U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Plasma Glucose

; ; .

Author Information and Affiliations

Last Update: February 27, 2024.


Glucose is a monosaccharide sugar that our bodies obtain from food and use as our principal energy source.[1] The basic molecular form of glucose is C6H12O6. The sugar is ingested in several forms, such as fructose and galactose, which are monosaccharides and isomers of glucose. These monosaccharides can combine to form disaccharides such as lactose and sucrose.[2] Larger polymers of glucose are the polysaccharide forms, including starch, glycogen, and cellulose. Our bodies must break down complex sugars into glucose, fructose, and galactose for absorption and metabolism.[1] The glucose concentration in the blood is regulated by the interplay of multiple pathways modulated by several hormones.[3] Glycogenesis is the conversion of glucose to glycogen. The reverse process involves the breakdown of glycogen into glucose and other intermediate products, termed glycogenolysis. Gluconeogenesis is the formation of glucose from non-carbohydrate sources, such as amino acids, glycerol, or lactate. The conversion of glucose or other hexoses into lactate or pyruvate is called glycolysis.[4] Further oxidation to carbon dioxide and water occurs through the Kreb (citric acid) cycle, and the mitochondrial electron transport chain couples to oxidative phosphorylation, generating energy as adenosine triphosphate (ATP).[5]

Etiology and Epidemiology

Plasma glucose is measurable in several ways, and the measurement is most important for screening, diagnosing, and monitoring diabetes and metabolic dysregulation in conditions such as metabolic syndrome.[6] These conditions result in pathological hyperglycemia or high glucose levels. The latest data released by the Centers for Disease Control (CDC) indicate that nearly 37.3 million Americans have diabetes, and almost 96 million people aged 18 years or older have prediabetes (38.0% of the adult US population). Approximately 90% to 95% of all US diabetes cases are type 2. Type 2 diabetes is undiagnosed in at least 30% of the US population.[7] Hence, adequate monitoring of plasma glucose in high-risk or pre-diabetic individuals helps guide lifestyle interventions that effectively reduce the risk.[8]


Absorption of glucose into cells depends on specific transporters. Some require sodium (Na+) as a cotransporter, while others do not. The Na+-dependent transport of glucose uses the Na+/K+ ATPase pump to generate a negative potential gradient that drives the passive transport of Na+ into the cell.[9] This gradient also allows molecules, such as glucose, to be transported into the cell against their concentration gradients. In particular, glucose in the lumen of the gut and renal tubules gets absorbed via sodium-glucose cotransporters (SGLTs). The expression of these transporters changes depending on the body’s glucose needs.[10]

Once glucose enters these cells, Na+-independent glucose transporters transport glucose into the blood. Na+ independent glucose transport refers to specialized transporters that vary in type depending on specific tissues.[11] The glucose transporter type 1 (GLUT1) is found in red blood cells and the brain and is not subject to regulation by insulin.[12] GLUT2 is in the intestinal epithelium, liver, kidney, and, notably, the pancreas. These transporters are regulated by different hormones to control the level of plasma glucose as needed.[13]

Glucose homeostasis in the plasma depends on the balance of the hormones glucagon and insulin. Both hormones (insulin from β-cells found in the islet of Langerhans and glucagon from α cells) get released from the pancreas in response to plasma glucose levels.[14] In response to high glucose levels, insulin promotes glucose uptake into glucose transporter type 4 (GLUT4) cells in adipose tissue and skeletal and cardiac muscles.[15]

Insulin exerts its effects by binding to insulin receptors, which possess tyrosine kinase activity, and activation of a series of downstream events beginning with insulin substrate-1 (IRS-1) culminates in the increased expression of GLUT4.[16] Additionally, insulin can down-regulate its receptors, which may contribute to the pathophysiology of insulin resistance (receptor and post-receptor defects) in the metabolic dysregulation of obesity and diabetes mellitus (DM). In particular, insulin receptors are decreased in obesity and increased in starvation.[17] Insulin stimulates glycogenesis and fat deposition in liver and muscle tissues and inhibits glycogenolysis and gluconeogenesis to modulate blood glucose levels.[18]

The target organ for glucagon is the liver, which binds to a specific G protein-coupled receptor, expressed abundantly in the liver and kidney and, to a lesser extent, in other tissues, including the heart, adipose, pancreas, and brain. Glucagon stimulates the production of glucose in the liver predominantly by glycogenolysis.[19] Gluconeogenesis is also activated, and glycogenesis is inhibited. Glucagon secretion is regulated primarily by plasma glucose concentrations, with low and high plasma glucose being stimulatory and inhibitory, respectively. Long-standing DM impairs the glucagon response to hypoglycemia, increasing the incidence of hypoglycemic episodes. Stress, exercise, and amino acids induce glucagon release.[20]

Insulin inhibits glucagon release from the pancreas and decreases glucagon gene expression, attenuating its biosynthesis.[21] Increased glucagon concentrations, secondary to insulin deficiency, are believed to contribute to the hyperglycemia and ketosis of DM. In addition to the effects on glycemia, glucagon directly regulates triglyceride, free fatty acid, and bile metabolism. For example, it enhances fatty acid oxidation and ketogenesis in the liver.[17]

Importantly, plasma glucose levels undergo regulation through a few key pathways: glycolysis, gluconeogenesis, and glycogenesis. Insulin can affect glycolysis and gluconeogenesis through dephosphorylation of the phosphofructokinase-2 enzyme (PFK-2), which increases levels of fructose 2,6-bisphosphate (F-2,6-BP).[22] This molecule directly increases the activity of the enzyme PFK-1, which converts fructose-6-phosphate to fructose 1, 6-bisphosphate, commits glucose to the glycolysis pathway, and directs it away from gluconeogenesis. In contrast, glucagon similarly influences glycolysis and gluconeogenesis through the phosphorylation of fructose 2,6-bisphosphatase, which decreases levels of F-2,6-BP and, subsequently, the activity of PFK-1. This activity shunts glucose away from glycolysis and towards gluconeogenesis and glycogenolysis.[23]

Other hormones that influence glucose homeostasis include incretins such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). Incretins potentiate the release of insulin in response to oral glucose. Other hormones that influence glucose metabolism include pancreatic amylin, glucocorticoids (increase insulin resistance and gluconeogenesis), thyroid hormones (promote glucose absorption, glycogenolysis, gluconeogenesis), growth hormones (inhibit glucose uptake into cells), and epinephrine.[24]

Epinephrine (adrenaline), a catecholamine secreted by the adrenal medulla, stimulates glucose production (glycogenolysis) and decreases glucose use, increasing blood glucose concentrations. The hormone also stimulates glucagon secretion and inhibits insulin secretion by the pancreas.[25] Epinephrine is key in glucose counter-regulation when glucagon secretion is impaired (eg, in type 1 DM. Physical or emotional stress increases epinephrine production, releasing glucose for energy. Tumors of the adrenal medulla, known as pheochromocytoma, secrete excess epinephrine or norepinephrine and produce moderate hyperglycemia as long as glycogen stores are available in the liver.[26]

DM is a disorder in regulating blood glucose levels and is associated with genetic and lifestyle factors, such as family history, race, obesity, and diet. DM resulting from other causes include monogenic diabetes (such as neonatal diabetes), maturity onset of diabetes in the young (MODY), gestational diabetes, pancreatic insufficiency, or drug-induced. High blood glucose levels characterize the disorder due to insulin resistance and ultimate insulin deficiency.[27]

DM occurs most commonly in two main types: type 1 or type 2.[28] Type 1 occurs in younger patients due to an autoimmune pathology where the immune system attacks β-cells of the pancreas, resulting in a loss of insulin.[29] The autoimmune process leading to type 1 DM begins months or years before the clinical presentation, and an 80% to 90% reduction in the volume of β-cells is required to induce symptomatic type 1 diabetes.[30] The rate of islet cell destruction is variable and more rapid in children than adults.

The most practical markers of β-cell autoimmunity are circulating antibodies, which are detected in the serum years before the onset of hyperglycemia. Almost 85% of type 1 diabetes patients have circulating islet cell antibodies, most of which are directed against β cell glutamic acid decarboxylase (GAD).[31] Individuals with specific human leucocyte antigens (HLAs) have a high risk of developing type 1 diabetes.[32] There is a well-recognized association between type 1 diabetes and other autoimmune endocrinopathies, such as hypothyroidism, Addison disease, and pernicious anemia. Without insulin, the body loses the primary stimulus to transport blood glucose into cells.[29] These patients require lifelong injections of insulin to replace their deficiency.[30]

Type 2 diabetes occurs in the majority of patients with weight gain. This type is more strongly associated with obesity, progressive metabolic dysregulation, and insulin resistance.[33] The body produces insulin in type 2 diabetes, but the cells are less sensitive to insulin; hence, a higher insulin level is needed to stimulate cells to take up glucose.[34] The insulin resistance syndrome (also known as syndrome X or the metabolic syndrome) is a constellation of associated clinical and laboratory findings, consisting of insulin resistance, hyperinsulinemia, obesity, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol), and hypertension. Individuals with this syndrome are at increased risk for cardiovascular disease.[35]

In DM, glucose is elevated outside the cells, resulting in starved cells and high glucose levels in plasma.[36] Cells switch to protein and fatty acid catabolism, which can increase urea and ketones. High glucose levels in the plasma can harm nerves osmotically, leading to peripheral neuropathies. Moreover, the levels can impede wound healing and increase inflammation by creating oxidative stress and inflammation reactions. These reactions also modify to form advanced glycation products (AGEs), contributing to microvascular and macrovascular complications.[37]

Notably, glucose can react with the amino group of a protein non-enzymatically, forming compounds such as fructosamine that reflect the level of glucose control over 2 weeks.[38] Clinical presentation includes polydipsia, polyuria, and weight loss with polyphagia. Hence, the widespread elevation of glucose in plasma can lead to irreversible organ damage over time, and control of glucose levels is crucial to preventing adverse long-term outcomes.[39]

Specimen Requirements and Procedure

In individuals with normal hematocrit, fasting whole blood glucose concentration is approximately 10% to 12% lower than plasma glucose. Although glucose concentrations in the water phase of red blood cells and plasma are similar (the erythrocyte plasma membrane is freely permeable to glucose), the water content of plasma (93%) is approximately 11% higher than that of whole blood.[6] Most clinical laboratories use plasma or serum for glucose testing. However, self-monitoring methods use whole blood samples but can measure the glucose concentration in the plasma phase. For DM diagnosis, venous plasma is recommended.[40]

During fasting, capillary blood glucose concentration is only 2 to 5 mg/dL (0.1 to 0.3 mmol/L), higher than venous blood. After a glucose load, however, capillary blood glucose concentrations are 20 to 70 mg/dL (1.1 to 3.9 mmol/L), mean approximately = 30 mg/dL (1.7 mmol/L); equivalent to 20% to 25% higher than concurrently drawn venous blood samples.[41]

Glycolysis decreases serum glucose by approximately 5% to 7% in 1 hour (5 to 10 mg/dL; 0.3 to 0.6 mmol/L) in normal uncentrifuged coagulated blood at room temperature. Leukocytosis or bacterial contamination affects in vitro glycolysis, with some studies observing a higher rate and others slightly decreasing.[42] In separate, non-hemolyzed sterile serum, the glucose concentration is generally stable for 8 hours at 25 °C and 72 hours at 4 °C; variable stability is observed with longer storage periods.[43] Plasma, removed from the cells after moderate centrifugation, contains leukocytes that metabolize glucose, although cell-free sterile plasma has no glycolytic activity.[44]

Glycolysis is inhibited, and glucose is stabilized for 3 days at room temperature by adding sodium fluoride (NaF) or, less commonly, sodium iodoacetate to the specimen.[45] Fluoride ions prevent glycolysis by inhibiting enolase, an enzyme that requires Mg2+. This inhibition is due to forming an ionic complex consisting of Mg2+, inorganic phosphate, and fluoride ions; this complex interferes with the interaction of enzyme and substrate.[6] Fluoride is also a weak anticoagulant because it binds calcium; however, clotting may occur after several hours. It is, therefore, advisable to use a combined fluoride-oxalate mixture, such as 2 mg of potassium oxalate (K2C2O4) and 2 mg NaF/mL of blood, to prevent late clotting. Other anticoagulants (eg, EDTA, citrate, heparin) are also used.[45]

Fluoride ions in high concentration inhibit the activity of urease and certain other enzymes; consequently, the specimens are unsuitable for determining urea in procedures requiring urease and for the direct assay of some serum enzymes.[46] Potassium oxalate (K2C2O4) causes cell water loss, diluting the plasma. Therefore, samples collected in these tubes should not be used to measure analytes other than glucose.[47] Although fluoride maintains long-term blood glucose stability, the rate of decline in the first hour after sample collection is not altered, and glycolysis may continue for up to 4 hours.[48]

Diagnostic Tests

Plasma glucose is measured with high precision and accuracy using enzymatic methods such as glucose oxidase and hexokinase. Many point-of-care testing analyzers, including blood-gas instruments, measure glucose concentrations using the glucose oxidase method.[48] HbA1c is specific for DM but not very sensitive and has greater utility in monitoring control over 2 to 3 months. The value is falsely elevated with iron deficiency and, hence, not appropriate or cost-effective for the developing world.[49]

Testing Procedures

Glucose Meters 

Portable meters for measurement of blood glucose concentrations are used in 3 major settings: in acute and chronic care facilities (at the patient’s bedside and in clinics or hospitals), in clinicians’ offices, and by patients or their caregivers at home, work, and school.[50] To perform the measurement, a sample of blood (usually from a finger stick, but anticoagulated whole blood collected in ethylenediaminetetraacetic acid [EDTA] or heparin) is placed on the test pad, which is attached to a plastic support. The test strip is inserted into the meter. (In some devices, the strip is inserted into the meter before applying the sample.) After a fixed period, the result appears on a digital display screen.[51]

These meters use reflectance photometry or electrochemistry to measure the reaction rate or the products' final concentration. Reflectance photometry measures the light reflected from a test pad containing a reagent. In electrochemical systems, the enzymatic reaction in an electrode incorporated on the test strip produces a flow of electrons.[52] The current, directly proportional to the concentration of glucose in the sample, is converted to a digital readout.[53] Large variability has been noted among current meters as to the volume of blood required (0.3 to 1.5 μL), test time (5 to 45 seconds), and the claimed reading range: 30 to 500 mg/dL (1.7 to 27.8 mmol/L) to 0 to 600 mg/dL (0 to 33.3 mmol/L).[54]

Calibration is automatic on some devices, whereas others use lot-specific code chips or strips. All manufacturers supply control solutions. Recent advances in technology facilitate data analysis and sharing.[50] Some meters have Bluetooth capabilities (enabling data transmission to a smartphone or computer). These cellular connections automatically send data to the “cloud,” USB ports, and/or communication with an insulin pump.[51]

Strict adherence to the instructions is necessary to obtain accurate results.[52] Some meters have a porous membrane that separates erythrocytes, and analysis is performed on the resultant plasma. Whole blood glucose concentrations are approximately 10% to 15% lower than plasma or serum concentrations, but meters are calibrated to report plasma glucose values, especially when the sample is whole blood.[53]

Laboratory Assessment of Glucose

Current laboratory recommendations for plasma glucose measurement are to draw fasting blood samples in the morning rather than later, as glucose levels tend to be higher in the morning than in the afternoon.[6] These samples should be placed on ice to minimize glycolysis and quickly processed (via plasma separation within 60 minutes) as glucose concentrations decrease at 5% to 7% per hour. If plasma separation cannot occur within 60 minutes, the lab tech can add a glycolytic inhibitor such as fluoride.[55]

Oral Glucose Tolerance Test (OGTT)

Serial measurement of plasma glucose before and after a specific amount of glucose should provide a standard method to evaluate individuals and establish values for healthy and diseased subjects.[56] Although more sensitive than fasting plasma glucose determinations, glucose tolerance testing is affected by multiple factors that result in poor reproducibility.[57] Unless results are grossly abnormal initially, the OGTT should be performed on 2 separate occasions to establish the diagnosis of DM.[58]

The following conditions should be met before an OGTT is performed: discontinue, when possible, medications known to affect glucose tolerance; perform in the morning after 3 days of unrestricted diet (containing at least 150 g of carbohydrate per day) and activity; and perform the test after a 10- to 16-hour fast only in ambulatory outpatients (bed rest impairs glucose tolerance). The patient should remain seated during the test.[56]

Glucose tolerance testing should not be performed on hospitalized, acutely ill, or inactive patients. The test should begin between 7:00 am and 9:00 am. Venous plasma glucose should be measured while fasting and 2 hours after an oral glucose load. For nonpregnant adults, the recommended load is 75 g, which may not be a maximum stimulus; 15 g for children, 1.75 g/kg, up to 75 g maximum, is given. The glucose should be dissolved in 300 mL of water and ingested over 5 minutes.[58]

Intravenous Glucose Tolerance Test

Some patients cannot tolerate a large oral carbohydrate load or may have altered gastric physiology (eg, after gastric resection). In these patients, an intravenous glucose tolerance test may be performed to eliminate factors related to the rate of glucose absorption.[59] In addition, measurement of the first-phase insulin response can identify the subgroup of individuals with increased concentrations of multiple autoantibodies at the most significant risk of progression to type 1 diabetes.[60]

The preparation of patients is the same as for the OGTT. The dose of glucose is 0.5 g/kg of body weight (maximum 35 g), given as a 25 g/dL solution. The dose is administered intravenously over 3 minutes ± 15 seconds, and blood is collected every 10 minutes after the mid-injection time for 1 hour.[61] A single forearm vein cannula may be used for infusion and sampling, but it should be flushed with saline after infusing the glucose. Dead space should be cleared with several volumes of blood before each sample is drawn. If insulin assays are performed, a specimen is also obtained 5 minutes after the start of the injection.[62]

Interfering Factors

When checking plasma glucose levels, the essential factor is when the patient last consumed anything caloric. Plasma glucose levels tend to be lowest before meals or when fasting.[6] In addition, evidence suggests that fluctuations in glucose levels throughout the day may contribute to a missed diagnosis of DM. Hence, recommendations are to check fasting plasma glucose in the mornings when endogenous glucose levels predominate compared to later in the day.[55]

When processing a plasma glucose sample, limiting the amount of glycolysis after drawing a sample is crucial.[40] To limit glycolysis in a sample, process the sample within the hour or use a glycolytic inhibitor to stabilize the sample. Additionally, some glucose measurement differences depend on the blood processing method.[45]

Results, Reporting, and Critical Findings

The diagnosis of DM has serious consequences. DM confers a risk of long-term diabetic complications, including blindness, renal failure, and amputations, as well as an increased risk of cardiovascular disease. The condition also entails a lifetime of dietary restrictions and medications and can seriously curtail lifestyle and employment prospects.[37] The diagnosis may be suggested by the patient’s history or by the results of dipstick tests for glucose on urine specimens. However, urine glucose measurements are inadequate for diagnosing DM.[63] They potentially yield false-positive results in subjects with a low renal threshold for glucose. A patient with DM may deliver false-negative results if the patient is fasting.[64]

A provisional diagnosis of DM must be confirmed by laboratory measurements on blood specimens. Normal plasma glucose levels are defined under 100 mg/dL during fasting and less than 140 mg/dL 2 hours postprandial. Additionally, glucose levels in healthy individuals can vary with age.[37] Fasting plasma glucose in adults increases with age, starting in the third decade of life, but does not increase significantly beyond 60 years. Normal HbA1c is lower than 5.7%.[64]

Diagnosis depends on plasma glucose, which is measurable during fasting, the oral glucose tolerance test (OGTT), or the A1c criteria.[65] Fasting plasma glucose measurements show glucose levels at the point in time, whereas HbA1c measures the average amount of glycation to hemoglobin, accumulating over 2 to 3 months. According to the American Diabetes Association (ADA), fasting (at least 8 hours of no caloric intake) plasma glucose greater than or equal to 126 mg/dL is diagnostic.[64]

Confirmation of the diagnosis requires 2 abnormal test results from the same or 2 separate samples.[63] Other equivalent diagnostic criteria include 2-hour plasma glucose greater than or equal to 200 mg/dL during OGTT or A1c greater than or equal to 6.5% (performed in an accredited laboratory). Clinically, a patient with hyperglycemic crisis symptoms and random glucose greater than or equal to 200 mg/dL also meets the diagnostic criteria.[37]

Patients at the borderline of these criteria for DM are considered prediabetic.[66] The ADA criteria define prediabetes as impaired fasting glucose (IFG) defined as fasting plasma glucose of 100 to 125 mg/dL or impaired glucose tolerance (IGT) 2-hour plasma glucose (in OGTT) of 140 to 199 mg/dL or A1c of 5.7% to 6.4%. Patients with prediabetes are at high risk of progressing to DM. In particular, a systematic review found that increased A1c from 6% to 6.5% correlated with an increased 5-year incidence of DM.[65]

Hypoglycemia is generally plasma glucose under 70 mg/dL, but symptoms may not occur until plasma glucose is less than 55 mg/dL. Such low levels of plasma glucose indicate a dangerous, potentially life-threatening situation characterized by seizures and coma.[67] Plasma glucose reference values for hypoglycemia vary widely, and diagnosis largely relies on clinical presentation.[68]

Reactive hypoglycemia can present in gastric surgery patients and usually occurs 90 to 150 minutes after a meal, especially if it is high in sugar or other carbohydrates. Because of the reduced stomach size, glucose is rapidly transported into the small intestine, where incretins are released, leading to excessive insulin response and hypoglycemia.[69] Symptomatic hypoglycemia is sometimes recorded in normal individuals if an OGTT is sampled beyond 2 hours. Still, it must be stressed that an OGTT, consisting of rapidly ingesting a drink containing 75 g of glucose, is hardly physiological.[70]

Factitious (or non-physiological) hypoglycemia occurs when insulin or sulphonylurea is taken or administered deliberately. The condition is difficult to diagnose and is usually associated with psychological problems in the patient or involved caregivers. If a confirmed hyperinsulinaemic hypoglycaemic sample has a low c-peptide level, then the insulin will likely be exogenous.[71] If a sample's c-peptide level is high, then the insulin is likely endogenous, and a sulphonylurea screen should be performed. A positive screen indicates the raised insulin is due to sulphonylurea administration.[72]

Symptoms of hypoglycemia vary among individuals, and none is specific. Epinephrine produces the classic signs and symptoms of hypoglycemia: trembling, sweating, nausea, rapid pulse, lightheadedness, hunger, and epigastric discomfort.[68] These autonomic (neurogenic) symptoms are nonspecific and may be noted in other conditions, such as hyperthyroidism, pheochromocytoma, or anxiety. Although controversial, it is proposed that a rapid decrease in blood glucose may trigger the symptoms, though it may not reach hypoglycemic values. In contrast, the gradual onset of hypoglycemia may not produce symptoms.[73] Hypoglycemia frequently occurs in both type 1 and 2 diabetes, and it is the limiting factor in the glycemic management of DM. Patients using insulin experience approximately 1 to 2 episodes of symptomatic hypoglycemia per week, and severe hypoglycemia (ie, requiring assistance from others or associated with loss of consciousness) affects about 10% of this population annually.[74]

CSF glucose concentrations should be approximately 60% of plasma concentrations and must be compared with concurrently measured plasma glucose for adequate clinical interpretation. Glucose in the CSF of neonates varies much more than in adults, and the CSF-to-serum ratio is generally higher than in adults.[75] CNS infections can cause lowered CSF glucose levels, although glucose levels are normal in viral infections. Normal glucose levels do not rule out infection because up to 50% of bacterial meningitis patients will have normal CSF glucose levels.[76] Chemical meningitis, inflammatory conditions, subarachnoid hemorrhage, and hypoglycemia also cause hypoglycorrhachia (low glucose level in CSF). Elevated glucose levels in the blood are the only cause of an elevated CSF glucose level. There is no pathologic process that causes elevated CSF glucose levels.[77]

Clinical Significance

Measurements of plasma glucose levels are essential for screening metabolic dysregulation, pre-diabetes, and diabetes. Evidence finds that the onset of type 2 diabetes can occur as early as 4 to 7 years before clinical diagnosis. Additionally, plasma glucose levels can monitor diabetes, screen for hypoglycemic episodes, guide treatment or lifestyle interventions, and predict risk for comorbidities like cardiovascular or eye and kidney disease.[78] In particular, evidence reports that plasma glucose level monitoring in patients with type 2 diabetes can predict complications and mortality. Higher glucose correlates with more significant comorbidities and risk for mortality.[79]

In a 15-year study of 1939 patients with type 2 diabetes, patients with fasting plasma glucose equal to or greater than 140 mg/dL showed a significantly increased risk of death.[80] Similarly, type 2 diabetic patients with fasting plasma glucose equal to or greater than 140 mg/dL were found to have increased cardiovascular mortality.[81] Other studies also report the risk of a first myocardial infarction increases with higher fasting plasma glucose levels.[82]

Quality Control and Lab Safety

The purpose of a clinical laboratory test is to provide information on the pathophysiologic condition of an individual patient to assist with diagnosis, to guide or monitor therapy, or to assess risk for developing a disease or for the progression of a disease. Quality control (QC), also called internal QC, monitors a measurement procedure to verify that results for patient samples meet performance specifications appropriate for patient care or that an error condition must be corrected.[83] QC samples are measured at intervals along with patient samples. For non-waived tests, laboratory regulations require, at the minimum, analysis of at least 2 levels of control materials once every 24 hours. If necessary, laboratories can assay QC samples more frequently to ensure accurate results.[84] 

Quality control samples should be assayed after calibration or maintenance of an analyzer to verify the correct method performance. To minimize QC when performing tests for which manufacturers’ recommendations are less than those required by the regulatory agency (such as once per month), the labs can develop an individualized quality control plan (IQCP) that involves performing a risk assessment of potential sources of error in all phases of testing and putting in place a QC plan to reduce the likelihood of errors.[85]

Westgard multi-rules are used to evaluate the quality control runs. If a run is declared out of control, investigate the system (instrument, standards, controls, etc.) to determine the cause of the problem. Do not perform any analysis until the problem has been resolved.[86] Per Centers for Medicare & Medicaid Services (CMS) regulations in the United States, laboratories are typically mandated to participate in external quality assessment (EQA) programs.

External quality assessment, or proficiency testing (PT), is an assessment process in which samples are received from an independent external organization, and the laboratory does not know the expected values. The results for the EQA/PT samples are compared with target values assigned to the samples to verify that a laboratory’s measurement procedures conform to expected performance.[87] The criteria for acceptable performance for glucose assay by the Clinical Laboratory Improvement Amendments (CLIA) and College of American Pathologists (CAP) proficiency program is within ± 6mg/dL or ± 10% of the mean value of laboratory peer groups.[88]

Ensuring safety within clinical laboratories is a foundational element of healthcare, guaranteeing the welfare of both healthcare providers and patients.[89] Consider all specimens, control materials, and calibrator materials as potentially infectious. Exercise the normal precautions required for handling all laboratory reagents. Disposal of all waste material should be under local guidelines. Wear gloves, a lab coat, and safety glasses when handling human blood specimens.[90] Place all plastic tips, sample cups, and gloves that come into contact with blood in a biohazard waste container. Discard all disposable glassware into sharps waste containers. Protect all work surfaces with disposable absorbent bench top paper, and discard into biohazard waste containers weekly or whenever blood contamination occurs. Wipe all work surfaces weekly.[91] By adhering to these measures, clinical laboratories play a pivotal role in furnishing precise, dependable, and secure diagnostic services, significantly contributing to the quality of patient care.

Enhancing Healthcare Team Outcomes

Routine screening of plasma glucose levels in at-risk patients would aid early diagnosis and intervention to limit the complications and mortality risks of DM. In particular, continuous glucose monitoring in intensive care patients helps prevent severe hyperglycemia, hypoglycemia, and associated mortality risks. Continuous glucose monitoring (CGM) can detect hypoglycemia or hyperglycemic episodes early and provide guidelines for rapid insulin or interventional adjustments. Hence, real-time access to accurate glucose measurements alerts health professionals to treatment efficacy and helps decrease the risk of missed episodes of hypoglycemia or hyperglycemia.[92][93]

If elevated, serum glucose monitoring can inform and direct care for several potentially deleterious sequelae. As a result, everyone on the interprofessional healthcare team is involved in the testing, patient education, monitoring, and therapy when appropriate. This includes clinicians, specialists, nurses (including specialty-trained nurses), and pharmacists.

Review Questions


Holesh JE, Aslam S, Martin A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 12, 2023. Physiology, Carbohydrates. [PubMed: 29083823]
Qi X, Tester RF. Fructose, galactose and glucose - In health and disease. Clin Nutr ESPEN. 2019 Oct;33:18-28. [PubMed: 31451258]
Röder PV, Wu B, Liu Y, Han W. Pancreatic regulation of glucose homeostasis. Exp Mol Med. 2016 Mar 11;48(3):e219. [PMC free article: PMC4892884] [PubMed: 26964835]
Dashty M. A quick look at biochemistry: carbohydrate metabolism. Clin Biochem. 2013 Oct;46(15):1339-52. [PubMed: 23680095]
Akram M. Citric acid cycle and role of its intermediates in metabolism. Cell Biochem Biophys. 2014 Apr;68(3):475-8. [PubMed: 24068518]
Kim HS. Blood Glucose Measurement: Is Serum Equal to Plasma? Diabetes Metab J. 2016 Oct;40(5):365-366. [PMC free article: PMC5069392] [PubMed: 27766243]
Rowley WR, Bezold C, Arikan Y, Byrne E, Krohe S. Diabetes 2030: Insights from Yesterday, Today, and Future Trends. Popul Health Manag. 2017 Feb;20(1):6-12. [PMC free article: PMC5278808] [PubMed: 27124621]
Deshpande AD, Harris-Hayes M, Schootman M. Epidemiology of diabetes and diabetes-related complications. Phys Ther. 2008 Nov;88(11):1254-64. [PMC free article: PMC3870323] [PubMed: 18801858]
Abdulla H, Phillips B, Smith K, Wilkinson D, Atherton PJ, Idris I. Physiological mechanisms of action of incretin and insulin in regulating skeletal muscle metabolism. Curr Diabetes Rev. 2014;10(5):327-35. [PubMed: 25323297]
Norton L, Shannon CE, Fourcaudot M, Hu C, Wang N, Ren W, Song J, Abdul-Ghani M, DeFronzo RA, Ren J, Jia W. Sodium-glucose co-transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects. Diabetes Obes Metab. 2017 Sep;19(9):1322-1326. [PubMed: 28477418]
Solini A, Rossi C, Mazzanti CM, Proietti A, Koepsell H, Ferrannini E. Sodium-glucose co-transporter (SGLT)2 and SGLT1 renal expression in patients with type 2 diabetes. Diabetes Obes Metab. 2017 Sep;19(9):1289-1294. [PubMed: 28419670]
Triplitt CL. Understanding the kidneys' role in blood glucose regulation. Am J Manag Care. 2012 Jan;18(1 Suppl):S11-6. [PubMed: 22559853]
Ghezzi C, Loo DDF, Wright EM. Physiology of renal glucose handling via SGLT1, SGLT2 and GLUT2. Diabetologia. 2018 Oct;61(10):2087-2097. [PMC free article: PMC6133168] [PubMed: 30132032]
Ojha A, Ojha U, Mohammed R, Chandrashekar A, Ojha H. Current perspective on the role of insulin and glucagon in the pathogenesis and treatment of type 2 diabetes mellitus. Clin Pharmacol. 2019;11:57-65. [PMC free article: PMC6515536] [PubMed: 31191043]
Huang S, Czech MP. The GLUT4 glucose transporter. Cell Metab. 2007 Apr;5(4):237-52. [PubMed: 17403369]
Mayer JP, Zhang F, DiMarchi RD. Insulin structure and function. Biopolymers. 2007;88(5):687-713. [PubMed: 17410596]
Niswender KD. Basal insulin: physiology, pharmacology, and clinical implications. Postgrad Med. 2011 Jul;123(4):17-26. [PubMed: 21680985]
Thevis M, Thomas A, Schänzer W. Insulin. Handb Exp Pharmacol. 2010;(195):209-26. [PubMed: 20020367]
Kleinert M, Sachs S, Habegger KM, Hofmann SM, Müller TD. Glucagon Regulation of Energy Expenditure. Int J Mol Sci. 2019 Oct 30;20(21) [PMC free article: PMC6862306] [PubMed: 31671603]
Zeigerer A, Sekar R, Kleinert M, Nason S, Habegger KM, Müller TD. Glucagon's Metabolic Action in Health and Disease. Compr Physiol. 2021 Apr 01;11(2):1759-1783. [PMC free article: PMC8513137] [PubMed: 33792899]
Mathieu C, Gillard P, Benhalima K. Insulin analogues in type 1 diabetes mellitus: getting better all the time. Nat Rev Endocrinol. 2017 Jul;13(7):385-399. [PubMed: 28429780]
Young A. Effects on plasma glucose and lactate. Adv Pharmacol. 2005;52:193-208. [PubMed: 16492547]
Geidl-Flueck B, Gerber PA. Insights into the Hexose Liver Metabolism-Glucose versus Fructose. Nutrients. 2017 Sep 16;9(9) [PMC free article: PMC5622786] [PubMed: 28926951]
Kuo T, McQueen A, Chen TC, Wang JC. Regulation of Glucose Homeostasis by Glucocorticoids. Adv Exp Med Biol. 2015;872:99-126. [PMC free article: PMC6185996] [PubMed: 26215992]
Stumvoll M, Chintalapudi U, Perriello G, Welle S, Gutierrez O, Gerich J. Uptake and release of glucose by the human kidney. Postabsorptive rates and responses to epinephrine. J Clin Invest. 1995 Nov;96(5):2528-33. [PMC free article: PMC185914] [PubMed: 7593645]
Walters JM, Ward GM, Kalfas A, Best JD, Alford FP. The effect of epinephrine on glucose-mediated and insulin-mediated glucose disposal in insulin-dependent diabetes. Metabolism. 1992 Jun;41(6):671-7. [PubMed: 1640854]
Cloete L. Diabetes mellitus: an overview of the types, symptoms, complications and management. Nurs Stand. 2022 Jan 05;37(1):61-66. [PubMed: 34708622]
Kaul K, Tarr JM, Ahmad SI, Kohner EM, Chibber R. Introduction to diabetes mellitus. Adv Exp Med Biol. 2012;771:1-11. [PubMed: 23393665]
Gillespie KM. Type 1 diabetes: pathogenesis and prevention. CMAJ. 2006 Jul 18;175(2):165-70. [PMC free article: PMC1489998] [PubMed: 16847277]
Acharjee S, Ghosh B, Al-Dhubiab BE, Nair AB. Understanding type 1 diabetes: etiology and models. Can J Diabetes. 2013 Aug;37(4):269-276. [PubMed: 24070892]
Bluestone JA, Herold K, Eisenbarth G. Genetics, pathogenesis and clinical interventions in type 1 diabetes. Nature. 2010 Apr 29;464(7293):1293-300. [PMC free article: PMC4959889] [PubMed: 20432533]
Barnett R. Type 1 diabetes. Lancet. 2018 Jan 20;391(10117):195. [PubMed: 30277879]
Brunton S. Pathophysiology of Type 2 Diabetes: The Evolution of Our Understanding. J Fam Pract. 2016 Apr;65(4 Suppl) [PubMed: 27262256]
Fletcher B, Gulanick M, Lamendola C. Risk factors for type 2 diabetes mellitus. J Cardiovasc Nurs. 2002 Jan;16(2):17-23. [PubMed: 11800065]
Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training. Compr Physiol. 2013 Jan;3(1):1-58. [PMC free article: PMC4129661] [PubMed: 23720280]
Guthrie RA, Guthrie DW. Pathophysiology of diabetes mellitus. Crit Care Nurs Q. 2004 Apr-Jun;27(2):113-25. [PubMed: 15137354]
American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2011 Jan;34 Suppl 1(Suppl 1):S62-9. [PMC free article: PMC3006051] [PubMed: 21193628]
Tripathi BK, Srivastava AK. Diabetes mellitus: complications and therapeutics. Med Sci Monit. 2006 Jul;12(7):RA130-47. [PubMed: 16810145]
Cole JB, Florez JC. Genetics of diabetes mellitus and diabetes complications. Nat Rev Nephrol. 2020 Jul;16(7):377-390. [PMC free article: PMC9639302] [PubMed: 32398868]
Sacks DB, Bruns DE, Goldstein DE, Maclaren NK, McDonald JM, Parrott M. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Clin Chem. 2002 Mar;48(3):436-72. [PubMed: 11861436]
Kotwal N, Pandit A. Variability of capillary blood glucose monitoring measured on home glucose monitoring devices. Indian J Endocrinol Metab. 2012 Dec;16(Suppl 2):S248-51. [PMC free article: PMC3603039] [PubMed: 23565391]
Gupta S, Kaur H. Inhibition of Glycolysis for Glucose Estimation in Plasma: Recent Guidelines and their Implications. Indian J Clin Biochem. 2014 Apr;29(2):262-4. [PMC free article: PMC3990791] [PubMed: 24757316]
Uchida K, Matuse R, Toyoda E, Okuda S, Tomita S. A new method of inhibiting glycolysis in blood samples. Clin Chim Acta. 1988 Feb 29;172(1):101-8. [PubMed: 2966020]
Turchiano M, Nguyen C, Fierman A, Lifshitz M, Convit A. Impact of blood sample collection and processing methods on glucose levels in community outreach studies. J Environ Public Health. 2013;2013:256151. [PMC free article: PMC3556871] [PubMed: 23365588]
Chan AY, Swaminathan R, Cockram CS. Effectiveness of sodium fluoride as a preservative of glucose in blood. Clin Chem. 1989 Feb;35(2):315-7. [PubMed: 2914384]
Li G, Cabanero M, Wang Z, Wang H, Huang T, Alexis H, Eid I, Muth G, Pincus MR. Comparison of glucose determinations on blood samples collected in three types of tubes. Ann Clin Lab Sci. 2013 Summer;43(3):278-84. [PubMed: 23884222]
Shi RZ, Seeley ES, Bowen R, Faix JD. Rapid blood separation is superior to fluoride for preventing in vitro reductions in measured blood glucose concentration. J Clin Pathol. 2009 Aug;62(8):752-3. [PubMed: 19638548]
Janssen K, Delanghe J. Importance of the pre-analytical phase in blood glucose analysis. Acta Clin Belg. 2010 Sep-Oct;65(5):311-8. [PubMed: 21128557]
Weykamp C. HbA1c: a review of analytical and clinical aspects. Ann Lab Med. 2013 Nov;33(6):393-400. [PMC free article: PMC3819436] [PubMed: 24205486]
Zhang L, Gu C, Ma H, Zhu L, Wen J, Xu H, Liu H, Li L. Portable glucose meter: trends in techniques and its potential application in analysis. Anal Bioanal Chem. 2019 Jan;411(1):21-36. [PubMed: 30280228]
Amalfitano E, Karlikow M, Norouzi M, Jaenes K, Cicek S, Masum F, Sadat Mousavi P, Guo Y, Tang L, Sydor A, Ma D, Pearson JD, Trcka D, Pinette M, Ambagala A, Babiuk S, Pickering B, Wrana J, Bremner R, Mazzulli T, Sinton D, Brumell JH, Green AA, Pardee K. A glucose meter interface for point-of-care gene circuit-based diagnostics. Nat Commun. 2021 Feb 01;12(1):724. [PMC free article: PMC7851131] [PubMed: 33526784]
Lunt H, Florkowski C, Bignall M, Budgen C. Capillary glucose meter accuracy and sources of error in the ambulatory setting. N Z Med J. 2010 Mar 05;123(1310):74-85. [PubMed: 20360781]
Hellman R. Glucose meter accuracy and the impact on the care of diabetes in childhood and adolescence. Pediatr Endocrinol Rev. 2011 Mar;8(3):200-7. [PubMed: 21525796]
Thompson H, Chan H, Logan FJ, Heenan HF, Taylor L, Murray C, Florkowski CM, Frampton CM, Lunt H. A glucose meter evaluation co-designed with both health professional and consumer input. N Z Med J. 2013 Nov 22;126(1386):90-7. [PubMed: 24316996]
Sacks DB, Arnold M, Bakris GL, Bruns DE, Horvath AR, Kirkman MS, Lernmark A, Metzger BE, Nathan DM., National Academy of Clinical Biochemistry. Evidence-Based Laboratory Medicine Committee of the American Association for Clinical Chemistry. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Diabetes Care. 2011 Jun;34(6):e61-99. [PMC free article: PMC3114322] [PubMed: 21617108]
Hagura R. [Oral glucose tolerance test (OGTT) for diagnosis of diabetes mellitus]. Nihon Rinsho. 2005 Feb;63 Suppl 2:372-5. [PubMed: 15779406]
Flores-Arguedas H, Capistrán MA. Bayesian analysis of Glucose dynamics during the Oral Glucose Tolerance Test (OGTT). Math Biosci Eng. 2021 May 27;18(4):4628-4647. [PubMed: 34198457]
Phillips PJ. Oral glucose tolerance testing. Aust Fam Physician. 2012 Jun;41(6):391-3. [PubMed: 22675678]
Cunningham VJ, Heath DF. An interpretation of the intravenous glucose tolerance test in the light of recent findings on the kinetics of glucose and insulin in man. Clin Sci Mol Med. 1978 Feb;54(2):161-73. [PubMed: 340115]
Valdes CT, Elkind-Hirsch KE. Intravenous glucose tolerance test-derived insulin sensitivity changes during the menstrual cycle. J Clin Endocrinol Metab. 1991 Mar;72(3):642-6. [PubMed: 1997519]
Taniguchi A, Nakai Y, Fukushima M, Doi K, Tokuyama K, Kawamura H, Suzuki M, Higaki Y, Tanaka H, Sakai M, Nagata I. Intravenous glucose tolerance test-derived glucose effectiveness in bulimia nervosa. Metabolism. 1997 May;46(5):484-6. [PubMed: 9160811]
Silber HE, Nyberg J, Hooker AC, Karlsson MO. Optimization of the intravenous glucose tolerance test in T2DM patients using optimal experimental design. J Pharmacokinet Pharmacodyn. 2009 Jun;36(3):281-95. [PubMed: 19554431]
Kerner W, Brückel J., German Diabetes Association. Definition, classification and diagnosis of diabetes mellitus. Exp Clin Endocrinol Diabetes. 2014 Jul;122(7):384-6. [PubMed: 25014088]
Rossi G., American Diabetes Association. [Diagnosis and classification of diabetes mellitus]. Recenti Prog Med. 2010 Jul-Aug;101(7-8):274-6. [PubMed: 20842952]
American Diabetes Association. (2) Classification and diagnosis of diabetes. Diabetes Care. 2015 Jan;38 Suppl:S8-S16. [PubMed: 25537714]
American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2004 Jan;27 Suppl 1:S5-S10. [PubMed: 14693921]
Umpierrez G, Korytkowski M. Diabetic emergencies - ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nat Rev Endocrinol. 2016 Apr;12(4):222-32. [PubMed: 26893262]
Scheen AJ. [Diagnosis and assessment of hypoglycemia in patients with diabetes mellitus]. Rev Med Liege. 2014 Feb;69(2):110-5. [PubMed: 24683833]
Hofeldt FD. Reactive hypoglycemia. Endocrinol Metab Clin North Am. 1989 Mar;18(1):185-201. [PubMed: 2645126]
Brun JF, Fedou C, Mercier J. Postprandial reactive hypoglycemia. Diabetes Metab. 2000 Nov;26(5):337-51. [PubMed: 11119013]
Kittah NE, Vella A. MANAGEMENT OF ENDOCRINE DISEASE: Pathogenesis and management of hypoglycemia. Eur J Endocrinol. 2017 Jul;177(1):R37-R47. [PubMed: 28381450]
Bauman V, Sturkey AC, Sherafat-Kazemzadeh R, McEwan J, Jones PM, Keating A, Isganaitis E, Ricker A, Rother KI. Factitious hypoglycemia in children and adolescents with diabetes. Pediatr Diabetes. 2018 Jun;19(4):823-831. [PMC free article: PMC5938100] [PubMed: 29464887]
Iqbal A, Heller S. Managing hypoglycaemia. Best Pract Res Clin Endocrinol Metab. 2016 Jun;30(3):413-30. [PubMed: 27432075]
Ardigo S, Philippe J. [Hypoglycemia and diabetes]. Rev Med Suisse. 2008 Jun 04;4(160):1376-8, 1380-2. [PubMed: 18630059]
Yin L, Han Y, Miao G, Jiang L, Xie S, Liu B. CSF leukocyte, polykaryocyte, protein and glucose: Their cut-offs of judging whether post-neurosurgical bacterial meningitis has been cured. Clin Neurol Neurosurg. 2018 Nov;174:198-202. [PubMed: 30273842]
McLaughlin WN, Lamb M, Gaensbauer J. Reassessing the Value of CSF Protein and Glucose Measurement in Pediatric Infectious Meningitis. Hosp Pediatr. 2022 May 01;12(5):481-490. [PubMed: 35373285]
Tamune H, Kuki T. CSF/blood glucose ratio and bacterial meningitis without pleocytosis in a potentially immunocompromised host. Am J Emerg Med. 2016 May;34(5):922. [PubMed: 26922639]
Lotfy M, Adeghate J, Kalasz H, Singh J, Adeghate E. Chronic Complications of Diabetes Mellitus: A Mini Review. Curr Diabetes Rev. 2017;13(1):3-10. [PubMed: 26472574]
Feng Y, Fang Y, Wang Y, Hao Y. Acupoint Therapy on Diabetes Mellitus and Its Common Chronic Complications: A Review of Its Mechanisms. Biomed Res Int. 2018;2018:3128378. [PMC free article: PMC6217896] [PubMed: 30426006]
Sasaki A, Uehara M, Horiuchi N, Hasegawa K, Shimizu T. A 15-year follow-up study of patients with non-insulin-dependent diabetes mellitus (NIDDM) in Osaka, Japan. Factors predictive of the prognosis of diabetic patients. Diabetes Res Clin Pract. 1997 Apr;36(1):41-7. [PubMed: 9187414]
Andersson DK, Svärdsudd K. Long-term glycemic control relates to mortality in type II diabetes. Diabetes Care. 1995 Dec;18(12):1534-43. [PubMed: 8722048]
Gerstein HC, Pais P, Pogue J, Yusuf S. Relationship of glucose and insulin levels to the risk of myocardial infarction: a case-control study. J Am Coll Cardiol. 1999 Mar;33(3):612-9. [PubMed: 10080459]
Loh TP, Lim CY, Sethi SK, Tan RZ, Markus C. Advances in internal quality control. Crit Rev Clin Lab Sci. 2023 Nov;60(7):502-517. [PubMed: 37194676]
Bugni E, Cohen R, Mazellier C. IQC Laboratory management strategy for medical biology. Ann Biol Clin (Paris). 2017 Dec 01;75(6):637-645. [PubMed: 29072175]
Kinns H, Pitkin S, Housley D, Freedman DB. Internal quality control: best practice. J Clin Pathol. 2013 Dec;66(12):1027-32. [PubMed: 24072731]
Peng S, Zhang J, Zhou W, Mao W, Han Z. Practical application of Westgard Sigma rules with run size in analytical biochemistry processes in clinical settings. J Clin Lab Anal. 2021 Mar;35(3):e23665. [PMC free article: PMC7957980] [PubMed: 33270940]
James D, Ames D, Lopez B, Still R, Simpson W, Twomey P. External quality assessment: best practice. J Clin Pathol. 2014 Aug;67(8):651-5. [PubMed: 24621574]
Zneimer SM, Hongo D. Preparing for Clinical Laboratory Improvement Amendments (CLIA) and College of American Pathologists (CAP) Inspections. Curr Protoc. 2021 Dec;1(12):e324. [PubMed: 34958716]
Ménard AD, Trant JF. A review and critique of academic lab safety research. Nat Chem. 2020 Jan;12(1):17-25. [PubMed: 31740762]
Asiry S, Ang LC. Laboratory Safety: Chemical and Physical Hazards. Methods Mol Biol. 2019;1897:243-252. [PubMed: 30539449]
Meisenhelder J, Bursik S, Lunn G, Strober W. Laboratory safety. Curr Protoc Hum Genet. 2008 Apr;Appendix 2:Appendix 2A. [PubMed: 18428418]
Bochicchio GV, Joshi M, Bochicchio KM, Pyle A, Johnson SB, Meyer W, Lumpkins K, Scalea TM. Early hyperglycemic control is important in critically injured trauma patients. J Trauma. 2007 Dec;63(6):1353-8; discussion 1358-9. [PubMed: 18212660]
Krinsley JS, Chase JG, Gunst J, Martensson J, Schultz MJ, Taccone FS, Wernerman J, Bohe J, De Block C, Desaive T, Kalfon P, Preiser JC. Continuous glucose monitoring in the ICU: clinical considerations and consensus. Crit Care. 2017 Jul 31;21(1):197. [PMC free article: PMC5535285] [PubMed: 28756769]

Disclosure: Purnima Gurung declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Zubair declares no relevant financial relationships with ineligible companies.

Disclosure: Ishwarlal Jialal declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK541081PMID: 31082125


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...