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose rate requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism.
The other important clue to the cause of hypoglycemia is blood (the critical specimen) obtained at the time of the hypoglycemia. Hormone levels obtained at the time of hypoglycemia can provide information that would otherwise require a thousand-dollar admission and unpleasant starvation testing.
For an infant or child with hypoglycemia, the serum should be used for as many as possible of the following, roughly in order of importance:
Glucose is needed for the interpretation of insulin, cortisol, GH, glucagon, and epinephrine levels.
Insulin levels range from undetectable to several hundred μU/ml and can change as rapidly as glucose. It is usually the highest priority test, but is of no value if not obtained simultaneously with a low blood sugar. Levels above 10 μU/ml at the time of hypoglycemia implicate hyperinsulinism as the probable cause of hypoglycemia. As some infants with hyperinsulinism may have levels only slightly above this, the insulin/glucose ratio (in μU/ml and mg/dl, respectively) may be more discriminant. I/G ratios repeatedly above 0.4 during hypoglycemia are strong evidence of hyperinsulinism.
Cortisol should rise above 10 mg/dl in response to hypoglycemia at any age. Weight loss, vomiting, dehydration, and (sometimes) hyperpigmentation are suggestive of primary adrenal failure. Micropenis, hyperbilirubinemia, absent septum pellucidum, midline defects and/or optic nerve abnormalities in the newborn suggest congenital hypopituitarism.
Growth hormone should rise above 10 ng/ml in response to hypoglycemia at any age. It is especially important in young children with growth failure and morning ketotic hypoglycemia. Other features of congenital hypopituitarism are listed in the previous paragraph.
Urine and serum ketones (acetone, acetoacetate, and β-hydroxy¬bu¬ty¬rate) normally rise as insulin levels fall (e.g., prolonged fasting and most types of hypogly¬cemia). Standard laboratory measurement of Aserum ketones@ in 0.2C0.5 ml provides a rapid but semiquantitative titer of acetone and acetoacetate but not β-hydroxybutyrate (see below). Because the kidneys actively transport and concentrate them, ketones can be detected by dip strip in urine even when the blood level is below the threshold of detection. The absence of ketosis at the time of hypoglycemia usually indicates hyperinsulinism or defective ketogenesis (as in certain disorders of mitochondrial fatty acid oxidation described below).
Electrolytes do not necessarily need to be obtained as part of the critical specimen (because they do not change so rapidly) but should be part of the initial tests for the ill-appearing patient. Various patterns of abnormality may reflect major organ system dysfunction. Hyponatremia can occur with adrenal insufficiency or hypopituitarism. Metabolic acidosis is also consistent with adrenal insufficiency, as well as numerous other conditions (severe gastroenteritis, sepsis, renal failure, etc.). A metabolic acidosis with a large anion gap may indicate lactic acidosis (a common accompaniment of disorders of gluconeogenesis such as type I glycogenosis) or poisoning (e.g., ethanol, salicylate).
The following tests also must be obtained at the time of hypoglycemia to be interpretable, and may be essential for certain diagnoses. Because they require larger amounts of blood or special tubes, or are useful in only a few circumstances, they should be chosen more selectively.
Lactic acid (or lactate) can be measured in 0.7 ml of serum. It is most likely to be useful in ill-appearing young children with vomiting, hepatomegaly, or prior episodes. Fasting levels should be less than 2.5 mmol/l in infancy, 2.0 in early childhood, and under 1.0 in older children and young adults. Levels are lower when fed and slightly higher after prolonged starvation. Lactic acidosis occurs with (a) circulatory failure and (b) many metabolic disorders, especially those involving gluconeogenesis (e.g., type I glyco¬genosis).
Free (or non-esterified) fatty acids rise during fasting as a result of lipolysis. Typical FFA levels after overnight fasting are 0.5C1.5 mmol/l in infants and young children. Levels are slightly lower in older children and young adults, and somewhat higher with prolonged fasting. Demonstration of inappropriately low levels at the time of hypoglycemia may help corroborate a diagnosis of hyperinsulinism.
β-hydroxybutyrate is one of the ketone bodies described above. βOHB is typically less than 1 mmol/l after an overnight fast in infants and young children, and less than 0.5 in older children and young adults. Levels rise three- or four-fold with more prolonged starva¬tion. Post-prandial levels should be nearly undetectable. Low levels accompanying hypoglycemia sug-gest hyperinsulinism.
Alanine is the principal amino acid substrate for gluconeogenesis. Alanine values vary by age, dietary protein, time since meal, and laboratory from as low as 135 μmol/l to above 700. Levels tend to be higher in infants than adults. Alanine levels decline during fasting due to consumption by the liver for glucose production. In the work-up of hypoglycemia in young children, alanine levels obtained at the time of low glucose can occasionally be useful, but must be interpreted with caution and consideration of other laboratory evidence. Alanine levels above 480 μmol/L often occur with defects of gluconeogenesis other than type I glycogenosis. Levels below 200 occur with ketotic hypoglycemia.
Glucagon should rise above 120 pg/ml in any type of hypoglycemia. Despite glucagon's crucial role in regulating glycogenolysis, clinically significant deficiency (except in long-term diabetes) is so rare that this test is among the least important.
Epinephrine (adrenaline) is an important mediator of both glycogenolysis and lipolysis in response to hypoglycemia of any type, usually rising above 100 pg/ml. It is worth measuring mainly in suspected autonomic failure, and provides little additional information when prominent adrenergic symptoms and signs confirm autonomic function.
C peptide is released as a byproduct with endogenous insulin. Because C-peptide is not present in animal or synthetic human insulin products, measurement during hypoglycemia can help distinguish endogenous from exogenous hyperinsulinism. Levels of 1-2 ng/ml occur with significant endogenous insulin secretion. A significant insulin level with undetectable C-peptide indicates exogenous hyperinsulinism (insulin-dependent diabetes, malicious or factitious insulin injection).
Proinsulin is cleaved to produce C-peptide and insulin in beta cells and is normally present in the circulation in amounts under 20% of the insulin level. Disproportionate levels in hypoglycemic patients with endogenous hyperinsulinism indicate an insulinoma. Proinsulin has not been found to be elevated in the most common types of hyperinsulinism in young children.
Ethanol ingestion can cause severe hypoglycemia and metabolic acidosis in a previously healthy toddler.
Causes of hypoglycemia
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.
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
Hypoglycemia in young children
Hypoglycemia in adolescents 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 the peak age for idiopathic postprandial syndrome, and recurrent "spells" in this age group represents 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
- Addison's disease
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.
Starvation, Inadequate Intake Or Absorption
The younger the child, the shorter the time it takes fasting to lead to hypoglycemia although most infants can maintain a low normal glucose for 18-24 hours or more. Adults in ordinary health and nutritional status should be able to fast longer than 36 hours without becoming hypoglycemic.
Major Organ Failure & Critical Illness
Hypoglycemia occurs in adults in the setting of failure of most major organ systems, including brain, heart, liver, and kidneys. In an intensive care unit, solitary causes of hypoglycemia are less common than combinations of contributing factors.
Hypoglycemia has been reported in association with many different types of solid tumors which do not produce insulin. Suspected mechanisms have included increased glucose utilization by a large or active tumor, cachexia and depletion of glycogen reserves, inhibited hepatic gluconeogenesis or glycogenolysis, blunted counterregulatory hormone responses, autoimmune stimulation of insulin receptors, and production by the tumor of peptides (e.g., insulin-like growth factor 2) or antibodies capable of activating insulin receptors.
- Hypoglycemia due to endogenous insulin
- Congenital hyperinsulinism
- Transient neonatal hyperinsulinism
- Due to maternal factors
- Due to infant factors
- Malposition of umbilical catheter
- Focal congenital hyperinsulinism
- Paternal SUR1 mutation with clonal loss of heterozygosity of 11p15
- Paternal Kir6.2 mutation with clonal loss of heterozygosity of 11p15
- Diffuse congenital hyperinsulinism
- Donohue syndrome (leprechaunism)
- Acquired tumors and hyperplasias of pancreatic beta cells
- Islet cell adenoma
- Islet cell carcinoma
- Multiple endocrine adenomatosis syndrome
- Pluriglandular syndrome of islet, pituitary, parathyroid hyperplasia
- Autoimmune insulin syndrome
- Reactive hypoglycemia (postprandial hypoglycemia syndrome)
- Dumping syndrome
- Drug induced hyperinsulinism
- Hypoglycemia due to exogenous (injected) insulin
- Insulin self-injected for treatment of diabetes
- Excessive insulin dosage or accelerated absorption
- Excessive activity
- Inadequate food or delayed or decreased absorption
- Drugs which contribute synergistically
- Development of concurrent disease
- Acquired endocrinopathies
- Renal, cardiac or liver failure
- Factitious & malicious insulin injection
- Insulin tolerance test for pituitary or adrenergic response assessment
- Treatment of hyperkalemia
- Insulin potentiation treatment (cancer quackery)
- Insulin-induced coma for depression or psychosis treatment (insulin shock)
- Defective glycogenolysis or glycogen accumulation
- Galactose-1-phosphate uridyl transferase deficiency (galactosemia)
- Defects of gluconeogenesis or substrate supply
- Fructose-1,6-diphosphatase deficiency
- Isovaleric acidemia
- Phosphoenolpyruvate carboxykinase deficiency
- Pyruvate carboxylase deficiency (Leigh syndrome)
- Fructose-1-phosphate aldolase deficiency
- Defects of mitochondrial beta-oxidation and fatty acid metabolism
- Systemic carnitine deficiencies
- Enzyme deficiencies
- Carnitine palmitoyltransferase I
- Carnitine palmitoyltransferase II
- Carnitine acyltransferase
- Butyryl CoA dehydrogenase
- Hydroxymethylglutaryl CoA lyase
- Methylcrotonyl CoA carboxylase
- Medium chain acyl CoA dehydrogenase
- Short chain acyl CoA dehydrogenase
- Long chain acyl CoA dehydrogenase
- Multiple acyl CoA dehydrogenase (glutaric aciduria type II)
- Long-chain 3-hydroxyacyl-CoA dehydrogenase
- Short-chain 3-hydroxyacyl CoA dehydrogenase
- Carnitine/acylcarnitine translocase
- Enoyl CoA hydratase
- Succinyl CoA:acetoacetate transferase
- Defects of amino acid metabolism
- Miscellaneous metabolic defects
- Defective type I glucose transporter in brain
- Methylglutaconic aciduria
- Glycerol intolerance
- Rare variants of galactose intolerance
- Other rare or poorly defined congenital metabolic defects
Drugs And Toxins
- Insulin, antidiabetic agents (see above)
- Drugs associated with hypoglycemia alone
- Drugs which lower glucose in diabetics
- Enlapril and captopril
- Sulfa antibiotics, including SMX/TMP (especially in renal failure)
- Monoamine oxidase inhibitors
- Medicines not available in U.S.
- Azapropazone, buformin, carbutamide, cibenzoline, cycloheptolamide, glibornuride, gliclazide, mebanazine, metahexamide, perhexiline, sulphadimidine, sulphaphenazole, Nigerian cow urine medicine
- Environmental toxins
- Amanita phalloides toxin
- Abractylis gummifera (Mediterranean plant)
- Hypoglycin from unripe ackee fruit (Jamaican vomiting illness)
- Vacor rat poison
Idiopathic And Miscellaneous
- Ketotic hypoglycemia
- Identifiable hormone and enzyme deficiencies
- Idiopathic hypoglycemias, etiologies undetermined
- Antibodies to insulin
- Antibodies to insulin receptor
- Stimulating antibodies to islet cells
- Thyrotoxicosis (extremely rare)
- Extreme exercise
- In vitro glucose consumption after blood drawing
- Leukemic WBC's may consume glucose in vitro
- Polycythemia of infancy (RBCs consume glucose in vitro)
- Inaccuracies of blood drop strips
- Inherent variation inaccuracy at low end
- Inadequate drop
- Excessive wiping
- Short time interval
Reactive, Functional, Postprandial, Etc.
- Prediabetes (both categories controversial & may not be valid)
- Juvenile diabetes (rare, anecdotal reports)
- Adult onset diabetes (in early stages)
- After intravenous glucose load
- Abrupt discontinuation of parenteral nutrition or i.v. glucose
- After exchange transfusion with ACD preserved blood in neonate
- Alimentary (rapid jejunal emptying with exaggerated insulin response)
- Post fundoplication for gastroesophageal reflux
- Post gastrectomy dumping syndrome
- Short bowel syndrome
- Idiopathic gastrointestinal motility disturbance
- Alternate day growth hormone therapy
- Idiopathic reactive or functional hypoglycemia (hypoglycemia documented at time of symptoms: rare)
- Idiopathic postprandial syndrome (hypoglycemia never documented: common)
The main cause of hypoglycemia is intentional or accidental overdose of antidiabetic medication, insulin or oral drugs, or failure to eat as planned after taking those medications. There are other causes as well, both in diabetic or non-diabetic people.
Another serious cause of hypoglycemia is the 'insulinoma', a pancreatic tumor that is derived from B (beta) cells of islets of Langerhans. These tumours are hormonally active, producing and releasing insulin into bloodstream. C-peptide levels can distinguish between abnormally high insulin levels that result from overproduction, and those caused by administration of exogenous insulin.
Hypoglycemia can differ in both its causes and treatments depending on whether or not the person has diabetes.
Hypoglycemia can occur in people with diabetes who take certain medications to keep their blood glucose levels in control. Usually hypoglycemia is mild and can easily be treated by eating or drinking something with carbohydrate. But left untreated, hypoglycemia can lead to loss of consciousness.
Two types of hypoglycemia can occur in people who do not have diabetes: reactive (postprandial, or after meals) and fasting (postabsorptive). Reactive hypoglycemia is not usually related to any underlying disease; fasting hypoglycemia often is.
In reactive hypoglycemia, symptoms appear within 4 hours after you eat a meal. Not all causes are not well understood, though some are. Researchers are still debating which causes are more prevalent.
Fasting hypoglycemia is diagnosed from a blood sample that shows a blood glucose level of less than 50 mg/dL after an overnight fast, between meals, or after exercise. Causes include certain medications, alcohol, critical illnesses, hormonal deficiencies, some kinds of tumors, and certain conditions occurring in infancy and childhood.
Hypoglycemia is usually divided into "reactive hypoglycemia" and "functional hypoglycemia." Reactive hypoglycemia refers to hypoglycemia caused by external influences, like diet and medication use. This type is more amenable to management or cure. Functional hypoglycemia refers to hypoglycemia caused by a malfunction, possibly metabolic, within the sufferer. This type is harder to manage. Functional hypoglycemia is caused by an overproduction of insulin, or a malfunctioning of the body's insulin-management system (insulin resistance). Hypoglycemia is also known as idiopathic if no physical cause for the bloodsugar drop can be discerned.
For a hypoglycemic episode, if the patient is conscious, eating or drinking something that is rich in simple carbohydrates, such as fruit juice, hard candy, 4 oz. of non-diet soda, etc. can be enough. If not, intravenous injection of glucose and/or injection of glucagon that is a hormone with antagonistic properties counteracting the hypoglycemic state. When injecting anything to a diabetic patient under a state of Hypoglycemia, one must be careful not to inject insulin accidentally, under the typical confusion this type of emergency brings. This would cause the diabetic person immediate death.
For long-term treatment, of reactive hypoglycemia, some experts recommend:
- eat small meals and snacks about every 3 hours
- exercise regularly
- choose high-fiber foods
- avoid or limit foods high in sugar, especially on an empty stomach
- eat a variety of foods including:
- meat, poultry, fish, or nonmeat sources of protein
- starchy foods such as whole-grain bread, rice, and potatoes
- dairy products
Treatment for fasting hypoglycemia varies a great deal by cause. See a medical professional to further examine the cause so an appropriate treatment option can be used.