Differences among IVUS, TD-OCT, and FD-OCT
\r\n\tThis book will provide an insights in different aspects of hygiene in correlation to human health with special emphasis on cross contamination and cross infections with pathogens transmission. Basic principles of prevention, control and procedures for best hygiene practice are described with aim to deliver comprehensive overview of the current state-of-the-art in hygiene for human health.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"8b691145a9a17f8f0362d48b6e9909ce",bookSignature:"Ph.D. Urška Rozman and Prof. Sonja Šostar Turk",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/6867.jpg",keywords:"Personal Hygiene, Environmental Hygiene, Food Hygiene, Water Hygiene, Drinking Water, HACCP, Quarantine, Medical Waste",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"August 12th 2019",dateEndSecondStepPublish:"September 2nd 2019",dateEndThirdStepPublish:"November 1st 2019",dateEndFourthStepPublish:"January 20th 2020",dateEndFifthStepPublish:"March 20th 2020",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"189776",title:"Ph.D.",name:"Urška",middleName:null,surname:"Rozman",slug:"urska-rozman",fullName:"Urška Rozman",profilePictureURL:"https://mts.intechopen.com/storage/users/189776/images/9462_n.jpg",biography:"Urška Rozman is Assistant Professor of Biology at the Faculty of Health Sciences, University of Maribor, Maribor, Slovenia. Dr. Rozman has a university degree in Biology and Chemistry and a master’s in Biology. She obtained a PhD in Ecology from the Faculty of Natural Sciences and Mathematics, University of Maribor, with study on molecular methods in microbiology for purposes of hospital hygiene. She participates in study programmes of Nursing, Bioinformatics, and Food Safety covering environmental factors affecting human health. 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She was also involved in seventy-five national and international projects; most notably ten EU projects. She carried out preliminary studies for industry and health institutions. She is participating in study programmes of Nursing, Bioinformatics, and Food Safety covering subjects in the field of environmental factors affecting human health and hygiene. She has also participated in several research projects focusing on environmental health, hospital and waste water hygiene, and nutrition.",institutionString:"University of Maribor",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"16",title:"Medicine",slug:"medicine"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"301331",firstName:"Mia",lastName:"Vulovic",middleName:null,title:"Mrs.",imageUrl:"https://mts.intechopen.com/storage/users/301331/images/8498_n.jpg",email:"mia.v@intechopen.com",biography:"As an Author Service Manager, my responsibilities include monitoring and facilitating all publishing activities for authors and editors. 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The high-resolution images of OCT produce an intense interest in adopting this imaging technique for both clinical and research purposes.
In clinical aspects, OCT imaging for undergoing percutaneous coronary intervention (PCI) is feasible and provides superior resolution of arterial pathology than IVUS. During PCI, OCT can assess pre-procedural coronary plaque morphology and acute effects of coronary intervention (dissection, tissue prolapse, thrombi, and incomplete stent apposition (ISA)). Moreover, OCT provides more useful information to consider PCI strategy, such as distal protection, optimal stent landing zone.
In research aspects, OCT provides characterization of coronary plaque to assess factors associated with acute coronary syndrome (ACS) and vessel healing process after stent implantation. Recent studies have shown that OCT is useful for the assessment of coronary atherosclerotic plaques (plaque rupture, erosion, thin-cap fibroatheroma (TCFA), and intracoronary thrombi) in patients with ACS. In addition, OCT can detect the proliferation of vasa vasorum and the distribution of macrophages surrounding vulnerable plaques. OCT provides cardiologists with the tool they need to better understand the pathological condition of ACS.
According to vessel healing after stent implantation, OCT can provide stent strut coverage, ISA, and restenotic tissue characteristics at follow up. Previous OCT studies have shown that delayed neointimal coverage after drug-eluting stent (DES) implantation vs. bare metal stent (BMS) implantation. Pathological studies have indicated that the proportion of delayed neointimal coverage represents the best morphometric predictor of late stent thrombosis. Recent OCT studies demonstrate that restenotic tissue characteristics is completely different between BMS and DES. Therefore, OCT can play an important role to assess the safety profile of novel DES systems.
Finally, we introduce usefulness of 3-dimensional reconstruction of the OCT images and 1-μm resolution OCT.
\n\t\tOCT is an optical analog of IVUS, used to examine the coronary arteries. There is a pressing need for improved characterization of coronary pathology to better recognize the factors associated with coronary vessel disease and to guide the selection of better interventional strategies. The resolution and contrast of OCT is attractive for these applications and suitable catheters to access the coronary arteries in detail. There are several differences between IVUS and OCT, as shown in Table 1 [1]. The resolution of OCT (10-20 μm) is 10-fold higher than that of IVUS (100-150 μm), but the penetration depth is lower with OCT (1-2 mm) than with IVUS (4-8 mm) [2]. According to other important difference between IVUS and OCT, the removal of blood is not need for IVUS examination but OCT examination. To examine coronary arteries, blood must first be removed during an OCT examination because of the strong attenuation of light by blood [3].
OCT imaging uses an interferometry technique based on time-delay measurements of the light reflected or backscattered from the tissues [4]. We can use two processing modes used for intracoronary OCT imaging, the first generation time-domain OCT (TD-OCT) imaging systems and the more recently available second generation frequency-domain OCT (FD-OCT) imaging systems [5, 6].
The first-generation OCT (ImageWire and M2/3 OCT system; LightLab Imaging, Inc., Westford, Massachusetts) incorporated both an OCT imaging wire and an over-the-wire occlusion balloon. To deliver the image wire and remove blood from the target lesion, an over-the-wire occlusion balloon catheter was used. The OCT imaging procedure started with advancing a 0.014-inch coronary guide wire distal to the target lesion. The occlusion catheter is passed along the guide wire through the lesion. After the guide wire and OCT image wire were exchanged, the occlusion balloon is pulled back proximal to the lesion. Then, ringer’s solution was continuously flushed at 0.5–0.6 ml/s through the occlusion catheter lumen using a power injector, and the balloon was inflated to 0.3–0.5 atm by an inflation device to block blood flow. When an OCT image well appeared, a motorized pullback was initiated from the imaging system console. The first-generation OCT was not user-friendly and had several disadvantages of complex procedure, such as balloon occlusion and relatively short length of image acquisition due to the limited frame rate. To improve these disadvantage, a new generation of OCT systems, termed FD-OCT imaging methods, has been developed.
FD-OCT imaging methods, utilize a light source with variable wavelength that is tuned to continuously oscillate between 1250 and 1350 nm, a so-called wavelength swept laser, instead of the broadband light source used in TD-OCT. As a result, FD-OCT system can enable faster image acquisition and greater scan depths compared with TD-OCT system. Intravascular OCT examination has been frustrated by requiring blood removal. However, FD-OCT system can enable faster image acquisition and greater scan depths compared with TD-OCT system. As a result, only intermittent injection of transparent fluid through guiding catheter for a few seconds enables to obtain entire coronary images [6, 7]. FD-OCT system has been developed (Dragonfly imaging catheter and C7- XR OCT system; LightLab Imaging, Inc., St Jude Medical,St Paul, Minnesota, USA). Differences between TD- (M3) and FD-OCT (C7-XR) systems are shown in Table 1 [8]. This advance may provide dramatic improvements in understanding coronary atherosclerosis and response to intravascular interventions such as angioplasty and stenting.
\n\t\tIn clinical aspects, OCT imaging for undergoing PCI is feasible and provides superior resolution of arterial pathology than intravascular ultrasound. During PCI, OCT can assess pre-procedural coronary plaque morphology.
Regarding to plaque characterization, OCT can differentiate three types of coronary plaques, such as fibrous, calcified, and lipid-rich. Fibrous plaque is characterized by a homogenous high signal region with low attenuation, calcified plaque by a well-delineated, low-signal region with sharp borders, and lipid-rich plaques as a low-signal region with diffuse borders [9]. Importantly, a histology-controlled OCT study showed >90% sensitivity and specificity for detecting lipid-rich plaque in comparisons with pathological specimens. [9, 10]. Moreover, OCT can recognize vulnerable plaques, such as plaque rupture, erosion, intracoronary thrombus, TCFA.
Assessment of plaque characteristics before PCI is useful to choose optimal interventional strategy. Tanaka et al. showed that TCFA was often observed at target lesions of the patients with no reflow after PCI compared with good reflow (50% versus 16%,
Another aspect, plaque type at the stent edges has an impact on the occurrence of edge dissections. Gonzalo et al. showed that presence of edge dissection was significantly more frequent when the plaque type at the edge was fibrocalcific (43.8%) or lipid rich (37.5%) than when the plaque was fibrous (10%) [12]. This study demonstrated that complex plaque type at the stent edge might influence on the presence of edge dissections from OCT observation. The OCT guide stenting might be a useful assistance to achieve optimal landing zone.
After PCI, OCT can assess acute effects of coronary intervention (dissection, tissue prolapse, and ISA). Dissection, tissue prolapse, and ISA were observed more often with OCT than with IVUS [13, 14]. Coronary dissection is frequently observed at the distal stent edge because of the oversized stent diameter or complex types of plaque at the stent edge by OCT. When there is no limited coronary flow by angiography and adequate area of the true lumen by OCT, no additional procedure might be necessary for the treatment of coronary dissection [15].
There are 2 types of tissue prolapse, plaque prolapse or thrombus prolapse. OCT can distinguish between plaque prolapse and thrombus prolapse. Plaque prolapse is characterized by smooth surface with no signal attenuation, and thrombus protrusion by irregular surface with significant signal attenuation. Minor tissue prolapse identified by IVUS was not found to be associated with angiographic in-stent restenosis [16]. However, the relationship tissue prolapse identified by OCT and angiographic in-stent restenosis has not been elucidated.
ISA by OCT was identified as clear separation between at least one stent strut and the vessel wall. To check the stent apposition to the vessel wall, the distance between surface of stent strut and adjacent inatima border should be measured because of differences of stent and polymer thickness [8]. Small ISA, which is detected by only OCT but not by IVUS, could disappear by neointimal growth during follow-up period [15].
\n\t\tIn research aspects, OCT can provide characterization of coronary plaque to assess factors associated with ACS and vessel healing process after stent implantation.
The first OCT study to assess in vivo culprit lesion morphology in patients with ACS showed that higher frequency of TCFA in ACS compared with stable angina pectoris (72% in acute myocardial infarction (AMI), 50% in unstable angina pectoris, and 20% in stable angina pectoris;
OCT has been proposed as a high resolution imaging modality that can identify vasa vasorum as microchannels with tiny black holes (50-100 μm). The proliferation of vasa vasorum has been identified recently as a common feature of vulnerable plaque [18]. Kitabata et al. demonstrated increase of microvessels counts in TCFA [19]. An observational study of OCT revealed that the presence of microvessels in the plaques was also associated with positive remodeling and elevated high-sensitive C-reactive protein levels [19]. The OCT evaluation of microvessels counts might be helpful for assessing plaque vulnerability.
Moreover, the other unique aspect of OCT is the detection of macrophages. Degradation of the fibrous cap matrix by macrophages is associated with atherosclerotic plaque instability [20]. Macrophages detected by OCT were observed as a ‘bright spot’, with a high signal variance from the surrounding tissue. Tearney et al. [21] and MacNeill et al. [16] descried OCT is capable to evaluate cap macrophage content accurately. High degree of positive correlation was observed between OCT and histological measurements of macrophage density in fibrous cap (
According to vessel healing after stent implantation, OCT can provide stent strut coverage, ISA, and restenotic tissue characteristics at follow up. Previous OCT studies have shown that delayed neointimal coverage after DES implantation vs. BMS implantation [22]. Pathological studies have indicated that the proportion of delayed neointimal coverage represents the best morphometric predictor of late stent thrombosis [23, 24]. Recent OCT studies demonstrate that restenotic tissue characteristics is completely different between BMS and DES [21, 25]. Therefore, OCT can play an important role to assess the safety profile of novel DES systems.
\n\t\tRecently, a second-generation OCT technology, termed FD-OCT, has been developed that solves the TD-OCT limitations by imaging at much higher frame rates with slightly deeper penetration depth and greater scan area. In combination with a short, non-occlusive flush and rapid spiral pullback, the higher frame rates generated by FD-OCT enable imaging of the 3-dimensional reconstruction of longer segments of coronary arteries. The 3-dimensional OCT can express all of the coronary microanatomy and pathology previously visualized by OCT, including lipid pools, calcium, macrophages, thin fibrous caps, cholesterol crystals, thrombus, stent, and stents with neointimal hyperplasia [26]. The 3-dimensional OCT may be useful as a research tool for assessing human coronary pathophysiology and as a clinical tool for guiding the management of coronary artery disease.
Progress in understanding, diagnosis, and treatment of coronary artery disease has been hindered because of inability to observe cells and extracellular components associated with human coronary atherosclerosis
The high resolution of OCT provides histology-grade definition of the microstructures of coronary atherosclerosis in vivo. Introduction of this attractive imaging method contributes significant progression in both clinical and research aspects. Clinically, OCT can provide more useful information to consider PCI strategy for getting the optimal interventional results. On the other hand, OCT is a useful imaging device for understanding, diagnosis, and treatment of coronary artery disease. In the future direction of OCT systems, 3-dimensional OCT and μOCT may be upcoming in the field of coronary artery disease. These novel OCT technologies will play an important role for investigation of coronary artery disease.
\n\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t
Axial resolution, μm | \n\t\t\t\t\t\t100-150 | \n\t\t\t\t\t\t15-20 | \n\t\t\t\t\t\t12-15 | \n\t\t\t\t\t
Lateral resolution, μm | \n\t\t\t\t\t\t150-300 | \n\t\t\t\t\t\t39 | \n\t\t\t\t\t\t19 | \n\t\t\t\t\t
Frame rate, fps | \n\t\t\t\t\t\t30 | \n\t\t\t\t\t\t20 | \n\t\t\t\t\t\t100 | \n\t\t\t\t\t
Pullback speed, mm/s | \n\t\t\t\t\t\t0.5-2.0 | \n\t\t\t\t\t\t0.5-2.0 | \n\t\t\t\t\t\t10-25 | \n\t\t\t\t\t
Scan diameter, mm | \n\t\t\t\t\t\t8-10 | \n\t\t\t\t\t\t6.8 | \n\t\t\t\t\t\t10 | \n\t\t\t\t\t
Penetration depth, mm | \n\t\t\t\t\t\t4-8 | \n\t\t\t\t\t\t1-2 | \n\t\t\t\t\t\t1-2 | \n\t\t\t\t\t
Balloon occlusion | \n\t\t\t\t\t\tUnnecessary | \n\t\t\t\t\t\tNecessary | \n\t\t\t\t\t\tUnnecessary | \n\t\t\t\t\t
Differences among IVUS, TD-OCT, and FD-OCT
IVUS, intravascular ultrasound; OCT, optical coherence tomography; TD, time-domain; FD, frequency-domain; fps, frames per second.
Modified from Terashima M et al, korean j intern med 2012;27:1-12.
\n\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t
Dissection | \n\t\t\t\t\t\t○ | \n\t\t\t\t\t\t◎ | \n\t\t\t\t\t
Tissue prolapse | \n\t\t\t\t\t\t△ | \n\t\t\t\t\t\t◎ | \n\t\t\t\t\t
ISA | \n\t\t\t\t\t\t○ | \n\t\t\t\t\t\t◎ | \n\t\t\t\t\t
Stent expansion | \n\t\t\t\t\t\t◎ | \n\t\t\t\t\t\t○ | \n\t\t\t\t\t
Lesion coverage | \n\t\t\t\t\t\t○ | \n\t\t\t\t\t\t○ | \n\t\t\t\t\t
Acute effects of coronary intervention between IVUS and OCT
IVUS, intravascular ultrasound; OCT, optical coherence tomography; ISA, incomplete stent apposition.
The human body is dependent on a tight control of its blood glucose levels to ensure normal body function. Survival of individuals, the conscious state, the integration of different types of internal and external stimuli, and appropriate responses to these stimuli depend on the proper functioning of the central nervous system, which puts intense activity in their cells. This requires the consumption of oxygen and glucose to obtain the energy that enables the activity of the central nervous system (CNS) and keeps the neurons in constant activity [1].
The lack of oxygen causes, in minutes, serious and irreparable damage to the central nervous system. However, the lack of glucose is tolerated for a longer time because in a deficit situation, the CNS itself makes autonomous adjustments leading to inactivity to other non-vital systems of the body and preserves for more time the availability of glucose for neurons, and ultimately, in multiday starvation states, it substitutes glucose for ketone bodies as a nutrient, which allows life expectancy to be extended during fasting. The availability of glucose in people is vital for a good quality of life, since it allows the lucid and full functioning of the CNS [2, 3].
The rest of the body’s cells also obtain energy through oxygen and glucose, thus enabling metabolism and cellular response. The main source of glucose is through food and specifically depends on the consumption of carbohydrates [4]. The use of this carbohydrate in the body is finely regulated by a hormonal system capable of always maintaining blood glucose (glycemia) in a concentration ranging from 4.0 to 5.4 mmol/L (72 to 99 mg/dL) [5]. The human body is prepared to store excess of glucose (glycogenesis) and use it in the future (glycogenolysis) when this is required and is also able to synthesize glucose from noncarbohydrate precursors (substrates) such as amino acids, lactate, and/or glycerol (gluconeogenesis).
The pancreas is the body in charge, among other functions, of maintaining glycemia at tolerable levels for the organism, through a system of hormones, where insulin is responsible for reducing glycemia in situations of postprandial hyperglycemia, while glucagon is responsible for reversing situations of hypoglycemia [6, 7].
The carbohydrates present in foods are primarily as polysaccharides that are digested by various digestive enzymes. Starch is the most common polysaccharide in foods and is metabolized to maltose by the enzyme alpha amylase present in saliva and secreted by the pancreas and this to glucose by the maltases in the microvilli of the duodenum. The lactose present in dairy products is metabolized by lactases in the intestinal villi to glucose and galactose. Sucrose is also metabolized in the intestinal microvilli in glucose and fructose.
The absorption of glucose and galactose is carried out by a secondary active cotransport of Na+ to the interior of the enterocyte and from there to the portal flow by facilitated diffusion through the GLUT2 glucose transporter (Figure 1). Fructose, on the other hand, is only entered into the enterocyte by facilitated diffusion through GLUT5 type transporters located on the apical side, and then they are poured into the portal circulation by the same carrier proteins that are also found on the basal side of the enterocyte.
Carbohydrate metabolism. Polysaccharides in food are digested, by several enzymes. The absorption is mainly in the duodenum. Glucose in the jejunum and ileum stimulates the release of GIP and GLP-1, and postprandial release of insulin is stimulated. Glucose in blood reaches the pancreas and undergoes glycolysis to generate pyruvate and then ATP; ATP closes K+ channels, and a depolarization begins. Next, voltage-gated calcium channels are open and exocytosis of insulin occurs. Insulin binds to its tyrosine kinase receptor and initiates a signaling cascade that rapidly produces the massive entry of glucose into the cell.
The duodenum has a very extensive contact surface, in order to take advantage of and absorb as much of these nutrients as possible. The excess, which passes to the jejunum, stimulates the release of the glucose-dependent insulinotropic peptide (GIP) from the K cells and the glucagon-like peptide type 1 (GLP-1) from the L cells. Both stimulate the postprandial release of insulin from the pancreas (Figure 1).
Absorbed glucose increases suddenly in the blood, reaching values above 90 mg/dL, and is transported by the GLUT2 carrier protein inside the pancreas where it undergoes glycolysis to generate pyruvate. This is used by the mitochondria for the production of ATP, which is released into the cytoplasm of the beta cells of the pancreas. This excess of ATP desensitizes the ATP-dependent K+ channels that close and prevent the migration of K+ ions to the extracellular fluid. With the intracellular increase of K+, a depolarization begins; this stimulates the opening of voltage-gated calcium channels, which finally ends with the exocytosis of insulin (Figure 1), peptide C, and amylin stored in the vesicles into the bloodstream.
The average life of this circulating insulin is 3–5 minutes; its main action is to stimulate the uptake of glucose from the bloodstream, mainly by the liver and muscle cells. The receptor for insulin in these cells is a tyrosine kinase that, when insulin binds, dimerizes and initiates a signaling cascade that rapidly activates the phosphatidylinositol-3-kinase (PI3K) pathway that translocates GLUT4 carrier to the cell membrane, which allows the massive entry of glucose into the cell. Then the same pathway activates the enzyme glycogen synthetase that converts excess of glucose into glycogen, activates Acetyl CoA carboxylase that stimulates lipogenesis, and finally, in the longer term, activates the pathway of the mitogen-activated kinases (MAP kinases) responsible for the expression of the protein synthesis (Figure 1).
C peptide is a small molecule that is released when proinsulin is metabolized to insulin; in spite of not knowing the specific physiological role of this molecule, in the clinical environment, it serves to correlate it with the quantity of insulin synthesized by beta cells, because for each molecule of insulin, there is a C peptide, and this remains in the bloodstream for a longer time. Amylin, a peptide hormone produced in the pancreas, and co-secreted with insulin, and in the brain, improves postprandial blood glucose levels by suppressing gastric emptying and glucagon secretion. Amylin also acts centrally as a satiation signal, reducing food intake and body weight.
In this way the glycemia values are usually maintained between 70 and 110 mg/dL; values below this range produce hypoglycemia that stimulates the release of the hormone glucagon from the alpha cells of the pancreas, which promotes anti-insulin effects in such a way to re-raise the glycemia values (Figure 2). To this is added a third pancreatic hormone, somatostatin, of paracrine regulation which collaborates to modulate the release of insulin and glucagon.
Regulation of plasma glucose level by insulin and glucagon. Hypoglycemia situations related to diabetes and not related to diabetes.
After intense physical activity, the adrenaline released by the stimulus of exercise and the increase of lactate and pyruvate in blood blocks insulin secretion and stimulates glucagon to always make glucose available to the body and avoid reactive hypoglycemia [6, 8, 9].
Insulin secretion from the beta cells of the pancreas is a standard response that is directly related to glucose absorbed from food. Thus, if the glycemia increases significantly after an intake, this results in a large insulin secretion, while if the glycemia remains within the normal range, the stimulus decreases and produces a pulsatile insulin secretion that favors the glycemia to remain within the physiological range.
In the case that the glycemia falls below 60 mg/dL, the signal to secrete insulin weakens and eventually becomes blocked. In contrast, this allows the alpha cells of the pancreas to release considerable amounts of glucagon (Figure 2). This hormone travels through the portal vein to the liver, where it activates signaling pathways to initiate glycogenolysis, which will cause the formation of glucose in the liver so that it is released into the bloodstream to immediately increase glycemia. Additionally, glucagon increases the recruitment of amino acids to the liver for gluconeogenesis that reinforces the effect of glycogenolysis [10].
Hypoglycemia is almost always related to a normal or increased amount of insulin as a direct response to glucose intake in food or other pathophysiological factors that induce an excessive increase in insulin secretion. A balanced intake of carbohydrates, fats, and proteins provides all the nutrients that the body needs for survival, but an inadequate diet, deficient in carbohydrates, leads to a reactive hypoglycemia.
The chronic and excessive intake of alcohol produces metabolic alterations in the liver that lead to decrease the synthesis and release of glucose from the liver to the blood and therefore a decrease in blood sugar (Figure 2).
In the case that the gastric emptying is accelerated (dumping syndrome), due for example, to a gastric resection, the digestion and absorption of carbohydrates are much faster than normal and also produce the early release of intestinal hormones, including the GIP, which leads to hyperinsulinemia and then the consequent hypoglycemia (Figure 2).
The alteration of various functions of the organism has as one of its consequences the reduction of glycemia to critical values, as occurs in the reduction of glucocorticoid secretion, such as cortisol, which causes an increase in glycolysis and reduced gluconeogenesis from amino acids. This in turn leads to a greater secretion of adrenaline that is contrasted in its effects to insulin. On the other hand, thyroid hormones regulate many cellular metabolic processes, including hepatic metabolism; therefore, in a situation of hypothyroidism, glycogenolysis and gluconeogenesis are drastically reduced (Figure 2).
An alteration in the hepatic metabolism of amino acids, either due to liver failure or due to specific enzymatic defects, such as that inducing high leucine level, has an effect on insulin secretion, which is increased producing hypoglycemia (Figure 2).
Hepatomegaly is usually caused by an increased hepatic storage of glycogen, known as glycogenosis, due to metabolic alterations produced by defective enzymes such as glucose-6-phosphatase, in Gierke’s disease, or a debranching enzyme in Cori Forbes disease, a phosphorylase in Hers disease, or a phosphoryl kinase in Huijing’s disease. This increase in hepatic glycogen deposition produces a marked hypoglycemia throughout the system (Figure 2).
Aberrations in the expression of certain genes in beta cells make them unable to relate the increase in lactate and pyruvate with the state of physical activity and therefore induce an increase in insulin secretion that causes significant hypoglycemia in the organism (Figure 2).
The development of tumors, of any type, entails an increase in the need for energetic molecules so that cell proliferation is possible. This added to the fact that the formation of tumors produces long-term hormonal disorders that keep oncological patients with hypoglycemia for a long time. This effect is compensated by lipolysis of the adipocytes in order to make more energetic molecules available, and finally the patient develops tumor cachexia [11, 12] (Figure 2).
One of the most common causes of hypoglycemia in diabetics occurs as a result of the excess administration of insulin or oral hypoglycemic drugs [13, 14]. Patients suffering from diabetes mellitus type 1 and whose treatment is based on the exogenous administration of insulin must previously corroborate the level of glycemia and then adjust the amount of hormone to be administered, considering that 100% of the dose, approximately half, is used to immediately regulate the metabolism of carbohydrates and the other half is to cover the metabolism at night or fasting hours. Therefore, the amount of insulin administered is higher than required, and if the necessary precautions are not taken, there is a high probability that the dose administered will produce a strong hypoglycemia, especially during sleep hours, known as the Somogyi effect. The amount of insulin units to administer considers the actual value of the glycemia, which forces the patient to measure it, compare and extract the difference with the theoretical optimum value of 120 mg/dL of fasting blood glucose, and divide it by the factor 50, since one unit of insulin reduces blood glucose by approximately 50 mg/dL (Figure 2).
Even so, the correct amount of insulin to be administered must also be defined by other factors, such as the total amount of carbohydrates ingested with food, the type of insulin to be administered, and the recommendations of the treating medical professional.
Oral hypoglycemic agents, used in the treatment of type 2 diabetes mellitus, can also lead to a strong insulin secretion. The large family of sulfonylureas (chlorpropamide, glibenclamide, gliclazide, glisentide, glipizide, gliquidone, and glimepiride) and the secretagogue glinides (repaglinide and nateglinide) are characterized by the ability to induce hypoglycemia and cause weight gain, due to the decrease in the lipolysis in the patients who use it for their treatment (Figure 2).
Another interaction with a high probability of producing hypoglycemia is the concomitant treatment with incretin analogues (exenatide) and inhibitors of dipeptidyl peptidases (vildagliptin) because it significantly increases the pancreatic β cell mass, which leads to greater insulin secretion and even with high risks of producing pancreatitis (Figure 2).
Diabetic women during pregnancy have poor control of carbohydrate metabolism and thus coexist with high blood levels of glucose and amino acids; this long-term hyperglycemia is transferred to the fetus and forces hyperplasia in fetal pancreatic beta-cell tissue, which finally predisposes the newborn to a greater secretion of insulin and the consequent hypoglycemia [15, 16, 17] (Figure 2).
The decrease in blood sugar below 60 mg/dL is known as hypoglycemia. In a first phase, this leads to a stimulation of the parasympathetic autonomic nervous system that causes a sensation of hunger and leads the patient to bulimia. In the second phase, the sympathetic autonomic nervous system is stimulated, producing the secretion of important quantities of catecholamines that activate their receptors in important target organs such as the heart, which produces an acceleration of the heartbeat, in sweat glands increases the production of sweat, and in the somatic nervous system causes tremors. It is frequent double vision, difficulty concentrating, loss of ease of speech, and confusion states. A hypoglycemia below 20 mg/dL induces a coma (Figure 3).
A summary of glycemia levels and clinical consequences.
The most serious effect is a marked cognitive dysfunction, since the supplies of nutrients, glucose, and ketones to the nervous system are markedly diminished; produce loss of consciousness, brain spasms, and epileptic seizures in children; and can potentially lead to irreversible neuronal damage [18, 19].
The treatment will depend on the degree of hypoglycemia that the patient develops. That, which does not pass the first phase of the clinical manifestation, requires rapid replacement of glucose from food. The CNS itself is the one that predisposes to this action by triggering bulimia in the patient. Most of the foods available to patients contain abundant amounts of carbohydrates that help to remedy hypoglycemia (Figure 3).
In cases where hypoglycemia is more pronounced, it is necessary to administer pharmaceutical preparations containing glucose, but this treatment should be monitored to avoid the opposite effect, i.e., hyperglycemia, especially in diabetic patients who triggered hypoglycemia due to excess insulin.
In patients with severe hypoglycemia crisis, which affects the conscience, it is necessary to act urgently administering parenteral glucagon preparations, or glucose will be administered directly, and the rapid recovery of the patient will be monitored [14, 15, 19, 20, 21] (Figure 3).
Hypoglycemia is generated by mechanisms directly related to an increase in insulin secretion or by metabolic disorders that require increased glucose consumption or by a deficient metabolic production of glucose by the body.
Hyperinsulinemia can be produced by various mechanisms, including high glucose intake in foods, an increased dose of oral hypoglycemic agents, as well as exogenous insulin administration without control, liver metabolic conditions that lead to an increase in the production of amino acids by this organ, tumors in permanent growth, and an abnormal increase in glucose and amino acids in the case of uncontrolled diabetic pregnant women that end up producing insulin hypersecretion in the newborn.
Work that requires high glucose consumption, more than what the body can supply, ends up in situations of hypoglycemia, as well as when there is a decrease in hormone antagonists to insulin, such as cortisol or glucagon. The state of hypoglycemia is generated by metabolic deficit in pathophysiological situations such as defects in enzymatic systems, alcoholic hepatitis, and insufficient diet.
The most characteristic symptoms include bulimia, fits of sweating, and tremors due to a strong activation of the sympathetic system. Primarily, the CNS is strongly affected by the lack of glucose, which is even more complicated because also hypoglycemia leads to a situation of decreased lipolysis and ketone bodies that finally seriously compromise the supply of energy to the central nervous system, producing loss of consciousness, spasms, and even irreversible brain damage.
The treatment of less severe hypoglycemic patients is preferably carried out with the rapid administration of carbohydrate-rich foods. For more serious cases, the use of pharmaceutical products that supply carbohydrates is resorted to, but the glycemia must be monitored to avoid hyperglycemia. Those patients who are much compromised, with loss of consciousness, should receive parenteral glucagon or glucose in an urgent way to recover them.
The authors declare that there is no conflict of interest regarding the publication of this chapter.
These Terms and Conditions outline the rules and regulations pertaining to the use of IntechOpen’s website www.intechopen.com and all the subdomains owned by IntechOpen located at 5 Princes Gate Court, London, SW7 2QJ, United Kingdom.
',metaTitle:"Terms and Conditions",metaDescription:"These terms and conditions outline the rules and regulations for the use of IntechOpen Website at https://intechopen.com and all its subdomains owned by Intech Limited located at 7th floor, 10 Lower Thames Street, London, EC3R 6AF, UK.",metaKeywords:null,canonicalURL:"/page/terms-and-conditions",contentRaw:'[{"type":"htmlEditorComponent","content":"By accessing the website at www.intechopen.com you are agreeing to be bound by these Terms of Service, all applicable laws and regulations, and agree that you are responsible for compliance with any applicable local laws. Use and/or access to this site is based on full agreement and compliance of these Terms. All materials contained on this website are protected by applicable copyright and trademark laws.
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\n\nThe following terminology applies to these Terms and Conditions, Privacy Statement, Disclaimer Notice, and any or all Agreements:
\n\n“Client”, “Customer”, “You” and “Your” refers to you, the person accessing this website and accepting the Company’s Terms and Conditions;
\n\n“The Company”, “Ourselves”, “We”, “Our” and “Us”, refers to our Company, IntechOpen;
\n\n“Party”, “Parties”, or “Us”, refers to both the Client and ourselves, or either the Client or ourselves.
\n\nAll Terms refer to the offer, acceptance, and consideration of payment necessary to provide assistance to the Client in the most appropriate manner, whether by formal meetings of a fixed duration, or by any other agreed means, for the express purpose of meeting the Client’s needs in respect of provision of the Company’s stated services/products, and in accordance with, and subject to, the prevailing laws of the United Kingdom.
\n\nAny use of the above terminology, or other words in the singular, plural, capitalization and/or he/she or they, are taken as interchangeable.
\n\nUnless otherwise stated, IntechOpen and/or its licensors own the intellectual property rights for all materials on www.intechopen.com. All intellectual property rights are reserved. You may view, download, share, link and print pages from www.intechopen.com for your own personal use, subject to the restrictions set out in these Terms and Conditions.
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\n\nIn no circumstances shall IntechOpen or its suppliers be liable for any damages (including, without limitation, damages for loss of data or profit, or due to business interruption) arising out of the use, or inability to use, the materials on IntechOpen's websites, even if IntechOpen or an IntechOpen authorized representative has been notified orally or in writing of the possibility of such damage. Some jurisdictions do not allow limitations on implied warranties, or limitations of liability for consequential or incidental damages; consequently, these limitations may not apply to you.
\n\nIntechopen.com website content and services are provided on an "AS IS" and an "AS AVAILABLE" basis. Material appearing on www.intechopen.com could include minor technical, typographical, or photographic errors. IntechOpen may make changes to any material contained on its website at any time without notice.
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\n\nIntechOpen may revise its Terms of Service for its website at any time without notice. By using this website, you are agreeing to be bound by the current version of all Terms at the time of use.
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