Hypoglycemia

Last Updated: September 2, 2004

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Synonyms and related keywords: glucopenia, low serum glucose, hyperinsulinism, glycogen storage disease, excessive glucose utili ation, glucose underproduction, !etotic hypoglycemia, glycogen storage disorder, "ree "atty acid metabolism de"ect, mild hyperinsulinism
Author# Robert Hoffman, MD, Associate $ro"essor, %epartment o" $ediatrics, &hio State 'niversity College o" (edicine Robert )o""man, (%, is a member o" the "ollowing medical societies# American Academy o" $ediatrics, American %iabetes Association, Christian (edical * %ental Society, Endocrine Society, and Society "or $ediatric Research Editor+s,# Karl S Roth, MD, Chair, $ro"essor, %epartment o" $ediatrics, Creighton 'niversity School o" (edicine- Robert Konop, harmD, Clinical Assistant $ro"essor, %epartment o" $harmacy, Section o" Clinical $harmacology, 'niversity o" (innesota- Stephen Kemp, MD, hD, $ro"essor, %epartment o" $ediatrics, Section o" $ediatric Endocrinology, 'niversity o" Ar!ansas and Ar!ansas Children.s )ospital- Merrily oth, MD, $ro"essor, %epartment o" $ediatrics, 'ni"ormed Services 'niversity o" the )ealth Sciencesand !eorge "hro#sos, MD, $%% , $%" , M%"& , Chie", $ediatric and Reproductive Endocrinology /ranch, $rogram %irector, $ediatric Endocrinology, 01C)%201)- Clinical $ro"essor, %epartment o" $ediatrics, 3eorgetown 'niversity (edical School 'ackgro#nd: )ypoglycemia may be termed a biochemical symptom, indicating presence o" an underlying cause4 Since glucose is the "undamental energy currency o" the cell, disorders that impact its availability or its use can cause hypoglycemia4 1t is, there"ore, a common clinical problem in neonates, although it is less common in in"ants and toddlers and rare in older children4 1t can be caused by a variety o" di""erent conditions4 5he most common cause o" mild or severe hypoglycemia in childhood is insulin6treated type 7 diabetes and a mismatch among "ood, exercise, and insulin4 Clinical symptoms o" hypoglycemia may be subtle or overt but are not speci"ic to hypoglycemia and "re8uently are attributed to other disorders by the unaware physician4 5his is particularly true i" the patient has had another neurologic insult such as head trauma or hypoxia4 athophysiology: 5he body normally de"ends itsel" against hypoglycemia by decreasing insulin secretion and increasing glucagon, epinephrine, growth hormone, and cortisol secretion4 5hese hormonal changes combine to cause

increased hepatic glucose output, increased alternative "uel availability, and decreased glucose utili ation +See 1mage 7,4 5he increase in hepatic glucose production comes initially "rom the brea!down o" liver glycogen stores due to lower insulin and increased glucagon4 9hen glycogen stores become depleted and protein brea!down increases due to increased cortisol levels, hepatic gluconeogenesis replaces glycogenolysis as the primary source o" glucose production4 5his brea!down o" protein is re"lected by increased plasma levels o" the gluconeogenic amino acids, alanine, and glutamine4 %ecreased peripheral glucose use again occurs initially because o" a "all in insulin levels and later because o" increases in epinephrine, cortisol, and growth hormone4 All : events increase lipolysis and plasma "ree "atty acids, which are available as an alternative "uel and competitively inhibit glucose use4 1ncreased plasma and urinary !etone levels indicate the use o" "at as an energy source4 $lasma "ree "atty acids also stimulate glucose production4 )ypoglycemia occurs when one or more o" these counterregulatory mechanisms "ail, either through glucose overutili ation as in hyperinsulinism, underproduction as in the glycogen storage diseases, or a combination o" the two as in growth hormone or cortisol de"iciency4 Mortality(Morbidity: )ypoglycemia has both acute and long6term conse8uences4 (ost o" the acute conse8uences are listed immediately below in the Clinical section o" this discussion- however, in"ants and children with asymptomatic hypoglycemia have been shown to have neurocognitive de"ects at the time o" hypoglycemia, including impaired auditory and sensory evo!ed responses and impaired test per"ormance4 ;ong6term conse8uences o" hypoglycemia include decreased head si e, lowered 1<, and speci"ic regional brain abnormalities seen with magnetic resonance imaging4 (any o" the etiologies o" hypoglycemia may have the same conse8uences, ma!ing the causal distinction very di""icult4

History: 1n normal situations, glucose is the primary source "or brain energy use4 5he brain also can use !etones, but this transition ta!es time4 Symptoms o" hypoglycemia re"lect 2 ma=or clinical pathways4 5he "irst pathway is caused by activation o" the autonomic nervous system, which causes symptoms o" sweating, trembling, "lushing, anxiety, heart pounding, and hunger4 5he second group o" symptoms is due to neuroglycopenia and includes inability to concentrate, con"usion, tiredness, "eeling tear"ul, di""iculty spea!ing, behavioral changes, incoordination, wea!ness, and drowsiness4 0onspeci"ic symptoms include mouth tingling, dry mouth, blurred vision, headache, and nausea4 5hese symptoms, o" course, vary according to the age o" the sub=ect as listed below4

0eonates

o o o o o o o o o o o o

5remulousness /ris! (oro re"lex ;ethargy $oor "eeding 1rritability )ypothermia Respiratory distress Apnea /radycardia Sei ure Coma Sudden death

&lder children
o o o o o o o o o o o

%i iness Sweating )unger Anxiousness Con"usion ;ethargy $oor "eeding 1rritability Sei ure Coma Sudden death

hysical:

)ypoglycemic reactions usually, but not always, are accompanied by an increased heart rate with bounding pulse due to increased epinephrine secretion4 1n"ants, i" awa!e, may be irritable, tremulous, and cran!y4 1" the brain energy supply is severely impaired, the patient.s mental status is li!ely to be impaired with extreme inappropriate a""ect and mood, lethargy, or coma4 ;arge body si e "or age in the neonate or older child suggests hyperinsulinism, while decreased subcutaneous "at suggests inade8uate glucose stores4 $oor linear growth may point to growth hormone de"iciency, and midline "acial and cranial abnormalities suggest pituitary hormone de"iciencies4 ;iver si e should be assessed to loo! "or evidence o" glycogen storage diseases4

"a#ses: %isorders o" excessive glucose utili ation

o

)yperinsulinism +in"ant o" a mother with diabetes, persistent hyperinsulinemic hypoglycemia o" in"ancy, insulin6producing tumors, child abuse,# )yperinsulinism causes excess glucose utili ation primarily by its stimulatory e""ect on glucose upta!e by s!eletal muscle4 1n in"ants, hyperinsulinemia may be present due to a genetic activating de"ect in the sul"onylurea receptor causing persistent insulin secretion4 5his disorder is !nown as endogenous6 persistent hyperinsulinemic hypoglycemia o" in"ancy +previously called nesidioblastosis,4 1n"ants o" mothers with diabetes also have high insulin levels a"ter birth due to the high glucose exposure in utero- the poorer the glucose control during pregnancy, the greater the li!elihood o" hyperinsulinism in the in"ant4 1n older children, hyperinsulinemia is rare, but an insulin6producing tumor is the most common cause4 Exogenous administration o" insulin or oral hypoglycemic agents, either accidentally or due to abuse, must be considered4 %e"ects in glucose utili ation +>rebs cycle de"ects, respiratory chain de"ects,# 5hese disorders are rare but inter"ere with the ability to appropriately generate A5$ "rom glucose oxidation4 ;actate levels are high4 %e"ects in alternative "uel production +carnitine acyl trans"erase de"iciency, hepatic hydroxymethyl glutaryl coen yme A +)(3 CoA, lyase de"iciency, long6 and medium6chain acyl6coen yme A dehydrogenase de"iciency, variably in short6chain acyl6coen yme A dehydrogenase de"iciency,# 5hese disorders all inter"ere with the use o" "at as energy supply so the body is dependent on glucose

only4 5his becomes a problem during periods o" prolonged "asting that "re8uently accompany gastrointestinal illness4
o

Sepsis or other hypermetabolic state, such as hyperthyroidism4

%isorders o" glucose underproduction

o

1nade8uate glucose stores +prematurity, small "or gestational age in"ants, malnutrition, !etotic hypoglycemia,# 5hese disorders are the most common causes o" hypoglycemia apart "rom insulin treatment in diabetes but to a large degree are diagnoses o" exclusion once other causes o" hypoglycemia are ruled out4 5he "irst : should be readily apparent "rom the clinical situation4 5he last +ie, !etotic hypoglycemia, usually occurs in children who are thin and small between the ages o" 7? months and @ years and usually occurs when "ood inta!e is disrupted "or some reason4 %isorders o" hepatic glucose production +glucose6@6phosphatase de"iciency Atype 7 glycogen storage diseaseB, debrancher de"iciency Atype : glycogen storage diseaseB, hepatic phosphorylase de"iciency Atype @ glycogen storage disease, glycogen synthase de"iciency, "ructose 7,@ diphosphatase de"iciency, phospho6enol pyruvate de"iciency, pyruvate carboxylase de"iciency, galactosemia, hereditary "ructose intolerance, maple syrup urine diseaseB,# 5hese disorders all inter"ere in glucose production through a variety o" de"ects including bloc!age o" glucose release or synthesis, or bloc!ing2inhibiting gluconeogenesis4 Children with these diseases may become adapted to their hypoglycemia because o" its chronicity4 )ormonal abnormalities +panhypopituitarism, growth hormone de"iciency, cortisol de"iciency Aprimary or secondaryB,# As described earlier, growth hormone and cortisol play important roles in generating alternative "uels and in stimulating glucose production4 Since they are easily treatable abnormalities, it is important that they be recogni ed early4 5oxins and other illnesses +ethanol, salicylates, propranolol, malaria,# Ethanol inhibits gluconeogenesis by the liver and can thus cause hypoglycemia4 5his is particularly true in patients with insulin6 treated diabetes who are unable to reduce insulin secretion in response to developing hypoglycemia4 Salicylate intoxication causes both hyperglycemia and hypoglycemia4 5he latter is due to augmentation o" insulin secretion and inhibition o" gluconeogenesis4

D)$$&R&*+)%LS
Section , of

-ther roblems to be "onsidered: Addison Adrenal Exogenous insulin Multiple acyl-CoA dehydrogenase Sepsis .#ick $ind

disease crisis administration deficiencies

Lab St#dies: %etection o" hypoglycemia

o

5o be !ept uppermost in mind is that hypoglycemia should be considered as an indication o" some abnormality in counterregulation or lac! o" alternative substrate4 )ence, the "inding should prompt a thorough investigation o" its cause4 $lasma glucose concentrations should be measured in all neonates and children with the above6mentioned symptoms with due consideration given to the temporal relationships o" the test samples4 %ebate continues as to what exact glucose level constitutes hypoglycemia, particularly in neonates4 &lder literature suggests levels above 74C mmol2; are acceptable in this age group4 0ewer publications suggest levels below 24D mmol2; are inappropriate4 5he presence o" symptoms and a low plasma glucose concentration plus relie" o" symptoms by correction o" hypoglycemia constitute 9hipple triad4 5his documents the presence o" hypoglycemia and its symptomatic conse8uences4 (easurement o" the plasma glucose concentration ideally should be per"ormed with a laboratory6based glucose analy er4 1" this is unavailable, the home blood6glucose monitors may be usedhowever, their accuracy in the low range is uncertain, and they have been shown to miss and overdiagnose hypoglycemia4

Screening

Screening "or hypoglycemia in the asymptomatic neonate may be controversial4 (ore recent reviews suggest screening is appropriate in in"ants o" mothers who are diabetic, in"ants who are large or small "or their gestational age, and in"ants who are premature4 Screening should begin within the "irst 26: hours o" li"e and continue throughout the "irst 24 hours o" li"e4 1n"ants who are premature and those small "or their gestational age should be given intravenous or oral "eedings shortly a"ter birth to prevent hypoglycemia4

Critical sample
o

Sorting through the di""erential o" hypoglycemia depends on obtaining the critical sample at the time o" hypoglycemia4 5his sample measures the various metabolic precursors and hormones involved in glucose counterregulation and includes the "ollowing# glucose, insulin, growth hormone, cortisol, lactate, pyruvate, beta6 &)6butyrate, "ree "atty acids, carnitine, and branched6chain amino acid levels4 A urine sample "or organic6acid analysis is also o" critical importance4

Easting study
o

1" the above measurements are not available at the time o" initial presentation, the hypoglycemia must be reproduced4 5his is usually completed through a closely monitored "ast4 5his "ast should be conducted in a center that can respond 8uic!ly and appropriately should signi"icant hypoglycemic conse8uences develop4 9hen the plasma glucose concentration "alls below 24D mmol2;, the "ast is ended and the critical sample is drawn4 (aximum length o" the "ast is dependent on the age o" the child4 Conservative recommendations "or maximum lengths o" "asting are as "ollows# younger than @ months, ? hours- @6? months, 72 hours?672 months, 7@ hours- 762 years, 7? hours- 26C years, 20 hoursolder than C years, 24 hours4

1nterpretation o" critical sample +1mage 2,

o

(etabolically, plasma "ree "atty acids and beta6&) butyrate should increase to more than 04D mmol2; and more than7 mmol2; to provide alternative "uel4 A "ailure o" both to increase is consistent

o o o o

with hyperinsulinemic lipolytic suppression4 A de"ect in "atty acid metabolism is suggested by an increase in "ree "atty acid +F: mmol2;,, but not by beta6&)6butyrate levels4 )igh plasma lactate levels suggest de"ects o" gluconeogenesis, glycolysis, or respiratory6chain de"ects4 $lasma insulin levels should be suppressed +G:0 pmol2; AD m'2m;B,4 Cortisol levels should increase +FDD0 nmol2; A20 mcg2d;B,4 3rowth hormone levels should increase +F@ mcg2;,4

&ther laboratory studies

o

/e"ore per"orming a "asting study, some authors have suggested measuring "ree carnitine, total carnitine, and acyl carnitine species in order to detect medium6chain acyl6CoA dehydrogenase de"iciency in advance, since this may prevent the occurrence o" li"e6 threatening hypoglycemia and hyperammonemia during the "ast4 (easurement o" insulinli!e growth "actor6binding protein 7 +13E/$6 7, be"ore and a"ter the "ast may also be use"ul4 13E/$67 levels are suppressed by insulin and there"ore increase during "asting in healthy individuals but decrease or remain stable in hyperinsulinemic individuals4 A glucagon stimulation test at the end o" the "ast also may be use"ul4 1n most individuals, the glucose level should not increase "ollowing hypoglycemia, since the glycogen stores are signi"icantly depleted be"ore the development o" hypoglycemia4 )yperinsulinemia, however, suppresses endogenous glucagon secretion and glycogenolysis4 1n this situation, the plasma glucose concentration increases +change F74H mmol2; A:D mg2d;B, "ollowing glucagon administration4 At no time will glucagon increase blood glucose concentration in patients with type 1 glycogen storage disease4 (easurement o" sul"onylurea, ethanol, or salicylate levels is appropriate i" it is suspected that that hypoglycemia is secondary to their ingestion4 $resence o" a low C6peptide level with a high insulin level documents exogenous insulin administration4 &ral glucose tolerance tests are o" no use in the diagnosis o" hypoglycemia because many healthy sub=ects have low plasma glucose concentrations "ollowing such a large glucose bolus4 1n addition, a low plasma glucose concentration during an oral glucose tolerance test does not prove that the patient is hypoglycemic when symptoms occur4

Medical "are: Acute treatment o" hypoglycemia consists o" an intravenous bolus o" dextrose 70I 24D m;2!g, "ollowed by intravenous in"usion to match normal

hepatic glucose production4 1n an in"ant, this is approximately D6? mg2!g2min and about :6D mg2!g2min in an older child4 5his should be ad=usted to maintain the plasma glucose above 24D mmol2;4 Children with hyperinsulinemia may have much higher needs4 ;ong6term care o" children with hypoglycemia varies with the etiology4 Eor many o" the disorders, such as !etotic hypoglycemia, glycogen storage disorders, de"ects o" "ree "atty acid metabolism, and mild hyperinsulinism, hypoglycemia can be avoided by "re8uent "eedings with speci"ically designed diets and a rapid response with parenteral dextrose when "eeding is inade8uate because o" gastrointestinal problems or other illnesses4 Avoidance o" "ructose is necessary in the child with "ructose diphosphatase de"iciency4 Eor hyperinsulinism, a hierarchical approach is used4 As mentioned, the "irst step is usually "re8uent "eeding4 5he next step is usually dia oxide4 &ctreotide is usually the second6line medical therapy4 5he calcium channel bloc!er ni"edipine also has been shown to be use"ul4 Surgery is recommended i" these treatments "ail or i" an insulin6producing tumor is suspected4 3rowth hormone and2or cortisol replacement are speci"ic treatments "or children with hypoglycemia and hypopituitarism or adrenal insu""iciency4 1n"ants who are born prematurely and those small "or their gestational age should be given intravenous or oral "eedings shortly a"ter birth to prevent hypoglycemia4 Eor hypoglycemia in patients with diabetes, treatment depends on the patient.s mental status4 1" the patient is awa!e and alert, then 7D g o" simple carbohydrate +4 o o" most "ruit =uices, : tsp o" sugar or glucose tablets, by mouth should be su""icient4 1t is important to wait at least 7D minutes a"ter the initial treatment be"ore retesting because overtreatment o" low blood sugars in patients with diabetes is a "re8uent cause o" hyperglycemia4 1" more than an hour will pass be"ore the next regularly scheduled meal, an additional 7D g o" complex carbohydrate with additional protein +bread, crac!ers, peanut butter, may be warranted4 1" the patient.s mental status is altered so that aspiration is a concern, treatment depends on the patient.s setting4 At home, 1( glucagon is the best choice, and "amilies or close associates o" all insulin6treated patients with diabetes should have this available4 1n the hospital setting, intravenous dextrose 2DI is appropriate treatment4 %extrose is not associated with the nausea and vomiting that may "ollow glucagon administration4 3lucagon should be used i" venous access is a problem4 A"ter treating the low6sugar reaction, the patient.s insulin, diet, and activity patterns should be examined to determine the cause4 Ad=ustments should be made to prevent hypoglycemia "rom recurring4 S#rgical "are: Surgery "or hyperinsulinism is usually underta!en when medical therapy "ails or when the patient is an older child with a possible insulin6 producing tumor4 5he usual initial operation in the in"ant with persistent hyperinsulinemic hypoglycemia o" in"ancy is to remove HDI o" the pancreas4 1" this is unsuccess"ul, drug therapy may be added or a complete pancreatectomy may be per"ormed4 1n the child with an insulin6producing tumor, only the tumor is removed4 5umors are best located intraoperatively by the surgeon through palpation or intraoperative ultrasound4

"ons#ltations: Evaluation and treatment o" a child with hypoglycemia re8uires a team approach4 'sual consults include a pediatric endocrinologist "or initial evaluation and treatment depending on the results o" the evaluation4 1t is also help"ul i" a geneticist "amiliar with the various metabolic disorders is available4 A nutritionist is necessary to provide input and instruction regarding treatment "or the various metabolic disorders and to ensure proper caloric inta!e in children with inade8uate stores4 (ost medications used to treat hypoglycemia are hormonal and either replace a hormonal de"iciency, cortisol or growth hormone, or suppress excess hormone production +octreotide,4 %ia oxide is an antihypertensive agent that also suppresses insulin secretion4 %rug Category# Insulin secretion inhibiting agents 66 1nsulin secretion may be altered by various mechanisms4 %ia oxide inhibits pancreatic secretion o" insulin, stimulates glucose release "rom the liver, and stimulates catecholamine release, which elevates blood glucose levels4 &ctreotide is a peptide with pharmacologic action similar to somatostatin, which inhibits insulin secretion4 A5$6sensitive potassium channels +composed o" the sul"onylurea receptor A SURB and the potassium channel pore protein A Kir6.2B, are believed to "unction abnormally in nesidioblastosis4 5hese channels initiate depolari ation o" the beta6 cell membrane and opening o" calcium channels4 5he resultant increase in intracellular calcium triggers insulin secretion4 Calcium channel bloc!ers bloc! the action o" these calcium channels, decreasing insulin secretion4 0i"edipine is the only calcium channel bloc!er that has been reported in clinical trials in humans4 Dr#g *ame %ia oxide +$roglycem, 66 Eirst6line medical treatment "or hyperinsulinism4 %ia oxide inhibits insulin release "rom the pancreas4 %d#lt Dose :6? mg2!g2d $& divided tid ediatric Dose 0eonates# 7D620 mg2!g2d $& divided tid &lder children# :6? mg2!g2d $& divided tid "ontraindications %ocumented hypersensitivity to dia oxide, thia ides, or other sul"onamide derivatives- also avoid in patients diagnosed with aortic coarctation, arteriovenous shunts, pheochromocytoma, and aortic aneurysm )nteractions %ia oxide may decrease serum hydantoins, possibly resulting in decreased anticonvulsant action- conversely, thia ide diuretics may potentiate the hyperuricemic and antihypertensive e""ects o" dia oxide regnancy C 6 Sa"ety "or use during pregnancy has not been established4 reca#tions Adverse e""ects include edema, hypotension, and excessive hair growth- when given prior to delivery, it may produce "etal or neonatal hyperbilirubinemia, thrombocytopenia, altered carbohydrate metabolism, and other adverse reactions Dr#g *ame &ctreotide +Sandostatin, 66 'sually the second6line therapy "or hyperinsulinism, octreotide is a synthetic polypeptide that inhibits the release o" many biologically active substances including insulin4

ediatric Dose Starting dose# D mcg2!g2d SC divided 846@halternatively, may be administered as an continuous in"usion- dose usually must be increased because o" development o" tachyphylaxis "ontraindications %ocumented hypersensitivity )nteractions (ay decrease the e""ect o" cyclosporine regnancy / 6 'sually sa"e but bene"its must outweigh the ris!s4 reca#tions (a=or adverse e""ects are gastrointestinal with loose stools- un"ounded concern that growth might be inhibited since it suppresses growth hormone secretion as well as insulin secretion Dr#g *ame 0i"edipine +Adalat, $rocardia, 66 Acts to bloc! calcium in"lux, which stimulates insulin secretion4 %d#lt Dose 70 mg $& tid initial- may gradually titrate upward to ?0 mg $& tid as determined by blood glucose ediatric Dose Starting dose# 04: mg2!g2d $& divided in 4 doses, may increase to 04C604? mg2!g2d "ontraindications %ocumented hypersensitivity )nteractions Caution with coadministration o" any agent that can lower /$, including beta6bloc!ers and opioids- )2 bloc!ers +cimetidine, may increase toxicity- may increase serum levels o" digoxin or 8uinidine- ni"edipine levels may be a""ected by CJ$:A4 inhibitors +eg, erythromycin, itracona ole, or inducers +eg, carbama epine, ri"ampin, regnancy C 6 Sa"ety "or use during pregnancy has not been established4 reca#tions (ay cause lower extremity edema or hypotensionallergic hepatitis have occurred but is rare %rug Category# Dextrose and glucose stimulators 66 $rompt acting gluconeogenesis is achieved with glucagon4 Emergent blood glucose elevation re8uires 1K dextrose4 Dr#g *ame 3lucagon 66 Eirst6line home treatment o" severe hypoglycemic reactions in patients with diabetes4 3lucagon may cause vomiting "or 46@ h a"ter administration4 3lucagon promotes glycogenolysis and gluconeogenesis, resulting in elevation o" blood glucose levels4 %d#lt Dose 7 mg 1( prn ediatric Dose GD years# 04D mg 1( prn FD years# 7 mg 1( prn "ontraindications %ocumented hypersensitivity )nteractions Enhances anticoagulation e""ect o" war"arin- propranolol partially inhibits the hyperglycemic e""ect- phenytoin may inhibit the action o" glucagon regnancy / 6 'sually sa"e but bene"its must outweigh the ris!s4 reca#tions 'se with caution in patients with a history o" insulinoma and2or pheochromocytoma- some o" the more common adverse drug reactions include nausea, vomiting, and urticaria Dr#g *ame %extrose +%6glucose, 66 'sed to promptly elevate serum glucose4 (onosaccharide absorbed "rom the intestine and then distributed, stored, and used by the tissues4

%d#lt Dose 7062D g 1K bolus- may "ollow with continuous 1K in"usion according to patient re8uirements ediatric Dose Acute treatment# 24D m;2!g +70I dextrose, 1K bolus"ollowed by 1K in"usion to match normal hepatic glucose production +approximately D6? mg2!g2min "or in"ants and approximately :6D mg2!g2min "or older children ,- ad=usted to maintain the plasma glucose above 24D mmol2; "ontraindications Anuria- do not administer to a patient in diabetic coma i" blood sugar levels are extremely high, and avoid in severely dehydrated patients- do not administer a concentrated solution i" intraspinal or intracranial hemorrhage is present- avoid in dehydrated patients diagnosed with delirium tremens, hepatic coma, or glucose6galactose malabsorption syndrome )nteractions Caution with coadministration with drugs that may increase blood glucose regnancy C 6 Sa"ety "or use during pregnancy has not been established4 reca#tions (ay cause nausea, which also may occur with hypoglycemia- 1K dextrose solutions may result in dilution o" serum electrolyte concentrations, or overhydration when there is "luid overload- caution in patients su""ering "rom congested states or pulmonary edema- hypertonic dextrose given peripherally may cause thrombosis +administer instead through central venous catheter,- caution in subclinical diabetes mellitus or carbohydrate intolerancethere is increased ris! o" inducing signi"icant hyperglycemia or hyperosmolar syndrome i" solution is administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance- concentrated solutions should not be administered SC or 1(- rates o" dextrose in"usion higher than 04D g2!g2h may produce glycosuria- at in"usion rates o" 04? g2!g2h the incidence o" glycosuria is DI- monitor "luid balance, electrolyte concentrations and acid6base balance closely- dextrose administration may produce vitamin /6complex de"iciency "omplications: (any o" the etiologies o" hypoglycemia may have conse8uences, ma!ing the causal distinction very di""icult4

the

same

1n"ants and children with asymptomatic hypoglycemia have been shown to have neurocognitive de"ects at the time o" hypoglycemia, including impaired auditory and sensory evo!ed responses and impaired test per"ormance4 ;ong6term conse8uences o" hypoglycemia include decreased head si e, lowered 1<, and speci"ic regional brain abnormalities seen with magnetic resonance imaging4

Medical(Legal itfalls: (any physicians may overloo! hypoglycemia either acutely or chronically4 $lasma glucose levels should be tested in any patient who presents with

neurologic de"icits at the time the de"icits are present4 1n the child who presents initially with sei ures, this may prevent prolonged, inappropriate, ine""ective anticonvulsant therapy4 (ore acutely, "ailure to recogni e hypoglycemia can lead to permanent impairments or death i" not treated4 Several case reports exist in which hypoglycemia was "ound in individuals who were thought to be comatose secondary to head trauma4

A second area o" medical6legal concern is the child who has hypoglycemia due to abuse or (unchausen syndrome by proxy4 5he possibility o" exogenous insulin administration must be considered and, i" "ound, reported to the appropriate authorities4

"aption: $icture 74 )ypoglycemia4 0ormal hypoglycemic counterregulation4

ict#re +ype: 3raph "aption: $icture 24 )ypoglycemia4 1nterpretation o" critical sample4

ict#re +ype: 3raph ')'L)-!R% H/

Section 00 of 00
/ibliography

/ibliography

al Luayyan 0A# 1solated adrenocorticotropin de"iciency as rare cause o" hypoglycaemia in children4 Eurther studies and a report o" an additional case4 )ormone Research 7HHD- 44# 2:?62404 al Rabeeah A, al6Ashwal A, al6)erbish A, et al# $ersistent hyperinsulinemic hypoglycemia o" in"ancy# experience with 2? cases 4 L $ediatr Surg 7HHD- :0# 777H67727A(edlineB4

Aynsley63reen A# 3lucose, the brain and the paediatric endocrinologist4 )ormone Research 7HH@- 4@# ?62D4