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=== Hypoglycemia in Newborn Infants === | === 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. | 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: With loss of the continuous transplacental supply of glucose, plasma glucose concentration in the healthy term newborn falls during the first two hours after delivery | *Transient neonatal hypoglycemia: With loss of the continuous transplacental supply of glucose, plasma glucose concentration in the healthy term newborn falls during the first two hours after delivery.<ref name="pmid25819173">{{cite journal| author=Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW et al.| title=Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management. | journal=J Pediatr | year= 2015 | volume= 166 | issue= 6 | pages= 1520-5.e1 | pmid=25819173 | doi=10.1016/j.jpeds.2015.02.045 | pmc=4659381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25819173 }}</ref> | ||
*plasma glucose concentration is maintained by glycogenolysis during the first 8 to 12 hours then by gluconeogenesis.<ref name="pmid10202173">{{cite journal| author=Stanley CA, Baker L| title=The causes of neonatal hypoglycemia. | journal=N Engl J Med | year= 1999 | volume= 340 | issue= 15 | pages= 1200-1 | pmid=10202173 | doi=10.1056/NEJM199904153401510 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10202173 }}</ref> | |||
* [[Prematurity]], [[intrauterine growth retardation]] and [[perinatal asphyxia]]. | * [[Prematurity]], [[intrauterine growth retardation]] and [[perinatal asphyxia]]. | ||
* Maternal hyperglycemia due to [[diabetes]] or iatrogenic glucose administration | * Maternal hyperglycemia due to [[diabetes]] or iatrogenic glucose administration. | ||
* [[Sepsis]] | * [[Sepsis]] | ||
* Congenital hypopituitarism: cortisol and growth hormone regulate glucose level. | * Congenital hypopituitarism: cortisol and growth hormone regulate glucose level. | ||
* Maternal treatment with beta-sympathomimetic agents (eg, terbutaline and beta-blockers), which interrupts glycogenolysis by blocking epinephrine's effect | * Maternal treatment with beta-sympathomimetic agents (eg, terbutaline and beta-blockers), which interrupts glycogenolysis by blocking epinephrine's effect.<ref name="pmid27577580">{{cite journal| author=Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A et al.| title=Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia. | journal=Pediatrics | year= 2016 | volume= 138 | issue= 3 | pages= | pmid=27577580 | doi=10.1542/peds.2016-0731 | pmc=5005024 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27577580 }}</ref> | ||
* Hypothermic infants who have diminished availability of glucose and increased rates of glucose utilization | * Hypothermic infants who have diminished availability of glucose and increased rates of glucose utilization. | ||
* Severe hepatic dysfunction due to impairment of both glycogenolysis and gluconeogenesis | * Severe hepatic dysfunction due to impairment of both glycogenolysis and gluconeogenesis. | ||
*[[Congenital hyperinsulinism]]: | *[[Congenital hyperinsulinism]]: | ||
**Infant of a diabetic mother is the most common cause of hypoglycemia due to hyperinsulinism. Prolonged intrapartum hyperglycemia in fetus leads to hypertrophied and hyperfunctioning beta cells causing hyperinsulinsim. It is transient and resolves two to four days after birth. | **Infant of a diabetic mother is the most common cause of hypoglycemia due to hyperinsulinism. Prolonged intrapartum hyperglycemia in fetus leads to hypertrophied and hyperfunctioning beta cells causing hyperinsulinsim. It is transient and resolves two to four days after birth. | ||
**[[Beckwith-Wiedemann syndrome]] | **[[Beckwith-Wiedemann syndrome]] | ||
**[[Persistent hyperinsulinemic hypoglycemia of infancy]]: mutations in genes encoding enzymes that control intracellular metabolic pathways of the pancreatic beta cell. The genes most often affected control the sulfonylurea receptor that control the functional ATP-dependent potassium channel in the beta cell membrane. | **[[Persistent hyperinsulinemic hypoglycemia of infancy]]: mutations in genes encoding enzymes that control intracellular metabolic pathways of the pancreatic beta cell. The genes most often affected control the sulfonylurea receptor that control the functional ATP-dependent potassium channel in the beta cell membrane. | ||
**Excess exogenous insulin given to newborns with hyperglycemia may result in hypoglycemia | **Excess exogenous insulin given to newborns with hyperglycemia may result in hypoglycemia.<ref name="pmid19588439">{{cite journal| author=Sinclair JC, Bottino M, Cowett RM| title=Interventions for prevention of neonatal hyperglycemia in very low birth weight infants. | journal=Cochrane Database Syst Rev | year= 2009 | volume= | issue= 3 | pages= CD007615 | pmid=19588439 | doi=10.1002/14651858.CD007615.pub2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19588439 }}</ref> | ||
**Neonatal conditions associated with excess insulin secretion include alloimmune hemolytic disease of the newborn, heart failure and sepsis. These conditons increase anaerobic glycolysis due to decreased tissue perfusion. | **Neonatal conditions associated with excess insulin secretion include alloimmune hemolytic disease of the newborn, heart failure and sepsis. These conditons increase anaerobic glycolysis due to decreased tissue perfusion.<ref name="pmid10331464">{{cite journal| author=Sue CM, Hirano M, DiMauro S, De Vivo DC| title=Neonatal presentations of mitochondrial metabolic disorders. | journal=Semin Perinatol | year= 1999 | volume= 23 | issue= 2 | pages= 113-24 | pmid=10331464 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10331464 }}</ref> | ||
**polycythemia may result from greater glucose utilization by the increased mass of red blood cells. | **polycythemia may result from greater glucose utilization by the increased mass of red blood cells. | ||
*[[Inborn error of metabolism|Inborn errors of carbohydrate metabolism]]: | *[[Inborn error of metabolism|Inborn errors of carbohydrate metabolism]]: | ||
**Disorders of gluconeogenesis: fructose-1,6-bisphosphatase deficiency, pyruvate carboxylase deficiency. | **Disorders of gluconeogenesis: fructose-1,6-bisphosphatase deficiency, pyruvate carboxylase deficiency. | ||
**Disorders of carbohydrate metabolism: hereditary fructose intolerance, galactosemia. | **Disorders of carbohydrate metabolism: hereditary fructose intolerance, galactosemia. | ||
**Disorders of fatty acid metabolism: medium or long-chain acyl-CoA dehydrogenase deficiency). | **Disorders of fatty acid metabolism: medium or long-chain acyl-CoA dehydrogenase deficiency).<ref name="pmid7726385">{{cite journal| author=Worthen HG, al Ashwal A, Ozand PT, Garawi S, Rahbeeni Z, al Odaib A et al.| title=Comparative frequency and severity of hypoglycemia in selected organic acidemias, branched chain amino acidemia, and disorders of fructose metabolism. | journal=Brain Dev | year= 1994 | volume= 16 Suppl | issue= | pages= 81-5 | pmid=7726385 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7726385 }}</ref> | ||
====Hypoglycemia in Young Children==== | ====Hypoglycemia in Young Children==== | ||
Revision as of 18:50, 17 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Carlos A Lopez, M.D. [2] Mohammed Abdelwahed M.D[3]
Overview
Is when blood sugar decreases to below normal levels. This may result in a variety of symptoms including clumsiness, trouble talking, confusion, loss of consciousness, seizures, or death. Some causes of hypoglycemia are chloramphenicol, addison's disease, acute fatty liver of pregnancy and sepsis.
Causes
Life Threatening Causes
Common Causes
Causes
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: With loss of the continuous transplacental supply of glucose, plasma glucose concentration in the healthy term newborn falls during the first two hours after delivery.[1]
- plasma glucose concentration is maintained by glycogenolysis during the first 8 to 12 hours then by gluconeogenesis.[2]
- Prematurity, intrauterine growth retardation and perinatal asphyxia.
- Maternal hyperglycemia due to diabetes or iatrogenic glucose administration.
- Sepsis
- Congenital hypopituitarism: cortisol and growth hormone regulate glucose level.
- Maternal treatment with beta-sympathomimetic agents (eg, terbutaline and beta-blockers), which interrupts glycogenolysis by blocking epinephrine's effect.[3]
- Hypothermic infants who have diminished availability of glucose and increased rates of glucose utilization.
- Severe hepatic dysfunction due to impairment of both glycogenolysis and gluconeogenesis.
- Congenital hyperinsulinism:
- Infant of a diabetic mother is the most common cause of hypoglycemia due to hyperinsulinism. Prolonged intrapartum hyperglycemia in fetus leads to hypertrophied and hyperfunctioning beta cells causing hyperinsulinsim. It is transient and resolves two to four days after birth.
- Beckwith-Wiedemann syndrome
- Persistent hyperinsulinemic hypoglycemia of infancy: mutations in genes encoding enzymes that control intracellular metabolic pathways of the pancreatic beta cell. The genes most often affected control the sulfonylurea receptor that control the functional ATP-dependent potassium channel in the beta cell membrane.
- Excess exogenous insulin given to newborns with hyperglycemia may result in hypoglycemia.[4]
- Neonatal conditions associated with excess insulin secretion include alloimmune hemolytic disease of the newborn, heart failure and sepsis. These conditons increase anaerobic glycolysis due to decreased tissue perfusion.[5]
- polycythemia may result from greater glucose utilization by the increased mass of red blood cells.
- Inborn errors of carbohydrate metabolism:
- Disorders of gluconeogenesis: fructose-1,6-bisphosphatase deficiency, pyruvate carboxylase deficiency.
- Disorders of carbohydrate metabolism: hereditary fructose intolerance, galactosemia.
- Disorders of fatty acid metabolism: medium or long-chain acyl-CoA dehydrogenase deficiency).[6]
Hypoglycemia in Young Children
Single episodes of hypoglycemia due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism
- 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
- 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
- Disorders of fatty acid oxidation
- Medium chain acylCoA dehydrogenase deficiency (MCAD)
- Accidental ingestions
- Sulfonylureas, propranolol and others
- Ethanol (mouthwash, "leftover morning-after-the-party drinks")
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
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
- Drugs: they are the most common cause of hypoglycemia.[1]
- Insulin or insulin secretagogue: sulfonylureas, glyburide and less common glipizide or glimepiride due to longer duration of action. [30]. They suppress hepatic glucose production and stimulate glucose utilization causing hypoglycemia.
- Other drugs in non-diabetic patients: quinolones, pentamidine, quinine, beta blockers, angiotensin-converting enzyme inhibitors, and IGF-1 especially in in older patients with underlying renal or hepatic dysfunctions. [32]
- Alcohol: due to hepatic glycogen depletion in fasting patients. Alcohol can induce hypoglycemia alone or associated with other hypoglycemic drugs.
- Critical illnesses: hepatic, renal, or cardiac failure, sepsis. [34] It occurs due to impaired liver gluconeogenesis. Sepsis induced cytokines secretion cause supression of gluconeogenesis. 36
- Hormone deficiency: cortisol in acquired adrenal insufficiency or acquired hypopituitarism
- Nonislet cell tumor: Hypoglycemia usually occurs as a result of tumor production of IGF-2. 1
- Insulinoma
- Reactive hypoglycemia: there are different kinds of reactive hypoglycemia:[1] Alimentary Hypoglycemia (consequence of dumping syndrome; it occurs in about 15% of people who have had stomach surgery) Helicobacter pylori-induced gastritis. Congenital enzyme deficiencies (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood). Idiopathic reactive hypoglycemia Late Hypoglycemia (Occult Diabetes; characterized by a delay in early insulin release from pancreatic B cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test).
- Post gastric bypass hypoglycemia: rapid jejunal emptying with exaggerated insulin response.
- Insulin autoimmune hypoglycemia: it occurs in patients who have antibodies directed to endogenous insulin or to the insulin receptor. 41
- Accidental, surreptitious, or malicious hypoglycemia
References
- ↑ Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW; et al. (2015). "Re-evaluating "transitional neonatal hypoglycemia": mechanism and implications for management". J Pediatr. 166 (6): 1520–5.e1. doi:10.1016/j.jpeds.2015.02.045. PMC 4659381. PMID 25819173.
- ↑ Stanley CA, Baker L (1999). "The causes of neonatal hypoglycemia". N Engl J Med. 340 (15): 1200–1. doi:10.1056/NEJM199904153401510. PMID 10202173.
- ↑ Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A; et al. (2016). "Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia". Pediatrics. 138 (3). doi:10.1542/peds.2016-0731. PMC 5005024. PMID 27577580.
- ↑ Sinclair JC, Bottino M, Cowett RM (2009). "Interventions for prevention of neonatal hyperglycemia in very low birth weight infants". Cochrane Database Syst Rev (3): CD007615. doi:10.1002/14651858.CD007615.pub2. PMID 19588439.
- ↑ Sue CM, Hirano M, DiMauro S, De Vivo DC (1999). "Neonatal presentations of mitochondrial metabolic disorders". Semin Perinatol. 23 (2): 113–24. PMID 10331464.
- ↑ Worthen HG, al Ashwal A, Ozand PT, Garawi S, Rahbeeni Z, al Odaib A; et al. (1994). "Comparative frequency and severity of hypoglycemia in selected organic acidemias, branched chain amino acidemia, and disorders of fructose metabolism". Brain Dev. 16 Suppl: 81–5. PMID 7726385.